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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.

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Although the World Health Organization only recently declared the end of the mpox global emergency, the virus is not gone. Chicago health authorities, for one, have identified up to 31 cases of the disease formerly known as monkeypox since the beginning of April, and the Centers for Disease Control and Prevention is raising awareness ahead of the summer. 

A full schedule of two doses of the Jynneos vaccine can be up to 89 percent effective, but the CDC urges high-risk communities to take extra precautions to avoid a health crisis like we had last summer. Understanding how the virus spreads and how to prevent infection is key to complementing the protection provided by vaccines.

It’s worth noting that mpox seldom requires hospitalization and is rarely lethal: The US reported 30,235 confirmed cases between May 2022 and March 2023, with 38 deaths, the majority of both among Black people. Last year, access to treatment was limited, but there’s no reason to believe that will be the case this year, especially in major cities, as the health system is currently better equipped to respond to new mpox surges. But prevention is still crucial as the skin lesions that are one of the most common symptoms of the virus can be extremely painful without proper medication. 

Matching last year’s domestic and international trends, the recent small surge in Chicago has mainly been concentrated within the community of gay, bisexual, and queer men who have sex with other men (GBMSM, in short), and their sexual network. Whether you identify as such or are currently at low risk of contracting the virus, you should know how mpox spreads and how to stay safe.  

“​​Let’s say you touch a lesion and the virus gets on your hand. Unless you have a break in the skin, you should be ok,” says Scott Roberts, assistant professor of infection prevention at Yale University’s School of Medicine. The problem is that we tend to touch our mouths, eyes, and faces throughout the day, which means you can infect yourself with viruses lingering on your digits, he explains. 

“The reason that we’re seeing the spread through sexual contact is not that it’s a sexually transmitted infection, but rather the close, prolonged contact in an intimate encounter, where you’re touching parts of the skin, kissing, sharing bodily fluids,” Roberts says. “All of that is a good scenario for a virus to spread.”

Several studies have found traces of the mpox virus in semen, but only one of them, published by Italian researchers in The Lancet Infectious Diseases, showed the virus in the sample could replicate and actually infect another person. Unfortunately, there still isn’t enough evidence either way, so we still don’t know if mpox can spread directly through the exchange of semen, feces, or vaginal fluids.

Keep in mind that skin-to-skin contact doesn’t mean you’ll get infected by shaking hands with someone who has mpox—you’d need a high viral load for that to happen. 

“It definitely requires a much longer time of close and prolonged contact if you don’t touch somebody’s lesions,” says Roberts.

But mpox is not airborne, and it doesn’t behave like COVID-19, where microscopic droplets can infect you if enough of them get into your nose and mouth. Researchers including those who worked on the Lancet study have said that the viral load in a mpox patient’s airways is nowhere near as high as the one from lesion secretions. That means transmission from respiratory fluids may be possible, but a lot less likely.

How to prevent mpox

As mentioned above, because the current and 2022 outbreaks have been mostly contained within the GBMSM community, authorities have given its members priority access to vaccines and treatment options. But even with that and greater availability of inoculations compared to last year, the CDC says only one in four people eligible to get the Jynneos shots actually have received them. 

It’s because of this low vaccination rate, aggravated by the fact that vaccines are not 100 percent effective, that even if you’ve received your two doses, you should still strive to reduce your own risk of contracting mpox as much as possible.

You should also keep in mind that there are a lot of ways to have sex, and some don’t require touching or even being in the same room with your partner. Take this as an opportunity to be creative and explore these options as sexual alternatives.

Anonymity is another problem. We know the thrill of having sex with strangers is, well, the “strangers” part. But it’s better to stay in the know when it comes to stopping the spread of a virus. Anonymous sex rarely gives people the chance to have honest conversations about their levels of mpox exposure, potential symptoms, and vaccination status. Talking to someone before tearing off their clothes will allow everyone involved to stay safer, make informed decisions, and clearly establish how much risk you’re comfortable with. 

And since you’re already having a conversation, don’t forget to exchange real names and contact information with potential partners. These include people you kiss, have penetrative sex with, and do everything in between. This will make it easier to get in touch if you end up with mpox symptoms in the future. 

And if you don’t trust yourself to break the spell of anonymity, try to avoid contexts where anonymous sex is most likely to happen, like sex clubs, sex parties, and any other contexts where on-site casual sex is common.

“Mpox is actually a pretty easy virus to kill,” Roberts says. “Alcohol wipes, soap and water, disinfectant, all of that really easily kills the virus.”

In general, you should regularly disinfect surfaces like kitchen counters, door knobs, and light switches, the CDC says. You should also wash your hands frequently with an alcohol-based sanitizer, or soap and water. If you’re not sure whether your cleaning products will do the trick, the Environmental Protection Agency has a list of approved disinfectants. 

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But before you start, there are a few things you should keep in mind before you craft homemade hand sanitizer. First, it’s crucial that you understand that proper hand washing will always be better than simply rubbing your digits with hand sanitizer. Using the right amount of alcohol-based disinfectant (3 milliliters) for 25 to 30 seconds is fine in a pinch, but soap, water, and a good scrub are the absolute best way to protect yourself against contagious diseases.

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Knowing how to make hand sanitizer is useful if you ever find yourself in the middle of a health emergency like the COVID-19 pandemic. But these and other DIY recipes are only for extreme cases when hand washing is not an option and supplies are low. Professionals use these formulations in underserviced healthcare settings, and if at some point hand sanitizer is not available at local stores, you can use them too.

Lastly, your homemade hand sanitizer won’t last forever. The main active ingredient in the recipes below is isopropyl alcohol, a volatile compound that will evaporate over time and compromise the effectiveness of your hand sanitizer. When alcohol concentration drops below 60%, your hand sanitizer won’t be able to kill COVID-19 or influenza, for example. The shelf life of store-bought hand sanitizers can vary—the industry standard is three years, but it can go up to five. How long your DIY hand sanitizer lasts will depend on the type and size of the container you use and how often you open it, along with room temperature and humidity. Unfortunately, all of these factors make it hard to predict exactly how long your hand sanitizer will be good for, so proceed with caution. 

The WHO has a comprehensive guide on how to make hand sanitizer—the only problem is that if you follow their instructions, you’ll end up with a lot of it. Like, exactly 2.6 gallons of it. If you want to make enough to last you, your family, and all your friends through a zombie apocalypse, you definitely can. But if you want to keep things on a smaller scale, we’ve adapted the measurements for you.

5. Sanitize your spray bottles and pour in your hand sanitizer. Spray some of your leftover alcohol into your bottles and let them sit until the alcohol has evaporated. Then pour in your sanitizer.

6. Label your bottles. Hand sanitizers pose a real risk of involuntary alcohol poisoning, especially among children, who were largely affected by it during the first months of the COVID-19 pandemic. You don’t want anyone to accidentally ingest your newly made hand sanitizer. Take the time to label your bottles with their contents and the date, and keep them away from unsupervised kids.

6. Label your containers. Hand sanitizers pose a real risk of involuntary alcohol poisoning, especially among children, who were largely affected by it during the first months of the COVID-19 pandemic. You don’t want anyone to accidentally ingest your newly made hand sanitizer. Take the time to label your bottles with their contents and the date, and keep them away from unsupervised kids.

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Over the first two years of the COVID-19 pandemic, the coronavirus directly or indirectly killed about 15 million people worldwide, according to estimates from the World Health Organization. In the United States, more people died in 2020 and 2021 than during the 1918 influenza pandemic, which was widely called the most deadly in recorded history. 

The word “deadly” certainly applies to the virus that causes COVID-19. And yet, epidemiologists hesitate to give SARS-CoV-2 the superlative of deadliest virus in human history. To them, the raw number of mortalities caused by a given virus doesn’t always paint the full picture of a pathogen’s danger—especially when comparing viral outbreaks across time.

Raw mortality numbers have to be taken in the context of the world’s total population, says Jennifer Nuzzo, professor of epidemiology and director of the Pandemic Center at Brown University School of Public Health. “A lot of people talk about how COVID deaths eclipsed what we saw in 1918,” she says. “It’s really important to remember that the population of 1918 was a fraction of what it is today.” In that context, the flu of 1918 rises back up in the ranks in terms of deadliness.

Using the “case fatality rate” metric to determine what virus is the deadliest, rabies would likely come out on top. That’s because, if an infection becomes symptomatic, rabies is fatal to humans in more than 99 percent of cases. Globally, approximately 59,000 people die from rabies every year. Very few of those deaths—an average of two in the US—occur in the developed world because of rabies vaccines for household pets and swift medical interventions after bites.

But “a virus doesn’t have to have a very high case fatality ratio to cause a tremendous amount of death and disruption,” Nuzzo says. “It’s more about looking at the environments in which the viruses are spreading, and our social and human vulnerabilities to it.” 

A virus with a lower case fatality rate can kill more people if it’s highly transmissible, with a long period of time before severe or obvious symptoms set in. This allows an infected person to expose many others. That’s why SARS-CoV-2 caused such a rapid and devastating outbreak around the globe. It’s easily transmitted via airborne droplets, and doesn’t always or immediately cause severe illness. 

[Related: Can viruses be good for us?]

Globalization sped it along, too. “When a virus spreads at the pace of a human being walking, that’s very different than when you can hop on an airplane and be anywhere in the world in 36 hours,” Nuzzo says. 

During large outbreaks such as epidemics or pandemics, epidemiologists look at another metric, called excess deaths: how many more people died during a period of time than typically do over that same window. Excess deaths can account for other indirect ways that a virus causes death, Nuzzo says, such as patients who need critical care but can’t get it in overburdened hospitals.

Here’s how some of the most devastating viruses in human history tell different stories of how high a death toll can rise:

Influenza

The 1918 influenza pandemic still far and away ranks as the deadliest global outbreak of the 20th century. Thought to be caused by an H1N1 virus, it spread globally in 1918 and 1919. An estimated 500 million people were infected (approximately a third of the global population) and 50 million people died worldwide, about 675,000 of whom were in the United States, according to the Centers for Disease Control and Prevention. 

Without sophisticated testing and tracking, death toll estimates rely heavily on excess death calculations. Some suggest the true toll was closer to 17 million, while others set it much higher at 100 million. William Schaffner, professor of preventive medicine and professor of medicine in the division of infectious diseases at the Vanderbilt University School of Medicine, cautions against over-interpreting comparisons between the historic flu data and modern viral outbreaks.

[Related: Can you get diseases from bad bathroom smells?]

 “We are determining cases and even counting deaths with much more precision now than we did then,” he says. At the time, there were also no flu vaccines and no antibiotics to treat secondary bacterial infections, which likely drove the excess death toll higher.

Today, the youngest and oldest people are most likely to die from influenza. But during the pandemic over 100 years ago, Schaffner says, deaths bore a different signature: mortality peaked among young and middle-aged adults, too. Why that happened is still unclear, he says, but it contributed to the historic toll of that pandemic.

Influenza continues to hold its place as one of the deadliest viruses, despite the availability of vaccines. Variants of the influenza virus have led to other pandemic-level events, such as the 2009 outbreak colloquially called the swine flu pandemic. But the virus is also endemic in our society, and infects an estimated 1 billion people globally every year, according to the World Health Organization. Of those cases, the WHO reported in 2019, somewhere between 290,000 to 650,000 result directly or indirectly in deaths. 

An estimated 40.1 million people have died from AIDS-related illnesses since the start of the epidemic, according to the Joint United Nations Program on HIV and AIDS. That is nearly half of the number of people estimated to have become infected with HIV since the start of the epidemic, at an estimated 84.2 million. 

The case fatality rate of HIV/AIDS was historically quite high. Some estimates put it around 80 percent without treatment. But much has changed since the 1980s. Today, there are ways to manage HIV and mitigate the immunodeficiencies associated with an infection, and most patients are diagnosed sooner after an infection. In the United States, the rate of HIV-related deaths fell by nearly half from 2010 to 2017, according to the CDC. 

That excess deaths metric likely reached a much higher number by the time officials declared the public health emergency over in early May. The Omicron wave that swept around the globe in late 2021 and early 2022 saw one of the largest surges in cases of COVID-19 and, although the variant didn’t seem to be more deadly than previous variants, with millions of people infected, a high death toll in the hundreds of thousands was inevitable. 

Early in the pandemic, the case fatality rates calculated for SARS-Cov-2 varied considerably. Many estimates were likely higher than the true number, as researchers scrambled to devise tests for the virus and milder cases slipped through the cracks. In early 2020, estimates of the case fatality rate by country ranged as high as 25 percent or more. Since then, case fatality rates have dropped, and now, according to Johns Hopkins University, they are as high as 4.9 percent. In the US, the case fatality rate is 1.1 percent. 

Mortalities continued to stack up into the 20th century, with an average of three out of every 10 people infected dying. The disease, which is caused by variola virus, is estimated to have killed more than 300 million people from 1900, until a global vaccination campaign halted its path of devastation in 1977. It was the first disease ever to be eradicated. 

[Related: The first honeybee vaccine could protect the entire hive, starting with the queen]

But it was the very thing that made it particularly fearsome that was its downfall, Schaffner says. “It created such a distinctive rash that people could identify it and fear it. And that was one of its Achilles heels,” he says. Because it was so easily identifiable, and spread so slowly, vaccinating the local population near an outbreak swiftly curtailed transmission. Such an approach, he says, was part of the vaccination strategy that eradicated the great pestilence. 

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A phase 3 trial found that a new meningococcal disease vaccine is safe and effective and also induces a strong immune response across five strains of meningococcal bacteria. The results were published May 24 in the New England Journal of Medicine. The vaccine could be a useful tool in eliminating meningitis in African countries including parts of Senegal, Mali, and Ethiopia.

[Related: A once-forgotten antibiotic could be a new weapon against drug-resistant infections.]

Meningococcal disease is a cause of meningitis and blood poisoning. According to the World Health Organization, meningitis caused an estimated 25,000 deaths in 2019. While vaccines are readily available in wealthier countries, vaccinating the more vulnerable regions has been a challenge, largely due to cost. Developing affordable vaccines that provide broad coverage against meningococcal disease strains is a key part of the World Health Organization’s Defeating Meningitis by 2030 Global Roadmap.

The trial compared the immune response generated by a new pentavalent, or 5-in-1, vaccine  called NmCV-5 against that of the licensed quadrivalent, or 4-in-1, MenACWY-D vaccine. The participants included 1,800 healthy two to 29-year-olds in Mali and The Gambia in western Africa. The vaccinations occurred in June 2021, and the trial didn’t find any safety concerns with NmCV-5. 

After 28 days, the immune responses generated by one dose of NmCV-5 were generally higher than those generated by the 4-in-1 vaccine across all age groups. The 5-in-1 vaccine also induced a strong immune response across meningococcal bacteria strains A, C, W, and Y and the emerging X strain. Currently, there is no licensed vaccine against the X strain, which may be the cause of meningitis epidemics in sub-Saharan Africa.

“Meningitis is a deadly disease with the ability to spread like wildfire in the event of an outbreak, this affects all ages most especially within the meningitis belt region,” study co-author Ama Umesi said in a statement. Umesi is a clinical trial coordinator and clinician from the Medical Research Council’s Unit The Gambia at the London School of Hygiene & Tropical Medicine. 

“Epidemic preparedness is the way forward in providing available, affordable and accessible vaccines relevant to regions prone to meningitis outbreaks. Having meningitis vaccines should be a public health priority to prevent catastrophic outcomes during an outbreak and would be a game changer in the fight against meningitis,” Umensi said.

Issues with supply and affordability have limited the use of 4-in-1 meningococcal vaccines across a portion of sub-Saharan Africa called the meningitis belt. This region is at high-risk of epidemics of both meningococcal and pneumococcal meningitis. The NmCV-5 vaccine was developed by the Serum Institute of India and PATH, the global division of the Bill & Melinda Gates foundation. It follows the successful Meningitis Vaccine Project that developed an effective meningococcal A vaccine called MenAfriVac.

[Related: Ghana is the first country to approve Oxford’s malaria vaccine.]

According to the study, the new NmCV-5 vaccine can be made available at lower cost than existing 4-in-1 vaccines with more cost-effective production methods. The trial was designed to provide the World Health Organization with the evidence it needs to license the new vaccine for future epidemic control.

“As a researcher in the continent, I am hopeful that relevant vaccines for the common strains within the meningitis belt region will be readily available for timely interventions due to the collaboration and teamwork of multicentre trials like ours,” Umesi said. “Together we can defeat meningitis,” Umesi said. 

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This article originally published on The Conversation.

Intestinal infections take a heavy toll on impoverished Black communities that have out-of-date sewage systems. These infections often spread through contaminated soil and water and are among the most common diseases worldwide.

Approximately one-quarter of the global population is infected with soil-transmitted helminths, intestinal parasitic worms that can cause serious health problems.

Additionally, up to 50% of people around the world are infected with Helicobacter pylori, bacteria that live in the stomach and can cause ulcers and cancer.

I am a biological anthropologist, and it is clear to me that these two types of infections contribute to systemic health inequities, especially among communities of color in which limited access to medical care and inadequate sanitation systems may both increase exposure to pathogens and lead to worse outcomes.

Historically, intestinal infections have been prevalent in parts of the U.S. where high poverty rates and environmental factors – such as flooding and warm, humid summers – favor infection spread.

Although many Americans believe these diseases now exist only in lower-income countries, research that my colleague and I have conducted challenges this assumption.

Renewed interest in US intestinal infections

Launched in 2019, the Rural Embodiment and Community Health Study started with the goal of measuring current infection rates and determining which living conditions contribute to infection risk.

Though national infection rates remain unclear because of the absence of large-scale studies, our preliminary work in 2019 found that 38% of children sampled in a predominantly Black Mississippi Delta community had intestinal parasitic infections.

Moreover, 80% of those children exhibited high levels of intestinal inflammation. Those levels are much higher than those observed in other populations and may lead to several poor health outcomes, including impaired intestinal ability to absorb nutrients and stunted growth.

Our more recent analyses from 2022 focused on adults living in the Mississippi Delta and Southwestern Illinois, two areas that experience regular flooding.

Among those adults, 73% displayed elevated intestinal inflammation, while 45% were infected with H. pylori, the bacteria that can cause ulcers and cancer.

Taken together, those results demonstrate widespread intestinal infections and inflammation at all ages in these low-income, mostly Black communities.

Long-lasting intestinal infections and associated inflammation can lead to nutritional deficiencies, restricted growth, reduced educational attainment, decreased work productivity and increased risk for serious diseases later in life, including certain cancers).

A legal challenge in Alabama

The Rural Embodiment and Community Health Study is not alone in recognizing the impact of intestinal infections on Black communities. One of the most widely publicized recent research studies investigating intestinal infections focused on the health effects of poverty and crumbling sanitation infrastructure in Lowndes County, Alabama, a region characterized by a history of racial segregation and inequity.

Researchers found that more than 1 in 3 people tested in Lowndes County were infected with hookworm, an intestinal worm spread through sewage exposure that lives in soil and infects people by burrowing into bare feet.

This 2017 study has since led to legal action.

In a landmark May 2023 court ruling, the Biden administration found that Alabama’s public health department had discriminated against Black residents by denying access to adequate sanitation systems and imposed fines for resulting sewage issues.

This decision is being hailed by environmental justice advocates as a transformative environmental justice agreement that may increase public awareness of the ongoing health crisis that results from infrastructure neglect and associated pathogen exposure.

Community activists – such as Catherine Coleman Flowers, founder of the Center for Rural Enterprise and Environmental Justice – said they hope the federal government continues to intervene, leading to similar results in other affected communities.

“This country’s neglect of wastewater infrastructure in majority Black communities, both urban and rural, is resulting in a hygienic hell for far too many people, a hell that climate change is only making worse,” Flowers said in a March 2023 interview.

Why are there still parasites in the US?

The story of parasite infection in the U.S. is two-sided.

On one hand, the U.S. has successfully controlled many parasite infections. Malaria is one of them.

In addition, advancements in sanitation infrastructure and household construction mean that many Americans do not generally have to worry about parasite infections.

But this national success is not complete, as demonstrated by the recent findings in low-income Black communities across the country.

Limited awareness of the continued threat posed by neglected intestinal infections has made it more difficult to identify and treat these diseases in the U.S. than in lower-income nations.

For instance, in many countries the drugs needed to treat hookworm infections cost mere cents, but in the U.S., where drug prices are unregulated by the federal government, these same medications can cost hundreds of dollars.

The recent court decision in Alabama represents an important step toward increased national recognition of the role intestinal infections play in perpetuating racial health inequities.

Increased awareness will ideally result in improved access to testing and treatment in affected communities. But more work is needed to assess the full extent of these infections across the U.S.

Even if medical treatment is accessible and affordable, vulnerable individuals are often reinfected, as these pathogens continue to spread through the environment. Structural changes are needed to break the cycle of infection and poor health.

Current federal investment in community infrastructure – including water quality – is encouraging but does not go far enough. Ultimately, a concentrated nationwide effort to update and maintain sanitation systems is the best way to finally halt infection transmission and support health equity across the U.S.

Theresa E. Gildner, Assistant Professor of Biological Anthropology, Arts & Sciences at Washington University in St. Louis. This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Humans are born with instincts for crying and smiling, but not for kissing. Sometime in the past, our ancestors had the idea to smack their mouths together and call it romantic. And though we may not know who gave the first smooch, ancient records of these steamy sessions are helping us piece together when people started locking lips. 

The generally accepted earliest evidence we have of making out is religious text written in India in 1500 BCE. And while there was no official word for kissing back then, sentences like “young lord of the house repeatedly licks the young woman” and lovers “setting mouth to mouth” implied more than platonic relationships. But whether this was when kissing all began is still up for debate. In fact, an overlooked collection of written texts from ancient Mesopotamia (modern-day Iraq and Syria) suggests people were kissing further in the past. 

Citing those texts, authors of a new perspective article published today in the journal Science argue romantic kissing occurred 1,000 years earlier than historians first predicted. And as kissing became more of the norm, old medical records reveal the widespread transmission of viruses that spread through lip-to-lip contact.

“Given what we know about the history of kissing in humans and the myriad of similar kissing-like behaviors observed around the animal kingdom, I’m not surprised by these findings,” says Sheril Kirshenbaum, the author of The Science of Kissing, who was not involved in the study. “Whether romantic or not, kissing influences our bodies and brains in so many meaningful ways by guiding our emotions and decisions.”

[Related: Scientists think they found a 2,000-year-old dildo in ancient Roman ruins]

Clay tablets left behind by ancient Mesopotamians in 2500 BCE describe two types of kissing. The first was the friendly-parental kiss. People kissed the feet of their elders or the ground as a sign of respect or submission. 

The second was the lip kiss with a more erotic and intimate overtone. However, there were a few cultural expectations when it came to this type of kissing. Romantic kissing was an action reserved for married couples, as people frowned upon any PDA in Mesopotamia. Kissing among unmarried folks was taboo, considered to be giving in to sexual temptation. People not meant to be sexually active, such as priestesses, were thought to lose their ability to speak if they kissed someone. “The need for such norms indicates that romantic kissing must have been practiced in society at large,” explains lead author Troels Pank Arbøll, an assyriologist (a person studying the language and civilization of ancient Mesopotamia) at the University of Copenhagen.

As more people adopted the practice of kissing on the lips, ancient medical texts described illnesses whose symptoms resemble viral infections spread through mouth-to-mouth contact. The authors note this aligns with DNA analysis from ancient human remains detecting viruses such as herpes simplex virus 1, Epstein-Barr virus, and human parvovirus. All three viruses transmit through saliva.

One example is a disease that the ancient Mesopotamians labeled bu’šānu. The infection involved boils in or around the mouth area. Its name also implies that the infected person might have stunk. While Arbøll says bu’šānu shares several symptoms with herpes, he warns people not to make any assumptions. “As with all ancient disease concepts, they do not match any modern diseases 1:1, and one should be very careful when applying these modern identifications. A disease concept like bu’šānu likely incorporated several modern diseases.”

Mesopotamians likely did not think infectious diseases were spread through kissing, since it is not listed anywhere in the medical texts. However, they had some religiously influenced ideas of contamination, which spurred some measures to avoid spreading the disease. For example, a letter from around 1775 BCE describes a woman in a palace harem with lesions all over her body. Assuming it was contagious, people avoided drinking from any cups she drank, sleeping in her bed, or sitting on her chair.

[Related: When you give octopus MDMA they hug it out]

The findings show that this form of kissing did not originate in a single place. Mesopotamia, India, and other societies separately learned to associate pecks on the lips as romantic. Arbøll says it’s possible other areas also learned about kissing but didn’t have the writing tools to record this behavior. This opens the question of how widely sexual kissing was practiced in the ancient world. 

Some experts are less convinced that kissing was a universal behavior. William Jankowiak, a professor of anthropology at the University of Nevada, Las Vegas, who was not involved in the study, points out that written records of kissing often occurred in complex societies and less so in people living in smaller foraging groups. It’s also difficult to know if romantic kissing was practiced in more than one class or reserved for elite groups in ancient civilizations. Additionally, other factors, such as living in tropical versus colder regions, could influence whether people wanted to lock lips. 

There’s still a long way to go in understanding the ancient history of kissing. But the study does clear up one thing—all the smooching our ancestors did is probably why oral herpes and other kiss-transmitted diseases are a global problem today.

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Doctors may have a new tool to protect patients against multi-drug resistant bacterial infections. But the new defense against increasingly difficult-to-treat bacteria isn’t a brand new development—it is an 80 year-old antibiotic. A study published May 16 in the open access journal PLOS Biology looked at a natural product made in soil called nourseothricin that was discovered in 1942.

[Related: Kids all over the US are getting strep, but antibiotics are hard to come by.]

The rise of antibiotic-resistant bacterial infections has encouraged a search for new antibiotics. Antibiotic resistance is a very serious and growing medical problem—according to the Centers for Disease Control and Prevention, antimicrobial resistance killed at least 1.27 million people worldwide and was associated with close to 5 million deaths in 2019. In the United States, more than 2.8 million antimicrobial-resistant infections occur each year, and over 35,000 people die as a result.

Nourseothricin contains multiple forms of a complex molecule called streptothricin. There were high hopes that the streptothricin inside would be a powerful agent against bacteria called gram-negative bacteria. These bacteria, such as E.coli., have a thick outer protective layer and are particularly hard for antibiotics to kill. 

Unfortunately, nourseothricin was toxic to kidneys according to the results of an unpublished limited human trial sometime in the 1940’s and its development was dropped. The team in this study decided to go back and take a second look at nourseothricin.

“We started searching around for drugs that we could use, and it turns out these super resistant bugs were highly susceptible to streptothricin, so we were able to use it as a selection agent to do these experiments,” study co-author and pathologist at Harvard Medical School James Kirby said in a statement. “What scientists were isolating in 1942 was not as pure as what we are working with today. In fact, what was then called streptothricin is actually a mixture of several streptothricin variants. The natural mixture of different types of streptothricins is now referred to as nourseothricin.”

Kirby is also the director of the Clinical Microbiology Laboratory at Beth Israel Deaconess Medical Center.

In the earlier studies on the antibiotic, nourseothricin suffered from incomplete purification of  streptothricin which was likely causing the toxicity. A study published in 2022 showed that multiple forms of streptothricin actually have different toxicities. 

One called streptothricin-F was significantly less toxic while also working against present day pathogens that are resistant to multiple drugs. 

[Related: Raw dog food can harbor antibiotic-resistant bacteria.]

In this study, the team looked closely at streptothricin-F and also streptothricin- D. Streptothricin-D strain was also highly selective for the gram-negative bacteria and was even more powerful than streptothricin-F against drug-resistant Enterobacterales and other bacterial species. However, it caused renal toxicity at a lower dose. 

The team used cryo-electron microscopy to show that streptothricin-F bound extensively to a subunit of the bacterial ribosome. This binding causes translation errors in the bacteria, which helps antibiotics inhibit the spread of a bacterial infection.  

“It works by inhibiting the ability of the organism to produce proteins in a very sneaky way. When a cell makes proteins, they make them off a blueprint or message that tells the cell what amino acids to link together to build the protein. Our studies help explain how this antibiotic confuses the machinery so that the message is read incorrectly, and it starts to put together gibberish. Essentially the cell gets poisoned because it’s producing all this junk,” said Kirby.

The team is still trying to figure out the mechanism behind how nourseothricin works, but found that it acts differently than other antibiotics. Kirby will continue studying nourseothricin with collaborators at Northwestern University and Case Western Reserve University Medical Center to dive deeper and understand how it actually works.

“We have great collaborators that have allowed us to pursue a project that crosses multiple fields. This work is an example of collaborative science really at its best,” said Kirby. 

The post A once-forgotten antibiotic could be a new weapon against drug-resistant infections appeared first on Popular Science.

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This article was originally featured on KFF Health News.

What use could health care have for someone who makes things up, can’t keep a secret, doesn’t really know anything, and, when speaking, simply fills in the next word based on what’s come before? Lots, if that individual is the newest form of artificial intelligence, according to some of the biggest companies out there.

Companies pushing the latest AI technology — known as “generative AI” — are piling on: Google and Microsoft want to bring types of so-called large language models to health care. Big firms that are familiar to folks in white coats — but maybe less so to your average Joe and Jane — are equally enthusiastic: Electronic medical records giants Epic and Oracle Cerner aren’t far behind. The space is crowded with startups, too.

The companies want their AI to take notes for physicians and give them second opinions — assuming they can keep the intelligence from “hallucinating” or, for that matter, divulging patients’ private information.

“There’s something afoot that’s pretty exciting,” said Eric Topol, director of the Scripps Research Translational Institute in San Diego. “Its capabilities will ultimately have a big impact.” Topol, like many other observers, wonders how many problems it might cause — like leaking patient data — and how often. “We’re going to find out.”

The specter of such problems inspired more than 1,000 technology leaders to sign an open letter in March urging that companies pause development on advanced AI systems until “we are confident that their effects will be positive and their risks will be manageable.” Even so, some of them are sinking more money into AI ventures.

The underlying technology relies on synthesizing huge chunks of text or other data — for example, some medical models rely on 2 million intensive care unit notes from Beth Israel Deaconess Medical Center in Boston — to predict text that would follow a given query. The idea has been around for years, but the gold rush, and the marketing and media mania surrounding it, are more recent.

The frenzy was kicked off in December 2022 by Microsoft-backed OpenAI and its flagship product, ChatGPT, which answers questions with authority and style. It can explain genetics in a sonnet, for example.

OpenAI, started as a research venture seeded by Silicon Valley elites like Sam Altman, Elon Musk, and Reid Hoffman, has ridden the enthusiasm to investors’ pockets. The venture has a complex, hybrid for- and nonprofit structure. But a new $10 billion round of funding from Microsoft has pushed the value of OpenAI to $29 billion, The Wall Street Journal reported. Right now, the company is licensing its technology to companies like Microsoft and selling subscriptions to consumers. Other startups are considering selling AI transcription or other products to hospital systems or directly to patients.

Hyperbolic quotes are everywhere. Former Treasury Secretary Larry Summers tweeted recently: “It’s going to replace what doctors do — hearing symptoms and making diagnoses — before it changes what nurses do — helping patients get up and handle themselves in the hospital.”

But just weeks after OpenAI took another huge cash infusion, even Altman, its CEO, is wary of the fanfare. “The hype over these systems — even if everything we hope for is right long term — is totally out of control for the short term,” he said for a March article in The New York Times.

Few in health care believe this latest form of AI is about to take their jobs (though some companies are experimenting — controversially — with chatbots that act as therapists or guides to care). Still, those who are bullish on the tech think it’ll make some parts of their work much easier.

Eric Arzubi, a psychiatrist in Billings, Montana, used to manage fellow psychiatrists for a hospital system. Time and again, he’d get a list of providers who hadn’t yet finished their notes — their summaries of a patient’s condition and a plan for treatment.

Writing these notes is one of the big stressors in the health system: In the aggregate, it’s an administrative burden. But it’s necessary to develop a record for future providers and, of course, insurers.

“When people are way behind in documentation, that creates problems,” Arzubi said. “What happens if the patient comes into the hospital and there’s a note that hasn’t been completed and we don’t know what’s been going on?”

The new technology might help lighten those burdens. Arzubi is testing a service, called Nabla Copilot, that sits in on his part of virtual patient visits and then automatically summarizes them, organizing into a standard note format the complaint, the history of illness, and a treatment plan.

Results are solid after about 50 patients, he said: “It’s 90% of the way there.” Copilot produces serviceable summaries that Arzubi typically edits. The summaries don’t necessarily pick up on nonverbal cues or thoughts Arzubi might not want to vocalize. Still, he said, the gains are significant: He doesn’t have to worry about taking notes and can instead focus on speaking with patients. And he saves time.

“If I have a full patient day, where I might see 15 patients, I would say this saves me a good hour at the end of the day,” he said. (If the technology is adopted widely, he hopes hospitals won’t take advantage of the saved time by simply scheduling more patients. “That’s not fair,” he said.)

Nabla Copilot isn’t the only such service; Microsoft is trying out the same concept. At April’s conference of the Healthcare Information and Management Systems Society — an industry confab where health techies swap ideas, make announcements, and sell their wares — investment analysts from Evercore highlighted reducing administrative burden as a top possibility for the new technologies.

But overall? They heard mixed reviews. And that view is common: Many technologists and doctors are ambivalent.

For example, if you’re stumped about a diagnosis, feeding patient data into one of these programs “can provide a second opinion, no question,” Topol said. “I’m sure clinicians are doing it.” However, that runs into the current limitations of the technology.

Joshua Tamayo-Sarver, a clinician and executive with the startup Inflect Health, fed fictionalized patient scenarios based on his own practice in an emergency department into one system to see how it would perform. It missed life-threatening conditions, he said. “That seems problematic.”

The technology also tends to “hallucinate” — that is, make up information that sounds convincing. Formal studies have found a wide range of performance. One preliminary research paper examining ChatGPT and Google products using open-ended board examination questions from neurosurgery found a hallucination rate of 2%. A study by Stanford researchers, examining the quality of AI responses to 64 clinical scenarios, found fabricated or hallucinated citations 6% of the time, co-author Nigam Shah told KFF Health News. Another preliminary paper found, in complex cardiology cases, ChatGPT agreed with expert opinion half the time.

Privacy is another concern. It’s unclear whether the information fed into this type of AI-based system will stay inside. Enterprising users of ChatGPT, for example, have managed to get the technology to tell them the recipe for napalm, which can be used to make chemical bombs.

In theory, the system has guardrails preventing private information from escaping. For example, when KFF Health News asked ChatGPT its email address, the system refused to divulge that private information. But when told to role-play as a character, and asked about the email address of the author of this article, it happily gave up the information. (It was indeed the author’s correct email address in 2021, when ChatGPT’s archive ends.)

“I would not put patient data in,” said Shah, chief data scientist at Stanford Health Care. “We don’t understand what happens with these data once they hit OpenAI servers.”

Tina Sui, a spokesperson for OpenAI, told KFF Health News that one “should never use our models to provide diagnostic or treatment services for serious medical conditions.” They are “not fine-tuned to provide medical information,” she said.

With the explosion of new research, Topol said, “I don’t think the medical community has a really good clue about what’s about to happen.”

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.

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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.

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COVID-19 is no longer a public health emergency in the US. The Biden administration’s deadline follows the World Health Organization’s announcement last week that removed COVID’s status as a global health crisis.

Infectious disease experts tell Popular Science that it’s an encouraging step and a sign that we are in a very different place than where we were in 2020. And while the recent decisions in no way mean the virus is gone—it’s expected to be endemic like the flu—access to COVID testing, treatments such as Paxlovid, and the vaccines have put the US in a position to coexist with it.

That said, managing your safety will come at a higher cost now. In one of the biggest changes from ending the federal emergency response, insurances are no longer required to cover the costs of COVID testing or reimburse people if they bought an over-the-counter home COVID-19 test. The federal government is also ending its free COVID-test program over the mail. 

As the financial burden of testing shifts to families and individuals, knowing where and when to get tested will keep you protected as the country transitions into this new stage of the pandemic. “We’re still seeing up to 1,000 deaths a week in the US from COVID for people that are older and at risk,” warns Del DeHart, a medical director of the infectious diseases department at the University of Michigan Health-West. “For those people, COVID is still not over and so testing for early treatment is going to be critical.”

Where to get COVID tests

There are still options for getting free COVID tests around the US The last day to order four free at-home COVID tests from the government is May 31, but local community clinics can give away free COVID tests or at a lower cost until supplies run out. 

Access to free testing might also depend on where you live. David Souleles, the director of the COVID-Response Team at the University of California, Irvine, says some state governments are taking measures to avoid financial barriers with COVID testing. California, for example, issued a mandate for health insurances to continue providing reimbursement for eight monthly at-home tests. Check your state government’s website to see what policies are in place following the end of the public health emergency.

If you are uninsured, the US government will continue to provide access to swabs through the Increasing Community Access to Testing Program. This government program partners with specific healthcare sites such as Walgreens and Quest Diagnostics to provide no-cost COVID tests with priority for people with a known exposure to the virus or who are showing symptoms.

[Related: An at-home test for both COVID-19 and the flu gains approval]

At-home rapid tests and PCR laboratory testing will still be available at your local pharmacies and doctor’s office, but it’s up to your insurance company if they want to bear the cost or require a copayment. What’s more, insurance companies may charge different prices for COVID tests; if they cover the cost, they may set limits on how many tests they will cover per individual. 

Prices for COVID test kits in stores like CVS range from $9.99 to $28.99, meaning testing can quickly get expensive. DeHart is concerned that the prices will create a financial barrier that will deter people from getting tested. If affordability becomes a question, it’s important to make every COVID test you take count.

When it’s still important to get tested for COVID

While most COVID mandates have lifted around the country, some employers and places might require you to get tested. For instance, healthcare workers employed in facilities like nursing homes will likely continue routine COVID testing. And as of now, many hospitals still require routine COVID testing for admitted patients, though it remains unclear whether the hospitals will cover the cost or if the test will be added to a person’s medical bill.

For voluntary testing, it’s important to evaluate your risk of having a severe COVID infection. DeHart says individuals above the age of 65 and those with immunosuppressive conditions should get tested regularly, along with loved ones in close contact with those that fall under this category. Souleles also recommends taking a test before visiting a relative in assisted living or anyone who is considered at high-risk of exposure. 

Other scenarios may apply, too, Souleles adds. “We would still encourage people to test before and after travel and before and after gatherings if they have the ability to do so. Anytime that you have the ability to test before you’re going to be around lots of people is great, and anytime you have the ability to test three to five days after being around a lot of people, that’s also a good thing.”

[Related: Long COVID recovery is finally getting the attention it deserves in the US]

If you have COVID-like symptoms, get tested before going out in public, even if the side effects seem mild. Testing early will give you more chances to get Paxlovid, which is most effective when taken within the first five days of seeing symptoms, and potentially avoid life-threatening complications. 

If you need to purchase a COVID test, treat it like you would any other over-the-counter goods. This includes checking the expiration dates to avoid a false positive or false negative result. You will also want to throw out any recalled COVID tests. If purchased for a later date, keep COVID tests at room temperature and away from the hands of pets and young children.

What to do if you test positive for COVID

If the test comes out positive, follow the Centers for Disease Control and Prevention’s (CDC) guidelines. Stay home and isolate yourself from others in the household for five days. People experiencing moderate symptoms like difficulty breathing should isolate for 10 days. Monitor your condition and go to the hospital if there are any severe or life-threatening complications. 

If you must go outside, wear a high-quality mask and avoid going to places where you would have to take it off. Also contact your doctor to see if you are eligible for any COVID-19 treatments and start those as soon as possible.

You can stop isolating after five days if you have no symptoms. If you continue to show symptoms, the CDC says you should stay put until your symptoms improve or you are fever-free for 24 hours without using medication.

[Related: Getting COVID more than once might be even worse than we thought]

Keep in mind that COVID tests are only one of the many tools available to reduce your risk of severe infection and death. Both DeHart and Souleles strongly urge people to get vaccinated and get their booster shot when eligible. Insurers will still be expected to cover the bivalent COVID vaccine as a routine immunization, and the Biden administration’s Bridge Access Program for COVID-19 Vaccines and Treatments will continue to provide vaccines free-of-charge to the uninsured.

“Stay up to date with your vaccines,” says Souleles. “It’s still the most important tool that we have right now.”

The post Your guide to COVID testing for the unforeseeable future appeared first on Popular Science.

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With the federal public health emergency for COVID-19 set to expire at the end of the day on May 11, take a few minutes today to order the handful of free at-home COVID-19 tests the US government is holding for you. Don’t procrastinate: guaranteed insurance coverage for tests ends with the emergency, so they might not be free starting on May 12.

For now, every residential address in the US, Puerto Rico and other US territories, as well as those linked to overseas military and diplomatic personnel, can request four free rapid antigen tests from the federal COVID tests website. Although coverage may change when the public health emergency ends, the US Department of Health and Human Services says the government will continue to distribute tests via that website through the end of May.

And if you still have tests you ordered at any point since the program launched in January 2022, don’t throw them out—use the Food and Drug Administration’s searchable at-home test database to see if their expiration dates have been extended. Studies have shown that repeat COVID-19 infections increase the risk of hospitalization and death, so it’s worth hanging onto as many usable tests as you can. It’ll help you avoid spreading it among your family, friends, and community.

What’s changing with insurance coverage for COVID tests

The end of the public health emergency also means private insurance is no longer required to cover COVID tests without cost-sharing. The Biden administration has encouraged health insurers to continue, but after May 11, you may have to pay for any tests you order or pick up. To understand exactly what to expect, you’ll need to check with your plan to see how it will handle COVID tests.

If you’re insured by a state Medicaid program, though, you’re in luck. These are required to cover COVID tests without cost-sharing until September 30, 2024, the HHS says. After that, coverage may vary by state.

Medicare coverage, meanwhile, is a mixed bag. Anyone with traditional Medicare can continue getting PCR and antigen tests with no cost-sharing when the lab tests are ordered by a doctor and some other health care providers. If you’re enrolled in Medicare Advantage, cost-sharing may change when the health emergency ends, so the HHS recommends you check with your plan after May 11.

Despite the end of the health emergency, the government may continue to distribute free tests from the national stockpile through states and communities. If you’re looking for a free COVID tests, you can check the Centers for Disease Control and Prevention’s no-cost COVID-19 testing locator.

Those living in multi-family, co-living, or other shared living spaces can place more than one order as long as the USPS knows the address houses multiple unrelated families, but may be unable to if the government doesn’t know several families live there. If that happens, you can file a service request or call the USPS help desk at 1-800-ASK-USPS (1-800-275-8777) to try to get it fixed.

If you need help placing an order, you can call 1-800-232-0233 Monday through Friday between 8 a.m. and 8 p.m. Eastern Standard Time, or between 8 a.m. and 5 p.m. on the weekend, for assistance in English, Spanish, and more than 150 other languages. There’s also a teletype (TTY) or text telephone number at 1-888-720-7489 and the aforementioned USPS help desk.

People with disabilities can call the disability information and access line at 1-888-677-1199 between 9 a.m. and 8 p.m. EST, Monday through Friday, or email DIAL@usaginganddisability.org.

If you provide an email address when you order, you will get shipping notifications and can track the package on the USPS website. You can’t pick the tests up anywhere, even your local post office—they will always come to the address you provided, the agency says.

As long as your tests haven’t expired, the government recommends you take them if you begin having COVID symptoms like a fever, sore throat, runny nose, or loss of taste or smell; at least five days after you are in close contact with someone who has since tested positive for COVID; or before you gather with a group, especially if that group includes people at risk of severe disease or who aren’t up to date on their vaccinations (keep in mind that you may not know who’s at risk, either).

It’s also worth noting that you should let your tests come to room temperature before using them—especially if they were delivered in freezing or blistering hot temperatures. Although the tests are built to survive a range of conditions, they might not work as well if they’re cold, the government says. Generally, rapid antigen tests are meant to be used in an environment that’s somewhere between 59 and 86 degrees Fahrenheit (15 to 30 degrees Celsius), but your tests should come with specific instructions about this. The government recommends letting the unopened package sit indoors for at least two hours before opening and using any of the tests inside.

How to take a rapid antigen test

Each test kit comes with directions for how to use it, and they all involve swabbing the inside of your nose. You should get results within 30 minutes and you won’t have to leave your home. If you don’t follow the instructions, the result could be wrong. For visual learners, the Centers for Disease Control and Prevention has a how-to video, and it also has one for people who use American Sign Language.

[Related: The Postal Service helps keep millions of Americans alive and well]

If the results come out negative, the test didn’t find COVID in your body, and you might have a lower risk of spreading the disease. It’s worth noting that these at-home antigen tests generally aren’t as accurate as PCR tests, for example, which are processed by laboratories. So if you think you got a false negative, the government suggests testing again within a few days, leaving at least 24 hours between tests.

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Scientists in Australia have just begun vaccinating wild koalas against chlamydia. This field trial in the state of New South Wales is an effort to protect one of Australia’s most beloved animals against the disease that can cause blindness, infertility, and death. The chlamydia epidemic in koalas has been ravaging populations of the marsupial since the 1990s. 

[Related: A new vaccine may curb the koala chlamydia epidemic.]

Koalas along the east and southeast Australian coasts have been particularly affected, with some populations having infection rates of up to 100 percent. In 2021, Australia Zoo Wildlife Hospital veterinarian and research coordinator Amber Gillett called chlamydia one of the most significant threats to koalas and treatment after infection is not enough to save them. “Although many koalas with chlamydia can be treated using traditional antibiotics, some animals cannot be saved due to the severity of their infection. Having a vaccine that can help prevent both infection and the severity of the disease is a critical element in the species’ conservation management.”

While origins of the disease is koalas aren’t fully confirmed, but scientists believe that marsupials possibly caught the disease from exposure to the feces from infected cattle and sheep. Chlamydia then spread via sexual contact or was passed from mother to offspring.  

This single-shot vaccine has been designed just for koalas and was tested in a few hundred fluffy specimens in wildlife rescue centers. For this new field trial, the team hopes to catch, vaccinate, and subsequently monitor about half of the koala population living in the Northern Rivers region of New South Wales–about 50 koalas. 

“It’s killing koalas because they become so sick they can’t climb trees to get food, or escape predators, and females can become infertile,” Samuel Phillips, a microbiologist at the University of the Sunshine Coast who helped to develop the new vaccine, told the Associated Press.

The first koalas were caught and vaccinated in March, and the effort is expected to last for three months. To find them, the team spots koalas in eucalyptus trees to then build circular enclosures around the base of the trees with doors that lead into cages. Eventually, the koalas climb down from one tree to get more eucalyptus leaves from another tree and wander into the traps.

They are then given a check-up to assess their health and given anesthesia before getting the vaccine. They are kept under observation for 24 hours after waking up to check for unexpected side effects, according to Jodie Wakeman, the veterinary care and clinical director at Friends of the Koala. The nonprofit organization runs a wildlife hospital where the koalas are getting vaccinated.

[Related: How to handle a koala-chlamydia epidemic.]

The koalas are marked with a pink dye on their backs so that the same animals are not caught twice before being released back into the wild. 

Australia’s federal government declared that the koalas in the eastern regions of New South Wales, Queensland, and the Australian Capital Territory were endangered. A 2020 report from the New South Wales government found that the unique creatures could become extinct by 2050 due to disease, road collisions, and habitat loss. Climate change is only exacerbating the problem.

The trial was approved by multiple Australian governing bodies balancing the risk of disturbing the marsupials against the danger of allowing chlamydia to continue to spread unchecked. It is one of only a few worldwide examples of scientists attempting to inoculate endangered wildlife for the purposes of conservation. In 2016, a team began to vaccinate Hawaiian monk seals morbillivirus and in 2020, biologists in Brazil started vaccinating golden lion tamarins against yellow fever.

“Vaccination for wildlife is certainly not routine yet,” Jacob Negrey, a biologist at Wake Forest University School of Medicine told the AP. “But whether it should be used more often is a fundamental question that conservation biologists are really wrangling with right now.”

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On May 5, the The World Health Organization (WHO) announced that we are no longer in a global COVID-19 emergency. The emergency was first declared over three years ago in the early days of the pandemic. During the 15th meeting of the International Health Regulations Emergency Committee regarding COVID-19, the members highlighted a decreasing trend in deaths, decline of COVID-19 related hospitalizations and intensive care unit admissions, and higher levels of population immunity to the virus as the basis of their decision. 

“With great hope, I declare COVID-19 over as a global health emergency,” WHO director general, Tedros Adhanom Ghebreyesus announced during a media briefing. 

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

However, Tedros stressed that just because the global emergency declaration is ending, it does not mean that COVID-19 is not still a threat to public health. “As we speak, thousands of people around the world are fighting for their lives in intensive care units. And millions more continue to live with the debilitating effects of post-COVID19 condition,” Tedros said. 

The WHO first made the emergency declaration on January 30, 2020, when only 213 people were known to have died from the novel virus. The declaration was a signal to the international community that COVID-19 posed a threat to the whole world and that they should begin to prepare. 

The WHO will continue to list COVID-19 as a pandemic, similar to how they designate HIV. While it acts as a symbolic milestone, this decision does not change much, but it is a significant moment in the evolving human relationship with the novel virus that brought life to a screeching halt in 2020 after it first emerged in China in December 2019.

Many countries, including the European Union, have already ended their COVID-19 states of emergency and have moved away from mitigation efforts. The United States is scheduled to lift its COVID-10 emergency on May 11.

The WHO decision was not welcomed by all public health experts. Respiratory physician and member of Brazil’s National Academy of Medicine Margareth Dalcolmo told The New York Times that it was too soon to lift the emergency, due to the urgent tasks such as research into COVID variants and development of better vaccines. She added that the designation of a global public health emergency also creates leverage for lower-income nations to access needed treatments and support.

Around the world, 765,222,932 confirmed COVID cases, including 6,921,614 deaths, have been reported to the WHO as of May 3. However, these figures are likely a vast undercount of the pandemic’s true toll on human life. In 2022, the WHO said 15 million more people had died in the first two years of the pandemic than they would have in normal times, with developing and indigenous nations experiencing the worst of the devastation. Close to eight million more people than expected died in lower-middle-income nations by the end of 2021.

[Related: White House invests $5 billion in new COVID vaccines and treatments as national emergency ends.]

“One of the greatest tragedies of COVID-19 is that it didn’t have to be this way. We have the tools and the technologies to prepare for pandemics better, to detect them earlier, to respond to them faster, and to mitigate their impact But globally, a lack of coordination, a lack of equity, and lack of solidarity meant that those tools were not used as effectively as they could have been,” Tedros said.

Additionally, on May 4, the United States Centers for Disease Control and Prevention released provisional data that COVID-19 dropped to the fourth leading cause of death in the US in 2022, falling behind heart disease, cancer, and unintended injuries like shootings, car accidents, and drug overdoses. In 2020 and 2021, only heart disease and cancer were ahead of COVID-19 as leading causes of death.

Death rates due to COVID-19 fell for nearly all Americans and the virus was the underlying cause of roughly 187,000 deaths in the US in 2022.  According to the CDC, the highest COVID-19 death rates were in the South and in the adjacent region that stretches west to Texas, Oklahoma, and New Mexico.

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After 60 years of trial and error, the Food and Drug Administration (FDA) approved the first vaccine to prevent respiratory syncytial virus (RSV) on May 3. More preventative shots for the respiratory virus are on the way.

[Related: How our pandemic toolkit fought the many viruses of 2022.]

The FDA approved Arexvy from pharmaceutical company GSK. The vaccine is designed to protect those over 60 in a single dose. A vaccine from Pfizer is currently under consideration for older adults and pregnant people as a maternal vaccination to protect newborn babies. Sanofi and AstraZeneca’s monoclonal antibody treatment for babies that offers vaccine-like protection during RSV season is also under consideration by the FDA. Additionally, a late-stage trial of an RSV vaccine that uses mRNA technology from Moderna showed promise in late-stage trials. 

The vaccine could be available as soon as this fall, pending a recommendation for its use from the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, which will meet in June. GSK says it has “millions of doses ready to be shipped,” according to a recent earnings presentation.

“Older adults, in particular those with underlying health conditions, such as heart or lung disease or weakened immune systems, are at high risk for severe disease caused by RSV,” said Peter Marks, director of the FDA’s Center for Biologics Evaluation and Research, in a statement. “Today’s approval of the first RSV vaccine is an important public health achievement to prevent a disease which can be life-threatening and reflects the FDA’s continued commitment to facilitating the development of safe and effective vaccines for use in the United States.”

RSV can affect all age groups, but it is particularly worrisome in babies and older adults. It is a highly contagious virus that causes infections of the lungs and breathing passages. According to the Centers for Disease Control and Prevention (CDC), RSV leads to approximately 60,000 to 120,000 hospitalizations and 6,000 to 10,000 deaths among adults 65 years of age and older every year. It is also a common cause of lower respiratory tract disease in older adults. This disease affects the lungs and can cause life-threatening pneumonia and bronchiolitis.

The virus circulates seasonally, usually beginning in the fall and peaking in the winter. The 2022-2023 RSV season started particularly early and flooded hospitals and pediatric wards across the United States, leading pharmacies to limit the sales of children’s medicines.

According to the results of a clinical trial of close to 25,000 older adults, the GSK vaccine was 83 percent effective at preventing lower respiratory tract disease by the virus. It was 94 percent effective at preventing severe disease in seniors. In the trial, severe disease was defined as the need for supplemental oxygen or a mechanical help to breathe. The results were published in the New England Journal of Medicine in February. 

[Related: Fighting RSV in babies starts with a mother’s antibodies.]

The vaccine works by using a small piece of the virus called a fusion protein, or F-protein. The F-protein sticks out on the virus’ surface and helps it latch onto cells in the upper airway and infect them. The F-proteins were made in a lab with specially programmed cells. 

In 2013, researchers at the National Institutes of Health discovered how to freeze the normally wiggly and shape-shifting F-protein in the shape that it takes before it fuses onto a cell. When it’s in this shape, the body can produce antibodies against it. The GSK vaccine uses this pre-fusion form of the F-protein and an ingredient called an adjuvant that can boost immune activity.

The search for a vaccine to RSV began in the 1960s, but has been mired by tragedy. Two toddlers died after receiving an experimental shot in the 60’s after it unexpectedly caused them to contract a very serious version of the virus. Many of the safety measures currently in place during vaccine trials were put in place after the failures of the RSV vaccine.

Barney Graham, a vaccine scientist at Morehouse School of Medicine worked alongside Jason McLellan, a structural biologist at the University of Texas at Austin, and Peter Kwong, a vaccine scientist at the National Institutes of Health, to jump-start the RSV vaccine field after decades of failure.

“This is my life’s work, so it’s kind of amazing to see it come to this point,” Graham told The Washington Post.  “It’s exciting for me to see this happening because of all the other people who’ve come before me working on RSV, some of whom are no longer with us. I wish they could see this is happening. It’s been a long struggle.”

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Deep beneath the Pacific Ocean, the edge of one tectonic plate was being jammed beneath the tectonic plate that held Japan. This wasn’t news. It had been happening at a rate of three inches a year since long before humans had invented the concept of news. But that March, it became news in the biggest possible way, when a chunk of the underlying plate suddenly gave way, causing the seafloor to pop up by about 15 feet and the plate holding parts of Japan to suddenly drop by about three feet. The magnitude 9 Tohoku earthquake was so big it shunted Japan eight feet to the east. It was so big it shifted the Earth six inches on its axis. It was so big it sped up the rotation of the planet
(only by 1.8 microseconds a day, but still—your days are now just a tiny bit shorter. Thanks Obama!). The earthquake and resultant tsunami also wreaked havoc on human systems—transportation systems, energy systems, water systems, telecommunication systems, and that most important of all human systems, the biological system that allows us to slobber, reproduce, and contemplate the irrationality of high baby-formula prices (usually in that order).

The tsunami killed more than twenty thousand people and caused multiple nuclear meltdowns, a disastrous toll for everyone except sellers of supplements, who pivoted to prey on the baseless fears of Americans living thousands of miles away from the radiation. Toby McAdam, still selling his RisingSun products, told the local newspaper that he doubted the radiation would drift to Montana—“but it could.” He recommended that his “Lugol’s Iodine solution” be applied to the skin daily as “an ounce of prevention.” Though public health officials said people self-treating with iodide supplements were more likely to harm than help themselves, orders spiked so sharply that Toby’s website crashed.

The multifaceted nature of the tsunami-caused chaos makes it perhaps appropriate that the event also marked the beginning of the United States’ descent into a full-blown zombie apocalypse.

The June following the earthquake, the CDC began a conversation about emergency preparedness on Twitter that led to a handful of people jokingly tweeting that they would like the CDC to weigh in on a catastrophic zombie attack.

This led to the predictable wave of lols, rofls, and laughy-face emoticons, but it also sparked an idea for Dave Daigle (a CDC communications administrator) and Dr. Ali S. Khan (a CDC expert in disaster preparedness).

With Daigle’s input, Khan wrote a piece for the CDC website explaining how to prepare for a zombie apocalypse. This neatly demonstrated the humanity of the person on the other side of the icy-cold stethoscope even as it leveraged the innate appeal of zombies to teach real-life strategies to cope with actual disasters.

It turned out people were hungry for messaging about people hungry for brains. The CDC zombie apocalypse preparedness plan was an instant hit, racking up so many views that the CDC server froze up, overwhelmed by all the traffic.

This bit of fun was so successful that a team of researchers from the University of California, Irvine, published a congratulatory paper in the journal Emerging Infectious Diseases urging other public health officials to follow suit. It argued that zombies were an opportunity “to capitalize on the benefits of spreading public health awareness through the use of relatable popular culture tools and scientific explanations for fictional phenomena.” They proposed that the medical establishment build o those efforts to stimulate the conversation and do better public education on a variety of health topics.

Suddenly, zombies were everywhere in public health and safety. The CDC, the Department of Homeland Security, and the Federal Emergency Management Agency all published in-depth zombie-related literature. Finally, public officials were seizing the initiative and taking back the cul tural space they had inadvertently ceded to promoters of One True Cures.

Also in 2011, a Harvard Medical School physician and aspiring nov elist named Steven Schlozman appeared on the radio show Coast to Coast AM, which spun tales of conspiracy and paranormal phenomena to a large and credulous national audience from 2 a.m. to 4 a.m., seven days a week. Because Coast to Coast AM was the most popular late-night radio show in the country, with ten million listeners, it was a great opportunity for Schlozman, who was there to promote his latest work, The Zombie Autopsies: Secret Notebooks from the Apocalypse. In the book, Schlozman drew on his medical knowledge to describe “Ataxic Neurodegenerative Satiety Deficiency syndrome” as the medical cause
of zombies (it was of course a fictional work of fictitious fiction). The format of the show required that Schlozman spend the opening stretch talking about the events of his novel as if they were real, before shifting to an acknowledgment that it was all pure fantasy.

Daigle, Khan, and Schlozman were helping people learn a bit of science in a fun way.

But their efforts quickly ran up against a problem: there is more than one way to view a zombie apocalypse.

One fact that the CDC and its fellow agencies failed to fully appreciate was that, in zombie properties like 2009’s feature film Zombieland and 2010’s hit television series The Walking Dead, very little
screen time is given to public health concepts like water sanitation. The action takes place after most health authorities have had their faces eaten, leaving individual survivors to run around attacking infected people with baseball bats, crossbows, and shotguns as a means of self-preservation.

That’s why other groups were quickly lining up to enlist the hot new cultural craze into their own, very different agendas. Zombies became the centerpiece in gun advertisements and were a major part of the NRA’s annual conventions, where shooting at the undead carried none of the moral baggage that came with shooting at human targets.

“Because the zombie canon focuses so squarely on the apocalypse, its spread into popular culture can erode faith in the resiliency of civilization,” wrote Daniel Drezner, the Tufts University professor and zombie expert. “The zombie narrative, as it is traditionally presented, socially constructs the very narrative that agencies like the CDC and FEMA are trying to prevent.”

Drezner documented the way that zombie references became a sort of dog whistle for gun rights—those on the outside glossed over a quirky head-scratcher while targeted audiences became fired up, even though they would clearly never need to shoot a zombie in real life.

Until some Americans began to ask, Will I need to shoot a zombie in real life?

Toby McAdam had told me about the 2012 Miami incident in which a man bit the face off a homeless man and then was himself described by authorities as slow to die after being shot. But Toby was not the only person fascinated by that attack. It let the undead cat out of the bag.

Soon after the news broke, a self-described Bitcoin evangelist and promoter of alternative-health supplements doctored a Huffington Post article about the incident so that it attributed the cause of the face eating to “LQP-79,” a virus that destroys internal organs and makes the host hungry for human flesh.

The fake article went viral, blitzing digital media feeds so thoroughly that LQP-79 was soon the third-most-searched term on the CDC website, forcing the agency to officially deny the existence of a zombie virus.

Around then, communities of zombie-themed survivalists and militias sprang up all across America. One was an offshoot of the well-established Michigan Militia, while others had names like the Kansas Anti Zombie Militia, the Anti Zombie Unified Resistance Effort (AZURE), Zombie-Fighting Rednecks, the Zombie Eradication and Survival Team, Postmortem Assault Squadron, and the US Department of Zombie Defense.

One, a loosely affiliated national group called the US Zombie Outbreak Response Team (ZORT), popularized a strange mishmash of survivalism and cosplay. Its website features pictures of preppers in tactical gear and tinted sunglasses using stickers and goofy accessories to trick out their trucks as zombie-fighting vehicles that would be equally at home in Ghostbusters or Mad Max universes. It was in some ways good fun. But they also carried real firearms. And engaged in real postapocalyptic survival exercises.

“A Zombie could be anything from a person infected by a pandemic outbreak to a crazy nut job, criminal or gangster who wants to hurt your family and steal your food and preps,” reads ZORT’s promotional material.

Though ZORT purports to be simply providing tongue-in-cheek cover for legit training that would be helpful in a natural disaster, of course the real difference between zombies and hurricane survivors is that one must be shot in the head and the other should be given a hot toddy and a shower.

Did any of these folks actually believe in zombies?

Probably not. But there was potential.

Drezner cited research showing that when considering paranormal ideas, people look less to the logical evidence and more to whether other people believe in the ideas. This means that even if no one believes in zombies, if some people believe that other people believe in zombies, then some people will believe in zombies. The gaslighting became so effective that the gaslit then gaslighted others, until fear of actual zombies took on an undead life of its own—call it masslighting.

And really, the online picture was becoming quite blurry. At the CDC, Daigle and Khan began getting inquiries about their Zombie Preparedness Plan from concerned citizens who wanted to know what sort of firearm was recommended to repel undead invaders. Meanwhile, after his Coast to Coast AM appearance, Schlozman got emails from listeners who wanted to know what medicines could stave off a zombie infection, and whether he had recommendations for how to protect one’s home. China’s state media had to formally debunk a robust rumor that Ebola victims were rising from the dead as zombies. And in 2014 in the Florida statehouse, a representative formally proposed “An Act Relating to the Zombie Apocalypse” as the name of a bill that would allow citizens to carry firearms without a permit in an emergency.

Shockingly, a 2015 survey showed that 2 percent of American adults thought the most likely apocalyptic scenario would be one caused by zombies.

And zombie references kept popping up in unexpected places. People downloaded audio fitness tracks in which joggers were kept motivated by imaginary zombie antagonists that pursued them as they ran.

A man named Vermin Supreme, who sought the 2016 Libertarian Party nomination for president, added a platform plank on “zombie apocalypse awareness.” He also advocated using zombies for renewable energy. Even Big Tech was in on it. Buried in Amazon’s user agreement for a game-development engine, clause 57.10—a gag, probably?—read that the software should not be used in life-and-death situations, such as in medical equipment, nuclear facilities, spacecraft, or military combat operations. “However, this restriction will not apply in the event of the occurrence (certified by the United States Centers for Disease Control or successor body) of a widespread viral infection transmitted via bites or contact with bodily fluids that causes human corpses to reanimate and seek to consume living human flesh, blood, brain or nerve tissue and is likely to result in the fall of organized civilization.”

With zombie stories saturating popular culture, the lore in TV and film began to expand beyond the simple trope of shambling brain eaters. There were zombie rom-coms and zombie mockumentaries. On the CW Television Network, a show called iZombie tells the story of a Seattle morgue worker infected by a zombie virus. In this world, zombies retain their personality and capacity for reason, as long as they are well fed (on brains). During the third season, which aired in 2017, a militant group of zombies releases a deadly flu virus in Seattle; local public health officials announce a mandatory flu vaccination, only to find that the zombies have tainted the vaccines with a substance that will turn the vaccinated into zombies.

Vaccines that zombified ordinary citizens?

Luckily for public health, no one would believe that in real life.

Buy If It Sounds Like a Quack by Matthew Hongoltz-Hetling here.

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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.

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Archaeologists in Rome have unearthed a treasure trove of Renaissance-era medical supplies inside the Forum of Caesar. Among the “golden” finds are 500 year-old medicine bottles and urine flasks. In a study published April 11 in the journal Antiquity, the authors believe that the containers were used to collect pee for medical analysis and diagnosis. 

According to the researchers, the pathogens that could have been present in these bottles helps uncover how urban waste was managed.

[Related: Pee makes for great fertilizer. But is it safe?]

The current excavation initially began in 2021 and is part of an international collaboration called the Caesar’s Forum Excavation Project. The 16th century medical dump was found inside Caesar’s Forum, which was built centuries prior in 46 BCE. About 1,500 years later, a guild of bakers used this space to build the Ospedale dei Fornari or Bakers’ Hospital. According to the authors, the waste dump was then created by the hospital’s workers. 

The archaeologists also found rosary beads, broken glass jars, coins, a ceramic camel, and a Renaissance-era cistern full of ceramic vessels. The team of researchers from institutions in Italy and Denmark believes that the objects were likely related to patient care in the hospital. Each patient at the hospital may have been given a basket with a bowl, drinking glass, jug, and a plate for hygiene purposes. 

The glass urine flasks are called “matula” in medieval Latin medical texts and were likely used for the practice of uroscopy. This was a diagnostic tool for physicians during the Middle Ages and Renaissance. Urine was also once believed to be a cure for motion sickness. 

The authors believe that doctors would use the flasks to observe urine’s sedimentation, smell, color, and even taste. This would help the physicians diagnose ailments like kidney disease, jaundice, and diabetes. The excess glucose in diabetic urine gives it a saccharine quality. English physician Thomas Willis was credited with discovering this during the 17th Century and described the pee as “wonderfully sweet as if it were imbued with honey or sugar.”

[Related from PopSci+: What’s in a packrat’s petrified pee? Just a few thousand years of secrets.]

Also included in the cistern were lead clamps that were associated with wood treated with fire. According to the study, this may be evidence of burning objects brought into the hospital from houses with known plague cases. Italian physician Quinto Tiberio Angelerio wrote this in a series of rules for preventing the spread of the contagious disease in 1588, which included burning objects touched by plague patients. Plague killed roughly 25 million people throughout the 14th century alone as it spread across Eurasia, North Africa, and eventually the Americas for 500 years.

Once the cistern was full, it was likely capped with clay While landfills existed at this time outside the city walls of Rome, “the deposition of waste in cellars, courtyards, and cisterns, although prohibited, was a common practice,” study lead author Cristina Boschetti told Live Science. 

The unique find sheds more light on how hygiene practices and controls in European medical settings progressed during the early modern era. 

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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.

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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. 

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On April 26, the Food and Drug Administration approved the first pill for fecal transplants. The pill is made from healthy bacteria found in human waste which can help fight dangerous infections in the gut.

[Related: The FDA approved a fecal transplant treatment for the first time.]

According to the FDA, the pill from Massachusetts-based Seres Therapeutics provides doctors and patients with a simpler, and rigorously tested version of the procedure that has been used for just over a decade. Previously, when a patient experienced a Clostridium difficile infection or CDI, doctors would perform a fecal transplant using the stool from a healthy donor. Donor bacteria can help restore the balance of bacteria in the gut and prevent reinfections.  

The new treatment will be sold under the brand name Vowst as four daily capsules for three consecutive days. Vowst was cleared for adults 18 and older who face risks from repeat infections from C. diff, and have already received antibiotic treatment. A CDI can cause severe nausea, cramping, and diarrhea, and is dangerous when it reoccurs. CDI’s lead to roughly 15,000 to 30,000 deaths per year. 

While C. diff can be killed with antibiotics, the drugs can also destroy the beneficial bacteria that live inside the gut, leaving  it more susceptible to infections in the future. People over age 65 are at an increased risk for contracting an infection, but other risk factors include hospitalization, a weakened immune system, and a previous history of infection. Some patients may get the infection again following recovery, and the risk of additional recurrences increases with each infection. 

The FDA approved Vowst based on a study of 180 patients wherein nearly 88 percent of the patients taking the capsules did not experience a reinfection after eight weeks. About 60 percent of those who received dummy pills did see a reinfection. Some of the common side effects included abdominal swelling, constipation and diarrhea.

According to Seres, via reporting from the Associated Press, manufacturing the pills relies on the same techniques and equipment that is used to purify both blood products and other biologic therapies. It starts with stool from a screened group of donors that is tested for potential infections, viruses, and parasites. The samples are then processed to remove the waste and isolate the healthy bacteria,killing any lingering organisms. 

In the approval announcement, the FDA warned that the drug “may carry a risk of transmitting infectious agents. It is also possible for Vowst to contain food allergens.”

[Related: What to know about fecal transplants in the wake of the first death.]

In late 2022, the FDA approved Rebyota, the first pharmaceutical-grade version of a fecal transplant treatment from Ferring Pharmaceuticals. This product must be delivered via the rectum. 

The approvals of both Rebyota and Vowst are the product of years of pharmaceutical research into the bustling community of fungi, bacteria, and viruses that lives in the gut called the microbiome.

A network of stool banks from hospitals and medical institutions across the US have provided most fecal transplants. However, that growing number of fecal transplant practitioners and stool banks around the US has created a regulatory mess for the FDA, since the agency doesn’t traditionally regulate medical procedures performed by doctors. As long as stool donors are carefully screened for any potential infectious diseases, the FDA has rarely intervened in using the procedure.

In response to these new FDA-approved options, the largest stool bank in the US called OpenBiome said it will keep serving the patients like children and adults with treatment-resistant cases who are not eligible for the new treatments. Since 2013, OpenBiome has supplied more than 65,000 stool samples for CDI patients.

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A common diabetes drug has become trendy because of its use as an off-label weight loss drug. From tech moguls to influencers, this drug has become the latest “celebrity secret” for shedding the pounds. 

Ozempic, and a similar medication called Wegovy, are brand names for an injectable medicine called semaglutide. This drug is the synthetic version of a hormone called glucagon-like peptide-1 (GLP-1), which belongs to a class of medications known as GLP-1 agonists. 

The chemistry explains how Ozempic works and what its main side effects are. GLP-1 is a compound that increases insulin production and lowers blood sugar. After we eat, GLP-1 also signals to the brain a feeling of fullness. Meanwhile, GLP-1 agonists slow down the rate at which food empties out of the stomach, further promoting a feeling of satiety. This prevents cravings and overeating, which can result in weight loss. 

While Ozempic and Wegovy are now lumped together with weight loss fads, these medications are not diet hacks. Instead, they are medications proven to lower weight in certain patient populations. 

Despite this, there is a growing concern that these drugs are misused and overprescribed in individuals who casually use them for aesthetic reasons. There’s concern this type of use is resulting in repercussions like unmanaged side effects and drug shortages. Here are some proven facts and common misconceptions surrounding Ozempic. 

Fact: Ozempic’s side effects include weight loss, but it’s not a weight loss drug

This distinction is important. Ozempic is only approved by the Food and Drug Administration (FDA) for Type 2 diabetes. It is intended to help diabetes patients control their blood sugar. While it is not a weight loss drug, diabetes patients on Ozempic may lose weight as a side effect because of the way the medication works. Losing weight can improve insulin production and, in turn, benefit some individuals. Meanwhile, Wegovy is FDA-approved for chronic weight management in adults with obesity.

[Related: There’s still a lot we don’t know about the new generation of weight loss pills.]

Swetha Bhat, a primary care physician in the California Bay Area, prescribes Ozempic and Wegovy to patients who meet the criteria. She tells PopSci she has denied requests for semaglutide for weight loss because patients don’t qualify. 

“I can’t prescribe medications to someone who doesn’t meet the FDA indication,” Bhat says. “There are med spa clinics run by dermatologists or plastic surgeons who prescribe semaglutide and that is simply out of scope for their practice.”

Fact: Ozempic and Wegovy are the same medication

Ozempic and Wegovy are two names for the same injectable drug manufactured by Novo Nordisk: semaglutide. But they are approved for different conditions and administered at different dosages.

Ozempic first received FDA approval as a treatment for type 2 diabetes in 2017 at a maximum dosage of 1 milligram once weekly, and was approved again in 2022 for a larger maximum dose of 2.0 milligrams. 

Wegovy received FDA approval in 2021 for adults who are obese or overweight with at least one weight-related condition (high blood pressure, type 2 diabetes, or high cholesterol). People taking Wegovy start at a dose of 0.25 milligrams once a week and increase the dose every four weeks until they reach the full dose of 2.4 milligrams.

Despite the recent Wegovy approval, there’s already a new drug on the block, which seemingly packs even more punch. In 2022, Eli Lilly launched its first in-class diabetes drug called Mounjaro (generic name tirzepatide), which activates both GLP-1 and GIP receptors for increased blood glucose control. According to the FDA, the average weight loss on Mounjaro at the maximum dose is 12 pounds more than with semaglutide. 

Fact: Ozempic has other side effects, but they’re not the same for everyone

There are some reports that Ozempic use results in a side effect called “Ozempic face,” in which the face becomes noticeably more gaunt and sunken due to the drastic weight loss. 

[Related: Experts rank the raw food diet as the worst of 2023.]

However, the term “Ozempic face” is misleading. It’s not necessarily a side effect of Ozempic, but a general possible side effect of weight loss. Sometimes a large weight reduction can result in excess skin in the face among other places. But not everyone who uses Ozempic will experience this, and it’s not a clinically proven side effect.

The most common side effects of taking GLP-1 agonists are nausea and diarrhea. Another common side effect is lack of appetite, to the point where some patients need to remind themselves to eat.

Fact: The Ozempic shortage was caused by the weight loss fad—and many other reasons 

There are several reasons for the Ozempic shortage. Novo Nordisk stated the shortage was due to issues with manufacturers coupled with the increase in demand for both on-label and off-label use. Pharmacies also tend to not stock Ozempic as it is expensive with poor cost-benefit. 

Meanwhile, social media increased interest in semaglutide among people who wouldn’t qualify for the drug for FDA-approved reasons. For example, a TikTok of Chelsea Handler went viral after she was unknowingly given Ozempic by her “anti-aging doctor.” This is referred to as “off-label” prescribing—when a doctor uses their best judgment to prescribe a medication for which the drug isn’t FDA approved.

[Related: Weight might not be the best way to detect diabetes early.]

Digital health companies, meanwhile, have made it easy for people who want the drug to access it. This has contributed to drug shortages.

A retail pharmacist in Central California, who did not want their name published, spoke about the opposite end of the experience with PopSci. “At first we were getting an influx of patients who were diabetic and we saw how much it helped. Then all of a sudden there was a surge of non-diabetic patients and we could not get semaglutide for our diabetic patients.”

Now, most practitioners have to provide a diabetes diagnosis when prescribing Ozempic for insurance reasons, they explain. “At the same time, the supply chain was also a major contributor to the shortage. For a while, we couldn’t get the drug at all through McKesson [a drug distributor] and our diabetes patients suffered. We had to switch them to Trulicity [the brand name for the drug dulaglutide] and even that went out of stock for a while.”

Fact: Ozempic is made from lizard lips (kind of)

In a recent episode of the pop culture podcast “Psychobabble,” hosted by Tyler Oakley and Korey Kuhl, the duo giggled in wonderment after reading on Twitter that Ozempic was made from “Gila monster spit.” 

GLP-1 agonists are derived from the venomous saliva of the Gila monster, a giant lizard that lives in US and Mexican deserts. In 1990, an endocrinologist named John Eng researched both the toxic and nontoxic chemicals produced by the species for medicinal use. He discovered that Gila monsters went long periods without eating and slowed down their metabolism while maintaining constant blood sugar levels. 

The peptide that allows them to do this is called Exendin-4 and is strikingly similar in both structure and function to human GLP-1. So Exendin-4 was derived to make the first synthetic GLP-1 drug, called Exenatide.

Fact: Ozempic can be a life-changing medication for the right patients

GLP-1 agonists, including Ozempic, continuously prove to be powerful blood glucose and weight-lowering medicines. They are also one of the few classes of diabetes drugs that have a significant clinical benefit in patients with a cardiovascular disease history and chronic kidney disease, which are risk factors for diabetes. 

With so many headlines and news outlets, the amount of information the average individual has to filter through can be overwhelming, especially when it comes to health. The Ozempic craze is a fantastic example of pop culture amplifying potentially misleading information. It is important to weed out the fact from fodder to avoid an unwarranted bias against a possible life-saving medication for the right candidate.

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This article originally appeared in Knowable Magazine.

The seizures started when Samantha Gundel was just four months old. By her first birthday, she was taking a cocktail of three different anticonvulsant medicines. A vicious cycle of recurrent pneumonia, spurred on by seizure-induced inhalation of regurgitated food, landed the young toddler in and out of the hospital near her Westchester County home in New York State.

Genetic testing soon confirmed her doctors’ suspicions: Samantha, now age 4, has Dravet syndrome, an incurable form of epilepsy. Her brain was misfiring because of a mutation that is unlike those responsible for most genetic diseases; it’s a type that has long eluded the possibility of correction. Available drugs could help alleviate symptoms, but there was nothing that could address the root cause of her disease.

That’s because the mutation at the heart of Dravet creates a phenomenon known as haploinsufficiency, in which a person falls ill if they have only a single working copy of a gene. That lone gene simply can’t produce enough protein to serve its molecular purpose. In the case of Dravet, that means that electrical signaling between nerve cells gets thrown out of whack, leading to the kinds of neuronal shock waves that trigger seizures.

Most genes are not like this. Though the human genome contains two copies of almost every gene, one inherited from each parent, the body can generally do fine with just one.

Not so for genes such as SCN1A, the main culprit behind Dravet. For SCN1A and hundreds of other known genes like it, there’s a delicate balance of molecular activity that is needed to ensure proper function. Too little activity is a problem — and oftentimes, so is too much.

This Goldilocks paradigm partially explains why conventional gene therapy strategies are ill-suited to the task of haploinsufficiency correction. With therapies of this kind — several of which are now available to treat “recessive” genetic diseases such as the blood disorder beta thalassemia and a form of inherited vision loss — the amount of protein made by an introduced gene just needs to cross a minimum threshold to undo the disease process.

In those contexts, it’s not a problem if the added gene is overactive — there’s a floor, but no ceiling, to therapeutic protein levels. That is simply not the case with many dosage-sensitive diseases like Dravet, especially for brain disorders in which too much protein can overexcite neuronal activity, says Gopi Shanker, who served as chief scientific officer of Tevard Biosciences in Cambridge, Massachusetts, until earlier this year. “That’s what makes it more challenging,” he says.

Adding to the challenge: The special types of modified viruses that are used to ferry therapeutic genes into human cells can handle only so much extra DNA — and the genes at the heart of Dravet and many related haploinsufficiency disorders are much too big to fit inside of these delivery vehicles.

Overlooked no more

Faced with these technical and molecular hurdles, the biotechnology industry long ignored haploinsufficiencies. For more than 30 years, companies jostled to get a piece of the drug development action in other areas of rare genetic disease — for cystic fibrosis, say, or for hemophilia — but conditions like Dravet got short shrift. “It’s one of the most neglected classes of disorder,” says Navneet Matharu, cofounder and chief scientific officer of Regel Therapeutics, based in Berkeley, California, and Boston.

Not anymore. Thanks to new therapeutic ideas and a better understanding of disease processes, Regel, Tevard and a group of other biotech startups are taking aim at Dravet, with experimental treatments and technologies that they say should serve as testing grounds for going after haploinsufficiency diseases more broadly.

Currently, there’s little to offer patients with these maladies other than drugs to aid with symptom control, says Kenneth Myers, a pediatric neurologist at Montreal Children’s Hospital who cowrote an article about emerging therapies for Dravet and similar genetic epilepsies in the 2022 issue of the Annual Review of Pharmacology and Toxicology. But thanks to new advances, he says, “there’s a huge reason for optimism.”

Samantha, for one, now seems to have her disease under control because of a drug called STK-001; it is the first ever to be evaluated clinically that addresses the root cause of Dravet.

Between February and April 2022, doctors thrice inserted a long needle into the young girl’s lower spine and injected the investigational therapy, which is designed to bump up levels of the sodium-shuttling protein whose deficiency is responsible for Dravet. It seemed to work. For a time, Samantha lived nearly seizure-free — presumably because the increased protein levels helped correct electrical imbalances in her brain.

She went from epileptic attacks every 7 to 10 days, on average, to nothing for months on end. Her verbal skills improved, as did her physical capabilities. Her gait improved and her tremors disappeared.

Eventually, as the therapy wore off, Samantha began to backslide, with seizures returning every couple of weeks or so. But she started receiving additional doses of STK-001 under a new trial protocol in October 2022, and since then has experienced only two epileptic episodes over the span of six months. “It’s really pretty amazing,” says her mother, Jenni Barnao.

“Is it a cure? No.… But this is absolutely our best shot,” Barnao says. “There’s definitely something with this drug that’s very good. Her brain is just working better.”

Give a boost

The STK-001 treatment relies on the fact that the normal activity of genes is somewhat inefficient and wasteful. When genes get decoded into mRNA, the resulting sequences require further cutting and splicing before they’re mature and ready to serve as guides for making protein. But often, this process is sloppy and doesn’t result in usable product.

Which is where STK-001 comes in.

A kind of “antisense” therapy, STK-001 consists of short, synthetic pieces of RNA that are tailor-made to stick to part of the SCN1A gene transcript and, as a result, make productive cutting and splicing more efficient. The synthetic pieces glom on to mRNA from the one working version of the gene that people with Dravet have and help to ensure that unwanted bits of the mRNA sequence are spliced out, just as a movie editor might cut scenes that detract from a film’s story. As a result, more functional ion channel protein gets made than would otherwise happen.

Protein levels don’t get completely back to normal. According to mouse studies, there’s a 50 percent to 60 percent boost, not a full doubling of the relevant protein in the brain. But that bump seems to be enough to make a real impact on patients’ lives.

Stoke Therapeutics, the company in Bedford, Massachusetts, that is behind STK-001, reported at the American Epilepsy Society’s 2022 Annual Meeting that 20 of the first 27 Dravet patients to receive multiple doses of the therapy in early trials experienced reductions in seizure frequency. The greatest benefits were observed among young children like Samantha whose brains have accumulated less damage from years of debilitating seizures and abnormal cell function. Larger confirmatory trials that could lead to marketing approval are scheduled to begin next year.

Stoke is hardly alone in its quest to fix Dravet and haploinsufficiency disorders more generally. Several other biotech startups are nearing clinical trials with their own technological approaches to enhancing what working gene activity remains. Encoded Therapeutics, for example, will soon begin enrolling participants for a trial of its experimental Dravet therapy, ETX-001; it uses an engineered virus to deliver a protein that ramps up SCN1A gene activity so that many more mRNA copies are made of the single, functional gene.

And if any of these companies succeed in reversing the course of Dravet, their technologies could then be adapted to take on any comparable disease, says Orrin Devinsky, a neurologist at NYU Langone Health who works with several of the firms and is involved in Samantha’s care. “An effective therapy would provide a potential platform to address other haploinsufficiencies,” he says.

New targets, new tactics

Stoke will soon put that idea to the test.

Buoyed by the early promise of its Dravet therapeutic, the company developed a second drug candidate, STK-002, that similarly targets splicing to turn nonproductive gene transcripts into constructive ones. But in this case, it’s designed to tackle an inherited vision disorder known as autosomal dominant optic atrophy, caused by haploinsufficiency of a gene called OPA1. In this disease, a single working copy of OPA1 is not enough to sustain proper nerve signaling from the eyes to the brain.

Clinical evaluation of STK-002 is expected to start next year. Meanwhile, in partnership with Acadia Pharmaceuticals of San Diego, Stoke is also exploring treatments for Rett syndrome and SYNGAP1-related intellectual disability, both severe brain disorders caused by insufficient protein levels.

Stoke’s splice-modulating approach flows naturally from the success of another antisense drug, Spinraza. Developed by Ionis Pharmaceuticals in collaboration with Biogen, Spinraza also works on splicing of mRNA transcripts to promote production of a missing protein. In 2016, it became the first therapy approved for treating a rare neuromuscular disorder called spinal muscular atrophy (SMA).

SMA is somewhat different, though. It isn’t a haploinsufficiency — it occurs when both gene copies are defective, not just one — but it’s an unusual disease from a genetics standpoint. Because of a quirk in the human genome, it turns out that people have a kind of backup gene that doesn’t normally function because its mRNA undergoes faulty splicing. With Spinraza acting as a guide to help the mRNA splice correctly, that backup gene can be made operational and do the job that the damaged gene copies can’t do.

Few diseases are like this. But Stoke’s scientific cofounders, molecular geneticist Adrian Krainer of Cold Spring Harbor Laboratory in New York (who helped to develop Spinraza) and his former postdoctoral researcher Isabel Aznarez, realized that there was a whole world of other ailments — haploinsufficiencies — for which this type of splice modulation could be beneficial.

Spinraza was the prototype. Stoke’s portfolio is full of the next-generation editions. “We brought it to the next level,” says Aznarez, who now serves as head of discovery research at Stoke.

Striking a balance

There was a time when Dravet researchers were more focused on traditional gene replacement therapies. They aimed to insert a working version of the SCN1A gene into the genome of a virus and then introduce the engineered virus into brain cells. The problems proved manifold, though.

For starters, the virus vehicles generally used in gene therapy strategies — adeno-associated viruses (AAVs) — are too small to hold all 6,030 of the DNA letters that constitute the SCN1A gene sequence.

Researchers tried a few potential workarounds. At University College London, for example, gene therapist Rajvinder Karda and her colleagues split the SCN1A gene in half and delivered both parts into mice in different virus carriers. And at the University of Toronto, neuroscientist David Hampson and his group tried introducing a smaller gene that would fit in a single AAV vector and compensate for the SCN1A deficiency in an indirect way.

But none of those efforts advanced past mouse experiments. And while it is technically feasible to deliver the entire SCN1A gene into cells if you use other kinds of viral vectors, as researchers at the University of Navarra in Spain showed in mice, those viruses are generally considered unsafe for use in people.

What is more, even if gene replacement could be made to work, there are many reasons to think it would not be ideal for diseases like Dravet in which the underlying defect is mediated by an imbalance of protein levels. The amount of protein produced by those kinds of gene therapies can be unpredictable, and so are the types of cells that end up manufacturing the proteins.

To get protein levels just right, scientists say, it is best to follow the cell’s own lead, tapping into the ways that it naturally produces the protein of interest only in certain tissues of the body, and then providing a therapeutic nudge to aid the process along.

CAMP4 Therapeutics, for example, is using antisense therapies, like Stoke. But instead of targeting the splicing of gene transcripts, CAMP4’s drugs are directed at regulatory molecules that act like rheostats to control how much of those transcripts are made in the first place. By blocking or stabilizing different regulatory molecules, the company claims it can ramp up the activity of target genes in a precise and tunable way.

“It’s basically teaching the body to do it a little bit better,” says Josh Mandel-Brehm, president and CEO of CAMP4, which is based in Cambridge, Massachusetts.

In theory, the gene-editing technology known as CRISPR could obviate the need for all of these therapeutic approaches. Gene editing allows you to perfectly correct a mistake in a gene — so one could edit a faulty DNA sequence to correct it and render kids with Dravet or some other haploinsufficiency disease as good as new.

But the technology is nowhere near ready for prime time. (Some of the first CRISPR therapies to be tested in children have failed to demonstrate much benefit.) Plus, any gene-correction therapy would have to be tailored to the unique nature of a given patient’s mutations — and there are more than 1,200 Dravet-causing mutations in the SCN1A gene alone.

That’s why Jeff Coller, an RNA biologist at Johns Hopkins University and a scientific cofounder of Tevard, prefers therapeutic strategies that can address all manner of disease-causing alterations in a gene of interest, as most companies are doing now. “Having a mutation-agnostic technology is a way of going after the entire cohort of patients,” he says.

Tevard, whose mission is to “reverse” Dravet syndrome (the company’s name is Dravet spelled backward), is approaching this challenge in various ways. Some involve engineered versions of other RNAs that are key for protein production; known as “transfer” RNAs, they help to ferry amino acid building blocks to the growing protein strands. Others are intended to help bring beneficial regulatory molecules to sites of SCN1A gene activity.

But all of Tevard’s therapeutic candidates remain at least a year away from clinical testing, whereas STK-001 is in human trials today. So the company’s chief executive, Daniel Fischer — who, along with board chair and cofounder Warren Lammert, has a daughter affected by Dravet — is considering enrolling his child, now 13, in the Stoke trial rather than waiting for his own company’s efforts to bear fruit.

“We’re open to any approach that would help our daughters,” Fischer said over lunch last November at the company’s headquarters.

“And help people with Dravet generally,” added Lammert. “We’d love to see many of these things succeed.”

Editor’s note: This article was amended on April 14, 2023, to correct Gopi Shanker’s relationship with Tevard Biosciences. Shanker is Tevard’s former chief scientific officer; he is now chief scientific officer with Beam Therapeutics.

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

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This article originally appeared in Grist.

A new report by the American Lung Association found that more than one in three Americans were exposed to unhealthy levels of air pollution between 2019 to 2021. Released on Wednesday, the 24th annual State of the Air report grades Americans’ exposure to two of the nation’s most pervasive air pollutants: ground-level ozone, an air pollutant that forms smog, and particle pollution, also known as soot. 

The report found that while overall smog and soot pollution continues to decrease across the U.S., racial and geographic disparities are rising. As climate-fueled wildfires and drought increase and intensify, more people living in the West face potentially deadly particle and ozone pollution compared to their Eastern counterparts.

People of color were found to be 64 percent more likely than white people to breathe unhealthy air, compared to 61 percent in last year’s report. They are also 3.7 times more likely than white people to live in a county that received the American Lung Association’s lowest rating for all three pollution metrics that the group examined: ozone pollution, annual particle pollution, and short-term particle pollution. The report’s ratings were informed by national air quality standards set by the U.S. Environmental Protection Agency. Last year, people of color were 3.6 times more likely to live in a county that received a failing grade on all three measures.

Paul Billings, national senior vice president of public policy for the American Lung Association, said that those findings reflect the continued impact of systemic racism. Pollution sources ranging from refineries to highways are disproportionately sited in communities of color — a persistent legacy of racist housing policies such as redlining. “The benefits of clean air have not been equally shared, and in fact, we’re seeing in this report an even wider disparity than we saw last year,” he said. 

Ozone causes what experts describe as a “sunburn of the lungs,” causing shortness of breath and wheezing and increasing the risk for asthma and respiratory infections. And particulate matter pollution bypasses the human body’s natural defenses to enter the deepest part of the lungs. Even short-term exposure to fine particles — those smaller than 2.5 microns across, also known as PM 2.5 — can lead to a host of health harms, including asthma attacks and heart attacks. 

The number of people experiencing 24-hour spikes in particle pollution rose to the highest levels reported in the last decade. Close to 64 million people lived in counties with failing grades for those daily spikes, according to the report. “That’s nearly a half a million more than we saw in last year’s report,” said Billings.

One major contributor is more frequent and intense wildfires linked to climate change, which spew smoke and fine particles.

Billings said that when the American Lung Association started issuing its State of the Air reports 24 years ago, the organization noticed a much broader spread of communities across the U.S. experiencing high levels of pollution. Now, because of wildfires and increasingly hotter and drier weather, Western states are dominating the lists of top 25 cities most impacted by pollution. 

California cities make up four out of the top five in the lists of cities most impacted by annual particle pollution and ozone pollution. 

“We really see this marked shift, and a lot of that we think is due to climate change, not only for the wildfires but also the hot conditions that create the opportunity for ozone formation,” said Billings. 

Ozone forms when nitrogen oxides and other pollutants “cook” in the sun through a series of chemical reactions. According to the EPA, ozone is more likely to form “on warm, sunny days when the air is stagnant.” 

Those hotter days have become more frequent as a result of climate change, leading to “the number of unhealthy ozone days being higher than it would otherwise be,” the report says. “Simply, climate change is undercutting the progress we would have made.”

In response to these challenges, the American Lung Association and other public health groups are calling on the EPA to further limit ozone and particle pollution by significantly strengthening national ambient air quality standards under the federal Clean Air Act passed in 1970. The agency is currently reviewing both the particulate matter and ozone standards. 

Billings said tightening those limits would fulfill the central promise of the Clean Air Act to provide everyone with clean, healthy air. “While we’ve made progress — no question about it — here we are more than 50 years later looking in the rearview mirror, and we still have more than 1 in 3 living in this country, living in a county that has unhealthy air,” Billings said. “No child born in 2023 should have to breathe air pollution that can make them sick.” 

This article originally appeared in Grist at https://grist.org/health/pollution-smog-wildfires-1-in-3-americans-breathe-unhealthy-air-new-report-says-strong/. Grist is a nonprofit, independent media organization dedicated to telling stories of climate solutions and a just future. Learn more at Grist.org

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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.”

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This article was originally published on Undark.

Approximately 300 miles south of New Zealand, the Auckland Islands lie in a belt of winds known as the Roaring Forties. In the late 19th century, sailing ships departing Australasia would catch a ride back to Europe by plunging deep into the Southern Ocean to ride the westerlies home.

But these seas were poorly charted, and weather conditions frequently horrendous.

Sometimes, navigators miscalculated the islands’ position and, too late, found their vessels thrown upon the islands’ rocky ramparts. Ships were torn to pieces and survivors cast ashore on one of the most remote and inhospitable places on the planet. These castaways soon found out they were not alone.

The main land mass in the Auckland archipelago, Auckland Island, was — and still is — home to pigs, initially introduced in the first half of the 19th century by European hunters and explorers, as well as a group of Indigenous New Zealanders fleeing conflict.

The pigs have no natural predators, and over time, they have wrought destruction upon Auckland Island’s flora and fauna. Government conservationists now want them gone — but there’s a twist: These once domesticated farm animals have evolved into ultra-resilient, disease-free pigs that have caught the eye of scientists who study xenotransplantation, a type of medical procedure in which cells, tissues, or organs from one species are transferred into another species.

Last year, for the first time, surgeons transplanted pig hearts and pig kidneys into humans. Such procedures have not yet been tested in clinical trials, and they are not approved by the U.S. Food and Drug Administration or regulatory agencies in New Zealand. But researchers say that xenotransplantation could eventually prove effective at treating a range of conditions and may alleviate the huge global need for donor organs. The Auckland Island pigs, with their unique genetics, may be especially well-suited for this purpose.

Some of the hardy quadrupeds are now housed in a research facility on the New Zealand mainland. Meanwhile, conservation authorities are preparing a massive effort to eradicate those left in the wild.

The first European ship to reach the Auckland Islands (known as Maukahuka or Motu Maha in the Māori language) was the whaler Ocean, in 1806. The ship’s captain returned the following year to drop off a team of seal hunters. During this visit, pigs were first released as a food source. Subsequent introductions continued, and in the late 1800s, with the tales of shipwreck and survival piling up, the New Zealand and Australian governments got involved, releasing additional pigs for the castaways.

The pigs, which were of mostly European and Asian origin, had to learn to live with the persistent cold, rain, and wind — far from ideal conditions for animals bred for sheltered barnyards. But because pigs produce up to two litters each year, they can adapt relatively quickly, said Michael Willis, of the Rare Breeds Conservation Society of New Zealand. Soon, Auckland Island’s pigs formed one unique strain.

In the winter, they survived by eating the island’s endemic plants and scavenging carrion. In the summer, their fortunes changed, and they gorged on plump albatross chicks and protein-filled penguin eggs. Twenty-five species of seabird breed on the Auckland Islands, but after two centuries of pig predation, their numbers have fallen. New Zealand conservationists are increasingly wary of the porcine prowlers.

The archipelago is “an immensely special place,” said Stephen Horn, a project manager at New Zealand’s Department of Conservation. It’s the biggest remaining stronghold of the yellow-eyed penguin, the world’s rarest penguin species, and the Gibson’s wandering albatross, which breeds there exclusively. (Currently, said Horn, seabirds on Auckland Island nest only on the precipitous edges of the land, where even the most tenacious pig won’t venture.)

The pigs have also taken a toll on the spectacular flowering plants known as megaherbs, which are now “almost non-existent” on Auckland Island, Horn said. “They’re absent until you get to the extremely steep cliff areas. Then you can see patches of green that are out of reach” of the pigs.

Horn believes there are between 700 and 1,500 pigs on the island, with the population fluctuating widely. Survival to breeding age, he said, is low. Those that do make it have to be tough and adaptable. “On one hand, super admirable,” he said, “the way they’re able to adapt and survive in those conditions.” And on the other hand, incredibly damaging. “They use the coastline pretty heavily,” he said. “They’ll eat anything that turns up, scavenging things like dead whales and seals or even krill and squid.”

Mindful of the Department of Conservation’s long-held wish to eradicate the pigs, the Rare Breeds Conservation Society sent a team to retrieve some in 1999. Using dogs, they managed to catch 17. “Hunger appeared to be the pigs’ constant companion,” wrote team member Peter Jackson for New Zealand Geographic. “The suckling sows had only two or three teats producing milk, which told how few piglets survived.”

The team loaded the pigs on a boat and brought them back to the southern New Zealand town of Invercargill. There, the animals were put into a quarantine facility, intended to protect the country’s domestic pig herd from potential diseases.

Keeping the pigs in quarantine required money the Society didn’t have, so they prevailed upon Invercargill’s then-mayor, Tim Shadbolt, a colorful former left-wing activist, who dipped into his contingency fund for the approximately 2,300 in today’s New Zealand dollars, or $1,400, needed to feed them.

During the first year of quarantine, the pig population ballooned. “They dined on porridge and swedes and they became raging sexual beasts, producing larger litters than they did on the Auckland Islands,” Shadbolt recalled in a 2008 article in the Otago Daily Times. The pig’s food bill increased tenfold — an expenditure that whipped up a political storm in Invercargill, with councilors and constituents railing against what they characterized as a scandalous waste of public money. Shadbolt was unceremoniously stripped of his contingency fund.

The mayor, though, would be vindicated. These pigs from a previous century soon found an unlikely home in the futuristic world of xenotransplantation.

Globally, the demand for transplant organs is overwhelming. Every year, thousands of people die waiting for a new heart, liver, kidney, or lung that never arrives. In the United States alone, around 17 people on the organ waiting list die every day. For decades, xenotransplantation has been seen as a possibility to bridge this shortfall.

Since the 1960s, surgeons have transplanted chimpanzee and baboon parts into a small number of humans with life-threatening conditions, but these efforts have had little success. The biggest challenge is getting the human body’s immune system to accept the new organ.

The use of non-human primates for biomedical research is controversial, so over time, researchers looked to pigs. “Their organs, their tissues, and their physiology are sufficiently close to humans,” said Paul Tan, founder and CEO of New Zealand xenotransplantation research company NZeno. “Their cells function in a manner that is very close to humans. So their blood sugar levels and our blood sugar levels are pretty close.”

In the late 1980s, New Zealand pediatrician Bob Elliott and colleague David Collinson started a company called Diatranz to investigate whether pig islet cells could be used to treat Type-1 diabetes. For Collinson, the quest was personal. His son suffered from the disease.

Islet cells are found in the pancreas and produce insulin, but in Type-1 diabetes patients, are destroyed by the immune system. Trial transplants of human islet cells had met with mixed results, and in any case, with millions of Type-1 diabetes sufferers globally, there were nowhere near enough human donors to meet demand.

Diatranz aimed to surgically implant pig islet cells, encapsulated in a seaweed-derived polymer that shielded them from the human immune system, into the pancreases of diabetes patients. In the 1990s, though, the work stalled amid fears of disease.

Xenotransplantation, of both cells or organs, carries the risk of bacterial or viral infections crossing from the donor animal into humans. Pigs are not as closely related to humans as apes and baboons, a circumstance that makes transplanted pig parts less likely to spread disease to humans. Still, the risk persists.

While common diseases might be eliminated with medicines, a more serious risk was thought to come from viruses that essentially gatecrash the genetic material of the host animal. These are called retroviruses; they include HIV as well as viruses that cause certain cancers.

Some retroviruses, called endogenous retroviruses, have, in the deep past, even insinuated themselves into the DNA of sperm and egg cells — they are therefore part of the animal’s genetic makeup, replicated in every cell in the body and passed down through generations. There is currently no medication to eliminate retroviruses.

The concern was that pig tissues could secrete infectious particles of a porcine endogenous retrovirus, or PERV, which could then infect human cells to create a new, transmissible human disease. In the worst-case scenario, it was feared, such an event could trigger a global pandemic.

In the late 1990s, a London-based research team confirmed that, in a laboratory setting at least, PERVs could infect human cells.

The discovery, for a time, “killed xenotransplantation,” said Björn Petersen, a xenotransplantation researcher with the Friedrich Loeffler Institute, the German government’s animal-disease research center. “Pharmaceutical companies withdrew their money from the research.”

Around the world, the hunt was on for pigs that were as disease-free as possible.

In 1998, Diatranz partner Olga Garkavenko turned on her radio and got wind of Invercargill’s new arrivals. She decided to investigate.

The company obtained tissue samples from the quarantined pigs for analysis. The islands’ harsh conditions, it seemed, had been tough on disease.

“They remained isolated and therefore they remained free of a lot of common infections that you have in pigs,” said Tan. “The pigs that were weak were probably wiped out. Only the fittest survived.”

The pigs also have an unusually low number of retrovirus copies in their genome. Petersen noted that the population is also completely free of a type of PERV called PERV-C, which may pose the biggest risk to human transplant recipients. This was possible “because they were isolated for a long time and they never had contact with other pigs.”

Joachim Denner, a xenotransplantation researcher from the Free University of Berlin, said the Auckland Island pigs had another major advantage over other pig breeds — their small stature. At around 90 pounds in weight, he said, “they are the right size for transplantation.” A domestic pig weighs 300 to 700 pounds, and its organs, he added, are too large.

In 2004, Elliott, Tan, and others set up a company called Living Cell Technologies, or LCT, which absorbed Diatranz and took over the pigs’ care, building an expensive facility near Invercargill to keep them in medical-grade isolation while they were selectively bred for xenotransplantation.

The animals housed in quarantine were suddenly reputed to be worth hundreds of thousands of dollars each, much to then-Mayor Shadbolt’s barely-concealed glee.

The project brought jobs and millions of dollars of investment to Invercargill. “It has all come to fruition,” Shadbolt said in the 2008 Otago Daily Times article. “I rub it into those people who didn’t support me at every opportunity.”

By the 2010s, concerns around PERVs were lessening, as multiple clinical trials of cell transplants suggested not only that pig cells could be effective in treating diabetes, but also that PERVs weren’t passing to humans. New gene-editing technology also meant that retrovirus genes could be rendered non-functional before an animal was born.

With these advancements, the race to successfully implant pig organs in humans has gathered pace. Groups around the world now breed pigs for this purpose. It’s big business — a recent report estimated the global xenotransplantation market could be worth $24.5 billion by 2029.

In January 2022, a University of Maryland group, using a pig organ from the U.S. company Revivicor, conducted the first successful transplant of a pig heart into a living patient. The patient survived for two months. While the cause of his death is still being examined, evidence of a disease called porcine cytomegalovirus was found during the autopsy. The pig used in the transplant, said Tan, would have been rigorously screened for the virus, which, he added, shows the importance of breeding pigs that are genuinely free from such diseases.

Paul Tan now runs NZeno, which has taken over the breeding and keeping of the Auckland Island pigs. LCT, meanwhile, has switched its focus to Parkinson’s disease and recently began clinical trials of a treatment that involves inserting capsules containing pig brain cells into the human brain to repair nerve damage.

NZeno supplies pig cells to LCT and is also trying to establish itself as a major player in the organ game. “We like to think that our strain of pigs, derived from the Auckland Islands, further developed at Nzeno, would be the ideal pig strain for human organ xenotransplantation,” said Tan. Their cells, he noted, have already been used in humans for years, and have a very good track record of safety. The small number of retrovirus copies in the pigs’ genomes, he said, also require less gene editing compared to other breeds.

NZeno recently provided its pig cells to a team at Ludwig Maximilian University in Munich, which aims to have a genetically-modified pig ready for a pig-human heart transplant by 2025. NZeno is also working with another xenotransplantation group in China that aims to develop kidneys for transplant.

Petersen agreed that there is a solid rationale for minimizing gene editing. “The more genetic modifications you do,” he said, “the more side effects you can maybe expect.” But, he added, there may be cases in which it doesn’t make sense to prioritize the minimization of gene editing. For example, “if you want to have a universal donor” — an animal that can supply a variety of suitable organs or cells for human transplant — “then you need to have a pig with more genetic modifications right from the beginning.”

Denner said the Auckland Island pigs, which he describes as the most disease-free pigs in the world, may yet prove their true worth. But he cautioned against viewing them — or any pig — as a silver bullet. “All these studies have limitations,” he said. “The real effect of PERVs on humans, we will see when we perform the first transplants of organs.”

For now, wild Auckland Island pigs continue to run free in their storm-battered home, but the clock is ticking. Over the last five years, New Zealand’s Department of Conservation has been preparing for eradication.

Stephen Horn leads the team charged with this enormous task. Previous work attached GPS trackers to pigs, trying to learn their movements, and Horn’s team has trialed various methods of killing them. The plan is to wipe out the pigs using a combination of traps, poisoning, and hunters shooting from helicopters and on foot.

“The approach is really high intensity, as quickly as possible,” said Horn, “and try to keep the population as naive as possible.

“You need a suite of tools,” he continued, “because pigs are smart. Not every pig is going to be vulnerable to the same technique.”

Compounding the difficulty is the island’s size and isolation. It is several days’ dangerous sail from the mainland and, aside from a few uninhabitable hut shelters, the islands have no infrastructure to support human life. Once ashore, movement through the dense undergrowth and shoulder-high grasses is extraordinarily difficult.

“It’s rugged, remote, and massive,” said Horn. “It’s pretty overwhelming when you’re looking at it through a lens of animal pest control.”

Not everyone is thrilled at the prospect of the pigs’ demise. The animals are “very much part of our heritage,” said Willis of the Rare Breeds Conservation Society. The organization argues more effort should be made to preserve at least some of them. Perhaps the pigs could be fenced off, so as not to disrupt the entire island, said Willis. Or some could be relocated to another island, where they might not pose as much of a problem. As far as he is aware, however, these options are not being considered.

Paul Tan said he would also jump at the chance to retrieve more pigs.

The Department of Conservation, said Horn, has fielded inquiries about recovering pigs, but the logistics of retrieving them from the Auckland Islands, as well as the enormous costs involved in quarantine, are major hurdles to overcome.

Horn said that while staff are actively discussing options for retrieving pigs, their focus is eradication. With a plan in place, the department just needs to secure enough funding to make it happen, he said, “to undo some of the damage that was done by people, on what is an extremely fragile, but important place.”

Bill Morris is a documentary filmmaker, wildlife cameraman, and science journalist based in Dunedin, New Zealand. He is a regular contributor to New Zealand Geographic magazine and his work has also appeared on the BBC and Animal Planet.

This article was originally published on Undark. Read the original article.

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Ghana is the first country to approve a malaria vaccine for young children, who have the highest risk of death from the disease. Some scientists have called the new vaccine a potential “game-changer” in the fight against the disease that is the leading cause of child death in Africa.

This new vaccine, called R21, has an efficacy rate of 77 percent, according to a September review in the journal The Lancet. One approved Malaria vaccine already exists, called Mosquirix, which has a 30 to 60 percent efficacy rate. 

Late stage testing is still underway in Burkina Faso, Kenya, Mali, and Tanzania. It’s unusual for a country to approve a vaccine before clinical trials are completed, according to WHO guidelines, and the World Health Organization has yet to approve it. 

Oxford researchers shared the mid-stage data with regulatory authorities in Ghana over the past six months and their new data suggests similar performance as in earlier trials, according to Oxford Professor and Chief investigator of the R21/Matrix-M programme, Adrian Hill. The results of R21’s final trials are expected to be published in the coming months. 

[Related: New four-dose malaria vaccine is up to 80 percent effective]

Oxford researchers shared the mid-stage data with regulatory authorities in Ghana over the past six months and their new data suggests similar performance as in earlier trials, according to Oxford Professor and Chief investigator of the R21/Matrix-M programme, Adrian Hill. The results of R21’s final trials are expected to be published in the coming months.

The R21 vaccine is designed to stop disease and death, not prevent transmission, although vaccines that prevent transmission between people are currently in the works at Oxford, Hill said in a press interview.

“The main idea now is to get R21 out there as soon as possible, and then add a transmission blocking vaccine,” Hill said. “That will allow us to use vaccination, not just for disease control, but for initial disease elimination, and then eventually global eradication.”

Ghana’s Food and Drug authority approved its use for children aged five months to three years, but rollout will be delayed until the WHO approves it. Once it is approved, Ghana’s drug regulator has a deal with the Serum Institute of India to produce up to 200 million doses of R21 a year. Each dose is expected to cost a couple dollars, per the BBC.

The mosquito-borne disease kills about 620,000 people globally each year, and 77 percent of those deaths are children. That translates to a death toll of over one thousand children each day, nearly one child lost per minute, according to UNICEF.

Malaria is a parasitic disease transmitted by mosquitoes, most often seen in tropical and subtropical climates. It is preventable and curable. Symptoms range from mild to life-threatening, including tissue inflammation in the brain, kidneys, and lungs. In extreme cases, leading to cerebral malaria, kidney failure, and acute respiratory distress syndrome. Children, pregnant women, and immunocompromised individuals are most at risk.

The parasite responsible for Malaria is the unicellular plasmodium. There are multiple plasmodium species known to cause the disease, each with its own unique characteristics. Unfortunately, the most common species in sub-saharan Africa, Plasmodium falciparum, is also the most deadly. 

Vaccinations are a relatively recent method of treatment for malaria. Since Mosquirix was introduced in 2019, 1.4 million children across Ghana, Kenya, and Malawi were vaccinated, resulting in a 10 percent drop in child mortality. A lack of funding and commercial potential has prevented drugmakers from producing adequate amounts of Mosquirix.

The release of the R21 vaccine “marks a culmination of 30 years of malaria vaccine research at Oxford with the design and provision of a high efficacy vaccine that can be supplied at adequate scale to the countries who need it most,” Hill said in a statement.

There are multiple reasons why a Malaria vaccine is hard to develop—including the complex life cycles of the parasite and its ability to evade immune responses. 

However, the biggest barrier is not biological, it’s financial. Malaria is most prevalent in sub-saharan Africa, making up 95 percent of all malaria cases and 96 percent of malaria deaths. This region is also home to low-income countries, which have limited resources for research funding and vaccine development. 

[Related: White House invests $5 billion in new COVID vaccines and treatments as national emergency ends]

“Malaria is a life-threatening disease that disproportionately affects the most vulnerable populations in our society and remains a leading cause of death in childhood,” Adar Poonawalla, CEO of the Serum Institute of India, said in a press release statement. 

“We remain steadfast in our commitment to scaling up production of the vaccine to meet the needs of countries with high malaria burden and to support global efforts towards saving lives,” he said.

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Sitting for too long is harmful to your health—even if you don’t feel it at the moment, your body will remember. Staying motionless for at least four hours has been linked to an increased risk of blood clotting in humans. 

But there are some exceptions. People with permanent paralysis don’t show an elevated risk for blood clotting while those who are temporarily immobile—like being stuck in a hospital bed or in a cramped airplane seat—are more susceptible to clot formation. 

A new study published today in the journal Science probes this blood-circulation question in brown bears, a species known to withdraw in their dens for five to eight months out of the year and emerge clot-free. Hibernating bears avoided blood clots by reducing a protein in their body that triggers the blood clotting process. Humans also have this protein, it turns out, and can regulate it under certain circumstances.

[Related: Scientists stuck grizzly bears on treadmills and confirmed they hate hills as much as we do]

“I would have never thought to go to bears, but it’s an excellent idea to turn to nature for studying human biology,” says Mirta Schattner, the director of the Instituto de Medicina Experimental del CONICET in Argentina who wrote an accompanying perspective piece on the study, but wasn’t involved in the research. 

An international team led by scientists from Ludwig-Maximilians-University of Munich ran tests on brown bears and people who have long-term mobility issues to compare anti-clotting strategies. They collected blood samples from 13 free-ranging brown bears during hibernation and again when they were awake during spring. When analyzing the contents of the blood samples, the authors noticed hibernating bears showed more signs of an anti-clotting mechanism. It worked by lowering several protein levels, including heat shock protein 47 (HSP47), which regulates immune responses. Reducing HSP47 tamps down inflammation that would have otherwise started the process of blood clotting.

To see if chronically immobilized humans have a similarly helpful reaction, the authors extracted blood from 23 people with spinal cord injuries and compared it to the blood of 23 able-bodied adults. Just like with the hibernating bears, people with spinal cord injuries showed a decrease in HSP47 levels and fewer clumped platelets that form clots. 

The similar process in bears and humans suggests prolonged immobility is the trigger that switches on the anti-clotting strategy. In situations where you might be bedridden for only a couple of days, Schattner says the inflammatory proteins are more powerful than this protective mechanism. “It would be interesting to know if it’s worth blocking the clotting mechanism in patients with acute immobilization,” she theorizes. “It’s a new pharmacological target to access.”

[Related: Heart disease-related deaths rise in extreme heat and extreme cold]

Anti-clotting mechanisms are one of many adaptations biologists can study from bear hibernation. The ursine body has developed different tactics to remain dormant throughout the winter without waking up to a horde of health problems. For example, bears use their fat to break down energy without reducing their muscle mass. They also limited the renewal of damaged bone cells to prevent osteoporosis in their sleep. Another feature includes changing biological processes like heart rate when entering hibernation. Studying how bears lower their heart rate for months at a time could help doctors better understand the mechanisms that drive cardiac diseases in humans.

But the opportunity to look at these body-regulating strategies might be short-lived. Warmer temperatures and shorter winters from climate change are affecting bear hibernation patterns, says Heather Johnson, a wildlife biologist for the United States Geological Survey Alaska Science Center who was not involved in the study. “We’re seeing that bears are hibernating for a shorter period and having longer active periods.” The warmer winters signal to bears that there is less of a need to sleep when the conditions are fine to go foraging for food. 

There have also been a few anecdotal observations of bears not needing to hibernate at all, for example, because they have access to human food all winter. Johnson says that while it’s too soon to predict how climate change will affect bear survival, we are already seeing indirect effects by having more bears awake during open hunting season and getting into more conflicts with humans. As bears adjust to the changing climate, there’s no telling how their bodies will adapt. The anti-blood-clotting mechanisms they have today may be gone tomorrow—a disadvantage for the animals and a loss for potential thrombosis treatments.

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The national COVID-19 emergency is drawing to a close, which means certain treatments and tests that have previously been available without cost is soon to change. However, working on effective vaccines and therapies for COVID-19 is far from over. The federal government recently announced plans to spend over $5 billion in order to speed up new vaccines and treatments, according to a Department of Health and Human Services (HHS) spokesperson and a Biden administration official.

The plan, called Project NextGen, was first announced in the Washington Post on April 10 and aims to provide better protection from future coronaviruses that could become public health threats. It is the follow-up to the Trump Administration’s Operation Warp Speed, which sped up the production of COVID-19 vaccines in 2020. Project NextGen would take a similar approach by partnering public and private-sector organizations to accelerate development of different vaccines and therapies in an ever changing virus. 

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

“It’s been very clear to us that the market on this is moving very slowly,” White House coronavirus coordinator Ashish Jha, the White House coronavirus coordinator, told the Post on April 10. “There’s a lot that the government can do, the administration can do, to speed up those tools … for the American people.”

According to Jha, Operation Next Gen will have three main goals: creating long-lasting monoclonal antibodies, speeding up the development of mucosal vaccines to possibly reduce transmission and infection risks, and speeding efforts to develop a universal coronavirus vaccine that protects against COVID-19 and other coronaviruses. 

Medical treatments for COVID-19 have lost effectiveness as the virus has continued to evolve. Even once-hailed “miracle” monoclonal antibodies are no longer effective in the face of the Omicron variant. 

“Our ability to develop … vaccines that generate mucosal immunity will have very large benefits for other respiratory pathogens we deal with all the time, like flu and RSV,” Jha said.

Mucosal vaccinations given in the nose can provide patients “sterilizing immunity” against the virus. Some of these types of vaccines are already in development around the world, with China and India rolling out the nasal vaccines, but it is not clear how well they are working. The ChAdOx1 vaccine failed to induce nasal immunity in a phase 1 trial late last year, but a nasal vaccine in Germany has shown some promise after experiments with hamsters. 

[Related: China approves world’s first nasal COVID-19 vaccine booster.]

Michael Osterholm, an epidemiologist who worked with the administration to develop the new program, told USA Today that the rapidly developed current vaccines are “really good, but they’re not great. There is a substantial amount of work [to be done] to take these good vaccines and hopefully achieve better vaccines,” he added.

Jha did not announce a timeline for when the new products will be available to the general public, but did note that it would be based on factors including drug manufacturer production plans and Food and Drug Administration (FDA) reviews. 

Previous vaccine funding requests have been repeatedly denied by Congress, with Republicans insisting that the Biden Administration use funds left over from previous pandemic aid packages. The White House directed HHS to free up $5 billion for Operation Next Gen and the agency responded by shifting funds from testing and other priorities. 

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A new report from the Centers for Disease Control and Prevention (CDC) reports that cases of infections from A Streptococcus (commonly called strep-a or strep throat) have surged this past winter. During the time period while most COVID-19 mitigations were still in place, cases dropped by about 25 percent, but now cases are above pre-pandemic levels. 

Across the US, the CDC report found that the most severe cases of invasive group A strep infections have been seen in children. Caitlin Rivers, an epidemiologist at the Johns Hopkins Center for Health Security, told NPR that in an invasive strep infection, the bacteria has spread to other parts of the body instead of just staying in the throat. It can spread to the bloodstream, cause rashes on the skin, and even infect the body’s organs. 

[Related: Strep throat is figuring out how to beat our go-to antibiotics.]

The recent spike in strep throat cases coincides with a shortage of amoxicillin, an antibiotic commonly used to treat strep throat, especially in children. Rivers also recounted the difficulty her own family and patients have had finding the antibiotics needed to treat strep cases. “We had to visit several pharmacies to find the medication that we needed,” she tells NPR. “It just adds another burden on what’s already been a really difficult winter respiratory season for families.”

Health officials in Illinois warned parents in March to be vigilant, as five pediatric deaths were reported in the state. Illinois Department of Public Health Director Sameer Vohra warned that cases of strep throat infections that lead to severe complications were on the rise in the state “with more cases reported in 2023 than in any of the past five years.”

In October 2022, the Food and Drug Administration (FDA) added amoxicillin products to its list of drug shortages.  Some amoxicillin medications are still not widely available. The shortage is linked to the lack of liquid versions of products  that are easier for children to consume The shortage is affecting multiple generic brands, including Teva and Sandoz.

The current shortage appears to be a demand issue and not a quality issue. “Companies typically look to see what their sales were the prior year. They might make a little bit of an adjustment,” Erin Fox, a national expert on drug shortages at the University of Utah, told NPR. “But with the really severe respiratory season we’ve had this year, it just simply was a mismatch between what people manufactured and what was available.”

[Related: Tik Tokers are taking a diabetes drug to lose weight. Now it’s in short supply.]

Fox also added that while a popular strength of amoxicillin – 400 mg/5mL – isn’t always available, pharmacists have other options, like giving a lower dose at a greater volume. Shortages of many commonly used prescription medications, including adderall and some diabetes drugs, have been common throughout the United States over the past year. Increases in demand and supply chain issues being partially to blame. 

Strep throat cases are typically most common from December through April, however the pandemic has thrown seasonal infection cycles off their usual track. RSV surged especially early and severely in late summer and fall 2022 along with norovirus.

Some of the most common strep throat symptoms include pain, fever, swollen tonsils, and tiny spots at the roof of the mouth called petechiae. Infected patients should see a healthcare provider if the symptoms become serious, get worse, or if they do not go away after two weeks of initial treatment.

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This article was originally featured on Hakai Magazine, an online publication about science and society in coastal ecosystems. Read more stories like this at hakaimagazine.com.

Microplastics wreak havoc on fish in myriad ways, disrupting everything from eating behavior to brain development. While it’s clear these pesky particles can cause animals a world of trouble, scientists have found it much harder to pin down exactly how they cause so many problems.

“We know that if you expose animals to plastics, then oftentimes we’ll see pathology,” says Andrew Wargo, a disease ecologist at the Virginia Institute of Marine Science (VIMS). “But what we don’t really know are the secondary effects.”

That, however, is starting to change.

In controlled laboratory experiments, Wargo and his VIMS colleagues have shown how microplastics leave rainbow trout more vulnerable to a common salmonid disease, infectious hematopoietic necrosis virus (IHNV). The effect can be dramatic: by exposing trout to a high concentration of either polystyrene beads or nylon microfibers for one month and then subjecting them to IHNV, the scientists found that fish were three to six times more likely to die, respectively, than IHNV-infected fish that hadn’t been exposed to plastics.

As well as increasing the lethality of IHNV, the microplastics also caused the exposed fish to have higher viral loads and shed more virus.

Taking tissue samples from the fish at different points in the experiment, the scientists found that the plastics were damaging the fish’s gills and provoking an inflammatory response. This likely makes it easier for the virus to invade the fish’s body, leading to more severe disease.

“There’s this kind of priming happening with some plastics,” says Meredith Evans Seeley, an environmental chemist at the National Institute of Standards and Technology and the study’s lead author. “That allows the pathogens to be more successful at colonizing the host.”

“Understanding the mechanism of how microplastics can increase the virulence of a virus? That’s pretty new,” says Bettie Cormier, an aquatic ecotoxicologist at the Norwegian University of Science and Technology who was not involved in the work.

The deadly synergy between microplastics and viruses could be especially troubling in aquaculture operations, Wargo says. Infections spread easily on fish farms, and farmed fish frequently encounter plastics such as nylon and polystyrene, which are used for buoys and nets.

Wild fish encounter microplastics and viruses, too, Cormier adds, so similar interactions between microplastics and pathogens could be having ecosystem-level effects.

“Plastics and pathogens are everywhere,” Wargo says. “I think if we want to understand the effects of both, we probably need to consider them together.”

This article first appeared in Hakai Magazine and is republished here with permission.

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Preeclampsia is a very serious high blood pressure condition that can arise during pregnancy and is a leading cause of maternal deaths. Defined as blood pressure greater or equal to 140/90 mm Hg, the condition affects as many as 1 in 25 pregnancies in the United States and complicates eight percent of births worldwide. 

It is typically diagnosed after 20 weeks of pregnancy and symptoms can include vision changes, headaches, and swelling in the hands, feet, face or eyes of the mother, or a change in the unborn baby’s well-being.  

[Related: The important difference between postpartum psychosis and postpartum depression.]

A study published April 10 in the journal Hypertension found that more than half of all preeclampsia cases that occurred during an at term birth (37 to 42 weeks) may be prevented with a timed birth. Timed birth methods include a labor induction with oxytocin or a surgical Cesarean section.

A preterm delivery may already be considered for patients who develop preeclampsia during weeks 20 to 36 of pregnancy, but most preeclampsia cases occur during 37 to 42 weeks gestation. “Timed birth is achievable in many hospitals or health centers,” study co-author and professor of obstetric medicine at King’s College in London Laura A. Magee said in a statement. “So our proposed approach to prevent at-term preeclampsia has huge potential for global good in maternity care.”

For the study, a team of researchers in the United Kingdom looked at more than 10 years of health records from King’s College Hospital in London and Medway Maritime Hospital in Gillingham. Most of the patients in the dataset were in their early 30s and self-identified as white. Roughly 10 percent self-identified as smokers and less than three percent had a medical history of high blood pressure, Type 2 diabetes, or an autoimmune disease. Only 3.9 percent reported any known family history of preeclampsia.

The dataset included 57,131 pregnancies with health records at 11 to 13 weeks gestation. Of these, there were 1,138 cases of at-term preeclampsia. In the 35 to 36 weeks timeframe, there were 619 cases of at-term preeclampsia.

The researchers evaluated the risk of preeclampsia and potential benefits of a timed birth for both groups, using the standard critical criteria for the condition and a risk prediction model that uses a patient’s individual factors to assess risks. 

[Related: Miscarriages could become more dangerous in a post-Roe world.]

They found that at term preeclampsia occurred with a similar frequency when the patients screened during their first trimester to those screened during their third. On average, the patients included in the study delivered at 40-weeks. Two-thirds of all participants experienced spontaneous onset of labor and about one-fourth of the patients had Cesarean deliveries.

Additionally, their analysis indicates that when using a risk model in place of standard clinical screening, a timed birth may be an effective intervention for reducing the risk of at-term preeclampsia by more than half.

“Our findings suggest that over half of the cases of at-term preeclampsia may be prevented by timed (planned) birth,” said Magee. “It is important to note that being at higher risk of at-term preeclampsia was associated with earlier spontaneous onset of labor, so women at the highest risk were already less likely to deliver close to their due date.”

Some of the limitations of the research included that the preeclampsia risks were only calculated through risk modeling, and that the study didn’t look at the potential for preeclampsia after delivery which, while rare, can occur up to six weeks after birth.  Additionally, randomized clinical trials are needed to evaluate the safety and effectiveness of timed birth as an appropriate intervention to reduce at-term preeclampsia.

For pregnant people with risk factors, the Cleveland Clinic recommends some preventative steps to lower risk. These include managing blood pressure and blood sugar, getting enough sleep, and maintaining a regular exercise routine. Taking a baby aspirin daily also might decrease the risk of developing preeclampsia by 15 percent, according to the Cleveland Clinic.

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This article was originally featured on KHN.

Nothing prepared Linda C. Johnson of Indianapolis for the fatigue that descended on her after a diagnosis of stage 4 lung cancer in early 2020.

Initially, Johnson, now 77, thought she was depressed. She could barely summon the energy to get dressed in the morning. Some days, she couldn’t get out of bed.

But as she began to get her affairs in order, Johnson realized something else was going on. However long she slept the night before, she woke up exhausted. She felt depleted, even if she didn’t do much during the day.

“People would tell me, ‘You know, you’re getting old.’ And that wasn’t helpful at all. Because then you feel there’s nothing you can do mentally or physically to deal with this,” she told me.

Fatigue is a common companion of many illnesses that beset older adults: heart disease, cancer, rheumatoid arthritis, lung disease, kidney disease, and neurological conditions like multiple sclerosis, among others. It’s one of the most common symptoms associated with chronic illness, affecting 40% to 74% of older people living with these conditions, according to a 2021 review by researchers at the University of Massachusetts.

This is more than exhaustion after an extremely busy day or a night of poor sleep. It’s a persistent whole-body feeling of having no energy, even with minimal or no exertion. “I feel like I have a drained battery pretty much all of the time,” wrote a user named Renee in a Facebook group for people with polycythemia vera, a rare blood cancer. “It’s sort of like being a wrung-out dish rag.”

Fatigue doesn’t represent “a day when you’re tired; it’s a couple of weeks or a couple of months when you’re tired,” said Dr. Kurt Kroenke, a research scientist at the Regenstrief Institute in Indianapolis, which specializes in medical research, and a professor at Indiana University’s School of Medicine.

When he and colleagues queried nearly 3,500 older patients at a large primary care clinic in Indianapolis about bothersome symptoms, 55% listed fatigue — second only to musculoskeletal pain (65%) and more than back pain (45%) and shortness of breath (41%).

Separately, a 2010 study in the Journal of the American Geriatrics Society estimated that 31% of people 51 and older reported being fatigued in the past week.

The impact can be profound. Fatigue is the leading reason for restricted activity in people 70 and older, according to a 2001 study by researchers at Yale. Other studies have linked fatigue with impaired mobility, limitations in people’s abilities to perform daily activities, the onset or worsening of disability, and earlier death.

What often happens is older adults with fatigue stop being active and become deconditioned, which leads to muscle loss and weakness, which heightens fatigue. “It becomes a vicious cycle that contributes to things like depression, which can make you more fatigued,” said Dr. Jean Kutner, a professor of medicine and chief medical officer at the University of Colorado Hospital.

To stop that from happening, Johnson came up with a plan after learning her lung cancer had returned. Every morning, she set small goals for herself. One day, she’d get up and wash her face. The next, she’d take a shower. Another day, she’d go to the grocery store. After each activity, she’d rest.

In the three years since her cancer came back, Johnson’s fatigue has been constant. But “I’m functioning better,” she told me, because she’s learned how to pace herself and find things that motivate her, like teaching a virtual class to students training to be teachers and getting exercise under the supervision of a personal trainer.

When should older adults be concerned about fatigue? “If someone has been doing OK but is now feeling fatigued all the time, it’s important to get an evaluation,” said Dr. Holly Yang, a physician at Scripps Mercy Hospital in San Diego and incoming board president of the American Academy of Hospice and Palliative Medicine.

“Fatigue is an alarm signal that something is wrong with the body but it’s rarely one thing. Usually, several things need to be addressed,” said Dr. Ardeshir Hashmi, section chief of the Center for Geriatric Medicine at the Cleveland Clinic.

Among the items physicians should check: Are your thyroid levels normal? Are you having trouble with sleep? If you have underlying medical conditions, are they well controlled? Do you have an underlying infection? Are you chronically dehydrated? Do you have anemia (a deficiency of red blood cells or hemoglobin), an electrolyte imbalance, or low levels of testosterone? Are you eating enough protein? Have you been feeling more anxious or depressed recently? And might medications you’re taking be contributing to fatigue?

“The medications and doses may be the same, but your body’s ability to metabolize those medications and clear them from your system may have changed,” Hashmi said, noting that such changes in the body’s metabolic activity are common as people become older.

Many potential contributors to fatigue can be addressed. But much of the time, reasons for fatigue can’t be explained by an underlying medical condition.

That happened to Teresa Goodell, 64, a retired nurse who lives just outside Portland, Oregon. During a December visit to Arizona, she suddenly found herself exhausted and short of breath while on a hike, even though she was in good physical condition. At an urgent care facility, she was diagnosed with an asthma exacerbation and given steroids, but they didn’t help.

Soon, Goodell was spending hours each day in bed, overcome by profound tiredness and weakness. Even small activities wore her out. But none of the medical tests she received in Arizona and subsequently in Portland — a chest X-ray and CT scan, blood work, a cardiac stress test — showed abnormalities.

“There was no objective evidence of illness, and that makes it hard for anybody to believe you’re sick,” she told me.

Goodell started visiting long covid web sites and chat rooms for people with chronic fatigue syndrome. Today, she’s convinced she has post-viral syndrome from an infection. One of the most common symptoms of long covid is fatigue that interferes with daily life, according to the Centers for Disease Control and Prevention.

There are several strategies for dealing with persistent fatigue. In cancer patients, “the best evidence favors physical activity such as tai chi, yoga, walking, or low-impact exercises,” said Dr. Christian Sinclair, an associate professor of palliative medicine at the University of Kansas Health System. The goal is to “gradually stretch patients’ stamina,” he said.

With long covid, however, doing too much too soon can backfire by causing “post-exertional malaise.” Pacing one’s activities is often recommended: doing only what’s most important, when one’s energy level is highest, and resting afterward. “You learn how to set realistic goals,” said Dr. Andrew Esch, senior education advisor at the Center to Advance Palliative Care.

Cognitive behavioral therapy can help older adults with fatigue learn how to adjust expectations and address intrusive thoughts such as, “I should be able to do more.” At the University of Texas MD Anderson Cancer Center, management plans for older patients with fatigue typically include strategies to address physical activity, sleep health, nutrition, emotional health, and support from family and friends.

“So much of fatigue management is about forming new habits,” said Dr. Ishwaria Subbiah, a palliative care and integrative medicine physician at MD Anderson. “It’s important to recognize that this doesn’t happen right away: It takes time.”

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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Roughly one in six people (17.5 percent) around the world are affected by infertility, according to a new report from the World Health Organization (WHO). The report is described as a “first of its kind in a decade,” analyzing infertility data from 1990 through 2021. This  includes data from 133 previously published studies on the prevalence of infertility. 

Infertility is defined as not being able to conceive after one year or more of unprotected sex. The WHO called these new numbers “staggering.” Infertility affects both the male and female reproductive system and can cause significant emotional distress and financial hardship, and is still stigmatized and understudied.

[Related: These urologists are setting the record straight about penises and COVID.]

According to the Centers for Disease Control and Prevention (CDC), roughly one in five married women between 15 and 49 years of age experience infertility.

“The report reveals an important truth: infertility does not discriminate,” said WHO Director General Tedros Adhanom Ghebreyesus in a press release. “The sheer proportion of people affected shows the need to widen access to fertility care.”

The report found little variation in fertility rates across income levels in the new report. Higher-income countries experience infertility rates of roughly 18 percent and low- to medium-income countries see rates of close to 17 percent. 

The report, however, did find differences among how much money people are spending on treatments and how accessible they are. Those in the poorest countries spent a significantly larger proportion of their annual income on one single cycle of in vitro fertilization (IVF) or other fertility care compared to those in wealthier countries. IVF is becoming increasingly unaffordable in the US, and just one cycle of IVF can cost between $10,000 and $25,000, according to reporting from The Washington Post,

Additionally, there was limited data available for countries in Africa and across southern Asia, further emphasizing the unequal access to fertility care and the “persistent need” for better data collection methods in those regions.

While there was some regional variation in infertility at the regional level, the WHO said that the differences were either not substantial or conclusive. The highest lifetime prevalence was found in the Western Pacific (23.2 percent) and the lowest was in the Eastern Mediterranean (10.7 percent).  

[Related: Why birth rates are falling, and why it’s no big deal.]

The report did not determine whether the global infertility rate is increasing or decreasing. The WHO also noted that most of the studies used in this report contained estimates based on female respondents, despite infertility being a condition experienced by both sexes. According to the CDC, hormonal disorders, disruptions to ejaculatory or testicular functions, and genetic disorders may result in infertility in males. Lifestyle factors like smoking and excessive alcohol or drug use, age, and body weight can also undermine the ability to conceive in both sexes.

Asima Ahmad, an endocrinologist and fertility expert who serves as chief medical officer and co-founder of Carrot Fertility, told CNN that the new report shows more people need fertility coverage and access to high-quality healthcare, and that inequities need to be addressed.

“These inequities, I’m not surprised that they exist on a global level, because we already see the inequities in the United States domestically, with how infertility impacts different populations and how some populations have limited access. And even with the access that they finally get, they, for example, will have a lower rate of success or even a higher rate of miscarriage,” said Ahmad, who was not involved in the new WHO report.

Ahmad also cited a lack of access to “clinically vetted evidence-based information” about the causes of infertility and how to recognize and treat it and that access to employer-provided fertility benefits is also a significant barrier to care in the United States.

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The waste honeybees discard in their hives could hold valuable insight into the public health of our cities. In a study published this week in the journal Environmental Microbiome, scientists shared a new method for collecting microbial information from the environment using honeybee debris. Identifying germs in a city gives researchers a snapshot of the diversity of a city’s microbiome, which could lead to better health outcomes. The technique might also help in surveilling illness-causing bacteria and viruses among bees and humans. 

While we can’t see microorganisms, they play a critical behind-the-scenes role in shaping our survival. For example, microbes in the human gut support digestion, help keep our immune system healthy, and are the first line of defense from “bad” bacteria that cause food poisoning and other infections. Typically, the more diverse a person microbiome, the greater their health and well-being. One way to increase said variety is interacting with outside surroundings.

[Related: A link to depression might be in your gut bacteria]

“A lot of [microbes] are beneficial to human health,” says lead study author Elizabeth Hénaff, an assistant professor at the center for urban science and progress at New York University. “The goal of this study is understanding the whole breadth of diversity of microbiomes and the ones we’re interacting with in urban environments.” 

Hénaff and her colleagues knew they wanted to create microbial maps of different cities to get a better sense of  the diversity in each area. However, they weren’t sure what was the best way to move forward. One idea was swabbing noses, but it would be impractical to swab everyone in a broad and diverse area. The urban microbiomes might also differ from block to block, requiring extensive swabbing. Another option was wastewater surveillance, but the researchers wanted to look at everything urbanites came into contact with—not just what they digested. Then came the aha moment: they could study bee hives.

Because honeybees constantly interact with the environment when they forage for nectar, and they often carry back some bacteria, fungi, and other microorganisms from their travels  when they return to the hive. “As bees are foraging, they’re traversing all of these microbial clouds related to other aspects of the built environment,” explains Hénaff. “They’ve traversed the microbial cloud of a pond, a body of water, and groups of human beings if they happen to be in the same park where they’re going.”

The scientists used a technique called metagenomic sequencing to study all the genes found in a single environmental sample. This allowed them to match genes to different microbial species related to hive health and, in turn, learn the health status of the bees. But first they had to figure out what sample should be collected from the hive.  

In a pilot project in Brooklyn, New York, the scientists worked with local beekeepers. They took swab samples of honey, propolis (a resin-like material used to cover the inside of hives), debris, and bee carcasses—anything that could provide the most information on microorganisms.

Subsequently, they discovered that the microbes found in honey and propolis were similar across hives. “Bees are really good at controlling the microbial environment of their own beehives,” adds Hénaff. The only material that differed from hive to hive was the debris left at the bottom of the hive, and this became the source they collected in the next set of experiments.

To profile urban microbiomes, the team took samples of debris from 17 tended hives from four cities across the world: Sydney and Melbourne in Australia, Tokyo, and Venice. The DNA extracted from the bee debris contained material from different sources, including plants, mammals, insects, bacteria, and fungi in the area. 

Each city carried a unique microbial profile that gave a snapshot of how life is like there. The single Venice hive used in the study was filled with wood-rotting fungi. Hénaff says the findings makes sense since most buildings are built on submerged wood pilings. In Australia, the two Melbourne hives had large amounts of eucalyptus DNA, while Sydney’s revealed high levels of a bacterium called Gordonia polyisoprenivorans, that breaks down rubber. Tokyo’s dozen hives displayed genetic hints of lotus and wild soybean—a common plant found in Eastern Asia. There were also high levels of a soy sauce fermenting yeast called Zygosaccharomyces rouxii. 

“Most interesting to me was that [the results] didn’t feel like a disjoint metric from all the other things we know about these cities and their culture, but it actually felt like a puzzle piece we didn’t know existed that fit into our general understanding of these cities,” says Hénaff.

The debris were also helpful in identifying microbes involved in bee health. The team found three honeybee crop microbial species—Lactobacillus kunkeii, Saccharibacter sp. AM169, and Frishella perrara—along with five species related to the insects’ gut health. Three honeybee pathogens were also identified across cities. 

Next, the study identified the human pathogens bees could pick up when venturing outside. The researchers focused on the hive information collected in Tokyo because it had more hives than the other cities, and so had more data for DNA sequencing. They detected two bacteria: one that could cause bacillary dysentery and another involved in cat scratch fever. They then took the pathogen behind cat scratch fever, Rickettsia felis, and reconstructed the genome. Doing so allowed them to not only confirm the species was in the city, but that it had the bacteria-associated molecules to allow it to spread disease. 

[Related: 5 ways to keep bees buzzing that don’t require a hive]

Profiling the microbiome of different cities may be an additional tool for detecting potentially harmful pathogens in humans, says Hénaff. It could also open up new ways of surveying airborne pathogens—a growing interest since the recent arrival of SARS-CoV-2.

Jay Evans, a research entomologist at the US Department of Agriculture who was not involved in the study, says the new approach is “fine” and can help in identifying at least the microorganisms found in urban floral environments. However, he expressed reservations about overvaluing some results. Evans notes that one of the species genome-mapping algorithms used in the study is known to be “a bit greedy,” matching the best microorganism available at the moment. This suggests some genetic matchups to bacteria may not actually be the right fit, and that further tests would be needed to confirm their presence. Because bees can pick up non-living hitchhikers like pesticides, Evans also says it would be nice for the researchers to contrast these biological results with pesticide-specific studies and how that affects hive microbiomes.

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Following its March meeting, the World Health Organization’s Strategic Advisory Group of Experts on Immunization (SAGE) has revised their global COVID-19 vaccination recommendations. The new vaccine guidelines focus on group risk levels and are based on current conditions. These are subject to change as the pandemic and virus evolve. 

For high-risk and high-priority groups, SAGE recommends an additional booster dose of the COVID-19 vaccine six to 12 months after their last dose. This group includes immunocompromised people of any age, those roughly over 60 years-old, front-line health workers, and pregnant people six or 12 months after their last booster.

[Related: The FDA says get used to COVID-19 vaccine boosters.]

For medium risk individuals, like children and adolescents who have health risks, and healthy adults under about age 60, the group recommends the primary vaccination series and first booster doses, but not routine additional boosters.  

For the lowest-risk groups, SAGE recommends that countries vaccinate based on cost-effectiveness and disease burden. This group includes healthy children six months to 17 years-old. 

“The public health impact of vaccinating healthy children and adolescents is comparatively much lower than the established benefits of traditional essential vaccines for children – such as the rotavirus, measles, and pneumococcal conjugate vaccines,” SAGE wrote in a statement.

The new guidelines come as higher income countries are taking different approaches to future vaccinations. The United Kingdom and Canada are currently offering high-risk individuals another dose of bivalent boosters six months after their last dose.

Health officials in the United States are still weighing this option, but the new WHO advice contrasts with the Food and Drug Administration’s proposed plans to treat COVID-19 boosters like annual flu shots. In those plans, new formulas based on dominant circulating strains would be offered to ever fall, possibly regardless of risk status. 

“Countries should consider their specific context in deciding whether to continue vaccinating low risk groups, like healthy children and adolescents, while not compromising the routine vaccines that are so crucial for the health and well-being of this age group,” SAGE Chair Hanna Nohynek said in a statement.

The group also called for urgent global efforts to catch up on routine vaccinations for preventable diseases like measles, mumps, and tuberculosis that have been missed due to the pandemic.

[Related: A good night’s sleep could help vaccines work better.]

“As we all know, the COVID pandemic has taken a heavy toll on immunization programs,” said SAGE Chair Hanna Nohynek said on Tuesday, according to CNN. “It’s been a tremendous effort, and many countries have done very well reaching high coverages, but it is still requiring efforts to reduce the inequities, and we need to reach the high-priority groups, and we need to close the coverage gaps.”

Nohynek cited rising cases of measles in regions that the World Health Organization tracks. Measles is called a “tracer,” or a sign that other vaccine-preventable diseases are present. Polio is also already circulating in several countries, with new samples detected in New York’s wastewater. To combat this, SAGE recommends strengthening vaccine coverage and supplementing with a dose of injectable polio vaccine in places with  “persistent poliovirus circulation.”

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The Health Resources and Services Administration (HRSA) recently announced plans to overhaul the country’s Organ Procurement and Transplantation Network (OPTN). The changes include better and more transparent data,  modernizing the entire system, providing more funding for organ procurement and transplantation, and even breaking up the monopoly power of the United Network for Organ Sharing. The nonprofit organization has run the system for the entire US for 37 years.

The United Network for Organ Sharing has been under contract with the federal government for decades and coordinates matching candidates with donated organs. The nonprofit holds a $6.5 million annual contract with HRSA, and has faced numerous problems such as  discarding or damaging too many organs during transit, as well as using faulty technology.

[Related: Who gets an organ transplant? Waitlist rules are complicated.]

The Biden Administration states that they hope these changes will encourage competition in a system that has effectively operated as a monopoly for decades, thereby improving  outcomes. For years, patients and families have said that the system lacks oversight, efficiency, and discriminates against people of color. Black Americans were four times more likely to have kidney failure than white patients and Latinx Americans were 1.3 times more likely than white peers, according to the results of a public comment period by the Health and Human Services Department. Despite the increased risk, Black and Latinx patients on dialysis are less likely to get on organ donation lists and receive transplants.

Additionally, a 2022 report by the National Academies of Sciences, Engineering, and Medicine called the system “demonstrably inequitable” and found that one in five donated kidneys is not used. 

Federal government data shows that more than 100,000 people in the US are awaiting organ transplants, and about 6,000 Americans per year die while waiting for lifesaving organs. 

“Every day, patients and families across the United States rely on the Organ Procurement and Transplantation Network to save the lives of their loved ones who experience organ failure,” HRSA Administrator Carole Johnson said in a press release. “At HRSA, our stewardship and oversight of this vital work is a top priority. That is why we are taking action to both bring greater transparency to the system and to reform and modernize the OPTN. The individuals and families that depend on this life-saving work deserve no less.”

In response, the United Network for Organ Sharing said that it supports HRSA’s plan and that numerous components of the plan also align with the organizations new action agenda published in January 2023. 

[Related: Space might be the perfect place to grow human organs.]

The federal proposal would also change the entire network’s structure,installing a board of directors that is independent of the United Network for Organ Sharing to bring more transparency. 

The Biden administration has committed $67 million (nearly double the current budget) towards modernizing the transplant network in its proposed fiscal budget for 2024.

The overhaul received early bipartisan support from Congress, including Sen. Charles E. Grassley (R-IA) saying and Sen. Elizabeth Warren (D-MA).

Richard Gilroy, a transplant hepatologist and Intermountain Health’s liver transplant medical director, welcomed the new guidelines in an email to PopSci, but stressed that the proposal brought up more questions, namely if a new system can fix issues and immediately manage the complexities of organ donation.

“If appropriately listed for a transplant, patients either get a transplant or they die. For liver transplants, the very sickest patients are the first on the allocation run,” said Gilroy. “But with that, the sickest patients also need to be well enough to survive post-transplant. A lot of people die or are removed from the list before they get a chance at a transplant.”

Gilroy added that the current policy has created waste and diminished efficiency in organ placement and increased costs overall, which harms outcomes across the board. 

“As physicians, we strive to help all patients and want everyone to get a life-saving opportunity. Increasing the number of donors is critical to that goal,” said Gilroy. “However, a process that ensures equity in access to a waiting list is more important (big cities list more people and have advantages over residents of smaller remote towns that list less). Healthcare equity is needed now.”

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Tick season is not only starting sooner—it’s becoming a year-round event. While April through September are usually the most active months, the pesky eight-legged parasites are biting people and animals much earlier in the year than expected. The increasing tick bites are leading to a rise in a variety of tick-borne diseases, including some that were previously uncommon.

One reason for the hike in tick-transmitted diseases like Lyme disease and babesiosis is because humans are expanding towns and cities into previously forested areas. Andrew Handel, a pediatric infectious disease specialist in Stony Brook Medicine, says cutting down forests creates an edge habitat—when one habitat type meets another—which presents more opportunity for common tick hosts such as deer and mice to interact with humans. 

[Related: A guide to the tick species every American should know]

Climate change is another culprit. Changes in rain and temperature have morphed regions with low rates of tick-borne diseases into a more palatable place for the parasites to live. What’s more, warmer conditions are getting ticks to wake up earlier from their winter sleep and have more time to bite nearby mammals. “As we see more mild winters, we’re absolutely going to see more tick-borne diseases,” says Handel.

The best thing to do is to stay aware of how ticks are circulating in your area. Even if you don’t live in the Northeast, you may be at risk for other tick-borne diseases. Knowing what to watch out for in spring, summer, and even other seasons can help treat and potentially prevent future tick bites—and the diseases that follow.

Babesiosis

Babesiosis is a parasitic infection transmitted by the bite of deer ticks (also known as black-legged ticks). These ticks are about the size of a poppy seed and found on small mammals like the white-footed mice living in the Northeast and upper Midwest. Minnesota and Wisconsin are two Midwestern states with endemic transmission of babesiosis.

Once the Babesia parasite enters the human body, it targets red blood cells. The parasites infect and destroy red blood cells by forcing their cell membrane to break open. A tremendous loss of red blood cells can, over time, cause hemolytic anemia. “It’s actually the same way that malaria works, and is why it’s called ‘the malaria of the Northeast,’” says Handel.

Babesiosis is treatable. Your doctor would prescribe a seven- to 10-day course of antibiotics if you are severely ill. Some people are at a higher risk of complications from anemia—people who are immunocompromised, those without a spleen, and newborn babies—and may need to get blood transfusions or other supportive care.

Lyme disease

Lyme disease is also spread through deer ticks. “These ticks carry and spread multiple diseases,” explains Chad Cross, a researcher at the University of Nevada, Las Vegas who studies parasites and vector-borne diseases. “If you are bitten by one, there’s always the possibility of being infected by more than one disease agent at the same time.”

While the CDC estimate shows 476,000 Lyme disease cases in the US each year, Cross states there are “at least 10 times more cases of Lyme disease than are actually reported” to the department. One reason for the discrepancy is that most cases are asymptomatic. When people do show symptoms, the fatigue and chills they exhibit can be mistaken for another condition. If left untreated, there is a risk of developing neurological problems such as facial paralysis and nerve damage to the limbs. Chronic lyme can lead to a host of persistent issues, too, many of which are still less understood. 

Most early Lyme disease cases are curable with a two- to four-week regimen of oral antibiotics such as doxycycline and amoxicillin. However, some patients may continue to experience pain, fatigue, and concentration issues six months after treatment. 

Anaplasmosis

Anaplasmosis manifests as a flu-like illness in humans. The bacterium is present in deer ticks in the Northeast and Midwestern US. The Western blacklegged tick, most prevalent around the coast of California, Oregon, and Washington, can also spread the pathogen. There has been an upward trend of anaplasmosis cases from 348 cases in 2000 to 5,655 cases in 2019.

Similar to Lyme disease, people who develop anaplasmosis develop nonspecific symptoms such as fever and muscle aches. If left untreated, it may turn fatal with some developing severe bleeding problems and organ failure. Handel says doxycycline is the most effective treatment option.

Powassan virus infection

Three tick species carry the Powassan virus: the groundhog tick, the squirrel tick, and the deer tick. Of those, the deer tick is the one that often bites and infects humans. Nearly all cases of this rare virus have occurred in the Northeast and Great Lakes region.

The virus causes mild symptoms such as headache, vomiting, and fever. By the time a diagnosis is made, Handel says about half of the patients present some type of neurologic deficit. People may also continue to show neurological problems, such as chronic headaches and memory problems after recovery.

Because there are only about 20 to 30 cases a year, Handel says there’s not a lot of medical research on how to treat it. There is no cure or antivirals to treat Powassan virus. Instead, infected individuals are given fluids, over-the-counter medications, and other supportive care to ease symptoms while the immune system fights off the infection.

Rocky Mountain spotted fever

There are two main ticks responsible for spreading rocky mountain spotted fever: the Rocky Mountain wood tick and the American dog tick. Cross says the American dog tick is very common out East while the Rocky Mountain wood tick is found in the West. Despite its name, Cross says Rocky Mountain spotted fever is being found more in the East and South than in the actual Rocky Mountain region. The less-common brown dog tick has also caused several cases along the US-Mexico border. The disease is part of a larger class of illnesses that strike thousands of people in the states each year.

The most noticeable sign is a rash that looks like red splotches or pinpoint dots in the first three days after getting bit. If treated with either doxycycline or an antibacterial agent within the first one to four days, the symptoms won’t worsen. Otherwise, the disease can be fatal. After a week, Cross says that people can develop swelling in the brain, life-threatening respiratory problems, and a coma-like state. Those who recover from severe illness may be left with permanent disability, such as paralysis or amputation of limbs.

Alpha-gal syndrome

A bite from the lone star tick can make you allergic to red meat for life. The unusual condition takes root when someone becomes highly sensitive to a sugar molecule called alpha-gal that’s found in most mammals. People who develop the allergy cannot eat red meat (fish and birds are safe to consume) or mammal-based products like dairy and gelatin. They may also be restricted in using certain medication such as heparin, which uses pig intestines. An allergic reaction can range from hives and nausea to more life-threatening reactions like anaphylactic shock.

Alpha-gal syndrome has been a rare but increasing tick-borne condition. In 2009, there were only 24 alpha-gal cases reported in the US. By 2021, the number was estimated to be around 34,000. While saliva from the lone star tick seems to trigger the mammalian allergy, deer tick bites are suspected of also causing it. According to the CDC, lone star ticks have concentrated in large numbers across the country. They are found in the southeastern, eastern, and south-central US states extending from Maine to central Texas and Oklahoma. 

There is no cure for alpha-gal syndrome. Instead, people need to learn to avoid certain foods and mammal-based products. Symptoms are managed using antihistamines and corticosteroids.

Reduce your chances of tick infections

These days, ticks are a threat across most of the US and in practically every season. Experts warn that cases will only continue to rise as ticks expand to previously uninhabitable areas. 

[Related: Climate change could introduce humans to thousands of new viruses]

Your best bet at avoiding tick-borne diseases is to keep the pests off your body. Rather than staying indoors for the rest of your life, both experts recommend spraying tick and mosquito repellant. “DEET is what we usually recommend at 20 to 30 percent,” says Handel. If you’re going to be hiking or spending a lot of time outside, learn how to handle an insecticide called permethrin. Handel advises leaving your clothes overnight in the solution to kill any insect on contact. The repellency lasts for up to 10 washes. But make sure to only use it on your clothes or gear—it’s not meant to be sprayed directly on human skin.

Remember, you can pick up ticks even if you’re not an avid hiker or camper. Ticks tend to live on tall grass, meaning they might climb on you at the park or even on your own property. Avoid rubbing up on any tall grass and keep to the middle when walking down a path. Wearing long sleeves and tucking your pants inside your socks further prevents any openings for the pests to crawl into if they latch on your clothes. 

Once you get home, immediately wash your clothes in high heat and perform a tick check for any stragglers. If you take your pet outdoors (even if it’s just the yard), you’ll want to check them daily for ticks as well. There are also topical medications that you or a vet can apply to your pet to control for any external parasites. If you or any members of your household are feeling unwell, always let your doctor know that you’ve been in wooded areas or places with high tick circulation.

“These tick-borne diseases have been around for a long time and they’re going to become more common over time,” says Handel. “But by following these steps you can keep yourself safe and still enjoying the outdoors without having to have too much anxiety about catching one of these infections.”

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This article was originally featured on KHN.

Consider three hypothetical women in their mid-70s, all living alone in identical economic circumstances with the same array of ailments: diabetes, arthritis, and high blood pressure.

Ms. Green stays home most of the time and sometimes goes a week without seeing people. But she’s in frequent touch by phone with friends and relatives, and she takes a virtual class with a discussion group from a nearby college.

Ms. Smith also stays home, but rarely talks to anyone. She has lost contact with friends, stopped going to church, and spends most of her time watching TV.

Ms. Johnson has a wide circle of friends and a busy schedule. She walks with neighbors regularly, volunteers at a school twice a week, goes to church, and is in close touch with her children, who don’t live nearby.

Three sets of social circumstances, three levels of risk should the women experience a fall, bout of pneumonia, or serious deterioration in health.

Of the women, Ms. Johnson would be most likely to get a ride to the doctor or a visit in the hospital, experts suggest. Several people may check on Ms. Green and arrange assistance while she recovers.

But Ms. Smith would be unlikely to get much help and more likely than the others to fare poorly if her health became challenged. She’s what some experts would call “socially vulnerable” or “socially frail.”

Social frailty is a corollary to physical frailty, a set of vulnerabilities (including weakness, exhaustion, unintentional weight loss, slowness, and low physical activity) shown to increase the risk of falls, disability, hospitalization, poor surgical outcomes, admission to a nursing home, and earlier death in older adults.

Essentially, people who are physically frail have less physiological strength and a reduced biological ability to bounce back from illness or injury.

Those who are socially frail similarly have fewer resources to draw upon, but for different reasons — they don’t have close relationships, can’t rely on others for help, aren’t active in community groups or religious organizations, or live in neighborhoods that feel unsafe, among other circumstances. Also, social frailty can entail feeling a lack of control over one’s life or being devalued by others.

Many of these factors have been linked to poor health outcomes in later life, along with so-called social determinants of health — low socioeconomic status, poor nutrition, insecure housing, and inaccessible transportation.

Social frailty assumes that each factor contributes to an older person’s vulnerability and that they interact with and build upon each other. “It’s a more complete picture of older adults’ circumstances than any one factor alone,” said Dr. Melissa Andrew, a professor of geriatric medicine at Dalhousie University in Halifax, Nova Scotia, who published one of the first social vulnerability indices for older adults in 2008.

This way of thinking about older adults’ social lives, and how they influence health outcomes, is getting new attention from experts in the U.S. and elsewhere. In February, researchers at Massachusetts General Hospital and the University of California-San Francisco published a 10-item “social frailty index” in the Proceedings of the National Academy of Sciences journal.

Using data from 8,250 adults 65 and older who participated in the national Health and Retirement Study from 2010 to 2016, the researchers found that the index helped predict an increased risk of death during the period studied in a significant number of older adults, complementing medical tools used for this purpose.

“Our goal is to help clinicians identify older patients who are socially frail and to prompt problem-solving designed to help them cope with various challenges,” said Dr. Sachin Shah, a co-author of the paper and a researcher at Massachusetts General Hospital.

“It adds dimensions of what a clinician should know about their patients beyond current screening instruments, which are focused on physical health,” said Dr. Linda Fried, an internationally known frailty researcher and dean of the Mailman School of Public Health at Columbia University.

Beyond the corridors of medicine, she said, “we need society to build solutions” to issues raised in the index — the ability of seniors to work, volunteer, and engage with other people; the safety and accessibility of neighborhoods in which they live; ageism and discrimination against older adults; and more.

Meanwhile, a team of Chinese researchers recently published a comprehensive review of social frailty in adults age 60 and older, based on results from dozens of studies with about 83,900 participants in Japan, China, Korea, and Europe. They determined that 24% of these older adults, assessed both in hospitals and in the community, were socially frail — a higher portion than those deemed physically frail (12%) or cognitively frail (9%) in separate studies. Most vulnerable were people 75 and older.

What are the implications for health care? “If someone is socially vulnerable, perhaps they’ll need more help at home while they’re recovering from surgery. Or maybe they’ll need someone outside their family circle to be an advocate for them in the hospital,” said Dr. Kenneth Covinsky, a geriatrician at UCSF and co-author of the recent Proceedings of the National Academy of Sciences article.

“I can see a social frailty index being useful in identifying older adults who need extra assistance and directing them to community resources,” said Jennifer Ailshire, an associate professor of gerontology and sociology at the University of Southern California Leonard Davis School of Gerontology.

Unlike other physicians, geriatricians regularly screen older adults for extra needs, albeit without using a well-vetted or consistent set of measures. “I’ll ask, who do you depend on most and how do you depend on them? Do they bring you food? Drive you places? Come by and check on you? Give you their time and attention?” said Dr. William Dale, the Arthur M. Coppola Family Chair in Supportive Care Medicine at City of Hope, a comprehensive cancer center in Duarte, California.

Depending on the patients’ answers, Dale will refer them to a social worker or help modify their plan of care. But, he cautioned, primary care physicians and specialists don’t routinely take the time to do this.

Oak Street Health, a Chicago-based chain of 169 primary care centers for older adults in 21 states and recently purchased by CVS Health, is trying to change that in its clinics, said Dr. Ali Khan, the company’s chief medical officer of value-based care strategy. At least three times a year, medical assistants, social workers, or clinicians ask patients about loneliness and social isolation, barriers to transportation, food insecurity, financial strain, housing quality and safety, access to broadband services, and utility services.

The organization combines these findings with patient-specific medical information in a “global risk assessment” that separates seniors into four tiers of risk, from very high to very low. In turn, this informs the kinds of services provided to patients, the frequency of service delivery, and individual wellness plans, which include social as well as medical priorities.

The central issue, Khan said, is “what is this patient’s ability to continue down a path of resilience in the face of a very complicated health care system?” and what Oak Street Health can do to enhance that.

What’s left out of an approach like this, however, is something crucial to older adults: whether their relationships with other people are positive or negative. That isn’t typically measured, but it’s essential in considering whether their social needs are being met, said Linda Waite, the George Herbert Mead Distinguished Service Professor of sociology at the University of Chicago and director of the National Social Life, Health, and Aging Project.

For seniors who want to think about their own social vulnerability, consider this five-item index, developed by researchers in Japan.

(1) Do you go out less frequently now than last year?

(2) Do you sometimes visit your friends?

(3) Do you feel you are helpful to friends or family?

(4) Do you live alone?

(5) Do you talk to someone every day?

Think about your answers. If you find your responses unsatisfactory, it might be time to reconsider your social circumstances and make a change.

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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Roughly 1.4 million Americans are diagnosed with diabetes every year, and 96 million Americans over the age of 18 had prediabetes in 2019. It’s a major public health issue, and early diagnosis can prevent serious complications from the disease.

However, when it comes to diagnosis, a study published March 24 in the American Journal of Preventive Medicine found that focusing on age and not weight captures the greatest number of people in all ethnic and racial groups who have prediabetes and diabetes. The team found that this age-focused approach will also maximize the ability to diagnose prediabetes and diabetes.

[Related: Fatphobia and medical biases follow people after death.]

Currently, the US Preventive Services Task Force (USPSTF) recommends screening those who are 35 to 70 years-old who have a body mass index (BMI) above 25 for diabetes, partially because BMI is considered a risk factor and predictor for the disease. But different racial and ethnic groups develop diabetes at lower body weights, so making screening decisions solely based on weight alone can miss them, according to this study. 

“All major racial and ethnic minority groups develop diabetes at lower weights than white adults, and it’s most pronounced for Asian Americans,” Matthew O’Brien, a co-author of the study and physician with Northwestern University Feinberg School of Medicine, said in a statement. “It might sound counterintuitive because we think of being overweight or obese as the primary cause of diabetes.”

In the study, the team examined the clinical performance of the 2021 USPSTF prediabetes and diabetes screening recommendation, as well as alternate age and BMI cutoffs. The performance was assessed in the entire US adult population and also separately by race and ethnicity.

When looking at a national survey of blood sugar levels, the team found that 2021 guidelines do detect a greater share of people with people with prediabetes or diabetes, but the percentage of cases found in Asian Americans is significantly lower than from other groups. The study found an estimated 6 million Asian Americans have prediabetes or undiagnosed diabetes.

The study then examined the number of cases that would have been detected if all adults ages 35-70 were screened, regardless of BMI. Using age as a criteria detects the most cases within a broad population, hitting closer to an equal percentage point across racial groups.

When looking at lowering the minimum screening age to 18, they found that it increases the amount of cases, which results in large differences in diabetes detection. However, when expanding a test pool for screening, there is also a greater chance of testing those who do not have prediabetes or diabetes.

[Related: Why we should be looking out for diabetes in young people with COVID.]

”Diabetes is a condition in which unacceptable racial and ethnic disparities persist,” O’Brien said. “That’s why we need a screening approach that maximizes equity. If we can find everyone earlier, it helps us reduce these disparities and the bad outcomes that follow.” 

Some scientists say that there is evidence that health care providers are already doing a good job at screening and diagnosing diabetes in the United States. Elizabeth Selvin, an epidemiologist at Johns Hopkins Bloomberg School of Public Health adds that this new study also did not take into account the costs associated with expanding screening, in an interview with STAT News. A 2022 study she conducted found that the proportion of undiagnosed cases has declined substantially over the last three decades. 

Additionally, the USPSTF guidelines do suggest that clinicians consider earlier screening in racial and ethnic groups with high diabetes risk at younger ages or lower BMI. Still,  these alternatives were not formally included in their list of recommendations. 

“It’s imperative that we identify a screening approach that is equitable across the entire U.S. population,” O’Brien said. “Our findings illustrate that screening all adults aged 35 to 70 years, regardless of weight or body mass index, performs equitably across all racial and ethnic groups.”

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Swifties, Jerry Garcia’s Deadheads, and Beyoncé’s BeyHive have nothing on Symphony No. 5 in C Minor composer Ludwig van Beethoven’s fandom. The composer is considered one of the most influential musicians of all time and he defied the onset of deafness in his mid-20s and went on to compose 722 works of music, including 16 string quartets, 35 piano sonatas, and 9 symphonies.

Thanks to locks of hair saved by his devoted fans and collaborators, a team of researchers have analyzed his DNA to learn more about the composer’s ailments, almost 200 years after his death. The research is detailed in a study published this week in the journal Current Biology.

Starting at the end of the 1790s, Beethoven started losing his hearing for unknown reasons. In 1802, 25 years before his death, Beethoven asked that his doctor describe his progressive hearing loss to the world so that “as far as possible at least the world will be reconciled to me after my death.” He was also plagued with gastrointestinal ailments and jaundice. 

[Related: Oldest DNA ever sampled paints a lush portrait of a lost Arctic world.]

Beethoven’s desire for a postmortem description of his illness inspired a team of scientists in Europe to pursue this study. Improvements in DNA analysis enabled them to completely sequence a genome from small quantities of very old hair. 

“Our primary goal was to shed light on Beethoven’s health problems, which famously include progressive hearing loss, beginning in his mid- to late-20s and eventually leading to him being functionally deaf by 1818,” said study co-author Johannes Krause from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, in a statement. 

Saving locks of hair of the deceased was a common mourning practice in the Nineteenth Century. In 1804, Treasury Secretary Alexander Hamilton was famously killed in a duel with his political rival Aaron Burr and his wife Eliza clipped a lock of her late husband Alexander Hamilton’s hair and kept it in a ring. 

The team on this study first analyzed the locks of hair attributed to Beethoven, soon finding five others that were confirmed to come from the same European male. They deemed that the five locks were “almost certainly authentic” and then sequenced the composer’s Beethoven’s genome.

While the team was unable to find a definitive cause for the musician’s gastrointestinal problems or deafness, they did find evidence of a hepatitis B infection and a number of significant genetic risk factors for liver disease. These factors together with his overconsumption of alcohol likely contributed to his death at the age of 56. Earlier medical biographers had suggested that Beethoven may have had substantial inherited health troubles, but they did not find any evidence of this in his genome. 

[Related: Autopsies are more important than ever. Here’s what they can tell us.]

They also uncovered another surprise locked within the composer’s DNA. Beethoven’s Y chromosome does not match the Y chromosome of any of the five living relatives who share the same last name and common ancestor on Beethoven’s paternal line. There likely was an extramarital “event” on Beethoven’s father’s side.

“This finding suggests an extrapair paternity event in his paternal line between the conception of Hendrik van Beethoven in Kampenhout, Belgium in c.1572 and the conception of Ludwig van Beethoven seven generations later in 1770, in Bonn, Germany,” said study co-author Tristan Begg, now at the University of Cambridge, in a statement. 

The DNA they found in Beethoven’s hair is genetically most similar to that of people living in the present day state of North Rhine-Westphalia, in the western Germany. 

Additional studies of the hair samples may help clarify when Beethoven was infected with hepatitis B. Further studies of his close relatives might also help to clarify his biological relationship to living descendants of the Beethoven family.

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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.”

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We aren’t in an apocalyptic The Last of Us scenario, but there’s still plenty of fungus to be wary of. The Centers for Disease Control and Prevention (CDC) announced on March 20 that a deadly and highly drug resistant fungus is spreading at “an alarming rate” in nursing homes, long-term care hospitals, and other medical facilities that treat very sick patients.

Data from the CDC shows that infections from Candida auris (C. auris) tripled nationally from 476 infections in 2019 to 1,471 in 2021. Additionally, cases where a person carries the fungus but is not infected almost quadrupled from 1,077 in 2019 to 4,040 in 2021. Their early data suggests that these numbers have continued to increase. The CDC’s findings were published in a paper in the Annals of Internal Medicine on March 21. 

[Related: The deadly combination behind the surge of ‘superbug’ fungus outbreaks.]

“The rapid rise and geographic spread of cases is concerning and emphasizes the need for continued surveillance, expanded lab capacity, quicker diagnostic tests, and adherence to proven infection prevention and control,” Meghan Lyman, a CDC epidemiologist and co-author of the new paper, said in a press release.

The fungus primarily affects older patients with weakened immune systems. However, the fungus is resistant to some common antifungal medications, making it particularly dangerous.  A 2020 report found that 86 percent of the germ samples tested by the CDC were resistant to a broad class of drugs known as Azoles. Additionally, 1.3 percent of C. auris samples were resistant to echinocandins. These drugs are often the first treatment against the fungus, and if resistance grows as the germ evolves, C. auris could become extremely difficult to treat. 

C. auris was first reported in the United States in 2016 and public health officials hoped that it could be contained (primarily in Illinois and New York) through intensive screening and infection control in healthcare settings.

Now, C. auris can now be found in half of the 50 states, with higher concentrations in California, Texas, Florida, and Nevada. The strain on healthcare systems due to the COVID-19 pandemic may have also worsened the spread of the fungus.

According to the CDC, case counts may have increased due to enhanced screening efforts, including colonization screening. This is a test to see if a patient has the fungus somewhere inside of their body, but does not have the symptoms of infection. Symptoms include chills and fever that intensify without treatment, which are common to other fungal infections. 

While scientists believe that C. auris is not a threat to those with immune systems that can fight it off, it poses a danger to medically fragile individuals, including patients on ventilators, cancer patients on chemotherapy, and nursing home patients. It forms in medical equipment and is estimated to be fatal in between 30 to 70 percent of hospitalized people who develop bloodstream infections.

[Related: A killer fungus could help the US South fight back against insatiable ants.]

Robust cleaning of medical supplies and screening will be needed to help stop the spread since it tends to cling to protective gear like nursing gowns and gloves. These items should be changed frequently, but were reused due to supply shortages brought on by the pandemic. It can also attach to medical equipment like ventilators.

“If [the fungi] get into a hospital, they are very difficult to control and get out.” William Schaffner, a professor of medicine in the infectious diseases division of Vanderbilt University Medical Center, told The Washington Post,“They can persist, smoldering, causing infections for a considerable period of time despite the best efforts of the infection control team and everyone else in the hospital.”

However, it’s not a hopeless situation, Lyman told The New York Times. She cited intensive efforts by Illinois and New York to stop the spread that appear to be effective within health care settings.

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A class of compounds known as PFAS, or so-called forever chemicals, have made the headlines many times in the past few years—they are difficult to remove or break down, leading to pervasiveness in nature and toxic health implications for our own bodies. In fact, last year the EPA found that the chemicals cause harm at even extremely low levels, noting that any exposure could be unsafe.

And while the European Union and other governments have made steps to reduce their presence, the US has been slower to regulate them until quite recently. 

On Tuesday, the Biden administration debuted a new action to protect communities against this pollution, notably by making the nation’s first drinking water standard for PFAS, technically known as per- and polyfluoroalkyl substances. This proposal would be one of the first new standards to update the Safe Drinking Water Act since 1996, and is even more ambitious than EPA suggested limits proposed in 2016. 

[Related: PFAS are toxic and they’re everywhere. Here’s how to stay away from them.]

“I am thrilled to announce that EPA is taking yet another bold step to protect public health,” EPA administrator Michael Regan said at a news conference on Tuesday. “Folks, this is a tremendous step forward in the right direction. We anticipate that when fully implemented, this rule will prevent thousands of deaths and reduce tens of thousands of serious PFAS related illnesses.”

The proposal goes after six chemicals—specifically targeting PFOA and PFOS at 4 parts per trillion. Additionally, there would be limits set on the total mixed amount of four other similar chemicals, known as PFNA, PFHxS, PFBS, and GenX. If finalized, these regulations would require public water systems to monitor these compounds and notify the public if limits are exceeded. 

“Regulating these six highly toxic PFAS chemicals in drinking water is a historic start to protecting our families and communities,” Anna Reade, a senior scientist with the Natural Resources Defense Council, an environmental group, told the New York Times. “We cannot safeguard public health until we get off this toxic treadmill of regulating one PFAS at a time when thousands of other PFAS remain unregulated.”

Unsurprisingly, not everyone is on board. According to the New York Times, members of the Association of Metropolitan Water Agencies are concerned about high expense of compliance, estimating it would cost $43 million for just one utility in Cape Fear, North Carolina, to filter out PFAS. On the other hand, the American Chemistry Council noted to the Times that two of the chemicals mentioned in the new proposal had already been phased out of production by some manufacturers eight years ago. 

[Related: The right kind of filter can keep microplastics out of drinking water.]

A few experts also pointed out that cleaning up water is only so effective—to preserve human and environmental health, corporations must stop manufacturing these harmful chemicals altogether. While some companies have made promises to stop producing PFAS, they are hardly universal. “You have to turn it off at the source,” Carol Kwiatkowski of the Green Science Policy Institute, an environmental advocacy organization, told the BBC. “It doesn’t make any sense to keep cleaning them out of the water if we keep putting them back in.”

The Biden administration has been laying the groundwork for such a move for over a year. In 2021, Biden’s Bipartisan Infrastructure Law passed, which included $10 billion of funding to address emerging contaminants including PFAS. As of February 2023, $2 billion of that will go towards addressing pollutants in drinking water across the country.

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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.”

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Nearly 16 million Americans suffer from chronic obstructive pulmonary disease (COPD). The often severe respiratory issues can dramatically influence patients’ day-to-day lives, making even once-simple physical tasks like walking and going to the store incredibly difficult, and sometimes even life-threatening. 

While there are a number of treatments and medications available, the therapies are often expensive, complicated, and time-consuming. Recently, however, researchers designed a cheap, simple, tiny tool that could not only alleviate COPD patients’ breathing issues, but offer relief for others dealing with anxiety and stress, as well as aid practitioners of meditation and yoga.

[Related: Seniors are struggling with chronic anxiety, but don’t seek treatment.]

As detailed in a new paper published in the journal, Respiratory Care, a team at the University of Cincinnati have created a new positive-expiratory pressure (PEP) device roughly the size and shape of whistle that attaches to a lanyard for users to keep on them during their everyday activities. Unlike existing PEP products that are often handheld, bulky, and expensive,  Muhammad Ahsan Zafar and Ralph Panos’ PEP Buddy aid only costs around $25, and includes no electronics.

Because of their respiratory system degradation and weaker air tubes, it often takes COPD sufferers longer to exhale while breathing. When their breath quickens, such as during physical activities or while stressed, more and more air stays within the lungs, causing “dynamic hyperinflation” that leads to breathlessness and lower oxygen levels. This compounds over time, and often restricts or discourages further physical movement and exertion, which then can worsen existing COPD symptoms.

[Related: How to make the most of meditation with science.]

To combat these problems, users put the device in their mouth just as they would a whistle when needed, then breathe through their nose and exhale through the product. PEP Buddy’s design simply relies on creating a slight back pressure while users breathe out, thus slowing down their exhalations to better regulate air flow. In their studies, Zafar and Panos found that around 72-percent of patients utilizing PEP Buddy over a two-week period reported a “significant impact” in reducing shortness of breath while also improving their everyday living. What’s more, over a third of those participating in the study showed no signs of dropping oxygen levels while PEP Buddy was in use.

Because there are no respiratory medications involved, the PEP Buddy can also be used by anyone looking to simply better regulate their breathwork following intense exercise or while practicing mindfulness and meditation exercises. Going forward, researchers hope to oversee a long-term study to see PEP Buddy’s potential in conjunction with rescue inhalers, alongside emergency room visits and usage within pulmonary rehabilitation programs.

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As a New Yorker, there’s a difference in whether it’s cold or “brick” outside. Cold weather is when you throw on a sweater before heading out. When it’s brick, you try to stay home as much as possible to avoid ending up like a human glacier. But the local lingo didn’t apply much this winter, with record-low snowfall and above-average temperatures across New York City.

A warm winter is more than just losing a few snow days. It’s knowing that the world will be dealing with more scorching heat waves and droughts, and natural disasters like the deadly flooding caused by Hurricane Ian in Florida and Cuba last year.

Climate change is only one of humanity’s long list of problems. This month we mark the third anniversary of the COVID pandemic, a disease that has killed millions worldwide and is becoming more chronic like the flu. On top of that, Turkey and Syria are still facing the aftershocks of a historically deadly earthquake, and soaring food prices from Russia’s invasion of Ukraine could worsen global hunger for years to come. 

[Related: How to manage your mental health as traumatic events pile up]

There seems to be no shortage of community-wide tragedies. Likewise, these events are taking a toll on people’s psyches. Whether conscious or subconscious, you might mourn a loss of safety and security, on top of the more obvious layers of sorrow. But these feelings can also help you be the change you need to move forward in this ever-evolving world.

Collective grief is both a shared and unique experience

Some tragedies, like a mass shooting or police brutality, resonate among an entire group of people. “Grief is a normal reaction to loss,” says Kriss Kevorkian, a thanatologist and founder of the counseling service, A Grieving World. “When it’s collective grief, we’re experiencing that on a larger scale with more people.”

Collective grief can take hold even if you don’t personally know the people directly affected. When the Uvlade school shooting occurred, there was a nationwide outpouring of anger and sorrow over the murders of the teachers and children. Violent events like these force you to rethink life and the safety of your family, says Kevorkian.

Younger generations have become the most vulnerable to collective grief, especially with environmental anxiety. Kevorkian says that government failure to stop climate change has caused children to become more helpless and apathetic. When young people like Greta Thunberg do speak out on climate change, they are mocked and subject to verbal abuse.

Your brain and body on grief

Grief doesn’t stay in one corner of your body—it consumes your entire being. You might feel more tired than usual from tossing and turning all night. Maybe you’ve lost your appetite or have trouble keeping food down. Research shows that the first few months of grief can affect your body’s immune system activity and increase your risk of blood clots.

When your mind is weighed down by sadness, anger, and loneliness, there is little space to focus on other matters. Having “grief brain” can make it feel like you’re in a fog. Everyday tasks such as watering the plants or taking out the trash become really challenging. As you try to process your loss, you might forget things like where you placed your keys or an important doctor’s appointment. 

Grief brain happens because your mind recognizes the stress and emotional trauma as a threat, triggering the entire body’s fight-or-flight response. Brain regions like the amygdala signal the alarm through stress hormones that elevate your heart rate and increase your blood pressure, upping your anxiety and panic to keep tabs on the stressor. 

When you don’t deal with the heavy emotion, your brain protects itself by going into constant survival mode. Believing it’s in danger, it allocates more energy and resources to fear centers like the amygdala. Your brain might also decide to escape the stressor by metaphorically running away. It might dissociate from daily happenings, for example, to give you a mental break from negative emotions. “Deciding how to approach your grief can foster healing as opposed to delaying it when we try to ignore or deny reality,” says Jasmine Cobb, a social worker specializing in grief and trauma at Visual Healing Therapeutic Services in Texas.

Consume your grief before it consumes you

The good news is that grief-related stress on the brain is reversible. Meditation and mindfulness can train you to focus on the present moment instead of reliving the past or dissociating from future threats. Going outside for a 30-minute walk instead of doom-scrolling or watching the news can help clear and calm the mind. Crying can also be a healthy release of stress as it releases feel-good hormones such as oxytocin and endorphins. 

There is no normal amount of time you’re supposed to grieve. You can spend months or years mourning, only for a news story or movie to trigger your pain all over again. “There are three words I really can’t stand, ‘get over it,’” says Kevorkian. “Grief never ends.” 

While time can help with the grieving process, it’s important that you’re actively working on your emotions and any unresolved issues related to the loss. Cobb says speaking with someone you can confide in is important, whether it’s a family friend, therapist, or a spiritual leader. There is also power in shared grief. People who have gone through a similar experience can help provide support in overcoming your grief. “Find your community who can hold a torch for you when you’re unable to do that for yourself,” advises Cobb.

Turning collective grief into collective action

Grief is one of life’s greatest teachers, says Kevorkian. It shows you how to live in the present and appreciate all that you have right now. Beyond acceptance, taking action can help you wrestle with some of the hopelessness you might feel when dealing with events out of your control, Kevorkian explains.

[Related: The biggest tool we have to fight climate anxiety is community]

One example of a group turning pain into lasting change is Mothers Against Drunk Driving (MADD). In 1980, 13-year-old Cari Lightner was killed by a drunk driver—a man who had just gotten out of jail two days after his fourth DUI arrest. For the next few years, Cari’s mother, Candace, used her daughter’s photo and story of her accident to raise awareness and change California traffic safety laws. Candace went on to form MADD, a political-advocacy group that gives other grieving parents the opportunity to feel like their tragedy was not in vain. 

“It’s easy for us to stay in bed under the covers and wallow in despair,” says Kevorkian. But finding the courage to take action can help you get out of your head and connect with others sharing similar distress. Hopefully, with time and work, the world will seem a little less bleak.

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For the roughly 94 million Americans with high cholesterol, 90 percent are prescribed a class of drugs called statins. These drugs help lower low-density lipoprotein (LDL)—commonly called the “bad” cholesterol—in the blood, but can trigger muscle pain, increase blood sugar or occurence of type 2 diabetes, and occasionally cause liver damage or neurological issues. An estimated 10 to 30 percent of patients stop taking them due to these unwanted side effects.  

However, a different medication already used around the world might be a solid alternative for those who can’t take statins. A large study published on March 4 in the New England Journal of Medicine found that bempedoic acid can lower LDL levels by 21.7 percent.

[Related: A super-sharp gene editing tool could tackle high cholesterol and other common ailments.]

While statins are considered both safe and effective, they don’t work for everyone. In 2020 the Food and Drug Administration approved bempedoic acid—sold under the brand name Nexletol—to treat patients who can’t or won’t take statins. There was a lack of data from randomized controlled trials on the drug’s effects on heart health, despite studies showing it could lower LDL by 17 to 28 percent. The new research was funded in part by Esperion Therapeutics, the Michigan-based maker of Nexletol.

Bempedoic acid works by drawing cholesterol out of the waxy plaque that can build up in artery walls and interfere with blood flow, the same way that statins do. Too much plaque buildup can lead to strokes and heart attacks. According to the authors, bempedoic acid is activated in the liver and not the muscles, so it is unlikely to cause musculoskeletal pain the way statins can. 

The study included 13,970 patients from 32 countries with an average age of 65 years old. Every participant had experienced musculoskeletal adverse effects from statins, and required alternative treatment. There were roughly the same number of men and women in the trial, but 91 percent were white and 17 percent were Hispanic or Latinx.

The participants were randomized into two groups: one took bempedoic acid and the other was given a placebo. The researchers followed up with the patients for up to five years and found that the drug was well-tolerated and reduced LDL cholesterol by 21.7 percent compared with the placebo. Additionally, the risk of cardiovascular events was 13 percent lower with bempedoic acid over a median of 3.4 years compared with the placebo. By comparison, some statins can lower LDL levels by as much as 50 percent.

According to the authors, the drug worked in patients who’d previously experienced a cardiovascular event or were at risk of a first event. The study also included multiple diabetics, and did not observe any blood-sugar increases from the treatment. There were a few more cases of gout and gallstones in the group that took bempedoic acid than in the placebo group, but one of the authors told CNN that lowering the risk of a heart attack outweighs a possible gout attack.

[Related: Millions of Americans take aspirin to prevent heart disease—but should they?]

In an editorial accompanying the study, John H. Alexander, the director of cardiovascular research at Duke Clinical Research Institute, wrote, “The benefits of bempedoic acid are now clearer. It is now our responsibility to translate this information into better primary and secondary prevention for more at-risk patients, who will, as a result, benefit from fewer cardiovascular events.”

However, proving that a medication can lower cholesterol does not automatically mean it will improve cardiac health. In 2020, a drug made by Eli Lilly called evacetrapib dramatically lowered LDL cholesterol, but doubled “good” high-density lipoprotein (HDL) and did not prevent heart attacks. The new bempedoic acid study was also not conducted long enough to get a sense of how many deaths it did or did not prevent.

The positive findings are just the first step in getting the statin alternative to be more widely accepted by physicians. The study’s co-author Steven Nissen, the chair of cardiovascular medicine at the Cleveland Clinic, told The Washington Post that unless there is critical “outcome data” showing that bempedoic acid reduces heart attacks, doctors are not as likely to prescribe the treatment and insurers may not cover it. 

“In the current era where we have other cholesterol-lowering drugs, people are not going to use a drug that does not have demonstrated outcome benefits. People want evidence. Everybody has been waiting for this trial,” Nissen said. 

NYU Langone Health cardiologist Howard Weintraub commented that while some will not consider a medication successful unless it reduces mortality, he believes that is short-sighted. “I think there’s more to doing medicine than counting body bags,” he told CNN. Weintraub was not involved in this specific study, but was pleased with the results, especially for those who could benefit from lowering cholesterol but can’t take statin medications. “Preventing things that can be life changing … and certainly change your quality of life forever going forward,” he said, “I think is a good thing.” 

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The month of March brings with it the third anniversary of COVID-19 shutdowns beginning in the United States. The year 2020 became synonymous with change and fear, as major sporting events were canceled, thousands were infected with the novel virus and died, and work and school shifted online for millions. The world changed forever–especially for children.

In a survey of parents conducted in the fall of 2022 by Pew Research Center, 48 percent of parents with children in grades K-12 said that the first year of the pandemic had a very or somewhat negative impact on their children’s emotional well-being. Additionally, a 2022 review of survey studies by the National Institutes of Health (NIH) found that “the impact of the COVID-19 pandemic on mental health of children and adolescents is multifaceted and substantial,” and urged more well-designed studies looking at the mental health effects of the pandemic. 

[Related: COVID-19 vaccines are still essential in preventing death in children and teens.]

Now, a group of researchers in Sweden is turning to children’s drawings and their own explanation of what they drew to get a better sense of their feelings, beliefs, and ideas about COVID-19. A small study published March 2 in the journal Acta Paediatrica found that the common themes were detailed images of canceled activities, illness, and death, and the children had quite a bit of knowledge about the disease.

The team collected 91 drawings from kids between the ages of four and six years-old that were submitted to the Swedish Archive of Children’s Drawings between April 2020 and February 2021. The project was part of investigations into children’s voices in the public space during the pandemic.

“It was a very fun study to carry out. I was actually quite uncertain as to whether a medical journal would publish the article, but they did, including the children’s drawings and everything,” co-author Anna Sarkadi said in a statement. Sarkadi is a physician specializing in children’s health and social medicine from Uppsala University in Sweden

They analyzed the drawings using a type of visual analysis called semiotic visual analysis which looks at the image’s denotation (what images represent and how) and connotation (the associated meaning). The analysis also looked at the child’s own explanations accompanying the drawings.

The findings revealed that even the youngest children were strongly affected by the pandemic. In addition to canceled plans and images showing sick and dying people, fear, worry, and missing grandparents were common themes among them. Coronavirus was often described as a monster, while other children described how to protect themselves from the virus. One drawing even showed two children in a sword fight against a giant virus.

[Related: It’s harder for kids with food allergies to catch COVID.]

“The drawings were often covered in a lot of snot. On one drawing, a child wrote, ‘You throw up, then you cough, then you feel better or die,’ with extremely clear illustrations,” explained Maria Thell, a co-author and doctoral student at Uppsala University, in a statement. 

The study found that the children also know quite a bit about the virus, including how it spread and its symptoms. Out of 91 drawings, 14 showed hand washing, 17 showed symptoms like coughing, and 44 showed a depiction of the virus itself. 

“As a researcher with a background in child and youth science, I would love to develop this method further,” said Thell.

This team’s research will continue and the drawings from seven to 11 year old children will be studied next. 

“By encouraging young children to draw pictures using open prompts, such as how a disease feels, looks like or what is different now, it is possible to understand their interpretations of a situation and related emotions,” the authors write in the study. 

Additionally, they write that pediatricians can use children’s drawings to gage emotional response to COVID-19 in addition to other health issues and get a unique glimpse into their world. This can help adults have a better idea of what kids understand or don’t understand and detect any “unhelpful fantasies’ they may have conjured up. 

A survey of children in the United Kingdom found that seven to 11 year-olds were highly aware of the social restriction, illness, and death caused by the virus and similar reviews of children’s drawings have been conducted in Spain and Greece.

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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.”

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Many Americans remained locked down and logged online throughout 2021, changing the way people shopped for countless goods and services. Initial coverage frequently focused on the ensuing supply chain woes, but new research is showcasing another grave consequence to all that consumption—the ocean shipping industry boom generated massive amounts of greenhouse gasses. 

Although their pollution statistics rarely make into the news as much as everyday cars, “dirty cargo ships” running on fossil fuels bring an estimated 40 percent of America’s goods into the country each year, and are a major impediment towards transitioning to a greener society. Because individual ships are often connected to dozens of international companies, it is often difficult to assign emissions regulation responsibilities. Meanwhile, thousands of ships burn sulfur-heavy “bunker fuel” that, while sometimes “scrubbed” via exhaust cleaning systems, still produces hazardous waste often dumped into oceans.

[Related: Is acid rain forming from the Ohio train derailment site?]

Commissioned by Ship It Zero, a coalition advocating for ocean freight companies’ transition to clean-energy, the “All Brands on Deck” report analyzes 2021’s international imports from 18 of America’s foremost retailers, including Walmart, The Home Depot, Target, Amazon, and Samsung. The findings aren’t pretty—an estimated 4.7 million containers traveling aboard over 1,650 ships generated approximately 3.5 million metric tons of greenhouse gas emissions in 2021 alone. That’s equivalent to the carbon dioxide belched from 754,000 traditional gas-powered cars, or the energy required to power 440,000 US homes. As Canary Media also notes, “ships spewed enough smog-forming nitrogen oxide to equal the annual emissions of seven coal-fired power plants.”

Most of these imports entered the country through a few major port hubs: Los Angeles and Long Beach, California, alongside Houston, Texas, and Savannah, Georgia. The report explains that due to port  locations, much of the ocean vessels’ asthma- and cancer-causing pollutants most often affect port-adjacent and coastal communities with disproportionately Black, Indigenous, and Brown working class populations.

Walmart, Target, and Home Depot were among the worst offenders analyzed. Their combined  shipping contracts generated over 1.7 million metric tons of CO2 and 33 metric tons of methane in 2021. “Buoyed by reliance on the cheapest, most deadly fossil fuels on the planet, international shipping companies and the corporations that rely on them make billions while treating our oceans, health and climate as externalities,” explains the report’s authors. “For far too long, they’ve gotten away with it.”

[Related: Breathe easier during wildfires with a DIY air purifier.]

Ship It Zero hopes that highlighting these troubling figures and increasing pressure on corporations will spur them to speed their transitions towards cleaner shipping options, like fuel cells, marine batteries, and wind harnessing equipment. Currently, both Walmart and The Home Depot have made no public commitments to fossil fuel-free maritime shipping plans, despite generating “the highest levels of carbon dioxide, methane and carcinogenic particulate matter pollution of all companies studied,” the report reads.

As part of their suggested path forward, Ship It Zero urges these companies to ask ocean carriers to demonstrate immediate and year-over-year emission reduction efforts during contract negotiation periods. “Any ship on the water today could be retrofitted with wind- assist propulsion or other emissions reducing technologies,” argues the authors. “[P]ublic health and the climate cannot wait for an entirely new generation of vessels.”

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This article was originally featured on KHN.

There’s no cure, yet, for Alzheimer’s disease. But dozens of programs developed in the past 20 years can improve the lives of both people living with dementia and their caregivers.

Unlike support groups, these programs teach caregivers concrete skills such as how to cope with stress, make home environments safe, communicate effectively with someone who’s confused, or solve problems that arise as this devastating illness progresses.

Some of these programs, known as “comprehensive dementia care,” also employ coaches or navigators who help assess patients’ and caregivers’ needs, develop individualized care plans, connect families to community resources, coordinate medical and social services, and offer ongoing practical and emotional support.

Unfortunately, despite a significant body of research documenting their effectiveness, these programs aren’t broadly available or widely known. Only a small fraction of families coping with dementia participate, even in the face of pervasive unmet care needs. And funding is scant, compared with the amount of money that has flooded into the decades-long, headline-grabbing quest for pharmaceutical therapies.

“It’s distressing that the public conversation about dementia is dominated by drug development, as if all that’s needed were a magic pill,” said Laura Gitlin, a prominent dementia researcher and dean of the College of Nursing and Health Professions at Drexel University in Philadelphia.

“We need a much more comprehensive approach that recognizes the prolonged, degenerative nature of this illness and the fact that dementia is a family affair,” she said.

In the U.S., more than 11 million unpaid and largely untrained family members and friends provide more than 80% of care to people with dementia, supplying assistance worth $272 billion in 2021, according to the Alzheimer’s Association. (This excludes patients living in nursing homes and other institutions.) Research shows these “informal” caretakers devote longer hours to tending to those with dementia and have a higher burden of psychological and physical distress than other caregivers.

Despite those contributions, Medicare expected to spend $146 billion on people with Alzheimer’s disease or other types of dementia in 2022, while Medicaid, which pays for nursing home care for people with low incomes or disabilities, expected to spend about $61 billion.

One might think such enormous spending ensures high-quality medical care and adequate support services. But quite the opposite is true. Medical care for people with Alzheimer’s and other types of dementia in the U.S. — an estimated 7.2 million individuals, most of them seniors — is widely acknowledged to be fragmented, incomplete, poorly coordinated, and insensitive to the essential role that family caregivers play. And support services are few and far between.

“What we offer people, for the most part, is entirely inadequate,” said Carolyn Clevenger, associate dean for transformative clinical practice at Emory University’s Nell Hodgson Woodruff School of Nursing.

Clevenger helped create the Integrated Memory Care program at Emory, a primary care practice run by nurse practitioners with expertise in dementia. Like other comprehensive care programs, they pay considerable attention to caregivers’ as well as patients’ needs. “We spent a great deal of time answering all kinds of questions and coaching,” she told me. This year, Clevenger said, she hopes three additional sites will open across the country.

Expansion is a goal shared by other comprehensive care programs at UCLA (the Alzheimer’s and Dementia Care Program, now available at 18 sites), Eskenazi Health in Indianapolis, the University of California-San Francisco (Care Ecosystem, 26 sites), Johns Hopkins University (Maximizing Independence at Home), and the Benjamin Rose Institute on Aging in Cleveland (BRI Care Consultation, 35 sites).

Over the past decade, a growing body of research has shown these programs improve the quality of life for people with dementia; alleviate troublesome symptoms; help avoid unnecessary emergency room visits or hospitalizations; and delay nursing home placement, while also reducing depression symptoms, physical and emotional strain, and overall stress for caregivers.

In an important development in 2021, an expert panel organized by the National Academies of Sciences, Engineering, and Medicine said there was sufficient evidence of benefit to recommend that comprehensive dementia care programs be broadly implemented.

Now, leaders of these programs and dementia advocates are lobbying Medicare to launch a pilot project to test a new model to pay for comprehensive dementia care. They have been meeting with staff at the Center for Medicare and Medicaid Innovation and “CMMI has expressed a considerable amount of interest in this,” according to Dr. David Reuben, chief of geriatric medicine at UCLA and a leader of its dementia care program.

“I’m very optimistic that something will happen” later this year, said Dr. Malaz Boustani, a professor at Indiana University who helped develop Eskenazi Health’s Aging Brain Care program and who has been part of the discussions with the Centers for Medicare & Medicaid Services.

The Alzheimer’s Association also advocates for a pilot project of this kind, which could be adopted “Medicare-wide” if it’s shown to beneficial and cost-effective, said Matthew Baumgart, the association’s vice president of health policy. Under a model proposed by the association, comprehensive dementia care programs would receive between $175 and $225 per month for each patient in addition to what Medicare pays for other types of care.

A study commissioned by the association estimates that implementing a comprehensive care dementia model could save Medicare and Medicaid $21 billion over 10 years, largely by reducing patients’ use of intensive health care services.

Several challenges await, even if Medicare experiments with ways to support comprehensive dementia care. There aren’t enough health care professionals trained in dementia care, especially in rural areas and low-income urban areas. Moving programs into clinical settings, including primary care practices and medical clinics, may be challenging given the extent of dementia patients’ needs. And training needs for program staff members are significant.

Even if families receive some assistance, they may not be able to afford necessary help in the home or other services such as adult day care. And many families coping with dementia may remain at a loss to find help.

To address that, the Benjamin Rose Institute on Aging later this year plans to publish an online consumer directory of evidence-based programs for dementia caregivers. For the first time, people will be able to search, by ZIP code, for assistance available near them. “We want to get the word out to caregivers that help is available,” said David Bass, a senior vice president at the Benjamin Rose Institute who’s leading that effort.

Generally, programs for dementia caregivers are financed by grants or government funding and free to families. Often, they’re available through Area Agencies on Aging — organizations that families should consult if they’re looking for help. Some examples:

• Savvy Caregiver, delivered over six weeks to small groups in person or over Zoom. Each week, a group leader (often a social worker) gives a mini-lecture, discusses useful strategies, and guides group members through exercises designed to help them manage issues associated with dementia. Now offered in 20 states, Savvy Caregiver recently introduced an online, seven-session version of the program that caregivers can follow on their schedule.
• REACH Community, a streamlined version of a program recommended in the 2021 National Academy of Sciences report. In four hour-long sessions in person or over the phone, a coach teaches caregivers about dementia, problem-solving strategies, and managing symptoms, moods, stress, and safety. A similar program, REACH VA, is available across the country through the Department of Veterans Affairs.
• Tailored Activity Program. In up to eight in-home sessions over four months, an occupational therapist assesses the interests, functional abilities, and home environment of a person living with dementia. Activities that can keep the individual meaningfully engaged are suggested, along with advice on how to carry them out and tips for simplifying the activities as dementia progresses. The program is being rolled out across health care settings in Australia and is being reviewed as a possible component of geriatric home-based care by the VA, Gitlin said.

We’re eager to hear from readers about questions you’d like answered, problems you’ve been having with your care, and advice you need in dealing with the health care system. Visit khn.org/columnists to submit your requests or tips.

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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On Wednesday, pharmaceutical company Eli Lilly announced a series of price cuts that would lower the price of the most commonly used forms of its insulin by 70 percent. The company will also cap the out-of-pocket cost of insulin at $35 per month for those who have commercial insurance and use participating pharmacies.

The cost cap will come through the expansion of the company’s Insulin Value Program, which caps out-of-pocket costs at $35 or less per month for people who are uninsured. 

[Related: From the archives: How a medical ‘outsider’ discovered insulin.]

As of May 1, the company says it will drop the list price of its non branded insulin to $25 a vial from its current list price of $82.41 for a vial. 

Lilly will also lower the list price of Humulin and Humalog, which are its branded injections, during the fourth quarter of 2023. Humalog is the company’s most commonly prescribed insulin and the list price for one vial is currently $274.70 and the new price cuts will drop that down to $66.40. 

This change puts Eli Lilly in line with a provision in the Inflation Reduction Act of 2022 that imposed a $35 monthly cap on the out-of-pocket cost of insulin for senior citizens enrolled in Medicare Part D.

About three in 10 diabetics in the United States rely on insulin made by three companies that control the market–Eli Lilly, Novo Nordisk, and Sanofi.  Eli Lilly was the first company to commercialize insulin 100 years ago and has since become one of the biggest players in the market. 

Insulin manufacturers have faced ongoing criticism for their prices, forcing some patients to ration insulin or reduce their use. Insulin rationing can be life threatening because it can cause dangerous spikes in blood sugar.  Some advocacy groups say that unaffordable insulin may be a human rights abuse. At least 16.5 percent of people in the US have reported rationing insulin due to cost. 

In November 2022, Eli Lilly’s stock price dropped dramatically after a tweet from a fake account  falsely claimed that the company was making insulin free, which renewed focus on the cost of insulin. 

Other manufacturers have created additional programs to help consumers. Sanofi’s Insulin Valyou Savings Program that began in 2019 charges uninsured patients $35 and commercially insured patients up to $15 for a 30-day-supply of insulin, regardless of income. Novo Nordisk created a similar program called My$99Insulin in 2021 and the Danish company also collaborated with retail giant Walmart to sell discounted private-label analog insulin. According to Walmart, ReliOn NovoLog vials and FlexPens save customers 58 to 75 percent off the cash price for branded insulin.

[Related: TikTokers are taking a diabetes drug to lose weight. Now it’s in short supply.]

Insulin is also relatively inexpensive to manufacture. Yet the average price of insulin almost tripled between 2002 and 2013, according to the American Diabetes Association. Research from prescription drug website GoodRx found that that trend has only continued, with the average retail price of insulin increasing 54 percent between 2014 and 2019.

People with diabetes need insulin because their bodies have stopped producing enough of the hormone or aren’t using insulin efficiently to convert food into energy. After eating, the body breaks down food, mostly into sugar. The sugar enters the bloodstream, which signals the pancreas to release insulin. Insulin allows sugar to energize the cells, but if diabetes keeps sugar in the bloodstream too long, it can lead to problems like blindness, nerve damage, kidney disease, and heart disease. 

Diabetes has become the fastest growing chronic disease in the world and has doubled in the United States alone over the past 20 years. Centers for Disease Control and Prevention (CDC) data shows that more than 37.3 million people have the disease, and another 96 million Americans have prediabetes. Prediabetes is a condition where blood sugar levels are higher than normal, but are not high enough to be diagnosed as type 2 diabetes and can lead to the development of the disease.

According to the American Diabetes Association, diabetes was the seventh leading cause of death in the US in 2019.

Correction (March 8, 2023): The prices of insulin under Sanofi’s program have been corrected from $99 to $35 and $15 for uninsured and insured patients, respectively.

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A popular artificial sweetener, erythritol, has been linked to blood clotting, heart attack, stroke, and death, according to a study published February 27 in the journal Nature Medicine. Individuals with elevated factors for heart disease–such as diabetes–were twice as likely to have a heart attack or stroke if their blood contained high levels of erythritol in their blood.

Erythritol and other artificial sweeteners like aspartame and saccharin are common replacements for table sugar in low-calorie, low-carbohydrate, and “keto” branded products. “Sugar-free” products like those containing erythritol are often recommended for individuals with diabetes, metabolic syndrome, or obesity and are looking for options to help manage their sugar or calorie intake. 

The product, which can be called a “natural” sweetener because it is made in very small amounts by the human body and in fruits and vegetables, has increased in popularity in recent years. A 2022 report from research firm NielsenIQ found that sales growth for products with erythritol grew by 43 percent over two years and products that claim to have “natural sweeteners” in them grew by 91 percent.

[Related: What we know about diet soda’s connection to heart disease, stroke, and early death.]

“Sweeteners like erythritol have rapidly increased in popularity in recent years but there needs to be more in-depth research into their long-term effects,” said senior author Stanley Hazen, chairman for the Department of Cardiovascular & Metabolic Sciences in Lerner Research Institute and co-section head of Preventive Cardiology at Cleveland Clinic, in a statement. “Cardiovascular disease builds over time, and heart disease is the leading cause of death globally. We need to make sure the foods we eat aren’t hidden contributors.”

In the study, the researchers looked at over 4,000 people in the United States and Europe who were undergoing cardiac evaluation. They found that subjects with higher blood erythritol levels were at elevated risk of experiencing a heart attack, stroke, or death. 

In preclinical studies, they also found some evidence erythritol increased the formation of blood clots. To do this, the team looked at the effects of adding erythritol to either whole blood or isolated platelets. These are the cell fragments that clump together to stop bleeding and contribute to blood clots. They found that erythritol made platelets easier to activate and form a clot.

“The degree of risk was not modest,” Hazen told CNN. “If your blood level of erythritol was in the top 25 percent compared to the bottom 25 percent, there was about a two-fold higher risk for heart attack and stroke. It’s on par with the strongest of cardiac risk factors, like diabetes.”

Erythritol is produced by fermenting corn and is about 70 percent as sweet as sugar. After it is eaten, it is poorly metabolized by the body and goes into the bloodstream instead. It leaves the body naturally through urine and the human body does create low amounts of erythritol naturally, so any additional consumption through diet can accumulate in the body.

[Related: Sorry, but artificial sweeteners won’t help you lose weight.]

The study’s authors note that follow-up studies are needed to confirm their findings in the general population. Additionally, the point to several limitations in the study, including that clinical observation studies demonstrate association and not causation.

“Our study shows that when participants consumed an artificially sweetened beverage with an amount of erythritol found in many processed foods, markedly elevated levels in the blood are observed for days – levels well above those observed to enhance clotting risks,” said Hazen. “It is important that further safety studies are conducted to examine the long-term effects of artificial sweeteners in general, and erythritol specifically, on risks for heart attack and stroke, particularly in people at higher risk for cardiovascular disease.”

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On February 24, the Food & Drug Administration (FDA) authorized what the agency says is the fist at-home test for detecting both COVID-19 and the flu.

The test uses one nasal swab to collect a sample from the nose and generates results in roughly 30 minutes. It can be purchased without a prescription and is authorized for use in anyone over 14 years-old, or in children two to 14 with the help of an adult. It is made by Lucira Health, a biotech company based in California’s Bay Area. 

[Related: Airplane toilets are a surprisingly good place to track COVID outbreaks.]

“Today’s authorization of the first OTC test that can detect Influenza A and B, along with SARS-CoV-2, is a major milestone in bringing greater consumer access to diagnostic tests that can be performed entirely at home,” said Jeff Shuren, director of the FDA’s Center for Devices and Radiological Health, in a statement. “The FDA strongly supports innovation in test development, and we are eager to continue advancing greater access to at-home infectious disease testing to best support public health needs. We remain committed to working with test developers to support the shared goal of getting more accurate and reliable tests to Americans who need them.”

According to the FDA, The Lucira COVID-19 and Flu Home Test can recognize positive results for influenza A with more than 90 percent accuracy and negative results with over 99 percent accuracy. For influenza B, there were not enough cases for a clinical study while Lucira was testing the product. However, in lab tests, it was 99.9 percent accurate in detecting negative results. 

With COVID-19, it is 99.9 percent accurate for a negative result and more than 88 percent accurate with a positive result. 

“As with all rapid diagnostic tests, there is a risk of false positive and false negative results. Individuals who test positive for either flu or COVID-19 should take appropriate precautions to avoid spreading the virus and should seek follow-up care with their physician or healthcare provider as additional testing may be necessary,” the FDA wrote.

The COVID-19 pandemic has changed some doctor’s hesitations regarding testing being performed by patients. A 2020 study found that people do not require medical training to test themselves for respiratory illnesses like COVID-19 and the flu.

[Related: How our pandemic toolkit fought the many viruses of 2022.]

Wilbur Lam, a pediatric hematologist and bioengineer at Emory University who helped federal officials with test development and validation, told The New York Times that this new test is the first in a series of tests that was taken for multiple illnesses at once. 

“Now we’re in this new era that’s honestly pretty exciting,” said Lam. “It’s exciting for a health care provider, it’s exciting for the technology developers, and I think exciting for the public because we have this new test. And this is only the beginning.”

According to the US Centers for Disease Control and Prevention, the US saw 236,131 new cases, 2,407 deaths, and an average of 3,461 hospitalizations last week. After getting off to an explosive and early start, flu activity is low around the country.

The post An at-home test for both COVID-19 and the flu gains approval appeared first on Popular Science.

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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.

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Centuries before COVID-19 brought the world to a screeching halt in March 2020, a tiny bacteria called Yersinia pestis–AKA the plague–killed roughly 25 million people throughout the Fourteenth Century alone as it spread across Eurasia, North Africa, and eventually the Americas for 500 years. Plague still exists today, particularly in the American west, and parts of Africa and Asia, but it can be treated with antibiotics. 

Now, a team of scientists studying the origins and evolution of the plague are using human teeth from Denmark to help them answer burning questions on how it arrived, persisted, and spread in Scandinavia.

[Related: What a 5,000-year-old plague victim reveals about the Black Death’s origins.]

Their study, published February 24 in the journal Current Biology, focused on a timeline of 800 years (1000 to 1800 AD) and used almost 300 samples collected at 13 archeological sites around Denmark. They used the samples from the teeth to reconstruct Yersinia pestis (Y. pestis) genomes that were present at the time. Teeth can preserve traces of blood-borne infection for centuries and proved to be a valuable resource for this kind of genetic detective work. 

What they found is that the plague was reintroduced to the Danes in multiple ways over that time period via human movement. 

“We know that plague outbreaks across Europe continued in waves for approximately 500 years, but very little about its spread throughout Denmark is documented in historical archives,” said study co-author Ravneet Sidhu, a graduate student at McMaster University’s Ancient DNA Centre, in a statement.  

The analysis was conducted at McMaster and the team worked with historians and bioarchaeologists in Denmark and Manitoba, Canada to examine how the different strains of the plague that were present in Denmark during this period of time were related.

After reconstructing the genomes, the team then compared these older specimens with each other and their modern-day Y. pestis relatives. They found samples positive for plague in samples from 13 individuals who lived over a period of 300 years. From this pool, nine samples had enough genetic information to make evolutionary conclusions about how the plague persisted in Denmark, showing how urban and rural populations alike faced constant waves of the disease.

“The high frequency of Y. pestis reintroduction to Danish communities is consistent with the assumption that most deaths in the period were due to newly introduced pathogens. This association between pathogen introduction and mortality illuminates essential aspects of the demographic evolution, not only in Denmark but across the whole European continent,” said Jesper L. Boldsen, the skeletal collection curator and paleodemographer at the University of Southern Denmark, in a statement.

[Related: These skeletons might be evidence of the oldest known mercury poisonings.]

The analysis also showed that Y. pestis sequences from Denmark were interspersed with medieval and early modern strains that originated in other European countries, including the Baltics and Russia, instead of coming from a single Denmark specific cluster that reemerged from natural virus reservoirs over time.  

“The evidence for plague in Denmark, both historical and archaeological, has been far more sparse than in some other regions, such as England and Italy. This study identified plague for the first time from medieval Denmark, therefore enabling us to connect the experience in Denmark to disease patterns elsewhere,” said co-author and University of Manitoba anthropologist Julia Gamble, in a statement.

The study proposes that the earliest known appearance of Y. pestis in Denmark dates back to 1333 in the southwestern town of Ribe around the time of the Black Death. It appeared in rural areas like Tirup and disappeared by 1649. Most of the places hit in Denmark were port cities, but one of the final outbreaks hit smaller rural sites in the central portion of the country that did not have access to water for transportation. The team believes that this suggests that humans were moving the pathogens around via rodents or lice.

“The results reveal new connections between past and present experiences of plague, and add to our understanding of the distribution, patterns and virulence of re-emerging diseases,” said Hendrik Poinar, a study co-author and director of the McMaster Ancient DNA Centre and an investigator with the Michael G. DeGroote Institute for Infectious Disease Research, in a statement. “We can use this study and the methods we employed for the study of future pandemics.”

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On Thursday, the Centers for Disease Control and Prevention (CDC) reported the results of a small trial that investigated the wastewater from lavatory bathrooms on international flights for SARS-CoV-2 (the virus that causes COVID-19 infections). For most of the samples, which all came from France, the United Kingdom, and the Netherlands, COVID-19 was onboard—at least in the bathroom.

[Related: COVID-19 testing scientists are the unsung heroes of the pandemic.]

For the study, conducted by the  agency along with biotech company Ginko Bioworks, the authors tested wastewater samples from 80 flights that landed in John F. Kennedy International Airport in New York City between August 1 to September 9, 2022. The team found that 65 sewage samples (81 percent) were positive. They also were able to get 27 genome sequences of WHAT from 25 of the samples and found evidence of  BA.5, BA.4.6, and BA.2.75–all sublineages of the Omicron subvariant. 

The testing added roughly three extra minutes to aircraft maintenance, did not require swabbing passengers, can be scaled up as needed, and is also relatively inexpensive. 

“This investigation demonstrated the feasibility of aircraft wastewater surveillance as a low-resource approach compared with individual testing to monitor SARS-CoV-2 variants without direct traveler involvement or disruption to airport operations,” the authors wrote in their conclusion.

The study provides an example of how aircraft and airport wastewater surveillance can help monitor the spread of pathogens around the globe. In the case of SARS-CoV-2, Viral shedding of SARS-CoV-2 can begin in feces early in an infection, potentially before a person shows symptoms like coughing or fever. 

To track the spread of COVID-19, and give communities early warnings of spikes in the virus, the CDC launched the National Wastewater Surveillance System (NWSS) in September 2020. It works for other pathogens as well and does not rely on people getting tested themselves to detect the presence of the virus. Wastewater surveillance detected the spread of polio in New York in August 2022. 

In January, some public health officials,  concerned over a COVID-19 surge in China and expressed interest in surveilling wastewater on flights from China for new variants. Citing the success of the pilot study at JFK, the CDC and Ginko Biotech gave indications that they were open to expanding the program.

[Related: How do we track COVID as people get tested less?]

“Just like we have radar to look for airplanes to make sure we know what’s coming into our country, or we take swabs and samples to make sure somebody walking through security doesn’t have explosives on their hands, this is the same thing for pathogens or viruses or bacteria,” Ginkgo Bioworks general manager, Matthew McKnight, told Politico.

Additionally, the CDC’s The Traveler Genomic Surveillance program (TGS) runs in partnership with Ginkgo Bioworks and XpresCheck, a COVID-19 testing company, to directly test some travelers in an effort to detect new variants and fill gaps in global surveillance. 

Some of the limitations of testing wastewater on aircrafts come down to flight length—testing waste is most beneficial on longer flights where passengers are more likely to use the restroom. It also remains unclear how many airlines will be willing to participate, and connecting flights will hinder tracking the origins of variants as they arrive in the United States. 

Despite the limitations, the authors found that this could be a useful public health tool for tracking pathogens. “In combination with traveler-based surveillance, aircraft wastewater monitoring can provide a complementary early warning system for the detection of SARS-CoV-2 variants and other pathogens of public health concern,” the authors wrote. 

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This article is excerpted from Sian E. Harding’s book “The Exquisite Machine: The New Science of the Heart.“ It was originally featured on The MIT Press Reader.

Nothing shows more clearly the perfect engineering of the heart than our own failed attempts to imitate it. This history of the total artificial heart is punctuated with both brilliant innovation and continual clinical failure. In 1962, John F. Kennedy challenged the scientific community to land a man on the moon and return him safely to Earth by the end of the decade. In 1964, cardiovascular surgeon Michael DeBakey persuaded President Lyndon B. Johnson to fund a program to develop the first functional self-contained artificial heart, launching a race to successfully make one before the moon landing. In 1969 both aims were apparently achieved, with the Texas Heart Institute implanting the first total artificial heart just three months before the launch of Apollo 11. However, while the moon landings have led to the Space Shuttle, Mars Rover, and International Space Station, and (despite a long lull) the newest aims to develop a moonbase to bring us to Mars, a reliable off-the-shelf total artificial heart is still just out of reach.

At the outset, the artificial heart was aimed to be a lifetime replacement for the failing organ. This was a high bar to reach, since the first design had an external compressor with an air line through the skin into the patient’s body. Compressed air inflated and deflated Dacron pouches or sacs, which collapsed and expanded to displace blood from a surrounding sac. While having the compressor outside the body was useful, since the mechanical parts (which were most susceptible to wear) could be easily replaced, it would make for a bulky piece of equipment to be wheeled about with the patient. It was difficult to see how this could be given to a patient and expect them to live an even partly normal life for many years.

However, the history of the artificial heart is also intertwined with that of the heart transplant. This was again only a hopeful dream in the early 1960s, but by 1967 cardiac surgeon Christian Baarnard in Capetown performed the first successful transplant. Now, the purpose of these first artificial hearts was changed. They did not need to be suitable for a lifetime; their purpose was to keep the patient alive until a transplant donor could be found. As with many highly experimental therapies, the first case was done on a patient who had run out of options. A 47-year-old man was being operated on to repair a huge aneurysm of the left ventricle that had thinned and swollen the heart wall. He was being supported by a heart-lung machine, which bypassed the heart and kept blood flowing through the body. However, he could not be weaned from the machine at the end of the operation as his heart was too weak. He desperately needed a transplant. Denton Cooley, DeBakey’s associate, offered him the new experimental total artificial heart and he accepted. The patient was kept stable with the new device for 64 hours until a matching donor heart was found and then transplanted.

This seemed at first a triumph for the total artificial heart, but tragically the patient died 32 hours later from sepsis. Not only that but the device had damaged both the blood and the kidneys, and the walls of the expandable sacs were coated with blood clots. This heralded a series of problems that would continue to thwart the scientists and engineers wrestling with this procedure. Infections and sepsis are a continual challenge to any device where there is a wire that must permanently cross the skin. Devices that move the blood will alter its composition and the foreign surfaces will cause the blood to clot, resulting in strokes and blood breakdown. The first Jarvik heart, one of the next iterations, was implanted in five patients and one lived for 620 days. But two of the patients had severe strokes, and eventually all died of either sepsis or blood problems.

Heart transplantation also had a shaky start, with Baarnard’s first patient dying after only 18 days. The first patient in the UK, whose transplantation was performed by cardiothoracic surgeon Donald Ross at London’s National Heart Hospital, survived for only 45 days, and the general success rate remained disappointing. The problem here was not the mechanics of the operation or the initial performance of the new heart. It was the mismatch of the immune system of the recipient to that of the donor heart. Even though the donor heart is matched as closely as possible to the patient with the major tissue types, the immune system must be suppressed to stop the heart being rejected. Drugs to suppress the immune system were not very sophisticated in the early days, but the development of ciclosporin in the early 1980s produced a revolution in immunosuppression that dramatically improved the success of heart transplantation. Now, it is a victim of its own success, with many more people in need of a transplant than there are donors. Only about 200 transplants are carried out in the UK each year despite more than 750,000 living with heart failure, and similar figures are seen worldwide. To fill this gap, scientists have been genetically modifying pigs to make their hearts compatible with the human immune system so that they can be transplanted to patients without being rejected. This has proved very complex and challenging, but first clinical transplants started in 2022.

The success of heart transplantation, however, had reinvigorated the search for the total artificial heart, with the more achievable goal of keeping the patient alive until a donor is found, or “bridge to transplant” as it is called. For decades, the artificial heart technologies have improved through changes to more biocompatible materials, better valve design, and more efficient handling of blood flow. Successes have been achieved: one study saw 80 percent of patients on the artificial hearts surviving for over a year, and some for 6 years. The longest time a patient was supported to transplant was 1,373 days. But severe infectious complications were still common, and the goal of a complete “destination” therapy for artificial hearts was still a distant dream.

Meanwhile, the urgent need to bridge to transplant had taken the technology in another direction. Rather than replacing the failing heart completely, the idea was to support it by assisting the blood flow. The ventricular assist device, or VAD, took blood out of the ventricle of the heart by a completely different route and pushed it into the aorta at high pressure. This added to the blood being ejected from the heart and thereby magnified the effective cardiac output. It also solved another problem encountered by the engineers of total artificial hearts — how to balance the right and left heart-blood flow. The amount of blood circulating in the left ventricle/body loop must be very close to that in the right ventricle/lung loop. With 100,000 beats a day, even a teaspoon of difference at each beat would add up to 500 liters of blood in the wrong place. The heart has evolved complex biological mechanisms to make sure this does not happen, but the engineers were having huge battles to try to do the same with feedback systems. For VADs, either the right (or more usually) the left ventricle can be independently supported, taking this problem away.

Left ventricular assist devices, or LVADs, have produced a revolution in care for end-stage heart failure. More than 15,000 LVADs have now been implanted worldwide, and around a third of patients with end-stage heart failure are now supported on LVADs. The intention is usually to bridge the patients to transplant, but in fact the shortage of donor hearts means that patients can often stay on LVAD support for years. Survival rates of over 50 percent are seen at seven years, and there are reports of patients living up to 13 years on these devices. LVADs have therefore become by default a therapy in themselves. Again, technology has progressed, with newer LVADs performing better. A breakthrough idea was to stop imitating the heart, with its pulsing action, and move to constant flow of blood. Rotating paddles (impellers) push the blood along in a continuous motion, creating a smooth unbroken stream. This has the curious side effect of creating a patient without a pulse, which can be disconcerting for the unsuspecting physician as well as producing some unwanted side effects as the body adapts to the new flow. External battery packs are still an inconvenience and a source of infection, but systems are being developed that transfer energy transcutaneously (across the skin) based on induction (like domestic induction stoves). The LVAD units would still need a small, implanted battery in case of a temporary device failure — and it has been known for external battery packs to be snatched from patients by handbag thieves!

The search for a completely implantable total artificial heart continues. Trying to develop external transcutaneous units to fully power the demands of the heart is the biggest barrier. Specifications for a total artificial heart require it to pump eight liters per minute of blood against a blood pressure of 110 mmHg. (The biological power storage molecule adenosine triphosphate [ATP] would be needed in quantities greater than half your body weight per day to power your own heart to do that, if ATP were not continually renewed in cells.) Compressors have been miniaturized to be more portable, but it has been a struggle to make them completely implantable. Here it seems that the VAD technology may hold a solution, dispensing with compressors altogether and using instead the impeller devices, with dual right and left VAD working together.

Solutions seem tantalizingly close, but no one is anticipating an easy ride. The many failures over the years have certainly produced in scientists a humility and awe for the natural engineering of the heart.

Sian E. Harding is Emeritus Professor of Cardiac Pharmacology in the National Heart and Lung Institute at Imperial College London, where she led the Division of Cardiovascular Sciences and the BHF Centre for Cardiac Regeneration. She is the author of “The Exquisite Machine,” from which this article is excerpted.

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Norovirus—an unpleasant and contagious stomach virus—is spreading in the United States, even closing a school in suburban Detroit for days last week. Data from the Centers for Disease Control and Prevention (CDC) shows that positive tests are at a seasonal high throughout the country, with the test positivity spikes in the Northeast (over 16 percent) the South (also over 16 percent positive), the West (over 12.5 percent), and a small dip from over 17 percent positive to under 15 in the Midwest. Currently, 14 states are reporting outbreaks of the virus and cases have also been rising in the United Kingdom and Canada.

Norovirus is commonly called called the “stomach flu,” but is not related to the influenza virus. It generally causes nausea, diarrhea, vomiting, and stomach pain, and a mild fever and arches are also possible. It is usually spread through contaminated foods, surfaces, hands, or water and is also the annual leading cause of foodborne illness. The virus is extremely contagious and is often found on cruise ships, at schools, and in other environments where people share close quarters.

[ Related: Want to stay healthy? Learn to wash your hands the right way. ]

While norovirus can be contracted at any time of year, instances of the illness are most common from November to April in countries above the equator and between April and September in regions below the equator. One wildcard for 2023 is that changes in behavior due to the COVID-19 pandemic have interrupted natural cycles of many viruses. Since people have behaved differently since 2020, viruses do not travel the globe in their usual patterns, and population level (not individual immunity) is likely reduced, so we’re more susceptible to viruses and in different patterns.

Infectious disease specialist Dr. Daniel Kuritzkes from Brigham and Women’s Hospital in Boston, Massachusetts told NBC10 Boston, “The recent norovirus cases are probably another example of seeing re-emergence of common infections as we continue to emerge from our COVID-19 shells… There were periodic localized outbreaks of norovirus infection all the time pre-COVID, so not surprising that we’re seeing them again.”

[Related: Restaurants could save a lot of dough by letting sick employees stay home. ]

According to the Mayo Clinic, norovirus symptoms usually last for only a few days; those infected should stay hydrated as much as possible, since dehydration can cause complications and possible hospitalization. It is also important to isolate and stay home from work or school, if possible, to avoid infecting others since the virus spreads so quickly.

“Set a timer on your phone if you must to say it’s time to try to eat something, or it’s time to at the very least to drink something to remain hydrated. If you can’t keep water down after 24 hours, it’s important to seek help,” says Dr. Jay-Sheree Allen, a Mayo Clinic family medicine physician. “If you are able to keep some things down, but your symptoms persist after 48 to 72 hours, it’s also a wise idea to seek help from a medical professional.”

Norovirus is a difficult virus to kill, so washing hands with soap and water is an important prevention method, since as hand and sanitizer is not as effective against norovirus. Some other prevention tips include washing your fruits and vegetables before eating them, not sharing utensils with those who are sick, avoiding contact with people who are infected, and throughly washing clothes, especially if they’re soiled.

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Moderna announced that it will keep its COVID-19 vaccine free of charge for even after the federal government stops paying for it.

“Everyone in the United States will have access to Moderna’s COVID-19 vaccine regardless of their ability to pay,” the pharmaceutical company wrote in a statement. “Moderna’s COVID-19 vaccines will continue to be available at no cost for insured people whether they receive them at their doctors’ offices or local pharmacies.”

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

In their statement, the company also claimed that its patient assistance program will provide free vaccines for the “uninsured and underinsured,” after the federal government’s public health emergency expires, which should be in May. The company did not say how long the vaccines would remain free. 

Moderna faced criticism in January after it announced it was raising the market price from about $26 per shot to as much as $130. The vaccine was developed with the help of billions of federal tax dollars and private donations. Moderna CEO Stéphane Bancel is scheduled to testify before the Senate health committee on March 22 regarding the price for its COVID-19 vaccine when they are sold on the private market.

[Related: The FDA says get used to COVID-19 vaccine boosters.]

Moderna’s announcement of a potential price hike coincided with the Biden Administration informing Congress last month that it was moving towards ending the national public health emergency on May 11, 2023. This change would limit or end federal dollars towards the shots and leave uninsured Americans paying out of pocket for future boosters. 

The federal government had been paying for all COVID-19 vaccines despite insurance status, but ending the public health emergency means funds for federal support for programs aimed at serving the uninsured and those that explained testing, treatments, and Medicaid will dry up. Moderna says its patient assistance program is scheduled to be available after the public health emergency expires, though it is unclear for how long. 

The public health emergency was first declared by Health and Human Services Secretary Alex Azar on January 21, 2020. The national emergency was later declared by Former President Donald Trump in March 2020. President Biden has repeatedly extended both the national and public health emergencies since taking office in January 2021 and has extended them as recently as January 11.

In January, the World Health Organization (WHO) said that the coronavirus remains a global health emergency, despite a key advisory panel for the group finding that the pandemic may be nearing an “inflexion point” where higher levels of immunity could lower virus-related deaths. 

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This article was originally featured on Undark.

At Singapore’s National Environment Agency, more than a million mosquitoes buzz inside plastic boxes in a breeding room that smells of fermented sugar. The male insects, which don’t bite, feed on plant juices in the wild, but here, they nourish themselves on sugar water. Meanwhile, their female counterparts lay eggs on paper-like strips half submerged in trays of water. Each week, the insects inside this facility produce 24 million tiny black eggs.

The NEA’s mosquitoes are all Aedes aegypti, a species that can transmit viruses to humans, including dengue — a growing global threat which, by some estimates, infects 100 to 400 million and kills about 21,000 people each year. These captive insects are disease-free, however, and they are being bred to stop the spread of the viral illness. Specifically, the insects in the NEA lab have been infected with a bacterium called Wolbachia, which they will pass on to the next generation of mosquitoes.

The Wolbachia bacterium is ubiquitous in nature: It can be found in as many as 60 percent of insect species, from butterflies and wasps, to bees, dragonflies, and some species of mosquito. However, these bacteria do not naturally occur in Aedes aegypti. When scientists infect Aedes aegypti with Wolbachia, the insects no longer transmit dengue readily to humans. Additionally, under some circumstances, the bacterium can interfere with mosquitoes’ ability to reproduce. (The precise mechanisms behind these changes are not fully understood.)

Wolbachia-based protocols for insect control have been used in countries across the globe for more than a decade, and in many cases, they have reduced the incidence of mosquito-related disease. But scientists are still learning the best ways to employ these methods at scale. Wolbachia-infected insects are difficult to mass produce, and NEA’s researchers have responded by automating some of the steps that were previously done by hand. Even so, it would be tough to cover “the billions of people, living in the 10,000s of towns and cities in more than 100 countries, that are at risk of dengue,” Jérémie Gilles, the director of production development and supply at the not-for-profit World Mosquito Program, said in an emailed response to Undark.

The WMP and other research organizations use an alternative Wolbachia-based approach — one that doesn’t require such large numbers of lab-bred insects. Thus far, the approach has been effective and cost-efficient, though more time is needed to monitor the long-term outcomes, including the possibility that dengue may evolve to evade the bacterium.

Despite the challenges, officials in Singapore have been game to try Wolbachia to fight dengue — a common scourge in this densely-populated city-state that offers a perfect breeding ground for Aedes aegypti, which favor urban environments and warm climates. Singapore’s National Environment Agency has fought the virus for decades: spraying insecticides, advising people to avoid getting bitten, providing detailed instructions for preventing mosquitoes from reproducing inside one’s home, and fining those who fail to comply. Yet all these efforts are like chasing a runaway train, experts say, which is why the government turned to Wolbachia.

Since 2016, NEA scientists have been setting free male Wolbachia-carrying mosquitoes around Singapore. Though the program started small, by 2019, the NEA was releasing up to 2 million insects per week. Thanks to automation, that number increased to as many as 5 million per week in 2022. So far, at intervention sites, this has led to dramatic reductions of wild Aedes aegypti populations — and far less dengue.

Once the insects have laid their eggs in the mosquito breeding room, the NEA researchers move the millions of tiny black dots down the hall to a hatchery — a bright, hot, humid place that stinks of fish. The eggs are placed in small, water-filled trays, waiting to hatch into larvae.

By releasing male Wolbachia-infected mosquitoes into the community, Singapore is following a protocol that aims to suppress the population of native mosquitoes. When such males mate with local Wolbachia-free females, the females lay eggs that won’t hatch, and in time the number of mosquitoes decreases. This suppression method is tricky. As it happens — and for reasons that are not well understood — mosquitoes can successfully breed when both partners are infected with Wolbachia. To prevent this, NEA scientists separate the females from the males before the latter are released.

But first, the larvae need to be counted and transferred to a rack with larger trays, each holding precisely 26,000 larvae. The exact number is important for keeping the rearing conditions constant, and initially, NEA staff would manually count all the hatched larvae. It took a sharp-sighted lab assistant two hours to count just 4,000 larvae, said the NEA’s senior research officer, Deng Lu. Now, the tally is automated: Pour millions of larvae into a machine, and within minutes it will count the 26,000 needed to fill one tray.

Once in their new, larger trays, the larvae are kept at a water temperature of 80 degrees Fahrenheit and fed a customized mixture of fish meal, carbohydrates, and fats (hence the smell). In nature, male pupae are generally smaller than females, but the difference is not large and it can be hard to distinguish males from females. To solve this issue and make separation by sex a bit easier, NEA scientists have perfected the larvae-rearing process. The diet, the temperature, and the humidity have to be kept perfectly constant, Deng said, to ensure that the females and males end up as different in size as possible.

Separating male from female pupae also used to be done by hand, a job that was both tedious and prone to error. Now, however, NEA scientists are helped by another new technology: the pupae sex sorter. Here, the process starts with scanning a batch of pupae — basically, taking pictures of each individual and gathering its measurements. An AI-based computer system will then draw a type of graph called a distribution curve. If everything up to now has been done correctly, the graph on the screen will show two clearly separated peaks: a small upward curve indicating males to the left and then another, larger bump, indicating females, to the right.

Scientists can calculate the male-female size differential in a particular mosquito batch by measuring the distance between the two peaks. “In this batch, the male and female distance is about 200 microns,” Deng said. “So we actually can do the female separation.” Based on that 200-micron distance, he picked up a sieve that would only let the smaller pupae through and inserted it into the sorter, a white machine shaped like a mini-fridge. After the pupae are poured in, the females will stay on the sieve while the males pass through into a container underneath. The whole process takes about 10 to 12 minutes.

Singapore is not the only country that fights dengue by releasing Wolbachia-infected male mosquitoes. A facility run by Verily Life Sciences — formerly Google Life Sciences — which bred mosquitoes for release in a trial in Fresno, California, can produce close to 3 million males per week, also with the help of AI and automation. The world’s largest mosquito factory in Guangzhou, China, can churn out even 10 times as much.

Automation and AI may have allowed some laboratories to produce huge batches of mosquitoes, but these tools are not cheap. (The NEA would not divulge its budget.) This is one reason why many efforts use a different Wolbachia-based method, known as population replacement, which does not require sex sorting and can work with fewer factory-bred mosquitoes. This method aims to replace native populations with one that is unable to transmit dengue.

Scientists begin by infecting both male and female mosquitoes with Wolbachia. For reasons that are so far unclear to scientists, the bacterium impairs females’ ability to transmit certain viruses, dengue included. A non-randomized study conducted in Yogyakarta City, Indonesia, showed that two years after initiating a population-replacement protocol, dengue incidence in the intervention area fell by 73 percent compared to a control area. A similar study conducted in Brazil showed a 69 percent reduction in dengue incidence and a 56 percent reduction in cases of another virus called chikungunya.

Though male mosquitoes do not bite — and therefore can’t spread dengue — it’s still important to infect them with Wolbachia and release them along with the infected females. When Wolbachia males mate with wild infection-free females, the eggs will not hatch, and over time, there are fewer infection-free females to compete with their lab-produced counterparts. At the same time, as the Wolbachia females mate with both wild and lab-bred males, the eggs will hatch and the offspring will carry Wolbachia. The hope is that ultimately the native Aedes aegypti mosquito population will be made up of individuals infected with the bacterium.

This makes the approach simpler than Singapore’s because there’s no need for sex sorting.

Additionally, population replacement requires considerably fewer lab-grown mosquitoes. “The aim is to get Wolbachia to spread into that population rather than to suppress it, and so the numbers of mosquitoes that need to be released are an order of magnitude lower than with a male-only suppression program,” said Steven Sinkins, a professor of microbiology and tropical medicine at University of Glasgow.

In the Yogyakarta City study, only 1.7 million mosquitoes were released over a 7-month period — compared to Singapore’s 5 million per week. This makes the method more affordable. “Where the budget is restricted, the health budget, we would definitely be recommending the replacement approach because of the smaller scale of releases needed,” Sinkins said.

What also potentially makes the replacement method easier to employ is that it’s designed to be self-sustaining. “If you’ve done it correctly, it will be a discreet period of releases and then you can stop. The Wolbachia will be at a high stable frequency and it will stay there and block dengue transmission long term,” Sinkins said. In Australia, where Wolbachia-mosquito releases to fight dengue were conducted in 2011, the first replacement project in the world, the bacterium was still stable in the Aedes aegypti population nine years later.

The simplicity and affordability of the replacement method is one reason why it was chosen by the World Mosquito Program, which has launched Wolbachia programs in 12 countries, from Brazil and Mexico to Vietnam and Australia. “We aim to simplify our production process as much as possible,” Gilles wrote in an email. “We try to minimize automation throughout our program.”

Why did Singapore choose the suppression method, then? One reason, according to Ng Lee Ching, director of NEA’s Environmental Health Institute, is the issue of bites. To replace a mosquito population, researchers need to release those pesky females. “Our people are not used — not comfortable with mosquito bites, so I think the public acceptance for the replacement approach would not be as high,” she said. After decades of various mosquito control programs on the island, there simply aren’t many mosquitoes flying around Singapore anymore. And for reasons that will be obvious to anyone who has ever been swarmed, local residents are not keen to bring the insects back.

On a November morning, Matthew Verkaik arrived in the Singaporean town of Yishun to release about 4,400 lab-reared male Aedes aegypti. Yishun used to be a dengue hotspot, brimming with mosquitoes. Now, after six years of releases, the local Aedes aegypti population is down by as much as 98 percent, and dengue cases are down by 88 percent. “The before and after is very startling,” said Verkaik, a senior research officer at the National Environment Agency. “You don’t pay attention until you are like, ‘Okay, wait. There’s no mosquitoes. What’s going on?’”

He picked up a basket containing 22 black canisters, each filled with about 200 Wolbachia-infected males, and walked to the first release spot located at the back of a 12-floor apartment block. The place was not random — Verkaik chooses these spots carefully. In general, he freed about six mosquitoes per inhabitant, and did so at even intervals alongside the buildings, both on the ground floor and on higher ones, too.

Standing by the building’s trash chutes, Verkaik grabbed a canister, opened the lid, and gave it a shake. The insects emerged as a cloud of tiny black shapes. A few open containers later and the mosquitoes were everywhere: buzzing around, sitting on walls. In general, the locals seemed not to mind, as the program has strong community support. In a 2021 study, 92 percent of households reported no concerns with releases in their neighborhoods.

According to Sinkins, replacement projects also tend to be welcomed by the public, biting females notwithstanding. “I think mainly because we’ve been targeting areas that have high dengue transmission rates,” he said. “The community acceptance has been very good because nothing else has really been working.”

Reducing mosquito bites, however, is not the only reason why Singapore chose the suppression method over population replacement. The other one is the potential risk of viral evolution, Ng said. Just like Covid-19, dengue is caused by an RNA virus that can evolve relatively quickly. Replacement areas still have a lot of mosquitoes, and there is always the risk of sporadic dengue infections occurring in a small number of the insects. Such breakthrough infections might provide opportunities for dengue viruses to evolve and adapt to the bacterium.

Virus evolution is something that concerns some experts. “It’s a risk, ” said Kat Edenborough, a microbiology research fellow at Monash University in Australia, the institution that owns the World Mosquito Program. “It’s something that we’ll be actively surveying.” She noted, however, that unlike SARS-CoV-2, which can evolve as it spreads person-to-person, dengue needs two species to serve as hosts: the mosquito and the human. This, according to Edenborough, should slow down the viral evolution. A recent study in which researchers passed the dengue virus 10 times through Wolbachia-infected cells of Aedes aegypti did not show signs of the virus adapting.

While Wolbachia programs have gained momentum over the last few years, there is still a lot of ground to cover. Scientists want to understand how exactly Wolbachia works inside mosquitoes, how it evolves, and whether it pushes viruses to fight back. And researchers want to find out if Wolbachia can help fight other diseases, such as malaria. (There are some indications that it might.) The World Health Organization has set a goal to lower the incidence of dengue by 2030 by 60 percent compared to 2016 numbers. “To get to that point,” Edenborough said, “we need to just be using everything that we can.”

UPDATE: A previous version of this piece incorrectly stated that the male mosquitoes at Singapore’s National Environment Agency are infected with Wolbachia after they are sorted from the female mosquitoes. In fact, the males are infected with the bacteria prior to this sorting. The story has been corrected.

This article was originally published on Undark. Read the original article.

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Equatorial Guinea has confirmed their first outbreak of Marburg virus disease, according to the World Health Organization (WHO). This Ebola-related virus is responsible for at least nine deaths and 16 suspected cases in the small country located in western Africa.

Laboratory samples confirmed the outbreak after an alert from a local health official on February 7. The WHO is sending medical experts to the country to help stop the outbreak in addition to personal protective equipment (PPE) for medical workers.

[Related: WHO announces that Uganda’s months-long Ebola outbreak is over.]

“Marburg is highly infectious. Thanks to the rapid and decisive action by the Equatorial Guinean authorities in confirming the disease, emergency response can get to full steam quickly so that we save lives and halt the virus as soon as possible,” said Matshidiso Moeti, WHO Regional Director for Africa, in a statement.

African fruit bats are believed to be the natural host of the virus, which sometimes spillover into humans and other primates via close contact with bodily fluids or surfaces. It is in the same family as the virus that causes Ebola and symptoms include high fever, muscle pain, fatigue, diarrhea, and vomiting. 

According to the Centers for Disease Control and Prevention (CDC), diagnosing Marburg virus disease, “can be difficult” since many of the symptoms and signs are similar to typhoid fever, malaria, and Ebola. 

While Marburg is rare, it is an extremely serious disease. It can have a fatality rate of up to 88 percent if left untreated. In 2004, a Marburg outbreak in Angola, killed 90 percent of the 252 people infected. There were two reported Marburg deaths in Ghana in 2022. 

Currently, there are no authorized vaccines or drugs, but rehydration treatments that alleviate symptoms can improve the chances of survival. The results of a small, first-in-human clinical trial showed that an experimental vaccine was safe and induced an immune response. There are plans to conduct further vaccine trials in Ghana, Kenya, Uganda, and the United States.

[Related: The deadly Marburg virus—a close cousin of Ebola—reemerges in Ghana.]

Health experts recommend that people in the area avoid mines and caves that may be occupied by bats and avoid eating or handing bush meat, or to thoroughly cook meat before consumption to minimize the risk of catching and spreading the virus. The virus primarily spreads among humans through close contact with bodily fluids and surfaces. Burial ceremonies involving direct contact with the body of the deceased can also contribute to the transmission of the virus.

The virus was first identified in 1967 after it caused simultaneous outbreaks in laboratories in Marburg, Germany and Belgrade, Serbia. There were seven fatalities in those who were exposed to the virus while conducting research on monkeys. 

Due to the outbreak, the WHO is set to hold an urgent meeting today to discuss the vaccine candidates and treatment options.  

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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. 

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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.

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More than four dozen Jamaican fruit bats destined for a lab in Bozeman, Montana, are set to become part of an experiment with an ambitious goal: predicting the next global pandemic.

Bats worldwide are primary vectors for virus transmission from animals to humans. Those viruses often are harmless to bats but can be deadly to humans. Horseshoe bats in China, for example, are cited as a likely cause of the covid-19 outbreak. And researchers believe pressure put on bats by climate change and encroachment from human development have increased the frequency of viruses jumping from bats to people, causing what are known as zoonotic diseases.

“Spillover events are the result of a cascade of stressors — bat habitat is cleared, climate becomes more extreme, bats move into human areas to find food,” said Raina Plowright, a disease ecologist and co-author of a recent paper in the journal Nature and another in Ecology Letters on the role of ecological changes in disease.

That’s why Montana State University immunologist Agnieszka Rynda-Apple plans to bring the Jamaican fruit bats to Bozeman this winter to start a breeding colony and accelerate her lab’s work as part of a team of 70 researchers in seven countries. The group, called BatOneHealth — founded by Plowright — hopes to find ways to predict where the next deadly virus might make the leap from bats to people.

“We’re collaborating on the question of why bats are such a fantastic vector,” said Rynda-Apple. “We’re trying to understand what is it about their immune systems that makes them retain the virus, and what is the situation in which they shed the virus.”

To study the role of nutritional stress, researchers create different diets for them, she said, “and infect them with the influenza virus and then study how much virus they are shedding, the length of the viral shedding, and their antiviral response.”

While she and her colleagues have already been doing these kinds of experiments, breeding bats will allow them to expand the research.

It’s a painstaking effort to thoroughly understand how environmental change contributes to nutritional stress and to better predict spillover. “If we can really understand all the pieces of the puzzle, that gives us tools to go back in and think about eco-counter measures that we can put in place that will break the cycle of spillovers,” said Andrew Hoegh, an assistant professor of statistics at MSU who is creating models for possible spillover scenarios.

The small team of researchers at MSU works with a researcher at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Montana.

The recent papers published in Nature and Ecology Letters focus on the Hendra virus in Australia, which is where Plowright was born. Hendra is a respiratory virus that causes flu-like symptoms and spreads from bats to horses, and then can be passed on to people who treat the horses. It is deadly, with a mortality rate of 75% in horses. Of the seven people known to have been infected, four died.

The question that propelled Plowright’s work is why Hendra began to show up in horses and people in the 1990s, even though bats have likely hosted the virus for eons. The research demonstrates that the reason is environmental change.

Plowright began her bat research in 2006. In samples taken from Australian bats called flying foxes, she and her colleagues rarely detected the virus. After Tropical Cyclone Larry off the coast of the Northern Territory wiped out the bats’ food source in 2005-06, hundreds of thousands of the animals simply disappeared. However, they found one small population of weak and starving bats loaded with the Hendra virus. That led Plowright to focus on nutritional stress as a key player in spillover.

She and her collaborators scoured 25 years of data on habitat loss, spillover, and climate and discovered a link between the loss of food sources caused by environmental change and high viral loads in food-stressed bats.

In the year after an El Niño climate pattern, with its high temperatures — occurring every few years — many eucalyptus trees don’t produce the flowers with nectar the bats need. And human encroachment on other habitats, from farms to urban development, has eliminated alternative food sources. And so the bats tend to move into urban areas with substandard fig, mango, and other trees, and, stressed, shed virus. When the bats excrete urine and feces, horses inhale it while sniffing the ground.

The researchers hope their work with Hendra-infected bats will illustrate a universal principle: how the destruction and alteration of nature can increase the likelihood that deadly pathogens will spill over from wild animals to humans.

The three most likely sources of spillover are bats, mammals, and arthropods, especially ticks. Some 60% of emerging infectious diseases that infect humans come from animals, and about two-thirds of those come from wild animals.

The idea that deforestation and human encroachment into wild land fuels pandemics is not new. For example, experts believe that HIV, which causes AIDS, first infected humans when people ate chimpanzees in central Africa. A Malaysian outbreak in late 1998 and early 1999 of the bat-borne Nipah virus spread from bats to pigs. The pigs amplified it, and it spread to humans, infecting 276 people and killing 106 in that outbreak. Now emerging is the connection to stress brought on by environmental changes.

One critical piece of this complex puzzle is bat immune systems. The Jamaican fruit bats kept at MSU will help researchers learn more about the effects of nutritional stress on their viral load.

Vincent Munster, chief of the virus ecology unit of Rocky Mountain Laboratories and a member of BatOneHealth, is also looking at different species of bats to better understand the ecology of spillover. “There are 1,400 different bat species and there are very significant differences between bats who harbor coronaviruses and bats who harbor Ebola virus,” said Munster. “And bats who live with hundreds of thousands together versus bats who are relatively solitary.”

Meanwhile, Plowright’s husband, Gary Tabor, is president of the Center for Large Landscape Conservation, a nonprofit that applies ecology of disease research to protect wildlife habitat — in part, to assure that wildlife is adequately nourished and to guard against virus spillover.

“Habitat fragmentation is a planetary health issue that is not being sufficiently addressed, given the world continues to experience unprecedented levels of land clearing,” said Tabor.

As the ability to predict outbreaks improves, other strategies become possible. Models that can predict where the Hendra virus could spill over could lead to vaccination for horses in those areas.

Another possible solution is the set of “eco-counter measures” Hoegh referred to — such as large-scale planting of flowering eucalyptus trees so flying foxes won’t be forced to seek nectar in developed areas.

“Right now, the world is focused on how we can stop the next pandemic,” said Plowright. “Unfortunately, preserving or restoring nature is rarely part of the discussion.”

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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For patients experiencing conditions like kidney failure, treatments such as hemodialysis or dialysis can filter toxins from the blood when the kidneys can no longer keep a person healthy. It’s life saving, but it comes with the risk of dangerous staph infections in their blood, which can cause blood, skin, joint, and bone infections and pneumonia.

There are also some serious racial and economic discrepancies in the level of risk during dialysis treatments, according to the Centers for Disease Control and Prevention’s (CDC) Vital Signs Report released on February 6. Hispanic, Latino, and non-Hispanic Black Americans, as well as patients with a low socioeconomic status experience a higher rate of infection. 

The findings highlight well-documented healthcare inequities in the United States where race and socioeconomic status directly impacts health. 

The report used data from 2017 to 2020 to pinpoint common patterns among patients who contracted bloodstream infections. It found that in 2020, roughly 14,800 bloodstream infections were reported and 34 percent of them were caused by Staphylococcus aureus (S. aureus)—the bacterium that causes staph infections. The procedure relies on needles and catheters to circulate a patient’s blood through a machine that cleans it.

[Related: These doctors are fighting to make the kidney-donor system less racist.]

“Germs like staph can get into the patient’s bloodstream via these access points,” said acting principal deputy director of the CDC Debra Houry, in a briefing on February 6. “These infections can be serious or deadly, and some are resistant to some of the most common antibiotics used to treat them.”

Patients undergoing dialysis had an annual rate of staph infections that was 100 times higher than adults who are not on dialysis.

While the study found that staph infections dropped 40 percent between 2014 and 2019, it still shows that there’s a lot of work left to make dialysis treatments safe for all patients in the United States.

Hispanic, Latino, non-Hispanic Black Americans were disproportionately affected by dialysis-linked bloodstream infections, since there are race, ethnicity, and social determinants of health affect the development of end stage kidney disease. These populations are at a higher risk for kidney disease partially due to higher rates of diabetes and hypertension.

“Overall for Hispanic patients after adjusting for other factors, we found a 40 percent higher risk of bloodstream infection for that group,” said study author Shannon Novosad, dialysis safety team lead in the CDC’s Division of Healthcare Quality and Promotion, during the briefing. 

[Related: The US’s healthcare system discourages people from getting care, new study says.]

The type of access used in dialysis treatment was also important, as patients who were connected to a machine with a central venous catheter had a higher risk of infection. Using this method, a thin tube is directly inserted into a vein, typically in the neck or chest. The other end of the tube is outside of the body, where it can be exposed to germs. 

“Our data confirm this use of a central venous catheter as a vascular access type has six times higher risk for staph bloodstream infections, compared with the lower risk, lowest risk fistula access,” said Novosad. 

Using grafts (small, plastic tubes that are connected to an artery and a vein) and fistulas (which join an artery and a vein directly) were deemed to be safer methods by the report.

“Removing barriers to lower risk vascular access types for dialysis treatment is a critical step for preventing infection,” said Novosad. “It is vital to coordinate efforts among patients nephrologists, vascular access, surgeons, radiologists, nurses, nurse practitioners and social workers to reduce the use of central venous catheters for dialysis treatment. It’s also critical to educate patients on potential treatment options and vascular access types before they develop end-stage kidney disease.”

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This article was originally featured on Undark.

When Sandy Bagwell began fostering a three-week-old baby in 2019, she knew there was a chance he might have been exposed to drugs or alcohol in the womb. His birth mother, Bagwell said, had struggled with substance use disorders for years. So Bagwell, who later adopted the boy, made sure early on that he saw doctors and therapists.

When her son was about 18 months old, Bagwell said one of his therapists mentioned fetal alcohol spectrum disorder, or FASD, a developmental disorder that can happen after a fetus is exposed to alcohol. At the time, Bagwell said, “I was really ignorant about it.”

Bagwell managed to find the only doctor in her area who specialized in diagnosing such disorders. After a six-month wait and a 10-minute appointment, she recalled, the doctor eventually diagnosed her son with FASD at the age of 2 and a half. That doctor has since passed away, so Bagwell’s son has spent a year on a waiting list for a more complete assessment at Cook Children’s, which is about a five-hour drive from their home in northwestern Texas.

Since the initial diagnosis, Bagwell said her son has had physical therapy, speech therapy, and occupational therapy, and he’s on a waitlist for parent-child interaction therapy. The treatments have helped, she said, but he’s starting to develop behavioral problems serious enough that he may not be able to stay in daycare.

The disorder is not rare, but Bagwell’s story — receiving a diagnosis so early in her son’s life — is. Because there are so few specialists, patients mostly go undiagnosed or misdiagnosed. While research-based dietary and behavioral interventions have been available since the 1990s and 2000s, respectively, patients — including, so far, Bagwell’s son — almost never get these specialized treatments.

Advocates are currently pushing for bills that will make support for children with FASD and their families more widely available, but experts say much more is needed in order to connect them with resources. “People need to see the advantages of learning programs specifically for FASD and why that would matter,” said Christie Petrenko, an FASD specialist at the Mt. Hope Family Center in Rochester, New York. “And they have to recognize that they actually are seeing FASD in the clients they already have.”

It’s been half a century since Kenneth Jones and David Smith, researchers at the University of Washington School of Medicine, demonstrated that alcohol can disrupt fetal development. By 1981, Kathleen Sulik, with colleagues at the University of North Carolina at Chapel Hill, recognized fetal alcohol syndrome, or FAS, as a specific set of traits including unique facial characteristics — a smooth philtrum (the vertical crease under the nose), a flat nasal bridge and midface, and small eyelid openings — and intellectual challenges.

FAS tended to occur in people who were exposed to alcohol between gestational weeks seven and 12, but not long after Sulik’s work, scientists began to realize that exposure to different amounts of alcohol at different points in gestation could cause a range of disruptions, without the distinctive facial characteristics.

More recently, researchers have begun to find evidence that even moderate doses of alcohol, equivalent to one or two drinks, consumed at vulnerable points in gestation may disrupt development, although heavier drinking is associated with a higher likelihood of more serious developmental disruptions. Brain scans of 22- to 36-week-old human fetuses revealed brain differences in those whose mothers reported drinking less than a drink per week on average, according to data presented at a conference in 2022. A study published in 2022 in rats suggested that a moderate dose of alcohol, approximately equivalent to a single drink for humans, given at day 12 of gestation — akin to the start of the second trimester in humans — could lead to lasting social deficits and anxiety. This time is especially important, according to the study’s lead author, Kathryn Przybysz, now a postdoctoral psychiatry researcher at the University of Illinois at Chicago, because “it could be when women don’t know they’re pregnant and are still drinking.”

FASD is thought to impact 1 to 5 percent of people in the United States, according to a study of more than 13,000 first graders. Depending on the genes and nutrition of the mother and fetus, as well as the timing of the exposure and the amount consumed, alcohol can have a range of effects on a developing fetus from social deficits to autoimmune disorders. Scientists see some of the most common effects in areas of the brain that handle short term memory, coordination, and attention and planning. Individuals with FASD may seem forgetful, have difficulty anticipating consequences, and need extra time to process information.

Diagnosing FASD, however, has proven elusive. While researchers are actively searching for biomarkers in blood, teeth, and brain scans, none are currently validated. Typically, to get a true diagnosis patients need to be evaluated by FASD specialists, and there aren’t many of them.

Patients don’t just go undiagnosed, but often are misdiagnosed, said Annika Montag, an epidemiologist and public health scientist at the University of California San Diego. She and her team conducted a study, published in September 2022, for which they screened kids who were receiving services at their local community center for diagnoses such as autism or ADHD, and found that about 7 percent of them likely had an undiagnosed FASD. “The takeaway is children have not been diagnosed with FASD, despite being under medical care,” said Montag. “They’re not getting optimal care.”

In the late 1980s, researchers at Columbia University were finding that supplements of choline, a nutrient found in eggs, beef, soybeans, and codfish, seemed to improve learning and memory in rats by facilitating long-term changes in the structure of the hippocampus, a part of the brain known to be responsible for forming short-term memories. Later studies in humans have supported these early findings.

Given the challenges people with FASD faced with short-term memory and attention, Jennifer Thomas, a neuroscientist at San Diego State University, wondered if choline could help mitigate the effects of in-utero alcohol exposure. In 2000, she fed alcohol to a group of pregnant rats. After the pups were born, she gave some of them large doses of choline and found that days after having received it, the rats performed significantly better on a task that tested their ability to associate light with a reward compared to their counterparts who had been exposed to alcohol but hadn’t received choline.

“The really fascinating thing that she showed was that even after those rodents were born, the choline was still somewhat effective, because the brain is still developing,” said Jeffrey Wozniak, a neurobehavioral development researcher at the University of Minnesota. “That really gave us a model that we could use in humans.”

Over the past two decades, scientists have continued to study choline in humans and have found that if it is given to a pregnant mom after the exposure, or even to children during their first few years of life, the nutrient can reduce the effects of alcohol. Children who received choline between the ages of 2 and 3 showed improvements in memory and attention even four years later, according to a 2020 trial by Wozniak and his team.

Still, choline isn’t a drug; it’s a nutritional supplement, explains Wozniak. While a drug would undergo clinical trials, then be evaluated and approved by the Food and Drug Administration, there’s not an obvious pathway through which choline will become a standard treatment. Although the treatment is largely safe, very high intake of choline (five to 10 times the recommended amount) can lead to a fishy odor, liver damage, low blood pressure, vomiting, or heart disease.

“We’re continuing to do the studies to demonstrate the effects and to put it out into the literature so that people pick it up and say, ‘Okay, this is something we can use as a tool,’” said Wozniak.

Bagwell told Undark that she never had guidance from doctors or other experts on choline. But she did find some of the relevant studies on her own before her son was formally diagnosed with FASD and started giving him the supplement daily when he was 2 years old. “I read so many good things about it, a lot of the studies,” she said.

Researchers have also developed behavioral interventions for both people with FASD, as well as their teachers and caregivers. Two popular programs are the Families Moving Forward and the Math Interactive Learning Experience programs. Providers need about a week of specialized training to offer FMF, but to implement the MILE program, teachers and community centers can learn from resources available online.

FMF is a nine-month program for caregivers of children with FASD. Caregivers attend 90-minute weekly or biweekly sessions with mental health professionals who help them understand their child’s challenges and offer practical strategies to help them thrive, including effective communication and identifying and avoiding triggers that lead to outbursts or difficult behaviors.

In self-reported, validated surveys, caregivers who participate in FMF have said that they felt better equipped to parent and that their children also engaged in fewer problematic behaviors after the program.

The MILE program helps teachers instruct young children with FASD in math, one of the areas in which these individuals tend to struggle the most. The technique uses tools and toys to help kids conceptualize math, but it also addresses emotional regulation in problem solving. Rachelle Feiler, a teacher and researcher in California, explains that anxiety escalates very quickly in many children with FASD. In addition to slowing down and repeating concepts to help children with short term memory deficits or slow processing speeds, the intervention aims to reduce anxiety. For example, she told Undark that when a student asks her if their answer is correct, she used to try helping the child develop their own understanding of math by asking, “Well, what do you think?” But that can cause a lot of anxiety for a child with FASD. Now, she said, she’ll start by saying “You’re right,” or “that’s really close,” before asking, “how did you get that answer?”

After six weeks of tutoring with the MILE program, nearly 57 percent of children with FASD improved their math skills by at least a full standard deviation, according to a 2008 study from the Centers for Disease Control and Prevention, compared to about 23 percent of children in a control group who received standard math tutoring.

While interventions specifically designed for people with FASD and their families exist, they are not consistently available across the country. “There are pockets,” said Wozniak.

Advocates are working at the national and local levels to try and get more consistent recognition and resources. FASD United, a national advocacy organization, has been advocating for Congress to pass the 2021 FASD Respect Act. The act would re-institute the FASD Center for Excellence, which initially opened in 2001 with support from the Substance Abuse and Mental Health Services Administration to identify and disseminate best practices, but lost funding in 2016.

At the state level, California recently passed a bill that adds FASD as a diagnosis that qualifies a child for special education support. Feiler called the passing of the bill “huge.”

“If you’re trying to match a strategy to a student, you’ve got to know what you’re looking at,” she said. “I’ve seen students I thought might have FASD but I’ve never had an IEP, an individualized education plan, come to me with that diagnosis in it. Ever.”

In New York, Petrenko said, most people with FASD don’t qualify for disability services such as therapy, career counseling, and respite for caregivers. “There was a kid here or there,” who might get approved for such services, she said, and usually they had a separate qualifying intellectual disability, but most people whose only diagnosis is FASD are denied.

Working with a government relations officer at the University of Rochester, Petrenko got the attention of a state senator and assemblyman who proposed a bill adding FASD to the mental hygiene law in January 2022. “It actually got unanimously approved in the state senate last session. But they couldn’t push it through the assembly,” she said.

Recognizing that resources for in-person interventions are scarce, some researchers are trying to help patients more directly. For instance, in Minnesota, the American Institute for the Advancement of Forensic Studies offers virtual and in-person training sessions for caregivers, health care professions, and law enforcement about how to better understand and communicate with people who have FASD, autism, and more. And Petrenko and her team have developed a cell phone app that allows caregivers to work their way through the FMF program on their own.

So far, Petrenko has published a pilot study to show feasibility of using the app, but she’s just finished collecting data on her larger trial. The preliminary data, she told Undark, suggests that the app is improving parent satisfaction and child behavior, although not necessarily to the same degree as the in-person program. “But for an app to have any measurable impact is a pretty big deal,” she added. “Because even just a little bit of improvement over a lot more people does have a pretty significant public health impact. So we’re pretty excited about that.”

This article was originally published on Undark. Read the original article.

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The first three episodes of HBO’s The Last of Us have a lot to say about fungi. The series begins with a warning, as a gray-haired epidemiologist played by actor John Hannah cautions us that some fungi, including Ophiocordyceps, “seek not to kill but to control” the behavior of the animals they infect. Later, a mycologist at the University of Indonesia, played by Christine Hakim, explains that there is no medicine nor vaccine to fight off such a fungus in humans. What she proposes next—that our only solution to an emerging fungal epidemic is to “bomb this city and everyone in it”—is prime cinematic hyperbole. Although we fight these infections with intravenous therapy, not incendiary devices, there’s still real cause for concern when it comes to fungi.   

The fungi that colonize our vast planet, though mostly a far cry from the phantasmic organisms that transform people into zombies, can pose serious threats to agriculture, biodiversity, and human health, especially in an increasingly warmer world. These fungi are precisely the ones you should be familiar with and, in some cases, fear.

[Related: Ancient frozen viruses don’t pose a threat to your health—yet]

Common human-associated fungi, which the public perceive as “bad” or “gross,” such as the ones that cause athlete’s foot, dandruff, run-of-the-mill yeast infections, and toenail fungus, are not the ones that keep doctors awake at night. But you can’t sell what you can’t see so Hollywood continues to play up the behavior-modifying properties of a few exceptional fungi at the expense of the truly invasive ones that are responsible for hospital stays and a majority of patient deaths. 

“From a clinical perspective, the impact of these fungal diseases is really underappreciated,” says Bridget Barker, an associate professor of mycology at Northern Arizona University. “The patients get really sick before they get intervention.” Because many fungi opportunistically infect already sick patients, it complicates our understanding of their role in patient deaths and probably helps explain their near absence from the public conversation.  

Even for physicians, especially those in many parts of the world where some of these fungal infections are most prevalent, “the biggest challenge is making the diagnosis,” says Ilan Schwartz, a physician at Duke University in North Carolina who specializes in fungal diseases. 

In some places, clinicians still lack even the most basic tests, which can lead to an incorrect determination. By the time they realize a fungus, not a bacterial infection like tuberculosis, is causing the disease, treatment is generally less effective and can unfortunately lead to death.  

But, if caught early enough, therapies can be very effective.             

Tried-and-tested fungal treatments

There are three main classes of antifungals, medications that kill or suppress fungi, according to Schwartz. Of these, only one (azoles) can be taken as a pill outside the hospital setting. The negative side effects of the other two, echinocandins and polyenes, require professional medical oversight. “Any resistance to any one of these classes is hugely important and really restricts our ability to treat patients,” Schwartz explains.      

And just how far-fetched is the emergence of fungi that resist our best drugs? One soil-dwelling fungus that also causes lung infections, Aspergillus fumigatus, shows resistance in 10 to 15 percent of isolates in some locations, Schwartz says. “The azoles they use in the field [to combat plant pathogenic fungi] are structurally very similar to the one we use in the clinic.” So what Joel told Ellie in the third episode of The Last of Us is right: Fungi are mutating. Though many have mastered the art of invading animals long ago, including people, they are becoming harder to fight once they are inside us.                        

Killer fungi outside of fiction

Some might argue that the fungi that live rent-free in our bodies are far more alarming than Ophiocordyceps. This includes fungi that cause Valley Fever, a disease in the southwestern US that is expanding northward and westward as the climate warms. Two closely related soil-inhabiting fungi responsible for this disease, Coccidioides posadasii and Coccidioides immitis (simply called “Cocci”), are a major concern. “We’re already seeing increases in areas in California where they hadn’t seen very many cases,” says Barker, who is among the world’s experts on Cocci. The Onygenales, the larger group of fungi that includes Cocci, are “concerning,” she notes, “because they cause disease in otherwise healthy people.” And because this particular group is co-evolving with mammals, “this is probably where the future threats will come from.”                

Schwartz has his own concerns about Cocci. “The environment that favors the growth of this fungus is also the environment that favors wildfires,” he explains. The epithelial changes that occur with wildfire exposure dramatically increases the risk of Valley Fever.” When the ash settles in our lungs, so too may these fungi.

[Related: Soil fungi are spreading lung infections to new territories]

Cocci is far from the only fungal infection showing up in the clinic. In fact, outside of specific geographic areas where they are endemic, few cases of Cocci or its Onygenales counterparts are reported nationwide. “What I see as a clinician on a day-to-day basis is primarily invasive candidiasis and aspergillosis,” Schwartz says. These fungal diseases affect people with weakened immune systems, many because of cancer or a viral infection, including HIV/AIDS, COVID-19, or flu. The human immune system can also be weakened by treatment with corticosteroids and immunosuppressant drugs, like ciclosporin (coincidentally, a drug naturally produced by a close relative of Ophiocordyceps). “Viruses themselves cause various forms of immunoparesis [or dampened immune response] that then allow secondary infections to come in and basically run amuck,” Schwartz explains.

Lessons from epidemics in wildlife

Fungi infect animals, too—with their own implications for human health. Some recent large-scale fungal disease outbreaks among wildlife include mass die-offs of amphibians, due to chytridiomycosis, and bats, due to white-nose syndrome. An unchecked fungal animal pandemic can look apocalyptic: a dark backwater bloated with hundreds of frogs floating belly up, for instance, with their fungus-stiffened legs rising out of the water.

Prior to the 1990s, only a handful of mycologists knew anything about these bizarre aquatic fungi we call chytrids. The most famous among them, Batrachochytrium dendrobatidis or Bd, is responsible for the extinction of some 90 amphibian species with another 124 species experiencing global population declines of 90 percent or more.

[Related: Tri-colored bats are imperiled by deadly fungal disease]

Why should we care about frog-killing fungi? Well, like with human pathogens, climate change can accelerate spread in areas where the fungus was previously kept in check according to Rabern Simmons, a chytrid expert and curator of fungi at Purdue University Herbaria. More importantly, we are just now beginning to see the “hidden human welfare costs” of biodiversity loss, he says. In Costa Rica and Panama, an area hard hit by chytridiomycosis, Bd-driven collapse of amphibians has led to more mosquitoes and malaria cases in humans, as per a 2022 study. “We are seeing human health implications because of a microscopic aquatic mobile fungus that hardly anybody knew about,” says Simmons.

There is nothing fictional about the threat some fungi pose to us. While Ophiocordyceps fungi will continue to manipulate and kill insects, as it has done over millions of years of co-evolutionary history with their invertebrate hosts, the human fungal epidemic on the horizon likely will not bother to modify our behavior. Our history is more likely to intersect with an unassuming mold lurking quietly in the soil or forming a biofilm in a hospital sink: ever adapting to our dwindling lines of defense. Though a world where we do too little to stop a rising tide of fungal pathogens is a horrific prospect, our collective failure to recognize the interconnectedness between pathogens, people, animals, and plants could be more terrifying.          

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On Monday, President Joe Biden informed Congress that he will end the two national emergencies currently addressing the COVID-19 pandemic 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: A quick look at Biden’s new COVID preparedness plan.]

The announcement comes as lawmakers have already ended elements of the emergency protocol, such as changes in policy that have kept millions of Americans insured since the pandemic began in 2020. Removing federal dollars would also shift the development of future vaccines and treatments away from direct management by the government and more towards the private sector.

The public health emergency was first declared by Health and Human Services Secretary Alex Azar on January 21, 2020. The national emergency was later declared by Former President Donald Trump in March 2020. President Biden has repeatedly extended the emergencies since taking office in January 2021 and has extended them as recently as January 11.

According to the Centers for Disease Control and Prevention (CDC), more than 1.1 million people in the United States have died from COVID-19 since 2020, including roughly 3,700 last week.

Everyday Americans will see these changes directly through more expensive vaccines. The cost is expected to skyrocket when the federal government stops purchasing them, and vaccine manufacturer Pfizer says it could charge as much as $130 per dose. Additionally, those with private health insurance will have to pay some out-of-pocket costs for vaccines, especially if seeing an out–of-network provider, according to Larry Levitt, the executive vice president for health policy at Kaiser Family Foundation.

Hospitals will no longer receive extra payments for treating COVID-19 patients. Some hospitals have been receiving a 20 percent increase in Medicare’s payment rate, which could lead to higher consumer costs. The cost of COVID-19 testing and treatments like Paxlovid will also be more complicated. Charges will depend on whether they have private insurance, Medicare, Medicaid, or no health insurance and what state they live in could also affect costs.

[Related: Long COVID recovery is finally getting the attention it deserves in the US.]

Flexibilities for telehealth were extended for another two years, leading health care systems around the US to regularly deliver remote care.

Additionally, the World Health Organization (WHO) said on Monday that the coronavirus remains a global health emergency, despite a key advisory panel for the group finding that the pandemic may be nearing an “inflextion point” where higher levels of immunity could lower virus-related deaths. 

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Men taking erectile dysfunction pills may be adding years to their life, suggests a sweeping observational study published in early January. The research, published on January 13 in The Journal of Sexual Medicine, reported cardioprotective effects from sildenafil, the generic name for Viagra and Revatio. Sildenafil was originally developed as a heart medication before eventually becoming approved for ED. The findings support earlier claims during the drug’s development that it possesses cardiac benefits.

“In general, these drugs appear to be safe in regards to major adverse cardiovascular events,” says lead study author Robert Kloner, a professor of medicine at Keck School of Medicine at the University of Southern California, chief science officer at Huntington Medical Research Institutes, and lead author of the study. However, he cautions that the study only showed an association, not a causal relationship, between the drug and lowered risk of heart problems and mortality. The research was partially funded by Sanofi, a pharmaceutical company that produces the erectile dysfunction medication Cialis.

[Related: Viagra could have been a groundbreaking cure for period cramps]

Sildenafil is a phosphodiesterase type 5 (PDE5) inhibitor. It works by blocking an enzyme in the walls of blood vessels, which allows them to relax and widen, increasing blood flow, most notably in the penis. But it can also improve blood flow to other areas of the body and is currently approved as a treatment for pulmonary hypertension for both men and women in the US. Decades of research in men taking PDE5 inhibitors for erectile dysfunction suggests that the drug could also help treat other heart problems, although most of these studies lacked control groups and involved small sample sizes. Kloner and his colleagues were interested in studying other health benefits the drug provides in a much larger pool that would be more likely to use it—men with ED living in the US.

The study authors analyzed 14 years of medical records of men 18 years and older diagnosed with erectile dysfunction for at least one year. The patients were classified into two groups: The first group included more than 23,000 men who spent one or more years using PDE5 inhibitors like sildenafil, and the second group was made up of more than 48,000 men with no record of ever using these drugs.

Men who had taken PDE5 inhibitors showed a 13-percent lower chance of future heart problems that involve reduced blood flow to the cardiac muscle, such as a heart attack, stroke, or chest pain, versus men who have never taken the medications. What’s more, PDE5 users were 39 percent less likely to die from a cardiovascular-related death, and 25 percent less likely to die from any cause compared to the non-exposed group. 

The amount of pills they took also mattered. Men with ED prescribed the most PD5 inhibitors (an average of 191.2 tablets) showed the most reduced risk of heart issues (55 percent) and premature death (49 percent) than those given the lowest amount of pills (an average of 5.5 tablets). “The encouraging aspect of the study was that nearly all the endpoints were improved in the same direction that is in favor of PDE-5 inhibitor exposure. This finding was consistent across the study,” says Kloner.

At first glance, the positive results might make it seem like everyone should take ED treatments to stay heart-healthy. But that’s not the case, as the observational study design makes it difficult to rule out any other explanations. For one, it only measured the number of pills given to patients, not the number actually taken, says Rigved Tadwalkar, a cardiologist at Providence Saint John’s Health Center in California who was not involved in the research. “Filling a medication does not necessarily equal taking the medication.”

Men who chose to take Viagra could have also been heart-healthier from the start. A doctor may feel hesitant to prescribe the drug to someone with a history of poor cardiovascular health, says Rena Malik, a urologist and associate professor of surgery at the University of Maryland School of Medicine who also was not involved in the study. “When does sex become risky? It’s usually when you have really poor cardiac health, and that’s when you shouldn’t be having much sex.” What’s more, for those engaging in between-the-sheets activity, it may be the exertion itself that’s providing cardiovascular benefits. People who often have sex may already be fitter than someone who is not, Malik explains. “It’s possible they have less chronic pain, are more mobile, and are flexible.” Additionally, being intimate with someone could imply that they’re less lonely than someone without a partner. “We know loneliness is associated with mortality and poor heart health outcomes” Malik notes, all of which could contribute to a higher risk of cardiac-related mortalities.

But both Tadwalkar and Malik agree that the study findings shouldn’t be dismissed, even if there are several confounding variables. “There are many factors that could play a role, but PD5 inhibitors are vasodilators that allow for blood flow, so it makes sense that these could also be protective,” says Malik. She and Tadwalkar further noted that the study was well-executed and adds a lot of value to what we already know about PD5 inhibitors. Tadwalkar underscores that doctors may be more willing to use these drugs in patients with cardiovascular problems who want to take Viagra if there are no significant and harmful reactions to the drug. 

[Related: Research on aphrodisiacs is kind of unsatisfying]

PD5 inhibitors could also be prescribed to protect the heart health of women. While female patients were not part of the study, Kloner says the drugs have the capability of relaxing blood vessels and reducing mortality for them, too. A randomized, placebo-controlled clinical trial will be needed, however, to expand the findings to other populations and make more conclusive recommendations around PD5 inhibitors and any potential cardiac benefits.

“The issue is who is going to pay for a [clinical trial],” says Kloner. Because the drugs are generic, he says there has been low interest from pharmaceutical companies and the government to support a large erectile dysfunction-related analysis that isn’t based on preexisting data. “But perhaps with our study, there will be renewed interest in funding such a study,” he states, “[and possibly] allow for new indications for these drugs for the practice of preventative cardiology.”

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For many of us, coffee is an essential. But the research on its role in a healthy diet is still pretty confusing. It wakes most of us up so we’re ready to face the day, can lower the risk of dementia, and may increase longevity. However, too much can lead to headaches, stomach aches, an increased heart rate, and more. 

One key to balancing this out may lie in what goes into the caffeinated beverage: milk. A study published January 30 in the Journal of Agricultural and Food Chemistry, finds that a milk and coffee combo might have an anti-inflammatory effect. 

[Related: Coffee and tea could lower your risk of dementia.]

Inflammation occurs when foreign substances, bacteria, or viruses enter the body and inflammatory cells are released as a defense. It also happens when tendons or muscles are overloaded, like after a workout. Chronic inflammation is a  symptom of diseases like Alzheimer’s disease and rheumatoid arthritis, which can cause pain, fever, and damaged joints.

In a new study, a team of researchers from the University of Copenhagen in Denmark investigated how antioxidants called polyphenols behave when combined with amino acids, the building blocks of proteins. 

Polyphenols are naturally found antioxidants in lots of fruits and vegetables, tea, coffee, red wine and beer, but there are still many unknowns about the substance. 

“In the study, we show that as a polyphenol reacts with an amino acid, its inhibitory effect on inflammation in immune cells is enhanced,” said study co-author Marianne Nissen Lund from the University of Copehahagen’s Department of Food Science, in a statement. “As such, it is clearly imaginable that this cocktail could also have a beneficial effect on inflammation in humans. We will now investigate further, initially in animals. After that, we hope to receive research funding which will allow us to study the effect in humans.”

The team applied artificial inflammation to immune cells to investigate what kind of anti-inflammatory effect occurs when polyphenols and proteins are combined. One group of cells received various doses of polyphenols that had reacted with an amino acid. Another group only received polyphenols in the same doses and a control group didn’t get anything.

They found that the immune cells that were treated with the combination of polyphenols and amino acids were actually twice as effective at fighting inflammation as the cells to which only polyphenols were added.

[Related: Should pregnant people not drink coffee? The answer is complicated.]

“It is interesting to have now observed the anti-inflammatory effect in cell experiments. And obviously, this has only made us more interested in understanding these health effects in greater detail. So, the next step will be to study the effects in animals,” said co-author Andrew Williams of the university’s Department of Veterinary and Animal Sciences, in a statement.

Previous research has found that polyphenols bind to proteins in beer, meat products, and milk, and beer. In a separate new study Nissen Lund tested whether the molecules also bind to each other in a coffee drink with milk. 

“Our result demonstrates that the reaction between polyphenols and proteins also happens in some of the coffee drinks with milk that we studied. In fact, the reaction happens so quickly that it has been difficult to avoid in any of the foods that we’ve studied so far,” said Nissen Lund.

More work is needed on the major advantages of polyphenols and the team’s next steps include figuring out how to add the right quantities of polyphenols to foods to achieve the best quality.

“Because humans do not absorb that much polyphenol, many researchers are studying how to encapsulate polyphenols in protein structures which improve their absorption in the body,” said Nissen Lund. “This strategy has the added advantage of enhancing the anti-inflammatory effects of polyphenols.”

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On Thursday, the Food and Drug Administration’s (FDA) Vaccines and Related Biological Products Advisory Committee unanimously voted to support a new plan simplifying future COVID-19 vaccines, making them similar to annual flu shots.

At the meeting, the advisory panel said that a single annual vaccine would be less confusing and more effective to health care workers and patients alike. 

In a 21 to 0 vote, the panel voted to direct Moderna, Pfizer/BioNTech, and Novavax to “harmonize” the first doses (or primary vaccination series) with the new bivalent booster shots that protect against the original strain of the virus and the newer Omicron variant. 

[Related: What’s really going on with myocarditis and COVID vaccines.]

“This is a consequential meeting to determine if we’ve reached the point in the pandemic that allows for simplifying the use of current COVID-19 vaccines,” said FDA’s David Kaslow, the Director of the Office of Vaccines Research and Review..

Under previous guidance, patients must first get two shots of the original vaccines (spaced weeks apart) and then a bivalent booster tailored to protect against the Omicron variant two months later. 

Members of the advisory panel were also supportive of a new approach that is more like the strategy seen with the annual flu vaccine. Currently, the annual flu vaccine is created each year to match whatever strain of the virus is circulating. This way, patients and healthcare professionals wouldn’t have to worry about how many shots they’ve already gotten and when they were administered. 

“I think this is a reasonable approach. We have to keep reminding ourselves that this is not influenza and we need to keep paying attention to that to make sure we don’t just follow that dogma because we’re used to doing it,” said Bruce Gellin, a temporary voting member of the panel and chief of global public health strategy for the Rockefeller Foundation’s pandemic prevention institute. “We’ll try this this time. I don’t think we’re setting it in stone and we’ll see how it goes. We may need to adjust along the way.”

The agency also addressed varying risks to people with different health status and ages in briefing documents released ahead of the meeting. ​“Most individuals may only need to receive one dose of an approved or authorized COVID-19 vaccine to restore protective immunity for a period of time.  Two doses of an approved or authorized COVID-19 vaccine may be needed to induce the expected protective immunity for those who have a low likelihood of prior exposure (the very young) or those who may not generate a protective immune response (older and immunocompromised individuals),” the FDA wrote.

If a more dangerous COVID variant were to emerge, the FDA said it might reconsider the strain used in the vaccine at other times of the year on an “as-needed and emergent basis.”

Additionally, the timing of annual boosters was debated since COVID-19 hasn’t fallen into a seasonal pattern like the flu—instead  COVID-19 waves emerge periodically year round.  Peter Marks, the director of FDA’s Center for Biologics Evaluation and Research said that there is some evidence SARS-2 is developing a seasonal pattern, but that comment was not universally agreed upon in the meeting. 

“When do we have to worry about the worst overwhelming of the hospitals? It will be when we have influenza, RSV, and potentially covid at the same time,” said Marks.

There is also a debate among scientists if updating the COVID-19 vaccines really does make them more effective and some critics of the FDA’s proposed new strategy argue that investing in developing better vaccines that are more appealing to people, such as intranasal vaccines that could also help curb transmission of the disease, and more robust vaccination campaigns might be more effective.

[Related: Omicron boosters are the future of COVID vaccines in the US.]

“Particularly now when Congress is not allocating new funds for COVID response, we have to be especially judicious in how we spend our money and what would be most cost-effective,” Celine Gounder, a senior fellow at the Kaiser Family Foundation, told NPR. “It’s unclear whether updating the booster formulations and repeatedly boosting people is the most effective approach to controlling COVID at this stage.”

Uptake of vaccine boosters remains slow. Roughly 40 percent of adults over 65 and only 16 percent of those 5 years and older have received the latest COVID-19 booster. 

In a separate development on Thursday, the FDA also halted the emergency use authorization (EUA) of Evusheld, a monoclonal antibody treatment used to prevent COVID-19 in immunocompromised people who are less likely to generate a robust immune response from vaccination. The treatment does not appear to protect against the variants currently circulating.

The agency advised those who are infected to seek medical care and ask about antiviral treatments like Paxlovid, remdesivir, or molnupiravir, which do work against currently circulating variants.

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Adapted from the book WHAT’S GOTTEN INTO YOU by Dan Levitt. Copyright © 2023 by Dan Levitt. Courtesy of Harper, an imprint of HarperCollins Publishers.

By the late 1800s, scientists had identified four of the basic substances that make up our bodies: protein, fat, carbohydrates and minerals. These four kinds of molecules form the scientific basis of the ingredient list in the first baby food: Liebig’s Soluble Food for Babies, “the most perfect substitute for mother’s milk.” Unfortunately, no one suspected that Liebig’s list was incomplete, which would explain why babies raised solely on his formula did not thrive. It turns out that we have to eat one more type of molecule to assemble ourselves.

   Unhappily, a lack of this last kind of substance was responsible for four exceptionally gruesome diseases. In the seafaring age between 1500 and 1800, scurvy killed about two million sailors, many more than the who died in battle. Throughout Asia, a pernicious disease called beriberi sporadically paralyzed and killed millions. Pellagra, memorably known for its four “D”s—dementia, dermatitis, diarrhea, and death—afflicted the poor in Europe and America, particularly many in the American South who primarily ate bacon, cornbread, and molasses. Rickets deformed the bones of the children of rich and poor alike. Growing up in Arkansas during the Great Depression, my own mother-in-law’s sisters were stricken by it. Until scientists could discover the reason for these inexplicable ailments, countless victims would suffer and die hideous deaths.

Some clues, however, had long been visible, including a particularly promising one that appeared half a century before Liebig was even born. In 1747, a 31-year-old British naval surgeon named James Lind stood one day on the rolling deck of the HMS Salisbury, a three-masted ship of war outfitted with fifty cannon. As they patrolled the Bay of Biscay, off the coast of France, Lind relished the fresh air, a welcome relief from the stagnant hold below and the vexing mystery he faced there.

It had been only eight weeks since they’d left port, and already forty of the three hundred sailors on board had contracted scurvy. The men limping to Lind’s sick bay had putrid gums and red, blue, or black spots resembling bruises on their skin. They were lethargic and losing the strength to walk. He knew that, if the disease grew too advanced, he would have to cut away their grossly swollen gums just so that they could swallow their food.

In the British navy, this was hardly unusual. Scurvy was common on longer voyages. Lind was all too aware of the single worst incident, as it had happened just seven years earlier. The navy had dispatched a squadron of eight ships under the command of Sir George Anson to attack Spanish galleons in South America. Three and a half years later, Anson returned with a treasure so vast, he needed thirty-two wagons to haul it to the Tower of London. But only about 400 of his 1,900 men returned with him. Most had died of scurvy.

It was not that the navy completely ignored the disease. The problem was, there was no agreement on how to cure it.

Yet, this knowledge had once been known, at least by some. Two hundred years before, many ship captains could have told you that scurvy breaks out on long voyages that deprive sailors of fresh fruit and vegetables. The writer Stephen Bown observes that in the seventeenth century, captains made mad dashes from port to port in an attempt to outrun the disease. It was also known that lemon juice could prevent or cure it. In his 1617 textbook, The Surgeon’s Mate, John Woodall recommended lemon juice daily. The Dutch East India Company even established plantations in the Cape of Good Hope and Mauritius to provide lemons for their crews.

Over time, unfortunately, the knowledge of lemon juice’s beneficial properties somehow vanished. The reasons were many, including simple complacency. When the incidence of scurvy grew worse again, there was resistance to citrus. Lemon juice was expensive and some shipowners suspected that merchants touted the imaginary medicinal powers of lemons just to drive up the price. At the same time, physicians were peddling a confusing variety of many other supposed cures. As author David Harvie observes, there were even “anti-fruiters,” who claimed that lemons hurt rather than helped sailors on some expeditions.

Lind had seen relatively little scurvy himself until, on their tenweek voyage the previous summer, eighty of his crew had been laid low. As he cast about for an explanation, he noted that the rainy cold weather they encountered had made it hard for the crew to dry out and fostered stale air in the hold. Lind wondered if this bad air was the culprit. He also contemplated the possibility that the lack of a proper diet was to blame. Yet that seemed unlikely. “They had been afflicted by scurvy,” he would write, “even though the captain supplied the crew with mutton-broth fowls and meat from his own table.” On Lord Anson’s ships, Lind noted, scurvy had broken out in spite of a plentiful supply of what he believed to be adequate provisions and good water.

Despite Anson’s staggering loss, the brass in the British Admiralty displayed a disastrous lack of urgency. There was a great difference of opinion about its cause. Was it overcrowding? An excess of salt? Bad air? Some believed that only sluggish and lazy sailors succumbed to it. Moreover, even if they were to accept that for some strange reason lemons helped prevent it, carrying large crates of lemons on long voyages would entail great expense and was impractical besides, because lemons and lemon juice spoil. Perhaps most important, scurvy usually passed over the officers and higher-ranking seamen. So it simply seemed more expedient to replace casualties by pressing more unwitting men into service (often through trickery or kidnapping) than it was to shoulder the burden and expense of trying to prevent the disease.

Lind, newly promoted to ship’s surgeon, was horrified by scurvy. Having a sound scientific mind, he requested permission from his captain to search for a remedy by conducting an experiment that is considered by some to be the first clinical trial in all of medicine. Lind divided twelve sailors suffering from scurvy into six pairs and lodged them in hammocks in the ship’s forehold. He doled out a different remedy to each: either cider, sulfuric acid, vinegar, seawater, or oranges and lemons. The unfortunate sixth pair received a formulation that one of Lind’s colleagues recommended: an unappetizing paste of garlic, mustard seed, dried radish root, a tree resin known as balsam of Peru, gum myrrh, and for good measure, an occasional dose of barley water with tamarind along with cream of tartar to purge the system. After a week, he ran out of fruit and had to end his trial. It was by now evident that only two of the remedies had any effect. The cider appeared to help a little bit, while, incredible as it seemed, the citrus largely cured the disease—so much so that one sailor returned to duty, and Lind put the other to work nursing his companions.

You might think that Lind would immediately jump up and down yelling “Eureka,” because he had just proven, for all time, that something in citrus fruit cured scurvy. Not a chance. The unfortunate Lind was mired up to his hips in intellectual quicksand—the confusing medical theories of his day.

Lind gave himself time to make sense of his work. He retired from the navy, earned a medical degree in Edinburgh, and established a practice as a physician. Then he settled down to review many accounts of scurvy by others, before finally and conclusively explaining it.

In 1753, six years after his landmark experiment, Lind published a 456-page opus. Although the results of his experiment may seem clear-cut, his conclusions could have been, well, more conclusive. This is the point in our story where one wants to say, “Wait, wait! Can’t you see?” After perceptively reviewing fifty-four other works on scurvy, he only gets around to his own trial a third of the way through the book—and devotes just five paragraphs to it. He was confident he had shown that citrus could cure scurvy, yet he struggled to explain the malady’s cause. Concepts of disease at the time were a complete mess.

They were dominated by Galen’s idea that sickness resulted from an imbalance of bodily humors. So Lind concluded that on ships, a combination of poor diet and moist cold air blocked perspiration, and this trapped putrid unwholesome humors inside the body. He explained that citrus could open up the skin’s pores, but in a later edition he conceded that other medicines could also do the same. “I do not mean to say,” he opined, “that lemon juice and wine are the only remedy for the scurvy. This disease, like many others, may be cured by Medicines of very different and opposite qualities to each other, and to that of lemons.” As the author Frances Frankenburg observed, “If there was ever a researcher who doubted his own findings, it was James Lind.”

On the bright side, Lind did recommend that sailors use lemon juice to prevent the disease. But he followed that sound suggestion with an uncharacteristically sloppy error. To prevent the juice from rotting, he suggested it should be heated to make a syrup—little suspecting that heat destroys the juice’s curative powers. To add to the confusion, many distinguished physicians championed other cures that were entirely ineffective. One sea surgeon wrote sourly, “Dr. Lind reckons the want of fresh vegetables and greens a very powerful cause of the Scurvy; he might with equal reason, have added fresh animal food, wine, punch, spruce beer, or whatever else is capable of preventing this disease.” Lind’s critic went on to recommend rice as a remedy, or a mixture of one-fourth brandy and three-fourths water. Scurvy rampaged on, unabated.

In 1756, three years after Lind published his treatise, the Seven Years’ War broke out between Britain and France. Of the 184,899 sailors who enlisted or were pressed into the Royal Navy, only 1,512 were killed in action. Another 133,708 expired from disease—primarily scurvy. Scurvy continued to hamstring the British navy during the American Revolution that followed soon after. If the Admiralty had provided lemons to their crews, some argue, the British might have prevailed against the colonies, or at least held off France’s navy and negotiated a more favorable settlement.

It wasn’t until 1795, a year after Lind’s death, that the Royal Navy began issuing lemon juice to sailors. For a time, scurvy actually ceased to be a problem. But after taking one fruitful step forward, the navy leaped two steps back. Eighty years later, they switched to limes, which they could buy more cheaply from plantations in the British West Indies. Henceforth, British sailors were, of course, known as limeys. But regrettably, limes were much less effective at preventing scurvy, and this cast doubt on the value of any citrus juice as a cure. Even in the early twentieth century, when doctors agreed that fresh fruit and vegetables could treat scurvy, they still could not agree on the disease’s cause, which is why, in 1912, scurvy plagued the British explorer Robert Scott’s meticulously planned expedition to the South Pole. His conviction that bacterial food poisoning was to blame likely hastened his own demise. After hundreds of years, scurvy’s cause still remained a mystery.

Buy What’s Gotten Into You by Dan Levitt here.

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In the two years since the COVID vaccines became available to the public, they have become a popular target for misinformation. Anti-vaccine activists have made some wild claims—the vaccines alter DNA, cause infertility, and implant magnetic devices for the government to track your every move—with no credible scientific evidence. But they have managed to accomplish one goal: More Americans than ever are hesitant about getting a vaccine.

So whenever a person has a rare side effect from the COVID vaccines, news spreads rapidly. For example, Florida’s surgeon general recommended boys between 18 to 39 should not get the mRNA shots, citing a questionable state analysis that claimed the risk of cardiac death jumped up by 84 percent after immunization. More recently, people were quick to blame Buffalo Bills player Damar Hamlin’s sudden cardiac arrest in early January on the NFL’s mandatory COVID vaccine requirement. Cardiologists, however, were just as quick to debunk the notion with more realistic medical explanations.

Infectious disease experts have been investigating the risk of myocarditis since the beginning of the pandemic. Thousands of studies have been published on COVID, and some have found a connection between myocarditis with both the virus and the vaccines. Here are the answers we have so far.

What is myocarditis?

Myocarditis is a disease that causes inflammation in a middle layer of the heart muscle called the myocardium. The inflammation affects muscle cell function and the heart’s electrical system, causing irregular heart beats and interfering with pumping blood to and from the body. The inflammation results from your body’s immune response overreacting to an infection it’s currently fighting. Viruses are the common cause of most myocarditis infections and are responsible for 1.5 million cases every year.

A majority of myocarditis cases are mild and self-resolving, says Keren Hasbani, a pediatric cardiologist at Pediatrix Pediatric and Congenital Cardiology Associates of Texas. Most go away in less than two weeks without complications or need to go to the hospital. 

[Related: A good night’s sleep can boost cardiac health]

Myocarditis persisting for longer than two weeks is considered chronic and can create severe complications. The longer inflammation stays in the heart, the weaker the muscle becomes. Continued injuries to heart cells can lead to permanent scarring of cardiac tissue, which can cause the condition to come back and increase the risk of stroke, heart attack, heart failure, or death.

Myocarditis can strike anyone, at any age. However, the heart condition appears to occur at twice the rate in young men than women.

What does myocarditis feel like?

In some myocarditis cases, it is possible for a person to go about their day without knowing that their heart is inflamed. When there are symptoms, they could mimic those of a viral infection, including fever, vomiting, headaches, and a sore throat. 

The most common presenting sign of the condition is a discomfort or a feeling of tightening in the chest area. Hasbani says the pain can happen anywhere between your left side to the chest bone area. Rather than the soreness you feel when you pull a pectoral muscle, Hasbani says myocarditis chest pain is often described as aches originating from a place much deeper inside the body. “People usually say it’s different from any kind of chest pain they’ve felt before.”

Individuals with myocarditis also tend to describe rapid or abnormal heart beats because the inflammation affects the heart’s electrical system. Since the organ is not functioning to its full potential, blood is not being properly distributed to other parts of the body. This can lead to symptoms such as shortness of breath, especially as the chest pain makes it difficult to take big deep breaths. The lack of oxygen can then spur on lightheadedness and fainting spells. Less common symptoms include swelling in the legs, ankles, and feet from the lack of blood distribution.

While Hasbani says it’s extremely rare, myocarditis can be life-threatening when the weakened heart cannot meet the demands of the body. In these scenarios, a person would need to be hospitalized and given medication such as adrenaline to keep the heart pumping. Doctors may also have to provide a life support machine to oxygenate and pump the blood. This allows the heart to rest and recover from the damage myocarditis inflicted. 

Is there a relationship between myocarditis and COVID?

COVID infections can cause severe and life-threatening cases of myocarditis, but the overlap is still slim. Forty out of every 1 million people are estimated to develop myocarditis 28 days after testing positive. The chances of inflammation increases among people with severe COVID illness that requires hospitalization and people with preexisting health conditions such as high blood pressure and obesity.

A 2021 study from the Centers for Disease Control and Prevention (CDC) found the risk of myocarditis is 16 times higher among unvaccinated people with COVID than unvaccinated people who have never had the disease. It also found that men and adults 50 years and older are more vulnerable to the condition. Among unvaccinated children under 16, myocarditis risk was 37 times higher in those with COVID infection than their healthy peers. 

[Related: What patients find at long COVID clinics: rejection, outdated therapies, and unanswered questions]

Hasbani says the reason why people with myocarditis from a COVID infection have more serious complications is because the body is already overworked from dealing with the extensive damage the virus is causing to other organs like the lungs, kidneys, and GI tract. Inflammation in the heart may take a backseat to all the other ongoing bodily issues and take longer to resolve. In children under 16, the CDC speculates that COVID-induced myocarditis might actually be a sign of multisystem inflammatory syndrome, which is a potentially deadly condition associated with the coronavirus. 

Can COVID vaccines cause myocarditis?

Yes, but the chances are extremely rare. One August 2022 study in England calculated the rate of hospitalizations and deaths related to myocarditis in more than 42 million people 13 and older. The subjects consisted of two different groups: individuals fully vaccinated with either the AstraZeneca, Moderna, or Pfizer-BioNTech vaccines, and unvaccinated individuals who tested positive for COVID. The researchers found a 0.007-percent chance—that’s 2,681 out of 43 million vaccinated adultsof being hospitalized or dying from vaccine-related myocarditis. Only 0.001 percent occurred within 28 days of receiving a COVID vaccine or booster. A separate study from October 2022 estimated that the myocarditis risk is seven times greater in unvaccinated versus vaccinated individuals. 

So far only the mRNA vaccines have been associated with myocarditis. The risk appears to be higher in people with a second dose of the Moderna shot than the Pfizer-BioNTech one, says Jayne Morgan, a cardiologist and clinical director of the COVID task force at Piedmont Hospital in Atlanta. The large-scale study done in England last year showed more overlap of myocarditis cases with a second Moderna dose. Meanwhile, another 2022 study measured a two- to threefold higher chance of developing myocarditis after a second Moderna vaccine, with the association being the strongest among men and people between 18 to 39. Still, Morgan warns that the rate is small compared to that of unvaccinated populations with COVID.

[Related: The truth about COVID, vaccines, ED, and infertility]

Though incidence is low, research points to young men under 40 having the highest risk of developing myocarditis, says Morgan. A September 2022 study in Israel reported 28 mild cases of myocarditis after a the Pfizer-BioNTech booster shot—out of nearly four million adults. The results showed that men between the ages of 16 to 19 had the highest risk of myocarditis (a 1 in 15,000 chance), followed by men between the ages of 20 to 24. All individuals made a full recovery after spending an average of 3.5 days in the hospital.

There is no official explanation for why young men have a greater risk of myocarditis. Some COVID researchers have hypothesized that the SARS-CoV-2 spike protein that the mRNA vaccines were designed from might trigger an overly active immune response that causes inflammation in the heart. That doesn’t mean the vaccine causes the infection, warns Hasbani: Instead, the immune system is responding to the vaccine in a way that also happens to react with heart cells in the myocardium. The effect is nearly always temporary.

Myocarditis existed well before COVID vaccines

Hasbani says any medical treatment, including vaccines, has side effects, including ones that involve the heart. The smallpox vaccine, for example, helped eliminate smallpox worldwide in 1980, but was later found to have a 10-percent risk of mild myocarditis.

One likely reason we know more about the risks of myocarditis for the COVID vaccine is that “we haven’t vaccinated this amount of people this quickly for one specific illness, and followed a large population this closely,” Hasbani explains.

With all the facts, both experts stress that the small risk of myocarditis does not outweigh the severe complications you can get from a SARS-CoV-2 infection. For instance, long COVID remains an issue for millions of patients and has been associated with far more persisting heart problems. “Giving you and your family a vaccine is much safer than taking your chance on COVID,” Hasbani adds.

If the vaccine does cause cardiac inflammation in someone, there is little chance the condition would cause a heart failure. A January 2022 analysis of more than 17 million people found just 627 cases (or 0.0035 percent) of COVID vaccine-related myocarditis. Of those, 626 individuals fully recovered and one individual died. To put that into perspective, the National Institute of Health website states: “Your chance of getting myocarditis after getting a COVID vaccine is less than the chance of being struck by lightning during your lifetime.”

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The National Institute of Allergy and Infectious Diseases (NIAID) announced on January 18 that a Phase 3 clinical trial of a human immunodeficiency virus (HIV) vaccine in development from Johnson & Johnson (J&J) has failed. The vaccine proved to be ineffective at preventing infection.

Janssen, the vaccine division of J&J, began running this trial in 2019. It was stopped after a scheduled review, which revealed that there were roughly as many new HIV infections among people in the vaccine arm as in the placebo arm.

The trial, which is part of the Mosiaco study, had 3,900 volunteers across multiple countries, including Argentina, Brazil, Italy, Mexico, Peru, Poland, Puerto Rico, Spain, and the United States. The trial focused on cisgender and transgender people who have sex with men due partially to these populations’ vulnerability to the virus.

[Related: The first woman has been cured of HIV using donor stem cells.]

“We are disappointed with this outcome and stand in solidarity with the people and communities vulnerable to and affected by HIV,” said Penny Heaton, Janssen’s head of global therapeutics and vaccines, in a statement. “Though there have been significant advances in prevention since the beginning of the global epidemic, 1.5 million people acquired HIV in 2021 alone, underscoring the high unmet need for new options and why we have long worked to tackle this global health challenge. We remain steadfast in our commitment to advancing innovation in HIV, and we hope the data from Mosaico will provide insights for future efforts to develop a safe and effective vaccine. We are grateful to our Mosaico partners and the study investigators, staff and participants.”

This vaccine was given in four injections over one year and was based on “mosaic” immunogens, where the vaccine is built using components (or pieces) that feature elements of multiple HIV subtypes. The goal was for the vaccine to start an immune response to a broad range of HIV strains and used a common cold virus (adenovirus 26) to deliver antigens. This is the same the same antigen delivery system that J&J’s COVID-19 vaccine used. It was the only HIV vaccine in late-stage clinical trials.

In an interview with The New York Times, former NIAID director Anthony Fauci said that the news is “disappointing, but it isn’t the end of the effort toward developing a vaccine. There are other strategic approaches.”

Multiple HIV vaccine candidates have stalled over the past few decades. In 2021, Imbokodo trial (a Phase 2b trial of a similar vaccine candidate) stopped when data indicated that it was not preventing infections. The vaccine was being studied in women in sub-Saharan Africa.

According to some experts, this defeat sets progress towards a vaccine back by three to five years, but other options are in early-stage trials. In January 2022, Moderna began Phase I clinical trials for an HIV vaccine that uses the same mRNA technology as the pharmaceutical company’s COVID-19 vaccine.

Additionally, a small phase 1 clinical trial of another experimental two-dose HIV vaccine found that it could induce crucial broadly neutralizing antibody precursor B cells in 97 percent of study participants without significant side effects. These results were published in the journal Science in December 2022. “At the most general level, the trial results show that one can design vaccines that induce antibodies with pre-specified genetic features, and this may herald a new era of precision vaccines,” said William Schief, study co-author and researcher at The Scripps Research Institute, in a December press release.

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

HIV is no longer a death sentence in wealthy countries due to medications that reduce viral load, or the amount of the virus in the blood. There are currently pills and bimonthly injections that can prevent infection in HIV negative individuals. However, these medications can be inaccessible to the people who need it most, and HIV treatment must be taken for the rest of a patient’s life after diagnosis.

HIV still infects about 1.5 million people each year and kills roughly 650,000. The virus attacks the body’s immune system and destroys white blood cells, weakening immunity against other opportunistic infections.

“The ultimate prevention modality for any infection, particularly viral infection, is a vaccine that’s safe and effective,” Fauci said. “That’s the reason why the field is going to continue to pursue very active research in that area.”

According to the Centers for Disease Control and Prevention (CDC), some of the best ways to prevent HIV infection using wearing condoms during sexual intercourse, not sharing needles, and continually testing for sexually transmitted disease and infections.

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On January 17, Moderna announced that data from a late-stage clinical trial for the company’s experimental messenger RNA (mRNA) vaccine for respiratory syncytial virus (RSV) was 83.7 percent effective at preventing at least two symptoms, such as cough and fever, in adults 60 and older.

“RSV significantly affects the health of older and high-risk adults, particularly those with comorbidities,” Abdullah Baqui, a principal investigator for the study sites in Bangladesh and professor at Johns Hopkins Bloomberg School of Public Health, said in a statement. “This trial will help to understand the role of severe acute respiratory infections in older adult populations and inform the future implementation of vaccines in adults in lower-resource areas.”

[Related: Is it flu or RSV? It can be tough to tell.]

The study was conducted in roughly 37,000 participants age 60 and older and the data analysis was performed after 64 of the participants contracted the virus. Moderna plans to release the full data at an upcoming medical meeting and will seek approval from the Food and Drug Administration (FDA) during the first half of 2023.

“Today’s results represent an important step forward in preventing lower respiratory disease due to RSV in adults 60 years of age and older. These data are encouraging, and represent the second demonstration of positive phase 3 trial results from our mRNA infectious disease vaccine platform after, Spikevax, our COVID-19 vaccine. We look forward to publishing the full data set and sharing the results at an upcoming infectious disease medical conference,” said Stéphane Bancel, Moderna’s Chief Executive Officer, in a statement.

Currently, there is no vaccine to prevent RSV infection and Moderna, Pfizer, and GSK are working to get their vaccines out to the public. In 2022, Pfizer and GSK filed applications for regulatory approval in the United States and late-stage trial results found that Pfizer’s RSV vaccine was 66.7 percent effective in preventing two or more symptoms.

[Related: How our pandemic toolkit fought the many viruses of 2022.]

In Europe, an antibody treatment called nirsevimab from Sanofi and AstraZeneca gained the European Commission’s marketing authorization to prevent the virus in newborns and infants. This treatment is under review by the FDA for use in the US.

While RSV produces symptoms similar to a cold, it can be fatal for young children and older adults. According to the CDC, about 60,000 to 120,000 older adults are hospitalized and between 6,000 to 10,000 die due to RSV infection every year.

Cases of RSV began appearing earlier than usual during the 2022-2023 RSV season, but cases have ticked downward after peaking in November 2022. RSV surged in the US and Europe this alongside the flu and COVID-19 as part of a “tripledemic” that has been straining hospitals and has even caused shortages of children’s pain relievers and fever reducers.

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This article was originally featured on KHN.

MALMO, Minn. — Eight women, all 73 or older, paced the fellowship hall at Malmo Evangelical Free Church to a rendition of Daniel O’Donnell’s “Rivers of Babylon” as they warmed up for an hourlong fitness class.

The women, who live near or on the eastern shore of Mille Lacs Lake, had a variety of reasons for showing up despite fresh snow and slippery roads. One came to reduce the effects of osteoporosis; another, to maintain mobility after a stroke.

Most brought hand and ankle weights, which they would use in a later portion of the program focused on preventing falls, known as Stay Active and Independent for Life, or SAIL. The class meets twice a week in Malmo, a township of about 300 residents. It is run by Juniper, a statewide network of providers of health promotion classes.

A few years ago, older adults who were interested in taking an evidence-based class like SAIL — meaning a class proved by research to promote health — had only one option: attend in person, if one was offered nearby.

But then the covid-19 pandemic and physical distancing happened. Along with social isolation came the rapid introduction of remote access to everything from work to workouts.

After widespread lockdowns began in March 2020, agencies serving seniors across the U.S. reworked health classes to include virtual options. Isolation has long since ended, but virtual classes remain. For older adults in rural communities who have difficulty getting to exercise facilities, those virtual classes offer opportunities for supervised physical activity that were rare before the pandemic.

And advocates say online classes are here to stay.

“Virtually the whole field knows that offering in-person and remote programming — a full range of programming — is a great way to reach more older adults, to increase access and equity,” said Jennifer Tripken, associate director of the Center of Healthy Aging at the National Council on Aging. “This is where we need to move together.”

Since April 2020, the National Council on Aging has organized monthly conference calls for service providers to discuss how to improve virtual programs or begin offering them.

“We found that remote programming, particularly for rural areas, expanded the reach of programs, offering opportunities for those who have traditionally not participated in in-person programs to now have the ability to tune in, to leverage technology to participate and receive the benefits,” Tripken said.

In 2022, at least 1,547 seniors participated in an online fitness program through Juniper, part of a Minnesota Area Agency on Aging initiative. More than half were from rural areas.

Because of grant funding, participants pay little or nothing.

Juniper’s virtual classes have become a regular activity both for people who live far from class locations and others who because of medical needs can’t attend. Carmen Nomann, 73, frequented in-person exercise classes near her home in Rochester before the pandemic. After suffering a rare allergic reaction to a covid vaccine, she’s had to forgo boosters and limit in-person socializing.

Virtual classes have been “really a great lifeline for keeping me in condition and having interaction,” she said.

Since 2020, Nomann has participated in online tai chi and SAIL, at one point logging on four days a week.

“Now, we would never go away from our online classes,” said Julie Roles, Juniper’s vice president of communications. “We’ve learned from so many people, particularly rural people, that that allows them to participate on a regular basis — and they don’t have to drive 50 miles to get to a class.”

When seniors drive a long way to attend a class with people from outside their communities, “it’s harder to build that sense of ‘I’m supported right here at home,’” she said.

Roles said both virtual and in-person exercise programs address social isolation, which older adults in rural areas are prone to.

Dr. Yvonne Hanley has been teaching an online SAIL class for Juniper since 2021 from her home near Fergus Falls. She had recently retired from dentistry and was looking for a way to help people build strength and maintain their health.

At first, Hanley was skeptical that students in her class would bond, but over time, they did. “I say ‘Good morning’ to each person as they check in,” she said. “And then during class, I try to make it fun.”

AgeOptions, an Illinois agency serving seniors, has seen similar benefits since introducing virtual fitness programs. Officials at the agency said last year that their operations “may have changed forever” in favor of a hybrid model of virtual and in-person classes.

That model allows AgeOptions to maintain exercise programs through Illinois’ brutal winters. Organizers previously limited winter activities to keep older adults from traveling in snow and ice, but now AgeOptions leans on remote classes instead.

“If the pandemic didn’t happen, and we didn’t pivot these programs to virtual, we wouldn’t be able to do that,” said Kathryn Zahm, a manager at AgeOptions. “We would just potentially spend months limiting our programming or limiting the types of programming that we offered. So now we can still continue to offer fall-prevention programs throughout the year because we can offer it in a safe way.”

But the new approach has challenges.

AgeOptions has identified increasing access to technology as a funding priority for the next few years, to ensure seniors can sign on.

The agency found that for many “folks in rural communities it was a challenge not only for them to have the device but to have the bandwidth to be able to do video conference calls,” Zahm said.

Tripken said providers and participants need guidance and support to facilitate access to virtual classes.

“For older adults in particular, that includes ensuring those with vision loss, those with hearing loss, those with low English proficiency” can participate in virtual classes, she said.

Some programs have created accommodations to ease the technology barrier.

Participants in Bingocize — a fall-prevention program licensed by Western Kentucky University that combines exercise and health education with bingo — can use a printed copy of the game card mailed to them by AgeOptions if they lack the proficiency to play on the game’s app. Either way, they’re required to participate on video.

The mail option emerged after Bingocize fielded requests from many senior service organizations trying to figure out how to offer it remotely, said Jason Crandall, the creator and international director of Bingocize.

Crandall designed Bingocize as a face-to-face program and later added the online application to use during in-person classes. Then covid hit.

“All of a sudden, all of these Area Agencies on Aging are scrambling, and they were scrambling trying to figure out, ‘How do we do these evidence-based programs remotely?’” Crandall said.

He said Bingocize was one of the few programs at the time that could quickly pivot to strictly remote programming, though it had never done so before.

“From when the pandemic began to now, we’ve come light-years on how that is done,” he said, “and everybody’s getting more comfortable with it.”

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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A large comprehensive study published January 16 in BMJ Global Health is shedding light on the risks of COVID-19 infection during pregnancy.

The study of over 13,000 pregnancies across 12 countries found that those infected with COVID-19 were seven times as likely to die during childbirth and are more than three times more likely to be admitted to an intensive care unit during during pregnancy, compared to COVID-free pregnant people. About 2,000 patients had a confirmed or probable case of COVID-19.

[Related: COVID deaths in pregnant people in the US are flying under the radar.]

“This study provides the most comprehensive evidence to date suggesting that COVID-19 is a threat during pregnancy,” Emily R. Smith, an assistant professor of global health at the George Washington University Milken Institute School of Public Health and lead author of the study, said in a statement. “Our findings underscore the importance of COVID-19 vaccination for all women of childbearing age.”

The researchers also found that when compared to uninfected pregnant people, those who have the the virus were 15 times more likely to require a ventilator and fives time more likely to develop blood clots that can cause swelling, pain, or other life-threatening complications. 

Babies born to those infected with COVID-19 were almost twice as likely to be admitted to a neonatal intensive care unit (NICU) after birth and were at a higher higher risk of being born prematurely. According to Smith, preterm babies are also at high risk of having lifelong health problems including delays in early childhood cognitive development.

“This study shows the risk of getting COVID-19 for both mother and baby,” Smith said. “All countries, including the United States, should make access to COVID vaccines an urgent priority in order to save lives and prevent health problems.”

The study did not look at the benefits of vaccination in pregnancy, but other studies have shown decreases in the risk of stillbirth, preterm birth, and severe disease or death.

[Related: The CDC is urging pregnant people to get COVID-19 vaccines. Here’s how we know it’s safe.]

Division director of Maternal Fetal Medicine at the Cleveland Clinic Justin Lappen praised the study in an article for CNN, saying the findings reinforce and advance previous research that highlights the importance of preventing and treating the virus in pregnant people. Lappen wasn’t involved in the BMJ study.

There are some caveats on this study, namely that the data used in this research was conducted relatively early in the pandemic when many people were still unvaccinated and uninfected. The people in the study were likely at higher risk not just because of pregnancy, but because pre-existing immunity to fight the virus was non-existent.

According to the CDC, more than 72 percent of pregnant people in the US have had their primary series of COVID-19 vaccines, and about 95 percent of Americans are estimated to have had the virus at least once or have been vaccinated against it.

The best ways to prevent COVID-19 infection, whether pregnant or not, remain getting vaccinated, waring a high-quality face mask when indoors or in crowds, and practicing good hygiene.

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As more and more adults have jobs that require them to be sitting at a desk most of the day, the phrase “sitting is the new smoking,” can feel quite haunting. According to the Mayo Clinic, sitting for long periods of time can increase the risk of cardiovascular disease, increased blood pressure, cancer, and other health concerns.

However, a small study published January 12 in the Medicine & Science in Sports & Exercise, the journal of the American College of Sports Medicine, finds that taking a five minute walk for every 30 minutes of sitting can offset some of the worst effects of prolonged sitting. It builds on a growing body of research into the health benefits of shorter walks or bursts of activity throughout the day.

[Related: How to sit ergonomically without expensive equipment.]

The study tested five different exercise “snacks,” or short bursts of activity: one minute of walking after every 30 minutes of sitting, one minute after 60 minutes; five minutes every 30; five minutes every 60; and no walking. 

“If we hadn’t compared multiple options and varied the frequency and duration of the exercise, we would have only been able to provide people with our best guesses of the optimal routine,” said study co-author Keith Diaz, an associate professor of behavioral medicine at Columbia University Vagelos College of Physicians and Surgeons, in a statement.

Each of the 11 adults who participated in the study sat in an ergonomic chair for eight hours in Diaz’s lab. The participants (all in their 40s, 50s, and 60s and most didn’t have hypertension or diabetes) could read, work on a laptop, and use their phones and were provided standardized meals.

They stood up only for their prescribed exercise snack of walking on the treadmill or for restroom breaks. The research team monitored that each participant din’t over or under exercise and measured blood pressure and blood sugar-two key indicators of cardiovascular health.

Five minutes of walking every 30 minutes was the only amount that significantly lowered both blood pressure and blood sugar levels in the participants. This regimen also affected how the participants’ bodies responded to large meals and reduced blood sugar spikes by 58 percent compared with sitting for eight hours. 

[Related: Walking correctly takes work—here’s how to improve every step.]

One minute walking breaks every 30 minutes also provided some modest benefits to blood sugar levels throughout the day, but walking for either one minute or five minutes after 60 minutes of sitting didn’t appear to provide any benefits to blood sugar.

As far as blood pressure levels, all amounts of walking reduced blood pressure by 4 to 5 millimeters of mercury (mmHg) compared with sitting all day. “This is a sizeable decrease, comparable to the reduction you would expect from exercising daily for six months,” said Diaz. 

Levels of mood, fatigue, and cognitive performance was also measured during the testing. Every regimen except for walking one minute every hour led to decreases in fatigue and boots in moods. Cognition wasn’t influenced by any of the walking regimens.

“The effects on mood and fatigue are important,” said Diaz. “People tend to repeat behaviors that make them feel good and that are enjoyable.” 

The team is now testing 25 different doses of walking and exercise “snacks” and testing a wider variety of people.

“What we know now is that for optimal health, you need to move regularly at work, in addition to a daily exercise routine,” said Diaz. “While that may sound impractical, our findings show that even small amounts of walking spread through the work day can significantly lower your risk of heart disease and other chronic illnesses.”

You don’t even need to get a standing desk (which aren’t necessarily better) to help prevent some of the negative effects of sitting all day. Some tips on how to increase your movement during the work day include holding walking meetings with co-workers, taking the stairs instead of the elevator, setting reminders in your phone or watch to get up and move, and listening to music while walking to stay motivated and entertained. You can also try box squats, where you get up and down in your chair gently, or do some push ups and planks.

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On January 11, the World Health Organization (WHO) and the Ministry of Health-Uganda declared that the country’s recent Ebola outbreak is over. An epidemic can be declared over by the WHO when no confirmed or probable cases are reported for twice the incubation period for Ebola infections, or 42 days.

The outbreak in Uganda was officially recognized on September 20, 2022 and saw 164 confirmed or likely infections, 55 lab-confirmed deaths, and 22 suspected deaths due to the virus.

[Related: Uganda’s Ebola outbreak is ‘rapidly evolving,’ according to WHO.]

The last recorded victim was a stillborn baby at 28 weeks gestation that tested positive for the virus. Previously, the baby’s mother had been infected with the virus, but recovered and was reportedly in good health. Scientists are studying both cases to understand vertical transmission, or whether the virus could have crossed the placenta to infect the baby. This kind of transmission hasn’t been a known risk with Ebola before.

The outbreak was caused by the Sudan Ebola virus, one of five known strains of the virus. According to the WHO, the Sudan strain is a severe and frequently fatal illness that is contracted through the bodily fluids of infected animals. It and all Ebola viruses spreads between humans via direct contact with infected bodily fluids. Some of the best prevention methods for Ebola are good hand washing, avoiding contact with infected bodily fluids and items that could become contaminated, and avoiding eating meat from infected animals.

There are therapeutics and a vaccine against another type of Ebola virus (Ebola Zaire), but vaccines or treatments do not currently exist against Ebola Sudan. Three vaccines are undergoing trials in Uganda and this recent outbreak was the country’s first of this strain since 2012.

Since the effects of Ebola infections including eye problems, headaches, muscle and joint pain, and fatigue can last years, the 87 documented survivors will continue to need ongoing care and will be monitored. It is also possible that they’re carrying active virus in certain parts of their bodies that could spark a new outbreak under the right conditions and circumstances.

[Related:Ebola vaccines in African countries successfully produced antibodies in kids and adults.]

“While we expanded our efforts to put a strong response in place across the nine affected districts, the magic bullet has been our communities who understood the importance of doing what was needed to end the outbreak, and took action,” said Jane Ruth Aceng Acero, Uganda’s Minister of Health, in a statement.

Matshidiso Moeti, WHO regional director for Africa added that only two short months ago, “it looked as if Ebola would cast a dark shadow over the country well into 2023, as the outbreak reached major cities such as Kampala and Jinja, but this win starts off the year on a note of great hope for Africa.”

A lockdown was imposed from mid-October to mid-December in two districts at the epicenter to try to stop the virus from spreading from the outbreak’s epicenter and tried and true virus control measures are credited with helping stop the outbreak.

“The Ugandans, they’ve been dealing with Ebola responses for going on decades now. And they’ve always managed to control them and prevent them from spilling outside their borders. But they managed to do that through just very basic control measures,” Joel Montgomery, chief of the CDC’s Viral Special Pathogens Branch, told CNN. “That’s eventually how this outbreak ended. We had really good contact tracing, really good Ebola treatment units that had been set up and then really, really good laboratory diagnostics,” he said.

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This article was originally republished from The Conversation.

Bringing a new drug to market costs billions of dollars and can take over a decade. These high monetary and time investments are both strong contributors to today’s skyrocketing health care costs and significant obstacles to delivering new therapies to patients. One big reason behind these barriers is the lab models researchers use to develop drugs in the first place.

Preclinical trials, or studies that test a drug’s efficacy and toxicity before it enters clinical trials in people, are mainly conducted on cell cultures and animals. Both are limited by their poor ability to mimic the conditions of the human body. Cell cultures in a petri dish are unable to replicate every aspect of tissue function, such as how cells interact in the body or the dynamics of living organs. And animals are not humans – even small genetic differences between species can be amplified to major physiological differences.

Fewer than 8% of successful animal studies for cancer therapies make it to human clinical trials. Because animal models often fail to predict drug effects in human clinical trials, these late-stage failures can significantly drive up both costs and patient health risks.

To address this translation problem, researchers have been developing a promising model that can more closely mimic the human body – organ-on-a-chip.

As an analytical chemist, I have been working to develop organ and tissue models that avoid the simplicity of common cell cultures and the discrepancies of animal models. I believe that, with further development, organs-on-chips can help researchers study diseases and test drugs in conditions that are closer to real life.

What are organs-on-chips?

In the late 1990s, researchers figured out a way to layer elastic polymers to control and examine fluids at a microscopic level. This launched the field of microfluidics, which for the biomedical sciences involves the use of devices that can mimic the dynamic flow of fluids in the body, such as blood.

Advances in microfluidics have provided researchers a platform to culture cells that function more closely to how they would in the human body, specifically with organs-on-chips. The “chip” refers to the microfluidic device that encases the cells. They’re commonly made using the same technology as computer chips.

Not only do organs-on-chips mimic blood flow in the body, these platforms have microchambers that allow researchers to integrate multiple types of cells to mimic the diverse range of cell types normally present in an organ. The fluid flow connects these multiple cell types, allowing researchers to study how they interact with each other.

This technology can overcome the limitations of both static cell cultures and animal studies in several ways. First, the presence of fluid flowing in the model allows it to mimic both what a cell experiences in the body, such as how it receives nutrients and removes wastes, and how a drug will move in the blood and interact with multiple types of cells. The ability to control fluid flow also enables researchers to fine-tune the optimal dosing for a particular drug.

The lung-on-a-chip model, for instance, is able to integrate both the mechanical and physical qualities of a living human lung. It’s able to mimic the dilation and contraction, or inhalation and exhalation, of the lung and simulate the interface between the lung and air. The ability to replicate these qualities allows researchers to better study lung impairment across different factors.

Bringing organs-on-chips to scale

While organ-on-a-chip pushes the boundaries of early-stage pharmaceutical research, the technology has not been widely integrated into drug development pipelines. I believe that a core obstacle for wide adoption of such chips is its high complexity and low practicality.

Current organ-on-a-chip models are difficult for the average scientist to use. Also, because most models are single-use and allow only one input, which limits what researchers can study at a given time, they are both expensive and time- and labor-intensive to implement. The high investments required to use these models might dampen enthusiasm to adopt them. After all, researchers often use the least complex models available for preclinical studies to reduce time and cost.

Lowering the technical bar to make and use organs-on-chips is critical to allowing the entire research community to take full advantage of their benefits. But this does not necessarily require simplifying the models. My lab, for example, has designed various “plug-and-play” tissue chips that are standardized and modular, allowing researchers to readily assemble premade parts to run their experiments.

The advent of 3D printing has also significantly facilitated the development of organ-on-a-chip, allowing researchers to directly manufacture entire tissue and organ models on chips. 3D printing is ideal for fast prototyping and design-sharing between users and also makes it easy for mass production of standardized materials.

I believe that organs-on-chips hold the potential to enable breakthroughs in drug discovery and allow researchers to better understand how organs function in health and disease. Increasing this technology’s accessibility could help take the model out of development in the lab and let it make its mark on the biomedical industry.

Chengpeng Chen, Assistant Professor of Chemistry and Biochemistry, University of Maryland, Baltimore County. Chengpeng Chen receives funding from the NIH.

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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.

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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.

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Every new year, many people vow to lose weight—and 2023 is no different.  Pledging to eat healthy or hit up the gym are two of the top resolutions among Americans this year. If you’ve been scrolling through TikTok, however, you might have seen a third option for your weight loss goals: several TikTokers are injecting themselves weekly with a Type 2 diabetes drug called Ozempic, claiming it can help quickly trim your tummy. Kim Kardashian is rumored to have used the drug to fit into Marilyn Monroe’s dress for the Met Gala (though she has denied this) and Elon Musk has tweeted that he’s a fan.

Now, Ozempic’s newfound status as a weight loss hack has infiltrated TikTok, which is causing the drug to fly off the shelves. But the increased demand for the injection has also sparked a drug shortage worldwide, leaving people with diabetes without a means to get their prescribed medication. As the trend takes off, multiple health professionals are questioning the safety of using an off-label drug and its long-term effectiveness for keeping the weight off.  

For people just looking to get skinny, quick, “it’s not meant to be a short-term solution to weight loss, and it’s very expensive with people paying close to $1,000 [if not covered by insurance],” explains Rose Lin, an endocrinologist at Providence Saint John’s Health Center in Santa Monica. Lin advises the drug is not medically necessary for people without diabetes or obesity when diet and exercise can give better results for your overall health. 

[Related: ‘Hormone diets’ might work—but not for the reason you think]

Ozempic is the brand name for a drug called semaglutide. It’s approved by the Food and Drug Administration (FDA) as a once-weekly injection to control blood sugar levels in people with Type 2 diabetes. It is also approved as a treatment to reduce the risk of heart problems for people with Type 2 diabetes and known heart disease.

Semaglutide mimics a hormone called glucagon-like peptide-1 (GLP-1) that binds to GLP-1 receptors. The activated receptors stimulate the pancreas to release insulin when blood sugar levels rise. GLP-1 also has a secondary role in appetite control. Like GLP-1 hormone, semaglutide slows down the digestive process so food sits in the stomach for longer periods of time, giving you the sensation of feeling full. This feeling of satiety sends a message to the brain which blocks the release of hunger hormones that cause food cravings. 

Weight loss is a known side effect of diabetic patients who are on semaglutide drugs. However, Ozempic, in particular, is not prescribed for weight loss purposes. There is another version of semaglutide called Wegovy that was FDA approved in 2021 as a weight management injection for adults with obesity. “Generally this would be for people carrying excessive weight,” explains Lin. People who are prescribed Wegovy are considered obese (a BMI of 30 or higher) or overweight (BMI of 27 or higher) with a secondary condition or disease that may cause obesity. A 68-week clinical trial found that middle-aged adults with obesity who took weekly injections of Wegovy lost an average of 35 pounds, while participants in the control group only lost an average of 6 pounds.

Semaglutide is an effective weight loss mitigation strategy for people with obesity, but experts warn that being skinny does not equate to being healthy. “There are no easy fixes for weight loss,” says Silvana Obici, chief of endocrinology and metabolism at Stony Brook Medicine. 

[Related: Why most diets don’t work—and what to try instead]

If you don’t need to be on the medication to manage diabetes, you probably shouldn’t be using it as semaglutide does pose some safety risks. One common side effect of semaglutide is nausea from having food stay in your stomach for long periods of time. “I’ve had patients have nausea to the point of vomiting or dry heaving,” describes Lin. Other common side effects of semaglutide drugs include stomach pain, diarrhea, and constipation. While rare, there is a possibility of developing thyroid tumors, as a past study in rodents found them after semaglutide injections. Carcinogenic effects in humans remain under dispute. There have also been reports of gallbladder problems in people taking semaglutide with symptoms ranging from yellowing of the skin or eyes, upper stomach pain, and fever.

Obici also warns that Ozempic is not very effective for sustaining long-term weight loss. People using the drug will not be able to maintain the weight loss without a healthy diet and regular exercise. “An unhealthy lifestyle when taking Ozempic might obliterate the beneficial [weight loss] effects of the drug,” she says. A 2021 clinical trial found people regained most of the weight they lost after discontinuing semaglutide injections. 

Due to this temporary weight loss, it may cause people to continue to use semaglutide drugs like Ozempic for extended periods of time. Obici and Lin are concerned that long-term reliance on Ozempic for weight loss will exacerbate the global drug shortage. It’s a serious problem for diabetic patients who are struggling to access the drug. “We’ve had people over the past month or two calling in and telling us they cannot get the drug for their diabetes,” says Lin. “We’re giving them samples when we can, but a lot of times there’s just no supply.”

There are alternative drugs that people with diabetes can take instead, but the shortage of Ozempic is causing a ripple effect with other injectable GLP-1 agonist drugs. The FDA has reported a shortage of other diabetic drugs such as Tirzepatide and several doses of Trulicity. Novo Nordisk, the pharmaceutical company that manufactures both Ozempic and Wegovy, announced they have Wegovy back in stock and are working to resolve the Ozempic shortage by early 2023.

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This article was originally featured in Undark.

Brad Fuller was a toddler when he contracted polio in 1952 and was sent to a hospital miles from his northeast Pennsylvania home. He stayed there for nine months, enduring long stints in an iron lung, a large metallic ventilator that helped him breathe. Fuller’s parents were allowed only rare visits. His earliest memory is of a nurse holding him in a mineral pool, instructing him to kick his legs.

That year marked the epidemic’s peak, when roughly 58,000 American children and adults developed polio and 3,000 of them died. In this respect, Fuller was lucky. The disease spared him, leaving only a weakened left leg and right arm. He was able to play tennis and football and train as a clinical psychologist. He built a career leading non-profits while teaching part time at St. Joseph’s University in Philadelphia. Despite his childhood ordeal, Fuller said, he felt invincible.

Then, in his 40s, a new doctor offered to treat his post-polio. Fuller was taken aback. It was the first time he’d heard the term. But the symptoms, like increased muscle weakness and poor balance, had been creeping up. At one point, he’d fallen and injured his knee. He now wears a full leg-brace and because he falls so often, he has taught himself to land easily. “I think if I was a typical person” — a person without a background in mental health — “I would have immediately gone into denial,” he said.

Scientists believe that the poliovirus has been around for thousands of years, but it did not cause epidemics until the late 1800s, when countries like the United States and the United Kingdom began to experience waves of increasing severity. By the 1940s and early 50s, the polio terror was killing or paralyzing more than a half million people globally each year. To treat the overwhelming number of sick people, hospitals created the first intensive care units. Many of those ICU patients were children and young adults.

Then came a pair of highly effective vaccines, the first of which was licensed in 1955. Case rates plummeted within a matter of years, and the virus was soon eradicated from entire countries. The vaccines are widely viewed as a triumph of public health. “My mother would have given anything to have a vaccine” for her children, recalls Fuller. But for those who had already been infected and survived, there was a downside. Polio “supposedly disappeared,” Fuller said. “That means research stopped.”

This history is bittersweet for patients who now struggle with post-polio syndrome, or PPS, which affects 25 to 40 percent of survivors. As adults, these individuals face an array of new symptoms stemming from their initial infection — everything from pain and renewed muscle weakness to fatigue to problems speaking and swallowing. PPS affects up to 300,000 people in the U.S., and globally the figure could be as high as 15 to 20 million people, according to some estimates. Most polio survivors in developed countries are 65 and older, said Marny Eulberg, a physician with PPS who ran one of the first dedicated clinics in the U.S. Survivors in the developing world are often younger.

Fuller was fortunate in another respect. His physician recognized the signs of PPS. Many patients struggle for years to find an explanation for their various symptoms, only to find out, once they receive a diagnosis, that there are no approved treatments and few specialists who can help them manage their condition. The exact cause of PPS remains unknown, and it has confounded researchers seeking a cure. Further research could elucidate polio’s long-term effects and stall patients’ physical decline, say the handful of scientists still studying the condition, but funding is scarce.

“The sentiment in all the funding bodies is polio has disappeared. So are we going to put money in it?” said Frans Nollet, a leading figure in European post-polio research who heads a specialty clinic at Amsterdam University Medical Centers. “It’s difficult,” he continued. “People think the disease has vanished, but the patients are still here.”

Like polio itself, post-polio syndrome is thought to have been around since ancient times. But it didn’t capture the medical world’s attention until the generation of young polio patients from the 1940s and 50s reached adulthood.

That’s when Marilyn Fletcher, a physician and polio survivor, approached the National Institutes of Health for help. In 1982, after repeated phone calls and visits to the federal agency, Fletcher landed a meeting with the neurologist Marinos Dalakas. At least 20 polio survivors in and around Washington D.C. were experiencing new symptoms, she told him. These individuals had even coined a new term, “post-polio syndrome,” to describe their condition. Thousands of people across the U.S. could have similar symptoms, Fletcher maintained. Those in D.C. were frustrated that the medical community was ignoring them.

Dalakas was initially skeptical and took no action. But a month later, he received a call to meet Fletcher at the Surgeon General’s office. Everett C. Coop, newly appointed to the position, “expressed his concern about the emerging phenomenon of PPS as described by Dr. Fletcher,” wrote Dalakas in a 1995 paper. Soon thereafter, Dalakas headed up a first-of-its-kind survey to learn more.

The survey was sent to 2,800 individuals with medical records indicating a polio-related disability. At least 2,500 people replied, often sending letters and personal photographs along with their questionnaires. “Many of the responses contained details which were highly emotional and stimulating,” Dalakas recalled in an email to Undark. For example, a 50-year-old man who’d contracted polio at 19 was struggling to drive or even dress himself. The devastating toll of PPS quickly became clear to Dalakas.

But how to define this new condition was less obvious. Collectively, the study participants reported a wide variety of ailments, with the onset of new symptoms occurring years to decades after the initial infection, often when survivors were in their 30s, 40s, or 50s. Because of this heterogeneity, experts disagree even today about what constitutes PPS. An official diagnosis requires a 15- or 20-year period of stability without new weakness or impaired movement.

Yet Frances Quinn, who contracted polio as a 1-year-old, said her symptoms have never truly been stable. At age 14, she felt growing weakness in her upper right arm and in her thumb. Her health care provider, she said, attributed these changes to adolescence and her accompanying loss of baby fat. “There’s a lot of stuff said about PPS that’s not really based on good science,” said Quinn, who worked as a physicist in the U.K. government for most of her life. “PPS is diagnosed when the patient decides that something is wrong and also finds someone who will listen to them.”

Katharina Stibrant Sunnerhagen, a professor of rehabilitation medicine at the University of Gothenburg in Sweden, raised similar objections. “My problem is that, for instance, if you had polio as a 1-year-old, when is your condition steady?” Childhood and adolescence encompass periods of rapid physical growth and development. Strictly speaking, an individual who survives polio as a baby must wait until the completion of puberty before their 15- to 20-year period of stability can even commence.

PPS was formally redefined by the World Health Organization in February of 2022, when it updated its International Classification of Diseases. The WHO now calls PPS “post-polio progressive muscular atrophy.” Critics have argued that the redefinition does not reflect the spectrum of symptoms patients may endure, increasing the risks that patients will receive the wrong sort of care. Why change it at all? asked Quinn. “It took 40 years of work to get PPS recognized and creating more names only adds to confusion.” Some sufferers also worry that disability payments could be affected although, for now, practitioners in the U.S. and U.K. still refer to the older classification.

Government recognition of PPS as a disability has been important because symptoms often appear in mid-life, making it difficult for some patients to sustain their careers. Carol Ferguson, a polio survivor and mother, used to work at a Pennsylvania bed-and-breakfast but was obliged to quit when she could no longer stand all day. “My physicians made it very clear that that part of my life was over,” she said.

Some post-polio patients originally had mild symptoms. Others needed leg braces, calipers, or an iron lung. For the latter group, the reemergence of symptoms can feel like a deal gone sour. Eulberg contracted polio in 1950, when she was four. She recalls being promised that if she just worked hard enough, she would be able to walk without a leg brace. In junior high that promise was fulfilled. But decades later, her muscles started to weaken and she realized she needed a brace again. It “felt like a failure,” she told a Medscape reporter in 2020.

There are also unexpected risks. In rare instances, anesthesia can prove fatal for those with PPS, who may need as little as half the dose of typical adults because of an increased sensitivity to sedatives and other drugs. They may have difficulty breathing or swallowing, or be slow to rouse after treatment, possibly having the same vulnerabilities as other patients with neuromuscular disorders. John MacFarlane, a campaigner and former president of the European Polio Union, had given a talk about PPS to the British Medical Association. While leaving the conference building, his wheelchair tipped into a pothole and toppled over. He later needed an operation to pin and plate his arm. He told Undark that it took him 14 hours to wake up after surgery.

For many years, Ferguson, the former B&B worker, didn’t even realize that she’d been infected with the poliovirus. When she came down with a fever at the age of two, just a year before vaccines became available, she recalls, her parents assumed it was a “summer flu.” Ferguson developed a drop foot at age 11, and a doctor suggested polio as the possible cause. But Ferguson’s mother was dubious, and the disease was not mentioned again. Feelings of self-blame may have contributed to the situation, said Ferguson. At the time, many parents believed that if they simply kept a clean house, their children would not fall ill.

Ferguson grew up a clumsy kid who stumbled a lot. As an adult, she fell while ice skating and had to undergo a minor surgery. She woke up three days later in intensive care. The anesthesiologist, she recalls, probed for details that might explain why it had taken so long for her to wake. When she mentioned her summer flu, he warned, “Don’t ever leave that out of your medical history again.” The physician suspected that the flu had actually been polio and that Ferguson was experiencing the condition’s lingering effects. But he did not provide an official diagnosis of PPS.

For that, patients must undergo a battery of blood tests, scans, and X-rays to rule out other health conditions. Ferguson recalls starting along this path and encountering several doctors who thought she had multiple sclerosis; another was sure she had a brain tumor (“That’s the kind of thing that really messes with your head,” she said). When those conditions were eventually ruled out, a neurologist at the University of Pennsylvania conducted a diagnostic test called an EMG, which evaluates the function of motor neurons. Ferguson recalls lying in bed with needles in her leg, her husband holding her hand to ease her pain as the test recorded electrical activity in her muscles. She told Undark that partway through, the physician called his students to the room to show them what a case of “old polio” looked like.

For Ferguson, it was a moving moment. Her journey to diagnosis had come to an end. “We finally had it,” she said. “Everything else had been ruled out.”

For help managing her symptoms, which included deepening fatigue and a weak leg, Ferguson went to a polio clinic in Englewood, New Jersey. Like other clinics, this one provided access to an array of specialists, including rehabilitative physicians, occupational therapists, physical therapists, nutritionists, and orthotists — specialists who make braces and splints. Ferguson had been walking 10,000 steps a day, trying to keep healthy. At the clinic, she learned that she was over-using frayed muscles. This kind of insight, and the clinic’s care more broadly, are what ultimately “saved me,” Ferguson said.

Despite their benefits, polio clinics have been shutting down, said Carol Vandenakker-Albanese, a professor of health sciences who runs a clinic at UC Davis. Many physicians who once specialized in treating the disease have retired, she said, estimating that only about two dozen polio specialists currently practice in the U.S. With most survivors now in their 60s and 70s, few young clinicians want to take up the mantle.

Four specialists told Undark that there is a concerning lack of knowledge among their medical colleagues about PPS. Despite a steady trickle of published studies since the 1980s, many doctors are too busy to keep up with the science and simply “don’t believe in PPS,” said Richard Bruno, who trained in psychophysiology and led the Englewood clinic where Ferguson was treated. In Sweden, a patient told Sunnerhagen that when she asked her family physician if ankle pain could stem from childhood polio, the doctor replied, “Polio is a vaccine.”

Ferguson now volunteers with a Pennsylvania-based support group that she helped establish, which offers a list of recommended specialists and publishes newsletters and personal stories. Support groups exist in other states too, providing patients with an opportunity to swap details about symptoms and possible treatments and share tips for educating their doctors and advocating for themselves. In Germany, a doctor with PPS has argued that patients could benefit from medical cannabis, and he has developed a protocol to help patients with their symptoms. But, he said, insurers and other physicians are reluctant to accept the therapy.

Brad Fuller, the survivor whose first memory is of being in a mineral pool, would like to see the U.S. government offer more support to PPS patients. Some of them need braces or wheelchairs in order to continue living productive lives, but such mobility aids, he said, are “outrageously expensive.”

“Basically,” said Eulberg, who councils patients at the clinic she founded in Wheat Ridge, Colorado, “we’re telling polio survivors, ‘Yes, it would be wonderful if every health care provider you encountered knew a lot about polio, but that ain’t going to happen. You’re going to have to be your own advocate.’”

In 2001, Antonio Toniolo, a microbiologist and physician, experienced a serious car accident. To recover from his injuries, he spent two years visiting a rehabilitation clinic, where he encountered middle-aged polio survivors who were seeking help for their muscle weakness. At the time, Toniolo was working at the University of Insubria Medical School in Italy. The survivors, he recalls, started referring to him as “Doctor” and asking, “What do you know about polio?”

Then, as now, the cause of PPS was not well understood. Researchers know that the initial infection kills some of the body’s motor neurons, the cells that facilitate communication between muscles and the brain. Over time, some of these neurons regrow dramatically, reaching 7 or 8 times normal size, but they are unable to maintain themselves and eventually start to die off. But why this die-off happens, and why some patients are more affected than others, remain a mystery.

Throughout the 1980s and 90s, researchers focused on defining PPS and on trying to understand its underlying causes. After studying that literature, Toniolo began to wonder if the poliovirus might still be present in the blood of survivors — something earlier research had suggested — and causing their new symptoms. In 2013, he gathered blood and spinal fluid from 100 post-polio patients and compared the samples with those from a control group of about 50 survivors who weren’t experiencing PPS. He found traces of poliovirus in samples of about two-thirds of the PPS patients, compared with very few of the control group’s samples. The still-circulating virus, he posited, could cause inflammation or even cell death in those patients. This would mean the condition might respond to antiviral drugs.

Toniolo shared this preliminary data at a couple of PPS-related events and in a mid-study report published in 2015. But the research was never finalized or published in a scientific journal. “This was expensive research that needed funds and competent people,” he wrote to Undark in an email. “Thus, due to lack of funds and my retirement at the end of 2018, the work has not been completed.”

As of yet, nobody has tested whether PPS might respond to antivirals. A major multi-center study led by Dalakas is focusing on whether certain proteins in the blood of healthy donors could help neutralize proteins called cytokines that scientists have detected in the blood and spinal fluids of some PPS patients. Researchers hope that the therapy, called IVIG, will calm the cytokines and stabilize the immune system, thereby improving patients’ quality of life.

The treatment has been trialed in Sweden without conclusive results and was available for a while in some countries, Nollet from the Amsterdam University Medical Centers said, but because it was considered not sufficiently proven, insurers were reluctant to cover it. Whatever the outcome of this study — which is sponsored by a Spanish company, Grifols — it will be helpful for patients to know whether it works or not, said Nollet, whose clinic is among those taking part.

The Swedish government is rearranging care of rare diseases so that polio survivors will be treated at expert centers, a decision driven by recent events: Last summer, health officials reported that the poliovirus had paralyzed an unvaccinated man living in an under-vaccinated community in New York. It was the first U.S. case in years. As of early October, the virus still appeared to be spreading in several under-vaccinated parts of the state. In 2022, for the first time in decades, poliovirus was also detected in Israel, Malawi, Mozambique, and the U.K., alarming public health officials and spurring calls for vaccination campaigns.

Observing the cases in New York helped the Swedish government understand that a polio outbreak “is something that can actually happen again, even here,” said Sunnerhagen, whose own PPS research is part of an application for special status at her university hospital. Her clinic serves about a thousand post-polio patients, a largely Swedish cohort alongside a younger group of individuals who immigrated to Sweden from countries where the disease was never eradicated. “We need to spread the knowledge,” she said, to draw attention to the fact that polio patients are still present in society. Sunnerhagen doesn’t expect all physicians to be experts in the condition but she hopes that they will at least know to make the referral.

For now, patients are still driving much of their medical care.

Ferguson said she understands why a physician might be stumped by a multi-symptom disease triggered by a long-ago infection. “But to totally deny that this exists is heartbreaking,” she said. “I’m a living example that a very mild or unapparent case of a virus can leave lifelong damage.”

This article was originally published on Undark. Read the original article.

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Gas stoves have been used to cook food in American homes since the 1800s, so they are nothing new. An estimated 40 million homes still use them over a century past their introduction. However, scrutiny over the popular appliances for their environmental and health impacts has been steadily building over decades.

A new study published in the International Journal of Environmental Research and Public Health in December 2022 finds that 12.7 percent of cases of childhood asthma in the United States could be due to gas stoves in the home. The researchers from the US and Australia estimate 650,000 people under 18 could be affected. Gas stoves can produce and emit dangerous levels of carbon monoxide, methane, benzene, and nitrogen dioxide, especially if they are used in poorly ventilated spaces and aren’t properly maintained. According to a study published in January 2022, they can leak methane (a planet-warming gas) even when they are turned off.

[Related: Your gas stove could be hurting everyone around you.]

Brady Seals, manager of the carbon free buildings program at RMI and a co-author of the study, told The Guardian that the prevalence of asthma due to gas stoves is similar to the amount of asthma caused by secondhand smoke. She called these findings “eye popping,” adding, “We knew this was a problem but we didn’t know how bad. This study shows that if we got rid of gas stoves we would prevent 12.7 percent of childhood asthma cases, which I think most people would want to do.”

The study used 2019 US Census data to determine the proportion of children exposed to pollution from gas stoves, borrowing this method from a 2018 analysis that found that gas cooking ranges in Australia could be attributable for 12.3 percent of childhood asthma cases. The team also used data from an analysis in 2013 that found children in homes with gas stoves were 42 percent more likely to have asthmatic symptoms.

“It’s like having car exhaust in a home,” Seals told The Washington Post. “And we know that children are some of the people spending the most time at home, along with the elderly.”

With this analysis, the authors do mention that their findings are based on multiple assumptions, so there is a possibility that the dangers might be either understated or overstated and that principal axis factoring (PAF) analysis does have limitations.

[Related: Gas stoves are bad for the environment—but what if the power goes out?]

The gas industry has also pushed back against this study, with the American Gas Association saying it used a “headline-grabbing approach” that lacked scientific rigor and that “the claims made in this paper are clearly driven by simple advocacy-based modeling and hypotheticals over the deep and sophisticated analysis we should see in sound science.”

Industry lobbyists and Republican led legislatures have also pushed back hard against plans to phase out the use of gas stoves. Some states and cities like New York have banned the use of gas hookups in new buildings, while others have prevented these changes.

In December 2022, US Consumer Product Safety Commission head Richard Trumka announced that the agency will put out a formal request for information on hazards associated with gas stoves and possible solutions by March.

“We need to be talking about regulating gas stoves, whether that’s drastically improving emissions or banning gas stoves entirely,” Trumka said. “And I think we ought to keep that possibility of a ban in mind, because it’s a powerful tool in our tool belt and it’s a real possibility here.”

The move aligns with efforts to help lower income households and those who rent replace gas stoves. The Inflation Reduction Act of 2022 does include a rebate of up to $840 for the purchase of new electric induction cooking appliances.

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This story was originally featured on KHN.

Larry McMahon, who turned 80 in December, is weighing whether to undergo a major surgery. Over the past five years, his back pain has intensified. Physical therapy, muscle relaxants, and injections aren’t offering relief.

“It’s a pain that leaves me hardly able to do anything,” he said.

Should McMahon, a retired Virginia state trooper who now lives in Southport, North Carolina, try spinal fusion surgery, a procedure that can take up to six hours? (Eight years ago, he had a lumbar laminectomy, another arduous back surgery.)

“Will I recover in six months — or in a couple of years? Is it safe for a man of my age with various health issues to be put to sleep for a long period of time?” McMahon asked, relaying some of his concerns to me in a phone conversation.

Older adults contemplating major surgery often aren’t sure whether to proceed. In many cases, surgery can be lifesaving or improve a senior’s quality of life. But advanced age puts people at greater risk of unwanted outcomes, including difficulty with daily activities, extended hospitalizations, problems moving around, and the loss of independence.

I wrote in November about a new study that shed light on some risks seniors face when having invasive procedures. But readers wanted to know more. How does one determine if potential benefits from major surgery are worth the risks? And what questions should older adults ask as they try to figure this out? I asked several experts for their recommendations. Here’s some of what they suggested.

What’s the goal of this surgery? Ask your surgeon, “How is this surgery going to make things better for me?” said Margaret “Gretchen” Schwarze, an associate professor of surgery at the University of Wisconsin School of Medicine and Public Health. Will it extend your life by removing a fast-growing tumor? Will your quality of life improve by making it easier to walk? Will it prevent you from becoming disabled, akin to a hip replacement?

If your surgeon says, “We need to remove this growth or clear this blockage,” ask what impact that will have on your daily life. Just because an abnormality such as a hernia has been found doesn’t mean it has to be addressed, especially if you don’t have bothersome symptoms and the procedure comes with complications, said Drs. Robert Becher and Thomas Gill of Yale University, authors of that recent paper on major surgery in older adults.

If things go well, what can I expect? Schwarze, a vascular surgeon, often cares for patients with abdominal aortic aneurysms, an enlargement in a major blood vessel that can be life-threatening if it bursts.

Here’s how she describes a “best case” surgical scenario for that condition: “Surgery will be about four to five hours. When it’s over, you’ll be in the ICU with a breathing tube overnight for a day or two. Then, you’ll be in the hospital for another week or so. Afterwards, you’ll probably have to go to rehab to get your strength back, but I think you can get back home in three to four weeks, and it’ll probably take you two to three months to feel like you did before surgery.”

Among other things people might ask their surgeon, according to a patient brochure Schwarze’s team has created: What will my daily life look like right after surgery? Three months later? One year later? Will I need help, and for how long? Will tubes or drains be inserted?

If things don’t go well, what can I expect? A “worst case” scenario might look like this, according to Schwarze: “You have surgery, and you go to the ICU, and you have serious complications. You have a heart attack. Three weeks after surgery, you’re still in the ICU with a breathing tube, and you’ve lost most of your strength, and there’s no chance of ever getting home again. Or, the surgery didn’t work, and still you’ve gone through all this.”

“People often think I’ll just die on the operating table if things go wrong,” said Dr. Emily Finlayson, director of the UCSF Center for Surgery in Older Adults in San Francisco. “But we’re very good at rescuing people, and we can keep you alive for a long time. The reality is, there can be a lot of pain and suffering and interventions like feeding tubes and ventilators if things don’t go the way we hope.”

Given my health, age, and functional status, what’s the most likely outcome? Once your surgeon has walked you through various scenarios, ask, “Do I really need to have this surgery, in your opinion?” and “What outcomes do you think are most likely for me?” Finlayson advised. Research suggests that older adults who are frail, have cognitive impairment, or other serious conditions such as heart disease have worse experiences with major surgery. Also, seniors in their 80s and 90s are at higher risk of things going wrong.

“It’s important to have family or friends in the room for these conversations with high-risk patients,” Finlayson said. Many seniors have some level of cognitive difficulties and may need assistance working through complex decisions.

What are the alternatives? Make sure your physician tells you what the nonsurgical options are, Finlayson said. Older men with prostate cancer, for instance, might want to consider “watchful waiting,” ongoing monitoring of their symptoms, rather than risk invasive surgery. Women in their 80s who develop a small breast cancer may opt to leave it alone if removing it poses a risk, given other health factors.

Because of Larry McMahon’s age and underlying medical issues (a 2021 knee replacement that hasn’t healed, arthritis, high blood pressure), his neurosurgeon suggested he explore other interventions, including more injections and physical therapy, before surgery. “He told me, ‘I make my money from surgery, but that’s a last resort,” McMahon said.

What can I do to prepare myself? “Preparing for surgery is really vital for older adults: If patients do a few things that doctors recommend — stop smoking, lose weight, walk more, eat better — they can decrease the likelihood of complications and the number of days spent in the hospital,” said Dr. Sandhya Lagoo-Deenadayalan, a leader in Duke University Medical Center’s Perioperative Optimization of Senior Health program.

When older patients are recommended to POSH, they receive a comprehensive evaluation of their medications, nutritional status, mobility, preexisting conditions, ability to perform daily activities, and support at home. They leave with a “to-do” list of recommended actions, usually starting several weeks before surgery.

If your hospital doesn’t have a program of this kind, ask your physician, “How can I get my body and mind ready” before having surgery, Finlayson said. Also ask: “How can I prepare my home in advance to anticipate what I’ll need during recovery?”

What will recovery look like? There are three levels to consider: What will recovery in the hospital entail? Will you be transferred to a facility for rehabilitation? And what will recovery be like at home?

Ask how long you’re likely to stay in the hospital. Will you have pain, or aftereffects from the anesthesia? Preserving cognition is a concern, and you might want to ask your anesthesiologist what you can do to maintain cognitive functioning following surgery. If you go to a rehab center, you’ll want to know what kind of therapy you’ll need and whether you can expect to return to your baseline level of functioning.

During the covid-19 pandemic, “a lot of older adults have opted to go home instead of to rehab, and it’s really important to make sure they have appropriate support,” said Dr. Rachelle Bernacki, director of care transformation and postoperative services at the Center for Geriatric Surgery at Brigham and Women’s Hospital in Boston.

For some older adults, a loss of independence after surgery may be permanent. Be sure to inquire what your options are should that occur.

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

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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.

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As multiple respiratory viruses circulate in the United States, a subvariant of Omicron named XBB.1.5 appears to be poised to dominate other strains of the virus. Estimates from the Centers for Disease Control and Prevention (CDC), find that XBB.1.5 has risen from about 4 percent to 41 percent of new COVID-19 infections over the month of December. The CDC estimates that it’s causing 75 percent of new cases in the northeastern US.

[Related: Omicron boosters are the future of COVID vaccines in the US.]

“For a few months now, we haven’t seen a variant that’s taken off at that speed,” Pavitra Roychoudhury, director of COVIC-19 sequencing at the University of Washington School of Medicine’s virology lab, told CNN.

It is not yet clear where this version of Omicron came from, but it may have arisen in the United States. In late October 2022, it was first detected in Connecticut and New York, according to GISAID, an international effort to catalog and track COVID-19 variants.

XBB.1.5 was created by recombination that occurred when two descendants of Omicron’s BA.2 subvariant swapped pieces of their genetic code. The result was 14 new mutations to the virus’ spike proteins compared with BA.2 and a new sublineage named XBB.

XBB drove a wave of COVID-19 cases in Singapore during the fall of 2022. In the US, XBB faced competition from co-circulating variants that have each evolved some of the same mutations. According to the World Health Organization (WHO), XBB has been found in at least 70 countries.

[Related: Omicron variants keep getting better at dodging our immune systems.]

One of XBB.1.5’s main differences from the earlier XBB variant is that it can attach itself to cells more efficiently. “The virus needs to bind tightly to cells to be more efficient at getting in and that could help the virus be a little bit more efficient at infecting people,” Andrew Pekosz, a virologist at Johns Hopkins University, told CNBC.

Another concern surrounding this new strain is waning immunity. Vaccination or previous COVID-19 infection appear to only prevent reinfection for a few months in some cases, and the virus’ evolution adds an additional immunity challenge. There has also been limited uptake of the bivalent booster, that is targeted to fight both the original strain of COVID-19 and Omicron. Only 17 percent of adults have received this updated booster, despite evidence showing that it increases protection against severe illness and death.

While it is not completely clear if XBB.1.5 causes a more severe form of the illness or will increase hospitalizations, data shows that hospitalizations in the US are about to surpass the number seen during a spike of the virus in summer 2022. Multiple factors from this continued evolution of the virus and holiday gatherings appear to be driving transmission and the increase is a sign that an anticipated winter COVID-19 wave has begun.

The best ways to prevent infection include wearing a high-quality mask, especially in crowded indoor settings, regularly testing for COVID-19, and staying up to date on vaccinations.

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Following an abrupt end to the Chinese government’s strict lockdowns and “zero COVID” policy in December 2022, its citizens will be allowed to travel abroad for the first time since the pandemic began in 2020. In response, over a dozen countries have announced testing requirements and other restrictions on travelers from China.

The United States, Canada, Spain, France, Japan and the United Kingdom have cited concerns about a surge of COVID-19 infections in China, the potential risk of new variants emerging from its outbreak, in addition to a perceived reluctance by the Chinese government to share data with other countries among their reasons for implementing the testing policy.

[Related: What’s next for China’s zero COVID policy.]

Chinese government officials are pushing back against these restrictions. “Some countries have no scientific basis for restricting entries from China, and some excessive practices are even more unacceptable,” said Mao Ning, a foreign ministry spokeswoman, speaking at a news conference in Beijing on January 3. “We firmly oppose the practice of manipulating COVID prevention and control measures to achieve political goals, and will take corresponding measures in accordance with the principle of reciprocity according to different situations,” she added.

On December 28, the Centers for Disease Control and Prevention (CDC) announced that travelers from China, Hong Kong, and Macau will be required to present a negative COVID-19 test before entering the United States beginning on January 5, 2023. The CDC says the requirement for testing applies to air passengers regardless of their vaccination status and nationality, and will apply to travelers from China entering through a third country or those who connect through the US to other countries.

“Variants of the SARS-CoV-2 virus continue to emerge in countries around the world. However, reduced testing and case reporting in the PRC and minimal sharing of viral genomic sequence data could delay the identification of new variants of concern if they arise,” wrote the CDC in a statement. “Pre-departure testing and the requirement to show a negative test result has been shown to decrease the number of infected passengers boarding airplanes, and it will help to slow the spread of the virus as we work to identify and understand any potential new variants that may emerge.”

Similar restrictions have already been imposed in Italy and Japan, while India has mandated negative COVID-19 test reports and random screening for passengers arriving by air from China, Japan, South Korea, Hong Kong, and Thailand.

[Related: China approves world’s first nasal COVID-19 vaccine booster.]

The World Health Organization (WHO) has also urged Chinese officials to be more transparent on the country’s current surge of COVID-19 infections. The WHO requested more genetic sequencing data, data on hospitalizations, ICU admissions, and deaths, in addition to data on both the number of vaccinations delivered and vaccination status, especially in vulnerable people and those over 60 years old.

This lack of transparency surrounding COVID-19 data has health experts particularly concerned. “For the most part, we really don’t know what variants are circulating in China,” Andy Pekosz, a virologist at Johns Hopkins University in Baltimore, told CBS News. “That represents sort of a black box in terms of what we might be concerned about in terms of new variants in that country.”

However, Pekosz doesn’t believe that testing alone will be enough to stop a new variant from entering the US. “What you really need is a holistic approach. You need to know the sequences of the viruses that are there,” he said. “You need to know case numbers and hospitalization rates and how they are related to new variants. All of that information helps us to then prepare for a new variant if it were to arrive. Testing alone isn’t going to prevent a new variant from arriving here in the US.”

Parts of China have been fighting outbreaks of COVID-19 since the policy shift in December, but the severity of the outbreaks have been a guessing game.

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Drinking more water and staying hydrated is a good way to achieve that New Year’s resolution of living a more healthy lifestyle. According to the Cleveland Clinic, water is essential for multiple functions in your body, including digestion, creating hormones and neurotransmitters, and delivering oxygen, and up to 60 percent of the adult human body is made of water. 

It can also help with healthy aging, according to a study published Monday in the journal eBioMedicine. The research from the National Institutes of Health (NIH) found that well-hydrated adults appear to develop fewer chronic health conditions (heart diseases, lung disease, etc.), have a decreased risk of dying early, and are generally more healthy. 

[Related: The truth about hydration hacks like IV therapies, alkaline water, and more.]

The study looked at health data gathered from 11,255 adults over 30 years and looked at links between serum sodium levels and other indicators of health. Typically, serum sodium levels increase when fluid intake decreases.

The researchers assessed information shared during five medical visits for each participant—the first two when patients were in their 50s and the last when they were between 70 and 90 years-old. Adults who had high levels of serum sodium at their baseline check-in or those who had underlying conditions that can affect serum sodium levels, such as obesity, were excluded to allow for a better comparison of how hydration is correlated with health outcomes.

Then, the team evaluated how serum sodium levels correlated with biological aging, using 15 health markers, including systolic blood pressure, blood sugar, and cholesterol.  The study also adjusted for demographic and health factors, including age, race, biological sex, smoking status, and hypertension. 

The results found that adults on the higher end of normal level of serum sodium had a 10 to 15 percent greater chance of being biologically older than their chronological age, when compared with participants in the mid-normal range. Additionally, participants at greater risk of aging more quickly also had a 64 percent higher risk for developing chronic diseases such as stroke, heart failure, atrial fibrillation, chronic lung disease, peripheral artery disease, dementia, and diabetes.

The study did not have information on how much water participants drank and does not prove a causal effect, according to the researchers.

“The results suggest that proper hydration may slow down aging and prolong a disease-free life,” said Natalia Dmitrieva, a study author and researcher at the NIH’s Laboratory of Cardiovascular Regenerative Medicine at the National Heart, Lung, and Blood Institute (NHLBI), in a statement.

This new study expands on research this team of scientists published in March 2022, which linked higher ranges of normal serum sodium with an increased risk of heart failure. Both studies also used data from the Atherosclerosis Risk in Communities (ARIC) study. 

“This study adds observational evidence that reinforces the potential long-term benefits of improved hydration on reductions in long-term health outcomes, including mortality,” Howard Sesso, an associate professor of medicine at Harvard Medical School and associate epidemiologist at Brigham and Women’s Hospital in Boston who was not involved in the study, told CNN. He added, “it would have been nice to combine their definition of hydration, based on serum sodium levels only, with actual fluid intake data from the ARIC cohort.”

[Related: This device will allow the marines to make drinking water from thin air.]

The National Academies of Medicine suggests that most women consume around 6 to 9 cups of fluids per day and men drink 8 to 12 cups.  Some ways to add more fluids beyond drinking water include drinking juice or eating fruits and vegetables with higher water content, according to the researchers.
“On the global level, this can have a big impact,” said Dmitrieva. “Decreased body water content is the most common factor that increases serum sodium, which is why the results suggest that staying well hydrated may slow down the aging process and prevent or delay chronic disease.” 

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COVID-19 caused headlines again this year, but it was matched by a slew of other newsworthy viruses: the adenoviruses suspected to be behind the rise in hepatitis cases in early spring, the outbreak of mpox—formerly known as monkeypox—in the summer, an early surge in respiratory syncytial virus (RSV), and a peak in influenza cases following the Thanksgiving holiday season. Each of these viruses has tested clinicians, epidemiologists, and virologists. But these experts have responded by employing some of the tools that were built during the COVID pandemic.

The beginning of 2022 brought the first trial run for our toolkit: huge numbers of COVID cases, caused by the emergence of the highly transmissible Omicron variant. Virologists had to re-enact the early days of the pandemic: identifying the strain, testing its disease severity, and understanding its ability to escape the immune system. The available COVID vaccines were pitted against Omicron, and thankfully, showed good efficacy. By now, these studies were familiar, and early results were shared quickly to inform how public health officials around the world acted to protect populations.

After the initial surge of cases, in spring of 2022, many jurisdictions began to reduce COVID testing and tracing. The Centers for Disease Control and Prevention (CDC) changed its guidance on face coverings, so fewer people wore masks out and about. Still, researchers continued to track Omicron and its subvariants, and those who’d worked at speed to understand the latest strain would get little respite—2022 had more pathogens to throw at them yet.

Genome sequencing predicts viral spread

Monitoring mutations is a virus-fighting tool that had been employed early in the pandemic, because it’d been proven to help many times before. Since 2008, researchers sequencing all types of viruses have been able to upload whole genomes to GISAID, a science surveillance initiative. Their work had allowed for quick research at the start of the H1N1 flu pandemic in 2009 and during the 2013 bird flu epidemic. 

“When the unknown coronavirus emerged in January 2020, GISAID had already played a key role in influenza surveillance for 12 years,” says Sebastian Maurer-Stroh, executive director of the Bioinformatics Institute in Singapore and a collaborator with GISAID. The collaborative’s array of tools, though designed for tracking flu viruses, had been built in connection with the research community and large organizations like the World Health Organization (WHO). These tools were relatively easy to adapt to track the spread of COVID, Maurer-Stroh says. 

[Related: The World Health Organization officially renamed monkeypox to mpox]

GISAID’s database of SARS-CoV-2 genomes has helped research into the pathogen’s spike protein, the area on the virus that affects how it enters our cells and causes infection. It’s also meant that countries can monitor the rise and fall of different strains in their populations and make changes to guidelines accordingly. Though submissions of new SARS-CoV-2 genomes started to trail off in early 2022, GISAID and the WHO are still tracking Omicron and the emergence of subvariants. 

But in May 2022, GISAID researchers noticed a new genome being uploaded. The hMpxV virus and the disease it caused, mpox, was already endemic in countries in Africa, but rarely caused infections outside the continent. GISAID surveillance showed that there were new lineages spreading rapidly, and by July the virus was present in 75 countries. That month, the WHO declared the outbreak to be a public health emergency. Cases have been steadily dropping since then, though the WHO reports that seven countries are still seeing new cases. As of December 15, there have been more than 80,000 mpox cases worldwide.

Wastewater provide breadcrumbs for disease outbreaks

At the same time as GISAID was monitoring DNA sequences of the mpox virus, researchers were employing another surveillance tool used during the pandemic. Wastewater taken from July to October in  New York showed that poliovirus was circulating in six of 13 sampled counties.

Wastewater sampling had detected COVID in sewers back in April 2020; in September of that year, the CDC launched the National Wastewater Surveillance System (NWSS) to monitor virus levels. Compared to mass-scale PCR testing, testing wastewater offered an easy and unobtrusive way to find out where there were hotspots of virus activity. 

“You can track a lot of viruses in the wastewater, and what we’re seeing with COVID is that it may be an easier way of doing epidemiology, at least on a bigger picture scale,” says virologist Michael Teng, of the University of South Florida Department of Molecular Medicine. Wastewater surveillance can’t pinpoint individuals, so it won’t help identify potential “superspreaders” before they infect others. But it’s a great tool for virologists to see general geographical trends in virus levels.

[Related: Polio is officially circulating in the US again]

The poliovirus spread in the state was “silent,” but posed a real threat. Cases of polio had been basically non-existent in the US since the introduction of the polio vaccine, which has an average uptake of 92 percent in kids across the country—though some counties’ rates of vaccination are as low as 37 percent.

Vaccines fight viruses in and across individuals

As evidenced by the pandemic, vaccine uptake is one of the–if not the–best tools for stopping the spread of a virus. COVID vaccines protect against infection, and if you do get the disease, you’re less likely to have severe illness if you’ve been vaccinated.

So when researchers predicted a tripledemic of COVID, the flu, and RSV heading towards the US, the message was clear: Get your flu shot and COVID booster. But with no RSV vaccine available, case numbers quickly rose in young children and elderly population.

“We had a COVID vaccine within about 11 months of when the first virus sequence came out well, but RSV was first identified in 1957, and since then we have not really had good vaccines,” says Teng, whose focus is on the respiratory pathogen. “But one of the really exciting stories for this year is that Pfizer [who developed one of the COVID vaccines] along with GSK have had really good results in tests for an RSV vaccine for the elderly.”

[Related: Fighting RSV in babies starts with a mother’s antibodies]

Teng says the purchase of COVID vaccines led to an infusion of capital in companies like Pfizer and Moderna, the latter of which has been able to invest into research it began long before the pandemic. This money meant Moderna could move forward with several vaccines in development, according to Teng, including one for HIV.

These important elements of tackling viruses in 2022—genomic monitoring, wastewater surveillance, and vaccine development—are just part of the huge fight against infectious diseases. There is, of course, still a lot we don’t know about COVID and other viruses, and we cannot predict what 2023 will bring. But researchers are armed with more information about the spread of viruses than ever before, and they’ve already begun putting the pandemic’s teachings into practice.

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This article was originally featured on Undark.

In November 2016, virologist David Evans traveled to Geneva for a meeting of a World Health Organization committee on smallpox research. The deadly virus had been declared eradicated 36 years earlier; the only known live samples of smallpox were in the custody of the United States and Russian governments.

Evans, though, had a striking announcement: Months before the meeting, he and a colleague had created a close relative of smallpox virus, effectively from scratch, at their laboratory in Canada. In a subsequent report, the WHO wrote that the team’s method “did not require exceptional biochemical knowledge or skills, significant funds, or significant time.”

Evans disagrees with that characterization: The process “takes a tremendous amount of technical skill,” he told Undark. But certain technologies did make the experiment easier. In particular, Evans and his colleague were able to simply order long stretches of the virus’s DNA in the mail, from GeneArt, a subsidiary of Thermo Fisher Scientific.

If DNA is the code of life, then outfits like GeneArt are printshops — they synthesize custom strands of DNA and ship them to scientists, who can use the DNA to make a yeast cell glow in the dark, or to create a plastic-eating bacterium, or to build a virus from scratch. Today there are dozens, perhaps hundreds, of companies selling genes, offering DNA at increasingly low prices. (If DNA resembles a long piece of text, rates today are often lower than 10 cents per letter; at this rate, the genetic material necessary to begin constructing an influenza virus would cost less than $1,500.) And new benchtop technologies — essentially, portable gene printers — promise to make synthetic DNA even more widely available.

But, since at least the 2000s, the field has been shadowed by fears that someone will use these services to cause harm — in particular, to manufacture a deadly virus and use it to commit an act of bioterrorism.

Meanwhile, the United States imposes few security regulations on synthetic DNA providers. It’s perfectly legal to make a batch of genes from Ebola or smallpox and ship it to a U.S. address, no questions asked — although actually creating the virus from that genetic material may be illegal under laws governing the possession of certain pathogens.

Whether that’s a legitimate cause for alarm is under debate. Some experts say that creating a virus from synthetic DNA remains prohibitively difficult for most scientists, and that fears of an attack are often overblown. At the same time, new nonprofit initiatives, fueled by money from Silicon Valley philanthropists, and at times evoking worst-case scenarios, are pushing for more stringent protections against the misuse of synthetic DNA. Implementing effective security, though, is tough — as is enforcing any kind of norm in a sprawling, multinational industry.

“It’s not that I’m worried about something happening tomorrow. But the reality is, this capability is increasingly powerful in terms of how long the DNA fragments can be, what you can create with them, the ability of recipients to then assemble the DNA fragments into a new virus,” said Gregory Koblentz, a biodefense researcher at George Mason University. “This is the kind of thing that we really should be more proactive on — and try to get ahead of the curve.”

Perhaps the most prominent scientist sounding warnings about the danger of unchecked DNA synthesis is Kevin Esvelt, a biotechnologist at MIT. In conversation, Esvelt moves quickly between technical detail and Cassandra-like alarm. He often talks about Seiichi Endo, a Japanese virologist who, in 1987, joined the apocalyptic Aum Shinrikyo sect. Endo helped carry out a poison gas attack on the Tokyo subway, and the group tried — but seemingly failed — to obtain Ebola virus.

Since then, creating pathogens has gotten easier, thanks in part to the wider availability of synthetic DNA. “It’s really hard for me to imagine a graduate-trained virologist from Kyoto University being unable to assemble an influenza virus today,” Esvelt said.

As Esvelt describes it, the problem of synthetic biology is about power: New technologies have handed a group of scientists the keys to build unfathomably dangerous bugs. Very few — perhaps none — of those scientists has any wish to exercise this grim superpower. But, Esvelt argues, it’s only a matter of time before the next Endo comes along.

By Esvelt’s back-of-the-napkin estimate, perhaps 30,000 scientists worldwide have the skills to build a strain of pandemic influenza, provided they can find someone to synthesize the DNA for them. The consequences of unleashing such a pathogen could be catastrophic.

“No individual can make a nuke,” Esvelt said. “But a virus? That’s very doable, unfortunately.”

Not everyone buys those figures. “There are 1000s of virologists, but far fewer with these skills,” virologist Angela Rasmussen wrote on Twitter in November, in a thread suggesting that Esvelt’s work overstates the risks of a bioterror attack. “Infectious clones aren’t something you can whip up in a garage,” she continued — even with a full set of DNA on hand.

Zach Adelman, a biologist who studies disease vectors at Texas A&M University, echoed those points — and questioned Esvelt’s broader approach. “It sounds like his typical scare tactics,” he wrote in an email to Undark. “Could a single, dedicated, malicious individual still make their own flu strain while avoiding detection? Maybe, but even in ideal circumstances these experiments require a substantial amount of resources.”

Even if someone manages to illicitly make a virus, carrying out a bioterror attack is still difficult, said Milton Leitenberg, a biosecurity expert at the Center for International and Security Studies at the University of Maryland. “All of this is unbelievably exaggerated,” he said, after reviewing testimony Esvelt delivered to a U.S. House of Representatives subcommittee in 2021 about the the risks of deliberately caused pandemics.

Still, while experts may differ about the degree of risk, many agree that some kind of security for synthetic DNA is warranted — and that current systems may need an upgrade. “I do think that it’s worthwhile having a way of screening synthetic DNA that people can order, to make sure that people aren’t able to actually reconstruct things that are select agents, or other dangerous pathogens,” Rasmussen told Undark.

For years, some policymakers and industry leaders have pushed to beef up security for DNA synthesis.

In the 2000s, when the gene synthesis industry was in its early days, policymakers grew concerned about potential misuse of the companies’ services. In 2010, the U.S. government released a set of guidelines, asking synthetic DNA providers to review their orders for red flags.

Those guidelines do not have the force of law. Companies are free to ignore them, and they can ship almost any gene to anyone, at least within the U.S. (Under federal trade regulations, exporting certain genes requires a license.) Still, even before the government released its guidelines, major synthetic DNA providers were already strengthening security. In 2009, five companies formed the International Gene Synthesis Consortium, or IGSC. “The growth of the gene synthesis industry depends on an impeccable safety record,” the then-CEO of GeneArt wrote in a statement marking the consortium’s launch.

Consortium members agree to screen their customers. (They won’t ship, for example, to P.O. boxes.) And they agree to screen orders, too, following standards that Koblentz says are actually stricter than the federal guidelines.

But some companies never joined. According to one commonly cited estimate, non-IGSC members account for approximately 20 percent of the global DNA synthesis market. That’s little more than an educated guess. “We don’t really know, to be honest,” said Jaime Yassif, who leads the biological policy team at the Nuclear Threat Initiative, a think tank in Washington, D.C. And some companies, she and other analysts say, appear not to be screening at all.

Indeed, spend a few minutes on Google searching for synthetic DNA, and it’s easy to find non-IGSC companies advertising their services. It’s difficult to tell what kind of security measures — if any — those companies have in place.

In a brief phone call, Lulu Wang, an account manager for the Delaware-registered company Gene Universal, said the company did screen orders. She did not provide details, instead referring additional questions to an email address; the company declined to answer them. KareBay Biochem, a provider registered in New Jersey, did not reply to emailed questions. A man who answered the company’s phone, upon learning that he was talking to a reporter, said “Sorry, I have no comments,” and hung up.

Azenta Life Sciences, a Nasdaq-traded company, provides “complete gene synthesis solutions,” according to its website, after acquiring the synthetic DNA provider Genewiz in 2018. Nowhere does its website mention biosecurity. In an email, Azenta director of investor relations Sara Silverman wrote that the company “performs a biosecurity screen,” but declined to provide details. She did not answer a question about why Azenta had not joined the IGSC.

The industry as a whole has uneven security. “There’s no standardization process, there’s no certification, there’s no outside body checking to see how well your system does,” said James Diggans, head of biosecurity at Twist Bioscience, who currently chairs the board of the IGSC. As a result, he said, “companies invest along a broad spectrum of how much they want to put effort into this process.”

There are also financial incentives to cut corners. Existing DNA screening systems take a strand of DNA from an order and compare it against a database of so-called “sequences of concern.” If there’s a match, a bioinformatics expert reviews the order — a process that is expensive and time consuming. “It is certainly an unfair competitive advantage,” Diggans said, “if you decide not to invest in security, or if you decide to invest minimally in security.”

One solution, some experts say, is to use free, simple, high-quality screening software. In the coming months, two such initiatives are slated to launch.

One system, called SecureDNA, launched as a limited-access pilot this month, with plans to be widely available by the end of 2023. At its core is a database of billions of very short pieces of genetic information, the exact contents of which are a closely guarded secret. A small group of scientists — Esvelt, who is part of the SecureDNA team, calls them “curators” — will eventually maintain and update the tool, which is based in Switzerland. Orders are encrypted and routed to the SecureDNA servers. There, an automated system looks for matches between the order and the database. From initial tests, the SecureDNA team reports in a recent paper, the model is difficult to fool, and the researchers predict it will rarely produce false alarms. (The team plans to submit the paper to peer review after testing SecureDNA on more real-world orders.)

Whether companies will actually get on board remains unclear. In order to maximize security, the system is a bit of a black box. No company so far has committed to turning over its screening process to SecureDNA, Esvelt said, although some companies have agreed to test it.

In 2020, Yassif, at the Nuclear Threat Initiative, began developing a different screening tool in partnership with the World Economic Forum and an advisory panel of experts. Called the Common Mechanism for DNA Synthesis Screening and slated to launch in 2023 under the auspices of a new international organization, the tool will be distributed to companies, who can then use the software to search orders for potential red flags.

“The basic idea is, if we give a tool to companies to make it cheaper and easier to do the right thing, then it’s going to be very appealing for them to just take it,” said Yassif.

Government officials are also moving to encourage more robust screening. Two years ago, the U.S. Department of Health and Human Services began the process of updating its 2010 guidelines, which experts say have become dated. The new guidelines are slated to come out in 2023. Among other changes, they are likely to ask companies to start screening orders for shorter pieces of DNA, rather than just focusing on orders for longer stretches of genetic material. (The goal is to prevent people from buying many short pieces of DNA and then stringing them together into something high-risk.)

In August 2022, California Gov. Gavin Newsom signed into effect a bill requiring the California State University system to only buy synthetic DNA from companies that screen their orders, and requesting that the University of California system do the same.

“This is the first legal requirement in the U.S. for a user of synthetic DNA to pay attention to the security safeguards that are in place for what they’re ordering,” said Koblentz, the George Mason University expert, who consulted on the bill.

Ultimately, Koblentz said, the federal government should do more to incentivize good screening. For example, major federal science funders could give grants on the condition that institutions buy their DNA from more secure providers, using their market power, he said, “to require researchers to use biosecurity safeguards.”

So far, there appear to be no plans to apply those kinds of incentives. “Adherence to the revised guidance, like adherence to the 2010 guidance, is voluntary,” wrote Matthew Sharkey, a federal scientist working the new guidelines, in an email. And, he added, “no federal agency currently requires compliance with them as a condition for research funding.”

Amid other pressing global concerns, biosecurity experts have sometimes struggled to draw attention to the issue. A 2020 essay Koblentz wrote for The Bulletin of the Atomic Scientists is titled “A biotech firm made a smallpox-like virus on purpose. Nobody seems to care.”

Recently, much of the urgency around synthetic DNA security has come from the effective altruism community: A loose-knit movement, centered in Silicon Valley, that aims to take a rational approach to doing the most good possible. Supporters often throw their energy behind pressing public health issues like malaria treatment, as well as more rarefied concerns, such as rogue artificial intelligence or governance in outer space.

The movement has grown in prominence in the past decade, becoming a major funder of initiatives to prevent human-caused pandemics. Two effective altruism groups, Effective Giving and Open Philanthropy, are underwriting Yassif’s project. Yassif used to work at Open Philanthropy, which is also backing SecureDNA. (In August, Esvelt told Undark that the group was in talks to receive funding from the FTX Future Fund, an effective altruism venture linked to the cryptocurrency exchange FTX. They did not finalize an arrangement, according to Esvelt, and FTX collapsed spectacularly in November amid allegations of misusing customer funds.)

Despite these concerns about bioterrorism, the risks remain largely theoretical. Leitenberg, the Maryland biosecurity scholar, began working on biological weapons issues in the 1960s. In a 2005 paper, he argued that people in the field often overstate the risks posed by bioterrorists.

As Leitenberg argues, the U.S. has spent billions of dollars in the past two decades preparing for a bioterrorism attack — but the threat, at least so far, has not materialized. “The real bioterrorists,” he said, “still haven’t made a single thing.” Lab accidents, he argues, pose a far greater risk than a rogue actor.

What’s clear is that the challenge of regulating the synthetic DNA industry is only compounding — in particular because it’s getting easier to manufacture DNA. If DNA synthesis companies are printshops, a new generation of startups are now making at-home printers: so-called benchtop machines, some retailing for under $100,000, that make it possible to custom-print DNA in the laboratory.

Both SecureDNA and the Common Mechanism hope to one day allow companies to incorporate security tools directly into benchtop devices, so that they can remotely block the production of certain sequences.

The new benchtop technology, said Yassif, has the potential to dramatically expand the circle of people with access to custom-made DNA. The technology, she cautioned, is still in its infancy. “I don’t think the sky is falling today,” Yassif said. But, she added, “I think it’s a wakeup call that we need to be thinking about this now, and building in security now.”

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Due to increased demand, pharmacy chains CVS and Walgreens have limited purchases of children’s pain relievers and fever reducers. The demand comes amid a “tripledemic” surge of respiratory infections including flu, respiratory syncytial virus (RSV), and COVID-19. Particularly vulnerable to RSV, the virus has hospitalized more than four out of every 1,000 children under the age of five this season, according to the CDC.

In November, the spike in illnesses led to a 65 percent increase in the sale of children’s fever reducers and medications compared to November 2021, according to the Consumer Healthcare Products Association (CHPA). The association represents some of the companies that make the medications including Tylenol manufacturer Johnson & Johnson, Haleon the maker of Advil, and Perrigo, which manufacturers generic store brands.

[Related: Is it flu or RSV? It can be tough to tell.]

In a statement, CHPA said that it doesn’t yet have a timeline for when the supply may catch up with demand and stressed that the manufacturers were working to replenish the medications as quickly as possible.

At Walgreens, customers are limited to online purchases of six over-the-counter fever reducers per purchase, but the company does not currently have an in-store limit.

“Due to increased demand and various supplier challenges, over-the-counter pediatric fever reducing products are seeing constraint across the country,” said Walgreens, said in a statement. Walgreens added that the limits are, “in an effort to help support availability and avoid excess purchases.”

CVS also cited the increased demand for these items for their two-product per person limit on both online and in-store purchases. A spokesperson for CVS told The New York Times, “We can confirm that to ensure equitable access for all our customers, there is currently a two (2) product limit on all children’s pain relief products. We’re committed to meeting our customers’ needs and are working with our suppliers to ensure continued access to these items.”

The American Academy of Pediatrics (AAP) is urging parents “not to panic” if they are unable to find fever-reducing medicine. “These medicines are not curative. They don’t alter the duration of the illness or anything like that. They are essentially purely for comfort,” Sean O’Leary, chair of the Committee on Infectious Diseases for the AAP, told NPR earlier in December. “Fevers from common respiratory viruses in and of themselves are not harmful.”

[Related: No, you can’t get the flu from a flu shot.]

While weekly RSV hospitalizations have recently decreased, the number hospitalizations is still higher than normal for this time of year.

Daniel Ganjian, a pediatrician at Providence Saint John’s Health Center, told PopSci in October that RSV exposure early in life helps train the immune system and most RSV infections occur in babies whose immune systems are still developing. Beginning in early 2020, children did not attend as many in-person activities, which lowered their chance of infection and the creation of an appropriate immune defense. “They have zero antibodies because these kids, who were 1 and 2 during the pandemic, were not exposed to RSV,” Ganjian said. “Now they’re getting it for the first time and they’re getting severe reactions,” he said. Infected infants may cough and wheeze for about two weeks, but most babies make a full recovery. A 2022 study in The Lancet estimates that RSV caused 7 percent of infant deaths, with most occurring in children under 3.

Wearing a face mask, staying up to date with flu and COVID-19 vaccination, good hand-washing, and other general health practices can help prevent infection from respiratory infections.

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Chestnuts roasting on an open fire and the smell of cookies wafting through the air can only mean one thing—the holidays are here. For many, this is a time to see family and get some much needed R&R. But for people with diabetes, the food-filled celebrations can be a bittersweet reminder of what you can and can’t eat.

Having Type 1 or Type 2 diabetes doesn’t mean you have to miss out on all the goodies, however. Popular Science spoke with diabetes experts who agree that you can treat yourself this season—as long as you do it in moderation. “It’s okay to indulge on the holidays. They’re special,” says Carolyn Maxwell, an endocrinologist at Stony Brook Medicine in New York.

[Related: FDA approves first drug that can delay onset of Type I diabetes]

Read on for the diabetes do’s and don’ts of navigating merry feasts and festivities. 

Do plan ahead

If you’re going over to a friend’s or family’s holiday dinner, there are several ways to prepare. For example, you can snack throughout the day so you’re not starving when it comes time for the big meal: Having something in your system makes you less likely to binge eat unhealthy foods, says Melissa Gaynor, a dietitian at the Pediatric Diabetes Center at NYU Langone’s Hassenfeld Children’s Hospital. You’ll also want to avoid an excess amount of carbohydrates in your main course. Holiday dinners often have turkey, stuffing, and mashed potatoes in their lineups—all of which are high in glucose-producing molecules. Gaynor says that eating a large amount of these savory dishes at one time can make it tricky to control blood sugar levels, even if you’re regularly taking insulin. 

While a few carb-loaded bites won’t severely harm your health, says Gaynor, you might want to ask the host for the recipes in advance so you can keep track of what you’re eating. “There are so many websites and apps where you can type in the ingredients of a recipe and it will tell you the nutritional content and the carbs so you don’t have to guess,” she adds. Foods with a low glycemic index—a measure of how quickly they affect your blood glucose levels—are typically healthy for diabetes.

If you want more options at a communal meal, Gaynor recommends making your own dish. Not only would you have something you can definitely eat, but you’ll also know the nutritional contents without extra research. Consider bringing a veggie platter or a side such as roasted cauliflower to the party. 

Don’t drink sugary cocktails

For those who want to fully get into the holiday spirit, having two or three glasses of alcohol at a party is not too bad for your diabetes, says Maxwell. Imbibing too much, however, can lower your inhibitions and make you more likely to indulge in food.

[Related: The best non-alcoholic drinks to sip soberly this holiday]

If you do decide to stir up a drink, skip the cocktails: They’re chock-full of liquid carbs from added juice and syrup, which can spike your blood sugar. Instead, Gaynor recommends making a mixed drink using diet or zero-calorie soda, ginger ale, or seltzer. Be sure to stay hydrated in between drinks—water and other unsweetened beverages can dilute the amount of sugar circulating in your bloodstream, keeping your glucose levels in a healthy range. 

Do eat protein and fiber-rich foods

While both experts say it’s okay to have some carbs, you’ll want most of your plate made up of protein, vegetables, and high-fiber foods that “are going to have less of an effect on blood sugar,” explains Gaynor.

Fibrous fare like artichoke hearts and beans will satisfy your hunger faster, and slow down any spikes in blood sugar because the body can’t break the plant-based nutrients down. Proteins are also super filling and have a minimal effect on raising blood sugar. You can find tasty protein-rich foods in the cheeses of a charcuterie board, olives, and deviled eggs, to name a few. 

Don’t go overboard with dessert

When it comes to sweet treats, it’s all about portion control. If you’re going to gift yourself a small slice of cake, Maxwell recommends pairing it with fresh fruit. “There is sugar in fruit, but it’s almost always going to be better for you than everything else on the dessert table,” she notes.

[Related: How to avoid added sugars]

For heavy dishes like pie, it’s tricky to know how many carbs you’ll end up consuming. Gaynor says this is when it’s important to talk to the host about nutritional details. Even if you cut yourself a piece, be mindful of the serving size, she adds. And remember, you can bring your own dessert, too. Opt for something made with ingredients that have a low glycemic index, like almond or whole grain flour. “You’ll know exactly what ingredients went into that dish,” Gaynor says, “and you can pre-slice it so the portions are set.”

Do take a walk after dinner

Both experts recommend getting some light exercise after a meal at the end of the day. Not only would it help with digesting a big feast, but being active helps with lowering glucose spikes. That doesn’t mean you have to leave the party to hit up the gym: Research shows just a two- to five-minute walk around the block can make a noticeable difference in your blood sugar levels.

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As an outbreak of Ebola virus disease continues in Uganda, there is some progress in preventing future outbreaks. The results of two randomized, placebo-controlled trials analyzing three Ebola vaccine administration strategies published Wednesday in the New England Journal of Medicine show promising results.

According to the National Institutes of Health (NIH), “antibodies were produced in response to the vaccine regimens beginning at 14 days after the first vaccination and continued to be detectable at varying levels—depending on the vaccine and regimen used—in both children and adults for one year.”

[Related: Uganda’s Ebola outbreak is ‘rapidly evolving,’ according to WHO.]

Enrollment for these trials began in 2017, and the volunteers for the study are from Guinea, Liberia, Sierra Leone, and Mali. One of the study’s main goals was to identify the best vaccination strategies to curtail future Ebola outbreaks. The trials were conducted simultaneously and shared a placebo arm. A total of 1,400 adults and 1,401 children (age 1 to 17 years-old) were randomized to receive two injections of either placebo or Ebola vaccine in one of three different regimens.

One vaccine regimen was a dose of the Johnson & Johnson vaccine followed by a booster dose of a vaccine supplied by Bavarian Nordic eight weeks later. A second regimen was two doses of a vaccine made by Merck, given eight weeks apart. The third regimen included one dose of the Merck vaccine followed by a placebo injection eight weeks later.

All of the regimens produced antibodies 14 days after the first of two shots and these antibodies were detectable at varying levels in both children and adults for one year, depending on the vaccine and regimen.

[Related: Ebola hasn’t been cured yet, but two experimental drugs are showing significant progress.]

“The researchers say this finding is notable because vaccines against Ebola virus disease are typically administered during an outbreak and so information about how rapidly a vaccine produces an antibody effect is of potential use in efforts to protect at-risk populations,” wrote the NIH in a statement.

However, these vaccines target the Zaire strain of the virus, not the Sudan strain of Ebola. The Sudan strain is behind Uganda’s current outbreak that began in September and has caused at least 55 deaths and 142 confirmed cases, according to the The World Health Organization (WHO). There are signs that the outbreak is easing, including a hospital discharging the last known patient with Ebola on December 2. Uganda additionally received doses of a vaccine that targets the Sudan strain for use in a clinical trial last week.

The agency stresses that the results aren’t able to assess protection from the disease because the level of antibody response that correlates with vaccine-induced protection against infection or disease is not currently known. “As no participants contracted Ebola virus disease during the trial, the investigators were not able to assess protection from disease,” the NIH writes.

According to the researchers in this study, some of the strength of the trials include outstanding retention of volunteers throughout the process, community engagement ,and trust-building efforts. “Long-term follow up of the participants in this trial is taking place to determine if and when booster doses might be needed,” Brian Greenwood, a study co-author from the London School of Hygiene & Tropical Medicine, told Reuters.

In 2019, European regulators approved and the WHO prequalified Merck’s Ebola vaccine Ervebo. Johnson & Johnson’s vaccine Zabdeno received clearance from European regulators in 2020 and clearance from the WHO in 2021. Mvabea, made by Bavarian Nordic and used in the used in the Johnson & Johnson regimen, also received approval in 2020 and prequalification in 2021.

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HUMAN HEARING has its limits. Frequencies as high as 20,000 hertz (think of an anti-loitering alarm) can cause a pair of young ears to perk up. Any vibes above that fall into the range of ultrasound, meaning they don’t register to us at all. But gadgets like full-spectrum recorders and radio scanners have upped our auditory sensitivity and let us explore new worlds of information. Here are five shrill and mysterious noises that we’ve harnessed in some form.

A singer’s impossible peak

You might imagine Mariah Carey or Maria Callas would top the scales, but Brazilian soprano Georgia Brown set the bar by hitting a G in the high 10th octave. Musical experts later confirmed the note, which translates to about 25,000 hertz, earning Brown a Guinness World Record in 2004.

A medical device’s dramatic whine

Ultrasound machines create energy waves so fast and furious that they can pass through bone, fat, tissue, and other masses. The intensity of the transmissions depends on the medical application: Prenatal checks are usually set at 2.5 million hertz, breast scans at 5 million hertz, and skin-inflammation screenings at 100 million hertz. In some cases, extreme frequencies heal too: Pulses at 1 million to 3 million hertz have proven therapeutic for knee injuries like MCL sprains.

The cosmos’s cryptic message

In general, the universe operates in low frequencies (NASA recently recorded a black hole “screaming” at 57 octaves below the average adult voice). A mysterious radio signal from an unknown extraterrestrial location, though, screeches at such a high pitch that astronomers haven’t been able to precisely measure it. Nicknamed the “space roar,” this intense but diffuse energy wave could top out at 3 billion hertz.

A bat’s remarkable song

A diverse collection of creatures communicate in ultrasound, including katydids and hummingbirds. One species, however, takes it to a whole other level. The clear-winged woolly bat of Southeast Asia has one of the widest vocal ranges ever measured. Its echolocating buzzes can reach 250,000 hertz—more than 10 times higher than a human’s top shriek. Biologists hypothesize that the night flyers are locked in an evolutionary war with tasty moths: The higher the mammals raise their voices, the lower the chance their prey will hear them coming.

The body’s telling thrum

Heart murmurs can be a benign quirk or the sign of a deadly health condition. Family doctors might listen for them with a stethoscope, but a test called a Doppler ultrasound shows these irregular blood flows can whoosh around at up to 410 hertz, which is more than double the usual pitch. As a murmur courses through the arteries in the chest at varying speeds, the frequency of its sound changes, giving cardiologists a clue to the source’s severity.