The patient: A 65-year-old woman in Michigan

The symptoms: The woman arrived at the emergency room via ambulance and asked to see a psychiatrist for her visual hallucinations. "I'm seeing dead people," she told clinicians, adding that she'd even fired a gun at her hallucinations in one instance, according to a report of her case. (The report does not describe what the hallucinations looked like.)

Despite this reaction to her hallucinations, she was calm and alert during her physical exam, with normal vital signs other than high blood pressure. She reported a history of high blood pressure, diabetes, heart failure and chronic back pain but no prior psychiatric history.

What happened next: Since the woman had no past psychiatric history, doctors opted for a medical assessment before consulting a psychiatrist. A blood test revealed mild metabolic acidosis, meaning her blood was too acidic. A toxicology screen detected high levels of salicylates, a class of compound that includes acetylsalicylic acid, better known as aspirin.

The diagnosis: When questioned, the woman acknowledged that she had been taking over 15 aspirin pills a day for multiple weeks. Each of these pills, marketed for back and body pain, contained 500 milligrams of aspirin.

Upon further questioning, the woman confirmed that she had tinnitus (ringing in her ears), which is a classic symptom of salicylate toxicity. In other words, she'd overdosed on aspirin.

The treatment: Doctors consulted experts at Michigan's poison control center, who recommended intravenous (IV) treatment with sodium bicarbonate (the chemical name for baking soda). This treatment alkalinizes blood and urine, meaning it makes them less acidic. This enables more salicylate to be excreted through the kidneys, allowing the drug to be eliminated through the urine.

After 11 hours of the IV treatment, the woman's blood salicylate levels dropped from 28.8 milligrams per deciliter (mg/dL) to 18.3 mg/dL. Her hallucinations ceased and the tinnitus improved within 48 hours of her arrival at the hospital. She was discharged without having seen a psychiatrist.

What makes the case unique: Aspirin is generally safe when used in doses indicated on the bottle or advised by a person's doctors. However, taking too much aspirin can irritate the gastrointestinal tract, as well as disrupt the activity of parts of the nervous system.

At high enough doses, salicylates can stimulate part of the brain called the medulla, which regulates breathing. This results in hyperventilation that causes the body to lose too much carbon dioxide, and at first, the blood becomes more alkaline. This process is known as respiratory alkalinosis.

However, salicylates also disrupt metabolism, leading to metabolic acidosis from a buildup of lactic acid in the body, as the woman experienced. When metabolic acidosis overwhelms the respiratory alkalinosis and causes the blood to acidify, organ damage can occur. These metabolic effects may also explain the tinnitus, as it drives increases in arachidonic acid that stimulate receptors in the inner ear.

The woman's daily intake of roughly 75 milligrams of aspirin per kilogram of body weight was about half the typical dose associated with acute salicylate poisoning. However, it was still a large amount to take every day for weeks, and older age is also a risk factor for severe outcomes of acute salicylate toxicity.

The authors of the case report noted that although she had tinnitus, she lacked many other hallmark symptoms of salicylate overdose, such as nausea and fever.

To the clinicians, the woman's case served as a reminder that long-term aspirin toxicity may result in different symptoms than acute poisoning does. In past case reports, other patients with chronic salicylate toxicity have also reported visual hallucinations. But that potential symptom is not as well understood as more common symptoms like tinnitus.

The case report authors added that longer-term exposure to aspirin may be associated with more neurological symptoms because chronic exposure increases the odds of the drug crossing the blood-brain barrier — a gatekeeper that allows only certain substances from the blood into the brain. They added that doctors should consider poisoning, including salicylate toxicity, for patients with psychotic symptoms with no clear cause.

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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Emerging treatments aim to reverse or stall signs of aging in the body and thus cut the risk of age-related diseases. One of those signs is an accumulation of "zombie cells" — damaged cells that spew harmful substances rather than dying off and getting cleared away by the immune system.

Some scientists are designing treatments aimed at killing those zombies directly. But what if we instead helped the body's cleanup crew get rid of them?

"I think rejuvenating the immune system could rectify a lot of problems," said Roel de Maeyer, an immunologist at the University of Oxford. "We know hospitals are full of older people suffering from infections that younger people don't need to go to [the] hospital for."

The aim of these rejuvenating therapies would be to help people live healthier for longer, he told Live Science.

How do cells turn into zombies?

The immune system constantly gets rid of old, dysfunctional and dead cells to keep tissues healthy, but that cleanup gets less effective with age.

When cells die, they display proteins on their surfaces that act as "eat me" signals for immune cells, called macrophages, to engulf and destroy them. However, some cells refuse to die and instead become senescent. These zombified cells can lurk in tissues for years, releasing chemicals that drive inflammation and damage.

Senescent cells can form due to DNA damage from oxidative stress, radiation, or even normal cell division. Cells lose bits of DNA each time they make copies of themselves, and they have intricate mechanisms to decide when it becomes a "bit too dangerous to keep dividing," de Maeyer said. If a cell can no longer divide, it usually undergoes a process called programmed cell death or becomes senescent, he said.

Senescence can be beneficial in some contexts; it helps heal wounds, for example. But an accumulation of senescent cells is linked to damaging inflammation and impaired organ function.

"If there are many senescent cells in a tissue, that's usually a bad sign," de Maeyer said. The number of senescent cells goes up with age and is linked to many age-related conditions, such as heart disease and dementia.

Slaying zombies

Studies in mice have shown that using drugs to kill senescent cells can reverse inflammation and some signs of cellular aging. These drugs, called senolytics, force senescent cells to enter programmed cell death, thus reducing their numbers, said Jure Povsin, a biochemist at the Max Planck Institute of Biochemistry in Germany. This ultimately reduces inflammation and improves tissue function, he told Live Science.

But while senolytics can help rid the body of zombie cells, it's not clear why the immune system fails to eliminate senescent cells in the first place. To find answers, scientists began looking at macrophages, the cells tasked with devouring dying cells.

Research pointed to a receptor on macrophages called EP2. One study, published in July in the journal Science, found that old macrophages have a greater number of these receptors and cannot eat senescent cells effectively.

Genetically deleting the EP2 receptor in lab mice restored the macrophages' function and reduced the number of senescent cells. Compared with normal mice of the same age, the genetically tweaked mice showed less cognitive decline, muscle loss, cardiac dysfunction and systemic inflammation.

On some of these metrics, such as the ability to remember familiar objects, the modified mice were comparable to younger mice.

A problem with energy

Why is the EP2 receptor at the root of this problem? Scientists found a clue in a huge study of older adults.

A molecule called PGE2 plugs into the EP2 receptor. It's a type of prostaglandin — a molecule that helps cells communicate during stress and injury and contributes to fever, pain and swelling. Drugs such as ibuprofen reduce inflammation by blocking prostaglandin production.

In 2001, a large study uncovered a connection between these prostaglandin-blocking drugs and Alzheimer's disease: People ages 55 and older who routinely took the drugs for at least two years had a lower risk of developing Alzheimer's than nonusers did. The study could not prove that the drugs directly prevented the disease, but it added to growing evidence that inflammation related to EP2 activity plays a role in Alzheimer's.

This caught the attention of Dr. Katrin Andreasson, a neurologist at Stanford University and co-author of the recent Science study.

"I thought, 'Wow, this is interesting,'" she told Live Science. "I wondered if there's a connection."

Andreasson and colleagues had an important breakthrough in 2021: They found that aging macrophages had higher levels of the EP2 receptor and that increased EP2 activity disrupted how the cells used their energy. Instead of burning glucose to produce energy like young macrophages do, these cells stashed it away.

As a result, the cells could not do their job properly, as "gobbling up cells requires a ton of energy," Andreasson said. Blocking the EP2 receptor restored normal energy use in the macrophages. In old mice, it also led to reduced inflammation and better scores on cognitive tests, compared with mice in which EP2 activity remained high.

Making senescent cells vulnerable

In their recent study, Andreasson's team uncovered another consequence of aging: Old mice accumulated many senescent neutrophils, a type of short-lived immune cell that acts as the body's first line of defense against germs. Neutrophils normally die within days and are then cleared away, but with age, they become more prone to senescence and accumulate.

"I think that's kind of an odd concept because they're [usually] very short-lived cells," said de Maeyer, who was not involved in the Science study. "Neutrophils are inherently quite inflammatory, so wanting to clear them from tissues is very valuable."

Old mice have too much EP2 activity in their macrophages, and that means they can't get rid of these neutrophils, Andreasson's team found. That may be why deleting EP2 seems to have anti-aging effects in multiple organs, they concluded.

But increased EP2 activity is just one side of the story; some studies suggest that zombie cells actively suppress macrophages' ability to eat them. They do this by using a tricky protein called CD47.

CD47 is a "don't eat me" signal that stops macrophages from destroying cells, Povsin said. "It signals that the cell is healthy, alive and doesn't need to be eaten."

However, that signal gets amplified in senescent cells, Max Planck researchers showed in a 2023 study. That means that, when macrophages interact with senescent cells, macrophages' function becomes impaired. Afterward, they even lose the ability to engulf dying, nonsenescent cells. This allows a ton of cellular debris to accumulate.

So, rather than just blocking EP2, it could also be beneficial to reduce that "don't eat me" signal in senescent cells, this research hints. But CD47 is found on all living cells, so scientists can't just deplete its numbers across the body.

A specific enzyme modifies CD47 on senescent cells, and in the 2023 study, blocking the enzyme helped spare macrophages from the effects of CD47. Therefore, blocking the enzyme could be a more selective approach to weaken the "don't eat me" signal on senescent cells, Povsin said.

A long road to treatments for people

Translating these ideas into anti-aging treatments for humans would be a major success in the science of aging, but experts say there are significant problems to overcome.

Although blocking EP2 had consistent results in lab mice, the rodents are genetically identical and bred in controlled environments. Humans are inherently more variable in their biology and the environmental factors they're exposed to, introducing confounding factors that would need to be addressed, de Maeyer said.

Additionally, in clinical trials, EP2-blocking drugs have so far been explored as cancer treatments, but they are "underexplored" in the context of aging, he added.

Drugs targeting CD47 are in an even earlier stage of development. In the 2023 research from Max Planck, the team used both human and mouse macrophages in their experiments, but the approach has not been tested as an anti-aging treatment in living mice or humans yet.

In 2020, de Maeyer's team used a different strategy to rejuvenate macrophages in older adults. They blocked a protein called p38, whose activity was high in the macrophages of older adults. Blocking the protein helped macrophages better recognize and eat dying cells in specific tests.

In that study, the team gave adults ages 65 and up an experimental drug called losmapimod to block p38. Although it helped restore their immune cell function, it was not suitable for long-term use because it caused liver problems in later trials, de Maeyer said.

In their mouse studies, Andreasson's team was able to block EP2 without causing any negative side effects. But she cautioned that we "really need to drill down on the research and confirm all this stuff in humans."

"The next logical step," she said, "would be to figure out how to inhibit this receptor in a safe way."

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

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Rosalind Franklin, whose photographs of the molecular structure of DNA led to a 1962 Nobel Prize for three other scientists, knew that her famous images held the secret of the double helix, new research suggests.

An examination of archival material reveals that Franklin's Photograph 51, which was taken in May 1952 and later published to show the double-helix structure, was specifically taken for the purpose of publication — not, as some narratives have held, an experimental shot that Franklin believed was insignificant. The new research revealed that Photograph 51 was a new exposure of a sample Franklin had already photographed. She started Photograph 51 the same day she saw that photograph, Photograph 49.

"She took it because she wanted to get a really refined version," said study co-author Alistair Sponsel, a historian of science at the Science History Institute in Philadelphia. Making the effort to take a better photograph of the same sample is "a sign she knew she had something really important on her hands," Sponsel told Live Science.

Francis Crick, James Watson and Maurice Wilkins shared the Nobel Prize in Medicine for the discovery of the double-helix structure of DNA in 1962. As Watson told it in his 1968 autobiography, "The Double Helix: A Personal Account of the Discovery of the Structure of DNA," Franklin's photographs were his "aha" moment: "The black cross of reflections which dominated the picture could only arise from a helical structure," he wrote.

Watson further implied that Franklin was a laboratory automaton, good at the X-ray crystallography techniques used to capture the images of the DNA molecule but bad at interpreting her own data. The new archival work, published Monday (Oct. 5) in the Journal of the History of Biology, suggests otherwise.

Franklin's dearth of published notes about Photograph 51 has been used to suggest she missed a major discovery. But Sponsel said her journals show she noted the possible helical shape and rich structural data in her notes for her first picture of the sample, Photograph 49, which she followed up with the more refined image in Photograph 51.

"In Franklin's mind, they were two different types of scientific image," Sponsel said. Photograph 49 was the experimental image revealing exciting new data. Photograph 51 was the showpiece to convey these findings with the most clarity and sharpness possible.

This new understanding of the relationship between the two images, and how Franklin perceived them, is the most important feature of the new work, Sponsel said, which he conducted with molecular biophysicist Brian Sutton of King's College London. The project began when the Science History Institute acquired a new collection of archival material from Rosalind Franklin and her graduate student Raymond Gosling. The two researchers also combed through the archives at King’s College London, where Franklin was working when she took the famous photos.

Sponsel and Sutton think that Franklin's notes and actions reveal why she didn't rush to publish Photograph 51 right away. Her scientific goals, laid out in a report she wrote in February 1952, were to understand the two separate structures of DNA, then known as A and B. Structure B, illustrated in Photographs 49 and 51, turned out to be the double helix that occurs in nature. Structure A is a form DNA takes when it's dehydrated in the lab.

Structure A, when photographed, appeared more data-rich, so Franklin decided to characterize that structure first before studying structure B. But while she did this painstaking work, Wilkins showed Watson her photographs of structure B. The two scientists, together with Crick, then built a detailed model of DNA's double helix and scooped the discovery from under her nose.

Those three men shared the Nobel Prize for the work less than a decade later. Franklin died of ovarian cancer in 1958, making her ineligible for the prize — and leaving her insights to come to light only much later.

Editor's note: This article was updated at 3:23 p.m. ET to fix the caption and subhead, noting that Rosalind Franklin had likely discovered DNA's helical, but not double-helix structure. Also, the top photo is not Photograph 51, but another photo taken by Franklin.

Mpox spread across the world in 2022, triggering tens of thousands of cases in countries where the infection was once rarely seen. Although the disease has since fallen out of news headlines, mpox (formerly called monkeypox) continues to circulate. Now, recent data suggests that the viral illness may soon be endemic to the United States, meaning it will circulate in the country consistently.

Previously, mpox cropped up sporadically in the U.S. via travelers who had visited African countries where the disease is endemic, as well as imported, infected animals that spread the virus to people. Cases have fallen substantially since the peak of the outbreak in 2022, but they haven't disappeared. A report published in August found that there were 2,800 cases in 2024 and over 2,500 in 2025, with only a small fraction being tied to travel. Nearly all of the viral samples analyzed were descendants of the strain that sparked the 2022 outbreak. In short, once the virus arrived, it never went away.

"There's no set threshold for what constitutes endemicity of monkeypox virus (MPXV) in the United States," Ryan Standford, an epidemiologist in the Centers for Disease Control and Prevention's (CDC) Poxvirus and Rabies Branch and co-author of the report, told Live Science in an email. "But each year provides further evidence of this transition."

Why is mpox still spreading in the U.S., and what can be done to snuff it out? It's likely that too few people have received two doses of the mpox vaccine JYNNEOS, which together are 66% to 90% effective. But beyond low vaccination, there may be other, less-understood factors that are contributing to the continued spread, experts told Live Science.

"We don't quite know how it's able to persist at such low numbers across the entire country," said Joel Wertheim, a professor of medicine in the Division of Infectious Diseases and Global Public Health at the University of California, San Diego.

At the same time, public health efforts around mpox have dwindled. Without a sustained effort on that front, it's unlikely the disease will be eliminated from the U.S.

"We have vaccines, testing, and a much stronger understanding of the disease than we did in 2022," Dr. Demetre Daskalakis, chief medical officer of Callen-Lorde, a LGBTQ+ community health center in New York City, told Live Science in an email. "Our focus now should be making sure those tools remain accessible, especially for communities that continue to face ongoing risk," said Daskalakis, who coordinated the nation's mpox response during the previous presidential administration.

"People at increased risk should know that mpox has not disappeared."

Who is at risk of mpox in the U.S.?

In the U.S., mpox is predominantly affecting men who have sex with men, and current vaccine recommendations are aimed at this group and their sexual partners. Mpox mostly spreads from person to person through close contact, and transmission during sex is playing a major role in the ongoing spread in the U.S.

Men who have sex with men are not more prone to mpox infection than anyone else. Rather, this transmission pattern stems from the outbreak beginning within a specific sexual network and then continuing to persist within the same network. "The mpox virus rediscovered the same transmission network that HIV had explored decades earlier," Wertheim said.

In a paper published in 2025, Wertheim and colleagues described the transmission dynamics of mpox in New York City during the 2022 outbreak. Similar to how HIV previously spread, mpox triggered "densely connected" clusters of infection. Then, as people in the network gained immunity via infection and vaccination, the cases petered out, decreasing to the persistent trickle we see now.

Wertheim noted that he's not surprised that mpox has remained largely confined to the same network, rather than leaping into new groups.

"From an evolutionary, ecological perspective, it's not hugely successful," Wertheim said. "It's sort of barely hanging on as an STI."

Why is mpox still circulating?

So if mpox is not hugely successful and we have a vaccine, how has the virus continued to circulate? One big factor is that too few at-risk people have been vaccinated, experts said.

The CDC's Center for Forecasting and Outbreak Analytics has crunched the numbers to see what percentage of that at-risk group needs to have immunity to stop mpox transmission, Daskalakis said. The at-risk group is estimated by counting the men who have sex with men who are either taking HIV-preventing medicines or have HIV, and then adding 25% to that total to account for additional people in the same sexual network. That estimate comes out to about 2 million people.

To prevent an outbreak bigger than the one in 2022, between 21% and 35% would have to have immunity through vaccination or a past infection. If over 50% of the group had immunity, that would mean there's a "very small probability" of sustained local transmission, the CDC's modeling suggested.

The current case counts suggest we haven't hit the 50% mark, or a total of roughly 1 million complete vaccinations or past infections.

Data from the August report on mpox seems to support the idea that too few people are vaccinated. That said, information about vaccination status was missing for about 62% of the reported cases. Among the remaining cases, 76% were unvaccinated, while 10% had gotten one dose and 14% had gotten two.

In a subset of 860 cases, the effect of vaccination was striking: Unvaccinated people had nearly 10 times higher odds of hospitalization due to mpox than fully vaccinated people did.

Waning public health attention

It's difficult to pin down exactly how many at-risk people are vaccinated, given that that data is no longer tracked at the national level. "My understanding is that there's no mandatory reporting on mpox vaccination data," Wertheim said.

The CDC previously monitored national vaccination trends, comparing the number of people vaccinated to the overall at-risk population. But that tracking stopped in early 2024, when about 23% of the at-risk population had been fully vaccinated.

Some states, such as New York, previously mandated that clinicians provide their state health department data on the number of people given mpox vaccines. But that reporting is now voluntary, a spokesperson for the New York State Department of Health told Live Science in an email.

Meanwhile, "as the emergency phase faded from public attention, awareness and risk perception may have declined," Daskalakis said. Public health messaging about the virus and vaccination has also waned.

"In recent weeks, HHS [the Department of Health and Human Services] has pulled down some of the plain-language guidance, which is not helpful in supporting messaging," Daskalakis noted. This decision to remove online resources about mpox reflects the federal government's current stance against addressing issues that affect LGBTQ+ health, he told Live Science.

Complicating factors

Although JYNNEOS substantially lowers the risk of severe mpox infection, the vaccine is not perfect, said Rachel Roper, a professor of microbiology and immunology at East Carolina University.

The virus typically enters the body through broken skin, the respiratory tract or mucous membranes (thin tissues found in the eyes, nose, mouth, anus and genitals). The mpox vaccine is good at generating systemic immunity, but it's not as good at guarding against the virus's immediate effects at those mucous membranes, said Roper, who studies poxviruses and vaccines against them.

Because mpox is largely spreading through sexual contact that involves those membranes, that slight gap in protection may also help to explain some of the ongoing spread, she suggested.

Plus, "there are also some data supporting asymptomatic infection as a possible route of transmission, making it more difficult to eliminate local transmission of mpox," Daskalakis said.

What can be done?

Given that mpox is already well established within some sexual networks in the U.S., "preventing endemicity entirely may be increasingly difficult," Standford told Live Science.

And notably, some federal funding cuts could undermine efforts to address mpox, Daskalakis said. These include cuts to Medicaid, mental-health services, housing programs, and HIV services such as the Ryan White HIV/AIDS Program.

Thankfully, looking at current mpox trends, "there's no indication we're returning back to 2022 levels," Wertheim told Live Science. So far in 2026, just under 1,000 mpox cases have been reported, according to the CDC. Month over month, the number of cases is generally trending downward. So, at a glance, the current situation seems better than it was in 2025, he said.

"We sort of seem to be on this razor's edge between endemicity and extinction," he said. "And it's not really clear which way it'll go."

Tipping the virus toward extinction will require healthcare providers to be informed and equipped to spot and manage cases, Daskalakis said. And communicating the importance of vaccination is key.

"One lesson from 2022 was that trusted messengers matter," he said. "We [at Callen-Lorde] work closely with LGBTQ+ communities and make information and vaccination opportunities available in settings where people already receive care." The clinic integrates conversations about mpox vaccination into routine health visits, sexual health services, HIV prevention programs and community outreach activities.

Beyond vaccinating at-risk populations, educating patients about how mpox spreads and how to reduce their risk is also key, Standford noted. "Vaccination coverage is a very important factor, but it is not the only one," he said.

Tipping mpox toward extinction will also require enough investment to maintain the disease surveillance, vaccination, testing and treatment capacity that the federal government helped to expand in 2022, Daskalakis said. The vaccine itself is now commercially available to clinics and in adequate supply, he emphasized.

"The fact that we're seeing ongoing circulation underscores the need for sustained prevention efforts rather than viewing mpox as a resolved public health issue," he said. "Infectious diseases don't disappear simply because public attention shifts."

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

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Mpox is an infectious disease caused by a poxvirus, meaning a virus in the same family as smallpox. The infection was formerly known as monkeypox.

Historically, mpox was endemic to Africa, and the virus consistently spread in the continent's central, eastern and western regions. In 2022, an unprecedented global outbreak spurred the widespread transmission of mpox in places that had seen only sporadic cases in the past.

Today, many countries affected by that outbreak — including Germany, Portugal and the United States — are still contending with local mpox transmission. Here's what to know about the virus, how it spreads and how to prevent infection.

What to know about mpox in the U.S.

Mpox is still spreading at low levels in the United States and may soon be considered endemic to the country. While case counts have fallen dramatically since the peak of the global outbreak in summer 2022, some people are still advised to get vaccinated against the virus.

Who should get vaccinated for mpox?

The mpox vaccine currently used in the U.S. is called JYNNEOS. One dose is about 35% to 86% effective, while the complete two-dose series is 66% to 90% effective. (The effectiveness varies, in part, because some studies include people with HIV and people without HIV, and inadequately treated HIV can undermine the body's response to vaccines.)

The JYNNEOS vaccine is not currently recommended for routine use in the general population because, beyond vulnerable groups, the risk is not high enough to warrant a universal vaccination strategy. The current outbreak is primarily affecting men who have sex with men, and those sexual networks are the primary targets for JYNNEOS vaccination.

However, not all men who have sex with men need to be vaccinated, according to the Centers for Disease Control and Prevention (CDC). Instead, vaccination is recommended for a specific subset of the group, including those who, in the last six months, have had more than one sex partner, have had sex at commercial sex venues, or have been diagnosed with other sexually transmitted diseases.

Nonbinary and transgender people with these risk factors are also recommended to get two doses of JYNNEOS, as are any sexual partners of anyone in the above groups.

Vaccines are also recommended after a suspected exposure to mpox, as they can help prevent or reduce the severity of the infection.

"For those who are eligible and have not yet completed vaccination, now is a good time to talk with a healthcare provider about getting protected," Dr. Demetre Daskalakis, chief medical officer of Callen-Lorde, an LGBTQ+ community health center in New York City, told Live Science in an email.

With the exception of laboratory researchers who work with mpox, people who have received two doses of JYNNEOS are fully vaccinated and do not need a booster, he said. And if a person has caught mpox in the past and recovered, they do not need to get a vaccine, he added.

About the virus

The poxvirus family also includes smallpox, which has been eradicated worldwide. Mpox and smallpox cause some similar symptoms, but mpox tends to be far milder than smallpox. However, the viruses are closely related enough that vaccines designed to prevent smallpox can also protect against mpox.

Mpox was initially named monkeypox because the virus behind the disease was discovered in captive monkeys in Denmark. But monkeys are not the main hosts of the virus in the wild; rodents and small mammals mostly found in West and Central Africa likely are. Health officials changed the name to mpox in 2022.

There are two major branches of the mpox family tree, called clade I and clade II. These clades were historically thought to have very different death rates, with clade I being the deadlier of the two. The case-fatality rate (CFR) of clade I has been estimated to range from 1.4% to over 10%, depending on the outbreak, while the CFR for clade II has been estimated at between 0.1% and 3.6%.

However, as both clades have spread beyond Africa, data suggests that the CFR for clade I may be lower than once thought, said Joel Wertheim, a professor of medicine in the Division of Infectious Diseases and Global Public Health at the University of California, San Diego.

The features of a given outbreak — such as the surrounding health infrastructure, patients' access to timely medical care, and the population's underlying risk factors for severe disease — likely play a big role in determining the virus's death toll, Wertheim told Live Science. In short, rather than being an immutable feature of the virus itself, the CFR is dependent on the underlying health of and resources available to a given population.

How mpox spreads

Mpox can spread from infected animals to humans through the animals' bites or scratches. Additionally, people can get the virus when they come into close contact with animals and/or their bodily fluids during hunting, skinning, trapping, cooking, eating animals or handling carcasses, the World Health Organization (WHO) notes.

The virus also spreads from person to person, primarily through very close contact, including intimate contact during sex. The virus typically enters the body through broken skin, the respiratory tract or mucous membranes (thin tissues found in the eyes, nose, mouth, anus and genitals), spreading via bodily fluids such as spit, mucus or blood. People can also pick up the virus via objects, such as clothing or linen, that are contaminated with the bodily fluids of an infected person.

The virus can spread through small respiratory droplets expelled during speaking or breathing. However, this is thought to be a less-common transmission route than close contact. There is also evidence that asymptomatic spread sometimes occurs, though it's unclear how frequently that happens.

Mpox can spread from mother to baby during pregnancy or birth. This route of infection can result in pregnancy loss, stillbirth, death of the newborn, or complications for the mother.

Symptoms of mpox

Symptoms of mpox typically appear within a week of a person being exposed to the virus, but they can sometimes take up to 21 days to develop. Once they emerge, symptoms last about two to four weeks, although the illness can linger longer in people with weakened immune systems.

Common symptoms include rash (see images), fever, sore throat, headache, muscle aches, back pain, swollen lymph nodes and low energy. Often, mpox rashes first appear on the face and then spread to other parts of the body; however, if a person becomes infected during sex, the rash may instead start around their genitals. The rashes begin as flat, discolored patches of skin and then progress into raised bumps, blisters, and large, pus-filled pimples that eventually scab over and fall off.

Some people with mpox develop painful swelling of the rectum (proctitis), while others have pain and difficulty when peeing (dysuria) or when swallowing.

Mpox rashes can make people vulnerable to bacterial skin infections, which can cause abscesses or other serious skin damage. Additional complications of the illness include pneumonia, infection of the cornea that can cause vision loss, and vomiting and diarrhea that causes dehydration or malnutrition. Mpox can also lead to blood infections, the intense immune reaction sepsis and, rarely, brain infections (encephalitis) or heart inflammation (myocarditis).

Children, pregnant people, and people with weakened immune systems, including from HIV infection, have a higher risk of serious illness and death from mpox.

Mpox prevention measures

Beyond vaccination, other strategies to decrease the risk of mpox infection include washing hands frequently, avoiding contact with contaminated objects and materials used by people with mpox, avoiding contact with other people's scabs or rashes, and using condoms, although they may only reduce, not eliminate, the risk of mpox exposure during sex.

Mpox treatment

Mpox treatment aims to manage a person's rashes and pain while also preventing complications. "Early and supportive care is important to help manage symptoms and avoid further problems," according to the WHO.

There is no antiviral drug approved for use in mpox, although some are available for emergency use in various countries. For example, the U.S. allows the use of certain smallpox medicines for mpox.

Severe mpox infections also may be treated with vaccinia immune globulin intravenous, which contains antibodies taken from the blood of people who were immunized against smallpox.

People who have recently been exposed to mpox can be given an mpox vaccine to reduce the severity of their symptoms or to prevent the illness altogether. This approach is known as post-exposure prophylaxis, or PEP.

"Post-exposure vaccine should be given as soon as possible, ideally within 4 days of exposure; administration 4 through 14 days after exposure may still provide some protection against monkeypox," the CDC states.

About 1 in 8 cancer cases are caused by infections with viruses, bacteria or parasites, a new study finds, suggesting that one of the most effective ways to reduce cancer rates might be to prevent common infections.

In a new analysis published Sept. 28 in the journal The Lancet Oncology, researchers mapped the global impact of 12 cancer-causing pathogens. They estimate that infections drove about 2.3 million new cancer cases in 2024, or about 12% of all cancer cases diagnosed that year.

The study highlights that a large fraction of cancer cases could be avoided if these underlying infections were prevented, Dr. Prashant Mathur, director of India's National Centre for Disease Informatics and Research, who was not involved in the study, told Live Science in an email.

"When combined with other risk factors such as tobacco use, alcohol consumption, appropriate diet, physical activity, and environmental pollution, it is estimated that about 50 to 60 percent of all cancers in India are avoidable," he said. Past studies suggest that similar figures hold on a global scale.

In the new study, the researchers used the Global Cancer Observatory's GLOBOCAN database, which combines data from various cancer registries to estimate that about 20 million new cancer cases were diagnosed in 2024. The team combined that information with other published data examining the prevalence of different infections in people with specific cancers. This enabled them to estimate how many cases were attributable to each infection.

Their analysis focused on 12 pathogens tied to cancer, including human papillomavirus (HPV), hepatitis B and C, HIV and Epstein-Barr virus (EBV), the virus behind mononucleosis. The resulting breakdown revealed that just four pathogens accounted for roughly 92% of the cancer cases caused by infections.

A bacterium called Helicobacter pylori, which infects the gastrointestinal tract, accounted for 760,000 cases, primarily gastric cancers. The other three leading cancer triggers were viruses. HPV accounted for 750,000 cases, including cervical, penile, throat and mouth cancers. The liver-attacking hepatitis B virus was responsible for 360,000 cases and EBV drove 260,000 cases. (EBV is known to increase the risk of throat cancers, as well as certain lymphomas and stomach cancers.)

The scale of the burden contrasts with gaps in prevention. In 2024, just 31% of eligible adolescent girls worldwide received at least one dose of the HPV vaccine, well below the 90% target, the World Health Organization reports. The degree of protection provided by the vaccine is striking in countries that have achieved higher coverage.

"We have now achieved the critically important milestone of cervical cancer starting to disappear in countries that quickly achieved vaccination rates of over 80 percent," said Dr. Rebecca Perkins, an obstetrician-gynecologist at Tufts University School of Medicine who was not involved in the study. "Research from Australia, England, and Finland have shown zero cases of HPV-related cancers or deaths in young adults who received vaccination by age 13," Perkins told Live Science in an email.

But these successes are concentrated in wealthy nations. The Lancet study found that low- and middle-income countries bear 77% of the global infection-driven cancer burden. For example, about 81% of HPV-linked cancers occurred in these countries.

Perkins pointed out that shifting from the standard two-dose HPV vaccine series to a single-dose regimen using the same vaccines could make mass campaigns easier worldwide by lowering costs and eliminating the need to track patients for follow-ups. The single-dose approach has been backed by recent trials.

In the U.S., progress has been uneven across states with some boasting high vaccination rates and others lagging behind. One barrier is that some children's caregivers feel the shots are unnecessary or that their kids are too young to receive it. "The biggest misconception from families is that the HPV vaccine is not needed or that it can wait," Perkins noted. "The reality is that you can't vaccinate too early, only too late."

There is also a highly effective vaccine for hepatitis B, and health officials recommend giving children their first dose as soon as possible after birth. (The U.S. Centers for Disease Control and Prevention recently made the decision to stop recommending universal vaccination at birth, which experts say could raise the country's rates of hepatitis B infections and related cancers.)

While the challenge with HPV and hepatitis B is getting their vaccines into widespread use, there isn't an approved vaccine for EBV yet.

"The biggest hurdle has been the complexity of the virus," said Claire Shannon-Lowe, a tumor virologist at the University of Birmingham in the U.K. who was not involved in the study. "Unlike many other viruses that use just one or two virus proteins to enter cells, EBV uses multiple proteins ... and it hides inside cells for our entire lifetime."

Epstein-Barr infections are also incredibly common, with up to 95% of people infected by adulthood; most people infected with the virus don't develop a related cancer, but it's still a major contributor to the global cancer burden. The germ has also been tied to several autoimmune diseases, which may help spur the development of a vaccine, Shannon-Lowe suggested.

"With the increased impetus following EBV's association with multiple sclerosis and lupus, we may finally have a potential vaccine in sight that could not only prevent virus infection but could help treat EBV-associated cancers," she said.

For H. pylori, meanwhile, researchers are pursuing population-wide testing for and treatment of the infection to help prevent gastric cancer, while vaccine development remains an area in need of further investment.

The true scale of the infection-related cancer burden may be even larger than the study suggested. Some of the registries used in the new research cover only about 19% of the global population, and only 2% of Africa's population. More high-quality data is needed to fill in these gaps.

For Mathur, though, the bottom line is that cancer prevention makes economic sense.

"Studies have clearly demonstrated that the return on investment of prevention on cancers is much higher than on its treatment in the long run," he said. "Preventive aspects must be strengthened for long-term gains."

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

Could a psychedelic drug help the brain recover from mild injuries? New research suggests that psilocybin, the mind-bending ingredient in magic mushrooms, might protect the brain from the damage caused by minor head impacts.

Even mild head impacts that don't count as concussions can raise the risk of neurodegenerative disorders such as chronic traumatic encephalopathy (CTE), so finding an effective treatment for these blows could be useful for warding off debilitating conditions down the line.

The new research, published in the journal Communications Biology, included only lab rats, so there's more work to be done to translate the findings to humans. But the early results hint at a new application for psilocybin — a drug that's already been explored for a range of other conditions, including depression, PTSD and anorexia.

Live Science spoke with study co-author Argel Aguilar-Valles, an associate professor of neuroscience at Carleton University in Ontario, about the new study and how the research might eventually translate to treatments for repetitive head injuries.

Nicoletta Lanese: In this new study you focus on mild head trauma. Why does that minor level of injury still raise concern?

Argel Aguilar-Valles: This work was spearheaded by our collaborator, Dr. Craig Ferris at Northeastern University in Boston. The idea was to focus on the cumulative effect of those milder head hits, or injuries, that happen quite commonly; a lot of children and older adults can have repeated instances of these events of head trauma, and it doesn't necessarily lead to any immediate treatment or hospitalizations because they are considered fairly mild.

But over time, there's evidence that this can lead to cumulative and long-term effects that can affect the health outcomes of these individuals, particularly as we age. It's a risk factor for several forms of dementia. So the idea was to try to model this with a milder version of head injury [in lab rats].

So it's repeated — it's three hits — they're controlled, they're fairly mild. And they produce some alterations in the brain networks that are evident in using either MRI [which looks at the brain's structure] or functional MRI [which analyzes brain activity] analysis.

NL: So these are head impacts that don't come with the symptoms associated with concussions?

AAV: It's always difficult to compare [what a rat is experiencing] to what a human might experience, especially here. One good way to put it is that there's no loss of consciousness ‪—‬ so in those instances where the hits happen but you don't black out.

NL: Is there anything available now to manage and treat these mild impacts?

AAV: Well, as far as I'm aware, there's not really an intervention. I've experienced this secondhand with my children. Sometimes, they will come back from school and then they [the teachers] say, "OK, they had a hit on the head; there's a bump, but they didn't lose consciousness or anything."

Then sometimes, you go to the doctor concerned and typically you're told, "OK, just keep them under observation." If there's no vomiting, nausea, if there was no loss of consciousness, typically they just send you home and say keep an eye. Put some ice on it. Maybe don't overexert yourself in the next few days — and that's about it.

There is no intervention — for instance, if we do this [treatment], it's going to prevent you from developing dementia 50 years down the line. There's obviously nothing like that, particularly when you have repeated instances and the effects are cumulative.

NL: What made psilocybin seem like a potentially promising treatment for head trauma?

AAV: My group specifically has had an interest in testing the ability of molecules collectively known as psychoplastogens. We didn't coin the term, but it basically refers to all of these drugs that produce these brain-plasticity effects [changes in the brain's structure and activity]. These include serotonergic psychedelics [such as psilocybin and LSD, which affect serotonin receptors], and also things like ketamine or even MDMA.

We observe changes in cultured neurons in response to these drugs, in terms of dendritic complexity and increased synaptic spine density [changes in neurons' incoming and outgoing wires]. And in vivo [in live animals], you also observe functional reorganization of networks. All of these drugs have the ability to trigger these mechanisms. They do it through different pharmacological targets, but they all converge on some of these plasticity effects.

There are deficits in this plasticity in psychiatric illnesses, but also, obviously, in neurological disorders and even neurodegenerative disorders, where these plasticity mechanisms are completely nonfunctional.

So, we wanted to test the limit of the ability of these molecules to rescue, or to provide some therapeutic relief, in conditions where you have physical damage or neurodegenerative pathological mechanisms underlying the disorders. We observed — and not only us, but several other labs have also observed — that some of these molecules do seem to provide some level of therapeutic relief. [Editor's note: The current study looked only at physical trauma, but other labs have started to explore psilocybin for neurodegenerative disorders.]

It's still unclear if they're disease-modifying, in the sense they could provide lasting changes that can modify the course of the disorder. But so far, the evidence indicates that they can at least help to ameliorate some of the negative consequences of either neurodegeneration models or physical trauma, like in this case.

NL: Psychedelics have been more thoroughly studied for conditions like depression. In both depression and head trauma, could similar mechanisms explain the drug's potential benefits?

AAV: Some of the cellular effects might be similar. But the underlying condition can look quite different. Even if you think of two cases of depression, they can look very, very different. The drugs are going to be engaging similar mechanisms, but also the context in which these mechanisms are occurring will probably affect the outcome. What is remarkable about these drugs is that they seem to be working in both cases, so they're certainly tackling something that might be common in both situations.

We don't know the limits of these drugs yet. I'm not trying to imply that they don't have limits; what I'm trying to say is that our knowledge is incomplete. We don't know when they will work better than other potential treatment options.

I feel that will come when their clinical use is more widespread and we have a better idea of how they work in the heterogeneous populations that clinicians have in real life. In our animal models, conditions are very, very controlled and homogeneous, so they respond in a certain, similar way, whereas in the clinic, you observe huge disparity [in responses].

NL: Is there reason to think that psilocybin would be more promising than other psychoplastogens?

AAV: I think a lot of the focus on psilocybin has been because it's one of the psychedelics that's been more widely tested both in clinic and preclinical settings.

I'm not a clinician, but one of the reasons why psilocybin is favored over others is the length of the psychedelic trip. It's a few hours. If you go with something like LSD, it will last much longer. While the person is under the influence of the drug and undergoing the trip, there needs to be clinical supervision, so it becomes really challenging logistically to arrange sessions with psychedelics that last a long time.

That's also motivated preclinical research, like ours, to focus on this drug, as opposed to others that may have similar effects. From a potential translational perspective, it might be a safer bet to study this drug.

NL: In clinical trials of psychedelics, scientists often use a very small dose to try to avoid triggering strong hallucinogenic effects. Was that a goal with the rats?

AAV: No, they're probably experiencing something — this is a relatively high dose. A lot of people use 1 milligram of psilocybin per kilogram of body weight. In this case, they were using 3 milligram per kilogram, and it was based on previous imaging studies where they looked at the effects of this drug.

One measure we use is the "head twitch response," which is a behavioral measure that we commonly use in rodent work to test the hallucinogenic potential of a drug. This is a very rapid head movement that occurs in response to the serotonergic psychedelics. It's a behavioral response that correlates with hallucinogenic potential, and not perfectly.

For psilocybin, it's been very well characterized in the sense that it's mediated by the serotonin 5-HT2A receptor [in rodents], which is the same receptor that mediates hallucinations and the psychedelic trip in humans.

NL: What notable changes did you see in the rats in this study?

AAV: The measurements were done nearly three weeks after the injury. It's relatively short if you think of a human, but for a mouse, things happen much faster metabolically and physiologically. There was at least evidence of increased phosphorylation of tau [changes in a specific brain protein tied to Alzheimer's], and that was reversed by the treatment with psilocybin. That was certainly one surprising finding, and it's worth following up, I believe.

But also the hyperconnectivity — the brain's functional connectivity was really dramatically affected in the treated rodents with the head hits. They not only recovered but went to higher levels than the control-group animals.

We don't really know what the meaning of that is, but certainly it's quite remarkable how the networks became hyperconnected. And hopefully that means something positive for the animals. But it was certainly surprising, the level of recovery of that particular measure.

NL: And these effects were seen throughout the brain?

AAV: There were effects in a lot of brain regions — the thalamus, the hippocampus, the basal ganglia, and all different parts of the cortex, etc. One of the things that stands out from this study was the connectivity of dopaminergic nuclei [hubs of dopamine production in the middle of the brain]. Their connectivity is really fundamentally changed by the hits and then by the treatment with psilocybin.

These modulatory regions, the dopaminergic regions, are concentrated in one part of the brain, but they affect overall brain function because they have these widespread connections. So they're really crucial for a lot of functions, and we're seeing effects in these regions — that's really intriguing.

NL: Is it known whether the strength of the psychedelic trip has anything to do with the degree of benefit?

AAV: It is currently a hotly debated topic in the psychedelic field, whether the intensity of the psychedelic experience has anything to do with the beneficial effects or not. You can envision situations like psychological trauma, as opposed to physical trauma, where that trip might be part of the therapeutic mechanisms. It becomes evident in the debriefing sessions after psychedelic treatment, where it seems like in some cases, the psychedelic experience is fundamental.

But these are fairly correlative measures — if the two happen at the same time, it doesn't mean that they are linked together causally. So that's something that is being tested actively. One of the ways is the development of these non-hallucinogenic analogues that seemingly trigger similar plasticity mechanisms as their psychedelic counterparts do [without causing a trip].

I don't think we've had the first clinical trial with these drugs yet. Some of them may have undergone Phase I clinical trials just for safety, but I believe none of them have been tested in Phase II trials yet [in which their effectiveness is explored for specific conditions].

NL: Given this work is in rats, what are the next steps to translate this into a treatment for people?

AAV: Extending the observations, like other groups have done — looking at what happens if you do give this treatment months after the events. It's still unclear to me if, with this model we have, you will have effects months later.

We have some correlative measures that potentially BDNF expression [a gene for brain-derived neurotrophic factor, which helps neurons grow connections] is increased, and also the levels of its receptor, called TrkB. That is a possibility that needs to be further investigated, trying to find out whether these neurotrophic factors are crucial for the effects that we're seeing.

And obviously, the psychedelic trip is still a potential issue. But testing whether these non-hallucinogenic derivatives have the same lasting effects as their hallucinogenic counterparts do — that will be crucial and that can, in some cases, potentially facilitate the translation [into treatments]. Because not every person reacts the same way to these hallucinogenic compounds, and not everybody has the same risks.

NL: I assume the non-psychedelic options might be better for children, for instance?

AAV: We don't know what the consequences [of psychedelic use] are in a developing brain. There's not enough data. That will be obviously a big thing to sort out before recommending the use of these drugs, and maybe some of those non-hallucinogenic derivatives may hold the answer for that — for those cases where you really don't want to induce a full-on psychedelic experience.

There's also schizophrenia and a bunch of other psychiatric diagnoses with psychosis associated with them — from bipolar or psychosis-like events or episodes — where you might not want to apply a serotonergic psychedelic.

NL: Looking ahead to the next five to 10 years, what do you hope to see in the field?

AAV: There's a lot of enthusiasm in the field and a lot of push to try to characterize and understand better these drugs, from a basic perspective or a cellular level up to a brain wave level and then also the psychological effects. So there are a lot of different disciplines implicated in studying these drugs, and I think that's really exciting. That will hopefully lead to a wealth of knowledge about these drugs — not only their effects but also their limitations and their potential risks.

Hopefully we will have a balanced approach as scientists, to be able to really tease apart in which cases it [psychedelic treatment] will be really useful and in which cases the risks outweigh the benefits. That will be crucial to understand.

There's a lot of potential there, but we should proceed with caution.

This interview has been condensed and edited lightly for clarity. This article is for informational purposes only and is not meant to offer medical advice.

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A new AI tool that analyzes speech could give users a glimpse of how they are aging and whether they're at risk of dementia, a new study suggests.

The tool analyzes hundreds of speech and language patterns to estimate the user's chronological age from the way they talk. In a study involving nearly 3,000 Spanish-speaking adults, those whose estimated age was higher than their actual age were more likely to have cognitive problems, dementia and signs of accelerated biological aging, researchers reported Wednesday (Sept. 30) in the journal Science Advances. They were also more likely to have less favorable social and economic circumstances than other study participants.

This voice-analyzing tool is similar to other "aging clocks," which use various biological markers to predict people's risk of age-related diseases.

"Existing aging clocks are very powerful, but many of them rely on brain scans or blood tests that are expensive, invasive or difficult to repeat regularly," said study co-author Adolfo García, director of the Cognitive Neuroscience Center at the University of San Andrés in Argentina. "All of these limitations can be overcome with speech," he argued.

However, the approach still needs to be tested over time and in other languages before it can be used to assess individual patients' risk of dementia, an expert told Live Science.

How the speech clock works

Researchers used data from the ReD-Lat consortium, a large dementia research project in Latin America. The analysis included over 2,900 Spanish-speaking adults from Argentina, Chile, Colombia, Mexico and Peru; their ages ranged from 18 to 88. Of them, about 1,500 were cognitively healthy; the others had mild cognitive impairment (usually marked by mild memory problems and trouble thinking), Alzheimer's disease or frontotemporal dementia.

Each person completed seven tasks, such as describing an animated video; naming as many words, vegetables or animals as possible in 60 seconds; and retelling a short story immediately after hearing it and then again 20 to 30 minutes later. The scientists took recordings, transcribed them, and then identified more than 700 distinct features of the recordings, including pauses, speaking speed, pitch, vocabulary and emotional expression.

They trained a machine-learning model using those features and the participants' chronological ages, teaching it to estimate age from the way a person spoke. The model generated a predicted age for each participant, and researchers compared it with each participant's actual age to calculate what they called a "speech-age gap."

Some people's speech appeared older than expected for their age, the AI tool determined. Cognitively healthy people had the smallest gaps between their true age and the age the AI assigned them, while people with mild cognitive impairment or dementia had larger gaps. The largest gaps were seen in people with language-dominant frontotemporal dementia, which primarily affects communication.

People with older-sounding speech also performed worse on various tests of memory, language and attention, and they had more difficulty with everyday function. Blood tests showed a similar pattern: Larger gaps were associated with greater age acceleration on three epigenetic clocks, which estimate a person's biological age by looking at chemical tags on top of their DNA. These epigenetic markers affect which genes can be switched on and to what degree.

Among people with Alzheimer's disease, larger gaps were also linked to higher levels of p-tau217, a protein associated with the disease.

Larger gaps were also correlated with various risk factors for dementia, such as having financial difficulties, food insecurity, limited healthcare, difficult childhoods or less education. The pattern was similar across all five countries, despite their social and cultural differences, García noted.

What the speech clock cannot tell us yet

The approach is "a huge leap toward making brain health assessments accessible to everyone," said Dr. Manisha Parulekar, co-director of the Center for Memory Loss and Brain Health at Hackensack University Medical Center in New Jersey, who was not involved in the study.

But the speech clock is not a crystal ball. "The human voice is incredibly sensitive to our overall well-being, which means a person's speech could sound 'older' simply because they are severely depressed, exhausted, or navigating serious life stress," Parulekar told Live Science in an email. "As a clinician, I wouldn't use this tool to definitively diagnose someone with dementia in isolation."

Instead, the speech measure could serve as an additional tool that prompts doctors to take a closer look at a patient's cognitive health, she suggested.

In the study, many participants were assessed at a single point in time rather than monitored over a longer period. The researchers therefore could not determine whether an older-sounding voice can predict whether a patient will soon experience cognitive decline, or whether certain voice changes occur as dementia progresses. Plus, the model was trained and tested only in Spanish-speaking participants from five Latin American countries.

"We cannot just take the Spanish model and plug English into it," Parulekar said. The language-specific features would need to be adapted and tested in other populations, she explained.

The researchers now plan to test the approach with other languages and follow people over time to see whether changes in speech can signal future cognitive decline.

"I truly believe that there is a very, very strong signal in speech to anticipate dementia and conversion in the future," García said, "but we need many more diverse studies."

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

It's well-known that regular exercise comes with health benefits, but exactly how those benefits manifest at the cellular level isn't clear. Now, researchers have identified a series of changes in metabolism and the immune system that differentiate regular exercisers from people with sedentary lifestyles.

The findings, published Sept. 18 in the journal Science Advances, point to potential pathways for managing chronic diseases, such as diabetes, heart disease and cancer, the scientists say.

The team of researchers analyzed data from the Chinese Immune Multi-omics Atlas (CIMA), which includes data from 400 adults who gave blood samples and answered an in-depth questionnaire about their lifestyles.

To capture the biggest possible effects of exercise, the team included only data from participants who did the most or least exercise. One group worked out at least three times a week, racking up more than 150 minutes of moderate exercise or 75 minutes of high-intensity exercise in that timeframe. The sedentary group said they did not work out at all.

The researchers then analyzed their volunteers' blood samples for physiological markers, such as blood sugar and fat levels. They found that the participants who exercised more had signs of boosted sugar and fat metabolism, stronger muscle metabolism, and higher levels of antioxidant molecules, which combat cell-damaging processes.

Many of these systems and their links to exercise were already known, said Dr. Michael Siebers, a researcher at the University of Duisburg-Essen who wasn't involved with the study. The study's real step forward was its subsequent cellular analysis, he said.

"It's a really good paper, which is showing, for the first time, what is really happening when you're doing sports on the intercellular level," he said.

How exercise changes the immune system

This analysis used a multiomics approach, meaning it combined data from multiple biological sources. These included metabolites (the byproducts of metabolism), fats, proteins and RNA (a cousin of DNA that helps build proteins).

The team also studied a feature of DNA called chromatin accessibility. Our genes are wound onto DNA helices, creating structures that resemble tightly packaged spools of film. Higher chromatin accessibility means that the spool is less tightly wound, so the individual images on that film can be seen more easily. Ultimately, those genes are more easily switched on. In cells, this mechanism is essential for enabling genes to be transcribed and translated into the proteins that help the body function properly.

Together, these analyses enabled the research team to closely examine how cells in people who exercise regularly functioned differently from people with sedentary lifestyles. This deep dive showed multiple changes in immune cells.

The activity of exercisers' immune foot soldiers — including cytotoxic T cells and natural killer cells — was boosted compared with those of participants with sedentary lifestyles. Additionally, naive immune cells, which act as nonspecialized reservists that can be recruited to the immune infantry, had greater chromatin accessibility in genes needed to fight off threats. That meant they were more ready to enlist.

The team also noted changes in cells that are in charge of alerting the rest of the immune system to threats, called immune monocytes and B cells. In people who regularly exercised, these cells had increased expression of alarm-sounding genes.

The findings suggest that regular physical activity may make the immune system better prepared to fight potential threats, the researchers wrote in their study. It's already known that not exercising is a risk factor for chronic health conditions, including type 2 diabetes, and that working out reduces these risks. The study gives "a molecular perspective on [exercise's] systemic health benefits," the researchers wrote.

That said, there were limitations to the study. Siebers pointed out that, beyond the number of minutes participants worked out, the study didn't record what type of exercise they did and had little information about the participants' physical makeup.

The researchers also couldn't show that the regular exercise caused the immune improvements. It's possible that the reduced activation in sedentary participants' immune systems made them less able to exercise.

Despite the limitations, these types of deep dives into the cellular basis of exercise are important for furthering our understanding of why working out feels good, Siebers said. "This is really deep stuff."

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

The patient: A 50-year-old woman in New York

The symptoms: The woman went to the hospital because she could not bend her legs, walk or sit up. She also had chronic lower-back pain, recurring episodes of fever and chills, and unexplained weight loss of more than 30 pounds (14 kilograms).

What happened next: The patient told doctors that, one month earlier, she had visited another hospital due to persistent back pain, stiffness in her knees, fever and significant weight loss. However, she noted that she'd actually begun feeling discomfort in her knees and back about five years before that.

Over time, increased rigidity in her right leg began affecting her balance and caused frequent falls. Doctors prescribed her ibuprofen and physical therapy, but the stiffness and pain continued.

During the patient's first hospital visit, blood tests had revealed that her white blood cell count was normal, suggesting that she was not fighting an infection. She was not producing antibodies that might have suggested she had rheumatoid arthritis, an autoimmune disease that causes joint stiffness. Nor did she have antibodies associated with other several conditions that can cause pain, numbness or stiffness in the extremities, such as HIV, Lyme disease or the autoimmune condition Sjögren's disease.

Nevertheless, over the next month, her symptoms steadily worsened until she couldn't get out of bed; she was also unable to sit up or turn to either side.

At her second hospital visit, the patient's arm had normal movement during an exam, but her leg stiffness prevented doctors from testing the range of motion in her lower extremities. When the doctors tried to flex the woman's knee, it caused contraction in her quadriceps — the large muscle in the front of the thigh — and "was painful for the patient," the doctors wrote in a report of the case.

The diagnosis: Based on her earlier test results and her past and current symptoms, the doctors suspected that the woman had developed an extremely rare autoimmune neurological disorder: stiff person syndrome (SPS).

Autoimmune disorders are characterized by the immune system attacking healthy tissues in the body. In the case of SPS, this rogue immune response targets nerve cells that control muscle contraction. Destruction of these cells disrupts signals to the muscles, causing painful muscle spasms and contractions that affect a person's balance and restrict their movement.

A clue from the woman's blood tests hinted at this condition. Doctors found high levels of antibodies that block the enzyme glutamic acid decarboxylase (GAD). Elevated levels of these antibodies are seen in up to 80% of people with SPS. The anti-GAD antibodies prevent the enzyme from producing a chemical messenger called GABA, which acts like a brake on nerve cell activity. Without enough GABA, the nerve cells that control how muscles move can go into overdrive, which can cause spasms and prevent muscles from relaxing as they normally would.

The treatment: There is no cure for SPS, but medication can help slow the disease's progression and manage symptoms. This patient received intravenous immune globulin, an antibody treatment that regulates the immune system and is often used to treat autoimmune disorders. She also received rituximab, another type of antibody that targets specific immune cells to pare down their activity.

In addition, her doctors prescribed the steroid prednisone, the anticonvulsant gabapentin and the sedative diazepam, along with a regimen of physical therapy to help relax the woman's spasming muscles.

Within a few days, the woman's condition had significantly improved. "Prior to discharge, the patient could turn in her bed unassisted, could flex her left hip and knee fully, could flex [her] right hip fully and right knee with assistance to 110 degrees, and could stand with assistance," the report authors noted.

At a three-month checkup after being discharged, the patient could stand unassisted and walk using a rolling walker. The doctors started reducing her steroid dose, but she continued taking diazepam and gabapentin as prescribed, along with a monthly dose of immune globulin and a maintenance dose of rituximab every six months.

What makes the case unique: Just 1 to 2 in 1 million people are thought to be affected by SPS each year, although by some recent estimates, that number is higher. Its rarity and the slow development of symptoms make the condition challenging for health professionals to recognize and treat. What's more, the mechanisms and progression of the disease are "incompletely understood," the case report authors noted.

Often, SPS is misidentified as other conditions, including psychiatric disorders, Parkinson's disease, multiple sclerosis, or a neurological disorder called dystonia, which causes muscle spasms.

On average, the diagnosis of SPS takes about seven years from the start of symptoms, according to the Stiff Person Syndrome Research Foundation. It is most commonly diagnosed in people ages 40 to 50, but SPS can also appear in older adults and in children. It affects about twice as many women as it does men, according to the National Institute of Neurological Disorders and Stroke.

One well-known person with SPS is singer Celine Dion. She publicly shared her diagnosis in 2022, after her illness led her to cancel multiple shows in 2021. Dion told People magazine that she was experiencing "severe and persistent muscle spasms" and that the pain caused by her condition eventually became so intense that she was sometimes unable to walk.

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!

Millions of Americans are diagnosed with common conditions like cancer and diabetes — but some 10% of the population live with rare diseases that doctors often struggle to diagnose. On average, those with rare diseases will spend five to seven years searching for answers and see 12 specialists before they arrive at a diagnosis.

In the process, they may be subject to incorrect, ineffective or even harmful treatments.

"Any medicine that you prescribe has a one-third chance of working, a one-third chance of doing nothing, and a one-third chance of hurting you," said Dr. Ada Hamosh, a geneticist and the center director for the Johns Hopkins Medicine-Kennedy Krieger Institute National Organization for Rare Disorders (NORD) Rare Disease Centers of Excellence Network. "I do not want to understate this: The right diagnosis is unbelievably powerful, even if you can't do something."

Emerging data suggests that genetic testing could speed the diagnosis of rare conditions, which each affect fewer than 200,000 people in the United States. If employed widely, such testing could help diagnose the majority of rare diseases, most of which are genetic in cause, experts told Live Science.

"Now, with the wide availability of vast, somewhat inexpensive, genetic testing and whole genome sequencing available, we're really at the point of understanding a lot more about these rare and ultra-rare diseases," said Danielle Carnival, CEO of the Undiagnosed Diseases Network Foundation (UDNF), a nonprofit supporting patients with rare and undiagnosed diseases.

"And then hopefully, that turns into the ability to treat them," she told Live Science.

Uncommon disorders, many patients

Researchers have documented more than 10,000 rare diseases and less than 5% of them have a treatment approved by the U.S. Food and Drug Administration. On average, 250 new rare diseases are discovered each year, Hamosh said.

Although each individual disease affects relatively few people in the population, collectively, they are not rare. In the U.S. alone, it is estimated that there are more than 30 million people living with a rare or undiagnosed disease.

"So many people know someone living undiagnosed or with a rare or ultra-rare disease, even if they don't know it," Carnival said.

About 80% of rare diseases are genetic in origin, while the other 20% are caused by environmental factors, such as a toxin exposure or viral infection, said Emily Glanton, a genetic counselor and associate director at the Undiagnosed Diseases Network Data Management Coordinating Center, a central hub for the National Institutes of Health's Undiagnosed Diseases Network.

There's a lot of overlap between rare and undiagnosed diseases, but they're not always the same. Some undiagnosed diseases can be unusual manifestations of common conditions, such as long COVID, or alternatively, they may be common conditions that doctors frequently struggle to diagnose, like endometriosis. Still, it's thought that up to 50% of people with rare diseases are undiagnosed.

"We certainly don't have a way to know [exactly] how many people have a disease that we haven't even discovered the name or cause of," Dr. Jacqueline Harris, a pediatric neurologist and director of Kennedy Krieger's Epigenetics Clinic in Baltimore, told Live Science.

Patients sometimes miss out on a diagnosis because clinicians are unable to piece together their symptoms and clearly link them to one condition. Such patients may receive multiple distinct diagnoses over time.

"A lot of times what happens with undiagnosed patients is that they end up with a little bit of a diagnosis. And I always say, it's like the umbrella is missing. We've got lots of little rain hats or visors on, and those are the diagnoses," said Kelly Kemper, whose son has an undiagnosed disease and who is a member of the UDNF patient advisory council. "But we don't have something overall that says: 'Okay, this is what it is.'"

Isolating experience

Searching for a diagnosis can be an isolating, frustrating experience.

Kemper, for instance, has spent the last five years looking for an explanation for her son's rare form of dystonia, which causes muscle spasms. He still doesn't have a diagnosis.

"We joke about this in the undiagnosed disease world: We are the only people who are consistently praying for positive test results," Kemper told Live Science.

Negative test results can be a relief, but it can be frustrating when doctors and specialists can't explain what's going on. Hearing the phrase "your labs look normal" often invalidates the symptoms a patient is experiencing, she added.

And though this process of elimination rules out conditions her son does not have, it doesn't always feel like they're getting closer to something that can be named, she said. There have been specialists who have also refused to see her son because they don't know what else to try.

"There was, like, a little bit of hope that you're gonna see the specialist and then they decline the appointment," Kemper said. "That's a hard one."

Between a multitude of doctor appointments and insurance claim denials because no diagnosis has been made, the journey has been isolating, Kemper said.

The promise of genetic testing

The American College of Medical Genetics and Genomics (ACMGG) recommends genetic testing for patients with congenital anomalies — meaning birth defects — before age 1, as well as those who have any developmental delay or intellectual disability that was recognized in childhood. ACMGG recommends both exome sequencing, in which all the genes that code for proteins are examined, amounting to approximately 2% of our DNA, or whole genome sequencing, in which every letter of DNA is sequenced, as first-line genetic testing, Glanton told Live Science.

As of yet, there are no clinical guidelines surrounding exome and genome sequencing testing for people with undiagnosed and rare diseases.

To help solve some of these medical mysteries, research groups such as the Undiagnosed Diseases Network have partnered with 24 clinical centers across the country to test new diagnostic technologies.

In late 2025, the network evaluated over 3,000 patients with undiagnosed diseases and ultimately diagnosed 30% of them. Getting to answers involved several strategies: whole genome sequencing; model organisms screening, in which scientists use DNA from flies, worms and zebrafish to find gene variants that might be tied to disease; and RNA sequencing, which reveals which genes are active in different cells.

Additionally, the network also frequently utilized trio genetic testing, in which both patients and their biological parents are tested to see which gene variants they carry.

The findings suggest that at least some of these undiagnosed diseases can be diagnosed with a comprehensive suite of genetic testing.

Limits of testing

But genetic testing isn't a silver bullet. After all, the network found diagnoses for less than one-third of the patients whose cases they evaluated.

A 2025 study that looked at 400 undiagnosed patients with a range of symptoms found that exome and whole genome sequencing were likelier to help for neurological symptoms, whereas patients with a complex presentation of symptoms are likelier to go undiagnosed despite these tests. Other research suggests that exome or genome sequencing that includes family members has a better success rate than testing only the affected individual.

And crucially, diagnosis is just the first step.

"We don't want to stop at a diagnosis. We really want to build a bridge for folks to be on a pathway to get a treatment that works for them," Carnival told Live Science. That wouldn't just benefit the patients themselves, it may also provide benefits for the wider community, she added.

"So often, the answers to diseases that impact more people start with understanding these very specific mutations or environmental impacts or immune responses in very few [people]," Carnival said. "The knowledge that's generated really tells us a lot about the systems of the body and what goes wrong in even broader diseases."

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.

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In modern times we tend to think of lithium as powering smartphones and cars, yet its historical fame comes from its role as a mood stabilizer.

Lithium was first used as a treatment for bipolar disorder in 1949. Yet despite decades of research and drug development, this simple medication remains the gold standard for treating one of the most complex psychiatric conditions. But why?

According to Becci Strawbridge, a senior lecturer in psychological medicine at King's College London, lithium's simplicity could be what helps it cut through the complexity of bipolar disorder, a lifelong disorder that affects about 36 million people worldwide.

Clinically, bipolar disorder is defined as a mood disorder characterized by specific, lasting changes to a person's mood and energy levels. Depending on the type of bipolar disorder, individuals can experience manic, hypomanic and depressive episodes — either individually, or in sequence.

However, "experiencing mania itself is sufficient to have a diagnosis of bipolar [disorder]," said Dr. David Cousins, a clinical senior lecturer and honorary consultant psychiatrist at Newcastle University in the U.K. "It's probably easiest to think of that as the opposite of depression — people become elevated in mood, extremely energized, driven, motivated, and engage in hedonistic behavior with lots of risk taking," he said. "It's a highly detrimental, highly damaging, highly disruptive state."

Treating an illness that operates at such extremes is a difficult balance to strike, with any intervention to treat one emotional state needing to factor in how it could impact the other. "For example, if you gave somebody antidepressants without an antimanic drug, you might either trigger mania or destabilize the illness," Cousins explained.

A combination of antidepressants, antipsychotics, and mood-stabilizing anticonvulsants are often prescribed in combination to juggle these highly variable symptoms. "There are really very few medications that have an overall effect against both poles," Strawbridge said. Once stabilized, the challenge then becomes preventing relapse back into this destructive cycle.

Lithium, by contrast, does not suffer from these limitations, Strawbridge added.

"It's often considered the gold standard for bipolar disorder; it's helpful for the depression and for the mania, but its main benefit overall is in preventing relapse, so stopping either of those two types of episodes from coming back."

Psychiatrists usually prescribe lithium as either lithium carbonate tablets or a lithium citrate liquid, both of which dissociate inside the body into lithium ions and their corresponding counterion (either carbonate or citrate). This simple active form is part of what gives lithium its powerful, broad-ranging mood-stabilizing effect, Strawbridge said.

"Because lithium is quite a simple ion, it's able to disguise itself as sodium, and that means it can slip inside of brain cells, whereas most medications act on the surface of cells," she explained.

Lithium's simple form enables it to spread throughout the brain and rest of the body. Once inside, it interacts with many cellular processes, but doctors still don't really understand the underlying mechanism behind its beneficial effects.

"We know that the monoamine system and the neurotransmitters in the brain that are involved in reward emotions and cognition are disrupted," Victoria Wing, a National Institute for Health and Care Research clinical lecturer at Newcastle University and CNTW NHS Foundation Trust, told Live Science. Included in this disruption is the regulation of crucial mood molecules, such as dopamine and serotonin, which may be underactive or overactive depending on the nature of the bipolar episode.

The same small lithium ion also blocks an enzyme called glycogen synthase kinase 3. This enzyme has wide-ranging downstream effects, such as controlling gene activity, regulating the body's circadian rhythms and managing inflammation and cell survival.

"Lithium can also help with autophagy, which is the clearance of debris and toxins in cells, and it has antioxidant effects and boosts mitochondrial function, which are important for cell energy processes," Wing said.

However, despite its manifold therapeutic benefits, lithium does have some drawbacks. While around one-third of people experience profound benefits from the drug, another close third only experience intermediate effects, and the final rough third don't respond at all.

This means it's vital to identify which patients respond well to the drug as early as possible, especially because the cyclic nature of the condition means it can take years to ascertain whether lithium is effective in preventing relapses in the long-term, said Cousins. The drug also has a narrow therapeutic window, which means it has a small margin of safety between doses that are high enough to be effective and those that are toxic to the kidneys and thyroid. Some patients who undergo lithium treatment also report having to urinate more frequently or experiencing slight tremors.

As with any medication, some side effects are unavoidable. The alternatives to lithium also carry their own risks. But if carefully and correctly managed, lithium medications can have a transformative impact for patients.

"I've met a lot of patients through patient involvement groups that have told me how effective and lifesaving lithium has been for them," Wing said. "We know it works, but can we fine-tune the use even better so more people can benefit from it?"

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 patient: A 16-year-old boy in India

The symptoms: The teen developed swelling on his left upper eyelid that persisted for a few months but was painless. However, he later noticed two sharp, white projections poking out from the skin above his eye.

About a month after these projections appeared, he went to a hospital.

What happened next: Doctors examined the teen's eyelid, noting that the spikes had a "fairly smooth surface and were hard on palpation," said Dr. Meghana Tanwar, a medical consultant at the Aravind Eye Hospital in India who co-authored a report of the case. The texture and color of the projections suggested they might be teeth, she told Live Science in an email.

Initially, the doctors thought the points also might have been related to a teratoma, a rare type of tumor that can include different types of tissue, including bone and tooth tissue. They also wondered if the projections might be a foreign body in the eyelid. They conducted a CT scan to take a closer look.

The diagnosis: The scan revealed that the projections were indeed part of a tooth.

"The structure of a lone tooth in the superior orbit was quite obvious," Tanwar said. "Superior orbit" refers to the upper eye socket, and the tooth had poked out in the small space between the boy's eyelid and eyebrow.

Teeth that develop and erupt in abnormal locations are known as ectopic teeth. This umbrella term includes teeth that are in the mouth but erupt outside their typical positions; for instance, in about 2% to 6% of people, their first permanent molars grow "out of place" in the expected line-up of teeth.

In this case, though, the patient had an ectopic tooth that appeared completely outside the dental arch, which is far rarer.

The treatment: The doctors surgically removed the ectopic tooth from the patient's eyelid and found that it was a mature canine tooth. It didn't have any features that suggested it was part of a teratoma.

"Since the imaging done did not show the presence of any other ectopic teeth, the likelihood of him having another one are unlikely," Tanwar noted.

What makes the case unique: This is not the first ectopic tooth in the medical literature, but it was in a very notable location.

"To the best of our knowledge this is the first and only ectopic tooth reported in the superior orbit," Tanwar said. Previously, they've been reported in the nasal cavity and the bottom of the orbit, under the eye, she noted. According to MedPage Today, they've also been found in the nostrils, chin and maxillary sinus, which is located inside the cheekbone.

"This was a first not just for us but the world over," Tanwar said of the case. "We were very surprised by it."

Prior to the case, Tanwar had personally seen a tooth in the bottom of the eye socket of a different patient, but it was part of a rare type of mass called an odontogenic choristoma.

In this teen's case, the underlying cause of the ectopic tooth was unknown. Hypotheses suggest that, in general, ectopic teeth may grow out of place due to developmental disorders, physical trauma, infection or genetic factors.

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.

Lab mice who spend time in space seem to bear offspring with reduced reproductive capacity, a new study suggests. But what that might mean for human astronauts and their families is still unclear.

The research, published June 30 in the journal PNAS, looked at female mice that had spent extended periods on the International Space Station (ISS). These mice had similar levels of fertility as Earth-bound mice. However, their children and grandchildren produced smaller-than-average litters, had fewer litters overall and had lower levels of key reproductive hormones, among other measurable differences.

"The offspring of those that came back from space were altered in their behavior, their muscle, their ability to reproduce further," study co-author Lane Christenson, a professor of cell biology and physiology at the University of Kansas Medical Center, told Live Science. And "just about every marker we looked at had some differences."

As the study was conducted in mice, it’s difficult to determine whether the effects might carry over to human astronauts. However, mice are good biological models for understanding the health impacts of space travel, given that they are mammals with a similar reproductive system to humans, experts told Live Science.

As scientists explore the feasibility of long-term space travel, this study highlights the need for further research on the impact of long-term spaceflight on the reproductive system, the study authors argue.

A "void" in research

Past research, such as the NASA Twins Study, has suggested that short-term spaceflight has modest effects on human health. That study compared astronaut Scott Kelly, who completed a year-long mission on the ISS, to his identical twin brother, Mark Kelly, who remained on Earth.

However, few studies have explored the long-term health impacts of spaceflight, including those that might affect reproduction.

A 2019 study looked at male mice that spent time aboard the ISS and found they could father healthy offspring. The new study, by contrast, was conducted to "fill a void" in research investigating how space travel might impact the female reproductive system, Christenson said.

Such investigations are especially important because hormones like estrogen affect more than just reproduction; they "influence almost all organ systems in the female body," he added. For example, estrogen supports processes like bone maintenance, too.

For the new study, 20 female mice lived on the ISS for 42 days. The female mouse reproductive cycle is very short, only about four to five days long, while the human menstrual cycle is 28 days on average, Christenson noted. "But a lot of the molecular background is very similar" in terms of how hormones fluctuate each cycle, he explained.

Upon their return to Earth, the mice could still get pregnant and give birth to live offspring. Their litters were slightly smaller than those of comparison groups of mice that did not spend time in space. But that difference was not statistically significant, meaning it could be coincidence.

Researchers saw clearer differences in the next generation of mice. The offspring of the spacefaring mice had about 15% less muscle strength than the control groups' offspring. Additionally, the female mice in that second generation were more prone to stress than the female offspring in the control groups, based on a behavioral experiment.

"We were pretty surprised that a relatively short period of time, 42 days, was able to induce these striking changes," Christenson said.

The second generation of mice could also get pregnant, but these mice had fewer litters and much smaller litters than the control mice did. Further testing also showed that the offspring of spacefaring mouse mothers had lower levels of anti-müllerian hormone (AMH), a hormone whose levels correlate to overall egg count. Higher AMH means higher egg reserves and vice versa. The subsequent third generation also had lower levels of AMH compared with mice in the control groups.

Christenson theorizes that this pattern may be the result of an "acceleration of aging" caused by the mice's predecessors being exposed to microgravity. Previous mouse and human-tissue studies have suggested that a lack of gravitational force may leave cells more vulnerable to stress. This has been tied to dysfunction in mitochondria, the powerhouses of cells that contain special DNA that's exclusively passed from mother to child.

This theoretical mechanism and its relationship to mice's reproductive capacity still needs to be confirmed, though.

For now, "this study adds to the growing body of literature on the effects of space travel in general on the reproductive system," said Dr. Ulrike Luderer, director of the Center for Occupational and Environmental Health at the University of California, Irvine, who was not involved in the research.

Luderer noted that, given that the research was conducted on the ISS, which has less exposure to cosmic radiation than deeper regions of space do, the impacts of traveling in deep space — say, on a journey to Mars — may be even more consequential. Earlier this year, Luderer published research that found that exposing mice to radiation levels similar to the ones an astronaut might experience on a trip to Mars lead to a "very significant decrease in the number of eggs and follicles in the ovaries."

She hopes that further research can focus on additional reproductive markers, such as hormonal levels, to pinpoint the long-term consequences of deep-space travel. Those will be especially relevant if "humans spend long periods of time in [space] or colonize some other planet."

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

How much do you know about the process of pregnancy? Find out with our pregnancy quiz!

Scientists built a swallowable paper battery that can power medical devices inside the body and then gradually break down after its job is done.

So far, the battery has been tested only in pigs, in which it powered devices for up to three days. If proven safe and effective in people, the battery could someday power temporary devices inside the gut while avoiding surgery to retrieve a conventional battery from the body when the device is no longer needed.

"I'm very excited about this work," said Reza Ghodssi, a professor of electrical and computer engineering at the University of Maryland who was not involved in the study. "The battery is one component that takes up most of the space in an ingestible device, so anything that can provide the required power while reducing the size of the capsule is very promising."

Examples of ingestible medical devices include those that detect bleeding, dispense medicines, or stimulate specific tissues or organs.

How does the battery work?

Conventional batteries used in ingestible devices are not only large; they also need to stay sealed to prevent their internal materials from leaking into surrounding tissue and causing damage. The new battery, described Monday (Sept. 21) in the journal Nature Chemical Engineering, is made from materials that gradually dissolve in the acidic gastrointestinal tract and can then be safely absorbed without leaving behind harmful fragments or toxic byproducts.

The battery is built in layers. A magnesium alloy forms the anode (the battery's negative terminal), while the cathode (positive terminal) contains molybdenum trioxide and activated carbon. Between the two sides is a biodegradable electrolyte that allows the battery to generate electric current. These materials have been used in earlier biodegradable battery prototypes for temporary medical and wearable electronics.

The new design adapts them into a thin, porous, paper-like battery using cellulose nanofibrils as a binder, whereas earlier versions used larger binders. "The paper structure improves the battery's strength and control over degradation while still allowing it to produce electricity," study co-author Giovanni Traverso, director of the Laboratory for Translational Engineering at MIT, told Live Science in an email.

To keep the battery from breaking down too quickly in stomach acid, the researchers coated it with beeswax. Some versions also got a layer of candelilla wax — derived from the desert shrub Euphorbia antisyphilitica — for longer protection.

"The wax coating is not simply packaging," Traverso said. "It is a key design element that controls the functional lifetime."

The team made two versions of the battery, including one that was small enough to fit inside a standard gelatin capsule. In lab tests, it produced about 1.77 volts and could store and deliver 2 milliampere-hours per square centimeter, which is enough capacity to power low-power electronics.

A larger version of the battery produced about 1.84 volts and had a maximum capacity of 3.5 milliampere-hours. That could power devices that need a bit more power. However, the battery's capacity is still low, Ghodssi noted. "They need to have an order of magnitude higher capacity for this technology to be even more promising," he said.

Testing the battery inside the body

The researchers placed the battery prototypes inside 3D-printed capsules and administered them to pigs orally using an endoscope — essentially a long tube. Both versions of the battery worked for up to three days, although their voltage and capacity dropped as they gradually degraded. The larger battery's voltage dropped from about 1.8 volts to 1.6 volts after one day and then down to about 1.45 volts by the third day, while the smaller battery fell from 1.7 volts to 1.35 volts over the same period.

The team used the batteries to power two types of medical devices inside the pigs. The smaller battery powered a wireless RFID (radio-frequency identification) tag. Similar RFID-based sensors have been tested in people before, but the one used in this study was experimental. Researchers positioned it in the esophagus, where the tag communicated with a receiver up to 5 feet (1.5 meters) away and allowed researchers to detect when the pigs swallowed a medication.

The larger battery powered a swallowable capsule that electrically stimulated the stomach; this increased levels of the hunger-stimulating hormone ghrelin in the blood without causing visible tissue damage at the stimulation site. Gastric electrical stimulation is already used in people with severe gastroparesis, a condition that slows the rate at which the stomach empties; the battery-powered capsule tested in this study is experimental.

"It's quite impressive that the battery can operate in a stable and reliable fashion as the overall device passes through the GI system in a large animal model," said John Rogers, a pioneer in bioelectronics and a materials scientist at Northwestern University who was not involved in the study.

The battery and its biodegradable components broke down, but the electronic circuit board used for the stomach-stimulation experiment did not; instead, the pigs passed it naturally. "Making every part of the device bioresorbable could eliminate the risk of a leftover component becoming lodged in the gastrointestinal tract," Rogers said.

The researchers' biggest remaining challenge is controlling the battery's working lifetime and making its breakdown more predictable, Traverso said.

The researchers also found some variability between the batteries, which they attributed to factors in their construction, including the amount of contact between layers, their electrolyte distribution, and differences in the thickness of the wax coating. The team is now working to standardize manufacturing and adjust the coating so the batteries can be designed to function for specific periods of time, ranging from hours to days.

The team also plans to conduct longer tests under conditions that more closely mimic the human gastrointestinal tract. They are working toward an initial clinical trial of the RFID system that could begin in about two years, Traverso said.

If your blond preteen seems to be turning into a brunette, you're not imagining things. For some children, hair that starts out platinum blond gradually becomes darker and may end up dark brown, or even black, as they grow.

So what causes this change?

The short answer is that hair color is controlled by a complex interplay of genes, pigment-producing cells and, later in childhood, hormones. Scientists understand many of the genes involved in hair color, but they are still trying to find out why some blond children's hair darkens while others' locks remain blond for life.

"It depends on their genetic inheritance," Desmond Tobin, a professor of dermatological science at University College Dublin, told Live Science in an email.

Hair gets its color from a pigment called melanin, which is produced by specialized cells called melanocytes in hair follicles. There are two main types of melanin: eumelanin, which produces brown and black shades, and pheomelanin, which contributes yellow and red tones to hair. The amount and type of melanin produced by a follicle largely determine the color of the hair that grows from it.

In general, more eumelanin means darker hair. For example, during pregnancy, high levels of estrogen and progesterone can encourage hair darkening as more eumelanin is produced.

The activity of hair follicles isn't necessarily fixed throughout childhood. As children grow, the biological signals controlling pigment production can change, too.

From blond to brown

For many blond children, the most noticeable darkening happens around puberty, typically between about 10 and 13 years old, Tobin said.

It is likely the hormonal changes during puberty, such as estrogens and androgens that stimulate an increased production of eumelanin, that gradually turn blond hair darker over time, he said. "Those that remain blond typically have a genetically determined reduction in eumelanin pigment formation," Tobin added.

Exactly how hormones might cause this change, however, is still something of a mystery.

One clue comes from a group of hormones called melanocortins. One of these, alpha-melanocyte-stimulating hormone (alpha-MSH), is involved in telling pigment-producing cells to make more melanin. In our skin, alpha-MSH is triggered by ultraviolet (UV) light. UV light can damage DNA in skin cells that, via a cellular signaling pathway, encourages the release of alpha-MSH to make the skin tan.

But in hair, things get, well, hairy. Scientists haven't shown that a rise in alpha-MSH, testosterone, estrogen or any particular hormone is what makes blond hair darken.

The melanocortin system shows that hormones can tell pigment-producing cells to make more eumelanin. What remains unclear is whether changes in this system are actually responsible for blond hair darkening during puberty.

"We haven't yet identified the genes that control this process," Wojciech Branicki, a researcher who studies the genetics of human pigmentation at Jagiellonian University in Poland, told Live Science in an email.

One possibility Branicki suggested is that hormones may affect children's hair follicles differently depending on their genetic background. For now, researchers don't know which genes are involved or how they interact with hormonal changes during puberty, as more research is needed.

Branicki posits that in some children, the hormones could induce the production of melanin or the transport of pigment within the hair follicle. In other words, two children could start out with similarly blond hair but respond differently to the hormonal changes as their bodies develop. One might continue producing relatively little eumelanin and stay blond, while the other's follicles might gradually ramp up pigment production, causing new batches of hair to grow darker.

"Research on human genome variation is quite advanced, but not all aspects have been explained yet," Branicki said.

Scientists have identified an inherited genetic mutation that greatly increases the risk of lung cancer, even in people who have never smoked.

The mutation involves the EGFR gene, which helps control cells' growth, division and survival. People who had never smoked and who had the genetic mutation — called EGFR T790M — were 62 times more likely to develop lung cancer than nonsmokers without the mutation, according to the new study, published Thursday (Sept. 17) in the journal Science.

By comparison, people who smoked but didn't carry the mutation were four times likelier to develop lung cancer than nonsmokers, so the mutation alone carried a higher risk of the disease.

Among people in the study who smoked and carried the mutation, T790M increased their cancer risk 11-fold compared with other smokers.

This is a "very important finding," said Chris Amos, a genetic epidemiologist at the Baylor College of Medicine who wasn't involved in the study. "The prevalence of the T790M variant and its impact on lung cancer risk has previously been poorly understood."

The study included over 3 million people of European ancestry, and the mutation showed up in 1 out of every 15,850 people. Given that it's relatively rare, it likely doesn't account for a large percentage of overall lung cancer cases, Dr. Stephen Chanock, director of the Division of Cancer Epidemiology and Genetics at the National Cancer Institute, who wasn't involved in the study.

However, Amos argued that it is important to test whether a patient has this mutation when they have a family history of lung cancer in nonsmokers, or when their relatives are known to have the mutation. Having the T790M mutation not only influences a person's risk of lung cancer, but also affects treatment decisions for those who already have cancer, he said.

Combining genetic, geographic and historical data

For the study, researchers analyzed DNA and health data from over 3.3 million people who used 23andMe's at-home genetic testing kits and who gave consent for their personal data to be used in research.

Two of the largest public genetic databases to date — called All of Us and the UK Biobank — contained just 19 and two individuals with the T790M mutation, respectively. But the 23andMe cohort included 641 individuals with the mutation, giving the researchers enough data to run reliable statistical analyses.

On average, people who had the mutation had about 25 times the odds of developing lung cancer compared with people who didn't have the mutation. That statistic includes both smokers and nonsmokers. T790M was not linked to any other type of cancer or noncancerous lung condition.

When the researchers looked at where the study participants were born, they found that the T790M mutation was much more common among those born in the Southeast, especially in Alabama, Mississippi and Tennessee. In those three states, the mutation showed up in 1 out of every 2,078 people who'd contributed data to 23andMe.

By referring to historical records, the researchers pieced together when and how the mutation likely spread. They think settlers from the British Isles first brought it to the U.S. in the early 1700s. Later, families with the mutation moved to southern Appalachia, where they were relatively isolated —‬ so the variant got passed down again and again within that area and became unusually common there.

The concentration of people with the T790M mutation in the Southeast‬ may help to explain why this region of the U.S. experiences elevated lung cancer rates, Chanock said. Statistics suggest that people in the region also have higher smoking rates than the U.S. average: approximately 20% of adults in Appalachia report smoking, compared to 16% of adults elsewhere in the U.S. So it's possible that those two factors interact.

Ongoing and future studies

Certain populations with a history of smoking are recommended to get screened annually for lung cancer using low-dose CT scans. A key question, Chanock said, is when and how often people with the T790M mutation should be screened.

The study found that people with T790M developed lung cancer about five years earlier than people without the mutation, on average. That finding highlights the "need to begin screen[ing] at an earlier age and irrespective of smoking status," Amos said.

A clinical trial is now underway to evaluate CT-based lung cancer screening in people with the mutation. The trial will also determine whether lung cancer risk increases with age in this population.

The researchers recommended that future studies unpack why the T790M mutation increases the risk of lung cancer, as well as investigate environmental risk factors that might interact with this genetic risk. Exposure to particulate-matter pollution in the air is one key factor to explore, they suggested. Future work could also look for other genetic mutations that might contribute to the inherited risk of lung cancer.

"Time will tell" whether additional lung-cancer-linked mutations will be identified, Chanock said. But personally, he fully expects scientists to find other very rare mutations that contribute to the risk.

"It is likely there are other variants of EGFR that increase lung cancer risk, but these may be even rarer than the one studied in this publication," Amos said. Finding these variants is important because it could enable people who carry them to proactively manage their risk for developing lung cancer, he said.

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

In a new study, scientists reared lab mice that were missing sections of their brains and then replaced the missing tissue with human cells.

The experiment represents a step forward in the study of human brain organoids ‪—‬ tiny models of the human brain grown from stem cells. In the long run, scientists aim to use organoids to better understand how the brain develops and how its structure and function change in the context of disease.

"It is definitely an advance in the field," said Dr. H. Isaac Chen, an associate professor of neurosurgery at the University of Pennsylvania Perelman School of Medicine. Chen was not involved in the current study but has conducted experiments transplanting human brain organoids into rodents' heads.

Organoids offer a window into early brain development that's impossible to observe closely in humans, namely because it unfolds inside developing fetuses. Although organoids are not perfect re-creations of full-size human brains, scientists think organoids are useful models for studying the developing brain in both health and disease.

The model in the new study "certainly creates some pretty interesting options in terms of modeling human neurodevelopment and various types of neurodevelopmental disorders," Chen said. "If you're looking for a model that really allows you to look at larger areas of human neural tissue from a cellular, molecular perspective, I think there's a lot that this model has to offer."

Making space for human cells

Often, brain organoids are grown outside living organisms, either in lab dishes or devices that keep these "minibrains" suspended in a solution. Multiple organoids representing different parts of the brain, or even different people's brains, can also be brought together to form more-complex structures.

Why, then, are some scientists growing human organoids inside mice? One reason is that there's a secret sauce inside living organisms that helps organoids mature better in animals than they do in lab dishes. In the body (in vivo), there are mysterious signals that help direct neurons' development and organization, and these signals are missing in lab dishes (in vitro).

"There are some cues that are present in vivo that are really important, and we simply don't know what to add in, in vitro," said study co-author Dr. Sergiu Pașca, a professor of psychiatry and behavioral sciences at Stanford University. The team demonstrated this phenomenon by transplanting organoids into lab rats in a study published in 2022; the transplanted organoids grew larger, formed better connections and were more active than organoids grown in dishes.

But transplanting human brain cells into rodents comes with different challenges. One is that human brains mature at a slower rate than rodent brains do. "Even when they're put in an animal, in a mouse or in a rat, they will still develop about 20 times slower than the mouse or the rat," Pașca told Live Science.

The host's brain cells quickly grow and form new connections, while the human cells lag behind and get outcompeted, Pașca explained. This limits the amount of space that the human cells can take up. As neurons mature, they become myelinated, meaning they gain fatty insulation that helps them communicate more efficiently. The rodent neurons become myelinated more quickly than the human cells do, and that fat creates a physical barrier that the human cells struggle to penetrate, Pașca said.

In their study, described Wednesday (Sept. 16) in the journal Nature, Pașca and colleagues aimed to give the human neurons a leg up. They couldn't solve the issue of human cells maturing slowly, but they could lend the cells extra space to grow in.

Through years of work, they developed a genetically modified mouse that develops only 2% of its cerebral cortex. The majority of its hippocampus — a major memory center in the brain — is also missing. Within a few days of the mouse's birth, the team transplants human neural tissue into that vacant space, and about 90% of the time, that human tissue integrates successfully and starts to grow, Pașca said.

"We just took cortical organoids, about four of them, and transferred them with a syringe into that vacant space," he said. "That's it. They go in there, they graft, and within a few weeks, they start to grow. And then within a few months, they've taken most of that volume."

In the weeks following the transplantation procedure, the human brain cells in the mice's heads grew, formed connections and extended projections into the underlying mouse tissue. The human tissue didn't organize itself into distinct layers as it normally would inside a human's head, but it included many cell types that are typically seen in the human cerebral cortex.

Future of the field

The researchers compared the mice imbued with brain organoids with mice that were missing the same amount of brain tissue but didn't get organoids. They also compared both groups to unmodified lab mice.

Perhaps surprisingly, the mice missing large chunks of their brains still functioned fairly well. "You look at them, and you can't really honestly tell," Pașca said. Upon closer inspection, though, the mice had subtle deficits in their fine-motor skills, working memory and socialization, he noted.

"From our perspective as humans, so much of what we do day to day depends on the cortex," Chen noted. But in a mouse, the cortex makes up a minority of the overall brain, and various studies have suggested that the animals can get by without it, he said. "I don't think the transplantation process itself is significantly hurting the animal," he added.

In the future, the ability to compare these three sets of mice — with organoids, without organoids, and unmodified — could help scientists tease apart how the human tissue is contributing to a given experimental result. Pașca envisions that the approach will be useful for studying the effects of insults to the brain, such as hypoxia (low oxygen) and exposure to toxins or drugs in the womb. Additionally, the genetics of the human organoids could be tweaked to see how those changes affect the brain's development, structure and function. That could be useful for studying cerebral palsy or autism, he suggested.

Chen expects that this new approach will be useful for studying aspects of early brain development at the molecular and cellular levels. The new model incorporates a larger volume of human tissue than models have done in the past, and that's an additional advantage. The human tissue doesn't organize itself into layers or lobes as you'd see in a real human brain, he noted, but he thinks there's still a lot that can be learned from it.

From an ethical standpoint, Pașca consulted with experts at Stanford and an external ethics committee regarding the welfare of the animals used in the study. Studies that involve putting human brain tissue into animals also raise questions about whether that added tissue could grant the animals new cognitive abilities — make them more human-like, in essence. The ethics committee fielded these concerns as well.

"We have not seen emergence of any new properties," Pașca noted. "It's not surprising because we're still at a very early stage of development." They grew the organoids for only six months, so the human organoids were roughly as developed as a 6-month-old fetus's brain tissue.

If the organoids matured to be more human-like — developing layers and lobes — that might present more of a concern. But both Pașca and Chen said that type of development might be hard to recreate in a mouse anyway.

Chen argued that the sheer size of the human brain contributes to its complexity, and it also contains specialized regions that work together to execute different tasks. A mouse's head cannot support the scale of a human brain, and at this point, organoids don't develop the same organization and specialization that we see in people, he said.

"It would be much more problematic if this was to happen in a species that has a larger brain and is closer to humans evolutionarily," Pașca argued. Pigs and nonhuman primates, such as monkeys, would be examples. Especially in regard to transplanting human organoids into monkeys, "that would be an experiment that I don't see is justified at this point," Pașca said.

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

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

The symptoms: The man went to an emergency department after fainting. He had felt nauseous just before the episode, which lasted about three minutes and was followed by a second fainting episode lasting about two minutes. He also had swelling around one eye.

His family told doctors that he hadn't shown any jerking movements, loss of bladder control or subsequent grogginess, which would have been telltale signs of a seizure.

What happened next: Because the man had fainted twice and had a history of heart disease, doctors first looked for problems affecting his brain and heart. An MRI of his brain, used to look for structural abnormalities that could explain the fainting, and an electroencephalogram (EEG), which records the brain's electrical activity, did not reveal a cause.

The man had persistently low blood pressure, the doctors observed, and this led them to move him to the intensive care unit. There, doctors carried out tests for infections and heart attack, but all came back negative.

Meanwhile, the swelling around one of his eyes spread to both eyes and then across his face, while his blood pressure continued to fall despite treatment with intravenous fluids.

The doctors probed further into the man's medical history and activities before the fainting episodes. They learned that he had applied an artificial hair dye two days before he became ill. Soon afterward, he developed itching on his scalp, neck and face. He self-treated with the allergy medicine cetirizine, an antihistamine, for two days. He also reported spending two to three hours outdoors in the sun each day after he'd applied the hair dye.

The diagnosis: Based on the man's recent use of hair dye, the itching that followed, his rapidly worsening facial swelling and his persistently low blood pressure, doctors concluded that he was experiencing anaphylaxis, a severe allergic reaction that can affect the whole body. The reaction can be life-threatening if left untreated.

The treatment: Doctors treated the man with epinephrine (also called adrenaline), a hormonal medication that rapidly reverses the effects of anaphylaxis. They also gave him antihistamines and steroids to help bring the allergic reaction under control, along with intravenous fluids to raise his blood pressure.

However, the patient's blood pressure remained dangerously low, so doctors continued giving him epinephrine through an intravenous drip for about 16 hours. Over the next three days of treatment, his blood pressure stabilized and the swelling in his face gradually subsided.

He was transferred to a general ward and treated there for another five days before being discharged. He was advised that he could have a similar reaction in the future and referred to a dermatologist.

What makes the case unique: Most allergic reactions to hair dye remain limited to the skin, causing itching, redness and swelling where the dye has touched it. Severe reactions affecting the whole body are uncommon, the man's doctors wrote in a report of the case.

The itching the man noticed shortly after applying the dye was likely an early, mild allergic reaction, his doctors wrote. That reaction later progressed to a much more severe one, they suggested, raising the possibility of a "biphasic" allergic reaction, an uncommon pattern seen in about 5% of patients with anaphylaxis. However, this remains only a possible explanation.

The doctors also noted that the man's prolonged sun exposure after he applied the dye may have intensified the reaction; they cited previous research that ultraviolet light can enhance the allergy-triggering effects of para-phenylenediamine, a common ingredient in hair dyes. In the report, the doctors did not identify the exact hair dye ingredient that triggered the reaction in this instance.

The case highlights the importance of asking about recent use of products such as hair dye when doctors evaluate patients with otherwise unexplained fainting, facial swelling or shock, the medical team concluded.

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!

In women's reproductive years, their brains are exposed to high levels of sex hormones, and their neurons may come to depend on those hormones to function optimally. But leading up to and after menopause, the ovaries produce far less estrogen and progesterone, raising concerns that this drop in hormones may contribute to women's dementia risk.

"We think that the loss of those hormones at menopause renders those neurons more vulnerable to age-related cellular decline and pathologies like Alzheimer's," said Karyn Frick, a neuroscientist and professor of psychological and brain sciences at the University of Wisconsin-Milwaukee.

So, if falling hormone levels are a risk factor for dementia, could replacing those hormones help stave off the disease?

While the idea sounds logical on its face, studies that have looked at hormone replacement therapy (HRT) for dementia prevention have had mixed results. There are early hints that restoring estrogen during early menopause may protect brain health, but ultimately, more gold-standard clinical trials are needed to know for sure, experts told Live Science.

Support for estrogen protecting the brain

The idea that estrogen could help ward off dementia is plausible. Women are more likely to develop Alzheimer's disease than men are, and scientists think the loss of estrogen during menopause may be partly to blame, said Jennifer Bruno, an instructor of psychiatry and behavioral sciences at Stanford University.

Lab and animal studies buttress the idea that estrogen could protect brain health.

In the brain, estrogens act as neuromodulators, or chemical messengers that alter how neurons behave. Estrogen also helps neurons keep their shape. Estrogen loss in female mice triggers a drop in the number of dendritic spines ‪—‬ the small, bud-like bumps on neurons that receive chemical messages.

Researchers think that estrogen may help prevent the formation of the abnormal proteins — including one called amyloid beta — that accumulate, disrupt communication between neurons and ultimately kill cells in Alzheimer's disease. Amyloid beta is produced when a larger protein is cut the "wrong" way by an enzyme, Frick explained. Estrogen promotes the "normal" cutting of this protein, thus reducing amyloid beta, studies in lab mice show.

And estrogen may limit the buildup of a second Alzheimer's-related protein, called tau, by preventing the chemical processes that cause the tau proteins to clump together. This helps prevent the formation of tau tangles, a hallmark of Alzheimer's disease.

The hormone may also support brain health indirectly by improving sleep quality.

"It's well documented that menopausal women have difficulty sleeping, whether it's due to hot flashes or insomnia," Frick said. Estrogen can ease those nighttime hot flashes, thus helping menopausal women get more, less-fragmented sleep. Deep rest may help the brain clean out toxic proteins, while research shows sleep deficiency is linked to Alzheimer's disease.

Mixed results with estrogen-only HRT

HRT for menopause comes in two main forms: treatments that include only estrogen, and combined therapies with both estrogen and progesterone. The treatment has a complicated history.

HRT was popular in the 1990s but fell out of favor after results from the Women's Health Initiative study were published in 2002. That study identified various risks tied to both estrogen-only and combined HRT options, some of which have since been overturned by newer data.

That said, the Women's Health Initiative study found that estrogen-only HRT came with an increased risk of endometrial cancers, and later analyses have backed up this idea. That's why today, clinical guidelines recommend that women who have not gotten a hysterectomy take combined HRT, while estrogen-only options are reserved for those who have had their uterus removed. (The added progesterone counteracts estrogen's thickening effect on the uterine lining.)

For the subset of women who take estrogen-only HRT, observational data published in August showed that this form of the treatment was linked to a reduced risk of dementia. The study, published in the journal Neurology, found that women who took estrogen-only HRT were less likely to show Alzheimer's-related changes in the brain than women who didn't take any HRT.

Estrogen-only HRT was also tied to better clinical outcomes: Treated women were less likely to be diagnosed with dementia, were less likely to show clinical and functional cognitive decline, and had better scores on memory tests, on average, compared with untreated women. These findings drew on two large, separate groups of older women, reporting data from 21,400 people in total, but they didn't include data on when each woman started HRT.

Whereas earlier studies of HRT and dementia risk relied on doctors' ratings of patients' symptoms, the Neurology study measured levels of Alzheimer's-related proteins in the brain after death. That's a more "definitive" marker of disease, said Bruno, a co-author of the study. However, the research was observational, so it can't say whether estrogen-only HRT directly causes the better brain outcomes the team observed, she stressed.

Although the Neurology study's findings are promising, they don't necessarily match the results of other studies of estrogen-only HRT and dementia. For example, a slightly larger observational study, published in 2023, found that estrogen-only HRT was associated with an increased dementia rate.

In that research, most of the women took a type of estrogen called estradiol, while Bruno's study included a greater variety of estrogens. That may have been the difference in the two studies' results, but teasing that out would require further study. Meanwhile, the conflicting findings muddy the waters of what estrogen-only HRT can do for brain health.

Does timing matter?

One big finding from the Women's Health Initiative study was that starting HRT — either estrogen-only or combined — after age 65 was associated with worse cognitive function and increased dementia risk, said Yuko Hara, director of aging and Alzheimer's prevention at the Alzheimer's Drug Discovery Foundation.

The same may not be true for people who start HRT earlier. For context, menopause starts around age 51 to 52, on average, and it's preceded by perimenopause, a transitional period when hormone levels begin to drop, typically around the mid-40s.

An observational study published in August in the journal Alzheimer's & Dementia found that starting HRT between ages 46 and 56 was linked to a reduced risk of dementia. That study did not differentiate between estrogen-only and combined treatment; it lumped all of the data together.

The protective link was especially strong in three groups: women with "surgical menopause," triggered by the removal of one or both ovaries; carriers of a certain variant of a gene called APOE that raises Alzheimer's risk; and women who had a relatively short time between their first period and menopause.

A 2024 meta-analysis of randomized controlled trials also found that HRT had a cognitive benefit for women with surgical menopause; that finding was tied mostly to estrogen-only therapies.

However, outside of that specific group, the idea of early HRT protecting brain health is far from settled.

Who might benefit, if anyone?

When it comes to using hormone replacement to protect brain health, the evidence isn't yet strong enough to recommend any kind of HRT as a way to protect the brain in all women, Hara said. Women who had one or both of their ovaries surgically removed are the exception to this rule.

"This is a distinct clinical population because the procedure can cause an abrupt, early loss of estrogen, rather than the gradual hormonal decline that occurs with natural menopause," Hara said.

For most women who have gone through natural menopause, "there is not enough evidence to recommend [HRT] specifically for preventing cognitive decline or dementia," she said.

HRT is not currently prescribed to prevent dementia — it is prescribed to ease menopause symptoms, such as hot flashes, night sweats and sleep disturbances. To settle the science on HRT and the brain, what's really needed is a well-designed clinical trial that follows women from perimenopause to postmenopause, Bruno said. That would reveal the effects of HRT on brain health and dementia risk more reliably than the studies done so far.

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

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Artificial intelligence (AI) algorithms that hunt for cancer may do a better job when they approach the analysis as if they were a human pathologist, a new study suggests.

Many AI systems analyze preselected regions of a tissue sample, or they split a whole pathology slide into patches of a fixed size. By contrast, a pathologist searches more dynamically, panning across the tissue, zooming in and out, and pausing over areas that raise red flags. A whole slide can contain billions of pixels, while the evidence of cancer may occupy only a tiny patch.

Study co-author Zhi Huang, an assistant professor of pathology and laboratory medicine at the University of Pennsylvania, compared the process to a search-and-rescue helicopter. "You don't start by inspecting one square meter of ground," Huang told Live Science. You scan the landscape first and then swoop in for a closer look.

In the new study, published in July in the journal Nature, Huang and colleagues demonstrated that cancer-detecting AI might work better when it takes this humanized approach.

Training AI to hunt for cancer

AI algorithms called vision language models (VLMs) struggle with the first step that Huang described — that initial, cursory scan. That's in part because many pathology AI systems learn from what pathologists leave behind at the end of that search: a labeled image pointing out where the cancer is or an official diagnosis.

Instead, the researchers trained their new AI on pathologists' search behavior. They called this approach to training "Pathology-CoT," short for "chain of thought." It turns observable actions, including where pathologists move around and zoom in on an image, into training data.

To collect the data, the team created a tool that recorded how pathologists moved around a slide and changed magnification. The raw logs, gathered from eight pathologists, were messy, as a given pathologist might drift across a slide, overshoot their intended region of focus or fiddle with magnification to adjust it to their liking.

To clean up the data, the researchers filtered out those incidental movements, focusing on moments that appeared to represent deliberate attention, such as lingering over one view or making a sustained pan. Then, they compared those regions with eye-tracking data to check that the software was capturing where pathologists were actually looking.

For each region a pathologist inspected, the VLM also drafted a short rationale explaining why the region was worth examining and what features were visible; human pathologists could then accept, edit, or reject the rationale, creating additional training data for the AI. In one example, the AI flagged a portion of a slide as potentially metastatic and suggested zooming in to look for atypical cells. Other inspected regions were flagged as healthy tissue.

Ultimately, the researchers used this training method to build a new tool called Pathology-o3. It scans a slide at low resolution, uses a model trained on pathologists' behavior to choose regions worth a closer look, then sends higher-resolution views of those regions to a VLM for analysis.

Putting it to the test

Huang said the goal of the new study was not to show that Pathology-o3 worked better than specialized AI models that are specifically built to detect specific types of cancer; those models are often trained disease by disease. Rather, the researchers wanted to see whether their new training approach could help a general-purpose AI navigate a pathology slide more effectively.

They compared Pathology-o3 to other general-use AI systems, such as OpenAI's o3, and asked the algorithms to examine slides containing lymph node tissue. These slides were collected from colorectal cancer cases and some contained metastatic cancer, which human pathologists had already labeled.

The algorithm correctly identified slides that were positive for cancer 100% of the time. However, of the slides it identified as positive, 15.5% were actually negative. By comparison, OpenAI o3 correctly identified slides that were positive for cancer 87.5% of the time. Of the slides it identified as positive, 53.3% were actually negative.

The researchers designed Pathology-o3 to err on the side of flagging something for another look, rather than potentially missing cancer. That might help to explain the rate of false positives, Huang said.

Whether that rate of false alarms is acceptable depends on how Pathology-o3 is used, said Mohammad Asadi, a data scientist at Stanford University who was not involved in the research. It's not precise enough for the AI to diagnose patients on its own, but it could still be useful for a system to point a human toward regions of a slide that are worth double-checking. It may be an advantage that the approach shows the pathologist a specific region to inspect rather than declaring an entire slide suspicious, he said.

The researchers tried repeating the test on an independent dataset that the algorithms hadn't seen before to see how well it worked on unfamiliar slides. Pathology-o3 correctly identified slides that were positive for cancer 97.6% of the time. Of the slides it identified as positive, 37.1% were actually negative. The finding is an example of how AI performance can change when the data source changes, even when the medical task stays the same.

Asadi explained this result suggests the system can still work with slides from a different source. But that result does not yet show that using this tool would make pathologists more accurate or efficient in practice.

Can it help pathologists?

The researchers applied their training approach to several existing VLMs, finding that the models' performance consistently improved after the training. That suggests that the navigation data from pathologists was useful across settings, Asadi said.

For Huang, that is the most important result. "The takeaway isn't our system," he said. "It's that the missing ingredient has been sitting in hospitals this whole time."

The study did not compare Pathology-o3 directly with human pathologists, but the researchers said that wasn't their aim.

"The right question isn't whether it beats a pathologist," Huang said. "It's whether a pathologist working with it catches more [cancer cases] and works faster." The current study did not address the latter question, either, but the team's next experiment is designed to test pathologists on the same cases with and without Pathology-o3, measuring what they catch and how long they take to do so.

The system's most plausible use is as a prescreening tool, Asadi said, but he stressed that the research has not yet shown that doctors who use it become faster or more accurate. Asadi wants an even tougher test: trials conducted across multiple hospitals that measure not just accuracy and speed but also pathologists' workloads. He wants the trails to assess the burden of false alarms from the AI algorithms and whether doctors recognize when the AI is wrong.

Importantly, cancer diagnoses can require information from multiple slides, stains and a patient's medical history, while the current system just reads one slide at a time. "I wouldn't claim it should diagnose on its own," Huang said.

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

The brain undergoes dramatic changes during puberty and pregnancy, but during menopause, the organ's structure remains remarkably stable, a new study suggests.

The research, published Sept. 8 in the journal Nature Communications, examined the brain's gray matter, which mostly includes the wrinkled outer surface of the organ, called the cerebral cortex. Past studies have found that the volume of gray matter shrinks markedly during puberty and pregnancy, likely reflecting a fine-tuning of neural circuits during those periods.

There's also a gradual decline in gray matter during adulthood that's seen as a normal part of aging, said study co-author Sophie van't Hof, a doctoral student in psychiatry at Amsterdam University Medical Center. However, during the transition leading up to menopause, that gradual loss of gray matter levels off temporarily, the study found.

"This study provides the first direct longitudinal comparison of brain structural changes across all three major female hormonal transitions," said Magdalena Martínez-García, scientific director of maternal health for the Ann S. Bowers Women's Brain Health Initiative, a brain imaging consortium headquartered at the University of California, Santa Barbara.

"I really appreciate the effort that went into finding and curating such an impressive longitudinal dataset of the female brain," Martínez-García, who was not involved in the study, told Live Science in an email.

Declines in puberty and pregnancy

For their analysis, the researchers gathered data from the UK Biobank, a biomedical database that contains information from 500,000 U.K.-based adults. That data includes MRI scans of people's brains, which the team used to study brain changes in menopause.

To look at puberty and pregnancy, the researchers pulled from several brain-scan datasets that had been compiled by Leiden University in the Netherlands.

In all, the study included data from 1,095 brains across the three life stages. They analyzed each participant's brain at two different time points, examining how each person's brain changed over time and how it compared to others' brains.

The youngest cohort included participants who hadn't started menstruating yet, as well as those who'd recently started and those who'd already had periods for an average of 19 months. The pregnancy cohort included 40 who'd had their first pregnancy during the study and 30 who'd had second pregnancies, as well as 40 women who'd never been pregnant, as a point of comparison.

As in previous studies, the researchers observed that both the girls entering puberty and the pregnant women lost gray matter. But scientists don't necessarily see these declines in gray matter at puberty and pregnancy as negative.

It’s a hypothesis, but "we actually see it as something positive," van't Hof said. "We see it as neural fine-tuning."

During puberty, that gray-matter loss is thought to be a normal part of the brain's development into adulthood. Its function in pregnancy is not well understood, van't Hof noted, but the evidence to date doesn't suggest that it contributes to "mommy brain" — the brain fog and forgetfulness some women can experience postpartum.

"I'm not saying that there's no neurobiological basis for this mommy brain, but up until now, we haven't found it," van't Hof said. "But what's really important is that gray matter decline is not equal to cognitive complaints."

Stability in menopause

The analysis included 120 women who entered menopause during the study. At the first time point, these women had not gone a full year without a period, but by the second time point about 3.5 years later, they had. Menopause is defined as the point at which a full year has elapsed since a person's final period.

The researchers compared these women to two other groups: about 50 women (average age 51) who had not had their last period yet and over 670 women (average age 55.5) who had already had their last period.

During late perimenopause — the final stages of the transition to menopause — the brain's gradual decline in gray matter paused, van't Hof said. Then, in postmenopausal women, that gradual decline of gray matter resumed. The exact timing of that pause differed for each woman, but it occurred consistently across the group, van't Hof noted.

The most striking finding was the lessening of the "ongoing age-related decline in brain volume during the transition into and out of menopause, compared with the more stable premenopausal and postmenopausal groups," Martínez-García said. This is an "interesting finding that adds to our understanding of how dynamic the female brain can be across the lifespan."

Factors such as whether participants had taken hormone replacement therapy for menopause and the number of children they had given birth to did not have a measurable impact on the results, the study authors noted.

In general, complaints of brain fog are widespread just before, during and after menopause, van't Hof said. This could be attributed to declining hormone levels and sleep disruptions.

"We have no clue if there's a neurological basis [for that brain fog], because, again, this is the first study to look at it," she said, adding that more studies are still needed to learn more.

"As with any study, there are some limitations to consider, but overall, I think the methods and conclusions are well supported by the data available," Martínez-García said. Both Martiniz-Garcia and van’t Hof said that they hope other researchers build on these findings to deepen scientists’ understanding of female neurobiology at every stage of life.

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!

Many people are familiar with melatonin, a hormone that helps ready the body for sleep. But there's another, lesser-known chemical in the brain, called orexin, that tips the scale in the other direction: waking the body up.

In 1999, two scientists independently uncovered the function of orexin and published papers about it. Dr. Masashi Yanagisawa, a molecular biologist and physician now at the University of Tsukuba in Japan, came across orexin while studying the interaction of receptors and chemicals in the brain. Dr. Emmanuel Mignot, now the director of the Stanford Center for Narcolepsy, homed in on orexin while studying narcoleptic dogs. (His Chihuahua, named Watson, has narcolepsy, and he previously had another dog with the condition, named Bear.)

This year, the pair of researchers won the coveted Albert Lasker Basic Medical Research Award for this fundamental finding that helped reshape our understanding of sleep. Their work has since led to the development of drugs for insomnia and narcolepsy.

Yanagisawa told Live Science that, at the start of his research career, he didn't expect to end up studying sleep. Mignot, on the other hand, had an early interest in understanding narcolepsy so that better treatments for the neurological disorder could be developed. Live Science spoke with Mignot about the discovery of orexin and how the field might progress in the future.

Nicoletta Lanese: What initially drew you to studying narcolepsy?

Dr. Emmanuel Mignot: There were three things that attracted me to narcolepsy: Number one, it was a human problem. It was already known [at the time] that it was not super rare. I'm not saying it's super common, but 1 person per 3,000, 0.03% ‪—‬ it's reasonably common. And nobody cared about it. I would talk to neurologists and they'd say, "Oh, I've never seen one case in my entire life." So I would say, "Yes, of course; you miss them all." That was the state of the play at the time.

Number two, was what this was a quintessential sleep disorder [in which sleep itself is disrupted]. I thought that if we found the cause of this disease, we could potentially discover something totally new about sleep — a fantastic entry point to a mystery.

The third thing that made me ready to go there was that it was tractable. A lot of problems are not tractable.

NL: Why did you start working with the dogs with narcolepsy?

EM: I studied the pharmacological basis because I was trained in pharmacology, and as a psychiatrist, and I discovered how this drug modafinil [a stimulant-based narcolepsy treatment] was working. But quickly, I realized I'm not going to find the cause by doing pharmacology. I'm only going to explore what's known.

That's when I started to fall in love with genetics, even though I was not trained as a geneticist. I said, "We have to find this gene in the dogs." It looks like they have all the symptoms. It was a huge bet, and it took me 10 years because I was definitely … overoptimistic. But it was worth the price at the end.

NL: And scientists already knew about narcolepsy in dogs at that time?

EM: The guy at Stanford that started the sleep program was called Dr. [William] Dement. He was a graduate student in Chicago in the 1950s, when [Eugene] Aserinsky and [Nathaniel] Kleitman discovered REM sleep. He had the foresight to understand that this was an important discovery.

[Later], he discovered that narcolepsy was really a disorder where people go into REM sleep and have this very abnormal dreaming. He came in 1970 to Stanford, and the first thing he did after his medical school was to start a clinic to see patients with narcolepsy. Around then, he spoke at an American Medical Association conference in San Francisco, and he discussed different sleep disorders, including narcolepsy. And then there was someone in the audience that said, "Oh my god; I have a dog with your disease. Every time it gets excited — boom — it collapses. And it sleeps all the time."

That dog had already been euthanized, but it still gave him the idea that these dogs have narcolepsy — maybe we should try to get some. So he went to a lot of veterinarians to talk to them about it, and they identified a whole series of dogs, including the first poodle, Monique, who had narcolepsy. And they started this little colony of dogs. Initially, they tried to breed them, but most cases of narcolepsy are actually not genetic. Then, in 1977, they got a whole litter of Dobermans, and then Labradors, that had some form that was genetic.

So when I arrived, it was in 1987. They already had the dog colony. I came to study the pharmacology, to try to find a better treatment for narcolepsy. But I did stand on the shoulders of giants.

NL: At that time, it's not like you had a complete dog genome. Did that make studying their genetics challenging?

EM: It was crazy. A couple of human genes had been isolated, and mouse genes, but it was a handful. We didn't even have the full genome map in humans. And meanwhile, dogs — no pun intended — were in no man's land. Very little was known.

It took me 10 years. I had times where some people didn't believe that the dogs had narcolepsy. There were a few depressing moments, but I was convinced that was the right thing to do.

NL: When you ultimately found the receptor for orexin, did it surprise you? It strikes me as surprising that there would be a discrete "switch" in the brain that controls wakefulness.

EM: I was lucky. Honestly, I had no idea. I got enamored with genetics because what I love [about it] is you can find something without any hypothesis. You just search for it, and what you find tells you what it is. You have no prerequisite for knowing what you would find.

I could have found something much less significant. That was a dream, to find a GPCR [G-protein coupled receptor, a protein on the outside of cells]. Can you imagine? A drug target.

Then, it turned out to be immediately applicable to humans. That, too, was a lot of luck; let's be honest. I was just trying to find the cause of one thing and one step at a time; it could have been something very complicated. It turned out to be simple.

Was I surprised? No, because I was not expecting one or another.

NL: Do you recall what the reception was like when the initial finding was published?

EM: It had an immediate effect, for several reasons. For example, I was seeing a lot of patients with narcolepsy at the time, but they were all old folks that had had narcolepsy forever. A lot of people would tell me, "I think I had it from when I was born, because I don't remember." We were never seeing children.

But after narcolepsy was described — the dog gene — suddenly narcolepsy became much more famous. And what happened is that people started to pay attention to narcolepsy, and we started to see kids. In kids, the picture is so much different. They gain an enormous amount of weight; it's very abrupt. It's a little bit different than what you see in adults, where they have adapted to it.

That was, I think, a practical consequence of the discovery. It really put narcolepsy on the map.

The second thing that happened is, all the drug companies started to develop hypnotics [sleeping pills], trying to block the orexin. They developed hypnotics relatively quickly, and they are very effective. They are probably safer than benzos [benzodiazepines] and so forth.

NL: Is it considered safer because the orexin blockers better replicate natural sleep?

EM: We know that the orexin definitely drops during sleep, so blocking it is definitely a way to recapitulate that drop; that's true. It's an awake-promoting system, so if you remove something that makes you more awake, it's safer than inducing sleep by shutting down the brain.

NL: As you moved to studying narcolepsy in humans, you found evidence that there might be an autoimmune response involved; it's been suggested that such a response may be harming the cells that make orexin in the brain. Was there suspicion that the condition had an autoimmune element previously?

EM: It's not something I 100% discovered. In 1983, before I came to study narcolepsy, there was a guy in Japan who I met, called Yutaka Honda. [Editor's note: Honda's research linked narcolepsy to the human leukocyte antigen (HLA) region of the genome, which helps regulate immune responses.]

The HLA is the way the immune system sees the world. That had just been discovered as very important for transplantation, because it's very polymorphic [takes on different forms] from one person to the next. They [Honda's group] found that all narcoleptics had a particular genetic variant, called HLA-DR2. This was a total surprise.

When I came, that was already known. But then people really looked and tried to see if the disease was autoimmune, but they couldn't find anything — no autoantibody, nothing. It was all negative.

I did a study with African Americans, and in African Americans, I found that this DR2 marker was not the best marker for narcolepsy. It was a gene just next to it that was called DQB1*06:02. [Editor's note: That HLA variant is now recognized as a strong risk factor for narcolepsy, particularly for narcolepsy type 1 (which involves a symptom called cataplexy).]

I'm very proud of that study because I think it's the first time that people used human diversity to actually map down a genetic factor more precisely, which now is used commonly. It's called transethnic mapping.

NL: New treatments that target orexin have just been approved. Do you see those therapies as an extension of your earlier findings?

EM: Of course. I was trained as a pharmacologist originally, so obviously, I do a lot of clinical trials. I see my patients totally transformed by this medication. It's just amazing. I'm so fortunate. How could you get a better reward than seeing your patients totally transformed by this medication?

It's going to have a lot of other applications [beyond narcolepsy]. Some people think it's going to be very helpful for ADHD; some people think it could be very helpful for depressed people with excessive sleepiness. We don't know, really; there's a lot of possibilities.

Another thing I'm excited about is that I have a few patients with [both] narcolepsy and schizophrenia. You cannot give them stimulants. If you give them modafinil or another dopamine stimulant [for narcolepsy], they have even more hallucinations. Often, they are sedated by their medication, and we are very poor at making people more motivated and active. These [orexin-activating] drugs seem to have effects beyond just waking people up. They seem to increase motivation.

You don't know until you try, but I'm sure it's going to have other applications.

This interview has been condensed and edited lightly for clarity. It is for informational purposes only and is not meant to offer medical advice.

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A family photo album can reflect how physical traits, such as blue eyes or lanky limbs, have been passed down — but a new analysis suggests that the way personality emerges across generations is far more complicated.

The meta-analysis, published Sept. 2 in the journal Nature, is the largest of its kind ever attempted. The work identified over 1,200 genes linked to five personality traits: extraversion, agreeableness, conscientiousness, openness to experience and neuroticism.

However, the scientists behind the study said its most important conclusion is that no single gene determines whether an individual will have a particular personality trait. Instead, thousands of genes exert tiny effects that are likely impossible to disentangle from environmental factors that shape our behavior.

Twins and DNA sequencers

Researchers have studied the link between genes and behavior for decades. Before the ability to analyze the genome in detail, many early studies looked to identical twins.

Knowing that identical twins share nearly 100% of their genetic material, scientists compared their traits with those of nonidentical twins and other siblings. Some studies compared twins raised in the same home with those raised in different homes in an attempt to separate the influence of upbringing from genetics. These efforts concluded that personality was roughly 50% heritable. ("Heritability" measures how much of the variance seen in a given trait can be explained by genes.)

The advent of gene sequencing enabled geneticists to calculate the influence of genes with greater precision than twin studies did. The most powerful tool in this arsenal is the genome-wide association study (GWAS), which can link traits to gene variants in detail. These statistical analyses require sample sizes in the millions, though.

The new study was a large collaborative project called the Revived Genomics of Personality Consortium, which brought together 46 cohorts of participants who'd had their genomes sequenced. Each person had been asked something related to one of the Big Five personality traits. The team had data from roughly 600,000 people about the first four traits — extraversion, agreeableness, conscientiousness, openness to experiences — and data from over 1.1 million people about their levels of neuroticism.

Generally, as geneticists have leveraged larger and more powerful GWAS, many traits have shown increased heritability because these bigger studies can identify more subtle genetic links, said Brent Roberts, a psychologist at the University of Illinois at Urbana-Champaign who was not involved in the new study. But "with personality, it was really clear from the get-go that it was different," Roberts said.

Earlier GWAS had suggested that the heritability of personality from common gene variants was roughly 5% to 15%, far lower than the estimate suggested by twin studies. The new work has confirmed those low numbers, said study co-author Michel Nivard, a genetic epidemiologist at the University of Bristol in the U.K.

It may be that GWAS do not capture extremely rare variants that might link personality traits in certain families, which means the heritability may be slightly underestimated, Nivard suggested. Additionally, twins are more likely to rate their personalities as similar for reasons unrelated to genetics, so the twin studies may have overestimated the heritability of personality, Nivard noted.

Cutting out confounders

It can be difficult to control for confounding factors in GWAS. For example, if scientists were investigating the influence of genes on academic achievement, genetics only tells part of the story; a person's socioeconomic status and access to books and tutoring also influence their education.

But in this case, Nivard and his colleagues did not find confounders in measuring personality. The researchers found that the genetic effects on personality are the same within families as they are among unrelated individuals.

"We've basically been able to rule out that there's any straightforward, simple social processes by which your parents directly influence your personality," Nivard said.

A key takeaway from the study should be not to focus too much on the different contributions of genes versus environmental factors in a trait as complex as personality, Roberts said. Our moods and minds are a collaboration between the two factors, not a tug-of-war, he argued.

A study to properly measure this interplay would be vastly expensive and would require following participants for decades. "This is where the limitation of human genetics research is really profound," Roberts said. Part of the problem, he added, is that while our DNA sequence is fixed, how the body accesses and reads DNA varies significantly depending on the environment a person finds themselves in. In other words, which genes get turned on and when are variable factors.

Assessing this enmeshed relationship using only the DNA code we are born with is like trying to predict every move of a couple's dance by looking at how they hold each other before the music starts up.

Nivard and his team can now use this powerful data source to learn more about personalities within groups of people, he said. Nivard predicted that, even once geneticists have mapped all the rare gene variants that may influence personality, some genetic influence will still go unaccounted for; processes such as the interaction between the environment and gene expression are still not fully understood. He called these the "unknown unknowns." Identifying these factors is the next frontier for the genetics of personality.

"It's where we're headed," Nivard said.

This year's Lasker Awards — coveted prizes for biomedical research that are sometimes called "America's Nobel Prizes" — have gone to scientists behind fundamental discoveries in sleep science and to researchers who developed a groundbreaking treatment for hemophilia.

Additionally, a Lasker Award for public service went to actor Michael J. Fox for his advocacy for patients with Parkinson's disease that has helped advance research into the neurodegenerative condition.

The prizes, each of which comes with an honorarium of $250,000, will be presented in person Sept. 17 in New York City. The awardees were announced Wednesday (Sept. 9) by the Lasker Foundation, which was established in 1942 by the philanthropists and health advocates Albert and Mary Lasker.

A deeper understanding of sleep

The first of the three awards, called the Albert Lasker Basic Medical Research Award, went to two scientists who independently discovered a key substance in the brain that helps control the sleep-wake cycle and is missing in people with some forms of narcolepsy — the neurological disorder marked by excessive daytime sleepiness and, sometimes, cataplexy (sudden episodes of muscle weakness).

The researchers — Dr. Emmanuel Mignot of the Stanford University School of Medicine and Dr. Masashi Yanagisawa of the University of Tsukuba in Japan — arrived at the discovery through different approaches. Mignot wanted to understand the underlying causes of narcolepsy, while Yanagisawa was investigating a curious class of receptors that were known as "orphans" because the chemicals that activated those receptors were unknown.

"We never thought we would end up in sleep," Yanagisawa told Live Science. "This was a kind of biochemical fishing expedition."

In particular, Yanagisawa was interested in proteins at the surface of cells called G protein-coupled receptors (GPCRs). When the right chemicals are plugged into these receptors, they trigger a chain of events within cells. Various compounds that activate GPCRs had already been found to be useful as drugs, but there were many receptors with unknown triggers.

Yanagisawa and colleagues went fishing for those triggering chemicals in rat brains, isolating substances called peptides from the tissue and then exposing GPCRs to those peptides. "We got very lucky, initially," Yanagisawa said. The fifth or sixth receptor they tested had a hit. Through further experiments, they landed on two closely related peptides as the trigger, and they found a second related receptor to match.

They discovered that the peptides came from a part of the brain called the hypothalamus, which was known to be involved in eating behaviors. So they named the peptides "orexins" after the Greek word for appetite, "orexis."

It turned out, though, that orexins' main job wasn't to control appetite; rather, they help promote wakefulness, the opposite of sleepiness. Mice without functional orexin genes would suddenly fall over and remain immobile for a minute or two, the researchers found. Peering into those mice's brains, they found that the animals were suddenly entering REM sleep, a phenomenon also seen in people with narcolepsy with cataplexy.

At the same time, Mignot, the other winner of the Lasker Award, was learning that orexin deficiency is also behind a form of narcolepsy seen in dogs. He then went on to study the mechanism in humans with narcolepsy.

"It became, suddenly, a very, very convincing story," Yanagisawa said of the researchers' converging findings. Previously, the study of sleep involved damaging parts of the brain and then seeing how a lab animal's sleep changed in response.

"There was no molecular level, genetic level, description of sleep regulation mechanisms at all," he said. "So our papers really shed new light on sleep regulation."

Together, the researchers' work paved the way to a new class of insomnia treatments, called orexin receptor antagonists, which promote sleepiness by turning down wakefulness. They have also led to new narcolepsy treatments called orexin receptor agonists, which boost wakefulness by increasing the receptors' activity. The first in the latter class of drugs was just approved in August.

A life-changing hemophilia treatment

The second award, called the Lasker~DeBakey Clinical Medical Research Award, went to three scientists affiliated with the Japanese drug manufacturer Chugai Pharmaceutical. These researchers — Kunihiro Hattori, Takehisa Kitazawa and Tomoyuki Igawa — created an antibody that interacts with key proteins in the blood that produce clots and thus stop bleeding.

This antibody treats hemophilia A, a severe bleeding disorder caused by a genetic mutation. That mutation causes the body to not make enough factor VIII, one of the key blood-clotting proteins. Normally, factor VIII grabs hold of two other clotting factors, and this enables a chain reaction that results in normal blood clotting. Without enough factor VIII, there is abnormal bleeding.

The severity of hemophilia A varies, but people with the disorder frequently experience blood pooling in their joints, which causes chronic pain and impairs mobility; they can also bleed uncontrollably even in the absence of trauma.

The antibody treatment works by binding two other clotting proteins — factors IX and X — to create a structure that fulfills the function of the missing factor VIII. Hattori, who is no longer at Chugai Pharmaceutical, initially launched the effort in 2000 after hatching the idea to use an antibody to bind several clotting factors together. Kitazawa and Igawa then brought the idea to fruition using pharmacology and chemical engineering, respectively.

The antibody, called emicizumab (marketed as Hemlibra), was approved by the U.S. Food and Drug Administration in 2017, and over 100 additional countries have approved the drug since. Over 30,000 people have received the antibody treatment to date, according to the award announcement.

Parkinson's disease advocacy

The third and final award — the Lasker~Bloomberg Public Service Award — went to Fox, actor and founder of The Michael J. Fox Foundation for Parkinson's Research.

Fox began experiencing symptoms of early-onset Parkinson's in 1990 at age 29. He publicly announced the diagnosis in 1998, sparking new discussions around the often-stigmatized disease. Through interactions with existing Parkinson's advocacy groups, Fox realized the field faced a lack of funding that likely hindered the pursuit of better treatments and a cure.

Since its inception in 2000, the foundation has funded more than $3 billion in Parkinson's research, according to the award announcement.

"When we launched the Foundation, our goal was simple, yet ambitious — cure Parkinson's," Fox said in a statement. "I am humbled to be recognized by the Lasker Foundation and jury. I accept this honor on behalf of everyone living with Parkinson's and everyone with us in our shared mission to end the disease."

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

The patient: A 55-year-old man in Bangladesh

The symptoms: The man went to the emergency room with severe abdominal pain that he said began five hours prior to his visit.

What happened next: During a physical examination, doctors noted that the patient's temperature and blood pressure were normal. His heartbeat was slightly elevated, at 110 beats per minute (bpm). (A typical resting heart rate for adults is 60 to 100 bpm.)

The man explained that one day earlier, an eel had "entered through his rectum accidentally," his doctors wrote in a report of the case. At the time of the encounter, the man was wearing a lungi — a type of long skirt often worn by Bangladeshi men — and he explained that the eel entered his lungi through the opening at the bottom and then wriggled into his anal canal.

He did not seek medical attention immediately after this happened, as he had hoped the fish would exit on its own.

When the doctors kneaded the patient's abdomen, it was rigid and tender. They ordered an X-ray, which revealed a dark, eel-shaped shadow on the right side of the abdomen.

The diagnosis: The X-ray showed a crescent-shaped gas shadow under the right part of the man's diaphragm and hinted that he had developed peritonitis — inflammation of a membrane called the peritoneum, which covers the abdominal organs. Peritonitis is usually caused by a bacterial or fungal infection, but it can also develop if fluids from other organs leak into the peritoneum.

If the condition is not treated quickly, it can lead to a life-threatening infection that can spread rapidly through the body.

The treatment: Doctors administered IV antibiotics, as well as fluids and anti-ulcer medications, which help repair injuries to organs' outer mucosal layers and prevent deeper tissue damage.

Due to the peritonitis, the doctors determined that the patient was at risk of septicemia, or "blood poisoning," in which pathogens invade the bloodstream. They decided to operate on the patient immediately and remove the eel via a laparotomy, a surgical technique that creates an opening in the abdominal wall and provides access to the pelvic organs.

After making an incision in the man's sigmoid colon — the S-shaped section of the large intestine adjacent to the rectum — the surgeons extracted the eel from the peritoneal cavity, the space surrounding the abdominal organs and encased by the peritoneum.

The eel measured nearly 2.2 feet (0.6 meters) long and was still alive. Perhaps, the doctors hypothesized, the eel was able to continue breathing by punching through the wall of the man's colon and squeezing into the peritoneal cavity, which contains a pale-yellow fluid that reduces friction between organs. This peritoneal fluid is mostly water, but it also contains glucose, electrolytes, proteins, enzymes, white blood cells and urea, a compound found in urine.

The surgeons then performed a sigmoid colostomy, creating an opening in the abdomen as an exit point for contents of the man's large intestine. In this way, they bypassed the damaged section of sigmoid colon to prevent leakage of fecal matter that could lead to further infection. Four days later, the man was symptom-free and was discharged from the hospital. The report did not document any follow-up visits.

What makes the case unique: Traumatic perforation of the intestine by foreign objects is uncommon, and cases involving live animals are "exceedingly rare," the authors wrote in the report. However, foreign objects often find their way into the human body through accidental ingestion or deliberate insertion into the rectum. Some deliberately inserted objects, such as vibrators, are designed for this purpose. Others are not; these have included chicken bones, light bulbs, metal rods, glass bottles and kitchen whisks.

Penetration of the colon by a live fish is an "unusual and scarcely documented event," the man's doctors added in the report. They noted one reference to such a case that appeared previously in scientific literature and involved a 50-year-old male patient in Hong Kong. In that case, the man knowingly inserted the eel — which measured more than 1.6 feet (0.5 m) long — into his rectum, allegedly in an attempt to relieve his constipation.

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!

Over a century ago, German pathologist Georg Schmorl documented a strange phenomenon: cells from fetuses that had moved into the mother during pregnancy. He had discovered microchimerism — where the cells from one individual move into another and set up shop.

In the past few decades, scientists' understanding of microchimerism has grown, thanks to technological advances. And the implications are wild.

Cells transferred during pregnancy could mean you have cells from your grandmother living inside you. A twin can be "absorbed" within the womb, leaving a genetic trace of the lost sibling. And after a bone marrow transplant, a man ended up with the donor's DNA in his blood and semen. These are just a few examples of how microchimerism opens a new way to understand immunology, genetics and evolution.

In her book "Hidden Guests: Migrating Cells and How the New Science of Microchimerism Is Redefining Human Identity" (Greystone Books, 2025), author and journalist Lise Barnéoud explores how the field emerged and developed as scientists grappled with understanding what was going on, and why — as well as the far-reaching implications of these minuscule interlopers.

"Hidden Guests" has been short-listed for the 2026 Royal Society Trivedi Science Book Prize.

Excerpt from "Hidden Guests": 'It doesn't lie. So who are you?': What happens when DNA tests show a woman is not the mother of the child she gave birth to?

Live Science spoke with Barnéoud about the book, why the idea of microchimerism resonates so deeply, and where the field could be headed next. "Hidden Guests" has been short-listed for the 2026 Royal Society Trivedi Science Book Prize.

Hannah Osborne: What first got you interested in microchimerism? How did your personal understanding change over the course of writing "Hidden Guests"?

Lise Barnéoud: The first time I heard about it, I was writing my previous book on vaccinations, and I had a chapter on our immunity, how our immune system works. I wanted to explain what we got wrong about how our immunity works. We are still learning — [we used to have this idea] that our immune system is kind of an army patrolling in our body and expelling any foreign elements. That's the image we have of our immune system. I wanted to tell another story, which is more accurate because we know now that it's not working like that.

I was looking for counterexamples, and, of course, one very famous counterexample is pregnancy. We tolerate the fetus that is half different than us. Another well-known counterexample is microbiota. Inside our body, we carry microbial cells as well as human cells ‪—‬ so cells coming from bacteria, viruses, fungi. We don't expel them; we need them. The third example I found was microchimerism.

The more I read about it, the more I was interested in it. It was challenging so many things. I've learned that the placenta is not that watertight barrier that we often think of, that the immune system is not as intolerant as we often think, and we can inherit cells from our kids like an inverted inheritance. All those elements popped up within my first reading, and I thought, "OK, I really need to dig more."

For your second question, I think the biggest change is that I realized those cells are not only kind of inactive tourists, just homeless drifters passively traveling in our body. They are really active. They can multiply, they can produce protein, they communicate with other cells, and they really influence our physiology, for better or for worse.

HO: We see how microchimerism is a relatively new field of research that has had lots of stops and starts. What was the biggest hindrance to the development of the field, and what changed?

LB: Maybe before speaking about the hindrances, just saying that the first time we discovered cells from other individuals within individuals was a century ago. The first one was in 1893, and it was a German pathologist who discovered cells from fetal origin in lungs from women who had died during pregnancy. Then it took a century to understand that this phenomenon happened to everyone and that it is of importance.

I think there are several hindrances. There's never one big one. The first one we can think of is the technology, because you need to study these microchimeric cells; you need tools that are able to study a tissue at the cellular level. This is quite new, so now we have these tools and we can make some progress. The second big hindrance is that this research field calls into question the traditional view of the immune system. If you see the immune system as a purely defensive and intolerant army, then you can't think of these foreign cells staying forever in your body, and that was a big hindrance, I think.

Maybe a third hindrance is that at the beginning of this field — I mean the new beginning in the '90s — they were mostly women working in this field. They told me that male colleagues often said, "Well, that's woman's stuff, you know; you're looking for some connection with your babies, but it's not really relevant," which is wrong, of course, because even men are affected by this phenomenon. They stayed nine months in the womb like us.

That might have, at least, challenged some of the first pioneers of the field. Now there are more and more men working in the field. In April, there was an international conference on microchimerism, and I think it was half women.

HO: The book includes many anecdotes about people directly affected by microchimerism. Which story were you most affected by, and why?

LB: I guess it'd be the story of Lydia Fairchild because she nearly lost custody of her children because of microchimerism. She was 26 and living in the U.S., and she applied for a welfare benefit to help her raise her kids. In the U.S., you need to undergo a maternity test for that, and her DNA test ends up showing that she could not be the mother of her kids. Of course she tried to argue; she had photos; she had testimonies. But she was always told, "DNA is 100% foolproof; DNA doesn't lie," which implied that she was lying. But she was not, so she called several lawyers. But at the beginning, they were all saying, "No, DNA doesn't lie."

At that time, she was pregnant with her third child, and they decided to do a test immediately after birth. Again, the impossible happened. This third child that just emerged from her womb was not her son — genetically speaking, at least.

In fact, she was harboring cells from her vanished sister inside her. Most of her eggs carried her sister's genetic signature, which means that the mother of her kids never lived. Isn't it amazing? That's maybe one of the stories that blew my mind.

HO: The section on DNA and how microchimerism complicates things is fascinating. How much of an impact do you think hidden cells have on the reliability of DNA evidence?

LB: The truth is that I think we don't really know. If you have only some microchimeric cells, among thousands of your own cells, then it won't change the reliability of the DNA test. But in some cases, these microchimeric cells can make up a significant part of an organ and sometimes even an entire organ. This proportion might depend on when you received those microchimeric cells. For instance, if you received those cells like Lydia Fairchild at the very, very beginning of your development, they might end up making up the entire organ where they landed first. But probably, we don't know which percentage of us start our in utero life with an evanescent embryo.

I looked for this number because I didn't really know about evanescent twins, so I wanted to know how many pregnancies started with several embryos and suddenly one disappeared. And I couldn't find any good number because, of course, it's quite difficult to put any imaging there at the beginning of the condition. Some articles say that up to 30% of pregnancies will start with several embryos, which means a lot of us are affected by evanescent twins. But let's say it might be rare that we have so many microchimeric cells in one organ that it completely changed a DNA test.

But there's another example in my book that took place in Alaska in 2004. After a rape, the forensic investigators collected the semen from the scene, and they discovered that the DNA in this semen matched with a man who was already in the database. But this guy was behind bars. He was in jail, the day of the rape, so he couldn't be the rapist.

Finally, investigators discovered that this guy, the prisoner, received a bone marrow transplant a few years ago from his brother, and the cells from the bone marrow of his brother didn't stay quietly in the bone marrow and blood. They go outside the marrow, and some end up in the semen. And the true rapist was the brother, the one who donated the bone marrow, and not the receiver. Without the alibi of the prison, the brother who received the transplant would have been charged, and the true rapist would have been left free.

I guess there are some cases where microchimeric cells can really change the result of a DNA test. But for now, it's not really studied. I've been contacted by some forensic investigators to learn more about microchimerism, so maybe things will change.

HO: You point out that microchimerism is used for both pro- and anti-abortion arguments, and it's used by "manosphere" influencers to promote ideologies. Why do you think microchimerism research is so open to interpretation and used in this way?

LB: Next time you're at a dinner, just try to explain microchimerism. You're a science journalist, right? Well, usually when you tell the story you're working on, people are saying, "Oh, yeah, OK." And they just turn to another conversation. If you try mentioning microchimerism in your next dinner, then you'll see. Everyone will try to make some hypothesis, some connection; some will be moved that it's possible to keep some cells from an unborn child or a lost child. Some will be disgusted by the idea that they keep cells from their mother, like having their mother on their shoulder all the time. It's really the first time as a science journalist I experienced such resonance with a story I was working on among people around me, people who are really not into science.

As soon as the door opened, it revealed the fears and the desires of people. So yes, some conservatives use microchimerism to fight against abortion because they say the cells from those aborted will haunt the women for the rest of their life. [But] I've met scientists explaining that if you receive a shot of cells of fetal origin, it can also help you to regenerate your organs. It can be used also by some other people to rejuvenate, to try to stay young.

It's because it's such a new field and you have such open questions, there's room for many interpretations, many hypotheses. I mean, that's fine; that's how science works. You should always have hypotheses and try to answer your hypothesis with new experiments. But it's true that sometimes I didn't know how to handle all those ideas at the beginning. Then I realized it was like a window open on the intimate — their fears and their desires — and it reveals what they really think about their connection to the world they are in. From a sociological point of view, it would be really interesting to study that.

HO: In the book, biologist and evolutionary theorist Amy Boddy warns that microchimerism researchers love to hypothesize. When the implications of the field are so far-reaching, how do we get past this? Which hypothesis do you find most intriguing?

LB: Many scientists told me that until 2021 or something like that, there was this hypothesis that those cells could come from another generation than the mother. We knew that the mother would give cells to the fetus and the fetus could give cells to the mother, but then people ask, because the mother can still carry cells from her mother, maybe she could pass those cells to the fetus. Until the 2020s, scientists were thinking, "Well that's a crazy hypothesis; that can't happen." There could be only a few cells that won't go through the placenta and integrate with the new fetus — until one scientist proved that a newborn can carry cells from the grandma.

In this field, you always have crazy hypotheses, and I guess until we haven't proved that this hypothesis is wrong, you can still leave the hypothesis on the table. One of the craziest hypotheses, the first time I encountered it, I thought, "OK, they've gone really too far."

This hypothesis is that we could inherit cells from our sexual partner. I thought it was not possible because I thought the semen was full of spermatozoa, that they are only like half cells having only half chromosomes, so they cannot survive. But actually in semen, you have a lot more cells than spermatozoids — you have immune cells, for example.

There are many cells in the semen, and we can think that if you have some, there could be some path for those cells to escape and go into your blood. It's not completely crazy. For now, there's no formal proof of this new source of microchimerism, but I recently heard that some scientists are working on the topic on mice.

We should be careful about those interpretations. But I think scientists are not the ones who should care about this interpretation; otherwise, they would prevent themselves from doing their research. They should open all the doors with all kinds of hypotheses. If we do it in a scientific way, meaning if we try to answer a hypothesis with good experiments, then I think everything is fine. You will never prevent people around you from using this information to distort the facts and tell another story. That's how life goes.

HO: What do you think the most promising use for microchimerism research will be over the next 10 to 20 years? How do you see it unfolding?

LB: I guess it will be in the regeneration field. We have discovered that those cells can participate to regenerate tissue. Some scientists around the world are doing clinical studies to see whether we could use these cells as a therapy either after an infarctus [heart attack], but also a vascular accident [stroke] or when you have a wound on your skin. The hope is that by either attracting microchimeric cells that are within our bodies, or injected, these microchimeric cells maybe can help this kind of tissue to repair. I think that might be one of the promising uses of these cells in the future.

Maybe also in the transplantation field; maybe we can think about using the knowledge of how microchimeric cells can induce tolerance to avoid [immunosuppressive] drugs. When you receive the transplant, you need to take drugs [that suppress the immune system] for the rest of your life, and those drugs are like really strong drugs. If we can use microchimeric cells before the transplant to allow better tolerance, then we could either not use any drugs or maybe use less drugs. That would be really interesting, too.

This interview has been condensed and edited lightly for clarity.

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People who are the exact same chronological age can undergo very different molecular changes as they grow older, a new study finds.

"Molecular aging is dynamic and unique to each person," said study co-author Julia El-Sayed Moustafa, a computational genomics researcher at King's College London. Even if you and your friend were born the same day, the activity of some of your genes might ramp up while the same genes in your friend dial down. The same is true for metabolites, which are small molecules produced during the body's chemical processes essential for health.

Genetics, environmental exposures and daily biological rhythms may help to explain some of those differences, the researchers say.

The findings, published Thursday (Sept. 3) in the journal Science, may complicate efforts to capture aging with a single metric. For example, "biological age" scores estimate the body's true cellular and physical health, judging how much "older" it is than your chronological age. Scientists have developed "aging clocks" that use molecular markers, such as chemical tags on DNA, to estimate biological age.

But this new study suggests that "biological aging is less like a fixed score and more like a changing set of molecular trajectories," said Raghav Sehgal, an associate research scientist at the Yale School of Medicine who was not involved in the new research. "No single number can fully capture the many systems that age at different rates," he told Live Science in an email.

More than a snapshot

In the study, researchers followed 335 women ages 32 to 80 from the long-running TwinsUK cohort for eight years. The cohort includes identical and fraternal twin pairs, along with detailed health and biological data gathered to investigate how genetics and environment can influence health.

Each woman had at least three clinic visits between 2009 and 2017, with a median of six years between their first and last visits. At each visit, researchers took blood samples and measured gene activity and levels of metabolites.

"Most aging studies take only a 'snapshot,' comparing different people at one point in time," El-Sayed Moustafa said. "In this study, we have multiple measurements, so we can see how gene activity and metabolite levels change over time within the same person."

Of more than 16,000 genes and 915 metabolites analyzed, 5,061 genes and 181 metabolites changed significantly over time. Of those genes, the vast majority — 5,036 — showed a consistent increase or decrease across the group. The same was true of 45 metabolites.

Many of these genes were involved in pathways linked to immune function, metabolism and age-related conditions, including heart disease and neurodegenerative disorders.

That said, "even when most people's genes or metabolites moved in one direction, we still found groups moving the opposite way," said study co-author Kerrin Small, a professor of genomics at King's College London. So even if, on average, certain genes' activity trended in the same direction, there were individuals who broke from the pattern.

Among 136 metabolites, for example, the levels changed from person to person. A metabolite that increased in one woman could fall in another, while some showed little change over time. One consistent pattern was that each woman's overall metabolite profile also became less similar to her earlier profile.

What might shape those changes?

Several factors appeared to shape these molecular changes. Identical twins tended to have more similar gene-expression patterns than fraternal twins did, suggesting that genetics plays a strong role. Different immune cell types also showed distinct patterns of gene activity with age, suggesting age-related changes in the immune system are not uniform.

The molecular signals also varied with the time of day and season in which the blood samples were collected. About a quarter of the genes and metabolites showed seasonal shifts, including changes linked to energy production and immune activity, while up to 40% of the metabolites varied with the body's 24-hour internal clock.

The researchers also found an unexpected decline in blood levels of per- and polyfluoroalkyl substances (PFAS), including PFOA and PFOS. Often called "forever chemicals," PFAS are synthetic compounds used in a variety of products, such as nonstick cookware and food packaging. Their decline in the study was likely due to restrictions on their use in the U.K., the study authors suspect. Blood levels of PFAS were also associated with changes in some genes and metabolites, although the study could not show that the chemicals themselves caused those changes.

The team found more than 100,000 associations between genes and metabolites, suggesting that changes in certain genes go hand-in-hand with changes in specific metabolites. This highlights how interconnected the body’s biological processes are and how complex aging really is.

"I would not call aging unpredictable, but it is certainly more individualized and context-dependent," Sehgal said. Understanding these individual trajectories could one day help researchers distinguish healthy aging from molecular changes linked to disease, but that application is still a long way off.

The study was observational, included only women and relied solely on blood samples, so larger and more diverse studies are still needed to see whether these patterns hold in broader populations. The researchers now plan to track molecular changes over about 15 years, up from eight in the current study. In the future, Sehgal suggested, aging assessments could combine broad, biological-age scores with more personalized measures of immune, metabolic, brain and cardiovascular aging.

Chemotherapy can save lives, but for many cancer patients, it leaves behind a painful legacy: damaged nerves that burn, tingle or go numb. Now, researchers report that a psychedelic compound may protect those nerves — not through its mind-bending effects, but by helping neurons keep their internal power supplies moving.

A new mouse study, published Thursday (Sept. 3) in the journal Science, suggests that psilocybin, the psychedelic compound in "magic mushrooms," may help prevent this painful and sometimes permanent side effect of chemotherapy, known as chemotherapy-induced peripheral neuropathy (CIPN).

In experiments in mice, psilocybin prevented nerve damage from CIPN that can cause pain, numbness and heightened sensitivity to cold and touch. Two doses of the drug given prior to chemotherapy garnered protection that persisted through as many as six rounds of the cancer treatment, according to the study.

CIPN affects roughly one-third to one-half of people receiving certain chemotherapies, said Dr. Thomas Strouse, a professor of clinical psychiatry and a neuropathy researcher at UCLA who was not involved in the study. In severe cases, the neuropathy can force doctors to reduce or stop chemotherapy. It can also contribute to mobility problems, which raise the risk of falls and fractures.

"It's a big deal, big problem," Strouse said. Researchers have been searching for a way to prevent it for a long time, he added.

Keeping nerve cells fueled

Initially, the researchers weren't looking for a neuropathy treatment, said study co-author Dr. Moran Amit, a cancer surgeon and researcher at The University of Texas MD Anderson Cancer Center. His team was investigating whether compounds that promote neuroplasticity — the nervous system's ability to change and adapt — might protect nerves and improve existing cancer treatments.

After testing several psychedelic compounds, they "very early on focused on psilocybin because this was the most effective one" for relieving neuropathy symptoms, Amit told Live Science. The psychedelic has been explored as a treatment for psychiatric disorders such as depression, in which it might promote "hyperconnectivity" between certain brain regions.

In the new study, protection against CIPN emerged as an unexpected effect of the drug.

To investigate how that protection worked, the researchers studied mice treated with cisplatin, a chemotherapy drug known to frequently cause neuropathy. Two doses of psilocybin — given nine days and two days before the first chemotherapy session, respectively — completely prevented the mice from developing hypersensitivity, and it also reduced cold sensitivity and preserved nerve endings in the skin.

The team then ran experiments using human sensory neurons and peripheral nerves that had been removed during surgery. These analyses pointed to a possible explanation: a process called mitochondrial trafficking.

Mitochondria generate the energy that cells need, but neurons present an unusual logistical challenge. Some peripheral nerves extend over enormous distances, so their mitochondria must be transported along structural tracks, called microtubules, to reach far-flung nerve endings. That in itself is an energy-intensive process.

Amit compared those microtubules to a railroad system: Chemotherapy can damage both the mitochondria themselves and the tracks they travel along.

In further experiments with human neurons, the team found that cisplatin depleted mitochondria and ATP (adenosine triphosphate) — cells' main energy currency — from the wires that extend from nerves. Psilocybin didn't restore the mitochondria's overall energy-producing capacity. Instead, it preserved their ability to travel and maintained their normal levels of ATP production, specifically within the nerve projections. That suggests the drug may help keep energy supplies where they're needed most.

The effect depended on the serotonin receptor 5-HT2A, which is responsible for many of psilocybin's psychedelic effects as well. Intriguingly, a compound called TBG — designed to activate 5-HT2A without causing hallucinations — also protected mice from neuropathy.

However, Amit cautioned that psilocybin's psychedelic effects may also be playing a neuroprotective role that we have yet to understand, so it's unclear if the effect should be avoided in humans.

A long way from patients

Strouse noted that mitochondrial damage in CIPN isn't a new idea. "What's novel is looking at psilocybin as a protectant," he said.

He also cautioned that different chemotherapy drugs may cause neuropathy through distinct mechanisms, so the protection demonstrated against one chemotherapy drug may not translate broadly.

Most importantly, the researchers have not shown that psilocybin prevents neuropathy in humans yet.

"The main thing is that it was never tested for this indication specifically in a systematic way in humans," Amit said. His team is now preparing a clinical trial at MD Anderson to test the approach. The research is part of MD Anderson's Cancer Neuroscience Program, a multidisciplinary effort that studies interactions between cancer and the nervous system, with an emphasis on improving patients' quality of life.

Human trials will need to establish both the effectiveness and safety of using psilocybin for this purpose, Strouse said, particularly before oncologists would consider giving a psychedelic drug alongside cancer treatment.

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

With only a couple of months to go before the harvest season for winter wheat in Colorado, the crop faced a whiplash: After a warm, dry winter, a cold snap plunged the plants into freezing weather for 12 hours, and temperatures soared to nearly 90 degrees Fahrenheit (32.2 degrees Celsius) two days later. When the final harvest numbers were tallied in July, 73% of the crops were in poor or very poor condition. According to early estimates by Colorado Wheat, 2026's winter wheat crop was the smallest in the state since 1965.

Pick a crop, any crop, and you'll hear a similar story: Extreme weather and climate change are rocking the food supply. The warming climate makes food less nutritious, threatens crop survival, and triggers tipping points that would upend farming as we know it.

The impacts will be felt most intensely in less-developed regions of the world, where many people can't afford imported food and climate-related famines and nutritional scarcity are already happening.

But the U.S. is facing big changes to its food systems too, and no one is immune. Humans have overcome looming agricultural disasters before, but experts say the challenge should not be underestimated.

"There are real food security and nutrition concerns," said Andrew Hultgren, an environmental economist at the University of Illinois, Urbana-Champaign, "especially under these high-warming futures."

Food is becoming less nutritious

As the planet warms, food crops are expected to become less nutritious. That's because, due to plant biology that's not yet fully understood, crops grown under higher levels of carbon dioxide are deficient in zinc, protein, magnesium, iron and other micronutrients. Crops are already less nutritious than they were in the 1950s, but this is partly due to breeding decisions that prioritize yield over nutrition. The carbon dioxide deficiencies will exacerbate this nutrition decline.

The global monthly average concentration of carbon dioxide in the atmosphere is now over 420 parts per million (ppm), well over the preindustrial average of 280 ppm. By the end of the century, those levels will increase to at least 550 ppm in all but the most optimistic scenarios.

That will mean an additional 175 million people will be zinc deficient and an additional 122 million people will be protein deficient by 2050, a 2018 study found. Zinc deficiency has consequences for immune and skin health and may lead to poor growth in childhood; protein deficiency can also cause stunted growth as well as fatigue, muscle weakness and stress fractures. Those figures account only for the effects of carbon dioxide. A cascade of climate shifts and extreme weather may also affect the number of nutrients (and calories) available to the world.

The threats are myriad: Rising sea levels may inundate farmland and lead to saltier soil in coastal regions where, for example, rice farming is common. Soil salinity can make it impossible to grow crops in some regions. Droughts, heat waves, storms or temperature swings like those seen in Colorado this year might take out certain crops in particular places, leading to year-by-year price spikes or shortages. In the U.S., the results might look a lot like the recent egg shortages triggered by bird flu; temporarily empty shelves, price spikes, or even restrictions on the amount a customer can purchase in a visit for an affected food.

Climate shifts that harm pollinators and fuel the spread and introduction of plant pathogens such as harmful fungi will also likely reduce crop yields.

Areas that depend on the ocean for food are also facing steep challenges, due to both ocean acidification and the degradation of coral reef ecosystems, which are sources of food for many coastal communities and form much of the base of food chains for the larger fish people eat.

Hotter weather also affects food safety, said Christopher Golden, a professor of nutrition and public health at the Harvard T.H. Chan School of Public Health.

"Increasing sea temperature and increasing sedimentation within seas could lead to harmful algal blooms or increasing food poisoning events from temperature-related food spoilage," Golden said. Algal blooms can contaminate shellfish like oysters or scallops with neurotoxins that can sicken and kill people who eat them. Food spoilage is a concern in regions such as Madagascar, where catches are brought ashore and readied for consumption in the open air.

Meanwhile, fish may move poleward to avoid the hottest sea temperatures, leaving the most vulnerable regions ‪—‬ such as Southeast Asia, the Caribbean, Africa, Central America and the Pacific ‪—‬ with fewer fish in their waters. How bad this looks depends on the extent of the climate swings, with research suggesting that without any mitigation, fishers could see their catches decline by 58% to 92% off small islands in the Pacific and by 70% to 86% in Southeast Asia. This would drive food insecurity and malnutrition in those regions. The U.S. will likely face impacts too, as most of its seafood is imported from subtropical or tropical waters elsewhere.

There may be shifts in trade networks that lessen the blow for U.S. consumers, Golden said, but it's hard to predict. Some possibilities include "price shifts or trade shifts that lead to changing dietary patterns or more shelf-stable and heavily processed items that we know aren't good for your health," he said. In other words, less fresh-caught snapper and more potted meats.

Changing foods on the table

Individual producers are adapting, sometimes in ways that may not be immediately obvious to consumers. "Climate change is bad in that it's a slow-moving wave," said Elizabeth Wolkovich, a professor of forestry at the University of British Columbia. "You don't really notice that it's shifting underneath you and that the apple you eat isn't the apple your granddaughter will eat."

On that note, growers in the Pacific Northwest and U.S. Northeast will face challenges getting apples to lunch boxes around the world. Fewer cold days and more extreme-heat days will likely reduce apple yields by affecting how and when trees go dormant and bloom. Because it takes five or more years to establish fruiting trees in new regions, this could mean a reduced apple supply and higher prices.

Today's smooth arabica coffee (Coffea arabica) varieties may get harder to find and more expensive as climate change forces coffee growers out of many of the places they used to farm and droughts reduce supply. Earthier, more bitter robusta coffee beans (Coffea canephora) do better in warming temperatures, but even those beans could struggle with increasing seasonal variability caused by climate change.

Climate has already shifted wines in favor of less-acidic and higher-alcohol varieties, Wolkovich said, but it's happened slowly enough that, unless you're a connoisseur, you may not have noticed. Wine lovers can expect more changes: Wolkovich has found that the varieties of wine grapes that growers can produce will shift with climate change. Wildfires in grape-growing regions like California can also produce an unpleasant acrid and smoky flavor in wine.

And it's not just flavors that will be affected. U.S. dairy cattle breeds originated in cool and cloudy Northern Europe, and their milk output goes down as temperatures climb. Such heat stress reduced annual milk yield by an average of 1% a year between 2012 and 2016 alone, and heat-related losses are expected to balloon by 30% by 2050.

Americans have long been drinking less milk from the glass, but their demand for yogurt and cheese is rising, said Jared Hutchins, an assistant professor of agricultural and consumer economics at the University of Illinois Urbana-Champaign and first author of the study on milk yield. Those products depend heavily on the fat and protein content in milk, which is the first thing to drop when cattle are hot. "Fat and protein are what deliver the cultured dairy products that are in high demand," Hutchins told Live Science.

The story repeats itself across agricultural products, Hultgren said. "For each degree of that global temperature rise, caloric output [from crops] drops by 120 kilocalories or U.S. calories per person per day," he said, "which is about 4.5% of a person's daily recommended caloric intake."

That calculation, published by Hultgren and his colleagues in the journal Nature in 2025, already accounted for adaptations that farmers can make to reduce crop losses. Without those adaptations, the number would be over 30% higher, he said.

Reductions in available calories will translate to food shortages in vulnerable places, such as the Horn of Africa or India, said Marina Romanello, executive director of a multinational research project that tracks the impacts of climate on health at University College London. In North America, "it would feel like inflation," Hultgren said ‪—‬ yet another factor driving up grocery prices.

Worst-case scenarios

For farmers, the year-by-year uncertainty of climate change is a problem. Will this year bring drought? Will there be a sudden storm or flood that will wash away the spring crop? Should they take a risk on a new heat-resistant plant or agricultural technique?

Similar uncertainty haunts the long-term forecast. Climate tipping points can lead to sudden, irreversible changes in the system. For agriculture, one of the scariest tipping points is the potential collapse of the Atlantic Meridional Overturning Circulation (AMOC). This pattern of ocean currents brings warm surface water north from the equator and circulates cold water south, warming Northern Europe and the northern parts of North America and cooling the Southern Hemisphere.

If this current were to collapse, northwestern Europe would cool dramatically, with studies suggesting that London could see temperature lows of minus 4 F (minus 20 C) ‪— ‬colder than the city's lowest temperatures on record. Precipitation would decline across Europe, leading to drought. Meanwhile, in the Amazon, the wet season could become the dry season and vice versa, said René van Westen, a climate researcher at Utrecht University in the Netherlands who has studied the impacts of an AMOC collapse.

On the other hand, if the AMOC doesn't collapse, London is expected to warm by 4.9 F (2.7 C) and see 15% to 18% more precipitation, depending on the season. The uncertainty in these predictions makes preparations difficult. There is still a lot of controversy over whether the AMOC will collapse and, if so, when. Should farmers plan for England to become increasingly toasty, or should they expect it to be plunged into a little ice age?

AMOC-related changes will take decades to centuries to unfold, even with a total collapse, van Westen told Live Science. But even so, they would require a total rewriting of agriculture in Europe and the northeastern U.S. "It will be very challenging to adapt to such a scenario," he said.

That doesn't mean a collapse of the world food system is inevitable. Farmers are already adapting to the early impacts of climate change by scaling back water-hungry crops in drought years and, in some places, testing new, heat-resistant varieties of crops in an attempt to stem the losses.

And humans have overcome looming disaster in agriculture before: In the 1950s and 1960s, new varieties of rice and wheat, along with the availability of synthetic nitrogen fertilizers, spurred the "Green Revolution," tripling the world's yield of cereal crops while expanding farmland by only 30%. Similar innovations could limit hunger even as the world warms.

But the biggest way to mitigate these impacts is the most obvious one. While Hultgren and his colleagues found that adaptation could cut caloric losses under climate change by 30%, mitigating warming by reducing emissions today could slash them by half. Similarly, the AMOC is on a path toward weakening, van Westen said, but as long as humans slow the pace of climate change, the current can recover.

"If you are cutting your emissions," van Westen said, "you can lower your risk."

Burning up — How can we adapt to a warming world?

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A fruit fly's brain is roughly the size of a poppy seed — and yet that tiny package contains over 100,000 neurons. A new map charts every single neuron in the male fruit fly brain, as well as the insect's equivalent of a spinal cord, totaling more than 166,000 neurons.

This new map joins a map of a female fruit fly brain that was unveiled in 2024 and covers about 140,000 neurons. These two wiring diagrams, also called "connectomes," can now be compared to see if there are differences between the sexes' brains that help to explain behavioral differences reflected during mating or in aggressive actions, including sex-specific fighting moves.

"It is the first time we can compare both sexes of an animal with complex social behavior," study co-author Gerry Rubin, head of biology and a senior group leader of the Howard Hughes Medical Institute's Janelia Research Campus, said in a statement. "Male and female flies have a lot of differences in their behavior, and neuroscientists want to understand how the brain controls those behaviors. This now allows us to easily home in on the neurons that are causing those differences."

Initially released as a preprint, the new fly brain map was published in the journal Cell and Current Biology Thursday (Sept. 3). The study describing the map was published alongside three other papers, each of which uses the new data to explore a specific aspect of fruit fly neurobiology.

"The fly nervous system performs remarkably sophisticated computations with relatively few neurons and little energy, and its architecture could suggest principles for designing more efficient artificial systems," said Carlos Ribeiro, a principal investigator at the Champalimaud Foundation in Lisbon, Portugal, whose team contributed to the brain map and led one of the related studies.

"This work also provides a technical roadmap for more ambitious connectomics projects in the future, such as those for mice and humans," Ribeiro said in a separate statement from the Champalimaud Foundation.

In the near term, the scientists aim to map the brains of larval zebrafish (Danio rerio) and adult danionin fish (Danionella). In the long run, the goal of this research is to understand how vertebrates' brains enable complex behaviors, and then use that knowledge to help unravel the basis of neurological and psychiatric disorders in humans.

The study led by Ribeiro and other Champalimaud Foundation scientists aimed to map the circuits in the fly brain dedicated to the insect's sense of taste. Fruit flies have taste receptors in many body parts, including their legs, wings, mouthparts and inside of the throat. The researchers identified these taste receptors and traced their connections back to the fly brain. From there, they examined how those circuits interacted with those that govern behaviors such as swallowing or walking. When it comes to eating behaviors, this circuitry helps the fly determine whether a given morsel is safe or harmful and ultimately choose whether to eat it, the researchers concluded.

This diagram of taste processing is a "hypothesis-generation tool," study co-author Inês de Haan Vicente, a research technician in Ribeiro's lab, said in the Champalimaud statement. "Suppose you are interested in how taste controls locomotion. Now you can go to the map and ask: which sensory neurons are connected to the neurons controlling locomotion? Which intermediate neurons should I manipulate? It gives you a place to start."

The other two papers published alongside the map respectively explore the circuits behind vision processing in the fly brain and sex-specific differences in male and female fly brains. The first showed that visual processing extends deep into the brain, involving more than half of the 11,000 or so types of neurons identified in the map. The latter study found a network of cells that's specific to the male brain and appears to coordinate male-specific behaviors, such as specific aspects of fly courtship and physical aggression. (For example, female flies tend to headbutt while males lunge at their targets.)

While there were some networks specific to each sex, the circuits for sensation and movement are largely shared between males and females, the research found. At times, specific switches within those circuits reroute signals to different destinations in the male and female brain; the consequences of that rerouting will be a focus of future investigations.

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

The patient: A 47-year-old woman in Canada

The symptoms: The woman underwent a lung transplant to treat interstitial lung disease, which involves harmful inflammation and scarring of lung tissue. While recovering in the hospital, she ate a bowl of breakfast cereal, which activated a nearly two-hour episode of flushing, itching, shortness of breath and low blood pressure.

This severe, life-threatening allergic reaction is known as anaphylaxis. A report of the woman's case does not mention specific treatment she received for this reaction, but it notes that it resolved after two hours.

(Treatment for anaphylaxis involves epinephrine (also called adrenaline), and it can also require antihistamines, cortisone, oxygen and beta-agonists, such as albuterol, which help improve breathing.)

What happened next: The woman experienced the same symptoms in the weeks after being discharged from the hospital — after eating a coconut cream pie and after having an almond candy bar.

The diagnosis: Two months after her lung transplant, the woman underwent a skin-prick allergy test, which revealed a sensitivity to peanut and pine nut allergens. She did not have an allergic response to tree nuts, such as the almonds in the candy bar, nor to coconut. None of the foods that triggered her symptoms were known to contain peanuts, but none were certified as peanut-free, either.

Notably, the woman's lung donor had been a 12-year-old boy with a known peanut allergy but no history of anaphylaxis. Her doctors theorized that the transplanted lung tissue contained immune cells from the donor that were sensitized to nut allergens.

The treatment: The woman did not receive a specific treatment to get rid of this new allergic response. However, the sensitivity subsided in follow-up skin-prick tests, and they had disappeared completely by a year after her surgery. She ate peanuts in a supervised setting a few months after the one-year mark and had no reaction.

The doctors reasoned that the sensitized immune cells from the donor must have cleared from her body.

What makes the case unique: Only one other case of peanut allergy following a lung transplant had been documented before the woman's case was published in 2011.

Scientists had only recognized the risk of allergies being passed from organ donors to recipients a little over a decade before the report, according to a 2025 review of such instances. Doctors had previously reported allergy transfer linked to bone marrow transplants, which makes sense given that bone marrow produces immune cells. But the first known donor-acquired allergy from a solid-organ transplant was observed in 1997 following a combined kidney-liver transplant from a donor who was allergic to peanuts.

The authors of the 2025 review noted that donor-acquired allergies are more commonly associated with lung and liver transplants than with transplants of other solid organs. That could be because these organs are rich in a type of immune cell that produces allergen-specific antibodies, called B lymphocytes.

Other potential culprits for donor-acquired allergies are mast cells and basophils, two types of immune cell that bind to those allergen-specific antibodies. The cells hold onto the antibodies, and when they encounter an allergen, they release the inflammatory compounds responsible for anaphylaxis.

In the woman's case, a blood test for peanut-specific antibodies came back negative. This suggested that her body was not continually generating the antibodies. That could serve as possible evidence that her reaction was caused by antibodies bound to mast cells or basophils within the donor tissue, rather than antibodies produced by lymphocytes.

That said, the woman's reaction to the skin-prick test could imply that lymphocytes were still involved in the allergic reaction, the doctors added, as they did not know whether mast cells or basophils could migrate to the skin the way circulating antibodies could.

Regardless of the cell type behind the woman's peanut allergy, the sensitivity faded after a year, consistent with other cases described in the 2025 review. Still, the review authors called for better donor allergy labels to inform allergy testing and treatment for organ recipients. The doctors in the case report came to a similar conclusion, noting that detailed donor allergy histories and skin-prick testing after organ transplant could help identify donor-acquired allergies.

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.

Football is a high-impact sport. A player may take hundreds of hits over the course of their career, including some that cause concussions. Other impacts may seem minor at the time, but there are concerns that repeated head blows can negatively impact long-term brain health.

Those worries gained new attention after a recent study estimated that at least 25% of recently deceased NFL players had chronic traumatic encephalopathy (CTE). CTE is a degenerative brain disease linked to repeated head impacts. Although the study doesn't necessarily mean that 25% of current NFL players have CTE, it does add to the growing evidence that repeated hits may carry serious consequences.

The NFL has taken steps to reduce those risks, including strengthening concussion protocols and investing in safer equipment, like Guardian Caps. But are those measures enough? With new research continuing to shed light on CTE, we want to know what you think. Weigh in via our poll below, and let us know your thoughts in the comments.

Yellow fever is appearing in regions that haven't seen cases of the disease in years, largely as a result of climate change.

Historically, the virus ravaged cities across the Americas, Europe and Africa, until a vaccine was introduced in 1937 and its range shrunk significantly. But now, as climate change creates favorable conditions for virus-carrying mosquitoes, scientists are seeing outbreaks in unexpected areas.

"Yellow fever is a highly deadly disease," Dr. Joelle Ivy Rosser, an infectious-disease researcher at Stanford University, told Live Science, "so any environmental pressures that increase the likelihood of future yellow fever virus outbreaks … is highly concerning."

How is climate change contributing to this pattern, and could it get worse in the future?

How rising temperatures impact yellow fever

Yellow fever is a mosquito-borne disease caused by the Orthoflavivirus flavi virus, better known as yellow fever virus (YFV). The infection causes fever, muscle aches, headaches and vomiting. About 15% of cases become severe, with patients showing jaundiced skin and eyes, bleeding from the mouth, eyes, nose and stomach, or organ failure.

Devastating yellow fever epidemics spread in the 17th to 19th centuries, before the development of a vaccine. Nowadays, an estimated 31,000 to 82,000 yellow fever deaths occur each year; severe cases have an estimated fatality rate of 20% to 50%.

Most yellow fever infections are a result of spillover from nonhuman primates; mosquitoes bite monkeys that carry the virus, such as howler monkeys, and then the infected mosquitoes bite humans. Several types of mosquitoes carry the virus, but the species Aedes aegypti is the main vector for yellow fever in cities, where high population density can make outbreaks especially severe.

Although there is an effective vaccine for yellow fever, cases have been on the rise in the past three decades. This led the World Health Organization (WHO) to set out a strategy in 2017 for eliminating yellow fever epidemics by 2026 through outbreak prevention and containment.

Climate-change-driven warming and extreme weather events may have heightened yellow fever risk over the past few decades, experts say. Rising temperatures make mosquitoes bite more because heat makes their metabolisms more active, said Dr. Seth Judson, an infectious-disease physician-scientist at UCLA. Warming also cuts down the virus's extrinsic incubation period, meaning the time it takes for the virus to replicate in a newly infected mosquito and then get passed on to another person, he told Live Science.

Weather patterns and deforestation

Changing weather patterns play a role, too. In 2017-2018, Brazil saw its first yellow fever outbreak in a city in almost a century. That outbreak, primarily in Belo Horizonte and São Paulo, was likely a result of drought, according to one study.

While heavy rainfall creates a breeding ground for mosquitoes, in this case, drought pushed forest-based mosquitoes — as well as YFV carriers like marmosets and howler monkeys — closer to cities as the animals searched for water. Drier conditions can also prompt dehydrated mosquitoes to bite more as they search for fluids, study co-author Jamie Caldwell, a disease ecologist at Princeton University, told Live Science.

"Extremes of weather in either direction" — very wet or very dry — "can exacerbate mosquito-borne disease transmission," Rosser said.

Parts of Africa and South America that were considered low-risk for yellow fever have already been seeing new outbreaks, Judson said, so maps of yellow-fever-affected areas have had to be updated. In research that's been released as a preprint but not peer-reviewed yet, Judson found that yellow fever is reemerging in an area of the Colombian Andes where it hadn't been reported since 1940.

Experts are paying particular attention to the edges of cities, where urban centers meet the forest. The risk of yellow fever transmission from monkeys to humans via mosquitoes is rising at these edges due to both climate change and deforestation.

"Humans are expanding the agricultural frontier and encroaching on forests where yellow fever mosquitoes … are found," Gabriel Parra-Henao, a biologist with the WHO, told Live Science in an email. "[This] results in more people being exposed to their bites."

Similar patterns have been seen with other mosquito-borne infections, such as malaria.

Could yellow fever return to the U.S.?

Climate change is expected to bring yellow fever to new areas. One study predicts that, under the most severe climate change scenario, nearly a billion people could face their first exposure to the mosquitoes that can carry YFV in the next century. While that worst-case scenario may not be the most likely, the mosquitoes' ranges are still expected to expand under less-severe conditions.

Europe is predicted to face the largest increase in exposure to Ae. aegypti mosquitoes compared to the rest of the world, and the U.S. and Canada are predicted to see increases too. In the U.S., the mosquito species already lives in a number of states, including Florida, Mississippi, Arizona and New Mexico. However, warming would increase the chances of mosquitoes surviving in locations further north, such as Philadelphia and New York, which suffered major yellow fever outbreaks in the past. One model predicts Ae. aegypti could spread as far north as Chicago by 2050.

Although the mosquito lives in the U.S. already, yellow fever cases are exceedingly rare within the country because the virus is not present in local populations. That's because of an international campaign that the U.S. spearheaded in the 20th century, which involved researching YFV, eradicating mosquito breeding grounds, and vaccinating people widely.

"If yellow fever virus reestablished itself in our local Aedes aegypti population, then that would be very concerning," Rosser said.

One way yellow fever could return to the U.S. would be via people carrying the virus home with them after traveling to regions where the disease regularly circulates. Local mosquitoes could then catch the virus by biting those infected people, and then pass it on to others.

For local transmission to take hold, "there needs to be significant numbers of infections [passed to locals], and infections among travelers," Judson said. "But … it's in the realm of possibility."

With climate change driving resurgences of yellow fever in more places, and more regions of the U.S. becoming hospitable to the mosquitoes, that reintroduction scenario may become more likely. But some scientists think that even if North American cities saw yellow fever outbreaks, the outcome would likely not be devastating. Infrastructure in wealthier cities could be the difference between a disaster and a manageable health concern.

"There's access to medicines and vaccines; we pipe water to our homes, so we don't have standing water around," Caldwell said. "So it is a concern, but it's never going to be the next COVID."

Other experts noted that diligent surveillance of yellow fever infections can help public health officials prepare. In places where yellow fever is circulating in forest primates, forest conservation can limit contact among humans, wildlife and the mosquitoes that spread diseases among them. It's also crucial to make vaccines widely accessible to people who live in the virus's endemic regions and to travelers who visit those regions.

The WHO's yellow fever campaign is set to conclude at the end of this year, and its next steps are unclear. There's ongoing discussion of what comes next, Judson said, with questions about whether the control of yellow fever outbreaks will rely more on national strategies than on international coordination via the WHO.

Whatever happens, this is a time for heightened awareness of the virus, Judson said.

"We think of yellow fever as this historic disease," he said. "I think many people don't realize that we're still seeing significant yellow fever outbreaks. … It's really important to be aware of the risks and think about how we prepare for that."

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

Of the former National Football League (NFL) players who died in recent years, at least 25% had brain changes related to chronic traumatic encephalopathy (CTE), a new study suggests.

The study, published Aug. 25 in the journal The BMJ, examined donated brain tissue from 338 former NFL players who died between 2008 and 2021. A total of 1,712 former players died in that time frame, so the analysis included only about 20% of the players' brains that could theoretically have been examined. Then, the researchers used that subset of brains to estimate the likely prevalence of CTE in the overall group.

Among the donated brains, over 93% showed physical signs of CTE, meaning an accumulation of abnormal proteins in specific places within the tissue. About 30% had stage IV CTE, the most severe form that comes with the most extensive brain changes.

These physical signs of CTE aren't always associated with overt symptoms, such as cognitive decline, mood and behavioral changes, or dementia. Only about 60% of the individuals with CTE-related brain changes were also diagnosed with dementia in this study. That said, those with stage IV CTE were more likely to have dementia, with 90% having a diagnosis.

Across the full study time frame, the researchers estimated that between 18.5% and 98.7% of the deceased players likely had CTE. Zooming in on the period with the highest number of brain donations — 2016 to 2021 — they estimated the rate to be between 24.5% and 97.7%. That latter time frame was likely the more representative sample, the researchers determined.

What can this study tell us about the CTE risk that current football players face, from youth sports to the professional level? To put the research into context, Live Science spoke with Thayne Munce, an associate professor and director of the Jayhawk Athletic Performance Laboratory at the University of Kansas, who was not involved in the BMJ study. Munce researches brain health and concussion in contact sports, primarily among young athletes. He cautioned that the BMJ study's findings shouldn't be extrapolated to all levels and ages of play, or even to today's NFL players.

Nicoletta Lanese: This study estimated the rate of CTE among this era of NFL players. Was the prevalence surprising to you, or in line with your expectations?

Thayne Munce: It's not surprising to me. This group and their colleagues have published previous work from donors — so these are former players who have donated their brains for research. They have reported even higher rates than 25% among just their donor sample [in this study]. This really high rate — over 90% of CTE cases in the donor group — is in line with what previous research has shown for these brain banks. So that's not terribly surprising.

What's different in this study is they compared the donors over a certain period of time versus all of the deaths among NFL players during that period of time and estimated the range based on how representative that donor sample was to the overall group of NFL players.

For example, if players just randomly selected to donate their brain to the brain bank and then they found that 98% of all of their samples had CTE — if that's representative of all the players from that era, then that's where you get the higher estimate. But if the majority of players that actually had CTE were the only ones who donated their brains because maybe they were showing outward signs or symptoms of dementia or cognitive decline or behavioral changes while they were living, then it becomes a very highly biased sample.

So that's where you get this big range. [The true prevalence] really depends on how representative that donor sample was to the peer group of players from that era.

NL: Does that broad range of estimates make it difficult to pin down the risk for current players?

TM: I think even more problematic than that big range is to understand that this is a historical study.

So these were players who died between 2008 and 2021, and the average age, I believe, was a little over 70 years of age. So if you extrapolate backwards, they probably played in the NFL starting around age 21 or 22 or 23 — that puts their playing days back in the '60s and '70s. So these were players who played in the NFL predominantly in the '60s and '70s, and would have played college and high school football in the '60s and '50s.

This is a different era of football. So we should not be making any estimations about what current CTE rates are based on this study, because a lot has changed in 50 years. It [the CTE rate] could be the same. It could be greater. It could be less. We really don't know.

I suspect, based on improvements in protective equipment and rules and advances in sports medicine, that the risk is likely lower. I don't have evidence that that's the case, but nobody does. We don't really know how the rates today compare to in the past, since CTE can't be diagnosed in the living. We can't take a sample of current players and look to see how many of them have CTE.

But that is the challenge of this study. It's interesting [in that] it gives us a range of what CTE may be in that group of former players. But it doesn't give us a lot of information about what rates are in current players in the NFL. And even more so, whatever the CTE rate is in professional NFL players does not translate to former collegiate, high school or youth football players, because CTE is an exposure-related disease. For players who have less exposure to these repetitive head impacts, it should follow that they have a considerably lower risk of CTE.

We don't want to confuse a range of CTE prevalence from players who played 50 years ago with contemporary NFL players and definitely don't want to conflate that with what CTE rates may be for current high school and youth players, who have far less levels of exposure.

NL: You mentioned that football has become safer over time. Could you spell out how the game has changed?

TM: We can look at different categories: With the rules back in that era, spearing — hitting with the crown of the head — was allowed, and oftentimes encouraged, as a style of play. That's now penalized and not taught, or shouldn't be taught.

There are changes in equipment, for sure. Modern football helmets — the material, the padding, the way in which these manufacturers are using head impact data to construct position-specific helmets and materials that are designed now to not just prevent catastrophic injuries, like skull fracture, but also to minimize the force from having repetitive head impacts — that's come a long way.

There's the Guardian Caps; you may have seen the NFL has adapted those. So they wear these soft-shell hats on their helmets during the preseason and during practices. That's now required for many of the position groups.

Virginia Tech has a helmet rating system where they test football helmets, and every year, the helmets score better on these tests. They now have star ratings for youth helmets, so manufacturers of youth football helmets are now being held to account, as well.

Maybe the most important thing is just the education around and recognition of concussion and brain injury in the sport. Now, when an athlete has a concussion, they are more likely to be recognized for having a concussion and be pulled from play and have an opportunity to recover before they return to the game. You hear anecdotal stories of former NFL players from that era, like the '60s and '70s, that suffered multiple concussions, oftentimes in the same game, and were not removed from play and continued to practice under those conditions. That medical recognition and treatment management of concussion and brain injury has moved ahead.

You look at the way in which practice was conducted, from full contact, two-a-day practices, which were common even in high school 15, 20 years ago. Now it's really not allowed at any level of play. So the amount of hitting that they do, the amount of contact that players are exposed to in practice and in the preseason is far less.

NL: When players weren't able to recover from concussions, did that likely increase their brain-injury risk?

TM: Theoretically, yes. There's evidence that if the brain is injured and then it's exposed to a second insult or injury before it's properly recovered, that makes the condition even worse.

There's actually a term called "second-impact syndrome," and it's very rare, so I don't want to scare people. But there have been instances where players — it's often, unfortunately, young players, high school players — who have had a concussion which, in retrospect, went undiagnosed and then there was a second concussive blow that led to brain swelling and death. That's the extreme, but there are cases of that [repetitive damage] happening even on a lower scale.

Even if you don't get another concussion, just those nonconcussive repetitive head impacts on top of an injured brain would not be good. It certainly is only going to delay recovery, likely is going to compound your inflammation and all of the downstream consequences of that initial injury.

I suspect that that was fairly common in years past, mainly because concussions generally weren't diagnosed. No one was looking for them, and players certainly weren't encouraged to report if they had the symptoms. So it's very likely that many of these players, including the players that were in the [brain donor] sample, had concussions and played through them and continued to receive additional trauma on top of a brain injury.

Now whether that leads to CTE, we can't really say. But I think it's reasonable to suspect that it probably would increase that risk.

NL: Could you explain whether the physical signs of CTE in the brain tend to come with symptoms, like cognitive decline? Or is the link more nuanced?

TM: So CTE is a neurodegenerative disease that can only be diagnosed by neuropathologists — people that look at slices of the brain and look for particular proteins that are present in certain regions of the brain. [This examination is done after death.] It's a pathological marker. It means that there are changes in the structure of the brain.

The clinical side of that is changes in mood, cognition, behavior, things like dementia or cognitive decline.

Even in the study, they showed that they [the CTE brain changes and symptoms] weren't necessarily linked. Now I believe they showed that for those who had more severe CTE — like the stage IV — that there was a pretty high rate of those individuals who also had subsequently diagnosed dementia. They had these clinicians that looked at the records and diagnosed them. That's a little bit of a limitation of the study: that a lot of the dementia cases were diagnosed after the person had passed away, based on medical records.

To your more immediate point, the presence of CTE: So the presence of these markers in your brain does not necessarily translate into a clinical disease or a clinical diagnosis. There can be signs or symptoms that somebody may have — let's say memory loss or changes in behavior — that may lead someone, like a former football player, to suspect that, "Oh, maybe I have CTE because I played football and I've heard that that's linked with dementia."

That may be true, but it may also be that it's due to old age, or it could be due to genetics or some other condition.

Many of these neurological diseases and conditions can be managed clinically, and there's treatment. There's therapy; there's pharmacological treatments. There's a whole toolbox available for people to seek help. That's, I think, an important message for former athletes or individuals who may be concerned about developing CTE, is to recognize that there is a disconnect between clinical disease and the pathological disease. Just because you have some outward signs or symptoms that doesn't mean that you have CTE.

NL: Since there was a higher likelihood of dementia in the stage IV cases, it seems like there's a stronger link between the pathological and clinical diagnoses at advanced stages. Is that a fair read?

TM: Again, from this study and other studies, just the presence of CTE does not necessarily mean that somebody's mood, behavior, cognition is altered. It seems to be more likely — it seems to be a tighter relationship at the more severe stages, which would kind of speak to what you're talking about. A certain threshold of disease progression seems to be more likely to manifest itself in clinical disease [with overt symptoms].

NL: What should current NFL players take from this study?

TM: I would go back to what we discussed earlier: just understanding the time frame in which the study was performed and when those players were in the NFL. I think we need to be cautious about projecting those rates; it's a pretty wide range of estimates, and it has to do with how representative the sample is. We need to use caution if we are trying to interpret those rates for the current players.

If anything, I think it probably validates all of these efforts that we discussed to try to improve brain health and minimize risk of exposure.

Even if the prevalence is on the low end ‪—‬ that 25% of players who played in the '60s and '70s developed CTE ‪—‬ that's pretty alarming. That in and of itself should get the NFL's attention. Players shouldn't have a 1-in-4 chance or greater of developing this disease.

So let's take steps to reduce that risk — and I think it validates all of the changes that have taken place over the last 50 years. I mean, a lot of them have taken place over the last 10 to 15 years. That's probably the biggest message: to say we were right to do these things and we need to continue to see if there are further opportunities to make the game safer.

Hopefully we've made a lot of progress and current-day rates are much lower than they were in the past. We don't know that, but let's not be idle. Let's continue to push forward to reduce as much risk as possible in a game where you can't completely eliminate the risk. That's something that I think everyone acknowledges; every player has to acknowledge that there is some risk.

NL: Looking forward, what further improvements could be made?

TM: There's a couple of areas that are really in the infancy stages right now. If you think about brain health as a continuum where you would have a disease like CTE on one end and then optimal health on the other end — let's say repetitive head impacts take away from your brain health and tip the scale in favor of developing disease, what are things we can do to tip the scale back in favor of improving brain health?

We know that sleep is really powerful and could learn more about that in and of itself. And what about nutrition? What about pharmacological interventions? Wouldn't it be great if we could develop a medicine, a drug at some point that could be taken preventatively to reduce athletes' inflammation? Really looking into ways in which we can optimally improve brain health as a countermeasure to the damage or the trauma that is occurring.

It's not just football where these treatments could be helpful; it's also with soccer, hockey, other sports and occupations where there is exposure to [head] trauma. I think that's a promising area.

And then, certainly, diagnostic techniques. We talked about CTE only being able to be diagnosed at death. It would certainly be a game changer if we could diagnose it convincingly in the living so it could be recognized early. People are going to have different risks, and some of that is probably genetically determined; some people are going to have the same level of exposure and develop CTE while some aren't. If we could identify individuals who are at higher risk or in the earliest stages of the development of the disease, you can then change lifestyle, behavior, exposure — that would be huge as well.

NL: To shift gears slightly, could you describe your own research in youth sports?

TM: Most of my work over the last 15 years has been focused on youth football players. That's been an interest in measuring repetitive head impacts and neurologic function in youth football players and some work in high-school-age players, as well. So a lot of that is focused around subconcussive injury [head trauma that does not trigger overt symptoms of concussion, like nausea, light sensitivity or thinking issues]. We're looking at the effects of these nonconcussive head impacts on brain health.

That ties into the CTE question in the sense that CTE is thought to be due to cumulative exposure to brain trauma — repetitive head impacts — and certainly most of the work, like in this study, has been done in NFL players. The question for a lot of the general population is, "What about youth players, high school players, that make up 90% of all football players?" So from a public health perspective, it's those younger players that I think we really need to be studying and concerned about.

That's not to say this study isn't really important. It certainly is, but my focus has been on that younger population. And then I do have some experience working more in a hospital background [on] clinical concussion management and [developing] objective pictures of concussion.

NL: With recent research, do we better understand how those nonconcussive impacts affect brain health?

TM: Going back maybe 15 to 20 years, people started to recognize that there were some cumulative effects of concussion. Those were some of the earlier studies showing that former NFL players who had multiple diagnosed concussions had worse outcomes later in life — that kind of put the spotlight on concussion. Concussion went to the forefront, in terms of how we thought about brain injury in football.

And then, over time, this recognition of what has been termed subconcussive or nonconcussive brain injury has emerged, as there's been some imaging studies in collegiate athletes, and even high school athletes, that have found that players who don't get concussed sometimes have changes in their brain, even over the course of the season.

That dovetails with some of the CTE research which has shown that history of concussions isn't necessarily predictive of who developed CTE. It's more of a cumulative effect of repetitive brain trauma. So the CTE researchers have essentially concluded that it's history of repetitive brain trauma, rather than history of concussion, per se, that's a leading risk factor for CTE.

With CTE, it's always looking backwards, because it's something that's diagnosed at death. For researchers like myself who study concussion, or study active football players, that has also then been a reaction of saying, "Well, if it is repetitive trauma, if it's repetitive head impacts, that is a risk factor for neurodegenerative disease such as CTE, then that makes it even more important to study it in active players." What does that head impact exposure look like at different ages, and how can we reduce that exposure? How can we reduce the number and severity of head impacts that players are experiencing?

So there's both the CTE angle, which is, again, retrospective — I'm looking at former players. And the contemporary issues of players who are currently playing and what's the risk for concussion, but also what's their exposure to repetitive head impacts? So it's really tied together.

That's why there's so much concern about repetitive head impacts and why there have been rule changes at the collegiate and high school level about the amount of contact and limiting those types of activities, with the idea of reducing that overall head-impact burden.

NL: When you talk about repetitive head impacts broadly, I assume that covers both concussive and nonconcussive impacts?

TM: Yep — so every hit would be considered a head impact, and then certain impacts are strong enough, or hit you in the right spot, to cause a concussion. The vast majority of impacts are nonconcussive.

NL: How do you speak to these athletes' families about the risks of concussion and CTE?

TM: When I do talk to players and coaches and parents, I often like to remind them that, generally, the benefits of playing sports, including tackle football, outweigh the risk. Oftentimes we get so concerned about the risk, which is real, that we forget about the benefits and about the alternatives of not playing. Almost always, the benefits — from the physical, the psychological and social components, the mental health components — are going to outweigh the risks. That's one thing to keep in mind.

Second, the risk of injury — in this case, CTE — is likely going to be far less in those younger players than older players, NFL players because their exposure, the number of impacts, the severity of impacts is far less. With my research, I've measured those head impacts and compared them to high school players and collegiate players, and extrapolated to NFL players because that data isn't available. And you see this big stepwise increase in exposure from the youth, the high school, the collegiate, to the NFL players.

[With parents], I'm reassuring them that the risk is far less for the younger players than what they hear about in this type of study. We're talking about an apples-to-oranges comparison.

I also like to remind them that, in my opinion, the game of football has never been safer. I've got a bit of a personal perspective on this as well, because I played football myself through college.

NL: Who did you play for?

TM: I played for a Division II school in South Dakota called — it's Augustana University now; it was Augustana College when I played there.

So I played 12 years of tackle football, and I can compare what tackle football was like when I was in fifth grade versus now — with the training that coaches have and the type of equipment they have and the way the practices are structured. It's completely night and day.

Even at the collegiate level, the way in which collegiate practices are conducted and the safety measures that are in place for current collegiate players is nothing like what we had when I was playing. So I like to reassure players that this is probably the safest time to be playing the sport of football.

At the same time, I acknowledge that this is an individual decision that parents need to make with their kids and evaluate that risk. One of my goals as a researcher is that I want to provide more empirical evidence so that they can make an informed decision, so that a parent would be able to say, "My son's risk of getting a concussion while playing youth football is 1 in whatever" — you know, 1 in 10, 1 in 5, or 1 in 100, whatever that case may be. And his risk of getting CTE by playing four years of youth football or four years of high school football would be this. Then you make an informed decision. Is that risk worth the benefit of participation?

Unfortunately, we don't know what that risk is [currently]. We can't tell parents, "Here's objectively what your risk of injury is going to be." It makes it tough for parents. So I like to reassure them that a lot of the concerns that are expressed for NFL players are greater than they should have as parents of youth players.

This interview has been condensed and edited lightly for clarity. It 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!

Earth's temperatures are steadily rising, with the past decade experiencing all 10 of the warmest years on record. As heat waves become more frequent and intense, concerns are growing about how this heat could impact people's health.

Higher temperatures can have serious effects on the human body, including dehydration, heat exhaustion and heatstroke. But extreme heat can also drive up the rates of heart attack and strokes due to ill health.

In a Live Science poll, we asked our readers how concerned they are about rising temperatures affecting their health and fitness, daily activities and the safety of their community. Over 170 people responded to the poll, which was published Aug. 26, with 67% of readers voting "Yes, I'm very worried about how extreme heat is affecting everyone around the world."

The comments from readers also reflected their concerns. One commenter wrote, "Too much of humanity is unaware that the Earth is a single organism. Everything is connected. El niño may begin off South America but its effects are eventually felt everywhere. There is only one ocean."

Another reader mentioned the daily challenges caused by the rising temperatures, saying, "I've been trying to make walking around the block of my neighborhood a regular thing, but when it gets too hot (and more precisely too humid) I prefer staying inside my house where I can be comforted by the AC."

So what do you think? After reading these responses, are you also worried about extreme heat? Let us know in the comments.

In 2013, MIT neuroscientists Steve Ramirez and Xu Liu published a paper detailing how they had created false memories in mice. They'd used optogenetics — where cells' activity is manipulated using light — to plant a fearful memory in the brain and then reactivate this memory with these pulses of light. The breakthrough helped to propel research in the field by showing that memories can be artificially constructed.

The initial experiments involved using a protein to tag brain cells in the hippocampus (a key memory center in the brain) that were active during the formation of a fearful memory. They then reactivated these "fear memory-bearing cells" while the mice were perfectly safe. The first four mice showed no response, but the fifth froze in fear. After analyzing the fifth mouse's brain, it turned out they had placed the protein in a slightly different location of the hippocampus to the others by accident — and inadvertently found the exact spot where the memory was stored — and that it could be manipulated and controlled.

In his book "How to Change a Memory: One Neuroscientist's Quest to Alter the Past" (Princeton University Press, 2025), Ramirez, now an associate professor at Boston University's Center for Memory and Brain,explores fundamental questions about memory: What is it, and can we manipulate it? He uses his personal experiences ‪—‬ including with loss, PTSD and addiction — to probe these ideas, asking whether this line of research could open new paths to treatments. He conceptualizes a world where memories could be manipulated to help ease a person's PTSD, or guard against dementia.

Live Science spoke with Ramirez about the book, the future of memory research, the ethics and implications for treating disease, and our brains' extraordinary power to recall our past. "How to Change a Memory" has been short-listed for the 2026 Royal Society Trivedi Science Book Prize.

"How to Change a Memory" excerpt: 'As if a shudder ran from its brain to its body': The neuroscientists that learned to control memories in rodents

Hannah Osborne: In the book, you reflect on your and Xu's major 2013 paper, noting that it was initially the result of a botched surgery in a single mouse. What if that little mistake hadn't happened?

Steve Ramirez: If we hadn't accidentally botched the surgery, I'd like to think we still would have gotten there, because what would have happened was that we would have done all the surgeries correctly, we would have hit the wrong spot, and everything would have been a negative result. And then, we would have said, "Maybe this is the wrong area to try to activate a memory." Now, where we would go next, I don't know.

I'd like to think that we would stay within the hippocampus and we would say, "Why not this other part or this other part?" Or maybe we would have moved to another brain area. But I think it would have delayed the inevitable by maybe six months or less.

Having hit the area, I think we realized that these mistakes — I shouldn't say mistakes; these unintended outcomes of an experiment — are certainly something that I think are pretty common. We just don't look for them often. A lot of times, we'll see a negative result and say, "OK, there's a million reasons why this experiment may not have worked as predicted," because it's very hard to touch base with reality and test the hypothesis. But I think it taught us to look a little bit more deeply when we see results that are either confusing or head-scratching.

The more I talk to people in science, I think everyone has this version of this one hiccup in an experiment [that] led us down a completely different rabbit hole that ended up being the basis of a paper or a series of papers ‪—‬ or, in mine and Xu's case, a career and then some.

I wouldn't say that they're universally common in every experiment, but I think that biology is so squishy, we're going to get things that kind of zig when we think that they're going to zag.

HO: Throughout the book, you talk about engrams. What are they, and why are they so important to memory research?

SR: An engram is a theoretical construct. It's a theoretical topic that certainly elicits every possible opinion out of memory researchers because it's kind of the holy grail of "what is memory." We think of an engram as whatever the physical basis of memory is.

It's almost like, what are the cellular building blocks of a memory in the brain? Whatever those building blocks are, that's what we consider an engram. And the reason I say that it's theoretical is because we don't really have a clean-cut "This is where an engram begins and ends in the brain."

We're not at the point where we have a Google Maps for an engram and we can zoom in to "This is the emotional part, and this is the smell associated with the memory." We have more of a zoomed-out satellite view of what an engram looks like. But we'll get there, and it's important, because if we have a full understanding of the physical manifestation of memory in the brain, then we have a way better chance of predicting what's going to happen when those building blocks break down and give rise to certain kinds of amnesia or cognitive impairments or memory loss.

By analogy, we have a pretty good understanding of how the heart works down to the physics of how a pump works, for example. Now that, thankfully, has enabled us over the past 200-plus years of cardiology, to have heart valves that we could 3D print or grow in pigs or things like that. With the brain, there's no law of physics saying that we can't get there to turn the brain into how we view the heart, where we can 3D print pieces to replace what was broken, or we understand a bit of clogging in this artery will lead to all of these different impairments.

We're only beginning to understand what those [metaphorical] clogged arteries look like in the brain, especially when it comes to memory. So if we have an understanding of the detailed physical picture of what an engram is, then we'll have a better shot of being able to predict what happens to ideally even prevent its breakdown, for example.

The goal is to understand the physical basis of memory and to use that understanding to try to enable well-being to an individual.

HO: In your experiments, you've used optogenetics to manipulate memories in mice, but that technique isn't widely used in human medicine yet. If you wanted to apply it in humans as a therapy, are there hurdles we'd need to get over? How are we going to be thinking about changing memories in 10 years?

SR: I'm so glad you asked, because I think it can go in two directions. Optogenetics is not really used in humans at all, except for maybe like eye retinal therapy, because you can flash light into the eyes and it's noninvasive and pretty straightforward. [Editor's note: Optogenetic retinal therapies are currently in clinical trials.]

There are groups working on some pretty remarkable technologies on being able to deliver [genetic] payloads into the brain, such as an optogenetic tool, but in a way that doesn't even require putting a virus in the brain [as is often done in gene therapies] or the optic fiber. There's groups working on giving even injections peripherally — like in the arm or in the rodent tail — and have that make its way into the brain, so it's way less invasive.

I'd like to think that technologically, we [researchers in the field] are working on trying to get optogenetic tools as noninvasively in humans as possible. But maybe the question becomes, do we want to do optogenetics in humans? And I just think that we may not have to, because there's so many other ways of doing what optogenetics does in rodents in humans, but especially with regards to memory.

In rodents, we have to go in and find those cells that hold on to a particular memory, that part of an engram, and activate those cells to get the animals to recall the memory. In humans, I can just ask you, "How was your night last night? How was your dinner? Did you have anything particularly savory or sweet?" Then, just through noninvasive verbal communication, a world of memory can come back in your mind.

I'd like to think of what we're doing in rodents as setting a blueprint for the kind of work that we could do in humans and that we can be clever about how to access things like memories in humans, where invasiveness like deep brain stimulation or transcranial magnetic stimulation is probably a last line of defense, whereas maybe the first lines of defense would be more cognitive behavioral [therapy, or CBT] because it requires no invasiveness into the brain at all.

HO: You look at the ethics around memory research a lot in the book. Where do you think the line is for whether we can apply memory manipulation, versus whether we should?

SR: I think there's two things happening simultaneously here. I don't think we should ever, for example, remove personal agency from the decision-making process here unless our personal agency has been removed by a particular disorder or something that can be medically considered [as having] robbed us of our ability to do the things that we want to do.

For instance, a patient living with depression, we may not just be able to tell them, "Think positive memories." Well, no, that's the very thing that we can't do, right? It's like asking someone with a broken leg to walk it off. So I think of it this way, where this kind of work can go with humans: we have to have some morally or ethically bounded goal of why we're doing what we're doing.

The goal of our research is truly to understand memory and to use that understanding to restore health and well-being to an individual. Now that's pretty arbitrary. That's human-made. We've made that up. We're the ones that made up this ethical boundary that this has to be used as a force for good — but by having that either ethically, or morally, or even medically bound goal, it can prevent us from derailing because we have a goal in sight that considers the overall well-being of people.

This is kind of like a sinister example, because people have compared this to the Manhattan Project. The goal was to build the bomb — it was to build or use nuclear fission; create it so that we can create a bomb. Now that's not necessarily an ethically bounded goal. The goal there is "win a war," and it's kind of the opposite of how I think about our research. The goal of our research is to prevent misuse by anticipating it first.

So what are the seat belts and what are the guardrails here? If we start by considering memory manipulation as part of our tool kit to help tackle disorders of the brain, then we have to use that inherently into some sense of good or medical good.

If we keep memory manipulation in the province of medicine, and in the clinic, then we can at least start in a way that takes the person into consideration first and foremost. We can study it to see, what are the side effects? Just like with any other drug, long-term use, is there desensitization? Are there clinics popping up everywhere that's doing this underground? We can anticipate all of this, right? Begin with it in the clinic, because we can have a kind of social infrastructure that can prevent its misuse and really hit the accelerator on using it for good.

The second part — and where I take my academic hat off and just become part of the public like everyone else — is, it's on us, society as a whole, to at least engage with some semblance of science literacy in a way that I think science can really be conveyed and used for good, whether it's storytelling or as a tool. Right now, it's so easy to fall under the traps of misinformation.

When we think of memory manipulation, everyone thinks Hollywood: "Eternal Sunshine [of the Spotless Mind]," "Total Recall." That's good for getting the conversation started and saying, what did "Total Recall" get right and wrong? What did "Eternal Sunshine" get right and wrong? But let's look at Hollywood, and let's use it as a case study of, where did memory manipulation go wrong here? Let's avoid that, or let's try to come up with some infrastructure that can avoid it. Where did memory manipulation go right? Let's try to do more of that and build some infrastructure around that.

HO: In the book, you note neuroscience is a relatively young discipline compared to things like astronomy. What do you think is the weirdest and most mind-blowing thing about memory that we still don't understand?

SR: The first thing that comes to mind is — I don't know how many memories we have, but let's just say we have a million memories or 10 million memories — that it's amazing to me that if I had 10 million memories, they all exist in my brain right now. They're all there. I can randomly think of the last time I ate steak, and my steak memories come up. Or I can randomly think of the last time I played a song on the piano, or me and Maple [his dog] going out for a walk, and then all of those memories come back.

So, 9,999,999 memories are quiet right now in my brain, except for one, which is me going out for a walk with Maple yesterday. But presumably, the other memories are still shaping me and sculpting my brain and influencing very much my biology, my sense of self, my personality, my identity, because they are me. They're just not bubbling into consciousness at the moment.

I think it's amazing that I can recall one memory and on the basis of what that memory is, I can either be moved to euphoria because I'm thinking of some of the happiest days of my life or be moved to tears because I'm thinking of more somber days of my life. And both of those can happen within like five seconds or less, depending on which memory I chose. I can experience the peaks of happiness or the valleys of sadness within five seconds or less. It's crazy that we can do that without really breaking a sweat.

What is everything else [the other memories] doing simultaneously? They might be helping to sculpt things like our imagination or our dreaming or our sense of self, which is an aggregate of all the sum of all of our experiences. I think that the fact that memories can move us through the entire landscape of emotion within seconds and that we have so many more memories that just fly under the radar of consciousness that are probably doing that and more is pretty remarkable. It's kind of scary, but it's kind of remarkable to think about it that way.

HO: On a related note, why do we wake at 3 a.m. and think of something stupid we did 20 years ago?

SR: As someone that wakes up like every other night at 3 a.m., I totally resonate here. There's a couple of theories. The first is less of a theory and more of a point. In terms of like the previous question about how remarkable memory can be, it's amazing that we have dormant memories that are decades old that, up until right now, we have every reason to believe we'd forgotten them. They don't exist anymore ‪—‬ out of sight, out of mind ‪—‬ and they're off into the ether now. But the fact that we can wake up at 3 a.m. and randomly remember something from 20 years ago is beautiful evidence that memories might go into dormancy for decades, but they may not actually be gone or erased or forgotten.

It's kind of wild, because I think that we have more possible connections in our brain than we do seconds of life. I don't think we would ever run out of space in our brain. I don't think that would ever happen.

But in terms of like waking up and the kinds of memory or waking up and recalling memories from the distant past, one theory is that whatever was happening when we formed that memory, there were particular sights and sounds and smells happening around us, and presumably we also felt a particular way during the formation of that memory, like our inner state was something when we were making that memory. Probably through random chance, when we wake up …our inner state happens to match the state that we were in when we made that memory, plus maybe a couple of more cues ‪—‬ a random song in the background that was playing that reminds us of it, or a particular odor, or maybe even something subtle like we saw a commercial an hour ago that just primed that.

I think it's evidence that some memories may truly live on in the brain for the entire life of a person, even though we don't recall them for decades, meaning we have access to an insane amount of memories in the brain that we don't always actually intentionally access.

We don't have an answer for it yet, but it gives me hope that some memories that are thought to be gone are not and actually way more restorable.

Hannah Osborne: It's a very personal and moving book, which you dedicated to Xu Liu, who passed away in 2015. What made you want to write it, and was it a difficult process?

Steve Ramirez: There's two things that made me want to write this book. The long-term reason was because I've always wanted to write a book since I was a kid. I do think that there's this inner 5-year-old core of me that thinks that if you're on a bookshelf, you matter somehow, like you did something that was important that all of humanity can read and presumably benefit from or learn from in some way, and I always found that cool as a kid.

More personally, in 2015, a book agent had reached out, asking if I was interested in writing a book. And I said, "Absolutely — but I have no idea about what." It wasn't until Xu passed away that all of the puzzle pieces clicked, [and] I was like, "I know what I want to write about" because I now have a real passion project. I knew that I always wanted to intertwine a bit of myself in this project because that's the way that I teach. In the classroom, I often bring my lived experiences.

More than anything, it was a way of honoring my friend, and that really felt like the purpose of the book — to honor my friend and, along the way, teach neuroscience, because that was kind of the basis of our friendship to begin with. I realized it's not so much that I want to as much as I have to write this book. That turned into very much benefiting from it in all of the weird ways that writing a book can change a person.

HO: Could you tell me about how you and Xu met and when your friendship clicked?

SR: Our friendship really did click on the first day that we met. We met in the lab, so we knew that science was going to be the common denominator of conversation, but it just so happened that there was a social that day for our building, which just meant free food and drinks for everybody. When we started chatting, we said, "Let's go; let's not miss the free drinks and food. Let's go to the social, and we'll continue our conversation there."

Then we spent the next couple of hours talking about all of these ideas of trying to artificially reactivate memories and why we thought they were important. It was such an easy conversation to have because I felt like I could let my academic guard down around him because, at least in the first year of grad school for me, it felt very stuffy and everyone at MIT was like an insane hotshot in some way and very intimidating. But Xu was just someone that I could level with; I could ask my quote unquote dumb questions, and I could just have a regular conversation about science.

When we were in the elevator ride back up to the lab, he mentioned just in passing that since it looks like we might be working together, we should just be co-first authors on everything that we do. It was just so perfectly emblematic of how our friendship would evolve, where all of our talks, all of our presentations, even awards, we were very like down the middle because there was no one without the other when it came to how we did our projects together. The combination of the scientific and the interpersonal made it easy. We were quite different people but very complementary, and I think that's what made it work.

This interview has been condensed and edited lightly for clarity.

There are many theories as to how the diabetes drug metformin lowers blood sugar levels, but now, scientists think they've discovered the main route.

It turns out that the drug, primarily used in type 2 diabetes, forces gut cells to absorb and burn extra glucose. It achieves this by messing with gut cells' mitochondria — their internal power generators.

Although metformin was first used in patients in the 1990s, scientists have been unsure of how it works.

"Every year there's a new mechanism for metformin that says last year's mechanism was wrong," said study co-author Navdeep Chandel, a biochemist at Northwestern University.

Part of the problem is that metformin affects several organs. "Metformin has a complex mechanism of action, with effects in several organs and on different aspects of metabolism, making it difficult to identify a single mechanism that explains all of its effects," Manuel Vázquez Carrera, a pharmacology researcher at the Sant Joan de Déu Research Institute who was not involved with the study, told Live Science in an email.

Some studies suggested that metformin causes intestinal cells to use up glucose, and an animal study released last year proposed that the drug causes glucose to move from the bloodstream into the intestines, where gut bacteria can then break it down. Other research pointed to the liver, proposing that the drug lowers blood glucose levels by inhibiting gluconeogenesis, a process in which the liver makes glucose from other molecules, usually to regulate sugar levels during fasting or exercise.

The scientists exploring the drug's action in the liver found that metformin interacts with a large complex of proteins inside mitochondria. Called mitochondrial complex I, it's a key player in generating cells' primary energy currency: the molecule adenosine triphosphate (ATP).

However, the theory that metformin mainly works by targeting this complex was quickly dismissed. That's because the drug's concentration in the liver is too low to exert an effect, Vázquez Carrera said.

But elsewhere in the body, it's a different story. In the recent study, published in May in the journal Nature Metabolism, Chandel and his colleagues found that metformin does work by targeting mitochondrial complex I — but it does so not in the liver but in the intestines, where the drug builds up to higher concentrations.

Their first clue came when they compared metabolites in the bloodstreams of people taking metformin and those unexposed to the drug. For one metabolite, called citrulline, they saw the biggest drop in concentration following a dose of metformin. This blood metabolite is produced almost exclusively by mitochondria in intestinal cells, revealing that the drug affects gut mitochondria.

In further experiments, the team genetically modified mice so they had a backup for complex I in the intestines. The backup was a different enzyme that performs a similar function but is not affected by metformin. That meant that if the drug works by inhibiting complex I, mice equipped with backups could bypass the drug's effects. When the researchers administered metformin to these mice, they found that the drug was much less effective at lowering citrulline levels in the blood, suggesting that metformin acts on complex I in intestinal cells.

Besides affecting citrulline, the genetic tweak also reduced metformin's effects on blood sugar by 80%, Chandel said. This means inhibition of complex I is probably the main mechanism behind the acute effects of the drug, he added.

Mitochondria can generate roughly 30 ATP molecules from one glucose molecule, but when these powerhouses are blocked, the cell tries to compensate by running a less-efficient ATP production line. This alternate pathway, called glycolysis, generates only two ATP molecules per glucose molecule. The researchers argued that by inhibiting intestinal mitochondria, metformin might force the cells to sequester and burn through as much glucose as possible with this less-efficient strategy. In turn, that lowers blood sugar levels.

They were able to show this in lab mice. Metformin caused glucose to accumulate in intestinal cells of normal mice, not the mice carrying backup enzymes, suggesting that the cells with blocked-up mitochondria usurp hoards of glucose to run glycolysis instead.

"Much of the mechanistic evidence comes from male mice, so it remains unclear how well the findings translate to humans and whether there are sex-specific effects," Vázquez Carrera noted.

Most of metformin's sugar-lowering activity — about 80% — involved complex I, but it's likely that the drug has additional targets. In future work, Chandel and his colleagues aim to explore how the drug affects other aspects of the body's biology, such as the liver or the gut microbiome.

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

Scientists may have found a way to regenerate the neurons that are lost due to conditions like Alzheimer's disease, a new laboratory study hints.

The research, published Aug. 26 in the journal Cell Biomaterials, suggests that reducing levels of a key protein in another type of cell in the brain, called astrocytes, may convert those cells into neurons. The adult brain has a limited capacity to produce new neurons, at baseline, and an even more limited ability to replace neurons lost to disease.

If successfully developed into a treatment for humans, this new approach could replenish lost neurons and thus restore brain function, the study authors say.

Astrocytes are abundant, star-shaped cells in the brain that protect and support the functions of neurons. A crucial protein for astrocyte development is called PTBP1, and previously, scientists suggested that eliminating this protein in astrocytes may convert them into neurons. In that study, researchers reported converting astrocytes in the mouse brain into neurons by eliminating the gene that coded for PTBP1.

However, later experiments contradicted these results, suggesting that newly formed neurons could not be traced back to the astrocytes. So Peisheng Xu, a co-author of the new study and a pharmaceutical scientist at the University of South Carolina, set out to investigate that contradiction.

"We felt it's strange [that] two groups of people got different conclusions," he told Live Science.

He used a technique called Nano-Eraser, developed earlier in his lab, to delete PTBP1 from astrocytes without editing any of their genes. The team accomplished this by packaging an antibody that targets PTBP1 into a polymer gel. That gel helped sneak the antibody across the blood-brain barrier, a gatekeeper that prevents certain substances in the bloodstream from entering the brain.

Once it reaches astrocytes in the brain, the antibody binds to PTBP1 and drives the cell's internal machinery to destroy the protein.

"I think it's quite interesting, intriguing and an innovative approach," said Dr. Christiane Wrann, a neuroscientist at Harvard Medical School, who was not involved in the study. "They show that [the gel] can cross the blood-brain barrier," which is important for developing therapies for the brain, she told Live Science.

The team first tested the gel in human astrocytes grown in lab dishes. Over the course of days, astrocytes exposed to the gel lost their characteristic star shape and started to form axons — the wires from which neurons send messages. Proteins typically found in neurons also became more abundant in the astrocytes.

The cells later showed electrical activity that further confirmed that they were functioning similarly to neurons and could fire synchronously. The gel also showed similar results in miniature models of the brain, called organoids, which had been grown from human stem cells.

The researchers then tested the gel in mouse models of Alzheimer's disease. These lab mice had lost neurons and had developed some characteristic features of Alzheimer's disease, such as inflammation, loss of cognitive function, and sticky clumps of a protein in the brain.

The team gave these mice two intravenous doses of the gel, eight days apart. Over the next four weeks, behavioral tests suggested that the treated mice's memories improved and they were able to build better nests than untreated mice; that's an indication of improved behavioral function. Later, the researchers examined the brains of the treated mice, finding that the density of their neurons had increased while their levels of inflammatory molecules decreased.

However, while the lab-dish experiments indicated that astrocytes converted into neurons, that finding has not been confirmed in live mice, Xu said.

"We observed that neuron density increased in treated mice compared to untreated ones," he said, "but we cannot yet eliminate the possibility that some other neural stem cells might have also converted into neurons."

Wrann agrees that additional experiments would have been required to see whether a particular astrocyte in the mouse brain changed into a neuron. While the results are "intriguing," a lot more research is needed to see the long-term effects of such a treatment on different types of brain cells, she said.

Xu and his team now plan to probe further into astrocyte conversion in live mice. Before they can move to clinical trials with people, he said, the safety and effectiveness of the treatment would need to be tested in nonhuman primates.

Notably, astrocytes themselves serve important functions in the brain. So there's a question about what having "chronically reduced PTBP1 could do to the brain," Wrann noted. She agreed that careful studies would be needed for this to translate to humans.

"That's something that needs to be tested step by step," she said.

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

Earth is getting hotter, and people across the world are starting to feel the effects. The past decade includes all 10 of the warmest years on record, and 2024 was the hottest year ever measured. As temperatures continue to rise and heat waves become more frequent and intense, that heat could severely impact people's health.

Extreme heat can affect the body in serious ways, such as dehydration and heat exhaustion, and it can lead to more severe conditions, like heatstroke or an increased strain on the heart and lungs.

How worried are you about these health effects as our planet heats up? Are rising temperatures changing the way you think about your health and fitness, daily activities, or the safety of your family and community? Answer our poll, and let us know what you think in the comments below.

The patient: A 41-year old man in Iran

The symptoms: The man visited an outpatient clinic after a week of experiencing extreme discomfort during urination and pain above his pubic bone. His urine stream was weak, and he was unable to empty his bladder.

What happened next: The patient told the doctors that about a month earlier, he had begun to develop incontinence. He self-treated for two weeks by inserting superglue into his urethra.

At first, the superglue seemed to help. But after four days, he began to produce less and less urine and urination became painful. By the time of his clinic visit — two weeks after he stopped applying the superglue — he was barely able to urinate at all and was in constant pain, his doctors wrote in a report of the case.

The diagnosis: During a physical examination, the doctors noted that the man's penis was erect and that they felt a solid foreign body in the penile urethra. They also observed "brittle fragments of superglue" on the opening at the tip of his penis, they wrote in the report.

The doctors attempted to perform a cystoscopy, a procedure in which a tube fitted with a lens enables doctors to look inside the urethra. But the obstruction prevented them from inserting the tube far enough to see anything, and they decided to perform emergency surgery to remove the mass of hardened glue.

The treatment: Surgeons made an 0.8-inch (2 centimeters) incision in the glans, the bulb at the end of the penis. For 15 minutes, they bathed the urethra with 0.8 gallons (3 liters) of saline solution to saturate the glue plug and thus separate it from the walls of the urethra ‪—‬ a feat they eventually accomplished through "certain maneuvers," they wrote.

Finally, the glue broke loose. The doctors extracted a rod-shaped solid glue block measuring nearly 4 inches (10 cm) long.

After the patient recovered from surgery, his urination and urine analysis were normal. He was discharged five days later with a catheter that remained in place for 10 days, and he received prescriptions for antibiotics to prevent infection. At a follow-up visit in the sixth week after surgery, his urination was normal and he had no further complications.

The doctors did not identify the cause of the patient's prior incontinence.

What makes the case unique: Application of superglue in body cavities typically occurs in the ear or nose, according to past case reports. Usually, the glue can be dissolved with solvents, such as acetone. However, three other case reports in the medical literature describe patients intentionally inserting superglue into their urethras, and all of those cases required removal with endoscopy or surgery, the doctors in Iran reported.

Urethra tissue is very delicate, and inserting anything into this sensitive tube risks damaging it, which can lead to serious infection. The insertion of foreign bodies into the urethra can also be painful, making the practice "relatively rare," the report's authors wrote.

If a person chooses to do this, they added, it may be to satisfy curiosity or as a result of intoxication or mental illness, but the most common motivation is sexual stimulation. Despite the risks, numerous case reports describe people pursuing pleasure by introducing a wide range of diverse objects into their urethras, including magnets, pencils, earphones, a dining fork, a thermometer, the ink chamber from a ballpoint pen, the metal tip of a screwdriver, a USB cable, a tree branch and three AAA batteries.

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!

President Donald Trump's recent executive order on childhood vaccines has generated a predictable and understandable debate around public health needs, parental autonomy and the scientific justifications for the directive. The order proposes, among other things, altering the U.S. childhood vaccine schedule and splitting up the combined MMR vaccine into multiple shots. As an immunologist, my view is that the order contradicts established scientific consensus and instead backs narratives that are not supported by evidence.

However, the more important issue with the order may be something more fundamental: What happens when vaccine policy is divorced from the scientific processes designed to guide it?

For many decades, the U.S. relied on a transparent process in which scientists, physicians, public health experts and vaccine specialists reviewed evidence and developed recommendations for who should receive a given vaccine and when. Through this process, there would be disagreements, which is not only expected but welcomed. Constructive debate on policy can lead to the development of better policies. But replacing expert scientific review with political directives risks creating a precedent that extends well beyond vaccines.

It's very possible that the immediate impact of the executive order will be limited. Many pediatricians, state public health agencies and professional medical organizations are likely to continue following established immunization schedules that were developed through decades of scientific review and real-world experience. The order itself does not magically change how vaccines work, how doctors practice medicine, or how states set school vaccination requirements.

Indeed, while the order says a lot, it doesn't hold direct authority to change vaccine recommendations. These, at least for now, are still protected by federal laws. The order can set direction but not policy.

Nevertheless, it would be a mistake to conclude that the order does not matter, because the true risk it poses is that it creates confusion and uncertainty for parents and caregivers, who only want to protect their children as best they can.

Vaccination programs rely on something fragile: the public's confidence. This confidence can be destroyed easily. Parents deserve to have trustworthy information when making decisions about the health of their children. Physicians, too, must trust that vaccine schedules reflect the best available science. Weakening those foundations of trust will further contribute to declining vaccination rates, even if no formal mandates change.

We are seeing this right now. U.S. kindergarten vaccination rates have continued to drop, falling farther below the thresholds needed for herd immunity. This is especially concerning at a moment when the U.S. is experiencing one of its worst measles outbreaks in decades, while other preventable infectious diseases are making a resurgence.

The executive order proposes separating the combined measles, mumps and rubella (MMR) vaccine into three individual vaccines — and this illustrates the problem. The proposal is framed as part of an effort to reduce the number of childhood immunizations, but it would do the opposite in practice.

Here's why. Today, during their first years of life, children receive two doses of the combined MMR vaccine, administered in two separate injections. Under the approach outlined in the executive order, children would need six separate injections to achieve the same protection.

The order also suggests that each immunization be administered at separate medical visits, thus tripling the number of visits needed to reach the same protection. For families, that translates into more time away from work, more missed school, more transportation costs, more co-pays for those whose insurance plans require them, and more opportunities for appointments to be postponed or missed altogether.

These practical consequences shouldn't be ignored. Every additional visit creates another chance for a child to fall behind on vaccinations. Every added logistical hurdle disproportionately affects families with fewer resources, less schedule flexibility or less access to healthcare.

What's more, the separate vaccines required to implement this policy are not even currently available in the U.S. Manufacturers would need to develop new production processes, conduct testing, navigate regulatory review and establish distribution systems for these separate vaccines, all to replace a combined vaccine with an extraordinary record of safety and effectiveness spanning more than half a century.

In short, the proposal would require substantial new costs and complexity just to replace a system that has been working exceptionally well and protecting children for decades. The combination MMR vaccine was developed precisely because combining vaccines reduces the number of injections, thus improving vaccination rates by ensuring children receive protection as early and efficiently as possible.

What is the rationale behind the executive order? Administration officials have pointed to differences between U.S. vaccine recommendations and those from some other developed countries, such as Denmark, which recommends fewer routine vaccines than the U.S. does. On the surface, that argument may sound reasonable — if another country administers fewer doses, why shouldn't the U.S.?

The answer is that the timing and number of vaccines are developed to suit different countries' wildly different healthcare systems and public health realities. Countries differ in disease prevalence, healthcare access, vaccination delivery systems, screening programs and population demographics. Some countries have more centralized healthcare systems that allow for easier preventive care follow-up, while others face different infectious disease risks than the U.S.

It is therefore unsurprising that schedules vary among nations, and the motivation to match other countries' schedules is arbitrary, rather than science-led. What matters more is whether recommendations are supported by evidence and whether they effectively protect children in America, specifically.

It may be months or years before we see the consequences of this executive order and the wider attacks on vaccines. It will be reflected through declining confidence in public health institutions, growing uncertainty among families, and increasing difficulty in maintaining high vaccination rates, leading to higher rates of disease and death.

That is why this executive order matters.

Whether formal policy changes will be implemented now or in the future is less the issue. What's more at stake is whether the order will drive Americans to rely less on scientific evidence and expertise when they're making decisions that affect their children's health.

I believe immunology is one of the critical scientific infrastructures that underpins modern medicine. Vaccine policy should be built on the foundations of that infrastructure, with the science and evidence guiding public health recommendations. When this fails, the results will be measured in the lives lost to preventable illness, and that's a future we must avoid.

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

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.

Two people in Lancaster County, Pennsylvania, have died of measles, marking the first measles-related deaths in the United States this year.

Neither individual was vaccinated against the disease, the Pennsylvania Department of Health (DOH) reported Tuesday (Aug. 25). Their deaths mark the first measles fatalities in the state in 35 years.

"To protect the privacy of the individuals and their families, DOH will not release any additional details that could personally identify these individuals and their families," DOH officials said in the statement.

Since the start of the year, there have been 393 confirmed cases of measles in Pennsylvania across 28 counties. Nationwide, 2,813 cases have been reported so far this year, according to the Johns Hopkins U.S. Measles Tracker. The 2026 nationwide total already exceeds the total number of measles cases reported in 2025, when 2,289 cases were reported, including over 240 hospitalizations and three deaths, according to Centers for Disease Control and Prevention data.

These totals represent both measles caught within the U.S. and imported cases from people who caught the infection elsewhere. Imported cases make up a relatively small proportion of the overall total, with most cases coming from local transmission, according to the tracker.

The two deaths in Pennsylvania come as the nation's vaccination rate for measles continues to fall among kindergarteners and as the proportion of kindergarteners with vaccine exemptions is rising. The U.S. is likely to lose its "measles elimination status" later this year, which would mean the same outbreak strain had been consistently circulating in the country for over 12 months. Essentially, this suggests that although the U.S. officially eliminated measles in 2000, the disease is likely back in regular circulation.

According to the tracker, nearly all of the measles cases reported this year — 96% — have been among unvaccinated people or people with unknown vaccination status. Two doses of either the MMRV vaccine (which protects against measles, mumps, rubella and chickenpox) or the MMR vaccine are about 97% protective against measles infections. (Both vaccines offer the same protection against measles, but the latter excludes protection against varicella, or chickenpox. Kids who receive the MMR shot get a separate chickenpox vaccine.)

Measles infections can cause rash; fever; cough; runny nose; and red, watery eyes. About 1 in 5 unvaccinated people who catch measles are hospitalized, and there's a risk of developing complications like pneumonia or brain inflammation. In the U.S., 1 to 3 in 1,000 people with measles die of the disease. Those who survive the infection can develop long-term health problems, such as neurological disease or "immune amnesia," where the immune system loses ability to fight off pathogens it's encountered in the past.

"Because measles was largely eliminated in the Commonwealth for more than three decades, people are not familiar with this disease and don't fully understand the potential severity of the illness," Dr. Debra Bogen, Pennsylvania's secretary of health, said in the statement. "We want to ensure every Pennsylvanian has the information they need to protect themselves, their loved ones and their communities."

The best way to protect against measles is to get fully vaccinated, DOH representatives said in the statement.

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