A once-daily pill cut the risk of death in half for a subset of patients with early-stage lung cancer who had undergone surgery. The results of a new clinical trial were presented on June 4 at the American Society of Clinical Oncology’s annual meeting and were published in the New England Journal of Medicine.

[Related: Poor lung cancer screening guidelines miss too many African American smokers.]

The pill named osimertinib and sold under the brand name Tagrisso is manufactured by drugmaker AstraZeneca, who funded the study. The pill is directed at a specific receptor that helps cancer cells grow. 

The study included a 682-patient trial that included patients diagnosed with non-small cell lung cancer, which is one of two main types of primary lung cancer that makes up 80 to 85 percent of all lung cancers. The participants in the study also had a mutation in the epidermal growth factor receptor (EGFR) gene. This gene codes for a protein that is found on the surface of cells. EGFR mutations can increase cancer’s ability to grow and spread throughout the body, which increases a patient’s risk of cancer recurrence after completing treatment. 

Roughly 10 to 15 percent of lung cancer cases in the United States have an EGFR mutation, however it is more common in Australia and Asia. The mutation is usually detected in those with little to no history of smoking. About two-thirds of the trial participants had no history of smoking, suggesting that it works for smokers and non-smokers diagnosed with lung cancer.

Osimertinib generally works by blocking the effects of these common EGFR mutations.

According to the results, five years after their diagnosis, 88 percent of those who took osimertinib were still alive, compared to 78 percent of the placebo group. The pill lowered the overall risk of death from lung cancer by 51 percent. This data is reportedly the first to show how targeted treatment for early-stage lung cancer can impact patient survival.

“Thirty years ago, there was nothing we could do for these patients,” study co-author and deputy director of Yale Cancer Center Roy Herbst said, according to The Guardian. “Now we have this potent drug. Fifty percent is a big deal in any disease, but certainly in a disease like lung cancer, which has typically been very resistant to therapies.”

[Related: 100 Years Of Smoking Studies In Popular Science.]

Over 100 countries have already approved osimertinib under the brand name Tagrisso, including the United States. The Food and Drug Administration (FDA) approved it in 2015 for those with more advanced lung cancer whose diseases worsened during or after other cancer treatments. In 2020, the FDA approved Tagrisso for early-stage versions of lung cancer.

Patrick Forde, an associate professor of oncology at Johns Hopkins Medicine who was not involved in the study told NBC News that before targeted treatments like Tagrisso were available, patients diagnosed with stage 1 to 3 lung cancer would typically receive chemotherapy after surgery. He estimated that the treatment would improve odds of survival by roughly five percent compared to those who did not receive chemo. 

“If you go back 15 years, for this patient population we would have expected maybe a survival of 50 percent at five years,” he said. “But because of the advances both for stage 4 cancer, and now this advance in earlier stage cancer, we’re up to 88 percent.”

Forde has consulted for AstraZeneca and obtained research funding from the drug company in the past.
Lung cancer accounts for about 1.8 million deaths per year and is the world’s leading cause of cancer death. More than 127,000 Americans die from lung cancer, according to data from the American Cancer Society.

The post A daily pill could cut lung cancer deaths in half, new study shows appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This article was originally featured on KFF Health News.

After spending 38 years in the Alabama prison system, one of the most violent and crowded in the nation, Larry Jordan felt lucky to live long enough to regain his freedom.

The decorated Vietnam War veteran had survived prostate cancer and hepatitis C behind bars when a judge granted him early release late last year.

“I never gave up hope,” said Jordan, 74, who lives in Alabama. “I know a lot of people in prison who did.”

At least 6,182 people died in state and federal prisons in 2020, a 46% jump from the previous year, according to data recently released by researchers from the UCLA Law Behind Bars Data Project.

“During the pandemic, a lot of prison sentences became death sentences,” said Wanda Bertram, a spokesperson for the Prison Policy Initiative, a nonprofit that conducts research and data analysis on the criminal justice system.

Now, Jordan worries about his longevity. He struggles with pain in his legs and feet caused by a potentially life-threatening vascular blockage, and research suggests prison accelerates the aging process.

Life expectancy fell in the United States in 2021 for the second year in a row, according to the Centers for Disease Control and Prevention. That decline is linked to the devastating effect of covid-19 and a spike in drug overdoses.

Some academic experts and activists said the trend also underscores the lasting health consequences of mass incarceration in a nation with roughly 2 million imprisoned or jailed people, one of the highest rates in the developed world.

A Senate report last year found the U.S. Department of Justice failed to identify more than 900 deaths in prisons and local jails in fiscal year 2021. The report said the DOJ’s poor data collection and reporting undermined transparency and congressional oversight of deaths in custody.

Thousands of people like Jordan are released from prisons and jails every year with conditions such as cancer, heart disease, and infectious diseases they developed while incarcerated. The issue hits hard in Alabama, Louisiana, and other Southeastern states, which have some of the highest incarceration rates in the nation.

A major reason the U.S. trails other developed countries in life expectancy is because it has more people behind bars and keeps them there far longer, said Chris Wildeman, a Duke University sociology professor who has researched the link between criminal justice and life expectancy.

“It’s a health strain on the population,” Wildeman said. “The worse the prison conditions, the more likely it is incarceration can be tied to excess mortality.”

Mass incarceration has a ripple effect across society.

Incarcerated people may be more susceptible than the general population to infectious diseases such as covid and HIV that can spread to loved ones and other community members once they are released. The federal government has also failed to collect or release enough information about deaths in custody that could be used to identify disease patterns and prevent fatalities and illness inside and outside of institutions, researchers said.

Over a 40-year span starting in the 1980s, the number of people in the nation’s prisons and jails more than quadrupled, fueled by tough-on-crime policies and the war on drugs.

Federal lawmakers and states such as Alabama have passed reforms in recent years amid bipartisan agreement that prison costs have grown too high and that some people could be released without posing a risk to public safety.

The changes have come too late and not gone far enough to curb the worst effects on health, some researchers and activists for reform said.

Still, no one has proven that incarceration alone shortens life expectancy. But research from the early 2000s did show the death rate for people leaving prison was 3.5 times higher than for the rest of the population in the first few years after release. Experts found deaths from drug use, violence, and lapses in access to health care were especially high in the first two weeks after release.

Another study found that currently or formerly incarcerated Black people suffered a 65% higher mortality rate than their non-Black peers. Black people also make up a disproportionately high percentage of state prison populations.

The enactment in 2000 of the Death in Custody Reporting Act, and its reauthorization in 2014, required the DOJ to collect information about deaths in state and local jails and prisons.

The information is supposed to include details on the time and location of a death, demographic data on the deceased, the agency involved, and the manner of death.

But a recent report from the Government Accountability Office found that 70% of the records the DOJ received were missing at least one required data point. Federal officials also lacked a plan to take corrective action against states that didn’t meet reporting requirements, the GAO found.

The deficiency in data means the federal government can’t definitively say how many people have died in prisons and jails since the covid-19 pandemic began, researchers said.

“Without data, we are operating in the dark,” said Andrea Armstrong, a professor at the Loyola University New Orleans College of Law, who has testified before Congress on the issue.

Armstrong said federal and state officials need the data to identify institutions failing to provide proper health care, nutritious food, or other services that can save lives.

The DOJ did not make officials available for interviews to answer questions about the GAO report.

In a written statement, agency officials said they were working with law enforcement and state officials to overcome barriers to full and accurate reporting.

“The Justice Department recognizes the profound importance of reducing deaths in custody,” the statement said. “Complete and accurate data are essential for drawing meaningful conclusions about factors that may contribute to unnecessary or premature deaths, and promising practices and policies that can reduce the number of deaths.”

Department officials said the agency is committed to enhancing its implementation of the Death in Custody Reporting Act and that it has ramped up its efforts to improve the quality and quantity of data that it collects.

The DOJ has accused Alabama, where Jordan was incarcerated, of failing to adequately protect incarcerated people from violence, sexual abuse, and excessive force by prison staff, and of holding prisoners in unsanitary and unsafe conditions.

Jordan served 38 years of a 40-year sentence for reckless murder stemming from a car accident, which his lawyer argued in his petition for early release was one of the longest sentences in Alabama history for the crime. A jury had found him guilty of being drunk while driving a vehicle that crashed with another, killing a man. If he were convicted today instead, he would be eligible to receive a sentence as short as 13 years behind bars, because he has no prior felony history, wrote Alabama Circuit Judge Stephen Wallace, who reviewed Jordan’s petition for early release.

With legal help from Redemption Earned, an Alabama nonprofit headed by a former state Supreme Court chief justice, Jordan petitioned the court for early release.

On Sept. 26, 2022, Wallace signed an order releasing Jordan from prison under a rule that allows Alabama courts to reconsider sentences.

A few months later, Jordan said, he had surgery to treat a vascular blockage that was reducing blood flow to his left leg and left foot. A picture shows a long surgical scar stretching from his thigh to near his ankle.

The Alabama Department of Corrections refused an interview request to answer questions about conditions in the state’s prisons.

Jordan said his vascular condition was excruciating. He said he did not receive adequate treatment for it in prison: “You could see my foot dying.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

The post The health impacts of incarceration don’t end after release appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

A new sound wave technique can help treat a deadly brain cancer called glioblastoma in only four minutes. The breakthrough report was published May 2 in the journal The Lancet Oncology and demonstrates the results of a phase 1 in-human clinical trial with 17 patients.

In the trial, the patients underwent surgery for resection, or removal, of their tumors and had an ultrasound device implanted. The device inside the skull opens the blood-brain barrier, repeatedly using sound waves to permeate the barrier and reach the brain tumor. IV chemotherapy is then able to reach the neurological tissues where the cancer can grow.

Treating this type of brain tumor, which has a 6.8 percent survival rate within the first five years of diagnosis, with the most potent types of chemotherapy is difficult. The strongest cancer medicines are typically unable to permeate the blood-brain barrier. The blood-brain barrier acts as a line of defense, making an extra wall around the brain to keep toxins and pathogens from getting into such a crucial area of the body. However, the repertoire of drugs that can be used to treat brain diseases is very limited. In 2014, scientists first found that sound waves could be used to permeate the blood-brain barrier and this study builds on that discovery.

[Related: Understanding glioblastoma, the most common—and lethal—form of brain cancer.]

“This is potentially a huge advance for glioblastoma patients,” co-author and Northwestern University neurosurgeon Adam Sonabend said in a statement. 

The study reports that using a novel skull-implantable grid of nine ultrasound emitters made by French biotech company Carthera can open the blood-brain barrier in a volume of the brain nine times larger than the small single-ultrasound emitter implants originally used. This importantly helps treat a large region of the brain next to the cavity that remains after glioblastoma tumors are removed.  

This is also the first study that shows how quickly the blood-brain barrier closes after being opened by the ultrasound. It closes in the first 30 to 60 minutes after the communication. and this will help scientists optimize what order to deliver the drugs to allow for better penetration of the brain. The procedure to open the blood-brain barrier only takes four minutes and is performed while the patient is awake. The new results show that the treatment is safe, well-tolerated, and some patients received up to six cycles of treatment. 

[Related: Scientists used Zika to kill aggressive brain cancer cells in mice.]

Opening up the blood-brain barrier led to a roughly four- to six-fold increase in the drug concentrations in the human brain. The team observed this increase with two chemotherapy drugs called paclitaxel and carboplatin. These drugs are typically not used to treat glioblastoma patients, because they typically do not cross the blood brain barrier in normal circumstances. 

According to Sonobend, the current chemotherapy used for glioblastoma (Temozolomide) does cross the blood-brain barrier, but is weak. Sonabend also said that previous studies that injected paclitaxel directly into the brains of patients with these tumors had promising signs of efficacy, but the direct injection was associated with toxicity such as brain irritation and meningitis.

A phase 2 clinical trial is already underway. “While we have focused on brain cancer (for which there are approximately 30,000 gliomas in the U.S.), this opens the door to investigate novel drug-based treatments for millions of patients who suffer from various brain diseases,” said Sonabend.

The post Scientists have developed a new way to fight a nearly untreatable brain cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

BUMS. HEINIES. FANNIES. DERRIERES. Few muscles in the human body carry as much cultural clout as the gluteus maximus. “Butts are a bellwether,” writes journalist Heather Radke in her 2022 book Butts: A Backstory. Radke goes on to explain that our feelings about our hindquarters often have more to do with race, gender, and sex than with the actual meat of them. Unlike with a knee or an elbow, Radke argues, when it comes to the tuchus, we’re far more likely to think about form than function—even though it features the largest muscle in the human body. 

For all the scrutiny we spare them (outside of when we’re trying on new jeans) our butts aren’t mere aesthetic flourishes. A booty is, in fact, a unique feat of evolution: Out of any species, humans have the most junk in their trunks. Many other creatures have muscle and fat padding their backsides, and some even have butt cheeks. But none pack anything close to the same proportions as us.

So why did our ancestors develop such a unique cushion? Evolutionary biologists’ best guess is that our shapely rears help us walk upright. The curved pelvic bone that gives the butt its prominence likely developed as our weight moved upward and our muscular needs shifted. Research increasingly suggests that more massive muscles in the vicinity of the buttocks make for faster sprinting and better running endurance too. “The butt is an essential adaptation for the human ability to run steadily, for long distances, and without injury,” Radke writes. 

That said, the gluteus maximus does more than just keep us on our feet. The fat that sits atop it affects how we feel whenever we sit or lie down. The organs nestled behind those cheeks also have a massive influence on our health and wellbeing. Here are a few of the ways our bums factor into scientific understanding, lifesaving medicine, and the future of engineering. 

Digging deep for ancient backsides 

For as long as humans have been making art, they’ve been thinking about bodacious butts. The 30,000-year-old Venus of Willendorf is a famous pocket-size figurine carved by a Western European civilization during the Upper Paleolithic. The statuette, which some archaeologists suspect served as a fertility charm, immortalizes a body too thick to quit.

Scientists also love peeping at the actual posteriors of our early ancestors, which hold a broader archaeological significance in telling the stories of ancient people and their lifestyles. Differences in the pelvis and other sat-upon bones have long been used to determine the sex of unearthed skeletal remains, though we know now there isn’t as clear-cut a binary as researchers long assumed. In 1972, anthropologist Kenneth Weiss flagged that experts were 12 percent more likely to classify skeletons found at dig sites as men versus women, which he blamed on a bias for marking indeterminate skeletons as male. Recent research bears that out, with anthropologists now designating many more remains as having a mix of pelvic characteristics (or simply being inconclusive) than they did historically. Still, while the distinction isn’t completely black and white, the signs of a body primed for or changed by childbirth are useful in figuring out the age and sex of ancient remains. Butt bones can also tell us about how people lived: This March, archaeologists published the oldest known evidence for human horseback riding in the journal Science Advances. They identified their 5,000-year-old equestrians—members of the Yamnaya culture, which spread from Eurasia throughout much of Europe around that same time—with the help of signs of wear and tear to hip sockets, thigh bones, and pelvises. 

Supporting heinies of all shapes and sizes

As Sharon Sonenblum, a principal research scientist at the School of Mechanical Engineering at Georgia Tech, puts it, “What could be better than studying butts?” The Rehabilitation Engineering and Applied Research Lab that she’s part of is perhaps more aptly referred to by its acronym: REAR. 

Stephen Sprigle, a Georgia Tech professor in industrial design, bioengineering, and physiology, started REARLab with better solutions for wheelchair users in mind. A decade ago, he and Sonenblum saw the potential for an engineering-minded solution to the serious clinical problem of injuries from sitting or lying down for extended periods. Pressure sores and ulcers are a risk whenever soft tissue presses against a surface for a prolonged time, and they become more dangerous in hospital settings—where antibiotic-resistant bacteria often lurk—and in people with conditions that hinder wound healing, like diabetes. 

Sonenblum recalls that they set out to answer a deceptively simple question: What makes one backside different from another? To answer it, they had to put a whole lot of booties into an MRI scanner. Those imaging studies and others (including some done on supine patients) have provided an unprecedented amount of data about butt cheeks and the stuff inside them. 

The big headline, Sprigle says, is that “we’re big bags of water. What the skeleton does in that big bag of goo is totally fascinating.” 

The work proved particularly humbling for Sonenblum, who’d intended to spend her career studying how the gluteus maximus affects seating. Instead, she and her colleagues figured out that humans don’t rest on muscle at all—the fat is what really counts. Sonenblum and the rest of the REARLab team are investigating how the natural padding in our rears changes over time, particularly in people who spend a lot of time sitting or supine.

Today, REARLab creates more precise computer models and “phantoms” to help cushion testing—mainly for wheelchair seats, but also for ergonomic chairs of all stripes—better account for real-world bums. Phantoms aren’t quite faux butts; they’re simple and scalable geometric shapes, almost like the convex version of a seat cushion designed for your tuchus to nestle into. They don’t account for bodies’ individual differences either. 

“Phantoms are always a tricky balance between time and representation,” Sonenblum says. “You want to represent the population well, but you can’t have too many or you’ll spend your entire life running tests.”

REARLab’s current approach is to use two shapes—elliptical and trigonometric—to represent a fuller backside and one more likely to pose biomechanical problems when seated, respectively. It would be reasonable to assume the trigonometric butt is the bonier of the two, Sonenblum says, but the reality isn’t so simple. Large individuals with lots of adipose tissue can still lose the round cushioning when they sit. 

“I’ve seen scans of butts that look like this, and when I do, I think, Wow, that’s a high-risk butt,” Sonenblum explains. It comes down to the quality of the tissue, she adds. “If you touch a lot of butts, you’ll find that the tissue changes for people who are at risk [of pressure injuries]. It feels different.”

Sonenblum and Sprigle hope that continued work on backside modeling, cushion-testing standards, and adipose analysis will help wheelchair users and patients confined to their beds for long stretches stay safer and more comfortable. But their work has implications for absolutely anyone who sits down. When asked what folks should take away from their studies, they’re both quick to answer: Move. People with limited mobility may not be able to avoid the loss of structural integrity in their butt tissue, but anyone with the ability to get up often and flex their muscles can keep that natural padding in prime health. 

Finding better bellwethers for bowel cancer

When it comes to protecting your posterior, it’s not just the bodacious bits of the outside that count. One of the biggest backside-related issues scientists are tackling today is the sharp rise in colorectal cancer, which starts with abnormal cell growth in the colon or rectum. It’s already the third most common cancer and second leading cause of cancer death, but it represents a mounting threat, especially for millennials. New cases of young-onset colorectal cancer (yoCRC)—defined as a diagnosis before age 50—have gone up by around 50 percent since the mid-1990s. 

Blake Buchalter, a postdoctoral fellow at Cleveland Clinic Lerner Research Institute focused on cancer epidemiology, says that the most troubling thing about this recent uptick in cases is how little we know about what’s causing it. He and his colleagues suspect that 35- to 49-year-olds who die from colorectal cancer may share many of the same demographics and risk factors—higher body weight, lower activity levels, smoking, alcohol use, and diets high in processed and red meats—seen in patients aged 50 and older. But those under the age of 35 don’t follow those patterns as closely as expected. 

“This indicated to us that mortality among the youngest colorectal cancer patients may have different drivers than among older populations,” Buchalter says. “Our future work in this space aims to identify underlying factors that might be driving higher incidence and mortality among certain age groups in particular geographic regions.” 

Buchalter hopes that more granular data will encourage more granular screening guidelines too. While he was heartened to see the US Preventative Services Task Force shift the recommended colon cancer screening age down from 50 to 45 in 2021, it’s clear that some populations are at risk for the disease earlier, he says. Buchalter and his colleagues hope to zero in on who should be getting screened in their 20s and 30s. 

But colonoscopies, the most commonly recommended form of detection, present a major hurdle in themselves. A 2019 study found that only 60 percent of age-eligible US adults were up to date on their colorectal cancer screenings, with others citing fear, embarrassment, and logistical challenges such as transportation to explain their delayed colonoscopies. At-home fecal tests offer a less invasive alternative, but research shows that fear of a bad diagnosis and disgust with the idea of collecting and mailing samples still keep many folks from using them. Blood tests and colon capsule endoscopy (CCE), in which patients swallow a pill-size camera to allow doctors to examine the gastrointestinal tract, both show promise in supplementing, and perhaps someday replacing, the oft-dreaded colonoscopy.

For now, it’s worth going in for the physical screening if you can manage it. While blood and stool tests can accurately detect signs of the cancer, colonoscopies can actually help prevent it. During a standard colonoscopy, gastro­enterologists are able to identify and remove potentially precancerous polyps known as adenomas on the spot. No DIY kit can manage that.  

Tracking microbiomes with futuristic commodes

Meanwhile, other researchers are uncovering health secrets from long-ago water closets. In 2022, archaeologists uncovered what they believe to be the oldest flush toilet ever found, in Xi’an, China. The 2,400-year-old lavatory features a pipe leading to an outdoor pit. Researchers believe the commode, which was located inside a palace, allowed servants to wash waste out of sight with buckets of water. Flush toilets wouldn’t appear in Europe until the 1500s, and wouldn’t become commonplace until the late 19th century. Up until that point, major US cities employed fleets of “night soil men” to dig up and dispose of the contents of household privies and public loos.

As far as we’ve come from the days of night soil, the future of the humble toilet looks even brighter. Sonia Grego, an associate research professor in the Duke University Department of Electrical and Computer Engineering, says she’s “super-excited” to see commodes enter the 21st century. 

“Smart” toilets boast everything from app-controlled heated seats to detailed water-usage trackers, and could grow into a $13.5 billion industry by the end of the decade. But Grego’s team—the Duke Smart Toilet Lab at the Pratt School of Engineering—is focused on turning waste flushed down porcelain bowls into a noninvasive health tool. She envisions a future in which your toilet can warn you of impending flare-ups of gut conditions like irritable bowel syndrome, flag dietary deficiencies, and even screen for signs of cancer. 

“When we first started to work on the smart toilet for stool analysis, laboratory scientists were skeptical that accurate analytical results could be obtained from specimens that had been dropped in a toilet instead of a sterile collection container,” Grego recalls. “The perspective is very different now.”

Drawing inspiration from wild butts 

Humans may be unusually blessed in the butt-cheek department, but that doesn’t mean other animals’ rears hold less scientific appeal. From modeling the evolution of the anus to cracking the code on climate-friendly gut microbes, scientists are keeping close tabs on all sorts of animal bottoms. Some researchers are even hoping to harness the power of butt breathing—yes, actually breathing through your butt—for future applications in human medicine. 

We’ll circle back to backside breathing in a moment. First, let’s consider the wombat. While it’s true enough that everybody poops, these marsupials are the only animals known to drop cubes. For years, no one was quite sure how they managed to get a square peg out of a round hole. Some even assumed the wombat must have an anus designed for squeezing out blocks instead of cylinders. In 2020, mechanical engineers and wildlife ecologists at Georgia Tech teamed up to publish a surprising new explanation for the shape in the aptly named journal Soft Matter. They’d borrowed roadkill from Australia to do the first-ever close examination of a wombat’s intestines. By inflating the digestive tract and comparing it to more familiar pig intestines, they were able to show that the marsupial’s innards have more variation in elasticity: Instead of being fairly uniform throughout, the organs have some inflexible zones. The team’s findings suggest that a few nooks within the digestive system—some stretchy, others stiff—provide a means to shape the refuse into a square. 

Wombat butts themselves, by the by, are veritable buns of steel. Their rumps contain four fused bony plates surrounded by cartilage and fat and can be used to effectively plug up the entrance to a burrow when potential predators come sniffing around. While this has yet to be caught happening live, some scientists think wombats can even use their powerful bums to crush the skulls of intruders like foxes and dingoes who manage to make it inside. 

So now we have more clarity on how wombats poop cubes, but the question of why remains unanswered. Experts have posited that wombats communicate with one another by sniffing out the location of poop cubes, making it advantageous to produce turds less likely to roll out of place. Others argue that the unusual shape is a happy accident: Wombats can spend as long as a week digesting a single meal, with their intestines painstakingly squeezing out every possible drop of moisture to help them survive the arid conditions Down Under. Their entrails, when unwound, stretch some 33 feet—10 feet more than typical human guts—to help facilitate the frugal squeezing. When the species is raised in captivity with loads of food and water, their poops come out moister and rounder. 

Elsewhere in the world of scat science, folks are working to understand the secrets of nonhuman gut microbiomes. Earlier this year, biotechnologists at Washington State University showed that baby kangaroo feces could help make beef more eco-friendly. Joey guts contain microbes that produce acetic acid instead of methane, which cows burp out in such abundance that it significantly worsens climate change. By reseeding a simulated cow stomach with poop from a newborn kangaroo, researchers say they successfully converted the gut to a factory of acetic acid, which doesn’t trap heat in the atmosphere. They hope to try the transfer out in a real bovine sometime soon. 

Going back to the butt breathing, scientists are hoping to suss out how to give humans a superpower already exhibited by catfish and sea cucumbers. In 2021, Japanese researchers reported in the journal Med that they’d been able to keep rodents alive in oxygen-poor conditions by ventilating them through their anuses. Inspired by loaches—freshwater fish that can take in oxygen through their intestines—the scientists are trying to find new ways to help patients who can’t get enough air on their own. They’ve moved on to study pigs, which they say do wonderfully with a shot of perfluorodecalin (a liquid chemical that can carry large amounts of oxygen) up the bum. 

From an evolutionary standpoint, it’s not all that surprising that our outbox can handle the same duties as our inbox. Though it’s still not clear which came first, it’s well established that the anus and the mouth develop out of the same rudimentary cell structures wherever they appear. Some of the most basic animals still use a single opening for all their digestive needs. And one creature—just one, as far as we know—has a “transient anus.”

In 2019, Sidney Tamm of the Marine Biological Laboratory in Woods Hole, Massachusetts, demonstrated that the warty comb jelly creates new anuses as needed. Whenever sufficient waste builds up—which happens as often as every 10 minutes in young jellies—the gut bulges out enough to fuse with the creature’s epidermis, creating an opening for defecation. Then it closes right back up. It’s possible that the world’s first anuses followed the same on-demand model, proving yet again that the butt and its contents are worthy of our awe, curiosity, and respect.  

Read more PopSci+ stories.

The post A scientific exploration of big juicy butts appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Three years ago, Nancy Klimas sat in an auditorium waiting to discuss her latest research progress. The audience was made up of the usual suspects at a scientific conference: doctors, scientists, and other academic colleagues. But this group was a bit different. The room was also packed to the brim with retired US veterans, all waiting to hear about any new developments over a “moonshot” idea that could be the closest attempt to a cure for Gulf War illness. 

Klimas, who serves as the director for the Institute for Neuro-Immune Medicine at Nova Southeastern University in Florida, has been studying this debilitating condition for three decades. The strange sickness affects 175,000 to 250,000 soldiers who were deployed in the 1990-1991 Persian Gulf War. For those veterans, nearly half of who are pushing 50 or above, life has been an uphill battle. There is currently no cure for Gulf War illness, and because it involves a cluster of symptoms—fatigue, joint pain, diarrhea, memory loss—attempts to treat it have come up short. “These people served our country and put themselves in harm’s way,” says Klimas. “Now they’re sick with a chronic illness that ruined their quality of life and ability to work for more than 30 years.” Exhausting her options, Klimas came up with a rather unconventional idea: use a well-established abortion drug to reset the body’s overwhelming response to chronic illness.

[Related: The PACT Act will take the burden of proof off US veterans exposed to burn pits]

Mifepristone, more widely known as the abortion pill, is capable of treating multiple illnesses. At low doses and when paired with another pill, misoprostol, the synthetic steroid binds to a protein in the uterus and stops the release of progesterone and other hormones needed to sustain pregnancy. But the drug has another effect, which Klimas is looking to tap. When taken at higher doses, mifepristone also blocks hormone receptors in the adrenal gland, which regulates the body’s stress response. The drug has already proven capable of doing this, and is currently approved as a treatment for the metabolic disorder Cushing’s syndrome. 

Based on that evidence, Klimas wondered if the medication could temporarily block the adrenal gland and rebalance the hormone signals that are blunted with Gulf War illness. Repurposing the FDA-approved drug would also save the 10 to 15 years it would take to develop and test a brand-new drug. Klimas is halfway through her phase 1 trial testing the safety of the drug at different dosages on veterans, and is making plans for the second phase of the study. 

The recent legal mess surrounding mifepristone access threw a wrench in Klimas’s plans, along with those of other researchers using mifepristone in their work. In early April, a federal circuit judge in Texas overturned the FDA’s 23-year-long approval of mifepristone, citing claims that the drug is unsafe for public use because abortion is now illegal in some states. And while the Supreme Court blocked the ruling that would have suspended mifepristone access across clinics, pharmacies, and mail orders, the future of the treatment remains uncertain in the US. “Obviously, we’re very concerned,” says Klimas, adding that mifepristone was already hard to get for research purposes. “Attempts to limit access to this drug has already had a splashback on the veteran population in these trials, as we’re delayed in rolling things out. How long will they have to wait for an effective therapy?”

Further constraints on mifepristone could impact medical progress on many other diseases and conditions as well. The medication is being studied as a potential treatment for diabetes in people without Cushing’s syndrome. It has also shown some potential in preventing weight gain caused by antipsychotic medication. Some ongoing clinical trials have found that mifepristone can be effective in slowing down the spread of breast cancer: The drug blocks progesterone receptors from releasing the hormone, which would normally stimulate tumor cell growth. And at different dosages, the pill can improve the quality of life of people dealing with painful uterine growths.

[Related: Abortion bans are impeding access to ulcer, arthritis, and cancer medications]

Banning mifepristone goes beyond stalling research—it puts any FDA-approved treatment at risk of being recalled. “You have a medication with an excellent track record of safety, efficacy, and high patient satisfaction,” says Carrie Cwiak, an OB-GYN at Emory Healthcare in Georgia. “The idea that the entire process for approving medication can be overturned [in court] is earth-shattering.” She says that restricting mifepristone opens a dangerous door to having people with legal power make treatment decisions based on their opinion and ideology rather than medical evidence. 

If the courts decide to bar or limit mifepristone use down the line, it would discourage pharmaceutical companies from spending money on producing new drugs that appear controversial. That could include contraceptives, hormone blockers, or treatments completely unrelated to reproductive issues. “If you were a pharmaceutical company and it was going to cost you $20 million to move a pipeline drug all the way up through phase three [clinical trials], would you want to invest the money for it if it’s possible the bench could reverse the authority of the FDA?” Klimas asks. 

Despite the setbacks on mifepristone access and potential legal battles, Klimas is optimistic that the research she is doing will help give veterans their long and overdue treatment. Her team is hoping to start their phase 2 trial soon and get as many results before politics interferes in science again. 

The post Banning the abortion pill would harm veterans, cancer patients, and many others appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Ozone is like Earth’s natural sunscreen, protecting living things from the sun’s harsh UV rays. But this sunscreen is running out. Greenhouse gases are thinning out the ozone layer, and our skin is starting to pay the price. According to the World Health Organization, losing an extra 10 percent of ozone levels will cause an additional 300,000 non-melanoma and 4,500 skin cancer cases.

With skin cancer as the most diagnosed cancer in America, the US Preventative Services Task Force (USPSTF) updated their screening recommendations earlier this month, emphasizing the need for people to get moles and other spots checked early for potential tumors. 

The quicker skin cancer is caught, the better your chances of recovering from it. And recent technological advances in skin cancer research is transforming the way doctors and patients approach this deadly disease. Here are five tech tools to keep an eye on.

Therapeutic skin cancer vaccine

As multiple companies experiment with cancer vaccines, Merck and Moderna are focusing theirs on melanoma. Their phase II clinical trial results, shared last week, showed a 44 percent decrease in risk of death or a melanoma relapse when pairing the vaccine with the immunotherapy Keytruda. Additionally, about 79 percent of people who took the vaccine plus immunotherapy stayed cancer-free for 18 months compared to the 62 percent who just took immunotherapy. The data shows enough promise for the companies to start a Phase 3 trial in adjuvant melanoma this year, and could compel them to rapidly expand the vaccine to other tumor types, including non-small cell lung cancer, Eric Rubin, a senior vice president at Merck, wrote in an email.

[Related: A vaccine trial targeting the most lethal breast cancer just took its next step]

The vaccine isn’t a preventative treatment, but is instead given to melanoma patients early in recovery. The researchers take tumor samples from biopsies and identify which proteins are most likely to be recognized by the human immune system. They then make a personalized mRNA vaccine (adapted from the technology behind Moderna’s COVID jab) using a certain number of these abnormal genes to boost an individual’s adaptive immunity. If the rest of the trials go as planned, the vaccine could be available as soon as 2025 or early 2026, says Eric Whitman, the medical director of Atlantic Health System’s oncology service line.

Genetic tests and personal risk scores

Precision prevention is when doctors use multiple tools to map out a person’s risk of cancer and use that assessment to tailor their treatment and risk-reduction strategy. Instead of following a standard guideline like an annual dermal exam, a person who is considered high-risk (like someone with a history of skin cancer) may need more frequent screenings and extra body imaging, says Meredith McKean, the director of melanoma & skin cancer research at the Sarah Cannon Research Institute in Tennessee. People with very low risk, on the other hand, may be encouraged to learn how to do their own self-checks at home. McKean adds that it’s really helpful “to stratify patients and really help them do the best that we can to prevent another melanoma or skin cancer [case].”

Genetic tests can also be used to identify people with a predisposition to skin cancer. A 2022 study in the journal Cancer Research Communications found that people who were told they had a MC1R mutation, which carries a higher risk for melanoma, made more of an effort to protect themselves against the sun and get regular skin checks. Some doctors even use AI technology to a personalized risk score for individuals based on photos of skin lesions and moles.

Melanoma sticker

The Dermtech SmartSticker is an easy precursor for checking suspicious moles for melanoma. A dermatologist places four skin patches on the potential tumor for less than five seconds, and ships the sample to a Dermtech lab in San Diego, California. The lab then tests for DNA from cancerous cells. If the results come back positive, the dermatologist would follow up with a biopsy. If not, this painful step can be avoided and the doctor would just continue clinically monitoring the patient. 

“It’s a very good test. If it comes up negative, there is a greater than 99-percent reliability that the mole is not melanoma,” says Emily Wood, a dermatologist at Westlake Dermatology & Cosmetic Surgery in Texas. She adds that patients in her clinic favor the stickers over biopsies because they’re painless, cost-effective, and quick. “We’re going to save lives in catching melanoma earlier. I think this will make a dramatic impact for patients long-term.” While the studies are ongoing, there is research suggesting the tool could extend to detecting non-melanoma skin cancer. 

Artificial intelligence apps

Medical researchers are now training computers to recognize patterns and atypical features associated with skin cancer. “AI picks up a lot more subtle changes than the naked eye,” says Trevan Fischer, a surgical oncologist at Providence Saint John’s Health Center. The high accuracy in AI deep learning can help doctors determine whether a mole is malignant and worth biopsying—saving patients from some unneeded discomfort.

The beauty of AI is that you can do a full home skin exam with a press of a few buttons. Popular smartphone apps like MoleMapper lets users upload a picture and have it analyzed for potential skin lesions. They also let you store photos to show your doctor and keep track of any changes to your mole. (Wood warns that a smartphone app is not meant to substitute in-person skin check-ups with your doctor.)

While these apps are useful, there’s always room for improvement. For example, the AI’s accuracy goes down when the view of the mole has shadowing, blurriness, hair, or if the image is rotated. There’s also been research showing that AI databases lack images of darker skin types that would teach the system to better detect skin cancer from people of color. If anything, Wood says the apps can encourage people to submit photos of suspicious moles and start the conversation early with their doctor. 

Millimeter wave imaging 

The same technology used in airport security scanners is getting revamped and used to detect skin tumors. Millimeter wave imaging is a non-invasive method and a low-cost alternative to biopsies that works by scanning a person’s skin for any biochemical and molecular changes related to a disease or disorder. The radio waves reflect differently when looking at benign versus cancerous moles. 

[Related: Everything you need to know about UPF sun protection]

While the approach is not yet available for clinical practice, there is evidence backing up the proof of concept. A 2017 study in IEEE Transactions on Biomedical Engineering found considerable differences when looking back at the scans of healthy skin and those for two common skin cancer types: squamous cell carcinoma and basal cell carcinoma. The study authors could see detailed changes in water molecules, glucose concentrations, and protein levels. A 2018 study in the same journal used ultra-high resolution millimeter wave imaging to identify early-stage skin cancer. Most recently, the diagnostic tool was studied on 136 people suspected of skin cancer. Ultimately, it found malignant tumors from various types of skin cancer on 71 patients, giving the tech a “high diagnostic accuracy.” 

“We’re really trying to leverage all the different ways that advanced technology can help us diagnose and treat skin cancer like melanoma,” Whitman from Atlantic Health Systems says. He emphasizes that most of these strategies weren’t imaginable 10 years ago. Using data to improve on existing AI technology and create new models for personalized medicine, he notes, “can really make a difference for people and their lives.”

The post 5 skin cancer-care tools you should look out for appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

New research from the University of Oxford in the United Kingdom found that while all hormone contraceptives carry a small “excess” risk of breast cancer, the overall risk remains low. 

The study was published March 21 in the journal PLOS Medicine and filled in research gaps on links between breast cancer and progestagen-only contraceptives. Progestagen-only contraceptives include birth control implants, intrauterine devices (IUD), contraceptive injections, and the minipill. Other kinds of hormonal birth control contain a combination of estrogen and progestagen and include the traditional birth control pill and patch. 

[Related: Where is all the hormone-free birth control?]

Importantly, the new study does not say that hormonal contraceptives cause breast cancer. It only investigated any potential links to the disease that affects about 264,000 women and 2,400  men every year. 

“Given that the underlying risk of breast cancer increases with advancing age, the absolute excess risk associated with use of either type of oral contraceptive will be smaller in women who use it at younger rather than at older ages,” the authors wrote in a statement.“These excess risks must, however, be viewed in the context of the well-established benefits of contraceptive use in women’s reproductive years.”

The study included data on roughly 10,000 women in the UK under age 50 who were diagnosed with invasive breast cancer between 1996 and 2017. They also looked at more than 18,000 subjects who did not have breast cancer. 

They found a relative increase of 20 to 30 percent in breast cancer risk with combined birth control (which also contain estrogen in addition to progestagen) and progestagen-only contraceptives. However, after five years of use, the 15-year absolute excess incidence of breast cancer was only 265 cases per 100,000 users at most. Earlier studies show that this excess risk disappears entirely about 10 years after stopping hormonal birth control. 

“These findings suggest that current or recent use of all types of progestagen-only contraceptives is associated with a slight increase in breast cancer risk, similar to that associated with use of combined oral contraceptives,” said co-author and cancer epidemiologist Kirstin Pirie, in a statement. 

The overall risk of breast cancer in hormonal contraceptive uses is low, particularly for younger users. Additionally, the team pointed to a lack of both a complete prescription history and family breast cancer history of the women as some of the limitations in this study.

[Related: Over-the-counter birth control pills could change reproductive care in the US.]

Progestogens, or progestin, are drugs that mimic a natural hormone called progesterone, which is crucial for both menstruation and pregnancy. Progestagen-only birth control options do not contain estrogen the way that combined hormone birth control pills do. They prevent pregnancy by thickening mucus in the cervix, which stops sperm from reaching an egg. It can also completely stop ovulation in some cases.  

According to the Centers for Disease Control and Prevention (CDC), the combined hormone birth control pill is the most popular form of hormonal contraception. More people have been choosing to use the IUD or an implant over the pill for at least a decade.

Claire Knight of Cancer Research UK, who funded this study, told The Guardian that this should not discourage women from taking birth control pills. “Women who are most likely to be using contraception are under the age of 50, where the risk of breast cancer is even lower,” Knight said. “For anyone looking to lower their cancer risk, not smoking, eating a healthy balanced diet, drinking less alcohol, and keeping a healthy weight will have the most impact.”

The post What we know about hormonal birth control and breast cancer risk appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The number of colorectal cancer diagnoses has nearly doubled in people younger than 55, a recent report from the American Cancer Society (ACS) warns. 

Colon cancer cases rose across the country from 11 percent in 1995 to 20 percent in 2019 people younger than 55.  There was an 8-percent jump in advanced cases across all ages since the mid-2000s. Most young people who were diagnosed had late-stage tumors. 

While the statistics are alarming, it doesn’t come as a surprise to doctors in the field who’ve noticed a trend in younger patients over the past few years. “This data is confirmation of that clinical observation,” says Deborah Nagle, the chief of colon and rectal surgery at Stony Brook Medicine in New York. 

Colonoscopies remain the gold standard for screening colorectal cancer. However, some might find the preparation, recovery, and procedure itself uncomfortable and time-consuming. Fortunately, there are other less invasive tools for detecting colon cancer, some of which you can access in the comfort of your own home. 

The reasons behind rising colon cancer rates

Why do some people get colon cancer over others? There’s “no smoking gun,” says Samir Gupta, a gastroenterologist and professor of medicine at the University of California, San Diego. Several causes factor into an individual’s overall risk.

One is antibiotics: The drugs might contribute to colorectal cancer by changing the composition of the gut microbiome that allows “bad” bacteria—those that lower a person’s immunity, create cancer-promoting metabolites, and damage DNA—to flourish. A 2021 study in Sweden found adults treated with antibiotics had a 17 percent risk of cancer in the ascending colon. The more antibiotics people took, the greater the risk. Gupta says there could also be a potential link between antibiotic exposure during infancy and future colorectal cancer. 

Obesity is another contributor for different kinds of cancers, including early-stage colorectal. Nagle says the obesity rate has significantly increased in the US in the past few decades. Nearly 42 percent of Americans have a BMI of or above 30. Excess body fat promotes inflammation and drives up the production of insulin and hormones, and in turn, can increase the number of cells that can lead to cancer. Additionally, inflammation from fat itself sometimes damages healthy cells and leads to cancerous mutations in cellular DNA.

While less studied in humans, chemicals put in food have also been seen as a potential cancer contributor. Dietary emulsifiers, which are usually added to processed foods to increase their shelf life, have been linked to colon cancer through animal research. In one 2022 study, titanium dioxide, a common food coloring in candies and baking products, helped promote colorectal tumor development in lab mice.

[Related: Two decades-long studies link ultra-processed foods to cancer and premature death]

Oncology researchers are also interested in looking at how big of a role genetics play in colorectal cancer formation. One in five people diagnosed with colorectal cancer carry a genetic mutation associated with tumor development.

Prevention is possible, however. At 91 percent, colorectal cancer has one of the highest five-year survival rates. The key is catching it in time. Both Gupta and Nagle recommend getting a colonoscopy screening to detect any early signs of cancer. A follow-up study in Europe last year showed that people who got a colonoscopy reduced their risk of colorectal cancer by 31 percent and the risk of dying from said disease by 50 percent.

When to get a colonoscopy

While there are standard guidelines for when you should get a colonoscopy, both experts urge anyone who experiences persistent rectal bleeding and changes in bowel habits to get immediate medical attention.

If you have no symptoms and no family history of colorectal cancer, the ACS recommends routine screenings starting at age 45. Those considered at high risk of colorectal cancer—family history of disease, history of radiation in the abdomen area to treat prior cancer, inflammatory bowel syndrome—are encouraged to get a screening before 45. 

People with Lynch syndrome, a hereditary condition that genetically predisposes a person to multiple types of cancer, are strongly urged to get a colonoscopy every one to two years starting in their early 20s or 2 to 5 years before the youngest case in the family.

Test your options

While colonoscopies are the go-to tool for colorectal screenings, says Nagle, they’re not all too popular among patients. The prep required for a colonoscopy—taking a laxative and adjusting your diet a few days before —can deter people. The procedure and recovery also takes up a huge chunk of time, which may not be doable for those who can’t take time off work. 

Stool-based tests like Cologuard offer an easier, at-home alternative. There’s no prep needed, and the results are generally accurate, though not on par with a colonoscopy. There are also fecal immunochemical tests (FIT) that look for hidden blood in your stool. This annual test can be done at home, though it is less accurate at detecting polyps smaller than 6 millimeters than colonoscopies.

A less invasive method some oncologists are turning to virtual colonoscopies. The procedure uses CT scans to create images of your large intestine to look for ulcers, polyps, and tumors.

[Related: First study of cancer-detecting blood test shows hopeful results]

There is ongoing research looking to improve screening results using a combination of these methods. Some involve using a person’s gut microbiome composition to identify the loss of certain “good” bacteria to predict their risk of precancerous tumors. Others include a multi-step screening process that still includes the recommended colonoscopy. A study from last spring suggests getting a colonoscopy after an at-home stool test; those who did not follow up were twice as likely to die from colorectal cancer.

“We have an opportunity to prevent some cancers from happening by doing the screenings,” says Gupta. “When people are diagnosed early, it’s more treatable.”

The post Colon cancer cases in younger generations are rising. When should you get screened? appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Catheters, stents, and other medical devices are instrumental in saving peoples’ lives, but the methods used to sterilize this equipment could be causing cancer in some parts of the country, most notably in Puerto Rico and the metro areas of Baltimore, Denver, and Richmond, Virginia. A colorless gas called ethylene oxide is used to decontaminate about 20 billion medical devices per year, about half of all medical equipment used annually. This process often happens within buildings that look like ordinary offices, lacking prominent exhaust pipes or billowing clouds often associated with chemical plants. 

The Environmental Protection Agency (EPA) classified ethylene oxide as a carcinogen in 2016, because it can cause lymphoid, breast, and other cancers if inhaled at low doses regularly or infrequently at particularly high levels. The chemical can also damage the brain and nervous system and irritate the eyes, skin, nose, throat and lungs. 

Puerto Rico, a US territory without voting power, has carried a disproportionate load of the country’s burden—both in terms of the number of plants and the effect on local communities. Its facilities tend to receive less legislative action than others, too.  When a sterilizer plant enters a neighborhood, the wealthier and whiter ones are more successful at getting it shut down, according to Adrian Wood, who works on community engagement at the University of Pennsylvania’s Center of Excellence in Environmental Toxicology, and the author of a 2022 research paper analyzing community and government responses to ethylene oxide emissions in the US and Puerto Rico.

Puerto Rico has seven sterilizer plants, including four of the most dangerous facilities, according to a new report from the Union of Concerned Scientists. “Only California and Texas, the two most populous states, have more sterilizers, even though Puerto Rico has roughly one-tenth the population of Texas and 1 percent of its land area,” the report states. The sterilizers are within five miles of more than 413,000 Puerto Ricans (roughly 13 percent of the population) and nearly 300 schools and childcare centers, according to the report.

Because most of Puerto Rico’s sterilizer plants are located in low-income and minority areas, many of the people who get cancer from the toxic fumes might not have access to hospitals with quality treatment. “It is incredibly tragic for people to get cancer and then find themselves being treated with the same materials that caused their cancer,” says Marvin Brown, an attorney for the nonprofit legal advocacy group Earthjustice. 

Accidents at these plants can be frightening. Two explosions at a Steri-Tech plant in Salinas, a small and low-income town in the south of the commonwealth, shook houses late last year and early this year. Residents told the Associated Press that the explosions were worrisome, and one woman said that several of her neighbors who lived nearby had died of cancer.

Then, last year, the EPA took air samples to measure the level of contamination across the island. The agency found extremely high concentrations of ethylene oxide in some areas, with one containing 121 micrograms per cubic meter of air, which is more than 400 times higher than the US national average of 0.3 micrograms. The four plants the EPA said posed the most elevated risks for cancer included Edwards Lifesciences Technology SARL in Añasco, Customed in Fajardo, Steri-Tech in Salinas, and Medtronic in Villalba.

Brown guesses that Puerto Rico might have so many sterilizer plants because of its sizable pharmaceutical industry. Eight percent of US pharmaceuticals are manufactured in Puerto Rico, according to the US Food and Drug Administration.

[Related: Pollution kills 1 in 6 people worldwide]

Sterilizer plants throughout the country are required by the EPA to have emissions controls, which reduce the amount of ethylene oxide diffused into the air above sterilization chambers, aeration room vents, and other parts of the plant. But Brown suspects that most of the ethylene oxide emissions may be produced elsewhere. Ethylene oxide may be released in uncontrolled settings, such as when  product ‘off-gasses,’ or continues to release chemicals, after sterilization.

Under the Clean Air Act, the EPA’s commercial sterilizer regulations must be updated every 8 years. But in 2019, the deadline the agency gave itself for new regulations, the agency failed to produce them. Earthjustice is suing the EPA to issue updated regulations and force the agency to adhere to a court-ordered deadline. The EPA hosted a community meeting on January 24 to address residents’ concerns, though the agency did not respond to request for comment by the time of publication.

Meanwhile, wealthier and whiter communities have used political pressure to shut down facilities that open in their neighborhoods. Wood’s research paper, which analyzed US states and Puerto Rico, found that sterilizer plants located in rich neighborhoods received the most aggressive response from the community, who in turn pushed the government. “The state [came] in quicker and more aggressive with testing and air monitoring, and [got] the facility to shut down in these wealthier suburbs,” she says. 

In two such suburbs, outside Chicago and Atlanta, new sterilizer plants were shut down within a few years. The EPA typically reacts much more slowly, Wood says. “But things did happen in those two areas,” she says. “So why couldn’t they happen in all the other areas, too?”

Researchers are studying other methods for sterilizing equipment. Right now, the Food and Drug Administration has approved three methods for sterilization: heat, steam and ethylene oxide. The problem with heat and steam is that they might melt certain medical equipment. The International Organization for Standardization published standards for hydrogen peroxide, another option for sterilizing these devices, although it hasn’t yet been approved by the FDA. 

[Related: California needs to stop saying everything causes cancer]

“Hydrogen peroxide, for example, appears to be less toxic to workers and the environment,” Darya Minovi, author of the Union of Concerned Scientists report, said in a blog post. “But the status of the FDA’s effort is unclear, and given what we know about ethylene oxide, we hope the agency is considering phasing out its use in medical device sterilization altogether instead of permitting its continued use.”

But the trade association AdvaMed claims the gas can decontaminate tools that other, rougher techniques would destroy. Hospitals and labs rely on ethylene oxide “to sterilize devices and equipment to protect millions of patients from the real risks of infectious diseases caused by bacteria, viruses, and fungi,” the group argues on its website. “For the majority of these products, [ethylene oxide] sterilization is the most effective and efficient—and often the only viable—sterilization technology.” 

Any update to EPA’s ethylene oxide regulations—which Earthjustice is suing for—would affect the commonwealth, too. “Everybody under the Clean Air Act deserves to breathe clean and safe and healthy air,” Brown says. “No part of the country should be a sacrifice zone for the rest of the country.”

The post A little-known form of medical pollution is costing Puerto Ricans their health appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This article was originally featured in Knowable Magazine.

Every four months, pathologist Aaron LeBeau scoops into a net one of the five nurse sharks he keeps in his University of Wisconsin lab. Then he carefully administers a shot to the animal, much like a pediatrician giving a kid a vaccine. The shot will immunize the shark against a human cancer, perhaps, or an infectious disease, such as Covid-19. A couple of weeks later, after the animal’s immune system has had time to react, LeBeau collects a small vial of shark blood.

Halfway across the country, immunologist Hidde Ploegh goes through the same steps, but with alpacas that live on a farm in western Massachusetts. The scientists are after the same thing: tiny antibodies, made only by certain animals, that may have big implications for human health.

Most antibodies — those molecules that course through our blood and tissues patrolling for pathogens — are fairly hefty as proteins go. But the antibodies made by camels and sharks and their close relatives are simpler and smaller. Since their discovery in the late 1980s, researchers have learned that these antibodies pack a big punch: They can latch onto hidden parts of molecules and can penetrate tissues more deeply, enhancing their potential as therapies. 

“They can get into little nooks and crannies of different proteins that human antibodies cannot access,” LeBeau says.

In the last decades, investigations of these diminutive antibodies have surged. Not only can they sneak into small places, they are also easy to work with — sturdier than their ordinary counterparts — and relatively cheap to make in large quantities. All these features make the antibodies promising treatments for a host of diseases, whether clotting disorders or Covid-19. Researchers are also exploring their use for diagnosing conditions such as cancer, and they’re becoming a key tool in other kinds of research, like mapping cells’ insides.

The full promise of these antibodies may still take years to realize, but researchers are very excited about their possibilities. “I think they have potential to save the world,” LeBeau says.

Luck of the blood draw

A group of biology students were the first to discover these unusual antibodies — quite by chance — back in 1989. The students of Free University in Brussels needed some blood for an exam in which they were tasked with separating an antibody into its two main parts: two heavy protein chains, which form a Y shape, and two light protein chains, which flank the prongs at the top of the Y.

Human blood seemed too risky to work with, given concerns at the time about potential HIV exposure, and the students didn’t want to kill a mouse. But the students’ professor, the late Raymond Hamers, happened to be studying sleeping sickness in large animals. He gave the students some blood from a camel, says immunologist Serge Muyldermans, who was then a post-doctoral researcher at the university.

Strangely, the students found only heavy chain proteins in the blood even though antibodies were supposed to also have light chains. As Muyldermans tells it, everyone thought that the camel antibodies had degraded — or that the students had done something wrong — so Hamers went to the Antwerp Zoo to collect fresh camel blood. But the students had not screwed up: Camels make antibodies with only heavy protein chains.

The potential applications of camelids’ small antibodies dawned on Hamers during those early years, says Muyldermans, who details their myriad uses in the 2021  Annual Review of Animal Biosciences. Like antibodies from people or mice, the camelid antibodies could be further pared down into even smaller, yet still effective, fragments — just the tips of the Y. These fragments, called variable domains, are the business end of any antibody — they act as the antibody’s “sensor” and can stick to parts of pathogens or toxins, whatever substance is recognized as foreign and a possible threat.

In standard antibodies (which camels also make), the variable domains come in pairs, one from the heavy chain and one from the light chain. But the variable domains of the camelid’s heavy-chain-only antibodies are singletons. The researchers realized these solitary fragments might be able to grab onto parts of foreign molecules that conventional antibodies were too bulky to reach.

In 1993, the team published the discovery in Nature. The next year, Hamers  patented the production of these camelid antibody fragments (they are also known as VHH antibodies or “nanobodies,” a trademarked term). A few years later, a different group of researchers reported that  sharks also make antibodies with only heavy chains and these have an even smaller tip (these shark end fragments are called variable new antigen receptors, or VNARs).

When the primary patent expired in 2013, research investigating the antibodies really surged, says Ploegh, an immunologist at Boston Children’s Hospital. “That’s sort of when the dam broke and a lot of folks got in on the game.”

Scientists have since learned a lot about the advantages of these mini antibodies. Some is practical: Unlike full-size antibodies, the fragments are stable at room temperature so there’s no need to keep them in a freezer or ship them cold. The mini antibodies of sharks can even be boiled with no effect on their function, LeBeau says. And while full-size antibodies require mammalian cells to be grown in a flask, which can be complicated and expensive to maintain, the fragments can be manufactured in large quantities using bacteria, saving time and money.

These mini antibodies also tend to self-assemble properly, keeping their correct shapes, making them a promising alternative to full-size antibodies, which have more pieces and thus can misfold. Such misfolding may expose parts that are more likely to be recognized by the immune system as foreign molecules, which can provoke a negative immune response in the body, with potentially serious consequences for patient health.

But the standout trait of the mini antibodies is their versatility. All antibodies, whether from human or shark, have variable domains at their tips, but those of sharks and camels have unique traits. They have an especially long, slender finger called a CDR3 loop that can poke into places that human antibodies can’t access. They appear to easily adopt different shapes — LeBeau describes that feature as “molecular yoga.” This means mini antibodies can get into tight spots, whether into tissues of the body or on minuscule parts of individual molecules.

Anti-cancer antibodies

Research into these unusual mini antibodies is now starting to bear fruit. In 2019, the first mini antibody medical treatment to be approved by the US Food and Drug Administration, called Cablivi, came on the market. It treats a rare blood disorder that leads to clots in small blood vessels. The treatment uses nanobodies to bind to a protein in platelets, which stops them from sticking together.

Mini antibodies could become a valuable tool for cancer treatment. Full-size antibodies are already used in immunotherapies to treat certain cancers; in some cases, the antibody tags cancer cells so that the body’s own immune system cells can then recognize and kill the rogue cells; in others, it might bring immune cells closer to the cancer cells so the body can better fight the cancer. The mini antibodies can do the same tasks, but can also be used in other ways, such as targeting proteins to reduce tumor growth or blocking blood vessels from feeding a tumor. And the smaller antibodies also may be less likely to trigger a negative immune response than full-size immunotherapy antibodies, which may lead to dramatic treatment improvements, Ploegh says.

LeBeau, for his part, is focused on developing mini antibodies targeted for prostate and lung cancer. The sharks in his lab, each named for James Bond bad guys — Goldfinger, Hugo Drax, Mr. Stamper, Oddjob and Nick Nack — keep him supplied with antibodies that he uses in lab experiments. His lab recently identified a shark antibody fragment that is specific for a highly aggressive, and currently untreatable, form of lung cancer. He’s hopeful that this new mini antibody could help combat the cancer, and has studies in progress to test it.

The mini antibodies are also helping physicians detect cancers more readily, pinpointing diseased cells with more precision. By attaching radioactive tracer molecules to specific antibodies that seek out cancer cells, physicians can locate cancerous cells on a PET scan, potentially with greater resolution than with standard antibodies because they can penetrate deeper into tissues. One such nanobody-based tracer detected several tumors in mice with  higher specificity than conventional imaging, a team reported in  PNAS in 2019.

Vanquishing viruses

Scientists are also harnessing mini antibodies to fight infectious diseases, including Covid-19. Wai-Hong Tham, an infectious disease researcher at the University of Melbourne and the Walter and Eliza Hall Institute of Medical Research, has been working to generate nanobodies that grab onto part of the spike protein of SARS-CoV-2, to prevent the virus from entering cells in the body.

In a preliminary study, published in PNAS in 2021, Tham and her colleagues identified several nanobodies from alpacas that interfered with the spike proteins’ ability to latch onto the molecular doorknob it uses to get into cells; cocktails of the nanobodies also reduced the amount of virus in experiments with mice. Ideally, Tham says, they could find a nanobody that universally blocks Covid-19 regardless of the coronavirus variant. Other nanobody cocktails also appear promising: Four nanobodies, mixed and matched in various combinations, disabled the spike protein in experiments in cells, a separate team reported in 2021 in  Science.

Mini antibodies might be delivered via mRNA technology so the antibodies assemble inside people’s cells, Tham says. Vaccine-like injections might work against other  infectious diseases, counter toxins such as  botulism, or even deliver therapeutics for cancer or other conditions.

And with a simple pill, mini antibodies could be delivered directly to the gut, which could help to block a number of pathogens, for example rotavirus, that enter the body through the digestive tract. Small microbes — such as yeast, bacteria and algae — can’t efficiently make full-size antibodies because these are too complex. However, researchers have proposed genetically engineering  spirulina (a blue-green alga that’s often sold as a nutritional supplement) or harmless bacteria called  Lactobacilli  or  Lactococcus that could deliver therapeutic nanobodies via a pill, which would be much more cost effective than producing a drug, Tham says.

Sleuthing cell mysteries

The diminutive antibodies are also a boon for scientists who study proteins and investigate interactions between molecules. The size and long finger of these antibodies can help solve protein structures, map proteins  inside cells and show how molecules within cells  interact with each other.

Researchers recently solved the structure of a human protein called ASIC1a, for example — it forms a type of channel that lets sodium into nerve cells and plays an important role in pain perception and several neurodegenerative diseases. Stabilizing the protein with a nanobody allowed the researchers to determine its structure with greater resolution, the team reported in 2021 in  eLife.

Single-domain antibodies “have the potential of mapping interactions that would be very difficult to study otherwise,” says Ploegh, coauthor of an overview of their traits in the 2018  Annual Review of Immunology. Scientists are even investigating their potential use in the brain — a tricky task because the blood-brain barrier likes to keep foreign molecules out. An international team recently reported using nanobodies as  sensors to study whether or not a protein in a mouse brain was activated, and where it was located.

Ploegh says that mini antibodies are exceptionally useful and have significant advantages over full-size antibodies, but they remain somewhat niche because of limited access to the animals that make them — not every researcher has nearby camels, llamas or, in LeBeau’s case, sharks. (“Probably very few people are crazy enough to actually build a shark tank and work with sharks. But we are,” LeBeau says.)

But this is starting to change as interest ramps up. Researchers are also developing new approaches, such as creating synthetic nanobodies and developing mice with “camelized” immune systems for research.

Scientists still don’t know why camelids and cartilaginous fishes, like sharks, are the only animals known to make heavy chain antibodies. Sharks are the most ancient living organisms to rely on antibodies as part of their immune systems, and their antibodies are more stable than those of camelids. Scientists speculate that sharks rely on these antibodies because of the high concentrations of urea in their blood, which would degrade the antibodies of most mammals.

Sharks evolved some 350 million years before camels, yet camelid heavy chain antibodies are also relatively ancient: They are found in both Old World camelids, like camels, and New World camelids, like llamas and alpacas, suggesting that the antibodies may have developed early in the lineage’s evolution. Perhaps “there are certain pathogens that are unique to the camelids that are best fought with these heavy chain antibodies,” Ploegh says.

The heavy chain antibodies of sharks might well be the most ancient immune molecules still in existence — but LeBeau is exuberant about what they could accomplish in the future. “Whenever you work with them, you see something new every day. And that’s really exciting,” he says.

And as for his two-foot-long sharks, when they outgrow their tank, they’ll retire to the local aquarium.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

The post Camels and sharks have small, sneaky antibodies that can help fight human diseases appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Researchers at Cleveland Clinic launched their next step in a study of a vaccine aimed at preventing triple-negative breast cancer. Triple-negative breast cancer is the most aggressive and lethal form of the disease, and accounts for roughly 10 to 15 percent of all breast cancers.

According to the American Cancer Society, the term “triple-negative breast cancer” means that the cancer cells don’t have estrogen or progesterone receptors (ER or PR) and also do not manufacture any or much of the protein called HER2. This means that the cells test negative on all three tests and these cancers don’t typically respond to hormonal or targeted therapies. These cancers are most common in patients under 40, who are Black, or who have a BRCA1 mutation. BRCA1 is a gene on chromosome 17 that typically helps to suppress cell growth and a person with certain mutations in the gene has a higher risk of developing some types of cancer. 

[Related: A single HPV vaccine dose can protect against cervical cancer.]

The new phase 1b study will enroll cancer-free individuals who are at a high risk for developing breast cancer. Participants have also decided to voluntarily undergo prophylactic mastectomy to lower their risk of developing breast cancer.

Higher risk individuals typically carry genetic mutations–such as BRCA1– that put them at risk of developing triple-negative breast cancer or have high familial risk for developing any type of breast cancer. 

The new phase of the trial will include roughly 6-12 patients and should wrap up by the end of 2023. Participants will receive three vaccinations administered two weeks apart and will be closely monitored for both side effects and immune response.

The vaccine is designed to work by targeting a lactation protein called alpha lactalbumin (α-lactalbumin). This protein is no longer found after lactation in normal, aging breast tissues, but is present in most triple-negative breast cancers. The vaccine is designed to prompt an immune response that attacks the tumor and keep it from growing if breast cancer develops. 

It is based on pre-clinical research led by the late Vincent Tuohy, who led breast cancer research at Cleveland Clinic’s Lerner Research Institute. It was his research with mice that showed that activating the immune system against α-lactalbumin was safe and effective in preventing breast tumors.

[Related: Personalized vaccines could help the immune system fight cancer.]

This study is funded by the United States Department of Defense and will be conducted at Cleveland Clinic’s main campus in Cleveland, Ohio. The phase 1b clinical trial is conducted in partnership with Anixa Biosciences, Inc. and follows the ongoing phase 1a study. The earlier phase began in 2021 and includes patients who completed treatment for early-stage, triple-negative breast cancer within the past three years and do not have tumors, but are at high risk of recurrence. The phase 1a study is also expected to be complete in the fourth quarter of 2023.

“Triple-negative breast cancer is the form of the disease for which we have the least effective treatments,” said G. Thomas Budd from the Cleveland Clinic’s Taussig Cancer Institute and principal investigator of the study, in a press release. “Long term, we are hoping that this can be a true preventive vaccine that would be administered to cancer-free individuals to prevent them from developing this highly aggressive disease.”

The first therapeutic cancer vaccine (Provenge) was approved by the Food and Drug Administration (FDA) in 2010, ushering in a new era of cancer treatment. Therapeutic vaccines work by using a patient’s own immune system to fight the disease and are preventative vaccines like those used for cervical cancer, measles, or hepatitis. 

The post A vaccine trial targeting the most lethal breast cancer just took its next step appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

On February 7, President Joe Biden gave his 2023 State of the Union Address to a joint session of a newly split Congress, with Democrats controlling the Senate and Republicans controlling the House. This is what he had to say on major science, tech, and health related issues. 

Health policy priorities—COVID and healthcare

Biden touted the progress made to combat COVID-19 since he first took office in January 2021, when the COVID-19 vaccine rollout was just getting underway since beginning in December 2020. “COVID no longer controls our lives,” he said, “while the virus is not gone, thanks to the resilience of the American people, and the ingenuity of medicine, we have broken COVID’s grip on us.” 

The administration stands to end the public health emergency on May 11. The change to formally end the national emergency declarations would restructure the federal government’s response to treating the virus as an endemic threat to public health that can be managed through normal authorities.

[Related: Biden will end COVID-19 national emergencies in May. Here’s what that means.]

He also pointed to several policies Congress can still achieve to deliver cheaper prescription drugs to the American people—for example continuing to expand Medicaid under the Affordable Care Act, and capping the cost of insulin at $35 for seniors on Medicare.

“But there are millions of other Americans who are not on Medicare, including 200,000 young people with Type I diabetes who need insulin to save their lives,” said Biden. “Let’s finish the job this time. Let’s cap the cost of insulin at $35 a month for every American who needs it.”

This was the first State of the Union after the Supreme Court overturned Roe v. Wade, and President Biden vowed to veto any national abortion ban. The Biden administration has taken steps to expand abortion access in the wake of the decision, including steps to make it easier to access the prescription pills used in a medication abortion. 

He touted the success of the PEPFAR program that has saved 25 million lives and transformed  the global fight against HIV/AIDS and the Cancer Moonshot program that Biden led while Vice President to Barack Obama. The program is a very personal initiative to the Bidens after their son Beau died of a brain tumor in 2015. 

“Our goal is to cut the cancer death rate by at least 50 percent over the next 25 years. Turn more cancers from death sentences into treatable diseases. And provide more support for patients and families,” said Biden.

When it comes to tech, CHIPS takes the spotlight

American ingenuity in tech was also on full display, with Biden highlighting the bipartisan Infrastructure Law and CHIPS and Science Act, especially when it comes to the jobs that will be created by investing in infrastructure and tech. The legislation devotes more than $50 billion intended to spur semiconductor manufacturing, research, development, and more in the United States.

[Related: Can the Chips and Science Act help the US avoid more shortages?]

“Semiconductors, the small computer chips the size of your fingertip that power everything from cellphones to automobiles, and so much more. These chips were invented right here in America. Let’s get that straight, they were invented in America,” said Biden. “America used to make nearly 40 percent of the world’s chips. But in the last few decades, we lost our edge and we’re down to producing only 10 percent.”

He also announced a new standard that will require all construction materials used in federal infrastructure projects to be made in America and stressed his administration’s commitment to providing Americans with universal access to high-speed internet. 

Climate and the environment—wins and losses

The Biden Administration’s recent flurry of environmental legislation amidst the past year’s spike in gas prices shifted the spotlight on his policies on climate change.  

“The Inflation Reduction Act is also the most significant investment ever to tackle the climate crisis. Lowering utility bills, creating American jobs, and leading the world to a clean energy future,” said Biden, before touting the investments aimed at modernizing infrastructure in the face of a changing planet from electric grids to floods and water systems and clear energy.

[Related: 4 ways the Inflation Reduction Act invests in healthier forests and greener cities.]

He also called the $200 billion in profits brought in by oil and gas companies during a global energy crisis “outrageous,” and proposed quadrupling the tax on corporate stock buybacks to encourage more investment in increasing domestic energy production and keeping costs down.    

High profile attendees included wildfire experts and cancer survivors

U2 frontman Bono, Tyre Nicols’ family, and Paul Pelosi were among the high profile guests for the 535 members of Congress. Several were innovators, activists, and scientists making a mark on the science and tech world. 

These included Jennifer Gray Thompson, the CEO of After the Fire USA,  Paul Bruchez, a rancher who has worked with other landowners to restore a part of the threatened Colorado River, Grover Fugate, the Executive Director of the Rhode Island Coastal Resources Management Council (CRMC), and  David Anderson, President and CEO of NY-CREATES and the Albany Nanotech Complex. 

Some of the guests invited to the First Lady’s Box included Maurice and Kandice Barron whose daughter Ava is a survivor of a rare form of pediatric cancer, Amanda Zurawski, a woman from Texas who almost lost her life to a miscarriage due to Texas’ abortion law, and Lynette Bonar, an enrolled member of Navajo Nation who helped open the first cancer center opened on a Native American reservation.

The post In the latest State of the Union, Biden highlights infrastructure, chips, and healthcare appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This article was originally featured on The Conversation.

Cell migration, or how cells move in the body, is essential to both normal body function and disease progression. Cell movement is what allows body parts to grow in the right place during early development, wounds to heal and tumors to become metastatic.

Over the last century, how researchers understood cell migration was limited to the effects of biochemical signals, or chemotaxis, that direct a cell to move from one place to another. For example, a type of immune cell called a neutrophil migrates toward areas in the body that have a higher concentration of a protein called IL-8, which increases during infection.

In the past two or three decades, however, scientists have started to recognize the importance of the mechanical, or physical, factors that play a role in cell migration. For example, human mammary epithelial cells – the cells lining the milk ducts in the breast – migrate toward areas of increasing stiffness when placed on a surface with a stiffness gradient.

And now, instead of focusing on just the effect of the “solid” environment of cells, researchers are turning toward their “fluid” environment. As a theoretician trained in applied mathematics, I use mathematical models to understand the physics behind cell biology. My colleagues Sean X. Sun and Konstantinos Konstantopoulos and I were among the pioneering scientists who discovered how water and hydraulic pressure influence cell migration through theoretical models and lab experiments. In our recently published research, we found that human breast cancer cell migration is enhanced by the flow and viscosity of the fluids surrounding them, clarifying one of the factors influencing how tumors metastasize.

How fluids affect cell migration

Cells in the human body are constantly exposed to fluids of different physical properties. Water is one such fluid that can direct cell migration. For example, we found that how water flows across the membranes of breast cancer cells influences how they move and metastasize. This is because the amount of water traveling in and out of a cell causes it to shrink or swell, inducing movement by translocating different parts of the cell.

The viscosity, or thickness, of body fluids varies from organ to organ, and from health to disease, and this can also affect cell migration. For example, the fluid between cancer cells in tumors is more viscous than the fluid between normal cells in healthy tissues. When we compared how quickly breast cancer cells move in confined channels filled with fluid of normal viscosity versus fluid of high viscosity, we found that cells in high viscosity channels counterintuitively sped up by a significant 40%. This discovery was unexpected because the fundamental laws of physics tell us that inert particles should slow down in high viscosity fluids due to increased resistance.

We wanted to figure out the mechanism behind this surprising result. So we identified what molecules were involved in this process, discovering a cascade of events that allow high viscosity environments to enhance cell motility.

We found that high viscosity fluids first promote the growth of protein filaments called actin, which open channels in the cell’s membrane and increase water intake. The cell expands from the water, activating another channel that takes in calcium ions. These calcium ions activate another type of protein filament called myosin that induces the cell to move. This cascade of events induces cells to change their structure and generate more force to overcome the resistance imposed by high viscosity fluid, meaning the cells aren’t inert at all.

We also discovered that cells retained “memory” after exposure to a high viscosity medium. This meant that if we put cells in a high viscosity medium for several days and then returned them to a normal viscosity medium, they would still move at a faster speed. How cells retain this memory is still an open question.

We then wondered whether our findings on viscous memory would remain true in animals, not just in Petri dishes. So we exposed human breast cancer cells to a high viscosity medium for six days, then placed them in a normal viscosity medium. We then injected the cells into chicken embryos and mice.

Our results were consistent: Cells pre-exposed to a high viscosity medium had an increased ability to leak into surrounding tissues and metastasize compared to cells that were not pre-exposed. This result demonstrates that the viscosity of the fluids in a cell’s surrounding environment is a mechanobiological cue that promotes cancer cells to metastasize.

Implications for cancer treatment

Cancer patients usually don’t die from the original source of the tumor, but from its spread to other parts of the body.

When cancer cells travel through the body, they move into spaces that will have varying fluid viscosity. Understanding how fluid viscosity affects the movement of tumor cells could help researchers figure out ways to better treat and detect cancer before it metastasizes.

The next step is to build imaging and analysis techniques to precisely examine how cells from various types of lab animals respond to changes in fluid viscosity. Identifying the molecules that regulate how cells respond to changes in viscosity could help researchers identify potential drug targets to reduce the spread of cancer.

Yizeng Li is an Assistant Professor of Biomedical Engineering at Binghamton University. Li receives funding from National Science Foundation.

The post A look at how cancer cells move and metastatize could help doctors stop them from spreading appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

It’s not a secret that diets high in sodium come with huge health risks, including high blood pressure, increased risk of stroke, heart disease, stomach cancer, and chronic kidney disease. The American Heart Association estimates that processed, packaged, and restaurant meals make up 75 percent of daily sodium intake in the United States.

In an effort to combat this, World Health Organization (WHO) recommends reducing the population-wide average sodium intake by 30 percent by 2025 in order to combat negative health outcomes. This limits total daily sodium intake to about per person to about 2,000 milligrams a day per person, compared to the estimated 3,400 mg of sodium consumed by the average American every day. The WHO also released guidance for sodium levels in food categories that are the biggest contributors to sodium intake such as processed meats, bread, and sauces in 2021.

[Related: Ancient poop proves that humans have always loved beer and cheese.]

Now, a study published January 10 in the journal Hypertension offers even more evidence of the positive health outcomes that sodium reduction could have. The paper details a voluntary effort by the Australian government to reformulate 27 packaged food categories across the continent. It found that removing some of the sodium from packaged foods could save about 1,700 lives per year and prevent nearly 7,000 annual diagnoses of heart disease, kidney disease, and stomach cancer in Australia.

“We had previously modeled the potential impact of the Australian program,” said the study’s co-lead author Kathy Trieu, lead author of the study and a research fellow in food policy at The George Institute for Global Health, and a lecturer at the University of New South Wales, in a statement. “In this study, we wanted to estimate the potential number of additional premature deaths, new cases of disease and years lived with disability that may be averted with the WHO sodium benchmarks, which are above and beyond the Australian government’s sodium reformulation targets.”

[Related: What happens if you eat too much salt?]

The team applied the same statistical model used in their previous study to estimate the potential impact of extending the Australian plan to include all of the 58 packaged food categories in the WHO’s benchmarks. They used national data from 2011 to 2012 on the amount of sodium in the food, how much was eaten nationwide, and sales data. Next, the team used published statistics about the relationship between sodium intake and high blood pressure, to calculate the potential effects of sodium reduction on rates of cardiovascular disease and chronic kidney disease. High blood pressure is a major risk factor for both conditions.

“Our findings indicate that compliance with WHO benchmarks compared with Australia’s current sodium targets may result in substantial health gains and prevent more than three times as many deaths and new cases of disease each year,” said Trieu. Trieu added that including more packaged food products and stricter sodium targets may have had a greater impact.

The team says that some of the limitations of this study include needing more recent data and that estimates of disease burden may be less accurate than estimates of more easily measured outcomes such as death.

According to the CDC, some ways to reduce sodium intake include buying fresh, frozen, or canned vegetables with no salt or sauce added, comparing the amount of sodium in different products by reading Nutrition Facts labels, and limiting sauces, mixes, and instant product.

The post Reducing sodium in packaged foods could reduce disease and save lives appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Since 2013, medical professionals have increasingly turned to a device called the iKnife for finding potential breast and brain cancers. The iKnife, an electric toothbrush-sized instrument that works by ingeniously combining electrosurgery alongside mass spectrometry. First developed by researchers at Imperial College London, the iKnife uses tiny electrical pulses to vaporize tissues, while a spectrometer array analyzes the ensuing smoke to detect potentially cancerous cells. The “smart” surgical tool has often shortened biopsy wait times while also allaying some of patients’ stress in the ensuing decade—and recently, Imperial College London’s iKnife team announced its capabilities are expanding.

[Related: More Americans are surviving cancer now than ever.]

As first reported by The Guardian, the iKnife’s technology shows promise in identifying patients’ endometrial cancers with an almost 90 percent accuracy rate. “The iKnife reliably diagnosed endometrial cancer in seconds, with a diagnostic accuracy of 89 percent, minimizing the current delays for [patients] whilst awaiting a histopathological diagnosis,” the team wrote in a paper published in the research journal, Cancers, adding that the innovation could “pave the way for new diagnostic pathways.”

Abnormal or irregular bleeding often occurs for postmenopausal people because of often benign reasons such as noncancerous polyps or a result of hormone replacement therapy. That said, postmenopausal bleeding is considered to be one of endometrial cancers’ major early indicators, and experts suggest patients always schedule medical examinations if bleeding begins. The iKnife’s potential new ability to near-instantly assess problematic tissue could drastically alleviate the stress that comes during these previously lengthy, sometimes weeks’ long wait periods, says Imperial College London’s research team.

[Related: Why doctors almost never say cancer is ‘cured.’]

Research lead, Sadaf Ghaem-Maghami, explained to The Guardian that with a positive predictive value of 94 percent, the iKnife could soon “immediately reassure” someone of an extremely low likelihood of cancer, while also expediting additional testing and treatment for those with potentially positive biopsies.

The researchers’ initial testing compared iKnife’s results with traditional diagnostic methods for 150 people’s biopsy tissue samples. Following a future major clinical trial, the iKnife’s newest capability could become yet another widespread feature for the smart device.

The post This surgical smart knife can detect endometrial cancer cells in seconds appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This story originally featured on ProPublica.

ProPublica is a nonprofit newsroom that investigates abuses of power. Sign up to receive our biggest stories as soon as they’re published. Also: Have you worked with hazardous chemicals? Our reporters want to hear from you.

Henry Saenz remembers when he first learned what even the tiniest bit of asbestos could do to his body. He was working at a chemical plant where employees used the mineral to make chlorine, and his coworkers warned him about what could happen each time he took a breath: Tiny fibers, invisible to the eye, could enter his nose and mouth and settle into his lungs, his abdomen, the lining of his heart. They could linger there for decades. Then, one day, he might develop asbestosis, a chronic disease that makes the lungs harden, or mesothelioma, a vicious cancer that ends the lives of most who have it within a few years.

By then, in the early 1990s, the dangers of asbestos were already irrefutable. The United States had prohibited its use in pipe insulation and branded it so risky that remediators had to wear hazmat suits to remove it. But unlike dozens of other countries that banned the potent carcinogen outright, the United States never did. To this day, the U.S. allows hundreds of tons of asbestos to flow in each year from Brazil, primarily for the benefit of two major chemical companies, OxyChem and Olin Corp. The companies say asbestos is integral to chlorine production at several aging plants and have made a compelling argument to keep it legal: Unlike in the horrific tales of the past, their current protocols for handling asbestos are so stringent that workers face little threat of exposure.

But at OxyChem’s plant in Niagara Falls, New York, where Saenz worked for nearly three decades, the reality was far different, more than a dozen former workers told ProPublica. There, they said, asbestos dust hung in the air, collected on the beams and light fixtures and built up until it was inches thick. Workers tramped in and out of it all day, often without protective suits or masks, and carried it around on their coveralls and boots. They implored the plant’s managers to address the conditions, they said, but the dangers remained until the plant closed in late 2021 for unrelated reasons.

It was hard for Saenz to reconcile the science that he understood—and that he believed OxyChem and government leaders understood—with what he saw at the plant every day. He did his best not to inhale the asbestos, but after a short time, he came to believe there was no way the killer substance was not already inside him, waiting, perhaps 30 or 40 or even 50 years, to strike.

Now, too late for Saenz, the Environmental Protection Agency appears poised to finally outlaw asbestos in a test case with huge implications. If the agency fails to ban a substance so widely established as harmful, scientists and public health experts argue, it would raise serious doubts about the EPA’s ability to protect the public from any toxic chemicals.

To fight the proposed ban, the chemical companies have returned to a well-worn strategy and marshaled political heavyweights, including the attorneys general of 12 Republican-led states who say it would place a “heavy and unreasonable burden” on industry.

Lost in the battle is the story of what happened in the decades during which the U.S. failed to act. It’s not just a tale of workers in hardscrabble company towns who were sacrificed to the bottom line of industry, but one of federal agencies cowed again and again by the well-financed lawyers and lobbyists of the companies they are supposed to oversee.

It’s the quintessential story of American chemical regulation.

For decades, the EPA and Congress accepted the chlorine companies’ argument that asbestos workers were safe enough, and regulators left the carcinogen on the list of dangerous chemicals that other countries ban but the U.S. still allows. The Occupational Safety and Health Administration even let OxyChem and Olin into a special program that limited the frequency of inspections at many of their plants. Along the way, the two companies proved that they didn’t need asbestos to make chlorine: They built some modern facilities elsewhere that didn’t use it. But they balked at the cost of upgrading the older facilities where it was still in use—even as they earned billions of dollars from chemical sales and raked in record profits this year.

OxyChem, owned by one of the country’s largest energy companies, Occidental Petroleum, declined requests for an interview. After ProPublica sent a summary of its reporting, company officials said the accounts from the Niagara Falls plant were “inaccurate” but declined to say what specifically was incorrect. In a statement, the company said it complies with federal regulations on asbestos and that workers who handle it are “trained, work in restricted areas of our plant, protected by personal protective equipment and are offered annual medical examinations.” The company also said it authorizes employees to stop work if they feel unsafe. “The health and safety of every plant worker and the people in our surrounding communities is our top priority,” the company said.

Olin did not respond to calls and emails sent over the course of a month.

It has been easy to minimize the toll asbestos takes on workers. Workers’ compensation cases are often confidential, and employees may fear speaking out and jeopardizing their livelihood. ProPublica reporters, however, found a unique opportunity to explore what it was really like to work at an asbestos-reliant plant after America’s longest-standing facility, the one run by OxyChem in Niagara Falls, shuttered last November. With their jobs no longer on the line, Saenz and 17 other former workers, some with institutional knowledge dating back to the 1960s and others with memories less than a year old, said they felt free to talk. They agreed to hours of interviews and dug through their homes for documentation to reconstruct their work lives in the decades they spent at the plant.

What they recounted—ever-present asbestos dust with scant protection—stunned six experts in industrial hygiene and occupational health who were consulted by ProPublica.

“Totally unacceptable,” said Rachael Jones, professor and chair of the Environmental Health Sciences Department at the University of California, Los Angeles.

“Fraught with danger,” said Dr. Philip Landrigan, a public health physician trained in occupational medicine and epidemiology who leads Boston College’s program for Global Public Health and the Common Good.

“It sounds like something that maybe would happen in the 1940s or the 1950s,” said Celeste Monforton, a lecturer in public health at Texas State University who studies occupational health and safety practices.

“It’s just so counter to everything that they put in the record about using [asbestos] safely,” Monforton said.

For more than a century, OxyChem’s plant on the Niagara River, just 3 miles upstream from the world-renowned falls, was a small city unto itself. It buzzed with workers day and night, and, in its heyday, had its own cafeteria, credit union and health clinic. A job there carried a certain cachet. Workers could make six figures, even without college degrees. But the plant had a dark legacy. Its previous owner, Hooker Chemical, had buried toxic waste in an unfinished aqueduct called Love Canal, then turned the property over to the city for development in the 1950s. After contaminated groundwater sickened the people who lived there, it became known as one of the worst environmental disasters in U.S. history.

Unlike many of the other workers who grew up in the shadow of the plant, following their fathers and uncles into jobs there, Saenz was originally from Northern California. But he fell in love with a woman from Niagara Falls and moved there to start a family with her, working at a hotel, delivering flowers and tending bar—anything to put food on the table, he said—before deciding OxyChem was the job he wanted to stay in.

He was hired in 1989 and soon after got a crash course in chemistry. A jolt of electricity, he learned, could turn a tank of salt water into three substances: chlorine, caustic soda and hydrogen. The chlorine could be sold for disinfecting water, the caustic soda for making paper, soap and aspirin. There was, however, a real danger: If the chemicals mixed, the tank could turn into a bomb. So each tank had a thick, metal screen inside to keep the chemicals apart.

The screen was coated with a layer of impenetrable asbestos. OxyChem used chrysotile, or white asbestos, the most common type. It showed up on trains in oversized bags that looked like pillows stuffed with down feathers. At OxyChem, there were about 200 tanks, called cells, each the size of a dining room table and containing a metal screen. When a screen needed to be recoated, a special team of workers removed it and brought it to the cavernous cell-maintenance building. There, they blasted it with a high-pressure water cannon until the old asbestos fell off. Then, they dipped the clean screen into a wet mixture containing new asbestos and cooked it in an oven until the asbestos hardened. They worked on one or two screens each day.

The asbestos job was one of the most hazardous at the plant, requiring special training. But it also provided a rare benefit. Unlike most positions, which forced workers to take afternoon and midnight shifts, the asbestos job was days only. Saenz, who initially worked in a different department, waited years for an opening on the team, eager to spend more time with his growing family. After his fourth child was born, a spot opened up.

The team was a small fraternity of eight or so men who ate lunch together in a special trailer. Some days, when their shift ended at 2 p.m., they would meet at JD’s, a dive bar near the plant. Other days, it was the wing joint down the street or the bar in Terry Cheetham’s basement. Cheetham was the big brother of the group; the guys called him Soupie. Reserved and shaggy-haired, garrulous only with a beer in hand, he’d dropped out of high school after his father’s death and gone to work for OxyChem. He wanted to help his mom support their family. Soon after Saenz joined the team, Cheetham tapped him on the shoulder. “We’re going for a ride after work,” he said. Later, they pulled up outside the local liquor store. As the new guy, Saenz had to carry the keg.

The guys raised their kids together, helped each other’s families through difficult times. At the plant, they always had each other’s backs. Certain hazards, like fires, were hard to miss. Others, like chlorine leaks, were more subtle. Then, there was the asbestos. As Saenz spent more time on the job, he began noticing just how much of it surrounded him.

Federal workplace safety standards require keeping asbestos fibers wet to prevent them from going airborne, having workers wear protective equipment and containing the asbestos inside certain areas. OxyChem had rules in place to meet those standards. But protocols failed to match reality at the Niagara Falls plant, according to more than a dozen workers.

Water-blasting the screens was like washing a car with a high-powered hose. Asbestos splattered everywhere. It wasn’t a problem when the asbestos was wet. But it would dry overnight, and the next morning, it would be stuck to the ceiling and the walls. Clumps would roll across the floor like tiny tumbleweeds. Floating particles would catch the light when the sun poured in. There was so much asbestos in the cell-maintenance building that it was impossible to keep it all wet, said Robert Cheff, who worked at the plant from 1981 to 2007. “We were constantly swimming in this stuff.”

Workers wore protective gear for certain tasks, like pressure washing and screen dipping. But they went into the building to carry out other tasks without special suits or anything protecting their faces, despite company requirements. One worker said managers enforced those rules. But a dozen others interviewed by ProPublica recalled that the bosses looked the other way. Suiting up was impractical, those workers said. It took time away from the tasks that needed to get done and was uncomfortable, especially on hot days, when the temperature inside could reach 100 degrees.

In the summer, the windows and doors were left open to keep the workers from overheating, allowing asbestos to escape outside. Wet asbestos splashed on their uniforms, coats, helmets and boots. One guy seemed to always have some on his mustache. It would dry and flake off their clothes wherever they went, they said. Saenz remembered walking into safety meetings in the administrative building with asbestos drying on his coveralls. The guys carried so much asbestos into the trailer where they ate lunch and took breaks that it needed to be replaced, former union leaders said.

Their uniforms sat in the laundry, caked with dry asbestos. When the union raised the problem in 2010, managers responded by giving the team its own hamper with a lid to contain the asbestos, said longtime union officer Mike Spacone. Only after union leaders threatened to call federal authorities did the company give the team its own laundry facilities, Spacone said.

On occasion, workers who handled asbestos would leave without showering in the plant’s locker room or wear their work clothes home. “My kids played sports,” recalled Dave Helbig, an employee from 1980 through 2021. “Sometimes I had to leave to get to their games.”

The company would have known employees were being exposed; workers with a high risk of exposure sometimes clipped a small monitor to their bodies to measure the amount of asbestos in the air around them. At least five times in 2001 and 2002, the levels around team member Patrick Nowak exceeded OSHA’s exposure limit, his company records show. “I failed so many times, they quit testing me,” he said. The records do not indicate if Nowak was wearing a protective mask known as a respirator, as some other employees’ records do.

Tony Garfalo wore a monitor seven times in 2001, and, on four occasions, the results exceeded OSHA’s limit, his records show. Once, the asbestos level was more than five times the allowable limit. The records say he was wearing a half-face respirator. Garfalo said his bosses promised to address the situation, but “nothing changed.”

He and the others knew all too well the damage asbestos could cause. Garfalo said his father, who worked the asbestos job at the plant, developed asbestosis. Employees in other departments got sick from a type of asbestos-containing pipe covering that once insulated the plant, longtime employees said and court records show. Cheff said his uncle died from asbestosis at 59. A millwright named Teddy Skiba was diagnosed with mesothelioma and later died.

In addition to those signature diseases, which are rare even among asbestos workers, the tiny strands can harm the body in other ways. They can put people at increased risk of heart disease by scarring the lungs, forcing the heart to work harder to pump blood through them to pick up oxygen. Some scientific evidence suggests an association between asbestos exposure and stroke. And battling all kinds of illnesses with damaged lungs can weaken the body’s ability to fight them; that damage can mean the difference between life and death.

One retired member of the team, Umberto Bernardone, died from an aneurysm in 2004 at age 77. He had long had trouble breathing, said his son, Mario, who also worked at the plant. X-rays showed that asbestosis had scarred his lungs. “The asbestos was with him all the time,” Mario said.

Not long after, another retired team member, Salvatore “Buddy” Vilardo, died from a blood clot, his son said. He was 62.

Cheetham, the group’s big brother, had just retired when he fell ill in 2004. A doctor in Buffalo said it was cancer. Cheetham told his daughter Keri that he was certain the asbestos was responsible and asked her to consult a lawyer after he died. When the guys found out he was sick, they showed up at his house. They found their friend in a bed in his living room, under the care of a hospice nurse, struggling to breathe.

Cheetham died five months before his 56th birthday. His autopsy surprised his family—it wasn’t asbestos after all; an aggressive form of skin cancer had killed him. His former co-workers weren’t told about the autopsy. For years, they believed his cancer had been brought on by asbestos exposure. The memory of Cheetham’s last gasps haunted the guys like a ghost, a harbinger of what their own futures might hold.

Elsewhere in the world, governments were taking action to protect their people. Saudi Arabia banned asbestos in 1998, Chile and Argentina did so in 2001, Australia in 2003. By 2005, asbestos was outlawed across the European Union. “It was a no-brainer,” said Tatiana Santos, head of chemical policy at the European Environmental Bureau, a network of environmental citizens’ groups.

America’s EPA could have banned asbestos. Congress could have banned it. But over and over, they crumpled in the face of pressure from OxyChem and its peers in the chlorine industry.

The EPA tried to enact a ban in the late 1980s, but the companies got ahead of it. Records from the time show corporations testified that removing asbestos from chlorine plants would not yield significant health benefits because workers were only minimally exposed; they also argued it would require “scrapping large amounts of capital equipment” and thus would “not be economically feasible.”

Under federal law at the time, the EPA was obligated to regulate asbestos in the way that was “least burdensome” to industry. That forced the EPA to make a cold calculation: Banning asbestos in chlorine plants would prevent “relatively few cancer cases” but increase the companies’ costs. So when the agency enacted an asbestos ban in 1989, it carved out an exemption for the mineral’s use in the chlorine industry.

The EPA made it clear that the companies should begin using alternatives to asbestos screens; in fact, according to company records made public through litigation and published as part of Columbia University and the City University of New York’s Toxic Docs project, OxyChem had already developed screens that didn’t need an asbestos coating. Still, the companies celebrated their immunity from regulation.

“WE HAVE A WIN,” a lobbyist declared in an internal communication included in the Toxic Docs project.

In the end, asbestos was never banned. The asbestos industry challenged the ban in court, and in 1991, a panel of federal judges deemed the rule too onerous and overturned it. The decision was a stinging blow to the EPA, several current and former employees told ProPublica. “I still remember the shock on the managers’ faces,” said Greg Schweer, an EPA veteran who ran its new-chemicals management branch before he retired in 2020. The office “was full of energized people wanting to make their mark. But things changed after that.” The agency shelved efforts to regulate other dangerous substances and wouldn’t attempt a similar chemical ban for 28 years.

Most industries stopped using asbestos anyway, a phenomenon experts largely attribute to a wave of lawsuits from people with asbestos-related diseases. But the chlorine industry kept using its asbestos screens. It continued importing hundreds of tons of the substance every year, more than the weight of the Statue of Liberty.

In 2002, Sen. Patty Murray a Democrat from Washington, tried to get a ban through Congress. She tried again in 2003 and again in 2007. That year, with Democrats in control of the Senate and House, her effort found some traction. OxyChem was keenly aware how much an asbestos ban would hurt its bottom line. Chlorine and caustic soda were the focus of its chemical operation, financial statements show, driving more than $4 billion in annual sales. Most of OxyChem’s plants still used asbestos; if they had to close, production would tumble.

Occidental Petroleum, OxyChem’s owner, was a force on Capitol Hill, with lobbyists that spent millions influencing policy and a political action committee that pumped hundreds of thousands of dollars into campaigns each election cycle. OxyChem was also a member of the American Chemistry Council, an influential trade organization that made campaign contributions of its own.

The industry had an ally in then-Sen. David Vitter of Louisiana; at the time, at least a quarter of the 16 asbestos-dependent plants in the country were located in the Republican senator’s home state, records show. At a hearing in June 2007, Vitter echoed the chlorine industry’s standby talking point, that its manufacturing process involved “minimal to no release of asbestos and absolutely no worker exposure.”

“Now, if this were harming people or potentially killing people, that would be the end of the argument, we should outlaw it,” he added. “But there is no known case of asbestos-related disease from the chlor-alkali industry using this technology.”

Then-Sen. Barbara Boxer, a California Democrat in favor of the ban, pushed back, saying the chlorine manufacturing process was “not as clean as one would think.” But to build support for the bill, proponents ultimately agreed to exclude products that might contain trace levels of asbestos, such as crushed stone, as well as the asbestos used in the chlorine industry.

The bill passed out of the Senate on a unanimous vote. But many of the public health advocates who championed the initial measure opposed the watered-down version, saying it had been practically gutted, and it failed to find support in the House. Vitter, who later went on to lobby for the American Chemistry Council, did not respond to requests for an interview.

In the 15 years that followed, congressional attempts to ban asbestos would continue to fall short.

Yet another federal entity had the power to protect the OxyChem workers. There was once a time when OSHA inspectors visited the Niagara Falls plant about every year. That ended in 1996, when the plant won coveted admission into an OSHA program that exempted it from such scrutiny.

The Star Program, created during the Reagan administration as part of OSHA’s Voluntary Protection Programs, allows plants that can prove they are model facilities to avoid random inspections. The theory behind the program is that motivating companies to adhere to best practices on their own is more effective than having underfunded government inspectors punish them.

At the Niagara Falls plant, former union leaders believed the program would protect jobs and make the facility safer, they told ProPublica. They worked with management on the application—a monthslong process that entailed updating the plant’s safety practices and submitting to a rigorous inspection. But what actually changed, the union leaders said, was that OSHA inspectors came far less frequently and announced their visits well in advance. When OSHA came to re-evaluate the plant, usually every three to five years, management spent months preparing, said Spacone, the union officer. “They would clean the hell out of the place. Everything would be spotless.” Work in certain areas came to a halt. Plant representatives tried to limit what the evaluators saw.

Even still, in 2011, evaluators found asbestos “scattered in certain areas of the floor” and covering much of the mechanical equipment, records show. “This contamination can spread easily when dry,” they wrote in a report. “Appropriate clean up procedures must be instituted to prevent airborne asbestos.” The evaluators did not give the plant an official citation. In the end, they applauded the plant’s “commitment to safety and health” and recommended it for continued participation in the program.

Three years later, evaluators identified another issue related to hygiene: Although the plant tested the air for hazards like asbestos, it wasn’t using the data to spot problems. What’s more, the person in charge of the program wasn’t properly trained. OSHA let the plant remain in the program on the condition that it fixed the problems within a year. The plant updated its software and the department leader took a 56-hour course, records show.

Apart from the re-evaluation visits, OSHA made just two other trips to the plant between 1996 and 2021, records show. Only one included a full inspection. On that visit, inspectors cited the plant for failing to protect workers from falls. The other visit did not result in any citations.

With OSHA largely out of the picture, the plant’s managers became more lax about safety, Spacone said. “I started thinking [that joining the Star Program] was a mistake,” he said. Debbie Berkowitz, a former chief of staff and senior policy adviser at OSHA during the Obama administration, said that, in her experience, it was possible for plants to stay in the program long after their commitment to safety had lapsed. “Once they’re in, they’re in,” she said. “In most cases, it is a total ruse.”

OSHA declined to make an official available for an on-the-record interview or comment on ProPublica’s findings at the Niagara Falls plant. A Department of Labor spokesperson said that plants can be terminated from the program and that unions can withdraw their support.

In the absence of government intervention, union leaders tried to tackle the asbestos problem themselves, four former union presidents told ProPublica. The union repeatedly asked management to expand the asbestos team and have certain people dedicated to cleaning. Plant leaders refused, they said. “It was a never-ending battle,” said Vincent Ferlito, one of the former presidents. “It always came back to the same thing: money.”

Fed up with the mess, Garfalo grabbed a roll of red caution tape one day in 2007 and wrapped it around the asbestos-soiled building where his team worked, to the amazement of his colleagues. He barricaded each doorway, then hung as many danger signs as he could find. The protest prompted his managers to hire professionals for a one-time clean, but they also warned him to never do it again, he said.

By 2011, a year after he’d retired, Garfalo couldn’t ignore a lingering cough that would occasionally startle him out of sleep. His doctor couldn’t tell whether his breathing difficulties were caused by asbestos or his smoking habit, but said that smokers who are exposed to the substance have an even higher risk of serious illness. Garfalo’s mind traveled back to a day, a dozen years earlier, when he climbed atop the cell-maintenance building to fix a fan, only to discover that the entire roof was coated in asbestos. Train cars parked beside the building were covered, too. He thought about the homes less than a half-mile away and wondered how far the fibers had traveled.

In August 2021, OxyChem announced it was closing the Niagara Falls plant, blaming “unfavorable regional market conditions” and rising rail costs in New York state. Over time, its workforce had dwindled from more than 1,300 to about 150. OxyChem’s chlorine operation was now mostly in Gulf Coast states with lower taxes and less regulation.

And a law that had once protected it from “burdensome” environmental rules had changed.

In 2016, Congress had updated the Toxic Substances Control Act, removing the requirement that the EPA choose regulations that burdened industry as little as possible. Though the change gave the agency another chance to ban asbestos, it wasn’t going to happen during the Trump administration; the former president once alleged that the movement against asbestos was “led by the mob” and had his face featured on the packaging of Russian-produced asbestos. Under the Biden administration, however, the EPA determined that all workers in asbestos-dependent chlorine plants faced an “unreasonable risk” of getting sick from it, citing a review of the companies’ own exposure-monitoring data. This April, EPA Administrator Michael Regan proposed a ban for the first time in more than three decades.

It could be eight months or more before the rule is finalized. Two trade associations, the American Chemistry Council and the Chlorine Institute, are imploring the EPA to reconsider. They are once again arguing that the companies use asbestos safely—and they’ve turned to industry-friendly scientists and consulting firms to accuse the EPA of overestimating the risk to workers.

When given a summary of ProPublica’s reporting on the Niagara Falls plant and asked to respond, Chlorine Institute Vice President Robyn Brooks said her organization had no knowledge of the situation and referred reporters to OxyChem. The American Chemistry Council pointed to the plant’s participation in the Star program as proof of its “record of performance.”

The industry groups have also made the case that a ban would jeopardize the country’s supply of chlorine and could even create a drinking water shortage. But the EPA and public health advocates contest those claims. They point out that only a small fraction of the chlorine produced by asbestos-dependent plants is used to clean drinking water and that OxyChem and Olin have voluntarily closed or reduced capacity at several of those plants in recent years without catastrophically disrupting the supply chain. In fact, OxyChem told investors in August that its plans to upgrade the asbestos-reliant technology at its largest chlorine facility next year would have “no impact on customers,” a transcript shows. For at least eight years, the company has been slowly upgrading some plants to a newer technology that uses a polymer membrane to separate the chemicals; it built a completely asbestos-free plant in 2014.

The U.S. Chamber of Commerce has come to the companies’ defense, saying asbestos is “tightly regulated” and “used safely every day” in the chlor-alkali industry. So have 12 Republican attorneys general, including Ken Paxton of Texas and Jeff Landry of Louisiana. In a letter, they questioned whether the EPA has the authority to pursue a ban, signaling a readiness to take the agency to court like the asbestos industry did in 1989. (The Chamber and most of the attorneys general declined to comment or did not respond to inquiries from ProPublica. A spokesperson for Nebraska Attorney General Doug Peterson called the situation at the Niagara Falls plant “very concerning” and said that it would be “completely misleading” to suggest that the letter implied approval of such circumstances.)

Industry leaders are confident they will prevail. “We’ve been engaged in this activity for quite a while and have pushed back on it,” Olin CEO Scott Sutton told shareholders on a July 29 earnings call. “I think you’re not likely to see a final rule come out that is as proposed.”

Michal Freedhoff, the EPA’s top chemical regulator, said she could not comment on what the final rule-making decision would be. But she said the agency was not backing down on the science and that ProPublica’s reporting underscores the need for decisive action.

Given the potential for litigation, lawmakers are renewing their effort to pass a law banning asbestos, which would be more difficult to challenge in court. “It is a brutal and painful fight,” said Linda Reinstein, a leading advocate who co-founded the Asbestos Disease Awareness Organization after her husband, Alan, died of mesothelioma in 2006. “We’re not going away.”

Hanging in the balance is the health of hundreds of workers at the eight remaining asbestos-dependent chlorine plants in Louisiana, Texas, Alabama and Kansas. ProPublica reached out to current and former employees at those facilities. At the OxyChem plant in Wichita, union president Keith Peacock said he was comfortable with the way asbestos was handled. “I don’t know of anyone who sees this as a health issue,” he said. “There are rules in place for it and everyone adheres to those safety guidelines.” But Chris Murphy, a former union president at Olin’s plant in Alabama, said the conditions there mirrored the ones described by the workers in Niagara Falls. He said he himself had seen asbestos caked on beams and cranes in recent years and been told to remove it with a putty knife. “There ain’t nothing to it,” he remembered his managers saying. “You’ll be all right. It ain’t that bad.” He wasn’t told to wear protective gear, he said, so he didn’t.

The former OxyChem workers who still live in Niagara Falls gather once a month to reminisce over Buffalo wings and beef piled high on salty kummelweck rolls. They can only wait and see if they develop symptoms as they enter the post-exposure time frame in which asbestos-related disease is commonly diagnosed.

Saenz left the plant with a bad back in 2016. Now a 64-year-old grandfather of two, he’s been having lung trouble and considering X-rays to see if there are signs of asbestos-related damage. “I’m wondering if I’m not headed down that road,” he said.

He sees the burden he now carries as a tradeoff for the lifestyle he was once afforded. “It was a great place to work. I was able to raise four children and buy a house and live the American dream.” He even gave his son Henry Jr. his blessing to start a job at OxyChem in 2013, so long as he stayed far away from asbestos. Saenz now wonders how much more time he has left with his family.

“It’s a nightmare,” he said. “It’s a price you pay, I guess.”

The post The US never banned asbestos. These workers are paying the price. appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

There’s a phrase that rings loudly in the heads of Popular Science editors any time we bring together a new Brilliant 10 class: “They’ve only just begun.” Our annual list of early-career scientists and engineers is as much a celebration of what our honorees have already accomplished as it is a forecast for what they’ll do next. To find the brightest innovators of today, we embarked on a nationwide search, vetting hundreds of researchers across a range of institutions and disciplines. The collective work of this year’s class sets the stage for a healthier, safer, more efficient, and more equitable future—one that’s already taking shape today. 

• Kandis Leslie Abdul-Aziz: Turning food waste into filters
• Sangeetha Reddy: Harnessing the power of immunotherapy for breast cancer
• Mohammad Hajiesmaili: Decarbonizing the internet
• Rachael Bay: Predicting how wildlife will adapt to climate change
• John Blazeck: Building an immune system from scratch
• Daniella Mendoza DellaGiustina: Spying our future in near-asteroid flybys
• Samitha Samaranayake: Making transit sustainable and equitable
• Chantell Evans: Finding the roots of neurodegenerative disease
• Aaron Streets: Mapping every human cell
• Daniel Larremore: Crunching the numbers to get ahead of outbreaks

Turning food waste into filters

After earning a bachelor’s in chemistry in 2007, Kandis Leslie Abdul-Aziz took a position at an oil refinery along the Schuykill River in South Philadelphia. Part of her job was to analyze refined petroleum products, like acetone and phenol, that other industrial manufacturers might buy. She was also tasked with testing the refinery’s wastewater—which, she couldn’t help but notice, flowed out right next to a residential neighborhood. “Literally, if you looked out past the plant,” she says, “you could see houses close by.”

That was more than a decade before an explosive fire forced the refinery to close and spurred an unprecedented cleanup effort. But the experience got Abdul-Aziz thinking about the life cycle of chemical byproducts and their potential impacts on human health. She went back to school for a PhD in chemistry, and her lab at the University of California, Riverside, now focuses on giving problematic waste streams—from plastic trash to greenhouse gases—a second life.

To start, Abdul-Aziz decided to investigate whether she could convert corn stover into something with economic value. The stalks, leaves, tassels, and husks left over from harvest add up to America’s most copious agricultural waste product. Much of it is left to rot on the ground, releasing methane and other greenhouse gases. A small percentage does get salvaged and converted into biofuels, but the payoff usually isn’t worth the effort.

Abdul-Aziz and her colleagues set out to test multiple processes for turning the refuse into activated carbon, the charcoal-like substance that’s used as a filter everywhere from smokestacks to your home Brita pitcher. Her analysis, published in 2021, looks at the activated carbon produced by various methods—from charring stover in an industrial furnace to dousing it in caustic substances—and the molecular properties that affect which contaminants it can soak up. The ultimate aim: Tell her what kind of chemicals you want to clean up, and she’ll create a carbon filter that can do the trick.

Abdul-Aziz has since applied to patent her customizable process, and is looking into other sources of detritus and use cases. Wastewater treatment companies have expressed interest, she says, in using her tools on environmental toxins such as PFAS—the stubborn, hormone-disrupting “forever chemicals” ubiquitous in household products and prone to contaminating drinking water. At the same time, she has also demonstrated that she can derive activated carbon from citrus peels, and is now investigating whether she can do the same with plastic trash.

She’s also exploring an even bigger swing. Earlier this year, the National Science Foundation awarded her half a million dollars to develop absorbent materials to capture carbon dioxide emissions and help convert them back into useful materials such as polymers and fuels. Abdul-Aziz wants to identify practical recycling processes that don’t require overhauling existing infrastructure. “For us it’s about trying to develop realistic solutions for these sustainability problems so they can actually be implemented,” she explains. It’s these small steps that she believes will move us toward a truly circular economy—one where materials can be reused many times. And with any luck, her innovations will help buffer the worst impacts of the very petrochemicals that inspired her quest.—Mara Grunbaum

Harnessing the power of immunotherapy for breast cancer

In recent decades, immunotherapy has been a game-changer in cancer treatment. Drugs that augment the body’s natural immune response against malignant tumors have dramatically improved survival rates for patients with diseases like lymphoma, lung cancer, and metastatic melanoma. But the method has been far less successful in breast cancers—particularly the most aggressive ones. Sangeetha Reddy, a physician-scientist at The University of Texas Southwestern Medical Center, is trying to change that. “We could do better,” she says.  

Reddy works with patients with triple-negative breast cancers, so-called because the malignancies don’t have any of the three markers scientists have historically targeted with anti-cancer drugs. Even with aggressive chemotherapy and surgery, the prognosis for these patients—who account for about 15 percent of breast cancer diagnoses worldwide—is relatively poor. Immunotherapies, in particular, often fail because breast cancers tend to hobble the body’s dendritic cells, the roving molecular spies that sweep up pieces of suspicious material and carry them back to immune system headquarters to introduce as the new enemy. When the body doesn’t know what it’s supposed to be attacking, boosting its power is of little use.

Reddy is therefore trying to figure out how to restore dendritic cell function. As a physician-scientist, she uses a relatively new approach that she describes as “bedside to bench and back.” She treats patients in her clinic, conducts in vitro and mouse experiments in her lab, and designs and manages her own clinical trials. This physician-scientist method enables a positive feedback loop: Reddy can analyze tumors excised from her own patients to assess whether treatments are working. Then she can test out new drugs on those same cancer cells. When she identifies a promising tactic, she can design clinical trials to test things like safety, dosage, and timing. At every step, she can find something in what she learns to incorporate back into her research or her patients’ care.

This cyclical strategy has led Reddy to the combination of three drugs that she’s currently testing against triple-negative breast cancer: Flt3-ligand, a protein that stimulates the proliferation of dendritic cells; a chemical that helps activate these cells and others; and anthracycline, a standard chemotherapy agent. In mice, this triad kept breast cancer tumors at least 50% smaller than chemotherapy alone. “A couple of our mice, we actually cured them,” says Reddy. A Phase-1 clinical trial investigating the safety and efficacy of the regimen in people began enrolling patients earlier this year.

Though it can take years to work out all the kinks in a new cancer treatment and clear the hurdles on the way to FDA approval, Reddy’s multi-pronged strategy should streamline this process as much as possible. Doing so will allow her to enable a transformation she’s been eyeing since she started to specialize in cancer treatment more than eight years ago. As a fellow at the MD Anderson Cancer Center, Reddy worked with melanoma patients in clinical trials of immunotherapy, which gave her a firsthand look at the treatment’s emerging potential. “We were taking patients who would have passed away within months and giving them ten years,” she says. “Just that hope that we can get there with [triple-negative breast cancer] led me to this path.”—M.G.

Decarbonizing the internet

The internet as we know it is inextricable from the cloud—the ethereal space through which all e-mails, Zooms, and Instagram posts pass. As many of us well-know, however, this nebulous concept is anchored to the Earth by sprawling warehouses that crunch and store data in remote places. Their energy demands are enormous and increasing exponentially: One model predicts they will use up to 13 percent of the world’s power by 2030 compared to just 3 percent in 2010. Gains in computing efficiency have helped matters, says University of Massachusetts Amherst assistant professor of informatics and computer science Mohammad Hajiesmaili, but those improvements do little to reduce the centers’ impact on the environment.

“If the power supply is coming from fuel sources, it’s not carbon optimized,” explains Hajiesmaili. But renewable power is sporadic, given its reliance on sun and wind, and geographically constrained, since it’s only harvested in certain places. This is the puzzle Hajiesmaili is working to solve: How can data centers run on carbon-free energy 24/7?

The answer involves designing systems that organize their energy use around a zero-carbon goal. Several approaches are in the works. The simplest uses schemes that schedule computing tasks to coincide with the availability of renewable energy. But that fix can’t work on its own given the unpredictability of bright sunlight and gusts of wind—and the fact that the cloud doesn’t sleep. Another strategy is “geographical load balancing,” which involves moving tasks from one data center to another based on local access to clean power. It, also, has drawbacks: Transferring data from one place to another still requires energy, Hajiesmaili notes, and, “if you’re not careful, this overhead might be substantial.”

An ideal solution, and the focal point of much of his work these days, involves equipping data centers with batteries that store renewable energy as a reserve to tap, say, at night. “Whenever the carbon intensity of the grid is high,” he says, “you can just discharge from the battery instead of consuming local high-carbon energy sources.” Even though batteries that are big enough, or cheap enough, to fully power data centers don’t exist yet, Hajiesmaili is already developing algorithms to control when future devices will charge and discharge—using carbon optimization as their guiding principle. This “carbon-aware” battery use is just one of many ways in which Hajiesmaili thinks cloud design should be overhauled; ultimately, the entire system must shift to put carbon use front and center. 

Most big technology companies have pledged to become carbon-neutral—or negative, in Microsoft’s case—in the coming decades. Historically, they have pursued those goals by buying controversial offset credits, but interest in carbon-intelligent computing is mounting. Google, for one, already uses geographical load balancing and is continuing to fine-tune it with Hajiesmaili’s input, and cloud-computer company VMWare has its own carbon-cutting projects in the works. In his view, though, the emerging field of computational decarbonization has applications far beyond the internet. All aspects of society—agriculture, transportation, housing—could someday optimize their usage through the same approach. “It’s just the beginning,” he says. “It’s going to be huge.”—Yasmin Tayag

Predicting how wildlife will adapt to climate change

Evolutionary biologists typically think about changes that took place in the past, and on the scale of thousands and millions of years. Meanwhile, conservation biologists tend to focus on the needs of present wildlife populations. In a warming world, where more than 10,000 species already face increased risk of extinction, those disciplines leave a crucial gap. We don’t know which animals will be able to adjust, how quickly they can do it, and how people can best support them.

Answers to these questions are often based on crude generalizations rather than solid data. Rachael Bay, an evolutionary biologist at the University of California, Davis, has developed an approach that could help make specific predictions about how at-risk species might evolve over the coming decades. “Injecting evolution into conservation questions is really quite novel,” she says.

The central premise of Bay’s work addresses a common blind spot. Conjectures about how climate change will affect a particular creature often assume that all of them will respond similarly to their changing habitat. In fact, she points out, it’s exactly the variation between individuals that determines if and how a species will be able to survive.

Take the reef-building corals she looked at for her PhD research: Thought to be one of the organisms most vulnerable to extinction as a result of warming oceans, some already live in hotter waters than others. Bay identified genes associated with heat tolerance in the coral Acropora hyacinthus and measured the prevalence of that DNA in populations in cooler waters; from there, she was able to model how natural selection would change the gene pool under various climate-change scenarios. Her findings, published in 2017 in Science Advances, made a splash. The data indicated that the cooler-water corals can, in fact, adapt to warming if global carbon emissions start declining by 2050; if they don’t, or keep accelerating as they have been, the outlook becomes grim.

Bay has continued her work on corals and other marine organisms, but she has also applied her method to terrestrial animals. In 2017, work she conducted with UCLA colleague Kristen Ruegg bolstered the case for keeping a Southwestern subspecies of the willow flycatcher on the US endangered list. Though the species as a whole is abundant, with a breeding range that spans most of the US and southwestern Canada, the subgroup that occupies southern California, Arizona, and New Mexico has struggled with habitat loss. The scientists demonstrated not only that the desert-dwelling birds were genetically distinct enough to merit their own listing, but also that individuals in that population have unique genes that are likely associated with their ability to survive temperatures that regularly top 100°F. Protecting this small subgroup—less than one-tenth of a percent of the total population—could help the entire species persist.

That kind of specific, forward-looking decision is exactly what Bay hopes to enable for other wildlife facing an uncertain future. Other recent work has focused on how yellow warblers, Anna’s hummingbirds, and a coastal Pacific snail called the owl limpet might shift their ranges in response to climate change. “The pie-in-the-sky goal is to make evolutionary predictions that can be used in management,” she says.—M.G.

Building an immune system from scratch

When a new pathogen invades, the immune system unleashes a suite of antibodies into the bloodstream—the bodily equivalent of throwing spaghetti at the wall to see what sticks. While most of those proteins will do an okay job of neutralizing the trespasser, a valuable few will zero in with deadly accuracy. The faster scientists can identify and replicate those killers, the better we’ll get at beating disease. Case in point: Antibody therapy helped many at-risk patients sick with COVID-19. The big challenge in studying the body’s natural response, however, is that in order to do so, people have to get sick.

John Blazeck, of Georgia Tech’s School of Chemical and Biomedical Engineering, is developing a workaround. Instead of using the human body as a “bioreactor” for antibodies, he wants to use microbes. That way, the repertoire that fires off in response to a pathogen can be studied in, say, a flask or a chip. The dream of a “synthetic immune system” has kicked around biotech circles for the last two decades, but Blazeck’s work is ushering it into reality. “We can have a million different microbes, making a million different antibodies that would mimic what a person would be doing,” he says.

His career began in synthetic biology, a field that involves sticking genes into microbes to make them do new things. Specifically, he tried to get them to pump out biofuels. His interest in advancing health, however, led him to use his expertise to fight disease in 2013, when he injected microbes with the human genes known to produce antibodies. Recreating the immune system in this way is a colossal undertaking. “The catch is that the process has been optimized for millions of years, so it’s very hard to make it happen,” he explains.

Nevertheless, his team has made foundational progress that could underpin the future of this research. Recently, they figured out how to efficiently mutate antibody DNA after it’s been inserted into microbes, which will help them select antibodies that bind more tightly to a given pathogen. The process is meant to mimic how the immune system uses its B cells—the body’s antibody factories—to self-select the proteins that generate the strongest defenses.

Building a synthetic immune system is only half of what Blazeck is doing to supercharge immunity. The rest builds on his postdoctoral research on engineering a means to thwart cancer cells’ defenses. Tumors secrete molecules that shut down immune cells trying to get in their way. Blazeck—with his former advisor George Georgiou, of the University of Texas, Austin—found an enzyme that can render those molecules harmless, allowing the immune system to do its thing. Ikena Oncology, a company specializing in precision cancer treatment licensed the enzyme, one of the first of its kind, in 2015. Both aspects of Blazeck’s work are at the forefront of burgeoning new fields, and he’s been heartened by the early response. “I hope that people continue to appreciate the value of trying to engineer immunity, and how it can contribute to understanding how to fight disease—and also directly fight disease,” he says.—Y.T.

Spying our future in near-asteroid flybys

The whole world will be watching when a 1,000-foot-wide asteroid called Apophis swoops by Earth in mid-April 2029. But Daniella Mendoza DellaGiustina, a planetary scientist at the University of Arizona, will be looking more closely than anyone else. Her gaze will be trained on what the space rock reveals about our past—and what it means for our future. “It’s going to captivate the world,” she says. In 2022, NASA named her principal investigator of the OSIRIS-APEX mission, which will send the OSIRIS-ReX spacecraft that sampled the asteroid Bennu in 2020 chasing after Apophis.

DellaGiustina wasn’t always interested in space, but as a “cerebral young person” gazing into the famously clear skies of the desert Southwest, she had a lot of big questions: Why are we here? How did we get here? A community college class in astronomy piqued her interest. Then, a university course on meteorites led to an undergraduate research position with Dante Lauretta, who later became the principal investigator of OSIRIS-ReX. DellaGiustina knew “very early on” that the research environment was right for her: “You’re actively pushing the boundary of human knowledge.” A master’s degree in computational physics led her to field work on the ice sheets of Alaska, which resemble those on other planets. Eventually, she returned to the University of Arizona, where completed a PhD in geosciences (seismology) while working on image processing for OSIRIS-ReX.

A belief that asteroids hold answers to the big questions of her youth drives her to understand them from the inside out. “They really represent the leftovers of solar system formation,” she says. “It’s kind of like finding an ancient relic.” So-called carbonaceous asteroids like Ryugu and Europa—rich in volatile substances, including ice—may explain how water and the amino acids that jumpstarted life once made their way to Earth. They may also offer a glimpse of the future: “Near-Earth asteroids, especially, hold tremendous potential for resource utilization,” DellaGiustina says, “but one might also take us out someday.”

Apophis is not considered dangerous, but it will swing by at roughly one-tenth the distance between Earth and the Moon. “If we ever have an incoming threat to our own planet, we need to understand ‘what’s the structure of this thing?’ so that we can properly mitigate against it,” she says. With DellaGiustina at the helm, the OSIRIS-APEX project will use this once-in-7,500-years chance to study how close encounters with planets can change an asteroid. Earth’s tidal pull, for example, is expected to “squeeze” Apophis—a tug DellaGiustina hopes to measure via a seismometer dropped on the surface.

Lauretta, who has worked with DellaGiustina since she was an undergraduate, jumped at the chance to nominate her to lead the next phase of the OSIRIS mission. She had always been keen on designing experiments—Lauretta seriously considered her proposal to equip OSIRIS-ReX with a dosimeter to measure the radiation risk for future asteroid-hopping astronauts. Her “decisive leadership is rare and critical for a program of this size,” he adds. On the off chance that an errant space rock ever threatens Earth, it’ll be a comfort to know she’s at work behind the scenes.—Y.T.

Making transit sustainable and equitable

Picture this: It’s Tuesday morning, and you’re planning to ride the train to work. Walking to the station takes 25 minutes, so you hop on the local bus. Today, though, the bus is delayed, and doesn’t reach the station in time to catch the train. You wait for the next one. You’re late for work.

If your boss is a stickler and you rely on public transit, a missed connection can be make or break. These are the kinds of problems that Samitha Samaranayake, a computer-scientist-turned-civil-engineer at Cornell University, has made it his mission to solve. He designs algorithms to help varied modes of mass transit work more seamlessly together—and help city planners make changes that benefit those who need them most.

Before Cornell, Samaranayake spent several years studying app-based ridesharing, including the potential of on-demand autonomous car fleets. In 2017, he co-authored an influential paper showing that companies like Uber and Lyft could reduce their contribution to urban congestion if cars were dispatched and shared efficiently. But he quickly became disillusioned with entirely car-centric solutions. “It’s convenient for people who can afford it,” he says, but when it comes to moving city-dwellers efficiently and accessibly, mass transit can’t be beat.

So Samaranayake began investigating how new technology can best be incorporated into city transit systems—and possibly solve some of their most-common pitfalls. Take the “last mile problem:” the challenge of transporting people from transit hubs in dense urban areas to the less-centralized places that they need to go—like their homes in far-out neighborhoods. If these connections aren’t quick and reliable, people may not use them. And if people aren’t using a neighborhood bus line or other last-mile service, says Samaranayake, a transit agency might cut it rather than run more buses, making the problem worse.

That’s where the technology developed by ride-sharing companies becomes useful, says Samaranayake. In recent years, he’s designed algorithms to integrate real-time data from public transit with the software used to dispatch on-demand vehicles. This could let transit authorities send cars to pick up groups of people, then deliver them to a commuter hub in time to make their connections.

This approach is known as “microtransit,” and after pandemic-related delays, a test project with King County Metro in Seattle launched earlier this year. It uses app-based rideshare vans to shuttle shift workers and others who live in the outskirts of the city to and from the regional rail line. Although it’s too early to measure success, Samaranayake has seen enthusiastic uptake from some commuters without many good alternatives.

That points toward his other goal: finding better ways to quantify how equitably transit resources are apportioned, so that city planners can ultimately design new systems that reach more people more efficiently. This social-justice element helps motivate Samaranayake to keep working on mass transit, even though funding has typically been more abundant for flashier technology like self-driving cars.

That could be changing: In recent years, Samaranayake and his collaborators have received nearly $5 million from the US Department of Energy and the National Science Foundation to pursue their vision. “Transit is not ‘cool’ from a research perspective,” Samaranayake admits. “But it’s the only path forward to a transportation system that is environmentally sustainable and equitable, in my view.”—M.G.

Finding the roots of neurodegenerative disease

Anyone who’s taken high school biology knows that mitochondria are the powerhouses of cells. While it’s true that these organelles are responsible for converting sugars into energy, they also have many less-appreciated jobs, including generating heat, storing and transporting calcium, and regulating cell growth and death. In recent decades, researchers have linked the breakdown of these functions to the development of certain cancers and heart disease.

When it comes to diseases like dementia, Parkinson’s, and ALS, however, Duke University cell biologist Chantell Evans thinks it’s time to look specifically at neurons. “Mitochondria are implicated in almost every neurodegenerative disease,” says Evans. By unraveling how neurons deal with malfunctioning mitochondria, her work could open up possibilities for treating many currently incurable conditions.

Evans’ work focuses on understanding a process called mitophagy—how cells deal with dead or malfunctioning mitochondria—in neurons. There are plenty of reasons to believe brain cells might manage their organelles in unique ways: For one, they don’t divide and replenish themselves, which means the 80 billion or so we’re issued at birth have to last a lifetime. Neurons are also extremely stretched out (the longest ones run from the bottom of the backbone to the tip of each big toe) which means each nucleus has to monitor and maintain its roughly two million mitochondria over a great distance.

Before Evans launched her investigation in 2016, research on epithelial cells—those that line the surface of the body and its organs—had identified two proteins, PINK1 and Parkin, that seem to be mutated in patients with Parkinson’s disease. But, confusingly, disabling those proteins in mice in the lab didn’t lead to the mouse equivalent of Parkinson’s. To Evans, that suggested that the story of neural mitophagy must be more complicated.

To find out how, she went back to basics. Her lab watched rodent brain cells in a dish as they processed dysfunctional mitochondria. Evans gradually cranked up the stress they experienced by removing essential nutrients from their growth medium. This, she argues, is more akin to what happens in an aging human body than the typical process, which uses potent chemicals to damage mitochondria.

Results she published in 2020 in the journal eLife found that disposing of damaged mitochondria takes significantly longer in neurons than it does in epithelial cells. “We think, because [this slowness] is specific to neurons, that it may put neurons in a more vulnerable state,” she explains. Evans has also helped identify additional proteins that are involved in the best-known repair pathway—and determined that that action takes place in the soma, or main body, of a neuron but not in its threadlike extensions, known as axons. That, she says, could mean there’s a separate pathway that’s maintaining the mitochondria in the axon. Now, she wants to identify and understand that one too.

Thoroughly documenting these mechanics will take time, but Evans says charting the system could lead to precious medicine. “If we understand what goes wrong,” she says, “We might be able to diagnose people earlier… and be more targeted in trying to develop better treatment options.”—M.G.

Mapping every human cell

It took the Human Genome Project a decade to lay out our complete genetic code. Since then, advances in sequencing technology have vastly sped up the pace by which geneticists can parse As, Gs, Ts, and Cs, which has allowed biologists to think even bigger—by going smaller. Instead of spelling out all of a person’s DNA, they want to create a Human Cell Atlas that characterizes the genetic material of every single cell in the body. Doing so will create “a reference map of what a healthy human looks like,” explains bioengineer Aaron Streets.

Understanding what makes individual cells unique requires insight into the epigenome—the suite of chemical instructions that tell the body how to make many kinds of cells out of the same string of DNA. “This is where the notion of the epigenome comes into play,” says Streets, who runs a lab at the University of California, Berkeley. All cells may be reading from the same book, but each one’s epigenome highlights the most relevant passages—essentially how and which genes are expressed. Streets is inventing the tools scientists need to zero in on those specifics.

Reading the epigenome is important, says Streets, because, in addition to showing why healthy cells act the way they do, it can also reveal why an individual one goes haywire and causes illness—cancer, for example. Once the markers of a rogue actor are known, he explains, researchers can develop therapeutics that address the question: “How can we engineer the epigenome of cells to fix the disease?”

Characterizing cells is highly interdisciplinary work, which Streets is perfectly suited for. He majored in art and physics but “just wasn’t good at” biology organismal studies. It wasn’t until graduate school, where he worked with a physicist-turned-bioengineer, that he realized how much insights gleaned from math, physics, and engineering could benefit the study of living things.

As a start, this year Streets and his colleagues published a protocol in the journal Nature Methods for reading particularly mysterious parts of the genome. The tool identifies sections within hard-to-read DNA regions that bind proteins—and thus have epigenomic significance—by bookending the strings with chemical markers called methyl groups. To James Eberwine, a pharmacology professor at the University of Pennsylvania and a pioneer of single-cell biology, “it is going to be very useful” for building a cell atlas.

Now, Streets’s lab is building new software to piece together the millions of sequences that comprise a single cell’s genome. And, because mapping every single anatomical cell will require a fair bit of teamwork, the programs they create are shared freely with other scientists who can use the tools to make their own discoveries. “If you look at really huge leaps in progress in our understanding of how the human body works,” says Streets, “they correlate really strongly with advances in technology.”—Y.T.

Crunching the numbers to get ahead of outbreaks

Like everyone in early 2020, Daniel Larremore wondered whether this virus making its way around the globe was going to be a big deal. Would he have to cancel the exciting academic workshop he had planned for March? What about his ongoing research on the immune-evading genes of malaria parasites?

As the answers became clear, so did his next big task: predicting the trajectory of the disease so that scientists and policymakers could get ahead of it. “You have a background in infectious diseases and mathematical modeling,” thought the University of Colorado Boulder computer scientist. “If you’re not going to make a contribution when there’s a global pandemic, when are you going to step up?” He put his work on the epidemiology of malaria on hold as he emailed colleagues studying the emerging outbreak to ask how his lab could help. “I sent that mid-March,” he says, “and didn’t stop working until early to mid-2021.”

Before coming to Boulder, Larremore had been a postdoctoral candidate at Harvard T.H. Chan School of Public Health, where he was first immersed in the world of infectious disease—how it was transmitted, how it evaded immunity, and how to model its spread. It prepared him well for the first wave of COVID-19 research questions, which were all about working around the shortcomings of antibody tests. At the time, they were the only tools available for counting infections, but their sensitivity and specificity varied widely. A paper he co-authored in those early months described how to estimate infection rate, a key metric in justifying public health measures like mask mandates and social distancing.

As the pandemic wore on, Larremore and his collaborators continued to think forward: “What’s the question we’re going to be asking six months from now that we’ll wish we had the answer to right away?” The research they conducted now underpins much of American COVID policy: Their modeling found that speed, not accuracy, in testing was more important for curbing viral spread; that the success of immunity passports depended on the prevalence and infectiousness of the virus; and that elderly and medically vulnerable people should be prioritized for vaccination. “Dan did a huge amount of work across a number of different disciplines, and I think the contributions he’s made have really been remarkable,” says Yonatan Grad, an associate professor at the Harvard T.H. Chan School of Public Health who frequently collaborates with Larremore.

While his work on COVID-19 winds down, Larremore is already helping develop a general theory of disease mitigation involving at-home testing. Through modeling, he’s hoping to find out how much testing might slow the spread of different infectious diseases—and how that changes with disease or the variant. He’s excited about leveraging the jump in public science literacy induced by COVID-19: “If you tell people to self-collect a nasal swab, they’ll do a great job at it,” he says. He imagines a world where the public can reliably self-diagnose common illnesses like flu, and take the appropriate steps (wearing a mask, opening windows) to protect others. “That just seems really empowering,” says Larremore. “And, potentially, a cool future.” —Y.T.

The post The Brilliant 10: The top up-and-coming minds in science appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

“An apple a day keeps the doctor away,” or so the old saying goes. Nutrition remains a powerful tool to prevent certain types of illness. The right food also play a role in helping serious or diet-sensitive diseases, like diabetes, HIV, and heart failure. A common way for those with illnesses like these is through medically tailored meals (MTM) customized and prepared for a patient’s needs. These meals can also be used for those facing food insecurity and those recently discharged from the hospital.

Meals catered to specific medical needs also have the potential to save a lot of money.

A study published today in JAMA Network Open finds that adding more programs that make and deliver MTMs could prevent hospitalizations nationally and save approximately $13.6 billion each year. The study used data from the 2019 Medical Expenditure Survey Panel Survey and other published research on the health impact of MTM programs. It found that implementing more of these programs around the country could also help prevent 1.6 million hospitalizations in addition to the huge cost savings. Most of the cost savings would occur within public programs like Medicare and Medicaid.

[Related: 5 nutrition goals that are better than weight loss.]

Kurt Hager, a PhD candidate in the Tufts University Friedman School of Nutrition and Science and Policy program led the study. “Currently, MTMs are not a covered benefit under Medicare or Medicaid, so they remain unavailable to the vast majority of patients who might benefit from them,” Hager said in a press release. “For people with chronic illness and physical limitations that make it difficult for them to shop and cook for themselves, these programs are a highly promising strategy for improving health and well-being. The estimated reductions in hospitalizations and associated cost savings reflect that.”

The majority of MTM programs around the country are run by organizations like Community Servings, God’s Love We Deliver, and Food is Medicine. Representative Jim McGovern, D-Ma has also introduced the Medically Tailored Home-Delivered Meals Demonstration Pilot Act of 2021, a pilot program for the the largest-ever MTM program under Medicare. They are currently funded though a mixture of by grants, donations, and Section 1115 waivers under Medicaid. The meals also often serve those with lower incomes and limited mobility, as well as individuals who regularly experience food insecurity. Most programs deliver five lunches and five dinner per week to eligible patients.

[Related: Unscrambling the health effects of eggs.]

“Food is not just for prevention–it can be used for treatment for people with debilitating conditions like heart failure, uncontrolled diabetes, HIV, and cancer,” Dariush Mozaffarian, a professor at the Friedman School and senior author on the paper, said in a press release. “With medically tailored meals, patients are treated using the power of food and put on a steady path toward healing. Our study suggests that expanding medically tailored meal programs nationwide—one key recommendation of the new Biden-Harris National Strategy on Hunger, Nutrition, and Health—would help reverse our ‘sick care’ system, keep people out of the hospital, and save billions of dollars each year.”

Researchers form Tufts University are now working with Community Servings and University of Massachusetts Chan Medical School on a multi-year evaluation of MTM programs in Massachusetts. The work will study how these MTM programs impact obesity, diabetes, nutrition insecurity, and health care utilization in the state.

The post Meals catering to different health needs could help save lives—and billions of dollars appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Colorectal cancer is the second most common cause of cancer death in the United States. A colonoscopy, a procedure which uses a camera to scope out the length of the large intestine and has long been considered to be the best way to detect the disease. It is recommended for all patients above the age of 45 in the US roughly every 10 years. However, a study published in the New England Journal of Medicine is casting some doubts on the effectiveness of the test.

The study was conduced by the Nordic-European Initiative on Colorectal Cancer (NordICC) and is the first randomized trial to directly compared patients who had undergone colonoscopies with those who had no cancer screening. It included more 84,000 men and women ages 55 to 64 from Poland, Norway, and Sweden who had never gotten a colonoscopy. The participants were randomly invited to have a screening between June 2009 and June 2014, or they were followed for the study without getting screened. About 42 percent of those invited to get a colonoscopy ended up receiving one.

[Related: You might not need a colonoscopy to be screened for colon cancer.]

The researchers found that receiving a colonoscopy was associated with only an 18 percent lower risk of getting colorectal cancer, and no significant reduction in the risk of cancer death.

Study researcher Michael Bretthauer, a gastroenterologist who leads the clinical effectiveness group at the University of Oslo in Norway, told CNN that he found the results disappointing, but physicians must follow the science. “So I think we have to embrace it. And we may have oversold the message for the last 10 years or so, and we have to wind it back a little.” Bretthauer said that the benefits of colonoscopy probably lie somewhere in the middle and expects that a screening colonoscopy potentially reduces a person’s chances of colorectal cancer by 18 to 31 percent, and their risk of death from 0 to as much as 50 percent.

Some experts say that the study has important limitations despite is methodology and sample size.

“It’s hard to know the value of a screening test when the majority of people in the screening didn’t get it done,” William Dahut, chief scientific officer at the American Cancer Society, said in a statement. “However, study patients who did undergo a colonoscopy had a 31 percent decrease in the risk of colorectal cancer as compared to those who were not screened. This result points to the value of continued screening.” Dahut who was not involved in the study.

Other doctors stress investigating this study’ limitation before giving new guidelines. Jason Dominitz, the national director of gastroenterology for the Veterans Health Administration, co-authored an editorial that ran alongside the study. “I don’t think anyone should be cancelling their colonoscopies. We know that colon cancer screening works,” he told CNN.

[Related: Why doctors almost never say cancer is ‘cured.’]

Previous research in the US have suggested that colonoscopy is the best way to screen for colorectal cancers. One study followed nearly 90,000 health care professionals for 22 years. Some of them chose to receive a screening colonoscopy, and some did not. It estimated that screening colonoscopy was associated with a 40 percent reduction in the risk of getting colon cancer and a 68 percent reduction in the risk of dying of colon cancer.

Regular colonoscopies beginning at age 45 are still recommended by the Centers for Disease Control and Prevention.

The post Colonoscopies still recommended for older adults, despite tepid new research appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The American Association for Cancer Research’s 12th annual Cancer Progress Report came with some welcome good news this year. Rates of cancer in the United States are falling steadily and more people are surviving the disease than ever before.

The number of cancer survivors (living people who have had a cancer diagnosis) has increased by over million in the past three years. As of January of this year, there are more than 18 million survivors, compared to only 3 million 1971. That number is expected to jump to 26 million by 2040, according to the association.

From 2011 to 2017 (the most recent data) the five-year overall survival rate for all cancer combined has increased from 49 percent during the mid-70’s to nearly 70 percent today.

Additionally, when adjusted for age, the overall cancer death rate is dropping. Between 1991 and 2019 nearly 3.5 million deaths were avoided.

[Related: Why doctors almost never say cancer is ‘cured.’]

“Basic research discoveries have driven the remarkable advances that we’ve seen in cancer medicine in recent years,” said AACR President Lisa M. Coussens in a press release. “Targeted therapies, immunotherapy, and other new therapeutic approaches being applied clinically all stem from fundamental discoveries in basic science. Investment in cancer science, as well as support for science education at all levels, is absolutely essential to drive the next wave of discoveries and accelerate progress.”

The association also pointed to declines in smoking and better early cancer detection and treatments for the decrease.

Coussens also noted that between August 1 and July 31, of this year alone the US Food and Drug Administration (FDA) approved eight anticancer therapeutics, expanded the use of 10 previously approved medications to treat new types of cancer, and approved two diagnostic imaging agents.

President Biden’s Cancer Moonshot initiative has a cornerstone of increasing funding for research. Biden lost his son Beau to brain cancer in 2015, and re-emphasized his goal is to cut cancer death rates in the United States by at least half in the next 25 years. The 2022 report urges Congress to fully fund and support Biden’s goal.

“The reignited Cancer Moonshot will provide an important framework to improve cancer prevention strategies; increase cancer screenings and early detection; reduce cancer disparities; and propel new lifesaving cures for patients with cancer. Actions will transform cancer care, increase survivorship, and bring lifesaving cures to the millions of people whose lives are touched by cancer,” the report says.

[Related: Oncologists are studying cancer in dogs and cats to help humans.]

Despite the tremendous reduction of cancer deaths, the report outlines the numerous challenges. More than 600,000 people in the US are still expected to die from cancer this year and the number of new cases is expected to reach nearly 2.3 million by 2040.

Additionally, health disparities that affect ethnic and racial minorities and the barriers to health, such as limited health insurance coverage and living in rural areas, remains a major issue. In a recorded statement played at the news conference about the cancer report, Representative Nikema Williams (D-Georgia) said that following her mother’s death from cancer, she learned that, “health care in America is not a human right yet. We have two health care systems in this country: one for people who can afford preventative services and quality treatment and one for everyone else.”

Rep. Williams is a co-sponsor of Medicare for All legislation, which aims to improve access to quality health care in the US.

The report also mentioned the ongoing COVID-19 pandemic decreasing cancer screening and the possible affect to cancer care due to the reversal of Roe v. Wade in June. “With the recent Supreme Court decision to overturn Roe v. Wade, which ends the constitutional right to an abortion, there is uncertainty surrounding how a particular cancer treatment may lead to the termination of a pregnancy. Such uncertainty may prohibit some physicians from prescribing a drug or performing other health services in a timely manner due to the potential legal consequences for both physician and mother,” said the report.

The post More Americans are surviving cancer now than ever appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

With about 10 million deaths worldwide in 2020, cancer remains one of the world’s leading causes of death. Early detection of the disease remains a key in increasing the chance of survival, but a recent review in the journal Science found that 50 percent of cancers are still diagnosed at the advanced stage. When cancer is caught early, treatment is more effective and cancer progression can even be slowed down or stopped.

However, early detection could get a boost from a new blood test that can screen for more than 50 types of cancer. In the first study results of the Galleri test, found that the tests detected a possible cancer “signal” in roughly 1 percent of the over 6,600 apparently healthy people aged 50 and older in the study. When followed by more extensive testing, cancer was diagnosed in 38 percent of those who had initially been detected for cancer using the initial Galleri blood test.

More than 90 percent of the patients with a positive blood tests had more than one imaging test (CT scan, MRI, etc.), while half had more than one invasive test (a biopsy, excision, etc.) that confirmed the results.

The trial showed that the tests identified the presence of 19 solid tumors in the breast, liver, lung and colon tissues. Additionally, the tests spotted ovarian and pancreatic cancers, which are typically detected at a late stage and have poor survival rates. The remaining cases detected in the trial were blood cancers. Out of the 36 types of cancers detected in total, 14 of them were early stage and 26 were forms that aren’t routinely screened for.

The findings are part of a study called PATHFINDER, which is being conducted across the US to evaluate Galleri. Biotechnology company GRAIL is both the maker of the Galleri test and funder of the PATHFINDER study. Galleri is one of a number of blood tests under development, with the ultimate the goal of providing “one-stop” screening for multiple cancers in the future. All of these tests work by looking at biological signals called biomarkers (tiny fragments of DNA shed by cancer cells, for example) that can signal that cancer is present in the blood stream.

[Related: We’re getting better at screening for cancer, and that could be a problem.]

“The PATHFINDER study is an exciting first step towards fundamental change in the approach to cancer screening. The study found cancer in about 1 percent of participants including types for which there is no established screening method. The study demonstrated the feasibility of this paradigm and solid test performance,” Deb Schrag, chair of the Department of Medicine at Memorial Sloan Kettering Cancer Center in New York said in a press release. “Although continued public health efforts to optimize adherence to existing screening strategies that have been proven effective are critical, this study provides a glimpse of what the future may hold—the opportunity for screening using blood tests to detect various types of cancers at their earliest and most treatable stages.”

The researchers also found that the blood test was correct 99 percent of the time when indicating that cancer was not present, an important finding due to the risk of a false-positive result in cancer screening. For example, a study published in March in the Journal of the American Medical Association Open Network (JAMA) found that half of all women undergoing mammograms experience a false positive after 10 years of annual screening.

[Related: Two thirds of cancer mutations result from completely random DNA mistakes.]

In an interview with US News & World Report, study co-author Catherine Marinac, a researcher at Dana-Farber Cancer Institute in Boston said “This is not ready for prime time. But if further studies confirm the blood test’s usefulness, she said, it could become a ‘game changer.'” She also stressed the importance of studying not only how well these multi-cancer early detection tests perform, but what happens when they are actually put into practice in real healthcare settings and if a screening test can actually prevent cancer death.

The results were presented yesterday at a meeting of the European Society for Medical Oncology in Paris, France. Studies released at meetings like this one are generally considered preliminary until they are published in a peer-reviewed journal. Currently, no multi-cancer early detection test is approved by the FDA, but Galleri is available for doctors to order, as a laboratory developed test. According to the US National Cancer Institute, the FDA has historically not regulated laboratory developed tests.

The post First study of cancer-detecting blood test shows hopeful results appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

While this upcoming long weekend may call for celebrations, this time around maybe reconsider breaking out the hot dogs, soda, and pre-packaged snacks. Two large-scale studies link overconsumption of “ultra-processed foods” to an increased risk of a number of ailments, including obesity, cancer, cardiovascular disease, early death, and more.

The authors defined ultra-processed food as “industrial formulations made entirely or mostly from substances extracted from foods (oils, fats, sugar, starch, and proteins), derived from food constituents (hydrogenated fats and modified starch), or synthesized in laboratories from food substrates or other organic sources (flavor enhancers, colors, and several food additives used to make the product hyper-palatable).” This definition is based on the NOVA Food Classification System.The paper published on August 31st in The British Medical Journal (BMJ) include two studies, one conducted in the United States and one in Italy.

The stateside study looked at 200,000 people (59,907 women and 46,341 men) for up to 28 years. Each study participant completed a questionnaire every four years, listing how often they ate about 130 different foods, ranging from non-processed foods like fruit all the way to ultra-processed like bacon. The long-range surveys found a link between ultra-processed foods and colorectal cancer in men, but not in women. Men in the highest quintile of ultra-processed food consumption had a 29 percent higher risk of developing colorectal cancer than those in the lowest quantile. The results of the Italian study found similar dangers in ultra-processed foods.

The reasons behind the differences between sexes is not yet clear.

[Related: Here’s why ultra-processed foods are so bad for your health.]

“We found an inverse association between ultra-processed dairy foods like yogurt and colorectal cancer risk among women,” said co-senior author Fang Fang Zhang, a cancer epidemiologist and interim chair of the Division of Nutrition Epidemiology and Data Science at the Friedman School, in a press release. Colorectal cancer is the third most diagnosed cancer in the US and is among the fastest-growing cancers in those under the age of 50.

Mingyang Song, co-senior author on the study and assistant professor of clinical epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, added that, “Further research will need to determine whether there is a true sex difference in the associations, or if null findings in women in this study were merely due to chance or some other uncontrolled confounding factors in women that mitigated the association.”

A wide body of research has associated processed meats (bacon, salami, beef jerky, etc.) with a higher risk of bowel cancer in both men and women. The connection remained even when accounting for factors like dietary quality and body-mass index. This new study found that all types of ultra-processed foods, not just meats, played a role to some extent.

“We started out thinking that colorectal cancer could be the cancer most impacted by diet compared to other cancer types,” said Lu Wang, the study’s lead author and a postdoctoral fellow at the Friedman School of Nutrition Science and Policy at Tufts, in the press release. “Processed meats, most of which fall into the category of ultra-processed foods, are a strong risk factor for colorectal cancer. Ultra-processed foods are also high in added sugars and low in fiber, which contribute to weight gain and obesity, and obesity is an established risk factor for colorectal cancer.”

[Related: The truth about counting calories.]

The researchers recommend that ultra-processed foods be replaced with unprocessed or minimally processed foods to decrease the risk.

The Italian study began in 2005 and followed 22,000 people in the country’s Molise region. It was designed to assess rick factors for cancer, heart disease, and brain disease. The researched also published in the BMJ also compared the role of nutrient-poor foods (high in sugar and saturated or trans-fats) with ultra-processed foods in the development of early death and disease.

“Our results confirm that the consumption of both nutrient-poor or ultra-processed foods independently increases the risk of mortality, in particular from cardiovascular diseases,” said Marialaura Bonaccio, epidemiologist of the Department of Epidemiology and Prevention at the IRCCS Neuromed of Pozzilli and lead author of the study, in a press release.

When the team compared the two types of food to get a sense of which contributed the most, they found that the ultra-processed foods were “paramount to define the risk of mortality,” according to Bonaccio. “This suggests that the increased risk of mortality is not due directly (or exclusively) to the poor nutritional quality of some products, but rather to the fact that these foods are mostly ultra-processed.”

The post Two decades-long studies link ultra-processed foods to cancer and premature death appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

My great-grandmother was a big proponent of wearing dark-colored, long-sleeved shirts in the middle of North Carolina’s scalding summers. Her reply whenever I’d ask her why she’d chosen that gardening outfit on a 95-degree day was always the same: “What keeps out the cold will keep out the sun.” 

Her ancestral wisdom was spot on. Ultraviolet radiation, of which the sun is a primary source, is thought to be a leading cause of skin problems in people—including wrinkles, sunburn, decreased immune function, irritation, and certain forms of cancer. Historically, humans have found ways to protect themselves from the sun. Indigenous populations in Alaska constructed snow goggles out of bone or wood to protect their eyes from UV rays reflecting off the snow. In Myanmar, thanaka, a paste of crushed tree bark, is still used. 

Consumer-wise, today there are two primary sun protectants on the market: sunscreens and UPF materials. The second is designed using “various weaving methods, dyes, and photo-protecting chemicals to impede ultraviolet light from penetrating through the fabric and damaging the skin,” says Travis W. Blalock, an associate professor of dermatology at Emory University School of Medicine. 

[Related: Your summer guide to sunscreen, from SPF to not-so-magic pills]

Basically, UPF is a grade given to clothing and other textiles specially designed to block UV rays from reaching the skin. According to outdoor retailer REI, even a plain white t-shirt provides a UPF rating of around 5, which isn’t much, but is better than your birthday suit.

While SPF and UPF products will defend your body from the sun, their levels of protection are not determined in the same way, explains Shadi Kourosh, the director of community health for the department of dermatology at Massachusetts General Hospital. A product’s SPF rating is based on how long someone can be in the sun with sunscreen on before their skin starts to redden, relative to how long they can be in the sun without it. For instance, if someone can be in the sun for 30 minutes before they start to burn, properly applied SPF 30 would allow them to stay outside for 30 times longer.

In comparison, UPF ratings are established by the percentage of UV rays that penetrate the material. If a shirt has a rating of UPF 50, it is thought to block 98 percent of ultraviolet A (UVA) and ultraviolet B (UVB) rays from reaching someone’s skin. (SPF only measures protection against UVB rays.) Officially rated UPF products range from 15 up to 50+.

I asked both Kourosh and Blalock about the benefits of UPF, how to tell if a product will offer good sun defense, and if SPF ratings serve as an effective guide for choosing the proper level of protection. Both interviews have been edited and condensed for clarity. 

Is UPF clothing and gear as effective as sunscreen?

Blalock: UPF is just one component of protecting the skin from the harmful effects of ultraviolet light. It does an amazing job of protecting the skin that it covers—however, I recommend using a broad spectrum sunscreen with an SPF greater than 30 to apply to areas not covered by UPF clothing. As a parent and a doctor, I am acutely aware of the benefit of UPF clothing, which does not have to be reapplied and doesn’t wash off during swimming. Sunscreen does have to be reapplied after a designated period, and spots could be missed if it is not applied uniformly. 

Kourosh: Even if you’re wearing a UPF fabric that blocks 99 percent of the sun’s rays, if you’re out for long enough, some of those rays still might get through. One concept discussed in the medical community, especially among dermatologists, is the percentage of body surface area covered by a garment and the weight of the garment itself. So it’s about how good the fabric is at blocking the sun, and how much of the body it covers. And there are other factors that affect its effectiveness—like the clothing should be loose rather than tight, and it should not be wet. 

So SPF is the superior choice between the two?

Blalock: I don’t typically think of SPF as being superior given that UPF and SPF focus on different aspects of photoprotection. I think of these concepts and measurements as complementary instead of comparative. However, as a practical matter, it is generally believed that UPF clothing may block out UVA more effectively than some sunscreens. 

How is the UPF level determined? 

Kourosh: While national and international health agencies like the Food and Drug Administration and the World Health Organizations recommend UPF as one of the pillars of sun prediction, there is no global standardization. Australia and New Zealand have done the best job of establishing guidelines and standards and having agencies for enforcement. But in the US, it’s not enforced, so that’s another reason why it’s a good idea to go for the maximum protection, because that gives you the best chance of getting the protection you’re hoping for. Australia and New Zealand also have a protection rating system corresponding to the percentage of rays that make it through the fabric.

What’s the right amount of sun protection then?

Kourosh: Usually, the protection we’re getting from either rating is less than we think. The estimate of SPF or UPF protection is based on the perfect world of lab settings. We’re probably outside for longer periods or in situations where the sun exposure is very intense, like at the beach. So we cannot assume that the conditions in which the testing was done are the same as what we are encountering in the real world. This is why I recommend that people get the maximum levels they can find on a product.

Blalock: My general advice to patients starts with an understanding that we know the negative impacts of the sun on your skin. Ultraviolet light can increase your risk of skin cancer, cause sunburns, and accelerate signs of aging, like wrinkles and spots. Thus, the more informed you are, the more likely you can make educated choices about protecting your skin. I recommend selecting sun protection that you are willing to use consistently. The skin is not protected by sunscreens or UPF clothing that aren’t used. 

How can people check if their UPF products are legitimate? 

Blalock: The easiest way for consumers to know is to purchase from a manufacturer that clearly indicates a UPF designation on the label. While certain types of fabrics are better at preventing ultraviolet light from getting to the skin—dark or bright colored clothing, densely woven fabrics, and loose-fitting clothing—there are no reliable ways for the consumer to know this unless they’re labeled as having a confirmed UPF. Companies that place this label on their clothing commonly do laboratory testing to evaluate sun- protective capabilities. This takes a lot of the guesswork out of the equation for consumers.

When should people wear or use UPF products?

Blalock: Minimizing UV damage to your skin is advised when sun exposure is likely to be high. You can monitor the UV index through your local weather report, or just be aware that the time with the most exposure is typically from mid-morning around 9 am to late afternoon around 4 pm. And there’s little downside to wearing or using sun protection outside of these times. Thankfully, as UPF clothing has become more mainstream and fashionable, I’m hoping we’ll see more of them worn at all times.

Which activities does UPF work best for?

Blalock: The big concern I hear most commonly regarding sunscreen is the need for reapplication. That might be common as people focus on their specific activities, like swimming in the ocean, engaging in athletics, or even going on a long hike. UPF clothing that is comfortable and not too uncomfortable provides the ability to engage in meaningful life activities without worrying about the reapplication requirements of sunscreen. 

Kourosh: Another issue that’s becoming increasingly important in the medical community is occupational exposure—so people who work in certain professions where they’re chronically exposed to heat and sunlight. Sunlight and heat are capable of causing certain skin problems, and that puts workers at risk. Some countries, like Germany, now have regulations around what we could call personal protective equipment against UV exposure, which employers must provide. 

There are also people who work in environments with snow, open water, white sand, asphalt concrete, or polished metal. These are reflective surfaces that intensify a person’s exposure to UV rays. They should opt for maximum-protection clothing and sunscreen, and seek shade as often as possible. 

The post Everything you need to know about UPF sun protection appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The e-cigarette brand Juul is on the verge of a nationwide ban on its sales of its products. Last Thursday, the Food and Drug Administration (FDA) ordered the company to stop selling its products and pull any items currently on the market, citing concerns on the products’ potential toxicity. But the day after, a federal appeals judge in D.C. temporarily suspended the ban, allowing the company to keep selling its e-cigarettes. Juul had until today at noon to respond to the FDA’s order for evidence that its products are not a severe health hazard and benefit public health. 

The FDA is enforcing new regulatory guidelines for electronic cigarettes currently for sale or planning to launch in the US market. Their decision involves reviewing data on safety and public health benefits to decide which products stay on shelves. Currently, the FDA has allowed the sale of 23 other e-cigarette products. The FDA’s decision to stop the sale of Juul e-cigarettes is because the company submitted insufficient data for government authorization that their product is good for people. The evidence presented to the FDA were considered “insufficient and conflicting.”  

[Related: The FDA is prepping its biggest cigarette crackdown since the ’60s]

E-cigarettes first made their US debut in 2007; by 2014 they were the most commonly used tobacco product among teenagers. As of 2018, 1 in 5 high school students and 1 in 20 middle school students use e-cigarettes. Juul’s e-cigarette products are commonly blamed for the teen vaping epidemic. One of the company’s most attractive features is that it offered kid-friendly flavors such as mango, fruit, and cucumber, which were banned in October 2019 because of an alarming increase in vaping use among teens. Still, Juul is the second best-selling e-cigarette brand today among teens and adults. 

Some studies suggest e-cigarettes and chemically damages a person’s DNA and contradictory results submitted to the FDA suggest chemicals from Juul’s e-liquid pods may do this. Other research has found conflicting results results on whether e-cigarettes truly help adult smokers quit using cigarettes. Therefore, the FDA concluded that it does not have enough data to undergo a complete assessment of the health risks Juul’s e-cigarettes pose to their users. As a result, the FDA issued a marketing denial order for all their products, meaning the company can no longer authorize sales without facing legal action.

The ban would affect the sale of all Juul e-cigarettes, not how a person uses them. In other words, you can keep using Juul products if you already have them in your possession and are 21 years of age or older. 

While Juul e-cigarettes have been overtaken in recent years by disposable vapes such as puff bars, the decision is expected to help reduce teen vaping overall. “FDA’s decision to turn down Juul’s application represents the most significant step FDA has taken to reverse the youth e-cigarette epidemic,” Matthew Myers, the president of the Campaign for Tobacco-Free Kids, told CNN.

[Related: Vaping harms more than just your lungs]

Some doctors, however, say the ban will have little effect if people can get their hands on other nicotine products. “This is one company out of hundreds that are now operating in this marketplace,” Jacob Kaslow, a pediatric pulmonologist at Vanderbilt University Medical Center, told said in an interview with WSMV4.

The ban is one small step toward a larger US crackdown on other nicotine-containing products. In early June, Biden administration said it set a maximum nicotine level for all smoking products to reduce the chances of addiction, lung cancer, and other illnesses. The timeline is May 2023, though, opposition to the policy may delay or prevent it from ever taking effect, according to according to The Washington Post. For a full list of symptoms linked to vaping and other forms of smoking, go to the Centers for Disease Control and Prevention website.

The post Why Juul vaping products might start disappearing from US stores appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

There’s no definitive cure for cancer, but a small clinical trial may lead the way to a powerful new treatment for rectal tumors. A study published Sunday in The New England Journal of Medicine found a 100 percent success rate in 12 patients with rectal cancer treated with the immunotherapy drug dostarlimab. The patients’ tumors disappeared—and there were no severe side effects or signs of the cancer returning.

Colorectal cancer affects about 5 percent of Americans over their lifetimes. Current treatments for rectal cancer can involve one or a combination of surgery, chemotherapy, and radiation therapy. These treatments have a risk of multiple side effects, however, that can lower a person’s quality of life. 

“Our first duty is to save our patient’s life. But the standard treatment for rectal cancer with surgery, radiation, and chemotherapy can be particularly hard on people because of the location of the tumor,” said Andrea Cercek, a medical oncologist at Memorial Sloan Kettering Cancer Center in New York and lead study author in a press release. “They can suffer life-altering bowel and bladder dysfunction, incontinence, infertility, sexual dysfunction, and more.”

The new study took a different approach from common therapies. The oncology team used an immunotherapy drug to boost a person’s immune system to help them get rid of cancer. The idea came from oncologist and study co-author Luis Diaz Jr., who found success using immunotherapy on people with colorectal cancer whose tumors had spread to other body parts. 

[Related: Why doctors almost never say cancer is ‘cured’]

The 5-year survival rate for people with cancer in the rectum is around 90 percent, according to the American Cancer Society. But if rectal cancer spreads to areas such as the lungs or bones, the 5-year survival rate falls to 17 percent. “We thought, ‘Let’s try it before cancer metastasizes as a first line of treatment,’” Diaz said in the press release.

The clinical trial enrolled 12 people with stage 2 or 3 mismatch repair-deficient rectal tumors. These types of tumors appear when the cell’s DNA repairing system malfunctions, spreading errors in the genetic code. This type of cancer is frequently resistant to chemotherapy and radiation, and treatment often requires surgery to remove almost all of the rectum.

All study participants were administered 500 milligrams of a drug called dostarlimab every 3 weeks for 6 months. The drug, known as a checkpoint inhibitor because it blocks proteins that turn off the immune response, allows immune cells to identify and attack cancer cells. While researchers expected most patients to require additional treatment with chemotherapy or radiation, they were surprised to find no trace of rectal tumors in all of the patients’ scans after a 6 month follow-up.

“The immunotherapy shrank the tumors much faster than I expected,” Cercek said in the press release. “Patients came to my office after just two or three treatments and said, ‘This is incredible. I feel normal again.’ ”

Two years later, none of the tumors reemerged, and the patients have had no need for chemoradiation or surgery.

While the findings are potentially practice-changing, it may be a while until dostarlimab replaces the standard treatment for rectal cancer. The study results were based on a small group of people, leaving a possibility that the outcomes may have been from chance. 

Hanna K. Sanoff, an oncologist at the University of North Carolina’s Lineberger Comprehensive Cancer Center who wasn’t part of the research team, wrote in an accompanying editorial that these preliminary results are compelling—but it’s too soon to tell whether dostarlimab can completely cure rectal cancer. Further research will need to enroll more patients to paint a complete picture of the treatment’s effects and how long remission lasts.

The post A new rectal cancer treatment eliminated all tumors in a small group of patients appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

One of the most misunderstood ideas in medicine is a single word: cure. With cancer, the idea of a cure is particularly strong. It can be a ritual that brings people together. It can be a source of focus for the mind, calm for the heart, and hope for the future.

But it is unlikely for a patient to hear that word from a doctor. “It’s very rare for us as cancer doctors to tell the patient, ‘You are cured.’ Right now the most that we can tell our patient is that they are in remission,” says Jason Aboudi Mouabbi, an assistant professor of general oncology and breast medical oncology at the University of Texas MD Anderson Cancer Center.

[Related: This chart shows how far we’ve come in fighting cancer]

Remission is when all signs and symptoms of cancer are completely gone, according to the National Cancer Institute; the cancer cells aren’t detectable by scans, exams, bloodwork, and other testing.      

“But that does not mean that cancer is completely gone—just we cannot see it. So we have to assume it’s gone,” Mouabbi says. “We don’t use the word cure until [you’re in] remission for five years.”

Even the five-year mark is an imperfect standard. The estimate may be less accurate for certain diseases, like breast cancers. And being “cancer-free” isn’t as straightforward as you might think, either. That phrase goes beyond remission: It means that there are no cancer cells in the body at all. Like a cure, this is essentially impossible to achieve. Though it’s unlikely cancer will come back after five years, there is always a chance it will return, because malignant cells may lay dormant and undetected.

When a person is sitting in a doctor’s office, holding their breath and their loved one’s hand, their goal isn’t to be cured, exactly. It’s to do whatever it takes to get better, despite many barriers, like the eye-watering cost of care. It’s to go into remission, after weeks and months of treatments. Here are the different strategies oncologists use to achieve that these days.

The latest options for cancer treatments

The legacy cancer treatment, of course, is chemotherapy. Beyond that, the major options are targeted therapy, radiation, surgery, and immunotherapy. The National Library of Medicine’s treatment list also includes hyperthermia, hormonal therapy, laser therapy, photodynamic therapy, and cryotherapy.                

Chemotherapy

Chemo, the oldest and often go-to strategy for tackling a wide variety of cancers, is getting an upgrade. “Many therapies [now] are targeted to genetic alterations within a cancer, and they would still fall under the class of chemotherapy,” Karen Knudsen, CEO of the American Cancer Society, says. For example, chemotherapy can directly attack colorectal and melanoma tumors linked to a mutation in a gene called BRAF.

Targeted therapies

“Even our cells have a shelf life,” Mouabbi says. “Eventually, they have to die off and new cells have to replace them.” But when the body tries to replenish cells and doesn’t follow the rules, the microscopic structures keep dividing. If they don’t stop, “that’s when cancer happens,” Mouabbi says. Targeted cancer therapies attempt to fix those errors at the genetic level, especially mutations.

[Related: A ‘living’ cancer drug helped two patients stay disease-free for a decade]

Targeted treatments called antibody-drug conjugates focus on cancer cells while leaving the rest of the body’s cells alone. Unlike chemo, this allows healthy cells to stay that way. “When it targets that protein [on the cancer cell], a payload gets released only to those cells that the antibody binds to,” Mouabbi says. It has revolutionized the management of breast cancer, he adds, and is being explored for other cancer types.      

Trastuzumab, commercially called Herceptin, is another targeted therapy that is informed by a patient’s biology. Some cancer cells create an excess of a protein called HER2. This therapy focuses on that protein, which causes an especially aggressive form of breast cancer, plus a type of stomach cancer and gastro-esophageal cancer.

Radiation

The Food and Drug Administration recently approved an innovative radiation therapy that targets prostate cancer, which accounts for 5.7 percent of all cancer deaths. It will kill an estimated 34,500 people this year, almost as many people as the residents of Beverly Hills, California.      

One of the more promising radiotherapies is proton therapy, which might be safer than photon therapy, a 2020 study of nearly 1,500 US patients found. Though both are radiation-based approaches, they work differently: Photon therapy beams high-energy X-rays or gamma rays into the body, while proton therapy uses positively charged particles to break up DNA. Proton therapy “has the potential to reduce harm to surrounding normal tissue,” Knudsen says (trials are still underway to investigate this).

Surgery

Cancer surgeries, which physically remove the tumor, “are constantly being upgraded,” Knudsen says. A major focus for medical researchers is to reduce side effects by improving the timing of chemotherapy before surgery. “For some cancers, [doing] chemotherapy upfront can shrink the tumor, which makes surgery easier to do with fewer adverse outcomes for the patient,” Knudsen adds.

Immunotherapy

This type of treatment trains the immune system to find and identify cancer cells, which guides medicine to get into the body to slaughter the invaders. The immune system’s job is to then find the cancer cells, but sometimes it doesn’t do this perfectly.

One type of groundbreaking immunotherapy is CAR (chimeric antigen receptor) T-cell therapy, which puts the immune system to work to fight cancer. T cells in blood are essentially trained to attack the cancer cells. A recently completed phase 3 clinical trial that studied 180 patients in the US over approximately two years found CAR-T therapy to be effective in individuals with large B-cell lymphoma (the most common type of non-Hodgkin’s lymphoma). When coupled with a dose of an mRNA vaccine, CAR-T therapy might one day work in patients with other types of cancer, another very early clinical trial suggests.

Another treatment removes the disguise that hides cancer cells from your immune system. “Checkpoint inhibitors block that cloaking process, so it allows your own immune system to potentially see the cancer—which is you, gone bad,” Knudsen says.

Preventing cancer before it attacks

Of course, the best way to fight cancer is to not let it develop and spread in the first place. Beyond lifestyle choices like diet and exercise, there are ways to reduce the risk of disease with a vaccine.

“We have a real opportunity to eliminate cervical cancer as we know it through HPV vaccination, as well as 50 percent of head and neck cancers,” Knudsen says. “This is something that we can control.”

[Related: A single HPV vaccine dose can protect against cervical cancer]

The Centers for Disease Control and Prevention recommends all pre-teens—not just girls—get vaccinated against HPV, the most common STD. It’s a “cancer vaccine,” Knudsen says. “No one wants to think that they will ultimately have their child or someone they love … develop that disease because they were not vaccinated.”

Meanwhile, researchers at Duke University are working on a different type of cancer vaccine that uses mRNA—just like COVID vaccines—to defeat a common type of breast cancer (HER2-positive). Rather than targeting an infectious agent like HPV or SARS-CoV-2, this immunotherapy vaccine technology, now in a phase 2 clinical trial, would protect people with genetic mutations that raise their risk of developing certain cancers. This covers a range of illnesses beyond breast cancers, including lung, prostrate, and colon cancers.

“We’re not really limited, if we can demonstrate the concept,” lead researcher Herbert Kim Lyerly, an immunologist at Duke University, says. “It’s almost like if you have one electric car—you can imagine a mini-van, a truck, a sports car. All these different versions can come out to be tailored for individual cancer types as we get successful with the prototypes we’re developing.”

The post Why doctors almost never say cancer is ‘cured’ appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Just a single dose of vaccine against human papillomavirus may be enough to protect against HPV and cervical cancer, according to new research. The HPV vaccine is normally administered in two- or three-dose regimens, but an effective single-dose schedule could make it easier for countries to vaccinate their populations of women.

Between December 2018 and June 2021, researchers randomly assigned 2,275 Kenyan girls and women between 15 and 20 years old to receive a dose of either the HPV vaccine or a different vaccine unrelated to HPV. They found that just one dose of an HPV vaccine was around 90 percent effective at preventing several strains of HPV after 18 months. The findings were published in the New England Journal of Medicine Evidence on Monday. 

The single-dose efficacy was so high—and comparable to that of multi-dose vaccines—that the findings support the adoption of a single-dose HPV vaccination campaign, Peter Dull, deputy director of vaccine development and surveillance at the Bill & Melinda Gates Foundation, which funded the study, said in a statement. Such a campaign could increase vaccine accessibility in low- and middle-income countries, he added, which would help the World Health Organization reach its goal to have 90 percent of 15-year-old girls vaccinated against HPV by 2030.

“I believe that I will see cervical cancer eliminated in my lifetime,” co-author of the study Maricianah Onono at the Kenya Medical Research Institute said in a statement. “So, let’s do this—one shot for every woman!”

[Related: HPV vaccination in the UK has prevented thousands of cases of cervical cancer]

Sexually transmitted HPV causes more than 95 percent of cervical cancer. It’s the fourth most common type of cancer in women globally, according to the WHO, and 90 percent of the women living with HPV are located in low- and middle-income countries. Although HPV vaccines are highly protective, and have been commercially available for more than 15 years, global uptake of the life-saving vaccine has been slow. In 2020, only 13 percent of eligible women and children worldwide had received two doses.

By comparison, in the United States, 77 percent of female adolescents aged 13 to 17 have received at least one dose of HPV vaccine, while 61 percent have received at least two, according to the Centers for Disease Control and Prevention’s most recent data from 2020. The version of the vaccine most widely available in the US today, Gardasil 9, is a two- or three-dose regimen, depending on how the shots are spaced, which protects against nine strains of HPV. According to the CDC, since 2006 “infections with HPV types that cause most HPV cancers and genital warts have dropped 88 percent among teen girls and 81 percent among young adult women.” 

Increasing equitable access for the HPV vaccine is a serious concern, says the WHO—especially when the vaccine prevents cancer so effectively. “We need political commitment complemented with equitable pathways for the accessibility of the HPV vaccine,” WHO Assistant Director-General Princess Nothemba Simelela said in a statement. “Failure to do so is an injustice to the generation of girls and young women who may be at risk of cervical cancer.”

The post A single HPV vaccine dose can protect against cervical cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

There’s a gap on the electromagnetic spectrum where engineers can not tread.

The spectrum covers everything from radio waves and microwaves, to the light that reaches our eyes, to X-rays and gamma rays. And humans have mastered the art of sending and receiving almost all of them.

There is an exception, however. Between the beams of visible light and the blips of radio static, there lies a dead zone where our technology isn’t effective. It’s called the terahertz gap. For decades now, no one’s succeeded in building a consumer device that can transmit terahertz waves.

“There’s a laundry list of potential applications,” says Qing Hu, an electrical engineer at MIT.

But some researchers are slowly making progress. If they stick the landing, they might open up a whole new suite of technologies, like the successor to Wi-Fi or a smarter detection system for skin cancer.

The mystery of the terahertz

Look at the terahertz gap as a borderland. On the left side, there are microwaves and longer radio waves. On the right side lies the infrared spectrum. (Some scientists even call the terahertz gap “far infrared.”) Our eyes can’t see infrared, but as far as our technologies are concerned, it’s just like light.

Radio waves are crucial for communication, especially between electronic devices, making them universal in today’s electronics. Light powers the optical fibers that underpin the internet. These realms of technology typically feed off different wavelengths, and uneasily coexist in the modern world.

[Related: An inside look at how fiber optic glass is made]

But both realms struggle to go far into the terahertz neutral zone. Standard electronic components, like silicon chips, can’t go about their business quickly enough to make terahertz waves. Light-producing technologies like lasers, which are right at home in infrared, don’t work with terahertz waves either. Even worse, terahertz waves don’t last long in the Earth’s atmosphere: Water vapor in the air tends to absorb them after only a few dozen feet.

There are a few terahertz wavelengths that can squeeze through the water vapor. Astronomers have built telescopes that capture those bands, which are especially good for seeing interstellar dust. For best use, those telescopes need to be stationed in the planet’s highest and driest places, like Chile’s Atacama Desert, or outside the atmosphere altogether in space. 

The rest of the terahertz gap is shrouded in mist. Researchers like Hu are trying to fix this, but it isn’t easy.

Engineering terahertz waves

When it comes to tapping into terahertz waves, the world of electronics faces a fundamental problem. To enter the gap, the silicon chips in our electronics need to pulsate quickly—at trillions of cycles per second (hence a terahertz). The chips in your phone or computer can operate perfectly well at millions or billions cycles per second, but they struggle to reach the trillions. The highly experimental terahertz components that do work can cost as much as a luxury car. Engineers are working to bring the prices down.

The other realm, the world of light, has long sought to make devices like lasers that could cheaply create terahertz waves at specific frequencies. Researchers were talking about how to make such a laser as early as the 1980s. Some thought it was impossible.

[Related: When light flashes for a quintillionth of a second, things get weird]

But MIT’s Hu didn’t think so.“I knew nothing about how to make lasers,” he says. Still, making this kind of laser became his quest. 

Then in 1994, scientists invented the quantum cascade laser, which was particularly good for making infrared light. All that Hu and his colleagues needed to do was push the laser out to the longer waves of the far infrared.

Around 2002, they succeeded in making a terahertz quantum cascade laser. But there was a catch: The system needed temperatures around -343 degrees Fahrenheit to actually fire. It also required liquid nitrogen to work, which made it difficult to use outside the lab or cryogenic settings.

In the two decades since, that temperature threshold has crept up. The latest lasers from Hu’s lab operate at a balmier 8 degrees Fahrenheit. That’s not quite room temperature, but it’s warm enough that the laser could be chilled inside a portable refrigerator and carted out of the lab. Meanwhile, in 2019, a team from Harvard, MIT, and the US Army created a shoe box-sized terahertz laser that can alter molecular gas.

In the time it took Hu to finetune his laser, electronics have made progress, too. Advances into how chips are built and the materials that go into them have pushed them to run faster and faster. (A nanoplasma chip made by a group in Switzerland in 2020 was able to transmit 600 milliwatts of terhertz waves, but again, only in the lab.) While electrical engineers want to see more progress, designing terahertz components isn’t the distant dream it once was. 

“Now we can really make really complicated systems on the chip,” says Ruonan Han, an electrical engineer at MIT. “So I think the landscape is changing.”

“What’s happened over the last thirty years is that progress has been made from both ends,” says Mark Sherwin, a physicist at the University of California, Santa Barbara’s Terahertz Facility. “It’s still relatively rare, but I would say, much, much, much more common … and much easier.”

Such decades-long timescales are common in a world where new technologies whirl about in cycles of hype and disappointment. Amongst engineers, terahertz is no exception. 

The future of terahertz technology

For now, the two realms trying to enter the terahertz dark zone from either end remain largely separate. Even so, they’re giving the science world new abilities in a broad range of disciplines.

Some of those abilities could speed up communication. Your Wi-Fi runs on microwaves: Terahertz, with higher frequencies than microwaves, could forge a better connection that’s orders of magnitude faster. Through a wire, it could also create a lightning-fast cross between USB and fiber optics.

Terahertz waves are also ideal for detecting substances. “Almost every molecule has a ‘fingerprint’ spectrum in the terahertz frequency range,” says Sherwin. That makes terahertz waves optimal for picking out chemicals like explosives and the molecules in medicines. Astronomers already use that ability to look at the chemical compositions of cosmic dust and celestial objects. Closer to Earth, Han envisions a terahertz “electronic nose” that could even discern odors in the air.

Those terahertz signatures also make the far infrared ideal for scanning people and objects. Terahertz waves can see through stuff that light can’t, such as clothes, with the bonus of avoiding potentially harmful ionizing radiation like X-rays. Security screeners have already shown interest in the tech.

The one scanning characteristic that terahertz waves lack is that they can’t get through water—in the air and in the human body. But that’s no obstacle for medicine. A doctor could use a terahertz device to screen for subtle signs of skin cancer that X-rays might miss; or a neuroscientist might use it to scan a mouse brain.

Hu thinks the research is still early days. “If we can develop tools that can really see something and not take forever to scan some area, that could really entice potential practitioners to play with it,” he says. “That’s an open-ended question.”

Much of the terahertz gap remains a blank spot on researchers’ maps, which means equipment using the coveted far infrared waves just isn’t common yet. 

“Researchers really don’t have a lot of chances to explore what [terahertz waves] can be good at,” says Han. So, for now, the faster, more sensitive world inside the gap remains largely in their imagination.

The post You’ve probably never heard of terahertz waves, but they could change your life appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This article was originally features on The Conversation.

Cancer is simultaneously one of the most common and devastating diseases in our society. So working out new ways to treat it is an enduring scientific challenge.

A protein called p53 plays a key role in the body’s immune response to cancer, and therefore makes an interesting target for cancer treatment. Specifically, our bodies rely on p53 to prevent cancer cells from growing and dividing uncontrollably.

P53 has been called the “guardian of the genome” because it can stop cells with DNA damage turning into cancer cells. Essentially, it shuts down the cell if it detects any damage that could cause cells to grow into tumours.

In up to 60% of all cancers, p53 is missing or damaged, making this the most common feature shared across human cancers. So introducing intact p53 protein into cancer cells would be an elegant way of treating the disease.

This is more difficult than it sounds, though. P53 is a relatively large and floppy protein, which means our cells do not produce large amounts of it, it can easily clump together and stop working, and it is quickly broken down once it has been made.

To find a possible solution to this problem, we looked at how nature deals with similar proteins. Somewhat unexpectedly, spidroins, the proteins that spiders spin into silk, are a bit like p53. They, too, are large, floppy, and easily clump together. But unlike p53, they are capped by a small, compact part (called a domain) that is very stable and can easily be made by the cellular protein production machinery.

In our study, which has recently been published in the journal Structure, we attached a small section of a spider silk protein—a domain—onto the human p53 protein. When we introduced this “fusion protein” to cells in the lab, we found that the cells produced it in very large amounts.

To understand why, we analysed the protein with electron microscopy, computer simulations, nuclear magnetic resonance, and mass spectrometry. These experiments tell us where the different parts of the protein are located, and how they work together, like parts of a robot.

It turned out that the floppiest part of the p53 protein was wrapped around the spider silk domain like a thread around a spindle. By “winding up” the protein like that, the spider silk domain pulled it out from the cellular production machinery, and as a result, more protein was produced.

Spider silk proteins could be the key to future cancer therapies

What now?

None of our findings so far amount to a new cancer therapy. But they do open up new possibilities: we could use this knowledge to design new protein domains that make p53 less floppy and easier to produce.

If we deliver the RNA, the genetic “blueprint” for how to make p53, into cells, we could include modified spider silk domains to increase the cells’ ability to make the protein.

As next steps, we will test how well healthy human cells tolerate the spider silk proteins, and whether this addition extends the lifetime of the p53 protein inside the cells.

The post Spider silk proteins could be the key to future cancer therapies appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Rodney Lee Page is a professor of Oncology, Colorado State University. This article as originally published at The Conversation.

Stunning advances have happened in medicine since President Richard Nixon declared the “war on cancer” just over a half-century ago.

But that progress is only the beginning. More is expected in the coming years and decades, particularly following President Biden’s recent announcement of a new “cancer moonshot” initiative, coupled with a pledge to “end cancer as we know it.”

One way to help make that happen is through the study of cats and dogs. As a professor of oncology and doctor of veterinary medicine who has been researching cancer in dogs for more than 40 years, I learned long ago that companion animals can teach us an enormous amount about how to prevent and treat cancer in people.

There are many reasons why this is true. Domesticated cats and dogs share approximately 85 percent of the same DNA as humans. And because both have been intimately associated with people for more than 10,000 years, they have become susceptible to some of the same diseases.

Remarkable similarities in cats, dogs and people

Over decades, researchers have accumulated what is now a treasure trove of cancer data on companion animals. This data holds clues—and perhaps, answers—to how and why pets can get cancer, and how to keep it in check or get rid of it.

But because of the remarkable similarities in the biology and habitats of cats, dogs and people, it’s possible researchers can also extract this data on pets and extrapolate it to humans. Therein lies the opportunity to discover biomedical innovations that benefit not only your pet, but you as well.

This approach cuts by decades the amount of time it takes for data to come in. Consider that veterinarians observe and care for cats and dogs as they age and die over a life span of roughly 10 to 15 years. In comparison, gathering similar data from humans over a lifetime takes from 60 to 100 years.

You may wonder if the same information could be gleaned from laboratory animals. After all, scientists have been obtaining important data from them for decades to develop new products. But cancer is induced in lab animals artificially, primarily through surgeries or injections; companion animals “naturally” develop disease, and data from them reflect more realistic estimates when serving as precursors to investigations in humans.

Dogs and cats as canaries in the coal mine

Cancer is a leading cause of death for cats and dogs. As with people, the disease develops over a long period of time, and the same conditions that create cancer in humans also apply to them.

Here are some examples: Scientists have long noted the similarities in mutations and biological changes in dogs and people with melanoma, lymphoma, and lung cancers. A growing segment of veterinarians, human medical doctors and cancer scientists are using these shared characteristics to develop improved therapeutics for pet dogs with cancer. Many researchers believe this will help them develop effective treatments for humans as well.

Studies show that asbestos exposure can lead to mesothelioma, a malignant tumor that forms on the lining of tissues throughout the body in both dogs and humans. Tobacco smoke can cause lung cancer in humans, lymphoma in cats and nasal cancers in dogs. Learning how to lessen toxin exposure in companion animals could speed up the use of similar strategies to keep humans healthy.

Work is underway to make this happen. In one study, researchers strapped silicon sensors to people and their pets to measure their exposure levels to pesticides and herbicides in the home and yard. The exposure levels between humans and their pets were strikingly similar. This study suggests our pets may serve as harbingers of harmful environmental exposures—the so-called canary in the coal mine.

Scientists are now starting to integrate the millions of human and canine datasets now available and compare them across species. The rapid and recent development of genetic sequencing technologies, along with the proliferation of electronic medical records, has also been tremendously helpful.

These factors will greatly accelerate significant insights into cancer risk factors for both companion animals and people. Already, large population studies of dogs have begun, with researchers collecting the animal’s genetic, environmental, lifestyle, and nutritional information.

The bone cancer connection

As previously noted, traditional lab animals don’t always make the best subjects for cancer research. The immune systems of mice and rats, for instance, are not as complex as that of humans; those of dogs and cats are far more like our own.

One example: Researchers combined a blood pressure medication, already generically available for humans and dogs, with a chemotherapeutic agent, also approved by the Food and Drug Administration for humans and dogs. Then they studied the repurposed product on pet dogs with bone cancer. The results were so positive that doctors initiated the same protocol in children with bone cancer. That clinical study is not yet far enough along to draw any conclusions.

But the proposition makes sense. Bone cancer in humans and dogs is genetically indistinguishable. If this approach works, it could cut by years, and with far less cost, the time it takes to develop a pharmaceutical product to treat children with bone cancer.

A rule of thumb: The traditional pipeline for a new cancer drug is at least 10 years at a cost of billions of dollars. But the bone cancer clinical trial on children began within five years—and cost $2 million.

What’s next

The people-pet connection is more than just the similarity in species. An extensive veterinary medical infrastructure now exists to support cats and dogs during cancer management. An ever-burgeoning technology and an abundance of data that crosses disciplines are there for the taking.

However, gaps still exist in our knowledge, particularly regarding our understanding of the immune system of companion animals. Additionally, the funding available to conduct clinical studies in companion animals is severely limited. Support from the National Institutes of Health, however, has been earmaked to overcome at least some of these obstacles.

When science learns more about how to prevent and treat cancer in our pets, it’s likely that we will minimize the burden of cancer for all species.

Disclosure statement: Rodney Lee Page previously received consulting funding from The Morris Animal Foundation as Principal Investigator of the Golden Retriever Lifetime Study. He has not received funding for 3 years. He is affiliated with The Dog Aging Project, Vaika Inc, and Embark Inc as a volunteer member of the scientific advisory board.

The post Oncologists are studying cancer in dogs and cats to help humans appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

A PAIR OF EMPTY DOCKS sit atop dried muck at an abandoned marina, glaring reminders that the largest saltwater lake in the Western Hemisphere is disappearing. Three main tributaries empty into Utah’s Great Salt Lake, but decades of their flows being diverted for agriculture, cities, and industry—along with prolonged drought—have starved the 1,700-square-mile body of its lifeblood. Last summer the inland sea made national headlines when it dropped to the lowest point ever recorded, exposing roughly 750 square miles of sediment to the same winds that carve hoodoos and sculpt arches to the south and east.

Despite much-needed rain on this early-October afternoon, only the slimmest sheen of water glistens where the lake should be—and it will disappear within days. The patches of bare earth it will leave behind can easily turn into dust that blows straight into Utah’s largest urban area, Salt Lake City, about 30 miles to the east. Making matters worse, that sediment is full of arsenic.

Kevin Perry, an atmospheric scientist at the University of Utah in Salt Lake City, has covered nearly every inch of this sandy terrain riding (sometimes pushing) a fat-tired bicycle to sample and identify the most erodible patches. Between 2016 and 2018, he pedaled 2,300 miles—dodging lightning, bullets from trigger-happy target shooters, and roaming bison on Antelope Island, a state park that juts into the southeastern corner of the lake. And he got caught in 15 or so of the increasingly frequent dust storms on the dried lake bed, or playa. “My legs were sandblasted,” he says. “Visibility reduced to feet in minutes. Sand was in my eyes.”

By documenting the amount of vegetative cover, the presence and thickness of any biological crust produced by bacteria, algae, or mosses, and the percentage of tiny dust-prone silt and clay particles, Perry determined that 9 percent of Great Salt Lake sediments readily blow away. But as much as 22 percent could—especially if human activities, such as the use of roving all-terrain vehicles or motorcycles, destroy the crust. Perry, a meteorologist by training, estimates Salt Lake City annually gets 10 to 15 notable dust events that reduce visibility to less than a mile, up from none only 15 years ago. He has to approximate because the sensors required to monitor air quality are few in number, not well placed for his purposes, and set to measure only one 24-hour period every three days, to keep costs low. Even if dust storms are happening all the time, you have only a 1-in-3 chance of being able to measure one, he says.

Perry is part of a team of six scientists aiming to track dust, both the extent to which it moves in acute storms and the incognito chronic creep of microscopic granules called particulates that can make one year dustier than the next—or alter the airborne earth’s long-term contribution to climate change. Their project, called Dust Squared, will over five years expand monitoring, assess the particles’ effect on water quality, and develop molecular “fingerprints” to better track, model, and ultimately predict their movement. Not only do they want to know where the stuff comes from, they want to understand what travels in it—and, once it settles, what impact it has on human health and ecosystem function. Efforts to quantify the amount emitted from the Great Salt Lake could better inform land and water management policies. The project is just one example of the alliances being built by US scientists to coordinate and prioritize research efforts to investigate the rising dust threat.

Dust may be one of the biggest environmental hazards routinely swept under the rug. A 2021 study led by environmental economists at Carnegie Mellon University found that a 9.7 and 12.2 percent increase in dust in the US West and Midwest, respectively, between 2016 and 2018 resulted in 9,700 additional premature deaths annually by 2018, translating to $89 billion in damages. While ongoing drought and land and water management are factors, other possible causes of the increase in airborne particulates range from greater wildfire activity to decreased enforcement of the Clean Air Act. Particulate matter 10 microns in diameter is called PM10. Anything smaller than that can damage lung tissue, cause lung cancer, and increase risk of death. Valley fever, a fungal disease that can infect the lungs once it gets kicked up by high winds, is on the rise. Dust-caused traffic fatalities garner the most attention, however. On a Sunday afternoon in late July 2021, in southwestern Utah, poor visibility led to a 22-car pileup that killed eight and sent 10 to the hospital. “It was an extremely tragic event—we had never seen that in Utah,” says Maura Hahnenberger, the Dust Squared team member who studies how meteorology shapes dust movement from the region to the Rocky Mountains.

Dry lake beds represent the West’s largest single dust source. The Great Salt Lake is just the latest so-called terminal lake—a water body that doesn’t empty into the ocean—to go parched. The most infamous is California’s Owens Lake, whose primary tributary was diverted in 1913 to supply Los Angeles with water. By 1987, when the EPA first found the lake violated National Ambient Air Quality Standards for particulate matter, it was the largest PM10 source in the nation.

[Related: Decades of US air quality improvements may be slowing

A study released by Brigham Young University in 2020 found that Utahns may be losing roughly two years each on their life expectancies due to poor air quality. Further, it costs the state about $2 billion a year in healthcare expenses, missed work time, lost tourism, and decreased growth.

Salt Lake City residents are concerned that potentially toxic desiccated sediments will worsen their already worrisome smog. The city sits in a bowl, known as the Great Basin, that stretches from California to western Utah; the lake, to the west, is its lowest point, and the Wasatch and Uinta mountain ranges that tower over the urban center form its eastern border. In the winter, the peaks cause inversions whereby warm air traps a polluted cold layer in the valley for extended periods. In the summer, warm, stagnant air causes spikes of ozone, and, increasingly, Utah gets California’s wildfire smoke. “Typically, spring and fall were when we had really good air quality,” says Perry, “but that’s when we get our big dust storms. They are closing our good air quality window—and that puts us all at risk for poor health outcomes over time.”

AT 7,800 FEET, citron-colored aspen trees encircle an 80-year-old weather station situated where the Wasatch and Uinta mountain ranges meet. Two Dust Squared team members are installing high-elevation collection devices before the first major storm of the season dumps more than a foot of snow

Jeff Munroe, a geologist at Middlebury College in Vermont and principal investigator of the project, pours black marbles into a simple, shallow plexiglass square with five separate troughs. Dust will get trapped below the spheres, while their dark surfaces will heat up and help evaporate any snow or rain that falls into the troughs. The decidedly low-tech device will sit undisturbed in the same location, accumulating particles until his team samples them in warm weather to collect the “winter” deposits and again in the fall to check the “summer” yield.

The Uintas are one of the few mountain ranges in the lower 48 with an unusual east-west orientation. As a result, Munroe says, they offer scientists a “ready-made experiment” to study how dust moves from the Great Basin to the Rocky Mountains. “It’s this nice kind of catcher’s mitt for stuff coming from the south or north,” adds colleague Greg Carling, a hydrogeologist at Brigham Young University in Provo. With some 18 such devices spread across the range, they can determine how much falls and from which direction.

Munroe is wrapping up his 25th season in the Uinta Mountains, where he first began studying how dust shapes high-elevation ecosystems, and where he deployed the first collection devices in the Wasatch in 2020. He and Carling began collaborating in 2015. In 2019, the duo published a first attempt at determining whether the playas or urban pollution is the primary dust source in the two ranges; they found that a startling 90 percent of the particles in the Wasatch came from the playas of the Great Salt Lake, roughly 75 miles east, and Sevier Lake, around 150 miles southwest. But they couldn’t distinguish between the two sources. Carling says the next step is to differentiate the playas, then consider additional sources, such as other playas, agriculture, and oil and gas development. Jumping at the opportunity to study dust “from source to sink,” Munroe and five Utah-based colleagues pulled together to form the Dust Squared crew after landing a $5 million grant from the National Science Foundation in 2020.

One of the big questions the team aims to tackle is what, if any, impact the minerals, metals, and microbes that hitchhike on dust can have on distant ecosystems. For example, Janice Brahney, a biogeochemist at Utah State University, looks at how phosphorous-laden dust alters pH and plankton growth in alpine lakes.

Carling, meanwhile, studies whether the metals carried along degrade water quality when snow flushes into mountain streams. “During snowmelt we see this increase in metal concentrations in the river,” he says. Using samples from the headwaters of the Provo River, near the weather station, Carling has detected lead, copper, beryllium, and aluminum—none of which could have come from local rock’s parent material, a simple quartzite. “Lead shouldn’t be in these samples,” he says. “It must have come from another source.” That finding turned attention to what the wind blows in. “There’s not a lot of work on the impacts of dust on water quality. We see it on the snowpack, but the next step is seeing where it goes, where it ends up in the watershed. It gets pretty messy.” To make those connections, Carling compares what’s in dust to what’s in the samples from the Provo, a source of drinking water.

Similarly, McKenzie Skiles, a snow hydrologist at the University of Utah, has been modeling dust impacts on snowmelt in the mountains to try to get a fix on how that affects the region’s water supply and quality. Eighty to 90 percent of Salt Lake City’s water comes from snow, Skiles says, “yet current snowmelt models do not account for dust impacts.” Her research suggests the airborne soil causes the white stuff to liquefy between one and three weeks sooner than it would otherwise. Instead of a steady trickle of water through spring, this earlier thaw leaves less to flow into rivers and groundwater during increasingly hot, dry summers. In the worst-case scenario, melting causes inundation that the soil—and reservoirs—can’t absorb and store. “It’s the mountains that provide all of our water,” she says.

The team’s real goal, though, is to inform policies that manage the amount of dust getting into the snowpack in the first place, which is why Carling looks for chemical fingerprints to connect what lands in the peaks to dried-out lake beds. In 2020, he showed that, although it’s slight, there is enough difference in their strontium isotopes to distinguish dust from the Great Salt Lake and sediments from the all-but-disappeared Sevier Lake. “That’s one fingerprint, but it would be better to have others,” he says. Carling and colleagues are also exploring whether they can find enough unique microbial DNA to distinguish whether their samples link back to sediment, soil, or mining.

Without fingerprinting, existing monitoring methods can miss a lot. Researchers can trace a bigger dust event back to the source, but it requires luck: A satellite must be in the right place at the right time to capture definitive images. When those images don’t exist, Skiles turns to a technique called “back-trajectory modeling,” which uses meteorological data to trace a parcel of air backward over time to see where it picked up particles. Using atmospheric computer models that determine the origins of air masses, Skiles tracked dust in the Wasatch Mountains to a single event in 2017 originating from the Great Salt Lake and desert. The model showed that event contributed roughly half of the snow’s total dust deposit.

Alternatively, the Dust Squared team can try to piece together information on events using EPA sensors, but those are limited too—down to only 19 such probes in Utah, 14 of which monitor PM2.5, the size that can most easily penetrate the lungs, and five of which track PM10. Their project will add another 550 low-cost sensors, most of them in urban areas, including PurpleAir monitors used by a popular real-time air quality smartphone app, to detect particulates below PM2.5. (About 80 percent of the state’s population lives in the urban-industrial corridor known as the Wasatch Front, extending from Brigham City to Provo and including Salt Lake City.) They also plan to install a dozen in more rural areas. In recent years, the EPA has gotten rid of PM10 sensors, since PM2.5 poses the greatest public-health concerns, but PM10 remains problematic, and without the ability to monitor it, the researchers can’t maintain a long-term record. “For dust research, it’s difficult not to have,” says Hahnenberger.

AT FIRST GLANCE, Owens Lake, 200 miles north of Los Angeles, east of the Sierra Nevada, looks like a crusty, pillaged landscape. An expanse of saline crystals covers most of the area, while streaks of crimson, salt-loving bacteria thrive in briny shallow pools. For decades, the dust generated here was hazardous to the area’s 40,000 permanent residents—and millions of visitors to the area’s national parks. By 2014, a court order required implementing dust-control measures to mitigate 44.2 percent of the 110-square-mile playa, the largest such project in the nation.

The EPA’s maximum National Ambient Air Quality Standard for coarse particulate matter is 150 micrograms per cubic meter of air during a 24-hour period, and amounts above 350 cause significant harm to human health. “At Owens Lake, we have had exceedances greater than 100 times the maximum standard,” says Phillip Kiddoo, the air pollution control officer now overseeing mitigation efforts on behalf of the state’s Great Basin Unified Air Pollution Control District. “Our highest day was around 20,000 micrograms.”

It’s taken three decades of experimentation with blankets of gravel, vegetative plantings, and shallow flooding to wrangle the dust. In the 1990s and early 2000s, the six lake sites monitored had dozens of exceedances each year; in 2020, the area topped federal limits on only eight occasions. It’s a mitigation success story, albeit one with a $2.5 billion price tag, and one that without a doubt will require ongoing maintenance. “We’ve learned that working with nature is much smarter than against nature,” says Kiddoo.

To avoid this kind of costly saga, Dust Squared’s Perry thinks it makes the most sense to keep the Great Salt Lake alive. In June 2021, during a brutal drought, water from the Bear River—the lake’s most significant source—stopped flowing into it, even as state legislators entertained proposals to divert more of its water for other purposes. Until the Great Salt Lake began to disappear, many locals considered it a nuisance. “The public thinks it’s salt water and can’t be used for anything, and that every drop of water that makes it in the lake is wasted,” says Perry.

But a 2012 state report said different. The inland sea generates $1.3 billion annually to Utah’s economy, including $1.1 billion from industry (largely mineral extraction), $136 million in recreation, and $57 million to raise brine shrimp for aquaculture feed. The state’s $1 billion ski industry also benefits from lake-effect snow. And the area is also a prominent pathway for migratory birds. One consequence of its disappearance, though, has even greater power to galvanize public attention: “The thing that unites everyone is air quality,” says Perry.

[Related: Living in the same city doesn’t mean breathing the same air]

Because of smog levels during winter inversions, the state fell out of compliance with National Ambient Air Quality Standards nearly a decade ago, forcing it to create a pollution mitigation strategy. But the plan doesn’t take into account dust coming off the Great Salt Lake. Now, with growing public outcry to save the lake, politicians have taken steps to find solutions. Utah congressional representative Blake Moore teamed up with a California congressman to introduce the Saline Lake Ecosystems in the Great Basin States Program Act in September of 2021. If passed, the legislation would direct the US Geological Survey to study how best to manage terminal water systems in the region—knowledge that could also benefit Lake Abert in Oregon and the Salton Sea and Mono Lake in California.

Perry’s previous research has shown that the most cost-effective way to prevent dust is to stop diverting freshwater, most notably to agriculture, and replenish flows into the Great Salt Lake. “Ten feet of water, and you could solve the dust problem,” he says.

The MIT Knight Science Journalism Fellowship Program funded travel for this story.

Correction February 28, 2022: An earlier version of this story mis-named Oregon’s Lake Abert as Lake Albert.

This story originally ran in the Spring 2022 Messy issue of PopSci. Read more PopSci+ stories.

The post Dust clouds are killing people out West—and the dangers could spread appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In 2010, three patients received an experimental form of immunotherapy for leukemia through a clinical trial at the University of Pennsylvania. Two of the patients went into complete remission—and stayed that way. 

The treatment, known as CAR T-cell therapy, is now FDA-approved to treat certain blood cancers. It involves engineering a patient’s own white blood cells to attack cancerous cells and then returning them to the body. Since clinical trials and FDA approval, CAR T-cell therapy has already been used to successfully treat and clear certain cancers. However, CAR T-cell therapy doesn’t lead to lasting remissions for every patient, and it can cause serious side effects. A new report offers clues about why the treatment is sometimes remarkably effective.

The two patients who responded well to CAR T-cell therapy in 2010 remained disease free for over a decade. One of the men, a Californian named Doug Olson, is now 75. The other, William Ludwig, died early last year of COVID-19. Researchers were able to detect CAR T-cells lingering in Olson and Ludwig’s bloodstreams long after their cancers disappeared, although the types of immune cells that persisted were slightly different than anticipated, the team reported on February 2 in Nature.

“Now we can finally say the word ‘cure’ with CAR T-cells,” Carl June, the principal investigator for the University of Pennsylvania trial, told The New York Times.

Olson and Ludwig were among the earliest recipients of CAR T-cell therapy, allowing clinicians a chance to track the patients’ cells and condition over the past decade. “To use the word ‘cure,’ you really need a long time to follow up to make sure people don’t relapse,” says David Maloney, the medical director of cellular immunotherapy at the Immunotherapy Integrated Research Center at the Fred Hutchinson Cancer Research Center in Seattle. “When we get these people out to 10 and 11 years post-treatment, that encourages us to be a little more forceful in saying that perhaps patients are cured in some cases.”

Steven Rosenberg, chief of the surgery branch at the National Cancer Institute’s Center for Cancer Research, is a little more hesitant about making similar declarations. He and his colleagues treated the first person to receive CAR T-cell therapy—a man with advanced lymphoma—in 2009; like Olson and Ludwig, the patient underwent a complete remission and has stayed disease-free. Still, it’s not impossible for a person’s cancer to come back after such a long time, Rosenberg says. 

While it may be too soon to know for certain that these patients are cured, Rosenberg feels, these cases are all very encouraging. “I think it’s a good step in that direction,” he says. “It certainly can last a very long time and provide a relatively normal life back to these patients.”

A living drug

Immunotherapy treatments harness a person’s immune system to fight cancer. The white blood cells known as T-cells, which form the basis of CAR T-cell therapy, play a variety of roles in the immune system, including attacking cells that have become infected by viruses or turned cancerous. However, the T-cells a person’s body makes naturally may not be equipped with the recognition tools, or may be too few in number, to vanquish their cancer.

The goal of CAR T-cell therapy is to genetically modify T-cells so they can effectively destroy cancerous cells. T-cells are edited to produce a lab-designed protein called a chimeric antigen receptor, or CAR, on their surface. The CAR is tailored to the type of cell that has gone awry. “[You] essentially insert a gene that could make all of the T-cells recognize the same thing,” Maloney says.

[Related: Why immunotherapy could be the cure to cancer we have all been waiting for]

For the clinical trials in 2009 and 2010, Rosenberg’s team and the University of Pennsylvania researchers independently engineered CAR T-cells that home in on a molecule called C19 that’s found on antibody-making B-cells—another immune cell known to become cancerous in certain leukemias and lymphomas. After being administered, the disease-fighting T-cells can multiply by up to 10,000 times over the course of several weeks, Rosenberg says. The patient is treated with their own cells.

“It’s a living drug,” Rosenberg says. “They can survive in the body for years, and they appear to be able to mediate complete, durable [remissions].”

CAR T-cell therapy is now used to treat certain forms of leukemia, lymphoma, and multiple myeloma. But, as the Times noted, it’s more effective against some blood cancers than others. Some people who go into remission later relapse. 

To understand why CAR T-cell therapy was so successful for Olson and Ludwig, June and his colleagues investigated the fate of the modified cells. “The surprising thing is that the types of CAR T-cells that actually persisted seemed to be slightly different than what people were anticipating would be the ones that would result in a long-term population,” Maloney says.

The cells that stuck around weren’t the so-called “killer” T-cells that attack diseased cells, but rather “helper” T-cells that are typically involved in coordinating the immune response. Laboratory experiments suggested that, intriguingly, these helper CAR T-cells retained their cell-killing ability. 

“We have long realized that there must be differences between CAR T-cells that persist for long periods and those that die within weeks to months from exhaustion,” John E. Levine, a professor of medicine, hematology, and medical oncology and of pediatrics at the Tisch Cancer Institute at Mount Sinai in New York, said in an email. “This paper now defines some of those differences.”

The reason for the lasting response, he said, may be that the CAR T-cells are kept stimulated by the B-cells constantly being made in the bone marrow. “These B-cells provide an endless source of targets for the few CAR T-cells that have the potential to stay healthy and live a long time,” Levine said. 

The results could help researchers identify CAR T-cell traits to emulate in the future. “This will lead to a lot of additional work to see how these cells arise and evolve over time after they’re infused,” Maloney says, adding that research clinicians could “potentially make cells that have these characteristics that might be associated with better outcomes.”

Another possible avenue for CAR T-cell research is to recreate the conditions that set these immune warriors up for success when they don’t occur naturally. For example, Levine said, researchers could “provide an artificial source that mimics the constant stimulation of CAR T-cells that seems to help keep them surveilling for malignant cells.”

Understanding more about how these treatments work could ultimately lead to patients receiving CAR T-cell therapy without having to wait until several other lines of treatment have failed. “As we get more data [and] we know how safe they are, we know how effective they are, we can start moving them up, and the future may be that this will be used much earlier in the course of cancer therapy than where we’re currently using them,” Maloney says.

Broadening the approach

One major drawback of CAR T-cell therapy is that it hasn’t been proven effective against solid tumors found in places like the colon, stomach, prostate, breasts, and uterus, which cause about 90 percent of cancer deaths in the US, Rosenberg says.

There are several reasons for this: “It’s a hostile environment, where the tumor is trying to kill the T-cells and trying to keep the T-cells out of the tumor so they…can’t actually get in there and attack the cancer,” Maloney says. Researchers are working on strategies to make T-cells more resistant to these blocking efforts, he says.

Another problem is that CAR T-cells kill healthy cells along with cancerous ones. When CAR T-cells demolish B-cells in people with blood cancers, the immune system can become more vulnerable to infections. To help avoid this, patients can receive antibody infusions and their antibody-making B-cells may replenish over time, Rosenberg says. 

With solid tumors it’s a different story. “You can live without B-cells during that interim by getting immunoglobulin infusions, whereas if you wipe out a liver or a lung or a heart or a brain, you can’t survive,” he says.

Fortunately, solid tumors are often somewhat vulnerable to naturally occuring T-cells, which recognize abnormal proteins specific to these cancerous cells. “The DNA in the normal cells has mutated in these solid cancers…and it turns out it’s the products of those mutations that conventional T-cells recognize,” Rosenberg says.

He and his colleagues have spent several decades investigating treatments that are similar in principle to CAR T-cell therapy to fight solid cancers.

One approach involves identifying which T-cells are best at recognizing a person’s cancer, multiplying these tumor-invading cells to much greater numbers in the lab, and transferring them back into the patient. Melanoma is a particularly appealing target for this treatment because it tends to have many mutations for T-cells to recognize. However, the experimental therapy shows promise for other types of cancer as well, including metastatic breast cancer.

The team is also testing techniques aimed at patients who don’t mount a strong enough immune response on their own. T-cells from these people are engineered to carry lab-made versions of naturally occurring T-cell proteins that will recognize mutations found on their cancer, much like CAR T-cells are equipped with synthetic proteins. 

These treatments can be more complicated to implement than CAR T-cell therapy because the T-cells recognize solid tumors by mutations that differ from one patient to the next, rather than a common molecule like CD19. “It’s a very highly personalized treatment, but we’ve shown it can be effective,” Rosenberg says. “The major challenge that we face now is increasing it from isolated cases to treatments that can be widely administered.”

The treatments he and his team are working on and CAR T-cell therapy are all forms of adoptive cell therapy, a branch of immunotherapy that involves multiplying or engineering immune cells from a patient to fight their cancer. The most promising avenue for adoptive cell therapy, Rosenberg feels, will be against the solid tumors in the future

“This entirely new approach of creating a drug for the patient using their own cells has resulted in these dramatic long-term responses that have returned people from being very ill to normal life and certainly is here to stay,” Rosenberg says.

The post A ‘living’ cancer drug helped two patients stay disease-free for a decade appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

A middle-aged, mixed-race woman is now the third person to be cured of HIV after receiving donated stem cells with an HIV-resistant mutation from umbilical cord blood. 

The woman, referred to as the “New York patient,” also had leukemia, and received the umbilical cord blood four years ago to treat her cancer. Since then, her HIV has been in remission. She is the first woman and the first mixed-race person to be cured of HIV through this blood transplant method, which is  a variation of a previously successful treatment. Two previous patients, Timothy Ray Brown or “the Berlin patient,” and Adam Castillejo or “the London patient,” received adult stem cell transplants in 2008 and 2016, respectively. Brown has since passed away from cancer—though his HIV stayed in remission.

Brown, Castillejo, and the New York patient all received transplants as part of their cancer treatment. All three developed immune systems that could fight off the virus, because the transplant donors had HIV-resistant mutations. This treatment has not been attempted in anyone with HIV who also does not have cancer. 

The woman who received cord blood also experienced smoother recovery than the two men who received adult stem cells—Brown and Castillejo both experienced graft versus host disease, in which the donated stem cells attack the host’s body. She was able to leave the hospital by day 17 after her surgery. 

Because umbilical cord blood is much more widely available than adult stem cells, the success of the New York patient’s transplant bodes well for future patients. Using umbilical cord blood is an innovation that could open up HIV treatment to many more patients of more racially diverse backgrounds, especially since cord blood does not need to be matched as closely to the recipient’s blood as other types of bone marrow transplants. 

[Related: The first people have received an experimental mRNA HIV vaccine]

A wider pool of patients could potentially receive this cord blood treatment as opposed to adult stem cells—donor registries are mostly Caucasian, which makes finding a donor (and especially one who has an HIV-resistant mutation) exceptionally difficult for people of color. 

“The fact that she’s mixed race, and that she’s a woman, that is really important scientifically and really important in terms of the community impact,” Steven Deeks, an AIDS expert at the University of California who was not involved with this patient’s case, told The New York Times. Globally, 52 percent of adults living with HIV are women, and yet women make up just 11 percent of participants in HIV treatment trials. 

Sharon Lewin, president-elect of the International AIDS Society, told The Washington Post that this is an exciting case, but ultimately not realistic for the masses of people dealing with HIV infections. “A bone-marrow transplant is not a viable large-scale strategy for curing HIV, but it does present a proof of concept that HIV can be cured,” she said. Not every patient will be able to undergo a bone marrow transplant, but for those who do, this is promising.

The doctors involved with the New York patient are nevertheless excited at the success and potential that umbilical cord stem cells offer for future treatments. “This provides hope for the use of cord blood cells … to achieve HIV remission for individuals requiring transplant for other diseases,” Yvonne J. Bryson, an infectious-diseases physician at the David Geffen School of Medicine at the University of California at Los Angeles who presented the case, told The Washington Post. 

Why this transplant with umbilical cord stem cells worked better than those with adult stem cells is still unknown. Perhaps they’re more adaptable, Deeks told The New York Times. “Umbilical stem cells are attractive,” he added. “There’s something magical about these cells and something magical perhaps about the cord blood in general that provides an extra benefit.”

The post The first woman has been cured of HIV using donor stem cells appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

This post has been updated to include additional context and background for several studies and sources cited. It originally published on January 13, 2022.

In July, chemical-manufacturing giant Bayer announced that home gardeners would no longer be able to buy products containing glyphosate, the active ingredient in the world’s most actively used weed-killer Roundup. It was the culmination of tens of thousands of lawsuits filed against Bayer and Roundup’s previous owner, Monsanto, for their alleged role in causing a form of cancer called non-Hodgkin’s lymphoma. So far, plaintiffs have been awarded hundreds of millions of dollars in settlements. In August, Bayer filed a petition to have the US Supreme Court review one of those cases.

The decision to remove glyphosate from the home-gardening market wasn’t an admission of culpability, and farmers will still use glyphosate-containing products. Bayer maintains that glyphosate is safe and doesn’t cause cancer. The most recent report from 2016 by the Environmental Protection Agency (EPA) supports Bayer’s view. The authors of the report concluded that glyphosate was an unlikely carcinogen and poses no known meaningful risks to human health.  These findings have been backed up by regulatory agencies across the globe, including the EU’s Assessment Group on Glyphosate (AGG), European Food Safety Authority (EFSA), European Chemicals Agency (ECHA), German BfR, Australian, Korean, Canadian, New Zealand,  Japanese regulatory authorities, and the Joint FAO/WHO Meeting on Pesticide Residues (JMPR). Still, authorities like WHO’s International Agency for Research on Cancer list glyphosate as a probable human carcinogen.

At the same time, scientists and economists raise doubts about the safety of Roundup and similar products—and the rigor of the research that’s gone into reports by Bayer and the EPA.

How Roundup became ubiquitous

When Monsanto first marketed Roundup in 1974, the company sold it as a breakthrough tool for agriculture: an herbicide that was safe for the environment and for humans. Unlike the pesticide DDT, which was banned by the EPA in 1972, Monsanto asserted that glyphosate wouldn’t linger in the environment or in human bodies. Studies suggest that within soil, glyphosate’s half-life, or the amount of time it takes for half of a particular application to break down, is between seven and 60 days. It leaves behind a chemical byproduct, AMPA, but neither glyphosate nor AMPA tend to accumulate in human cells. Instead, they’re excreted in urine and feces. 

[Related: Pesticides might be worse for bees than we thought.]

There’s also the mechanism by which glyphosate kills weeds: it inhibits the shikimate pathway, a system plant cells use to produce energy, by inhibiting an enzyme that helps them synthesize amino acids from carbohydrates. In essence, glyphosate starves plants. Human cells don’t have this same pathway to energy production. This detail sets glyphosate apart from other chemicals that cause genetic mutations and cancer, which tend to target pathways that also exist in human cells, says Jia Chen, a professor of environmental and public health at Icahn School of Medicine at Mount Sinai. “For that purpose, you would consider it quite harmless,” Chen says. 

While human cells don’t use the shikimate pathway, bacteria do. It’s possible that glyphosate’s apparent risk to human health is due in part to the chemical’s effect on the good bacteria in our guts. This community of good bacteria don’t just help us digest our food; they’re also vital players in our immune system. 

Studies on rats and bacteria cultured in labs suggest that glyphosate inhibits the composition of gut bacteria, possibly limiting their ability to modulate our immune systems. (However, we can’t know for sure based on these studies whether the same effects occur inside the human body.) Theoretically, glyphosate doesn’t have to stick around in our cells to have these effects; the chemical just needs to pass through. Imbalances in the microbiome create room for pathogenic bacteria, which could trigger inflammation. Researchers reason that both inflammation and immune-disruption are associated with increased cancer risk, according to a 2018 review published in the journal Carcinogenesis.

However, Bayer points out that when the European Food Safety Authority reviewed claims that glyphosate harms human gut microbiota, they found no evidence to support that assertion.

On top of that, research suggests that even at very low concentrations, glyphosate mimics human hormones, potentially triggering or speeding up the growth of tumors.

Nearly half a century after its introduction to agriculture the chemical is ubiquitous in the environment. “Glyphosate is, by far, the most heavily used and most profitable herbicide ever discovered,” says Charles Benbrook, an agricultural economist at the Heartland Health Research Alliance and a compensated expert witness in the ongoing Roundup litigation. As of 2014, 825,000 tons of the herbicide were used each year worldwide, according to an article published in the journal Environmental Health. 

Scientists have found glyphosate everywhere from tree roots to honeybee hives. In a study of 94 pregnant women who weren’t directly exposed to herbicides at work, Chen and a team of international scientists found traces of glyphosate in the urine of 95 percent of participants. “You can even detect it in surface water and rain,” Chen says, “Glyphosate is basically everywhere.”

The trouble with studying Roundup

Scientists have linked glyphosate and glyphosate-containing products to a number of conditions, from miscarriages to cancer. But you can’t randomly expose people to a potential toxin and compare them to an unexposed group, the way you would conduct clinical trials for a drug—doing so would be unethical for the former and pretty much impossible for the latter, given this compound’s ubiquitousness—so examining the effects of glyphosate in humans remains a challenge, Chen says. Scientists tend to study the effects of the chemical on human cells or other animals in the lab, or to retrospectively ask people about their exposure to glyphosate to find potential health correlations. Still, exposing lab mice to toxins won’t give you a clear image of what happens to humans, and people may bump into multiple potentially toxic substances throughout their lives that could damage their health. In other words, neither method is perfect.

In 2016, the EPA concluded that glyphosate was “not likely to be carcinogenic to humans.” 

[Related: Pesticides can hurt agricultural communities—so why do farmers fight back against bans?]

Scientists, regulators, and the popular press have all focused overwhelmingly on the link between glyphosate and cancer. “But from my point of view, I’m more interested in the non-cancerous outcomes. Because health is not just equal to cancer,” Chen says. This year, Chen’s pilot study on pregnant women, published in the journal Environmental Pollution, linked higher urinary concentrations of glyphosate to shorter pregnancies. All of the pregnant people in the study gave birth to full-term babies—in other words, gestation lasted 37 weeks or longer—but shorter pregnancies, especially those shorter than 37 weeks, are associated with complications in newborns, from breathing to gastrointestinal problems. The babies born to people who had more glyphosate in their urine also had greater distance between their anus and genitalia, which is associated with higher levels of male sex hormones. That finding suggested to Chen that glyphosate might interfere with the endocrine system—alarming, but not conclusive. Again, Bayer points out that no regulatory authority has ever found evidence that glyphosate acts as an endocrine disruptor.

Data on non-cancer outcomes isn’t the only information we lack, says Leland Glenna, a sociologist at Pennsylvania State University. Herbicide manufacturers aren’t required to share the inactive ingredients in their products, so scientists don’t really know what Roundup contains, aside from glyphosate. That makes it difficult to study. 

The data isn’t just incomplete. Glenna, who researches the role of science and technology in agricultural policy-making, believes much of it is unreliable. Much of the epidemiological data we do have comes directly from scientists employed by the companies producing herbicides—a potential conflict of interests. In that EPA report on glyphosate, 39 percent of the studies reviewed were produced by industry-funded scientists, according to an analysis published in Environmental Sciences Europe. 

“There’s a clear distinction between public science and private science,” Glenna says. That same analysis found that out of the 36 studies on pure glyphosate that were included in the EPA report, just two percent published by industry scientists found an association between glyphosate and cancer versus 67 percent of those published in peer-reviewed journals. But even that number may be unreliable. 

[Related: The main ingredient in RoundUp doesn’t just kill plants. It harms beetles, too.]

During the 2018 court case Johnson v Monsanto, evidence presented included leaked internal emails in which Monsanto employees discussed ghostwriting studies to support the claim that glyphosate is safe for human health.  This included discrediting the International Agency for Research of Cancer’s report that “glyphosate was a probable human carcinogen,” according to a 2021 review co-authored by Glenna and published in the journal Research Policy.

Still, scientists don’t have conclusive evidence that Roundup causes health problems. According to Chen, science has a long way to go before reaching any conclusion on the effects or Roundup—or lack thereof. She and other scientists are calling for more independent research, the release of information on inactive ingredients in these products, and a greater focus on complete herbicide formulations rather than just glyphosate. 

For now, Heartland Health Research Alliance’s Benbrook doesn’t advise consumers to renounce Roundup entirely. Instead, he says to take proper precautions: wear protective clothing when using the herbicide, take a shower immediately after any potential exposure, and avoid the product if you’re immunocompromised in any way. 

“There is some alarming evidence there, but nothing is concrete,” Chen says. “That’s why we need more research.” 

The post This Roundup ingredient is riddled with controversy—here’s why appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Emily Cataneo is a journalist and fiction writer whose work has been published in the New York Times, Slate, NPR, The Boston Globe, and Atlas Obscura, among other publications. Find her on Twitter @EmilyCataneo.

This story originally featured on Undark.

In the 1950s, Badin, North Carolina, was a segregated town divided by a titanic plant owned by the Aluminum Company of America. The company owned not just the plant, but also the schools, homes, and streets. On the town’s western side, known variously as West Badin or Negro Village, the alleyways went unpaved. Residents recall workers used a unique substance to tamp down the dust. “They would get PCB oils out of the power breakers and transformers,” says Macy Hinson, who grew up in West Badin. He remembers seeing trucks spread the oily concoction on the dirt.

As a youth, Hinson held the company, now known as Alcoa, in high regard. His family moved to Badin (pronounced Bay-din) in the 1940s to seek jobs at the plant. The Hinsons had been farmers, and Alcoa offered a lucrative and stable alternative to sharecropping. Black acquaintances from other parts of the country remarked on the presence of indoor plumbing in the Hinsons’ Alcoa-owned home, and Hinson grew up longing to work at Alcoa like his father and uncles. He started there when he was 19 and stayed for nearly 33 years.

“I thought Alcoa was the guardian savior,” he says.

Hinson, now in his 70s, is an affable, friendly man, wearing a t-shirt from a seafood restaurant in the next town over. He’s prone to such phrases as “if I can’t make you smile, I’ll leave you alone.” But talk of Alcoa darkens his mood. Years ago, Hinson saw a collection of obituaries kept by Valerie Tyson, another former Alcoa employee, outlining the causes of death for his friends and colleagues at the plant: cancers and breathing-related diseases.

While he couldn’t prove that Alcoa had caused these deaths, Hinson found it strange that so many of his coworkers had died of similar conditions. Hinson went on to learn that the toxic substances used in aluminum smelting are associated with the illnesses that killed his coworkers. PCBs, or polychlorinated biphenyls, for example, have been linked to an array of negative health effects in non-human animals, including cancer and nervous system issues. According to the U.S. Environmental Protection Agency, human studies suggest PCBs likely cause cancer in humans as well.

“I get angry when I think about some of this stuff,” Hinson says.

In 1980, Alcoa first applied for a hazardous waste permit from the EPA and the state of North Carolina. A series of rule changes by the EPA, however, initially left the company with little obligation to clean up sites around its plant. The following decade, Alcoa began working with the state to manage its waste. Since then, Alcoa has undertaken efforts to monitor and/or remediate dozens of sites and toxic runoff outfalls. In an email to Undark relayed through communications consultant Robert Brown, Alcoa director of transformation/asset planning and management Robyn Gross said the company is “doing everything we have been asked to do—and much more—to protect human health and the environment.”

But with other Alcoa smelting plants in Texas and New York having been extensively cleaned up, Hinson and a coalition of advocates, nonprofits, lawyers, and other residents say that Alcoa has not done enough in Badin. They say that some of these sites are still dangerous because they’re leeching substances such as fluoride and cyanide. They also point to runoff from decades of aluminum smelting dripping into nearby Badin Lake, as well as what they describe as racist decisions that put Black workers in the most dangerous jobs and Black-owned houses near the biggest waste dumps. Badin has become a crucible for questions about the legacy of industrialization, racial capitalism, and environmental justice in the American South, and for how choices made and prejudices fomented a century ago reverberate into the present — with the added complication that Badin was a company town.

Even after Badin incorporated as a town in 1990, its charter prohibited the local government from regulating or censuring any industry, and the present-day town government has not participated in the push for a cleanup. According to a body of social science research, the nature of company towns adds another layer to the already complicated relationship between workers and their employers in industrial America. Company towns were set up as paternalistic caretakers, saviors, and guardians against the cruel outside world. They proliferated in the late 19th century and saw their heyday in the early 20th, across industries ranging from railroads to coal; at their peak, there were 2,000 of these towns scattered across the United States. They ranged from seemingly idyllic communities, like the chocolate-producing town of Hershey, Pennsylvania, to exploitative, dangerous places, like those that dotted coal country in Appalachia.

Badin falls somewhere in the middle. Pavithra Vasudevan, an assistant professor of African and African diaspora studies at the University of Texas at Austin, interviewed Badin residents in the 2010s to understand Alcoa’s legacy. In a 2019 paper, she wrote that she had “expected narratives of exploitation, but was confronted everywhere by care.” Alcoa, she noted, was “ever the benevolent father.” The company gave residents schools, roads, jobs, an escape from sharecropping, and an identity. Efforts to confront and remediate the damage have moved slowly, in part, because residents didn’t want to believe that their beloved company could be harming them.

Although the definition of a company town varies, in its strictest form, a company town is a space where an industry owns and controls everything from shops to government. These towns “are the product of their designers’ hope that shaping the built environment in particular ways will allow them to further their political, economic, and cultural goals, whether these be exerting greater control over their labor force, ensuring the development of particular types of industrial relations, or, perhaps more altruistically, providing their workers with better housing than they might otherwise be able to secure,” according to the book Company Towns in the Americas: Landscape, Power, and Working-Class Communities.

By their nature, companies may control nearly every aspect of life in this kind of place. In the company town of Alcoa, Tennessee, for example, you couldn’t “sharpen a pencil without getting approval from a Company official,” Russell D. Parker wrote in the Tennessee Historical Quarterly in 1978.

The story of Badin as a company town begins during the aluminum rush in the late 19th and early 20th centuries, when companies sprang up all over the world to manufacture this lightweight, strong, versatile, rust-proof metal. Because aluminum smelting is energy-intensive, these companies turned to hydropower, a renewable resource. In the 1910s, there was a “global mad scramble” to find prime locations for factories, said Ryke Longest, co-director of Duke University’s Environmental Law and Policy Clinic.

In 1912, a group of Frenchmen decided to open a smelting plant in North Carolina, near the Yadkin River. They named the surrounding area after Adrien Badin, who became head of the firm in 1914, and started building a dam. But then World War I sent the French racing back to Europe. In 1915, Alcoa bought the unfinished dam, the plant, and the town, and began smelting two years later. The company cranked out aluminum through World War II with a near-monopoly. At its peak, the facility produced more than 125,000 tons of aluminum per year.

When Alcoa bought Badin from its French founders, the company added to the existing housing stock, building laborers’ cottages, bungalows, and superintendents’ houses, available at varying rental costs. All of this took place during the Jim Crow era. On the east side of the plant, white families took up residence on streets named after trees, while on the west side, Black families made their homes on streets named after presidents or Confederate generals. (Hinson was born on Lee Street.)

Producing aluminum is notoriously dirty. It first entails mining bauxite, a sedimentary rock that’s composed of aluminum hydroxides, iron oxide, silica, and other impurities. The crushed bauxite is then mixed with sodium hydroxide to extract aluminum oxide, leaving behind a highly toxic red sludge in the process. Workers place the aluminum oxide into steel cells—commonly known as pots—lined with carbon, where it gets converted into aluminum through an electrochemical process. Once impurities are removed from the molten metal, workers mold the aluminum into ingots, pieces of pure metal ready for the market. In the process, they run the risk of burns and exposure to a panoply of toxic materials.

According to researchers and former plant employees, Alcoa commonly employed Black workers in the plant’s most hazardous area—the place that contained the cells, known as the potroom. When the aluminum dropped to the bottom of these pots, it left behind a variety of toxins on the lining—cyanide, fluoride, “almost anything on the periodic table,” says Nancy Lauer, a geochemist by training who works as a lecturing fellow and staff scientist at the Environmental Law and Policy Clinic at Duke University. (Lauer doesn’t receive any compensation from the nonprofits or residents challenging Alcoa.)

According to Vasudevan’s interviews, potroom workers were colloquially called the bull gang because of the strength required to wield a sledgehammer and shatter the toxic crust that lined the pots. While Alcoa maintains that race was not a consideration in where employees were assigned, Vasudevan’s research suggests Black workers often received these jobs because many industrial employers at the time wrongly thought that Black bodies could withstand heat better than white bodies. One former white employee told Vasudevan that Alcoa sent recruiters to farms and cotton fields in search of Black workers to fill positions in the potroom, where it would get “hot, hot, hot.”

Hinson started out at Alcoa in the ingot department, toiling every day in noise and filth. Once, he says, higher-ups came in wearing hazmat suits, walking past him and the other workers in their normal clothes.

Meanwhile, Black workers and their families recall being exposed to toxins in their neighborhood, too. Hinson says ash billowed from smokestacks and settled over West Badin. Women scrubbed their husbands’ stained clothing, possibly contaminated with oil and asbestos. Kids played in a pool of muck that is now known to contain hazardous waste from the plant.

“I started realizing that the things they were doing and having people do, it was killing them,” Hinson says. (When asked about Hinson’s allegation, Gross replied: “Alcoa is a values-based company, and the safety and health of our employees is paramount. We are always working to ensure the protection of our employees, the communities where we are located, and the environment by complying with relevant rules and regulations. This includes taking steps to constantly improve working conditions. Alcoa is proud that we have been a leader in improving working conditions in the aluminum industry.”) Later Hinson started vying for new jobs, moving on to become a power dispatch operator before eventually finding a position as a dam supervisor.

The 20th century ended and the 21st started, and then, something happened that Hinson never thought he would see in his lifetime. Alcoa, the town’s backbone and raison d’etre, closed its plant. Badin transitioned from company town to regular town, albeit one run by a local government prohibited from regulating industry. Operations were shifted overseas to Iceland, where many aluminum smelters have moved over the past 20 years, enticed by the country’s low-cost hydropower and geothermal energy. (Alcoa does still operate some plants in the US.)

Badin’s population contracted, from 5,000 people at its 1920s heyday to less than 2,000 now, including the inmates at the nearby Albemarle Correctional Institution. The company left behind part of its giant plant, the town, and numerous waste areas. These dumps and contaminated sites are scattered across the area in pine copses and beneath the grass.

Today, Badin resembles many other rural American towns: good bones, a strip of brick buildings on a main street, and pleasant, leafy streets. There are more than a half-dozen churches and a smattering of businesses, including a pizza restaurant, a supper club, an antique store, and a Dollar General. The town is about half white and one-third Black, with many Black residents still living in West Badin.

According to the website for the Badin Business Park, a subsidiary established by Alcoa on the site of its former plant, “tremendous progress” has been made to identify and clean up the company’s past pollution. Starting in the 1990s, in accordance with a federal law called the Resource Conservation and Recovery Act, Alcoa says it has diligently worked with the state of North Carolina to identify and clean up waste areas stemming from its operations, through measures such as capping with soil or clay; implementing systems to collect seepage from the sites; and improving a channel to divert surface water around a landfill.

But Longest sees it differently. He said what’s happening in Badin is “just a slow and steady leeching of hazardous waste.”

For years, a series of citizens, environmental groups, and lawyers have challenged Alcoa’s narrative surrounding cleanup at the plant. It started with workers and family members filing compensation claims against Alcoa for the health impacts of working in an aluminum smelting plant. The following decade, during a relicensing process for the plant, a nonprofit called the Yadkin Riverkeeper noticed that Alcoa was failing to monitor and clean up pollution in nearby Badin Lake and sought pro-bono legal representation from the law clinic at Duke.

When Hinson heard about these efforts, he says nobody came into the Black neighborhood to ask its residents anything. “So we felt like we were left out of the process,” he says. He and others stepped forward to talk about their experiences with Alcoa, which led to Hinson’s founding a group called Concerned Citizens of West Badin in 2013. Hinson and the other concerned citizens, who numbered about 20 at their height, met regularly to advocate for themselves and for remediation in their community. In 2019, the Southern Environmental Law Center successfully negotiated a settlement on the citizens’ behalf, requiring the company to install a new stormwater system to manage the pollutants. More recently, however, an SELC lawyer told the policy news site NC Policy Watch that continued high levels of fluoride demonstrate that the new system isn’t effective.

The scientists and lawyers involved in monitoring Alcoa are concerned about two main environmental issues. First, the solid waste sites around Badin, which contain toxins from the spent potliner. And second, the PCBs polluting nearby Badin Lake.

Lauer, of the Duke Environmental Law and Policy Clinic, has been working with Longest for more than three years to monitor Alcoa’s cleanup effort. Her role is to examine Alcoa’s test results to ensure they support the company’s conclusions—and to make recommendations based on her review of data at the site.

“In my opinion, they do the bare minimum when it comes to testing,” she says. From Lauer’s perspective, when Alcoa finds contamination, they attribute it to other factors and abrogate responsibility. “Their data will say something, and their conclusions will say something different.” For example, one site deemed an “area of interest” by the Department of Environmental Quality is a former ballfield near Badin Lake, which Alcoa gifted to the town for a new park this past June. A July 2020 comment letter signed by Lauer and Longest stated that Alcoa’s testing of that area showed elevated levels of possibly carcinogenic chemicals called PAHs, but that Alcoa had concluded that the PAHs were simply “background soil concentrations.”

When asked why the company attributes these PAHs to background contamination, Gross replied: “Comparing study findings with the known presence of chemicals in the environment is a standard practice endorsed by state and federal environmental agencies and has been used in conjunction with comparison to state and federal criteria.”

In that July 2020 comment letter, Longest and Lauer further picked apart the results of Alcoa’s work plans to clean up three main areas, including the dump where Hinson once played and that ballfield. Lauer and Longest asserted that the data actually show ongoing, worrisome contamination at all of these sites. For example, surveys of the flood plains in the area indicate elevated levels of fluoride, cyanide, PCBs, and PAHs—suggesting these chemicals could stem from the Alcoa sites despite remediation efforts.

In studies of workers in Canada and Norway, aluminum smelting has been associated with higher rates of some cancers than in the general population. And a recent study published in Nature Communications also found that proximity to Superfund sites, highly contaminated sites managed by the EPA, decreased average life expectancy by about two months, a number that could grow to more than a year when combined with other factors such as low income or race.

A study on Badin itself bears out these adverse health outcomes. Work by health data analyst Libby McClure, who currently works at DataWorksNC and is also a postdoctoral researcher at the NC Occupational Safety and Health Education and Research Center, supports worker concerns that exposure to pollutants during the aluminum smelting process causes bladder and lung cancer. As her 2020 Ph.D. dissertation at UNC-Chapel Hill, McClure conducted a study of health outcomes for 754 union members employed at Alcoa between 1980 and 2007. The study found lower mortality rates than in the general North Carolina population—a fact that McClure attributes to high poverty in the rest of the state and “healthy worker bias,” wherein wages and retirement benefits elevated these workers above the average contemporary North Carolinian. But she also found higher rates of death by bladder cancer and mesothelioma among these workers, while noting the findings were based on just a handful deaths. McClure also found that workers employed in the potroom, more likely to be Black workers, were 1.5 times more likely to die of cancer than workers who were never employed in the potroom. In addition, she found that Black female workers at Alcoa experienced excess mortality relative to the general North Carolina population, and that Black male workers died of cancer at greater rates.

Gross said in an email that Alcoa disagrees with the assumptions in McClure’s conclusions, which were published in the American Journal of Industrial Medicine, pointing out that she uses the word “imprecise” to describe her own findings. (In an email to Undark, McClure explained that she “used the term ‘imprecise’ in a purely statistical way,” and that it “does not in any way reflect uncertainty in the number of deaths we documented in the analyses.”)

The story of Badin is in many ways the story of environmental justice concerns throughout the South. Vasudevan started her research career in Warren County, North Carolina, a majority-Black area that’s considered the birthplace of the environmental justice movement, and is familiar with environmental justice throughout the region, although Badin is the first company town she has studied.

“You start noticing a lot of the same patterns,” she says, including political and social exclusion for people of color, exclusion from decision-making processes, and connections between racism and environmental and workplace safety. She’s written about the similarities between Badin and Flint, Michigan, and she even drew comparisons to health outcomes in the Covid-19 pandemic, during which people of color were more likely to fall sick on the job.

These typical environmental justice narratives are compounded when they take place in a company town. Alcoa no longer owns Badin, but the legacy of that era of control lingers. In an email to Undark, Edgar Miller, the executive director of the nonprofit Yadkin Riverkeeper, wrote that Badin “is truly a company town and the local officials have been reluctant to criticize Alcoa and/or engage [with] their constituents who have concerns about the plant site.” He said he reached out to the mayor and a town council member earlier this year with a request for a spot on the agenda for the next council meeting, but when nothing came of it, he let it drop. Although many governments in many towns side with local industry, Badin is unusual because the town charter literally prohibits officials from regulating or taking action against Alcoa or other industry.

Jay Almond, the town manager of Badin since 2008, wrote in an email that while the town values “complete and accurate empirical data when compiled and fairly reported by reliable sources,” he and other officials are not worried about the pollution, because Alcoa and the NC Department of Environmental Quality have assured them that the site poses no risk to public safety. When asked about the town charter prohibiting regulation of Alcoa, he replied, “Rigorous regulatory standards of the state and county easily out-stride any opportunity for regulatory action by the town.”

The legacy of psychological control, too, lingers in Badin. When Vasudevan conducted her interviews with Badin residents in the 2010s, she found that “it’s very difficult for people to speak out” about company towns—a conclusion echoed by research of other company town residents around the world. To help further the dialogue, she turned their tales into a play, which professional actors performed at a church in neighboring New London in 2016. In an email, she wrote that the play, “catalyzed a public community conversation with some who may not have been interested in doing an interview with me (for a variety of reasons).” It explored stories from individual Alcoans and their families about their evolving relationship with the company, about the illnesses they endured after their employment there, and about the slow, fraught process of realizing that toxins and pollution may have damaged their environment and saddled them with breathing problems and a higher risk of cancer.

After the play, says Vasudevan, the audience engaged in a lively dialogue about what they’d seen; she says the former Alcoa employees were both delighted and saddened to see voice finally given to their stories, although she says that town officials in the audience did not comment or respond to the play.

Some Alcoa residents still feel protective of their erstwhile employer. At the Badin Museum, which houses a collection of ephemera from the town’s storied history, curator David Summerlin reminisced about his history with the plant. Now in his 80s, Summerlin started there as a hedge trimmer, left to join the Air Force, returned and worked there for more than 25 years, just like his father before him.

“I have nothing against Alcoa,” he says. “They were good to me all the way.”

Some of the residents who support Alcoa hope the company will bring jobs back to the area. Others have fond memories of their longtime employer. Many still feel a strong sense of gratitude. Vanessa Mullinix, now the owner of the 1913 Badin Inn, says she took a job in the potroom in 1994 and stayed for 10 years. “I knew it was a dirty, hot place. But they paid me well. I had good insurance,” she said.

“They got me out of what could have been poverty,” Mullinix adds. She thinks the allegations against Alcoa are blown out of proportion and that groups like Hinson’s have “been spitting in their face for 15 years. They have been fighting a company that brought education, that brought culture to this area.”

Hinson describes why many in town stay local to Alcoa: The company took care of their families and gave them high wages. Under those circumstances, “aren’t you going to protect them?”

Roger Dick’s grandfather was an early employee of Alcoa, working in a lab, and his father worked on the dam. Dick, now chief executive officer of a local bank, says that some residents focus on the company’s gifts to the town while not seeing the larger picture. Alcoa was drawn to Badin because of the river, a resource Dick saus the public had a right to. “They never really understood that,” he adds. Alcoa generated hydropower from the river to run its operations, yet “people will tell you how grateful they are that Alcoa just gave them a park,” says Dick, referring to the former ballpark where Alcoa testing confirmed the presence of contaminants.

On sunny days, Badin’s eponymous lake glimmers past the town’s trees and brick buildings. This 8-square-mile lake was birthed when the company dammed a local river in 1917, and now the lake’s northern points and coves are lined with vacation homes. Families, many of them Latino, drive in from Charlotte to bathe and boat at the sandy strip known as Badin Beach. Some people fish in the lake, either recreationally or potentially for sustenance.

Now, the lake is the site of a related contamination fight—one that speaks to another environmental justice issue, pertaining to whose concerns are taken seriously. Alcoa has discharged fluoride and cyanide into this lake and nearby Little Mountain Creek for years, said Lauer. And for years, the company failed to meet its permit levels for the creek. “They’re in noncompliance and they should get fined for it,” she said. “But instead they have been getting these special orders by consent to keep things business as usual.”

Alcoa applied for another such special order of consent in late 2020, asking the state to allow it to divert the discharge from the creek to Badin Lake, where it has a more lenient permit. When a group of neighbors living on the lake found out what was going on, they formed an organization called Protect Badin Lake. They started a petition that received nearly 5,000 signatures, and people sent more than 350 comments to the Department of Environmental Quality. The agency denied the special order of consent, although Alcoa may still submit another request. Miller of the Yadkin Riverkeeper wrote in an email to Undark that the organization is now “working with Alcoa to hire an independent facilitator to develop a stakeholder process to address issues” regarding the permit. “The facilitator,” he wrote, “has identified the Town of Badin as a key stakeholder in that process and will be invited to participate, mostly likely being represented by the Town Manager.”  

To Jen Caldwell, one of Protect Badin Lake’s founders, the idea of allowing Alcoa to divert the discharge into the lake is unthinkable. “If you let Alcoa, which has been getting away with this for 30 years plus, dump there, what is going to be their next step?” she said, adding that when she takes her boat across Badin Lake to pick up pizza, she has to walk right over that ballfield.

Concerned Citizens of West Badin and Protect Badin Lake are working together on their clean-up goals now, after Concerned Citizens learned about Protect Badin Lake in the course of being interviewed for this article. But some stakeholders expressed umbrage at how quickly Protect Badin Lake caught the attention of the Department of Environmental Quality, which has approved special orders of consent in the past. Lauer and Chandra Taylor, a lawyer who has represented Concerned Citizens of West Badin, attributed Protect Badin Lake’s organizing power in part to their race—many members are white.

“This is what happens,” says Taylor. “If we talk about the cause of environmental injustice, one of the factors is always either a lack of political power and influence or a perceived lack of connections that would build up social capital. That, to me, is at play here.”

Badin is not a lost cause. It’s possible to clean up sites with this kind of pollution and environmental damage, says the Duke experts.

Lauer says that in an ideal world, Alcoa would excavate all the hazardous waste and deposit it in a lined and permitted landfill. That could happen under the EPA: While the Alcoa site in Badin has been evaluated for listing under Superfund in the past, Alcoa has so far managed its own cleanup under an older framework established by the federal Resource Conservation and Recovery Act, administered by the North Carolina Department of Environmental Quality.

But critics, many of whom say the state has been too lax, want the EPA to list the area as a Superfund site.

“To leave hazardous waste in unlined landfill this close to bodies of water is just problematic in my opinion,” Lauer says. “We’ve seen that Alcoa has been able to excavate this at other sites and put it in a hazardous waste landfill. It’s entirely doable,” she said, adding that while Alcoa did not remove PCBs from the lake, they did cap them with sediment in 2013.

Alcoa has successfully cleaned up other sites that are comparable to Badin. In suing its insurers for exorbitant cleanup costs at dozens of facilities across the country in 1992, Alcoa highlighted smelting sites in Point Comfort, Texas; Massena, New York; and Vancouver, Washington. Alcoa opened its plant in Massena in 1903 (that plant is still in operation) and testing decades later revealed high PCB levels in fish, waterways, and on the property at the plant. The company was required to dredge and cap swathes of land and waterways around the site. In Point Comfort, where a smelting plant opened in 1948, the Texas Department of Health, now known as the Texas Department of State Health Services, found contamination in crabs and fish. Similarly, the EPA required the company to dredge and cap. The EPA listed the Vancouver site, where Alcoa operated until 1985, under Superfund in 1990. The company worked with the state to remove contaminated soil and the EPA delisted the site six years later.

The EPA, however, is not responsible for Badin. Point Comfort, Massena, and Vancouver were all designated federal Superfund sites, allowing the EPA to direct and oversee their cleanup. In Badin, the cleanup is proceeding under RCRA. Under this framework, Vasudevan said, Alcoa was able to designate itself a “responsible polluter” and take charge of its own cleanup. The company sets the tenor and pace of remediation, with NC DEQ providing supervision.

When asked why Alcoa cleaned up sites like Massena and Point Comfort more comprehensively, Gross said, “No two sites are the same. Each has its own unique set of requirements that need to be addressed in a responsible and comprehensive manner.”

McClure pointed out that the former Alcoa workers and the population of Badin include a higher percentage of people of color than the Massena and Point Comfort sites, although Massena is adjacent to the St. Regis Mohawk tribal lands. Vancouver’s population is also predominately white. But Vasudevan pointed out another reason: The American South has historically been a place of loose worker protections, as well as lax oversight of environmental issues and industrial shenanigans—part of the systematic issues underlying this whole controversy.

Lauer agreed that North Carolina is partly to blame. “The state has not really done what they need to do to hold Alcoa accountable,” she says. “Alcoa is seemingly able to get away with a lot.”

The successful clean-ups at Massena, Point Comfort, and Vancouver—at a cost of more than $240 million for the Massena site alone—means that Alcoa could conceivably clean up Badin too.

Alcoa is now conducting an ecological risk assessment for the former ballfield and the Alcoa/Badin landfill, but Lauer is unsure of how much human health will be considered. Ideally, she says, the company would look at the impacts of living, working, and vacationing in this area. What does swimming in the lake do to the human body over time? What about dust exposure? Having a home in West Badin? Eating the fish? A study like the one Lauer is proposing would systemically analyze all of these questions. But as of now, nobody has those answers.

On a hot June day this year, Hinson finished up work at Lowe’s, about 45 minutes away in Kannapolis, and then headed back to his house just outside of Badin. As the day dimmed, he drove down to Badin Lake, which is just across a highway from the old plant. Boats skimmed the surface of the lake, and happy vacationers bustled around with towels and swimwear, their hatchbacks popped and opened towards the shore. Others floated on tubes in the water. Near the boat launch lay that ballfield, gifted by Alcoa to the town.

“I thought they were here to save everyone in this area,” said Hinson. “And they were—so long as it benefited them.”

He pointed out a jumble of faded bricks on the shore. A train used to arc along the lake here, he said, and workers from the plant would dump bricks into the water. As far as he knows, no one has tested these bricks, so nobody knows if they’re contaminated or not, but either way, he said they’re waste from the former plant. Hinson looked down at these relics from the place where he, his family, and his friends spent their careers.

His message to Alcoa: “Clean it up and admit that you did it,” he said. “Apologize to whomever’s left.”

The post A North Carolina town struggles under the toxic shadow of the company that built it appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The Food & Drug Administration is finally allowing 23andMe to provide testing for the breast cancer-related genes BRCA1 and 2. Back in 2013, when the direct-to-consumer company originally starting selling the test, the FDA clamped down and forced 23andMe to verify its genetic health risk evaluations. 23andMe had to prove the genes they were testing for were related to a health condition, and show that the tests were accurate.

Now you’ll be able to buy your BRCA test online and get your results a few months later, all without ever seeing a genetic counselor or doctor. In some ways, this is a wonderful advent of technology. It democratizes health information. It empowers people to take control of their lives and mitigate risks.

But it also means we’re handing out data to people who might not be adequately prepared to hear it, and who might not actually understand what they’re getting. Testing positive for a genetic mutation often doesn’t mean you’ll get the associated disease, and we still don’t really understand how exactly genes impact your overall health. Before, when you had to get your genetic information through a counselor, a trained expert walked you through the process and explained the complex factors that go into disease risk. Now you get your answer from a website.

There’s a lot to unpack about this new BRCA test, so let’s take a few minutes to discuss what’s at stake here.

What is BRCA, anyway?

Inside your cells, you have a set of proteins whose only job is to identify and fix mistakes in your DNA. Every time your cells divide (which, by the way, happens millions of times a day), they have to replicate your genetic code to pass it along. Individual mutations—which is what we call any mistake in your DNA—happen all the time, but your repair proteins fix most of them before they cause any harm. Mutations most often come in the form of one DNA building block being swapped for another, but sometimes they occur because a DNA strand breaks, and the repair protein mends the strand imperfectly. Maybe a piece is lost, or the wrong end of the strand gets stuck back on. If just one strand snaps, the repair proteins can usually match the right end. But if both strands break at once, repair proteins struggle to make it right.

The BRCA1 and 2 genes produce some of these double-stranded DNA repair proteins. When they work normally, they can do the job pretty well. But if they have certain mutations, they stop being able to glue the broken DNA back together in the right orientation. This leads to a ton of glitches in the rest of your DNA, because the ends get stuck back in different spots. Cancer happens when you hit a critical mass of tumor-promoting mutations—tweaks that promote runaway growth—within a cell. So by increasing the odds and rates of mutations, faulty repair proteins can make you much more likely to develop cancer.

This is why the majority of women with BRCA1 and 2 mutations go on to develop breast cancer. In the general population, 12 percent of women develop the disease at some point in their life. But having certain BRCA1 or 2 mutations ups those odds to 72 and 69 percent, respectively. It also increases your chance of getting ovarian cancer, though not by nearly as much.

These mutations are inherited, so women with a strong family history of breast cancer—especially family members who got cancer in both breasts and/or at an early age—are often encouraged to get a genetic test. Being a carrier of these mutated genes doesn’t necessarily mean you’ll develop breast cancer, but it increases your odds so much that doctors tell people with positive results to get screened for cancer earlier and more often.

Does the 23andMe test work?

In order to get greenlit by the FDA, 23andMe had to prove that their test was clinically valid, meaning it can detects BRCA1/2 mutations with high accuracy and precision.

The big caveat here is that the 23andMe test only looks for three possible mutations out of more than 1,000 known variations. Not all of those are harmful, but many are, and the 23andMe test can’t tell you whether or not you have most of them. A negative result means you don’t have the three most common BRCA1/2 mutations, but you might have others.

It’s also worth noting that these three mutations are almost exclusively found in the Ashkenazi Jewish population. Though you may have Jewish heritage that you’re unaware of, most people not of Ashkenazi descent are going to test negative through 23andMe regardless of whether or not they’re actually a carrier for other BRCA mutations.

Should I get the 23andMe BRCA test?

Very few physicians would recommend BRCA testing for the broad population. Less than one percent of people have a BRCA1/2 mutation, so screening everyone isn’t practical or ethical. You’d end up with a lot of false positives—meaning the test says you have a mutation, even though you don’t—because no test is 100 percent accurate. But it is often recommended that you get a test if you have a family history of breast cancer, or if a family member has a known BRCA mutation.

Before home DNA tests, you’d have to go to a genetic counselor to discuss whether you should get a BRCA test at all. The National Society for Genetic Counselors argues that this should still be the standard. “Anyone who has a strong personal or family history of breast or ovarian cancer and is interested in finding out more about their individualized risk should consult with a genetic counselor to discuss their genetic testing options, or to discuss their results,” said Erica Ramos, President of the NSGC, in a statement. Though it’s never a bad idea to go talk to a counselor, not everyone still agrees with that idea.

“I have become more open to the fact that not every person who gets BRCA testing needs a pre-emptive counseling session with a certified genetic counselor,” wrote Leonard Lichtenfeld, Deputy Chief Medical Officer for the American Cancer Society, on his official ACS blog. “Even the genetic counselors have told me they have better things to do with their time, and that there are acceptable alternatives to informing those who want to know more about the test before they get it, such as computer-based information modules.”

The U.S. Preventive Services Task Force, which reviews evidence for various screening tests and offers a recommendation, says that women should first be screened for a family history of cancer and that “women with positive screening results should receive genetic counseling and, if indicated after counseling, BRCA testing.” They recommend against getting screened if you have no family history suggesting BRCA mutations.

“Given the importance of integrating medical and family history in understanding the implications of the results, it is similarly important that these be considered when deciding which tests are needed,” says Michael Watson, Executive Director of the American College of Medical Genetics and Genomics. “Not only is it important to have knowledgeable professionals involved in interpreting the clinical implications of the results of these tests for a specific individual, it’s equally important that these knowledgeable professionals be involved in informing people of which test is most useful for them, if any.”

He notes that many of the other health conditions that direct-to-consumer tests look at don’t have a lot of clinical relevance. If you find out you’re predisposed to certain eye diseases, it probably won’t change what your doctor recommends you do to stay healthy. But Watson explains that the BRCA mutations do change your situation. Some women will have preventative mastectomies or hysterectomies to confront an extremely high likelihood of cancer.

There’s no one right or wrong answer to the question of whether you should get the test or whether you should talk to a counselor. But it can’t hurt to talk to a medical professional.

It’s also worth keeping in mind that companies who profit from selling you a genetic test are the ones encouraging you to take said test. It used to be that DNA testing companies got their business through doctors and genetic counselors. Now those companies are coming directly to consumers, and we shouldn’t assume they have our best interests at heart.

23andMe receives a steady stream of income from selling customers’ genetic information. Some of it goes to research institutions, but they also sell to for-profit companies who use that data to try to develop new drugs. Though they may have nothing but good intentions, 23andMe only profits if people take their tests. It’s not in their interest to tell you that this may not be the right choice for you.

That being said, 23andMe is also a fairly cheap and easy way of looking at genetic markers for health risks. It’s probably not the ideal way to learn about those risks—that’s why we have counselors—but it’s not the worst. And if you’re unaware of your family history—if you’re adopted or estranged from your biological family—getting a test like 23andMe can be an accessible way to learn some basics.

What happens if my test says I’m positive?

Should your test say you have a BRCA1/2 mutation, now you should definitely talk to a genetic counselor. 23andMe doesn’t directly provide those services, so your best bet is to use the NSGC’s “Find a Counselor” tool. You’ll also probably want to talk to your primary care doctor about the results, since they should be aware of your situation. It’s possible they’ll ask you to consider some proactive treatments, depending on how high your risk is. And if you test positive for one of the common BRCA mutations, they’ll definitely want to put you on a more intense cancer screening regimen than the general population.

You may think that if you know what the results mean and don’t care to do anything about them, you don’t need to see a counselor. But here’s the thing: you don’t know what you don’t know. Genetic counselors are trained to talk to people who have just received what is, undeniably, life-changing news. They will know what you need to be aware of, and should you experience any anxiety or depression from the news, they’ll get you help. And perhaps even more importantly, they’ll know if you should follow your 23andMe results with a more in-depth genetic screening. There are many other mutations out there related to breast cancer, and some of them can raise your risk for other kinds of cancer, too.

23andMe repeatedly brings up the study they did showing that receiving a positive BRCA test didn’t have negative impacts on their customers. That may very well be true, but you should also know the conclusion came from interviewing just 32 people who responded to a request to participate in the study, out of 136 people who tested positive. Out of those, 16 were men. Male carriers still have a significantly elevated risk, but their lifetime risks of 1.2 and 6.8 percent for BRCA 1 and 2 respectively are still lower than the average woman’s breast cancer risk. It also slightly elevates the risk of prostate cancer.

When asked about their emotional response to the news, three women and one man reported that they were moderately upset, indicating they “couldn’t stop thinking about the result.” Another three women and 6 men were somewhat upset, meaning they felt “initial disappointment” or “felt anxious at first but then anxiety went away.” Nine women and eight men were neutral (some of these may have been people who already knew they were carriers, since five women reported they had already been tested).

None of this meant is to scare you away from getting the BRCA test if you want it. Plenty of people find out they’re carriers and continue to live perfectly happy lives. But some people don’t. This is just to prepare you for the idea that you could get a result that genuinely changes your outlook. It may help you better prepare for a day when you do get breast cancer, or it could give you anxiety about that possibility—or both. But you won’t know until you get the results. Just because you can now do it with a few clicks doesn’t mean it’s a test to be taken lightly.

And what if it’s negative?

Since the test only looks for three mutations, a negative result on the 23andMe test isn’t a guarantee of anything. If you have a family history of breast cancer, you should go to a genetic counselor and ask about getting a full screening. It’s only with a broader test that you’ll know whether you’re truly a carrier, which can inform your future plans for cancer screenings like colonoscopies and mammograms. So unless you also want to take 23andMe for other reasons, it doesn’t make much sense to use it for BRCA. Just skip right to talking to your doctor. 23andMe may be cheaper if you’re trying to get tested without insurance, but it’s still not going to do you much good when you’re left with incomplete results.

What if I don’t want to know?

Our healthcare system is trending toward more knowledge. In general, that’s great. Patients deserve to know all the information they want about their own health. And it’s absolutely true that having a full genetic panel can give you the sort of advance warning that might save your life.

But it’s also okay to want a bit of ignorance. Some people would rather not know. You can’t unring the bell that tells you you’re very likely to get cancer, and it’s understandable if you’d like to put off the looming specter for as long as possible. Of course you should do your best to follow medical advice based on your family history. But if you already know you need to be vigilant about mammograms and other tests, it’s okay to decide that’s enough. And if your family and personal medical history gives you no reason to think you’re at an elevated risk for breast cancer, there are many experts who would tell you that the slight chance of finding a dangerous mutation isn’t worth the risk of a false positive.

No genetic test is to be taken lightly, so everyone should consider the possible outcomes before they get one. Maybe it’s right for you, maybe it isn’t. Just think about it first. And if you’re at all willing or able to do so, talk to a doctor or genetic counselor, too.

The post 23andMe can now test for BRCA mutations. Here’s what you need to know. appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Ericka Johnson is a professor of Gender and Society at Linköping University in Sweden. She is the author of, among other books, Dreaming of a Mail-Order Husband: Russian-American Internet Romance, and A Cultural Biography of the Prostate, from which this article is adapted.

This excerpt originally featured on The MIT Press Reader.

Should I get a PSA test?” During the course of researching my book, I heard this question a lot. Even when it wasn’t asked straight out, I could feel it in the air, hovering above my conversations with men about their prostates.

“Is the test any good? What sort of number should I have? What sort of number do I want to have? Could I have cancer, or is it a false positive? Do I really need to take the test?” These questions were often asked through a haze of worry—so much so that I started to think of PSA as prostate-specific angst instead of prostate-specific antigen. And that the PSA test is causing the angst, not the prostate.

As it turns out, the prostate-specific antigen test—a simple blood test—is one of the most lauded yet also most controversial tests for prostate cancer.

But before I get into the social complexity of a simple blood test, let me provide a bit of background: prostate-specific antigen (PSA) is a proteolytic enzyme (an enzyme that breaks down proteins), secreted by the prostate into the ejaculate, that liquefies the seminal plasma, thereby allowing sperm to swim more freely. Small amounts of it also leak into the blood. Measuring this amount in the blood can indicate if there is an increased risk of cancer in the prostate.

The PSA test was first experimentally used to detect prostate cancer in the late 1980s, and in the mid-1990s it was approved for this purpose in the U.S. However, it is notoriously difficult to interpret, and can be connected to prostate size and age, and to other diseases like benign prostatic hyperplasia (BPH), inflammations, and infections. It can also be prone to false positives. Coupled with the digital rectal examination (the other dreaded test that involves feeling the prostate with a gloved finger), its reliability can be improved—a bit.

Results of PSA tests can—often do—lead to the next step: biopsy, which is often experienced as unpleasant, sometimes painful, and can lead to blood in the urine and, in some cases, infection. Biopsy following elevated PSA is, however, increasingly being replaced by MRI scans which are less cumbersome and might decrease the risk of unnecessarily detecting small, clinically insignificant, cancers. Nevertheless, results of PSA tests can also—and again, often do—lead to years of repeated, regular testing for the individual patient. And to years of repeated, regular PSA angst. Of course, the test can also lead to the detection of significant, potentially lethal, cancer, and the chance to save a life.

This is one of the paradoxes of the PSA test: People want it to find cancer and save individual lives, but they also critique it for finding too much cancer and destroying lives when applied across a whole population. If it is detected, the man and his family are placed in the shadow of cancer, faced with decisions about (and, in many countries, costs of) treatments with life-changing side effects. The man and his family are also thrown into a period of worry and anxiety, none of which would have occurred without the PSA test. For many individual men, even though they know that it might be the beginning of an extended rollercoaster ride of testing and more testing, there is still an almost irresistible impetus to know—and the hope that the test will prove they are—still—cancer-free.

It is this oscillation between hope and fear, combined with the continuous discursive shifting between the PSA as a test for individuals and the PSA as a screening tool for public health at the level of the population, that produces much of the debate about the PSA.

Complex, confusing … collective?

The preoccupation with mortality that emerges in the face of a blood test is not uniquely related to the PSA test—we are, after all, mortal. And especially at a certain age, most of us start to reflect upon this. However, as a medical sociologist, the angst I see men experiencing seems specifically generated by the threat of prostate cancer that the PSA test awakens. It is a test that congeals that angst into a worry which eats away at many of them.

When I am having these conversations—with friends, with colleagues, and with men I have interviewed—I tend to remember a urologist I met early on in this study, who admitted slyly that he didn’t get the PSA test for himself, to avoid, as he called it, “starting down that slippery slope.” He wasn’t the only urologist who admitted this to me during the course of my study, and his comment articulated a well-known phenomenon: that testing and screening can lead to a series of further tests, and a future of uncertainty. And sometimes it can generate pre-illness, proto-illness, or the idea of being a patient-in-waiting; even if you are not sick now, testing and screening can produce the feeling that you might become sick, that you might develop symptoms, and that in the future you will be struck by, in this case, prostate cancer. Then, once you have been tested, you as a patient are responsible for getting tested again, and keeping track of your numbers, following their ups (ideally not) or downs, or just their steady onward march through time.

The numbers become a visible way of knowing what is happening in your body, of trying to pin down risk and uncertainty. But because the PSA test can also be the first step in a series of more invasive tests, it is also cracking open the door to a future that threatens the side effects of prostate treatments, like impotence and incontinence and the feelings those possibilities evoke. It raises the specter of cancer and death.

Medical experts and policy-makers are aware that PSA testing is a source of anxiety for patients, but there is scant research on this, and what little there is tends to be mentioned but not considered seriously in debates about screening and testing decisions. This seems particularly poignant in recommendations that, more recently, have encouraged patient participation in deciding whether to test or not, a situation in which anxiety over results and potential false positives conflicts with the anxiety about refusing available medical tests and thereby missing a cancer.

This is amplified by the fact that the PSA test is purported to save lives by identifying tumors early, allowing for more successful treatments of smaller, contained cancerous tumors, and ultimately helping to reduce the number of men who die of prostate cancer every year. Public discussions about the PSA test are filled with survival stories from men who have found their cancer (often early, often when they were relatively young) and been successfully treated, so that they are alive today because of it. In these narratives, early detection is considered a good thing, because one is still alive; discussions of side effects are minimal. The PSA test allows medicine to come in and save a life rather than watching impotently by the patient’s side through the advanced stages of cancer.

Survival rates for prostate cancer have improved significantly over the last 30 years, but it is not clear if this is because of better treatment and primary care, or because of wider screening practices that allow earlier detection, or a combination of both. And while there is agreement that screening could save lives by detecting and treating prostate cancer earlier, it appears to entail the overtreatment of large numbers of men. This means that many men are unnecessarily subjected to surgery or radiation, and thereby have to deal with the severe side effects of treatment: pain, incontinence, bleeding, fistula formation, bowel trouble, sexual dysfunction, as well as the status of patient (including repeated PSA tests post-treatment to monitor if the cancer returns) for years to come.

And while the medical community is generally in agreement that many prostate cancers do not need to be treated (especially in men over 75), while others can benefit from active surveillance instead of immediate treatment, it can sometimes be hard to convince a patient of that. Cancer is terrifying. A patient who finds out they have cancer wants to get rid of it, and as quickly as possible. The concept of watchful waiting or active surveillance, however medically justified it might be, could quickly become an emotional nightmare.

The controversy about screening has become entrenched, as many national healthcare policy-makers have suggested that men should not be screened for prostate cancer with the PSA test. Pushing back against these decisions are national and international patient activism campaigns that try to raise awareness of the importance of screening, and encourage men to get tested. The importance of being tested — and possibly of screening populations of men — is a popular cause, for example, for many national prostate cancer patient groups — Europa UOMO; the French Association Nationale de Malades du Cancer de la Prostate; the German Bundesverband Prostatakrebs Selbsthilfe; the international Movember Foundation; the Swedish Prostatacancerförbundet — even if some countries’ patient groups are more reticent (like British Prostate Cancer UK), and even as the medical debate about its validity is still ongoing. Collectively, there are groups of men (and women, and cancer industry interests) promoting PSA and prostate cancer screening and testing, collecting research money for technological development, lobbying for screening programs, and enrolling men to participate in support groups and patient activism. And, of course, encouraging them to get tested.

All these voices, interests, and opinions are debating, promoting, rejecting, and encouraging the PSA test as a screening tool in the media around us. Especially in November. November — or Movember — has been the internationally successful flagship promotion campaign of a prostate cancer charity, encouraging men to get their PSA tested and asking them to take individual responsibility for the test rather than relying on national screening policies.

This is the message behind the mustache campaigns in November, for example, often fronted by famous people wearing mustaches, that pop up everywhere each winter. But notice the shifts I have made: from talking about individual men and their feelings about a simple PSA test to a discussion about the statistical life-saving it might achieve, to the response of governments and professional associations, to patient groups and charities who return the question to individual men and ways of encouraging them to be tested. The shifts from individuals to collectives and back to individuals in the debate can make one dizzy. It is no surprise that people become confused about the value of the PSA test, and its benefit to men.

How to embrace complexity

Healthcare as we know it today is governed with information sheets and short, simple sentences that simplify and flatten complexity in an attempt to achieve clarity. Often, this does away with complexity altogether. A lot of healthcare practice and policy is uncomfortable with recognizing death, fear, and vulnerability. And not just healthcare providers and policymakers: also people, us, everyone we know — the users and patients of modern healthcare are uncomfortable with recognizing death, fear, and vulnerability.

But how do you take something complex and make it simple, while maintaining the complexity? And how do you warn about the completely rational and expected worry about death that testing might trigger?

The PSA test involves many voices, perspectives, concerns, and stances. And there is no closure to the debates about its usefulness, even when there is a policy decision. This is because the medical evidence, should it ever become clear, is only one part of the answer. But this means that the question of PSA screening and PSA testing is more complicated than merely a question of whether the test is good enough or not. It is not only about the risk of false positives — though it is about that. It is not only about the risk of overtreatment — though it is about that, too. It is not only about the impossibility of screening men, finding cancer, and then being able to know which cancers are dangerous enough to warrant treatment and which are harmless enough to not bother about or embark upon active surveillance. And it is not only about the impossibility of reassuring someone with cancer that they can continue living with it, that they shouldn’t worry. It is about all of these things, entangled together.

The decisions about screening that we are living with today are historically formed and culturally embedded, and will always be so.

Judging by the countless discussions I’ve had with men when I wrote my book, and the voices raised for and against PSA screening in the media, it would seem as if our responses within this regime of anticipation are (at least also) colored by strong feelings of fear and worry about our mortality and vulnerability. They are emotional. And we are often caught in these knots of emotion, statistical risks, and prevention discourses, aided and abetted by well-meaning health promotion campaigns and evidence-based anticipation regimes, a situation that can easily become affective and infected. And a state of affect is not necessarily the most productive place in which to make a rational, calculated decision.

We assume that we are rational, calculating agents, making decisions based on objective facts, and we would like to believe that the answers to our screening questions could be based only on objective medical knowledge, because that would suggest that there should be a correct answer out there to questions of screen or test, when and how. But as the very idea of pure medical facts becomes tainted by the undercurrent of social context within which they are being produced, that option fades away. Those decisions about screening that we are living with today are historically formed and culturally embedded, and will always be so. They will engage our feelings of fear and worry specifically because they address mortality and death. This is the unavoidable “affective.” But instead of seeing that as a starting point for an infected debate, I suggest we embrace it. Perhaps recognizing those feelings and other social considerations in our decision-making will produce more humane, and ultimately more caring, policies for those we are trying to help.

The post Prostate exams can be lifesaving, so why are patients hesitant appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Cervical cancer is the fourth most common cancer in women around the world, affecting about 570,000 and killing more than 300,000 each year. Most cases are caused or at least triggered by human papillomavirus, or HPV.

The United Kingdom has been leading an HPV vaccination program since 2008, two years after a vaccine for cervical cancer first came onto the market. A new study out this week shows that the campaign has prevented thousands of cases of cervical cancer and precancerous conditions. Researchers examined UK cancer registry data from January 2006 to June 2019 and compared those who were vaccinated to those who were not—they found that by mid-2019, the vaccinated cohort had 450 fewer cases of cervical cancer and 17,200 fewer cases of pre-cancers than expected. The findings were published in The Lancet.

This new research is a landmark, the first to definitively illustrate the positive results of the vaccination campaign that began 13 years ago. Michelle Mitchell, the chief executive at Cancer Research UK, told The Guardian that “it’s a historic moment to see the first study showing that the HPV vaccine has and will continue to protect thousands of women from developing cervical cancer.”

In the UK, girls are offered the HPV vaccine between the ages of 11 and 13, and since 2019 it has been made available to boys as well. (In the US, the CDC recommends the vaccine for all kids between the ages of 11 and 12.) Given that the vaccine can prevent HPV infection but can’t do anything if the virus is already in the body, as well as the fact that the virus is so widespread, the vaccination program aims to reach children well before they’re sexually active.

[Related: Cervical cancer could soon be a disease of the past]

The study focused on women who received the vaccine as girls still in school. Now in their 20s, their rates of cervical cancer, and pre-cancerous conditions, are much lower than their unvaccinated peers. And the effect was more dramatic the younger they were when they got their shots.

“The impact has been huge,” Peter Sasieni, a co-author of the paper and cancer researcher at King’s College London, told the BBC. He added that these results are “just the tip of the iceberg”—the women observed are still young and not at high risk for cancer, as the years go by the benefits will compound.

Cervical cancer is one of the few cancers that are both preventable and curable (when detected early). The WHO Director-General announced a global call for action to eliminate cervical cancer in 2018, and the World Health Assembly adopted a global strategy for cervical cancer elimination in 2020. This means that, by 2030, they want 90 percent of girls fully vaccinated against HPV by age 15 and 90 percent of women with cervical disease (meaning cancer and precancerous conditions) to be receiving treatment. 

The study’s authors hope these nudge the UK population towards getting the vaccine. Co-author Kate Soldan from the UK Health Security Agency told the BBC, “we hope that these new results encourage uptake as the success of the vaccination program relies not only on the efficacy of the vaccine but also the proportion of the population vaccinated.”

The post HPV vaccination in the UK has prevented thousands of cases of cervical cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Home owners in the US will soon have to fight weeds with a different version of Roundup.

Bayer recently announced that it would change up the formula of the popular herbicide for lawn and garden care in 2023. The decision was motivated by questions around glyphosate, the main ingredient in Roundup, and whether it causes cancer in humans and harms wildlife.

The pharmaceutical and chemical company is facing tens of thousands of lawsuits and billions of dollars worth of settlements that claim health and environmental negligence from glyphosate use.

Roundup was first sold as an agricultural weed-killer in the 1970s by the biotechnology company Monsanto (now owned by Bayer). Since then, more than 19 million pounds of it have been sprayed by farmers, landscapers, and gardeners across the world. Nearly 20 percent of that share comes from the US.

Glyphosate, the acidic formula that makes Roundup so effective, is widely used in pest-control agents today. While the compound itself is thought to be non-toxic to humans, some research shows it has a potential to be carcinogenic when mixed with other herbicide ingredients. In the past two decades, more than a dozen studies have been linked glyphosate and Roundup exposure to higher risks of lymphoma in people and animals. Others have found links to male infertility, erratic honeybee behavior, and dwindling biodiversity in marine habitats.

[Related: Pesticides might be worse for bees than we thought]

In a statement that accompanied the announcement, Bayer wrote that, “this move is being made exclusively to manage litigation risk and not because of any safety concerns.” Last year, the US Environmental Protection Agency released a report saying that “there are no risks of concern to human health when glyphosate is used in accordance to its current label.” But a 2015 review by the International Agency for Research on Cancer concluded that there was strong evidence of genotoxicity, or DNA damage, from the agent—and limited evidence of carcinogenicity.

In the same statement where it said it would phase out glyphosate for residential use, Bayer noted that it would appeal a 2016 cancer lawsuit by a school groundskeeper in California up to the Supreme Court. Most of the other individuals who’ve sued Monsantor and Bayer over Roundup have been farmers.

In the 1990s, Monsanto started selling special strains of soy and other crops that were genetically modified to resist herbicides. Some experts say this encouraged more indiscriminate spraying of Roundup over the years. A handful of countries, including Vietnam, Mexico, and Germany, have either banned or set a timeline to phase out glyphosate-based herbicides. Some US cities have done the same, but there’s no federal legislation on the table just yet.

Correction August 9, 2021: After further clarification from Bayer, the headline and text of the article have been corrected to reflect that the company is changing the formula of some Roundup products, not phasing them out. The story has also been corrected to state that more than a dozen studies have found a link between lymphoma and glyphosate, not dozens.

The post Roundup is finally going to be made without glyphosate in the US appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Marc Gunther is a veteran reporter whose interests include philanthropy, psychedelics, animal rights, and tobacco. This story originally featured on Undark.

Not many scientists have fought harder against smoking than Stanton Glantz. As a professor of medicine at the University of California, San Francisco and founding director of its Center for Tobacco Control Research and Education, Glantz led campaigns to ban smoking in public places, exposed secret tobacco industry documents, and wrote or co-wrote five books and nearly 400 papers, most documenting the harm done by tobacco.

The cigarette companies despised him, and the feeling was mutual.

“I’d like to just destroy the tobacco industry,” Glantz once said. “It is an industry that kills 5 million people a year. It has no business existing. Make them go do something useful.”

In recent years, however, as a contentious debate over electronic cigarettes has fractured the community of tobacco researchers, many of Glantz’s former allies have turned on the 75-year-old scientist. His critics accuse him of exaggerating the dangers of e-cigarettes and downplaying their benefits. They say that his research into vaping has been driven by politics, not science. Some are even revisiting doubts about his earlier work, saying that his contempt for the cigarette manufacturers—and his activism against them—tainted his influential research into the dangers of secondhand smoke.

In the unkindest cut of all, these critics say that Glantz has become an unwitting ally of the tobacco industry. He has become one of “Big Tobacco’s little helpers,” as David Sweanor, a longtime anti-smoking activist, says.

How can that be? It stems from the belief held by many tobacco researchers, but not by Glantz, that e-cigarettes are safer than combustible tobacco. (Scientists do disagree about how much safer.) Many respected researchers—but again, not Glantz—also believe that e-cigarettes help smokers quit by delivering regular doses of nicotine in a way that won’t end up killing them.

Glantz and his powerful allies in the anti-tobacco movement—nonprofit advocacy organizations the Campaign for Tobacco-Free Kids and the Truth Initiative, as well as the American Lung Association, the American Heart Association, and the American Cancer Society—have mounted a campaign against e-cigarettes funded with $160 million from Bloomberg Philanthropies. Instead of inviting smokers to switch to vaping, Glantz and the nonprofits have promoted more traditional quitting strategies, including those involving the use of FDA-approved medications, while simultaneously working to ban e-cigarettes, tax them, prohibit the sale of flavored e-cigarettes, outlaw their use in smoke-free zones, and generally do whatever they can to stop both adults and children from vaping.

Glantz has made a variety of claims about e-cigarettes—that they are a gateway into smoking, that they don’t help smokers to quit, and that they raise the risk of heart attacks. All have been challenged, and one influential study has been retracted. But as Glantz’s work has been amplified by the nonprofits, they’ve helped turn public opinion against e-cigarettes. His critics say this bad science is driving bad public policy.

“They’ve convinced most of the public, including a majority of smokers, that vaping is as dangerous or more dangerous than smoking,” says Kenneth Warner, a founding board member of the Truth Initiative and former dean of the University of Michigan School of Public Health. “That’s crazy.”

“Stan has always been an advocate and ideologue willing to twist the science,” says David Abrams, a New York University professor and veteran tobacco researcher. He says that some scientists ignored flaws in his work when Glantz focused on combustible tobacco because they, too, strongly opposed smoking. “Frankly, none of us cared if he was a little bit sloppy with his research because the ends justified the means,” Abrams says.

Glantz denies that his research has been distorted by his activism. “That’s just bullshit,” he says. “It’s actually the other way around. The activism follows from the science.” He says the scientists favoring harm reduction—the claim, in the case of e-cigarettes, that vaping can reduce the damage of smoking—fail to grasp the dangers of vaping.

While Glantz retired from USCF last year, he remains the go-to scientist for the anti-tobacco movement and an honored figure on campus. “His research contributions in tobacco control are legendary,” said Pam Ling, who succeeded Glantz as head of USCF’s Center for Tobacco Control Research and Education, at a campus event earlier this year. Supporters and critics alike agree that his work has had an enormous impact on public policy.

For four decades, and especially during the early days of the US anti-smoking movement, Glantz was the “preeminent translator of the science of tobacco and disease into the public discourse of tobacco control,” wrote Michael Pertschuk, the former chairman of the Federal Trade Commission, in his 2001 book, “Smoke in Their Eyes.” The feisty academic became a “master of the sound bite” and a “tactical treasure,” according to Pertschuk’s account. Methodological questions aside, Glantz’s papers have been widely cited and publicized, and his relentless advocacy on behalf of smoke-free environments helped to curb smoking, save lives, and reduce the toll of disease. “He truly has been a hero in this global effort to fight the smoking epidemic,” says Clifford Douglas, director of the University of Michigan Tobacco Research Network.

And the impact of his work on e-cigarettes? That is decidedly more complicated.

On April 14, 1994, the CEOs of America’s seven largest tobacco companies stood before a congressional committee and a bevy of television cameras and swore under oath that they did not believe that cigarettes were addictive.

Less than a month later, a Federal Express package containing 4,000 pages of confidential tobacco industry documents arrived at Glantz’s office at UCSF. The return address: Mr. Butts, the name of a character in the comic strip “Doonesbury” who encouraged kids to smoke.

The four-foot-tall stack of papers showed that the tobacco CEOs had lied. “Nicotine is addictive,” said a 1963 memo from a vice president at Brown & Williamson, admitting the company was in the business of selling an addictive drug. The papers were rich with other insights; a letter from movie star Sylvester Stallone to Brown & Williamson promised to use its cigarettes in five movies, in exchange for $500,000.

Working with colleagues at UCSF, Glantz shared the papers with regulators, litigators, and reporters, published research to expose industry tactics, arranged to have the documents digitized, and over time raised millions of dollars to build a vast and valuable archive of materials created by the food, drug, and chemical industries, as well as the tobacco companies. Today, the tobacco archive alone contains more than 14 million items.

“The documents really transformed the whole tobacco issue,” Glantz says.

Big Tobacco and its allies hit back, hard. Brown & Williamson sued UCSF, claiming the documents were stolen. Californians for Scientific Integrity, an industry-funded group, sued the university system, accusing Glantz of scientific misconduct in connection with a study about the impact of smoking bans on the restaurant industry. Congressional allies of the tobacco industry tried unsuccessfully to terminate a National Cancer Institute grant to Glantz, and pro-smoking forces petitioned to cancel his consulting contract with the U.S. Occupational Safety and Health Administration.

In a letter to OSHA asking the agency to sever its ties with Glantz, the National Smokers Alliance called him “an avowed anti-smoking activist.” That was one charge that Glantz couldn’t deny.

Glantz was an anti-smoking activist even before embarking on his career as a tobacco researcher—and often in his career, he has played both roles simultaneously. In 1978, he volunteered to work on a statewide initiative to restrict smoking in public places in California that was defeated by the tobacco industry. “I just got sucked into the campaign leadership,” he says. He was a founder of Californians for Nonsmokers’ Rights, a nonprofit that incorporated in 1981 and grew into Americans for Nonsmokers’ Rights five years later. He helped to lead the 1983 campaign that made San Francisco one of the first major cities in the US to restrict smoking in public, a milestone that made national and international news.

Activism aside, Glantz has an unusual pedigree for a tobacco scientist. Most are physicians, epidemiologists, economists, lawyers, or psychologists. Glantz has a bachelor’s degree in aerospace engineering from the University of Cincinnati—he worked briefly at NASA—and a master’s and doctorate in applied mechanics from Stanford University. His Ph.D. thesis, a study of cardiovascular function, was titled “A mathematical approach to cardiac muscle physiology.”

His understanding of heart mechanics led him into tobacco research in the early 1980s. He found the tobacco work more rewarding, in every sense. Grants from the National Institutes of Health were available to study the effects of smoking, and funding for tobacco research would only grow. In 2009, Congress mandated that tobacco companies start paying annual user fees to finance regulation by the Food and Drug Administration and academic research overseen by the NIH. (The companies paid more than $700 million in 2020.) Private funders including the Robert Wood Johnson Foundation and the Truth Initiative also supported Glantz’s work, which has attracted well over $75 million to UCSF.

More importantly, tobacco research aligned with Glantz’s lifelong commitment to social change. His very first publication, which appeared in Science when he was a graduate student at Stanford, examined the influence of U.S. Department of Defense contracts on research at the university. He embraced his reputation as a rabble rouser, wearing a T-shirt given to him by colleagues that said, “Here Comes Trouble.”

He says his work to achieve a smoke-free society was especially satisfying. It’s easy to forget today that people used to smoke everywhere—at work, in restaurants, on airplanes, even in hospital waiting rooms. In his book, Tobacco War, Glantz recalled: “The executive director of the California division of the American Lung Association was a chain-smoker, and the American Heart Association distributed ashtrays and packs of cigarettes at its board meetings.”

With Glantz’s full-throated support, Americans for Nonsmokers’ Rights took the battle to towns and cities across the country. There, unlike in Washington, grassroots activists could defeat the tobacco industry. More than 400 localities passed laws restricting smoking.

The second-hand smoke issue transformed the politics of tobacco. No longer could the industry defend smoking as a matter of individual choice. Smoking was recast as indoor air pollution and a threat to the health of others. In a 1987 editorial in the journal Circulation, Glantz wrote: “The issue should be framed in the rhetoric of the environment, toxic chemicals, and public health, rather than the rhetoric of saving smokers from themselves or the cigarette companies.”

“Unquestionably, Stan was one of the major warriors in the fight against secondhand smoke,” says James Repace, a former official with the Environmental Protection Agency and one of the first scientists to analyze the health impacts of secondhand smoke.

The cigarette companies recognized the threat early on. In a 1978 report to the Tobacco Institute, the industry’s lobbying arm, a public opinion research group sounded the alarm: “This we see as the most dangerous development to the viability of the tobacco industry that has yet occurred.”

But how dangerous, really, was secondhand smoke? While experts agree that the risks of sustained exposure are high, especially for children, they may not be as high as many advocates claim. Despite lingering uncertainties, opponents of tobacco distilled the science into three words: Secondhand smoke kills. The Surgeon General said in 1986 “there is no risk-free level of exposure to secondhand smoke.” In an anti-smoking bus poster from 1997 depicting an elegantly dressed couple, the man asked: “Mind if I smoke?” The woman replied: “Care if I die?”

In December 2002, after a hard-fought battle, New York City’s then-mayor Michael Bloomberg signed a law that all but eliminated smoking in restaurants and bars. A few months later, Glantz presented the eye-popping findings of his latest study at a meeting of the American College of Cardiology: The rate of heart attacks in Helena, Montana, had fallen by nearly 60 percent after a six-month smoking ban in the small city.

“This striking finding,” he said at the time, “suggests that protecting people from the toxins in secondhand smoke not only makes life more pleasant; it immediately starts saving lives.” Glantz and two local physicians who worked with him on the study also reported that heart attacks returned to their historic levels when the ban was suspended because of a legal challenge.

The Helena miracle, as the study became known, generated global press coverage, including a New York Times op-ed. It was widely touted by anti-smoking groups. But it defied common sense. California had banned smoking in workplaces and bars, with no discernible impact on heart attacks. In other big cities with smoking bans, no one had noticed drops in heart attacks. The small sample size in Helena—four cases per month during the ban, compared to seven beforehand—should have raised red flags; random fluctuations could have explained the drop in hospital admissions.

When the study, which was funded by the National Cancer Institute, was published in the BMJ, the decline in heart attacks was revised downward to 40 percent—still an extraordinary outcome. Detractors pushed back. “I am truly amazed that a study of such poor quality was not only accepted for publication in a journal with the reputation of the BMJ but was accorded widespread coverage in the lay press,” wrote Henry Mizgala, an emeritus professor of medicine at the University of British Columbia, in a response to the journal. “This is, in my opinion, gross misrepresentation designed to provide maximal public impact in furthering the biased and unscientific opinions of these authors.” (Mizgala noted in a disclosure that he had “submitted affidavits on behalf of defendants in the tobacco litigation.”) Glantz’s former student, Michael Siegel of Boston University, was one of a few anti-smoking advocates to challenge the findings. In his own response to the BMJ, he wrote: “I am afraid that the credibility of tobacco control scientists and practitioners may be threatened if scientific claims are made that are not adequately justified.”

Subsequent research with larger sample sizes contradicted Glantz’s findings. England and New Zealand, both of which imposed national bans on smoking in public places, found much smaller impacts—a 2 percent reduction in heart attacks in England, no significant effects in New Zealand. A study by researchers at the Rand Corporation and elsewhere found that the reductions in Helena—which seemed to be confirmed by studies in other small cities, including Pueblo and Greeley, Colorado—were likely a result of their small sample sizes. The authors concluded: “We find no evidence that legislated US smoking bans were associated with short-term reductions in hospital admissions for acute myocardial infarction or other diseases in the elderly, children or working age adults.”

Glantz stands by his findings. (They’re cited in his current biography.) He points out the study found that at the 95 percent confidence interval the effect was real, but ranged from 1 percent to 79 percent, meaning that the reduction in heart attacks could have been much bigger or smaller. However, the caveat was never mentioned by those who cited the study to argue for smoking bans.

For their part, both the Institute of Medicine, now known as the National Academy of Medicine, and the Surgeon General have concluded that there is a causal link between smoking bans and a reduction in coronary events, including heart attacks—though the precise magnitude of the effect remains unclear.

The published version of the Helena study acknowledged its limits, noting the city’s small size. “There is always the chance,” the authors wrote, “that the change we observed was due to some unobserved confounding variable or systemic bias.” They concluded by making the modest claim that smoking bans “may be associated with an effect on morbidity from heart disease.”

When describing the study, though, Glantz showed no such restraint. In the original UCSF press release announcing the results, Glantz was quoted as saying: “Smoke-free laws save lives, and they do it quickly.”

This was the beginning of a pattern. Clive Bates, the former director of the London-based anti-tobacco organization Action on Smoking and Health, says Glantz habitually makes claims to the media or on his blog that go well beyond what his research says.

“We didn’t bother too much about it when he was doing things that we thought were good,” Bates said.

That changed with the arrival of the e-cigarette.

Glantz plays a cameo role in the origin story of vaping. To develop the device that became JUUL, the leading e-cigarette brand in the U.S., two Stanford graduate students dug deep into UCSF’s tobacco industry archives, studying earlier efforts by tobacco companies R.J. Reynolds and Philip Morris to design electronic cigarettes. The students approached Glantz, seeking his support for what they pitched as a tobacco cessation tool. He declined, warning that vaping would appeal to kids.

On that point, he was right. By 2018, after JUUL blitzed young people with marketing on Instagram, in magazines, and on billboards, one in five high school students had used e-cigarettes. The U.S. Surgeon General at the time decried what he called an “epidemic of youth e-cigarette use.” Then again, fewer young people than ever were smoking cigarettes. Some experts described vaping as a disruptive technology that was helping to drive smoking’s long-term decline.

The debate that ensued polarized the tobacco science community. In a commentary in Nicotine and Tobacco Research, nine early-career researchers led by Dana Mowls Carroll of the University of Minnesota expressed concern that “the continued promotion of select, polarized stances on e-cigarettes will threaten the integrity of research.” In a speech at a 2020 conference on e-cigarettes and public health, Steven Schroeder, the former president of the Robert Wood Johnson Foundation and a professor of medicine at UCSF, accused researchers on both sides of engaging in “strident discourse” and “troublesome activities.” He reserved his sharpest criticisms for the opponents of e-cigarettes. “In their anti-vaping advocacy, some have gone beyond the science, stretched the results, cherry picked the analyses, and skated around standard methodological practices,” Schroeder said.

Glantz staked out his position early, and he has stuck to it. In a background paper prepared for the World Health Organization in 2013—before the so-called epidemic of vaping began—Glantz and two UCSF colleagues called for an array of policies, including flavor bans, to curb e-cigarette use. Glantz has been in the thick of the debate ever since, producing several dozen scholarly papers on e-cigarettes, most in collaboration with others, some widely cited. His work has addressed the most important questions about e-cigarettes. He makes three broad claims, all of them sharply contested.

The first claim is that e-cigarettes encourage young people to smoke cigarettes. Glantz’s 2014 article in JAMA Pediatrics was the first national study to show that e-cigarettes were a “gateway to nicotine addiction for US teens,” according to a UCSF press release. His 2018 study in Pediatrics also claimed that e-cigarette usage encourages more young people to smoke. “I don’t know anybody credible who doesn’t accept the gateway,” Glantz says.

But neither study proved the existence of a gateway effect. The 2014 JAMA Pediatrics paper found associations between vaping and smoking, but there’s no way to know from the data whether young people first vaped and then smoked, first smoked and then vaped, or had a predilection for both. The 2018 Pediatrics paper claimed a gateway effect, but the alleged link between vaping and smoking disappeared when other teen behaviors, such as using marijuana, were taken into account.

The claims made in JAMA Pediatrics were publicly rejected by scientists at the American Cancer Society and the Truth Initiative, anti-smoking groups that for a brief time in the mid-2000s were open to the idea that e-cigarettes could reduce the harm from smoking. (Both now strongly oppose e-cigarettes.) “The data in this study do not allow many of the broad conclusions that it draws,” Thomas Glynn, a researcher who at the time was at the American Cancer Society, told The New York Times. The Journal of the American Medical Association, the parent publication of JAMA Pediatrics, published a critique of the study written by Glynn, Abrams, and Raymond Niaura, a colleague of Abrams at NYU and another longtime tobacco researcher. Bates, the British anti-smoking activist and persistent Glantz critic, called the study’s conclusions “false, misleading, and damaging” in an open letter.

The 2018 Pediatrics paper was also sharply criticized. Population studies provide the most compelling reason to reject claims of a gateway hypothesis, says Niaura—who, along with Abrams, was previously an unpaid member of the Scientific Technical Advisory Council for the Foundation for a Smoke-Free World, funded by Philip Morris International. “Cigarette smoking among kids is going down and down and down,” he adds. “If e-cigarette use was driving cigarette use, smoking would be going up.” (Glantz contends that e-cigarettes have slowed the decline.)

The second contested Glantz claim is that e-cigarettes, when sold as consumer products, don’t help smokers quit. Glantz made this case in two meta-analyses—studies that collect and combine data from other studies—one in The Lancet Respiratory Medicine in 2016, another in the American Journal of Public Health in 2020. “The irony is that quitting smoking is one of the main reasons both adults and kids use e-cigarettes, but the overall effect is less, not more, quitting,” Glantz said in a press release announcing the 2016 findings.

Meta-analyses can be problematic, particularly when they mix and match different kinds of research. They depend entirely on the quality of the underlying studies, and the Lancet research fell short in that regard, critics say.

In a submission to the FDA, scientists with the Truth Initiative (then known as the American Legacy Foundation) said the Lancet paper included studies that were “uninformative and marred by poor measurement.” They continued: “Quantitatively synthesizing heterogeneous studies is scientifically inappropriate and the findings of such meta-analyses are therefore invalid.”

Scientists in the United Kingdom, where health authorities promote vaping as a safer alternative to smoking, blasted the study as “grossly misleading,” “not scientific,” and a “major failure of the peer review system.” Ann McNeil, a professor of tobacco addiction at King’s College London, issued a response to the Lancet paper, saying that it included information about two studies that she co-authored that was “either inaccurate or misleading” and that in one instance Glantz and his co-author, Sara Kalkhoran, then a physician at UCSF, were told before publication “that they were misreporting the findings.” (Glantz says he doesn’t recall the specific details but that he and Kalkhoran would not have ignored such a warning.)

Plenty of countervailing evidence has surfaced since then. In 2015, Kalkhoran left UCSF for Harvard University where she and colleagues studied US adult cigarette smokers for two years. Using data from 8,000 adult smokers, Kalkhoran and her co-authors concluded that “daily e-cigarette use, compared to no e-cigarette use, was associated with a 77 percent increased odds of prolonged cigarette smoking abstinence.” (Kalkhoran did not respond to requests for comment.) Cochrane, an independent network of researchers, examined randomized control trials of e-cigarettes for smoking cessation and wrote: “We are moderately confident that nicotine e‐cigarettes help more people to stop smoking than nicotine replacement therapy or nicotine‐free e‐cigarettes.” In the UK, an estimated 3.6 million people use e-cigarettes, and nearly two-thirds are ex-smokers, according to Action on Smoking and Health.

None of that will end the debate over whether e-cigarettes can help smokers quit. But even Glantz and his co-authors, in their 2020 meta-analysis for the American Journal of Public Health, ceded some ground. “Daily e-cigarette use was associated with more quitting,” albeit under limited circumstances, they wrote. But Glantz continues to oppose vaping because, he says, the health risks are too great.

The third and final Glantz claim has attracted the most pushback: That e-cigarettes increase the risk of heart attack. In the space of less than a year, Glantz and colleagues produced two studies that led him to push this idea. In August 2018, he described the results from the first study in the American Journal of Preventive Medicine on his UCSF blog under the headline: “Risk of heart attacks is double for daily e-cigarette users.” Ten months later, when describing the second study, published in 2019 in the Journal of the American Heart Association, Glantz said it provided “more evidence that e-cigs cause heart attacks.”

“E‐cigarettes,” he asserted, “should not be promoted or prescribed as a less risky alternative to combustible cigarettes.”

This work was wildly influential with anti-vaping advocates and government health authorities. The American Journal of Preventive Medicine paper was cited by the WHO chief and the U.S. Surgeon General and covered in nearly 200 news stories. A New York Times article read: “Compared with people who never used e-cigarettes, daily users almost doubled their risk for heart attack.”

Critics pounced on what they called glaring flaws in the analyses. Some of the e-cigarette users had previously smoked, for example, muddying the correlation. Brad Rodu, a University of Louisville professor who has numerous and longstanding connections to the tobacco industry, dug into the raw data and found that at least 11 of the 38 heart-attack victims cited in the Journal of the American Heart Association study had suffered their heart attacks before they started vaping—some as many as 10 years before. Glantz was made aware of the temporality problem before publication because it was raised by a peer reviewer, the journal’s editor subsequently realized.

Sixteen tobacco researchers wrote to the journal editor asking for a retraction, and the Journal of the American Heart Association ultimately did just that—something it has done only a handful of times in its history. Its editor, though, was careful to state in a letter to Glantz that “the retraction notice is intentionally absent of any language suggesting scientific misconduct.”

The 2019 American Journal of Preventive Medicine paper came under pressure as well. Twenty-two tobacco scientists asked for a retraction, noting, among other things, that the association between vaping and heart attacks could be due to heavy smokers at risk of heart disease switching to e-cigarettes, or smokers who suffered heart problems then trying to quit with e-cigarettes. To assert or imply causation from the study is irresponsible, they wrote.

“It’s bad science,” says Niaura.

Matthew Boulton, the journal’s editor-in-chief, declined to retract the paper. But, in a letter to the 22 scientists earlier this year, he acknowledged that the paper suffered from “serious methodological issues,” including the fact that the database used by the researchers “makes it impossible to make causal claims.” The journal has asked new researchers to reexamine the issue in a paper that will be presented to readers as a cautionary tale to highlight how data can be misinterpreted.

Glantz remains unrepentant. On his blog, he blamed the Journal of the American Heart Association retraction on “pressure from e-cig interests,” naming Rodu. None of the other scientists who signed the letters seeking retractions appear to have financial ties to the industry. Abrams from NYU once contributed an op-ed to Filter, a publication owned by The Influence Foundation, which has received support from tobacco companies. (Abrams says he was not paid.)

Andrew Gelman, a professor of statistics at Columbia University who followed the controversy on his blog, was unimpressed with Glantz’s response to the retraction, calling it “anti-scientific.” He wrote: “If someone points out an error in your work, you should correct the error and thank the person. Not attack and try to salvage your position with procedural arguments.”

Last summer, Glantz retired from UCSF, where he had worked for 45 years. “I’m confident,” he wrote to colleagues, “that there will be more ways that I can keep contributing to fighting the tobacco industry and promoting public health.”

His last years at UCSF brought difficulties besides the controversies over his research. Three women filed complaints of sexual harassment against him and sued both Glantz and the Regents of the University of California, who fought the charges in court; the cases were eventually settled without an admission of guilt.

Meanwhile, there were worrisome signs that the campaign against e-cigarettes led by the Campaign for Tobacco-Free Kids and the Truth Initiative—which by this time had switched its stance on e-cigarettes—was having unintended consequences.

Minnesota enacted a steep tax on e-cigarettes that led to “increased adult smoking and reduced smoking cessation,” a study by researchers with the National Bureau of Economic Research found. In a story headlined “Smoking’s Long Decline is Over,” The Wall Street Journal reported that some e-cigarette users may have returned to combustible cigarettes “because of increased e-cigarette taxes, bans on flavored vaping products, and confusion about the health effects of vaping.” Public opinion polls showed that most people believed, wrongly, that vaping is as dangerous or more dangerous than smoking.

About the timing of his retirement, Glantz says he’d been planning for years to step away from UCSF. He’ll continue to produce academic research and engage in activism, he adds, speaking out on his blog and elsewhere. He says he is proud of having mentored dozens of researchers over the years: “It’s important to give opportunities to others.”

Siegel, one of those mentored by Glantz, has mixed feelings about his mentor. “I love him,” Siegel says. “He’s accomplished great things.” But Siegel says he no longer trusts Glantz and the anti-tobacco nonprofits. “The science is not driving the anti-smoking agenda,” he says. “Rather, the anti-smoking agenda appears to be driving the interpretation of the science.”

For his part, though, Glantz argues that the increasingly popular perception of e-cigarettes as dangerous is a positive development—and one backed by the science. “None of the people who are e-cigarette enthusiasts,“ Glantz says, “know anything about biology.”

Update August 6, 2021: A previous version of this article neglected to disclose that both David Abrams and Raymond Niaura of New York University were previously unpaid advisors for a smoking cessation organization funded by Philip Morris International. It also neglected to note that both the U.S. Surgeon General and the National Academy of Medicine (formerly the Institute of Medicine) have concluded that smoking bans do reduce coronary events, although the precise size and timing of such an effect is a matter of debate. The story has been updated to include these points.

The post What to know about the controversial tobacco scientist who wants to ban e-cigarettes appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Choosing a sunscreen used to be simple. You picked the cheapest or the nicest-looking bottle or just whatever happened to be at eye level (probably the most expensive one). But in the last few years there’s been a growing concern that sunscreens contain all kinds of chemicals that harm coral reefs—not to mention the fact that high SPF isn’t really that useful—and suddenly all the options in the sunscreen aisle seem pretty overwhelming.

Don’t worry, though, we’re here to help. Here are some of your burning sunscreen questions, answered.

Is higher SPF better?

You’ve probably heard that sunscreens with an SPF over 50 only provide a negligible increase in protection. This is mostly true, because SPF 50 already blocks 98 percent of UVB radiation. Going over 50 can only give you another percent or so of protection. But there are a few factors that complicate the issue.

One is that this idea is based on principle, not on actual experiments. There’s been only one randomized, double-blinded study of SPF efficacy in preventing sunburn, and it found that SPF 100 did prevent burns more effectively than SPF 50. That’s of course just one study, so it’d be irresponsible to draw sweeping conclusions from its results, especially because there are plenty of experts who say that anything over 50 isn’t offering an improvement. It’s also worth noting that sunscreens regularly test well below their listed SPF—24 out of 73 tested by Consumer Reports had less than half their claimed number. So the bottle promising you added protection might actually contain a product identical to the rest.

But the other issue is that most of us don’t apply the proper amount of sunscreen. Another study found that people routinely apply about one-third to one-half of what manufacturers base their SPF analysis on, which means few of us are even getting the full SPF listed on the bottle. Reapplying periodically (and especially after things like sweat and sea exposure help degrade your coverage) can help, but few of us bother. The American Academy of Dermatology recommends using enough sunscreen to fill a shot glass (about two tablespoons), and more if you’re a larger person. Any less and you’re decreasing the efficacy.

Buuuut there’s one more complicating factor: SPF doesn’t measure UVA protection. UVA radiation is what causes skin damage below the surface, whereas UVB is mostly responsible for the surface-level damage that produces burns. Though sunscreens do have to state whether they block one or both, in the US they’re not required to measure the extent of provided UVA protection. In Europe, all sunscreens have to provide at least one third as much UVA protection as UVB. Nearly half of the products sold stateside didn’t meet that requirement when tested in a study. Higher SPF sunscreens fared worse on the metric, though in absolute terms generally had a UVA protection factor (PF) equivalent to or higher than those with low SPF.

Unfortunately, it’s challenging for consumers to tell whether any particular brand fares well on the UVA PF front. Consumer Reports produced a lengthy report and ratings that includes UVA testing. If you have a subscription you can see the complete list, but for the rest of us, these lotions and spray-on products scored at the very top.

There’s also a report from the Environmental Working Group that gives an overall rating to how UVA-protective certain brands are. It doesn’t get into details on specific sunscreens, but Neutrogena, Coppertone, and Banana Boat all came in toward the top. The EWG Skin Deep database, which you can search for specific products, provides an overall score that they say encompasses UVA protection, but there’s no actual data provided. EWG is extremely cautious when it comes to including anything synthetic in skin products, which in some ways is a good thing—but it does mean that their barometer for safety may not align with the best scientific evidence available.

Which ingredients harm coral reefs?

In the last few years there’s been an increasing awareness of how much our sunscreen can potentially harm coral reefs. A common chemical called oxybenzone—along with a few others, including octinoxate—quickly bleach the coral and damage its DNA, according to research, and it only takes a single drop in 4.3 million gallons of water to do the damage. That’s why Hawaii has banned oxybenzone entirely—they’re trying to retain the reef they have left.

Unfortunately, it’s hard to avoid oxybenzone. The reason it’s so ubiquitous is that it’s highly effective at absorbing the sun’s rays, and there aren’t a lot of good alternatives at the moment. Mineral sunscreen, which works by reflecting the incoming radiation, is generally less effective. When Consumer Reports tested a variety of sunscreens, none of the mineral-based options deflected enough UV radiation to meet their requirements for recommendation.

To find a non-mineral option that won’t kill coral reefs, check out this list of sunscreens that EWG recommends. EWG can be more than a little sensitive to chemical in their evaluations, though, so while you can be pretty sure their top-rated products are free of any potential toxins, the absence of a sunscreen on such a list does not necessarily mean it’s actually dangerous.

You can also read the ingredients list on the back of any given bottle—tbut be aware that the reef-harmer in question sometimes goes under the name “benzophenone-3.” If you’re feeling overwhelmed by the sheer number of products, look at the baby options first: They tend to be gentler and less ingredient-dense, so they’re often oxybenzone-free.

As a final note, don’t think that you can avoid the problem by simply not swimming in the ocean. When you get home from the shore, you’ll wash that sunscreen down the drain, and all too often it ends up swirling around the nearest reef all the same.

Are spray-on sunscreens better or worse?

Setting aside the fact that sprayed sunscreen often ends up in the wind (or on your neighbor), misting a bunch of environmentally-hazardous chemicals into the air is never going to be a great idea. More could end up on the sand than your skin, and you’re also likely to inhale some of those particulates. The FDA is investigating whether the inhalation aspect is dangerous for human lungs, but in the meantime it’s better to be safe than sorry. And since we’re already terrible at putting on sufficient sunscreen to block incoming rays, it’s worth remembering that a fine mist is less likely to provide adequate coverage than a cream.

Can I just take a sunscreen pill?

No. Please don’t be fooled by the mysterious supplements claiming to protect you from UV radiation with a poppable pill. In 2018 the Food & Drug Administration sent warning letters to three of these companies to tell them to stop falsely advertising the “benefits” of their pills. None of these products—Advanced Skin Brightening Formula, Sunsafe Rx, Solaricare, and Sunergetic—can prevent sun damage. The FDA noted that “there’s no pill or capsule that can replace your sunscreen,” and to instead opt for one of the many available sunscreens on the market.

I scrolled down because I just want you to tell me what to buy!

Now that we’ve exhausted you with details, here’s a simple checklist for the next time you’re in your local drug store:

• Lotion, not spray-on
• Free of oxybenzone, and free of octinoxate and octocrylene if possible (this probably leaves you with only mineral options—you’ll have to decide personally whether you’d rather have a potentially less effective sunscreen or opt-in to the potentially reef-hazardous chemicals)
• At least SPF 50, but higher if you’re likely to not put on enough

And for reference, Consumer Reports recommends:

• Lotion: Coppertone Ultra Guard Lotion SPF 70, CVS Health Ultra Protection Sun Lotion SPF 70
• Spray-on: Trader Joe’s Spray SPF 50+, Neutrogena Beach Defense Water + Sun Protection Spray SPF 70
• Mineral: California Kids #supersensitive Tinted Lotion SPF 30+, Badger Active Natural Mineral Cream SPF 30 Unscented

If you happen to be in Europe, you can follow the same list, but rest easier knowing that you’re also getting better UVA protection.

The post Your summer guide to sunscreen, from SPF to not-so-magic pills appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

At the beginning of the movie 50/50, Adam Lerner is diagnosed with neurofibrosarcoma, a cancer of the spine’s nerve tissue. Adam sits in his doctor’s office while the doctor rattles off the word several times, but Adam has no idea what it means, or if there’s anything wrong with him at all. Eventually, his doctor uses the word “cancer,” and Adam’s perspective goes blurry, the doctor’s voice drowned out by a high-pitched ringing.

Many people have had real experiences like this one. Cancer is still one of the scariest words you can hear in a diagnosis. And chances are, you know someone who has heard it—almost 40 percent of adults are diagnosed with some form of it during their lifetime. Every patient’s story is different, and they don’t all have a happy ending. But because of decades of research into how cancer works, patients diagnosed with cancer today have a much better chance of survival than ever before.

Adam Lerner (Joseph Gordon Levitt) reacts to his diagnosis in 50/50

There’s something big going on in oncology right now. It seems like every day a scientific paper is published highlighting a new treatment or discovery; new documentaries or feature articles come out every week. But it’s difficult to understand this excitement without a firm grasp of how the meaning of cancer has changed for doctors and researchers today. Experts’ understanding of what cancer is, how to diagnose and treat it, has matured in recent years—and some of the things you may have learned in the past may no longer be true.

“Back in the 1970s we thought if we found every cancer early, we might be able to cure it. Now we have a much more mature understanding,” says Len Litchenfeld, the Deputy Chief Medical Officer for the American Cancer Society. “Our technology has allowed us to find many different cancers than we would have in the past. And our understanding of what cancer is and how it behaves is also evolving.”

Cancer isn’t just one disease—it’s actually hundreds of diseases. And these diseases don’t have much in common, except that they are caused by a genetic mutation that throws the cells’ normal process of growing and dying gets out of whack.

Cancer is actually hundreds of diseases. And these diseases don’t have much in common.

When people think of cancer, they imagine a scene much like the one in 50/50—a dreaded diagnosis. But in recent years oncologists have learned that cancers happen all the time in the body—the immune system is just usually able to fix the problem before it becomes overwhelming. “Most people are familiar with cancer diagnosed in our friends and family and colleagues, but not every cancer cell goes on to be a serious life-threatening cancer,” Litchenfeld says. Some cancers grow slowly and never become a problem; others are more aggressive and require immediate treatment. “There’s a wide spectrum,” he adds.

Since such a large percentage of the population is diagnosed with cancer, many people assume that cancer is more pervasive now than it has been in the past. But that’s not really true. “Cancer seems to be more pervasive, but that’s because we find more cancer in older populations,” Litchenfeld says. People are living longer, which means that they are more likely to develop age-related diseases like cancer—in fact, age is one of the biggest risk factors for developing cancer. “Sure, people are now living to 80 or 90, so it makes sense that we’re going to find more cancers in terms of numbers. But it’s important to look at the rate,” Litchenfeld adds. According to a National Cancer Institute survey, the incidence of cancer has decreased overall between 1975 and 2011, and cancer mortality has dropped even more. That’s not to say that we’re where we need to be in terms of fighting cancer, Litchenfeld notes, but there’s definitely been progress.

There are a lot of reasons why cancer mortality has dropped—both prevention and treatment have drastically improved because oncologists have a much better understanding of why people get cancer. But a big part of that decrease in mortality is because fewer people are getting tobacco-related cancers. Starting in the 1950s, researchers understood that smoking made cancers more likely, so urging people to stop (which didn’t work on a large scale until much later) was an important step to help them prevent it.

Cancerous HeLa cells that had recently divided

Though there’s a lot of misinformation surrounding some aspects of prevention (does drinking lots of coffee increase your risk of developing pancreatic cancer? Or decrease it?), doctors have a pretty good understanding of what works best to prevent cancer. “There are very few miracles out there. What we do know is that not smoking, weight loss, increased activity—those work, even if they’re tough to adhere to,” Litchenfeld says.

Because cancer prevention was not as well understood, doctors in the 1960s and ’70s spent a lot of their resources treating cancer. A lot of cancer treatment was left up to pure chance. Doctors would give patients chemotherapy and radiation in the hope of killing enough cells in their bodies so that the cancer could no longer survive. But in the mid-1970s researchers discovered the oncogene, genes that control the growth and death of cells that, if they have a particular mutation, can cause tumors. This discovery rocked the world of oncology, leading to new understandings of how environmental and lifestyle factors (like smoking) can make cancer-causing mutations more likely, and the discovery of many other genes related to cancer’s incidence and aggressiveness (like the BRCA-1 gene, which increases women’s chances of getting breast and ovarian cancer).

“As a result [of this research in the ’70s] we have a much greater understanding of the genetic abnormalities, the internal coding system, for what makes a cancer cell a cancer cell. That gives us targets at which we can aim new treatments,” Litchenfeld says.

That work has led to increasingly sophisticated treatments, and a whole new chapter of it is beginning now. Researchers are figuring out how to harness the immune system to fight cancer from within, which is called immunotherapy. Understanding the genetic drivers behind potentially life-threatening cancers, along with cheaper genetic sequencing, means that doctors can use treatments that target the mutation that’s driving the cancer, called precision medicine or personalized medicine.

This knowledge has also led doctors to diagnose and treat more selectively. “There’s the thought that early [cancer] detection always leads to a better outcome for the patient. But in some cancers that is less clear,” says William Dahut, the clinical director and deputy scientific director for the Center for Cancer Research at the National Cancer Institute. Take prostate cancer, for example. It’s the second leading cause of cancer death for men in the United States, and yet statistically a man diagnosed with prostate cancer is more likely to die with prostate cancer rather than because of it. If a cancer is just on the verge of being a health risk and doctors treat it too aggressively, the treatment can lead to other types of cancers, called secondary cancers—and the patient’s life suffers as a result. Too frequent screenings for other types of cancer, like breast cancer, may even increase a patient’s risk for the disease by exposing her to radiation.

Cancer cells found in human connective tissue, magnified

“Early detection may lead to side effects of treatment but it doesn’t always benefit the patient. You hear lots about screening, and sometimes there’s a significant benefit. But sometimes cancers that grow in between screenings are the ones that are the most virulent. And the ones [that doctors] pick up may not be the harmful ones,” Dahut says. After years of encouraging people to constantly get screened for cancer, some doctors and public health officials have started pushing for less frequent screenings for some kinds of cancer.

These substantial advances in oncology don’t mean that we now have all the answers—in fact, the more we learn about particular aspects, like the genes behind cancer, Dahut says, the more complex they become. “The idea [behind precision medicine] is that patients have a particular mutational profile, and hopefully that can be used to direct the cancer treatment. But the reality at this point is that it’s just more complicated than one would think,” Dahut says. Tumors often have several mutations that drive them, and even if oncologists could pinpoint them, there aren’t many drugs that target them, and even fewer that target several at once. The clinical trial system is designed to test treatments for the location of the cancer (lung, thyroid, and so on) and not specific mutations that drive them, though the Food and Drug Administration, which approves the drugs, is now starting to reform the structure to fit oncologists’ new understanding of how cancer works.

But researchers and doctors are still optimistic about what the next phase of research will bring. With a better understanding of how cancers form and how to treat them, doctors are finding new ways to talk patients about their cancer risks. Patients will start having earlier conversations with their doctors about their genetic mutations that may make them more likely to develop certain kinds of cancers so that they can take steps to prevent them. As researchers collect more data from cancer patients, they will get a better grasp of how mutations interact with one another to make cancer more or less aggressive, and will be able to develop treatments that target several of them at once. Figuring out how to combine these targeted treatments with immunotherapy is likely oncology’s next big advance, Dahut says. “It’s an incredibly exciting time in cancer treatment,” he adds.

A HeLa undergoing apoptosis, or cell death, under a scanning electron microscope

Litchenfeld is less certain about how quickly these cutting-edge treatments will be used for the average patient—especially given their astronomical cost. To him, the greatest strides can be made in patient care and improving the patient’s quality of life. There’s already a cultural shift—cancer is no longer the “c-word” with the stigma to match. A cancer diagnosis may no longer be a death sentence, but not everyone’s outcome is ideal yet, Litchenfeld adds. We need to make sure that people all over the country receive similarly high levels of care, and that they still have a high quality of life once they’re in remission—no bankruptcy from paying for medicine, no secondary cancers. “It’s not just about the science—it’s how we care for patients and their families,” Litchenfeld says.

Given the rate of advances in oncology, one thing is for certain: the survival rate in 10 years will surely be even higher than it is today. Treatment, prevention, and culture surrounding cancer are improving every day. But there’s a lot of misinformation in the popular media, and learning about the miracle cure of the moment can often be confusing and full of jargon, like starting a really technical movie halfway through.

In this series, A Future Without Cancer Popular Science explores the cutting-edge concepts and technologies pushing oncology forward, with the goal of helping readers understand this rapidly changing field.

The post How The Meaning Of Cancer Has Changed appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Mr. Frosty isn’t a snowman or a company that sells slushies, but a mutant leopard gecko that might help us better understand skin cancer. In 2015, a reptile breeder noticed one member of the colony was a little brighter than the others, with a yellow back and legs. That gecko, named “Mr. Frosty” for its distinct white undertones, went on to father hundreds of similarly patterned lizards (dubbed “Lemon Frost” geckos) that became a hit among pet shoppers. 

Over time though, a problem emerged: Hardened white spots frequently developed all over Lemon Frost geckos’ skin. Sometimes, the spots even expanded into large growths, which researchers identified as tumors made up of iridophores, a type of cell found in insects, reptiles, fish, and amphibians that’s involved in skin color. About 80 percent of Lemon Frost geckos go on to develop iridophoroma tumors, says Longhua Guo, a geneticist at the University of California at Los Angeles. 

Now, Guo and his colleagues have identified the gene likely responsible for both the Lemon Frost morph’s unique coloration and the tumors. They published their work this week in the journal PLOS Genetics. The findings highlight the importance of genetic studies in animals that science usually ignores, and offer a possible new model organism for the study of human skin cancer. 

Prior to his research on Lemon Frosts, Guo hadn’t even touched a gecko. In fact, he came to his study subject almost by accident, stumbling across an article about leopard geckos and being “captivated by how beautiful they look.” Having been bred for decades, these creatures come in an astonishing variety of colors, which is exciting from a genetics perspective, he says. “Nature is very colorful,” says Guo, but “we don’t know enough about how color is made.” 

[Related: Octopuses change color as the sleep]

Mammal skin and fur color are almost solely determined by melanophores—cells that produce melanin—but many other animals have more than one type of color cell, producing a variety of pigments which result in numerous skin and scale colors. For example, cephalopods like cuttlefish and octopus have at least three different types of cells involved in their magnificent color displays. Outside of mammalian melanophores, the genetic basis of animals’ color variations is poorly studied.

To find the gene or genes responsible for the Lemon Frost skin coloring, Guo and Leonid Kruglyak, professor of biochemistry and genetics also at UCLA, analyzed a record provided by a reptile breeder with information on the features of all the geckos in their colony and how each animal was related to one another. 

Using this record, the researchers identified a pattern of inheritance. They found that some of the breeder’s leopard geckos looked like Mr. Frosty, almost white with reduced spots and a yellow back and legs. But others had even more yellow coloration extending further onto their heads and tails, thickened skin, and more tumor development. This group was dubbed “Super Lemon Frosts.” A final set of geckos had the standard leopard gecko spots with beige colored skin surrounding them. This pattern revealed that the Lemon Frost traits could likely be traced to a single mutated gene, and that the mutated gene responsible was semi-dominant. Meaning, one copy of the mutation leads to changes in a gecko’s traits (more yellow coloration, tumor growth, thicker skin), but two copies results in even more intense differences.

The scientists separated these three groups of geckos and then sequenced and compared their DNA—looking for a gene matching the expected inheritance pattern. Once they’d identified a suspected region of the leopard gecko genome, the researchers went to the genetic database to compare their gene sequence with other well-mapped animal genomes. Through comparisons to chickens, green anole lizards, and humans, the scientists honed in on a gene called the SPINT1 gene. A mutated form of this SPINT1 gene, dubbed the Lemon Frost gene, seemed to cause the Lemon Frost skin, as well as the tumors. 

Mutations in the SPINT1 gene have previously been implicated in the development of skin cutaneous melanoma (SKCM), the most dangerous form of skin cancer in humans, and tumor growth in zebrafish.

[Related: Scientists are using gene editing to try to slow cancer growth]

But follow-up work is needed to confirm the link between SPINT1 and tumors in Lemon Frost geckos, says Craig Ceol, a geneticist at the University of Massachusetts studying melanoma using zebrafish as a model, who was not involved in the gecko work. Ceol explains that the researchers were careful in their methods and conclusions. Though he says usually, in similar genetic studies of more commonly used model animals, the next step would be to make transgenic geckos—testing the role of SPINT1 by inserting different versions of the gene and observing the effect on tumor growth. “You put in a normal copy of the gene, and then you would no longer get tumors. Or you would correct a mutation that’s there, and then we would no longer get tumors,” he says. “But I think that’s really, really hard to do in geckos.”

Model organisms are used to study human biology and disease because of the range of information and experimental possibilities they provide. “There’s a lot of experiments that we can do on model organisms that, you know, obviously, you can’t do on people,” says Ceol. “You can do these experiments where you give [animals] a cancer, and then look to treat it, or look to study the process by which the cancer arises, or by which it spreads.”

Geneticists usually focus their work in one of a few commonly used animal models like mice, zebrafish, and fruit flies. Leopard geckos aren’t one of those model organisms, and there are no reptiles at all commonly used in genetics research, says Doug Menke, a developmental geneticist at the University of Georgia, not affiliated with the new findings, whose own work focuses on anolis lizards. Yet Menke sees leopard geckos as a big opportunity for expanding genetic research and public understanding. “The standard leopard gecko is quite striking, and I think when you see images of how mutation can change the coloration or the pattern of the animal—there’s nothing like actually seeing with your own eyes, the sorts of changes that a genetic mutation or a genetic variant can cause.”

And studying a diverse array of model organisms is important, says Menke, because comparisons between lots of different animal genes can tell us more about the world and potentially help us to better understand our own genetics and diseases. He explains that comparing multiple, distantly related species can “help you understand what aspects of tumor formation and development are unique to an individual species, whether it’s a human or a gecko, and what’s shared across species.” He adds, “If you only study a single species to model human disease, you don’t always know how good that model or proxy for human disease is. How relevant is it? How similar is that disease state to the human state?”

But until relatively recently, scientists haven’t had the tools to study the genetics of non-model organisms. Identifying genes in previously unstudied animals required years of genome mapping (like the human genome project, which began in 1990 and only just reached completion a few weeks ago). Now though, new methods have allowed scientists to use other, well-mapped genomes as the jumping off point to learn more about less understood organisms like leopard geckos. Historically, the small number of genetically studied organisms posed “a huge limitation on the full range of phenomena that you can observe and study,” says Kruglyak. “It’s pretty exciting that the technologies are really democratizing this and extending it to a much broader range of species you can study.”

Because mutations in the SPINT1 gene cause cancer in both humans and geckos, the reptiles could act as a potential future model, studying ways to treat, prevent, or cure melanoma, according to Guo and Kruglyak. “I think it says geckos could be a potential model system for cancers and skin diseases,” agrees Ceol. For instance, he says leopard geckos could be useful for studying not just tumor emergence, but also metastasis, or cancer spread, which is difficult to study in other animals. 

The new findings suggest that the SPINT1 associated iridophoroma in Lemon Frost geckos could be metastatic, as the researchers documented instances of tumors in geckos’ livers and mouths as well as on the skin. Ceol points out, though, that “they haven’t formally shown [metastasis].” It’s possible the tumors observed on the gecko’s organs are still skin tumors, and genetic analysis is necessary to know for sure, he adds.

For now, Ceol says, he’ll be sticking to zebrafish. “I’m not sure that I would go out and adopt [leopard geckos] as a model myself.”

He adds, “Zebrafish have been worked on for a long time and a lot of people have developed good techniques for them. There’s a lot of advantages to working in the zebrafish system.”

But Guo hopes to continue exploring leopard gecko genetics for quite some time. He’s already working on his next project analyzing other color morphs. In the process, it’s possible other medically important genes will be uncovered, says Ceol. “There might be other mutations out there like it,” he explains. 

Finally, Guo hopes his recent finding will propel other geneticists to look into geckos and other non-model organisms in their research. “I just hope people can take advantage of our finding and move it forward.”

The post These popular pet lizards may hold the key to studying skin cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Brain surgery is notoriously complicated. Before surgeons go in to remove a tumor, they study the size and location of the tumor. But once they’re in, they have to rely on their fingers and eyes to distinguish tumor cells from healthy brain cells. Now researchers have developed a “paint” that can be injected into a patient’s veins to make tumor cells glow. After a number of successful studies in mice and dogs, the paint is now being tested in humans in California.

The paint is made from two chemicals. The first is chlorotoxin, a protein derived from scorpion venom, which targets the chloride receptors on the surface of tumor cells. The protein carries a second, non-toxic chemical that makes the cells fluoresce when they are exposed to near-infrared light.

Tests at this early stage are designed to make sure that the paint works as it’s supposed to, and initial results have been promising. Researchers injected the tumor paint into the patients’ veins and it was successfully able to cross the blood-brain barrier, which protects the brain from harmful chemicals that might be in the blood. The first few test subjects had tumors that were deep in the brain, so the surgeons had to remove a piece of the tissue before shining a light on it. “[T]he question was, ‘Does it glow?’ And when we saw that it glows, it was just one of those moments…’Wow, this works,'” Chirag Patil, one of the researchers behind the test at Cedars Sinai Medical Center in Los Angeles, told NPR.

The paint may also be used for other types of tumors in the future.

Ideally, doctors wouldn’t be using surgery at all to eliminate tumors–it’s still a “crude” technique, as one researcher said. But while surgery is still a standard treatment, tumor paint could help surgeons be much more precise.

A tumor glows thanks to tumor paint in a mouse brain.

The post Glowing ‘Tumor Paint’ Shows Surgeons Where To Cut appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In previous years, Australians might have been exposed to bushfire smoke for a few days, or even a week. But this bushfire season is extreme in every respect. Smoke haze has now regularly featured in Australian weather reports for several weeks, stretching across months in some areas.

What we considered to be short-term exposure we must now call medium-term exposure.

Given this is a new phenomenon, we don’t know for sure what prolonged exposure to bushfire smoke could mean for future health. But here’s what air pollution and health data can tell us about the sorts of harms we might be looking at.

Short-term effects

We know poor air quality is having immediate effects, from irritated eyes and throats, to more serious incidents requiring hospital admission—particularly for people with existing respiratory and heart conditions.

After the smoke haze hit Melbourne on Monday, Ambulance Victoria recorded a 51 percent increase in calls for breathing difficulties.

This aligns with Australian and international research on the acute effects of exposure to bushfire smoke.

But the long-term effects aren’t so clear.

Long-term effects: what we know

When considering the long-term health consequences of air pollution, we draw on data from heavily polluted regions, typically in Africa, or Asia, where people are exposed to high levels of airborne pollution for years.

It’s no surprise long-term exposure to air pollution negatively affects health over their lifetime. It’s associated with an increased risk of several cancers, and chronic health conditions like respiratory and heart disease.

The World Health Organization estimates ambient air pollution contributes to 4.2 million premature deaths globally per year.

A recent study in China reported long-term exposure to a high concentration of ultra-fine particles called PM2.5 (which we find in bushfire smoke) is linked to an increased risk of stroke.

We also know the dose of exposure is important. So the worse the pollution, the greater the health effects.

It’s likely some of these long-term effects will occur in Australia if prolonged bushfires become an annual event.

Experimental studies

Observational studies, like the Chinese one mentioned above, demonstrate the long-term health effects of extended exposure to air pollution. But we don’t really have any studies like this following populations which have experienced short- or medium-term exposure.

To explore the health risks of more limited exposure, we can look to experimental data from cell and animal models.

These studies follow the models for days (short-term) or weeks (medium-term). They show exposure to any type of airborne pollution—from traffic, bushfires, wood or coal smoke—is detrimental for health.

The results show increased inflammation in the body, and depending on the model, increased incidence of respiratory or heart disease.

What about bushfire smoke?

We don’t have a lot of experimental data on the effects of bushfire smoke specifically, apart from a few studies on cells in the lab.

In my lab we’ve found the short-term in-vitro effects of bushfire smoke are comparable to the smoke from cigarettes. This does not however mean the long-term heath effects would be the same.

If we think about what’s burning during a bushfire—grass, leaves, twigs, bushes and trees—it’s also reasonable to draw on experimental data from wood smoke.

Wood smoke contains at least 200 different chemicals; some of them possible carcinogens.

In one small study, ten volunteers were exposed to wood smoke for four 15 minute periods over two hours. Afterwards, participants experienced increased neutrophils, a type of aggressive white blood cell, in both their lungs and circulation. The concentration of particulate matter in the wood smoke was lower than the levels we’ve seen in Sydney.

These short term studies show bushfire smoke is toxic, and it’s this toxicity which is likely to cause long-term effects.

One review found lifelong exposure to wood smoke, for example from indoor heaters, is associated with a 20% increased risk of developing lung cancer. Though it’s important to remember this is long-term exposure; the risks associated with medium-term exposure are not yet known.

How can we apply these findings?

Taking data from one type of airborne pollution and applying it to different pollutants—for example comparing the smoke from only one type of wood to bushfire pollution—is complex. The chemical make up is likely to differ between pollutants, so we need to be cautious extrapolating results.

We also need to be wary about how we translate results from cell and animal studies to humans. Different people are likely to respond to bushfire smoke differently. Our genetic make up is important here.

And with variable factors like at what age the exposure starts, how long it lasts, and other factors we’re exposed to during our lives (which don’t exist in a petri dish), it’s difficult to ascertain how many people will be at risk, and who in particular.

Looking past the haze

The human body actually has a remarkable capacity to cope with air pollution. It appears our genes help protect us from some of the toxic effects of smoke inhalation.

But this doesn’t mean we’re immune to the effect of bushfire smoke; just that we can tolerate a certain amount.

So would a once in a lifetime medium-term exposure have a chronic effect? At the moment there’s no way of answering this.

But if, as many people fear, this medium term exposure becomes a regular event, it could cross into the long-term exposure we see in some countries, where people are exposed to poor air quality for most of the year. In this scenario, there’s clear evidence we’ll be at higher risk of disease and premature death.

For now, we desperately need studies to help us understand the effects of medium-term exposure to bushfire smoke.

Brian Oliver is a Research Leader in Respiratory cellular and molecular biology at the Woolcock Institute of Medical Research and Professor, Faculty of Science, University of Technology Sydney. This story originally featured on The Conversation.

The post We know wildfire smoke affects our health, but the long-term consequences are hazy appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The United States is on track to quash cervical cancer as a public health problem within two to three decades, according to a new report published February 10 in The Lancet Public Health.

Cervical cancer is one of the most preventable types of cancers. The disease is most often caused by the human papillomavirus virus, a type of sexually transmitted infection. With the advent of a vaccine that prevents the infection, which first came out in 2006, as well as regular screening to detect the HPV virus or abnormal cells that have not yet become cancerous, cervical cancer has become highly preventable. For the new analysis, researchers set out to estimate how many new cases of cervical cancer would emerge if more people are regularly screened or vaccinated.

“We found that, even without any new effort towards increasing vaccination or screening, we can achieve cervical cancer elimination…in roughly 20 years,” says Jane Kim, a professor of health decision science at the Harvard T.H. Chan School of Public Health. What’s more, she and her colleagues estimate, the disease could be eliminated 10 to 13 years sooner if people are screened more regularly.

“This study is really important because it says that if you implement screening and vaccination programs right now in 2020, that improvements in screening coverage would have a bigger impact on prevention of invasive cancer and associated death,” says Jennifer Smith, an epidemiologist at the University of North Carolina at Chapel Hill’s Gillings School of Global Public Health who was not involved in the research. “These should be complementary prevention strategies, but this data is highlighting that we really need to make sure that we’re very vigilant, as we’re rolling out important prevention programs with vaccinations, that we ensure that screening continues.”

Last year, the World Health Organization published a strategy for how cervical cancer might be vanquished around the globe. By their standards, the disease will be considered eliminated as a public health problem when there are four or fewer new cases of cancer per 100,000 women each year. Kim and her colleagues wanted to figure out how best to meet this ambitious goal in the United States.

According to the Centers for Disease Control, since the HPV vaccine was introduced, the kinds of HPV infections that lead to cancer and genital warts have dropped by 86 percent among teen girls in the U.S. And among vaccinated women, cases of abnormal cervical cells caused by the kinds of HPV most often linked to cervical cancer have dropped by about 40 percent. Currently in the United States, there are about seven new cases of cervical cancer per 100,000 women every year.

Kim and her colleagues used two mathematical models to investigate how quickly this incidence would drop under different scenarios in which screening, vaccination, or both were adopted more widely. Even if these prevention strategies aren’t scaled up, the two models estimated that the United States is on track to eliminate cervical cancer by 2038 or 2046.

Currently, the HPV vaccine is recommended for all people between the ages of 11 and 26. The researchers estimated that, based on current vaccination rates, around 75 percent of girls will be vaccinated by age 26 and 62 percent of boys would be vaccinated by age 21. When the researchers predicted what would happen if this already impressive rate of vaccine coverage reached 90 percent, they saw little difference in the timeline for how quickly cervical cancer could be eliminated.

On the other hand, if 90 percent of adult women (aged 21 to 65) were regularly screened starting in 2020, the researchers predicted that the disease would be eliminated significantly sooner and that around 1,400 to 2,088 new cases of cervical cancer would be averted every year.

“Screening will have a more immediate impact because you are basically intervening on the disease process much closer to…when the disease would be developing,” Kim says. By contrast, the HPV vaccine prevents infections that can take 20 to 30 years to develop into cancer.

“We’re not saying that screening is more important than vaccination; they’re both critical to reducing the burden of disease,” Kim says. “They just happen at different time points.”

The team hopes that the findings will galvanize public health authorities to understand how important it is to invest in these preventative strategies, Emily Burger, a research scientist at the Center for Health Decision Science at the Harvard T.H. Chan School of Public Health and another coauthor of the new study, told Popular Science in an email. However, she warned, “Any changes to current practice, such as lower HPV vaccination uptake, could disrupt or delay our projections of the timing of cervical cancer elimination in the US.”

The findings indicate that targeting women who are infrequently or never screened will have the biggest impact on eliminating cervical cancer.

People who fall through the cracks for cervical cancer screening tend to have lower incomes or be uninsured, Smith says. Her research focuses on how to identify women who are missing out on screening and make it easier for them to access the tests.

One possible strategy that researchers in the United States and Europe are investigating is giving women kits with little brushes that they can use to collect samples for an HPV test in the privacy of their own homes. Smith and her colleagues have found that these tests are effective and that the majority of women who participated in their studies in North Carolina followed through on mailing their samples back for testing.

Preventing cervical cancer (and other diseases caused by HPV, including cancers of the vagina, penis, anus, and throat) also means making sure that people are knowledgeable about current screening and vaccine recommendations. The Centers for Disease Control offers guidelines on when to get vaccinated against HPV and how often to get screened. The agency’s National Breast and Cervical Cancer Early Detection Program also provides free or low-cost screenings for people with low incomes or who are uninsured.

It’s also vital to follow up on any further diagnostic tests or treatment if your screens have abnormal results. “It’s only after completion of the whole screening process that you can prevent the disease,” Kim says. “We’ve had the luxury of really not seeing as many cases [of cervical cancer] as some of the other cancers…because we have screening options and now we have the HPV vaccination. But at the same time we can’t stop doing those things because the disease will come back.”

The post Cervical cancer could soon be a disease of the past appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

For February, we’re focusing on the body parts that shape us, oxygenate us, and power us as we take long walks on the beach. Bony bonafide bones. These skeletal building blocks inspire curiosity and spark fear in different folks—we hope our stories, covering everything from surgeries and supplements to good old-fashioned boning, will only do the first. Once you’ve thoroughly blasted your mind with bone facts, check out our previous themed months: muscle and fat.

Scientists have identified the oldest-known case of a unique kind of cancer in the tailbones of a duck-billed dinosaur. The abnormalities preserved in the ancient reptile’s bones match those seen in people today who are afflicted with this rare disease, the researchers announced February 10 in Scientific Reports.

Studying the fossilized traces of diseases in dinosaurs can shed light on how long certain maladies have existed and how they have changed over time, says Bruce Rothschild, a vertebrate paleontologist at the Carnegie Museum of Natural History in Pittsburgh and coauthor of the new study.

“This is not the first tumor that has been discovered in dinosaurs, but it’s the first of this particular variety,” he says. “When they occur in the dinosaurs, they don’t look any different than they do in us.”

Diagnosing illness in dinosaurs isn’t easy. Most of their soft tissue rotted away millions of years ago and the skeletons that remain are often incomplete. Still, paleontologists have been able to identify an impressive array of ailments, from gout to arthritis and cancer. The duck-billed dinosaurs, or hadrosaurs, seemed to be particularly prone to tumors for reasons that remain a mystery, Rothschild says. These herbivorous dinosaurs lived in large herds during the late Cretaceous and could grow to more than 30 feet long and weigh several tons.

Hadrosaur fossils have been found around the world but are particularly common in Alberta, Canada. When Rothschild examined fossils his colleague Darren Tanke, of the Royal Tyrrell Museum of Palaeontology in Alberta, had collected from this region, he noticed two vertebrae from a juvenile hadrosaur that bore distinctive signs of disease.

“This particular specimen had some features very different from what we had previously seen in dinosaurs,” Rothschild says. Within the hadrosaur bones were cavities that had an odd, meandering border reminiscent of those seen in people with a disease called Langerhans Cell Histiocytosis (LCH). “There’s very little else that does that, so it’s pretty characteristic.”

LCH is most commonly seen in children and causes immune cells to build up and form benign—but often painful—tumors in the skull, spine, other bones, or occasionally other parts of the body. When Rothschild and his colleagues examined the dinosaur bones under the microscope, they observed that the cavities had wrinkled bases that are unique to this rare disease.

The researchers then used a technique called micro-CT scanning to create virtual 3D reconstructions of the tumors. The team compared the dinosaur bones with vertebrae from people who had been diagnosed with LCH while alive, and found that the ancient reptilian tumors were “indistinguishable” from human ones. This means LHC has been afflicting the animal kingdom for more than 60 million years.

Investigating how dinosaur’s bodies were altered by disease can also give paleontologists a window into how they coped with adversity and how they survived despite challenges. Fossils might provide evidence about how often a dinosaur needed to eat and if it could wait to recover from an injury before hunting, Rothschild says, or whether a sick dinosaur could have survived with help from its pack-mates.

“When you look at dinosaurs, you recognize that they suffered the same types of problems [as humans].” Their resilience, he says, is quite impressive.

The post Duck-billed dinosaurs had the same bone tumors as people appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The current guidelines for lung cancer screening were established by the United States Preventive Services Task Force (USPSTF) in 2013 with pretty good reasoning: A national trial of over 50,000 former or current heavy smokers found that annual CT scans could better reduce the risk of dying from lung cancer compared with once-yearly chest x-rays. However, the guidelines are the same for everyone—even though only about 4 percent of participants in the original trial were African American.

Under these guidelines, far fewer African American smokers are eligible for lung cancer screenings, according to a new study. That may be because screening guidelines are based on the amount a person smokes or has smoked and their age. Research shows that African American smokers have different behaviors than white smokers—they tend to smoke fewer cigarettes, but have a higher risk of lung cancer. They’re also less likely to successfully quit smoking, and often are diagnosed with cancer younger than white smokers. Yet, a higher percentage of cancer cases occur in African American smokers ineligible for screening than in white smokers ineligible for screening.

“It emphasizes we have a long way to go to achieve equity in screening eligibility,” says study author Melinda Aldrich, assistant professor in the department of thoracic surgery at Vanderbilt University Medical Center. “I was quite surprised by how striking that disparity was.”

“The screening for the general population isn’t going to be specific enough,” says Eric Flenaugh, chief of pulmonary and critical care and interventional pulmonary medicine at Grady Hospital in Atlanta. “We already know [African Americans] are at a higher risk. They get cancer at younger ages, and at worse stages. You can’t really expect those criteria would work as well.”

The new study used cancer incidence data from nearly 50,000 smokers in the Southern Community Cohort Study. Just under 70 percent of African American smokers diagnosed with lung cancer were not eligible for screening, compared to 43 percent of white smokers diagnosed with lung cancer. African American smokers in the study were less likely to meet the benchmark for the amount smoked, and were diagnosed at a younger age.

“I was shocked by the disparity, but also by how many whites patient were ineligible,” says study author Kim Sandler, co-director of the Vanderbilt Lung Screening Program. If guidelines remain the same, the racial disparity will worsen, but a huge number of patients overall will not be screened. “As someone clinically trying to do this daily, it feels like we weren’t doing enough.”

Flenaugh published a similar study in February, using cancer data from the Surveillance, Epidemiology, and End Results Program and concluded that the age range of the USPSTF guidelines potentially miss lung cancer cases in African Americans. He conducted the analysis after noticing a pattern in the diagnoses made at his hospital, which serves a large African American population. “We were diagnosing a lot of people with lung cancer that didn’t meet the screening criteria.” Nearly 1 in 5 cancer cases were in people who wouldn’t have been eligible for screening, and whose cancer was found incidentally, he says.

The results from this research pushed Flenaugh to adjust his approach to treating African American patients, particularly those that are eligible for screening. “I’m on the lookout, even though I can’t officially screen for lung cancer and be reimbursed,” he says. “I have a heightened sense of urgency.”

The USPSTF is in the process of evaluating the lung cancer screening guidelines, Vanderbilt’s Aldrich says. “Our hope is that this is a piece of evidence that they would consider. We hope this emphasizes that current practices are insufficient.”

Ideally, Sandler says, lung cancer screening might be based on a risk prediction model that incorporates factors like age, race, socioeconomic status, family history, and other factors that can increase the likelihood that someone would develop lung cancer. That type of model would likely take time to develop—in the meantime, Aldrich says, reductions in the amount of smoking and age required for screening for African Americans would narrow the gap. “It would help lower the playing field,” she says. “Waiting is potentially the wrong thing to do.”

The post Poor lung cancer screening guidelines miss too many African American smokers appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Chernobyl has become a byword for catastrophe. The 1986 nuclear disaster, recently brought back into the public eye by the hugely popular TV show of the same name, caused thousands of cancers, turned a once populous area into a ghost city, and resulted in the setting up of an exclusion zone 1,000 mi² in size.

But Chernobyl’s exclusion zone isn’t devoid of life. Wolves, boars and bears have returned to the lush forests surrounding the old nuclear plant. And when it comes to vegetation, all but the most vulnerable and exposed plant life never died in the first place, and even in the most radioactive areas of the zone, vegetation was recovering within three years.

Humans and other mammals and birds would have been killed many times over by the radiation that plants in the most contaminated areas received. So why is plant life so resilient to radiation and nuclear disaster?

To answer this question, we first need to understand how radiation from nuclear reactors affects living cells. Chernobyl’s radioactive material is “unstable” because it is constantly firing out high energy particles and waves that smash cellular structures or produce reactive chemicals which attack the cells’ machinery.

Most parts of the cell are replaceable if damaged, but DNA is a crucial exception. At higher radiation doses, DNA becomes garbled and cells die quickly. Lower doses can cause subtler damage in the form of mutations altering the way that the cell functions—for example, causing it to become cancerous, multiply uncontrollably, and spread to other parts of the body.

In animals, this is often fatal, because their cells and systems are highly specialized and inflexible. Think of animal biology as an intricate machine in which each cell and organ has a place and purpose, and all parts must work and cooperate for the individual to survive. A human cannot manage without a brain, heart, or lungs.

Plants, however, develop in a much more flexible and organic way. Because they can’t move, they have no choice but to adapt to the circumstances in which they find themselves. Rather than having a defined structure as an animal does, plants make it up as they go along. Whether they grow deeper roots or a taller stem depends on the balance of chemical signals from other parts of the plant and the “wood wide web,” as well as light, temperature, water, and nutrient conditions.

Critically, unlike animal cells, almost all plant cells are able to create new cells of whatever type the plant needs. This is why a gardener can grow new plants from cuttings, with roots sprouting from what was once a stem or leaf.

All of this means that plants can replace dead cells or tissues much more easily than animals, whether the damage is due to being attacked by an animal or to radiation.

And while radiation and other types of DNA damage can cause tumors in plants, mutated cells are generally not able to spread from one part of the plant to another as cancers do, thanks to the rigid, interconnecting walls surrounding plant cells. Nor are such tumors fatal in the vast majority of cases, because the plant can find ways to work around the malfunctioning tissue.

Interestingly, in addition to this innate resilience to radiation, some plants in the Chernobyl exclusion zone seem to be using extra mechanisms to protect their DNA, changing its chemistry to make it more resistant to damage, and turning on systems to repair it if this doesn’t work. Levels of natural radiation on the Earth’s surface were much higher in the distant past when early plants were evolving, so plants in the exclusion zone may be drawing upon adaptations dating back to this time in order to survive.

A new lease of life

Life is now thriving around Chernobyl. Populations of many plant and animal species are actually greater than they were before the disaster.

Given the tragic loss and shortening of human lives associated with Chernobyl, this resurgence of nature may surprise you. Radiation does have demonstrably harmful effects on plant life, and may shorten the lives of individual plants and animals. But if life-sustaining resources are in abundant enough supply and burdens are not fatal, then life will flourish.

Crucially, the burden brought by radiation at Chernobyl is less severe than the benefits reaped from humans leaving the area. Now essentially one of Europe’s largest nature preserves, the ecosystem supports more life than before, even if each individual cycle of that life lasts a little less.

In a way, the Chernobyl disaster reveals the true extent of our environmental impact on the planet. Harmful as it was, the nuclear accident was far less destructive to the local ecosystem than we were. In driving ourselves away from the area, we have created space for nature to return.

Stuart Thompson is a Senior Lecturer in Plant Biochemistry, University of Westminster. This article was originally featured on The Conversation.

The post Plants couldn’t run away from Chernobyl—but that’s what saved them appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

When Hurricane Harvey struck Texas in 2017, it flooded MD Anderson Cancer Center—which meant patients had their scheduled appointments and treatments cancelled. Leticia Nogueira, who was part of the disaster response team, saw the disruption first-hand. “I saw the effect it had on the community,” says Nogueira, a researcher at the American Cancer Society.

It’s well-known that natural disasters can have devastating effects on the health of communities: They can spread disease, damage hospitals, and make accessing nutritious food and clean water difficult. However, most of what researchers know about those effects is generalized. Nogueira wanted to see how these catastrophes affect specific groups—and found, in a study published this week, that patients in treatment for non-small cell lung cancer during hurricane disasters have worse survival rates than those unaffected by hurricanes. “It shows that cancer patients are vulnerable in times of disaster,” she says.

The study, published in the Journal of the American Medical Association compared over 1,734 people undergoing radiation treatment when a hurricane disaster hit their area to 1,734 similar patients undergoing the treatment without an extreme weather incident. Patients who experienced a hurricane were in radiation treatment for longer, and had worse overall survival rates—including living an average of two months less. The risk of death for patients in storms increased as the length of the disaster increased—risks were 27 percent higher for disasters that lasted 27 days.

Delay in treatment is probably the major reason for worsened survival rates, Nogueira says—the treatment is usually provided daily. “It’s a very aggressive cancer, and if you have any issue with your treatment, we can see problems.”

In addition, she says, disasters are traumatic experiences. “Patients are displaced, they can impact mental health, and physical function.” However, treatment delays are a factor that can be targeted with interventions, she says. For example, patients with this cancer who are likely to be affected by a disaster could be identified by hospitals and clinicians during the lead up to a predicted storm or during hurricane season. They might then be able to be transferred to another location, Nogueira says, or insurance companies could waive out-of-network costs. “We can implement interventions,” she says.

These findings also highlight the importance of health care providers tailoring disaster response plans to specific patient groups, as well as taking an overall view of the patient population as a whole. This is the first study to show the direct effects of a disaster on people with one individual disease, Nogueira says. Future research, she says, should focus on other types of cancer patients receiving different treatments to help build a picture of the groups most vulnerable to disaster.

“The impacts of climate change are already here,” Nogueira says. They’re changing storm patterns and making storms worse, she says, making strategies to protect the health vulnerable groups, including cancer patients, even more important. “Physicians and facilities should have conversations, and think about their treatment plans in the event something happens. They need to make sure they know what the plan is, and if they’re prepared.”

The post People in cancer treatment during hurricanes have lower survival rates appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Doctors hope the future of cancer treatment is personal: Using genetics, they’ll be able to match patients with precisely the drug or treatment option that will fight their tumors. However, information on tumor genetics often isn’t linked with data on how well patients with those tumors did on particular treatments. This makes it difficult for researchers to tailor treatments to individual patients. “Sometimes all that’s known is how long patients lived who had a particular pathology, if that’s even known,” says Kenneth Kehl, a medical oncologist at the Dana-Farber Cancer Institute in Boston. “Asking questions like which mutations predict benefit from a particular treatment has been more challenging than one might expect.”

To help ease those challenges, Kehl worked on a team that developed a machine learning algorithm that could pull information from doctors’ and radiologists’ notes in electronic health records in order to identify how particular patients’ cancer progressed. Their tool, published this week in the journal JAMA Oncology, might in the future help identify patients who could benefit from clinical trials or other specific interventions—and it’s a piece of larger efforts to bring artificial intelligence into oncology.

Most of the information about the progression of tumors in cancer patients is contained in written notes from radiologists, who examine scans and track changes in the status of the cancer. Because it’s raw text—not choices from a drop-down menu or data points in a spreadsheet—most analytic methods can’t pull the relevant information. The tool created in this study leveraged improvements in machine learning for language to identify those details in electronic health records.

The machine learning system was able to identify cancer outcomes as well as human readers, and much more rapidly. Human readers could only get through three patient records an hour. The tool would be able to analyze an entire cohort of thousands of cancer patients in around 10 minutes.

Hypothetically, Kehl says, the tool could be leveraged to sweep the health records of every patient at an institution and identify those who are eligible for and would need clinical trials, and match them to the best possible treatments based on the characteristics of their disease. “It’s possible to find patients at scale,” Kehl says.

For this particular tool, the scans from cancer patients were initially read by human radiologists. But artificial intelligence and machine learning can read images, as well, and research shows that they can analyze scans of tumors as effectively as human radiologists. In another study published this month, radiologists and artificial intelligence experts partnered to develop an algorithm that could determine if lumps on a thyroid should be biopsied—and found that recommendations from the machine learning tool recommended biopsies similarly to expert radiologists using the American College of Radiology (ACR) system.

Assessing thyroid lumps can be time consuming, and radiologists can face challenges using the ACR system. “We wanted to see if deep learning can perform those decisions automatically,” says study author Maciej Mazurowski, associate professor of radiology and electrical and computer engineering at Duke University.

There’s more work to be done on artificial intelligence and scan analysis before these tools can take the place of radiologists, Mazurowski says, but recent research indicates that it’s possible for AI to perform at the level of radiologists. “The final question, even if we can show that these work as well as humans, will be whether and to what extent it will be adopted into the healthcare system. It’s not just whether it works.”

Visual analysis is further along in medicine and oncology than textual analysis, Kehl says, but both could be components of integration of machine learning into the normal practice of care. It might be possible, for example, to integrate machine interpretation of scans into the overall electronic health record analysis, he says. “That would mean looking at how much information we get from images themselves, how much do we get from human interpretation, and what could we get from the model looking at images,” he says. “The optimal strategy still isn’t known.”

It seems possible that, going forward, artificial intelligence might help identify and monitor cancer progress, Kehl says. “It’s figuring out how we can incorporate AI generally, and in imaging, pathology, and health records, into the clinical workflow,” Kehl says.

The post Artificial intelligence is taking an increased role in diagnosing and treating cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

When a person needs a bone marrow transplant, doctors must retrieve and harvest stem cells from that individual or a donor. That extraction process used to mean drilling deep into their hip bones and using an extra-long needle to pull out bone marrow, which holds the cells that can develop into all types of blood cells. Now, doctors use drugs, called granulocyte-colony stimulating factors (GCSFs), which are far easier to tolerate.

The process is safe, and though it has some side effects, it’s usually effective. However, it doesn’t work for everyone. “Not everyone is a good candidate for the regular standard of care,” says Stephanie Smith-Berdan, a research specialist at the University of California, Santa Cruz. “We as scientists should find alternatives.”

In a new study in mice, Smith-Berdan and her colleagues took the initial steps towards a new approach. The team found that a combination of Viagra and a stem cell mobilizer called Plerixafor were able to pull stem cells out of the bone marrow and into the bloodstream (like GCSF’s do), where they could be easily harvested. It worked quickly, and the cells could be extracted from the mice within two hours. It takes multiple days of injections with GCSF before stem cells can be harvested, under current clinical practice.

Although it’s too early to say if this treatment will work in humans, it’s a logical approach, says David Porter, the Jodi Fisher Horowitz Professor in Leukemia Care Excellence at the Perelman School of Medicine at the University of Pennsylvania, who wasn’t involved in the study. If the strategy proves effective and equally quick-acting in humans, it could have significant implications for stem cell donation and transplant, he says. “It may certainly make it easier to get stem cells where it is currently difficult.”

Right now, GCSFs don’t work for some patients who might benefit from autologous stem cell transplants—a procedure where doctors harvest a person’s own stem cells and use them to replace their unhealthy bone marrow, that’s used in conditions like Hodgkin’s lymphoma—because they often don’t work in people who have had chemotherapy in the past. The drugs also can’t be used in patients with sickle cell disease.

A fast process would also improve the experience for healthy donors who volunteer to give stem cells—which might attract more people. The low cost of Viagra could also be beneficial. “It’s cheap and it’s very simple,” says study senior author Camilla Forsberg, a professor of biomolecular engineering at the University of California, Santa Cruz. “The current standard is given by injection, and its five days of repeated injections. I would think people might have an easier time enticing donors if it’s a shorter process, that’s less invasive.”

Before Viagra made its money as a blockbuster erectile dysfunction drug, the medication was originally researched for its ability to dilate blood vessels. Smith-Berdan and Forsberg study the mechanisms that help stem cells move in and out of the bone marrow, and in previous research, found that the more permeable the blood vessels around the bone marrow were, the more easily stem cells moved into the bloodstream. As a result, they decided to test Viagra, which opens blood vessels and increases their permeability.

First, they tested Viagra alone in a set of mice, which didn’t have a large effect on the movement of stem cells. It’s probably a good thing that Viagra alone didn’t move stem cells into the bloodstream, Forsberg says. “That way you don’t have to worry about stem cells moving when you take Viagra for other indications,” she says. It might be that the drug is not strong enough—in early data, other, stronger vasodilators are enough to move the cells on their own.

Next, the team tested Viagra along with a single dose of Plerixafor, which mobilizes stem cells, in another set of mice—and the combination significantly increased the number of circulating stem cells in only two hours.

While the amount of circulating stem cells went up quickly, they dropped back off quickly, as well. That’s something to keep in mind if the procedure is tested in people, Porter says. “From a clinical and medical standpoint, something that has to be timed so carefully often is logistically difficult to manage.”

Forsberg and Smith-Berdan work in pre-clinical basic science, so they won’t try and test their drug combination in people themselves. However, Forsberg says she’s heard from other researchers who would be interested in running that type of study.

The drugs would likely be fairly easy to test, and test safely, in people, because the drugs used are already FDA-approved. “It’s not one of those very basic science approaches that you’ll never be able to give to people,” Porter says. “It’s intriguing, because it’s testable.”

The post Viagra might help make stem cell transplants easier appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

However much we might like to believe that a detox tea or a super-berry will prevent us from getting cancer, the truth is a more bitter pill: anyone can get cancer no matter what kind of lifestyle they follow, but eating healthy foods and exercising regularly is the best way to lower your risk.

But that’s so much less satisfying, isn’t it? “Eating healthy” is this ambiguous idea that might seem only tangentially related to cancer, whereas eating an antioxidant that supposedly blocks free radicals feels like much more direct action. And yet the truth is that just as many cancer cases are caused by poor diet as by drinking alcohol, and even more are tied to the excess body weight that comes with eating that poor diet.

Roughly two out of every five cancer cases in America are preventable by a modifiable risk factor, from alcohol consumption to physical inactivity and, of course, cigarette smoking. That’s more than 659,000 cases annually. Of those, a new study in the journal JNCI Cancer Spectrum estimates that more than 80,000 (at least in 2015) were attributable to suboptimal diet.

So what does that actually mean? How does diet influence our cancer risk? We’ll break it down for you.

How do certain foods affect my cancer risk?

Most of the breakdowns of diet and cancer focus on seven major food groups: fruits, vegetables, whole grains, processed meats, red meat, dairy, and sugar-sweetened beverages (sugar science is complicated, since fruits also have plenty of sugar, so researchers focus on sweet drinks since they’re unequivocally bad for you). Most Americans—in fact, most people around the world—don’t eat the right amount of any of these kinds of food. We consume far too much sugar and red or processed meat without getting nearly enough fruit, veggies, whole grains, or dairy.

Some of those food groups have a very direct influence on our health. The fiber in fruits, veggies, and whole grains, for instance, feeds a robust gut microbiome. Processed and red meats contain various molecules that promote cancer. But other foods, like sugar, are cancer-inducing in a less direct way: they make us gain weight. People who are considered overweight can be perfectly healthy, but on average, being obese comes with increased health risks—including a higher risk of cancer.

Here’s a more in-depth breakdown of how these foods influence our cancer risk, all courtesy of the World Cancer Research Fund’s thorough report on diet and cancer.

Whole grains

Processed grains, like those in white flour, don’t contain the whole grain kernel—but it’s the whole grain that contains all the nutrients. The bran and germ bits include nutrients like vitamin E, copper, zinc, and selenium, plus lignans and phytoestrogens that researchers think could have anti-carcinogenic properties. They’re also full of fiber, which feeds healthy gut bacteria, ferments into short-chain fatty acids that may help prevent cancer, and move your bowel contents along (which may decrease the chances that a mutagenic compound in your feces comes in contact with your intestinal cells).

All of this contributes to a healthy colon that’s low in inflammation. We hear a lot about inflammation and cancer—the basic idea is that inflammatory reactions are intended to kill potential invaders like bacteria, because generally your body is inflamed in response to a bodily threat. A cut on your hand, for instance, is less likely to get infected because your body produces chemicals that induce mutations in potential pathogens like bacteria. But those same chemicals damage your own cells. That’s not a problem on a small scale, but chronic inflammation ends up promoting cancer.

Diets low in whole grains tend to promote inflammation and lead to an unhealthy gut overall, which is why they’re primarily associated with colorectal cancer.

Dairy products

You might be used to thinking of dairy as bad because Americans have been told for decades that fat is evil. Fat is not wholly evil, and though it’s calorie-dense there are tons of dairy options that are lower in fat and quite healthy for you. For one, dairy is high in calcium, which research suggests could be protective for your colon (though it’s not clear exactly how). And then there are the lactic acid-producing bacteria that give yogurt and other fermented dairy products their characteristic tang. Those bacteria contribute to your gut microbiome and seem to inhibit cancer formation through a variety of pathways.

These factors all seem to help protect your colon cells from becoming cancerous.

There is one potential drawback to dairy (apart from saturated fat), which is that high calcium content might be associated with a slightly increased risk of prostate cancer. Greater milk consumption has been associated with a small elevation in levels of a growth factor called IGF-1, which in turn is associated with a higher risk of prostate cancer. For that reason, dairy isn’t often endorsed as wholly anti-cancer. On the other hand, calcium also appears to exert some protective effects by regulating vitamin D levels. Breast cancer risk seems to go down with higher calcium intake for this reason.

Processed and red meats

The carcinogenic effects of these meats are pretty much all tied to three types of molecules: heterocyclic amines, polycyclic aromatic hydrocarbons, and N-nitroso compounds. The first two form in red and processed meats during high-temperature cooking, while your colon produces the third when it’s exposed to high levels of heme iron (which is what gives red meat its hue). Processed meats also contain nitrates and nitrites, both of which may contribute to the formation of N-nitroso compounds.

These molecules contribute to cancer risk in multiple organs, including the colon, the stomach, and the pancreas, by directly causing mutations in cells that can add up over time.

Fruits and vegetables

Apart from all the aforementioned benefits of fiber, fruits and veggies also have tons of nutrients and phytochemicals that research suggests are anti-tumorigenic. These include everything from carotenoids to flavonoids to vitamins A, C, and E. A lot of the benefit from these compounds goes toward the various elements of your GI tract, from your mouth to your stomach to your colon. But they also help prevent others, like breast, lung, and bladder cancer, most likely through the same pathways.

Sugar-sweetened beverages

Unlike the rest of these dietary factors, sugar doesn’t have any direct cancer-causing or -preventing properties. Instead, it contributes by promoting weight gain. Though there are plenty of ways to get healthier if you’re overweight or obese (regular exercise can help your metabolism shift toward a heart-healthy level even if you don’t lose weight!), fat mass still contributes to cancer.

One method is that ol’ buddy inflammation. Body fat induces chronic inflammation through several pathways, including by directly producing pro-inflammatory chemicals, and is associated with higher levels of insulin, which can promote the excess cell growth that increases a person’s cancer risk.

Excess body fat also influences hormone levels, since fat cells are a significant storage site for hormones. This is especially true for postmenopausal women, who are no longer producing high levels of estrogens from their ovaries and thus get most of their sex hormone exposure from body fat.

Will eating healthier prevent me from getting cancer?

Yes and no. All of the mechanisms we’ve discussed so far do genuinely decrease your cancer risk, but it’s also important to know that a lot of what we know about how nutrition influences health comes from association studies. That means researchers look across a population to see, for example, who eats more fruits, and then figure out whether those people get fewer diseases like cancer. The trouble is that people who eat a lot of fruit probably also have other healthy habits, like exercising regularly, and they’re more likely to be of a higher socioeconomic status that affords them better healthcare.

This means that only taking one recommendation is unlikely to have a huge impact on your cancer risk. You can eat all the strawberries you want, but if you’re having bacon every day you’re unlikely to have a healthy colon. And if you’re a super-healthy eater, having a serving of bacon once a week as a treat isn’t going to greatly raise your cancer risk. But if you shift your whole diet toward more fruits, veggies, whole grains, and low-fat dairy—and away from red or processed meats and sugar—you have a better chance of staying healthy than if you ate carelessly. You’re even less likely to get cancer if you don’t drink alcohol or smoke, and if you get plenty of physical exercise.

Of course, many people follow all these recommendations and still get cancer. And some people will smoke and drink and eat chocolate bars every day of their lives and die at a ripe old age without ever developing cancer. It’s important to remember that neither end of that spectrum means that the recommendations are no good. Statistically, across an entire population, many tens of thousands fewer people would get cancer if everyone ate a healthy, balanced diet. And while cutting down on sugar and upping fiber intake isn’t a magical cancer prevention method, good nutrition definitely won’t do you any harm.

The post A bad diet really can raise your risk of cancer. Here’s how. appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Through a program called the National Air Toxics Assessment, the Environmental Protection Agency surveys overall air quality across the country, and calculates the cancer risk posed by the combined amount of chemicals in the air. It takes into account the effect of breathing in a mixture of all the air pollutants—because that’s how people are exposed to them in the real world.

However, research on pollutants and contaminants in drinking water has stuck with focusing on one chemical at a time: isolating it, and investigating the effects it has on health. Like with air, though, that’s not how people are exposed to these chemicals in real life—if they’re drinking a glass of water from the tap, it would contain all of the things the water system contains at once.

“Drinking water often contains more than one contaminant,” says Tasha Stoiber, senior scientist at the Environmental Working Group. In an effort to get a comprehensive look at the cancer risk of a water system, Stoiber applied a cumulative risk assessment to the water supply in California, which has data on the water supply easily available. “If we’re just thinking about drinking water, this kind of assessment more accurately reflects what you would see in real life exposures,” she says.

The analysis, published this week in the journal Environmental Health, estimated the number of additional cases of cancer that could be attributed to tap water in California between 2011 and 2015. They analyzed the information on contaminants that pose a cancer risk, including arsenic and the byproducts of disinfectants, in 2,700 water systems across the state. The combined levels of those contaminants were estimated to cause an additional 15,449 lifetime cancer cases, or 221 cases per year.

It’s important to note, Stoiber says, that the vast majority of California’s water systems meet legal standards for water contaminants. “Even at those legal levels, we calculated that there still is some health risk below those legally enforceable standards,” she says.

The study also showed that small communities had the highest exposure to waterborne contaminants. The water systems that posed the highest risk of cancer from arsenic exposure, for example, all served communities with fewer than 1,000 people.

“I’m sure that won’t be surprising to smaller communities affected by poor water quality,” Stoiber says. “They don’t have the resources available to larger communities to respond to drinking water problems.”

There’s a degree of uncertainty to these calculations, Stoiber says, because the researchers don’t know if and how any of the pollutants included in the assessment interact with each other. “The risk could be greater, or the risk could be less,” she says. The first step towards understanding a contaminant is to study it in isolation, and it’s a slow and complicated process to untangle how it might be exacerbated by another chemical.

The cumulative risk assessment applied in California could be easily applied to other states, too, if data was available, Stoiber says. And it’d be useful for policy: “It could be used as a decision making tool,” she says. People may underestimate the benefits of cleaning the water supply if they don’t consider the total group of contaminants that it would remove, she says. “If you’re just looking at one, and the health benefits of removing that, you’re missing the additional benefits of co-occurring contaminants.”

The study was an initial step towards looking at the cumulative impact of water contaminants on cancer risk, and there’s a lot of research to be done going forward, Stoiber says, and it’ll be a long and slow process to incorporate that research into regulations. “Certainly, we’re hoping that as we gain more information we can begin to asses and layer this work down the road to regulate contaminants,” she says. “We’re hoping this type of research is a step in opening dialogue towards that.”

The post California’s tap water could be a cancerous cocktail of pollutants appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

When they first came on the market, industry advocates originally touted vapes—electronic nicotine delivery systems such as a JUUL—as a smoking cessation aid. In the time since, they’ve exploded in popularity among young people, leading to worries that brands like JUUL are contributing to a new and dangerous nicotine addiction epidemic among teens who would never have thought to light up a traditional cigarette. E-cigarettes have public officials concerned, and a new study from Harvard researchers suggests there are two more reasons to worry: the presence of fungi and bacteria in vape juice and e-cigarette cartridges.

In the study, David Christiani and his colleagues tested 75 e-cigarette products in total for two contaminants: endotoxin, which is part of the cell walls of a class of bacteria, and glucan, which is part of the makeup of fungi. Chronic exposure to endotoxin is linked to asthma and reduced lung capacity; while the form of glucan they found is known to cause inflammation, which is a big problem in a sensitive system like your lungs. Both microbial products are found in many places out in the world. The issue here is that they’re in a substance that’s inhaled—and inhaled frequently.

Of the products they tested, of which about half were e-cigarette liquid and half were cartridges, they found endotoxin in 17 products, or 23 percent, of products. Eighty-one percent, or 61 products, contained glucan. Even though Christiani says the concentrations of these two microbial products “are not very high,” knowing they’re present “adds a couple more agents to the already long list of exposures from e-cigarette products,” Christiani says.

E-cigarettes work by heating up a nicotine-containing liquid so it vaporizes and can be inhaled by users. This liquid also contains flavorings, from the traditional (mint) to the avant-garde (banana.) The flavors are thought to be one of the reasons that e-cigarettes have become so popular among young people. Nobody really knows what happens to the juice chemically when it’s heated up.. Many compounds break down into dangerous chemicals when heated, and the researchers still don’t know very much about what’s in e-cigarette fluid.

Experts do know that some flavorings are linked to heart and blood vessel damage.) And there is a body of evidence showing that e-cigarettes product harmful carcinogens and other chemicals, as well as exposing users to metal byproducts from the devices themselves. However, because e-cigarettes are loosely regulated, with a huge diversity of products in the marketplace, it’s hard to definitively state what’s in them. It doesn’t help that the e-cigarette industry, like the traditional tobacco industry, has a stake in obscuring the health risks of their addictive (and lucrative) products.

This new study, which looked at brand-new products, also points to the fact that e-cigarette products are getting contaminated with microbes somewhere in the production process. In the case of cartridges, he speculates that the presence of microbial products may be the result of contamination on the cotton wicks that are part of the cartridge. But nobody knows yet, though his team is going to try and find out in further research.

Sanjay Sethi, a professor of medicine who specializes in lung health at the University of Buffalo, says the findings are “interesting, but not surprising.” Sethi was not involved with the study. He would like to see further research elaborating on how the levels of endotoxin and glucan in e-cigarettes stack up against those in traditional cigarettes, which he says would give the results more context. However, he agrees the current study’s findings are another reason for concern about e-cigarettes.

The post Vapes are full of flavors—and fungi appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

As if things in the world of healthcare weren’t chaotic enough, last week the FDA pulled the popular heartburn medicine ranitidine, brand name Zantac, from the shelves due to a possible cancer link. This follows months of investigation first prompted by Valisure, a small start-up pharmacy that looked into the chemistry of the popular medication.

Here’s what people with heartburn should know about the recall.

What is ranitidine?

Ranitidine is an H2 (histamine-2) blocker, which decreases the amount of acid created by the stomach, according to the FDA. This makes it a good fix for health issues like heartburn, sour stomach, or acid indigestion.

Some ranitidine drugs are available over the counter (Zantac can be found OTC), but others are prescribed for treatment and prevention of ulcers and treatment of gastroesophageal reflux disease.

Does Zantac cause cancer?

“It’s important to note that there are no data available linking ranitidine to cancer in humans,” Harvard epidemiology professor Joshua Gagne says, “only data showing that some ranitidine products that have been tested contain NDMA.”

If ranitidine is exposed to high temperatures, says Gagne, who has been writing about the drug on Harvard’s medical school blog, the drug can break down to form N-nitrosodimethylamine, or NDMA. This substance is classified as a possible carcinogen. But not all of the samples tested by the FDA were found to have an unacceptable level of the potential carcinogen.

“Long-term studies are needed to determine whether long-term use of ranitidine is associated with cancer occurrence in humans,” Gagne adds. “Nevertheless, I would not count on ranitidine returning to shelves.”

What is NDMA?

According to Gagne, NDMA is an environmental contaminant that can be produced by industrial processes like water treatment. Very low levels of NDMA can also be found in drinking water and certain foods like cured meats and dairy.

But before you lose your head about this scary-sounding molecule, it’s important to note that it’s classified right now as a “probable carcinogen.” This means there’s some evidence that it can cause cancer in animals, but the data on its relationship to cancer in humans is limited, Gagne says.

Ranitidine isn’t the only drug that has been linked with NDMA. Several blood pressure medications were recalled in July 2018 for a similar connection to the potential carcinogen.

I take Zantac. What now?

The FDA is telling consumers to stop taking any pills or liquid versions of ranitidine.

Luckily, there are lots of drugs that can help you out with heartburn struggles that don’t contain ranitidine. A few examples include famotidine (Pepcid), cimetidine (Tagamet), esomeprazole (Nexium), lansoprazole (Prevacid), or omeprazole (Prilosec). So if you’re a regular Zantec user, chat with your healthcare provider about another option that’s free of NDMA risks.

Gagne also suggests that lifestyle changes can be helpful for managing heartburn symptoms. Avoiding spicy foods, carbonated beverages, and smoking are just a few ways to try and prevent heartburn without stepping foot in your local pharmacy.

The post The FDA just pulled popular heartburn drug Zantac due to cancer risk appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Breast cancer is one of the most commonly diagnosed cancers in the United States, which is one reason why doctors encourage patients to get mammograms, which can identify problems before symptoms appear. But various medical associations, which put out mammogram guidelines and recommendations, don’t agree on how early or how often people with breasts should start being tested.

This week, the American College of Physicians (ACP) updated their screening guidelines to recommend that people with an average risk for breast cancer (meaning those who don’t have a personal or family history of breast cancer, dense breasts, or genes that increase risk) should have mammograms every other year starting at age 50. Between 40 and 49, they should discuss the risks and benefits of the screening procedure with a physician.

Previously, the ACP had set their mammogram start date at 40 for women without added risk factors. This update puts the organization in line with the recommendations from the U.S. Preventive Services Task Force, which also says regular mammograms should start at age 50, and that between 40 and 49, the choice should be made on an individual level. The American College of Obstetricians and Gynecologists, on the other hand, recommends annual screenings starting at age 40, as does the American College of Radiology. The American Cancer Society takes a hybrid approach, and says that people should start annual mammograms at 40 if they wish to do so, and if not, then at age 45.

Like with all screening tests, recommendations around mammograms require a complicated balancing act between the benefits of testing, like finding cancers, and the drawbacks of over testing—like the emotional harm of false positives, or providing unnecessary treatments for small tumors that might never have become dangerous.

People under the age of 49 are more likely to need follow-up screening, partly because their breasts are likely to be denser, making scans harder to read, says Linda Moy, a professor of radiology at NYU School of Medicine. They’re also more likely to have false positive scans, which can be anxiety provoking.

Recommending screening starts at age 50 means prioritizing the reduction of those additional tests and overdiagnosis, and is looking at the question from the societal, public health level: cutting down the amount spent on testing as much as possible without sacrificing care for the largest number of people. According to research from the New England Journal of Medicine, screening mammograms—which are ones conducted not to investigate symptoms but to monitor healthy people—is more likely to lead to overdiagnosis than to catch a dangerous tumor early.

In particular, mammogram screenings have increased the number of diagnosed cases of a non-invasive breast cancer called Ductal Carcinoma in situ (DCIS), which involves the cells that line the breasts’ milk ducts but rarely spread beyond them. The screening tests have been less able to detect early stages of other types of breast tumors that have the potential to metastasize and become deadly.

However, Moy thinks that the priority should be catching as many chances as possible, even if that creates more false alarms, and says screening should start at age 40. “We want to find cancers while they’re small. We need to call patients back because we want to be sure,” she says. That’s not to minimize the anxiety that follow up screening can cause, she says, but that anxiety level can vary patient to patient.

The physicians who are implementing these guidelines typically follow the recommendations of their own professional societies, Moy says: Radiologists follow the American College of Radiology guidelines, and gynecologists follow those from the American Congress of Obstetricians and Gynecologists. In 2017, a study found that over 80 percent of primary care physicians and gynecologists say that their patients should start mammograms at age 40. However, physicians who said that they trusted the U.S. Preventive Services Task Force recommendations were the least likely to recommend screening starting at age 40, indicating that the medical body guidelines play a role in the way physicians counsel their patients.

Many physicians, though, make their recommendations on a patient-by-patient basis, Moy says. “They might say, listen, there’s controversy over mammograms, they do find cancer earlier but they can also have false positives, what would you like to do?”

It’s ultimately a good thing to have that dialogue, and make decisions based on the patient. “We don’t want to be dogmatic. These doctors know their patients, and understand their history,” she says. “We try to be flexible.”

The post You might not need a mammogram until you turn 50 appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

At the National Republican Congressional Committee’s annual spring dinner, President Donald Trump claimed that the noise wind turbines produce causes cancer. This isn’t true—just ask anyone with a lawn mower, which are about as loud as a wind turbine, and much closer to people’s ears. It’s also not the only wind turbine myth in the popular consciousness, or the president’s public speeches.

That’s not to say that noise can’t cause humans physical harm. It’s just that the kind of sonic blasts that can produce nausea and impair breathing and vision, start at around 150 decibels. Even if you sat directly beneath a wind turbine, the sound produced would be about 105 decibels. That level of sound may be annoying, but the noise would not cause cancer. Scores of studies back this up. Some have found that the mechanical sounds wind power plants produce can interrupt people’s sleep, but none have linked the energy source to cancer.

That sets wind power apart from many of its fellow energy sources. Coal, for example, has been widely been proven to cancer as well as heart and lung problems. According to the National Cancer Institute, people who work in coal manufacturing have a higher risk of developing skin, lung, bladder, kidney, and digestive tract cancer. Byproducts of the industry impact public health, too. Coal- and oil-burning power plants release pollutants like mercury into the air. The neurotoxin makes its way into public water sources, while air pollution causes health problems including asthma and yes, cancer.

Coal- and oil-burning plants also contribute to climate change, which has its own consequences for human health. Carbon dioxide accounts for 65 percent of all greenhouse gas emissions. Fossil fuel use is the primary source of CO2 emissions, which heat the planet and exacerbate wildfires, rising sea levels, and hurricanes. Last year, the United States experienced 14 extreme weather events that each accrued $1 billion in losses. Together, these events killed 247 people. Renewable energy sources like wind and solar reduce greenhouse gas emissions that contribute to climate change.

The president also claimed wind energy creates “a graveyard for birds.” Wind turbines in the United States do kill somewhere between 140,000 and 328,000 birds every year. But studies have shown that the number of birds wind energy kills relative to the amount of power it produces is relatively low. One study found that fossil fuel plants actually pose a far greater threat to airborne wildlife than wind turbines, killing 17 times more per gigawatt hour than wind power. Birds get caught in oil pits and ponds that store toxic waste leftover from oil extraction and processing. Leaky chemical holding tanks have been known to poison fowl, while U.S. power lines kill as many as 64 million birds annually.

Scientists are working to further reduce bird-turbine collisions. This acoustic lighthouse, for example, emits a high-pitched sound that causes birds to slow down and look up. Since birds don’t typically look straight ahead while flying, they don’t see obstacles like skyscrapers, cell towers, and wind turbines. The alert system helps birds change course before it’s too late.

And those aren’t the only inaccurate claims the president has made regarding the science of wind power. In a speech he gave last month in Michigan, the president also suggested that homes that use wind power will not have electricity on calm days. But that’s not how renewable energy works. “Typically it’s not accurate to say that if your home runs on renewable energy that you won’t have power when it’s calm or cloudy,” says Johnathan Lamontagne, a systems analyst in the Department of Civil and Environmental Engineering at Tufts University. Large-scale renewable energy usually provides supplemental energy to a grid that has several input sources, so if one fails, there’s a backup to take its place.

The energy sector is dirty and dangerous, but wind power is not the problem.

The post Wind turbines do not cause cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In the United States, screening for colorectal cancer is usually unpleasant. A patient’s preparation begins with a liquid diet, laxatives, and the uncomfortable knowledge of where the colonoscopy camera is going to go.

But there’s another, effective way to screen for colorectal cancer: fecal immunochemical tests, or FITs, which detect blood in stool (an early sign of cancer). The tests can accurately identify cancer, according to a review and meta-analysis published in the Annals of Internal Medicine.

If the FIT comes back negative, the patient is in the clear until their next annual test. If it comes back positive, only then would they have a colonoscopy, says study author Thomas Imperiale, researcher at the Regenstrief Institute and the Indiana University Center for Health Services and Outcomes Research. “If the comparison is to do a colonoscopy on everyone, you can greatly reduce the use of colonoscopy by doing a FIT,” he says. “As long as it still enables you to detect most of those cancers.”

The latest study builds on a 2014 review of FIT performance. “At that time, there were fewer studies available,” Imperiale says. His team’s analysis looked at 31 studies which included a total of over 120,000 patients. They found that the tests had a moderate to high sensitivity for cancer, meaning they identified cancer when it was present, and had a low rate of false positives.

Different studies included in the meta-analysis had different thresholds for flagging a positive tests, which impacted the amount of cancers detected. When the test considered 20 micrograms per gram of blood in the sample as a positive, it identified three out of four cancers, with a low false positive rate, Imperiale says. But when the threshold was lowered to 10 micrograms per gram, the sensitivity goes up. “You can take the sensitivity up to identify 9 out of 10 cancers.” However, that generates more false positives.

The analysis showed that though a single FIT can identify cancer, it has a low sensitivity for abnormal growths, called advanced adenomas, which are considered precursors to colorectal cancer. This differs from a colonoscopy, which allows physicians to visualize everything from benign to cancerous growths.

But James Allison, emeritus professor at the University of California, San Francisco and emeritus investigator at Kaiser Permanente, isn’t worried. He says these adenomas grow very slowly, and only around 6 percent annually will actually become cancerous. Because FITs are intended to be used annually, a patient with a negative result would ideally be tested repeatedly, increasing their likelihood of detecting an adenoma. Colonoscopies, on the other hand, are only done every 10 years. “You have a long time, in a program of repeated screenings, before it hurts someone,” says Allison, who published an editorial on FIT that accompanied the new study. Not identifying them on the first test is not necessarily a problem, he says, because they’re slow growing, and if they’re discovered on a FIT a year later, they likely won’t pose a major problem.

The easy annual repeatability of FITs is one of the test’s major benefits, Imperiale says. “If you have repeated negative tests, you can start to stack meaningful results, and get away with not everyone needing a colonoscopy.” After all, only around 4 percent of people with adenomas get colorectal cancer. “95 percent of the population will never get it. Negative FITs will identify who those people are.”

Colonoscopies have been the standard screening for colorectal cancer in the United States, but the U.S. Preventative Task Force, the agency that produces medical screening guidelines,does not recommend colonoscopies over FIT, or vice versa. Instead, the organization says the goal is to get the highest number of people screened. In other countries, like Canada, FIT is always the first line screening for colorectal cancer. Patients cannot have a colonoscopy covered by insurance without first having a FIT.

The tests are also a lot cheaper than colonoscopies, notes Imperiale—and people are much more likely to do them than they might be to do a colonoscopy, which for many is uncomfortable and stressful.

FITs aren’t for everyone. Allison would not recommend the test for people with a family history of colorectal cancer or other significant risk factors. “I do not think a FIT is appropriate there,” he says. Imperiale agrees, and says that recognizing both options means patients with different risk factors can make informed choices with their doctors. A patient with some risk factors and who rarely goes to the doctor might be better off with a colonoscopy, he says. But for a marathon runner who stays on top of preventative check-ups, there aren’t a lot of upsides to colonoscopy. “Low-risk, compliant patients may do best with FIT,” he says.

To properly use FIT as a colorectal cancer screening strategy, hospitals and clinics must have systems in place to re-test people in the years after a negative result Imperiale says. “More importantly, people who are positive need to know that they need to go in for a colonoscopy,” he says.

There are multiple FITs available from different manufacturers, with varying amounts of information available, and patients should ask their doctors about the evidence behind the particular version they’re using, Allison says. The U.S. Preventative Task Force details the FITs with the best performance.

Ultimately, this study is a reminder that checking in with your gut doesn’t necessarily require a colonoscopy. “Non-invasive tests for colon cancer are a good option for average risk patients,” Imperiale says. “There are options, and the only wrong option is to go unscreened.”

The post You might not need a colonoscopy to be screened for colon cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

It’s hard to imagine a time before sunscreen. But it wasn’t that long ago that the only way to protect yourself from the sun’s powerful rays was to either stay inside or wear long sleeves. And it wasn’t until the 1970s that we started to see sunscreen lotions and sprays hit the market that looked anything like what we see today. Now, many Americans don’t think twice before slathering up to create a greasy barrier between themselves and the sun.

Behind the scenes, though, cosmetic companies and the Food and Drug Administration (FDA) must ensure that the stuff we use is not only doing its job but also not harming us in the process. And that’s been a slow operation. This week, the FDA made a big step forward, though, issuing proposed guidelines and regulatory regulations to better reflect what we know about sunscreen ingredients, how they work, and how they affect our health.

“Today’s action is an important step in the FDA’s ongoing efforts to take into account modern science to ensure the safety and effectiveness of sunscreens,” said FDA Commissioner Scott Gottlieb in an official statement release by the government agency.

As part of the report, the FDA re-examined all active ingredients currently present in sunscreens on the market today to determine if they’re still generally recognized as safe and effective or not. Of all 16 ingredients, just two met this “GRASE” standard: zinc oxide and titanium dioxide. Another set—PABA and trolamine salicylate—were deemed unsafe, and the other 12 had “insufficient safety data to make a positive GRASE determination at this time.”

None of this has any bearing on your favorite sunscreen—at least not yet. The FDA is now currently accepting comments from the public over the next several months to inform their research before they make recommendations that makers will have to follow. For now, here’s what you need to know.

What’s in sunscreen?

Sunscreen’s active ingredients are typically divided into two major categories: physical and chemical. Physical ingredients include both zinc oxide and titanium dioxide, which are easily recognizable for their characteristic white residue. They sit on the outside of the skin and work by literally deflecting ultra violet (UV) rays. Chemical ingredients, on the other hand, include PABA and trolamine salicylate (and the rest of the 12 yet-to-be determined safe ingredients). They are absorbed in your skin, and absorb the UV rays in return.

It’s no surprise, then, that the two ingredients that the FDA has deemed safe are the ones that rest on the surface of the skin only. For the rest, a main concern is whether and how much they enter the bloodstream—and what effect that might have on our health. Of note, studies have found many of the active chemical ingredients in breast milk, as well as urine and blood plasma. However, whether or not that is harmful to human health is still uncertain, though they have forced regulators to pause and take note. What will better help us determine the health effects are longer-term studies.

“These tests are critically important,” says David Andrews, a senior scientist at Environmental Working Group (EWB), a non-profit organization focused on consumer health, during a press call this week, “longer term cancer studies are essential to evaluate the long term impacts.” As such, because they are time intensive, he says, it is possible that an extension will be needed before final decisions are made.

Why are we questioning this now?

Over the last few decades, consumers have totally changed how they use sunscreen. Past regulations, according to the FDA, have reflected the fact that consumers had been using sunscreen for special occasions in which they would be exposed to a lot of strong UV rays, like a day at the beach. Now, many consumers use these products as a daily prevention not only against skin cancer, but also the effects of aging skin like wrinkles, discoloration, and blemishes. It’s far more common for other products like daily moisturizers to contain a sun protection factor, or SPF, than in the past.

More usage may be good for your skin, means more potential for the ingredients to be absorbed into the bloodstream and potentially cause health effects. Though, obviously, more research is needed to confirm potential effects.he FDA also plans to further scrutinize sunscreens in the form of powders and sprays, which are relatively new to the market, to determine their safety and effectiveness.

What sunscreen should I buy?

These new changes aren’t official yet, and it will likely be months before that happens, so it’s hard for anyone to make any official recommendations. One challenge going forward could be the white residue on physical sunscreens, which occurs on anything other than extremely pale skin. And is a detriment, for good reason, to wearing sunscreen. New innovations in finding ways to eliminate the white residue factor, could likely be an unmet need.

The post The FDA is questioning the safety of 14 common sunscreen ingredients appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Public health advances over the past decade have pushed down the rates of many cancers, particularly those—like lung cancer—caused by substances we now know are dangerous. On average, cancer deaths are trending downward. However, the rates of certain types of cancers linked to obesity, like colorectal and kidney cancer, are rising in young adults. People who are younger, reports a study published in The Lancet this week, have an increasing risk of developing these diseases.

The results of the study weren’t necessarily surprising, says Karen Basen-Engquist, director of the Center for Energy Balance in Cancer Prevention and Survivorship at the University of Texas MD Anderson Cancer Center. “We know that there are cancers that are linked to obesity; we know that obesity rates have been increasing. In some ways, we’ve been waiting for data to show that.” But the data, she says, were still striking. “Cancer is pretty rare in young people. When we see cancer rates rising in young people, it’s time to get worried.”

Research reliably shows the relationship between obesity and these types of cancers, Basen-Engquist says. For individuals, the strength of the link isn’t as strong as the one between smoking and cancer, for example—smoking is more likely to lead to cancer than obesity—but right now, she says, public health experts are more concerned about the population-level effect of obesity, because it affects more people.

Although it can reduce the risk of cancer (and other related health issues), losing weight and keeping it off is incredibly difficult. Barring that, though, people at risk for these types of cancers might be able to take other steps to stay healthier and reduce their cancer risk:

Maintain weight

Cancer risk tends to go up in lockstep with body mass index, Basen-Engquist says, so keeping weight from creeping up might be a good way to keep chances of developing cancer from going up.

It’s much easier, she says, to not gain wait than it is to gain weight and then try to lose it.

On average, American adults gain around one to two pounds per year. “If you spend your 20s doing that, by the time you’re 30, you’re 10 to 20 pounds heavier,” Basen-Engquist says. “It’s important for people to think about preventing weight gain no matter what they’re at.”

Eat well and exercise

One way to keep from gaining more weight is to get regular exercise, and eat a healthy diet, Basen-Engquist says. Although they might not lead to weight loss, both can still help reduce cancer risk: Exercise, for one, can independently help prevent cancer. Inactivity alone, she says, regardless of weight, is a risk factor for cancer. “Exercise can be a factor that protects against cancer, and also prevents weight gain.”

In addition, a diet high in fiber and vegetables, and low in red meat, is associated with a lower overall risk of cancer, she says.

Eating that sort of diet is easier said than done, especially in places with limited access to (often more expensive) healthy foods. In those situations, it’s important to find the factors that are controllable, Basen-Engquist says. “Sugar sweetened beverages are one big issue.”

For people struggling with weight or obesity, cancer isn’t the only elevated health risk, Basen-Engquist says. But this research provides another point for doctors to discuss with patients. “Having this data about cancer provides an additional motivation and conversation topic,” she says.

Those conversations, she notes, shouldn’t just be about weight loss, and should include the behaviors that can help manage weight. “No one can just turn down dial on their weight. It’s important for providers to talk about exercise, diet, portion control.” They should also be thoughtful, and consider using language that makes patients feel comfortable. “People should be making sure they’re talking to patient in a way you’d liked to be talked to,” she says.

The post Cancer rates are rising in young adults. Here’s how to lower your risk. appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Cancer is second only to heart disease in the number of people it kills annually in the US. For Hispanic and Asian Americans, and those under 80, it’s the leading cause of death. Millions of dollars, both public and private, get spent every year in a search for new cancer treatments, but since the 1980s there’s also been a focus on how to prevent cancer cases in the first place.

The American Cancer Society just updated its recommendations from its last publication in 2012, and though the guidelines are similar there are some key takeaways. Much of it may sound like common sense: Eat a healthy diet, exercise plenty, and don’t drink alcohol. But research shows that the risk factors associated with being overweight, eating a poor diet, drinking significantly, and having a sedentary lifestyle account for 18.2 percent of all cancer cases in the US, and nearly 15.8 percent of the deaths.

Here’s what the new guidelines—along with other world leaders in cancer research—say is best to prevent cancer.

Exercise more

The ACS now recommends 150 to 300 minutes of moderate-intensity or 75 to 150 minutes of vigorous physical activity every week, which works out to either 2.5 to 5 hours or 1.25 to 2.5 hours a week. Broken down even further, that’s an average of about 20 to 45 minutes of moderate exercise a day, or 10 to 20 of vigorous activity.

In the past, the ACS used to simply suggest that getting more than those lower baselines would be beneficial, but now the committee has taken a stronger stance: It now says it’s advisable to max out or even exceed the upper bounds. It’s worth noting that the type of activity seems less relevant. Kids, they say, should get an hour of activity every single day.

The ACS notes that there seems to be a linear relationship between the amount of exercise a person gets and their cancer risk—the more activity, the lower the risk. Meta-analyses have demonstrated that there’s a link between a higher risk of colon, breast (in women), and endometrial cancers and low physical activity. There’s also some evidence that suggests exercise can decrease a person’s risk of a wide variety of cancers.

It’s not exactly clear yet how physical activity might help prevent cancer, but researchers are starting to hone in on some reasons. Cancer is, at its core, a dysregulation of cellular division—cancer cells divide too frequently, which increases the rate of mutations that can lead to cancer. Exercise seems to have a beneficial effect on a lot of those mechanisms: Reducing inflammation, stabilizing the genome,controlling immune function and insulin activity, and reducing cellular (or oxidative) stress, among other things.

Drawing a clear, causational link is tough, but it’s becoming increasingly clear that regular exercise is an important part of cancer prevention.

Eat more whole foods and less processed stuff

Rather than specifying certain amounts of specific foods, or eliminating anything entirely, the ACS guidelines now suggest what it calls “a healthy eating pattern.” That means eating nutritious food, a variety of veggies, plenty of fruit, and lots of whole grains. It also means limiting or not eating red and processed meats, sugary drinks, and highly processed foods in general.

That’s because, despite what you might see in headlines, drawing links between specific foods and cancer risk is difficult to impossible. There’s no specific food that cancer researchers think prevents cancer. But it is abundantly clear that eating a healthy, well-rounded diet as a whole is a good cancer prevention strategy.

Fruit and vegetables have nutrients we need to keep our cells running. Whole grains have fiber that improve our gut microbiome. Conversely, processed foods are low in nutrients and fiber, yet high in fats and sugars. It’s not that you can’t ever eat candy again—it’s that a healthy diet overall means balancing that out with whole, nutritious foods.

The report also acknowledges that eating this kind of diet is hard for many people. Many Americans live in food deserts—areas with no grocery stores, or only stores that sell processed foods and little of the fresh stuff. Even those with access may have trouble paying higher prices for whole foods, or lack the time to prepare a meal when a fast food option is both cheaper and easier. Tackling those issues will require broader community and political action, but fixing the problems is crucial to US public health as a whole.

Don’t drink alcohol

This isn’t going to be a popular one, but here’s the painful truth: Alcohol consumption is the third-biggest modifiable risk factor for cancer after smoking and being overweight. At least seven types of cancers are directly linked to it, including oral cavity, colorectal, liver, and breast cancers. That’s because alcohol is a known carcinogen—it damages DNA, increases cellular division rates, and causes cellular (or oxidative) stress.

Despite these facts, more than 50 percent of the population over 12 drinks alcohol, and around a quarter qualify as binge drinkers (meaning they’ve had at least five drinks on the same occasion at least once in the past 30 days). And as a result, alcoholic beverages cause 5.6 percent of all cancer cases in the US and 4 percent of all cancer deaths. It’s why the World Health Organization lists lowering alcohol consumption as one of its “best buys” for interventions that would have substantial impacts on cancer rates.

Of course, most of the people reading this article are unlikely to stop drinking just because of these facts. Alcohol holds a huge place in cultures around the world, and certainly in the US, and quitting entirely is taken as a strong stance—Many people get pushback from their friends and family if they decide not to drink.

The ACS notes that if you do drink, your goal should be to limit yourself to no more than one drink a day for women, and two for men. That may be a lot lower than what you normally consume, but if you really want to reduce your cancer risk, this is one of the biggest impacts you can have.

The post The latest guidance on how to prevent cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Justice Ruth Bader Ginsburg had two cancerous nodules removed from her lung Friday at Memorial Sloan Kettering Cancer Center in New York, according to a press release issued by the Supreme Court.

Malignant nodules of this kind are among the earliest stages of lung cancer and are essentially round or oval-shaped growths in the lung. Doctors discovered the tiny growths in a CT scan Ginsburg had following a fall and subsequent series of rib fractures back in November.

Human lungs are divided into lobes (the right lung has three and the left has two). Those lobes are further sectioned off into segments and then into lobules. Ginsburg’s nodules were confined to the lowest lobe in her left lung. To excise them, doctors performed a lobectomy, which removes that entire section of the lung and the nodules with it. The other four lobes take over to keep the lungs functioning.

Pathologists identified both nodules as malignant, according to Bader Ginsburg’s thoracic surgeon Valerie W. Rusch, meaning they contained cancerous cells. Luckily, scans performed beforehand and medical evaluations conducted after showed no evidence of the disease anywhere else in her body.

Ginsburg is 85 years old. Pulmonary nodules tend to become more common as someone ages, according to the Mayo Clinic. (Those who smoke, or were previously smokers, are also at a higher risk than someone who has never smoked.)

For now, given the successful removal of the malignant nodules and no further evidence of cancer, Ginsburg’s next move is rest and recovery. Unfortunately, however, she isn’t completely out of the woods yet. During surgeries such as these, doctors take biopsies of surrounding lymph nodes—the pathway by which cancer likes to travel and spread—to confirm that the body is officially cancer-free. Those results won’t be ready for at least a couple of days. According to NPR, if those biopsies show no signs of cancer, Bader Ginsberg has an 80 percent chance of remaining cancer free for the next five years. If tests show there is cancer in the surrounding lymph nodes, those odds could drop to as low as 40 percent.

This is Ginsburg’s third time battling cancer, having survived bouts of both colorectal cancer in 1999 and pancreatic cancer in 2009. Despite this, her mind and body remain sharp and fit—an inspiration for us all to embrace as we face the New Year.

The post Ruth Bader Ginsburg just had cancer surgery—here’s why she should be okay appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The signature smell is hard to forget. Johnson and Johnson’s baby powder, a product that was once considered simple, benign, and ubiquitous among new mothers is now the subject of intense legal allegations. Over the past several years, the company has been struggling with claims that its powder, the main ingredient in which is talc, caused ovarian cancer in a number of women who had used the product for years. In July, Johnson and Johnson paid a group of plaintiffs $4.69 billion for the damage.

Most recently, this past week, Reuters reported that Johnson and Johnson had known since the 1970s that its baby powder might have contained or been contaminated with small amounts of asbestos, a known carcinogen.

But how talc, asbestos, and cancer all connect together is a far more complicated web to weave—and unravel.

What is talc—and how is it related to cancer?

Talc is a natural mineral found in metamorphic rocks around the world. The mineral is among the softest materials in the world so when ground into a powder, called talcum powder, it’s superb at absorbing moisture and reducing friction, and thus, helping to prevent diaper rash as well as chafing and other skin irritations.

In the United States, most deposits collect on the eastern side of the Appalachian mountains and in parts of the northwest and New Mexico. The substance is most often collected from open pit mines by drilling, blasting, and crushing the metamorphic rock material. Because talc isn’t the only substance found within these rocks, there’s a chance that the mined talc can be contaminated with other substances.

As it happens, talc and asbestos occur naturally together. And that’s a problem, because asbestos is a known carcinogen. It was often used in insulating buildings because of its strength and heat-resistant properties. But in the early 20th century, once it became clear that exposure to high levels scarred lungs, the substance was banned from use in construction materials.

Exposure to large amounts of asbestos, especially over long periods of time, has clear and documented health effects. But the asbestos exposure experienced by regular talc users is on an entirely different order. Women who used baby powder over a lifetime had trace exposure, but dosed out over decades. How that kind of slow-grade asbestos release affects human health is far less established.

Did the baby powder contain asbestos?

One of the main claims made against Johnson and Johnson’s baby powder was from women who used the talc powder routinely for feminine hygiene and claimed that routine exposure to the asbestos-laden product caused ovarian cancer. Back in July, a jury agreed with them, forcing Johnson and Johnson to over four billion dollars in damage.

But a jury’s verdict isn’t the same as a scientist’s. The big unknowns in this case were whether the product actually contained asbestos, and if it contained it in amounts that were high enough to cause cancer.Neither question can be answered in a clear-cut manner.

The recent Reuter’s report suggests that once it became clear that talc could be laced with asbestos, and that asbestos was an established carcinogen, Johnson and Johnson should have openly communicate results of internal testing on the amount of asbestos in its powder to both the FDA and the public, but they failed to do so.

What is the FDA’s role?

According to The New York Times, the FDA last tested commercial products that contain talc for asbestos back in 2010 and found no trace elements. However, private experts on behalf of lawyers for plaintiffs, have done independent tests and did detect asbestos in the talc products.

Routinely, the FDA does not test consumer products for safety. Because they are not prescription drugs and are not claiming to treat or cure a condition, these products do not need to comply with the same safety regulations as pharmaceuticals. Rather private companies typically comply with the Personal Care Products Council, which has stated that all talc products should be free of asbestos since 1976.

A major reason that none of this is clear cut is that it’s incredibly difficult to link the trace levels of asbestos in the amount that would be found in talc to cancer. Asbestos was originally tagged to cancer in relation to coal miners and construction workers who were exposed at far higher levels, often breathing in dusty air that contained the substance.

But the amount of the substance required to start cancer growth is near impossible to pin down. For example, research on the connection between ovarian cancer and the frequent and long-term use of talc-containing powder on the genitals has shown varied results, with some showing a slight increased risk and others showing no association at all. Further, as the American Cancer Society (ACS) points out, many of these studies are further complicated by the fact that the studies often rely on participants to recall years later exactly how much talc powder they used often years or decades earlier. Both the National Cancer Institute and the ACS conclude that research is ongoing and that any evidence of a connection—the strongest of which would be a very, very small increased risk— isn’t strong enough yet.

As PopSci reported back in August, this becomes even more complicated when you factor in how decisions about these connections are made by juries in a courtroom. A jury merely has to decide between two conclusions: Whether it’s more likely that talc caused the cancers or that it didn’t. Science, on the other hand, has a far higher bar to meet, and must be able to show, with high statistical certainty, that it’s nearly impossible that anything else could have caused the cancer other than the talc powder, which in many cases is near impossible to do.

Is baby powder actually useful for babies or adults?

For all it’s hype, baby powder is likely not worth the risk, talc aside. According to the Times, because of the risk of an infant choking on the powder, the American Academy of Pediatric recommends against using talc powders, and instead using an oil-based ointment, if necessary. For adults, a cornstarch-based powder is a good alternative for skin irritation or chafing.

The post The link between baby powder and cancer is easier to prove in a courtroom than in a lab appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Lonesome George died when he was roughly 101. He wasn’t especially old for a Galápagos tortoise, which can live to be 150 years old, nor was he especially large, weighing in at just 194 pounds compared to the standard weight of around 330 for his tortoise relatives. What makes Lonesome George worth studying wasn’t his physicality—it’s the fact that he was the last of his kind.

Giant tortoises used to roam, albeit slowly, across much of the world. Megalochelys atlas wandered the Punjab region of India and Hesperotestudo crassiscutata traversed Central America up into the southern United States. Their gigantism isn’t the result of living on islands—they were enormous back then, too. It’s just that the only giant tortoises that survived lived on remote spits of land isolated by oceans in fairly tropical parts of the world, where an evolving climate and the rapidly expanding human population could do relatively little damage to them.

We were too late to save George’s species, Chelonoidis abingdonii, but geneticists are still trying to piece together an understanding of these giants by looking at Lonesome George’s DNA. Even if he wasn’t exceptional, his genes are. As one of the longest-lived organisms on Earth, C. abingdonii and other giant tortoises are of interest to anyone who wants to understand how some animals are able to live for such extended spans.

That’s why this international group of geneticists and biologists collected samples from Lonesome George and another giant tortoise species, sequenced their genes, and compared them to a bunch of other creatures. They published their results in the journal Nature Ecology & Evolution. This comparison allows geneticists to figure out which genes occur at higher rates in long-living tortoises compared to other reptiles or to mammals (we call this positive selection). By looking at which bits of DNA are comparatively more common amongst giant tortoises, researchers can start to figure out which kinds of traits help animals live longer. It doesn’t mean that any of the specific genes they found are “the gene for living longer,” but it does mean that the sets of genes may tend to enable a longer life.

The classic example has to do with telomeres. At the end of all DNA strands are bits of repetitive sequences called telomeres that act like end caps for the individual strands. We all start out with very long telomeres because the cellular machinery that replicates DNA is imperfect and can’t replicate the entire strand—a small bit at the end gets cut off each time. If we were constantly cutting off bits of DNA that coded for important proteins, our cells couldn’t function for more than a few replication cycles. Instead, we cut off our telomeres, which don’t code for anything. The problem, of course, is that you can’t grow them back, and eventually your telomeres get so short that the cell can’t keep dividing. This seems to be a significant contributor to the process of growing old, so lot of anti-aging research centers around how to either slow telomere decline or regenerate them after they’re gone.

Giant tortoises, as this study identifies, have genetic variants in proteins that repair and maintain DNA, especially the telomeric portions. Researchers have taken that to indicate that telomere maintenance may play a role in keeping these turtles alive for so long.

But perhaps more interesting is how giant species like Lonesome George avoid one of the plagues of our modern existence: cancer. “An important trait of large, long-lived vertebrates is their need for tighter cancer protection mechanisms,” the authors write in the paper, citing something called Peto’s paradox.

You’ve probably never heard of Peto or his paradox, so allow us to elaborate.

Richard Peto is a Professor of Medical Statistics and Epidemiology at the University of Oxford who noticed that larger animals don’t get cancer at higher rates than smaller animals. That might not seem significant to you, but it is actually pretty surprising, because larger animals have more cells. Cancer is simply a disease of cellular division—every time a cell divides it must replicate its DNA, and that process is prone to mistakes. That means every division is an opportunity for a mutation to arise. More divisions leads to more mutations, and more mutations increase the risk that a cell will turn cancerous. Since larger animals have more cells, it makes sense that they should be more prone to cancer—they simply experience more divisions. But they don’t. Studies of body size and cancer risk show no correlation between species. Within a species is a different story, though. Taller humans seem to have higher cancer rates, even after controlling for potentially confounding factors. That’s not definitive proof, but it does add to the evidence. If even slightly larger humans seem to develop more cancers, then much larger species must have evolved ways to avoid cancer—otherwise every tortoise would die from it.

Tortoises, despite their enormous size, hardly ever seem to get cancer. And indeed, when these biologists took a look at giant tortoise genomes they found more copies of genes known to suppress tumor formation as well as duplications for other genes that may help the immune system identify and kill potential cancer cells. All of these changes are minor on their own, but together they suggest that giant tortoises are overall better able to avoid cancer.

We’re not going to get into all the other individual findings in this paper because there are a ton of them, most of which are incredibly detailed and esoteric. Tortoises seem to have slower metabolisms, for instance, which some scientists think may help slow aging. They also have mutations that may help them regulate glucose uptake better and resist hypoxia. All of it will require further research to determine exactly which genes contribute to a longer life and how—this research is just the first step. There’s a lot more work to do before these findings can help keep us young—or, more pressingly, help us save other species of Galápagos tortoise. For now, it’s just nice to know that Lonesome George could contribute something to our understanding of his kind even after he’s gone. He may have been the last C. abingdonii, but he was first in our hearts.

The post Lonesome George’s genes could reveal the secrets of longevity appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Over the past decade, researchers have developed nanoparticles to treat all sorts of medical conditions, from obesity to bleeding combat wounds. And although researchers have spent a lot of time figuring out how metal-based nanoparticles could diagnose or treat cancer, including types of cancer for which conventional treatments were largely ineffective, many of them were toxic — they would remain in the human body for a long time.

Now a team of researchers has developed metal nanoparticles that are non-toxic and make anti-cancer drugs more effective, according to a study published today in Nature Communications.

The nanoparticles are made of alloyed gallium indium, a metal known to be a stable liquid at room temperature. The researchers used ultrasound to turn the metal into particles each about 100 nanometers in diameter. Then, they used special molecules called “ligands” to stick molecules of doxorubicin, a common chemotherapy drug, to the metal particles.

The particles are small enough to be injected into the bloodstream. As they flow through the body, they encounter tumor cells, which absorb them thanks of another type of ligands on the surface of the metal particles. Most importantly, they don’t have any effect on non-cancerous healthy cells. Once the particles reach a tumor, they collect and form a liquid metal, allowing doctors to easily see them in scans.

The amalgamated metal has ions that that make the chemo drug towed along with the particles more effective. They also degrade the metal itself so that it can filter out of the body more quickly.

To see how effective the nanoparticles could be, the researchers tested them on mice models with ovarian cancer. They found that the nanoparticles made the chemo drug significantly more effective—so effective, in fact, that the researchers nicknamed them “nano-terminators.” Over the course of 90 days that they followed the mice, they didn’t see any signs that the metal had toxic effects (the researchers anticipate that the body filters out the metal within a few days).

Since the nanoparticles are so easy to manufacture, scaling up their production for widespread use wouldn’t be very challenging, the researchers write. This study was a proof of concept, the researchers write, but they hope to start trials in larger animal models—and even in humans—in the near future.

The post Liquid Metal ‘Nano Terminator’ Particles Could Fight Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The post Wriggling Away From Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Ten years, $30 million, and thousands of rodents later, the results from one of the largest studies on the relationship between the type of radiation emitted from cell phones and risk of developing cancer was published last week. It’s the latest (and one of the largest) studies looking at the link, and the National Toxicology Program, which ran the study, concluded that the data showed a small uptick in the development of two types of cancer in rodents that were exposed to the radio frequency radiation.

The results, though, aren’t likely any cause for alarm around human health—experts, including those who worked on the project, are quick to note that the study was done on mice, and used levels of radiation far above the amount generated by regular cell phone use, and cannot be directly translated to humans.

In addition, Christopher Labos, a physician and associate in the McGill Office for Science and Society, says that the noted increase in cancer may just be due to chance: In studies like these, researchers examine dozens of organs and tissues for tumors, so in thousands of rodents, actually finding some isn’t surprising. The rats that were exposed to the radiation also lived longer than rats that were not.

All this is to say that, overall, the results—and the decade of research that went into it—haven’t done a lot to crystalize the still-murky understanding of the role of cell phones in cancer development. The study itself was carefully planned and executed, says Kenneth Foster, professor emeritus of bioengineering at the University of Pennsylvania, but the results were weak and hard to interpret.

Research into the relationship between cell phones and cancer has been ongoing since the 1990s, when David Reynard sued a cellphone company after his wife developed brain cancer. Since then, the majority of results—both from animal studies and human epidemiological ones, which track the amount of cell phone use and risk of cancer development—have been difficult to make sense of. When relationships between the two have been identified in the data they’ve been far too small to confidently say what they mean, Foster says. “Dealing with smaller effects, you’re trying to juggle evidence from epidemiology that’s less than persuasive and animal studies that are less than persuasive,” he says.

Studies have also produced conflicting evidence: the 13-country Interphone study, for example, largely showed no increase in cancer, although one analysis did find a statistically significant (though hard to interpret) increase. One Swedish research group found a link, but large Danish and United Kingdom studies did not. Labos says the mixed results support the idea that there is not, in fact, an increased risk of cancer with cell phone use. “It usually implies that there is no effect. In random chance, you’d see a natural spread of data,” he says.

Based on the research prior to this new study, the International Agency for Research on Cancer, which classifies carcinogens, said that radio frequency radiation is a possible carcinogen—a label it gives to environmental factors that have limited or insufficient evidence linking them to cancer, but that haven’t been ruled out.

“It means that there’s some level of suspicion, but the evidence is not strong enough to draw a conclusion,” Foster says. “They’re not willing to say that there’s no risk, because you can’t prove that. But they’ve looked very carefully and don’t see evidence that there’s a big problem.” Foster doesn’t anticipate that major health agencies will change their recommendations as a result of the new study. The U.S. Food and Drug Administration, for example, did not move from their position that the cell phones are not a publish health risk after evaluating the results of this latest study.

When it comes to the difficulty of determining whether something causes cancer, cell phones are far from an isolated case, he says. In many cases, once research begins, it’s difficult to come to any definite conclusion. “Once these issues start going, they’re almost impossible to resolve,” Foster says. “You can’t prove something doesn’t cause cancer, but unless you have clear cut evidence that it does, you’re stuck in these gray areas.”

On top of that, it would also be nearly impossible to conduct a definitive, randomized, and controlled study on cell phones and cancer in humans. “You can’t take a group of people and say, you use cell phones, and take another group, and say you never use them,” Labos says.

The work on cell phones and cancer is similar, in some ways, to inquiries during the early 2000s into the relationship between childhood cancers and how close kids live to power lines, Foster says. Hundreds of epidemiological studies looked for a connection, but only found a small signal in the data. “It was a small signal that no one could explain, and that no one could explain away,” he says.

Consistent, small and difficult to interpret findings mean that the issues stay on the table until the researchers determine that it’s not worth continuing to run the same sorts of studies that will more likely than not likely result in the same, consistently puzzling and unclear results, Foster says. “They settle down, not because they’re settled scientifically, because there’s no benefit from pushing it.” That’s what started to happen with the power line research: “Health agencies are saying that if there’s something there, it’s probably so small that there’s not likely to be a large effect on the population,” Foster says. “They’d rather spend money on something else.”

Labos thinks that may happen for research on cell phones and cancer, as well. “There are a few other studies ongoing right now. If both fail to show an increased risk of cancer, it probably won’t be worthwhile to keep doing studies. At a certain point, you say enough is enough,” he says. “If there was a health effect we’d probably have seen it by now.”

If anything can be definitively concluded, it could be that cell phone use might have some small, theoretical link to cancer, but because of the extreme paucity of information, they probably aren’t a large risk to human health, Labos says. “If you go to the zoo, the bears pose a hazard to health. But the risk of actually being harmed by the bears is low,” Labos says. “The risk of you actually developing an illness from cell phones is low.”

There are other, more pressing dangers from cell phones to worry about, Foster says—namely, using the phone and driving. But if, despite everything, people are still concerned about their phone’s radiation, there’s an easy solution: using headphones or hands-free device for phone calls. “You can stick your phone someplace else and use those,” he says. “You don’t even have to have a good reason.”

The post Cell phones pose plenty of risks, but none of them are cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Diagnosing cancer can be a challenging task. Often, pathologists have to quickly decide whether a microscopic group of cells looks malignant or benign, or whether a small lump seen on a mammogram is suspicious. For this reason, pathologists go through four years and more of medical school and training. But it turns out that pigeons may one day be able to help out.

Researchers at the University of California, Davis and the University of Iowa wanted to understand how pathologists are able to refine their cancer-identification skills over time, and what are the most important features and properties that help them make an accurate diagnosis. To figure it out, the scientists trained pigeons to distinguish between healthy and malignant tissue, since humans and pigeons share many of the same visual systems. And the pigeons were surprisingly good at it, according to a study published today in PLOS One.

During the experiment, the scientists showed each pigeon a set of microscopic images of breast tissue. After staring at the image, the pigeon would then chose either a yellow- or blue-colored button that corresponded to either cancerous or non-cancerous. If the pigeon answered correctly, it was rewarded with a tasty treat. Each pigeon had 15 one-hour long sessions and by the end, they answered correctly about 85 percent of the time. Human pathologists are up to 97 percent accurate for more a difficult identification task where they were shown whole images instead of just small areas of interest.

In another task, in which the pigeons were asked to detect cancerous breast masses on mammograms, the pigeons were only able to memorize the correct answer–they couldn’t look at a new image and determine whether that mass was cancerous or benign. This is challenging task for even a group of pathologists who (as part of the study), viewed the same masses, and were only accurate 80 percent of the time.

While the pigeons’ results are impressive, they still aren’t as accurate as those of a trained pathologist. So, pigeons won’t become newly minted doctors anytime soon, but they can help researchers understand how pathologists get better overtime. The researchers found that while the color scheme and brightness of the images had little effect on the accuracy of the diagnosis (the researchers note that this makes sense since most pathology textbooks have until recently been in gray scale), they found that the birds were affected by how much the image had been compressed. At first, their accuracy was worse with highly compressed images; however, overtime, they were able to adapt to the compressibility and their results became more accurate. As the researchers note, this correlates with how pathologists learn overtime: “Humans can also learn to ignore compression artifacts and become accustomed to less-than-perfect visual images.”

So by figuring out what pigeons look at to make their diagnosis, that may allow researchers to train pathologists and computer systems in a better, more strategic way.

The post Pigeons Are Actually Pretty Good At Identifying Malignant Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The number of people dying from cancer every year has dropped to its lowest rate since 1991, according to a new study from the American Cancer Society and reported by Stat News.

In 1991, when death rates were at their peak, 215.1 people would die of cancer for every 100,000 members of the population. In 2012, the most recent statistics available, that number dropped to 166.4—a 23 percent decrease. That equates to more than 1.7 million deaths from cancer that were avoided, had that rate continued.

The numbers peaked in 1991 largely because of better diagnosis and screening, especially for prostate and colorectal cancers, according to the study. The authors have a pretty good reason why the death rates dropped, too—improvements in screening, prevention, and treatment have all helped fewer patients die of cancer each year. For example, fewer people smoke now than in the past because the habit can greatly increase the risk for many types of cancer.

But this decrease wasn’t universal across all types of cancers. While fewer patients are dying from colorectal and lung cancers, more are being diagnosed with thyroid, liver, pancreatic, ovarian, and breast cancer—some of the most fatal types of cancer. The researchers aren’t quite sure why these cancers seem more prevalent, but they think it might be due to a combination of overdiagnosis and environmental factors such as obesity.

Given all this progress, it may seem strange that the ACS is expecting the number of cancer deaths to increase this year to about 13,000 more than the 2012 numbers. This is because doctors have learned how to better manage heart disease, the most common cause of death in the United States. And while the number of cancer deaths is decreasing overall, cancer may soon overtake heart disease as the primary cause of death in some states.

While this progress is certainly impressive, it also shows just how far we have to go until doctors can better prevent cancer deaths. Cutting-edge treatments like precision medicine and immunotherapy, plus new screening tools, may contribute to a further drop in the near future.

The post Cancer Deaths Hit Lowest Rate In 25 Years appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

There was a moment during Obama’s valedictory State of the Union address last night that seemed uncharacteristically unscripted. Obama announced that he was putting Vice President Joe Biden in charge of “Mission Control”—that is, in charge of the initiative to cure cancer by 2020. There’s no audio of it, but if you can read lips, Biden seems to have leaned over to Speaker Paul Ryan and said, “That’s news to me.”

But despite all appearances, it seems Biden wasn’t surprised by the announcement; in conjunction with Obama’s speech, the Vice President’s office published a post on Medium outlining the roadmap towards a cure for cancer.

Cancer, as noted in the Medium post, is personal issue for Biden (his son, Beau, died from brain cancer at the age of 46 last May), but also for millions of Americans who have lost loved ones to different forms of cancer. Researchers have made amazing progress in the past few years, the post reads, and this is the moment to help scientists take advantage of that momentum and move towards a cure.

According to the post, Biden plans to:

The first point is probably not surprising—more money for cancer research means more researchers and more ideas. And that’s happening already—for 2016, Congress just allocated a budget of $5.21 billion to the National Cancer Institute, an increase of $260.5 million from 2015.

Biden’s second plan, of increasing collaboration among scientific institutions, is an idea that has been around, in one form or another, for quite some time. Last year researchers launched a new scientific journal intended draw in research across different specialties within cancer research. Promising new treatments such as immunotherapy and precision medicine have necessitated scientists to call upon colleagues with different expertise to work together to improve the method.

But scientific “silos” aren’t anyone’s fault—they’re a product of a rigid and specialized academic climate. The Vice President writes that the federal government will use “funding, targeted incentives, and increased private-sector coordination” along with collaboration from “data and technology innovators” to increase cooperation across disciplines. In practice, that might result in a data-sharing program that allows scientists to share data on a national scale, or increased federal support for gene sequencing, as Ars Technica writes.

Some experts think scientists would benefit more from Biden’s efforts if they were focused on increased sharing of genetic data across institutions, as STAT reports today. Sharing individuals’ genetic data is still an issue that is ethically and legally fraught, with no clean-cut solution in sight.

In the centuries in which scientists have sought a cure for cancer, we’ve come to understand a lot about how cancer works. One key component is that cancer isn’t just one disease—it’s hundreds of diseases that can endanger patients’ lives due to factors such as inherited genetics, environmental and lifestyle factors, and plain old bad luck. In some ways, these discoveries have discouraged researchers looking for a single cure for cancer. But Biden is right in this respect: If there’s ever a time to find that cure, this is it.

UPDATE: The Vice President explained his plan to Popular Science during a Twitter Q&A.

The post How, Exactly, Is Joe Biden Going To Cure Cancer? appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Mammogram

Last year, at the age of 43, Chicago-based writer Jessica Gardner had her first mammogram. She knew that most screening guidelines recommended that women of average risk for breast cancer receive annual mammograms starting at age 40, but Gardner procrastinated—because she didn’t have insurance when she turned 40, and because she was scared, she says. “When I was 41, my mom had breast cancer, and that scared the bejeezus out of me,” Gardner adds.

Once she got the mammogram, the radiologist saw an area of concern—there were some calcium deposits inside the breast tissue and, while it’s not uncommon, the doctors wanted to get a better look. There were more scans, a biopsy, and eventually a lumpectomy for some tissue that could become cancerous over time. Though Gardner considers herself of average risk for breast cancer, she is now a staunch advocate for breast cancer screening; in 2014, she wrote a blog post titled, “My first mammogram saved my life.”

Recently, the American Cancer Society changed its breast cancer screening guidelines; women should get annual mammograms starting at age 45, instead of at age 40. The U.S. Preventive Services Task Force, the other major organization that makes these recommendations, announced this week that it intends not to change its guidelines, recommending that a woman start thinking about breast cancer screening at age 40 based on her individual health profile, but definitely start screening by age 50. Though screening for cancer is just one tool in the increasingly sophisticated field of cancer prevention, early detection of breast cancer, like many other types of cancer such as those in the prostate and lung, could be essential for doctors to treat the disease before it threatens a patient’s life.

For women thinking about when to start screening for breast cancer, weighing the different guidelines can be a confusing and difficult experience. Most women want to know: Should I start at 45 or 50? Should I be screened every year or every other year? Am I ever supposed to stop? What is “average risk,” and do I have it?

Each organization gives a slightly different or nuanced answer to each of those questions. Why can’t experts agree on when to start screening and how often it should be done? What are the risks of over-screening, and, most importantly, how are patients supposed to parse through the noise to do what is right for them as individuals?

Why can’t experts agree?

The goal of cancer prevention is simple: prevent a patient from developing the disease, or dying from it. The field really took off in the 1990s, when public health officials urged people to stop smoking in order to prevent cancer, says Therese Bevers, the medical director of the MD Anderson Cancer Prevention Center and the chair of the National Comprehensive Cancer Network’s panel that creates guidelines for breast screening.

Screening tests are usually done on patients who don’t have symptoms. Doctors hope that, if screening is done consistently, it will catch lesions and polyps that may become cancerous. For some types of cancers, such as those in the cervix or colon, removing those non-cancerous growths early can mean that a patient never develops cancer at all.

“The general intent of screening is to catch disease early so that the treatment is less intensive, and then lower the chance of dying from cancer,” Bevers says.

Preventing cancer seems very straightforward, at least in the abstract. But every patient is a little different, with different family histories and past illnesses and lifestyle or risk factors. Those all affect a person’s likelihood of developing certain cancers over others, and can make it difficult for doctors to know which types of cancers to watch out for.

These guidelines are intended to provide patients with recommendations for cancer screening–what kind of screening, when to start, how often to get it–that will best help them prevent cancer. Insurance companies also use the guidelines to decide whether or not they will cover a patient’s screening. If people don’t screen for cancer early or often enough, there’s a greater chance that disease could grow unchecked, making it harder to treat later. Screen too much, though, and patients could overburden doctors, expose themselves to possibly harmful radiation, or undue stress. And though different organizations and agencies sift through dozens of scientific studies to create guidelines that streamline the science to best guide the public, the conflicting guidelines themselves might end up confusing more people than they help.

Making The Guidelines

Screening guidelines can provide a place to start for patients with average risk for certain types of cancer. Before issuing its screening guidelines, a committee of experts looks at scientific studies to determine what has been proven to work best for patients. They consider all the different technologies for screening (for breast cancer, they would weigh the evidence for mammograms versus self-exams) and only consider cancers in a particular region of the body. The committees want to know if patients lived longer if they received cancer screenings. If they did, how often should they get them, and at what ages are they most beneficial?

Randomized controlled trials—experiments that compare the health outcomes for randomly chosen patients who received the treatment to those who did not—are considered the highest quality evidence. Ideally, these trials would include hundreds or thousands of patients. But these trials are very expensive and take a long time, so there aren’t very many of them. It can be limiting to only consider these, says Kirsten Bibbins-Domingo, a professor of medicine at the University of California San Francisco, and the vice chair of the U.S. Preventive Services Task Force.

Many organizations take other kinds of studies into account, including observational studies, trials in which researchers track patients who received the treatment and those who didn’t to see if the treatment helped them live longer. Since the researchers aren’t trying to alter the outcomes themselves, these experiments can be done more quickly, which can help experts get a quicker assessment of new treatments. That can be useful, especially if the studies are done well, but they are considered weaker evidence than the randomized controlled trials—the researcher is only looking at one variable among many, and she is not herself adding an experimental variable. So these studies can’t absolutely determine the cause of an outcome, only what it’s likely to be based on correlation data.

Breast cancer from a mammogram

Why do different organizations issue different screening guidelines? In some cases, they’re not using the same studies, so it’s only natural that these organizations would reach different conclusions. For their breast cancer screening guidelines in 2009, the Task Force didn’t consider observational studies, Bibbins-Domingo says. But in response to public feedback, the organization has since incorporated observational studies.

Even while looking at the same evidence, however, experts can sometimes disagree. They may interpret the study’s findings differently, or, if two similar studies had disparate conclusions, they may find one more convincing than another based on the type of data or the study design. “If you look to experts in the field to see what they’re saying, there’s going to be disagreement still,” Bevers says. “But it’s important to get an understanding of why they disagree. It may be that there’s things they agree on.”

Why Not Just Screen As Much As Possible?

“Screening is a very blunt instrument in some ways,” says Robert Smith, the vice president of cancer screening at the American Cancer Society. “Screening tests are not diagnostic tests.” Though screening tests target the cancers that have higher mortality rates, doctors can sometimes uncover other cancers in the process. But the tests don’t show doctors if a cancer will progress or not. It’s then up to the doctor and patient to talk about treating the cancer, especially if it’s at an early stage.

Too-frequent screening comes with its own set of concerns. Despite years of debate, the low levels of radiation exposure involved in screening tests like mammograms, is no longer a big worry (the scientific consensus is that the benefits of screening far outweigh the risks), though the same may not be true for CT scans used to diagnose other types of cancers and to make 3D images of the breast. Some tests have a high rate of false positives, which cause patients unnecessary distress. One 2012 study estimated that around 20 percent of women will get a false positive result from a mammogram; earlier studies found even higher numbers.

MRI image

Even regular screening tests can lead to overdiagnosis, the diagnosis of condition that wouldn’t otherwise go on to threaten a patient’s life. “The real value of screening is in that early detection [of disease]. But that often leads to detection of other things that wouldn’t have caused a problem,” says Bibbins-Domingo. One study, published in August in JAMA Oncology, followed 100,000 women over 20 years and found that treating patients for the earliest stages of breast cancer didn’t make them any less likely to die from advanced stages of the disease.

As a result, doctors and patients feel compelled to treat the condition, and that’s not always what’s best for a patient, says Laura Shepardson, the associate director of breast imaging at the Cleveland Clinic. “When we catch disease early, we hit it with the biggest cancer treatment we have. And those can cause significant comorbidities [co-existing conditions] for a patient,” she says.

Treating a condition is not always what’s best for a patient.

There are dangers in using very aggressive treatment on such early stages of disease. Sometimes, radiation or chemotherapy used to treat these conditions can set the stage for cancers to develop later on. Preventative surgeries can have grisly side effects—men who have their prostates removed, for example, may be incontinent and impotent for the rest of their lives. And while some patients may be tempted to go under the knife at the first sign of disease, it may be more prudent to wait; while some types of prostate cancer progress quickly and cause thousands of deaths per year, overall men are more likely to die with prostate cancer than from it.

For all these reasons, organizations like the American Cancer Society and the Task Force are cautious with their screening recommendations. “There are trade offs between vigilance and precaution, and not wanting you to be overly preoccupied,” Smith says.

Overdiagnosis and overtreatment have been making headlines lately. “This concern is prompted by more studies that have come to light, as well as more discussion about what they mean, has led to an era where many things are shifting,” Bibbins-Domingo says. “We are living in a time when there is more aware of overtreatment. There’s more discussion among people who are doing treatment about what is the appropriate approach, when we should treat, et cetera.”

But not everyone agrees that overdiagnosis is a problem. “Careful studies that adjust for trends and incidence find very low rates of overdiagnosis,” he says, estimating a woman’s absolute risk of having an overdiagnosis of breast cancer at about one percent. The advantage, he adds, is that such early-stage cancers are much more treatable, giving a patient a better prognosis than a disease that’s even slightly more advanced.

If a physician catches early signs of cancer during a screening, for some low-risk patients the best recourse may be to continue screening more frequently and treat it only if the disease progresses, a tactic called watchful waiting. And though screening has undoubtedly saved or extended thousands of lives, it’s still not an exact science. And doctors and scientists alike still have a lot of questions that need to be studied before it can become more precise.

For example, many breast cancer experts are focusing on a condition called ductal carcinoma in situ (DCIS), in which abnormal cells line the milk ducts in the breast. It’s considered to be the earliest stage of breast cancer and doctors prescribe lumpectomies and other preventative treatments when they catch it (though she received the same treatment, Gardner had a different pre-cancerous condition). But they’re still not sure that DCIS is in fact a precursor to breast cancer, or that treating it does a patient any good. “Do we know for a fact that diagnosing DCIS is an overdiagnosis for breast cancer? We don’t have that answer yet. We may need to look at the disease differently,” Bevers says.

The Future Of Cancer Screening

Screening has come a long way in just a few decades (it’s been 40 years since mammograms became standard practice), producing high-quality images that help doctors treat patients. But it can still do better.

Researchers and biotech companies striving to reduce overtreatment and overdiagnosis come out with new screening tools all the time. But before they make their way into local hospitals, those tools need to be vetted by experts to ensure that the technology offers demonstrable benefits to patients. Tomography, which produces 3D images of the breast in addition to a conventional mammogram, is one such tool. Initial studies indicate that it’s pretty useful—it produces sensitive images that can reduce the number of patients who are called back for additional screening, saving doctors time and reducing patient anxiety. But researchers are still debating tomography’s benefits in the long term. “We’re figuring out how much better [tomography] might actually be,” Smith says.

3D mammography

Patients could receive better diagnosis and treatment without any new screening tools, if the systems could shift. In countries with nationalized healthcare systems, government organizations remind patients to get periodic screenings, ensuring that patients follow the recommended guidelines (some insurance companies in the U.S. do this, too, but it’s less consistent). Smith notes that a centralized screening organization could compile patients’ results in one place, providing researchers with data that could point to trends in patients’ risk factors, especially among underserved populations that don’t usually participate in clinical trials. It could even reveal weak points in screening practices—though images generated from screenings are fairly standard, radiologists’ interpretation of those images is still not consistent.

Even if screening were reorganized dramatically, there’s little doubt that more clinical trials are needed. Experts still have some fundamental questions about how cancer grows and spreads that need to be answered if screening—and early stage treatment—is to become more perfect. Is there a way to determine which early-stage cancers will progress into life-threatening diseases, and which will remain harmless? “We need to understand the diseases better—once you understand which will progress and which will not, then you can say this [pre-cancerous condition] isn’t the problem and doesn’t need to be treated,” Bevers says.

Some researchers think that precision medicine, a field that uses genetics to better identify and target cancer-driving mutations, could hold the key. The Holy Grail, from a screening perspective, would be finding a biomarker. With a simple blood test, that biomarker could show doctors that a patient runs a higher risk of developing a certain type of cancer, or could even help detect tumors before they can be seen in other screening tests. Ideally, it would be cancer-specific, not site specific—a particular type of breast cancer, not just cancer in the breast. To start to answer those questions, Bevers says, scientists need to conduct long-term, large-scale clinical trials. And those take a lot of time and money that, despite the billions of dollars spent annually on cancer research, are often not feasible.

Dense breasts

Given the information currently available, though, screening guidelines are less contradictory than they may appear. It may be easier to pick out the differences between screening guidelines suggested by the ACS and the Task Force, Bibbins-Domingo says, but the similarities are more useful because they highlight the fundamental principles that steered the experts to make them. “Where there are differences in guidelines, try to understand the underlying decisions about the recommendations,” Smith agrees.

As medicine becomes increasingly individualized, it’s more important to remember that recommendations are guidelines, not gospel. And because of how science works, the rules for screening may never be as firm as some might like. “The public needs to be reminded that science changes—we learn new things when we get new data. It’s iterative, and we learn things as we go along,” Smith says.

The best thing anyone can do is to understand the risk factors as we know them and talk to a doctor. If a woman believes she may have a higher risk of developing breast cancer, she should get her doctor’s opinion about starting to screen for it earlier, no matter what any guidelines tell her. “Women don’t make decisions [about screening] once in their lives, and each time those decisions are complex,” Bibbins-Domingo says. “We hope that women and their healthcare professionals are able to engage in this process to make the decision is right for them.”

“The only person who is going to advocate for your health is you,” Gardner says. “It’s our responsibility to take charge and to get the tests we need to sleep at night.”

Last month, Gardner had another lumpectomy, this time on her other breast, because her doctors found a small tumor inside her milk duct. The tumor was benign, but her doctors told her that over time these things can often turn into cancer, so she didn’t hesitate to get it removed. “I’m really grateful that they were able to find this because of mammography and other tests they did,” she says, adding that she intends to continue to get her annual mammogram. “If it had to sit there for a few more years, who knows what would happen.”

The post The Confounding Commandments Of Cancer Screening appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Scientists at the University of Michigan were experimenting with delicate silicone to better understand tissue scarring, but they had a problem: The molds in which the silicone needed to sit in were too hard and kept damaging the silicone. But they found a sweet solution: molds made of sugar that kept the silicone intact and could dissolve away after use, according to a recently published a paper in the journal Lab On A Chip.

In order to better understand how tissue scarring occurs on the cellular level, the researchers were testing cells inside of super-soft silicone that was less than a millimeter wide. To see how scarring might affect the individual cells, they squeezed the silicone with the cells inside to see how the hurt cells reacted and bounced back.

“We’re trying to measure the forces and movement of just a few cells,” says Shuichi Takayama, a professor of biomedical engineering at the University of Michigan, in a video from a university press release. “We could not get nice structures using conventional methods. We could mold the material but when we tried to remove the silicone from the mold, the structure would tear and rip and not hold its shape.”

What the researchers needed, he continues, was a mold that didn’t have to be peeled away from the silicone. Luckily enough, Takayama had an unlikely burst of inspiration when he tried to make cotton candy at home. He let sugar harden in a pan, and when he peeled it off, he found that the sugar retained the pan’s shape.

That ability worked perfectly for their molds. To test out their idea, the researchers poured a hot mixture of sugar and corn syrup into the shape they wanted and let it harden and cool. Next, they put the silicone medium in the sugary mold, baked the two for six hours so that the silicone sets, and then simply dissolved the mold away in a bath of warm water. The result was the silicone medium in exactly the shape they needed, ready for experimentation and chemically unaffected by the sugar.

The researchers hope to use these silicone models to understand how scarring happens both outside the body, as a result of trauma, and inside the body, which can result from conditions cancer or autoimmune diseases like fibrosis, as Smithsonian notes. Even after the body has healed, scarring can hamper organ’s function.

But this method has applications beyond the scope of the current research. By integrating soft materials more seamlessly into tiny devices and circuits, scientists may be better able to understand the tiniest developments of certain kinds of cells—for example, how cancer spreads or how stem cells differentiate into all types of cells in the body.

The post Scientists Use Hard Sugar To Create Dissolvable Mold For Delicate Research appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

There’s a lot we don’t know about organic food. But one thing we do know? That being a person who both can afford to buy organic and chooses to do so generally means you’re a healthier person.

Of course, that doesn’t necessarily mean organic food makes you a healthier person. That’s the central issue at the heart of a recent study published in JAMA that’s making headlines for purportedly showing that eating organic reduces your risk of cancer. Like so many studies claiming that any specific lifestyle choice will prevent cancer, there’s a lot more to this story.

What did the study actually say?

This is a classic case of association: French researchers asked 68,946 adults, also all French, to report how frequently they consumed organic food. They also asked everyone to report whether they had cancer, and at a five-year follow-up, asked again about any cancer diagnoses. On top of that data, the researchers collected information like whether the participant smoked, how much money they earned, how heavily they drank, and how much they exercised. Based on all that, they found a correlation between a lowered overall cancer risk and eating more organic food.

What’s getting slightly less attention in the media is what happened when the researchers broke down cancer risk into specific kinds of cancer. Eating organic food had no impact on participants’ risk for premenopausal breast cancer, prostate cancer, colorectal cancer, or skin cancer. It was only associated with a reduced risk for postmenopausal breast cancer, lymphomas, and non-Hodgkin lymphoma (a subgroup of lymphoma).

Where does the study fall short?

Potential confounding factors—like high income or physical activity level—are especially important when studying the health benefits of organic food, because eating organic is associated with lots of things that also help you live a longer, healthier life. In other words, people who regularly eat organic food tend to have other lifestyle factors and habits that could easily lower cancer risk as well. Even within just this one study, high organic food consumption was associated with higher income, higher occupational status (a “better” job, like being a manager or working an intellectual office job), more physical activity, eating more fruits and veggies, and eating less meat and processed food. Those are all things that make you more likely to stay healthy than those who can’t afford to take such good care of themselves.

And on top of those potential confounders, it’s very easy for people to misreport how much and what kind of food they really eat. “Organic food intake is notoriously difficult to assess,” notes an accompanying editorial in JAMA, “and its self-report is highly susceptible to confounding by positive health behaviors and socioeconomic factors.”

The researchers can try to control for these issues, which means doing statistical analysis to try to figure out the effect of organic food with all other factors being equal, but the problem with confounders is that it’s very difficult to control for all of them.

Controlling for higher income doesn’t quite cover all the benefits that having a higher income gives you, for example. People with more money can, for instance, go to the doctor more frequently, which makes them more likely to detect certain cancers early enough to treat them, and gives them an opportunity to be prescribed medication to treat chronic health issues. It also enables them to pay for high-quality treatment. It probably means they stress less about money, and we know that chronic stress has an overall deteriorating effect on health. They also tend to live in areas with lower levels of environmental pollutants and tend to get more sleep.

Having a higher income also means you can afford to buy organic food. On average in the U.S., organic food costs 45 percent more, and that means the people who consume the most organic food will tend to have more money (and likely less stressful jobs that afford them the time to exercise).

Is this study in line with what previous research has found?

Sort of yes, sort of no. There hasn’t been a lot of research on organic food and cancer risk, but the Million Women Study done in the U.K. was quite similar but reached slightly different conclusions. That research group also found that eating organic was associated with a reduced risk for non-Hodgkin lymphoma, but found no significant change in overall cancer risk. In fact, it found a slightly increased risk for breast cancer.

Why might cancer be linked to non-organic food?

Okay, so we’ve outlined all the ways in which this study does not mean that eating organic will keep you free from cancer. But if there is some connection, what causes the increase in risk? The main culprit researchers suspect here is pesticides. IARC, the International Agency for Research on Cancer, has identified three popular pesticides as “probably carcinogenic” (this doesn’t necessarily mean that they definitely cause cancer, it just means that it’s possible exposure to them has some effect on your risk of cancer). A lot of the data that went into making that decision came from occupational exposures—farmers or other agricultural workers who get much higher exposure than the average citizen, no matter what food you’re eating. All three of those pesticides have been associated with non-Hodgkin lymphoma, so it makes sense that this is the most consistent finding in large-scale dietary studies on cancer risk.

We do know that organic foods generally contain fewer synthetic pesticides than conventional produce, but “organic” doesn’t necessarily mean pesticide-free. The U.S. Department of Agriculture has a long list of permissible pesticides for certified organic farms. Still, fewer pesticides in our bodies would be a good thing, and studies in the last few years (like this one from 2015 and this one from 2016) suggest that consuming organic produce does decrease your pesticide exposure.

Should I be eating more organic produce?

We’ll defer to the JAMA editorial to summarize this one: “current evidence indicates that the benefits of consuming conventionally grown produce are likely to outweigh the possible risks from pesticide exposure.”

In other words: eat more fruits and vegetables, regardless of whether you can afford the organic versions. A 2017 meta-analysis of the health effects and nutritional differences between organic and conventional produce notes that though “there is some evidence for potential benefits of organic food consumption from human cohort studies,” that “considerable uncertainty/controversy remains on whether or to what extent these composition differences affect human health.”

So if you have the cash to spare, it’s probably a bit safer to buy organic in general, but as the editorial points out everyone would be better off in terms of cancer risk if they exercised regularly, ate less red meat, and increased their veggie intake—organic or otherwise. And of course, it’s important to remember that anyone can get cancer, no matter how healthy their lifestyle.

The post The truth about organic food and cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In Colombia in 2013, a man showed up to a hospital with a confusing array of symptoms. He was gaunt, having lost a lot of weight in the past few months. He was HIV-positive and hadn’t been taking his medication. He was fatigued, with a fever and a cough. Stool samples revealed that he was carrying the parasite Hymenolepis nana, a common type of tapeworm; strangely, a scan showed cancer-like nodes in his lungs and lymph nodes.

His doctors weren’t sure how to diagnose the man—the cells looked and behaved like cancer, but they weren’t the man’s own cells. The cancer seemed to be from another multi-celled organism. The disease progressed and 72 hours after he was admitted to the hospital, the man died.

Doctors determined that the man died from his tapeworm’s cancer—the first such case ever reported, according to the study published today in the New England Journal of Medicine. And that’s got some scientists asking questions about how much we know about what causes cancer in the first place.

Scientists have known for a while that some infectious agents such as parasites can cause cancer. Two types of parasitic flatworms that live in the liver have been connected with increased incidence of cancer in bile ducts found in the intestines; another called Schistosoma haematobium can be ingested through water and is known to cause bladder cancer. The hypothesis is that these parasites can cause inflammation in the host’s tissues, which causes them to reproduce faster and increase the likelihood of a mutation.

But this case is different—the cancer was in the parasite’s cells, not the man’s. To see what might have caused the tapeworm’s cancer, the researchers compared the genes of the worm’s normal and cancerous cells. The researchers found that several of the genetic mutations in the cancerous cells occurred in the same genes as malignant mutations in human cells.

That not only shows a level of biological commonality, one researcher told NPR, but this case also shows how cancerous cells can spread out of control when the immune system is compromised.

This strange case raises even more questions about possible misdiagnoses of cancer in developing countries, and about the role of the immune system in fighting or protecting the body against cancer. “The host–parasite interaction that we report should stimulate deeper exploration of the relationships between infection and cancer,” the study authors write.

And though the doctors weren’t able to act quickly enough in this case, answering these questions might lead to better cancer treatments in the future.

The post Case Study: A Man Dies From His Tapeworm’s Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In case you missed the news, Canada legalized marijuana last week, leaving the country’s 13 provinces and territories to each figure out how it will be sold in their jurisdiction, and pot users across the country wondering how they’ll buy it—legally—for the first time. They aren’t the only people with questions: researchers are wondering about the move’s potential public health effects, specifically in regard to the canonical way to ingest marijuana: smoking a joint.

Smoking is bad. Even smokers know this is so. In the years since the Surgeon General’s infamous 1964 report, billions of dollars have been spent making sure physicians and members of the public are aware that they’re unhealthy. You may not have the same opinion of marijuana, whether medical or otherwise—but researchers say that the health impacts of smoking pot warrant the same kind of consideration. In a new commentary published Monday in the Canadian Medical Association Journal, researchers Wan Tan and Don Sin make the case that we need to know more about how smoking weed affects the lungs.

Many people view marijuana as “a relatively safe drug,” they write, and there’s a lot of literature out there touting its health benefits and safety. But there are also concerns that there hasn’t been enough scientific research to really define the health problems that marijuana might present. Tan and Sin are specifically concerned about smoking the drug, and note in their commentary “that the overall health benefits of ‘medical’ marijuana have been overstated and the drug’s harms understated, as was the case for tobacco cigarettes before 1964.” That was the year that the United States Surgeon General issued a report definitively linking cigarette smoking and cancer. It’s seen as a major turning point in public health.

“We weren’t sure that the public actually knew some of the concerns that the scientific field had about greater use of smoked marijuana in Canadian society,” says Sin. “There’s been very little good research about the health impact of marijuana smoke on the lungs, which are the first point of contact for smoked marijuana.” Our lungs are efficient vehicles for substances to get into our bodies, which is why many drugs (tobacco included) are frequently inhaled as smoke or vapor. Other methods of ingesting marijuana don’t specifically concern Sin in regards to the lungs—he says edibles, for instance, will likely have little-to-no-effect on lung tissue.

The lack of research is associated with historical stigma, Sin says, in Canada as well as in the United States. In the U.S., of course, marijuana remains a Schedule 1 drug, even though numerous states have legalized it for personal or medical use. According to UCSF professor Stanton Glantz, the American research community has been asking the federal government for easier marijuana access for a long time. “Even if they want to keep it on schedule one, which is frankly ridiculous,” he says, researchers have been saying the government “should at least have some exception that makes it easier to do research on it.”

Given how widespread marijuana use is both in the United States and in Canada, there’s reason to call for more scientific inquiry. Biochemically, marijuana “is very similar to tobacco except for the active ingredient,” Sin says. In marijuana, it’s THC. In tobacco, it’s nicotine. But most of the other stuff in cigarette smoke is in marijuana too, he explains. That includes substances like formaldehyde, ethylene, and acetone. In Canada, at least, those substances have all been part of a graphic cigarette labelling campaign for almost 20 years.

There are more than 4,000 chemicals in tobacco smoke, Sin says, and nicotine is only one of them. Same goes for marijuana smoke, which has 4,000-5,000 chemicals in it, he says. Those non-THC chemicals potentially have tremendous impact on the lungs, just like cigarettes, he says.

“It is generally true that marijuana smoke is just as toxic as cigarette smoke,” Samuel Wilkinson, a resident physician at the Yale School of Medicine, told Popular Science in an email interview. “However, generally people expose themselves to less marijuana smoke,” he wrote. “It’s rare that someone smokes 20 joints per day, but it’s common that someone smokes a pack per day of cigarettes, which is 20 cigarettes.”

But while 20 joints per day does sound pretty implausible, Sin does worry that legalization will encourage more users to smoke heavily. Marijuana is known to be a potentially addictive substance, and it’s certainly a habit-forming one for some users. “Potentially many of these smokers will become perpetual smokers or constant smokers,” he says, though it’s impossible to know just how widespread such an uptick would be. There’s also the question of how habitual pot smoking, even at a rate that feels harmless to the smoker, might affect the body over the course of a decade or two. Because of the lack of research, such risks are poorly defined.

With the legalization of marijuana in Canada, Sin says, researchers there “have a tremendous opportunity, if not an obligation,” to study the substance and try to understand its effects. Easier access from a government-policed supply is likely to help, he says, partially because with legalization comes standardization, meaning Canadians—and researchers who study them—will have a better idea what they’re smoking. “With further research, the mysteries and myths behind marijuana can be resolved,” Tan and Sin concluded.

The post Nobody really knows what smoking pot does to your lungs appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Cancer is often considered a “disease of affluence”–a malady that mostly afflicts people in the world’s wealthiest countries, often as a consequence of over-consumption–but, as today’s infographic shows, the reality is not so straightforward: In the U.S., for instance, the rate of lung cancer is 26 times higher than it is in Tanzania, but Tanzania’s rate of cervical cancer is nine times higher than that of the U.S. And in Mongolia, liver cancer is 33 times more common than in Russia, the country’s northern neighbor.

This interactive graphic show the global footprints of the six most common types of cancer. The stark geographic patterns reveal both the role of lifestyle and the power of preventive measures, as well as the places where those measures remain out of reach:

[via Visual.ly]

The post Cancer Rates Around The World [Infographic] appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

If traditional cancer therapies like chemotherapy are the WMDs of medicine–powerful, indiscriminate killers–targeted drug therapies are the assassins, trained to seek out and destroy enemy cancer cells, one at a time.

Scientists recognize the clear advantage of the assassin approach, of course, and have successfully engineered several targeted cancer-killing drugs over the past few decades.

The problem is, assassins ain’t cheap. A single course of targeted drug therapy can cost upwards of $100,000. That’s largely because the drugs take a lot of effort to create–scientists have to first grow human antibodies capable of recognizing enemy cells, and then equip those cells with a weapon by attaching them to toxic molecules. The process is, apparently, as hard and time-consuming as it sounds.

But recently, a group of scientists at University of California, San Diego engineered algae to produce a human antibody with a built-in toxic weapon–a ready-made molecular cancer assassin. The researchers produced the new therapy by embedding the genetic code of the toxin P. aeruginosa into a human antibody gene, which they then spliced into the algae’s DNA.

In their research paper, the scientists note that this feat has been attempted before, using bacteria instead of algae, but the bacteria weren’t capable of folding the complex antibody into the right shape, so the method required a researcher to follow along behind and refold the proteins. The new therapy could not be produced by mammal cells, either, the researchers write, because the presence of the toxin would prohibit the engineered cells from reproducing.

If the new treatment is able to stand up to the battery of medical trials required by law, the targeted, assassin-style fight against cancer may soon get a lot more affordable.

The post Scientists Engineer Algae To Produce New Targeted Cancer Therapy appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

When your mother says eat your greens, you just might want to listen. It’s been known since the 1970’s that cruciferous vegetables, or cabbage family vegetables, such as broccoli, cauliflower, Brussels sprouts and kale, have anti-cancer benefits. But researchers at the University of California, Berkeley, who have studied the benefits of anti-cancer vegetables for 15 years, are the first to explain how an anti-cancer compound, indole-3-carbinol (I3C), found in broccoli and cabbage, works to slow down the activity of an enzyme linked to rapidly developing breast cancer.

In the study released online in the journal Proceedings of the National Academy of Sciences, Berkeley scientists honed in on how I3C inhibits elastase, an enzyme which at high levels in breast cancer cells reduces the effectiveness of cancer-fighting chemotherapy and endocrine treatments. They found that I3C prevents elastase from shortening cyclin E, a cellular chemical that controls the cell cycle.

At the moment, I3C is a supplement used as a treatment option for non-malignant tumors of the larynx. The Berkeley researchers say that now they have connected the dots on one extremely important pathway, scientists will be able to create an improved version of the I3C supplement to help fight against a broader range of breast and prostate tumors (and possibly against other types of cancer as well). Additionally, since I3C is derived from a natural source, it would have fewer side effects than traditional treatments, as well.

Via PhsyOrg

The post Veggies May Be the Key to Fighting Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Mole mapping, the process of charting your moles through regular skin checks, has just gotten easier—and potentially more reliable—thanks to MoleMapper. The app, which is free and available on iTunes, allows users to map, measure and monitor moles with the help of an iPhone camera and digitally share these images with a doctor.

“Being vigilant about your moles – the size, shape, color, and patterns—is the best way to catch melanoma when it’s most treatable and a cure is likely,” says Sancy Leachman, MD, Ph.D., director of the melanoma research program at Oregon Health & Science University (OHSU) in Portland.

Melanoma is the deadliest form of skin cancer. If it’s recognized and treated in its earliest stage, the five-year survival rate of people with melanoma is 97 percent. But once the cancer spreads to other parts of the body, that rate drops to as low as 15 percent.

The MoleMapper uses an Apple-Maps-like interface, allowing users to add and drag pins to chart each mole. After users take a close-up photo of a mole, the app then records the dimensions of each mole when compared to reference points—a dime, a penny, a nickel, for example—and alerts users to changes that may signal a malignancy.

Dan Webster, Ph.D., a research fellow in cancer biology at the National Cancer Institute, created MoleMapper for his wife, who is at high risk of developing melanoma. “She has several risk factors for melanoma, so we kept track of her moles by taking pictures between appointments. I wanted to empower others to do the same,” he said.

Webster then partnered with OHSU and Sage Bionetworks, non-profit biomedical research foundation in Seattle, to build an-app based study to quantitatively track moles and help detect early signs of melanoma. All app users are invited to take part in the study and given the opportunity to electronically consent to participate. Researchers hope that, by studying mole images from a large number of people, they can develop new ways of evaluating moles and potentially inform treatment options.

“We want to know if a regular iPhone camera could provide us with images that have value in determining moles that should be removed? If it can, we then want to know if we can train a computer to predict what moles should be removed based on how they look in a digital image,” said Andrew Trister. MD, Ph.D., senior physician at Sage.

Images and mole data from those who join the study data will have identity info removed before they are collected by Sage for use by the study team. These data will also be used in OHSU’s Melanoma Community Registry, a centralized resource of melanoma survivors and their families are interested in donating their health data to research. Study participants are also given the option to share their data more broadly with other qualified researchers.

“Right now it’s not possible to determine whether a mole should be removed by looking at a photo. There’s just not enough data, but this app changes the scale of the data we can collect,” said Dr. Leachman.

Researchers say data provided over time will prove particularly useful in contributing to knowledge about the disease. “What will really help is if people report back what moles they had removed because the size of the scars will indicate how big the melanoma was. This information will help us learn what moles actually are melanoma,” said Dr. Trister.

The MoleMapper is the latest addition to Apple’s ResearchKit, an open-source framework designed to help medical researchers expand their study candidate pools and collect more accurate data. Other ResearchKit apps include ones to better understand Parkinson’s disease and long-term health after treatment for breast cancer.

As with other apps included in the ResearchKit suite, the success of the MoleMapper study depends on broad participation. “Anyone with an iPhone and Internet connection can contribute to research on a disease,” said Leachman. “Everyone can do their part.”

The post A Selfie Could Save Your Life appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Yesterday, the Food and Drug Administration (FDA) announced that it had approved the drug Imlygic to treat late-stage melanoma on the skin and lymph nodes. The drug, which relies upon a genetically engineered herpes virus to attack and kill the cancerous cells, is the first virotherapy drug to gain approval, buoying researchers’ hopes that more will follow.

Since the 1800s, researchers have noticed that viruses could cause patients’ tumors to shrink or grow, but they weren’t sure why or how this happened. In recent years, scientists figured out that genetic tweaks to a virus could cause them to preferentially infect and kill cancerous cells without affecting the nearby healthy cells. And while malignant cancers often slip by the immune system, the virus’ presence ignites the immune response. Combined, these reactions mean that virology can successfully treat even some late-stage cancers that are often resistant to other treatment methods.

Before it was approved, Imlygic was tested in more than 400 patients with metastatic melanoma, which kills about 10,000 people per year in the United States, which had caused lesions in patients’ skin or lymph nodes. When the drug was injected into the cancerous sites over the course of six months, more than 16 percent of patients saw their lesions shrink.

So far, virology treatments haven’t worked as well in cancers in tissues deeper in the body—the drug has to be injected directly into the tumor site or the immune system will launch its attack too early, according to Nature News. But a number of drugs using different viruses and to treat several types of cancer are already in clinical trials. Now that the first virology cancer treatment has been approved, researchers hope that many more are to follow.

The post FDA Approves Use Of Engineered Herpes Virus To Treat Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Just like the X-Men, mutations endow cancer cells with unique abilities that normal, healthy cells just don’t have. For example, cancer cells, unlike normal ones, can invade other cells, causing the disease to metastasize to new tissues in the body and put the patient’s life further at risk. But the mechanism by which cancer cells are able to both multiply and invade new cells has been poorly understood, as scientists have been unable to find cells performing both those tasks simultaneously in a living organism. Now, researchers have found that cancer cells might divide and conquer at totally different stages of their development. According to a new study published today in Developmental Cell, researchers found that, at least in nematodes, cells that are dividing can’t also take over new cells–a discovery that could give researchers a new way to treat cancer by targeting the cells that are most likely to invade healthy cells.

Though a nematode doesn’t look much like a human, the two species have enough biological similarities that scientists often use nematodes to better understand human physiology. In this study, the researchers looked at the nematode’s anchor cell, which connects the worm’s uterus to its egg laying-structure during an essential stage in a nematode’s normal development. “That’s interesting because this process of connection involves an anchor cell invading through another cell’s basement [outside] membrane, which gives us a model for understanding cells’ invasive behavior,” says David Matus, a professor of biochemistry and cell biology at Stony Brook University and one of the study authors.

The researchers wanted to know which of the nematode’s genes made this process happen, so they tested about 850 of them and tried turning them off and on. One in particular acted like a particularly potent switch—normally, it’s turned on, which allows the anchor cell to invade another cell. But when the researchers turned it off, the anchor cell couldn’t break through the cell membrane. Instead, it divided and reproduced.

This is the first time that scientists have observed division and invasion as distinct, separate processes that can’t occur simultaneously. “We think of cancer as uncontrolled cell growth or division,” Matus says. “The idea that during metastasis, when cells form a tumor, and have to turn off cell division before they start to travel elsewhere, that’s not something that has been tested. [Scientists] have seen and made these observations in different ways in cancer, but no one has ever put the two together.” In nematodes, he adds, it can finally be tested.

These conclusions may mean that cancer treatments, many of which currently target rapidly dividing cells, could investigate the unique qualities of these invasive cells. If treatments could pinpoint those cells, they could slow or prevent metastasis, a process that makes a cancer significantly more deadly. “Our study gives one new avenue [to develop new] cancer treatments, allowing researchers to take advantage of the fact that the cells are not dividing and figure out what’s special about that,” Matus says.

The post Cells Can’t Divide And Invade At The Same Time appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In his 2017 budget that will be sent to Congress next week, President Obama is requesting another $755 million for Vice President Biden’s “moonshot” cancer initiative, White House officials said today. Congress has already allocated nearly $200 million to the program in last year’s budget, which will bring the total spending to almost $1 billion if they fulfill Obama’s proposal. Here’s an overview of how that money would be used.

The money would be allocated into six main research areas:

• Immunotherapy
• Technology to detect cancer earlier
• Vaccines for cancer-causing viruses
• More data sharing and scientific collaboration
• Genomic analyses
• Pediatric cancer

It would go to these institutions:

• The National Institutes of Health would receive the biggest chunk of funds
• The Food and Drug Administration would get $75 million, mostly for work with data, as Stat News reports
• The Department of Defense and the Department of Veterans Affairs would increase their number of long-term studies into risk factors for cancer
• Vice President’s Exceptional Opportunities in Cancer Research Fund, a new funding body that would back “high-risk, high-return research, as Reuters reports, as well as collaborations between businesses and non-profits

This announcement comes just a few weeks after the president announced the cancer moonshot initiative at the State of the Union address. He chose Biden to lead the charge; today, Biden is meeting with the members of the federal task force outlining that initiative, according to a blog post.

With this increased funding, officials hope to achieve a decade’s worth of scientific breakthroughs in half that time. But they’ve yet to outline, concretely, how the program defines success; though officials say the specific goals will be announced soon, critics have pointed to this fuzzy endpoint as one of the biggest weaknesses of the cancer moonshot effort.

The rest of the 2017 budget will be released on February 9.

The post White House Proposes Nearly $1 Billion For Cancer Research appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The Nobel Prize, though often questionable in its selections, captivates the world each year. While there are now scientific awards with larger monetary prizes, there is no prize so universally and immediately recognized as a sign of prestige.

The 2018 season kicked off on Monday with the Nobel Prize in Physiology or Medicine, which this year honors two researchers for their work on cancer therapy. James P. Allison, 70, born in Alice, Texas, and now affiliated with the University of Texas MD Anderson Cancer Center and the Parker Institute for Cancer Immunotherapy in San Francisco, splits the prize with Tasuku Honjo, 76, a professor at Kyoto University in Japan. Their joint prize includes 9,000,000 Swedish Krona, which is a bit more than $1,000,000 USD.

In the 1990s, Allison and Honjo did separate but parallel research on the use of the human immune system to fight cancer. Because cancer is a disease caused by the mutation of a body’s own cells, our immune systems rarely offer much assistance. Allison and Honjo showed how two different proteins can, in slightly different ways, pump the brakes on an immune system’s attempts to attack multiplying cancer cells. If someone disabled such brakes, their work suggested, the immune system might have a fighting chance against cancer. The work they and others did at that time led to the development of immunotherapy as a cancer treatment, which is now a quickly growing field. This was the first step toward cancer therapies more precise and less brutal than surgery, radiation, and chemotherapy.

This award is also the first Nobel Prize to be awarded to a cancer therapy. Past Nobels have been awarded to discoveries made to understand the mechanisms through which cancer cells work, but this is the first one that has directly translated into a clinical therapy to treat people with cancer.

Drugs based on these and similar proteins now help treat several types of cancer, and are known as immune checkpoint inhibitors.

“I’m so thrilled that a Nobel has been awarded for this game-changing cancer therapy,” Dan Davis of the University of Manchester told The Guardian. “It doesn’t work for everyone but lives have been saved, and it has sparked a revolution in thinking about the many other ways in which the immune system can be harnessed or unleashed to fight cancer and other illnesses. I think this is just the tip of the iceberg—many more medicines like this are on the horizon.”

At a press conference Monday morning in New York City, Allison said he was still in shock from the news (which he’d learned via a 5:30 a.m. wake up call from his son).

To him, he said, what’s so special about his now prized discoveries is the direct connection they make between basic research and clinical medicine. “I didn’t get into this to cure cancer, but to understand how T-cells work,” Allison said. “As a basic scientist, to see this work 20 years later really helping patients” has been the most rewarding, he said.

What does this mean for cancer patients now—and in the future?

Prior to Allison and Honjo’s work, the main pillars of cancer treatment were surgery to rid the body of as much of the cancer as possible, and chemotherapy and radiation to kill every remaining cancerous cell. What these discoveries did, Allison said, is bring a fourth pillar to cancer treatments’ arsenal in the form of immunotherapy. While it’s still not completely clear where immunotherapies will fit into more traditional treatments, Allison said, it will likely change the way we use our older arsenal.

For example, the process that jumpstarts the immune system’s fight against cancer starts with the death of some of those malignant cells. So if chemotherapy and radiation can initiate that process, then immunotherapy will have a chance to come in and enable the body to kill off the rest—and, theoretically, keep them gone for good.

“The traditional way of giving high doses of chemotherapy and radiation to kill every last cancer cell is no longer the goal, it should not be the goal. Kill enough tumor cells with chemotherapy and radiation and then come in with the immunotherapy to get the immune system going to get rid of every last one,” Allison says.

By showing that the immune system can be tweaked to ward off cancer cells, Allison and Honjo helped inspire the latest generation of gene-edited cancer therapies. Our 2017 Best of What’s New Awards honored Kymriah, the first FDA-approved treatment to utilize gene-edited white blood cells to fight the disease. Its results are astounding, but Kymriah still isn’t a magic bullet for all patients—or even for all types of cancers. Researchers are working on getting Novartis’ Kymriah and Kite Pharma’s Yescarta (two brands of the same therapy, generically known as CAR T-cell immunotherapy) approved for more varieties of the disease, but as PopSci reported back in December, the treatments have a long way to go. When they work, they often work miraculously. When they don’t, they can cause life-threatening side effects. And even patients who seem to do well aren’t always given the life-long bill of health they hope for.

But despite all the typical bumps in the road of a new form of medicine, immunotherapy is undoubtedly our best shot at making cancer—at least as we know it—a thing of the past.

“How dare I use the word cure,” Allison says, but “that’s the hope with these kind of therapies. Once you’ve got T-cells you’ve got them for the rest of your life. They don’t go away. If you give a chemotherapy drug, it’s gone in hours.”

And for what it’s worth, Allison may well be among the best harmonica players in Nobel history:

The post This year’s Nobel Prize in medicine is shared by a cancer-fighting (and harmonica-playing) Texan appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Last week, many news outlets reported that four people in Europe developed breast cancer after each received organ transplants from the same donor in 2007. Three have died from the disease so far.

The case report that detailed these findings, originally published in the American Journal of Transplantation earlier this year, explains how after a 53-year-old woman died of a stroke, she donated her heart, kidneys, liver, and lungs to four different transplant recipients. While the donor had no documented history of cancer when she died, DNA tests confirm the cancers in the recipients originated in the body of the donor.

Cancer spreading from a donor to a recipient is “extremely rare,” Dr. Frederike Bemelman, the author of the report, told CNN. Only about one in 5,000 people who receive a transplanted organ will get cancer from that organ.

But there is always an unknowable risk, says Nicole Ali, a transplant nephrologist at NYU Langone’s Transplant Institute. Infection and cancer are a constant concern. To protect patients and try to transplant as many donated organs as possible, specialists weigh the possible risks and benefits of each heart, lung, liver, intestine, pancreas, and kidney.

There’s a chronic shortage of donated organs in the United States. In 2016, more than 7,000 people died while waiting for an organ transplant, according to the United Network for Sharing Organs. This year, there are more than 114,500 people on the transplant waiting list. Only 24,000 have received new organs so far this year from 11,600 donors.

Once they receive a transplant, these patients take immunosuppressants—drugs that dampen the response of the immune system—to prevent their bodies from rejecting the new organs. Unfortunately, this makes transplant recipients much more susceptible to the rapid spread of cancers and viruses—including those that may lurk in their lifesaving new tissues.

To minimize risk, each donor goes through a careful screening process. But it’s easier to test living donors than deceased ones.

Healthy, living people can donate a kidney or part of their liver or, in rarer cases, a lung. Before these people go into surgery, however, they undergo rigorous testing as doctors try to learn everything about their bodies and medical history. The Organ Procurement and Transplantation Network sets the guidelines for all organ donations and recipients in the United States.

“We try to screen the living donors as much as humanly possible,” says Ali.

Doctors screen women for breast and cervical cancer and men over the age of 40 to 50 for prostate cancer. Anyone over the age of 45 (the guidelines recently moved up 5 years) will have to undergo a colonoscopy. Physicians will look out for skin cancer, abnormal blood work that could indicate something rarer like leukemia or lymphoma, and evaluate the health of the kidney or liver itself. If someone has a family history of lung cancer, they’ll check for that too, says Ali.

No one with an active malignancy or an inadequately treated cancer can donate an organ. But doctors approach people with a history of cancer on more of a case-by-case basis, with the transplant specialists consulting with oncologists to evaluate the risk of transmission.

For example, someone with a history of basal cell skin cancer would likely still be able to donate, says Ali, because basal cell is a simple cancer that rarely spreads to other parts of the body. Melanoma, on the other hand, tends to come back within a five-year window, so history of the disease tends to rule out a potential donor. Only if someone had been in remission for a long period of time—upwards of 15 years—would doctors consider it.

With diseases like breast cancer, it depends entirely on the type, whether and how much the cancer had spread throughout the body, and how long it’s been since cancer was treated without a recurrence, says Ali.

“With the living donor you have the benefit of time, and doing all this screening takes time,” says Ali. While there is still risk of disease or infection , doctors at least have time to do their homework.

“Some cancers have a very low risk of recurrence, or [happened] so long ago it’s not unreasonable to consider using those organs,” says Ali. “And cancer does rule out many, many organs, especially in the deceased donor population.”

With a deceased donor, someone who elected to be an organ donor and has been declared brain dead but hasn’t yet been taken off life support, everything happens much faster. Physicians have to quickly ask for the consent of the family, then harvest the organs and transplant them into the recipient. Many organs can only survive for a very short time out of the body, Ali explains. The doctors have to rely on the person’s existing medical history and information from family members.

In the case in Europe, the donor had no history of cancer or visible signs of disease when she died. The authors hypothesize the donor could have had micro metastasis of cancer throughout the body—cancer cells so small they went undetected during the woman’s life.

The authors of the report debate whether performing a CT scan on the body would have caught the cancer. If the micro metastasis theory is true, it likely would not have. There are many cancers a CT scan cannot detect, says Ali, but the machine could pick up on non-cancerous lesions that could rule out a donation unnecessarily. The author’s echoed these concerns in their report. Postmortem CT scanning, they warn, could shrink “the already scarce donor pool.”

Trying to treat as many people as possible as safely as possible is something transplant physicians have to think about every day. These complex considerations are all the more important in places like New York City, which has one of the lowest organ donation rates despite being one of the most populated cities in the country, says Ali.

“Everything we do in medicine is a balancing of risk and benefit,” she says.

The post Donated organs rarely spread disease, thanks to these protocols appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Fears of Zika have plummeted in the last year. New cases of the disease that plagued the Americas for nearly two years and infected hundreds of thousands of people are incredibly rare these days. Still, that doesn’t mean doctors have suddenly forgotten all about it. And in the process of developing and testing a working vaccine that can protect against the virus, new research suggests we may have come across a treatment for one of the deadliest forms of cancer that threatens humans.

In new findings published in the journal MBio a team of researchers from The University of Texas Medical Branch at Galveston and from China successfully used a Zika virus vaccine currently under development to kill glioblastoma, an extremely aggressive form of brain cancer that kills most patients in less than two years—the same type of cancer that recently killed Senator John McCain. Fewer than 3 to 5 percent of patients live past five years, and even when treated with surgery followed by high doses of radiation and chemotherapy, the cancer usually returns, likely because of an uncanny ability by glioblastoma stem cells to hide under healthy brain tissue.

“The truth is, if you take out the non-stem cells, which could be as much as 98 percent of the cancer, they can all eventually return,” says Andrew Sloan, a neuro-oncologist at Case Western Reserve University School of Medicine.

The pathology of Zika (caused by the ZIKV virus) to cause brain damage in fetuses is what made it an interesting candidate weapon against glioblastoma. “ZIKV targets normal stem cells in the developing fetal brain, yet has minimal effects on the adult brain,” explains Milan Chheda, a neuro-oncologist at Washington University in St. Louis, who was not involved with the study but has previously studied Zika’s interactions with glioblastoma. It turns out ZIKV especially likes to target neural stem cells that have not yet matured into fully-formed neurons. The brain of a growing fetus is obviously chock full of them. “Since glioblastoma stem cells share properties with neural stem cells, we wondered whether the natural honing and lytic [or rupturing] activity of ZIKV could be harnessed to target and kill cancer stem cells.”

Although purposely injecting someone with a disease as a medical treatment—virotherapy—can seem haphazard and dangerous, researchers have long worked on the development of viruses as cancer-fighting agents. “Using viruses as a form of cancer therapy has potential,” says Justin Lathia, a researcher at the Cleveland Clinic Lerner Research Institute who was not involved with the study. “The key advantages are the virus’s ability to simultaneously kill tumor cells directly as well as activate the immune system. But a major disadvantage is the ability to control viral replication. These approaches could still have off-target effects,” and essentially turn the virus against healthy cells in the body.

Chheda and his colleagues had previously published findings last year that showed Zika, in its normal state, could target and kill glioblastoma tumors cells in vitro. And when injected with Zika, mice afflicted with glioblastoma lived two to three times longer than without treatment—all while non-cancerous cells remained untouched.

Pei-Yong Shi, a UTMB geneticist who worked on that study, decided to take things a step further and see whether safer form of Zika could achieve the same sort of results without risking infection. So he and other colleagues turned to the ZIKV-LAV vaccine, which uses a living form of the virus attenuated to prevent Zika infection, with the goal of providing immunity to typical Zika strains.

The team tested that vaccine out on mice bred without an immune system and found that it did not cause infection, and did not damage the host brain or lead to behavioral problems. More importantly, the researchers also tested the vaccine out on mice grafted with one of two types of glioblastoma tumor lines originating from human patients. The vaccine managed to reduce tumor growth overall, and specifically target and kill off cancerous brain stem cells from both tumor lines, prolonging median rodent lives from 30 days to 48 days and 31 days to 53 days, respectively.

The results are greatly encouraging, but we’re still extremely far from successfully using Zika to eliminate the deadliest form of brain cancer. First and foremost, testing on mice never equates to testing on humans, and this study itself wasn’t a typical mouse study anyhow. “These findings are done in the absence of an intact immune system, so it’s unclear how the immune system would be altered, potentially in a positive manner to reduce tumor growth,” Lathia notes.

Sloan echoes those concerns, pointing out that often times, the other goal of virotherapy is to prime the immune system to target the tumor itself. “The problem in this mouse model,” he says, “is that if you activate the immune system too strong, there can be inflammatory effects that damage or kill the patient.”

We also still don’t know the exact mechanism by which ZIKV causes infection and spreads through the body, and until we characterize those processes and have robust ways to prevent transmission, there won’t be any Zika injections in humans to stop brain cancer, even if it is an attenuated form of the virus. As the study authors write, “an oncolytic virus must display a fine balance between efficacy and safety to be successful.” That’s often a hard balance to strike.

“While I do think it has an exciting potential, and I’m encouraged,” says Sloan, “I would not put patients on this quite yet.”

Still, considering how lethal glioblastoma is, it’s likely many patients would take their chances and elect a Zika-backed treatment, even with the risk of infection. There are few good options for patients, and any treatment that might reduce tumoral resurgence and prolong survival is certainly worth exploring.

The post Scientists used Zika to kill aggressive brain cancer cells in mice appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

In recent years, scientists have been finding new ways to treat cancer outside of the chemotherapy and surgery combination. One technique, called immunotherapy, has showed promising results by reprogramming the patient’s immune system to attack tumors. Researchers from the Fred Hutchinson Cancer Research Center in Seattle tested a version of immunotherapy on patients who had late-stage leukemia and lymphoma that had exhausted other treatment options—some weren’t expected to survive the experiment.

But the researchers were shocked to find that 27 of the 29 leukemia patients—that’s 94 percent of the study participants—went into complete remission and showed no more signs of the disease. Stanley Riddell, one of the researchers behind the trial, presented the unpublished results on Sunday at the annual AAAS meeting in Washington, D.C.

Our blood contains T cells, which are supposed to detect pathogens in the body. In this study, the researchers removed these cells from patient’s blood and tweaked their genes to recognize the cancer cells that would otherwise slip by the immune system.

The resulting T cells, called CAR-T cells because of the special receptors inserted into them, are then put back in the body. Researchers hypothesized that the CAR-T cells would give the patient a long-term immune response—indeed, a few small but promising trials have corroborated it—but in many cases the T cells end up being less effective over time, either because the cells themselves become exhausted or because the cancer cells inhibit detection.

The results of this trial were different. In addition to the stunning results from the leukemia patients, 19 of 30 lymphoma patients responded to the treatment as well, after just a single dose of CAR-T cells. Many of the patients who were not expected to live for more than a few months are still alive now, three years after the trial started. “This is unprecedented in medicine, to be honest, to get response rates in this range in these very advanced patients,” Riddell said, according to the New York Post.

To the researchers, this strengthens the evidence that CAR-T cells (and immunotherapy in general) might be a viable treatment for cancers beyond lymphoma and leukemia.

But the treatment isn’t perfect quite yet. During the trial, seven patients developed cytokine release syndrome, a life-threatening inflammation that results when too many cancer cells are killed at once, and two of the patients died as a result.

While that might be acceptable risk for a last-ditch effort for patients with terminal cancer, such dramatic side effects wouldn’t be acceptable for patients with earlier stage or less lethal cancers, as Ars Technica reports.

The researchers don’t yet know the best dose for the treatment that wouldn’t cause such a strong reaction but would still get rid of the cancer, and they don’t know how long the patients will remain in remission. But they are heartened and encouraged by the results.

The researchers have submitted a draft of their study to a journal and hope that it will be published soon so that they can continue their work with immunotherapy, according to a press release.

The post Here’s Why Scientists Are Shocked By The Results Of This Cancer Treatment Trial appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Cancer follows a fairly standard protocol: Cells multiply out of control until they take over key organs necessary for survival. Creatures across the animal kingdom from humans to birds to reptiles can all get cancer, and, as researchers report this week, so can dinosaurs that roamed the Earth millions of years ago. Knowing more about how and why the mysterious forms in these ancient creatures could help doctors prevent more animals from meeting the same fate.

Scientists from the Royal Ontario Museum and McMaster University have discovered that an ancient triceratops-like beast that lived over 75 million years ago developed an osteosarcoma tumor in its leg bone. They published their new findings in The Lancet last week.

The team of scientists, including health experts and paleontologists, had been searching for human-like diseases in ancient dinos by digging through old fossils at Canada’s Royal Tyrrell Museum and stumbled upon the fibula of a Centrosaurus apertus that had scientists had uncovered in Alberta thirty years ago.

Paleontologists at the time had diagnosed the malformed fossil as an oddly healed fracture. But a new team of researchers took a closer look, examining and running tests as they would if the bone belonged to a human patient. That meant coming up with a list of possible diagnoses, and eventually, biopsying slices of the bone under a microscope to take a closer peek.

“We had to do something called destructive analysis which is exactly what it sounds like,” says Seper Ehktari, an author of the study and orthopedic surgery resident at McMaster University.

With this closer examination, Ehktari and his team realized the destruction of the bone was caused by osteosarcoma which still impacts some 800 to 900 new human patients in the US yearly. Ehktari adds that it’s not only humans that get this disease, but other mammals and creatures more closely related to dinosaurs like chickens and cockatoos.

Jennifer Anne, a paleontologist at the Children’s Museum of Indiana not involved in the study, notes that this is not the first spotting of cancer in dinosaurs. There’s been a handful of known cases (a duck-billed dino has also had signs of bone cancer). However, it does open up a whole new group of dinosaurs to novel discoveries regarding cancer that we might’ve missed before.

“We are also gaining a lot more knowledge about cancer in non-human animals,” Anne says. “That information coupled with better access to new technology like CT scanners that can scan dense fossils means paleontologists are going to get better at identifying and, to the best of their ability, diagnosing paleopathologies.”

Beyond just satisfying our curiosity for the lives of the massive dinosaurs that once roamed our current-day backyards, discovering more about cancers in their ancient forms could help us diagnose and fight them in today’s creatures, including in us humans. Osteosarcomas in humans typically develop when people are growing at a super-fast rate, typically around age 10 to 20, says Ehktari.

Seeing as dinosaurs also grow rapidly from tiny babies to massive beasts is another reinforcement to the theory that rapid growth might have something to do with the rapid reproduction of cells, Ehktari says. After all, he adds, the more cells are growing and reproducing, the more likely it is that a handful of them could “go rogue.”

The post This triceratops cousin suffered from osteosarcoma, just like many humans do appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Corals in shallow water sometimes produce a fluorescent pigment that protects them from harmful solar rays, like a sunscreen. But when researchers from Israel and the U.K. found deepwater corals that produced a brilliant rainbow of hues, they were floored. “There might be something completely undiscovered in reefs that could be incredibly useful,” says Jörg Wiedenmann, an oceanographer at the University of Southampton.

The corals’ pigments, he says, might help in the lab. For example, one can change from green to red when exposed to near-UV light—a capability that could help researchers track cancer growth or test the effects of potential drugs on cell cultures.

This article was originally published in the October 2015 issue of Popular Science.

The post Corals Shine Light on Cancer Growth appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The above is a digital model of DNA, but it’s probably not the DNA you’re familiar with. The double-helix structure of DNA and RNA–two strings of nucleic acids spiraling around each other and held together by complementary base pairs–is both nearly universally recognized and central to its role as the fundamental vehicles for cell function. But it turns out that a square shaped, four-strand DNA structure (like the one above) is likely more common in our genomes than we previously thought, and that could have important implications for biology.

Four-strand DNA–or “G-quadruplex structures” (the G is for the base guanine)–is nothing new to genetic scientists. It can be easily conjured in the lab via guanine-rich strands of synthetic DNA, for instance, and it has long been thought to occasionally form naturally in biological cells. But a new study published online at the journal Nature Chemistry and conducted by University of Cambridge researcher Shankar Balasubramanian suggests that G-quadruplex structures are more common in natural genomes than we thought, and that they may carry out some important genetic business.

This has particular importance in the field of cancer research. Some researchers have previously suggested that these quadruplexes can be found in places along the genome where gene regulation occurs. Errors in gene regulation are, of course, one of the root causes of the kinds of abnormal cells that lead to cancerous cell replication. So the Cambridge researchers engineered an antibody designed specifically to seek out and bind to G-quadruplex structures while steering clear of double-helical structures. When introduced to human cells, the antibody bound itself to several sites along the chromosomal chain–not just in the few where the researchers expected it to–reinforcing the idea that G-quadruplex structures are more prevalent in more places than originally thought.

If researchers can figure out all the places where these structures are forming along the genome, they may be able to zero in on the places where genetic ailments like cancer get their starts and try to mitigate that process.

Nature

The post Oddly Shaped DNA Structures Found In Human Cells appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Logically, elephants should get cancer much more than humans do—elephants have 100 times more cells than we do and live just about as long, providing ample opportunity for cancer-causing mutations to occur. But in fact they have less cancer; an analysis of hundreds of zoo deaths found that only five percent of elephants die of cancer, whereas 11 to 25 percent of humans do, according to the New York Times. Scientists hypothesize that, in order to get so large and biologically complex, elephants’ bodes must have evolved a way to suppress cancer. But they weren’t sure quite how they kept the cancer at bay.

Now, two teams of scientists have figured out the gene that prevents elephants from getting cancer, according to a study published today in the Journal of the American Medical Association and another currently under review at eLife.

In both studies, the researchers turned to elephant genes. They analyzed the DNA of African and Asian elephants and discovered that both species had 20 copies of P53, a gene known to have tumor-suppressing qualities. The team from the University of Utah School of Medicine looked at the DNA of 60 smaller organisms, including humans, and found that most have only one copy of P53. The authors of the other study, led by researchers from the University of Chicago, analyzed the genes of elephants’ smaller ancestors, discovering that they contained fewer copies of P53. That implies that, as elephants evolved to be larger, their genetic code developed more copies of P53. When cancerous mutations occur, the genetic mutation causes them to quickly die, making them less likely to proliferate and form tumors.

The researchers are quick to point out that this discovery doesn’t answer all of scientists’ questions about P53—they still don’t know how it figures in to the genomes of other large mammals, like whales. And though researchers on the clinical side have already been studying P53 for a long time, using it in immunotherapy treatments to combat cancers that have sprung up in the body, other large and long-lived animals may have of their own ways of combatting cancer could be useful in humans. It’ll be decades before these discoveries become clinically useful, the researchers told Motherboard, but it’s not a bad idea to extrapolate some cancer-fighting tactics from other members of the animal kingdom.

The post Found: A Gene That Prevents Elephants From Getting Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

When Maggie Rogers was four and a half years old, her kidney ruptured. She was playing with her dad, she recalls, and was running to jump on him, and when she landed she found herself in immense pain. Her parents took her to the hospital where they told her that she would be just fine, but after getting a second opinion and a slew of tests, her doctors discovered a tumor the size of a softball on her kidney. She was diagnosed with stage 3 nephroblastoma, a kidney cancer diagnosed in just 500 kids per year. Maggie’s doctors removed her tumor and what was left of her kidney; she was then treated with radiation therapy and, over the next year and a half, received multiple rounds of chemo. She left preschool, only knowing that she was sick and needed strong medicine. And though she doesn’t remember everything because she was so young, Maggie recalls a certain amount of normalcy in her years of treatment. Every week, her mom drove her to get chemo, and they would stop by her favorite burrito place, which sold the only food that Maggie would eat. She had little games: as Maggie would get her blood drawn, her mom would ride up the elevator and see if she could be back before the phlebotomist finished. “When my hair would fall out, I would take clumps and throw them out the car window because I wanted birds to make a nest with it,” she says. She started kindergarten bald; her classmates nicknamed her “the bald eagle,” which she hated, so she became the class clown, “so that kids would laugh at me about something other than that.” At age six, Maggie went into remission. Her hair grew back, and her checkups became less frequent. “I remember it being a big deal when I graduated to one follow-up visit per year,” she recalls. Neither she nor her family came through the experience unscathed, but she had survived, enabling her to live a normal adult life.

Maggie is one of thousands of children who develop cancer and, through rigorous treatment and holistic care by doctors and families, beat the disease. Treatment for cancer has increased dramatically since the 1950s, and nowhere is that more evident than in pediatric oncology; of the thousands of children treated in the U.S. for cancer every year, 80 percent of them will go into remission and go on to live productive lives—significantly higher than the five-year survival numbers for general oncology, which are 63 percent chance of survival for female patients and 66 percent for men. This disparity exists in part because of biology—the types of cancers that kids get, the strength of their immune systems—and because pediatric oncologists treat patients very differently than do general oncologists. The field isn’t perfect; some of the kids who survive have health issues later in life, and curing the remaining 20 percent of patients won’t be easy. But general oncologists can learn a few things about how pediatricians achieved this remarkable cure rate, and may be able to collaborate with them to discover new, less toxic treatments to benefit patients of any age.

“Childhood cancer is a different animal. Even though it has a similar end point [as adult cancers], the body in which it occurs is quite different than that of an adult,” says Alan Gamis, a pediatric oncologist at Children’s Mercy Hospital.

A ‘Mistake Of Nature’

Both childhood and adult cancers are caused by genetic mutations that cause cells to grow uncontrollably, threatening the function of the rest of the body. Adult patients can be born with mutations that combine with environmental factors to later cause disease. But kids are born with these mutations through no action of their own. They didn’t smoke for 40 years and destroy their lungs, or spend too much time without sunscreen.

Childhood cancers are cases of unlucky genes, and as a result they are biologically different from those that occur in adults. The driving mechanisms are simpler, caused by only one or two mutations instead of the dozens that may be present in adult cancers.. They almost exclusively occur in rapidly dividing tissues, often in the blood, bones, kidneys, brain or nervous system. Since these tissues are no longer actively growing in adults, cancers that occur in the same organ in adults are often genetically different. “In [a child]’s proliferating tissue, a mistake occurs,” says James Downing, CEO of St. Jude Children’s Research Hospital and the chair of Childhood Cancer Treatment. Sometimes these “random mistakes of nature,” as Downing calls them, can occur even before a baby is born. And while most adult cancers grow so slowly that they can be checked every year or so, childhood cancers proliferate with terrifying speed because of the tissues in which they develop. Gamis mentions that he has seen children’s tumors double in size every eight or 12 hours.

But biology can work in favor of treating the disease, too; because of kids’ fast metabolisms and general lack of other health issues, kids can tolerate a much higher dose of treatment. “Kids are far more resilient,” says Andrew Kung, the head of the Pediatric Hematology, Oncology, and Stem Cell Transplantation Division at New York Presbyterian Hospital. “If you come to our clinic, you see the kids running around, and you would not know that these are kids with cancer, except that they are bald. Whereas adults getting the same kinds of therapies would be laid up in bed.”

Over time, researchers have found that this biology makes kids’ cancers much more treatable, contributing to the 80 percent cure rate. But to be able to leverage these elements of biology, researchers first had to discover viable treatments.

Seeking Treatment

Progress in treating childhood cancers has been swift. In the 1950s and early 1960s, children diagnosed with cancer would invariably die in a few months. But in the late 1950s, doctors discovered that radiation could stop cancer cells from proliferating; a few years later, in the early 1960s, others discovered that multiple rounds of aggressive chemotherapy could stop the cancer from coming back later. “In a generation, childhood leukemias went from uniformly fatal to curable most of the time,” says Douglas Hawkins, associate division chief of pediatric hematology/oncology at Seattle Children’s Hospital.

Since those early days, pediatric oncologists have been fine-tuning these treatments and discovering new ones to help more kids survive, and to do so with the fewest long-term complications. “The cure for cancer didn’t happen once—it’s a continuum of learning,” Hawkins says. “Gradually, over the course of decades, we learned that we could give kids less and less radiation through clinical trials.”

From the start, pediatric oncologists created a unique culture of collaboration that exists in few other places in medicine. Childhood cancers are rare diseases, affecting around 16,000 children and adolescents per year but making up only 2 percent of all cancer cases. Over the past three decades, this collaboration has coalesced most clearly in clinical trials. About 60 percent of all kids with cancer participate in clinical trials, and have done so for decades. “Every child we treat is an opportunity for us to learn and in that way continually optimize our treatments,” Kung says. Unlike for adult patients, fewer than 5 percent of whom are enrolled in clinical trials, these are the norm for children. This allows researchers to collaborate across institutions and disciplines of medicine, all in the hope of finding better ways to treat and support kids.

Experimental clinical trials are the norm for children.

This disparity between the enrollment of adults and children exists in large part because children are more often treated in university cancer centers; because there are so many more of them, adults are usually treated at their local hospitals. Adult patients often don’t even know that clinical trials are an option or if they are eligible; clinicians present less of a united front against a specific aspect of a particular disease. “We can’t get anything done as pediatric oncologists unless we work together, pool our results and talk to each other,” says Crystal Mackall, the chief of pediatric oncology at the National Cancer Institute. “Over and over again, the principles that childhood cancer teaches us turn out to be fundamental. This ability to use cooperative groups to learn about rare diseases is an important insight, as adult doctors are coming to understand.”

As a result of the systematic testing and constant collaboration, many of the treatments found to work in kids have been extrapolated to adults. In a sense, all cancer patients have benefitted from pediatric oncologists’ decades of work.

Stuck Numbers

20 years ago, Kung was working in Boston when he started treating a young man named Keith who was diagnosed with a rare leukemia called acute promylocitic leukemia. It’s a very treatable form of the disease, Kung says, but just two years after treatment, the disease came back. This time, it would be much harder to treat. As Keith’s doctors were contemplating which intervention to try next—maybe chemo again, or the more aggressive and invasive bone marrow transplant—Kung heard about a new, experimental treatment based on traditional Chinese medicine. The active ingredient was arsenic, which can kill a person with just a quarter of a gram. “It was a situation where people thought we were crazy—including Keith,” Kung says, but after going over all the details, Keith was on board. The treatment worked, and Keith went into remission. 18 years later, Keith is a full-grown adult and a long-term survivor of the disease. “I’ve subsequently been to his graduations, his wedding, his divorce,” Kung says, and arsenic is now a standard treatment for some types of leukemia. “That’s an example of why [pediatric oncologists] do what we do—to be able to treat these young children and really be able to impact them, not just prolong their lives, but cure them and have them return to a normal life.”

Those of us outside the field of pediatric oncology often assume that spending your career treating kids with cancer would be incredibly depressing. “When I’m at a cocktail party I say I’m a pediatrician,” Hawkins says, because he’s found that introducing himself as a pediatric oncologist tends to be a conversation-stopper. “But it’s an amazingly collaborative community. It’s incredible that people get up and speak so freely—it’s striking how willing they are to share information.”

Despite the hundreds of dedicated, smart people working hard to improve treatments for childhood cancers and a cure rate that has risen in jumps and starts over time, progress has stalled for the last decade. Clinical trials are still collaborative across fields and institutions, but the number of them has shrunk. Because childhood cancers are rare and the cure rate is so high overall, funding has dried up. And though 90 percent of children with some forms of cancer can be cured, the cure rate is much lower for some other types, like neuroblastoma or osteosarcoma, and hasn’t risen in decades. “There are some diseases in which we’ve made no progress in 39 years, and no one thinks that’s OK,” Mackall says. “If we had more resources, we could do better.”

“Even though cancer is rare in kids, and even though we do very well overall, there’s still a tremendous need in terms of research and funding,” Kung says. “It’s not just about doing better for the 20 percent that we’re not curing—even for the patients we do cure, over half ultimately have some sort of long-term effect attributable to the disease itself or to the treatments we have to use.” In other words, the cutting edge in pediatric oncology is two-fold: Improving the treatments already in use, and finding new treatments to cure those patients that are still slipping through the cracks.

The Good And Bad Of Treatment

As a junior in college, Maggie went to Prague to study abroad. On the fifth day of her program, she was preparing to go on a tour of a historic castle with her new friends, when she discovered that she was peeing blood. “Because I had kidney cancer and I only had one kidney left, peeing blood is really bad. I hadn’t even told my roommates yet [that I had had cancer],” she says. She spent a few days alone in the hospital in Prague and when they couldn’t figure out what was going on, her insurance company flew her back to the U.S. The issue was with her ureter, the duct that used to connect her bladder to her kidney before it was removed, and though Maggie’s doctors are still not quite sure what was wrong with it, they’re fairly certain that the issue was a result of the cancer treatment she received as a child. “It’s a medical mystery that I’m sure is related to the treatment somehow. I don’t know why else it would happen.” Later, she would have the ureter removed.

That was just one of the health complications that have arisen for Maggie as she’s grown up; she’s had several incidences of basal cell carcinoma, a skin cancer, on her abdomen where she received radiation therapy as a kid. And when she was 22, Maggie found out she won’t be able to have children. “Sure, there are other options, and I always wanted to adopt, but just having my options stolen from me was completely devastating,” she says.

As more childhood cancer survivors reach adulthood—some estimates that between one half and 1 percent of all kids who reach age 20 will soon be cancer survivors, Kung says—clinicians are discovering the long-term effects of these toxic treatments. “[Pediatric oncology’s] dirty little secret, and one that’s of great concern among those of us in this field, is that a sizable percentage of those children who are cured of their cancer will have lifelong side effects of their therapy. And a third of these side effects will be life threatening,” Mackall says.

Some chemo drugs have been shown to affect the function of a patient’s heart or result in neurological effects like decreased IQ or attention span. Girls who received radiation therapy as kids have higher incidences of breast cancer as adults. And for some patients like Maggie, when they grow up and are ready to have children, they find that they are not able—exposure to such noxious chemicals and energies during such an important period in their development has rendered their bodies unable.

Clinicians have been working to limit treatments’ effects by finding the lowest possible dose of a drug or using as little radiation as possible. But there’s only so far they can get with the same old treatments. “That’s the Holy Grail: more effective, less toxic therapies,” Mackall says. “The belief is that these will result from a biological understanding of the cancer itself.”

In theory, that biological understanding will lead to new paradigms altogether—which will be necessary, since most pediatric oncologists think that curing that last 20 percent of patients is going to be more difficult since the easiest solutions have already been exhausted.

General oncologists can learn from pediatrics, but information can also flow the other way. Some treatments that use small molecules, which are very effective in adults, have proven less so in kids. But researchers have seen promising results with kinase inhibitors, molecules that block the signals that tell cancer cells to divide and cause less damage to healthy parts of the body. This treatment is already known to work well on adults, but it has not yet been thoroughly tested in kids, and it’s not yet clear if the drugs will be as effective.

Another promising treatment is immunotherapy, a treatment in which a patient’s own immune system attacks the cancer that would otherwise slip past it. So far researchers are seeing some amazing results in using immunotherapy to treat certain types of leukemia, raising the cure rate from 90 percent to 100 percent, Mackall says. “Time will tell, but based on what we’re seeing on patients, they seem to be able to respond to immunotherapy even when they’re not responding to chemotherapy. It adds something completely different to the [treatment] portfolio,” she adds—if it works for other types of childhood cancers, Hawkins adds.

But an exciting new therapy isn’t a reason to throw the others out the window, Gamis cautions. Many cancers are very treatable with traditional chemotherapy; for now, new experimental treatments are just another tool in clinicians’ cancer-fighting toolbox. “Over the years we’ve seen paradigms come and go. So we have to be cautious about putting all our eggs in one basket,” he says.

Other clinicians like Downing intend to bring the most effective treatments to other countries where the cure rate for pediatric cancers is nowhere near 80 percent. The best way, he says, is to encourage the kind of collaboration—between healthcare providers within the same country and beyond—that enabled doctors to cure more American kids decades ago.

There’s no doubt that children diagnosed with cancer today fare better than those in decades past. And as more childhood cancer survivors grow up and have productive lives, clinicians see how their past treatment affects them in ways that are less tangible than physical scars. “There is a certain spirit factor, that’s what I call it, that the patients receive because of what they went through,” Mackall says. “They tend to have a very clear understanding of what life is all about and what really matters. And many of them will say that their lives have been enriched as a result. I’m not implying that they haven’t suffered, but there can be a positive psychological side.”

Maggie is one of those spirited people—she’s a normal, happy woman in her mid-20s. And yet her experience fighting cancer has become a part of her. After concentrating on gerontology in college, Maggie went on to earn her masters in public health in epidemiology and now works for a nonprofit focusing on palliative care. She can’t remember what she wanted to do with her life before she had cancer, but she thinks her career choice was shaped by both her intellectual interests as well as her own trajectory.

When Maggie tells people for the first time that she had cancer as a kid, she doesn’t talk about the ongoing health issues that resulted from it. “I don’t think they want to hear about the awful parts—they want to hear you’re all good now,” she says. And she hates when people tell her she’s so brave or an inspiration for surviving cancer treatment—she prefers that people say, “That really sucks.” “It shows empathy more than it shows sympathy,” Maggie says. “And, really, that’s what we all want to hear.”

Cancer research and treatment has changed drastically within the past decade. In this series, “A Future Without Cancer,” Popular Science provides a context in which to understand the breathtaking pace of progress, to help you get a picture of the current state of the art of cancer treatment, diagnosis, and prevention, and where it’s likely to go next.

The post Learning from the Children appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Overall recommendations on when and if to use sunscreen seem to be clear: always protect yourself from the sun, especially if you have a lighter skin tone. But for people with abundant melanin who often hear phrases like “Black don’t crack” or “Black don’t burn,” guidance around whether or not to wear sunscreen can be confusing.

The common misconception that people of color don’t have to wear sunscreen comes from the fact that high amounts of melanin, by way of its ability to absorb light, offers some degree of sun protection factor (SPF). Public figures have helped this belief take root—actress Angela Bassett (long revered for her seemingly flawless skin) said Black people have “natural sunscreen,” which might lead readers to believe her good looks come just from having dark skin.

But this is not the case. As Dr. Nada Elbuluk, associate professor of clinical dermatology at the Keck School of Medicine at the University of Southern California, explains it, individuals with medium to dark skin can often have natural protection equivalent to roughly SPF 8-15.

“This baseline SPF is not enough to provide adequate sun protection, which is why individuals of color of all shades still need to practice wearing sunscreen on a regular basis,” she says. (Bassett seems to know this, since she’s said she takes good care of her complexion, avoids the sun, and wears sunscreen every day.)

“There is also a myth that people with darker skin tones should not wear sunscreen because of vitamin D deficiency,” says Dr. Chesahna Kindred, associate professor at Howard University department of dermatology in Washington, DC. Studies show high amounts of melanin in the skin can prevent ultraviolet light from reaching the deepest layers of skin that create vitamin D, but in Kindred’s opinion: “The best source of vitamin D is in foods.”

Should people with skin of color wear sunscreen to avoid skin cancer?

Another misconception is that skin cancer prevention is the main reason everyone, regardless of the color of their skin, should wear sunscreen. But the relationship between the sun and melanin can’t be wrapped up in one tidy box that fits all groups, and many dermatologists specializing in skin of color are encouraging a more nuanced relationship with sun protection.

Though there is a clear link between UVB radiation (a type of UV radiation given off by the sun) and skin cancer in people with fair skin, this relationship is not as clear-cut in people with skin of color.

Skin cancers in this group typically appear on areas of the body that don’t see much sun, so campaigns that advise people with darker skin to wear sunscreen as protection against skin cancer are misleading, Kindred says.

Unclear information regarding the conditions affecting skin of color doesn’t stop here though—multiple studies have shown that there is a significant lack of images for certain skin conditions as they manifest in people of color. This lack of representation can negatively affect clinicians’ and dermatology students’ ability to accurately diagnose patients with skin of color, as well as public health resources that allow people to spot and recognize potentially concerning skin conditions in themselves.

“The gross lack of awareness is the reason skin cancers are deadlier in patients with darker skin tones,” says Kindred.

Also, most skin cancers affecting people with skin of color aren’t caused by UV exposure, which, contrary to popular belief, means sunscreen will do little to protect them.

In Black people, for example, skin cancers caused by inflammatory conditions are much more common, says Dr. Jenna Lester, an assistant professor of clinical dermatology at the University of California, San Francisco, and director of their Skin of Color program. Conditions such as Hidradenitis suppurativa—which affects hair follicles in typically unexposed areas like under the arms or in the groin—or discoid lupus, an autoimmune disease, can also cause skin cancers, and present a higher risk for Black patients than cancers usually caused by sun exposure.

To add a challenge to an already problematic situation, the majority of funding for dermatology usually goes to researching skin cancers caused by sun exposure, so the study of other skin cancer-causing conditions has become a struggle.

“Although these aren’t allocated to any specific race, this does mean that there is limited funding for skin cancer research in skin of color,” Lester explains.

There’s still much for us to explore in the relationship between the sun and skin of color, but there are plenty of benefits to sun protection besides skin cancer prevention. Lester says she generally recommends sunscreen to her patients with a darker skin tone to treat uneven pigmentation, while Kindred advices hers to wear it for anti-aging.

How to find the right sunscreen for your skin

The general rules for choosing the right form of sun protection are roughly the same across all skin tones. The American Academy of Dermatology recommends sunscreen that is SPF 30 or higher, broad-spectrum, and water-resistant. Kindred says you should also look for sunscreens with added antioxidants, which have been shown to be more effective that sunscreen alone in minimizing UV damage.

But when it comes to finding the right sunscreen for you, it’s helpful to know how it works.

There are two main types of sunscreen: chemical and physical. Physical or mineral sunscreens have ingredients such as zinc oxide or titanium dioxide that sit atop the surface of the skin and physically block out and reflect UV rays. Because they act as an actual barrier, physical sunscreens are easier to wash off with sweat or water, but they offer protection as soon as you put them on. Another major downside of physical sunscreens is the white cast they tend to leave upon application. This is especially noticeable on the darkest ranges of skin tones, and some people find it undesirable.

On the other hand, chemical sunscreens contain active organic compounds (usually avobenzone, oxybenzone, octocrylene, and/or ecamsule) that are absorbed into the skin, where they convert UV rays to heat. A substantial benefit of chemical sunscreen is that since the compounds in them are smaller, they can be formulated to be thinner and easier to spread, making them more convenient for day-to-day use. However, the compounds in chemical sunscreens may cause allergic reactions, and oxybenzone has recently been banned in Hawaii after studies found that even very low concentrations can cause bleaching in corals.

Both types of sunscreen are okay and generally safe to use across skin tones. If you have skin of color and want to avoid the white cast of mineral sunscreens, chemical ones might be best for you. However, if you have sensitive skin and have noticed a reaction to chemical sunscreens in the past, some companies have made transparent physical sunscreens that won’t leave a ghostly white cast. Whatever you decide to go for, be sure to read some reviews, ask around, and see what looks best on your skin.

When and where should you wear sunscreen?

When it comes to protecting yourself from UV rays, where and when to use sunscreen applies pretty consistently regardless of how much melanin you’re rocking, but many of us still don’t know when sunscreen is necessary, and when it’s not.

No matter what your skin tone, Lester says sunscreen should be worn wherever you’re exposed to UV rays. But that may mean something different than what you think. Though you might assume you can skip sunscreen when it’s cloudy out, it’s best to wear it regardless of the weather. Though thick cloud cover can generally absorb some UV radiation, rays still make it through, and studies have shown that light to thin cloud cover may have an enhancing effect on UV levels, making it even worse than a clear blue sky. Though we don’t definitively know why this is, it might be because thin clouds act like a lens, scattering solar radiation more strongly towards the ground, rather than diffusely into the atmosphere.

It’s also important to keep in mind that you can be exposed to UV rays in places and ways you wouldn’t normally expect. Lester notes that wherever you are exposed to sun rays, you are exposed to UV rays. So if you’re indoors by a window, you’re still exposed and should use sun protection.

To make things a bit more complicated, the risk for UV damage is not limited to solar sources. “Research shows that direct blue light from our devices is enough to cause skin damage. We’ve seen how this visible light can also trigger conditions like melasma, which people with darker skin are already predisposed to,” Lester says.

Not to worry though—recent research has also shown that wearing sunscreen can help mitigate the effects of UV exposure on melasma, and other hyperpigmentation conditions that disproportionately affect people with skin of color. And when it comes to UV protection, Lester notes that sun-protective clothing is also a great option.

When thinking about sun protection, it’s best to play it safe, so Kindred recommends her patients wear sunscreen “indoors, outdoors, rain, shine, winter, and summer.” And in the wise words of Beyoncé, “your skin shines and tells your story,” so be sure to care for it regardless of how much melanin you’re blessed with.

The post A guide to sun protection for people with darker skin appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The wait is over for chemistry enthusiasts: today the 2015 Nobel Prize in Chemistry prize was awarded to a trio of researchers, Tomas Lindahl of the Francis Crick Institute, Paul Modrich of Duke University and Aziz Sancar of the University of North Carolina School of Medicine, Chapel Hill, for their mechanistic studies of of DNA repair.

Once thought of as an extremely stable structure, DNA is actually under constant attack. It can undergo literally thousands of spontaneous and causal alterations in the course of a single day — more if you count the defects that can occur during normal cell division.

To repair themselves, cells deploy an army of enzymes that break open DNA and snip out the damaged part. Then they bring in a repair crew consisting of other enzymes.

In addition to occurring in normal cells, that repair process occurs in cancer cells exposed to UV radiation or drugs. Understanding how these repair mechanisms work on a molecular level is vital for the development of more effective cancer drugs, ones that can beat cancerous cells at the repair game.

Sancar is the leader of a research team at UNC that created a repair map of the entire human genome, an achievement that will enable scientists to pinpoint the exact location where repairs have occurred when DNA is damaged by UV radiation or chemotherapy.

He received the news through the time honored tradition of an after-hours phone call. Awoken by his wife, he described the experience to Nobel Media:

“I just got a call half an hour ago, my wife took it and woke me up . I wasn’t expecting it, I was very surprised. I tried my best to be coherent…”

For Nobel watchers who keep score by country, the award to Sancar marks the first time a Turkish-born scientist has won a Nobel prize (novelist Orhan Pamuk received the country’s very first Nobel in 2006, for Literature).

“I am proud for my family, my native country and my adopted country,” said Sancar.

Modrich has been a Howard Hughes Medical Institute (HMMI) investigator at Duke since 1994, with a particular focus on understanding the pathway behind hereditary colon cancer, which is caused by a rare but devastating condition in which the mismatch repair mechanism of DNA is inactive.

In normal DNA replication, the correct pairs of genetic bases, or “letters,” are opposite each other. If one gets misplaced, a mutation could occur. Modrich’s work describes the delicate choreography that occurs when cells are alerted to the discrepancy and take action:

Lindahl is considered a “father figure” in the field of DNA repair for his work dating back to the 1970s, when he first demonstrated that DNA constantly decays and repairs itself, a process called base excision repair.

When he received the news, he was preparing to spend a quiet day in seclusion. “I was going to do some writing at home today but after this message it was decided that a driver will take me to the laboratory,” Lindahl said.

Lindahl feels that the Nobel Prize will help people understand the importance of DNA repair mechanism research. According to Lindahl, by preventing cancer cells from repairing themselves, researchers can develop treatment regimens that enable people to manage their cancer as a chronic condition, similar to the way in which people can live with diabetes.

“It is a very hot topic, not only for cancer but for many diseases, “ he said. “We are getting away from finding a cure, and converting it to something we can live with.”

The post Nobel Prize In Chemistry Goes To 3 Scientists Who Uncovered DNA Repair appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

The hairy palms don’t sound so bad, and the blindness seems manageable. But cancer! It’s bad news for both Don Juans and subscribers to Swank Magazine, as a new paper in the British Journal of Urology International (BJU) reports a statistically significant correlation between the frequency of sex and masturbation to the early onset of prostate cancer.

But doctors disagree over the link between sexual activity and prostate cancer. While a 2002 paper in the journal Epidemiology backs the BJU study, a 2004 study in the Journal of the American Medical Association (JAMA) and a 2003 paper from the Australian Cancer Council Victoria claim that frequent masturbation and intercourse actually decreases the risk of prostate cancer.

The BJU study, conducted by a team from the University of Nottingham in England, looked at one group of 431 men who had been diagnosed with prostate cancer before the age of 60, and 409 men who did not have the disease. Of the 431 men with cancer, 40 percent of the men reported masturbating or engaging in sexual activity more than 20 times a month during their 20’s. Additionally, the cancer group also had a larger percentage of men who reported having more than six female partners in their life. And the men in the cancer group were also more likely to report having once had a sexually transmitted disease.

However, in the JAMA paper from five years ago, men who reported ejaculating more than 20 times a month showed a 33 percent lower lifetime risk for prostate cancer than men who reported only ejaculating between four and seven times a month. In contrast to the BJU study, which only looked at heterosexual sex and masturbation in 840 men, the JAMA study looked at all ejaculation for 29,342 men.

Similarly, the Australian study compared 1,079 prostate cancer patients and 1,259 healthy men, and found that the men who ejaculated at least once a day during their 20’s were a third less likely to develop prostate cancer.

With evidence on both sides of the debate, doctors seem to be hedging their bets. Michael Leitzmann, a doctor at the National Cancer Institute and the lead author of the JAMA study told Reuters that he didn’t believe his study should lead to men altering their sexual behavior, a position reiterated by the Mayo Clinic.

Since the jury’s still out on the effects of ejaculation on cancer risk, it might be premature to either hoard Viagra or to cancel the Playboy subscription. Of course, all you reading this online should still probably get at least your eyesight checked out. After all, we know what you really use the Internet for.

The post Drop that Sock! Masturbation May Cause Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Virtual reality headsets are not yet commonplace, but they already have the potential to revolutionize many aspects of our lives—how we view entertainment like movies and video games, how we see the world, and even how we do science.

Now researchers at Weill Cornell Medicine in New York City have started using the technology to better understand the genetic mutations that drive cancer. They’ve developed a new program for the Oculus Rift VR headset that lets users see and interact with 3D models of microscopic proteins. Called “IPM VR,” short for Institute of Precision Medicine VR, the program aims to make it easier for researchers to pinpoint where and how a person’s DNA has mutated to cause cancer. Their goal is to help doctors all over the country better understand the mutations in order to quickly find the best treatment to stop the disease.

A couple of us here at Popular Science recently got the opportunity to test IPM VR ourselves, as well as to learn more about the program from the researchers who developed it. Here’s what we discovered.

Why do we need to pay attention to proteins?

In order to understand the value of IPM VR in fighting cancer, you first need to know about how cancer is formed in the body. It all goes back to DNA, the blueprint by which your body, and the body of every living creature on Earth, manufactures proteins.

Everyone has some mutations in their DNA. Some are inherited, others are acquired from environmental factors such as smoking or sun, and others simply happen spontaneously new cells form. Most of these are benign, but the wrong combination of mutations can sometimes cause cells in a particular organ or area to grow out of control, which can eventually inhibit the normal functioning of the body. That runaway growth process is cancer, in all of its various forms.

Tumors usually contain about a thousand genetic mutations, but only a handful drive the cancer to grow and move throughout the body. Figuring out which mutations are the drivers of a particular cancer can be the genetic equivalent of a needle in a haystack. But if doctors can do it, they can target only those cells with that particular mutation, allowing healthy cells to continue to function — a better outcome for the patient overall. That’s the field of precision medicine.

It’s only by looking at proteins — the body’s molecular building blocks created from the genetic instructions in our DNA — that a genetic mutation becomes evident, says Olivier Elemento, a specialist in precision medicine at the Meyer Cancer Center at Weill Cornell. “A mutation at the DNA level does nothing—it’s only when the gene is transcribed and made into a protein that the mutation expresses itself, and the function of a mutation becomes important,” he says.

Proteins are three-dimensional structures, but they’re often depicted flat on paper. If clinicians don’t see the proteins in 3D, they can’t fully understand the role of the mutations, Elemento says. When clinicians are trying to determine if a new mutation could be driving cancer, they check to see if it’s close to a hotspot, a concentration of genetic mutations that indicates that the error is common in other patients with the same type of cancer.

“In a one-dimensional representation of a protein, if a mutation falls in a hotspot, it’s a no brainer—it’s important,” Elemento says. But because proteins fold, a mutation that might seem far away in a 2D representation could actually be positioned very close to a hotspot in the three-dimensional protein.

That might sound like a small difference, but the significance for the patient could be huge: It shows the clinicians that the mutation might be driving the cancer, and that knowledge might help them select a drug that could target it. It’s not an exaggeration to say that this information could make the difference between life and death for a patient.

Using virtual reality to look for cancer-causing mutations

Scientists at Cornell used an early developer version of the Oculus Rift VR headset and gaming software to develop IPM VR, giving researchers and clinicians an immersive way to explore a patient’s unique genetic mutations.

The Oculus Rift VR headset is equipped with a motion sensor that detects what direction you’re looking. IPM VR also relies on the presence of a few external cameras not included with the headset, which further track the motion of your body and hands.

After researchers sequence all the genes in a patient’s tumor, the software projects all of the mutations onto a particular protein, the shape of which the researchers downloaded from the protein data bank, a digital archive of 3D protein shapes.

The clinician wearing the headset can change the view to see only the mutation hotspot or only the mutation in question, navigating through the simulated protein with hand and arm gestures. For more information, the clinician can pull up two-dimensional “documents” pertaining to the patient—the report about the type of cancer, or the patient’s medical history from the electronic medical record.

In my brief time using it, it was a truly impressive piece of software to operate. It was my first time using an Oculus VR headset and I flailed clumsily to move through the protein, while my more VR experienced colleague Dave Gershgorn got his sea legs much quicker. He navigated to the mutation hotspots with ease. You can watch our experiences in the video at the bottom of this article.

If my ineptitude is any indication, it will take clinicians a little while to get used to IPM VR and the Oculus Rift headset more broadly. The researchers behind the software are still tweaking some of these features to see what best fits clinicians’ needs, says Alexandros Sigaras, a research associate in computational biomedicine at Weill Cornell Medicine. And though many researchers around the country are working on different aspects of precision medicine, Sigaras and Elemento believe that theirs is the only one integrating patient information into virtual reality.

How VR could become a game-changer for medical treatment

Right now this tool is primarily for research, Sigaras says, but the Cornell team is hoping that it will soon make its way to clinicians all over the country. “The idea of using Oculus is not to replace every computer—it’s to enhance information that would otherwise be very hard to get,” Sigaras says.

He’s aiming to make the complex information about genetic mutations and protein shapes instantly intuitive to clinicians, who wouldn’t have to learn to use another piece of software on their computers. Plus, clinicians would be able to collaborate more seamlessly—using their own headsets, specialists in different disciplines could see the same information to discuss a particular case.

Ideally, Sigaras would like the software to contain all of a patient’s information so that clinicians can analyze it without the distractions and technical requirements offered by a computer. That’s especially important for precision medicine, where the immense amount of genetic and health data can easily overwhelm doctors looking for the best way to treat a patient.

Of course, most doctors don’t yet have virtual reality headsets. But Sigaras, Elemento, and their team strongly believe that the platforms will soon be commonplace. “These Oculus devices are going to democratize themselves very quickly,” Elemento says.

Even at $599 for the recently announced Oculus Rift consumer edition, plus the separate high-powered graphics PC needed to run them, the setup isn’t very expensive compared to other medical equipment, he says. He and others believe that price is sure to drop, too, as more competitors enter the field of VR (though HTC’s upcoming Vive Pre VR headset is actually slightly more expensive at $699).

“I think that in maybe five years, maybe 10, every clinician will have one of these,” Elemento adds. He hopes that his team’s software will be among the first pioneers to make virtual reality attractive to doctors.

To get there, though, the precision medicine software needs to provide a clear advantage to clinicians, Sigaras says. They’re still figuring out just what kinds of information doctors would want to see in virtual reality, and what they prefer to see on a computer or even in hard copy.

The Oculus Rift VR headset is merely a means to an end to this team, which seems to be somewhat platform-agnostic. Sigaras has tested similar software on other virtual and augmented reality platforms including Google Glass, and even smartphone-powered VR headsets like Google Cardboard. He’s also trying to get a Microsoft HoloLens to try his software in augmented reality, too.

In the end, Sigaras and Elemento care most about getting more information to clinicians more quickly and intuitively. “The real question is: How do you make your clinician more productive?” Sigaras says. “We want to enable clinicians to go through an immense amount information at a faster pace.” More often than not, fighting cancer is a race against time, he adds, and if a virtual reality tool can give doctors an advantage in finding the right treatment more quickly, patients will reap the benefits.

The post Here’s How Virtual Reality Could Help Doctors Treat Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Researchers in the UK have found that the shape of a man’s urine stream can be analyzed for specific patterns that can be used to predict the maximum flow rate, a value that in turn can be used to diagnose developing urinary problems–including those associated with the prostate. This shape is caused by the surface tension in the urine and the urethra’s elliptical shape, the researchers say, and in their tests men were able to self-evaluate their arcs to determine whether their flow rates were indicative of some kind of urinary problem. Considering the majority of men in their 60s and 70s tend to experience some kind of urinary symptom that may be caused by an enlarged prostate, a non-invasive, self-evaluation could go a long way toward catching potentially life-threatening prostate problems early.

Queen Mary, University of London

The post The Shape Of A Man’s Urine Stream Can Diagnose Prostate Problems appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

It’s notoriously difficult to direct cancer drugs to only the cells you want to target—they often kill many healthy cells in the process, making the patient feel sicker, or the body attacks them assuming that they are invaders. For the past few years, researchers have been devising new ways to disguise drug molecules so that they will reach cancerous cells more efficiently. Now a team of researchers from the University of North Carolina, Chapel Hill may have found the best cloaking mechanism yet, masking drugs as blood cells, according to a study published yesterday in the journal Advanced Materials.

Platelets, a type of blood cell, are a good disguise for drugs because blood cells naturally stick to cancer cells, so the drugs can go directly to tumors or destroy cancer cells in the blood stream before they colonize new organs. Plus, since the platelets are derived from the patient’s own body, the immune system doesn’t immediately try to destroy them, allowing the drugs to stay in the system for longer, the study authors tell Science Beta.

A schematic of the cancer-fighting drug coated in platelet membrane

In this study, the researchers tested their method on 231 mice with tumors. They first separated the platelets from the blood drawn from each mouse, then removed the platelet membranes and combined them with two cancer-fighting drugs. The result was a sphere with a drug on the inside, surrounded by the platelet membrane. The researchers then injected the spheres into the mice’s bloodstream. They found that the particles stayed in the bloodstream for 30 hours, 24 hours longer than the particles not coated with platelet membranes, and that the coated molecules killed cancer cells and stopped tumor growth much more effectively.

Since this is a study in mice, this technology isn’t yet ready to be used in humans. And while it makes sense that blood cells would be a good disguise for drugs because of blood’s relationship with tumor cells, it’s unclear if the platelet membranes work better than similar efforts to camouflage drugs as innocuous viruses or bacteria. The researchers plan to answer some of these questions in future studies. They also anticipate that this method could be used to send other types of drugs to targeted places in the body to heal leaky veins or combat conditions like heart disease.

The post Drugs Disguised As Blood Cells Could Kill Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Your body has an excellent defense system for keeping toxins out of the brain: the blood-brain barrier. But this border patrol also keeps drugs out, which presents a real problem for treating tumors and other maladies.

In November, a team from Sunnybrook Health Sciences Centre in Toronto hacked the system by creating temporary new entrances. Doctors injected microscopic air bubbles into a cancer patient’s bloodstream, and then focused sound waves onto blood vessels near the growth. This caused the bubbles to vibrate violently, poking holes in the barrier just big enough for a chemotherapy drug to pass through. These holes closed back up hours later.

This method could also enable targeted drug treatments for diseases such as Alzheimer’s or Parkinson’s. “It opens up a whole world of possibilities,” says neurosurgeon Todd Mainprize, the team’s lead researcher. “We could treat things we couldn’t treat before.”

This article was originally published in the March/April 2016 issue of Popular Science.

The post A Trojan Horse In The War On Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.

Shawn Douglas grew up building R/C cars and planes, using skills he picked up from his repairman father. Two decades later, he’s still assembling machines—only they’re now a billionth the size, made from DNA, and designed to destroy cancer cells.

Other labs have worked with DNA to build distinct shapes—a process colloquially known as DNA origami—but most have produced nonfunctional objects. At the University of California at San Francisco, Douglas folds his to have a mission. “He is the first to have realized the dream of a truly programmable container for delivering therapies to cells in a targeted way,” says Paul Rothemund, a biochemical engineer at Caltech.

Shawn Douglas
Age 31
University of California at San FranciscoDouglas’s nanomachine looks like a clamshell, its halves clasped together by two sets of entwined double-stranded DNA and its interior filled with antibodies or drug molecules. When the DNA binds to proteins on target cells, such as cancer, the two double strands unzip and the clamshell swings open to unleash its cargo. Such targeted drug treatment would require lower doses of disease-killing chemicals—and thus produce fewer unpleasant side effects.

Douglas hopes nanotechnology will attract new generations of tinkerers. “I want to get college students to come with new ideas and do all sorts of exciting stuff,” he says. Last year, he launched BioMod, a competition in which students build their own nanomachines. So far 25 teams have already signed up.

Editors Note: Shawn Douglas did his pioneering work in DNA nanomachines while at the Wyss Institute for Biologically Inspired Engineering at Harvard University. Additionally, BioMod, the competition Douglas started, is still managed by the Wyss Institute. He has since moved to University of California at San Francisco.

Click here to see more from our 11th annual celebration of young researchers whose innovations will change the world

The post Brilliant 10: Shawn Douglas Programs DNA Nanorobots To Kill Cancer appeared first on Popular Science.

Articles may contain affiliate links which enable us to share in the revenue of any purchases made.