Want to speed up your recovery after an injury or a workout? Some influencers are fans of shots of BPC-157 and TB-500 for that. Want scar-free, youthful skin and thick hair? Reddit posts rave about GHK-Cu and KPV. Want to build beautiful, bulky biceps? Some fitness influencers swear shots of ipamorelin will do wonders. This is the world of peptides — an assortment of chemicals that promise to boost your body and health — and people are self-injecting them in a growing wellness trend.

Promoted by bodybuilders and influencers, supporters of the "Make America Healthy Again" movement and Silicon Valley early adopters, peptides promise results that leave people better than well, fitter than fit. Yet despite getting glowing reviews on social media, most peptides have limited clinical evidence to support health benefits, whether it's helping to heal a rotator cuff injury, improving libido or building muscles. There's not much information out there on the drugs' effectiveness and even less on their safety.

In 2023 the Food and Drug Administration banned several peptides, including BPC-157, GHK-Cu, KPV and ipamorelin, from being produced in the U.S. by compounding pharmacies — facilities that legally make non-FDA-approved medications for individual use — because of "significant safety risks." Many peptides are imported from outside of the country, and many made here are marketed for research use only. People who desperately want the promise contained in the tiny vials seek them out on online on legally dubious gray markets.

But accessing the shots might soon get easier. On the podcast The Joe Rogan Experience on February 27, Robert F. Kennedy, Jr., secretary of the Department of Health and Human Services, proposed legalizing the compounding of 14 peptides — and the FDA seems poised to grant his wish. Earlier this week the agency released plans to hold a meeting with independent advisers in July to review whether some U.S. pharmacies should be allowed to manufacture certain peptides, including BPC-157, TB-500 and KPV.

If the lift on peptides happens, a flood of people could start using the drugs, regardless of any safety concerns.

A Peptide by Many Names

A peptide is a chain of two or more amino acids — building blocks of proteins. The body's cells can produce numerous peptides, which perform various tasks or serve as signaling molecules.

Insulin is a peptide. So is human growth hormone — and semaglutide, the active ingredient in glucagonlike peptide 1 (GLP-1) receptor agonist drugs such as Ozempic and Wegovy. (GLP-1s are FDA-approved for managing type 2 diabetes and for weight loss). Buzzy new injections such as BPC-157 and GHK-Cu — touted for tissue repair — are derivations or synthetic versions of naturally occurring peptides. The public and online health retailers are starting to use "peptides" as a catchall term for any chemical taken for well-being, energy, exercise recovery, and more, says Luke Turnock, a criminologist who studies how people use enhancement drugs at the University of Lincoln in England.

And while people are using them as treatments, peptides aren't often described as drugs. "'Drug' has a certain stigma or negative connotation attached to it," Turnock says. The popularity of peptides has its roots in the bodybuilding and powerlifting communities, he explains, where "drug" has historically been tied to steroids — which are generally banned for professional athletes.

The term "peptides," meanwhile, stresses the natural origin of the molecules, says Flynn McGuire, who studies sports medicine at the University of Utah. "Because it's 'natural,' it is better or different, even though they're just drugs," McGuire says.

A Surge in Popularity

In the past few years, orthopedic surgeon Omar Rahman has seen a spike in interest in peptides. "I'm seeing more patients asking about peptides, often driven by the longevity and wellness space," says Rahman, who practices at Pacific Coast Sports Medicine in Los Angeles.

Because peptides encompass many products — some available by prescription, others on the gray market — the exact number of people trying them is hard to pin down. The subreddit r/peptides currently has more than 70,000 weekly visitors, and the related subreddit r/biohackers, which frequently hosts conversations on peptides, has more than 600,000. A scroll through TikTok offers pages of people sharing their "stacks" — combinations of injections people take to meet their personal goals, from muscle-building and exercise recovery to increased brainpower or a better tan.

"The real cultural tipping point in my mind seems to have been around 2022, when the GLP-1s really blew up," says Turnock, who is researching the peptide boom. He says injecting drugs became "normalized" when GLP-1 drugs approved to treat diabetes, such as Ozempic, were also shown to be effective for weight loss — and eventually became an approved treatment for obesity.

Some are turning to peptides because they feel doctors aren't giving them the help they need, says Dan Cushman, a sports medicine doctor at the University of Utah. Injuries to certain tissues, such as tendons, "are very slow to heal" with conventional treatments, he says. Mainstream treatment can also be expensive and painful. To someone desperate for relief, peptides might seem worth a try.

Peptide use is also linked to a growing interest in health autonomy, Turnock says. This is the idea "that doctors, if they're not prescribing what you ask for or they're not offering you these solutions, are acting as a barrier to your good health."

Stacking Up

McGuire, Cushman and colleagues published a review last year on one peptide they encountered frequently: BPC-157. The peptide is promoted as a way to stimulate multiple cellular pathways involved in blood vessel formation, cell growth, muscle repair and inflammation. Their review, however, found that most of the evidence of such health effects was from rodent studies, and only three small pilot studies had looked at BPC-157 use in humans.

In a regimen called the "Wolverine" stack, many people combine BPC-157 with injections of TB-500, another peptide that is supposed to promote healing but has even less research behind it. The "Wolverine" stack is named after the rapidly healing X-Men character. Add injections of GHK-Cu and KPV, and the stack is called "glow" or "KLOW." People claim that GHK-Cu increases wound healing, decreases scarring and helps regenerate collagen — and that KPV, derived from a hormone naturally found in the body, reduces inflammation. GHK-Cu is found in blood plasma and is an FDA-approved ingredient in topical antiaging cosmetics — but it is currently banned as an injectable because of safety concerns, such as the risk of immune reactions caused by impurities.

For muscle-building, the peptides ipamorelin and CJC-1295 are advertised as stimulating growth hormone release. Both have little clinical evidence behind them, however. Some people stack ipamorelin with GLP-1 drugs to try to lose fat while building muscle, though the effects of taking these injections together have not been studied.

Use at Your Own Risk

Clinical trial data for most of these peptides are thin. Not only are the effects anecdotal, but so are the doses. FDA-approved drugs, Cushman says, have been tested and reviewed not just for their efficacy but also for their safety. There is very little existing information on most of these peptides, he says, let alone on what happens if they are combined.

In many cases, the provenance of these peptides is even grayer than the gray market would suggest. "Patients are accessing peptides through online vendors, wellness clinics and compounding pharmacies," Rahman says. "That variability in sourcing is one of the biggest concerns, particularly when it comes to purity, dosing consistency and overall quality control."

The FDA does not allow production of BPC-157, GHK-Cu, KPV and ipamorelin in the U.S., for example, by compounding pharmacies because of safety concerns, so people are ordering them from overseas — usually from China. Some are buying peptides labeled as "for research only." Not all are stuck in the legal gray areas; other peptides are available from compounding pharmacies.

In Kennedy's February remarks about his aim to allow compounding of more than a dozen peptides in the U.S., he suggested that peptides made within the country would be safer than ones acquired abroad.

"Americans deserve to know the quality of the products they are buying and deserve drugs that have been proven to be safe and effective," an HHS spokesperson told Scientific American in response to questions about Kennedy's comment and the timing of the lift. "The FDA's goal is to ensure that patients can obtain FDA-approved products, and when those aren't available or can't work because of a patient's unique situation, are made by licensed U.S. pharmacies."

But even if Kennedy's plan to make some peptides easier to compound in the U.S. is enacted, it does not necessarily mean the drugs are safe or effective. The FDA does not approve or review drugs from compounding pharmacies — it just monitors the active ingredients the facilities use.

If peptides become more readily available in the U.S. market, Cushman predicts, more "people are going to just start trying [them]" — whether there are data to back them up or not. The public may experience any benefits — and perils — of peptides before scientists quantify them in the clinic.

This article was first published at Scientific American. © ScientificAmerican.com. All rights reserved. Follow on TikTok and Instagram, X and Facebook.

The hantavirus outbreak that struck a cruise ship in April, killing three people and sparking fears of further spread, is over, the World Health Organization (WHO) has announced.

"Today, the final contact of a person exposed to hantavirus on the cruise ship MV Hondius completed their quarantine period, tested negative and returned home. No further cases have been reported since the 25th of May," Tedros Adhanom Ghebreyesus, the WHO's director-general, said in his opening remarks at a news conference Thursday (July 2). "We are therefore very pleased to say that WHO considers the outbreak of hantavirus over."

The total number of cases linked to the outbreak was 13. All those affected were either passengers or crew on the ship.

The outbreak began aboard the Dutch-flagged cruise ship MV Hondius after it departed southern Argentina on April 1. It involved the Andes virus, the only known hantavirus that can spread between people.

Hantaviruses are rodent-borne viruses that are found in the Americas, Europe and Asia and spread to humans relatively rarely, usually via contact with the urine, droppings or saliva of infected rodents. The Andes virus, however, has sparked short chains of human-to-human transmission in the past.

Before public health authorities were informed of the cases on MV Hondius, several dozen people disembarked the vessel on the island of St. Helena. To find them, authorities launched an international contact-tracing operation, tracking down more than 650 contacts in total who were then followed by health authorities in 33 countries and territories, according to the WHO.

Additionally, health authorities coordinated the monitoring, care and transport of the remaining passengers and crew aboard MV Hondius.

Of these contacts, those considered at the highest risk of infection were then quarantined and monitored for up to 42 days, because sometimes, hantavirus symptoms don't show up until weeks after exposure to the virus. Depending on their jurisdiction and degree of exposure, some contacts quarantined at home while others stayed in specialized facilities.

The initial unchecked travel of some contacts, alongside the virus's long incubation period, prompted concern from the public that the cluster of cases could explode into an enormous outbreak, or even a global pandemic. Many infectious-disease experts emphasized that the Andes virus does not spread easily between people and that the containment effort was going well, so the risk of a large outbreak was low. Still, some experts raised concerns that the international travel of contacts could trigger pockets of the deadly disease, and some argued that the Andes virus does have "pandemic potential."

Now, with the final contact having completed their quarantine period and no further cases reported, the WHO has declared the outbreak over. All of the contacts who were repatriated to the U.S. completed their quarantine period by June 21.

"WHO will continue working with governments and partners to advance our understanding of this outbreak and of hantavirus more generally," Tedros said. "We are also coordinating a study involving 21 countries to understand how the disease develops, which will support the development of diagnostics, therapeutics and vaccines for future outbreaks."

Besides rigorous contact tracing, the WHO credited the coordinated actions of national public health bodies as being vital to preventing the further spread of the disease. These measures included the response of the Spanish government, which created a safe zone on the island of Tenerife for the ship's remaining passengers to disembark before they were repatriated under quarantine.

As the hantavirus outbreak concludes, there's an ongoing Ebola outbreak in the Democratic Republic of the Congo and an outbreak of the Marburg virus in Uganda. These and future outbreaks will require similarly robust international cooperation, the WHO emphasized.

"The outbreaks of hantavirus, Ebola and Marburg all show why there is no alternative to international cooperation in the face of international threats," Tedros said. "No country alone can fight."

This article is for informational purposes only and is not meant to offer medical advice.

An 11-year-old boy in Ontario, Canada, has died after being bitten by a rabid bat that was resting on his face as he slept. The boy had no obvious bite or scratch marks and didn't show symptoms for the first 19 days after the incident, his doctors report.

While on vacation with his parents at a cottage in northern Ontario in 2024, the boy was woken up in the night by a bat on his nose and mouth, according to a report published in the Canadian Medical Association Journal on June 29. His father caught the bat in a cooking pot and released it outside, and because the child had no visible injuries and the bat did not seem to be particularly aggressive, his parents decided not to seek a medical assessment, the report noted.

A few weeks later, the child began to experience tingling, numbness and swelling on the right side of his face. When he was examined at his local hospital his vital signs appeared to be normal, aside from an elevated heart rate and white blood cell count.

The next day, the boy's symptoms worsened: he lost feeling in the right side of his face and his speech was beginning to slur. While waiting in hospital, he developed a fever, confusion, hallucinations and difficulty swallowing, followed by excessive production of saliva.

After four days in intensive care at McMaster Children's Hospital in Hamilton, Ontario, the child tested positive for rabies, and after five days his brain stem reflexes were absent, indicating a total loss of brain stem function. Seventeen days after admission, following a consultation between his family and medical experts, he was taken off life support and died.

Rabies is a viral disease that primarily affects the central nervous system, according to the CDC. It is mainly spread through bites and scratches from infected animals, with bats accounting for the majority of cases in North America, according to the boy's doctors.

"Bats pose a particular risk because bites or scratches may be small and are easily overlooked, and patients may not recollect or recognize a bat exposure," the medical team wrote in their report.

According to a report in the Journal of Virology in 2013, silver-haired bats (Lasionycteris noctivagans), are responsible for the majority of rabies cases in Canada. Skunks, foxes and raccoons also often carry the disease.

The rabies virus must travel to the brain before symptoms can occur, but once a patient develops symptoms the infection is almost 100% fatal, with most deaths occurring within one to two weeks of symptom development. However, prompt treatment after exposure — including wound cleaning, antibody administration and a series of vaccines — is nearly always effective at preventing the disease, according to the CDC.

Rabies in humans is very rare in North America, with fewer than 10 deaths reported in the U.S. every year, according to the CDC. In Canada, only 28 human fatalities have been reported since 1924, according to the Canadian Veterinary Medical Association. Even so, the boy's doctors have emphasized the importance of prompt medical attention following exposure to bats and other animals that could carry the disease.

"Early recognition of exposure and timely PEP [postexposure prophylaxis] remain the only effective means of rabies prevention," they wrote. "Any direct human contact with a bat, even in the absence of a visible bite or scratch, is an indication for PEP."

They added that rabid bats do not always display the classic symptoms commonly associated with rabies, such as aggressive behavior and frothing at the mouth. "Any direct human contact with [a] bat is considered high risk," they added.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A man in his 20s in Edinburgh, U.K.

The symptoms: The man visited an eye clinic after noticing floaters — small, dark shapes drifting across his field of vision — along with brief flashes of light in his right eye for six days. He was otherwise healthy and had no history of eye disease, physical trauma to the eye, or drug use. He had mild nearsightedness, for which he wore glasses.

What happened next: Doctors performed a thorough eye exam while the patient wore glasses, finding that his corrected vision measured 6/6 in both eyes, the metric equivalent of 20/20. His eye pressure was also normal.

However, a closer examination of the patient's retinas, the light-sensitive layer lining the back of the eye, revealed significant damage in both eyes, according to a report of the case.

In the right eye, doctors found multiple retinal tears and bruising, as well as a retinal dialysis, a rare type of tear in which the retina begins to separate from its outer edge where it connects to other tissues of the eye. Without treatment, retinal dialysis can progress to full retinal detachment and cause permanent vision loss. The left eye also had bruising and six small, horseshoe-shaped retinal tears: three at the top and three on the side of the retinal tissue.

Since these injuries are typically caused by sudden trauma to the eye ‪—‬ from a punch or sports injury, for instance ‪—‬ doctors revisited the patient's history and asked whether anything unusual had happened involving his eyes.

The patient, described in the case report as a "hesitant historian," later disclosed that he had been using a percussive massage gun directly on and around his eyes for the past three months. He had bought the device himself and used it weekly for several minutes at a time without medical guidance, in an effort to relieve a "feeling of tiredness" in his eyes.

The diagnosis: Doctors concluded that the patient's retinal injuries were most likely caused by this improper use of the massage gun, according to the case report. These devices deliver rapid, high-frequency pulses of pressure that are intended to relieve muscle tension. However, they can cause severe damage to delicate tissues like those found in the eyes.

The eye is filled with a gel-like fluid that helps it maintain its shape. The case report authors suggested that, each time the device put the eye under pressure, it may have briefly distorted the eye's shape. Over time, this repeated stress may have placed strain on the retina, eventually leading to the small tears.

This pattern of injury was also different from what's seen in typical retinal dialysis cases, they noted. The condition most often occurs in the lower, outer part of the retina, along its bottom edge. In this patient, however, the injury was found in the retina's upper region, which his doctors said may reflect repeated forward pressure from the device rather than a conventional lateral impact, such as blow to the head.

The treatment: Around 8% to 15% of retinal dialysis cases can progress to retinal detachment, which can lead to vision loss. In this case, however, the patient's vision was preserved.

The retinal tears in both eyes were treated with laser therapy; targeted laser burns create scar tissue that helps seal the retina in place and thus prevent fluid from seeping underneath. The right eye's retinal dialysis was treated with "barrier laser therapy," which similarly creates a protective scar around the affected area to reduce the risk of progression.

At a follow-up six months later, the patient's condition remained stable, with no further damage or cataract formation (clouding of the eye's lens). Doctors reported that the positive outcome was "likely due to the patient's prompt presentation soon after noticing symptoms and the immediate initiation of treatment."

What makes the case unique: Eye injuries linked to massage guns are rarely reported. The small number of cases that appear in the medical literature suggest they can sometimes cause serious or permanent damage.

In one such case, a 69-year-old man developed severe eye complications, including lens dislocation and glaucoma (a sudden rise in eye pressure) after using a massage gun near his eye for several weeks. In another case, a 38-year-old woman developed a dense traumatic cataract — a type of cataract that forms due to physical injury — and severe vision loss after using a similar device over her temple and eye region.

The Edinburgh man's case is the first to report retinal dialysis and multiple retinal tears linked to massage gun use. Such injuries are usually associated with high-energy trauma, such as road traffic accidents, sports injuries or a direct blow to the eye, or they occur in people with underlying risk factors, including severe nearsightedness or age-related eye changes, the case report authors noted.

In this case, the young man had none of these known risk factors. The extent of the damage in the absence of these risk factors raises concerns about the effects of improper use of massage guns near the eyes, his doctors concluded.

Massage guns are widely sold for at-home use, but there are currently no standardized safety guidelines for using them on or near sensitive areas, such as the eyes. The authors of the case report said the man's case highlights the need for clearer manufacturer warnings and greater awareness of the potential risks of improper massage gun use.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

About a decade ago, the Japanese government spotted a worrying pattern: Pediatricians were doling out a ton of antibiotics, well beyond what should be needed to treat the bacterial infections coming through their doors.

Antibiotics treat bacterial infections, not those caused by viruses, fungi or parasites. Yet doctors were often sending young patients home with antibiotics for illnesses unlikely to be bacterial. Treating nonbacterial infections with antibiotics can fuel antimicrobial resistance (AMR) and the rise of superbugs by unnecessarily exposing bacteria to the drugs, pressuring those bacteria to evolve strategies to survive. Resistant bacteria can then spread their adaptations to others, thereby compounding the problem.

In the long run, resistance could make common infections impossible to treat with existing drugs, raising the risk of serious illness and death across the population.

When pediatricians in Japan did treat bacterial infections, they were overusing the antibiotics that are likely to fuel resistance — "broad-spectrum" drugs that target many bacteria at once. When compared against 35 other high-income countries in 2015, Japan ranked dead last in the appropriateness of antibiotic choices for kids under 5.

One way to slow the development of AMR is to get antibiotic prescriptions under control. So Japan focused on one of its biggest sources of problematic antibiotic use: pediatric outpatient clinics.

"The clinics are a particular problem," said Dr. Yusuke Okubo, chief of clinical epidemiology and health services research at the National Center for Child Health and Development, a research center and hospital in Tokyo. Looking at Japan's overall antibiotic use, "90% of prescriptions are [from] outpatient clinics, not hospitals," Okubo told me. (Outpatient practices account for a similar proportion of antibiotic prescriptions in the U.S.)

A large proportion of problematic prescriptions were being written for children under 3 years old, especially those with upper respiratory tract infections, which nine times out of 10 are caused by viruses, Okubo said. The stomach bug gastroenteritis was another biggie for overprescription, despite most often being caused by a virus.

Government officials hatched an idea: What if each time a pediatrician chose not to prescribe an antibiotic in these cases, they earned a small financial reward — a tip for making a better choice? Each tip would be small, amounting to about $5 per claim at today's exchange rate, but could translate to thousands of extra dollars of annual income for individual clinics. That's no small matter for Japanese pediatricians, who Okubo estimates earn roughly $90,000 to $100,000 a year.

This incentive program, rolled out in 2018, has proved a success, so much so that it's since been expanded to cover more patients, more clinics and a wider variety of diseases. But what made the program work? I went to Japan to find out what systemic and cultural factors contributed to the program's success. Ultimately, I wanted to see whether other countries, like the U.S., could learn from this nationwide experiment.

The quietly rising threat of resistance

With bacteria, as with animals, it's survival of the fittest. When exposed to antibiotics, a percentage of bacteria die, while others survive. That surviving population has traits that help them withstand the drug's effects, which are encoded in "resistance genes." Bacteria can transfer those genes to the next generation by multiplying, as well as physically pass those genes to nearby bacteria. Plus, they can pick up new resistance genes through random DNA mutations.

All antibiotics come with the risk of pressuring bacteria to evolve resistance — it's an inherent feature of the drugs. However, broad-spectrum drugs carry the greatest risk, because they place pressure on a wider variety of bacteria than narrow-spectrum drugs do. The 2015 cross-country comparison found that Japanese doctors prescribed antibiotics with the lowest risk of resistance only 35% of the time, meaning most antibiotic prescriptions were for broader-spectrum drugs.

It's sometimes necessary to use broad-spectrum drugs — such as when an infection is resistant to narrow-spectrum options — but using broad-spectrum antibiotics when they're not needed hastens the development of AMR. So does using antibiotics for nonbacterial infections. In both scenarios, you're introducing evolutionary pressure that could have otherwise been avoided.

Globally, resistance is rising among common disease-causing bacteria; it's far outpacing the development of alternatives to antibiotics. In 2021, resistant bacterial infections directly caused 1.14 million deaths worldwide and contributed to another 3.57 million deaths. Those numbers could climb dramatically by 2050 if swift action isn't taken now.

Common pathogens already show high rates of resistance in Japan, and resistant germs contribute to thousands of deaths each year, with most occurring among older adults. People over 65 make up about 30% of Japan's population. As that percentage grows in the coming years, AMR-related illness may also increase, health officials worry.

Japan's youngest residents are also at risk, though, as resistant bacteria can sometimes pass from mothers to newborns at birth and can cause serious complications, like sepsis. Resistance has also been detected among respiratory bugs that frequently infect kids, such as Mycoplasma pneumoniae, said Dr. Takemi Murai, deputy head of the Infectious Diseases Division at Nagano Children's Hospital in Azumino. "There have been outbreaks of Mycoplasma that are resistant to antibiotics," he said.

Yet not long ago, the unrestrained use of antibiotics was a mainstay of Japanese medicine. (I'll dig into the myriad reasons why in later installments of this series.)

National insurance data sampled from 2005 showed that 60% of patients in Japan with nonbacterial upper respiratory tract infections were prescribed antibiotics, mostly broad-spectrum ones like third-generation cephalosporins, macrolides and quinolones. Most of those prescriptions came from clinics.

Something had to shift.

Tips for appropriate treatment

In 2016, Japan got serious about reducing its antibiotic misuse, releasing its first National Action Plan on Antimicrobial Resistance. It aligned with a global plan from the World Health Organization, which aimed to raise awareness of AMR and optimize the use of antimicrobials, including antibiotics, among its member states.

Two of Japan's big goals were to slash overall antibiotic use by 33% and broad-spectrum antibiotic use by 50% by 2020. The country came very close to hitting those ambitious targets by the deadline, and doing so was no small feat. The tipping program was just one of a slew of initiatives introduced to improve AMR awareness and antibiotic use.

Prior to the incentive's introduction, Japan's Ministry of Health, Labour and Welfare (MHLW) — whose role is somewhat analogous to the U.S. Department of Health and Human Services — rolled out educational campaigns for doctors and patients and wrote a manual for antibiotic use, with the first edition directed primarily at outpatient doctors. It emphasized that most acute respiratory tract infections and acute diarrheal diseases don't require antibiotics.

Among kids, children under 5 saw the highest antibiotic prescription rates, often receiving the drugs for respiratory infections. Data showed this overprescription problem was the worst in children under 3 being assessed for upper respiratory infections or acute gastroenteritis. The government's solution? Pay doctors extra to withhold antibiotics when faced with cases that don't warrant them.

"If the clinicians provide more appropriate medical services, we add additional payment," said Dr. Takuma Kato, a counselor at the Permanent Mission of Japan to the United Nations who previously worked on the incentive program for MHLW. In this case, they pay "a little bit more" when doctors don't give patients antibiotics for illnesses that are likely viral, he said.

A "little bit more" is accurate. Each tip is 800 yen, equivalent to about $7.20 when the program launched in April 2018 and about $5 at today's exchange rate.

Here's how it works: A caregiver brings in their sick infant or toddler for an initial visit, and the pediatrician determines the child likely has an acute upper respiratory tract infection or gastroenteritis. These illnesses are typically caused by viruses, so the doctor decides not to provide an antibiotic. The doctor explains this rationale to the caregiver and provides guidance for home care. If the appointment checks those boxes, the clinic can claim an extra 800 yen when they seek reimbursement.

Because mild viral infections typically resolve on their own in a few days, a strategy called "watchful waiting" can help clarify if a bacterium is actually at fault. So if a doctor does prescribe an antibiotic at the first visit, they'll often encourage the caregiver to bring the child back if their condition remains the same or worsens within a few days. The incentive and this "waiting" strategy go hand in hand.

There are a few technicalities. For example, the children being assessed must have no underlying conditions that might complicate their case, such as a weakened immune system. If children test positive on a formal diagnostic test for influenza or COVID-19, the incentive cannot be claimed. To qualify for the incentive, clinics must specialize in pediatrics and use a "comprehensive" payment system, meaning patients pay a standardized amount for the whole appointment rather than the itemized "fee for service" that is ubiquitous in the U.S.

Despite this fine print, the perk is pretty appealing for the clinics that claim it. "I think pediatric doctor associations are really happy," Okubo said.

Doctors say "small incentives add up"

The Japanese government generally incentivizes doctors to adjust their behaviors, rather than penalizing them for poor practices, Okubo said.

"It's a constructive message from the government: 'You changed your behavior, so we'll pay something,'" Okubo said. "This constructive approach motivates physicians, especially pediatricians, to apply their common sense to their actual practice."

This system is readily accepted by Japanese doctors, who have historically held a lot of political power, Kato noted. Just like in the U.S., their professional groups, such as the Japan Medical Association, lobby the government and typically push against policy proposals that they view as potential threats to their bottom line.

By contrast, an incentivizing approach is "very, very welcome, especially by the doctors' associations," said Dr. Norio Ohmagari, director of disease control and prevention at the National Center for Global Health and Medicine, part of the Japan Institute for Health Security (JIHS) in Tokyo. Ohmagari also leads the AMR Clinical Reference Center, which collaborates with the WHO on AMR countermeasures.

Doctors I asked confirmed that they like the incentive, namely because it boosts their profits.

"I apply for the pediatric antibiotic appropriate use support premium each time" it's applicable, said Dr. Yusuke Shibata, who runs the Shibata Pediatric Clinic in Asakusa, a historic district in Tokyo's Taito ward. "I appreciate the premium, as pediatric clinics already have low profits" compared with clinics that care for adults, Shibata told me in an email after I visited his clinic.

For first visits with kids under 6, clinics are paid a base rate of 6,040 to 7,210 yen, or about $38 to $45 at current exchange rates. An extra 800 yen (about $5) increases that fee by more than 10% — "a huge amount," Okubo emphasized.

Shibata estimates that his clinic sees about 30 to 40 patients with an acute respiratory infection or diarrhea each week, depending on the season. He can potentially claim the incentive for the first visit with each of these patients, assuming they don't have any conditions that would disqualify the claim.

On the high end, Shibata estimates that he might claim the incentive 180 times in a single busy month, which would total 144,000 yen, or about $900.

Dr. Atsushi Miyahara, who runs the Karugamo Clinic in the Setagaya-ku ward in Tokyo, said he was already conservative about using antibiotics so the incentive rewards him for sticking with his status quo.

Fifteen years ago, when Miyahara opened his clinic, he noticed that other physicians prescribed a lot of antibiotics, and he questioned the practice due to the potential to fuel resistance. He provides his patients with informational flyers that explain the risks of resistance and how avoiding unnecessary prescriptions can reduce that risk. When antibiotics are needed, he predominantly uses narrow-spectrum drugs that pose a relatively low risk of resistance.

Miyahara said the local government and medical associations announced the antibiotic incentive when it was launched, and he felt its introduction has been very positive. It's increased his revenue and encouraged him to continue his stewardship practices. He estimates that for every 50 of his first visits with patients, he claims the incentive 10 to 15 times, so it applies to at least 20% of those visits.

The incentive's impact

Because some pediatric clinics qualified and others didn't — due to fee-for-service clinics being excluded — Okubo and his colleagues could directly measure whether the policy worked.

To assess the incentive's effects in its first year, the researchers looked at insurance claims from over 10,000 medical facilities from just before and after the policy's introduction. About 3,000 of the facilities qualified and claimed the incentive 316,770 times, totaling 253 million yen ($2.29 million at the time). These eligible clinics saw a 17.8% reduction in their total antibiotic use over a year without any negative effects for patients, such as higher hospitalization rates.

To see if those effects lasted, the team drew years of data from over 165,000 young children who went to either eligible or ineligible clinics. Within the first month of the policy's implementation, the former group of children saw a nearly 45% reduction in total antibiotic prescriptions, compared with the other kids. Cumulatively over the next four years, their overall antibiotic use and broad-spectrum-antibiotic use was 20% and 24% lower, respectively.

The decrease in antibiotic prescriptions did not come with an uptick in hospitalizations or healthcare costs, although there was a slight increase in the total number of doctor's visits. But that's what you'd expect as doctors track an infection over time, Okubo explained, meaning they likely employed the watchful-waiting strategy and had parents bring their kids back in if they didn't improve quickly.

Okubo's team has continued to track pediatricians' antibiotic use, and he noted that they're seeing "spillover effects" among age groups not covered by the incentive. In the under-20 age group, outpatient antibiotic prescriptions fell by 50% between 2011 and 2022. He thinks the incentive is a key driver of this trend, directly reducing prescriptions for the youngest kids while also triggering ripple effects in older groups. (This research will soon be published in a peer-reviewed journal.)

That said, there's room to improve doctors' selection of antibiotics when they are used, as the ratio of broad- to narrow-spectrum drugs is still too high. "Total antibiotic use was reduced, but its quality should be improved further," Okubo said.

The incentive's evolution

While the 800-yen tip has proved significant to clinicians, the incentive represents a very small slice of overall government healthcare spending, which totaled 468 billion yen ($3.1 billion) in 2022.

"This program is not large compared to the whole budget," Dr. Kosuke Sasaki, who works in the MHLW's health insurance bureau, told me. The program's budget has no upper limit, so if the number of claims from clinics increased, there isn't a cap on how many could be paid out. "The number of doctors using this program has increased while the number of antibiotic prescriptions has decreased since the start," Sasaki's colleague Dr. Tomonori Aoki added, noting that the government isn't concerned about how to pay that rising bill.

The program's measurable impact and low price tag may explain its growth over the years.

Every two years, Japan's Ministry of Finance hands the MHLW its slice of the government budget, and MHLW then revises the pricing for drugs, medical devices and healthcare services. The antibiotic incentive falls under this revision process and has been expanded several times.

During its first revision in 2020, the incentive was extended to children under 6. In 2022, ear, nose and throat specialists (ENTs) newly qualified for the incentive; like pediatricians, they treat many acute infections in kids and tend to overuse antibiotics, insurance data suggested. That same year, doctors could start claiming the fee for ear infections and sinus infections.

"I see a tendency for pediatric clinics to avoid prescribing antibiotics, but I do see some ENT clinics prescribing antibiotics carelessly," Shibata, the clinic owner in Asakusa, Tokyo, told me. So ENTs seem to be a logical next target.

In 2024, a separate, facility-level incentive was introduced as a complement to the 800-yen incentive. It encourages clinics to submit data to a government database that tracks antibiotic use. If first-line, narrow-spectrum antibiotics make up a certain percentage of the clinic's overall prescriptions, that clinic earns extra money, Okubo explained.

Ultimately, the 800-yen incentive helped put AMR on the radar of doctors who didn't take it as seriously as experts like Kato, who told me "AMR is kind of my life's work." Kato and researchers like Okubo see the program as a success, although they pointed to room for improvement in antibiotic selection. Ministry officials like Sasaki and Aoki said the program is easy to implement and makes a difference. Clinic doctors like Shibata and Miyahara appreciate the incentive and use it consistently. All in all, at just $5 a claim, the incentive has been remarkably effective.

In speaking with experts in Japan and the U.S., I've learned that U.S. doctors have historically faced the same pressures and showed similar lapses in antibiotic use that Japanese doctors have. However, the U.S. does not have an incentive program like Japan's. Should it launch one?

In the next installment of this series, I'll explore a central feature of this problem: the motivations behind pediatricians' antibiotic misuse. What are they, and do those motivations differ between doctors in the U.S. and Japan? Answers to those questions will help determine whether a similar incentive might have the same impact in both places.

Younger generations may be aging faster than their predecessors, and this may be linked to a rise in early-onset cancers, a new study suggests.

There have been recent increases in the rates of some cancers among adults under 50, including breast, colorectal, kidney and uterine cancers. One 2023 paper suggests that these early-onset cancer diagnoses rose by 25% globally between 1990 and 2019, and scientists are still investigating why.

"The trend of increased cancers at younger ages is very real, and it is not simply because of more efficient diagnosis, or diagnosis at earlier stages," said Dr. Jyoti Nangalia, a hematologist and cancer researcher at the Wellcome Sanger Institute in the U.K. who was not involved in the new study. "It is possible that we are being exposed to new cancer-causing risks or that [our] defences to them are somehow altered," she told Live Science in an email.

The new study, published June 22 in the journal Nature Medicine, suggests that younger generations may have a wider "gap" between their chronological ages and their biological ages — a measurement of how quickly the body's tissues and systems are aging — than older generations do. The greater gap among younger adults seems to be linked with a higher risk of developing cancer early in life.

The new study cannot prove that faster biological aging causes early-onset cancer, but it provides new clues for scientists trying to unpack what might be driving the worrying trend.

"This is really proof-of-concept," study co-author Yin Cao, a molecular and clinical epidemiologist at the Washington University School of Medicine and Siteman Cancer Center, told Live Science.

Concerning trends lurking in dense data

Chronological age is straightforward: It's the number of years that have passed since a person's birth. "Biological age," however, can vary wildly from one person to another. This catch-all term describes a range of metrics, including markers on DNA and in the bloodstream. These are often measured using "aging clocks," which aim to determine if the body is acting much older than its chronological age.

Scientists have increasingly used these summary measures in an attempt to understand why some people are more prone to age-related diseases than others. To check whether there could be a link between biological age and the rise in early cancers, the new study analyzed data from more than 150,000 adults in the UK Biobank, a long-running project that has been tracking the health of about half-a-million U.K. adults since the mid‑2000s.

The participants had provided blood samples, with many already measured for markers used to track biological aging. The study authors plugged these results into PhenoAge, a statistical model that estimates a person's "age gap" at a given chronological age. In essence, this model can compare snapshots of two 40-year-olds — one born in 1950 and the other in 1965 — and see if their blood markers suggest they're the same biological age.

"The traditional approach is really focusing on individual risk factors" for cancer, such as a history of obesity or a high intake of ultraprocessed foods, Cao said. "We are testing whether we can leverage these large biobanks and potentially find some biological imprint as a potential reflection of many exposures that can be linked with cancer risk," she said.

The analysis revealed a concerning pattern: UK Biobank participants born between 1965 and 1974 had a larger age gap than those born between 1950 and 1954 at the same chronological ages. Based on PhenoAge's metrics, the younger cohort had systemic aging levels about 0.23 standard deviations higher than the older cohort — a modest shift toward older-looking biology.

The researchers applied this same approach to about 10,000 participants in the U.S. National Institutes of Health's All of Us Research Program, another large biobank. There, they found a more pronounced pattern: People born between 1990 and 1999 had age gaps about 0.92 standard deviations higher than those born between 1965 and 1969.

Another blood-based aging clock, called the Klemera-Doubal method, showed broadly similar patterns to PhenoAge, albeit slightly weaker ones, the study found.

Real trend or data mirage?

In the UK Biobank cohort, the researchers found that participants with higher age gaps were more likely to develop early-onset solid cancers, meaning cancerous tumors that appear in tissues, rather than "liquid" cancers present in bodily fluids. This link was strongest for lung, gastrointestinal and uterine cancers. This finding was based on the patients' medical records.

When the participants were divided into three groups based on their biological ages, those in the highest group had a roughly 15% higher risk of early-onset solid cancer than those in the lowest group.

To probe deeper, the authors used a different model that estimates biological aging at the level of specific organs and systems, using patterns of proteins in the blood. In almost 20,000 UK Biobank participants, they found that markers suggesting an "older-than-expected" immune system were linked with a higher risk of early-onset lung cancer. Similarly, markers suggesting older-than-expected fat tissue were linked with a higher risk of early-onset colorectal cancer.

Does this mean younger generations are aging faster and that's causing the rise in cancers? Maybe, but maybe not — there are important caveats to the study's findings.

The patterns will need to be confirmed in other datasets and populations, Cao noted. Biological aging tests, including PhenoAge, are also relatively new, and their implications aren't fully understood. While they clearly capture something about health and risk at the population level, at the individual level, different biological age tests can give very different answers for the same person. That raises questions about what any single score really means for individual health.

It may be that the differences PhenoAge uncovered between younger and older people have to do with how the test was originally calibrated, Stephen Burgess, a professor of biostatistics at the University of Cambridge who was not involved in the study, told Live Science in an email. To know if that's the case, one would have to dig deeper into how PhenoAge scores are calculated and see if that might have skewed its assessment of the UK Biobank and All of Us cohorts, he said.

Cao added that, while PhenoAge scores have been tied to mortality risk across a range of adults, the test "requires further validations" when it comes to assessing cancer risk.

As with any observational study using large databases, it is hard to untangle cause and effect, Nangalia added.

"The main issue for this paper is one of correlation versus causality," she said. "Either way, it is useful — with the first, as a potential way of tracking population health and cancer risk, and with the second, as insights into cancer-causing mechanisms."

Cao hopes her team's approach will serve as another useful tool to figure out why more young people are getting cancer. " Hopefully this is just a starting point," Cao said.

With the aid of AI, scientists have identified a potential new antibiotic to treat gonorrhea, a sexually transmitted bacterial infection that's increasingly resistant to drugs. The newfound antibiotic has shown promise in lab experiments involving a "vagina on a chip," researchers report in a new study.

"There's an urgent need to address antibiotic resistance in gonorrhea, and discovering new antibiotics is one of the key strategies," Dr. Jeffrey Klausner, a clinical professor at the University of Southern California who was not involved with the work, told Live Science. "It's exciting to see the application of AI in this area of public health."

Every year, over half a million people in the United States catch gonorrhea, which causes symptoms such as pain and fluid discharge. In severe cases, untreated gonorrhea can lead to infertility. If it's acquired during pregnancy, the infection can pose risks of miscarriage and early birth, and if it's passed to babies, it can potentially cause sepsis or newborn blindness if left untreated.

Gonorrhea bacteria, called Neisseria gonorrhoeae, often carry mutations that confer resistance to one or more antibiotics, limiting treatment options. The widely used antibiotic ceftriaxone remains the go-to drug, but resistance to this drug is soaring globally. For now, only 0.1% of cases in the U.S. are resistant, but rates are as high as 10% in some Chinese provinces and 27% in Hanoi, Vietnam.

Scientists are searching for novel antibiotics to tackle resistant bugs. To pinpoint new drugs, they typically screen large libraries of compounds to find ones that kill the bacteria. However, these experiments are slow and don't keep up with the pace at which new resistant strains are emerging.

So, in a study published June 17 in the journal Science Translational Medicine, researchers instead harnessed AI to expeditiously wade through a bevy of antibiotic candidates. They trained the AI models to spot potential antibiotics by studying patterns in the chemical properties of 1,755 clinically approved drugs that either do or don't treat drug-susceptible gonorrhea.

Next, they ran their trained models on a different set of approximately 6 million compounds, finding 213 possible hits. They whittled down that list by process of elimination, first by excluding compounds that were too similar to existing drugs in modeling experiments. Those drugs might not have worked against drug-resistant superbugs. Next, through lab experiments, they removed compounds that weren't potent enough against gonorrhea or were too toxic to human cells.

One of the most promising compounds that emerged was called MP20, which the researchers then put to the test.

Scientists often use laboratory mice to study new drugs, but it's difficult to establish a gonorrhea infection in mice. That's because the bacteria are so adapted to humans, study co-author Dr. Melis Anahtar, a physician scientist at Massachusetts General Hospital, told Live Science. (She is listed as an co-inventor on a provisional patent for MP20.)

Additionally, "there is a large push, especially in the U.S. administration, to move away from animals and to use more human-organ-mimicking systems" to test new drugs, she added. (Many scientists are developing such laboratory models of the human body for drug testing, but those models aren't necessarily ready to replace animal testing yet.)

For this study, the researchers tested MP20 using a vagina-on-a-chip model. This small device contains a layer of cells that mimics the lining of the vagina and a layer of fibroblast cells, which are found deeper in the tissue. These layers are connected to a nutrient-filled flow channel that mimics the bloodstream.

The researchers added gonorrhea bacteria to the chip's first layer, mimicking how the bug is sexually transmitted. Then, they administered MP20 through the flow channel, mimicking body-wide administration of the drug, to see if the antibiotic could cross through these different tissues and reach the bacteria.

"It could actually get through all those epithelial barriers and accumulate at a concentration that was sufficient to kill the gonorrhea," Anahtar said. MP20 worked just as well as the existing drug ceftriaxone; no bacteria were detected at all after treatment with either drug.

More experiments are needed before MP20 could potentially reach the clinic and help patients. "You need to demonstrate these chemical compounds are safe and are not going to have any human liver toxicity, kidney toxicity or severe side effects," Klausner said.

He noted that an antibiotic's effectiveness depends on the anatomical site infected by the bug. So the researchers will need to assess how effectively their compounds, if delivered via the bloodstream, can reach the penis, rectum, throat and vagina to treat gonorrhea at any of those sites.

Anahtar thinks AI models will prove pivotal in the quest for new drugs, especially now that chemists can prepare a wider array of compounds than ever before. "In 2012, I think there were a million compounds that you could just buy from commercial vendors, and now it's more than 70 billion," she said. She aims to grow and improve her models to test even more compounds at once.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 61-year-old man in Japan

The symptoms: The man visited a hospital because two months earlier, some foods and beverages began to taste extremely unpleasant to him. Over time, more foods had become difficult for him to stomach. Sour and salty flavors were the first to trigger disgust. Oily foods were next, followed by fresh vegetables, cold water and juice, warm water and, finally, sweets.

The man ate less due to the taste aversions, and he unintentionally lost a few pounds. He told doctors at the hospital that he felt lethargic, they wrote in a report of the case.

What happened next: The patient, who was a physician himself, reported that eight years ago, he had been diagnosed with bipolar disorder. For the prior three years, he had been managing the condition with lithium, a mood stabilizer commonly used to treat bipolar disorder.

He was taking a prescribed dosage of 800 milligrams per day and historically hadn't had any unusual side effects. (This is slightly higher than the typical dose recommended for chronic management of bipolar disorder, but that said, doctors may tweak patients' doses based on their individual needs.)

The diagnosis: Doctors performed bloodwork and found that the level of lithium in the patient's blood was 1.28 milliequivalents per liter (mEq/L). Safe levels of lithium are between 0.6 and 1.2 mEq/L; any higher than that can cause a condition called lithium toxicity, which can be fatal if untreated.

When the doctors checked the man's medical records, they found that prior to the onset of his symptoms, the levels of lithium in his blood were between 0.4 and 0.9 mEq/L. In the report, the authors did not investigate the cause of the toxicity, nor did they hypothesize as to why lithium was accumulating in the patient's blood.

The treatment: The doctors told the man to stop taking lithium, and they instead prescribed another mood-stabilizing drug, called valproate. As the lithium levels in his blood dropped, the patient's energy returned and the foods and beverages that previously disgusted him recovered their normal flavors. Notably, this happened in the reverse order that their flavors had changed.

At a follow-up visit one year later, the man was still taking valproate and his symptoms of fatigue and taste changes had not returned.

What makes the case unique: Although they're uncommon, side effects of lithium use can include confusion, increased thirst, frequent urination, irregular or slow heartbeat, tiredness and weight gain. Rarer side effects include dizziness, headaches, vision problems and heat loss in the arms and legs. Lithium toxicity, also known as lithium intoxication, is known to increase the risk of these adverse symptoms.

Changes in a patient's sense of taste while taking lithium have been recorded in just a handful of reports dating to the 1970s and 1980s. One patient lost the ability to taste salt, while another "noticed a strange and unpleasant taste associated with butter and celery."

Nevertheless, "it has not been generally known that lithium can lose or change taste in some patients," the case report authors wrote. Based on their findings, they suggested that in the future, taste loss or changes in taste perception should be flagged as a potential indicator of mild lithium intoxication.

This article is for informational purposes only and is not meant to offer medical advice.

Using drugs to induce a hypothermia-like state may slow stroke-related brain damage, according to a new study involving lab animals and human patients.

The study used two existing drugs: the antipsychotic chlorpromazine and the sedative promethazine, called "C+P" when they're used together. This drug combo induced hypothermia and protected brain tissue in mouse and monkey models of stroke.

Additionally, an infusion of C+P was safe in an early trial including 32 human stroke patients, causing no notable side effects. However, no significant improvements in stroke outcomes were reported in a paper describing the results, which was published June 17 in the journal Science Translational Medicine.

More research is needed to determine what benefits C+P treatment may offer stroke patients. But the research sheds new light on the metabolic dynamics believed to be responsible for hypothermia's therapeutic effects, said Dr. Eric Landsness, an assistant professor of neurology at the Washington University School of Medicine in St. Louis who was not involved in the work.

"What's exciting about this study is that it's clear that it's not just the hypothermia, but it's the hypometabolism," said Landsness, who reviewed the paper before it was published.

Brain freeze?

The researchers tested C+P as a therapy for acute ischemic stroke, in which blood flow to the brain is blocked. Ischemic strokes are the most common form of stroke, accounting for over 85% of cases; "acute ischemic stroke" specifically refers to the medical emergency brought about by a sudden loss of blood flow to the brain and corresponding loss of neurologic function.

When blood flow is restored through a therapy called reperfusion treatment, "you can get significant injury from a lot of processes that were set in motion during the ischemia," said Dr. Patrick Lyden, a professor of physiology and neuroscience, neurology, and neurosurgery at the University of Southern California Keck School of Medicine who was not involved in the study.

To protect brain tissue from this double whammy of ischemia and reperfusion injury, some researchers have tried to harness hypothermia, which is "one of the most powerful ways of protecting the brain that we've ever studied in lab animals," Lyden told Live Science. "It's the standard by which all other brain protectants are measured."

In hypothermia, body temperature drops below 95 degrees Fahrenheit (35 degrees Celsius). Under normal circumstances, this can be very dangerous because the cold can slow down the heart and nervous system to the point that the body's cardiac and respiratory systems fail.

But one of the biggest theories for why hypothermia works in a therapeutic context is that it slows down our metabolism, similar to what's seen in animals during hibernation, Lyden said. "Because the metabolism is slowed, the death process in the brain is also slowed down."

Therapeutic hypothermia can protect the human brain following cardiac arrest, and it is also sometimes used to treat newborns with hypoxic ischemic encephalopathy, an injury that blocks blood and oxygen to the brain around the time of birth. However, studies of hypothermia in adult stroke patients have been less successful, Lyden said.

The C+P approach may be a more effective way to slow metabolism in stroke patients, the researchers hypothesized. In previous experiments, C+P reduced neuroinflammation in rodent models of stroke, possibly through changes in metabolic activity independent of hypothermia.

In the new study, the treatment was compared with two other methods of reducing core temperature in mice: a different drug, called adenosine 5'-monophosphate, and surface cooling using cold water and ice packs. While all three approaches induced hypothermia in the mice, only C+P treatment reduced their overall oxygen consumption and energy expenditure, two important indicators of slowed metabolism.

The paper highlights metabolism as more than a mere secondary effect of hypothermia, Landsness said; it's a process worth studying in its own right.

In mice, C+P treatment reduced the burning of sugar by the brain and brown fat, which burns fuel to generate heat. The treatment was also associated with less brain tissue damage and lactate accumulation, which can drive cell death, after stroke. These effects were also observed in rhesus monkeys treated with C+P.

According to the small safety trial with humans, the metabolic effects of C+P appear to extend to people.

The researchers measured lower levels of metabolism-associated proteins in the blood of patients who received the highest dose of the treatment tested. These were also the only patients to experience a significant decrease in body temperature at four hours after treatment, although their temperatures never dipped into true hypothermia. (Temperatures did fall that dramatically in the mice and monkeys.)

In people, C+P infusion did not reduce the degree of brain damage seen 72 hours after treatment, nor did it affect the participants' ability to perform daily activities without assistance after 90 days. Alongside the C+P treatment, the patients had also received standard reperfusion therapies.

The study authors, based at Capital Medical University in Beijing, did not respond to Live Science's request for comment. In their paper, they wrote that future trials could potentially establish the protective value of the C+P treatment in stroke.

In the current study, C+P did not trigger notable side effects in humans, but Lyden worried that the medications may still pose a risk of worrying effects. The two drugs could potentially interact in ways that cause symptoms like muscle spasms, seizures or changes in heart rhythm, for example. For that reason, it may be best to find different drugs that still slow metabolism but don't come with those risks, Lyden suggested.

To find an alternative to the C+P regimen, researchers will need a better sense of how the drugs exert their effects. The new paper "happened to fall upon a drug [combo] that happens to induce hypothermia and hypometabolism, but we don't necessarily know why," Landsness said. His lab is studying the neural circuits involved in hypothermia and hypometabolism, which could reveal new therapeutic targets.

This article is for informational purposes only and is not meant to offer medical advice.

See how much you know about the most complex organ in the human body with our brain quiz!

The causes of inflammatory bowel disease (IBD) are poorly understood, but now, scientists have pinpointed a runaway immune response that may underlie the condition in some patients.

IBD, which is characterized by chronic inflammation in all or part of the digestive tract, affects millions of people worldwide. Its principal forms are Crohn's disease, which can occur at any point of the gastrointestinal tract, and ulcerative colitis, which affects only the colon and rectum.

While IBD patients may experience similar inflammation, the underlying cause may be different. Understanding those differences could potentially unlock new, targeted angles for treatment, researchers concluded in the new study.

"Identifying these patients early could eventually allow clinicians to move more quickly toward therapies that address the specific mechanism of disease rather than relying on a trial-and-error sequence of medications," Dr. Brad Pasternak, medical director of the IBD Clinic at Phoenix Children's Hospital, who was not involved in the work, told Live Science in an email.

A potential subtype of IBD

The genetics of IBD are complex, with past studies linking the condition to 300 "hotspots" throughout the genome. The strongest known genetic risk factor for ulcerative colitis is a gene variant called HLA-DRB1*01:03, but how this variant contributes to IBD has been unclear.

The new study, published June 10 in The New England Journal of Medicine, helps connect the dots.

A major clue had emerged in previous research by the same team, which tested the blood of two children with IBD. The kids had autoantibodies — immune proteins that target the body itself rather than germs — that were neutralizing a key anti-inflammatory protein called interleukin-10 (IL-10).

IL-10 normally works by inhibiting the secretion of pro-inflammatory proteins, so patients whose bodies block IL-10 are effectively releasing a brake that should be holding off inflammation, Pasternak said.

The researchers suspected that these autoantibodies could be one factor causing IBD. In their latest study, they sought to find out whether more IBD patients had the same autoantibodies.

The study included data from over 4,900 people with IBD and over 1,000 without the condition. Using two separate lab tests, the researchers analyzed blood samples from both groups, finding the autoantibody in 173 of the IBD patients, or about 3.5%. The autoantibody was virtually absent from the blood of the comparison group.

Then, in lab experiments, the team exposed immune cells to blood from the IBD patients who carried the autoantibody. This lowered the amount of IL-10 while triggering a pro-inflammatory response.

Study co-author Dr. Holm Uhlig, a pediatric gastroenterologist at the University of Oxford, told Live Science that identifying what drives the formation of the autoantibodies will be "a question of intense interest." For now, though, their data suggests that patients carrying HLA-DRB1*01:03 are far more likely to have autoantibodies blocking IL-10 than those without the variant.

Historically, the variant has been associated with severe IBD that can require major surgery to treat. "Currently, autoimmune responses are not at all part of the therapeutic repertoire, and that's why we feel it's a relevant study," Uhlig said.

Uhlig also noted that the subgroup of 3.5% of patients they identified is a "significant number," given the large overall number of IBD patients worldwide.

In general, many IBD patients are currently treated with therapies that broadly suppress inflammatory pathways, Pasternak said, but not everyone responds to treatment. This study points to a potential way to someday tailor treatments to the mechanism driving specific patients' diseases, he said.

Aside from offering personalized treatments for IBD patients, Uhlig said their findings may improve diagnoses.

"Patients could undergo genetic testing already in the early stage of their disease diagnosis," he said, "and then it would determine their susceptibility to develop autoantibodies."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 29-year-old woman in Lithuania

The symptoms: The woman had been trying to conceive with her male partner but had not become pregnant. Two rounds of in vitro fertilization (IVF) also failed to produce a pregnancy, but gynecological exams did not find any underlying causes for why she was unable to become pregnant. (When the patient's doctors described the case in a report, they did not mention if any fertility tests were also conducted on her partner.)

However, the woman had a history of asthma and sensitivity to inhaled allergens, such as mold, cat fur and dust. So she visited a medical facility to see if her allergies might be affecting her fertility.

What happened next: At the facility, blood tests revealed that the woman had unusually high amounts of eosinophils, a type of white blood cell that defends the body against allergens. Skin tests showed that, in addition to the woman's known allergy triggers, she was sensitive to mites, pollen from weeds and grasses, and allergens from insects and dogs.

The patient was especially sensitive to a protein called Canis familiaris allergen 5 (Can f 5), which is found in dog dander and urine. Sensitivity to Can f 5 can also indicate sensitivity to similar types of proteins found in human semen, the doctors wrote in the report.

In an interview with an allergist at the facility, the patient confirmed that she experienced nasal congestion and sneezing after unprotected intercourse with her male partner. These symptoms were previously overlooked by other specialists during consultations about her inability to conceive, she reported.

The diagnosis: Doctors then conducted further allergy tests using samples of semen collected from the woman's partner. The patient's allergic response confirmed the doctors' suspicions that she had a human seminal plasma allergy. (Seminal plasma is the fluid component of semen that carries the sperm cells.)

Sensitivity to semen "is a potential cause of female infertility," because such allergies can trigger inflammation in reproductive organs, according to the report. It's not immediately clear if the allergy somehow complicated the woman's IVF treatments, as well, given semen would not have been present in the implanted embryos.

The treatment: Barrier contraception — namely, condom use — is the most common intervention for a semen allergy. However, the patient was still eager to conceive with her partner, so she rejected that strategy.

The only known treatment for reducing sensitivity to semen involves introducing the fluid into the patient's body in gradually increasing concentrations, to build up their tolerance to the allergens. But this course of treatment was unavailable in Lithuania, the doctors wrote. Instead, they recommended that the woman take antihistamine medication before intercourse to reduce the severity of her allergic reactions.

She followed their instructions but found this approach "ineffective," the doctors wrote. During a follow-up visit three years later, the woman said that she had still been unable to conceive. What's more, new allergic symptoms now appeared after contact with her partner's semen, including a burning sensation in her vulva, puffy eyelids and watery eyes. No further treatments were recommended, according to the report.

What makes the case unique: Worldwide, medical experts have documented about 80 cases of human seminal plasma allergy, and there is still much to be learned about its impact on pregnancy, especially in the presence of other health-related issues that could hinder conception.

The causes of infertility are often difficult to pinpoint. Therefore, "this case serves as a reminder that seemingly unrelated allergic conditions, when combined, can contribute to reproductive health challenges, warranting comprehensive evaluations," the woman's doctors wrote.

This article was first published July 23, 2025.

This article is for informational purposes only and is not meant to offer medical advice.

As summer in the U.S. heats up, people become more diligent about protecting their skin from the sun. Another option for doing so will soon be available.

On June 9, 2026, the U.S. Food and Drug Administration approved the first new sunscreen ingredient to be permitted for over-the-counter consumer use in the U.S. since 1999 — a chemical called bemotrizinol.

Bemotrizinol isn't new — consumers in Europe and Asia have used it for decades. Some are hailing its long-overdue approval and arrival onto the U.S. sunscreen scene.

I am a biomedical engineer studying skin science — including the damaging effects of the sun's rays. To understand what bemotrizinol does and how it fits in with products already available to consumers in the U.S., let's take a tour of the physics of sunlight and sunscreens.

A short primer on sunlight

Our planet is irradiated by a yellow dwarf star 93,000,000 miles away that we fondly call the sun. It radiates light from its surface at a temperature of about 10,000 degrees Fahrenheit.

The Earth's atmosphere blocks most of the sun's radiation. Of the rays that get through, about half consist of infrared light — which gives you that warm feeling you feel on a sunny day — and 40% visible light, which you are probably familiar with as daylight.

About 10% of those rays are ultraviolet, or UV, light. UV light has the shortest wavelengths of the three types. That makes it the most dangerous — it's invisible and can damage living tissue.

Ultraviolet damage

Physicists further categorize solar UV light into several types, based on the wavelength, which is measured in nanometers. About 95% of it is UVA (315-400 nm) and 5% is UVB (280-315 nm). Sunscreens need to be able to block those rays from penetrating the skin.

The sun also emits two other types of UV light — UVC (200-280 nm) and vacuum UV (100-200 nm) — but these are stopped by the atmosphere, so sunscreens do not typically need to be able to block them.

Scientists used to think only UVB was harmful because UVB rays cause sunburns. But today, researchers know both types of UV can damage the skin.

UVB, with its shorter wavelength, has more energy, but UVA can penetrate the skin more deeply. And all UV can degrade the integrity of your skin, damage the structure of your DNA and cause skin cancer.

The only natural safeguard your body has against UV light is a microscopically thin layer of a pigment called melanin in your epidermis. The skin produces more melanin when exposed to the sun — that's what tanning is.

This extra melanin does protect the skin, but not fully. That's why protecting your skin with sunscreen is so important.

Sunscreens old and new

Sunscreens come in two different forms — mineral and chemical.

The first chemical sunscreen, developed in 1891, was an ointment made from quinine — a plant-derived compound that makes tonic water bitter.

Chemical sunscreens cover the skin in a transparent coating, acting like a solar sponge. They absorb UV photons and undergo a harmless chemical reaction, then dissipate the energy as heat. Bemotrizinol falls into this category.

Mineral sunscreens such as zinc or titanium oxide ward off the sun's rays by forming a protective film that also absorbs most UV light, but reflects some of it. Unlike chemical sunscreens, the film absorbs the light naturally, without a chemical reaction — which is why they are often visible as a white film on the skin.

Chemical sunscreens that have been available in the U.S until now combine ingredients like avobenzone, the most widely used UVA filter, with UVB filters such as octinoxate, octocrylene octisalate and homosalate. Working together, these substances protect the skin against the broad spectrum of ultraviolet rays.

These sunscreens are only effective for a short time because they are degraded by the chemical reactions they undergo, which means they must be frequently re-applied.

Another important element of sunscreen — whether mineral or chemical — is its Sun Protection Factor, or SPF. This number tells you how well a sunscreen prevents your skin from burning — in other words, what amount of UVB rays it absorbs.

An SPF of 2 would mean a sunscreen cuts your exposure to UVB rays in half, filtering out 50% of those rays. An SPF of 30 means the sunscreen lets just 1/30 of the rays penetrate your skin - which is 3.3%. So it blocks about 97% of the UVB rays.

Dermatologists generally recommend using a sunscreen with an SPF of at least 30.

Benefits of bemotrizonol

Bemotrizinol, while new to the U.S., isn't a new compound. European regulators approved it in 2000. Chances are, if you brought back sunscreen from a vacation in Mexico, Europe, Canada or South Korea, you may even have some laying around your house.

One benefit of bemotrizinol is its ability to filter both UVA and UVB rays, so it doesn’t have to be mixed with other products to do the job.

It has some other beneficial features as well. First, its molecules prefer to sit on the surface of the skin rather than being more readily absorbed into the bloodstream, which can occur for some formulations.

Such absorption has raised concerns that sunscreens might be harmful — though this has not been demonstrated in people, it may discourage some people from using it.

Bemotrizinol also does not degrade as readily in the sun than other chemical sunscreen products. That photostability means it can last for four to eight hours, rather than having to be applied every two hours or so.

Regardless of the type, as a skin scientist I can say with certainty that any sunscreen is better than none. Your skin does an excellent job protecting you from the world outside — so make sure you protect it in return.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

For most people, a minor cut or scrape is no big deal — the body heals itself quickly, and antibiotics can deal with any infections. But some wounds, such as severe burns and diabetic ulcers, are prone to bacterial infections that can become resistant to antibiotics.

"Diabetic wounds are very difficult to heal and people live with these wounds for pretty much the rest of their life," says Vitaliy Khutoryanskiy, a materials scientist at the University of Reading in the United Kingdom.

To address this problem, scientists are developing new ways to treat infected wounds using specially designed nanomaterials that are activated with light and deliver precise antimicrobial action. The approach has shown promise in reducing infection and accelerating wound healing in experiments on mice and pigs but has not yet been tested in people.

Chronic, non-healing wounds offer ideal conditions for the formation of resilient biofilms, which delay healing and significantly raise the risk of amputation. The vast majority of such wounds — over 78 percent — have these stubborn layers of bacteria, which are often antibiotic-resistant.

The new light-activated nanomaterials offer a different way to eradicate bacterial infections, by converting light into localized heat, or by reacting with oxygen present in the tissues to produce toxic molecules that kill bacteria with minimal damage to the surrounding tissue.

Our skin can naturally absorb tiny amounts of radiation but with the help of specially designed nanomaterials, says Zhenpeng Qin, a materials scientist at the University of Texas at Dallas, "you can heat the tissue to a higher temperature." The heat weakens the bacteria and helps with tissue repair. Qin, who coauthored an exploration of the technique in the 2024 Annual Review of Biomedical Engineering, notes that similar, light-triggered therapies have been used to deliver toxins to target certain skin and esophageal cancers, but they have not been applied extensively to wound care.

In one promising study with wounds, Raffaele Mezzenga, a materials scientist from ETH Zurich, and his colleagues began with a naturally occurring antimicrobial protein called lysozyme, which was extracted from egg whites. They engineered the protein into a gel mixed with a light-absorbing dye. In the presence of near-infrared light, the dye heats up, melting the gel and releasing active lysozyme. When the light is turned off and the material cools, the lysozyme reverts to its inactive form.

When the team applied the gel to wounds in mice and pigs, they found it eradicated more than 95 percent of the bacteria present. The wounds also healed more quickly, because the lysozyme — which is toxic for healthy cells, too — was activated in the wound only when irradiated with light, saving the skin from overexposure. To boost healing still further, the team added magnesium ions to the gel, which prime immune cells called macrophages to shift from an inflammatory state to one that promotes healing. "The healing will be much faster because you kill the bacteria and heal the wound at the same time," says Mezzenga.

Since bacterial biofilms are especially persistent on the surfaces of medical implants — where they can cause recurring infections and sometimes require repeated surgeries or even amputations — the team also tested their gel on infected prosthetic joints in mice. They injected the gel around an infected implanted needle and shone near-infrared light through the skin. The treatment cleared biofilms and eradicated about 99 percent of bacteria around the implant, while preserving bone tissue.

In another recent study, scientists from Gannan Medical University and Shanghai University in China treated wounds using a nanomaterial made of gold nanoparticles and graphene-oxide "quantum dots," which are tiny, carbon-based semiconducting particles. When irradiated with blue light, the gold particles absorb the light energy and convert it into heat, while graphene oxide helps to transfer electrons across the material. This boosts reactions that produce toxic, unstable molecules called reactive oxygen species that react with structures on bacterial membranes and destroy them.

When the scientists added this material to a bacterial solution and shone blue light on it for 10 minutes, the mild heat and reactive oxygen species worked together to cause bacterial membranes to disintegrate. Using a stain that distinguished dead from living bacteria, the researchers confirmed that the treatment had killed 97 percent of the bacteria.

Testing the nanomaterial in mice revealed that after nine days, the wounds on treated mice showed 99 percent healing, while those of untreated mice showed only about 70 percent healing.

While these techniques have shown promise in the lab, further work will be needed before they can be applied to people. "There is still some way to go," says Lars Kaestner, a biologist at Saarland University in Germany. To be useful in a clinical setting, he notes, researchers would need to do extensive safety testing and lower the cost of the nanomaterials.

Nevertheless, the idea provides hope for patients with chronic wounds that fail to heal with conventional antibiotics, particularly as drug-resistant infections become more common in hospitals and diabetic care.

"It's a good concept," says Qin. "Wound healing and antibacterial resistance are very big challenges. And I think any advance that we can make in these areas would be welcome."

This article originally appeared in Knowable Magazine, a nonprofit publication dedicated to making scientific knowledge accessible to all. Sign up for Knowable Magazine's newsletter.

The patient: A 31-year old man in Louisiana

The symptoms: When the patient reached the hospital, he was bleeding from the mouth and had severe neck pain and stiffness. Upon examining the man, his doctors noted a tear in the back of his throat on the right side.

What happened next: The man, a sports fisherman, had been brought to the hospital by boat and helicopter after an accident during an ocean fishing trip. He had caught a white marlin (Kajikia albida), a type of large fish with a long pointy "bill," weighing approximately 60 pounds (27 kilograms). This species can grow up to 180 pounds (82 kg).

As the man leaned over the side of the boat to release the hook from the fish, it jumped and struck him in the mouth with its bill, sending the man tumbling backward into the boat. He felt pain in his neck, which then radiated into his spine.

At the hospital, an X-ray of the man's upper spine did not reveal any abnormalities. However, his intensifying spinal pain and neck stiffness prompted one of the doctors to order a computed tomography (CT) scan of the same area. In the CT scan, physicians noted "a wedge-shaped, hyperdense object," they wrote in a report of the case. The object had penetrated the back of the man's throat and entered his spinal canal. It stuck there, piercing the foramen magnum — a large hole at the base of the skull that the spinal cord passes through.

The diagnosis: The doctors immediately performed surgery on the man to remove the penetrating object. They administered general anesthesia, and the surgeon used retractors — instruments that hold wounds open — to expose the object, which turned out to be the broken tip of a fish bill.

The treatment: The sharp bill fragment was so firmly wedged in the man's skull that the surgeon had to make an additional incision above the man's topmost vertebra in order to remove it, pulling it out along the path of entry. It measured about 1.4 inches (3.5 centimeters) long.

After the fragment was removed, the patient was given five different types of antibiotics both to prevent infection from microbes found in the throat and from bacteria that are unique to marine environments. He was discharged eight days later and continued to take multiple antibiotics for the next two weeks.

At his final follow-up visit, the man had fully recovered and showed no lingering neurological symptoms.

What makes the case unique: In 1848, doctors published the first medical case study of a skull injury from a foreign object: a gunpowder explosion had sent an iron bar through the skull of railroad worker Phineas Gage. Gage recovered, but he exhibited personality changes that doctors attributed to his significant brain injuries.

In another notable case, published in 1895, a man had tripped and fallen face-first onto an oilcan. The spout penetrated his cheek and became stuck at the base of his skull, causing temporary incontinence and permanent memory loss.

Since those 19th-century cases, physicians have reported instances of cranial trauma in different parts of the skull and from a variety of objects, including a crochet hook, a pitchfork, a bike key and a harpoon.

This man's case is the first reported instance of an injury to the foramen magnum, as well as the first injury caused by a fish bill, according to the report.

This article is for informational purposes only and is not meant to offer medical advice.

It's after dark, and the lights go out; a thunderstorm has knocked out your power. At first, it's pitch-black. But slowly, after a while, the light from the moon makes it possible to see your surroundings. The light didn't change; your eyes did.

But why does it take our eyes so long to fully adjust to the dark?

It has to do with the types of cells in the eye and how they evolved, experts told Live Science.

Our eyes use two kinds of cells to sense light. These cells, known as photoreceptors, are called rods and cones, based on their shapes, Alapakkam Sampath, a retinal neuroscientist at UCLA, told Live Science.

Cones are responsible for color vision. Humans possess three kinds of cone cells, which detect red, green or blue light. The colors people can see are a mix of red, green and blue, Anand Swaroop, chief of the Neurobiology Neurodegeneration & Repair Laboratory at the National Eye Institute, told Live Science.

Rods cannot discriminate colors, but they are far more sensitive to light. Each is capable of detecting a single photon, or particle of light. "Rods are what allow you to see in dim light," Swaroop said.

The extraordinary sensitivity of rods has a price, though: Once each rod detects a photon, it can take up to an hour for it to regenerate its ability to see light, Johan Pahlberg, chief of the photoreceptor physiology group at the National Eye Institute, told Live Science.

The compound that helps rods sense light is called rhodopsin, which is derived from vitamin A, Sampath said. Once each rhodopsin molecule absorbs light, it gets "bleached," meaning it can no longer detect light.

Specifically, rhodopsin is made of two compounds: opsin and retinal, Pahlberg said. When rhodopsin absorbs light, the retinal changes from bent to straight and detaches from the opsin. This retinal eventually makes its way into a part of the eye known as the retinal pigment epithelium, where it can get repaired and resume a bent shape. This retinal can then make its way back to an opsin and reattach to create a functional rhodopsin.

If all of the rods in a human eye are bleached, it may take 45 minutes to an hour for all of them to regenerate, Pahlberg said. However, some rods may regenerate within 10 to 15 minutes to grant some level of vision in dim light, he added.

Rods and cones line the retina, the back part of the eyeball. Rods outnumber cones in most mammal retinas. "In each human eye, there are roughly 6 million cones and 100 million rods," Swaroop said. Sampath noted that "since it takes a lot of time for rods to regenerate, your eyes have a huge number of them to compensate."

Cones are found mostly in the center of the retina, where the eye's lens focuses most of the light it receives, while rods dominate the rest of the retina, Sampath explained. This reflects how during the day, we rely mostly on cone cells for our vision. "Rods are mostly not functional at all during that time," he said.

The human eye does have a quicker way to adjust somewhat to the dark. It can enlarge the pupil, the dark hole at the front of the eye, to let in more light, explained Mark Fairchild, professor of color science at the Rochester Institute of Technology in New York, in an article in The Conversation. However, the vast majority of the eye's adaptation to darkness is due to its rods, and the long amount of time it takes for rods to regenerate explains why it takes so long for eyes to fully adapt to the dark.

Before artificial lighting, humans would typically not experience quick shifts from light to dark. Instead, the ability for human eyes to adapt to the dark would have relied on the setting of the sun, which might take about the same time as rod cells take to regenerate. "There was no evolutionary pressure for it to be faster," Sampath said.

Rods are the most vulnerable cells in the retina to disease and dysfunction, Pahlberg said. This is why older adults often have trouble driving at night. "My colleagues are developing a diagnostic test as a normal part of an eye exam to measure the human adaptation to the dark to see how it changes with age," Sampath noted.

High estrogen in the brain's memory center may worsen one's resilience against traumatic events, swaying the tendency to develop memory problems or post-traumatic stress in the aftermath, a recent study in mice suggests.

The research, published in April in the journal Neuron, explored the effects of estrogen in the mouse brain. It zoomed in on the hippocampus, a key part of the brain involved in learning and memory. Both male and female mammals produce significant amounts of estrogen in the hippocampus, despite it often being framed as a "female" hormone.

"We're so biased to think of female high estrogen, male low estrogen," said study co-author Elizabeth Heller, an associate professor of pharmacology at the University of Pennsylvania Perelman School of Medicine. But "in this local brain region, where you have local production of estrogen, actually sometimes the males are higher than the females depending on the female's cycling," Heller told Live Science. Estrogen levels in the female hippocampus rise and fall in line with the body-wide hormone cycle, while its levels in the male hippocampus remain fairly steady.

The study suggests that these local estrogen concentrations may influence one's vulnerability to memory problems following major acute stress. Although the research was conducted in mice, the authors think it likely has relevance to humans.

"I think this is highly translatable," study senior author Dr. Tallie Z. Baram, a professor, developmental neuroscientist and child neurologist at the University of California, Irvine, told Live Science.

Estrogen isn't always a memory booster

Traumatic experiences can cause memory disturbances, including difficulty remembering specific personal experiences and having fearful reactions to formerly safe, familiar situations. When these issues persist and are accompanied by intrusive memories of the traumatic event, they are classified as post-traumatic stress disorder (PTSD).

About 10% to 12% of women experience PTSD in their lifetime, compared with 5% to 6% of men. Some of that difference may stem from variance in men's and women's lived experiences; for instance, women have higher rates of sexual assault at young ages than men do. Biological differences between women and men are another potential factor, but their contribution to the phenomenon is poorly understood.

The new study highlights hippocampal estrogen as one difference that might matter. "The research has uncovered important new avenues for research on PTSD," Victoria Luine, a professor emerita of psychology at Hunter College in New York City who wasn't involved in the work, told Live Science in an email.

In the study, researchers simulated acute traumatic events by exposing lab mice to multiple stressors at the same time, including bright lights, loud music and the odors of other stressed-out mice. They ran the mice through various memory tests before and after the stressful experience and compared these rodents with a group that did not experience such stressors.

Compared with unstressed mice, the stressed-out male mice performed worse on the various memory tests, and those deficits persisted for weeks. "Even a month later, they had a memory deficit — so it's a really perseverative effect," Heller said.

A similar pattern was seen in female mice that were stressed out during proestrus, the phase of their hormone cycle when estrogen peaks and the body prepares for ovulation. Both sets of mice learned to associate certain cues with the stressful experience and avoid them, with females being more sensitive to those cues than males were.

But interestingly, female mice that were stressed during estrus, when estrogen plummets and ovulation occurs, showed resilience. Their behavior and memory remained comparable to those of unstressed mice. "The female mice that had low levels of estrogen laughed it off — they were completely protected," Baram said.

Studies suggest hippocampal estrogen levels are similar in male and proestrus female mice, while estrus females have lower levels. The researchers confirmed this using a technique called mass spectrometry, finding that estrus mice had half the amount of hippocampal estrogen that the males and proestrus females did.

In this context, that lack of estrogen in the hippocampus appeared to guard against the negative effects of stress. This finding was surprising, Baram noted, because estrogen is generally thought to promote memory function in both sexes and declines in estrogen, as seen during menopause, are tied to memory problems. That said, menopause takes place over a much longer timeline than the female mouse hormone cycle, which takes only four or five days.

A connection to DNA

Why do estrogen levels matter for memory? "Estrogen receptors directly control gene expression," Heller said. By binding to its receptors, estrogen turns the activity of certain genes up or down.

Heller's lab studies mechanisms that control gene activity in the context of psychiatric disorders. One of those mechanisms is chromatin remodeling, meaning changes in how DNA is packaged in a cell that can shift which genes can be activated at a given time. A portion of the chromatin can be "open," exposing genes to machinery that turns them on, or "closed," which typically shuts genes down.

It turns out that the high hippocampal estrogen in male mice and proestrus female mice opens up their chromatin in a way that might leave them vulnerable to memory issues ushered by severe stress. Female mice in estrus, by contrast, have a totally distinct chromatin profile that appears to be protective.

"We can see that the function of many of those [open] genes relates to synapse biology," Heller said. Synapses are the points at which different neurons meet and exchange electrical signals, and they're central to the physical structure of memories in the brain.

It may be that, in most circumstances, it's useful to have high levels of hippocampal estrogen because they "open" the chromatin, enabling the hippocampus to forge new memories quickly in response to new experiences, Baram noted. But when these experiences consist of severe acute stress, "that same plasticity, that same ability of the brain to learn, turns problematic," she said. If the results carry over to humans, women may be particularly vulnerable to these memory impacts in certain phases of their menstrual cycles or points in their lifespans when estrogen is high.

In males and females, different flavors of estrogen receptor were responsible for the stress-induced memory issues. The reasons for this difference will be a matter of future study, Baram said. Additionally, future research could attempt to pinpoint exactly where the different estrogen receptors are located throughout the hippocampus, Heller said.

The study provides a "strong demonstration that estrogens drive sex-dependent, stress-induced changes in chromatin networks which can dramatically alter neural functions like memory," Luine said. What's more, "these results present cogent evidence that sex is a powerful biological variable."

Historically, female lab animals were excluded from studies because it was thought that their hormone cycles were too complex and would muck up the findings. The field of neuroscience exemplified this trend. In recent years, the U.S. National Institutes of Health (NIH) has required that scientists take sex differences into account when designing NIH-funded human and animal studies, but progress has been slow on both fronts — and current federal leadership has signaled a lack of support for the initiative.

It's important to include both sexes in research to truly understand how the brain functions and responds to external factors, like stress, Luine said. "An important aim of this and other studies is to protect humans against PTSD," she added, and this study strongly suggests preventive treatments for PTSD might need to be tailored by sex.

Beyond PTSD, Baram thinks the research could have implications for women's risk of aging-related memory problems and dementia.

The decline of estrogen in menopause is thought to raise this risk, but prior to menopause comes perimenopause — a period with massive spikes in estrogen. The study's findings hint that if stress shows up during perimenopause, the combination of stress and high estrogen levels may contribute to memory problems. Thus, perimenopause may represent another time when women are particularly vulnerable to memory disturbances, Baram suggested.

"We need to start thinking a little bit differently," she said. "What is it about women at that stage in life that makes them more vulnerable to memory loss with aging?"

This article is for informational purposes only and is not meant to offer medical advice.

This article was first published May 4, 2026.

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The patient: A 28-year-old woman in New Hampshire

The symptoms: In March 2020, the woman developed a high fever, chest tightness, shortness of breath and diarrhea, and she lost her sense of smell and taste. She also experienced coughing fits so intense that they caused her to faint. Based on these symptoms, her primary care provider diagnosed her with COVID-19, although she was not formally tested for the illness due to the lack of diagnostic testing available at the time.

After her diagnosis, she did not seek further medical care due to concerns about out-of-pocket costs, according to a report of the case.

What happened next: Three weeks after her symptoms started, the patient felt well enough to work from home. However, four weeks after that, many of her symptoms returned. She also noticed new feelings of disorientation and felt that "something was off with faces." Her primary care doctor suggested she go to an emergency room, where a CT scan was taken of her brain. The scan didn't show any active bleeding, the report notes, and she was discharged.

In June 2020, the patient spent time with family for the first time since catching COVID-19 and found she could not recognize her father or visually distinguish him from her uncle. She still recognized people by their voices, though.

The patient worked part time as a portrait artist; she used to be able to check her reference photos every 15 to 30 minutes but found she now struggled to hold the details in her mind. She told doctors that "faces are like water in my head," according to the case report.

The patient also had trouble doing everyday tasks, such as navigating her local grocery store or finding her way back to her car in a parking lot. In November 2020, she also started having balance issues and frequent migraines.

The diagnosis: Based on her wide-ranging and relapsing symptoms and her suspected history of COVID-19, doctors diagnosed the patient with post-acute sequelae of COVID-19 (PASC), now known as long COVID. They diagnosed her difficulties with recognizing faces as "face blindness," or prosopagnosia.

Roughly 2.5% of the general population is thought to be born with some degree of face blindness, while others can acquire the condition later in life. The exact number of people with acquired prosopagnosia is unclear, but some estimates suggest roughly 1 in 30,000 people in the U.S. are affected.

Many people with acquired prosopagnosia also have issues navigating familiar spaces. That was also the case with this patient, likely due to the "proximity of brain regions critical for scene and face processing," the case report authors noted.

To assess the extent of the patient's prosopagnosia, doctors had her complete several tests of facial memory, which asked her either to memorize strangers' faces or recognize celebrities' faces. The patient performed markedly worse on these tests than 10 women of similar age who were used as a comparison group.

However, she performed as well as the comparison group on other types of cognitive tests, suggesting her deficits were fairly specific to faces. She also got normal scores on tests of facial perception — the ability to recognize that a face is a face — so her face blindness seemed tied more to memory deficits for faces, the report authors said.

The treatment: The case report does not detail a specific course of treatment, and in general, few treatments exist for face blindness. If there's a clear cause for the deficit — such as a tumor in a key part of the brain for facial processing — addressing that underlying issue can help reverse acquired face blindness.

If the condition ends up being permanent, there are various strategies that can help patients cope. For instance, "perceptual training" can improve patients' ability to identify and remember the features of a person's face. Additional strategies include training people to use other cues, like voices and social context, to identify people.

What makes the case unique: In this patient's case, the report authors suspect that her COVID-19 infection triggered her face blindness either acutely or in the aftermath of the infection.

Various infections have been tied to face blindness; both bacterial meningitis and Whipple disease (caused by the bacterium Tropheryma whipplei) have been flagged as culprits, although such cases are uncommon. In a second known case involving COVID-19, a different person developed face blindness after an infection but had also had a stroke in the right hemisphere of their brain, a known cause of prosopagnosia.

The 28-year-old woman, by contrast, wasn't thought to have suffered a stroke, and it's unclear exactly how COVID-19 led to her facial processing issues.

The case report authors surveyed more than 50 other people with long COVID, to see if they also had signs of face blindness. While many showed general declines in visual recognition and navigational abilities, the group didn't have a specific problem with faces. So while long COVID is known to cause a range of neurological issues, it appears that face blindness is a rare consequence.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

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As the World Cup kicks off across the U.S., Canada and Mexico, scientists have predicted that extreme heat could play a decisive role in determining the outcome.

Nearly half of the scheduled matches — especially those in more southerly areas of the U.S. and low-lying parts of Mexico — have at least a 50% likelihood of "performance-impairing heat." To prepare, many teams have been training intensively in hot conditions, and during the tournament, they will have access to cold-water immersion tubs, ice vests and misting fans to help cool players down if they overheat.

Compared with these major sporting events, which have resources to adapt to extreme heat, community sports participants and recreational exercisers often have fewer options. This lack of adaptability may increasingly affect when, where and how people can safely exercise, especially as climate change makes extreme warming events more frequent and intense.

"The majority of people who play sport for competition or just for fun, recreation and leisure have a fraction of that power [of professional sports organizers] but face greater challenges and harms," Jessica Murfree, an assistant professor in the Department of Exercise and Sport Science at the University of North Carolina at Chapel Hill, told Live Science.

How hot is too hot for exercise?

Sports governing bodies typically use wet-bulb globe temperature (WBGT) to assess heat risk. It measures the combined impacts of temperature, humidity, direct sunlight and wind speed on the human body.

Taking humidity into account is key because, with more water in the air, it's harder for sweat to evaporate off the skin and cool the body. WBGT was developed by the U.S. military in the 1950s to prevent heat-related deaths in training camps. Nowadays, it also shapes safety guidelines for outdoor workers, as well as athletes.

The American College of Sports Medicine divides the U.S. into three regions to account for varying levels of heat acclimatization and defines WBGT ranges that pose a "very high" risk in each region. That threshold is a WBGT of 82.2 degrees Fahrenheit (27.9 degrees Celsius) or higher in Southeastern and Southwestern states, 79.9 F (26.6 C) in Central states, and 76.3 F (24.6 C) in Northern regions.

For unacclimatized individuals and those with poor physical fitness, the health risk jumps at lower thresholds.

Gulf Coast states — particularly Southern Texas, Louisiana, Mississippi, Alabama and Florida — tend to experience the highest WBGT values. High-risk conditions begin in May in South Texas and South Florida, before expanding northward and peaking in July and August. Studies suggest the number of extreme humid heat events has more than doubled in most parts of the U.S. since 1980, and that globally, climate change added roughly three weeks' worth of dangerous humid heat in 2024 alone.

An individual's overall health and fitness, hydration levels and amount of exertion need to be considered, and systemic factors like socioeconomic status also come into play, Murfree said. For instance, lower-income families are more likely to live in hotter urban environments and lack access to air conditioning, meaning they may already be experiencing heat stress at home.

While high humidity and heat make it so sweat can't evaporate easily, the body has other means to cool down. It also sends more blood to the skin, arms and legs, allowing heat to be released through the skin. But physical exertion in extreme heat makes this more difficult.

"We only have a limited amount of blood in our body, and we're simultaneously trying to use it to fuel the reactions in our muscles to be able to facilitate exercise, as well as send it to our skin to help us cool down," said Grant Lynch, a research fellow in the Heat and Health Research Centre at the University of Sydney.

When the body can no longer get rid of extra heat, symptoms of heat exhaustion ‪—‬ including dizziness, nausea, headache and muscle cramps ‪—‬ may set in. If the body continues to overheat, this can progress to heat stroke, a serious and potentially fatal medical emergency where a person's core body temperature rises to 104 F (40 C) or above. Heat stroke can cause central nervous system dysfunction and delirium, convulsions or coma.

In the U.S., exertional heat stroke is a leading cause of preventable death during sport and exercise and is a particular concern for youth athletes. Children, including teens, produce more heat relative to their body weight than adults do while sweating less. Additionally, they may feel less able to advocate for themselves on the playing field if they start to feel ill, Murfree said.

Reducing health risk in hot weather

The body can acclimate to extreme heat, to some extent. At the University of Sydney’s thermal ergonomics laboratory, researchers use a climate chamber to test the body’s capacity to adapt by increasing its blood plasma volume and lowering heart rate and resting temperature.

"We would have them come in for anywhere from five to 14 consecutive days of exposure," Lynch said. "They would be cycling or running for between 90 minutes to 2 hours every day, and the conditions would be [95 F to 104 F] 35 C to 40 C in the room for that entire duration."

The benefits achieved through this kind of heat acclimation aren't permanent. Research suggests that, for every two days spent in a cool environment, one day of heat acclimation is lost. For people exercising just a few times a week in hot weather, "it's pretty unlikely you are physiologically adapting as much as you think you are," Lynch said.

While WBGT is considered the "gold standard" for heat safety monitoring, the special device required to measure it may not be accessible to every community sports organization or individual person exercising. The danger, Lynch said, is that many people focus on ambient temperature alone to determine risk, when multiple factors are involved and can compound.

Sports Medicine Australia, the country's national body for sports medicine and sports science, developed a tool to calculate risk and suggest safety precautions. It combines data automatically extracted from weather stations — including ambient temperature, humidity, wind speed and solar radiation — with sport-specific information, such as typical uniforms and duration of activity.

Generally speaking, the sports body recommends staying hydrated before, during and after physical activity; wearing lightweight and breathable clothing; taking frequent rest breaks using ice towels and misting fans when possible; and delaying or cancelling games when the risk level gets too high. If someone begins to feel overheated, immediate action is important to prevent further heat strain.

"The most important thing to do, without a doubt, is to stop or reduce the intensity of the activity you're performing, seek shade, go into an area where you are not exposed to direct sunlight, and then douse the skin with water," Lynch said.

Heavy sweating, painful muscle cramps, nausea, dizziness, and cool, pale, clammy skin are all signs that someone may be suffering from heat-related illness. Heat stroke symptoms include a very high temperature; hot, dry skin or profuse sweating; confusion; and loss of consciousness. These symptoms should prompt immediate cooling with a cold water bath and emergency medical care.

While rescheduling events to cooler parts of the day is an option, heatwaves are already increasing in most regions and that trajectory is expected to continue as average global temperatures rise. So, some researchers and sports organizations are exploring infrastructure changes that could help: stadiums with shaded and green spaces, schoolyards with grass instead of concrete, and artificial turf with a built-in irrigation system for use in school sports fields.

Murfree said she would like to see heat safety training introduced in schools in areas prone to extreme heat in the U.S., similar to existing fire safety education.

"Sport often asks us to push ourselves harder, be faster and tougher," Murfree said. "It's OK to take breaks, stop, slow down, reschedule and advocate for our bodies and our wellness in the heat."

This article is for informational purposes only and is not meant to offer medical advice.

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The patient: A 44-year-old man in France

The symptoms: For two weeks prior to going to the doctor, the man had been feeling mild weakness in his left leg. There weren't any notable abnormalities in his medical history or neurological development, except for when a shunt had to be placed in his head when he was 6 months old. The shunt helped relieve fluid buildup in his brain, which had an unknown cause. When he turned 14 years old, the shunt was removed.

What happened next: When the man reported his leg weakness to medical practitioners, doctors ran CT and MRI scans of his head. They also performed neuropsychological testing, which revealed that the man's IQ was 75, below the average score of 100.

The diagnosis: Doctors determined that the patient was living with a brain that was at least half the average size.

The brain scans also revealed a large buildup of fluid in his brain, which allowed little room for tissue. This left the patient with just a thin sheet of brain tissue pushed up against his skull. The scans showed that the fluid-filled cavities in the brain — called ventricles — were extremely dilated. It's likely that this fluid accumulation drove the man's leg weakness.

The treatment: Doctors drained this excess fluid from the man's skull, which helped the patient regain some of his leg strength. In a case report published in The Lancet, the doctors wrote that a new shunt was also inserted inside the man's skull, and within a few weeks, the patient's neurological examinations — which were used to evaluate his leg weakness — returned to baseline. "The findings on neuropsychological testing and CT did not change," they noted, so the man's IQ remained about the same.

What makes the case unique: Over the course of evolutionary history, humans' brains became notably large compared with those of our relatives, leading to improved cognitive capacity and language acquisition. The exact reasons for this growth are not fully understood but are likely linked to a combination of environmental and dietary factors, among other pressures.

A human's brain also grows significantly within a person's lifetime, with the brain during adulthood typically being dramatically larger than the size of their brain as a newborn. In the man's case, it might have been expected that he would show deficits due to having a smaller-than-average brain. However, despite the smaller size of his brain, the man did not show any deficits and was working as a civil servant.

Had he not developed leg weakness, his small brain may well have gone unnoticed.

This article is for informational purposes only and is not meant to offer medical advice.

To our human eyes, a mouse's furred face doesn't betray much emotion. But if you watch the body language of a mouse who's reunited with one of her sisters after five days in a cage alone, you might suspect you know what she’s feeling.

The formerly isolated mouse chatters in squeaks too high for a human to hear. She follows her sister, crawling beneath the other mouse's body as if trying to get a hug. She looks like she's feeling what you or I feel when meeting a long-lost friend or a family member — maybe with more sniffing.

She looks like she's been lonely.

Loneliness isn't just for humans, and neither are its harms. Over the past decade or so, some researchers have come to believe that an animal's craving for the company of others isn't just a preference, but a basic, deeply held need. When we don't socialize enough, we feel the lack like hunger or thirst, they say. When we've had our fill of togetherness, we feel satisfied or quenched.

The amount of socializing a creature needs may be particular to that species, and even to that individual. Scientists have found within-species social differences in birds, monkeys, fish and even cockroaches.

Among humans, "you can feel lonely at a party, or you can feel fine alone in your office," says Kay Tye, a neuroscientist at the Salk Institute for Biological Studies in California. Whatever the ideal degree of togetherness, Tye and others think that an animal’s need to balance time alone and time with others represents a kind of homeostasis: an equilibrium that's critical for survival. Today, they are on a hunt to find where, in the brain, this equilibrium is controlled — and hoping their work will hold dividends for lonely humans.

A range of socializing

Beavers live with their immediate families. Starlings flock in huge murmurations. Adult male orangutans roam solo until it’s time to find a mate. What determines an animal's ideal amount of socializing?

Tim Clutton-Brock, an evolutionary biologist retired from the University of Cambridge, says several factors can push species to become more or less social as they evolve. One is the need to keep warm. Another is foraging: Does searching for food in a group make it easier for that animal to eat, or harder? What about predation — is there safety in numbers, or is it better to be alone and inconspicuous? Do females need help from others to raise their young?

"Dealing with the neighbors" is also important, Clutton-Brock says. For example, the meerkats he studies in the Kalahari Desert live in territorial groups, and constant conflict means it’s better to live in packs. A wild meerkat who's separated from the group is visibly distressed and looks around constantly. "They very clearly get extremely worried," he says.

Within each species, Clutton-Brock says evolution has probably allowed for a range of personality types around a certain species average. "There are costs to too much anxiety" about being alone, he says, "and costs to too little anxiety." A species may do best with a mix of social styles.

Whatever an animal's right amount of social activity, research suggests there can be dire consequences to mental and physical health when it's not met. People who are socially isolated, or feel lonely, die sooner. Poor social connections are linked to heart disease and stroke. Certain female rats, when housed alone, are more likely to develop cancer.

Tye started investigating loneliness well before the pandemic brought the subject to the forefront. In 2016, she showed that certain neurons in the brainstem — the deepest, oldest part of the brain — are active in male mice who are isolated for a day and then meet another mouse. When scientists inhibited those neurons, the formerly isolated mice were more standoffish; when scientists activated the neurons, the mice were more eager to seek out company.

The researchers realized they might be getting a glimpse, Tye says, of "the cellular substrate of loneliness."

In 2019, Tye and coauthor Gillian Matthews proposed that those brainstem neurons are part of a system of social homeostasis. Like a thermostat, they theorized, a mouse's brain senses how much company the animal has been getting, and measures that against an ideal. This ideal can also be called a set point. In the human body, for instance, the set point for temperature is around 37 degrees Celsius (98.6 degrees Fahrenheit); when we deviate from that we'll shiver or sweat. Likewise, the researchers suggested, the mouse's brain drives its behaviors to maintain the right balance of social activity.

The scientists hypothesized that other animals, including humans, share this system. Though it's not easy to test such a thing in people, Tye did team up with a research group at the Massachusetts Institute of Technology for an experiment in which people sat alone in a room for 10 hours.

Afterward, subjects reported craving social interaction. When they viewed pictures of people laughing together, their brains lit up in the same region as the brains of fasting subjects who viewed pictures of food: an area, also within the brainstem, packed with dopamine neurons that are involved in cravings.

For more evidence that this craving is part of a true homeostatic system, Catherine Dulac, a neuroscientist at Harvard University and the Howard Hughes Medical Institute, looked in another part of the brain: the hypothalamus, a deep region just above the brainstem that houses control centers for hunger, thirst and our need for sleep. It calibrates each of these basic needs using a kind of neural thermostat — or, as Dulac likes to call it, a "bean counter."

In the case of hunger, for example, scientists have found one set of neurons within the hypothalamus that drives appetite and tells an animal to eat. A separate set of neurons drives fullness — what biologists call satiety — and tells the animal to stop eating. Dulac guessed that she'd find a similar system in the hypothalamus for loneliness, comprising two sets of neurons: "one that encodes the need" for company, she says, "and one that encodes the satiety."

In a study published in 2025, she and her colleagues isolated adult female mice for five days. On days one, three and five, each isolated mouse got to have a 10-minute visit with her sister. Peering inside the heads of the mice undergoing these separations and reunions, the researchers saw just what they were looking for: One cluster of neurons in the hypothalamus started firing when animals were isolated, and turned off when they were reunited. A second cluster of neurons did the opposite.

What's more, when scientists used a technical trick called optogenetics to artificially activate the separation neurons every time the animals entered a certain chamber, the mice avoided spending time there. That suggested that these brain cells, when activated, give the mice a bad feeling. "It's unpleasant to be alone, in the same way it has been shown that it's unpleasant to be hungry," says Dulac, who coauthored an overview of social interaction as a fundamental need in the 2026 Annual Review of Neuroscience.

But activating the opposite cells — the reunion neurons — led the mice to spend more time in the chamber. These cells are connected to the brain's dopamine system, which doles out pleasure and rewards.

Aside from making us feel good or bad, Dulac says, the hallmark of a homeostatic system is a "rebound" effect — the greater the deprivation, the more an animal needs to make up for it. When we're parched, we drink more. And the researchers saw the same thing in their mice: The longer a mouse had been isolated, the more time she spent following, sniffing and squeaking to the other one.

Dulac says that her findings in the hypothalamus and Tye's in the brainstem probably represent different components of the same system. Other studies have found neurons in still more parts of the brain that may be involved.

Like our appetite for food, the mechanism for social homeostasis may be distributed through many parts of the brain, Tye says. After all, our brain needs to detect the amount of socializing we're getting, compare it to an ideal, and then drive our behavior so we get more or less company.

The scientists also believe that the circuitry that senses and manages loneliness is likely to be similar in the human and rodent brains. Unlike our more recently evolved cortex, our deep brain regions look much the same as what's inside a mouse's head. A lonely human may be feeling the effects of wiring laid down long ago in our evolution.

The importance of touch

After studying female mice, Dulac has now turned to studying male mice, who have competing social motivators because they're territorial toward other males.

Tye, for her part, has begun to look at females after studying males. So far, she's observed that they get more and more social over time — unlike the males, which become antisocial after two weeks in isolation and don't seem happy when reunited with other mice. "It's like avoidant, territorial, get-off-my-lawn vibes instead of wonderful-to-see-you-again vibes," Tye says. The scientists don't yet understand this fundamental sex difference.

Intriguingly, researchers have also observed an antisocial effect in human prisoners subjected to long-term solitary confinement. In addition to other psychological harms, prisoners may stop craving social contact, and start to fear it.

Besides attempting to understand the differences between chronic and short-term isolation, researchers are also trying to learn how creatures use their senses to gauge how much company they have.

In Dulac's experiments, vision didn't seem to be necessary: Blind mice reacted to separation similarly to sighted mice. Nor did scent or sounds hold the answer: When mice were physically separated by a perforated divider within the same cage — so they could still hear and smell their companions — they reacted as if they’d been fully isolated.

The only sense that seemed to matter was touch: The brush of another mouse's body told mice they had a friend nearby.

When the researchers lined a tube with soft cloth for mice to walk through, they saw that isolated animals preferred the soft tunnel to a hard one. Like a weighted blanket for humans, perhaps, the touch of the furry walls made the lonely mice feel a little better.

Ishmail Abdus-Saboor, a neurobiologist at Columbia University's Zuckerman Institute who studies touch and was a coauthor on Dulac's study, says the result didn't surprise him. "It is consistent with touch being perhaps one of the most essential sensations for well-being," he says.

Our sense of touch is not just one thing. Bodies have different pathways for processing different sensations, such as pain or itch — or social touches. We humans have specific neurons in the hairy parts of our skin, for example, that are activated by slow stroking. (Mice have related neurons.) And deep pressure, akin to a hug or a massage, activates a similar brain region to stroking touch.

Abdus-Saboor is now working with naked mole rats in his lab. These quirky, colony-living rodents are both the world's most social mammals, and conspicuously cuddly. He hopes studying them will provide more answers about the connection between touch and sociality. He even thinks they might be better models than mice for social touch in humans, because their nearly hairless skin is more similar to ours than a mouse's.

These social touch neurons may carry signals from an animal's skin to its brain that tell its bean counter it's not alone, making the animal feel better. "If we can hijack this pathway, can this be used as a therapeutic to promote health and well-being? I think so," says Abdus-Saboor, who wrote an overview of social touch research in the 2026 Annual Review of Neuroscience.

Even before scientists use this research to develop new treatments, Dulac says it highlights the danger of solitary confinement in prisons. "When individuals are left alone, their brain is just sending this danger signal: 'You should not stay alone,'" she says.

Tye imagines that if scientists better understood the brain's social bean counter, they could one day find a way to lessen the health effects of isolation. For now, she and coauthors suggest that spending time in a variety of social settings is the best way to buffer yourself against discomfort.

Before Covid, Tye recalls, she was always with other people. Then, "during the pandemic, I was alone a lot. And it was really stressful for me," she says. She thinks that giving ourselves regular alone time, as well as time in small and large groups, can make us more tolerant of changes.

Because we're not rodents, we might be able to get our social needs met — at least partially — in ways that they can't. We can connect with a loved one through a call or text. Still, Tye says, touch seems to be especially vital.

Abdus-Saboor, who is married with two children, says he's "very intentional" about touching his family: a supportive tap, a back rub. His kids are old enough to walk to school on their own, but he makes sure to check in before they go.

"It's like, 'Let me get that hug before you leave,'" he says.

This article originally appeared in Knowable Magazine, a nonprofit publication dedicated to making scientific knowledge accessible to all. Sign up for Knowable Magazine's newsletter.

If you've ever washed uncooked rice, you've seen the pale, milky-white water that rinses away. Billions of people across the world eat rice every day. So should everybody who cooks rice wash it beforehand?

This question has been the subject of a number of scientific studies, which have looked at how washing rice affects its texture, nutrition and how well it removes unwanted substances, such as dust, arsenic and microplastics.

Rice is traditionally grown in shallowly flooded fields, as it requires constant irrigation to grow. When the grains are ready, they are harvested and milled to remove the inedible hulls, yielding brown rice, which can be further milled to remove the bran layer, producing white rice.

The act of milling can damage rice kernels, leaving a layer of starch (the substance that makes up much of rice, potatoes and wheat) on the outside. When rice is rinsed, some of this starch is washed away.

In a 2017 study, scientists had speculated that washing rice might change the texture of cooked rice by rinsing off starch that would make grains stick together.

However, subsequent research found that "washing rice makes no difference to the stickiness of the cooked rice," Evangeline Mantzioris, an accredited practicing dietitian at Adelaide University in Australia, told Live Science.

Specifically, a 2019 study showed that "the stickiness of rice is not from the surface starch, amylose, but from another starch within the grain called amylopectin," Mantzioris said. "This is what leaches out during cooking and impacts the stickiness."

The 2019 study found the amount of amylopectin that leaches out of rice during cooking does not depend on whether it is washed. "It is the variety of rice that is important," Mantzioris said. In tests with 10-gram (0.4 ounces) samples of three kinds of rice that were all washed the same amount of time with increasing amounts of water and cooked for 30 minutes, the scientists found that "if you want sticky rice for your dish, you are best using glutinous rice. Medium-grain and jasmine rice are less sticky."

Traditionally, rice was washed for health and safety reasons, "to rinse off dust, insects, little stones and small parts of the husk," Mantzioris said.

However, nowadays, "rice sold in supermarkets and reputable retailers is generally produced under strict quality standards," Bo Wang, a food scientist at Adelaide University, told Live Science. "It is typically cleaned [with machines, such as sifters and blowers], dried, dehusked, milled, graded and packaged before reaching consumers. The drying step particularly reduces moisture content, helping maintain quality and limiting microbial growth during storage. As a result, rice is already a relatively safe product, and washing is generally not required to make it safe for consumption."

Still, "one additional consideration is that some rice may contain naturally occurring inorganic arsenic absorbed from soil and water," Permal Deo, a food scientist with a background in molecular biology at Adelaide University, told Live Science. "Rinsing may help remove some arsenic on the grain surface."

Rinsing rice can also rinse off microplastics, Mantzioris said. A 2021 study found that washing rice before cooking it reduced the amount of plastic contaminating it by 20 to 40%. (It remains uncertain what effect microplastics have on our health, although evidence is growing that microplastics could be harmful.)

Mantzioris noted that washing rice does reduce levels of some important nutrients that naturally dissolve in water, such as copper, iron, zinc and vanadium. However, rice at best offers only a small percentage of one's daily intake of these nutrients. Washing rice, therefore, "is unlikely to affect you nutritionally," she said.

"Long story short, for most consumers, a gentle rinse once or twice before cooking is usually sufficient," Wang said.

This article is for informational purposes only and is not meant to offer medical advice.

Do you know where pumpkins and blueberries come from? Find out with our fruits and vegetables quiz!

The United States successfully eliminated measles decades ago by taking measures to ensure the virus stopped spreading consistently within the country — but now, it's likely that measles is back.

Toward the end of 2025, experts cautioned that the U.S. could lose its "measles elimination status" within months as various outbreaks raged across the country. If the U.S. does officially lose this status — meaning the country will have experienced sustained measles spread for over a year — it would join a list of countries, including the U.K. and Canada, that have also seen local resurgences of measles as their vaccination rates have declined.

An assessment of the United States' elimination status is scheduled for November. In the meantime, experts have issued a progress report for the nation. Live Science spoke with two authors of the report from Boston Children's Hospital — Dr. Anne Bischops, a pediatrician and postdoctoral research fellow, and Maimuna Majumder, a distinguished scholar in the Computational Health Informatics Program — to understand where America's elimination status stands and what to expect in coming months.

Nicoletta Lanese: We saw measles cases start to rise in the U.S. around January 2025. Were you concerned at that point about the country losing its elimination status?

Maimuna Majumder: I've personally been working on measles for over a decade, and given that, what I will say is that my concerns around elimination status far predate even January 2025.

When January 2025 picked up, I felt like this might be the point of no return. But it was not in any way the first red flag. I do want to just stress that measles elimination has always been a tenuous prospect, and it is, by design, tenuous. Maintaining elimination status is, by design, difficult.

When you start to see these clusters turn into outbreaks that threaten to spill over into neighboring states, when you see the rapidity with which small outbreaks become larger outbreaks — those tend to be the signals that [say] "I don't think that we're going to be able to get the cat back in the bag here."

Dr. Anne Bischops: The trend of the increase of vaccine-preventable diseases has been ongoing for several years already, and it's something that has spilled into the daily life working in the ER. We've seen increasing cases of measles. And especially after the COVID-19 pandemic, we have this increase of vaccine fatigue adding to that.

This has been, globally, an increasingly important topic. For the current outbreak in the U.S., our study team has been closely monitoring that from the beginning.

NL: What factors set our current situation apart from past measles outbreaks?

MM: My very first domestic measles response was during the Disneyland measles outbreak in [late 2014 and] 2015. It was a different time. It was a radically different political administration; it was a radically different time, culturally, for how the United States felt about vaccines. It was an optimal time to make strides in policies that would help ensure that we didn't lose our elimination status.

In response to the Disneyland outbreak, we ended up passing SB-277 in California and a number of other important vaccination bills across the United States that allowed us to get rid of personal belief exemptions, for example. That really led to fantastic strides in reclaiming our measles protection, as a whole.

Now, in the 10 years that have since passed, a lot of things have changed. We are now in the second Trump administration, and there has been a massive pandemic in between that eroded the public's trust in public health and vaccines. A lot of that is driven by the pervasiveness of misinformation that's run rampant.

When the Disneyland outbreak happened, we largely had a feeling of hope that, "We can use this opportunity to pass bills that are going to protect the American people." What happened when the [2025] Texas outbreak started was the opposite of that. That's when the likelihood that you're going to lose your status becomes imminent, because the levers that you would typically use to rescue elimination status are no longer viable.

NL: In your report, you describe seven indicators that should be met for a country to achieve elimination status, noting that the U.S. has now missed — or essentially, failed — four out of seven. Why is it useful to define these indicators?

AB: The Pan American Health Organization [PAHO] has these recertification meetings [such as the one planned for November] where very detailed, granular data for every single transmission chain are presented, and this is very time-intensive.

We saw that the meeting had been moved from April to November, so our goal with the seven indicators was to provide an early warning framework ahead of that decision, using readily available data that we can use now. We have looked on the broad national level, using only national estimates. We really see it as a rapid assessment before then, in November, when a very detailed analysis will be done on the transmission-chain level, where every single transmission chain will be followed.

NL: For the indicators that haven't been "missed" yet, do we suspect they've been missed but just don't yet have the data to show that?

AB: Exactly. For example, for the genotyping criteria, we have some samples where we can already see that they all share the same genotype, but we are lacking the detailed genotyping data for every single transmission chain. So we can assume that this has been missed, but we need to confirm with the detailed analysis.

For vaccine coverage, we only have the kindergartners' estimates [regarding the percentage of kindergarteners who are up to date on measles vaccination], and we don't have immunity data. But based on the data available, we could think that has already been missed.

NL: Experts have said we're likely undercounting our current measles cases. Is that a fair assessment?

MM: I personally agree that it is very likely an undercount. One reason is that measles in general does not have to be super severe in pathology. So sometimes, kids will get sick and their parents may not take them in to get looked at. When we think about the way that infectious disease surveillance is done in the U.S., in order for mandatory reportable diseases like measles to be reported, there needs to be an encounter with the healthcare system. If you have a disease where that may not always happen, then certainly, by default, you're going to be undercounting the disease.

Our best indicator is wastewater surveillance [where germs are screened for in wastewater], and right now, we don't do a ton of wastewater surveillance for measles. The next question would be, how do we track this better? That is perhaps one of the better solutions.

NL: Do you think wastewater surveillance is something that could be feasibly expanded? I know our current coverage differs state to state.

MM: The technology is there, so this is possible. What is challenging — and this is true for all wastewater surveillance, not just measles — is that our interpretability of wastewater signals is, mind my language, still very much in the shitter.

We see numbers go up in the wastewater, so we know that numbers are going up in the community. To what degree that scaling factor is true is dependent on so many things that it's really difficult to have kind of a 1:1 [translation] based off of what the wastewater signal says — just how many cases there are in a given community at the time.

One of the big factors, of course, is that wastewater is very, very vulnerable to rainwater fall [in that rainfall dilutes wastewater and must be taken into account to interpret the results]. So there are a lot of physical engineering components to this that we have not fully figured out yet. It's harder to say, "Oh, there are exactly this number of cases because there's this much wastewater indication of this disease in this location." We can't do that yet, not in a meaningful way.

What we can do is use wastewater to predict when hospitalizations for respiratory disease will increase, when we might expect upticks and people seeking PCP [primary care provider] care for a given disease — this is something that the wastewater is very, very useful for. That is where I do believe that there is room for improvement, and this is something that can be done.

Massachusetts is one of the leaders in wastewater surveillance, and we have our own dedicated wastewater surveillance teams. So if I were to think of states that would probably be leaders in this, states like Massachusetts would probably be the most likely to pilot a measles wastewater program.

NL: Your report indicates we're on the brink of losing elimination status, and getting vaccination rates up is a key solution. Will that effort mostly be at the state and local levels, given the federal government's stance?

MM: All of our states operate as their own little entities that manage their own state's health, so we don't have a ton of programs that are universal, national. Even if Trump were not in office, we would expect most vaccination campaigns to happen at a more localized level. That has always been the case.

However, now you have a federal government that is pretty staunchly anti-vaccine, even when RFK Jr. is reneging and saying, "Actually, vaccines are alright." There's quite a bit of waffling even at the federal government level that we should acknowledge. I would not call it vaccine hesitancy at the federal government level; I would call it skepticism. What that does is that it seeds doubt. That has a trickle-down effect to the individual who is living in a given state.

The public discourse around vaccines is very, very heavily influenced by federal discourse.

While federal discourse does not affect states' rights to pass bills that are going to protect their public by encouraging more vaccination, what it does do is affect the way that individuals in those states perceive vaccines. The vast majority of people in this country are more aware about federal politics than they are about state politics; that is the reality of the situation that we live in.

You end up with a situation where, even though the federal government does not really have much control over what the state will mandate is required for a child to enter public schools, there is a control that is exerted through the communication strategy that is used by the federal government to reach individuals across the United States.

AB: From the pediatrician perspective, we can see day to day, there can be 10 positive vaccine-promoting campaigns, but it only takes one short online comment to spread doubts everywhere. So, for me as a pediatrician, it's very important to be very careful with health communication about that — I think we need efforts on all levels.

NL: Is there anything else you hope people take away from your progress report?

MM: Because we see this global resurgence of measles and we have a bunch of other countries that have also lost their status or who are also on the brink, we think that this [framework] might also be applicable to other countries who could use it as an early warning.

It's not just the U.S. that is dealing with this problem; it's not something that's happening in a vacuum.

The politics across most high-income countries are exhibiting similarities across the board that are absolutely influencing the pervasiveness of this issue, and the fact that many high-income countries have lost their measles elimination status in the last year is a very, very good indicator of that. But I'd like to stress that it's not entirely politics, either. Part of it is system memory.

What I mean by that is, the people that are having kids right now are people who have never known a person who has been gravely affected by measles. They have no clue that in previous generations, people died from this disease or were left with terrible post-acute conditions that have plagued them for the rest of their lives. That lack of exposure makes it seem like it's not that serious.

When public health works, nobody knows that it's working — that's a statement that we often make in this discipline. The reason nobody died from measles when I was a kid is because everybody was vaccinated. This particular thing is very difficult; it's very human to start questioning the severity of something when you haven't seen that severity yourself.

NL: To date, all signals seem to point to the U.S. losing its status in November. Would you agree?

MM: I would be very surprised to see it turn out otherwise. I would be delighted if we can turn it around, but it is unlikely.

Why that might happen is if we as a society decide that the strict criteria that we have been using to date are no longer the criteria we want to use. We could say we still have elimination status because we're changing what the criteria are; we're moving the benchmark. If that happens, I will be extremely unhappy.

Either we lose the status because we kept the criteria the same and nothing changed, which seems like the most likely circumstance, or we don't lose status because we changed the criteria, because we don't want to be seen as failures. The least likely but the most positive option is somehow we manage to get it together in the next six months and we don't change the criteria.

AB: There's no standardized criteria or cutoff points for deciding elimination status. In the end, it's completely up to the expert panel in November, so we don't know what exact cutoffs they will use. But based on the data we saw, for now, I think it's highly likely that we will, sadly, lose status.

NL: Could the expert panel move the benchmarks, like you said?

AB: So, the CDC [Centers for Disease Control and Prevention] has determined an expert panel that runs the analysis and will then present to the Pan American Health Organization meeting in November.

MM: That's why I'm saying that that second option is a possibility. There are people [on the panel] that can decide that the criteria are different.

NL: But if the PAHO doesn't think the presented data is valid, could they say that?

MM: They can do it — will they do it is a different question. The World Health Organization [WHO] and its ancillary branches [like the PAHO] are not typically shy about making statements when they believe that certain governments are not being truthful. This tends to happen in highly politicized situations where you are expecting that the data coming out of the country are not fully viable.

So the WHO has absolutely made statements in the past to this effect. The U.S. is a different type of entity though, right? I think that we're now getting into the question of "Does it harm the WHO and PAHO too much to take a stand against the CDC?" It's a very interesting question that I don't think that there is a very clear answer to yet.

To answer that question, can they do that? They can. There is precedent for other countries. But the U.S. is not just any country, and we need to acknowledge that.

As a region, we've already lost that status [given that Canada lost its elimination status already]. My hope is that that would make everybody more honest. I do feel that the situation would be significantly more tense if the U.S. was going to be the "make or break" for whether or not the Americas lost their elimination status.

Editor's note: This interview has been lightly edited for length and clarity. Live Science spoke with Bischops and Majumder in May, so the text may not reflect more recent developments.

This article is for informational purposes only and is not meant to offer medical advice.

For Sarah Hall, every mealtime was dangerous.

She has a rare condition called cardioinhibitory syncope, which causes overactive nerve signals to tell the heart to stop beating in response to subconscious bodily processes, such as swallowing. Swallowing food caused Hall's heart to stop beating up to 12 times a day, often making her faint.

Hall's condition wasn't improving with any treatments, but an innovative procedure has changed her life, as well as the lives of dozens of others.

In work presented at the British Cardiovascular Society's annual conference, scientists reported that 25 people with the condition dramatically improved after an experimental procedure. The early findings, which have not been peer-reviewed yet, are promising but require validation.

"It's important to note that this is still a relatively new therapy and that larger studies and longer-term follow-ups are still needed to provide a better understanding of its durability and help identify which patients benefit most," said Dr. Sirisha Vadali, a cardiologist at HonorHealth who was not involved in the research.

When "rest and digest" goes haywire

The autonomic nervous system handles the electrical signals the body relies on to complete subconscious, everyday processes, like eating or sleeping. This includes the body's complementary "fight-or-flight" and "rest-and-digest" responses.

The latter system send the bulk of its signaling through the vagus nerve, which starts in the brainstem and extends through the chest and abdomen. As the body senses changes, like food entering the throat or the legs bending into a crouch, the vagus nerve updates the brain on what's happening, enabling it to subtly alter digestion, breathing and heart rate in response.

In some animals, vagal activation is involved in a more dramatic bodily process: hibernation. Hibernating mammals, like bears, experience a strong wave of signaling through the vagus nerve when they enter their winter den, which lowers their metabolic rate for weeks.

People with cardioinhibitory syncope "go into a hibernation response" because their vagus nerve signals are too strong, Dr. Boon Lim, a consultant cardiologist at Imperial College Healthcare NHS Trust who led the new work, told Live Science.

The vagus nerve transmits signals to the ganglionated plexi, a web of nerve endings on the surface of the heart. The signals then reach the body’s built-in system for maintaining heart rate — and when they're too strong, it briefly shortcircuits this system, causing the heart beat to pause entirely.

There are many ways this hyperactive vagal response can be triggered. For 50-year-old Hall, the trigger was swallowing, while for others with the condition, sudden abdominal pain can flip the switch.

Why we faint

Syncope, the medical term for fainting, is common. Lim estimates that 40% of people faint at some point in their lifetimes, and for most, it is because signals from the vagus nerve temporarily reduce their blood pressure. Without enough blood flowing to the brain, people briefly lose consciousness.

But in cardioinhibitory syncope, the heart pauses entirely for a few seconds due to hyperactive vagal signaling. The strength of the vagus nerve's signaling to the heart is determined largely by genetics. Fewer than 5% of people who seek treatment for syncope have cardioinhibitory syncope.

The condition generally isn't life-threatening, Vadali said, but its unpredictability is highly disruptive. "Many patients may experience anxiety about when the next episode might occur," she said.

Boon described a patient named Rob, who had reported frequent fainting episodes. A diagram tracking the waves of Rob's pulse on a normal afternoon showed the churning rhythm of his heartbeat becoming still ‪—‬ one of several daily episodes. "It suddenly pauses for close to five seconds for no reason," Lim said.

For people with cardioinhibitory syncope, the best option previously had been to have a pacemaker implanted, Lim said. But this isn't a permanent solution; pacemaker batteries need to be replaced every decade or so. Patients who get pacemakers at younger ages can face long-term health risks as the devices deteriorate, and battery replacement operations can cause infections.

Now, Lim and colleagues have shown that a procedure called cardioneuroablation could drastically improve the lives of patients like Rob.

In the procedure, Lim snaked a thin wire through Rob's body that eventually reached his heart, specifically the ganglionated plexi on the organ's surface. Lim then delivered a pulse of radio-frequency energy to the plexi, which destroyed the tissue, thus reducing disruption of the heart's built-in pacemaker.

Lim's team carried out the procedure on 25 people at Imperial College London between 2013 and 2023. On average, the patients had had fewer than one fainting episode in the following year. This translated to significant improvements in the patients' quality of life, they reported.

Three patients required additional procedures, because the ganglionated plexi can sometimes regrow. The procedure is fairly invasive, but compared to repeated pacemaker maintenance, it could still offer a more appealing solution to patients, the researchers say.

By now, Lim's team has used cardioneuroablation to treat 52 people. Vadali said the early data presented at the conference is promising but more research is needed to see how well its effects last.

For Hall, the procedure changed her life. She has not fainted since, even at mealtimes.

"I can drive; I can work," she said in a statement. "It feels like everything has come full-circle."

What do you know about the body's hardest-working muscle? Find out with our heart quiz!

A century-old tuberculosis vaccine reduced insulin use in people with diabetes, new clinical trial results suggest. The catch: Research on this vaccine has divided the diabetes research community for years.

The Bacillus Calmette-Guérin (BCG) vaccine contains a weakened version of the bacterium Mycobacterium bovis, the germ that causes tuberculosis. Inside the body, the vaccine prompts a protective response against the bacterium. It's also approved to treat bladder cancer, acting as an immunotherapy that rouses an attack against tumors.

The leader of the trials, Dr. Denise Faustman of Massachusetts General Hospital, has long been the subject of controversy. Early on, critics argued that she falsely raised hope that her work could lead to a cure for those with long-standing type 1 diabetes.

On June 5, Faustman and colleagues presented results from two new clinical trials at the annual meeting of the American Diabetes Association in New Orleans. The results suggest the BCG vaccine may offer benefits to people with type 1 diabetes — not by curing the disease, but by improving blood sugar control or slowing the disease's progression, depending on the population. Here's what to know.

Another tool in the arsenal?

About 2 million Americans have type 1 diabetes, an autoimmune disease that destroys insulin-making cells in the pancreas. Patients monitor their blood sugar and inject insulin multiple times a day, carefully calculating every dose. Too much insulin and blood sugar crashes, causing shakiness, seizures or blackouts; too little, and chronically high blood sugar damages the heart, kidneys, eyes and nerves.

Early in the disease process, patients still have some insulin-making cells, but people with longstanding disease have almost none left. Curing type 1 diabetes in those with longstanding disease is a tough problem that requires stopping the immune attack and regenerating enough insulin-making cells to eliminate the need for injected insulin.

The new trial results do not show that level of improvement. However, "the new data suggests that BCG could reduce insulin resistance and decrease the amount of insulin needed in patients with both late-onset and juvenile-onset type 1 diabetes," said Dr. Gillian Goddard, a board-certified endocrinologist at NYU Langone Health who wasn't involved in the studies.

"These are phase 2 trials so further trials will be needed to fully understand the benefits of BCG in Type 1 diabetes," she told Live Science in an email, "but it could be another tool in our arsenal for improving the lives of patients with type 1 diabetes."

Others are more skeptical. Dr. John Buse, an endocrinologist at the University of North Carolina School of Medicine, cautioned that the improvements seen in these small trials may not hold up in a larger trial. The history of type 1 diabetes research "is littered with losers and no blockbuster successes," he told Live Science in an email.

Different trials, different benefits

In the trials, researchers tracked the effect of six doses of the BCG vaccine, administered over five years, on two separate groups of diabetes patients.

In one trial, 34 adults with childhood-onset type 1 received the BCG vaccine and 24 received a placebo. By five or more years later, the BCG group had measurable improvements in blood sugar levels and reduced insulin use, compared to the placebo.

This conclusion was based on hemoglobin A1C (HbA1c) tests, which measure a person's average blood sugar levels over the past two to three months. The vaccinated group went from an average 7.84% at the start of the trial to 7.30% five years later. Historically, a drop of 0.5% has been considered clinically meaningful enough to consider a therapy for approval.

The vaccinated group also spent more time in a healthy blood sugar range, up to 183% more often than they had at the start of the trial. They didn't experience more episodes of dangerously low blood sugar than the unvaccinated group.

The second trial focused on latent autoimmune diabetes (LADA). This is an adult-onset form of diabetes also known as "type 1.5." It's different from type 2 diabetes, which is not autoimmune.

Sixty-eight adults with LADA received the BCG vaccine and 27 received a placebo. The vaccine didn't lower blood sugar readings, but it appeared to slow the disease: Vaccinated patients showed preserved — and in some cases, partially restored — insulin production over five years, as measured by levels of C-peptide, a protein released by the pancreas alongside insulin.

Vaccinated patients also needed less insulin over five years, while those given placebo needed 22% more at the five-year mark than they did at the start of the trial.

"The results exceeded my expectations," Faustman told Live Science in an email.

How does it work?

In the LADA trial, the blood of the vaccinated group carried lower levels of two key antibodies that drive the attack on insulin-producing cells. This hints that the BCG vaccine may protect a person's remaining insulin-making cells from the immune system, the researchers think.

Faustman and her colleagues think that a different mechanism — one they proposed in a 2018 study — is at play in childhood-onset diabetes, where participants had little or no remaining insulin production in their pancreas at the start of the trial.

Uncontrolled diabetes forces cells to use fat for energy, instead of being able to efficiently switch between fat and sugar. From their 2018 study, the researchers concluded that BCG vaccinations specifically help shift immune cells, called regulatory T cells, out of a fat-burning state toward a sugar-burning state. Those immune cells then pull sugar out of the blood but stop once blood sugar declines, thus preventing dangerous crashes, Faustman explained.

Buse said that he can't personally judge whether these proposed mechanisms behind the vaccine's effects make sense. But he does suspect that BCG may work better for some diabetes patients than others; there could be responders and non-responders.

The evidence presented "suggests that there may be a benefit," he said, but the current data is probably not strong enough to say so definitively. "It would take a big program to develop proof and that is probably the biggest barrier to finding out whether it is in fact useful."

The only Food and Drug Administration-approved drug that delays insulin dependence is teplizumab, which is given early in the disease, before patients need insulin. BCG, by contrast, may offer benefits even to patients who have already been on insulin for years, Goddard said.

Faustman's team has now studied over 350 adults, following individual participants for up to eight years, and another trial involving 250 children is currently underway. "This is the next step to prove this safe, affordable and durable drug can work on all stages of T1D," she said.

Regardless of whether BCG improves blood sugar control in type 1, the "path of the future" is using combination approaches that treat the disease on multiple fronts simultaneously, Buse said. Whether BCG would be part of that mix remains to be seen, he said.

"It seems reasonable to proceed further [with research]," he said, "but funders will have to read the tea leaves to decide where to invest their resources among many options."

This article is for informational purposes only and is not meant to offer medical advice.

When the U.S. faces Paraguay in the World Cup in Los Angeles' SoFi Stadium on June 12, the teams will play on a natural-grass surface that, a month earlier, was carefully stitched together atop an underlying artificial-turf field. This "hybrid turf" installation was part of a broader effort in advance of the World Cup to ensure the world's best soccer teams played on predominantly natural-grass surfaces.

FIFA, the organization that oversees the World Cup, has prohibited the use of synthetic turf in World Cup games for years, mainly because of an increased risk of player injury, which has been well established. Synthetic turf is also notorious for causing nasty turf burns, as the material is a poor solar radiator and can reach up to 200 degrees Fahrenheit (93 degrees Celsius).

However, many people in the wider sports community worry that synthetic turf may pose more insidious harms, such as dangerous levels of exposure to heavy metals, cancer-causing chemicals and microplastics.

A recent, 10-year-long study from California found no significant risks from the chemicals in artificial turf. But experts aren't convinced the study has laid to rest concerns about artificial turf. Here's why.

Wonder of the Space Age

This infill is the crux of the issue: All those tire crumbs contain hundreds of chemicals and "created this exposure situation that had never existed previously," Rachel Massey, an environmental health researcher at the University of Massachusetts Lowell Center for Sustainable Production, told Live Science.

More than 95% of the 18,000 to 19,000 turf fields in the U.S. now include tire-crumb infills. AstroTurf has remained a dominant player offering 3G products. (Live Science reached out to AstroTurf to discuss the company's products but did not receive a response.)

Harmful chemicals?

Some researchers are concerned that turf contains nearly 400 chemicals that have been tied to various health risks, ranging from asthma to leukemia.

"None of those [risk assessment] studies dispute the fact" that those chemicals are present, Massey said. "So then all the debate is about exactly how much exposure there is."

To assess whether that exposure reached harmful levels, the California Office of Environmental Health Hazard Assessment (OEHHA), part of the California Environmental Protection Agency, undertook a study of the health impacts of chemical exposure due to synthetic turf.

"We identified as many chemicals as we could in the crumb rubber by doing non-targeted sampling and assessed as many chemicals as we could," said Amy Gilson, a spokesperson for the OEHHA.

They attempted to measure exposure to metals commonly found in turf infill, including lead, cadmium, manganese and zinc, with zinc being most frequently detected at concerning levels above U.S. regulatory guidelines. Although zinc is essential to the body, it can be harmful at high levels, with the potential to cause anemia, damage the pancreas, and reduce fertility.

They also looked at carbon black, a reinforcing tire filler material that has been shown to kill human cells in lab dishes; benzene, which has been linked to several types of leukemia; toluene, which is toxic to the nervous system, liver and kidneys; and polycyclic aromatic hydrocarbons, compounds that are most commonly found in tobacco and wood smoke and have been tied to cancer in animal studies.

Another potential concern emerged last year, when 1,3-dimethylbutylamine (1,3-DMBA), a stimulant banned by the World Anti-Doping Agency, was detected in post-match samples submitted by eight Norwegian female professional league soccer players from opposing teams. The artificial turf was found to be the source of the banned substance. With tire wear, 6PPD ‪—‬ a substance often added to tires to limit ozone-depleting emissions ‪—‬ can degrade into 1,3-DMBA, which was detected on the turf where the game was played.

The California EPA report also looked into the presence of microplastics in turf.

In 2023, the European Union announced a ban on the sale of products containing intentionally added microplastics, effective starting in 2031. Specifically, it named the granular infill within artificial turf as "the largest source of intentional microplastics in the environment." The U.S. does not have similar legislation.

Microplastics might harm human health by accumulating in various parts of the body through ingestion, skin contact or inhalation.

Early research in human cells in lab dishes hints that microplastics could damage the lining of blood vessels and promote the formation of atherosclerotic plaques and blood clots. Other studies have proposed potential links between microplastic exposure and asthma and inflammatory bowel disease. However, there is a lot of uncertainty about how microplastic exposure is measured and whether this exposure causes diseases or is simply a proxy for some other factor that causes these conditions.

"Negligible" long-term harm

The California EPA focused on chemicals in tire infill that could potentially cause harm at high doses. Then, it estimated the levels of exposure in players, referees and spectators through having direct contact with, breathing in, or inadvertently swallowing tire crumbs. First, they estimated exposure indirectly, by observing people.

"We actually had teams of people going out and videotaping players on the field," Gilson said.

The research team also collected samples of artificial turf and then put them in lab dishes with synthetic bodily fluids such as sweat, saliva and small intestine fluid and then measured the concentrations of dozens of potentially harmful chemicals within those fluids. To be more conservative, they assumed every chemical detected in their experiments would have been completely taken up by human cells, Jocelyn Claude, a toxicologist at the OEHHA who worked on the study, told Live Science.

The study found "no acute risks," meaning short exposure to this substance is unlikely to cause immediate harm, she said, and the risks of longer-term health effects, such as cancer or reproductive harm, "were negligible."

But some experts said the study methodology was flawed. Andrew Watterson, a professor emeritus of public health at the University of Stirling in the U.K., said the study should have taken urine or expelled-air samples directly from real people exposed to artificial turf, instead of estimating exposure in synthetic body fluids.

Wrong approach to risk assessment

For Massey and several environmental researchers Live Science spoke to, the bigger problem is that the underlying approach used by the California study — and most other environmental assessments done in the U.S. — is flawed.

Instead of asking whether an average person is at risk, society should aim to reduce exposure across the population, which also protects people at higher risk. Instead of asking, "Is this risk acceptable?" the latter approach asks, "How can we create the healthiest, safest playing surface for a child?" Massey said.

The California report included referees and spectators in addition to players, but it may have missed other at-risk groups, such as people exposed to chemicals that have leached into the water supply from synthetic turf, said Tracy Stewart, a Medway, Massachusetts resident who advocates against the use of artificial turf.

Another byproduct of 6PPD, the chemical tied to doping, has been shown to cause mass die-offs of coho salmon. So when dead salmon started turning up near an artificial turf field in Vancouver where scientists had detected 6PPD-Q and a range of other chemicals in the stormwater runoff, the community was worried.

The California study estimated 6PPD-Q exposure levels in synthetic bodily fluids, but it did not model how groundwater would be affected. And without well-established safe limits for this chemical, the California study couldn't make assessments of the risk it poses.

Beyond 3G turf

The attraction of synthetic turf is all about "increased hours of use," said Garnet Brownbill, a spokesperson for the Natural Turf Alliance, a nonprofit that advocates for alternatives to synthetic turf across Australia. "It's not impacted by the weather, it never closes, and people claim it's maintenance-free — it's not, by the way," he told Live Science.

However, in response to the looming EU ban on microplastics in infill, many scientists are working on alternatives that can provide that same advantage.

One material in development is hybrid turf, whose surface is "99.5% natural grass," with an additional 0.5% stitching material composed of either plastic or a biodegradable polymer, said Aaron Golembiewski, head of business development at Turftalents, a company that consulted for FIFA on the installation of hybrid turf at several U.S. stadiums. Hybrid turf is "stronger than if it's grass alone," Golembiewski told Live Science. "It increases [the] quantity of play."

It's also smoother than ordinary grass, which has naturally occurring bumps and divots. He noted that hybrid turf is cheaper to install from scratch than synthetic turf and lasts a few years longer, although it needs more maintenance.

Grass fields may be sufficient for many communities. While some stakeholders figure out how to maintain grass more sustainably, other scientists are working to improve the grass itself. "If the same amount of engineering went into natural grass, there's all of this stuff that we can do," Brownbill said. Not all grass is the same.

"There are high-heat-resilient grasses; there are shade-resilient grasses; there are high-wear grasses," Brownbill said. "[Municipalities] are basically using 100-year-old technology … the same grass cultivars that existed 100 years ago."

Editor's Note: This article was produced as part of the Dalla Lana Fellowship in Journalism and Health Impact program at the University of Toronto.

How much do you know about the greatest athletic feats of all time? Find out with our sports record quiz!

Emerging diagnostic tests for cancer aim to detect the disease in its earliest stages, to improve patients' chances of survival by enabling earlier treatment. Some of these diagnostics — called multi-cancer early detection (MCED) tests — screen for many cancers at once, which sounds great on paper.

However, in February, a flagship trial testing one such cancer test, called Galleri, failed to meet its primary endpoint: it didn't reduce the number of late-stage cancer cases identified. In May, at the American Society of Clinical Oncology (ASCO) meeting in Chicago, attendees got a closer look at some of the data behind the trial.

The trial was the biggest of its kind in the field to date and its high-profile failure drew a lot of attention. But experts told Live Science that it doesn't mean we should count out MCED technology.

Why Galleri was put to the test

The majority of cancer diagnoses and deaths are from cancers that have no well-established screening program, such as pancreatic cancer. Without these early-detection methods, like regular colonoscopies for colorectal cancer, many cancers are caught late.

The perfect MCED test could, in theory, make finding cancer a breeze. Such a test could use a single blood sample to screen for many cancers, detecting disease-linked changes in DNA and other cellular markers of disease floating in the bloodstream.

But designing a trial that proves that MCEDs can improve patient outcomes is difficult. Earlier diagnosis can be life-saving in some types of cancer, said Jessica Lloyd, a strategic evidence manager at the nonprofit Cancer Research U.K. Five-year survival rates drastically improve when lung or colorectal cancer are detected at an earlier stage. But for other cancers, such as melanoma, earlier diagnosis makes little difference to overall survival rates.

The ideal trial would follow a group of patients over many years; one half would receive MCED testing while the other would not. At the end of the trial, data would reveal whether overall cancer deaths were reduced in the group that received testing.

But there's already a lot of hype around MCED tests, and there's little appetite in the field to wait years for clear results that the tests improve outcomes, or to pay the high price tag that such long studies would incur.

Instead, the recent trial of Galleri, run in collaboration with the U.K.'s National Health Service (NHS), lasted only three years. It measured whether the test could identify cancers at an earlier stage, considering the early detection a proxy for mortality data. In other words, early detection was assumed to lead to lower death rates.

The trial recruited 142,000 healthy people ages 50 to 77. Participants had their blood drawn roughly once a year for three years. Each time, for a subset of participants, the Galleri test looked for markers linked to 12 different types of cancer. If a patient tested positive, they received further treatment. This tested group was compared to another that didn't have their blood tested.

The aim of the trial was to assess whether significantly fewer cases of late-stage cancers — meaning stages III and IV — would be detected in the test group; at that stage, disease has started spreading beyond the cancer's origin point to other tissue. The rationale was that the test would instead pick up these cancer cases in stages I and II, before the disease had spread. But Galleri failed to meet this endpoint.

Samantha Harrison, Lloyd's colleague and head of strategic evidence at Cancer Research U.K., said that the test's failure to reach its main target is "disappointing." However, she added that the trial's huge dataset hasn't been detailed in a peer-reviewed publication yet, which would shed more light on the trial's full value.

What went wrong for Galleri?

Galleri's problems were related to both the diagnostic test itself and the trial design, said Ruth Etzioni, a biostatistician at Fred Hutchinson Cancer Center in Seattle. Galleri caught an unexpected number of advanced cancer cases among the trial volunteers the first time they were tested.

These cases came as a surprise, because the volunteers recruited to the trial had not been diagnosed or treated for cancer over the previous three years. Etzioni said that if the trial were begun anew, these initial cases would likely be excluded from the analysis, which would have helped improve Galleri's performance.

But even with that adjustment, she added, it's unlikely the trial results would have significantly changed. That's because the test was unexpectedly bad at picking up early-stage cancer, she told Live Science.

"That's critical," she said. "You have to have an increase in stage I to II, and then that then coincides with the decrease in stage III to IV," she said.

The MCED test doesn't look for a lone marker that determines whether a patient has cancer or not. Instead, the various disease markers that the test looks for are weighed and a threshold is applied, above which the test yields a positive result. Etzioni said the test appeared to be conservative in how it registered these positive results; it applied a high threshold to deem a case "positive." That may explain why the harder-to-detect, early-stage cancer cases were not picked up.

But she added that some of the more dismissive commentary around Galleri's performance is "short-sighted."

"I don't think that this trial was a flop," she said. "I think it was hugely informative."

Galleri hopes that results from its upcoming Real-world Evidence to Advance Multi-Cancer Early Detection Health Equity (REACH) study, which has enrolled 50,000 patients in the U.S., will be more positive. The REACH trial has a slightly different endpoint in that it's measuring the test's ability to reduce stage IV diagnoses. The data from the NHS trial suggested Galleri did reduce these diagnoses, which was a secondary endpoint of the trial.

What does this mean for other MCED tests?

Galleri is just one of many MCEDs under development. What could the negative results from Galleri's initial trial mean for the future of cancer detection?

MCED tests are proliferating rapidly, and improvements to the panels used to detect cancer markers should enhance the performance of newer tests, said Etzioni. That said, she noted that, as these tests are closely guarded by manufacturers, it's hard to know exactly which markers would advance performance. Dozens of presentations at ASCO 2026 focused on other MCEDs in the field.

Galleri's results might mean a slightly longer wait before the tests are used widely, Etzioni said. She felt that some of the hype from GRAIL's earlier studies of the test has now dissipated. "They've maybe [previously] led the community to believe that the technology is more ready for prime time than it actually is," she suggested.

Harrison pointed to a position statement from the U.K. National Screening Committee (UK NSC), which provides advice to government ministers on implementing new disease screening programs. The statement, released in May, directly addressed so-called surrogate endpoints, such as the cancer stage-related endpoints used in the initial Galleri trial.

One concern, it pointed out, is that MCED tests may more easily detect aggressive cancers than slow-growing ones. So even if future trials show the tests find these cancers at earlier stages, patients may still die at similar rates because the types of cancer found at these early stages are harder to treat. So improvements in detection can't be assumed to translate to improvements in survival.

The UK NSC stated that further evaluation would likely be required before a MCED test would be adopted in widespread clinical practice, such as within the NHS. (For what it's worth, though, some MCEDs are available for direct-to-consumer purchase despite not proving their worth in gold-standard trials yet.)

The Galleri trial focused on the test's ability to identify cancer in a (presumably) healthy population, but this is just one potential use of the technology behind the tests. It could also be deployed to test people with non-specific symptoms that may hint at cancer or in populations who are known to be at high risk of the disease. Another NHS Galleri trial, called SYMPLIFY, suggested the test was accurate when used in symptomatic patient groups, Lloyd noted.

Galleri's results are not a reason to discount the value of MCED tests more widely, Etzioni said. She believes the tests will someday be used routinely for early cancer detection.

"This is just the beginning," she said.

This article is for informational purposes only and is not meant to offer medical advice.

Scientists genetically tweaked a tiny, worm-like parasite to produce a life-saving antitoxin from inside a living host.

In a first-of-its-kind study, researchers modified the hookworm Ancylostoma ceylanicum so that it produces antibodies that partially neutralize the potent pufferfish poison tetrodotoxin.

The approach has so far been tested in hamsters, but the ultimate aim is to use it in people. In fact, the study was funded by the U.S. Department of Defense with a view to developing protective treatments for military personnel exposed to chemical or biological threats, such as tetrodotoxin, study co-author Alex Loukas, director of the Australian Institute of Tropical Health and Medicine at James Cook University, told Live Science.

That said, future work could see these worms engineered to produce a variety of other medications and excrete them inside the human body, the study authors wrote in a report published June 3 in Nature Communications. For instance, they could deliver long-term treatments for chronic diseases, such as type 2 diabetes or inflammatory bowel syndrome, Loukas suggested.

From parasite to antitoxin factory

Hookworms are one of humanity's oldest parasites and infect upwards of 400 million people globally, primarily in tropical regions. Like an internal leech, these small intestinal worms latch on to the inner wall of the gut to feed on blood, simultaneously releasing a variety of anti-inflammatory and immunosuppressant compounds to prevent the body from flushing them out.

Each worm is about 0.4 inches (1 centimeter) long and consumes less than two drops of blood a day, and healthy hosts often don't experience any symptoms of infection. The hookworm used in this study, A. ceylanicum, infects humans, dogs and cats.

"The hookworm has spent millions of years perfecting how to assure long-term survival inside a human host and how to get molecules out of its body and into ours," study co-author Makedonka Mitreva, professor at Washington University School of Medicine in St. Louis, Missouri, said in a statement.

The cocktail of compounds produced by these parasites has already shown some promise in treating metabolic disorders such as metabolic syndrome and type 2 diabetes, as well as celiac disease. However, studies so far have been restricted to molecules produced by the hookworms naturally.

The new work pushes this concept one step further. "We asked: What if we could add one more molecule to the roughly 1,000 things the worm already secretes, something therapeutically useful to people?" Mitreva said. "This study shows that's not just a concept. It works."

Using CRISPR gene-editing technology, the team inserted a gene coding for an antibody known to counteract the deadly pufferfish poison tetrodotoxin into the hookworm's genome at the egg stage. Mitreva's team had to carefully consider the placement of the gene, ensuring it didn't interfere with other critical regions of DNA, yet still promoted production and secretion of the new protein.

The team then infected hamsters with 80 to 100 of the modified parasite larvae. Upon maturation, the adult worms containing the newly inserted gene were able to produce the antibody and then secreted it into the hamster's bloodstream. Blood samples later taken from the infected hamsters partially neutralized the tetrodotoxin poison in lab experiments, showing compounds produced by the worm were active in the hamster.

On paper, the same approach could be used to secrete other antibodies or peptide drugs — which are short bits of protein — to directly treat gastrointestinal disorders, Loukas said.

"We're thinking about actively introducing antibodies that neutralize inflammatory hormones or cytokines," to treat conditions such as inflammatory bowel disease, he said. "You can also think about the possibility of a worm that secretes very very small quantities of food allergens to desensitize the host for childhood food allergies,” he added.

Looking forward, the team wants to extend the durability of the therapeutic molecules the worms release, since they can only make so much at a time, he noted.

While it may sound counterintuitive to infect a person with a parasite to help them feel better, hookworms actually have an excellent safety profile, Loukas said. A quirk of their biology means there is no chance of the infection getting out of control.

Hookworm larvae enter the body through the skin and migrate to the small intestine where they mature into adults, often living for years without noticeably impacting the host. Any eggs the adult parasites produce must hatch outside of the host; they exit in the host's stool. That means the number of adult worms in the body remains fairly constant.

What's more, with a single dose of a standard anti-worming treatment, the infection clears within 24 hours. So any hookworm-based treatments could be easily cleared from a person's system.

"It's exciting and it's really opening up an entirely new way of delivering and producing therapeutic molecules," Loukas said.

The individual: A 78-year-old man in the United Kingdom

The discovery: The man donated his body after death. While dissecting the cadaver, medical students made a "serendipitous discovery" in the pelvis, according to a report of the case.

Inside the skin of the scrotal sac and adjacent to a primary external penis were two smaller penile structures. Only the primary penis was externally visible, but all three penises included a bulbous structure called a glans and a chamber of spongy tissue that would fill with blood to create an erection, known as the corpus cavernosum.

What happened next: Doctors measured the three penises, finding that the external penis measured about 3 inches (7.7 centimeters) long and was 0.9 inches (2.4 cm) wide. The second penis measured 1.49 inches (3.8 cm) long and was 0.51 inches (1.3 cm) wide, while the third penis was 1.45 inches (3.7 cm) long with a width of 0.47 inches (1.2 cm).

Upon closer examination, doctors saw that there was only one urethra — the tube that transports urine from the bladder — which followed a "meandering course" through the secondary penis and then into the primary penis, terminating in the external penis' urethral orifice. There were no branches in the tunnel, and no additional urethral tubes were found in the third and smallest penis.

The diagnosis: During fetal development, a structure called the genital tubercle arises and eventually develops into external genitalia, forming either a clitoris or a penis. "In this case, there may have been triplication of the genital tubercle," resulting in three penises, according to the report. Possessing three penises is called triphallia. (The more common variant of this anomaly is diphallia, referring to two penises.)

The urethra originated in the secondary penis, but changed course and redirected into the primary penis when the secondary one failed to fully develop, the authors suggested.

The analysis: Instructors and students at the medical school did not know the man's identity, nor did they have access to his records or medical history. As a result, they were unsure if the man knew about his condition. Nevertheless, they expressed doubts in the report that his triphallia went entirely unnoticed.

Had the man required a urinary catheter insertion, the procedure would have been extremely challenging due to "the tortuous nature of the urethra" winding around and through his second penis, doctors explained in the report. They also noted signs of scarring in the man's groin from an inguinal hernia, in which abdominal tissue oozes through an opening in the abdominal wall called the inguinal canal.

Internal pressure or friction from the presence of two additional penises may have weakened the man's lower abdominal wall and contributed to the hernia, the authors theorized. Medical attention for the damage could have led other doctors to discover the supernumerary penises, they added.

What makes the case unique: The development of more than one penis is extremely rare, appearing in approximately 1 in 5 to 6 million live births, according to a 2010 review of published case reports; these cases are predominantly diphallia. The man's case was the first discovery of a triple penis in a cadaver, and the second known example of triphallia documented in scientific literature, in general.

In most cases, extra penises are associated with medical issues such as sexual dysfunction, fertility problems and urinary tract infections. When supernumerary penises cause physical discomfort or medical complications, a common solution is to surgically remove them. Or, if they are externally visible, the patient may choose to remove them for cosmetic reasons, according to the report.

Perhaps in this case, the authors speculated, the man knew about his triphallia but opted to forgo surgery "due to the apparent lack of symptoms" and the "benign nature" of his condition.

This article is for informational purposes only and is not meant to offer medical advice.

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The Ebola outbreak in Central Africa was declared a public health emergency of international concern in May, and since then, over 900 suspected cases and 200 deaths have been reported in the Democratic Republic of the Congo (DRC) and Uganda.

With the majority of cases impacting the DRC, this marks the country's 17th Ebola outbreak since the discovery of the virus on the Ebola River in 1976. Most of these outbreaks were caused by the highly lethal Zaire virus, a species of Ebola virus that now has approved treatments and vaccines.

This newest outbreak, however, is being caused by the Bundibugyo virus, a more recently discovered species that is less lethal than Zaire but has no approved vaccines or treatments.

According to modeling published in the Morbidity and Mortality Weekly Report, this epidemic has the potential to become one of the largest Ebola outbreaks on record. It could exceed 20,000 cases in the next three months if effective intervention measures are not taken. Such efforts are underway, but they're complicated by conflict in the region and a dearth of international aid and health infrastructure.

Vaccines can help control Ebola outbreaks, as well as prevent future ones, by enabling health officials to inoculate the close contacts and potential contacts of confirmed and probable cases. Alternatively, all individuals in a given neighborhood or village might be vaccinated, if an outbreak is fairly concentrated. So now, a major effort is underway to craft brand-new vaccines for the Bundibugyo virus.

"The goal is to get a safe and effective Bundibugyo vaccine developed as quickly as possible," Dr. Richard Hatchett, CEO of the Coalition for Epidemic Preparedness Innovations (CEPI), told Live Science in an email.

Different virus, different challenge

Since the 2014-2016 Zaire virus epidemic ‪—‬ the largest Ebola outbreak ever recorded ‪—‬ scientists have learned a lot about how to control these epidemics. Tools such as rapid diagnostics, contact tracing, isolation, infection prevention, safe burials and prompt clinical care are key to reducing transmission and saving lives.

However, according to Dr. Anne Rimoin, chair of infectious diseases and public health at UCLA, there's much less field experience for this particular outbreak, as there have been only two recorded Bundibugyo outbreaks to date.

In addition, the Bundibugyo virus may have had a big head start before it was detected. Experts suspect that, although the outbreak was declared in mid-May, it likely began in February.

If new vaccines are approved, they could help to curb the outbreak using strategies like "ring vaccination." Through a combination of surveillance, contact tracing and rapid vaccination, health officials can vaccinate the close contacts of a person with a confirmed infection, thereby creating a "ring of protection." Potential contacts, and contacts of people with probable cases, can also be vaccinated under this strategy.

Other strategies include the targeted vaccination of populations with the highest transmission rates or phased rollouts of the vaccine that prioritize those at greatest risk of exposure. Even vaccination after exposure, if done quickly, can reduce the risk of severe illness and death.

Global efforts accelerate vaccine development

Scientists and vaccine manufacturers are now racing to design, test, manufacture and deploy vaccines that could help prevent this outbreak from persisting for several years, as previous outbreaks have.

CEPI, a global partnership to accelerate the development of vaccines and treatments against epidemic and pandemic threats, recently announced its support for the development of three vaccine candidates from three institutions: the International AIDS Vaccine Initiative (IAVI), the pharmaceutical company Moderna, and the University of Oxford. The vaccines will be manufactured by the Serum Institute of India.

"We are supporting three different vaccine platform technologies," Hatchett said. "All of these technologies have also been used to develop early-stage candidate vaccines targeting viruses that are closely related to Bundibugyo, so we have a lot of information about how they perform against other Ebolaviruses."

The IAVI vaccine employs rVSV vaccine technology, similar to what is used in the vaccine against the Zaire virus. rVSV stands for "recombinant vesicular stomatitis virus," and rVSV-based vaccines contain a weakened flu-like virus normally found in animals. This virus is tweaked so it makes proteins belonging to the target, in this case, Bundibugyo virus.

Previous Zaire vaccines made with this technology showed 95% to 100% effectiveness in preventing Ebola disease after just one dose ‪—‬ a feature that can be essential in controlling an outbreak.

Oxford's vaccine is using the same technology that forms the basis of the Oxford-AstraZeneca COVID-19 vaccine. Called the ChAdOx1 platform, it uses a harmless version of a common cold virus that infects chimpanzees as its base. This platform is easier to adapt to new strains than rVSV technology, and while rVSV vaccines need to be frozen, it can be transported at refrigerated temperatures.

Moderna — whose mRNA vaccine against COVID-19 was the first to enter human trials — is now using the same technology to design a Bundibugyo virus vaccine. This platform uses mRNA, a molecular cousin of DNA, which gives cells instructions to make small pieces of an inactive viral protein. Because of their production speed and design flexibility, mRNA vaccines have become the best way to rapidly design vaccines against specific viral species.

Preparing the vaccines

Once designed and tested in the lab, the vaccines will move quickly to early-stage clinical trials, in which they will be tested on a small group of healthy volunteers, according to a CEPI statement. These vaccine platforms have already been safely used against similar viruses in both trials and real-world scenarios.

If the safety trials are successful, late-stage trials will begin, with the goals of testing more volunteers and generating enough data for emergency use authorization and production.

According to the World Health Organization (WHO), this could take seven to nine months. The CEPI coordination effort aims to accelerate this timeline by providing funding for the late-state clinical trials. In previous outbreak scenarios, vaccine production often happens at the same time as safety testing to ensure quick deployment.

It is unclear which vaccine might be the most effective or deployed first, although the WHO thinks the IAVI vaccine is likely the most promising. In the meantime, coordinated efforts on the ground will likely make the biggest impact on how the outbreak progresses in the immediate future, experts told Live Science.

Deploying vaccines in an outbreak zone like the DRC presents many challenges. The DRC generally relies on the import of vaccines, but many regions don't have the refrigerated storage facilities required for certain vaccines. If they do, unreliable electricity grids and poor road networks still make it difficult to keep vaccines cold during transport. Vaccine hesitancy can also be high in certain areas.

"We have better tools and better knowledge than we had a decade ago, but all these tools only matter if they reach the front lines quickly, and if communities trust the response," Rimoin said. "So far, we've got a lot of issues with trust in this area."

While vaccines are great tools, researchers and responders must be realistic about timing, Rimoin added.

"These are certainly not going to be tools that are ready to change the course of the outbreak tomorrow," Rimoin said. "The response is going to be depending on the basics: finding cases and isolation, contact tracing, protecting healthcare workers and building community trust."

This article is for informational purposes only and is not meant to offer medical advice.

Polyendocrine metabolic ovarian syndrome (PMOS), previously called polycystic ovary syndrome (PCOS), is a common hormonal disorder in females. The condition has wide-ranging effects on the body, affecting metabolism, hair, skin and mental health, and sometimes making it hard to get pregnant, according to the Mayo Clinic.

PMOS affects over 170 million people of reproductive age worldwide, including up to 12% of U.S. women of reproductive age.

PMOS is characterized by high levels of androgens, the group of sex hormones that includes testosterone. It's often associated with resistance to insulin, a hormone that regulates blood sugar. The condition can come with a range of symptoms, including irregular periods, excessive weight gain and hair growth, and acne.

Many individuals with PMOS also have underdeveloped eggs, or "arrested follicles," lining the outer edges of their ovaries, which doctors previously labeled as cysts. However, calling these "cysts" was misleading, as people often thought they were the same as pathological noncancerous ovarian cysts, which can rupture, cause pain or bleed, and sometimes require surgery to treat.

The incorrect focus on so-called polycystic ovaries, which are neither necessary nor sufficient for a diagnosis, was part of the reason PCOS was officially renamed on May 12, 2026.

What causes PMOS?

Scientists don't know the root cause of PMOS, and there is probably more than one, Dr. Marie Menke, a reproductive endocrinologist at University of Michigan Health, told Live Science.

One possible cause is that the ovaries make excess levels of certain sex hormones, including testosterone and anti-Müllerian hormone, Live Science previously reported. This, in turn, may drive many of the other symptoms, so whatever is driving the excessive hormone production may be the key. Why some ovaries produce excess sex hormones, however, is unclear. Efforts to build better laboratory models of the ovaries could reveal the answers to some of these questions.

Obesity and insulin resistance ‪—‬ the body's inability to use insulin effectively — also may play a role in triggering PMOS, although whether these conditions are a cause or consequence of PMOS has been a matter of debate. Other studies have proposed that children who are exposed to high levels of androgens in the womb may go on to have the syndrome.

Genes play a role, too: PMOS tends to run in families, and a person whose family members have PMOS is more likely to develop it. People with a family history of type 2 diabetes are also more likely to develop PMOS, according to the World Health Organization.

PMOS and pregnancy

PMOS symptoms often start in early puberty and some persist through and after menopause. Many people find out they have the condition in their 20s and 30s, if they have trouble becoming pregnant. PMOS can make it difficult to become pregnant without fertility treatment because androgens prevent immature follicles from developing into mature eggs that can be released and develop into an embryo, according to the U.S. Office on Women's Health (OASH).

People who are hoping to get pregnant have a number of treatment options, including fertility medications, such as clomiphene (also known by the brand names Clomid and Serophene); or gonadotropins, such as follicle-stimulating hormone or luteinizing hormone, according to the OASH. Metformin, a type 2 diabetes drug, can also be used to promote ovulation.

PMOS symptoms

According to the OASH, PMOS may include these signs and symptoms:

• Infertility: People with PMOS do not ovulate regularly, so they have fewer chances per year to become pregnant
• Infrequent, irregular or absent menstrual periods
• Hirsutism, or increased hair growth on the face, chest, stomach, thumbs or toes, likely caused by excess androgens
• Ovaries that are enlarged or have many arrested follicles
• Acne or oily skin, also likely caused by excess androgens
• Weight gain or obesity
• Male-pattern baldness or thinning hair, another symptom of excess androgens
• Acanthosis nigricans: Thick, dark patches of skin on the neck, arms, breasts or thighs
• Skin tags, which are excess flaps of skin in the armpits or neck area

Diagnosis and tests for PMOS

Diagnosing PMOS can be challenging because symptoms vary a lot, Menke said. And many of them are nonspecific, meaning they're not uniquely tied to PMOS.

To be diagnosed with PMOS, a patient must experience at least two of the three main symptoms described below, Menke said:

1. Irregular menstrual cycles: Irregular, infrequent or no periods are caused by a lack of ovulation. For example, someone may have fewer than nine periods a year or have unpredictable periods.
2. Higher-than-normal levels of androgens.
3. Polycystic ovaries, identified by ultrasound. However, some patients with PMOS have normal-appearing ovaries, and other women with cysts (fluid-filled sacs) on their ovaries may not have PMOS.

Complications of PMOS

PMOS has been linked with a number of other health conditions, including:

• Metabolic syndrome: A group of risk factors for heart disease, stroke and diabetes that is twice as common in people with PMOS than the general population, according to the American Academy of Family Physicians
• Type 2 diabetes: More than half of people with PCOS develop diabetes by age 40, according to the Centers for Disease Control and Prevention
• Cholesterol abnormalities, such as high LDL ("bad") cholesterol and low HDL ("good") cholesterol, which can increase the risk for heart disease
• High blood pressure, which can affect the heart, brain and kidneys
• Sleep apnea, which can cause pauses in breathing during sleep
• Anxiety or depression
• Diabetes or high blood pressure during pregnancy

Treatment and medications for PMOS

It is difficult to treat all of the symptoms of PMOS at once, Menke said, so she typically asks her patients what their primary concern is and then focuses treatment on managing those symptoms first. For example, if someone's main concern is excess hair growth, Menke said she would typically prescribe birth control pills, which can help reduce levels of androgens.

There are treatment options to help manage the symptoms of PMOS, Menke said. According to the Mayo Clinic, treatment options may include the following:

• Birth control pills, which contain either a combination of estrogen and progestin or progestin only, can regulate menstrual cycles, reduce androgen production and help clear acne.
• Progestin hormone replacement therapy can also regulate menstrual periods. (It is not a contraceptive.)
• Fertility medications can stimulate ovulation in PMOS patients who wish to become pregnant.
• Weight-management drugs, such as GPL-1 agonists, which include medicines like Wegovy
• Anti-androgens, such as spironolactone or flutamide
• Diabetes medications, such as metformin, make the body more sensitive to insulin.
• Acne treatments and hair removal therapies, such as laser hair removal or electrolysis

This article is for informational purposes only and is not meant to offer medical advice.

Humans are not isolated, interchangeable biological machines. We seek medical care carrying complicated backstories, life experiences, and cultural perspectives that shape how we experience illness, communicate pain, and respond to treatment.

For decades, medicine ignored this fact and the cost fell heaviest on patients from marginalized groups. Study after study has documented the result: stark disparities in health outcomes that track closely with race, income, zip code, and immigration status.

Medicine has only recently begun to reckon with this blind spot. For the last few years, medical students across the country have been required to receive training in what are called "social determinants of health" to better understand how trauma, poverty, racism, and life experience shape what patients bring into the exam room and what they need from the people treating them.

But the board governing medical school accreditation no longer wants this training to be mandatory. This would be a big step back for medicine. Keeping these standards in place is essential for making a more effective medical workforce that can deliver the best care possible while doing no harm.

My experience with both sides of the medical system — as a second-year MD/PhD student and a patient — shows why this training is so necessary.

A few months after I turned 21, I went in for a routine checkup and was told by my physician that I needed my first Pap smear. I understood the importance of the test, but it wasn't something I had prepared for that day.

When the exam began, I flinched at the cold speculum. My physician noted my tension and said it was interfering with the exam. I tried to relax, but as a survivor of sexual violence, the sensation triggered memories I hadn't expected. I asked her to slow down and at some point, stop. Instead, one of the physician assistants held my legs open as the speculum moved further. As the exam wrapped up, the only sounds in the room were my occasional sniffles as I cried quietly.

My mother, too, has endured the experience of being unheard by physicians. An immigrant from Accra, Ghana, she had healthcare providers hear her accent and see her non-citizen status and make a quiet calculation: one that placed her judgment below theirs and created a lifetime of consequences she continues to deal with to this day.

At five years old, the phrases "structural violence" or "medical racism" were not yet a normal part of my vernacular, but I didn't need a college education to understand that my mother's immigrant identity shaped the care she received, or more accurately, the care that was withheld from her. Her experiences were the consequences of a system that delivers less attentive, less thorough, and less humane care to patients who are Black, low-income, or immigrant. It has done so for so long that the disparity reads as normal.

We've finally started to see a shift in that system, however slight. A year after the first Pap smear, I needed an additional one. Despite knowing this screening was essential for my health, I was still very hesitant and expressed my fears to my physician. This time, however, my physician used trauma-informed care throughout the procedure. She checked on me before we got started, narrated each step, and moved slowly so I could stop and breathe when I needed to. She gave me back the control and autonomy I had lost. Once we were done, she checked on me before letting me get dressed.

When the door closed, I let myself sob, not from pain, but because she cared. I mourned the version of me that wished she could have been granted that care the first time, and I found myself mourning my mother too, feeling a connection to her in the most unfortunate way.

The difference in my two experiences was not incidental. It is the result of training. Medical education now teaches future physicians to recognize how trauma, lived experience, and social context shape patient care, which collectively is called structural competency.

Such training equips future doctors to ask better questions, communicate more effectively, and avoid causing harm, even during routine procedures. Since starting medical school, I have seen how this training shapes the way my peers and I understand patients. A patient with uncontrolled asthma is not simply "noncompliant" with their treatment regimen, but may be living in substandard housing with mold exposure. A patient with poorly controlled diabetes may not lack "motivation," but may face food insecurity or unstable income.

Structural competency enables physicians to see the full picture and ultimately treat patients with the dignity they deserve. Rather than simply adjusting a medication dose or repeating discharge instructions, a structurally competent physician might coordinate with a social worker, connect a patient to community resources, or advocate for systemic changes that no prescription can address.

Research supports that structural competency training improves both how physicians practice and how patients fare. A 2016 pilot study in California found that such training led to better patient satisfaction scores, and a more recent study found that it increased residents' sense of competency.

The training curriculum has only been required for a few years, but some early evidence hints that it could yield positive patient outcomes. Physicians trained to recognize these factors are also more likely to advocate for policy changes related to housing, education, and income equality: key determinants that influence chronic disease prevalence, infant mortality rates, and overall life expectancy.

The American College of Physicians has formalized this thinking, publishing recommendations urging physicians to ask about and address social factors as a core part of patient care, and real-world implementation backs this up. One Michigan physician network that began systematically screening patients for social needs in 2017 conducted over 20,000 screenings and used the results to connect patients to social services.

This is partly why the Liaison Committee on Medical Education (LCME) that accredits med schools currently mandates that structural competency be taught in every school — but that's about to change. In the wake of the second Trump administration's attack on diversity, equity and inclusion efforts, the committee is indicating that it will likely no longer require structural competency training as a part of medical education.

It would be reassuring to think that even in absence of this training, nothing would change; that good physicians will remain attentive, and empathy will fill the gap. My mother's story and my own suggest otherwise. Medicine does not become neutral in the absence of this education. It defaults, reverting to entrenched habits of thinking that ignore the nuances of how a patient's background informs their care.

At a time when mistrust in medicine is already high, we cannot afford to strip away the training that helps rebuild it. So what can be done?

Medical students must advocate within their institutions to preserve and strengthen structural competency education. Faculty must keep such training in their medical curriculum, even if LCME doesn't require it. Most importantly, professional organizations from local institutions to national bodies like the American Medical Association, must speak out clearly and use their congressional lobbying powers to push for the LCME to reverse its decision.

I love medicine. I am training to become a physician-scientist because I want to help build a future where care is both innovative and just. But I will not stand by while medicine forgets its own history. We have made progress, inches in the right direction. So we must do all that we can to ensure that we don't fall back, because the consequences will ultimately be the trust, the support and the lives of our patients.

Opinion on Live Science gives you insight on the most important issues in science that affect you and the world around you today, written by experts and leading scientists in their field.

A deadly Ebola disease epidemic is rapidly unfolding in the Democratic Republic of the Congo (DRC) and Uganda. In May, the World Health Organization (WHO) declared the epidemic a public health emergency of international concern, citing a high risk of further international spread.

As of June 6, there have been 515 confirmed cases and 91 confirmed deaths in the DRC, according to the WHO, and 19 confirmed cases including two confirmed deaths in Uganda.

The outbreak is being caused by the Bundibugyo virus, one of three ebolaviruses known to cause large outbreaks. Unlike the Zaire ebolavirus, which caused the largest Ebola epidemic to date, the Bundibugyo virus does not have a licensed vaccine or medicines.

To get a better understanding of the outbreak and its global implications, Live Science spoke with Dr. Ali S. Khan, professor of epidemiology at the College of Public Health, University of Nebraska and former assistant surgeon general of the U.S. Public Health Service.

Khan has been involved in 25 international and domestic disease outbreak responses, including muliple Ebola outbreaks, during which he worked in the DRC and Uganda. He was director of the Office of Public Health Preparedness and Response at the Centers for Disease Control and Prevention from 2010 to 2014 and currently serves on the WHO Steering Committee for Global Outbreak Alert and Response Network.

Here's what he had to say about the Ebola epidemic and the future of public health threats.

Sophie Berdugo: This year's outbreak currently stands as the third-largest Ebola outbreak ever recorded, spreading faster in its early stages than the largest outbreak in 2014. What factors have made it so big?

Ali S. Khan: This outbreak is occurring in the midst of a political and humanitarian emergency that's going on in the Democratic Republic of the Congo, in an area with significant ongoing political violence, and fighting that is ongoing. That makes it very difficult. It's a remote area, it's an impoverished area. There's little to anything in the way of government services for health care or public health. So, it's not surprising that we see an outbreak there. This is the 17th outbreak in the Democratic Republic of the Congo.

But given the nature of where it is, it was identified late and so there have been multiple chains of transmission that have occurred before it was identified. It was late enough that now we're seeing what many would characterize as "community transmission." So that's why it's big.

Whether it's spreading faster is up for debate because they're still trying to understand where it is. It may just be spreading faster because they're identifying where all the cases are. So it may have already spread. Not that it's not going to spread further, but the early stages of the outbreak is just trying to get a handle on how many cases, who's infected, and where they're infected.

Fever, headache, muscle aches as an initial set of symptoms is not unusual in a country with a whole lot of malaria. So it can look like almost anything. Sick healthcare workers, dead healthcare workers act as a signal for a disease like Ebola.

And in this specific case, there was one final factor which is when they suspected the outbreak: the initial set of diagnostic testing they did, the tool they used, does not test for Bundibugyo. It only tests for Ebola Zaire. So the initial diagnostic testing to them suggested that this is just some other severe tropical febrile disease, and it's not Ebola.

Then when the right set of samples eventually went to the Ministry of Health where they had more sophisticated testing they could go "Wait, it is Ebola; it's just a different strain of Ebola."

SB: Will we need to control this Bundibugyo outbreak differently from previous Ebola epidemics?

AK: A response to an Ebola outbreak is the same as a response to any Ebola outbreak. It's all about excellent monitoring to identify cases, get them into a health care facility so they can no longer infect people within their community, and make sure they have great care. And then make sure there's good infection control so that you don't infect other healthcare workers. So that's step one.

The second step is [an] excellent follow-up of the contacts of infected people [to] find them and then make sure that they're quarantined in a humane way. And the third piece is safe burials. You want to ensure that if people die in the community that you have safe, dignified burial practices.

So those are the three critical components. Every [response to an] Ebola outbreak will do that.

This outbreak is challenging for two reasons. One is with Zaire, we now have drugs that can help a patient. We do not have similar drugs [for Bundibugyo]. So that makes it more difficult within the health care setting to save people's lives.

The other thing from the prevention standpoint is that we don't have vaccines. So for Zaire, you can vaccinate people. For example, you can vaccinate healthcare workers, we can vaccinate people who are contacts to decrease the likelihood of them getting infected.

So you really are completely relying on good old-fashioned, boots-on-the-ground public health. And that's difficult in a humanitarian crisis. And it's exacerbated by the lack of trust that there is for the government, which isn't there anyway, [and an] additional lack of trust for international partners.

Let's remember these people are dying every day of preventable diseases like malaria and nobody shows up, and the moment they have an "exotic disease" for the West, hundreds of millions of dollars and thousands of [medical] responders are showing up. It's very easy to see why there may be mistrust in this situation.

At the end of the day, the biggest factor in every outbreak is risk communications and community engagement. You can get an outbreak under control very fast if the community really is engaged and you communicate it well with them and they want to help make this happen.

SB: Do you have any concerns about the current approach the U.S. is taking to this outbreak? How may have cuts to the U.S. Agency for International Development (USAID) exacerbated it?

AK: I think it's fair to say that USAID has always been a critical partner in these outbreaks for logistics, for provision of personal protective equipment, PPE. So there's no doubt that we have lost that connection on the ground that the U.S. government used to have with these outbreaks.

That said, we do know that the U.S. is supporting the response from a financial standpoint. CDC and other partners have been engaged with WHO to help coordinate their actions and understand what's going on and how they can potentially help.

It's easier to say in the abstract than in the concrete because there's hundreds of partners during an outbreak. To say "this is not happening because this partner is missing" is difficult, but there's no doubt that the lack of USAID is going to impact any outbreak where in the past USAID has been such a critical partner on the ground.

People have asked in the past, "If USAID was there, would we not have heard about this outbreak earlier?" In the abstract, yes, but there's no concrete evidence of that. I mean, the truth is this outbreak occurred in the midst of a humanitarian crisis and the initial diagnostic testing didn't trigger an appropriate response. And there's always outbreaks in DRC of unexplained severe febrile illness.

I'm not sure if we can say the USAID and other cuts led to this outbreak. These outbreaks are going to happen: It's in the right part of the world for them to happen. For the animals being infected then infecting humans. [Humans can become infected when exposed to the bodily fluids of infected animals, such as fruit bats and chimpanzees.] There is little to no infection control in the healthcare setting, so the outbreaks are going to spread regardless.

SB: On that point, you said in a 2020 interview that a "disease anywhere is a disease everywhere," emphasizing the need for a global effort given diseases can be spread anywhere.

AK: Absolutely. We worry about these transboundary diseases for lots of reasons. One is the local impact in communities. We worry about large national and regional spread as we saw in Ebola in 2014. And then as with SARS-CoV-2 [the virus behind COVID-19] or the next influenza virus, we worry about global spread.

The best approach for all of us as global citizens is to rapidly identify a disease where it is and address it there so that it doesn't spread. And that takes multiple partners in communities, in partnerships with governments, to make that happen. And that remains more critical today than ever because of the speed at which diseases can travel.

So yes, a disease anywhere is a disease everywhere, but a disease anywhere can be a disease everywhere tomorrow morning.

Nowadays, I could get infected in Bunia [the capital city of Ituri Province in the DRC] today, and tomorrow evening, I could be sitting in New York City. I've got the virus inside of me but I'm not going to be sick for another week or so, but there's no way to know about that hidden infection because of the incubation period. Our speed of travel has become faster than this incubation period, and that has proven to be a downfall in terms of our ability to protect ourselves.

The old strategies of "lock down borders, keep ships from coming to your ports" — that doesn't work because it's probably already there by the time you decide that's what you need to do.

SB: This Ebola outbreak was reported within weeks of a cluster of hantavirus cases aboard a cruise ship. Are we heading into a world where the threats of epidemics, and possible pandemics, become more likely?

AK: Yes, without a doubt. They're becoming more likely for lots of reasons. One is, as humans move out into the environment, there's an increased opportunity for this human-animal intersection and then spillover into humans. So that risk remains and is probably increasing.

Climate change is also having its own impact as vectors — mosquitoes, ticks and rodents, etc. — move into new areas where they weren't previously. That puts people at risk. So that also helps exacerbate what's going on. Travel exacerbates what's going on because you could be infected and get somewhere faster than you ever could before.

And it's not just the U.S. that is cutting global funding. International development aid has been falling from Germany and other European countries also. So it's not just the U.S. But when you do that then it makes it more difficult for low- and middle-income countries to develop the systems they need to quickly identify these diseases and alert [local people and organizations about] these diseases so that either they take care of it themselves or they get international assistance to help take care of it.

SB: It doesn't look like any vaccines will arrive for nine months, according to the WHO. Is there any way to speed that up, now or in the future?

AK: Yes: Embrace mRNA technology and stop demonizing mRNA technology. Nothing's faster in getting a vaccine than mRNA technology. Nothing comes close. Think about how fast we got this COVID vaccine through FDA [Food and Drug Administration] approval in the United States: less than nine months. And a licensed vaccine with hundreds of millions of doses right off the bat.

We need to embrace new technology to make vaccines so that the moment you have a new pathogen you can spin up the vaccine production and have these vaccines available for people. In the United States, unfortunately we have been demonizing mRNA technology, which is unfortunate because that truly will be the technology that will help us get to a rapid vaccine for the next pandemic.

And I believe CEPI [Coalition for Epidemic Preparedness Innovations] in Europe has made a $10 million investment in mRNA technology for this new Bundibugyo strain. And then the two other vaccines that are being worked on are more classical methods. Those are established technologies that are being modified.

SB: What does the U.S.'s response to this outbreak tell us about its preparedness to face others?

AK: Globally, the fact that we left WHO — even though we are still talking to WHO — puts the U.S. government outside of the typical information loop and coordination loop of what's going on with pandemics. It's not as if we're not talking to WHO, I know that from all my CDC friends that we're talking to WHO.

The U.S. has been a leader over decades — we actually helped establish WHO — for pandemic preparedness, and that lack of global leadership will have an impact on our ability to rapidly recognize and respond to these diseases, which puts not just us but other countries at greater risk of transboundary diseases.

And that message is not just to the U.S., I think that [is a] message to every country in the world which has all of a sudden been up in arms about a dozen hantavirus cases which we knew, those of us in the field knew, posed no threat of a global pandemic.

Communities are understandably fearful when they hear about these sort of "exotic diseases" that are spread from person to person. It makes sense then for governments to help protect them by recognizing that global health security is also domestic health security.

They [disease outbreaks] don't always have to start in Africa and Asia; they could start potentially right here in the United States. And there's no doubt that we've eroded public health authorities since the COVID pandemic here in the United States. Eroding those public health authorities and the continued disinformation that we see weakens our ability to respond to the next pandemic.

Editor's note: This interview has been edited and condensed for clarity.

Flu drugs may help ward off the low-grade inflammation and related cognitive decline that can come with HIV infection, an early study suggests.

Upwards of 24% of people with HIV experience some degree of cognitive impairment that interferes with functions like attention, concentration and multitasking. These declines are often mild but can worsen quality of life, and they can happen even when a person consistently takes HIV medications that suppress the virus.

Understanding why this impairment emerges and how to prevent it is especially relevant as the population of people with HIV grows older.

"This is very important," study co-author Mohamed Abdel-Mohsen, an associate professor of medicine in the division of infectious diseases at Northwestern University Feinberg School of Medicine. "Despite the fact that people living with HIV live longer, so the lifespan is preserved, the 'health span' is not as preserved."

The new study, published Friday (June 5) in the journal Med, pinpoints a potential driver of this decline along with a strategy to reverse it. The scientists used mouse experiments and blood samples from HIV patients, so the work is at an early stage, but it could open the door to future treatments.

"Not only do they describe a mechanism, but they then report in animal models that this mechanism is something that potentially could be targeted by an intervention," said Dr. Alan Winston, a professor of HIV and genitourinary medicine at Imperial College and a consultant physician at St. Mary's Hospital in London. "That's really what's novel," said Winston, who was not involved in the study.

Anti-inflammatory sugars

HIV treatments are now so effective that people with the chronic viral infection can live nearly as long as people without HIV, provided they consistently take the medicines. In 2022 in the U.S., more than half of people living with HIV were over 50 years old, and that figure is expected to grow.

HIV treatment, called antiretroviral therapy (ART), suppresses the virus so that it can't multiply. This prevents the disease from progressing to AIDS while also driving down transmission rates, making the virus unable to spread via sex. But while ART wards off many symptoms of HIV/AIDS and extends an infected person's lifespan, it does not make the chronic infection completely benign. People with HIV still show various signs of accelerated aging, including earlier cognitive decline, in some cases.

"Before we had antiretroviral therapy, we saw profound effects of HIV in the brain," Winston noted. HIV-associated dementia is now rare, because its rates declined as the use of ART increased.

But some percentage of people still develop milder cognitive impairments, and "it can actually have quite a big impact on concentrating at work, for instance, and undertaking daily activities," he said. People have a higher risk of impairment when they've had a big gap between contracting HIV and starting ART, and interruptions in treatment can also raise the risk. However, the underlying cause of the impairments isn't fully understood, Winston said.

To unpack that mechanism, Abdel-Mohsen and colleagues investigated a clue that's recently emerged in the medical literature: sugar molecules called glycans.

These sugars are found throughout the body, including in the bloodstream, where they bind to proteins and fats. In circulation, they tag certain immune molecules to keep inflammation in check. But with age, the concentration of these inflammation-controlling glycans declines: This decline is fairly steady for males, while it has a sudden dip around menopause for females, Abdel-Mohsen said.

Scientists have previously explored how this decline might contribute to age-related diseases, including cancer, while Abdel-Mohsen and colleagues have investigated its relationship to HIV. In a 2024 study comparing people with and without HIV, they found that those with the infection show age-related shifts in their glycans at younger ages than usual. These shifts come with an increase in enzymes known to degrade the sugars, as well as increases in inflammation.

"While it's low-grade [inflammation], it's still damaging because it's continuous," Abdel-Mohsen said. "It's chronic; it doesn't get resolved."

Potential treatment?

In their latest study, the researchers wanted to see if they could connect the dots between the glycan loss, inflammation and cognitive decline.

They analyzed blood samples from more than 100 people with HIV who contributed data to the AIDS Clinical Trials Group, a global research network. All the individuals were taking ART and either had signs of cognitive impairment or did not, according to various assessments. The group with impairments showed greater losses in two glycans that help control inflammation: sialic acid and galactose. In particular, these losses were most pronounced in women, and they correlated with the degree of cognitive decline seen in a given person.

It's not clear why this pattern was more pronounced in women, and that remains a question for future study, Abdel-Mohsen noted. That said, it's known that glycans dip around menopause and that key immune cells bear estrogen receptors, so it's possible that estrogen levels play a role, he suggested. Winston wondered if the timing of diagnosis might also be relevant, since women tend to get diagnosed later than men and may therefore start ART later.

After studying the blood samples, the team used two models of HIV infection in lab mice. One enabled them to study the glycan changes and inflammation triggered by HIV, while the second let them examine signs of cognitive decline. They again found that infection was tied to a loss of glycans and increase in inflammation, as well as worse performance on cognitive tests.

Next, they set out to see if they could reverse those effects.

A class of drugs called sialidase inhibitors work by blocking the effects of enzymes that split sialic acid, one of the key inflammation-quenching glycans. These drugs include Tamiflu, because flu viruses rely on sialic acid to infect cells and spread through the body. The team found that, at least in mice, these flu drugs helped preserve sialic acid, prevent inflammation and improve cognition.

We saw that "this class of inhibitor could reduce inflammation caused by viral infection … and even more importantly, preserve cognition and and prevent memory deficits," Abdel-Mohsen said.

Abdel-Mohsen considers this work "proof-of-concept" that glycans may play a role in HIV-related cognitive decline, pointing to potential treatments. The end goal isn't necessarily to use flu drugs to treat cognitive impairment in HIV, but rather to identify compounds that could "either prevent the glycans from being degraded or just replace them," he said.

One limitation of the current study is that its definition of cognitive impairment was limited, Winston noted. It relied on cognitive test scores — how well participants solved various puzzles — and a standard "scoring" system that's used to assess a handful of cognitive functions. Including details of patients' symptoms and challenges they experience in daily life would have made the meaning of those scores more tangible, Winston said, and he would hope to see that in future work.

In the long run, Winston could see this research leading to a "precision medicine" approach in which patients' glycan levels are checked, and if they're low, they could get a treatment to address that. It's likely that different factors drive cognitive impairment in different people with HIV, so matching patients with the right treatment is imperative, he said.

And in theory, it may be that the loss of glycans also drives other issues seen in aging adults with HIV, such as increased rates of cardiovascular disease. If that's the case, the same treatments may serve multiple functions. "It will be definitely fantastic to study and see how targeting this mechanism could impact the multiple comorbidities," Abdel-Mohsen said.

This article is for informational purposes only and is not meant to offer medical advice.

A fly that deposits its parasitic, flesh-eating offspring inside cows has been detected in Texas for the first time in decades, the U.S. Department of Agriculture (USDA) reported Wednesday (June 3).

A second case in a cow in the same county was announced June 5, and two more cases — in a cow and dog — in other Texas counties were flagged on June 8. Another cow case was announced June 9, bringing the total to five.

Here's what to know about the New World screwworm (Cochliomyia hominivorax), a pest that was eradicated from the U.S. in the 1960s.

What is the New World screwworm?

New World screwworms are parasites that feed exclusively on the living flesh of warm-blooded animals, according to the American Society for Microbiology (ASM). The screwworms are the larvae, or maggots, of adult C. hominivorax flies.

The flies lay their eggs in animals' open wounds or body openings, such as the eyes, ears, nose, mouth or genitals. Once hatched, the maggots burrow into their host's flesh, using a screw-like motion that lends the species its name. The maggots have sharp mouth hooks that can cause extensive damage, deepening the wound and raising the chances of secondary infections. The infestation can be painful, cause swelling and bleeding, and can produce a foul smell.

After about a week of feeding, the maggots enter their next stage of development and exit the animal, burrowing into soil in order to "pupate" and mature into a fly.

Broadly, maggot infestations are known as myiasis, and myiasis caused by New World screwworms is a big problem for livestock agriculture. Across places where the fly species is endemic, or widespread, annual economic losses caused by the fly can amount to billions of dollars each year. The flies mostly infect large-hooved livestock, such as cows, sheep and horses. Less commonly, they can infect domestic dogs and wild mammals, such as deer, rabbits, opossums and birds.

Can the screwworm infect humans?

Yes, New World screwworms can sometimes infect humans, although it's fairly uncommon. The flies can potentially infect any warm-blooded animal, but livestock are most commonly affected.

People in endemic areas who work with livestock, have weakened immune systems, sleep outdoors, or have open wounds — however small — are most at risk for developing C. hominivorax infestations. As in animals, infestations in humans can be deadly, but they are treatable via physical removal of the maggots from the body.

Symptoms of infestation include feeling or seeing maggots move within a skin wound or sore, or in the ears, nose, eyes, or mouth; developing painful skin wounds or sores that worsen within a few days; bleeding from sores; and a foul-smelling odor at the site of the infestation.

The screwworms do not spread from infected animals to people or from person to person. Infestations start when a female fly lays eggs in a wound or bodily opening, like the eyes.

In 2025, the U.S. reported its first New World screwworm infection in a person in decades. That individual, in Maryland, had just returned to the U.S. after traveling to El Salvador, where the fly is endemic. That person recovered with treatment.

Can infected livestock be treated?

Yes, infected livestock with New World screwworms can be treated with antiparasitic medications. Treatment also involves physical removal of maggots from the flesh and disinfection of the wound sites. Treatment must be timely, as an infestation can kill livestock in 10 days, ASM notes.

Rather than culling whole herds — similar to what's done for commercial flocks infected with bird flu — affected farms are examined for additional cases and not allowed to move animals from the premises during that time, according to USDA. Infected animals are treated and quarantined until their wounds heal and they go a few weeks without any signs of reinfestation. Euthanasia for individual animals can sometimes be necessary if the infestation is too extensive.

If they meet all regulatory requirements, animals that have recovered from screwworm myiasis can enter the food supply, USDA says. Notably, screwworms do not infest dead meat, only healthy, living flesh. The screwworms thus pose a threat to food production but not to food safety.

Is it a big deal that it's been spotted in Texas?

Screwworm outbreaks can be incredibly costly if not snuffed out quickly — there's a reason the U.S. has poured so much effort into eradicating the pest. Experts estimate that, if a large outbreak took hold of the state today, the Texas economy could lose $1.8 billion due to disruptions to the livestock industry. Food prices would be expected to rise, in turn.

New World screwworms were declared eradicated from the continental U.S. in 1966, following an extensive effort that involved releasing sterilized male flies into the wild and breaking the species' reproductive cycle. Despite this local eradication, America still saw some major screwworm outbreaks due to flies and infected animals entering the country from Mexico. A 1972 outbreak was the worst recorded post-eradication, affecting multiple states and causing tens of thousands of cases in Texas alone.

A joint effort between the U.S. and Mexico was then established to prevent a similar outbreak from happening in the future, and the parasite had largely been eradicated in Mexico in the 1980s. But in recent years, there have been signs of a comeback. Cases have been moving northward from Central American countries, like Panama and Costa Rica, since 2023. In response, the U.S. has deployed a strategy, led by USDA, to drive cases back down.

"All models showed New World Screwworm entering the country in 2025," but these efforts likely bought the nation some time, USDA's June 3 statement notes.

So, the detection of C. hominivorax in a 3-week-old calf in Zavala County, Texas, was not necessarily surprising but it does require quick action. The case occurred in Southwest Texas about 50 miles (80 kilometers) from the U.S.-Mexico border. The maggots were seen around the calf's umbilical area. With treatment, the calf should recover, Agriculture Secretary Brooke Rollins told The Associated Press (AP).

"USDA urges residents to contact your veterinarian right away if you see any suspicious wounds, maggots, or infestations in your animals or herd," the agency said on X. "If you see signs of maggot infestations in live or very recently dead wild animals, especially in areas near the U.S./Mexico border, please call 866-4USDA-WS (866-487-3297) to report it to your local USDA Wildlife Services office."

The agency is now following strategies and actions outlined in the NWS Response Playbook to snuff out any potential danger in Texas. That includes establishing a quarantine zone around where the case was detected and limiting the movement of animals in that zone.

According to the AP, Rollins said the USDA is confident enough in its preparations that it believes "there is no threat of mass infestation." She added, "There is no reason to believe this incursion will result in establishment of the pest in our country."

Following the initial detection, USDA then detected a second screwworm case in Zavala County. The case was "within the established movement control zone and enhanced sterile insect dispersal area" that had been set up for the first case, Dudley Hoskins, Under Secretary for USDA's Marketing and Regulatory Programs, said in the June 5 statement.

On June 8, officials announced cases in a calf in La Salle County (just to the southeast of Zavala) and a dog in Andrews County (hundreds of miles northwest of Zavala), bringing the current total to four. Early reports indicate that the dog was recently in Mexico, hinting it may have caught screwworm there, but investigations are ongoing.

A case in another calf in La Salle County was reported June 9. Surveillance and response measures have been expanded in the area.

"While we address these instances that require immediate attention, and continue to sample suspected cases, we are simultaneously working to eradicate the pest entirely," Hoskins said in the June 8 statement. "We need the partnership of animal owners across the region — please stay vigilant, check your animals closely, and report anything that looks suspicious."

Editor's note: This story was updated June 9 with information about a fifth case. The article was first published June 4.

This article is for informational purposes only and is not meant to offer medical advice.

Google wants to release 64 million bacteria-riddled mosquitoes in California and Florida — but scientists aren't concerned.

The Environmental Protection Agency (EPA) is reviewing an application made by the tech giant for an experimental mosquito release permit, which, counterintuitively, could reduce mosquito populations that carry diseases.

The release is part of Google's Debug initiative, which aims to deploy millions of non-biting male mosquitoes infected with a bacterium called Wolbachia pipientis — commonly known as Wolbachia — into the environment. This bacterium doesn't harm infected males, but it does prevent any uninfected females they mate with from having offspring, thereby slashing mosquito populations over time.

In this case, Google is targeting southern house mosquitoes (Culex quinquefasciatus), an invasive species native to tropical and subtropical regions that can spread diseases like West Nile virus and St. Louis encephalitis in humans.

The proposal has scientists mostly buzzing with enthusiasm. Karthikeyan Chandrasegaran, an assistant professor at the University of California, Riverside, studies the ecology and behavior of mosquitoes in the context of public health, and told Live Science that using Wolbachia is a "reasonable" mosquito control approach, particularly when compared to the use of broad insecticides.

"Wolbachia-based strategies are generally species-specific and do not introduce novel toxins into the environment," Chandrasegaran said. "Importantly, Wolbachia is already widespread in many insect species and is a naturally occurring bacterial symbiont rather than a genetically engineered organism. From that perspective, they are among the more environmentally conservative mosquito control tools currently available."

The EPA has deemed Google's request to be of potential regional and national significance, and it will make a final decision whether to grant the permit following a public comment period ending on June 5. After this, the agency may give Google the greenlight to release up to 32 million mosquitoes in California and another 32 million in Florida over two years.

However, despite the scale of the proposed releases, Google's approach isn't new and has already been shown to work in another mosquito species.

"It is a technique that's been used actively to control mosquito populations since around 2011," Eric Caragata, an assistant professor at the University of Florida who studies Wolbachia for mosquito control, told Live Science.

Fighting mosquitoes with mosquitoes

Mosquitoes are the deadliest animal on the planet, according to the Centers for Disease Control and Prevention (CDC), killing between 500,000 to more than a million people a year by spreading harmful diseases. Given the blood-suckers are so small, widespread and numerous, reducing them at scale is tricky. Using insecticides can harm the environment and kill other pollinators, and increasingly, mosquitoes are building up a resistance to them.

"We have an ongoing battle with both mosquito-borne disease and insecticide resistance," Caragata said.

Wolbachia offers a potentially natural solution to these mosquito woes. The bacterium is common in insects but doesn't infect other animals, like humans. Through a process called cytoplasmic incompatibility, the bacterium creates a unique interaction between infected males and uninfected females.

In males, Wolbachia modifies the sperm genome in a way that kills embryos produced with that sperm. However, if a female also has Wolbachia and it's in the embryo, then the sperm genome impairment doesn't do any harm. This interaction means that if you release millions of infected males into a population, then the uninfected females will mate with them en masse and be unable to produce viable young.

"If a [female] mosquito has Wolbachia, that mosquito can mate and reproduce successfully with both infected and uninfected males," Caragata said. "All of her progeny will then have Wolbachia. However, if you have an uninfected female mosquito and she mates with a Wolbachia-infected male, none of her progeny will hatch."

Google is building machines to autonomously rear millions of infected mosquitoes, and then using artificial intelligence (AI) algorithms, sensors and other engineering to separate the males from the females.

Researchers have been using sterilized male mosquitoes to reduce populations for decades. Female mosquitoes bite humans because they need the protein and other nutrients found in blood to produce their eggs, but males get all their nutrition from flower nectar and fruit and not humans. So, releasing male mosquitoes theoretically poses no threat to people.

Most of the previous bacteria-based attempts have focused on Aedes aegypti mosquitoes, which carry diseases like Zika and dengue. In Singapore, where Google is also working, researchers have been using Wolbachia-infected males to fight dengue. Trials have found that the approach reduces the disease-carrying mosquito population by up to 90% and the subsequent risk of a person contracting dengue by 70%. However, Google's large-scale targeting of southern house mosquitoes is new.

More upsides than downsides

While there are some unknowns, neither Caragata nor Chandrasegaran expect any major ecosystem disruptions. Lots of animals feed on mosquitoes, but a sudden drop in southern house mosquitoes shouldn't result in lots of animals starving.

"Most predators that consume mosquitoes are generalists and feed on a broad range of aquatic and terrestrial insects," Chandrasegaran said. "Consequently, there is little evidence to suggest that local suppression of Culex quinquefasciatus would trigger substantial ecological cascades."

Chandrasegaran noted that ecosystems are complex, and so any large-scale intervention should be monitored. One potential consequence could be that reducing one mosquito species creates space for another, but Chandrasegaran thinks there will likely be more upsides than downsides.

"From a public health perspective, reducing Culex quinquefasciatus populations could yield meaningful benefits, as this species is an important vector of West Nile virus and several other pathogens," Chandrasegaran said. "If suppression can be achieved safely and sustainably, the public health benefits are likely to outweigh the ecological risks based on our current understanding."

In the U.S., West Nile virus is the leading cause of mosquito-borne disease. Around 2,000 people are diagnosed with the virus each year, with likely more infected but undiagnosed, according to the CDC. Most people don't develop symptoms and some experience mild flu-like symptoms; however, in some cases, it can result in severe illness and death. In California, there have been more than 8,000 human cases of the virus and more than 400 deaths since 2003 — none so far this year.

Internationally, C. quinquefasciatus and other Culex mosquitoes also play a major role in spreading Japanese encephalitis virus, which is a problem in Asia. There are an estimated 100,000 annual cases of Japanese encephalitis, for which the fatality rate can be as high as 30%, according to the World Health Organization (WHO).

Live Science reached out to Google for comment and was directed to a public statement about the Debug project.

A cheap, widely available painkiller used to treat conditions like arthritis can significantly reduce RSV in the human respiratory tract, an early-stage laboratory study suggests.

Respiratory syncytial virus (RSV) is the number one reason infants end up in the hospital in the U.S., with babies under 6 months old facing the highest risk of severe disease and death from RSV. It's also a serious health risk for adults over 65.

Currently, there are vaccines approved for pregnant people and older adults, as well as antibody-based drugs for children that can help prevent RSV infection. But there's no specific antiviral drug to treat the disease once someone is infected.

In the new study, published May 7 in the journal Virus Research, researchers found that the antiinflammatory drug indomethacin interferes with a key protein that RSV needs to invade human cells and spread. The finding hints that the drug could help treat RSV infections, but experts cautioned that laboratory findings don't always translate into real-world results.

"The way something behaves in a lab can sometimes be wildly different from how it behaves in real life," said Dr. Amy Edwards, a physician in the division of pediatric infectious diseases at University Hospitals in Ohio, who was not involved in the study. "Studies like this are very important first steps in understanding which therapeutics might be a target for future clinical trials but they are not sufficient to push for immediate use in clinical settings," she told Live Science in an email.

Dr. Aaron Glatt, the chief of infectious diseases at Mount Sinai South Nassau in New York, agreed that the findings are interesting but won't impact treatments in the short term. "It's a very preliminary paper suggesting something that is of potential great interest, but certainly is not something that's going to change one iota the practical care of patients with RSV tomorrow," said Glatt, who wasn't involved in the study.

One drug, different effects

Laboratory and clinical studies had previously shown that indomethacin has antiviral effects against a number of viruses, including herpesvirus, rotavirus and the coronaviruses behind SARS and COVID-19. In a small clinical trial, COVID-19 patients who received indomethacin got better faster than those taking acetaminophen, with most symptoms disappearing in half the time. To date, though, the drug has not been approved as an antiviral for any infections.

To test indomethacin's effects against RSV, the researchers infected cells from the human larynx (voicebox), bronchus (airway) and lungs with RSV and then treated the cells with indomethacin at various doses. The drug reduced the virus's ability to make copies of itself in all cell types and at very low doses, without harming the cells themselves.

The researchers found that indomethacin worked only when given after the virus had already entered cells. Giving it beforehand or during the brief window when the virus first attaches to cells had no antiviral effect.

The team also tested aspirin, which works in a very similar way to indomethacin as a painkiller; both drugs are nonsteroidal anti-inflammatory drugs, known as NSAIDs. Aspirin had no effect on RSV at all, suggesting that indomethacin's antiviral effect is separate from its pain-killing properties.

Indomethacin is already used in premature babies to help treat patent ductus arteriosus (PDA), a heart condition where a blood vessel that should close after birth fails to do so, Edwards said. (In that context, indomethacin is given intravenously.)

"There is a long history of it being used relatively safely in infants," Edwards said.

For short-term use, indomethacin is generally very safe, Glatt said. However, with higher doses and prolonged treatment, it can carry a risk of side effects, including kidney issues and bloody stool.

More research is needed to determine whether indomethacin benefits people with RSV. The researchers also point out that more work is needed to understand the exact mechanism whereby the drug stops the virus from multiplying and spreading.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: An 11-year-old boy in India

The symptoms: The boy's parents brought him to a hospital after he had several episodes of bleeding from his eyes, nose and ears. The episodes, which had occurred for about a month, seemed to start for no obvious reason, caused no pain and typically stopped on their own within minutes.

What happened next: While evaluating the boy, doctors witnessed active bleeding from his eyes and ears. However, examinations revealed no injuries or structural abnormalities that could explain the bleeding.

Tests showed that his blood counts were normal, as were his levels of von Willebrand factor, a protein involved in blood clotting. Meanwhile, tests of the secretions from his eyes and ears confirmed that they did indeed contain blood.

In the end, the doctors could find no evidence of a bleeding disorder, local injury, self-harm or other obvious medical cause for the bleeding. Because the boy's parents reported that the episodes often occurred during periods of "academic stress, peer pressure, or parental expectations regarding academic performance," doctors also arranged a psychiatric evaluation, they explained in a report of the case.

A psychiatrist interviewed the child and his parents and also made behavioral observations during consultations. This assessment supported the idea that academic stress and parental expectations regarding school performance may have been contributing psychological stressors.

The diagnosis: Since extensive testing failed to identify a physical cause for the bleeding, doctors concluded that the symptoms were consistent with stress-associated hematohidrosis. This is an extremely rare condition in which people appear to sweat or secrete blood through intact skin or natural body openings. The secretions are sometimes called "blood sweat," although evidence doesn't suggest the fluid passes through the sweat glands.

The treatment: Doctors treated the boy with propranolol, a beta blocker that can dampen the body's fight-or-flight response. They also set him up to start cognitive behavioral therapy, a common form of talk therapy, to help him manage stress and develop coping strategies for academic pressure. His parents received counseling as well, including guidance on reducing academic pressure and creating a more supportive environment at home.

Within two weeks, the boy's bleeding episodes had become much less frequent. Four weeks after treatment began, only occasional, mild episodes were reported. Three months after the start of treatment, he was symptom-free during his normal daily activities. (The case report doesn't note how long treatment continued.)

What makes this case unique: There are fewer than 50 cases of hematohidrosis reported in the medical literature, the boy's doctors wrote in the report of the case. Although the phenomenon has been reported for decades, its exact cause remains uncertain.

One proposed explanation is that intense emotional stress, fear, or psychological trauma triggers ruptures in tiny blood vessels surrounding sweat glands, allowing blood cells to leak into sweat ducts and emerge on the skin's surface. However, the existing research doesn't necessarily suggest that the secretions come from sweat glands.

The boy's doctors cautioned that these observations do not prove that psychological stress directly causes hematohidrosis, although the condition has been linked to stress in several previous reports.

For example, in a 2017 report, doctors described a 10-year-old girl who developed episodes of bleeding from her scalp after being punished at school and repeatedly criticized over her academic performance at home. Her symptoms eventually disappeared after psychotherapy, medication and changes in parenting strategies. A report published in 2022 described a 14-year-old boy whose bleeding episodes appeared to worsen around school examinations and anxiety about returning to class. After receiving stress-management therapy and treatment with antidepressants, he stopped experiencing the episodes.

Both of these earlier cases had also occurred in India, and in general, many documented cases have originated in Asia, particularly in India and Pakistan, the case report authors noted.

The doctors stressed that methodical and structured psychological and psychological assessments are required to better understand the underlying mechanisms of this rare condition.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

Heading a soccer ball just once is enough to temporarily release proteins into the blood that are associated with damage to brain cells, a new study suggests.

For two of the six proteins tracked, their levels rose higher the more frequently and the harder soccer players headed balls. The study authors say that while this could be evidence of acute brain injuries, further studies are needed to determine whether the cumulative effects of heading could increase a player's risk of developing a neurodegenerative disease like Alzheimer's.

In the research, published May 18 in the journal JAMA Neurology, researchers at Amsterdam University Medical Center found that amateur soccer players who headed balls had higher concentrations of the protein S100B in their blood right after a match compared with players who didn't perform headers. S100B, which is produced primarily by star-shaped cells called astrocytes, is widely used to assess for traumatic brain injury (TBI) and usually increases within one hour following a TBI.

Players who performed more than two headers, as well as those who struck multiple high-impact headers, also immediately experienced increases in a protein called p-tau217. This protein is one of the main blood-based signatures, or biomarkers, for Alzheimer's disease.

Tau is a protein that normally helps stabilize the internal scaffolding of neurons, but mechanical stress on the brain's transmission cables detaches it as enzymes then modify the protein, turning it into one of several forms of p-tau, including p-tau217.

Levels of p-tau217 and S100B returned to their original levels within 24 to 48 hours after each match, but the study authors said this does not exclude lasting harm.

"The evidence we have so far suggests that brain damage is occurring from heading soccer balls, both short and long-term," said Samantha Bureau, assistant executive director of the Concussion Legacy Foundation Canada (CLFC), who wasn't involved in the new study. "Long-term consequences are more difficult to track due to the latency between exposure and symptom onset, but several studies have raised concerns about the risks associated with heading in soccer," she told Live Science in an email.

This latest study in the Netherlands incorporated blood samples from 302 higher-level amateur male soccer players taken over the course of 11 matches ‪—‬ before, immediately after, and between 24 and 48 hours after each match. While 86 participants opted not to participate in the third blood draw, study co-author Marsh Königs, an assistant professor of developmental neuroscience at Emma Children's Hospital at Amsterdam UMC, told Live Science that this is unlikely to have affected the results. The study also relied on cameras to record how often each player headed the ball and to estimate the intensity of each header.

Königs said they don't know exactly how headers caused the two biomarkers to rise. However, there are a few potential explanations. The head's acceleration and deceleration within a short time frame could cause a "concussion-like" effect on a much smaller scale, Königs said. Another study, published in April, showed that when someone's head makes contact with a ball, a pressure wave travels through their head.

Regardless of the precise mechanism, scientists hypothesize that the effects of heading accumulate over time, contributing to neurodegenerative disease. A 2025 study found that years of repeated head trauma in soccer and football players kills neurons and leads to brain inflammation.

"It's not the rise in biomarkers itself but rather what it reflects, which is concerning," Königs said. What's more, Königs thinks repeating the team's study among the world's best soccer players would lead to more pronounced results.

Peter Theobald, a medical engineer leading research on brain biomechanics at Cardiff University who was not involved in the study, told Live Science in an email that soccer governing bodies, such as England's Football Association, are reducing the permitted practice loads for headers, despite a lack of meaningful evidence that prescribes a "safe"' level of heading. It is challenging to say whether the biomarker concentrations measured in the Dutch study were enough to cause concern, he added.

According to Königs, the elevations they observed do not exceed thresholds used in clinical settings to diagnose injuries. However, "these cutoffs are mostly designed to detect much more serious injuries, such as severe brain injuries or dementia," he noted. Königs is concerned that issues could arise if this action is repeated hundreds or thousands of times.

"This is a relatively strong study, as it also features athletes from non-contact sports and so does provide confidence that heading is the cause of change," Theobald said. "Tracking the same players throughout a season would have been interesting for example, as this would have enabled reporting of the cumulative effect of heading."

This article is for informational purposes only and is not meant to offer medical advice.

See how much you know about the most complex organ in the human body with our brain quiz!

Scientists have developed new eye drops that allow mouse eyes to perform certain steps of photosynthesis.

The drops, which contain photosynthetic machinery extracted from spinach leaves, use light-driven reactions to improve symptoms of dry eye disease, according to a study published May 15 in the journal Cell. Although the researchers tested the drops in mice, the hope is that with further testing, the therapy could be used in people someday.

The study is a "cool application" of engineering inspired by symbiotic relationships in nature, said Corey Allard, a cell biologist at Harvard Medical School who was not involved in the work.

Plants rely on photosynthesis to make energy, in the form of glucose, from sunlight. Organelles called chloroplasts conduct photosynthesis and give plants their green color. While no animals photosynthesize naturally on their own, a few have developed symbiotic relationships with photosynthetic algae that let them harness solar power. Some species of sea slug, including leaf sheep (Costasiella kuroshimae) and the mangrove leaf slug (Elysia bangtawaensis), even steal chloroplasts from algae they eat.

In the new study, David Tai Leong, a chemical engineer at the National University of Singapore, and colleagues tested whether mammal eyes could tolerate similar behavior, in hopes of pointing to a way to treat dry eye disease, which affects the film of tears covering the eye and produces oxidants and inflammation that can impair vision.

To create the eye drops, the team first removed stacked compartments called thylakoid grana from chloroplasts in spinach. Thylakoid grana are the chlorophyll-bearing structures inside chloroplasts where the first, light-dependent steps of photosynthesis occur. Then, the team encapsulated those thylakoid stacks in tiny packages to create a system they dubbed "light- reaction enriched thylakoid NADPH-foundry," or LEAF.

When incorporated into eye drops, LEAF reduced eye inflammation in mice induced to have dry eye disease. Along the path to making glucose, chloroplasts produce a chemical called NADPH at the thylakoid grana. NADPH acts as an antioxidant, and it helped to eliminate compounds that were exacerbating eye inflammation in the mice.

After five days, the mice treated with the LEAF eye drops were comparable to mice treated with an existing, commercially available medicine to treat dry eye disease. They showed greater tear production and reduced cornea damage compared with the mice that received only saline eye drops.

"The eye is uniquely suited for this type of strategy, since light is already an intrinsic component of its normal physiological function," Dr. Xianfeng Lin, an orthopedic surgeon at Zhejiang University School of Medicine in China, wrote in an email to Live Science. Although Lin wasn't involved with the new work, he and colleagues published a 2022 study in the journal Nature using a similar photosynthetic system to combat inflammation from arthritis in mouse knees.

"The work extends the role of light in the eye from being purely sensory to potentially contributing to local metabolic support and tissue repair," Lin said.

Even though the eye drops contain chlorophyll, the concentration is very low, and the drops appear transparent.

"We are able to use a highly optimized photosynthetic machine, so we do not need huge amounts of the LEAF system," Leong said. "Because it's so low concentration, you can't see the green color. So we won't have green eyes like the Incredible Hulk."

The eye drops aren't ready for human use yet; they still need to undergo extensive testing for safety and long-term efficacy. But the team is working to set up a clinical trial that will first look at safety, Leong told Live Science.

If approved for human use, the medicine would take advantage of how our eyes naturally work, since it only requires ambient light to activate. A patient would be "receiving a therapy that is aligned with how we normally go about our day," Leong said.

Most long-distance travelers have felt the discombobulation of changing time zones: being excessively tired during the daytime but struggling to sleep at night.

Jet lag often emerges when people hop several time zones. The majority struggle more when flying east because our body clock is typically just over 24 hours. "It's a little bit harder to shift earlier," Helen Burgess, a professor at the University of Michigan's Sleep and Circadian Research Laboratory, told Live Science.

So what's going on in our bodies when we have jet lag, and is there a way to prevent it?

What is jetlag?

Jet lag is a mismatch between our internal body clock and our time zone.

The term "jet lag" was coined in a 1966 Los Angeles Times article, in which journalist Horace Sutton described the symptoms experienced by long-haul jet-setters as "not unakin to a hangover."

"He said, at the time, that jet lag derives from the simple fact that jets travel so fast they leave your body rhythms behind," Dr. Charles Czeisler, a professor of sleep medicine at Harvard Medical School, told Live Science. Before flights, people traveled overland or via ship so slowly that their circadian clock didn't get out of alignment.

Jet lag is the body's normal response to skipping time zones. "If the circadian system is working correctly, you should have a problem with jet lag," Czeisler said.

But some populations — such as older people, frequent fliers or those with mood or sleep disorders — are more likely to feel symptoms.

Jet lag might seem trivial, but even a small dose can have serious health implications. When the clocks move forward — essentially causing an hour's jet lag — there's an increase in fatal car accidents, Czeisler said. Getting behind the wheel straight after a long-haul flight is dangerous because a lack of sleep is a known cause of car crashes. In fact, road accidents are the leading cause of non-natural death among U.S. citizens traveling abroad.

And shifting circadian rhythms can even "flip people into mania or depression," Czeisler said. According to one study, 186 people over two years were admitted to a psychiatric hospital from Heathrow Airport with jet-lag-related mental health conditions, such as depression and hypomania (a shorter, milder form of mania), while another study has shown that chronic jet lag could increase the risk of neurological disorders.

Minimizing jet lag

The best way to adjust to your new time zone is through light exposure. "Light is the strongest signal that shifts the timing of the clock," Burgess said.

But the timing has to be right: exposure to light at the wrong time can push your clock in the wrong direction, making jet lag last longer.

Around two or three hours before your usual wake-up time, your body clock switches from interpreting light as evening light, making you sleepy, to morning light — which wakes you up.

"Light before the crossover point will shift you later, and light after the crossover point will shift you earlier," Burgess said. This is why napping isn't always the right solution.

If you usually wake up at 6 a.m., your crossover point will be around 3 a.m. This means that if you travel to a time zone six hours ahead and land at 7 a.m., this would be around 1 a.m. for your internal clock, which is still on your original time zone. So, your body interprets all the morning light you take in while landing and going through security as evening light and it wakes you up again, pushing your clock later.

Knowing when to expose yourself to light requires planning. To get light when you need it, go outside, use light boxes, or put on wearable light therapy devices. To avoid light when it will push you in the wrong direction, nap, stay inside, or wear sunglasses or glasses that block blue light within a specific wavelength range (460 to 480 nanometers).

To minimize the effects of jet lag, stay hydrated, avoid alcohol, be mindful of not drinking too much caffeine — "maybe just one cup of coffee" at strategic times, Burgess said, adding that caffeine has a long half life so will stay in your body and make it harder to sleep — and adjust to local mealtimes as soon as possible. Some people may also speak to medical professionals about whether melatonin is suitable for them.

You can prevent jet lag by shifting your body clock to the new time zone before you arrive. "On average, we can only shift the clock earlier by about an hour and a half a day," Burgess said.

For instance, to adjust to a time zone 10 hours ahead, you would need to start shifting your light exposure timings a week before the flight. For example, if you usually sleep between 11 p.m. and 6 a.m., you'd be aiming to shift toward going to bed at 9 a.m. and waking up at 4 p.m — something not feasible for most people.

It works, Burgess said, but when she tried it, she felt disconnected from the world around her because everyone was asleep during her waking hours. "I just felt really, really isolated," she said.

Although it's impractical for most people, you wouldn't experience the symptoms of jetlag because of how gradually you'd be moving your sleep schedule toward the new time zone. "People do not experience jetlag symptoms because everything is being moved slowly together," Burgess said, not "yanked apart" in one flight.

If you don't want to become nocturnal before you leave, nudge yourself in the right direction by shifting your schedule earlier by around an hour each day for just a few days. In essence, if fully switching to the new time zone before you depart is too challenging, nudging closer to it before arrival will still be beneficial. "It can make a huge difference," especially for those flying east, Burgess said. "Take the five or 10 minutes to plan it out, and that's going to really help."

This article is for informational purposes only and is not meant to offer medical advice.

Imagine receiving a test result that tells you your body is biologically five years older than your chronological age. You exercise regularly, get good sleep, eat healthy meals and have a happy personal life. What have you been doing wrong? Can this test be trusted?

Dozens of companies are marketing products that promise to reveal a person’s "true" biological age — that is, how well your body is functioning — for a price ranging from around US$30 to over $1,000. These products are based on epigenetic aging clocks, which are research tools that estimate age based on a person's DNA. These clocks are reshaping how scientists study aging and how the public thinks about it.

But while epigenetic clocks are highly effective research tools to study aging at the population level, they aren't designed to make claims about the health of individuals.

We are biobehavioral health scientists who study how early development and environmental factors across the lifespan shape biological aging, influencing health and disease decades later. As researchers who use epigenetic clocks in our work, we have found them to be highly informative tools when studying large numbers of people. But these clocks can provide faulty results at the individual level, and they do not meet the standards required of common medical tests.

What are epigenetic clocks?

Measuring reversible chemical changes to DNA, known as epigenetic marks, can provide information about how your body is aging.

Using DNA obtained from routine blood draws, researchers can measure millions of these epigenetic marks in an individual. Running statistical algorithms on this information can produce a single value that represents that person's epigenetic age, analogous to chronological age.

Epigenetic clocks work because the chemical marks on DNA can shift over time and are influenced by lifestyle, stress and the environment. These changes capture aspects of aging that chronological age alone may not reflect.

In this way, epigenetic clocks help scientists identify the experiences, exposures and behaviors that may accelerate or slow biological aging.

Not for individual health decisions

Why can't epigenetic clocks provide reliable results about biological age for individual people?

First, there are dozens of different types of epigenetic clocks, each designed for a specific purpose. Some are used to predict a person's age, while others are used to predict how fast someone is aging or how many years until they die. These different clocks do not always agree with one another, even when used on the same person.

Second, epigenetic changes are dynamic, making age predictions sensitive to short-term fluctuations in diet, environmental exposures, illness, time of day and other transient factors. As a result, estimated age could vary substantially depending on when someone is tested.

Third, constructing epigenetic clocks is technically challenging, and there is no established gold-standard method for generating clocks across laboratories. For example, testing epigenetic age in saliva versus blood samples can yield substantially different results for the same person. The technologies used to measure epigenetic marks have also evolved over time and will likely continue to improve. As these methods change, the original algorithms designed for specific measurement platforms may not perform the same way.

Fourth, scientists do not universally agree on what aging means, in part because it is a very complex process. Reducing that complexity to a single number, such as an epigenetic age, can be misleading.

Finally, epigenetic clocks are influenced by a person's history of trauma, discrimination and early life adversity. This makes their use at the individual level potentially problematic. On average, marginalized communities tend to show signs of accelerated aging when assessed with epigenetic clocks. If insurance companies began using epigenetic age estimates to set premiums, many people could face higher costs for biological differences shaped by circumstances beyond their control, potentially deepening existing health disparities.

Studying how aging unfolds over time

While epigenetic clocks are not appropriate tools for individual health decisions, this does not mean they lack value.

Researchers have used epigenetic clocks to discover lifestyle habits that can, on average, slow down aging. Some examples include reducing daily calorie intake, exercising regularly, maintaining a healthy diet, getting enough sleep and avoiding smoking.

Epigenetic clocks can also help test new drug therapies aimed at slowing down specific aging processes. For example, researchers have shown that rapamycin, a drug connected to various aging processes, can reduce the epigenetic age of human skin cells. There is also some evidence that a treatment designed to regenerate the thymus may slow or even reverse epigenetic aging after one year of treatment. However, researchers have seen these effects only when looking at groups rather than individuals.

Epigenetic clocks are helping scientists advance scientific research on the aging processes, but they aren't medical tests to measure individual health. In the future, epigenetic measurements may play a useful role in guiding personal health decisions. But for now, epigenetic clocks sold as biological age tests are best used and refined by researchers who are studying populations rather than individual people.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Walk into any U.S. pharmacy, and you'll find a multicolored range of melatonin supplements marketed as sleep aids for adults and children alike.

The body-made hormone melatonin streams through our systems every evening, preparing us for rest. But while melatonin supplements claim to mimic this natural process, experts say bottles stamped with claims like "100% drug free" may be misleading.

Melatonin carries little risk when used correctly, but as a dietary supplement, it skirts the strong governmental regulation that's reserved for pharmaceuticals. This has led to inaccurate dosage labeling, incomplete safety information, and scant research into melatonin's long-term effects on kids, some scientists argue. Researchers worry that, given that many people perceive melatonin as harmless, some are misusing the supplement by taking unnecessarily high doses at improper times of the day.

"It's being promoted like there's absolutely no risk … [People say] 'It's all natural, and it just is a safe sleep aid,'" said Dr. Pieter Cohen, a Harvard Medical School researcher who studies supplements. "And that's where you can get into trouble."

The U.S. Food and Drug Administration (FDA) classifies melatonin as a supplement, while countries like the U.K. and Australia deem it a medication. This designation comes with a level of governmental oversight that U.S. supplements aren't subject to. Given melatonin's soaring popularity, some experts think the United States should follow suit and make melatonin an over-the-counter drug.

But if melatonin is already produced naturally by the body, why would the supplement version be riskier? Live Science spoke with experts to find out.

Supplements aren't well regulated

In the U.S., a 1994 federal law required that supplements be regulated as food, not drugs. The FDA doesn't assess the safety, efficacy or manufacturing quality of supplements before they're marketed but instead intervenes if harmful side effects are reported or if it's made aware of inaccurate labels. This largely leaves the supplement industry to self-regulate.

Cohen's research suggests that actual melatonin concentrations in products may range from 74% to 347% of what's reported on the label. Meanwhile, safety warnings and instructions on the best way to use melatonin aren't required on labels. Still, many popular brands adhere to voluntary melatonin labeling guidelines from the Council for Responsible Nutrition, a supplement trade organization. These guidelines include disclaimers like "may cause drowsiness" and "for occasional or intermittent use only."

Despite such disclaimers, nearly 1 in 5 school-aged children use it regularly as a sleep aid, a trend scientists are concerned by. Long-term safety data is lacking in kids, in part because melatonin hasn't gone through the safety trials required of new drugs. And melatonin isn't patented, so there's no strong incentive for drug companies to invest in safety studies, according to Debra Skene, a neuroendocrinologist at the University of Surrey in England. "There's no money in it," she said.

Many parents inaccurately view melatonin as akin to a "little glass of warm milk," Cohen said. But if parents give children high-dose supplements or multiple doses at once, "you're talking about side effects and getting sick and not helping sleep," he said.

Calls to U.S. poison control centers about melatonin poisoning in young children have shot up with the supplement’s popularity. This has been driven by accidental ingestions in children under 5, and in some cases, kids had serious symptoms, like respiratory failure or seizures. That said, some of those effects may be due to certain melatonin products' inclusion of serotonin, which can be dangerous if consumed in large quantities.

Evidence does suggest that melatonin can help children with attention-deficit/hyperactivity disorder and autism get to sleep, among whom sleep problems are common. But the potential benefits of melatonin for neurotypical kids are less clear.

One concern scientists have is that the regular use of melatonin may affect puberty. In various animal species, melatonin helps regulate reproduction, and supplemental melatonin can disrupt these effects. The few human studies that exist haven't shown clear effects on puberty, but there hasn't been an in-depth study tracking hormone levels in the blood, said Helen Burgess, who researches the circadian rhythm at the University of Michigan.

"I'm OK with intermittent short-term use," she said of melatonin supplementation in kids. But given the lack of data, she suggested that parents consult a pediatrician to look for another solution if their child needs melatonin regularly.

The lesser-known effect of melatonin

Supplements supercharge the body's supply of melatonin, said Margarita Dubocovich, who studies melatonin at the University at Buffalo. Supplement dosages generally range from 1 to 10 milligrams (mg), while adults produce about the equivalent of a 0.3-mg pill nightly, she said.

When taken orally, supplements and medications pass through the digestive tract before reaching systemic circulation, meaning the full dose of melatonin won't necessarily make it into the bloodstream. However, the amount that circulates will still be far higher than what's naturally produced in the body, said Skene.

Upping your melatonin dosage doesn't knock you out; the drowsiness triggered by the supplements is generally mild. The supplement also avoids the side effects of conventional sleeping pills: memory loss, gastrointestinal issues and next-day "hangovers."

However, melatonin has a lesser-known effect. Given its role in regulating the circadian rhythm — the 24-hour clock that regulates many bodily systems — it can scramble the body's sense of timing when regularly taken outside your bedtime, such as too early before bed or in the middle of the night.

That's why melatonin can help treat jet lag if taken for multiple days just before or after traveling. But if people take pills as they're tossing and turning throughout the night, this could throw off the circadian rhythm, Dubocovich said. This practice may induce a kind of jet lag (without the perks of international travel). In the short term, that can come with drowsiness during the daytime, irritability, upset stomach, brain fog and insomnia.

"I think that melatonin could be good if you take it in a controlled manner and the right dose," Dubocovich said, suggesting a few milligrams taken right at bedtime. "But how people are taking it [currently], they are intoxicating themselves."

Not all researchers agree that melatonin-induced jet lag poses a big risk, but taking more than 3 mg in the middle of the night still "isn't a good idea," said Burgess. This dose may linger in the body through the morning, she said, leading to next-day grogginess.

Burgess' research suggests that supplemental melatonin is most effective at shifting the biological clock forward in time, which happens when it's taken in the early evening. Still, she said the impact of melatonin on the circadian rhythm "just does not seem to be really recognized or understood by the public at all."

Should melatonin be a drug?

If melatonin were an over-the-counter medication, it would require clear labels with instructions and accurate dosing. "You should be able to know what dose you're getting, and it shouldn't be sold in whatever dose the manufacturer … decides to pour in on a given day," Cohen said.

Yet, reclassification could disrupt access to a relatively safe sleep aid that many consumers rely on, argued Jeff Ventura, a spokesman for the Council for Responsible Nutrition, the supplement industry trade organization that created the melatonin labeling guidelines. "Moving melatonin into the drug category would require formal FDA drug approval pathways, which could limit consumer access, reduce product variety, and significantly increase costs" for both manufacturers and consumers, he told Live Science in an email.

It's unlikely the supplement will be made an over-the-counter drug anytime soon. Cohen attributes the lack of a serious movement to the supplemental industry lobby, which includes the Council for Responsible Nutrition. "Any move to take such a great money winner like melatonin out of their hands would cause them to fight it tooth and nail," he said.

Burgess, who serves on the scientific advisory board for the melatonin brand Natrol, agrees that purity is an issue. However, she said she isn't too concerned about melatonin's availability, given its "pretty benign effects." Still, she suggests going with a big name brand with a US Pharmacopeia (USP) stamp verifying its listed ingredients are accurate; USP is a nongovernmental organization that sets quality standards for medicines, food ingredients, and dietary supplements.

After studying the hormone for 40 years, Dubocovich agrees that melatonin should be regulated as an over-the-counter medication.

"Melatonin can help support a good night’s sleep, especially in small doses that mirror the body’s natural rhythm," Dubocovich said. "But not all melatonin is created equal."

This article is for informational purposes only and is not meant to offer medical advice.

How much do you know about sleep and dreams? Find out with our sleep quiz!

The patient: A 23-year-old woman in Florida

The symptoms: The woman went to the emergency room with an itchy rash on her back that had lasted two days. The rash first appeared as isolated, inflamed regions on her upper back, which initially led her to seek treatment at an urgent care center. Despite treatment with steroids and antihistamines, however, the rash spread to the woman's lower back in grouped patterns of irregular stripes, which resembled lash marks made by a whip.

What happened next: When doctors examined the woman, they found "multiple streaked lesions on her back," according to a report of the case. The lesions were not blistered or peeling, and no other part of her body was affected.

The woman didn't report any other symptoms that are typically associated with an allergic reaction, such as difficulty breathing, throat irritation or swelling, or gastrointestinal distress. Nor was she experiencing body aches, joint swelling or any neurological symptoms. Her blood pressure, heart rate and respiratory rate were in the normal ranges, although her temperature was slightly elevated, at 99.1 degrees Fahrenheit (37.3 degrees Celsius).

In accordance with standard emergency-room procedures for patients with rashes, the doctors considered and eliminated possible causes for the lesions. The woman said the marks were not self-inflicted or made by someone else. She was not taking any medications besides those prescribed by the urgent care. She had not recently introduced potential skin irritants, such as new cosmetics, fragrances or detergents. She had not been bitten by insects and did not have a history of autoimmune disease or symptoms associated with meningitis, a disease that can cause rashes in addition to symptoms like neck stiffness and fever.

When the doctors asked the woman about foods she had eaten recently, she mentioned that the day before her symptoms appeared, she had eaten shiitake mushrooms.

The diagnosis: Although the woman had eaten shiitakes before and never had an adverse reaction, these mushrooms are known to occasionally cause a condition called shiitake dermatitis, a rash with a distinctive pattern that resembles whip marks.

Japanese researcher Takehiko Nakamura first described the condition in 1977, calling the lesions "flagellate dermatitis" after the flagellants, "a medieval religious sect whose members would whip themselves as a demonstration of their faith," according to the report of the woman's case.

The allergic response is thought to result from a compound in the mushroom called lentinan; in some people, lentinan causes the secretion of interleukin-1 and other cytokines, proteins that regulate inflammation as part of an immune response and can cause rashes. Researchers previously associated the rash with eating raw or undercooked shiitakes.

However, how the mushrooms are grown also may play a part, with log-grown shiitakes being more likely to cause a reaction than those grown on a substrate, the doctors noted.

The treatment: Doctors told the patient to continue using the medication that she received at urgent care: a topical cream containing hydrocortisone, a steroid to reduce inflammation; clotrimazole, which relieves fungal skin infections; and oral doses of diphenhydramine (an antihistamine) and methylprednisolone (a corticosteroid).

The woman was breastfeeding at the time, and she was worried that the cause of the rash might affect her breastmilk. However, the doctors reassured her that she could safely continue breastfeeding.

The medications provided some relief from her symptoms, which disappeared after about three weeks, she later reported at a follow-up visit. She also mentioned that she continued to regularly consume shiitake mushrooms and the whiplike rash did not reappear. (The authors of the report did not investigate or explain why she was not affected by shiitakes before or after this isolated incident.)

What makes the case unique: Shiitake dermatitis is rare, with approximately 100 reported incidents described in the scientific literature, according to the case report. Most of the reported cases occurred in Asia, and "although there have now been several cases in Europe and the Americas, it is still a relatively extraordinary occurrence in Western countries and the United States," the doctors wrote.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

Researchers have developed a system that uses short videos of the eye to estimate a person's levels of red blood cells — no needles required.

The technology, described in a paper published April 8 in the journal npj Digital Medicine, correctly identified anemia more than 80% of the time in a trial involving 224 participants.

This technology isn't ready to replace standard blood draws, the researchers behind the study cautioned. But they think it could potentially serve as a screening tool to flag people who may need a full blood test. This could be especially useful in low-income countries where access to laboratory testing can be scarce.

"Its potential utility may lie in enabling frequent, noninvasive longitudinal monitoring or early identification of patients requiring further investigation," said Dr. Christine Kiire, a consultant ophthalmologist at Oxford Eye Hospital and a visiting researcher in the artificial medical intelligence lab at the University College London Institute of Ophthalmology. If validated and made affordable, the system could make blood monitoring more accessible in resource-limited environments, Kiire, who was not involved in the study, told Live Science in an email.

The method could be useful in settings where it's burdensome to draw and analyze blood repeatedly, said Dr. Theodore Leng, an ophthalmologist and vitreoretinal surgeon at Stanford University who wasn't involved in the study. This could include outpatient screening, home monitoring, follow-up appointments for dialysis and cancer treatments, or pediatrics, he said in an email.

That said, the system is not ready for prime time yet. "It's great research but will take a lot of steps to be clinically available," Dr. Peter Campbell, an ophthalmologist at Oregon Health & Science University who wasn't involved in the study, said in an email.

How the needle-free system works

Noninvasive blood sensors already exist. In 2021, the Food and Drug Administration (FDA) approved a device, the Pronto-7, that measures levels of hemoglobin in the blood by shining light through the fingernail. Hemoglobin carries oxygen inside blood cells.

Unfortunately, Pronto-7's readings can be influenced by skin tone, meaning they're less accurate for people with dark skin. The white part of the eye, in contrast, contains very little pigment and looks roughly the same across different populations.

The new screening technique takes advantage of this. To build it, researchers used a microscope camera at 50x magnification to record 10-second videos of the whites of study participants' eyes. A software called Video-to-Vessels cleans the footage ‪—‬ removing blinks, eye movements and lighting changes ‪—‬ and converts the videos into time-lapse snapshots of the blood vessels within the eye.

Then, an AI model called VesselNet, which was trained on blood vessel snapshots paired with lab results regarding blood count, predicts the person's hemoglobin level and red blood cell count by analyzing patterns in the flow of blood cells.

"This paper is unique because it describes images of the front surface of the eye, rather than the retinal vasculature (at the back of the eye)," Campbell said. "So in theory it could be applied without expensive retinal cameras ‪—‬ even a smartphone."

The researchers tested the method on 224 people, including cancer patients with blood disorders and healthy volunteers, at Sheba Medical Center in Israel. They compared the model's predicted hemoglobin values with actual hemoglobin values measured using standard blood tests, finding that the model correctly identified whether a person had low hemoglobin about 83% of the time.

This falls short of what's needed for real-world use, Kiire said. For context, Pronto-7 scores between 80% and 88% for detecting low hemoglobin in men, and 84% to 87% in women.

"In practical terms, this sounds more like a great screening tool, rather than a technology ready to support dosing, transfusion decisions, or definitive hematology management," Leng said.

Additionally, whereas the eye-based method measures only two things — hemoglobin and red blood cell count — a standard blood test measures many more, Kiire said. The study authors think they may be able to count white blood cells, as well, if they design a camera with higher resolution and magnification.

Kiire also noted that certain conditions, such as pink eye and dry eye disease, as well as drugs such as medicated eye drops, may affect blood vessels in the eye and lead to false readings. On a practical level, getting good results "requires careful patient positioning and sufficient optical focus,"which aren't easy skills for clinicians to master and may limit the usability of the new method, she added.

The researchers plan to do studies involving larger and more diverse cohorts, including patients with iron-deficiency anemia, which were underrepresented in this study. They also aim to do repeated testing of their method, to validate and extend their findings.

This article is for informational purposes only and is not meant to offer medical advice.

The wind picks up dust from the unpaved road one afternoon in December as Jack van Honk turns into a ramshackle neighborhood in Lambert's Bay, on the west coast of South Africa. A stocky woman in a red patterned sundress steps out of a small home painted palest sea green, her ochre-dirt yard crowded with potted plants, many medicinal. She smiles broadly, deep wrinkles creasing a face that is cherubic and yet careworn beyond her 47 years. "Doctor! I missed you," she beams, her husky voice barely more than a hoarse whisper.

Maria carries a rare genetic mutation that is almost unknown outside of southern Africa. Its effects have been to calcify a part of the brain called the basolateral amygdala, and to thicken and scar the vocal cords. A friend of Maria with the same condition lives several hours inland, and sometimes they meet when van Honk brings them to Cape Town for brain scans and other tests. "It helps to know I'm not alone," Maria says.

By every measure of daily life — holding down a job, keeping a household running, raising two teenage sons — Maria is competent and engaged. "You talk to her, and you don't see anything wrong," says van Honk, a social neuroscientist at the University of Cape Town. She and others he knows with her condition, Urbach-Wiethe disease, "are kind, sweet people by nature." In an interview in her kitchen, Maria struggles to recollect even a fleeting moment of unhappiness — before mentioning that she kicked out her partner some years ago because of his drinking.

Yet on tests and questionnaires designed to shed light on moral choices, Maria and others with Urbach-Wiethe fail in perplexing ways that challenge one of neuroscience's most durable assumptions.

Fear factors

The amygdala, a brain region the size and shape of an almond, has long been described — almost mythologized — as the brain's fear center. That view emerged from early rodent experiments showing its role in defensive reactions. "There were a lot of discoveries linking the amygdala to fear conditioning," says Steve Chang, a neuroscientist at Yale University who studies social cognition and decision-making in monkeys. In such studies, mice and rats learn to associate a neutral cue — such as a tone — with a mild foot shock. Soon the sound alone makes them freeze in anticipation, a learned fear response that disappears after the amygdala is damaged.

But in recent years, studies in animals and humans have painted a more complex picture. Rather than a simple switch for fear, the amygdala is now understood as a Grand Central Station in the brain: a network of specialized nuclei that help detect what we care about so that we can make decisions, says Elizabeth Phelps, a psychologist at Harvard University who studies how emotions affect cognition. The rare cases of Urbach-Wiethe disease in South Africa offer a unique window into that circuitry. Because the condition appears to damage the basolateral amygdala while sparing other regions of the structure, it has helped to clarify how different amygdala neural circuits interact with each other and with other brain regions — not only in fear-learning, but in social judgment and decision-making.

Van Honk "is doing a really good job at linking his research to animal work to come up with a bigger theory," says Phelps, who is not affiliated with the project. The emerging picture is intriguing, she says, though not yet entirely convincing to her: Van Honk and his colleagues now posit that the basolateral amygdala functions primarily as a kind of social compass, helping to weigh the needs and intentions of others and decide who matters to us.

Earlier research had painted a simpler picture. Scientists in the 1990s unveiled the sensational case of a young woman with Urbach-Wiethe disease whose amygdala had almost entirely calcified, and she fit the prevailing fear-amygdala model. Unstintingly cheerful like Maria, S.M. (identified only by her initials) could not recognize fear in the facial expressions of others, neuroscientist Antonio Damasio and colleagues reported in Nature in 1994.

As the scientists got to know S.M., she confided repeatedly how she hated snakes and spiders and would try to avoid them. But when they took her one day to an exotic pet store, she gleefully held and stroked a snake for three minutes — remarking, "This is so cool!" — and had to be deterred from touching larger, more dangerous snakes. She was unflappable in a haunted house and unfazed by horror films. Damasio's team concluded that S.M. exhibited "a profound and pervasive impairment in the induction and experience of fear."

Like many in his field, van Honk, a young researcher at the time at Utrecht University in the Netherlands, was gripped by S.M.'s story. "She has to be the world's most famous living neurological patient," he says. Then in 2003, on van Honk's first visit to South Africa, clinical psychologist Helena Thornton of the University of Cape Town bent his ear about her efforts to track down people with Urbach-Wiethe in South Africa. She realized that the country offered something neuroscientists almost never encounter: not just one famous patient, but an entire cluster of people living with a rare neurological disorder.

Also known as lipoid proteinosis, Urbach-Wiethe disease was first described scientifically in 1929 by the Austrian medical researchers Erich Urbach and Camillo Wiethe. Medical sleuthing later traced back the disorder's presence in South Africa to a brother and sister, Jacob and Else Cloete, who had immigrated from Cologne, Germany, in the mid-1600s. The pair had married into a colony of Dutch settlers. Around the turn of the 19th century, a Cloete descendant transferred a gene for the trait into the mixed-race population of Namaqualand, the arid highlands in the Northern Cape, near the border with Namibia.

Urbach-Wiethe is recessive, which means that people must inherit copies of the defective gene from both parents to develop the condition. It has been associated with at least three dozen different mutations, all of them in a gene that carries instructions for a protein called ECM1, which is integral to the skin's connective tissue. Those with the mutation tend to have papery, inflamed skin and vocal cord lesions. They can have different patterns of calcification in brain regions, primarily in the amygdala, and in severe cases can suffer epilepsy, paranoia or other psychiatric symptoms.

Thornton and her colleagues found 34 Urbach-Wiethe individuals, most of them scattered across the rocky deserts of Namaqualand. Numbers had dwindled since the days of the Dutch colony — "a small community that suffered from inbreeding," van Honk says. Without close-kin marriages to sustain it, the condition was dying out. But with just 100-odd known cases globally, Namaqualand still had the most in the world.

The implications were extraordinary: a rare chance to study how selective damage to the amygdala shapes behavior. In 2005, the University of Cape Town organized another research trip to Namaqualand. Van Honk climbed aboard, and later recruited Utrecht social neuroscientist David Terburg, then a student. "We went into this research with the basic idea that the amygdala is the fear center, and we'd find fearless people, like S.M.," Terburg says. "But we got totally opposite results." Although individuals with Urbach-Wiethe disease in the Northern Cape appeared calm and good-natured, behavioral testing showed heightened fear responses and high rates of anxiety.

How could that be, the scientists wondered, if the brain region thought to govern fear had been compromised? At first, the revelations appeared to undercut the iconic case of S.M. and were coolly received by peers. "We spent five years to get those initial findings published," Terburg says. One clue to the apparent contradiction was that individuals in Namaqualand had a unique Cloete mutation not seen on other continents. Another clue came in 2007, after a powerful 3 Tesla MRI machine came to Stellenbosch University near Cape Town. "We were the first to use it," says van Honk. That's when the team discovered that the damage was concentrated in the basolateral amygdala. "Nothing like that had been seen before," van Honk says — in people, that is. Researchers had induced selective lesions to this and other parts of the amygdala in rats.

Rats are social creatures, and studies on these lesioned animals revealed that the basolateral amygdala helps them weigh outcomes and consequences; the central-medial amygdala, meanwhile, is more closely tied to fast, defensive reactions, such as freezing or fleeing from danger. It dawned on van Honk that the South Africans with Urbach-Wiethe disease were a kind of Rosetta Stone for seeing if what held for rats held for humans. Perhaps, he thought, different amygdala circuits might push human behavior in opposite directions, too.

Personal stakes

The brain had long fascinated van Honk, in part because of his own history. As a young adult, after his older brother died in a motorcycle accident, he struggled with mental health crises. The experience shaped how he related to the Urbach-Wiethe patients he later met — people whose raspy voices and visible skin changes often set them apart in their communities — and deepened his determination to unravel a living neurological mystery.

In 2008, after studying Urbach-Wiethe from afar, van Honk landed a visiting professorship in the University of Cape Town's department of psychiatry and mental health and moved from the Netherlands with his wife and their young children. He winnowed down the study population of people with Urbach-Wiethe, excluding individuals with afflictions such as alcoholism so that the team could be sure the effects they observed were truly due to the mutation. That reduced their pool of subjects to a handful of women, including Maria.

Then, to dive deeper into their behavior and cognition, van Honk and his colleagues turned to tools borrowed from economics and moral philosophy: simple games and thought experiments designed to reveal how people weigh risk, reward and responsibility. Classical economic theory assumes that humans shrewdly tally costs and benefits. Decades of behavioral research suggest otherwise: Decisions are often guided by gut feelings, impulses and social instincts that defy narrow self-interest.

In one widely used experiment known as the trust game, participants are given a sum of money and asked how much to invest with a stranger — with no guarantee of a return on that investment. Most people hedge their bets. The women with Urbach-Wiethe did not. Again and again, they invested generously with unfamiliar partners. With regard to their finances, their choices were reckless. To van Honk and his colleagues, the behavior suggested a diminished ability to flexibly weigh uncertainty, self-interest and the intentions of others — the kind of calibration they believe an intact basolateral amygdala normally helps provide.

A different pattern emerged in moral dilemmas. A classic thought experiment is the "trolley problem," in which a runaway trolley could kill five people, but intervening would mean you actively killed just one. When asked what they would do in variations on this theme, the women with Urbach-Wiethe disease consistently refused to endorse sacrificing a life, even as the numbers of people to be killed — were they not to intervene — grew extreme. "It's very nice to resist sacrificing a person, but if so many people were to die, it's a bit weird," van Honk says. "Something in the computation isn't working." The women understood the consequences but could not bring themselves to intervene. Some of them explained to the researchers that causing harm, even for the greater good, "hurts too much."

Intrigued, psychologist Tobias Kalenscher of the University of Dusseldorf in Germany took a sabbatical in 2023 to work with van Honk in South Africa. Kalenscher's team had earlier found striking behavioral changes in rats with lesions in their basolateral amygdala. Normally, when a rat is presented with two options — getting a treat just for itself, or the exact same treat for itself and for another rat — it often prefers the mutual reward. The rats with brain lesions couldn't care less about other rats, suggesting that the basolateral amygdala helps to assess the social value of a choice.

Social behavior in rats is only a rough proxy for humans. "Generosity is a genuinely human topic that you need to study in humans," Kalenscher says. He and van Honk asked the Urbach-Wiethe women in the Northern Cape to think of real people in their lives — those closest to them and those increasingly distant, all the way out to an anonymous stranger. For each person, the women were to decide how much money they were willing to share. A control group of women without the disease were asked the same questions. Generosity declined with distance in everyone, but among the Urbach-Wiethe women it dropped off far more steeply, the team reported in 2025 in PNAS.

The duo suspected that the women's behavior reflected a difficulty in balancing self-interest with concern for others, rather than a fixed tendency toward generosity or selfishness. So, starting in November 2025, they conducted a variation of the experiment that removed the need to divide resources. They asked Maria and others to squeeze a handheld device called a dynamometer. Pressing harder would generate more money for people at various social distances. In such tests, people without amygdala lesions are consistent: "They press much harder for people they love or feel close to than for strangers," Kalenscher says. The women with Urbach-Wiethe, by contrast, pressed just as hard for strangers as for loved ones — suggesting that they were not adjusting their behavior to social distance.

Across responses to threat, moral judgment and social decision-making, a striking pattern emerges. The women with Urbach-Wiethe are hampered in their ability to adjust their decisions as circumstances change. This suggests that the basolateral amygdala enables us to imagine others' outcomes and weigh them against our own when making decisions. "This is what we do, and I think what the Urbach-Wiethe patients cannot do," Kalenscher says.

In other words, while earlier theories framed the amygdala mainly as a detector of danger — a switch that turns fear on or off — the new evidence points to the brain region's broader role in calibration of behavior. Van Honk and his colleagues propose that the basolateral amygdala integrates emotional signals with possible consequences, allowing us to trade off our own gain against potential harm or benefit to others. The women with Urbach-Wiethe disease show what happens when that calibration system is disrupted: They are less able to reconcile competing considerations when making decisions. "It appears that they can't trade off their own benefit versus the benefit of others," Kalenscher says.

One possible explanation for that breakdown lies in how the basolateral amygdala interacts with the ventromedial prefrontal cortex, a region involved in evaluating reward and guiding decisions. In a healthy brain, the two appear to work together, integrating self-interest with concern for others into a single signal that guides behavior. When the basolateral amygdala is damaged, that communication may break down, leaving decisions to be driven by simpler, intact circuits. The idea remains speculative, Kalenscher says, but it fits with what is known about how these regions interact.

Translating the women's behavior in experiments into everyday life is a challenge. But Kalenscher says he sees clues in Maria. On the visit with her in January, she was caring for two orphaned children, apparently unrelated to her. From his brief window on Maria's day-to-day life, Kalenscher believes her computational deficit may translate into a kind of extreme altruism: a willingness to help others without the usual filtering of context. It makes her someone people can rely on, he says, but also someone who could potentially be taken advantage of. Echoing Maria's heroism is an observation about S.M. reported in 2018: S.M. told researchers how she'd once given her only coat and scarf to a homeless man she'd met under a freeway ramp in the dead of winter.

An enduring riddle

Every visit to the Northern Cape, it seems, brings to light another hidden oddity of Urbach-Wiethe disease. Sitting at Maria's kitchen table in Lambert's Bay, van Honk chats with his research subject as if she is an old friend — and, indeed, they've known each other for more than 15 years. As the visit winds down, he asks her about her sense of smell. "Yes, it's very good," she says, without hesitation. She talks easily about cooking, about knowing when food has gone off. Nothing in her answer suggests impairment.

Later, van Honk shows me unpublished results of a smell test he and colleagues recently ran with Maria and the others with Urbach-Wiethe disease. While their basic odor sensitivity is intact —they can detect smells just fine — the women struggle to identify what those smells are, a pattern that points to what the researchers call olfactory amnesia. "They understand the smell of fish, and coffee. But other smells they can't really differentiate," van Honk says. More striking, the women are unaware of the deficit, a phenomenon known as olfactory anosognosia.

In rodents, the basolateral amygdala plays a key role not in detecting odors but in learning what they mean — linking a smell to memory or consequence. When that region is damaged, animals can still sense odors, but they fail to learn that a particular scent predicts danger or reward. The Urbach-Wiethe data suggest something similar, the scientists say. Smell, one of the most ancient sensory systems, appears to rely on the same circuitry that helps humans learn from experience and revise their internal models of the world.

Despite the obstacles they face because of a steady, irrevocable loss of their basolateral amygdala, the women with Urbach-Wiethe in the Northern Cape cope and adapt, with resilience that impresses van Honk. And as they live out their lives, they gift science with a glimpse of how small changes in the brain can reshape how we fear, whom we trust and how far our concern for others extends.

This article originally appeared in Knowable Magazine, a nonprofit publication dedicated to making scientific knowledge accessible to all. Sign up for Knowable Magazine’' newsletter.

Epigenetics, which means "above genetics," results in changes to the way an individual's genes act without involving changes to the DNA itself. For example, by adding molecules called methyl groups to DNA — a process called DNA methylation — epigenetics may turn genes on or off, or increase or decrease their activity.

Environmental factors ‪—‬ such as stress, diet and smoking ‪—‬ can fuel epigenetic modifications which can, in turn, lead to conditions such as colorectal cancer and heart disease.

But some of these epigenetic modifications can be reversed. This means that epigenetics can reveal potentially new and targeted ways of modifying disease risk, Alika Maunakea, a professor of anatomy, biochemistry and physiology at the University of Hawaii at Manoa, told Live Science.

Having grown up subsistence-living on a homestead in Hawaii, Maunakea said he learned from a young age that the environment plays a major role in shaping the health of the community.

Now, Maunakea has been researching epigenetics for over 20 years and heads the Maunakea Lab, which focuses on how environmental and epigenetic factors act at the molecular level to fuel health disparities. Live Science spoke with Maunakea to unpack how epigenetics affects health and what his research is uncovering about how epigenetics plays a role in driving health disparities in Native Hawaiians.

Sophie Berdugo: Can you explain how genetics and epigenetics interact in a health context?

Alika Maunakea: It's a little complicated because there's a lot of nuanced differences and variability in understanding the context behind disease risk that's not just shaped by genetic predisposition but also environmental factors and lifestyle, and even things that our grandparents experienced. That's where epigenetics comes in.

Epigenetics is this intermediate state between the environment and the genome, and it helps to regulate the genome. So, even if you carry a genetic risk, it doesn't necessarily mean that risk will play out.

They [genetics and epigenetics] relate to each other because there are certain regions in the genome where if there's a polymorphism — a change — in the sequence, that can sometimes cause a change in the epigenetic patterning. So there's this intertwined connection between the two. In some cases, it's hard to separate completely the genetic variability that's conferring a risk of a particular outcome with epigenetic variability that's contributing to that same risk.

If a lot of the epigenetic variability is contributing to that risk — rather than genetic variability — then there's a chance that there are lifestyle changes, things that you can modify at the individual level to reshape the epigenome, that would then help to reduce that risk. So there's still a lot of work [to be done] around understanding that connection, and it will require a multidisciplinary approach and integrating multiple types of data.

SB: What got you interested in this field?

AM: My great-grandmother was a Hawaiian healer — what we call "kahuna la'au lapa'au" — and she taught me "nā mea Hawai'i," so "all the things Hawaiian." There was a deep understanding and recognition for how maintaining a healthy built and natural environment around us actually does shape our own health and well-being.

I was really interested in understanding why our population, Native Hawaiians, has a higher prevalence of specific chronic conditions which we never had before Westernization, and trying to understand, why do we see it earlier, at a younger age, in our population compared to other populations? That was something that really bothered me. I wanted to understand that more at the cell and gene level, so I think I just gravitated naturally towards epigenetics because I think it explains that phenomenon.

My main goal is really to apply that information into more of a clinical, community-based setting where that information can be used to enable tools and approaches that would help reduce the onset of these disorders in our community.

What we're learning now is that, indeed, epigenetic processes can precede disease symptoms. We can actually identify some of the earlier indicators of disease trajectories before our clinical diagnosis, using epigenetic analyses. Trying to understand how that can play a role in enabling prevention is a real big thing in my lab right now.

SB: Which health conditions do you look at in your research?

AM: One of the conditions that we're looking at is type 2 diabetes, which has such a high prevalence amongst Native Hawaiians. It's three times higher than in other populations in the state, as well as an earlier onset of disorder: about 10 to 15 years younger where Native Hawaiians are diagnosed with type 2 diabetes compared to other populations in the state. [They also have] higher rates of mortality due to type 2 diabetes and other chronic conditions.

Pre-colonization [pre-Western contact in 1778], we never had [chronic conditions like type 2 diabetes] as an issue in our population. Our "kahuna la'au lapa'au" [Hawaiian healer], like my great-grandmother, had to invent new terms for them based on the phenotype [how the condition is presenting]. So we call it [type 2 diabetes] "mimi koko," which is "sweet blood."

It's unclear how much of our genotype is really related to that disease risk, but we think that environmental factors and the changes that happened after colonization and Westernization, and the changes in our lifestyle and our society — disruption and especially displacement — really drove us to this state where there's this higher incidence now of these conditions. And so we're trying to understand what, at the molecular level, is shaping those outcomes and how we can use that information to prevent that from happening in the first place.

One of the questions that really immediately came out was, what's really behind the earlier age of onset? Why do we not only have a higher prevalence, but why is it happening at a younger age? That question still remains to be clarified, but we think that certain traits, like obesity, modify that risk.

To get at that question, then, we really need to understand, at the molecular level, are there disruptions to the aging process in this population? Are there differences in vulnerabilities to aging in this population versus other populations that might be influenced by these environmental factors?

There's a phenomenon called "epigenetic aging," which Steve Horvath back in 2013 initially published a paper around, and identified that there are certain sites in the genome that are epigenetically regulated — by DNA methylation, in particular — that correlate with chronological age really well in a healthy population.

But there were some individuals that exhibited what we would call outliers in this relationship, where there were cases where individuals seem to have higher estimated epigenetic age compared to their chronological age. So they would seem [to be] biologically aging faster than they should be normally. And then there were also people at the opposite end, where their estimated epigenetic age actually appeared younger than their chronological age. And we think that corresponds to health in general.

We found something similar in the Native Hawaiian population: There's a higher frequency of individuals in the Native Hawaiian population that seem to be, at the molecular level, aging faster than they should be compared to other populations, such as white populations and Japanese American populations in the state of Hawaii.

And we know that corresponds to the higher prevalence of these chronic conditions that we see, like diabetes in the Native Hawaiians compared to these other populations, as well as some of these risk factors, like obesity. And we've seen it in our community. Individuals that are in socioeconomically poorer neighborhoods tend to have this accelerated aging.

We're learning that there are certain individual-level lifestyle factors that can actually potentially modify that [epigenetic] risk. We have identified that even amongst Native Hawaiians that are living in socioeconomically poorer areas, at the individual level, if there's a higher degree of physical activity as well as education — and even in some cases, nutrition — there tends to be closer-to-normal biological aging amongst those individuals even within that population.

And so that told us that while there's a higher risk for individuals that have this accelerated aging of diseases like diabetes, that risk could be potentially modified by engaging in healthier lifestyle changes.

Now we're not only seeing that there's this disparity and potentially a mechanism that might underlie that disparity but some clues into potentially what types of environmental factors might be shaping that molecular process.

We have one pilot study that we published a few years ago showing clearly that amongst Native Hawaiians that are diabetic, when they engage in a lifestyle intervention that includes social support, in particular, they not only improve their glycemic control — which is the main purpose of this intervention, really — through this lifestyle modification over a 12-week period, but we also showed that the cells that relate to inflammation, the behavior of those cells, is actually modified by that intervention, and they actually seem to be less inflamed. [Glycemic control is the management of blood glucose levels.]

The epigenomes of those cells are also being modified to a pattern that's similar to a nondiabetic-like state.

So we think those cells play a role in the pathology and the etiology [cause] of the disease and metabolic dysregulation in diabetic individuals. But we also think that modifying their inflammatory state might actually help with improving the glycemic control. So we're trying to understand how much of the epigenetic patterning might be associated with that [inflammation].

We're finding very clear associations that indicate that potentially we can use that information also to identify more effective interventions that might actually target this [epigenetic] process, where we can reduce the inflammatory state of these individuals at the cellular and molecular level.

We're really hoping that it can be useful for prevention, because we can identify these really early, before the clinical diagnosis. [Editor's note: These findings have not been published in a peer-reviewed journal.] And we think that if we can do that at the individual level, especially in a high-risk population, then we can recommend appropriate interventions — or optimize those interventions that exist — to target changes in the epigenome that then have this effect on the physiology and the outcomes of the condition itself. So that's something we're trying to develop further.

SB: How resource-intensive is it to inspect an individual's epigenome?

AM: It is resource-heavy, unfortunately, at this stage. So I think that it will take time to develop new technologies and tools that are more targeted and that can be used in more of a clinical setting.

But with genome sequencing being more cost-effective than it ever was before and the reduced cost that it's now moving towards, that does increase the feasibility to adopt some of these approaches.

Editor's note: This interview has been condensed and edited for clarity.

Fingerprinting transformed police investigations by making it possible to place a suspect at a crime scene with physical evidence. Similarly, genome sequencing has changed how disease detectives study outbreaks by allowing them to read a pathogen's genes as a biological record of where it came from and how it spread.

One way to think about sequencing is to imagine a virus or bacteria's genome as a recipe book. Each gene is a recipe for making a protein. When scientists sequence a pathogen, they read the order of the genetic letters in those recipes.

Over time, small changes appear in the recipes as the pathogen mutates. By comparing those changes in samples collected from different places and times, researchers can determine which infections are related and estimate when and where the pathogen entered a population.

Scientists have used sequencing in this way to track outbreaks of COVID-19, Ebola, mpox and foodborne illnesses. This information helps public health investigators connect cases that might otherwise seem unrelated.

Still, genomic sequencing has limits. It can show that different pathogen strains are related, but it cannot fully explain why an outbreak began in one place, why it spread in a particular direction, or how human behavior shaped its course. Answering those questions requires combining genomic data with historical records, archaeological artifacts, trade records and epidemiological investigations.

I am a chemist and the author of "Diseases Without Borders: Plagues, Pandemics, and Beyond," a book for young adults on infectious disease and the ways it has shaped human history. In my research, I've found that while the genome can help researchers trace the evolutionary trail of a pathogen, other fields are needed to explain the environmental conditions that allowed this trail to become an outbreak.

Ancient DNA tells only part of the story

Advances in DNA sequencing and extraction over the past decade have made it possible to recover fragments of ancient DNA from bones and teeth. Researchers can use these genomes to study a metaphorical molecular fossil record of microbial evolution.

The Black Death, one of the deadliest pandemics in history, shows both the power and the limits of sequencing.

The infectious disease behind the Black Death, plague, is caused by the bacterium Yersinia pestis. DNA recovered from the teeth of people buried more than 5,000 years ago in what is now Sweden revealed the existence of an ancestral form of Y. pestis that had not yet adapted to fleas.

About 2,000 years later, the bacterium made an important evolutionary shift: It gained the ability to survive in fleas and pass back and forth between humans, rats and other mammals via flea bites. That change made the pathogen far more dangerous and helped pave the way for three great plague pandemics that followed: the Justinianic Plague from the sixth to eighth century; the Black Death and later waves from the 1300s into the 1700s; and the third pandemic from the 19th to mid-20th centuries.

But how and why did plague emerge and move through human societies with such devastating results? Genetic results alone are not enough to answer these questions.

When gravestones become genetic evidence

Geneticists needed archaeologists, paleoclimatologists and historians to complete the picture of the plague pandemics. The genome revealed the lineage. Other disciplines supplied the historical and environmental context.

Two 14th-century graveyards in what is now Kyrgyzstan provide a striking example of how historical evidence can guide genetic investigations into the origins of a pandemic.

Historian Philip Slavin noticed archival records pointing to an unusual number of gravestones from 1338 and 1339. Some of those tombstones explicitly referred to a pestilence as the cause of death.

That clue led to the next stage of the investigation, where archaeologist Maria Spyrou and her team extracted and sequenced ancient DNA from the skeletal remains of seven people buried in the graves and found genetic traces of Yersinia pestis in three of the skeletons. These strains were close precursors of the strain linked to the Black Death and ancestors of several modern Y. pestis lineages.

This major finding was still not the whole story. It could explain where the Black Death pandemic began but not how the disease spread across Asia to Europe. Researchers found a potential answer to this question in artifacts buried at the site, which included pearls from the Indian Ocean, Mediterranean coral and foreign coins. Those objects suggested that the region was connected to long-distance trade networks.

Once the gravestones, skeletal remains, written records and trade goods were considered together, a richer picture emerged. Researchers could place the pathogen in a specific time and place and connect it to the networks of human movement that may have carried plague westward.

Sequencing provided the biological clue, revealing the pathogen’s identity and ancestry. History and archaeology turned that clue into a plausible narrative.

From ancient DNA to modern outbreaks

Genomic sequencing isn't limited to examining outbreak cold cases. It is also researchers' tool of choice for understanding new diseases.

When the first reported COVID-19 cases emerged in 2019, researchers quickly sequenced the virus and found that it was closely related to the virus that caused the 2002 SARS outbreak. This placed the new virus within a known family of pathogens.

Later genomic sequencing helped reveal the scale of a major superspreading event: the 2020 Biogen conference in Boston.

The biotech company Biogen brought together about 175 European and American executives at a moment when COVID-19 was only beginning to spread in the United States. In Europe, COVID-19 was also escalating, with northern Italy reporting locally transmitted clusters just days before the meeting. After the meeting, many Massachusetts cases were linked to the conference.

Researchers then analyzed thousands of viral genomes from patients in Massachusetts and elsewhere. One viral genome carried a unique genetic signature traceable to a European attendee at the conference. It matched viruses circulating in Europe but also had an additional mutation that appeared to have arisen during the attendee’s travel to Boston or early in the conference.

Because that altered sequence appeared only in people with direct or indirect ties to the meeting, it served as a genetic marker for the COVID-19 strain originating at the Biogen conference. By comparing it with other viral sequences in national databases, researchers tracked the strain associated with the conference to 29 states and several other countries.

Interviews and contact tracing alone couldn’t have made that chain of infection so clear because people may not know exactly when they were exposed, especially when infections spread through brief encounters, via travel or large meetings.

When genomes join the investigation

Genome sequencing has rewritten the history of disease by giving scientists a way to read a pathogen's own record of change.

It can link ancient graves to later pandemics and trace a modern outbreak from one conference room to cases across a continent.

But the greatest strength of genome sequencing lies in partnership. Sequencing does not replace history, archaeology or public health investigation. It gives them a new molecular partner.

Combining work from these fields produces a fuller and more accurate account of how disease moves through the world.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

An Ebola epidemic in Central Africa has been declared a "public health emergency of international concern" by the World Health Organization (WHO).

As of May 22, over 800 Ebola cases have been reported in the Democratic Republic of the Congo, including more than 180 deaths; these counts include both suspected and laboratory-confirmed cases of the disease. There are also two confirmed cases and one death in Uganda, specifically among people who had recently traveled to the DRC.

A number of factors are making this outbreak very challenging to contain, experts told Live Science — here's what to know.

Current Ebola outbreak

WHO officials suspect the Ebola outbreak centered in the DRC may have begun about two months ago. The earliest suspected death occurred April 20, and it was likely followed by a superspreader event at a funeral or healthcare facility, officials say. Reuters also reported that medical personnel failed to escalate the first patient's samples for further tests after they came back negative one type of ebolavirus.

That virus — known as Ebola virus, or Zaire ebolavirus — is the most common culprit behind Ebola disease outbreaks and deaths. There are two other viruses known to cause outbreaks of Ebola disease: Sudan virus and Bundibugyo virus. The latter is driving the current outbreak.

With only a handful of travel-related cases in Uganda, as well as one American receiving care in Germany after being infected in Congo, the outbreak remains concentrated in the DRC. The WHO anticipates a high risk of international spread, though, which prompted the agency's leader to make an emergency declaration without first convening a committee to discuss the decision.

"In our view, the scale and speed of the epidemic demanded urgent action," WHO Director-General Tedros Adhanom Ghebreyesus said May 19.

A virus with no vaccine

Part of the challenge with containment is that there is no effective vaccine against Bundibugyo virus, the germ driving this outbreak.

There are approved Ebola vaccines. "However, these vaccines have been designed specifically to address the Zaire ebolavirus," which has historically caused more outbreaks than Bundibugyo virus has, said Dr. Madeline DiLorenzo, clinical coordinator of infectious diseases operations and an associate hospital epidemiologist at New York University (NYU) Langone's Tisch Hospital. The largest Ebola outbreak to date, which happened from 2014 to 2016, involved the Zaire ebolavirus.

Zaire ebolavirus and Bundibugyo virus are genetically distinct, sharing only about 60% to 70% of their genetic material. The protein targeted by the existing Ebola vaccines is encoded by a specific gene, and that gene's sequence differs between the two viruses, DiLorenzo explained.

Studies suggest that immune responses against filoviruses — the family of viruses that includes Zaire ebolavirus and Bundibugyo virus — show limited cross-reactivity, meaning the immune response is narrowly focused on just one type of virus. So the Zaire-targeting vaccines likely wouldn't help in this outbreak.

WHO officials have said there is a promising experimental vaccine against Bundibugyo virus, but there are no doses available for a clinical trial. It could take six to nine months to manufacture those doses, the WHO estimates. Another vaccine in development could take two to three months to produce, but its efficacy is unknown because scientists are still waiting on results from lab-animal tests.

In Ebola disease outbreaks, vaccines are used for ring vaccination, in which people exposed to a suspected or confirmed case are inoculated against the disease. They can also be used for "targeted geographic vaccination," in which everyone in a given area is vaccinated because the outbreak is relatively concentrated there or contact tracing is too difficult to conduct. Without a Bundibugyo vaccine, both of those strategies are currently off the table.

Lack of diagnostics and treatments

Ebola disease can be difficult to spot in its early stages, in part because the first symptoms are fairly generic: fever, fatigue, malaise, muscle pain, headache and sore throat. These symptoms appear within two to 21 days of exposure to an ebolavirus.

There are tests for Bundibugyo virus that look for the virus's genetic material in bodily fluids; this approach is known as PCR testing. "However, it is not widely available for the Bundibugyo virus, making it difficult to diagnose and, as a result, contain the virus," Dr. Jill Weatherhead, an associate professor of infectious disease and tropical medicine at Baylor College of Medicine, told Live Science in an email.

Even when such tests are available, it can take several days after a patient develops symptoms for the virus to be detectable in blood, DiLorenzo noted, so repeat testing can be necessary. The recommended samples for Ebola tests are whole blood or plasma for living patients and an oral swab for deceased individuals, the WHO says.

There are additional tests that can detect Bundibugyo virus, including some that determine whether a sample contains a filovirus that infects humans in general, without specifying which one is present. These rapid tests look for specific viral proteins. However, these tests are less sensitive and "may not pick up specific proteins associated with Bundibugyo," DiLorenzo said. "This may have contributed to delayed detection of the current outbreak in the DRC."

On top of these diagnostic challenges, there are no specific antiviral treatments for Bundibugyo virus. There are lab-made antibodies approved for Zaire ebolavirus, and they improve survival by binding to the virus's surface and blocking it from infecting cells. Similar treatments for Bundibugyo virus haven't progressed beyond lab research or early-stage human safety studies, Weatherhead said.

Conflict, declining foreign aid hinder containment

In the absence of vaccines and treatments, other strategies, such as quarantining close contacts of infected people, become key to containing the outbreak, Weatherhead said. Clinicians treating patients with suspected or known cases should also follow strict infection-prevention-and-control protocols to prevent further spread, she added.

Ebola spreads via contact with infected blood and other bodily fluids, as well as contaminated surfaces or materials, such as clothing and bedding. This means using personal protective equipment to block splashes or other contact with infected materials, among other protocols.

The strategies available to contain this outbreak — finding and isolating cases and employing tight infection-control protocols — require public health infrastructure to execute. But in the DRC, that infrastructure is severely compromised. The outbreak's epicenter is the Ituri province in the northeastern DRC, which has "experienced armed conflict for decades, making it challenging for health systems to function optimally there," DiLorenzo said.

Joshua Walker, director of programs of the Congo Research Group at NYU's Center on International Cooperation, told Live Science via email that the circumstances of the current outbreak resemble a 2018-2020 outbreak that centered on the North Kivu province, which borders Ituri to the south.

This time around, several cases have been reported in both North and South Kivu provinces, parts of which are essentially partitioned between the DRC government and a Rwanda-backed rebel group, called M23. And there's been increasing violence among armed groups in Ituri in recent months, Walker said. Meanwhile, development assistance for healthcare in the area has fallen substantially in recent years. Together, these factors "will make access and coordination of a single response more difficult," he said.

Recent cuts to foreign aid are only making things worse, Dr. Manenji Mangundu, DRC country director for Oxfam, which is coordinating on-the-ground responses to the outbreak, told Live Science in an email.

"USAID [the U.S. Agency for International Development] was the main donor in the DRC and many aid organizations depended on its funding to deliver life-saving support in a country already devastated by conflict," Mangundu said. "When USAID was shuttered last year, eastern DRC lost around 70% of its humanitarian aid."

More funding cuts from other donors followed, leading to the closure of medical centers, declines in medical supplies and community health workers, and reduced capacity to deal with outbreaks.

"Funding cuts directly do not cause outbreaks, but they do weaken the very systems that are meant to prevent small crises from becoming larger crises," Mangundu said.

In Ituri, residents have been repeatedly displaced due to the conflict and must shelter in crowded schools and churches with limited access to clean water, sanitation and healthcare. Funding cuts only compound these existing problems, he said.

In this setting, it can also be difficult to convince people to adopt safety measures to limit the spread of Ebola, he added. For example, "communities remain attached to their deceased relatives and continue to handle the bodies, which increases the risk of transmission."

Lessons from past outbreaks

Walker noted that the international response to the current outbreak will shape how it evolves.

"The 2018-2020 Ebola response effectively sidelined the local Congolese health system, viewing it as too fragile or weak to be an effective partner," he said, citing his past research. So the response was largely orchestrated by outsiders to local communities, which fostered suspicion.

"One hopes," Walker concluded, "that there have been some hard lessons learned by the international community since the last major outbreak."

As global health leaders warn that this outbreak could swell to impact more countries, Mangundu emphasized that much more support is needed to snuff out the epidemic in the DRC.

"There is capacity in the country to respond, but there are not enough resources to help control and prevent the spread," he said. "We need to fund humanitarian aid and support the people of DRC at this time before a preventable crisis turns into one with far wider, global consequences."

This article is for informational purposes only and is not meant to offer medical advice.

Two decades ago, a landmark study showed that the brains of kids with attention-deficit/hyperactivity disorder (ADHD) take longer to mature. But new research suggests that this result, which was based on brain scans from a few hundred children, was a mirage.

What was thought to be a hallmark of the ADHD brain, the study found, instead reflects average sex differences in how the brains of boys and girls develop over childhood. The earlier dataset, which used a smaller sample size, may have become skewed to more closely reflect the average boy's brain development, the new research suggested.

In 2007, a research project forged a new path in the study of ADHD. A team based at the National Institute of Mental Health showed that children with ADHD, who outwardly struggled with attention and impulsivity, had differences in their brains underlying these behavioral symptoms, compared with children without ADHD.

The team used MRI to look inside the brains of 223 children with ADHD and a similarly sized control group of children without the condition. The study found that the brains of children with ADHD developed differently than the brains of kids without ADHD. Throughout childhood, the thickness of the cortex — the outer layer of the brain — increases and then decreases. The team showed that this process was significantly delayed in kids with ADHD.

At the time, this finding made perfect sense, because it matched well with ADHD behaviors, said Matthew Albaugh, a clinical neuroscientist at the University of Vermont. "You see kids that maybe are acting a little younger than their chronological age," he told Live Science.

The 2008 paper was "foundational" in the field, Albaugh said. The study even showed that kids with ADHD had earlier maturation in the areas of the brain responsible for movement, which was thought to explain their hyperactivity. The work told a commonsense story, researchers thought at the time.

Sex differences undermine brain data

But science is rarely that neat. In their new study, published May 18 in the journal PNAS, Albaugh and his colleagues cast doubt on those earlier findings.

The new work exploited a powerful data source to show that the previously reported delayed maturation is likely a mirage in the data, caused by differences in how boys' and girls' brains develop. When these different patterns are taken into account, there's no difference between ADHD and non-ADHD brain maturation, the study authors wrote.

The team set out to replicate the 2008 paper, using data from the Adolescent Brain Cognitive Development (ABCD) study, a National Institutes of Health-funded project that is tracking over 11,000 9- and 10-year-olds for roughly a decade, said study first author Shannon O'Connor, a research project assistant at the University of Vermont. The study measures various behavioral traits and brain metrics and is the largest imaging study of its kind to follow people over time in the United States, O'Connor told Live Science.

The ABCD study asked parents to report any problems with their child's attention. When the researchers initially examined the relationship between attention problems and cortical thickness, they found the same associations as the original study uncovered nearly 20 years earlier.

But the team wanted to use the rich dataset provided by the ABCD to test what would happen if they accounted for other factors in the children's lives. O'Connor had noticed that, in other studies of the ABCD data, boys tended to show a lower rate of cortical thinning than girls. When the team accounted for these different rates, the associations between attention problems and brain structure disappeared.

"That's what made the whole house of cards topple," Albaugh said. Earlier studies had accounted for the differences between boys and girls at single snapshots, but not over time, he noted. As kids dropped out of these smaller studies, their carefully balanced analyses may have swung to disproportionately reflect boys’ lower rate of cortical thinning.

Digging further into the data, the team split the cohort into just boys and just girls. In both sexes individually, there was no relationship between cortical thickness and attention.

The replication crisis rolls on

Dr. Max Wiznitzer, a pediatric neurologist at Case Western Reserve University who was not involved with the new study, said it was "well designed" and "asked the right questions." The new findings were based on parent-reported attention problems rather than ADHD diagnoses, so Albaugh's team conducted a series of follow-up studies looking at subsets of the patients who were diagnosed clinically, which produced similar results.

The new findings add to the overall replication crisis affecting neuroscience. New, powerful datasets and more precise imaging techniques have undermined, rather than strengthened, notable neuroscience studies that have guided the field. Albaugh said these new datasets suggest that many of these early findings "may have been flukes."

Notably, the influence of sex differences has been largely overlooked in neuroscience, and this research highlights how acknowledging sex as a factor can refine a study's conclusions.

Albaugh was quick to emphasize that the findings don't change the underlying knowledge that ADHD is a biological condition that has a strong genetic component. But it does leave the field lacking reliable biological signatures for the condition, Wiznitzer said.

The study should encourage researchers in the field to seek biological signatures that can be used to guide the diagnosis and treatment of individual patients rather than groups, he added. Cortical thickness was never used in those ways.

"If I put someone on medication and their behavior improves, in a way, it doesn't matter what their cortical thickness is," Wiznitzer said. "Clinically, there's the improvement, which is what you're after."

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A common asthma drug could be repurposed to help tackle hard‑to‑treat cancers, such as triple‑negative breast cancer, an early study suggests.

The research finds that cysteinyl leukotriene receptor 1 (CysLTR1), a protein found on many cells, may be hijacked by tumors to turn important immune cells into sleeper agents that work for the cancer instead of against it. Those immune cells, called neutrophils, would normally directly kill tumor cells, help to rally other immune cells against cancer, or boost the effects of certain cancer therapies.

However, research increasingly suggests that the cells are an important player in how cancers resist immunotherapy. Under certain conditions, they help build and maintain a tumor-promoting environment.

If the new study's finding is confirmed in future research, an existing medication could offer a way to target this receptor and thus reverse cancers' resistance to common immunotherapies. There's already a drug on the market that can block CysLTR1, called montelukast, which has historically been used to treat asthma and allergies.

The work suggests that "you can repurpose these drugs to revive or to reprogram those neutrophils to become immune stimulatory cells that basically sensitize tumors to immunotherapy," study co-author Dr. Bin Zhang, a professor of cancer immunology at Northwestern University Feinberg School of Medicine, told Live Science. The research, published Tuesday (May 19) in the journal Nature Cancer, could also help to explain why some patients don't respond to immunotherapy, a treatment that redirects the immune response toward cancer cells.

"There are not many options available for patients who are resistant [to immunotherapy]," Zhang said. "But now, using this drug, it seems like they [could] start to respond to the treatment."

Immune cells called to the dark side

CysLTR1 is an important actor in immune responses; it helps recruit immune cells to a site of infection and prompts the lungs to produce mucus and cough out any invading microbes, for instance.

The problem comes when that reaction gets out of hand. In asthma, blocking CysLTR1 can do wonders, alleviating symptoms like wheezing, breathlessness and allergy‑related nasal symptoms. The drug montelukast does just that, and it has been approved by the Food and Drug Administration (FDA) since 1998 to treat asthma and hay fever.

The new research suggests that CysLTR1 can also be co‑opted by tumor cells to cause neutrophils to adopt "tumor‑promoting" behavior. By releasing chemicals that tweak the behavior of immune cells — cytokines and cysteinyl leukotrienes — tumor cells encourage neutrophils to release powerful molecules that help cancer cells invade surrounding healthy tissue. They also help tumors ward off attacks from other immune cells that would normally seek out and help kill cancerous tissue.

"We identified this molecule plays a very important role in controlling neutrophils, which is one of the most abundant immune populations in the circulation, particularly in cancer patients," Zhang said.

When researchers blocked CysLTR1 in lab mice, by either turning the gene off or using montelukast, they found that they could slow tumor growth, increase the mice's survival time, and make previously resistant tumors respond better to immunotherapy drugs.

Blocking CysLTR1 worked across several tumor types in mice, including breast, colon and melanoma‑like cancers. It was particularly strong when combined with a common type of immunotherapy called "checkpoint blockades," causing once-resistant tumors to shrink under treatment.

This is important because some cancers, such as triple‑negative breast cancer, don't tend to respond well to checkpoint blockades, Zhang said. At least from preclinical models, we suggest that when checkpoint blockades and montelukast are combined together, "you see beautiful results reflected by increased survival" across multiple tumor types.

"It's a very amazing result," he said.

Turning science into treatment

In experiments with human cells, the team found that blocking CysLTR1 in human blood reduced neutrophils' ability to shut down cancer‑killing immune cells. It also stopped neutrophils from maturing into this tumor‑helping, immune‑suppressing state, suggesting that the same pathway the team saw in mice is also active in people. Using a genetic analysis, the team unraveled the chain of events that CysLTR1 triggers to switch into this "cancer-promoting" mode.

They then uncovered clues that this same mechanism had left traces in large cancer datasets. They found that patients whose tumors had more of the receptor tended to do worse overall and responded less well to checkpoint blockades.

Shakti Ranjan Satapathy, a postdoctoral researcher at Lund University in Sweden who studies this field but was not involved in the new research, said the study was "important and timely" and "moves the field forward."

Zhang is hopeful that the team will be able to launch a clinical trial on the back of their results."It's not easy, sometimes, doing a clinical trial, but in this case, it may be a little bit less challenging because those drugs are available," he said.

The team also suggests that doctors screen for this receptor to determine whether patients are likely to resist immunotherapy. "We are probably the first to demonstrate [CysLTR1 as] maybe a functional biomarker that could be linked to the patient prognosis and help predict the immunotherapy resistance," Zhang said. Still, there is a lot to be tested before this drug can be confidently rolled out in the context of cancer, he said.

"'Quickly move into trials' should not be confused with 'ready for routine cancer treatment,'" Satapathy cautioned. "Repurposing an approved drug still requires an appropriate dose, dosing schedule, patient selection strategy, safety monitoring, pharmacodynamic readouts, and evidence of benefit in combination with immunotherapy."

For one, montelukast is occasionally linked to substantial neuropsychiatric side effects when used for hay fever, including suicidal thoughts and mood changes, leading the FDA to raise a boxed warning in 2020. One alternative, Zhang said, might be to test whether the receptor could be targeted directly with an antibody, which could potentially cause fewer side effects, rather than a chemical, though further research will be needed to assess if this is the right path.

"Hopefully, we can have a real clinical impact," he said, "but that's too early to say."

This article is for informational purposes only and is not meant to offer medical advice.