There has been talk of "rescheduling" cannabis for years, a regulatory move that would significantly ease federal restrictions on the drug. Now, with a recent push from the White House to expedite the rescheduling process, we may see that change come to pass.

Moving cannabis to Schedule III — a less-restrictive classification for drugs — would represent a very important shift in how the federal government treats cannabis research, in that it would officially state that cannabis has medical use. This landmark decision would encourage some of the largest scientific investment in cannabis research to date and help build some of the strongest evidence of the value of cannabis-based therapies.

However, the move to Schedule III should be viewed as a transition rather than an endpoint.

How cannabis is regulated, today

Cannabis has existed in a complicated space in medicine, policy and public perception for decades.

More than 6 million Americans are registered to use cannabis through state medical programs. Clinicians participating in state medical cannabis programs generally "certify" and "recommend" specific cannabis products to certain patients, rather than write traditional prescriptions. Additionally, a handful of cannabis-derived and cannabinoid-based medications have received formal Food and Drug Administration (FDA) approval.

However, since the Controlled Substances Act was enacted in 1970, cannabis has been classified as a Schedule I substance. This category is associated with the highest level of restriction, including substances such as heroin, MDMA, and LSD.

Under federal law, Schedule I drugs are defined as having a high potential for abuse and no currently accepted medical use. Given some cannabis-derived drugs are FDA approved, it may seem contradictory that cannabis remains a Schedule I substance. The key is that federal drug scheduling, FDA drug approval and state cannabis laws are separate legal and regulatory systems.

Federal law classifies cannabis as a Schedule I drug. Separately, the FDA evaluates and approves individual cannabinoid medications for specific medical conditions. Independently, states can authorize cannabis for medical or adult use under their own laws, even though cannabis remains illegal under federal law.

This three-tiered regulatory landscape can be confusing for patients, clinicians and the general public alike.

Rescheduling would be a boon for research

For a few years, federal officials have recommended moving cannabis to Schedule III, which includes drugs with accepted medical uses that are subject to fewer federal restrictions. Ketamine and anabolic steroids, like testosterone, are examples. Compared with Schedule I substances, Schedule III drugs are considered to have a lower potential for abuse and can be prescribed for accepted medical uses under federal law.

Rescheduling cannabis would thus create a regulatory environment that's more favorable to research, which could support the development of future FDA-approved cannabis-based medicines. Researchers are already exploring cannabinoids as potential treatments for conditions including chronic pain, post-traumatic stress disorder, inflammatory bowel disease and sleep disorders, but the available evidence remains limited for many uses.

Evidence is limited, in part, because for decades researchers studying cannabis have faced regulatory hurdles that extend beyond those encountered with many other controlled substances.

Studies using cannabis often require additional federal, institutional and local approvals, compared to research with less-restricted drugs. They have extra requirements around securely storing and handling cannabis. They require detailed record-keeping to document how research materials are received, stored and used, as well as Drug Enforcement Administration registration for the principal investigator conducting Schedule I research.

Additionally, federal restrictions have historically limited researchers' access to cannabis products that reflect those people regularly use, such as commercially available flower, vape products and edible formulations.

This regulatory burden has historically discouraged some universities, healthcare systems and funding organizations from investing in cannabis research. These hurdles have made cannabis studies slower, more costly and smaller in scale than those conducted with more loosely controlled drugs.

Shifting cannabis to Schedule III would help to reduce these barriers, opening opportunities for more universities and healthcare systems to conduct much-needed clinical studies for medical cannabis. It could help researchers conduct the larger, more rigorous clinical trials needed to determine which therapies are truly safe and effective — and which are not.

Such gold-standard studies would better evaluate cannabis' potential benefits and risks, as well its effects in specific medical conditions and appropriate dosing for each. This evidence could, in turn, help reduce the stigma associated with cannabis use.

What rescheduling won't accomplish

Rescheduling cannabis will not automatically make cannabis more accessible to patients or immediately establish where cannabis is beneficial, what doses are most appropriate or which patients are most likely to benefit.

It would not automatically convert existing state cannabis programs into the conventional prescription model used for most Schedule III drugs. And it would not immediately resolve the complexities surrounding state medical cannabis programs, which operate outside the traditional FDA-approved medication pathway.

Unlike most prescription drugs, medical cannabis is an umbrella term that includes hundreds of products that differ in cannabinoid content, formulation, dose and route of administration. Most of those products have not been approved by the FDA, so rescheduling would not automatically place them into the traditional prescription drug system or immediately resolve many of the financial and access barriers patients face when trying to use them.

Without robust follow-up research, rescheduling alone would do little to resolve the uncertainty surrounding many cannabis products.

In short, the greatest benefit of moving cannabis to Schedule III would not be the policy change itself; it would be the opportunity to build a stronger evidence base for cannabis science and medicine. Policymakers may open the door to Schedule III, but researchers, clinicians and regulatory agencies will determine whether this opportunity will actually lead to the appropriate and meaningful advances in cannabis science and medicine.

The value of rescheduling will be measured not by how quickly it changes patients' access to cannabis, but by whether it helps create the scientific foundation needed to guide responsible medical use.

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

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It's a Tuesday morning, and you're getting your toddler ready for daycare. But as you brush her hair into a ponytail, you notice that her cheeks are flushed, her nose is runny and her breathing is phlegmy. Instead of daycare, you head to your pediatrician, who offers a solution: a prescription for antibiotics.

This scenario has played out many times in clinics around the world. The problem is that most common childhood infections are caused by viruses, which antibiotics don't treat. In the long term, unnecessary antibiotic prescriptions can foster resistance in bacteria, thereby reducing the drugs' potency and fueling the rise of dangerous superbugs.

That's why, in recent years, there's been a huge push in many countries to raise awareness of antibiotic misuse among doctors and to reduce the overprescription of these drugs. In Japan, the government noticed that the country's pediatricians were prescribing too many antibiotics, especially to young children, and offered them a financial incentive to break the habit.

It's been working remarkably well. Among young kids directly affected by the incentive, it slashed antibiotic prescriptions by 20%; it also contributed to a spillover effect in older kids and teens, as under-20s have seen a 50% reduction in prescriptions in recent years. I went to Japan to examine why the program has been so effective and to learn whether similar approaches could work in the U.S.

Understanding why a fairly modest incentive of 800 yen (about $5) a visit is so effective requires unpacking why Japanese doctors overused antibiotics in the first place. If doctors face similar pressures stateside, maybe the same strategy could work here too.

A culture of overprescription

Japan started out with a big problem of antibiotic misuse, especially among prescriptions for kids. From 2013 to 2016, over 30% of children with respiratory tract infections were given antibiotics, despite most of those infections being viral. (The U.S. started at a slightly better baseline regarding antibiotics given for respiratory conditions, with about 23% of outpatient prescriptions being unnecessary.)

For decades, it was common in Japan to routinely prescribe antibiotics for sniffles and tummy bugs, Dr. Takemi Murai, deputy head of the Infectious Diseases Division at Nagano Children's Hospital in Azumino, told me. That's in part because medical education there didn't emphasize the risk of "superbugs," meaning bacteria that can withstand many antibiotics.

"When I trained, antimicrobial stewardship wasn't yet a formalized part of the curriculum in the way it is now," said Murai, who finished medical school in 2006.

There also may be a generational divide, Dr. Tatsuki Ikuse, a pediatric infectious disease specialist at the National Center for Child Health and Development in Tokyo, told me. Ikuse, who finished medical school in 2013, suspects that older doctors "experienced many cases of bacterial infections when there was no vaccination."

Now that vaccines for whooping cough, diphtheria and pneumococcal disease are routine, children face a lower risk from the bacteria that cause those illnesses. But those early experiences treating children with serious bacterial infections may still be shaping doctors' prescribing patterns, even decades later, Ikuse thinks.

Surveys conducted in Japan suggest that doctors under 50 are more likely than doctors over 50 to see antimicrobial resistance as an urgent issue. Clinic doctors — those likeliest to see kids as outpatients for acute illnesses — also skew older than doctors in hospitals; in 2024, clinic doctors averaged about 60 years old, while those in academic and nonacademic hospitals averaged 40 and 48 years old, respectively.

Historically, Japanese doctors also had a strong bias toward prescribing antibiotics for "feverish" diseases, noted Dr. Norio Ohmagari, director of disease control and prevention at Japan's National Center for Global Health and Medicine.

Murai agreed with that sentiment. "If doctors saw a fever and a high CRP level [a sign of inflammation], they prescribed antibiotics," Murai said. "Doctors were following such a practice for a long time, so they didn't question it."

Concerns over secondary infections were also a big driver of unnecessary antibiotic use, said Dr. Masahiko Sakamoto, a hospital pediatrician in Saku, a highland city about an hour northwest of Tokyo by bullet train. Even if doctors suspected a viral infection, like the common cold, they worried that the illness could open the door for secondary bacterial infections, such as bacterial pneumonia. However, recent studies suggest this scenario is uncommon and shouldn't prompt doctors to use antibiotics preventatively.

Is antibiotic misuse still a problem in the U.S.?

Young children in the U.S. were once the most likely group to receive unneeded antibiotics, but now, those unnecessary prescriptions have "dropped dramatically," Dr. Sarah Kabbani, director of the U.S. Centers for Disease Control and Prevention's (CDC) Office of Antibiotic Stewardship, told me in an email.

Between 2011 and 2016, children's antibiotic prescriptions decreased 13% overall. "Overall declines in antibiotic use over the past decade have been driven in large part by reductions in prescribing for children," Kabbani noted.

Japan has also decreased its overall antibiotic use in younger populations, halving its outpatient prescription rates for patients under 20 between 2011 and 2022, Dr. Yusuke Okubo, division chief of clinical epidemiology and health services research at the National Center for Child Health and Development in Tokyo, told me.

The decrease in antibiotics overuse syncs with parents' lived experiences in both countries.

"I was taking antibiotics quite often" as a kid, Tatsuya Kanno, a software engineer and father of two in Tokyo, told me. "Nowadays, we don't get really prescribed those antibiotics easily."

"It has definitely been different from my childhood," said Gabby Brown, an apparel consultant and mother of two in Littleton, Colorado. "There was always a bottle of pink stuff in the fridge, you know? And now they're very hesitant to give it out."

Brown's pediatrician actually has an explicit policy on their website stating that they don't overprescribe antibiotics and instead follow evidence-based guidelines to determine when the drugs are truly necessary. I've found a number of other U.S. pediatric clinics that do the same.

One reason U.S. pediatricians have been able to improve several key metrics of antibiotic use is that the issue has been on their radar for a while.

"Antibiotic stewardship was a core tenant of my residency training 20 years ago," Dr. Morgan Leafe, a U.S.-based pediatrician who worked in inpatient and outpatient settings for 11 years after residency, told me in a direct message. "So I would say it's not new in pediatrics."

But there remains room for improvement.

Prescription rates vary widely among states and among different types of outpatient facilities, such as community practices versus those affiliated with academic medical centers. Rural communities often use antibiotics at higher rates and log more inappropriate use, compared with urban areas. These regional variations are "not explained by clinical factors," said Julia Szymczak, a medical sociologist and associate professor in the Division of Epidemiology at the University of Utah School of Medicine.

Nowadays in the U.S., urgent care clinics might be a hotspot for antibiotic misuse. These and other walk-in clinics serve an increasing number of pediatric patients, with an estimated 26% of children visiting one in the past 12 months. Urgent cares may prescribe antibiotics to children at a higher rate than other ambulatory settings do; in one study, 42% of the children seen at urgent cares were prescribed antibiotics at their visit, while the national average across all pediatric ambulatory visits is 21%.

It may be that urgent cares are more likely to prescribe antibiotics for conditions that they're explicitly not recommended for. One national analysis found that urgent cares prescribed antibiotics for 20% of allergy cases, 42% of viral upper respiratory infections and 52% of uncomplicated ear infections, while doctor's offices wrote far fewer of these inappropriate prescriptions. Other studies highlight similar patterns.

Among children, inappropriate prescriptions are less likely at urgent cares that specialize in pediatrics, highlighting doctors at general clinics as a potential population to target. Additionally, research has found that visits with nurses or physician assistants are more likely to end in an antibiotic prescription than those with doctors. (Only licensed doctors can write prescriptions in Japan, so this factor is more unique to the U.S.)

Different systems, similar pressures

Japan's nationalized healthcare provides a staggering degree of choice, because insurance coverage doesn't tie you to specific clinics or require you to get referrals to access certain care. Young children's care is virtually free thanks to national and local subsidies. So on paper, parents can easily shop around for a pediatrician that best suits their family's needs, as well as pop into any healthcare facility with flexibility should the need arise.

While this system is convenient, it has its downsides, some parents told me.

"In the U.S. and in Switzerland, they try to get to know you and know your child," said Reid, a fundraiser and father of two based in Okinawa, who recently moved to Japan with his sons and husband. "They don't at all in Japan."

In contrast, about 9 in 10 children in the U.S. have a primary care provider, although that percentage has fallen in recent years as the use of urgent care has increased. Primary care providers can be a go-to for sick visits as well as an ongoing monitor of kids' health via annual check-ups. (Annual check-ups in Japan are handled by local municipalities, not by children's regular doctors, Reid noted.)

In some ways, pediatric clinics in Japan can be considered more analogous to urgent care in the U.S., in that they're intended to address acute cases of illness as they emerge. For more serious illnesses, caregivers bring their children to hospitals, parents in Japan told me.

Diagnostic uncertainty

For a typical respiratory or tummy bug, doctors in both the U.S. and Japan make diagnoses based largely on a patient's symptoms and timeline of illness. In the U.S., most minor infections are "generally assumed to be viral unless certain criteria are present," Leafe said. These criteria are spelled out in manuals used by pediatricians.

The criteria enable doctors to "feel reassured" that they've correctly classified an infection as viral or bacterial, even in the absence of a highly sensitive diagnostic test, said Dr. Ilan Shapiro, a community pediatrician at AltaMed Health Services, a nonprofit health network in Southern California.

Rapid tests are available for only a handful of bacteria, including Streptococcus pyogenes (also called group A strep), a common culprit behind strep throat and scarlet fever. These tests are "definitely underutilized" by Japanese clinics, Ohmagari noted, while U.S. clinicians are encouraged to use them more widely.

"For strep throat, we never treat [give antibiotics], now, without a positive test," said Dr. Jennifer Shu, a pediatrician with Children's Medical Group, a group of pediatric offices in the Atlanta metropolitan area. (That said, electronic medical records suggest that not all doctors' offices use these tests before prescribing antibiotics, despite these recommendations.)

In both countries, doctors can use rapid tests to diagnose common viral infections, such as influenza and RSV. But those tests don't always catch every case. And even if they come back positive, they can't rule out the possibility of simultaneous infections with viruses and bacteria, Shu noted.

Shu's practice also uses a 45-minute test that looks for multiple viruses and bacteria in the nose and throat, including the bacteria behind whooping cough and Mycoplasma, which causes "walking pneumonia." Not all clinics use this type of test, though, because they require a special certification and equipment to run on-site, Shu said.

Such panel tests can be helpful but also tricky to interpret. Bacteria can sometimes be detected in a patient's nose without being the cause of their symptoms. "That's where clinical judgment comes in," Shu said, emphasizing that a doctor must combine test results with the timeline of a patient's symptoms.

Time crunches

The lack of quick, surefire diagnostic tests for bacterial infections can leave doctors with a degree of uncertainty, which can sometimes prompt unnecessary prescriptions, Szymczak said.

"Our number one motivation is to not harm somebody; that's the main thing," said Dr. Shruti Gohil, an infectious-disease specialist at UCI Health who designs interventions to improve doctors' antibiotics use. Worries about potential missed diagnoses can prompt doctors to reach for an antibiotic now "in exchange for a potential future, untoward consequence," such as a greater chance of resistant infections, she said.

In both countries, doctors must make diagnoses and treatment plans in a limited amount of time. "Pediatric outpatients in Japan are very busy and can only secure a few minutes for each patient," Ikuse told me.

Such time crunches are common in the U.S., too.

"I had a pediatrician who said they had — I can't remember the figure — but it was like 800 seconds for a sick visit," said Szymczak, who studies the factors that drive clinicians to misuse antibiotics. "They broke it down into seconds."

Given that antibiotics are generally very safe drugs, pediatricians can be tempted to prescribe them "just in case" in these situations, even if the need isn't certain, a 2019 review found. In these scenarios, patients end up taking courses of antibiotics they likely don't need.

Doctor shopping and bad reviews

One factor driving antibiotic misuse that might be unique to Japan is the competition between clinics and the customer service culture it motivates.

Japan's mandatory national health insurance makes it easy to "doctor shop." Depending on where a family is based, there may be a glut of pediatric specialists to choose from — as in metropolitan centers like Tokyo — or very few. For instance, in Okinawa, general family doctors are easier to come by than pediatricians, said Sandra Miller*, a researcher and mother of one based in the prefecture.

But across all settings, families can still flexibly choose which clinic they go to. Meanwhile, pediatricians in Japan, who make less than their peers who care for adults, can worry about losing clients to nearby practices.

Japanese clinicians used to worry that, after being denied antibiotics for their sick kids, dissatisfied parents would leave poor reviews online — particularly in Google Reviews — and thus drive away business, Okubo said. "They feared such clinic reviews."

Parents frequently used to demand antibiotics from their children's pediatricians, Okubo added. "Ten years ago, it was a common situation," he told me.

Among the clientele of Shu's Atlanta clinic, she's "seeing a trend where people aren't asking for antibiotics as much." But still, parents sometimes request the drugs when she's determined they're not needed. These requests often stem from the parents' past experiences.

"They'll say, 'Well, last time they took an antibiotic they got better faster, the next day,'" Shu said. Because mild viral infections often go away on their own in a few days, that timing could have just been a coincidence, but it leaves an impression on the caregiver nonetheless.

A parent in Japan told me about the other side of this conversation.

Kanno once brought his daughter into a clinic after she developed a bad cough after catching the flu. Their doctor prescribed antibiotics, and the cough resolved within days. Later, Kanno's son had similar symptoms, but the doctor didn't recommend an antibiotic in his case. When his son's coughing and wheezing persisted, "I asked him to prescribe that antibiotic, the same one that my daughter took," Kanno said.

The pediatrician said it likely wouldn't help but didn't explain why. The doctor said he would provide the antibiotic if the family wanted it. He ultimately prescribed it, and it didn't help. "He got my trust after that," Kanno said.

Szymczak's research has identified this "it-helped-last-time" bias as a common driver of patients' antibiotic requests that can be difficult for doctors to negotiate.

Parents' understanding of antibiotic resistance

In Japan, parents' awareness of antibiotic resistance has grown in recent years, Japanese doctors told me, but research suggests many still don't know much about it.

"I don't think parents generally understand that antibiotics don't work for colds, much less [understand] antibiotic resistance," said Dr. Yusuke Shibata of the Shibata Pediatric Clinic in Tokyo. "Explaining antibiotic resistance to parents is difficult," though he still tries to do so, he told me in an email after I visited his clinic.

Studies of U.S. parents suggest that many don't understand resistance or proper antibiotic use and that a misunderstanding of the purpose of antibiotics can drive requests for the drugs. In my interviews, I found that parents in both countries had some grasp of the concept of antibiotic resistance, but the depth of that understanding varied.

Tomomi Sato*, a New York City-based teacher and mother of two who lived in Japan as a child, said she'd heard that taking antibiotics too often could make it so your body didn't respond to them well in the future. She likened it to an urban legend about roaches that she heard from her mother and others from her hometown of Tokyo.

"You know how they talk about, in Japan, roaches are getting bigger and bigger?" she said. "They just build immunity … they don't respond to the old type of roach spray, so you have to get a new version."

Some parents are cautious about overusing medications in general but don't worry about antibiotic resistance, specifically.

"I want them to recover by trusting their own immunity, rather than relying on medication," said Risa, an HR representative and mother of two in Saku, Japan. But that said, "if it's something that's difficult to heal naturally, I think professional judgment and a prescription are necessary," she added.

Risa told me she thinks antibiotics may be medically appropriate when an illness is particularly severe or prolonged. She doesn't weigh whether the cause is likely viral or bacterial, even though antibiotics don't treat viral illnesses.

"I think that's probably the general mindset," said Fumie Kuchiba, a mother of one in Saitama, Japan, who previously worked as a registered pharmaceutical salesperson.

Other parents have a clear sense of the threat resistance poses.

"Resistance is a threat because if something is powerful enough to beat our current modern medicine, then it can wreak real havoc," said Malcolm, an editor and father of one in Atlanta. On the individual scale, he knows that resistance can emerge within an individual, potentially raising their personal risk of resistant infections. But on a global scale, he thinks of resistance as a threat as formidable as that posed by viral pandemics, such as COVID-19.

Difficult conversations

When parents seek an antibiotic that isn't medically needed, that can prompt difficult conversations with their children's doctors.

A Philadelphia-based doctor summed up the dynamic in an interview with researchers: "If patients feel like they need an antibiotic, it's very, very hard to talk them down from that. So, antibiotics are definitely overprescribed. And, you know, it's easier to say yes rather than taking time and, like, so much time to say no." This doctor and several other participants in that study felt they had "little autonomy to stand up to patient demand."

Some studies find that, when a pediatrician withholds antibiotics and a parent questions them, doctors can perceive that as negative pushback and give the drug against their initial judgment. But if a pediatrician denies antibiotics while also providing guidance for symptom relief, that conflict can be avoided and prescription becomes less likely.

Shapiro, the pediatrician in California, told me he handles such requests by walking parents through his diagnostic process and explaining the downsides of using unnecessary prescriptions. He also offers options for seeking further care — via phone, telehealth or an in-person visit — should the infection not improve as expected.

These conversations take time, and they can stir up conflict, which Shapiro said he's grown more comfortable navigating over his career. Early on, "you don't want conflict; you feel that conflict is bad, and you want everybody to be happy," he said. But ultimately, "the objective is for them to be healthy."

Multiple parents in Japan told me their doctors don't usually talk through their reasoning for checking for a given symptom or prescribing X drug over Y. "If we don't ask, he won't explain," Kanno said of their current pediatrician; but if prompted, their doctor provides good explanations, he said.

Similarly, Japanese parents told me their doctors don't often say whether or why they suspect an infection is viral or bacterial — a clarification that might help caregivers feel more comfortable forgoing an antibiotic.

Notably, Japan's antibiotic incentive program, which allows pediatricians to earn "tips" for withholding unnecessary antibiotics, provides the payment only if the doctors also explain responsible antibiotic use to children's caregivers. That requirement may be necessary to prompt that conversation.

Some doctors in Japan who claim the incentive provide verbal explanations about resistance or give parents a slip of paper that explains the basics and includes links to further information. Dr. Atsushi Miyahara of the Karugamo Clinic in Tokyo told me that, over time, his clients have become more knowledgeable about antibiotics, and insurance data related to the incentive also hints that this learning takes place. But it's unclear if these interactions can always move the needle.

Fielding parents' concerns

Shu, the Atlanta-based pediatrician, finds that some parents ask for antibiotics because they think the drugs will speed their child's recovery, without considering whether a bacterium is the culprit. Caregivers in both the U.S. and Japan also told me that they know parents who seek antibiotics as a quick remedy for illnesses.

Parents I spoke to who understood that antibiotics only treat bacterial infections added that it can be frustrating that there aren't many medicines available for viral ailments. Waiting for an infection to clear up can be stressful because you don't want your child to suffer, parents said, and the sickness also disrupts the family's normal routine of work, school or daycare.

"When your kid gets sick, things just kind of fall apart, and you need your life to get back to normal," said Katie, a journalist and mother of one in Jacksonville, Florida, who added that many parents may lack support that would help them take time off to care for their kids.

In both countries, pediatricians feel pressure to leave caregivers satisfied. While clinics in the U.S. aren't necessarily competing for patients in the same way Japanese clinics are, there is still a degree of customer service at play, Szymczak said. "That clinical encounter is very transactional, particularly in the United States," she said.

Doctors want to provide something of value — a diagnosis, medicine, reassurance — in exchange for the caregiver's time and money. Sometimes, pediatricians assume that what the caregiver wants is antibiotics, when really, they want a treatment plan to help their child, Szymczak said.

Could incentives motivate change?

While the U.S. has made progress in curbing antibiotic misuse, there's room for improvement. Could we close those gaps by using a similar approach to Japan's 800-yen incentive?

Similar dynamics are at play in both countries, with parents and pediatricians in both places dealing with similar issues. But while these pressures are similar in the clinic, a key difference sets America's situation apart: Our complex healthcare system, funded through a patchwork of insurers, can be difficult for patients and doctors to fully trust.

In the final installment, I'll talk with U.S. doctors to see what they think about Japan's approach and explain solutions that would suit our own fragmented healthcare system.

Editor's note: The names of some parents quoted in this story have been abbreviated or changed to protect their privacy. Altered names are marked with asterisks (*).

In the weeks around the 2026 annual meeting of the American Society of Clinical Oncology, my phone kept buzzing with alerts about GLP-1 drugs and cancer. The headlines were everywhere — from NPR and The Washington Post to Substack and heated exchanges on social media — all circling the same claim: Ozempic might lower the risk of cancer.

Behind those headlines is a real wave of studies, involving millions of patients. I'm a physician and clinical epidemiologist, and my team and I design and interpret these same kinds of studies that test what widely used drugs actually do.

The excitement around the idea that GLP-1 drugs can prevent cancer is running well ahead of the evidence. Not wrong, necessarily. Just not yet earned.

Cancer is among the hardest things to study, because it is not one disease but more than a hundred. Breast cancer, lung cancer and blood cancers are not variations of the same disease; each has its own distinct biology and its own mix of genetic, environmental and behavioral risks.

A single drug never gets one verdict on how it affects cancer. It gets a hundred, raising the risk of some, lowering it for others and leaving most untouched.

The early cancer concerns

Before the current buzz that GLP-1 drugs could reduce cancer risk, the worry ran in the opposite direction: that they might raise cancer risk.

Researchers were originally concerned about thyroid cancer. Studies in rodents found that Ozempic caused thyroid C cell tumors, which is why U.S. regulators added a black box warning in June 2026 to the drug that advises against its use among those with a personal or family history of related conditions.

But rodents are not people. Human thyroid C cells are less sensitive to GLP-1 drugs compared to rodent C cells because they have far fewer GLP-1 receptors. Long-term studies in monkeys did not show the same abnormal thyroid cell growth seen in rodents.

A 2025 analysis of data from 93 clinical trials found no clear link between taking certain GLP-1 drugs and thyroid cancer. European regulators reached the same conclusion in 2023 after reviewing available research on GLP-1s.

Pancreatic cancer was another concern. Here, too, researchers found no consistent increased risk from taking GLP-1 drugs in a 2025 analysis of data from 62 studies.

The reassurance is real but provisional. These drugs are young, and cancer can take decades to surface.

The cancer story turns on its head

GLP-1 drugs, once scrutinized for possibly causing cancer, are now being discussed as drugs that might prevent or even treat cancer.

A 2024 study of more than 1.6 million people with Type 2 diabetes found lower rates of 10 out of 13 obesity-related cancers in people treated with a GLP-1 drug compared to insulin.

A 2025 study of about 87,000 adults found that overall cancer rates among those who started a GLP-1 drug were roughly 17% lower, with the clearest reductions in endometrial and ovarian cancers as well as a type of brain cancer called meningioma. The risk of kidney cancer was 38% higher among patients taking GLP-1 drugs, though larger studies are needed to confirm its significance.

A 2026 study of more than 110,000 women undergoing breast imaging found a roughly 30% lower risk of breast cancer among those who use GLP-1 drugs compared to those who do not.

Researchers are also studying how GLP-1 drugs affect a patient's chances of surviving cancer. Among more than 6,800 colon cancer patients in a 2024 study, around 16% of the 103 on a GLP-1 drug died within five years compared to 37% of those who were not taking one. A study presented at the 2026 American Society of Clinical Oncology reported a 34% lower risk of death across six cancer types for those taking GLP-1 drugs.

Why the evidence is so easy to misread

While these findings are exciting, studies on the effects of GLP-1 drugs on cancer risk have three features that make them especially easy to misread.

The first is healthy user bias. People who start a GLP-1 drug tend to be healthier and wealthier than those who do not. A person with obesity who has insurance, sees doctors regularly and can afford Ozempic is far more likely to start the drug than someone with the same height and weight who lacks those advantages.

Healthy user bias is very difficult to scrub out of observational studies, which compare people as they are treated in real life rather than assigning the drug at random. The very advantages that made it possible to receive a GLP-1 prescription, not the drug itself, may be what lowered a patient's cancer risk.

The second is the choice of the comparison drug. To understand the effect of a drug, it has to be measured against something else. What it's measured against will shape the results of the study. The 2024 study reported that patients taking GLP-1 drugs saw large reductions in cancer risk compared to those taking insulin. But comparing patients on GLP-1 drugs with patients taking the diabetes drug metformin showed no clear reduction in cancer risk.

Insulin is reserved for patients with more advanced diabetes, a condition that is itself a risk factor for cancer. In these studies, patients on insulin start out with a higher risk of cancer. Measured against a group at higher risk of developing cancer, almost anything can look protective. The apparent benefit came from the comparison drug, not the GLP-1 drug.

The third is timing. It is not so much another source of bias as a clue that other biases may be at work. Cancer can take decades to develop, yet most GLP-1 studies follow people for only a handful of years. In some studies, the apparent cancer benefits of GLP-1 drugs show almost immediately. But prevention doesn't work that quickly. A drug that truly lowered the risk of developing cancer would show its effect gradually as fewer tumors surface over time, not within the first few months of taking a drug.

When cancer risk appears to drop almost as soon as a patient starts treatment, the speed is not a magical triumph of GLP-1 drugs. Rather, in my view, it is the tell: People who start these drugs were already at lower cancer risk, and the GLP-1 drugs are getting credit for that preexisting advantage.

Moreover, almost all of this research comes from a handful of high-income countries, even as uptake of these drugs is increasing globally and the burden of cancer has disproportionately grown in lower-income countries. The idea that GLP-1s may reduce cancer risk for much of the world is being inferred from data generated almost entirely in a few rich ones.

What do randomized trials show?

The cleanest way around these study biases is randomized trials, which by design make comparison groups alike from the start.

Available clinical trials tell a quieter story than the headlines. Two 2025 meta-analyses, which pool data from multiple studies — one covering 50 trials and a second covering 48 — found little evidence that GLP-1 drugs either raise or lower cancer risk.

The findings of these meta-analyses are generally more reliable than those of observational studies because their total amount of data increases their statistical power. Despite their strengths, these analyses inherit the limitations of the trials they include. Most of the trials in these 2025 studies had a short follow-up of a year or two and recorded too few cancer cases to settle the question.

Randomized clinical trials designed to answer the question of whether GLP-1 drugs affect cancer risk would need to enroll tens of thousands of people and follow them for many years. Short of that, the next best evidence will come from observational studies designed to emulate randomized trials.

Until then, the idea that GLP-1 drugs lower cancer risk is a hypothesis worth testing but not a conclusion to act on.

The bottom line

Based on the available evidence, the clearest conclusion is the reassuring one: GLP-1 drugs do not appear to raise overall cancer risk. However, more ambitious claims that GLP-1s actively prevent cancer or improve survival after diagnosis remain unproven.

Suppose GLP-1s do have an effect on cancer risk. Researchers still would not know where that effect comes from: weight loss itself, broader improvement in metabolic function, or a more direct effect on inflammation, the immune system or tumors.

The surest thing I can say is also the least satisfying: It's still too early. These drugs are far younger than the cancers they are being credited with preventing.

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

The use of nicotine pouches is increasing among teenagers and young adults in the U.S. As researchers who study nicotine use among young people and develop strategies to prevent it, we worry these discreet products might be driving a new public health crisis. It may be that more and more teens are becoming addicted to nicotine pouches under our watch.

To stop that crisis in its tracks, we need to act now. Myriad strategies would help, including eliminating flavored pouches and reducing the amount of nicotine in the products, as well as regulating their marketing and stopping companies from making deceptive claims. And while we await such regulation, informing educators, parents and teens about the harms of nicotine pouches will be key.

Why worry now? Nicotine pouches — small, pillow-like products that users place between their gum and lip — are now the second most used tobacco product among U.S. adolescents. In a recent survey, 2.3% of high school and about 1% of middle school students, an estimated 460,000 students total, reported using a pouch in the past month. More than 9 in 10 pouch users opted for flavored pouches, with mint being the most popular.

While rates of pouch use remain behind e-cigarette use, more students reported using pouches than cigarettes, cigars, smokeless tobacco or any other form of nicotine. Nicotine pouches were the only product whose use increased in the survey, while the popularity of other products declined or remained stable.

What makes nicotine pouches particularly tricky is how invisible they are to the outside observer. Unlike cigarettes, they produce no smoke. Unlike e-cigs, they generate no visible aerosol. They are small and easy to conceal. That invisibility is not a coincidence; it's part of big tobacco companies' intentional design. An adolescent can use nicotine pouches during class and no one around them would know.

Each pouch contains nicotine powder that is either derived from tobacco plants or synthetically produced, as well as other ingredients like acidity regulators and flavorings. Those flavors can be dessert-like, fruity, minty, and reminiscent of coffee or cocktails — all of which appeal to young people.

The amount of nicotine per pouch varies by brand, but generally, using one pouch is roughly equivalent to smoking one to four — or more — cigarettes. That's a problem because, although pouches don't produce smoke, nicotine is still very addictive and harmful to the developing brain.

Nicotine use can negatively affect teens' attention and impede their impulse control, hurting their academic performance and mental health. In regards to physical health, data suggest that smokeless oral nicotine products may harm some aspects of heart health and raise the risk of death in people with existing heart disease.

It may be tempting to wave away concern because the percentage of adolescents using these pouches appears relatively small. However, that would be a mistake, as doing so would mean watching history repeat itself.

Rates of e-cigarette use also started low, and by the time national data finally showed a clear increase, their use was already a deeply entrenched behavior among adolescents, with many addicted. Furthermore, national surveillance studies are, by design, snapshots in time and often lag behind what is happening in real time in classrooms and communities.

We're concerned that more teens are becoming addicted to nicotine pouches, now, and want to curb the trend. At Stanford Medicine's REACH lab, we work with thousands of schools and teachers across the U.S. every year, providing free, evidence-based tobacco prevention curriculums. We've spoken with hundreds of educators, parents and students across the country who have raised significant concerns about nicotine pouches, and presented talks to over 1,200 people on the subject.

It became clear that we must create a specific approach to prevent teens from using pouches — so, we created a course called Not So Sweet: Oral Nicotine and Smokeless Tobacco Prevention Curriculum.

The free course is designed to be used in schools or by anyone who works with teens. It explains the different types of oral nicotine and smokeless tobacco products and their many health effects, including addiction. It also lays out the marketing tactics employed by the tobacco industry to attract youth in the first place. In just a few short weeks of releasing the curriculum, we already have over 1,500 active users.

We're heartened that people are already engaging with the course, because we might already have a public health crisis on our hands.

Today's nicotine pouch market in the U.S. is dominated by three brands: the top seller, ZYN; On!; and VELO. These brands are owned by Philip Morris International, Altria, and British American Tobacco, respectively. The companies have decades of knowledge in marketing nicotine products that they are now deploying to sell nicotine pouches.

They're falling back on successful advertising tropes, telling consumers that nicotine pouches could help them socialize, unwind, or appear cool to potential romantic partners. Ads also emphasize the discreet nature of the pouches, which allows them to be used anywhere without drawing too much attention.

Through these marketing strategies, nicotine pouches have soared in popularity and sales, Zyn has become a household name, gaining nicknames like Zynnie, Zynfluence and Zyndulgence. Zyn has effectively become the "Coke" of colas, the Kleenex of tissues, the Juul of e-cigs.

What's more, the Food and Drug Administration just authorized various Zyn products to be marketed with the claim that using Zyn instead of cigarettes puts you at a lower risk of mouth cancer, heart disease, lung cancer, stroke, emphysema and chronic bronchitis. But when it comes to teenagers, we see many using Zyn or other nicotine pouches alone or alongside other nicotine products that aren't cigarettes. Unlike adult smokers who may be switching to pouches, teens may be newly introduced to nicotine addiction through products like Zyn.

It is not a matter of cigarettes versus Zyn for many teens; it is Zyn versus nothing.

Nicotine pouches might come in tantalizing flavors, but they are not sweet — they are dangerous, especially for adolescents. Reminiscent of what we've seen for decades with cigarettes and over the last decade with e-cigarettes, we once again have a nicotine product that is very appealing to and being increasingly used by young people. Yet, they contain a great deal of nicotine and are unsafe. We need to work together, now, to ensure we don't perpetuate another generation of addicted kids.

Editor's note: Bonnie Halpern-Felsher has served as an expert witness in litigation against various tobacco companies.

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.

On paper, doctors should know better — antibiotics treat only bacterial infections, and yet, physicians sometimes give them to patients who have viral infections. For patients, an unnecessary antibiotic can mean short-term side effects, like diarrhea, or more-persistent impacts, like microbiome disruption. But on a grand scale, the overuse and misuse of antibiotics pressure bacteria to gain resistance, the ability to thwart the drugs intended to kill them.

That can fuel the evolution of "superbugs" that evade most, if not all, antibiotics. In the worst-case scenario, this could contribute to tens of millions of extra deaths over the next 15 years, caused by illnesses that were once easily treated.

Given that antibiotic resistance is one of the world's leading public health threats, earlier this year, I went to Japan to investigate a program that has been remarkably effective at curbing the overuse and misuse of the drugs. I wanted to understand why doctors sometimes prescribe antibiotics when they're not needed and what approaches have been shown to improve their prescribing habits.

To answer those questions, I took a deep dive into the research on the topic and found the work of Julia Szymczak, a medical sociologist at the University of Utah School of Medicine, whose studies shed light on why doctors prescribe these medicines when they're not needed. I spoke with Szymczak about the complex social dynamics behind this behavior and whether there are reliable strategies for reining in antibiotic misuse.

Nicoletta Lanese: Could you explain the focus of your work?

Julia Szymczak: All of my work is really focused on two things. One, understanding why it is difficult for clinicians in real-world practice to use antibiotics the way that medical guidelines or evidence suggests they should be used. And then, more recently in my career, it's focused on developing interventions or strategies to help clinicians apply evidence that's informed by all that work.

I think about the decision-making about how an antibiotic is used as not simply a decision that is about pathophysiology or microbiology — it's about social dynamics. Clinicians are sensitive to a lot of other features in the care delivery environment beyond what they know to be true about antibiotics, what they know to be true or apparent about the potential infection that a patient has.

NL: What are some factors that shape that dynamic?

JS: Diagnostic uncertainty is a major challenge for clinicians. Differentiating viral versus bacterial is not [straightforward] — you don't have a slam-dunk perfect test. There are attempts to develop things to help, but the diagnostic uncertainty piece is really challenging.

Then there's the organizational characteristics around clinician decision-making, which is that everybody is incredibly time pressured, and so decision-making about antibiotics happens very quickly.

In the ambulatory or the outpatient setting, where the vast majority of human antibiotic use occurs, one of the more common themes that you will hear when you talk to clinicians is that patients often want antibiotics that are not needed. That relationship is more complicated than it appears on its face, but that is a major pressure point for clinicians.

NL: Are there other pressures that are unique to the outpatient setting, where most antibiotics are used?

JS: The major one is time pressure. I had a pediatrician who said they had — I can't remember the figure, but it was like 800 seconds for a sick visit. They broke it down into seconds. Their experience of time in the outpatient setting is so intense. Certainly clinicians in the inpatient setting [hospitals] feel time pressure, but the decision-making is distributed over an admission, which still might only be two days, but two days is different than literally five minutes.

The other thing is your interaction with that patient. That clinical encounter is very transactional, particularly in the United States, particularly for those clinicians who work in, for example, telemedicine, which is a whole other context but has similar features to urgent care or sick visits. This idea that "I'm trying to provide you with something of value" [is a big factor]. That could be a proper diagnosis. That could be the provision of a prescription. It could be reassurance that you're going to be fine. In some scenarios, people are looking for information that they can share with their employer.

Someone is coming to you to get something for a problem. Oftentimes, your assumption is that what they're coming to you for is an antibiotic. The encounter is already shaped by the patient's expectation — or your [the doctor's] expectation of the patient's expectation. There's literature that shows that, in many scenarios, clinicians might perceive that a patient wants an antibiotic when the patient actually doesn't.

Oftentimes, clinicians will say that [when] somebody has what is very likely a viral infection and they don't need antibiotics, the act of explaining why they don't need antibiotics is very difficult, particularly if they seem to want them or if they've had multiple similar episodes and they've always gotten antibiotics in the past. That discussion, the literal conversation, is difficult. It takes time. It's draining.

Then, you're in an environment where there are competing priorities around how that patient is going to evaluate your care. If a patient is unhappy because you didn't give them an antibiotic and you're concerned about the patient-satisfaction score, which is being watched by your leadership, but no one's monitoring your antibiotic use, that could tip you into the prescription of an antibiotic that isn't needed.

Then, of course, there's also the fear of missing something. On the off chance the patient has an infection and it helps them, that staves off a whole bunch of other imagined or real bad scenarios down the line.

NL: You said it's often difficult for doctors to explain their reasoning around antibiotics. Do you think that's because the technicalities of resistance are hard to explain, or something else?

JS: I don't think it's necessarily that they aren't confident in the medical explanation. A paper of mine called "I Never Get Better Without an Antibiotic" goes through all the reasons why the discussion is difficult.

Briefly: The biomedical stuff is often not the hard part. What's difficult is countering a patient who you think has already made up their mind about what they need and convincing them that they don't need it. It involves not just the provision of microbiological facts but having to explain why their past diagnoses might not have been accurate or their previous clinicians didn't make a good decision. Or people might talk about their social network: "Well, so and so got antibiotics for that." And it's like, I'm not their doctor. I didn't see them. I'm making a decision about you.

There are social reasons why that discussion is just difficult, and then you throw that into the time pressure and potentially add in even the glimmer of antagonism or conflict, and people just don't want to go there because they're exhausted.

I don't think it's about the education, about the likelihood of this being viral and "antibiotics don't work for viral infections." It's a lot more countering beliefs that aren't necessarily accurate [such as antibiotics always being needed for certain symptoms] and dealing with social awkwardness.

NL: I feel like that breaks with the common stereotype of doctors being very cold, calculating and logical.

JS: In my life of explaining to people, mostly clinical and epidemiologic audiences, there is a bit of a professional pride about evidence-based practice. Clinicians are educated deeply, and they're experts; they should be applying this evidence to every patient every time. But I always start [by saying], "You guys are human too, right?"

With antibiotics, emotions play a large role in how people are using these drugs. I've had many clinicians describe antibiotics as some of the best anti-anxiolytics — so like it's an anti-anxiety medicine for the clinician.

This idea of the cold, logical, rational actor, I mean, doesn't apply anywhere in medicine. But in particular, I think this is a great [example of a] scenario where that perfect model of decision-making just gets completely upended by contextual and structural factors, as well as social and emotional factors.

NL: Are there additional factors to consider in the context of pediatrics?

JS: A lot of my portfolio is in pediatrics, and in fact, that's where I started my work. I was a postdoctoral fellow at the Children's Hospital of Philadelphia, so I have spent a lot of time doing pediatric research.

As pediatricians say, "We have two patients: there's the child and the caregiver, the parent or the guardian." Maybe two. And so you're navigating the patient and their parents, and the interactions have a lot of complexity. There's often the challenge where the patient can't communicate what's wrong; it's difficult to convey symptoms. It adds a layer to the diagnostic uncertainty.

Then, of course, the fragility of children [is a factor], and the concern of the illness going off the rails. That feels more fearful than it does for a middle-aged adult.

But I would say one thing with pediatrics is that parents are more open to the idea of not wanting to give their kids medication that they don't need. The origins of that may come from different places than what an antibiotic steward would necessarily think of as the main reason why you want to avoid antibiotics, because it's often just about avoiding any medication. But I think that parents can be a partner in stewardship, engaging with clinicians around whether or not an antibiotic is necessary or potentially being open to this "watch and wait" — this idea of holding off to see if the body fights off the infection on its own.

When you look nationally [in the U.S.], pediatricians have done the best at improving their prescribing. Some of the biggest leaps and bounds in outpatient stewardship, it started in pediatrics. So pediatricians tend to be on the cutting edge, I would say.

NL: In pediatric outpatient settings, are there any strategies that work really well?

JS: One of the most common ones is the use of "audit with feedback," this idea of prescribing report cards where you give clinicians information at regular intervals about how well they use antibiotics and then compare it to their colleagues in their practice or in their entire health system. That's been demonstrated to work, but not in isolation.

[Editor's note: Szymczak's research suggests that certain social factors make this approach more likely to work. For instance, clinicians who respond best trust that the data they're being given is accurate, feel supported by their leadership, don't feel overly stressed or surveilled by the feedback, and are comfortable fielding patients' demands for antibiotics.]

Another piece that has been demonstrated to work, if clinicians use it, is that many electronic health records have pathways or order sets or guidelines embedded. So, if a clinician's like, "I'm going to diagnose [urinary tract infection] UTI in this patient," there's a UTI pathway that they can click on that will give them evidence-based laboratory testing and management strategies. It takes them fewer clicks to get the stuff that they need.

So, it's multifactorial, but [effective stewardship] usually involves some combination of data, education and making the right choice the easy choice.

NL: When it comes to interventions for outpatient settings, are there strategies that just don't seem to work?

JS: Education on its own, targeting clinicians or patients, is not sufficient to move the needle on prescribing.

NL: Could you elaborate on why educating patients isn't the best approach?

JS: Patient education is important but has not been demonstrated to move the needle very much. I think partially that is because the approach we have taken to education has been connected to abstract concepts like antimicrobial resistance, which is important at the population level, of course, but can be difficult to understand for the lay public and can be less motivating [for them to change their personal behaviors].

I do think we are seeing more interest from the lay public in things like the microbiome and gut health and the role of antibiotics in potentially disrupting those things. I think education to the public that directly connects to individual-level harms is more motivating than population-level harms.

NL: When it comes to interventions, do you think the surrounding cultural context affects which strategies work best? I'm thinking of the U.S. versus Japan, for instance.

JS: I do think that the surrounding cultural context will always play a role, to some degree, in how interventions to improve clinical decision-making will fare. I have also written a bit about that in another commentary that delves into the observation in the United States that we have considerable regional variation in antibiotic use that is not explained by clinical factors.

I am cautious, though, about how we think about the concept of "culture" in relation to clinical decision-making. When it comes to antibiotic prescribing, I do think there are universal factors that shape how people respond to efforts to intervene, including the management of diagnostic uncertainty; fears of missing something, leading to "just in case" prescribing; a desire to offer patients something of value; and the difficulty explaining why antibiotics are needed or not.

NL: Regarding Japan's incentive program, which pays pediatricians "tips" for improving their antibiotic use, do you think a similar approach would be motivating for U.S. pediatricians? Would it be feasible to implement that kind of strategy here?

JS: I think it could be difficult to implement here, but the details of how the program is operationalized would be very important.

We know, in general, that financial incentives have [a] mixed impact on physician decision-making. You especially have to be careful about unintended consequences. For antibiotics, it would be very important to have a clear definition of the outcome that will be incentivized and how it would be measured. With antibiotics, there can be gray areas and you don't want to incentivize undertreatment, especially if it is individual-level financial incentives.

A better approach may be in aggregate and [to] reward health systems or clinics for improved antibiotic use for conditions in which antibiotics are never needed, for example.

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

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

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

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

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

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

A Peptide by Many Names

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

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

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

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

A Surge in Popularity

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

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

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

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

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

Stacking Up

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

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

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

Use at Your Own Risk

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The quietly rising threat of resistance

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

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

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

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

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

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

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

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

Something had to shift.

Tips for appropriate treatment

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

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

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

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

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

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

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

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

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

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

Doctors say "small incentives add up"

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

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

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

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

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

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

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

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

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

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

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

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

The incentive's impact

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

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

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

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

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

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

The incentive's evolution

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Brain freeze?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Another tool in the arsenal?

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

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

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

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

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

Different trials, different benefits

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

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

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

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

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

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

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

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

How does it work?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

From parasite to antitoxin factory

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Different virus, different challenge

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

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

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

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

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

Global efforts accelerate vaccine development

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

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

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

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

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

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

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

Preparing the vaccines

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

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

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

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

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

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

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

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

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

A cheap, widely available painkiller used to treat conditions like arthritis can significantly reduce RSV in the human respiratory tract, an early-stage laboratory study suggests.

Respiratory syncytial virus (RSV) is the number one reason infants end up in the hospital in the U.S., with babies under 6 months old facing the highest risk of severe disease and death from RSV. It's also a serious health risk for adults over 65.

Currently, there are vaccines approved for pregnant people and older adults, as well as antibody-based drugs for children that can help prevent RSV infection. But there's no specific antiviral drug to treat the disease once someone is infected.

In the new study, published May 7 in the journal Virus Research, researchers found that the antiinflammatory drug indomethacin interferes with a key protein that RSV needs to invade human cells and spread. The finding hints that the drug could help treat RSV infections, but experts cautioned that laboratory findings don't always translate into real-world results.

"The way something behaves in a lab can sometimes be wildly different from how it behaves in real life," said Dr. Amy Edwards, a physician in the division of pediatric infectious diseases at University Hospitals in Ohio, who was not involved in the study. "Studies like this are very important first steps in understanding which therapeutics might be a target for future clinical trials but they are not sufficient to push for immediate use in clinical settings," she told Live Science in an email.

Dr. Aaron Glatt, the chief of infectious diseases at Mount Sinai South Nassau in New York, agreed that the findings are interesting but won't impact treatments in the short term. "It's a very preliminary paper suggesting something that is of potential great interest, but certainly is not something that's going to change one iota the practical care of patients with RSV tomorrow," said Glatt, who wasn't involved in the study.

One drug, different effects

Laboratory and clinical studies had previously shown that indomethacin has antiviral effects against a number of viruses, including herpesvirus, rotavirus and the coronaviruses behind SARS and COVID-19. In a small clinical trial, COVID-19 patients who received indomethacin got better faster than those taking acetaminophen, with most symptoms disappearing in half the time. To date, though, the drug has not been approved as an antiviral for any infections.

To test indomethacin's effects against RSV, the researchers infected cells from the human larynx (voicebox), bronchus (airway) and lungs with RSV and then treated the cells with indomethacin at various doses. The drug reduced the virus's ability to make copies of itself in all cell types and at very low doses, without harming the cells themselves.

The researchers found that indomethacin worked only when given after the virus had already entered cells. Giving it beforehand or during the brief window when the virus first attaches to cells had no antiviral effect.

The team also tested aspirin, which works in a very similar way to indomethacin as a painkiller; both drugs are nonsteroidal anti-inflammatory drugs, known as NSAIDs. Aspirin had no effect on RSV at all, suggesting that indomethacin's antiviral effect is separate from its pain-killing properties.

Indomethacin is already used in premature babies to help treat patent ductus arteriosus (PDA), a heart condition where a blood vessel that should close after birth fails to do so, Edwards said. (In that context, indomethacin is given intravenously.)

"There is a long history of it being used relatively safely in infants," Edwards said.

For short-term use, indomethacin is generally very safe, Glatt said. However, with higher doses and prolonged treatment, it can carry a risk of side effects, including kidney issues and bloody stool.

More research is needed to determine whether indomethacin benefits people with RSV. The researchers also point out that more work is needed to understand the exact mechanism whereby the drug stops the virus from multiplying and spreading.

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

Walk into any U.S. pharmacy, and you'll find a multicolored range of melatonin supplements marketed as sleep aids for adults and children alike.

The body-made hormone melatonin streams through our systems every evening, preparing us for rest. But while melatonin supplements claim to mimic this natural process, experts say bottles stamped with claims like "100% drug free" may be misleading.

Melatonin carries little risk when used correctly, but as a dietary supplement, it skirts the strong governmental regulation that's reserved for pharmaceuticals. This has led to inaccurate dosage labeling, incomplete safety information, and scant research into melatonin's long-term effects on kids, some scientists argue. Researchers worry that, given that many people perceive melatonin as harmless, some are misusing the supplement by taking unnecessarily high doses at improper times of the day.

"It's being promoted like there's absolutely no risk … [People say] 'It's all natural, and it just is a safe sleep aid,'" said Dr. Pieter Cohen, a Harvard Medical School researcher who studies supplements. "And that's where you can get into trouble."

The U.S. Food and Drug Administration (FDA) classifies melatonin as a supplement, while countries like the U.K. and Australia deem it a medication. This designation comes with a level of governmental oversight that U.S. supplements aren't subject to. Given melatonin's soaring popularity, some experts think the United States should follow suit and make melatonin an over-the-counter drug.

But if melatonin is already produced naturally by the body, why would the supplement version be riskier? Live Science spoke with experts to find out.

Supplements aren't well regulated

In the U.S., a 1994 federal law required that supplements be regulated as food, not drugs. The FDA doesn't assess the safety, efficacy or manufacturing quality of supplements before they're marketed but instead intervenes if harmful side effects are reported or if it's made aware of inaccurate labels. This largely leaves the supplement industry to self-regulate.

Cohen's research suggests that actual melatonin concentrations in products may range from 74% to 347% of what's reported on the label. Meanwhile, safety warnings and instructions on the best way to use melatonin aren't required on labels. Still, many popular brands adhere to voluntary melatonin labeling guidelines from the Council for Responsible Nutrition, a supplement trade organization. These guidelines include disclaimers like "may cause drowsiness" and "for occasional or intermittent use only."

Despite such disclaimers, nearly 1 in 5 school-aged children use it regularly as a sleep aid, a trend scientists are concerned by. Long-term safety data is lacking in kids, in part because melatonin hasn't gone through the safety trials required of new drugs. And melatonin isn't patented, so there's no strong incentive for drug companies to invest in safety studies, according to Debra Skene, a neuroendocrinologist at the University of Surrey in England. "There's no money in it," she said.

Many parents inaccurately view melatonin as akin to a "little glass of warm milk," Cohen said. But if parents give children high-dose supplements or multiple doses at once, "you're talking about side effects and getting sick and not helping sleep," he said.

Calls to U.S. poison control centers about melatonin poisoning in young children have shot up with the supplement’s popularity. This has been driven by accidental ingestions in children under 5, and in some cases, kids had serious symptoms, like respiratory failure or seizures. That said, some of those effects may be due to certain melatonin products' inclusion of serotonin, which can be dangerous if consumed in large quantities.

Evidence does suggest that melatonin can help children with attention-deficit/hyperactivity disorder and autism get to sleep, among whom sleep problems are common. But the potential benefits of melatonin for neurotypical kids are less clear.

One concern scientists have is that the regular use of melatonin may affect puberty. In various animal species, melatonin helps regulate reproduction, and supplemental melatonin can disrupt these effects. The few human studies that exist haven't shown clear effects on puberty, but there hasn't been an in-depth study tracking hormone levels in the blood, said Helen Burgess, who researches the circadian rhythm at the University of Michigan.

"I'm OK with intermittent short-term use," she said of melatonin supplementation in kids. But given the lack of data, she suggested that parents consult a pediatrician to look for another solution if their child needs melatonin regularly.

The lesser-known effect of melatonin

Supplements supercharge the body's supply of melatonin, said Margarita Dubocovich, who studies melatonin at the University at Buffalo. Supplement dosages generally range from 1 to 10 milligrams (mg), while adults produce about the equivalent of a 0.3-mg pill nightly, she said.

When taken orally, supplements and medications pass through the digestive tract before reaching systemic circulation, meaning the full dose of melatonin won't necessarily make it into the bloodstream. However, the amount that circulates will still be far higher than what's naturally produced in the body, said Skene.

Upping your melatonin dosage doesn't knock you out; the drowsiness triggered by the supplements is generally mild. The supplement also avoids the side effects of conventional sleeping pills: memory loss, gastrointestinal issues and next-day "hangovers."

However, melatonin has a lesser-known effect. Given its role in regulating the circadian rhythm — the 24-hour clock that regulates many bodily systems — it can scramble the body's sense of timing when regularly taken outside your bedtime, such as too early before bed or in the middle of the night.

That's why melatonin can help treat jet lag if taken for multiple days just before or after traveling. But if people take pills as they're tossing and turning throughout the night, this could throw off the circadian rhythm, Dubocovich said. This practice may induce a kind of jet lag (without the perks of international travel). In the short term, that can come with drowsiness during the daytime, irritability, upset stomach, brain fog and insomnia.

"I think that melatonin could be good if you take it in a controlled manner and the right dose," Dubocovich said, suggesting a few milligrams taken right at bedtime. "But how people are taking it [currently], they are intoxicating themselves."

Not all researchers agree that melatonin-induced jet lag poses a big risk, but taking more than 3 mg in the middle of the night still "isn't a good idea," said Burgess. This dose may linger in the body through the morning, she said, leading to next-day grogginess.

Burgess' research suggests that supplemental melatonin is most effective at shifting the biological clock forward in time, which happens when it's taken in the early evening. Still, she said the impact of melatonin on the circadian rhythm "just does not seem to be really recognized or understood by the public at all."

Should melatonin be a drug?

If melatonin were an over-the-counter medication, it would require clear labels with instructions and accurate dosing. "You should be able to know what dose you're getting, and it shouldn't be sold in whatever dose the manufacturer … decides to pour in on a given day," Cohen said.

Yet, reclassification could disrupt access to a relatively safe sleep aid that many consumers rely on, argued Jeff Ventura, a spokesman for the Council for Responsible Nutrition, the supplement industry trade organization that created the melatonin labeling guidelines. "Moving melatonin into the drug category would require formal FDA drug approval pathways, which could limit consumer access, reduce product variety, and significantly increase costs" for both manufacturers and consumers, he told Live Science in an email.

It's unlikely the supplement will be made an over-the-counter drug anytime soon. Cohen attributes the lack of a serious movement to the supplemental industry lobby, which includes the Council for Responsible Nutrition. "Any move to take such a great money winner like melatonin out of their hands would cause them to fight it tooth and nail," he said.

Burgess, who serves on the scientific advisory board for the melatonin brand Natrol, agrees that purity is an issue. However, she said she isn't too concerned about melatonin's availability, given its "pretty benign effects." Still, she suggests going with a big name brand with a US Pharmacopeia (USP) stamp verifying its listed ingredients are accurate; USP is a nongovernmental organization that sets quality standards for medicines, food ingredients, and dietary supplements.

After studying the hormone for 40 years, Dubocovich agrees that melatonin should be regulated as an over-the-counter medication.

"Melatonin can help support a good night’s sleep, especially in small doses that mirror the body’s natural rhythm," Dubocovich said. "But not all melatonin is created equal."

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

How much do you know about sleep and dreams? Find out with our sleep quiz!

The patient: A 6-month-old boy in Bangkok

The symptoms: The child was brought to a hospital after he'd had a fever and cough for 24 hours.

What happened next: Doctors tested the boy for COVID-19, and the test came back positive. They prescribed favipiravir, a broad-spectrum oral antiviral that is frequently used to treat RNA viruses, such as influenza, Ebola and some enteroviruses. Coronaviruses are also RNA-based, and doctors first started using it to treat COVID-19 in 2020.

The plan was for the child to be administered favipiravir tablets on the first day of hospitalization and then given the drug in liquid form for the next four days. But about 18 hours after he began the treatment, the boy's mother noticed that his eyes, which were normally dark brown, had turned bluish-purple.

The corneas — the transparent, dome-shaped barriers covering the fronts of the eyes — appeared blue in sunlight. There was no visible discoloration of his skin, nails or hair, according to a report of the case.

The diagnosis: Doctors suspected that favipiravir might be causing the blue tint.

A year earlier, in 2021, physicians in Goa, India, described the case of a 20-year-old man who also developed a bluish tinge in his corneas after he began favipiravir treatment for COVID-19. The side effect had never been documented before, they wrote in a report of his case. In that case, the doctors advised the man to stop taking the drug, and his corneas returned to their normal color the next day.

This unusual eye color change may stem from how the body breaks down the antiviral medication, releasing fluorescent chemicals that collect in the cornea, Dr. Vik Sharma, an eye surgeon at the London Ophthalmology Centre who was not involved in either case, previously told Live Science in an email.

Four female COVID-19 patients in Turkey developed similarly fluorescent features, physicians in Istanbul reported in January 2021. All of the patients had taken favipiravir and developed a glowing blue-green tint in their hair and fingernails that was visible under a Wood's lamp, which uses long-wave ultraviolet light to detect fluorescence.

In July 2021, another team of Turkish researchers documented fluorescence in whole favipiravir tablets and in tablets that had been dissolved in water. This "signified a robust association between the fluorescence of the ocular surface and favipiravir," the child's doctors wrote in their report.

The treatment: After three days of favipiravir treatment, the child's COVID symptoms improved, and on the fifth day, a pediatrician advised discontinuing the drug. The child's corneas reverted to their normal color five days later.

Two weeks after that, an ophthalmologist examined the child's eyes and found that they appeared normal, with a clear cornea and no sign of a bluish color. Nor was there any fluorescence in the cornea.

The disappearance of the blue took several days in the child's case, while the 20-year-old man's discoloration vanished almost immediately. Doctors did not know the reason for the delay, but they proposed that the patient's age and the medication dosage could be factors.

It's also possible that the baby was urinating less frequently — a potential side effect of favipiravir, which elevates levels of uric acid in the body — which meant that the compounds affecting his eye color lingered in his tissues.

What makes the case unique: Side effects of favipiravir are uncommon, but may include diarrhea, high levels of uric acid in the blood, and lower levels of neutrophils, a type of white blood cell that helps the body fight infection. Other less-common side effects include abdominal pain, nausea and a low level of platelets, blood cells that assist with clotting.

Although this child's case is not the first example of favipiravir triggering corneal discoloration, it is the first recorded instance of a pediatric patient developing blue eyes in response to favipiravir therapy, the doctors noted in the case report.

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!

The patient: A 68-year-old woman in the U.S.

The symptoms: Over the course of six weeks, dark patches appeared on the woman's arms and legs. The splotches ranged from a bruise-like dark blue and purple to jet-black.

What happened next: While examining the patient, doctors noticed blue-gray "hyperpigmentation" on the woman's forearms and shins, as well as on the sides of her tongue. The woman noted that the patches had first appeared on her legs before cropping up elsewhere.

She also told doctors that, two weeks before the patches appeared, she'd started a course of minocycline, an oral antibiotic.

She had been prescribed a daily 100-milligram dose of the drug to treat symptoms of rosacea, which causes chronic inflammation and redness of the face. This inflammation can drive the formation of small, red bumps and pus-filled pimples on the skin, and evidence suggests that antibiotics like minocycline can help eliminate those bumps. In addition to killing bacteria, the drug is known to have anti-inflammatory effects, the latter of which may best explain how it treats rosacea.

The diagnosis: A well-established side effect of minocycline is hyperpigmentation, in which patches of skin become darker than the skin surrounding them. In this case, the woman was diagnosed with type II minocycline-induced hyperpigmentation, which is "defined by blue-gray discoloration of normal skin on the extensor surfaces of the arms and legs," according to a report of the case.

The antibiotic can also trigger two other types of hyperpigmentation. Type I shows up as blue-black discoloration on scarred or inflamed skin on the face, rather than on healthy skin on the limbs, and type III appears as muddy-brown pigmentation on sun-exposed areas of the body.

The treatment: Doctors advised the patient to stop taking minocycline and to avoid sun exposure, as ultraviolet light is thought to worsen hyperpigmentation in these cases. Six months later, the hyperpigmentation in her limbs had "abated somewhat" but was still visible.

What makes the case unique: Hyperpigmentation is not necessarily uncommon for minocycline users with rosacea; one frequently cited study estimates that the side effect shows up in about 28% of people in this population, although that research included only a small number of patients. The true incidence of the side effect is unclear.

This woman's case was notable, in part, because of how quickly the discoloration developed ‪—‬ within two weeks of starting minocycline. While type I minocycline-induced hyperpigmentation can show up soon after a person starts taking the drug, type II and type III usually take longer to appear.

"It typically develops after months of treatment but may rarely occur with shorter courses," the case report authors noted. Type II and type III are thought to be dose-dependent, in that a certain amount of the drug needs to build up in the body before the dark patches show up.

The cause of minocycline-induced hyperpigmentation isn't fully understood, but it's thought to result from how the antibiotic gets broken down in the body. The metabolites, or byproducts, created in this process bind to iron and are then picked up by immune cells called macrophages, in which they accumulate. Additionally, the drug may drive up the activity of cells that make melanin — the pigment that gives skin its color — while also binding to melanin, thereby creating complexes of dark pigment that linger in the skin.

Once a person stops taking minocycline, the pigmentation can take months to years to dissipate, reports suggest. In type III cases, it sometimes never goes away.

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!

The weight-management drug Wegovy has become widely used and now comes in a convenient pill form — but recently, a study flagged that the popular medication may carry a risk of "eye stroke," also called ischemic optic neuropathy (ION), which can cause rapid vision loss.

But Wegovy users shouldn't panic, experts told Live Science. For now, the link between the drug and eye stroke is far from confirmed and the overall rate of the condition is extremely low. In the study, published in March in the British Journal of Ophthalmology, ION occurred in less than 1% of patients who reported experiencing side effects when taking Wegovy.

Because ION is this rare, the risks "do not outweigh the benefits of semaglutide," the active ingredient in Wegovy and Ozempic, Dr. Amanda Adler, a professor of diabetic medicine and health policy at the University of Oxford who was not involved in the study, told Live Science in an email.

She added that the U.K.'s Medicines and Healthcare products Regulatory Agency — the U.K. equivalent of the Food and Drug Administration (FDA) — is informing people who use semaglutide to "seek urgent medical care if they notice their eyesight getting worse quickly."

A potential signal

This isn't the first time a connection has been drawn between weight-loss drugs and eye health concerns.

A review of the medical literature published in 2025 flagged a potential risk tied to semaglutide. In clinical trials and observational studies, the drug carried a slightly higher risk of eye stroke in those using it for diabetes management compared with non-users. That risk wasn't seen in patients using the drug for weight loss, though, and the overall rate of eye stroke in semaglutide users was still low.

The new BJO study takes this existing work and delves deeper into Wegovy, one of the most common drugs taken for chronic weight management. The findings showed a connection between Wegovy and ION, which is caused by interrupted blood flow to the optic nerve, causing damage that can lead to rapid vision loss.

"This is a very sudden and painless way to lose your eyesight," Barbara Pierscionek, deputy dean of research and innovation at Anglia Ruskin University in the U.K., told Live Science. "You can lose vision in one of your eyes or both of them. We're not quite sure exactly how it happens, but it is essentially a blockage of the blood vessels in the eye," said Pierscionek, who was not involved in the new study.

The team behind the study wanted to understand if certain weight-loss drugs presented a higher risk of ION than others. To find out, they scoured reports of side effects associated with medicines that were submitted to the U.S. FDA between December 2017 and December 2024.

They identified 31,774 reports that involved semaglutide-based drugs; of those, 3,070 were attributed to Wegovy and 20,608 to Ozempic. Twenty-eight of the Wegovy reports noted ION, compared to 47 of the Ozempic reports.

Ozempic has been on the market longer than Wegovy, having been approved in 2017 while Wegovy was approved in 2021. Factoring in this time difference, when it comes to ION, the proportional risk was higher with Wegovy than Ozempic, the study authors concluded.

A lesser-known semaglutide drug called Rybelsus, which is approved for diabetes management, had no notable association with ION in the study.

Weaknesses of the study

Importantly, the side effect reports reviewed in the study are not verified by experts. Instead, they serve to provide early hints about users' experiences with a given drug after it's been approved.

"The research did not study patients directly," Brian Woods, an ophthalmology expert at the University of Galway who wasn't involved with the study, told Live Science in an email. "Instead, it analyzed reports submitted to a large US drug safety database where suspected side effects are logged. These systems are useful for detecting possible warning signals but they cannot determine how common a complication actually is."

If a concerning pattern crops up in the database, regulators can then launch a formal investigation to see if the drug's use or approval status should be adjusted.

"The [BJO study's] findings are based on fewer than 100 reports of ION among tens of millions of entries," Woods said. "Such reports are not independently verified and lack important medical details." So while this data hints at a link between Wegovy and eye-stroke risk, more research is needed to know if the drug directly causes the condition.

"The adverse effect observed may be causal or may be because semaglutide is offered to people already at higher risk of ION, that is," Adler said. For instance, high blood pressure and cardiovascular disease are risk factors for ION, she noted. That said, diabetes is also a risk factor for ION, and Ozempic is specifically approved for people with diabetes, while Wegovy is not, though some people with diabetes may still be eligible for it. So presumably, Ozempic and Wegovy users both may be likely to have a slightly elevated risk of ION at baseline.

One difference between Wegovy and Ozempic is that the former contains a higher dose of semaglutide, but it's unclear if that affects ION risk.

"While it is biologically plausible that dose alone could be causing this, it remains unproven," Woods said. "At this stage, there is a significant likelihood that differences may be confounded by baseline risk and metabolic dynamics rather than dose alone. So, for now, the jury is still out on this key factor."

If the higher dose is relevant, that could be a concern because Wegovy just announced a higher-dose alternative of its drug.

"An increased dose would cause an increased risk, but only to those who are vulnerable," Pierscionek said. "Not everybody is at risk of ION when taking these drugs," she emphasized.

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

A new blood test can detect a precursor to liver disease, which can in turn be a harbinger of cancer. The hope is that the test could help prevent liver cancer before it occurs.

The test uses a machine learning model to analyze free-floating genetic material circulating in the blood. In the new study, researchers used it to detect bits of DNA that point to early-stage liver scarring, or fibrosis. This early scarring, if left untreated, can develop into severe liver scarring, called cirrhosis, and eventually cancer.

The test still needs to go through follow-up testing to show it accurately flags early cases of fibrosis without falsely flagging people without the condition. But the current study's results raise the prospect that the test could eventually identify people at risk of liver cancer before it emerges, said study lead investigator Dr. Victor Velculescu, co-director of the cancer genetics and epigenetics program at the Johns Hopkins Kimmel Cancer Center.

"The best way to intervene in liver cancer is not to detect liver cancer early, but to detect early liver disease," Velculescu told Live Science.

Once detected, fibrosis can be reversed with antifibrotic medications, lifestyle changes and other treatments, he added. Cirrhosis, by contrast, is largely irreversible.

Signs of disease written in the blood

Millions of Americans have liver fibrosis but don't know it. Risk factors for developing this scarring include liver inflammation (hepatitis), diabetes, high blood pressure and obesity. When caught early, liver fibrosis is reversible.

But currently, the traditional clinical assessments — such as the fibrosis-4 (FIB-4) blood test that uses age, liver enzymes and platelet blood counts to estimate liver scarring levels — fail to detect early-stage liver disease, Velculescu said.

In the new study, published March 4 in the journal Science Translational Medicine, Velculescu and colleagues first looked at blood samples from 423 people with and without liver disease. By analyzing tens of millions of fragments of cell-free DNA in the blood, they uncovered markers that could distinguish patients with early liver scarring from those without any degree of liver disease.

Also called free-floating DNA, cell-free DNA includes small snippets of genetic material that are released into the blood when cells regenerate and die. Instead of looking for specific mutations, or changes in the letters of DNA, the team used a computer model that looked for larger, genome-wide patterns across all the free-floating DNA shed by cells.

"We're trying to pick up on changes that are potentially occurring in disease that can occur across the entire genome," study first author Akshaya Annapragada, an MD/PhD student in Velculescu's lab, told Live Science. "So, you have more opportunities to find something."

They identified several factors that were collectively tied to early liver disease. These included the length of the DNA fragments and how often cells shed repetitive sequences of DNA. They also spotted key epigenetic changes, or marks on the genome that change gene activity without altering the underlying DNA code.

With these factors in hand, they built a test that looked for these patterns in blood.

To then assess how well the blood test worked, the team evaluated it in another 221 participants: 30 with early liver disease, 85 with advanced liver disease and 106 with no liver disease. The test detected 50% of the early liver disease cases and about 78% of the advanced cases.

It correctly identified disease-free people in 83% of cases, meaning it falsely flagged liver disease 17 times out of 100.

By using machine learning to spot patterns across the whole genome, the new research enables the team to analyze billions of fragments at once, said Alain Thierry, a professor and research director at INSERM, the French National Institute of Health and Medical Research, who was not involved in the study.

This is an advantage over earlier blood tests that looked for only specific mutations or disease markers, and had to sequence the genome thousands of times to get enough DNA to interpret, Annapragada said. By contrast, "this test only sequences the genome only, like, one to two times, so it's much cheaper and more efficient."

The next steps are larger clinical trials to validate the machine learning models that can detect liver fibrosis, Velculescu said

The researchers said they hope tests like theirs eventually pave the way for noninvasive methods of screening for many diseases from a single blood test, which would enable earlier diagnosis and treatment of diseases before they become chronic and irreversible.

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

A new synthetic opioid designed to relieve pain could hold promise for replacing addictive painkillers like morphine or fentanyl in patients, a study in lab rats suggests.

The research hints that the new opioid carries a lower risk of addiction — though it's likely not completely risk-free.

Opioids are very effective at treating severe pain associated with surgery, physical trauma and disease. But they can also cause euphoria, which increases the odds that patients will become addicted and abuse these drugs outside a medical setting. When they use opioids regularly, users can develop tolerance and often increase their dosage to compensate; high doses, in turn, can slow down breathing and lead to a fatal overdose.

In the 1950s, a class of highly potent opioids called nitazenes was developed and offered 1,000 times more relief than morphine, but they carried a much higher risk of overdose. Michael Michaelides, a pharmacologist at the National Institute on Drug Abuse, told Live Science in an email that "research using nitazenes was stopped and they were largely forgotten until they re-emerged as street drugs a few years ago."

But now, in a study published April 1 in the journal Nature, Michaelides and his colleagues developed a new patented nitazene called DFNZ that offers pain relief without slowing down breathing as sharply as other nitazenes do. That makes it much less likely to cause an overdose.

Additionally, while many opioids cause euphoria by flooding the brain with the neurotransmitter dopamine, DFNZ did not trigger a large surge of the chemical. That suggests it might not cause euphoria and thus may carry a lower risk of addiction.

Measuring addiction risk

To demonstrate that DFNZ could be less addictive than other opioids, the team allowed rats to self-administer the drug and use it as much as they liked. To do so, they inserted a catheter tube into the rodents' jugular veins and hooked up the tube to a lever that the rats could press to get a hit of DFNZ. They also ran the same experiment with morphine.

Regardless of whether the rats were hooked up to a morphine lever or a DFNZ lever, they would repeatedly self-administer the drug, which suggests both drugs have the potential to cause addiction.

Next, the researchers halted drug administration via the lever to assess whether the rats experienced withdrawal symptoms. Looking for signs like teeth chattering, jumping or paw tremors, they found that rats cut off from morphine experienced worse withdrawal than rats denied DFNZ. They also found that rats coping without morphine would futilely press the defunct lever over and over in hope of a fix, whereas rats discontinuing DFNZ were quicker to give up this behavior. That suggests DFNZ might be less addictive than morphine.

"The studies are good at suggesting that it has a weaker addictive potential than some of the other drugs out there," said Natashia Swalve, an assistant professor of behavioral neuroscience who studies drug addiction at Grand Valley State University and was not involved with the work. However, she cautioned that the self-administration test "still leads me to believe that there is a potential for an addictive profile."

In another experiment, the researchers wanted to see whether DFNZ might be useful for treating heroin addiction. They administered heroin to rats, provided them with a lever to self-administer more heroin, and then treated them with either DFNZ, fentanyl or a placebo drug. Rats receiving the placebo pressed the lever significantly more times than rats treated with either fentanyl or DFNZ, suggesting these opioids tempered the urge to use heroin.

Based on these results, "DFNZ could potentially be used for the treatment of opioid use disorder similar to how methadone or buprenorphine are used," Michaelides suggested. "But rigorous multi-phase clinical trials would have to first demonstrate its safety and efficacy, and it would need to receive regulatory approval."

In their paper, the researchers noted that they didn't study the impact pain could have on the addictive potential of DFNZ. In other words, there's a worry that the pain relief provided by the drug could pose a higher risk of addiction, even in the absence of euphoria.

With aspirations that the new opioid may one day be used to treat chronic conditions such as cancer or post-surgical pain, it's important to determine whether rodents in constant pain are more likely to repeatedly press the lever even when DFNZ is withdrawn.

Swalve added that the researchers only tested the addictive potential of a pain-relieving dose of the drug. They should also assess higher doses, she said, because people could potentially take larger volumes than prescribed.

With multiple safety tests and clinical trials still to run, Swalve expects it would take at least a decade before DFNZ reaches the hospital.

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

An experimental treatment has doubled one-year survival rates for pancreatic cancer, one of the deadliest types of cancer, a new study reports.

The drug, called elraglusib, targets the protective web that pancreatic tumors build around themselves, thus helping immune molecules and chemotherapy better penetrate the tumors. The results of the trial showing elraglusib's safety and efficacy were published April 14 in the journal Nature Medicine.

"We're starting to see, for the first time, drugs that are effective outside of the standard chemotherapy that we have used for pancreatic cancer for the last two decades," said study co-author Dr. Devalingam Mahalingam, an oncologist at Northwestern University Feinberg School of Medicine.

A rare win in pancreatic cancer treatment

Pancreatic cancer has one of the poorest prognoses of all cancers, with patients who are newly diagnosed having only a 13% chance of surviving five years with the disease. Often, the problem is that pancreatic cancer is not detected until it has progressed substantially,

"Most patients, unfortunately, present with advanced disease," Mahalingam told Live Science. "There are no screening tools to pick things up earlier."

In addition, the region surrounding the tumor, called the tumor microenvironment, poses problems for pancreatic cancer treatment. "It's very dense and fibrous," he said, which reduces the effectiveness of typical treatments for the condition, like chemotherapy.

Elraglusib addresses this problem by suppressing a protein called glycogen synthase kinase-3 beta (GSK-3 beta).

Petri-dish studies had previously shown that GSK-3 beta helps keep pancreatic cancer cells alive by boosting the activity of a protein called nuclear factor κB, which helps pancreatic cells resist programmed cell death — essentially a cellular "self destruct" button. The drug also suppresses molecules that make the tumors resistant to the immune system.

Elraglusib boosts survival time

Past work showed that elraglusib was safe for patients with a range of cancers, but to see whether it improved pancreatic cancer outcomes, Mahalingam and his colleagues tested the drug in 286 people who had been recently diagnosed with pancreatic cancer. The patients received chemotherapy with or without elraglusib. Nearly all of the patients in the trial had advanced, metastatic disease, meaning the cancer had spread to other parts of the body beyond the pancreas.

Half of the patients given elraglusib and chemotherapy were still alive after 10.1 months, while half of the patients given chemotherapy alone were still alive after 7.2 months. Of the patients given elraglusib, 42% lived a year after their diagnosis, compared with 22% of those who received only chemotherapy.

Although elraglusib increased overall survival time, it didn't lengthen the amount of time that patients lived without their cancer growing or spreading to new areas.

The trial's protocol required patients to stop receiving treatment if their disease progressed, and Mahalingam said the trial's extremely sick cohort meant the chances of progression were high. As a result, some patients were switched to palliative care before the drug's effects became obvious. These patients may have lived longer if they had stayed on the trial and received more doses of the drug, Mahalingam speculated.

Future treatment options

In lab-dish experiments and animal testing, elraglusib also made the environment surrounding the tumor more permeable to immune cells and chemotherapy, and it reduced tumor cells' ability to fight off immune cells once they infiltrated the tumor.

These abilities, combined with the drug's safety, could make it a useful complement to other pancreatic cancer therapies, such as immune checkpoint inhibitors, which enhance the immune system’s ability to recognize and kill tumor cells, or KRAS inhibitors, which stop mutant proteins that drive tumor growth, Mahalingam said.

Elraglusib could potentially treat other types of cancer in combination with chemotherapy, Mahalingam noted. A decade ago, other GSK-3 beta-targeting drugs were tested against other solid tumor cancers but never made it past the early stages of clinical testing. But therapeutic doses of those drugs didn't reach the tumors — an obstacle elraglusib has overcome, Mahalingam said.

The new study is also notable because the drug was developed without the involvement of large pharmaceutical companies.

"It's never easy to develop a drug from an academic institution," he added. "It's nice to see some that come true."

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

A common antiseptic used to clean hospital patients' skin can linger on surfaces for hours, creating breeding grounds for bacteria to become tolerant, or even gain resistance, to chemicals that usually kill them.

Once they develop "tolerance," bacteria can survive certain concentrations of chemicals more easily than their peers do, but they can still be killed by the doses of antiseptics typically used for cleaning. Antiseptics include chemicals, such as alcohol, iodine or hydrogen peroxide, that are used to disinfect surfaces or the skin. "Resistance" is a greater concern because it enables bacteria to grow even when exposed to concentrations of an antiseptic that would typically kill them.

According to a study published April 2 in the journal Environmental Science & Technology, as they learn to tolerate faint traces of antiseptics, bacteria might be swapping bits of DNA with each other. That same DNA might also help them dodge drugs designed to treat bacterial infections — namely antibiotics.

The study adds to a growing body of research mapping the hidden environmental stressors that can encourage bacteria to evolve these tolerance and resistance genes.

"Antimicrobial resistance comes from a lot of different places," said lead author Erica Hartmann, a professor of civil and environmental engineering at Northwestern's McCormick School of Engineering. "To really tackle the problem, we need antimicrobial stewardship, responsible use in agriculture, and we need to think about responsible use of chemicals in other environments, as well," she told Live Science.

Practicing stewardship means using antimicrobial agents like antibiotics and antiseptics sparingly in order to prevent bacteria from evolving tolerance or resistance.

Tolerant bacteria travel by air

In the study, Hartmann and her colleagues tracked bacteria with tolerance to chlorhexidine, a commonly used chemical applied to patients' skins before surgery or catheter insertion. They searched for these bacteria in an intensive care unit in an Illinois medical center.

Researchers swabbed 219 samples from bedrails, nurse call buttons, door sills, keyboards, light switches, and sink drains in six locations around the ICU in 2018. The rooms were quite clean, they found, but they were able to isolate about 1,400 bacteria and they found that 36% showed some tolerance to chlorhexidine.

In the lab, the researchers applied chlorhexidine to common materials — plastic, metal and laminate — and then tracked how long the antiseptic lingered on the surfaces, including after they cleaned the materials with water and other chemical cleaners. They found that, even after cleaning, traces of the antiseptic persisted on surfaces for at least 24 hours.

These lingering traces weren't strong enough to kill bacteria. But these types of microenvironments, in which bacteria are exposed to non-lethal doses of a chemical that usually kills them, always raise alarm bells.

In these settings, the bacteria that thrive are those that carry genes that help them survive the chemical's effects. These tolerant bacteria outcompete those that lack tolerance genes and thus grow more abundant. The worst case scenario would be that bacteria become so used to fighting off a chemical — and so good at it — that they become resistant to its effects.

The team found chlorhexidine-tolerant bacteria throughout the hospital rooms, even though the antiseptic was applied only to patients' skin. The sink emerged as a hotspot for these bacteria.

Hospital sinks have become a focus for those studying antimicrobial resistance in recent decades. Bacteria love the humid, warm U-bends found in sinks, and they will do what they can to stay there, even if they are exposed to watered-down chemicals that get washed down the drain. This creates a perfect environment for tolerance and resistance to emerge.

Sinks can also spread bacteria by generating aerosols, or tiny particles that can float through the air; as water leaves the tap, hits standing water, or splashes against the drain, these particles can fly through the air. The researchers' swabs showed that tolerant strains could be found on door sills, suggesting they traveled through the air and settled up there.

Antiseptics still work really well

Some of the antiseptic-resistant bacteria carried a plasmid — a small DNA loop that can be transferred between bacteria — that not only helped them tolerate chlorhexidine but could also help them resist antibiotics, such as carbapenems. This type of gene transfer is a well known way that bacteria gain resistance to antimicrobials, and it can take place between bacteria of totally different species.

That is "really quite important," said Danna Gifford, a lecturer in antimicrobial resistance at the University of Manchester in the U.K., who wasn't involved in the study. This finding suggests that antibiotic resistance could be accelerated "without the use of antibiotics," she said, driven by antiseptic exposure alone.

But let's be clear: chlorhexidine is still highly effective at killing germs. The bacteria observed in the study could only survive very low concentrations of the chemical, far below the amounts used to clean patients' skin.

"I don't think that this supports a really conservative approach" to using chlorhexidine, said Gifford, adding that limiting the antiseptic's use in high-risk settings like ICUs, without proper clinical evidence, could put vulnerable patients at risk of infections. But this work, alongside other recent research, still raises the question of whether we need to be more cautious about our use of antiseptics, Hartmann and Gifford agreed.

Further studies should look into whether these effects can be seen in other settings — for instance, in the home or in veterinary clinics — to better understand how these antiseptic residues affect bacteria, the study authors wrote.

Whether we should be reserving antiseptics for "high-risk situations" is "probably worth more investigation," said Gifford. Often for household cleaning, "plain soap and water are more than sufficient for our cleaning and hygiene," Hartmann noted, so that might be a setting where antiseptic use can be reduced.

In the meantime, "we are running out of antibiotics that work effectively," she said. "We are not quite fully there yet, but if we don't intervene in the things that we do now, we're going to end up in a situation in the future where we can't do simple things like treat dental infections or do surgery because we can't then give patients antibiotics after treatment."

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

Imagine a single vaccine that protects against the flu, COVID-19, lung-invading bacteria and seasonal allergens all at once.

Scientists recently developed a nasal spray to protect against multiple respiratory diseases, including seasonal influenza and COVID-19, which they've so far tested in mice over a three-month period. They call the promising invention a "universal respiratory vaccine," though it doesn't stimulate the immune system the way classic vaccines do.

So, how far away are we from a truly universal vaccine that can target all respiratory bugs? Experts told Live Science that while the new research is interesting, a truly universal vaccine is still years away.

Chasing universal protection

Flu and COVID-19 shots need to be updated every year to remain protective, because influenza viruses and coronaviruses are constantly mutating.

"As they circulate, viruses mutate in big and small ways," said Dr. Alfredo Mena Lora, medical director of infection control at Saint Anthony Hospital in Chicago, Illinois. "So antibodies that worked last season may not bind as well this season, leaving more people vulnerable to infection."

What's more, there are myriad respiratory viruses, bacteria and allergens floating around that aren't the target of any existing vaccines. These problems have driven research into "universal" vaccines that could provide broader, longer-lasting protection against multiple respiratory insults — including even seasonal allergies.

This push for universal vaccines accelerated after the COVID-19 pandemic exposed how vulnerable the world is to new respiratory pathogens, as well as how quickly existing vaccines become obsolete in the face of mutations. Since then, researchers have focused on developing vaccines that could last longer and protect against more variants, potentially reducing the need for frequent updates of vaccine formulas.

Universal vaccines in the works

Many universal vaccines in development aim to target parts of viruses that change very little across strains.

For example, for influenza, researchers are targeting the hemagglutinin protein that sticks off the viral surface, but they are focusing on the "stalk" rather than the "head" of this protein, because the stalk mutates more slowly. The National Institutes of Health's (NIH) FluMos-v2, which targets hemagglutinin from six flu strains, recently completed early-phase human trials and generated encouraging immune responses.

The NIH's Generation Gold Standard initiative also aims to develop universal vaccines to protect against multiple viruses that are likely to spark future pandemics. One intranasal flu vaccine is already in later-stage human trials. It uses whole, inactivated viruses to spur the body to make antibodies, which block infection, and T cells, which attack infected cells. This approach could provide broad protection against multiple influenza strains and potentially block transmission — something current flu vaccines do not do.

Meanwhile, some scientists are working on pancoronavirus vaccines to protect against current and future coronaviruses, while others are exploring AI-designed vaccines. They build these by using computational tools to pinpoint regions of virus proteins that mutate very slowly and appear in many viruses. Both these efforts are still in early, experimental stages.

With no universal respiratory vaccines yet on the market, most of the R&D efforts have focused on developing vaccines for specific groups of viruses, such as influenza viruses or coronaviruses. The recent nasal spray study is unique in that it aims to protect against viruses, bacteria and allergens, rather than just one pathogen family.

Rousing innate immunity

Unlike traditional vaccines, the experimental nasal spray does not teach the immune system to recognize select proteins on a specific antigen, the researchers reported Feb. 19 in the journal Science. Rather, it revs up the immune system's first-line defense, known as the innate immune system, study senior author Bali Pulendran, a pathologist at Stanford University, told Live Science in an email.

This acts like an early warning system in the lungs, ready to detect and respond quickly to a wide range of pathogens, even ones the body has never encountered before.

"These [lung] cells are the first to sense infection and help determine how the immune response unfolds," said Pulendran. "And we've learned over the past decade that innate immune cells can also be 'trained' to respond faster and more effectively to future threats."

The concept builds on research with the Bacillus Calmette-Guérin (BCG) vaccine, which prevents tuberculosis. In 2023, Pulendran and colleagues found that mice given BCG saw T cells flock to the lungs. There, they released signals that kept innate immune cells active in the lungs for months, protecting the mice against both COVID-19 and influenza.

This new nasal spray rouses similar immune protection. It combines two adjuvants, or substances that trigger an immune response, to activate T cells and draw them to the lungs. These T cells send chemical signals that mimic natural infection cues, keeping the lungs' innate cells activated and on high alert. If a pathogen makes its way into the lungs, innate immune cells will be primed to nip the infection in the bud.

In experiments, mice received four doses of the nasal spray, spaced one week apart, and were exposed to coronaviruses 21 days to 3 months after their final dose. Vaccinated mice had about 700 times less virus in their lungs than unvaccinated mice and also maintained their weight and survived the infections. Unvaccinated mice, in contrast, lost significant weight, experienced lung inflammation, and, in some cases, died.

The vaccine also helped mice fight off bacterial infections caused by Acinetobacter baumannii and Staphylococcus aureus weeks to months after dosing. For example, levels of S. aureus in the kidneys were about 200 times lower in vaccinated mice than in unvaccinated mice.

The vaccine also reduced the severity of allergic reactions caused by house dust mites. The vaccine seeds the lungs with long-lived T cells that alter the lung environment such that it suppresses the immune pathway behind allergies, the researchers reported. As a result, when vaccinated mice encountered dust mites, their immune systems didn't recruit inflammation-driving cells or generate mucus as they might have otherwise. Removing the T cells abolished this protection.

From mice to humans

"This concept sets up a stronger, faster immune posture in the respiratory tract," Mena Lora, who was not involved in the study, said of the nasal spray. Although the results are still early, he added, the work offers an important proof-of-concept.

The study only tested a handful of pathogens, so although the vaccine raises broad defenses, it's too early to declare it a universal respiratory vaccine. And in the long run, translating these findings to humans will be complex.

"The human immune system varies greatly," said Mark Cameron, an associate professor of population and quantitative health sciences at Case Western Reserve University School of Medicine. "Whether this vaccine can generate broad protection without side effects will require careful clinical trials," said Cameron, who was not involved in the study.

Pulendran agreed, adding that spurring the immune system in this way carries potential risks, such as triggering excessive inflammation. "In our animal studies, we did not observe pathological inflammation, but these questions will need careful examination in human studies," he cautioned.

The team is now preparing for early-stage trials in humans. The exact timeline to potential approval remains uncertain.

"If successful, such a vaccine could reduce hospitalizations, ease ICU [intensive care unit] strain, and protect populations during seasonal outbreaks and future pandemics," saidMena Lora.

The World Health Organization estimates next‑generation or universal influenza vaccines could prevent up to 18 billion flu cases and save millions of lives globally if widely used from 2025 to 2050. However, as no universal flu vaccine has reached the market yet, these ambitious goals are still on hold.

"Their ultimate impact will depend on effectiveness, duration of protection, and performance in diverse populations," Mena Lora emphasized. "The more tools we have — different platforms, targets, and delivery methods — the better our chances of developing broadly protective vaccines, while still refining pathogen-specific shots for high-risk groups."

Antibiotic-resistant bacteria may have an Achilles' heel: a unique sugar molecule found only on the outsides of bacterial cells.

Targeting this molecule can make the bacteria vulnerable to the immune system, which can then destroy the germs and clear infections, recent research in mice shows.

If the same effect can be demonstrated in humans, targeting this sugar molecule could offer a new approach to tackling a wide array of superbugs — including notorious species like Acinetobacter baumannii, Helicobacter pylori, and Campylobacter jejuni. That's according to the researchers behind the study, which was published Feb. 4 in the journal Nature Chemical Biology.

"The next stage in the development of this concept is to produce an antibody that is suitable for use in humans," said study co-author Ethan Goddard-Borger, who studies the role of sugars called glycans in disease at the Walter and Eliza Hall Institute of Medical Research in Australia.

This would involve either "humanizing" the antibody used in their mouse study or identifying a human equivalent that is similarly potent, Goddard-Borger told Live Science in an email.

Sugars on superbugs

Antibiotic-resistant ​​bacteria​​ pose a critical threat worldwide, and Gram-negative bacteria are a particular problem. Bacteria within this group sport tough protective layers that make them especially hard to treat with many existing drugs. The pathogens A. baumannii, H. pylori and C. jejuni belong to this group.

These bacteria often employ a "sugar coat" to help them evade the immune system and resist the effects of antibiotics. The sugar coating essentially mimics sugars seen on human cells, tricking the immune system into ignoring the bacteria.

Past research showed that a sugar called pseudaminic acid (Pse) is found exclusively on the outsides of bacterial cells, and that it differs significantly from sugars found on human cells. Theoretically, this could make Pse a safe way to target infections that are resistant to antibiotics, by helping flag the bacteria as "foreign" so the immune system can attack them.

However, previous research was limited in that scientists struggled to extract enough of the sugar to study it effectively. So in the new study, the researchers ​​made Pse sugar molecules in the lab.

They used the tailor-made molecules to develop specialized proteins that latch onto them. These proteins, called monoclonal antibodies, ​​act like a highly specific biological targeting system, designed to home in on the Pse sugars.

In lab experiments, ​​the team tested these antibodies against H. pylori, C. jejuni, and A. baumannii and found that ​​they​​ tightly bound Pse across all of those bacterial species. The antibodies worked even when the sugars differed in structure between the bacteria.

Next, they tested the sugars in mice with antibiotic-resistant A. baumannii infections. They found that tagging Pse with antibodies​​ made the infections visible to the immune system, enabling immune cells to find, engulf, and destroy the bacteria.

In an experiment, 10 mice that didn't receive the antibodies died of their infections within a day. Mice treated with the antibodies had 100% survival through a full week of observation.

A new approach to beat antibiotic resistance?

The study authors think that, in the future, these antibodies could be given to vulnerable hospital patients to help prevent infections. Since Pse is absent in human cells, they expect such a therapy would specifically target bacteria without harming healthy human cells.

In the long term, the authors propose, these antibodies could potentially be utilized to develop vaccines that offer broad protection against Gram-negative bacteria.

The immediate next step, though, involves adapting these antibodies for potential human use. "I do think that it may be possible to develop monoclonal antibodies that target shared sugars across multiple bacteria to be used as a therapeutic," said Brian Luna, assistant professor of molecular microbiology and immunology at the University of Southern California, who was not involved in the study.

"However, the main limitation is that the sugars, including pseudaminic acid in this case, are not expressed on all bacteria," Luna told Live Science in an email. "So while this antibody may hit some specific strains across different bacterial species, additional work would be needed to show that these antibodies bind a high percentage of clinical isolates tested for this specific antibody to be reasonably considered as a potential therapeutic."

In short, much more work is needed to demonstrate that such antibodies could help treat and prevent a wide range of bacterial infections in people.

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

Scientists have found a way to get treatment for a rare type of cancer into the back of the eye without damaging the nearby structures: by using a particle derived from pig semen.

The approach, which was tested in mice, targets a cancer called retinoblastoma and takes advantage of sperm's ability to penetrate barriers. If the new technique can be demonstrated as safe and effective in people, it could help retinoblastoma patients, who are mostly young children, receive chemotherapy without having to face painful and potentially eye-damaging injections.

"Given that the majority of affected patients are young children, eye-preserving and toxicity-minimizing therapies are critically important for their lifelong well-being," said study co-author Yu Zhang, a pharmaceutics researcher at Shenyang Pharmaceutical University in China.

Retinoblastoma affects 1 in 18,000 children. Almost all are under 5 years old, and two-thirds are younger than 2. In retinoblastoma, the tumor is at the very back of the eye. For a drug treatment to get there, it needs to pass through either the cornea — the protective layer at the front of the eye — or the side of the eyeball. Chemotherapy for this condition is usually injected, but this can damage the eye.

To get around this problem, Zhang's team wanted to design a safer, painless way to deliver chemotherapy to the retina. They considered what natural biological systems were particularly good at getting material across barriers and found inspiration in sperm exosomes.

Exosomes are tiny fat bubbles that cells use to send proteins or other materials from a cell's interior to its outer membrane. In semen, exosomes are carried in the seminal fluid and ferry proteins that help the sperm cell pass through the protective layer of cells around the egg to fertilize it. Even though the cells in the eye are very different, the mechanics of passing this biological barrier appeared similar to Zhang's team. "This led us to explore whether semen-derived exosomes also possess the ability to penetrate ocular barriers," Zhang told Live Science.

They tested this with pig semen, because pigs are already widely used in biology research and material from pigs is generally safe to use in clinical research. Zhang's team gave mice eye drops with pig seminal extracellular vesicles (SEVs), or exosomes, and showed that they could deliver a potential retinoblastoma treatment to the back of the eye.

This proof-of-concept delivery system was used to ferry carbon dots, or nanostructures made of carbon atoms, to the back of the mouse eye. Carbon dots are not routinely used in cancer treatment yet, but other researchers have studied how these tiny structures could be used to kill tumor cells by producing high levels of "reactive oxygen species," which destroy the cells' DNA. To ensure that the exosomes targeted tumor cells and not healthy eye cells, their lipid layer included additional molecules that ramped up reactive-oxygen-species production in the presence of hydrogen peroxide, which cancer cells crank out at high levels to grow and spread.

In the new study, which was published March 27 in the journal Science Advances, Zhang and colleagues showed that the eye drops permeated the layers of the mouse eye to kill tumor cells. After 30 days, the tumors were only 2-3% of the size of those in untreated mice.

This work provides some interesting insights into the application of this technique, Owen Davies, an expert in extracellular vesicles at Loughborough University in the U.K., told Live Science in an email. But he noted that other types of exosomes, such as those derived from stem cells, might work as well.

Zhang, for his part, thinks exosomes could be used to deliver other treatments for eye conditions beyond retinoblastoma, such as macular degeneration.

Dr. Shiri Zayit-Soudry, an ophthalmologist at the Rabin Medical Center of Tel Aviv University who was not involved in the study, agreed, saying in an email that the new technique "holds genuine transformative potential." However, she cautioned that this would still require extensive testing to show if it can be used to treat other diseases and any potential applications would have to go through human clinical trials.

Editor's Note: This story was updated on Tuesday, March 31 at 9:15 a.m. EDT to change references to exosomes as individual molecules. Each exosome is an organelle composed of many molecules.

"I was completely surprised."

When psychiatrist Dr. James Murrough teamed up with dermatologist Dr. Emma Guttman-Yassky to investigate how the immune system might contribute to depression, he didn't expect to find a promising treatment.

In their study, published in February in the journal Molecular Psychiatry, Murrough, Guttman-Yassky and their colleagues uncovered similarities in the immune systems of people with depression and people with eczema, the most common form of which is called atopic dermatitis. Those similarities showed up in the "type 2 pathway," an immune response that involves immune cells called T helper 2 (Th2) cells. When working well, type 2 immunity wards off parasites. But in inflammatory conditions like allergies, asthma and eczema, the pathway's activity goes haywire in the absence of a parasitic infection.

Seeing that this pathway was also ramped up in depression, the team then used computer modeling to predict which existing drugs might subdue that activity. They tested a few promising medicines in lab animals. Ultimately, they found that dupilumab — an antibody used to treat eczema and other inflammatory conditions — helped resolve the symptoms in a mouse model of depression.

Live Science spoke with Murrough, who directs the Depression and Anxiety Center for Discovery and Treatment at the Icahn School of Medicine at Mount Sinai, and Guttman-Yassky, the health system chair of the department of dermatology at Mount Sinai. Their team is now preparing to launch a small trial of dupilumab in people with treatment-resistant depression, whose conditions haven't improved with other forms of therapy. Information about the trial will soon be available on the Mount Sinai website.

The scientists chatted with us about their recent study, upcoming trial and long-term hopes for this research.

Nicoletta Lanese: Prior to your new study, what was known about the role of the immune system in depression?

Dr. James Murrough: Going back a couple of decades, there started to accumulate evidence implicating the immune system in depression, or at least in some types of depression.

People that have some type of disorder of inflammation — whether it's rheumatoid arthritis or an inflammatory skin disease — have a higher incidence of co-occurring depression than you would predict based on the general background population. This is the epidemiologic evidence. So, there's some connection, but we don't know, "Does A cause B, or is there some underlying factor that's causing both?"

Stress of different types — psychological stress, stress from the environment, things like job losses, divorce, marriage, moving — can precipitate an episode of depression. When I was in medical school, we didn't really learn about it, but it turns out that the immune system is sensitive to stress. This has been shown in people and other animals, model systems, that psychological stress, social stress, isolation, bullying, trauma ‪—‬ you name it ‪—‬ it drives high the immune system.

A classic finding that you do learn about in medical school is that hepatitis C used to be treated with things that are pro-inflammatory — cytokines, something called interferon alpha. No one really understood why, but a significant proportion of patients that had hepatitis C and got the treatment for it developed depression. This was well known, and people would put them on antidepressants beforehand.

And a lot of studies now have shown, if you look at common markers in the blood of inflammation … patients with depression reliably show small but statistically significant elevations in these pro-inflammatory factors.

NL: And what prompted your recent study, which also looked at inflammatory markers in the blood?

Dr. Emma Guttman-Yassky: James had an idea that maybe some inflammatory markers are involved in depression and came to me. Then together, we came up with an idea that it would be nice to compare patients with intractable depression to those patients with psoriasis and atopic dermatitis ‪—‬ and, of course, healthy controls ‪—‬ to understand where depression falls. That's when we understood that, in depression, the Th2 immune pathway likely plays a role, and we also associated it [its activity] with the severity of depression.

The magnitude of dysregulation is greater in patients with eczema —‬ so patients with eczema have more systemic inflammation than patients with depression. But overall, the patients with depression still had significant elevations [of inflammatory markers] in their circulation compared to controls.

And then we did something actually quite novel: We took the [immune] signature of depression and the signature of what dupilumab does in atopic dermatitis patients, and we put the latter on top of the depression signature. We saw that actually, if we extrapolate, dupilumab is likely able to reverse the [immune] phenotype of depression.

That, plus the mouse model experiments, led us to think that probably the type 2 pathway, and maybe inflammation in general, likely play a role in depression. This led to this very novel trial designed by James that, if successful, I think could revolutionize, completely, the way we treat depression.

NL: With your mouse model of depression, were you surprised to see dupilumab have such a strong effect?

JM: I was very surprised. We hadn't used that technique before, the so-called in silico [computer] modeling technique. This study was also made possible with the recent development of being able to look at, in this case, close to 400 proteins in the blood. That probably led to uncovering some of these pathways that hadn't been previously reported in the literature. No one had really honed in on this particular IL-4 target, the Th2 pathway.

[Editor's note: IL-4 is a signaling protein that interacts with and is produced by Th2 cells, and it plays a central role in eczema. Dupilumab blocks receptors that respond to IL-4.]

We worked with Scott Russo, who's been a big part of this research and has contributed substantially to understanding the biology of the immune system in stress using animal models. His lab went back and did the validation studies. We identified the target in the human, went back to the mouse, and then were able to show that, if you gave a drug against the IL-4 receptor, you could block the depression-like behavior that develops in the context of stress, which is a common animal model.

NL: Could you explain what the role of type 2 immunity is in the body, usually?

EGY: When it's working well, it wards off parasites.

But in these patients, the type 2 immunity is misbehaving. In patients with eczema; asthma; allergy, including seasonal allergies; eosinophilic esophagitis; hives ‪—‬ they all have very high elevation of this pathway. But it's important to understand that, when you use drugs that target Th2, you do not increase the risk of infections, including those parasite infections.

NL: Does that suggest that the drugs bring the pathway into a "normal" range, rather than completely suppressing it?

EGY: Yes, you stole my thought. I explain to my patients that the old treatments [for eczema] — like cyclosporine, methotrexate, oral prednisone — these were really immune suppressants. Now we are dealing, I think, with immune "correction" rather than immune suppression.

NL: In depression, why might that kind of immune modulation be helpful?

JM: Inflammation has been shown to suppress the brain's response to reward. So that's a hint as to why being inflamed might make you feel depressed. That's been worked out also in stress models in animals, and we can use technology like functional brain imaging to look at markers of that in the brain. We're also going to be doing that [in our upcoming trial].

We think that the suppression of the reward system is a key factor, but we know there are other effects. For example, we did some prior studies in people with depression and looked at their inflammation, and we were able to show that the higher their inflammatory markers in the blood, the less responsive their brain was during a standard reward-activation task. That's in a part of the brain called the nucleus accumbens, [within] the ventral striatum.

One way we think of depression is you have this group of symptoms related to lack of effort, lack of motivation, lack of response to pleasure. There are brain systems that we feel pretty confident are connected to that, but why they're suppressed, often, we don't know. Maybe the immune system is a piece of that.

But then you have other parts of the brain, like the amygdala, which is more attuned to threat. People with depression have been shown to have abnormally reactive amygdala responses, specifically to negative information or threats — sad faces, fearful faces, things like that. So, there's evidence for blunted positive responses, but then also, abnormally reactive responses to negative information in the world. We did a study that showed that the higher the inflammation in the blood, the greater their reaction in the amygdala, even though at the same time, it's reduced in the reward center.

NL: To clarify, as we're thinking about using immune modulation as a depression treatment, would it likely be helpful to all patients, or only a subset?

JM: We don't know. It's likely that only a subset — only some patients that carry a diagnosis of major depression will have an abnormality in their immune system, at least one that's relevant for treating.

EGY: We hypothesize now, starting with the study soon, that treating with an immune-based treatment that targets this pathway may be able to reverse part of the phenotype of depression and ameliorate [symptoms in] these patients.

I think time will tell what will be the improvement and what is the right patient, and so on.

JM: As our knowledge evolves, some people are starting to talk about an immune subtype of depression. It doesn't currently exist; it's not recognized in the textbooks yet. It's not in our "bible of psychiatric illnesses," the DSM [Diagnostic and Statistical Manual of Mental Disorders]. But there are proposals, and folks are gearing up to write the next DSM. It's on the table; it's gaining some traction. The challenge is, how should it be defined?

We hope that one day a patient [with depression] will get a blood test that can say, "OK, you have a blood marker that indicates dysfunction in your immune system — or even better, a specific component of your immune system. Now, we're going to give you a medicine that targets that." We'd like to be able to personalize our treatment based on known, underlying biology. So, instead of just saying a patient has depression, we'd like to be able to say, "You have this type of depression, and therefore, you need that treatment."

There's a lot of detail trying to be worked out, but there is clearly a link between what's going on in the body and these brain systems that support our emotions, our emotional health. I think psychiatry is advancing to the point where we're going to start to understand our illnesses in terms of specific pathways and brain systems, which, of course, is not always how it's been understood.

We're right at that cusp of, hopefully, a lot of fundamental biology and neuroscience knowledge starting to spill into how we actually practice the treatment of psychiatry. We're trying to move towards that in the next few years.

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

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

What if a single vaccine could offer protection against a range of disease-causing bacteria, common allergens and respiratory viruses? A new mouse study highlights an experimental vaccine that could potentially offer that elusive "universal" protection.

As it's been tested only in lab animals, the vaccine must still pass a number of trials in people before it can be proven safe and effective.

The new study, published Thursday (Feb. 19) in the journal Science, describes a nasal-spray vaccine that works differently than most vaccines.

Conventionally, vaccines train the immune system to recognize a specific antigen, such as a protein on a virus's surface. The immune system then trains cells to remember and attack that antigen if they encounter it. This results in a robust, but fairly narrow immune defense — one which can be thwarted if the target antigen mutates over time.

Some scientists are working on vaccines that target antigens that are "highly conserved" between viral strains, meaning the antigen doesn't change much over time and looks similar from virus to virus. Such shots could potentially target many flu viruses or many coronaviruses at once, for example. But the scientists behind the new nasal-spray vaccine took a different approach: Rather than targeting only the "adaptive" immune system, which remembers specific antigens, it also revs up the innate immune system, a generic, first-line defense.

"What's remarkable about the innate system is that it can protect against a broad range of different microbes," senior study author Bali Pulendran, a professor of microbiology and immunology at the Stanford University School of Medicine, said in a statement.

The idea of a vaccine activating both innate and adaptive immunity is not completely new. It's well known that the tuberculosis vaccine, called Bacillus Calmette-Guérin (BCG), triggers this dual protection. In fact, because of that effect, scientists tested whether BCG could offer broad protection against COVID-19 in the early days of the pandemic.

Pulendran and colleagues had previously studied the BCG vaccine in mice and found that the shot caused immune cells in the lungs to spew specific signals. These signals prompted innate immune cells in the lungs to stay active for several months, rather than calming down after just days.

The new nasal-spray vaccine — called GLA-3M-052-LS+OVA — works by mimicking those special signals. It also contains a harmless egg-protein antigen that helps summon the right immune cells to the lungs. The team found that mice given three doses of the vaccine over three weeks were protected against SARS-CoV-2 (the virus that causes COVID-19) and other coronaviruses, the bacteria Staphylococcus aureus and Acinetobacter baumannii, and an allergen from house dust mites for at least three months afterward.

When exposed to these germs and the allergen, vaccinated mice were protected by the primed innate immune response and also quickly mounted an adaptive immune response against the insults. By comparison, unvaccinated mice fared much worse — in response to viruses and bacteria, they showed higher lung inflammation, weight loss and risk of death, and in response to allergens, they had more pronounced allergic reactions and mucus buildup.

"This is a really exciting piece of research," Daniela Ferreira, a professor of respiratory infection and vaccinology at the University of Oxford who was not involved in the study, told BBC News. It could "change how we protect people from common coughs, colds and other respiratory infections" if the results are confirmed in human studies, she said.

Pulendran also emphasized that, so far, the tests of the vaccine have been in lab animals and more work is required to translate the research to humans.

"If it ultimately proves safe and effective in humans, the potential impact could be transformative: simplifying seasonal vaccination and improving readiness for emerging respiratory threats," Pulendran told Genetic Engineering and Biotechnology News. Pulendran thinks two doses of the vaccine would likely be protective in people, according to the Stanford statement.

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

For many people with diabetes, managing their blood sugar levels requires daily insulin shots — but now, scientists have invented a new polymer-based gel that can deliver insulin through the skin without needles.

The gel, described in a November study in the journal Nature, normalized the blood sugar levels of diabetic mice and pigs within one to two hours of application. The animals' blood sugar then stayed in a normal range for approximately 12 hours.

The gel's speed and long-term effects are comparable to that of "basal" insulin shots, which deliver a steady dose that stabilizes blood sugar between meals and overnight. These are typically used together with fast-acting insulin that's used just before, during or after meals to control big spikes in blood sugar triggered by food.

The gel is "mechanistically elegant," said Suchetan Pal, an associate professor and head of the Biomaterials Laboratory at the Indian Institute of Technology Bhilai, who was not involved in the research.

However, for now, it is still strictly experimental. To date, the gel has been tested only on mice and pigs and not on people, Pal told Live Science in an email. Human skin — which is variable in its thickness, fat content and pH — may behave differently than animal skin.

How the gel slips past the skin's defenses

Human skin's outer layer, the stratum corneum, is only about 10 to 15 micrometers thick, thinner than a human hair. But the dead cells and fats that make up the layer form a shield that's tough to penetrate. While some small molecules can cross this barrier, larger proteins, like insulin, normally cannot.

The team behind the study overcame this challenge by engineering a pH-responsive polymer, which they call OP.

At a pH of around 5, the skin's surface is acidic, while deeper layers of the skin are closer to a neutral pH of 7. At the skin's surface, the OP polymer becomes positively charged. This positive charge helps it stick to the fatty acids within the skin, much like opposite ends of a magnet attract each other.

As the pH gradually increases in deeper layers, the OP polymer changes to a neutral state that enables it to diffuse through fats in the skin. Insulin, which is chemically linked to the polymer, is thereby carried through skin layers that it wouldn't normally be able to penetrate on its own.

Lab tests with mouse and pig skin confirmed that OP penetrates all layers of the skin, whereas insulin alone remains stuck on the surface. The researchers then tested whether applying the OP-insulin gel to animals' skin could lower their blood sugar.

In a mouse model of diabetes, applying the gel once lowered their blood glucose to a normal range in about an hour and maintained it within that range for roughly 12 hours. However, Pal noted that this effect required a very high OP-insulin dose of 116 units per kilogram of body weight (U/kg) — far beyond a typical human dose of insulin. ​​This could raise a concern that the insulin delivery through the skin might not be efficient enough.

But notably, the researchers were able to use a lower dose in diabetic miniature pigs, whose skin closely resembles that of humans. Using a single dose around 7.25 U/kg, the gel restored the pigs' blood glucose to normal levels. And using the gel repeatedly caused no skin irritation or inflammation, the team found.

More research needed

If these animal results translate to people, the needle-free insulin gel could potentially help patients with a fear of or aversion to needles, thus helping improve their treatment adherence and easing the burden of diabetes management.

The 12-hour effect suggests the gel could serve as a long-acting insulin to provide "background" blood-sugar control, although patients would still need fast-acting doses at mealtimes. Because the gel's absorption into the bloodstream is slower and steadier than that of an injection, it cannot quickly reverse high blood sugar in an emergency, Pal noted.

The authors hope this polymer approach could extend beyond insulin delivery, as they're working to adapt OP to carry GLP-1 agonists, such as semaglutide (Ozempic), and other therapeutic proteins. However, experts cautioned that hurdles remain before the gel could be approved for human use.

"The polymer hasn't shown any side effects in mice or pigs," said lead study author Youqing Shen, a professor in the School of Chemical and Biological Engineering at Zhejiang University in China, told Live Science in an email. "But humans have used insulin for decades, so we need to investigate long-term toxicity."

Shen also said the insulin dose delivered through the gel must be carefully controlled, since too much can result in dangerously low blood sugar. In sum, developers would need extensive preclinical safety studies, an Investigational New Drug (IND) filing with the Food and Drug Administration, and human clinical trials before a skin-based insulin therapy could reach patients.

While the pig experiments offered a better model of human skin than the mice did, Pal also cautioned that the lower dose of insulin had lower efficacy. This underscores the amount of development still needed to achieve effective insulin delivery at safe and clinically relevant human doses.​​ The long-term safety of using the gel repeatedly is also unknown.

Looking forward, the team will need to figure out the optimal formulation and dosing for the gel; devise a way to scale up its manufacturing; and run clinical trials, Pal said. Nonetheless, he finds the idea exciting and believes it could create an avenue for needle-free diabetes care.

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

Patients undergoing in vitro fertilization (IVF) must give themselves daily hormone shots in weeks leading up to having eggs collected for the procedure. Now, a research team has developed what it calls a painless, automated way to deliver these hormones using a light-activated microneedle patch.

A preliminary study conducted in rats has shown that delivering the hormone leuprolide from a patch could be done painlessly and without releasing foreign substances into the body. A light can be preprogrammed to turn on at specific times, such that the patch releases the hormone at the correct cadence.

These results, published in the journal Small in November 2025, suggest that the patch could someday help address two of the challenges of IVF: the pain of the hormone shots and the inconvenience of self-administering the shots at the same time daily for two weeks, said lead study author Marta Cerruti, a materials chemist at McGill University in Montreal. Most patients report feeling a brief, pinching pain when administering the shots, but the pain level can vary depending on a given patient's anxiety level with needles.

Vivienne Tam, who was a doctoral student at the time of the study, suggested the potential of their research for helping IVF patients, Cerruti said. The group had previously been thinking about using the patch for administering cancer drugs to patients, Cerruti said.

"From what we read, one of the main reasons for the failure of IVF is that the drug is not given consistently," she told Live Science. The hope is that, someday, the patch could solve that challenge.

Designing a hormone-delivery system

In the new study, the team incorporated prior discoveries made in two separate labs at McGill and the INRS research center in Quebec.

The patch is composed of tiny needles that contain nanoparticles, which are packed with the hormone leuprolide. The researchers had already developed a potential coating for the nanoparticles that breaks down when exposed to low-energy light, called near-infrared light (NIR). Upon NIR exposure, the nanoparticles then spill their contents.

How this works is that the NIR is converted to higher-energy ultraviolet (UV) light by the nanoparticle's core. This UV light can then break the bonds in the coating of the particle, releasing the molecules held inside. "We had this coating that we knew worked," Cerruti said.

Other researchers had shown that the nanoparticles, which are made of rare-earth materials, are nontoxic in animal tests. To then make their patch, the team incorporated the nanoparticles into microneedles made of a nonsoluble, synthetic polymer, which should not degrade, Cerruti said.

The needles prick microscopic holes in the outer layer of the skin, called the stratum corneum, which is made up of dead skin cells. These pricks are painless because the needles do not penetrate deep enough to reach the sensory nerve endings housed in deeper layers of the skin, Tam said.

In rats, the NIR successfully released the drug from the microneedles without releasing any foreign substances — namely, the nanoparticles themselves — into the body, Cerruti said. If the nanoparticles had entered the body along with the hormones, they would have accumulated in the liver and other organs, she said, but the team didn't observe that in tests.

The new findings show that the hormone went into the rats' circulatory system as intended, but researchers have yet to test whether this delivery method has the desired effect of encouraging egg maturation, Cerruti said.

The biggest hurdle for any nanoparticle-based therapy is biocompatibility, said Lifeng Kang, an associate professor at The University of Sydney School of Pharmacy who was not involved in the study. That means the material must be compatible with living tissue and not cause toxic effects or harmful immune reactions. The researchers "must prove these nanoparticles are either safely excreted or remain inert in the skin without long-term toxicity," he said.

While the researchers did not study whether the microneedles themselves release pieces of polymers in the bloodstream, the polymer the microneedle patch is made of is known to be highly durable, Cerruti said.

Before moving on to studies in larger animals, she added, the researchers want to conduct additional rat studies to determine the efficacy of this hormone-delivery system.

In their initial experiments, the team released only a small dose of the hormone. For the dose to be equivalent to that used in IVF, they would need to use more patches on a given mouse, or include more nanoparticles in a given patch, Cerruti said. They could also increase the size of the patch, so the number of nanoparticles scales up.

One of the "biggest barriers to overcome before eventual clinical translation is the limited dose of the drug available in the bloodstream," Cerruti said.

Editor's note: This story was updated on Jan. 29 to clarify comments from Cerruti.

Imagine going to the hospital for a bacterial ear infection and hearing your doctor say, “We’re out of options.” It may sound dramatic, but antibiotic resistance is pushing that scenario closer to becoming reality for an increasing number of people. In 2016, a woman from Nevada died from a bacterial infection that was resistant to all 26 antibiotics that were available in the United States at that time.

The U.S. alone sees more than 2.8 million antibiotic-resistant illnesses each year. Globally, antimicrobial resistance is linked to nearly 5 million deaths annually.

Bacteria naturally evolve in ways that can make the drugs meant to kill them less effective. However, when antibiotics are overused or used improperly in medicine or agriculture, these pressures accelerate the process of resistance.

As resistant bacteria spread, lifesaving treatments face new complications – common infections become harder to treat, and routine surgeries become riskier. Slowing these threats to modern medicine requires not only responsible antibiotic use and good hygiene, but also awareness of how everyday actions influence resistance.

Since the inception of antibiotics in 1910 with the introduction of Salvarsan, a synthetic drug used to treat syphilis, scientists have been sounding the alarm about resistance. As a microbiologist and biochemist who studies antimicrobial resistance, I see four major trends that will shape how we as a society will confront antibiotic resistance in the coming decade.

1. Faster diagnostics are the new front line

For decades, treating bacterial infections has involved a lot of educated guesswork. When a very sick patient arrives at the hospital and clinicians don’t yet know the exact bacteria causing the illness, they often start with a broad-spectrum antibiotic. These drugs kill many different types of bacteria at once, which can be lifesaving — but they also expose a wide range of other bacteria in the body to antibiotics. While some bacteria are killed, the ones that remain continue to multiply and spread resistance genes between different bacterial species. That unnecessary exposure gives harmless or unrelated bacteria a chance to adapt and develop resistance.

In contrast, narrow-spectrum antibiotics target only a small group of bacteria. Clinicians typically prefer these types of antibiotics because they treat the infection without disturbing bacteria that are not involved in the infection. However, it can take several days to identify the exact bacteria causing the infection. During that waiting period, clinicians often feel they have no choice but to start broad-spectrum treatment – especially if the patient is seriously ill.

But new technology may fast-track identification of bacterial pathogens, allowing medical tests to be conducted right where the patient is instead of sending samples off-site and waiting a long time for answers. In addition, advances in genomic sequencing, microfluidics and artificial intelligence tools are making it possible to identify bacterial species and effective antibiotics to fight them in hours rather than days. Predictive tools can even anticipate resistance evolution.

For clinicians, better tests could help them make faster diagnoses and more effective treatment plans that won’t exacerbate resistance. For researchers, these tools point to an urgent need to integrate diagnostics with real-time surveillance networks capable of tracking resistance patterns as they emerge.

Diagnostics alone will not solve resistance, but they provide the precision, speed and early warning needed to stay ahead.

2. Expanding beyond traditional antibiotics

Antibiotics transformed medicine in the 20th century, but relying on them alone won’t carry humanity through the 21st. The pipeline of new antibiotics remains distressingly thin, and most drugs currently in development are structurally similar to existing antibiotics, potentially limiting their effectiveness.

The antibiotic discovery void

To stay ahead, researchers are investing in nontraditional therapies, many of which work in fundamentally different ways than standard antibiotics.

One promising direction is bacteriophage therapy, which uses viruses that specifically infect and kill harmful bacteria. Others are exploring microbiome-based therapies that restore healthy bacterial communities to crowd out pathogens.

Researchers are also developing CRISPR-based antimicrobials, using gene-editing tools to precisely disable resistance genes. New compounds like antimicrobial peptides, which puncture the membranes of bacteria to kill them, show promise as next-generation drugs. Meanwhile, scientists are designing nanoparticle delivery systems to transport antimicrobials directly to infection sites with fewer side effects.

Beyond medicine, scientists are examining ecological interventions to reduce the movement of resistance genes through soil, wastewater and plastics, as well as through waterways and key environmental reservoirs.

Many of these options remain early-stage, and bacteria may eventually evolve around them. But these innovations reflect a powerful shift: Instead of betting on discovering a single antibiotic to address resistance, researchers are building a more diverse and resilient tool kit to fight antibiotic-resistant pathogenic bacteria.

3. Antimicrobial resistance outside hospitals

Antibiotic resistance doesn’t only spread in hospitals. It moves through people, wildlife, crops, wastewater, soil and global trade networks. This broader perspective that takes the principles of One Health into account is essential for understanding how resistance genes travel through ecosystems.

Researchers are increasingly recognizing environmental and agricultural factors as major drivers of resistance, on par with misuse of antibiotics in the clinic. These include how antibiotics used in animal agriculture can create resistant bacteria that spread to people; how resistance genes in wastewater can survive treatment systems and enter rivers and soil; and how farms, sewage plants and other environmental hot spots become hubs where resistance spreads quickly. Even global travel accelerates the movement of resistant bacteria across continents within hours.

Together, these forces show that antibiotic resistance isn’t just an issue for hospitals – it’s an ecological and societal problem. For researchers, this means designing solutions that cross disciplines, integrating microbiology, ecology, engineering, agriculture and public health.

4. Policies on what treatments exist in the future

Drug companies lose money developing new antibiotics. Because new antibiotics are used sparingly in order to preserve their effectiveness, companies often sell too few doses to recoup development costs even after the Food and Drug Administration approves the drugs. Several antibiotic companies have gone bankrupt for this reason.

To encourage antibiotic innovation, the U.S. is considering major policy changes like the PASTEUR Act. This bipartisan bill proposes creating a subscription-style payment model that would allow the federal government up to US$3 billion to pay drug manufacturers over five to 10 years for access to critical antibiotics instead of paying per pill.

Global health organizations, including Médecins Sans Frontières (Doctors Without Borders), caution that the bill should include stronger commitments to stewardship and equitable access.

Still, the bill represents one of the most significant policy proposals related to antimicrobial resistance in U.S. history and could determine what antibiotics exist in the future.

The future of antibiotic resistance

Antibiotic resistance is sometimes framed as an inevitable catastrophe. But I believe the reality is more hopeful: Society is entering an era of smarter diagnostics, innovative therapies, ecosystem-level strategies and policy reforms aimed at rebuilding the antibiotic pipeline in addition to addressing stewardship.

For the public, this means better tools and stronger systems of protection. For researchers and policymakers, it means collaborating in new ways.

The question now isn’t whether there are solutions to antibiotic resistance – it’s whether society will act fast enough to use them.

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

A pill version of the popular weight-management drug Wegovy has been approved by the Food and Drug Administration (FDA) and is now available through various pharmacies and telehealth services in the U.S.

The drug has been available by prescription as a once-weekly injection in the U.S. since 2021. Like the injection, the new Wegovy pill contains semaglutide, the same active ingredient as Ozempic. It works by mimicking a hormone in the body — glucagon-like peptide-1 (GLP-1) — that helps control appetite and blood sugar levels.

Both forms of Wegovy are approved to help adults with obesity — as well as adults who are overweight and have related health conditions, like high blood pressure — lose weight and keep it off, in combination with a reduced-calorie diet and increased physical activity. However, only the injectable version is approved for children 12 and up with obesity; the pill version is not yet cleared for that age group.

Here's what to know about the new Wegovy pill and who might benefit most from it.

Do semaglutide pills work as well as injections?

The main difference between the Wegovy pill and the injection is how the drug enters the bloodstream.

When semaglutide is injected under the skin, it is absorbed directly into the blood. When taken as a pill, however, the drug must first pass through the stomach and intestines, where some of its active ingredient is broken down by digestive enzymes before it can be absorbed through the gut lining and into the blood.

Because of this, "only a small fraction [of the pill] reaches the bloodstream," explained Dr. Chika Anekwe, obesity medicine clinical director of the Massachusetts General Hospital Weight Center and an instructor in medicine at Harvard Medical School. This is an expected difference between injected and oral medications, in general.

Although the pill exposes the digestive tract to more semaglutide than the injection would, its local effects on the gut are minor, Anekwe explained. That's because the "key effects still require absorption and systemic signaling," so they only kick in once the drug reaches the bloodstream, she said.

To make up for that digestive process, the pill version of Wegovy is taken at a much higher dose than the injectable form. The highest dose of the pill is 25 milligrams, compared with 2.4 milligrams for the weekly injection, Anekwe told Live Science in an email.

The pill also comes with strict instructions for when you should take it, Anekwe said. It should be taken on an empty stomach in the morning with a small amount of water, and patients must wait at least 30 minutes before eating, drinking or taking other medications, its drug label says. This ensures that the medication will be properly absorbed at the intended dose. The injectable version does not have these restrictions; it can be taken at any time of day and with no fasting required.

Dr. Priya Jaisinghani, an endocrinologist and obesity medicine specialist at NYU Langone Health, discussed the effectiveness of the two formulations during an Endocrine Society webinar about GLP-1 pills in December 2025.

So far, "there has been no long-term, head-to-head trial" that has compared the once-daily 25-mg pill with the once-weekly 2.4-mg injection in adults with obesity, Jaisinghani said. However, results from clinical trials that tested the drugs separately suggest the two versions lead to very similar weight loss when taken as instructed.

In the STEP-1 trial, a study of 2.4-mg injectable semaglutide, participants lost an average of about 14.4% of their body weight. In the OASIS 4 trial, a study of the 25-mg pill, participants lost an average of about 13.9% of their body weight. Jaisinghani said these results indicate that the pill and the injection "offered comparable efficacy for weight management."

Is the Wegovy pill as safe as the injection?

The trials also suggest that Wegovy pills and injectables have similar side effects.

"Oral and injectable Wegovy have very similar, predominantly gastrointestinal side effects," Anekwe said. These include nausea, diarrhea, vomiting and constipation, for example.

About three-quarters of Wegovy users experience mild-to-moderate gastrointestinal symptoms, Anekwe said. But for both forms of the drug, a minority of patients — around 7% to 10% — stop taking the medication because of these effects, according to trial data.

(Some real-world data suggest that a higher percentage of patients stop taking GLP-1s within a year of starting them, but that may be due to a mix of factors, including both side effects and medication cost.)

Who might benefit more from the pill or the injection?

Patients considering Wegovy may opt for the pill or injection for different reasons. For instance, "the pill may be better for someone who is averse to using injections," Anekwe said.

The pill version may also be more appealing to people who do not have reliable access to refrigeration, such as frequent travelers, she said. That's because the pill can be stored at room temperature, unlike the injection, which must be refrigerated. Generally, the Wegovy injectables should be kept between 36 and 46 degrees Fahrenheit (2 to 8 degrees Celsius). And if needed, the pens can be stored at 46 to 86 F (8 to 30 C) for up to 28 days, if their caps haven't been removed.

That said, the strict daily schedule of taking a pill on an empty stomach with restrictions on food timing may be challenging for some people to stick to. Those individuals may prefer the convenience of a once-weekly injection.

Cost and insurance coverage may also influence which version people choose. The pill may be better for someone who doesn't have insurance coverage because it has a lower out-of-pocket cost, Anekwe said.

And besides lifestyle factors and cost, there is another important difference that determines who can use each version: Unlike the injectable form of Wegovy, which is approved for adolescents ages 12 and older with obesity, the Wegovy pill is currently approved only for adults.

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

An iridium metal complex has been identified as a promising, if unconventional, new antibiotic drug, a new study finds.

The compound is one of more than 600 produced in a study published in December in the journal Nature Communications. The researchers used a robot to synthesize the compounds, combining metal and organic molecule building blocks to generate a huge chemical library in just a week.

This streamlined approach, which also produced five other potential antibiotics, could dramatically accelerate both drug discovery and parallel areas of chemical research, study lead author Angelo Frei, an inorganic chemist at the University of York in the U.K., told Live Science.

As the prevalence of drug-resistant bacterial infections increases, there's a need for new, effective antibiotics that can kill germs that no longer respond to existing drugs. So far, the search has focused on organic — meaning carbon-based — molecules, leaving metal complexes almost completely unexplored.

These metal-containing compounds significantly differ in shape compared to their flatter organic alternatives; and their three-dimensional shapes give rise to distinct chemical and biological properties. This attribute, combined with their ease of synthesis, makes these molecules an exciting potential source of future antibiotics, the study authors say.

But as there's little existing data on the antimicrobial properties of metal complexes, Frei's team needed an efficient method to rapidly make and test as many compounds as possible. Their solution was to merge straightforward and robust chemistry with state-of-the-art automation.

The team began by creating a panel of 192 different ligands, the organic molecules that bind to the metal center and determine the overall complex's final properties. They did so by using a liquid-handling robot to perform "click chemistry." This robust reaction fuses two types of starting materials — called azides and alkynes — to construct nitrogen-containing rings known as triazoles. These nitrogen rings bond strongly to metals.

In the next step of the process, the robot combined each of the 192 ligands with five different metals to generate a total of 672 metal complexes.

"We opted to use liquid-handling robots to do the chemistry because it's just combining different reagents in the right ratios," Frei said. After making the azides, "then we added the alkynes and the catalyst to do the click reaction, and then we used those ligands on different metals. It can all be done in one pot with robots," he said.

Each product was analyzed to confirm the expected complex had formed and then immediately tested for antibacterial activity and potential toxicity to human cells. In this way, the team quickly identified the safest and most potent compounds, without wasting time on lengthy purification steps.

"It allows us to go from hundreds of compounds to maybe dozens of compounds that are interesting," Frei explained.

Complexes containing iridium and rhenium exhibited particularly high levels of antibacterial activity. Overall, 59 of the iridium compounds and 61 of the rhenium compounds inhibited the growth of Staphylococcus aureus, an important cause of hospital-associated infections that can range from mild to deadly. For both metals, the toxicity toward human cells was variable. From these initial screening results, the team selected the six compounds that most effectively balanced antibacterial activity with low toxicity for further study.

"When we have identified those really promising ones, we can then go back to the bench and remake them, isolate them, and characterize them, to confirm what we saw previously with the [unpurified] mixture," Frei said.

In this second round of tests, one of the iridium complexes was the clear standout winner. The compound was about 50 to 100 times more active against bacteria than it was toxic to human cells. This large difference is vital to ensure that the complex is simultaneously effective in treating an infection but safe to use on human tissues.

Mark Blaskovich, a molecular bioscientist at the University of Queensland in Australia who wasn't involved in the work, was impressed by the efficiency of Frei's approach and the diversity of the compounds created by the automated synthesis. However, substantial work remains to transform their antibiotic candidates into viable clinical drugs, he said.

The "most important next steps" are to show that the most promising compounds have drug-like properties, meaning they are chemically stable and don't have a lot of off-target effects on the body, he told Live Science in an email. In addition, research needs to demonstrate how these compounds work in a living body, "ideally in the 'gold standard' mouse models of infection," he said.

In order to get these potential antibiotics approved for clinical use, eventually, studies in lab animals would be followed by clinical trials that could definitively show the drugs are both safe and effective for people.

For the time being, though, Frei intends to build upon this initial library of compounds, leveraging artificial intelligence to help target specific properties.

"We can use this data to make smarter decisions," he said. "So we can do machine learning and train models to correlate which structural features lead to good activity and low toxicity and then have the model predict for us which compounds we should make next."

The U.S. federal government has rewritten its childhood vaccine schedule, reducing the number of shots universally recommended to kids 18 and under from around 17 to 11.

This policy change effectively downgrades the recommendations for several shots, such as those against rotavirus, the flu and hepatitis A. Rather than being recommended to all children by default, those vaccines will now be recommended to only certain "high-risk" groups or will be accessible through "shared clinical decision-making" between parents and providers.

The concept of shared clinical decision-making emphasizes that, if a child's caregivers wish to give them a routine vaccine, they should first consult with a medical provider. While that idea may sound benign, it could sow confusion around which vaccines are considered effective and medically necessary, Dr. Daniel Jernigan, former director of the Centers for Disease Control and Prevention's (CDC) National Center for Emerging and Zoonotic Infectious Diseases, told STAT. And it could introduce logistical hurdles to accessing vaccines.

"By making these vaccines a shared clinical decision making, it introduces one more barrier that prevents a child from getting a life-saving vaccine," Jernigan said.

The new recommendations

The new recommendations group vaccines and immunizations into three categories:

• Those recommended for all children
• Those recommended for certain high-risk groups
• Those that can be given based on "shared clinical decision-making"

Federal guidance still recommends that all children receive shots against 11 diseases: measles, mumps, rubella, polio, pertussis, tetanus, diphtheria, Haemophilus influenzae type B (Hib), pneumococcal disease, varicella (chickenpox), and human papillomavirus (HPV). However, HHS is recommending only one dose of HPV vaccine instead of the usual two, STAT reported.

Certain "high-risk" populations are recommended to be immunized for RSV, hepatitis A, hepatitis B, dengue, and two types of meningococcal disease. (Note that immunizations against respiratory syncytial virus, or RSV, include a prenatal vaccine given to mothers and antibody drugs given to kids. There is no RSV vaccine available for children.)

Vaccines against meningococcal disease and hepatitis A and B are also listed under the "shared decision-making" category, as are shots against rotavirus, COVID-19 and the flu.

"Abandoning recommendations for vaccines that prevent influenza, hepatitis and rotavirus, and changing the recommendation for HPV without a public process to weigh the risks and benefits, will lead to more hospitalizations and preventable deaths among American children," Michael Osterholm of the University of Minnesota's Center for Infectious Disease Research and Policy, told The Associated Press.

'Dangerous and unnecessary' changes

Stakeholders had been bracing for this policy change for several weeks by the time it was announced Monday (Jan. 5).

In early December, President Donald Trump called on federal officials to compare the U.S. childhood vaccine schedule to that of "peer nations," implying that other countries have superior policies. In mid-December, Politico reported that Robert F. Kennedy Jr., the head of the Department of Health and Human Services (HHS), had intended to make the U.S. vaccine schedule more like that of Denmark — which recommends shots against only 11 diseases in its schedule.

Comparable countries often recommend vaccines and immunizations against about 12 to 15 pathogens, while Austria and the U.S. have historically sat on the high end at around 17.

Experts have emphasized that the United States' vaccine schedule has been rigorously tested and that the decision to change it was not made using new data on its safety or effectiveness. They also noted that the policies of Denmark — a small country of roughly 6 million people with universal health care and a fairly homogenous population — may not serve the U.S. population, given that it's much larger and contends with a splintered health care system and greater health inequities. (The U.S. population is roughly 340 million.)

"The truth is that while vaccine guidance is largely similar across developed countries, it may differ by country due to different disease threats, population demographics, health systems, costs, government structures, vaccine availability, and programs for vaccine delivery," the American Academy of Pediatrics (AAP) noted.

These location-specific factors weigh upon which vaccines health officials recommend to a given country's children. But despite the differences between America and Denmark, federal officials are now claiming that Denmark's approach is the superior one regardless of context.

Officials had already been shifting away from giving full-throated recommendations of routine vaccines. For example, HHS previously recommended "shared clinical-decision making" for giving COVID-19 vaccines to kids and providing hepatitis B vaccines to infants of mothers who test negative for the virus.

Various stakeholders are expected to break with the CDC's new recommendations. For instance, medical societies, city and state health departments, and regional health alliances have rejected the CDC's other vaccine policy changes, and the AAP has sued HHS for allegedly violating established rules around vaccine regulatory changes when the agency tweaked its COVID-19 vaccine guidance.

"Today's announcement by federal health officials to arbitrarily stop recommending numerous routine childhood immunizations is dangerous and unnecessary," AAP president Dr. Andrew Racine, said in a statement, according to the clinical news source Contemporary Pediatrics.

"The longstanding, evidence-based approach that has guided the U.S. immunization review and recommendation process remains the best way to keep children healthy," Racine said, "and protect against health complications and hospitalizations."

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

An experimental drug compound could prevent and treat some complications of diabetes, such as poor wound healing and rampant inflammation. And it works regardless of blood sugar control, a new study in mice and human cells suggests.

The cornerstone of diabetes care is keeping blood sugar in check through diet and exercise, by maintaining a healthy weight, and by injecting the hormone insulin to help shuttle glucose out of the bloodstream. But while maintaining blood sugar levels in a target range reduces the chance that diabetes complications will emerge, it doesn't eliminate the risk.

"The complications of diabetes — which really are the issues that make people sick, that reduce their lifespan, and that just make them unwell — are only partly mitigated by tight control of the blood sugar," said study co-author Dr. Ann Marie Schmidt, a professor of medicine at the NYU Grossman School of Medicine and director of the Diabetes Research Program at NYU Langone Health.

That raises questions about what the other drivers of diabetic complications might be and whether they can be treated.

For decades, Schmidt and colleagues have sought to answer those questions, and their efforts have led to the development of the new experimental drug. In their latest work, published in October in the journal Cell Chemical Biology, the team tested the drug's effects in lab mice and human cells.

The results show that such a drug has "great potential" for limiting or preventing several complications of diabetes, Timothy Perkins, an assistant professor of pathology at the University of Pittsburgh, wrote in a commentary on the study.

Blocking complications at the source

The new drug compound takes aim at a protein called RAGE, which interacts with a second protein called DIAPH1. Schmidt and colleagues first described RAGE in the 1990s, finding that it plays a role in the vascular complications of diabetes, such as heart disease.

The RAGE protein is found in many types of cells, including immune cells and the cells that line blood vessels. It spans the cell membrane, with one end interacting with substances on the outside of the cell and the other relaying signals inside the cell. The external bit of the protein interacts with advanced glycation end products (AGEs) — proteins with sugars stuck to them.

"Once they're stuck on there, they have a gain of function where they can actually perturb and damage endothelial cells, the cells that line every blood vessel in our body," Schmidt told Live Science. It's known that AGEs accumulate in the body with normal aging, and in the context of certain chronic diseases, including diabetes, they build up more quickly than usual.

RAGE, which stands for "receptor for AGEs," is activated by this buildup of sugar-coated proteins, and this kicks off harmful changes inside the cell, including processes that ramp up inflammation. It turns out that those changes rely on RAGE's interaction with a second protein inside the cell: DIAPH1. (The team had previously tried blocking AGEs from plugging into RAGE, but didn't find success with that approach.)

With guidance from co-author Alexander Shekhtman, a structural biologist at the State University of New York at Albany, the researchers took a closer look at the interaction of RAGE and DIAPH1. They built a detailed model of how the two proteins interact in the presence of AGEs, and also investigated the downstream cellular consequences of that exchange.

They showed that, at baseline, DIAPH1 starts with a cellular brake engaged that holds back its activity, but after it interacts with RAGE, those brakes are ripped off. The full consequences of that aren't yet understood, Schmidt noted, but from what we know, it "appears to have pathological outcomes."

Schmidt, Shekhtman and their team had previously looked for molecules that could block the interaction of RAGE and DIAPH1. Among 58,000 molecules, the team zeroed in on one that looked promising and found in initial mouse experiments that it curbed diabetes complications such as kidney disease and heart ischemia. An analogue of that original molecule was used for the new study, as tests suggested it has a better safety profile.

In cells from patients with type 1 diabetes, the drug compound blocked the interaction between RAGE and DIAPH1 and subsequently reduced inflammatory signals. In lab mice with diabetes, applying the compound topically to mice's wounds helped to both tamp down inflammation and speed up healing. The researchers also showed that the drug could reduce inflammation in mice with allergies when given by mouth, but they didn't test this oral delivery in diabetic mice.

Looking forward, it will be important to study RAGE in many cell types, because it likely does different things in different types of cells, Perkins noted in his commentary.

Much more work is needed before the drug can be tested in humans, including more tests in lab animals, Schmidt emphasized. But she suggested that, if the drug makes it to approval, it would be best for patients to start using it soon after being diagnosed with diabetes. Ideally, RAGE therapy should be paired with tight blood sugar control, before the snowball effect of AGEs building up could get started, she said. You'd want to "mitigate that spiral of constantly making more AGEs," she said.

Beyond diabetes, RAGE is also known to contribute to inflammatory diseases of the lungs, such as asthma and chronic obstructive pulmonary disease (COPD), Perkins noted. He suggested that those might be additional contexts where drugs that disrupt the RAGE-DIAPH1 interaction might be helpful.

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

More than 300,000 snakebite cases occur in Africa annually, resulting in at least 7,000 deaths, as well as numerous amputations and injuries. Now, scientists have invented a new nanobody-based antivenom that shows promise against 17 dangerous African snake species.

Until now, the mainstays of treatment have been antivenoms created by exposing horses to particular venoms and then isolating protective antibodies from the animals' blood. These traditional antivenoms can occasionally cause allergic reactions in patients, and they are effective against only one or a few of related snake species.

Now, in a study published in October in the journal Nature, scientists report creating an antivenom that targets most of Africa's deadliest elapids, meaning cobras, mambas, and the rinkhals, also called ring-necked spitting cobras. Instead of horse serum, the antivenom uses eight engineered nanobodies that are essentially tiny antibody fragments designed to block key toxins in the snakes' venoms.

Juan Calvete, director of the Evolutionary and Translational Venomics Laboratory at the Biomedicine Institute of Valencia, who was not involved in the study, said the new nanobody-based antivenom is "a remarkable advance in the development of synthetic antivenoms." However, he noted that in its current form, the antivenom may be expensive to make, and thus challenging to use in poorer regions.

To create the new antivenom, researchers exposed an alpaca and a llama to venoms from 18 African snakes, including cobras, mambas, and the rinkhals. These snakes' venoms are potent and can cause serious problems, such as paralysis and tissue damage, and they also contain a diverse range of toxins.

The llama and alpaca exposed to the venoms produced special, tiny antibodies, known as nanobodies. The compact size of these nanobodies enables them to diffuse quickly through tissues and bind toxins at hard-to-reach sites in the body, the study authors noted.

The researchers collected the animals' blood and used a technique to find nanobodies that stick well to various venom toxins. The nanobodies that latched on most effectively were then made in the lab and tested for their ability to block the venoms' effects. Finally, eight of these engineered nanobodies were combined into a powerful mix to create the new antivenom.

In lab tests in mice, this nanobody serum prevented death from 17 of the 18 target snake venoms; the venom of the eastern green mamba (Dendroaspis angusticeps) was the only one not fully neutralized. Further analyses suggested that the antivenom neutralized seven toxin families found within the venoms and that it reduced tissue damage from venoms known to kill cells.

The antivenom outperformed a commonly used antivenom designed to target multiple toxins: Mice given the nanobody mix survived multiple venoms with fewer symptoms than did mice treated with the traditional horse-antibody-based serum.

"The main advance of our work is showing that an effective recombinant antivenom can be made with a surprisingly small number of nanobodies that outperform existing ones," senior study author Andreas Hougaard Laustsen-Kiel, a biotechnologist at the Technical University of Denmark, told Live Science in an email. The new antivenom was better at preventing both lethal effects and tissue damage, and it could theoretically be "produced at large scale in bioreactors, independent of snakes and horses," he said.

The next steps include testing the antivenom's effects in larger animals to estimate what dose a human might need and optimize the process to scale up production. "We are also testing some of these nanobodies, and new ones, against Asian cobra venoms to develop cocktails with broader species coverage and geographical relevance," Laustsen-Kiel said.

The idea of a broad-spectrum — or even "universal" — antivenom has recently gained traction. A notable 2025 study published in the journal Cell used human antibodies from a snakebite survivor to protect mice from multiple cobra and mamba venoms. Yet practical and economic barriers remain to developing such an antivenom and manufacturing it affordably and scalably.

Calvete called the new nanobody venom a significant advance, but he cautioned that dosing requirements in humans might complicate things. "A therapeutic dose to treat envenomings from all target snakes could require up to 50 grams of nanobodies," he suggested. (That said, tests to officially determine human dosing have yet to be conducted.)

He added that improving the pharmacokinetics of the antivenom — that is, how the treatment interacts with the human body — would likely increase production costs beyond what was seen in this proof-of-concept study. "The most powerful of all the 'omics' — economics — may once again represent an insurmountable obstacle to fighting the most neglected of tropical diseases," he concluded.

In theory, the new nanobody mixture could represent a promising step toward safer, scalable snakebite therapies, but further testing, manufacturing optimization, and regulatory validation will be crucial to getting it into human patients.

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

Scientists have reported the discovery of the first in a promising new class of antibiotics — and the find was unexpected, as they hadn't set out to find new drugs.

The new antibiotic compound shows promising activity against drug-resistant infections, including methicillin-resistant Staphylococcus aureus (MRSA) and Enterococcus faecium, germs that are notorious for causing resistant infections in hospitalized patients.

The discovery of the novel molecule, called pre-methylenomycin C lactone, was reported Oct. 27 the Journal of the American Chemical Society and "can be considered the first in a new class" of antibiotics, Lona Alkhalaf and Greg Challis, chemists and lead authors of the study, told Live Science in an email.

However, the team's initial aim wasn't to discover new drugs. Instead,the researchers were investigating how a known antibiotic, methylenomycin A, gets made by a soil-dwelling bacterium called Streptomyces coelicolor.

Plants and microorganisms produce a host of complex compounds known as secondary metabolites, many of which happen to have useful medicinal properties in humans. Understanding how these compounds are made within these organisms and how they interact with human cells can help scientists develop effective drugs from these natural products.

The blueprints for producing these different biological molecules are held in specific collections of genes, called "biosynthetic gene clusters." By deleting individual genes from these clusters, Alkhalaf and Challis could remove specific enzymes involved in the synthesis of methylenomycin A. This research technique enabled them to halt the reaction sequence at key points to study it more closely — and it led them to spot extract previously unobserved intermediate compounds that get produced along the way.

This systematic approach allowed the team to isolate two never-before-seen molecules, which they named pre-methylenomycin C and pre-methylenomycin C lactone. After using an array of techniques to thoroughly characterize the structures of these compounds, they investigated the molecules' biological activity against a panel of bacterial strains.

Pre-methylenomycin C lactone proved particularly promising. "[It] is active against a range of Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA) and a multidrug-resistant strain of Enterococcus faecium," Challis and Alkhalaf told Live Science. "[It] is 100x better at killing drug-resistant bacteria than the original antibiotic."

But perhaps more importantly, the new compound doesn’t appear to induce antibiotic resistance in the treated strains.

Repeated exposure to antibiotics can trigger the evolution of defense mechanisms in some bacteria, eventually leading to drug resistance that makes future infections extremely difficult to treat. In a 28-day experiment, E. faecium bacteria were exposed to increasing concentrations of pre-methylenomycin C lactone, providing the perfect opportunity for resistance to develop. But over that period, the team did not observe any change in the minimum inhibitory concentration — the amount of drug needed to produce a visible effect. In short, the antibiotic retained its infection-killing activity, and the bacteria did not evolve any problematic resistance mechanisms.

Expanding this line of research — both to include more bacterial strains and to study the drugs' effects over a longer time frame — will be two important next steps for the team to demonstrate the full potential of the new molecule.

"It's a really nice study and I think this is a lesson: if you isolate novel molecules then look for novel activities with those molecules," said Stephen Cochrane, a medicinal chemist at Queen's University Belfast in Ireland who was not involved with the work. However, he cautioned that there is a significant difference between a compound with antibacterial activity and an antibiotic used to treat disease.

"The big challenge is translating this into a viable drug — something that persists long enough in the body, isn't toxic to humans, and is not prone to resistance," he said.

For Alkhalaf and Challis, this is exactly the direction they hope to pursue next. They are now collaborating with David Lupton, a synthetic chemist at Monash University in Australia, to develop a chemical route to pre-methylenomycin C lactone. This would enable them to produce the molecule from scratch via chemical synthesis, rather than relying on microbes to make it. In turn, this would provide larger volumes of the compound for studies aimed at understanding how the molecule works and how it might affect human cells.

"It would be useful to identify the biological target(s) of the compound in susceptible bacteria and develop a better understanding of how changes to the compound's structure affect target binding and biological activity," Alkhalaf and Challis said. Such insight might inform the design of related compounds with even more potent antibiotic activity.

On Dec. 31, 2019, the first reports emerged about a mysterious pneumonia of unknown cause circulating in China. On March 11, 2020, the World Health Organization declared COVID-19 a pandemic.

On March 16, the first COVID-19 vaccine entered clinical trials.

And by Dec. 14, members of the American public were getting the first doses of COVID-19 vaccines outside of trials.

The first coronavirus vaccines were paradigm-shifting because they went from conceptualization to mass production in mere months. But they were also unique because they used a new way to stimulate the immune system — one that had been thoroughly studied for decades in order to be ready for deployment at this crucial moment.

The key to these vaccines was messenger RNA (mRNA), DNA's less-famous cousin. The power of the mRNA platform is that vaccines can be produced exceptionally quickly once a pathogen's genetics have been analyzed; conventional vaccine manufacturing takes months or years whereas mRNA vaccines can be made in mere weeks. So while it was once the subject of high school biology classes and niche pockets of biomedical science, mRNA was suddenly thrust into the public eye — and once there, it inspired relentless misinformation and controversy.

While mRNA-based COVID-19 vaccines are the best known application of the molecule, researchers around the world have found additional uses for mRNA technology beyond the realm of vaccines. They're exploring its use for groundbreaking treatments for cancer and autoimmune disease, as well as for gene-editing therapies for genetic disorders. But that promise may be unrealized in the United States, where the federal government has declared war against this promising technology.

This new stance runs counter to the Trump administration's prior embrace of mRNA vaccines.

"We do really have to give President Trump credit for introducing the mRNA platform to the world through his leadership in Operation Warp Speed," said Jeff Coller, the Bloomberg distinguished professor of RNA biology and therapeutics at Johns Hopkins University. "The president should be taking a victory lap." But instead, the second Trump administration is actively dismantling this legacy, Coller told Live Science.

Vaccine skeptic Robert F. Kennedy Jr. now heads the Department of Health and Human Services (HHS), and opponents of both conventional and mRNA-based vaccines hold seats on the country's most influential vaccine advisory committee. Since Trump's inauguration, federal scientists have faced mass layoffs, funding freezes, and memos warning them to disclose their involvement in research areas the administration has targeted, including mRNA vaccines.

These actions had an immediate chilling effect on mRNA research and development in the U.S., Coller told Live Science. And then, in August, HHS canceled nearly half a billion dollars of investment into mRNA vaccine development.

"I was shocked to see this, frankly," said Jordan Green, head of the Biomaterials and Drug Delivery Laboratory at Johns Hopkins, whose lab is developing both mRNA therapies and delivery systems to get the molecule into the body.

The cuts are sending ripples through biotech, making stakeholders question whether it's safe to set up shop in the U.S., or whether their mRNA investments would be better spent abroad. "It's just a shame because it's an unforced error; there's no reason," Green said.

For now, HHS appears to be retreating primarily from mRNA vaccines; it noted "other uses of mRNA technology" would not be affected by the cuts. But "the industry doesn't trust that," Coller told Live Science.

According to Grant Witness, a project tracking scientific grants under the Trump administration, mRNA research unrelated to vaccines has already been hit by grant terminations and funding freezes. So even if it's not being explicitly targeted, it's not necessarily being preserved. The project's database shows that the National Institutes of Health (NIH), part of HHS, terminated grants for projects developing mRNA-based treatments for cancer, Alzheimer's, pulmonary arterial hypertension and HIV, as well as grants for basic research about how mRNA works in healthy and diseased cells.

Here's what the United States stands to lose if the federal government broadly divests of mRNA medicines after spending decades readying the technology for prime time.

Cancer treatment

On a molecular level, mRNA is a close cousin of DNA — and human cells are stuffed with it. These ubiquitous "messengers" copy instructions from DNA and relay them to other locations in the cell — namely, to protein-construction sites where the complex molecules that do most of the work in cells get made. mRNA also performs other key jobs in cells, such as helping control which genes are switched on and to what degree.

For decades prior to the pandemic, dedicated scientists pored over mRNA, learning how this class of molecules works in the body and how it might be leveraged to heal the sick and guard against disease.

"I started doing this when I was like 21, back in the '90s, back when about 10 people on Earth knew what mRNA were," Coller said. Findings from Coller's lab later helped inform the development of Spikevax, the COVID-19 vaccine made by Moderna. But while COVID-19 vaccines are the best-known application of mRNA to date, they're far from the first.

The first mRNA therapeutics company was founded in 1997, and rather than targeting infectious disease, it had its sights set on cancer treatment. Its approach ultimately hasn't panned out in human trials, but in the meantime, other approaches to mRNA-based cancer treatment have gained traction.

Cancer vaccines are a standout example, but in this context, the term "vaccine" is "a bit of a misnomer," said Dr. Vinod Balachandran, a pancreatic cancer surgeon-scientist and director of The Olayan Center for Cancer Vaccines (OCCV) at Memorial Sloan Kettering Cancer Center. Rather than being given preventatively, like a COVID vaccine, cancer vaccines are "given to patients as a treatment; it is a therapy," he said.

These therapies are similar to conventional vaccines in that they train the immune system to recognize antigens, which are substances that act as "red flags" for foreign invaders, toxins or diseased cells. These include, for example, the spike protein of SARS-CoV-2 — the virus that causes COVID-19 — and certain molecules on cancer cells. Balachandran and colleagues have focused on pancreatic cancer, which has a five-year relative survival rate of only 13% — meaning people newly diagnosed with pancreatic cancer are about 13% as likely to survive the next five years compared with the general population.

The researchers have found that, in the rare long-term survivors of pancreatic cancer, the immune system can recognize the cancer and fight off its recurrence. The team hoped to re-create that immune recognition in other patients by analyzing the genetics of their tumors to see what unique antigens they express. They then create customized vaccines that target those molecules.

"We felt at the time [when we started this work] — this is back in 2017 — that the best technology for rapid custom cancer vaccination for patients was to use RNA," Balachandran said. Once you know a given patient's cancer genetics, a personalized mRNA vaccine that targets multiple antigens can be crafted in a matter of weeks. Conventional vaccines that require the antigens to be grown in the lab and purified would take many months to make.

"For cancer vaccination, speed is essential," Balachandran said. "These are patients who are facing deadly cancers, who require rapid treatment. So we do not have the luxury of waiting."

So far, the team has seen some success. In an early-stage trial, they treated 16 patients who had undergone surgery for pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, which has a five-year survival rate of about 10% to 12%, though they fare a bit better when their cancer can be surgically removed.

Within nine weeks of surgery, Balachandran said, each patient's tumor tissue was analyzed and a personalized vaccine was crafted and delivered alongside post-surgery cancer treatments, like chemotherapy. Half of the patients responded to their vaccine, producing immune cells that have persisted for nearly four years so far, and estimates suggest they could last an average of seven years, "with some lasting even beyond a decade," Balachandran said.

The vaccine responders had a significantly lower risk of recurrence in the following three years than those who didn't respond, with six showing no signs of recurrence in that time frame. A mid-stage trial is now testing the vaccine in about 260 people to see how well it delays or prevents recurrence compared with standard treatment.

"Anything we can do to improve outcomes for these patients who really need help I think will be transformative for the field, for them, for their families — it will mean a lot," Balachandran said. "All other immune therapies and all other therapies have largely failed."

In this initial trial, vaccine production took over two months, in part because samples had to be shipped to overseas collaborators at BioNTech. "We are confident this can happen much faster" in the future, perhaps within a month, Balachandran said.

Other scientists are working on off-the-shelf cancer vaccines that can help bridge the gap until a patient gets a personalized one. These vaccines use a mix of mRNA molecules to stir up a generic, first-line immune defense against cancer. In mice with different kinds of solid tumors, researchers led by Dr. Elias Sayour, a pediatric oncologist at the University of Florida, demonstrated that such a vaccine triggers anti-cancer responses by itself. And when used in combination with another cancer treatment, the mRNA mix can boost the effects of that therapy, Sayour's team has found.

That team has now moved on to human patients, with a two-pronged approach: an off-the-shelf cancer vaccine, followed by a personalized one. They have also run trials of personalized vaccines for the deadly brain cancer glioblastoma, finding that the shots mount a strong, targeted immune response against these tumors that are usually difficult for the immune system to "see." Meanwhile, at another lab, scientists are testing a personalized vaccine in late-stage trials for the skin cancer melanoma and non-small cell lung cancers.

Pancreatic cancer has historically been an elusive target for the immune system because, compared to cancers like melanoma, its cells carry relatively few antigens, Balachandran explained. But pancreatic cancer can be targeted with these vaccines. That bodes well for using mRNA approaches to treat potentially many other cancers, and "I think that's really the most exciting take-home," he said.

Beyond cancer vaccines, Green and colleagues are leveraging mRNA to fight the disease in a different way: by forcing tumors to raise their own red flags to the immune system. Using mRNA packaged inside nanoparticles, the researchers introduce immune-cell genes into cancer cells, prompting tumors to expose their antigens and secrete molecules that call immune cells to the area.

"We can program that tumor cell to now act like an immune cell that helps teach other immune cells what its antigens look like, how to recognize it, how to destroy it," Green told Live Science. In mouse models of breast cancer and melanoma, they combined this approach with an existing immunotherapy and found that it helped shrink and clear tumors from the body while also extending survival.

If shown to work in people, "this could just be off the shelf," he said. It would be one injectable that could work on any patient's solid tumor, he said.

Immune reprogramming

In cancer, scientists are exploring different ways to launch an immune attack against tumor cells, whether by igniting a generalized response or enabling cells to spot specific red flags. But in some diseases, the immune system itself is the culprit — and in those instances, mRNA can help rein in turncoat immune cells.

"Autoimmune diseases — type 1 diabetes, multiple sclerosis, Crohn's, colitis — these can be treated with these mRNA and genetic-based therapies," potentially, Green said. The goal of these treatments would be to "tune the immune system" so it stops attacking healthy tissues.

In type 1 diabetes, for example, the immune system attacks beta cells, which make insulin, leaving the body too little of the hormone to control blood sugar. Green and colleagues are in the early stages of developing an mRNA medicine to reprogram the immune system so it better tolerates beta cells, rather than attacking them. They aim to do this by targeting special immune cells in the liver that promote a tolerant environment in the organ.

The liver is constantly exposed to antigens from food and from microbes in the gut, so immune activity is dialed down to prevent an overreaction. The team's idea is to deliver mRNA that codes for beta-cell proteins to the liver, essentially marking those beta-cell proteins as "safe" to the immune system. This, in turn, can increase the number of regulatory T cells that recognize the proteins as safe; regulatory T cells keep other immune cells in check, and could thus help ward off further attacks on beta cells.

"The problem with autoimmunity is that [the immune system] thinks parts of its own body are foreign," so it's trying to attack them, Green explained. The hope is that "we can use these mRNA medicines to train the immune system so that it sees, 'Oh no, this is fine.'" The work is currently in preclinical stages, as the team runs experiments with cells and lab mice to refine their mRNA nanoparticles.

Green calls this approach of fine-tuning specific cells' activity "genetic surgery." Rather than using a "blunter instrument," like immunosuppressive drugs, to broadly suppress the immune system, the surgery makes a precise change to counter only harmful immune activity. In the long run, the lab is looking to apply this same approach to other autoimmune diseases beyond diabetes, such as multiple sclerosis, in which immune cells target myelin, the insulation surrounding nerve fibers in the brain and spinal cord.

Meanwhile, BioNTech has published data from its own early tests of an mRNA vaccine designed to quell autoimmunity against myelin. In mice, the vaccine expanded populations of immune cells that then kept the myelin-attacking cells in check, suppressing their activity without hobbling the immune system as a whole.

Elsewhere, researchers including Dr. Samira Kiani of the University of Pittsburgh School of Medicine and Kathryn Whitehead of Carnegie Mellon University are using mRNA to counter off-the-rails immune responses, such as the extreme inflammation seen in sepsis. Their approach, described in a preprint, packages mRNA inside a tiny bubble of fat called a lipid nanoparticle (LNP), which then ferries the mRNA into immune cells. From there, the mRNA instructs the cells to make proteins called "zinc finger repressors," which latch onto genes and suppress their activity. In this case, they repressed a key gene involved in the immune signaling that can lead to runaway inflammation.

In experiments with cells in lab dishes and with mice, this type of "epigenetic engineering" showed promise as a potential method for tuning the activity of the immune system. One perk of mRNA is that it degrades quickly in the body, the study authors wrote, so in theory, once the harmful inflammation is subdued, the immune system can get back to defending the body against germs.

Gene editing

mRNA is also being used in tandem with the gene-editing system CRISPR to revolutionize treatments for genetic disease.

Classical CRISPR systems use molecular scissors to snip through DNA strands and enable scientists to tweak specific segments of the molecule. And now, a modified system called base editing can be used to precisely change just one "letter" in DNA's code.

But if you want to use CRISPR for gene therapy, you must first get the scissors, as well as a "guide" molecule that directs them to the right spot — into human cells. And, ideally, the scissors enter only the cells you need to edit, said Giedrius Gasiūnas, a senior researcher in the Life Sciences Center at Vilnius University in Lithuania.

That's where mRNA packaged in nanoparticles could be a game changer.

"This technology could be important for in vivo delivery," meaning the delivery of gene editors directly into the body, said Gasiūnas, who is also chief scientific officer of the biotech company Caszyme.

The first CRISPR-based therapy approved in the U.S. involved editing cells outside the body. The therapy treats two blood disorders by disabling a gene called BCL11A; patients have blood-making stem cells removed from their bone marrow, edited in the lab and then returned to their bodies. But this complex treatment involves a month-long hospital stay, during which the edited stem cells give rise to new blood cells. By comparison, mRNA approaches to gene therapy would be easier to administer and thus more likely to be scalable, Gasiūnas said.

mRNA isn't the only vehicle for getting CRISPR therapies into the body. Some existing gene-editing treatments instead use harmless viruses, such as adeno-associated virus (AAV) vectors, and this same approach is being applied to CRISPR in some emerging therapies. But mRNA packaged inside nanoparticles is emerging as a key player in the field.

This application made headlines in the case of KJ, an infant who became the first person to receive a personalized CRISPR treatment. "The CRISPR technology was introduced as an mRNA," Coller said. "That is the critical feature that was necessary to get this to work."

KJ was born with a severe form of carbamoyl phosphate synthetase 1 (CPS1) deficiency, an inherited disease that causes ammonia to accumulate in the body and affects an estimated 1 in 1.3 million people worldwide. The condition arises from mutations in the CPS1 gene, but in different patients, the gene is broken in different ways. To fix KJ's specific mutation, scientists developed a customized gene therapy consisting of a guide and an mRNA that carried instructions for a base editor into his liver cells, where CPS1 is most active.

"The editor is so large that it cannot easily be accommodated by an AAV vector," said Dr. Kiran Musunuru, co-developer of the therapy and a professor at the University of Pennsylvania's Perelman School of Medicine. Because other potential delivery systems are too early in development, "LNPs are currently the best option," Musunuru told Live Science in an email.

The therapy was ready to administer within six months of KJ's birth. By 9 months old, he had received several doses of the therapy and was thriving; he was hitting milestones he may have never reached otherwise, his medical team reported in May. Had he not received the treatment, he would have needed a liver transplant once he got big enough.

Promising technology at risk

When it comes to the future of mRNA medicines in the U.S., vaccines for infectious disease currently have the bleakest outlook due to political barriers being raised around the technology. Among mRNA tech, vaccines have been the primary target of the federal government's ire, despite experts' warnings that abandoning the shots will leave us vulnerable to pandemics.

"It's foolish to condemn mRNA because people didn't like vaccine mandates or mask mandates or whatever they didn't like," Dr. Seth Berkley, an epidemiologist and senior adviser to the pandemic center at the Brown University School of Public Health, told Live Science. "What we need to do is improve upon them [mRNA vaccines] and understand what the best use of them is," which can only be accomplished through investing in further research.

For now, other applications of mRNA don't appear to be a focus for funding cuts, although some projects have nonetheless been caught in the crosshairs of reduced federal spending. For his part, Musunuru told Live Science he's been in discussions with the Food and Drug Administration regarding ways to get more patients access to personalized gene therapies like KJ's, so that the technology isn't used only in a handful of special cases. When asked about potential funding cuts, he added, "Vaccines and therapies are so different that I do not expect the latter to be affected."

Green, however, anticipates that divestments from vaccines would have unanticipated impacts across the field, because mRNA therapies and vaccines are ultimately composed of very similar genetic molecules and delivery systems.

Regarding nanoparticles, "the vaccine development is … at the pioneering edge of this technology platform," Green said. He argues that cuts to vaccine R&D will inevitably undermine the development of nanoparticles that could be really useful in treating cancer or genetic disease. "It's going to set us back in a very broad way," he said.

The hits to vaccine research also aren't happening in isolation. Myriad federal science grants have been terminated or frozen; NIH agencies may be facing steep funding cuts; and the government shutdown ushered mass layoffs across leading health institutions. Sayour, the oncologist whose lab is developing personalized and universal cancer vaccines using mRNA, said federal grants have historically been critical to his research.

"None of this would be possible without the support of the federal government," Sayour told Live Science. "That is most certainly, 100% true." And that goes for every stage of research, from studies in lab dishes to large clinical trials.

These widespread cuts and more-targeted cuts to mRNA vaccines will not only starve the academic environments where new biotechnologies are typically nurtured, Coller said; they will also drive prospective talent, investors and industry stakeholders in the mRNA space away from the U.S. "In biotech, we're going to see, over the next five to 10 years, a significant 'brain drain,' where other countries build up their infrastructure," he said.

Coller knows this because he is a founding member of the Alliance for mRNA Medicines (AMM), a global organization aimed at advancing and advocating for mRNA medicines. In the spring, AMM surveyed over 100 leaders in the field. They primarily represented U.S.-headquartered pharmaceutical and biotechnology organizations but also included some based in Europe, Canada or Asia. Even prior to the major HHS cuts in August, these stakeholders were feeling squeezed; nearly half reported "already experiencing direct impacts" from federal policy changes tied to mRNA funding.

The cuts caused projects to be scaled back, partnerships to be terminated, and jobs to be lost. About 30% of respondents said that, if faced with further cuts, they might pivot away from mRNA, and 30% said they'd consider moving their operations to other countries. Over 80% agreed that anti-mRNA policies would drive talent away from the U.S. and toward other locales.

Even as scientists contend with these big-picture problems on the national and international stage, skirmishes have also been unfolding at the state level. These battles primarily concern public access to mRNA vaccines but could potentially have broader ripple effects.

A bill still in committee in Iowa would make administering an mRNA vaccine in the state a misdemeanor with a fine of $500 for each shot given. Another bill in committee in South Carolina would prohibit the use of mRNA-based "gene therapies" in the state, but makes an exception for therapies for noninfectious diseases, such as cancer.

It may be that most bills of this ilk never become law and some, like the one raised in South Carolina and two dead bills in Texas, purposely make exceptions for certain uses of mRNA. However, others have been worded in ways that made it unclear whether any mRNA medicine is permissible. If any of such bills ultimately pass at the state level, that could sway where mRNA companies can manufacture products and run clinical trials, Coller said. So, while an exodus of expertise unfolds at a national level, we may see an echo of that at the state level.

The future of mRNA medicine in the U.S. rests on many "ifs," and the worst-case scenario may not come to pass. But in the face of staggering uncertainty, researchers in the field are starting to look for better bets.

"Let's not fool ourselves: mRNA is one of the three most important molecules in the body, with the other two being DNA and protein. It's the intermediary between them," Coller said. "When the federal government sends a message that mRNA-based medicine and research is not wanted, you're basically saying that there's a whole branch of science that is no longer welcome within the U.S."

Months before COVID-19 was officially declared a pandemic, public health leaders were poring over the early data coming out of China and preparing for the worst.

Dr. Seth Berkley — a renowned infectious-disease epidemiologist and former CEO of Gavi, an international organization aimed at improving children's vaccine access — was among those leaders. In January 2020, Berkley and colleagues were working to establish an infrastructure so that, if and when scientists created vaccines for this novel virus, the shots wouldn't be hoarded by high-income countries and denied to poor nations.

Now, Berkley has released a new book — "Fair Doses: An Insider's Story of the Pandemic and the Global Fight for Vaccine Equity" (University of California Press, 2025) — that recounts how that initiative unfolded and what lessons were learned through the process, while underscoring why the broader fight for vaccine equity is far from finished.

On January 23, 2020, I was high up in the Swiss Alps in Davos, attending the World Economic Forum (WEF). I was at Davos as the CEO of Gavi, the Vaccine Alliance, the largest purchaser of vaccines in the world and which worked to provide new and underutilized vaccines to children in developing countries — countries in which about half the world's children live. As usual, I was preoccupied with how we could do a better job protecting the world with vaccines for new and old diseases. And there were murmurs of a new epidemic of respiratory disease caused by a novel coronavirus in China on the horizon.

At the bar of the Hard Rock Hotel my wife, Cynthia [an academic physician and consultant], and I met with Richard Hatchett, CEO of the Coalition for Epidemic Preparedness Innovations (CEPI). Over nachos and drinks, we started to talk through what was likely to happen with the new coronavirus, which would later be named COVID-19. Discussion about the disease hadn't really reached a high political level and was not formally on the Davos agenda, but concern was growing, and many people during that week asked us our opinions.

The first question we discussed was whether this was just going to be a worrisome outbreak or the Big One that epidemiologists had long warned might come. So far, we only had official confirmation of a point outbreak, spreading from animals at the Wuhan live animal market to humans. But on the nerdy LISTSERVs about infectious disease and epidemics, there was already a lot of chatter about how the virus might be spreading from person to person, which is a huge red flag in our field. We agreed that there was potential for the new virus to spread dramatically. Regardless of whether this was or was not the Big One, we needed to prepare.

Such a scenario creates a problem for all countries, even those with access to the vaccines. But to me a far bigger concern was the unfairness of high-income countries' self-interest. People in developing nations without access to vaccines were historically already the most vulnerable to disease and the most likely to suffer complications if they got sick. They already had limited access to the most basic medical treatment.

Improving the delivery of existing vaccines and building up better delivery systems is the best way to detect outbreaks early, prepare communities for outbreaks of disease, and ensure health systems aren't overwhelmed in an emergency — as well as strengthen our epidemic stockpiles.

If vaccines against the disease could be made — and at the time, we were far from certain they could be — we knew that stocks would be quickly bought up by the richest countries. The logical conclusion was that the bulk of the world's population, and most especially those in lower income, developing countries, would be locked out of these deals, and so denied timely access to whatever vaccine supplies became available.

That was where we thought we could help. So, Richard, Cynthia, and I talked through a rough outline of what would be needed to ensure equitable access to any COVID-19 vaccines that emerged and the roles that various organizations — such as CEPI, Gavi, UNICEF, and WHO — as well as the pharmaceutical companies might play to make that happen.

Imagining ourselves in the place of government decision-makers, we envisioned that they would have an incentive to participate in a mechanism that pooled risk by making advance purchase commitments for a wide variety of candidate vaccines. Their buy-in could help us pool demand, generating enough scale to incentivize increasing production and to negotiate the best prices on everyone's behalf. We wanted to promote solidarity, to publicize and meet lower-income country needs, and to create an early, strong global movement for equitable access.

Richard went from Davos back to London and talked with the CEPI team, I went back to Geneva to talk to the Gavi team and our Alliance partners WHO and UNICEF, and we started our collaboration. That joint effort became COVAX [COVID-19 Vaccines Global Access, an initiative to ensure equitable access to COVID-19 vaccines].

Our small team working on COVAX undertook what I believe was the most ambitious public health effort of the 21st century so far. The first COVAX dose was delivered to a COVAX-supported country 39 days after the first jab in the United Kingdom. Due to the time required for WHO to prequalify the vaccine, 43 days later the first doses were administered in Africa, in Ghana and Côte d'Ivoire. Forty-two days later, COVAX vaccines had been distributed to 100 countries. There were many delays due to export bans, vaccine nationalism, and manufacturing delays. But by the end of 2021, close to 1 billion doses had been distributed; by the end of 2022, COVAX had delivered more than 1.6 billion doses to people in the world's poorest countries and was estimated to have averted 2.7 million deaths in those countries. That's the fastest rollout of vaccines to developing countries ever.

WHO estimates that some 16 million people died during the first two years of the pandemic; we are still counting, and that number will doubtlessly grow. And COVID-19 is by no means the only infectious risk: Currently, about one in seven deaths, accounting for more than 7 million people a year, is due to an infectious disease. Millions of people die from diseases for which we already have vaccines.

It's hard to put numbers on the deaths that have been prevented by vaccines, but some estimates say that vaccines have saved more than half a billion lives over the past 70 years, the time period they have been routinely available. And this only covers the 30 or so vaccines we have against the more than 300 infectious diseases known to plague humanity.

More and better vaccines need to be developed, particularly for major killers such as tuberculosis, malaria, and HIV, and, hopefully, more cancers. And in the meantime, the risks for infectious diseases are shifting.

Even those of us who had been working in the field for years were surprised at how poorly prepared the world was for an emergency of this magnitude. What's more, we faced the perils of vaccine nationalism, vaccine diplomacy, and the sometimes-selfish behaviors of manufacturers and world leaders. It was clear from the start that we wouldn't be able to do this work perfectly. But we did our best, and I've sought to set down both what we did and what I wish we could have done differently so that we can learn from our history.

As the world continues to recover from the worst of the pandemic years, we may not relish thinking about another pandemic ahead. We face complacency, fatigue, and a growing distrust of both science and institutions, fed by intentional disinformation that spreads rapidly online. But we also have an opportunity to harness what we've learned to do better next time — and there is epidemiologic certainty that a next time will come. When it does, we need to have robust public health systems in place, and ideally, vaccines.

Reprinted from Fair Doses: An Insider's Story of the Pandemic and the Global Fight for Vaccine Equity by Seth Berkley, MD, courtesy of University of California Press. Copyright 2025.

Within weeks of the first cases of a "mysterious pneumonia-like illness" being reported in Wuhan, China, public health leaders were convening to assess the threat and shore up systems to mitigate the potential harm to come. This work started unfolding months before COVID-19 would be officially declared a pandemic.

Dr. Seth Berkley — a renowned infectious-disease epidemiologist and former CEO of Gavi, an international organization aimed at improving children's vaccine access — was one figure at the forefront of the effort to ensure future COVID-19 vaccines would be distributed to the world's poorest nations. In his new book "Fair Doses: An Insider's Story of the Pandemic and the Global Fight for Vaccine Equity" (University of California Press, 2025), Berkley recounts those pandemic-era efforts and reflects on what went right and what went wrong.

Live Science spoke with Berkley about the book and the lessons we should take forward into the world's next big outbreak — the emergence of which, Berkley argues, is a matter of "when," not "if."

Nicoletta Lanese: What was the impetus to write this book?

Dr. Seth Berkley: When the book was written, the real purpose of it was to capture the experience [of the pandemic], post-COVID and post-COVAX. COVAX [COVID-19 Vaccines Global Access] was an initiative we put together when we realized that this looked like it was going to become a more severe infection. In doing that, we had all kinds of problems, but in the end, we did do the fastest and largest rollout of vaccines in history. We ended up with 57% of people in the developing world, the poorest 92 countries, getting coverage with primary doses, versus 67% globally — so not perfect equity, but better than it had ever been done before.

What I was worried about is [that] people wouldn't capture the lessons learned, both good and bad. The book tries to explain what it took to get there, and also who were the good players, who were the bad players.

Now, since the book was written, the world has changed dramatically. I couldn't — I mean, I suppose I could have ripped the book up and started writing again. I didn't do that, but I did have a chance to say in the preface, and then later on at the end of the book, how much had changed, given the intense anti-vaccine attitudes that we're seeing right now in the U.S. government, particularly in the secretary of health and human services [HHS], Robert Kennedy Jr., who is a long-term vaccine skeptic and a conspiracy theorist on these things.

It's obviously quite concerning in regard to how that may affect Americans. But also it's important for Americans to understand that the vaccine work that's done in other countries also affects America, because the diseases we get come from both inside and outside.

NL: On that point, we've seen the U.S. withdraw support from initiatives that support vaccine equity globally. What are the potential impacts of that?

SB: So if we go back — I'll use a period of 50 years, for convenience — less than 5% of people in the world received even a single dose of vaccine. Not all the doses that were recommended — a single dose. And we've gone from that level up until vaccines, now, are the most widely distributed health intervention in the world. Along with that, we've seen a 70% reduction in vaccine-preventable disease deaths, and we've seen a more than 50% reduction in under-5 child mortality, directly as a result of this type of work.

So this is a really big deal. We've also seen control of many infectious diseases: the eradication of smallpox, the almost complete elimination of wild polio, the control of measles in many countries, etc. etc. Those are the successes. But the idea now is that we back away from this, when we have these infectious diseases that are still a risk — and as we've recently seen in the U.S., we've had some big measles outbreaks.

The U.S. actually had received the status of having eliminated endogenous measles infections, meaning that when new infections would occur, they had to come from outside. Now, the U.S. is at risk of losing that designation. This is why it's so important to think about it globally, because if we see many more measles infections occurring in other countries and given the movement of people, you're eventually going to see those cases in the United States if vaccine rates go down. And they are going down.

We've got a situation where people are discrediting experts and putting people in place who do not have expertise and have preconceived notions on vaccines. They say they're trying to increase trust, but I don't see how that increases trust. And we're now fractured in the U.S.; you've seen most recently this idea that states are coming together to put out their own recommendations. Professional societies are putting out recommendations, instead of having one definitive set. In the end, I don't think that helps with confidence.

NL: Do you feel these shifts in the U.S. stem from an amplification of an old problem we've had, or more from a brand-new issue?

SB: It's a little of both. Vaccine hesitancy has existed from the first vaccine, which was in the 1700s smallpox right after the original vaccine was shown to work. There were cartoons showing — because the vaccine was derived from cows — there were pictures of people with cow horns growing out of their heads and all kinds of things like that. So this is not a new problem.

What is new is having the intense politicization of this — the idea that one political party more than another political party has these beliefs and therefore acts on them, so there are different coverage slates for vaccines for different parties. And then finally, [there's] the fact that you've got government leaders that are pushing these conspiracy theories and discrediting institutions that have scientific professionals and mechanisms that have been set up to try to have the best science possible.

During COVID, we saw Russian bots and Chinese bots that were providing disinformation, and of course, this spread like wildfire. But also for the first time that I know of, we had the U.S. government, the Defense Department, putting out misinformation to try to discredit the Chinese vaccine. So this is a kind of warfare that's going on that has some terrible effects. … This is a completely different level of anti-vaccine engagement than we've ever seen before.

NL: You often hear the argument that, because vaccines have worked so well, people lack a fear of vaccine-preventable diseases. Do you see any validity to that?

SB: When you look at this new era of misinformation — as I said, there's always been vaccine misinformation. But the difference is, if you are in a country that has very high vaccination rates and therefore the diseases have virtually disappeared, it's very easy for a parent to say, "I don't want my kid to be injected with something. … I don't know anything about these diseases. I've never seen them. How bad can they be?" So that's one side of it.

When you're living in a developing country and these diseases are still there, you see kids that have morbidity from these diseases. You see people paralyzed from polio. You see people who are blind or deaf from German measles [also called rubella]. And so your benefit-harm ratio is seen as different in these different populations. And it's the job of science to ask the question, what is the benefit-to-cost ratio of these products?

The other thing that's really hard is, because we don't see these diseases, you don't know the kind of really severe side effects that occur. In measles, there's a disease called subacute sclerosing panencephalitis. It's a fairly rare disease — but when it happens, the child's brain dissolves, and there is nothing you can do.

The challenge is that you don't want people to live in fear all the time, but no parent wants that to happen to their child. It's about how you can both educate and have people aware of the side effects of these diseases, and even ones that are rare. That's really the challenge right now. I think the only way to solve that is education.

NL: Another focus of the book is a roadmap to global vaccine equity. What do you see as the biggest obstacles to that goal?

SB: First of all, the stuff we've just discussed, which is having awareness of the value of vaccination, and that's critical for populations everywhere in the world. And obviously keeping that knowledge up even when the diseases get rarer and rarer is really important.

The second critical point is having access to vaccines. What Gavi was able to do was, by consolidating the buying power of many different countries, we were able to drive the price [of routine vaccines] down 98% from that of what it cost in the United States, which makes it really affordable. Vaccines are cost-effective even at higher prices, but obviously the more affordable they are, the better it is. So a priority is making sure that those products are available and that they are being produced in the quantities they need.

The third part of it is having delivery systems in place, and this is really a challenge. As I mentioned at the beginning, vaccines are the most widely distributed health intervention, and about 90% of families in the world have access to routine vaccines. … Reaching [the last 10%] with that system not only provides vaccines but also provides health access, and it also means there is an early warning system to make sure that there are health workers for everybody — so that if there are outbreaks or weird diseases that appear, you have a system that can report back.

Lastly, I'd say that there's importance in having global surveillance for new infections. It's evolutionarily certain we're going to have new outbreaks and new pandemics, and that warning system is critical for everybody in the world. Building this prevention system, which is very cost-effective, is the right thing to do everywhere, and it's a matter of making that a priority.

NL: I want to come back to the point that epidemics and pandemics are essentially inevitable. With that in mind, how do we prepare?

SB: Epidemics are evolutionarily certain — certainly, that's true. So the first part of that is, how do we prepare for things that we know, like flu, like COVID, like hemorrhagic fevers? These are things that we now have interventions for. And how do we make sure that the world is ready, that there are systems of laboratories, that there are stockpiles of vaccines ready to go, and [that there's] the ability to scale them up?

Unfortunately, a lot of that is now being broken apart. At this moment in time, we [the United States] are firing people in major health agencies. We're pulling out of the World Health Organization. We're changing our development assistance and stopping training of scientists, etc. etc. So we are breaking down the systems that exist to deal with that [preparation for known threats], which is a real problem.

Then, when you get to the "unknown unknowns," you also want to have the science ready to go. There's a good example right now, of pulling out of mRNA vaccines. [The HHS recently pulled funding from research-and-development projects focused on mRNA vaccines.] mRNA vaccines may not be perfect; they may not even be the best vaccines for some diseases. But they are the fastest, because you can make them very quickly from the genome. Then you can, in essence, "print" the vaccine and scale it up very quickly.

In the case of a very severe pandemic that has a very high mortality rate, that is the best way: to make an mRNA vaccine to deal with it. The idea that we would not want to continue to work on mRNA — improving it, making it better — and instead we're just pulling research out seems to me to be very, very shortsighted indeed.

NL: To continue on mRNA, would you say that in a pandemic scenario, it's speed that's the most crucial element of the vaccine? Or are there other advantages to the mRNA platform?

SB: The absolute advantage there is speed. And remember, COVID had a mortality rate of about 1.5%, 2%. Some of the other diseases that we know of, that potentially could spread, have mortality rates of 20%, 30%, 40%, 50%. If you had something like that — that's a respiratory pathogen spreading quickly with very high mortality rates — every hour counts in terms of speed.

So mRNA is the fastest. … It may be that, once you have mRNA vaccines, you may want to shift to other vaccines that may give longer duration of protection, give better immune responses, etc. [for a given pathogen]. But you can't make those in the same time frame, so it may be a handoff from one to another.

One of the challenges in COVID was that there were over 200 different vaccines that were made, but mRNA was so fast out of the block that others really didn't get a chance to become successful. If I use an example, the Novavax vaccine, which is a protein[-based vaccine], never really got global traction, even though it was a very effective, very safe vaccine that maybe had a longer duration of protection.

The challenge is, how do we, in that setting, have comparative science to say which are the best products? That will not be done by the pharmaceutical sector because they don't have any incentive to do head-to-head comparisons. That needs to be done by international agencies or by governments.

NL: What else can readers expect from "Fair Doses"?

SB: The book is also filled with lots of interesting nuggets of stories of who behaved well and who didn't behave well during the pandemic, and that includes political leaders, that includes pharmaceutical companies, that includes agencies. So it gives a nuanced understanding of what that time really looked like.

We came together, along with our partners, to try to see if we could change the normal dynamic that occurs in a pandemic, which is wealthy countries buy all the doses and there's no doses available for anybody else. That was our goal going into it, and the book tells the story of how we put together this initiative, how we raised the $12.5 billion necessary to buy vaccines, how we ultimately delivered more than 2 billion doses to 146 countries.

One of the questions is, how do we do better? What do we learn from that? And that's something we try to explore in the book.

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

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

When the first cells appeared on Earth approximately 3.8 billion years ago, viruses were already here to greet them. Ever since, viruses have been devising ways to infect cells, and cells have been responding by evolving ways to stop these infections. This evolutionary dance eventually led to the development of your immune system.

A key aspect of your immune system is to distinguish "self" from "nonself" so it can destroy and remove foreign materials from your body. While this immune reaction protects you from viruses, it also has implications for how well foreign materials such as medications work.

I am a researcher studying ways to make drugs work better, including how to get them to the site of disease within the body before being removed or destroyed. One way to do this is to encapsulate drugs in nanoparticles — materials small enough to be taken up by cells. While these materials still trigger an immune response to get them out of the body, scientists like me have found that this reaction could actually be used to improve the effectiveness of cancer treatment.

The immune system and drug delivery

In addition to detecting pathogens, your immune system also responds to tissue damage. You might observe this reaction as inflammation — such as redness and swelling — when drugs are injected into your body with a needle.

Typically this inflammatory response is minimal. But the potential for a sustained reaction increases when drugs are administered slowly over a prolonged period of time, such as during chemotherapy infusions that can take an hour or more. For this reason, some patients are given anti-inflammatory medications before infusion to reduce the potential for an adverse immune response during treatment.

The most recent breakthroughs in getting drugs into the body is using nanoparticles. These materials — which can be made from lipids, proteins, gold or other components — have the advantage of being very small: The diameter of a typical nanoparticle is about 10-thousandths of a millimeter. Their small size allows diseased cells to easily take them up. So when nanoparticles contain drugs, they can act as a drug delivery system.

Despite being so small, nanoparticles can hold a large number of drug molecules, allowing them to deliver a potent cargo of treatment directly into a cell. They can also deliver drugs made of DNA and RNA. The most well-known example of this technology is the COVID-19 vaccine, which uses nanoparticles made of modified fat molecules to deliver mRNA that teaches the immune system to protect itself against COVID-19 infection.

Your innate immune system also identifies nanoparticles as foreign invaders when they are injected into your body. As a result, some patients experience an initial inflammatory reaction when the body tries to attack the nanoparticle.

But what if this reaction could actually be used to improve treatment?

Exploiting the innate immune response

For the past 30 years, my laboratory at the University of Colorado has been studying how nanoparticles deliver drugs. More recently, we have focused on understanding how the innate immune system responds to an injection of nanoparticles. While this immune reaction is typically considered a drawback, we wanted to explore whether it could enhance therapy.

In a 2022 study on how nanoparticles affect the immune response in mice, we found that the innate immune response triggered by an initial dose of nanoparticles carrying a drug will also reduce the effects of a second dose if it is injected shortly afterward — typically within days. It does this by clearing the drug out from the body more quickly. This reaction is similar to how an initial viral infection would trigger a short-term protective response against a subsequent infection from another virus.

One critical aspect of this protective effect involves the production of a protein called interferon lambda. This molecule "interferes" with the infection process by restricting viruses from gaining access to different tissues in the body. Researchers have previously tested this protein as a potential antiviral drug to treat COVID-19.

Similarly, the interferon lambda made in response to the first dose of nanoparticles limits the ability of the second dose to deliver the drug to healthy tissues in the body. However, it did not affect the nanoparticle's ability to access tumors, possibly because tumors can impair the immune response.

In conventional cancer treatment, chemotherapy drugs are used to kill the tumor. Because these drugs are also toxic to healthy cells, patients often experience side effects such as hair loss, gastrointestinal problems and skin rashes. Using nanoparticles to deliver cancer treatment could help reduce these side effects, and combining them with interferon lambda could allow the nanoparticle-encapsulated drug to stay in the body long enough to have its full effects.

Our team is studying whether directly injecting interferon lambda before chemotherapy with nanoparticles could help limit the amount of drug that ends up in healthy tissues while increasing their concentration in tumors. In an initial test of this strategy in mice with colon cancer, all mice that received interferon lambda saw increased survival time and reduced weight loss. A better understanding of how this effect happens could help researchers eventually test this approach to cancer treatment in human patients.

Scientists have a long way to go in developing nanoparticles that are as efficient as viruses at getting into cells. But our hope is that exploiting an immune response that evolved approximately a billion years ago to prevent viral infections could help reduce the toxic side effects from treatment while improving its effectiveness.

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

Mamba snakebite symptoms sometimes worsen in patients after antivenom is administered — and scientists may finally know why.

The complex interplay of toxins and antivenom in the body unmasks hidden neurological symptoms from specific toxins in the venom. These masked symptoms appear once the effects of other, equally dangerous toxins are neutralized.

These findings, published in Sept. 26 in the journal Toxins, could help improve treatments for these deadly snakebites.

There are four species of mamba snakes, which belong to the genus Dendroaspis. Mamba bites are critical medical emergencies in sub-Saharan Africa, especially those of the black mamba, which is considered one of the world's deadliest snakes because its bite is 100% fatal unless treated immediately.

Without quick intervention, the neurotoxins in mamba venom can cause death from respiratory paralysis and cardiac arrest within an hour, contributing to the 30,000-plus snakebite deaths in the region annually.

Mamba toxins attack the nervous system, mostly by "hacking" nerve receptors on muscles, study co-author Brian Fry, a molecular biologist at the University of Queensland, told Live Science. This blocks nerve signals from the brain from reaching the muscles.

"You wouldn't even know that's happening unless you try to do something, like walk or breathe," Fry said. This effect — characterized by the inability of muscles to contract — is known as limp or flaccid paralysis, and existing antivenoms work well against the symptom. This form of paralysis is triggered by the venoms of three of the four mamba species: the western green, Jameson's mamba, and black mamba.

But there is a second way that mamba venoms act, which has the opposite effect: it overloads the muscle with nerve signals, thus causing uncontrollable spasms. This is called rigid or spastic paralysis. "Instead of not being able to breathe because their diaphragm is completely limp, [now the patient] can't breathe because their diaphragm is completely contracted," Fry said.

Historically, scientists believed that the neurotoxins behind rigid paralysis were present only in the fourth species, the eastern green mamba venom. Venoms of the other three mambas were thought to cause only limp paralysis. "What wasn't known is that [rigid paralysis] has always been happening in the background with the other species as well," Fry said.

Fry and colleagues tested how venoms of the four mamba species attack the nervous system, as well as how well three antivenoms commercially available in Africa subdue these effects. They ran these tests using neuromuscular tissue from lab animals, which enabled them to chemically or electrically stimulate a piece of muscle. Introducing eastern green mamba venom caused spasms in the tissue, while venoms of the other mambas triggered no visible response — that is, until they attempted to stimulate the muscle and got no response because the venoms were preventing the muscles from contracting.

The three antivenoms successfully treated the limp-paralysis effects across all the mamba species, enabling the muscles to contract again. However, at that point, rigid paralysis set in in some cases, and the antivenoms showed poor effectiveness against that. In people bitten by mambas, "spastic paralysis can be fatal but the flaccid paralysis is more dangerous as its typically a more potent effect," Fry noted.

The researchers also noted that the venom of the black mamba — able to kill with just two drops of venom — varied between snakes hailing from Kenya and South Africa. The venoms varied both in how they affected the tissue and how they responded to antivenoms.

"Knowledge on geographical venom variation is needed in order to design antivenoms that contain antibodies against all medically relevant toxins from species, no matter where the species comes from," Andreas Hougaard Laustsen-Kiel, a biotechnologist at the Technical University of Denmark who wasn't involved with the study, told Live Science in an email. "The significance of the study is that it shows that antivenoms must be optimized to neutralize both toxin types to be effective."

Fry next wants to take a more comprehensive and wide-ranging look at the black mamba.

"We'd like to map more precisely which antivenom performs better in a particular region," he said, "which gives the doctors the kind of data that's crucial for evidence-based design of clinical management strategies."

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

Editor's note: On Oct. 6, 2025, the CDC adopted the new recommendations set forth by ACIP, which are described below.

Staff changes at the U.S. Centers for Disease Control and Prevention (CDC) ushered in changes in which populations were advised to get this year's updated COVID-19 vaccine. People under age 65 faced confusion and uncertainty over whether they and their children were eligible for the 2025-2026 shot, where they could get it and whether their health insurance would cover the cost.

On Friday (Sept. 19), an influential CDC committee — the Advisory Committee on Immunization Practices (ACIP) — said that everyone over 6 months old can get this year's COVID-19 vaccine and have the cost covered by insurance, provided they or their caregiver talk with their pharmacist or another health care provider about the shot's risks and benefits.

This was an unexpected result after an at times contentious and confusing two-day meeting, during which the ACIP members weighed heavily restricting American's access to COVID-19 vaccines. They debated whether to require everyone to get a prescription prior to seeking the shot, for instance.

Here's what to know about the ACIP's recommendation and what it might mean for people seeking the vaccine this year.

Related: Have you gotten this year's COVID vaccine? (Poll)

• Asthma
• Blood cancers
• Blood disorders (including sickle cell disease)
• Cerebrovascular diseases
• Chronic kidney disease
• Some chronic lung diseases
• Some chronic liver diseases
• Cystic fibrosis
• Type 1 and 2 diabetes
• Gestational diabetes
• Disabilities, including Down syndrome, ADHD, autism, cerebral palsy
• Heart conditions
• HIV or tuberculous infection
• Mood disorders, including depression and schizophrenia
• Dementia or a neurologic condition
• Parkinson's disease
• Obesity
• Physical inactivity
• Chronic liver disease
• Kidney disease
• Current or recent pregnancy
• Primary immunodeficiencies
• Tuberculosis
• Current or former smoking
• Substance use disorder
• Solid organ or blood stem cell transplant recipients
• Use of immunosuppressive drugs

As of Sept. 16, Blue Cross Blue Shield said its current vaccine coverage aligns with the most recent recommendations from multiple medical groups and includes COVID-19 vaccines, a spokesperson told Live Science in an email. The company bases its coverage decision on the recommendations made by professional associations such as the AAFP and AAP, as well as the CDC's ACIP.

Aetna CVS Health provides coverage for approved vaccines, including COVID-19 shots, in compliance with applicable state and federal cost-sharing requirements, a spokesperson told Live Science in an email. Its members who are eligible may be vaccinated against COVID-19 at no out-of-pocket cost to them.

In addition, state pharmacy laws govern where CVS Pharmacy can vaccinate, a spokesman said via email. Based on Food and Drug Administration (FDA) approval and recent regulatory action by certain states, CVS Pharmacy currently can offer COVID-19 vaccines in 43 states without a prescription from an outside provider, not including the following: AZ, DC, FL, GA, LA, OR, UT and WV. If the ACIP recommendations are approved, a prescription will no longer be required for the vaccine in those last seven states.

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

Editor's note: On Oct. 6, 2025, the CDC adopted the new recommendations set forth by ACIP, which are described below.

An influential Centers for Disease Control and Prevention (CDC) committee has announced new recommendations for the combined measles, mumps, rubella and varicella (MMRV) vaccine.

The members of the committee, called the Advisory Committee on Immunization Practices (ACIP), was recently changed under the leadership of Department of Health and Human Services Secretary (HHS) Robert F. Kennedy Jr. All 17 previous members were removed and then replaced with a new group, which includes several prominent anti-vaccine advocates.

The ACIP is meeting Thursday and Friday (Sept. 18 and 19) to discuss the COVID-19 vaccines; the hepatitis B vaccine; and the combined measles, mumps, rubella, varicella (MMRV) vaccine. They will also discuss recommendations regarding respiratory syncytial virus (RSV), which has a vaccine available to adults and an antibody treatment available to kids.

As of Thursday at 5:30 p.m. ET, the committee had so far voted on only the MMRV vaccine, CBS reported. In a vote of 8 to 3, with one abstention, the members voted to say that the combined MMRV vaccine is not recommended before age 4. Instead, they are recommending that this age group be given the MMR shot — which guards against measles, mumps and rubella — and the varicella shot, which protects against chickenpox, as two separate injections.

This latter option — sometimes known by the shorthand MMR+V — was already the option recommended for kids under 4. It's just that the ACIP is moving to take the MMRV option off the table for many children.

Previously, the CDC's recommendations stated that, at 12 to 15 months old, children can either get one MMRV shot or one MMR shot along with the chickenpox vaccine. The MMRV shot comes with a slightly higher risk of febrile seizures in 12- to 15-month-olds, compared with getting the MMR and varicella vaccines separately, so the latter option is preferred and recommended for that age group.

Related: RFK's handpicked advisers are coming for the childhood vaccine schedule. Here's what to know.

However, the previous guidelines allowed caregivers to choose to give their kids the MMRV shot. They might opt for that if they wanted to reduce the number of total shots given at their child's appointment, for instance. Doctors helped caregivers weigh the risks and benefits of the two options. Although scary for kids and their caregivers, febrile seizures are fairly rare, typically harmless and quick to resolve, and the MMRV raises the risk of the events by a small degree.

Following their first dose of either the MMRV or the MMR+V, kids get a second dose at age 4 to 6. At that age, both options come equally recommended, so it comes down to preference and availability.

At Thursday's ACIP meeting, some experts argued that recommending only the MMR+V option for kids 12 to 15 months old takes away a choice from caregivers, and could also have implications for how government insurers cover the shots, CBS reported. Others noted that the increased seizure risk is small, has been known about for nearly 20 years, and is discussed with caregivers as a standard of care. Presenters at the meeting also noted that, currently, 85% of caregivers opt for separate shots for their kids, while 15% choose the combo MMRV option, independent health journalist Liz Szabo reported.

The ACIP's recommendations are important in part because they determine which shots are included under the Vaccines for Children (VFC) program, for which about half of children in the U.S. are eligible. Kids covered by the program include those who are uninsured and underinsured; on or eligible for Medicaid; or are American Indian or Alaska Native.

There was some apparent confusion among the ACIP members about the VFC program, Medscape reported.

On Thursday, the ACIP committee voted on whether the MMRV should no longer be covered for under-4s in the program, to bring its coverage in line with their new recommendation. The members rejected making any change, with some abstaining because they said they weren't sure what they were voting for. But on Friday, the vote was reopened and the members voted to change the VCP coverage so MMRV is no longer covered for that age group, CNN reported.

The committee's recommendations must be reviewed and approved by the CDC director to become official guidance, but the director most often approves the recommendations.

Meanwhile, America's Health Insurance Plans (AHIP), a trade group of private insurers, announced in a statement on Sept. 16 that insurers would continue to cover vaccines that were recommended as of Sept. 1, 2025, until at least the end of 2026.

The ACIP also discussed the hepatitis B vaccine Thursday but has moved to delay their vote about the shot. The committee plans to both discuss and vote on the COVID-19 vaccine recommendations Friday.

Following leadership changes at HHS and CDC, the American Academy of Pediatrics issued its own recommended child and teen immunization schedule and said it would not endorse the recommendations of the CDC.

Editor's note: This story was updated on Sept. 19, 2025, at 10:50 a.m. ET to note that the ACIP twice voted on their VFC recommendations, flip-flopping their decision in doing so.

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

An influential Centers for Disease Control and Prevention (CDC) vaccine advisory committee that has been reconstituted by Health and Human Services Secretary (HHS) Robert F. Kennedy, Jr. will meet Thursday and Friday (Sept. 18 and 19) to discuss changes to the childhood vaccine schedule.

These changes, experts say, could make American children less healthy.

The Advisory Committee on Immunization Practices (ACIP) meeting starting Thursday will focus on the hepatitis B vaccine, as well as the MMRV vaccine — a version of the measles, mumps and rubella (MMR) vaccine that also protects against varicella, or chickenpox. The first dose of the hepatitis B vaccine is currently recommended at birth, while the first dose of the MMRV vaccine is recommended at age 12 to 15 months.

The discussions being raised by the ACIP are alarming outside experts, who say there is no new data suggesting these recommendations are problematic — and that the current schedule is well studied and highly effective at preventing these dangerous infections.

"It's brilliantly successful," Dr. William Schaffner, a professor of preventive medicine at the Vanderbilt University School of Medicine, said of the recommendation to vaccinate everyone against hepatitis B at birth. Schaffner an ACIP member in the 1980s and was a liaison to the committee for various organizations between 1986 and 2024. "If we change it, we will start to see transmissions again," he said.

Hepatitis B protection for infants

Kennedy is the founder of Children's Health Defense, a nonprofit known for campaigning against childhood vaccines, and he stepped down as chairman of the group prior to assuming his role at HHS. In June, he fired the 17 sitting members of the ACIP and has since replaced them with new members, some of whom rose to prominence by promoting unproven treatments for COVID-19 and criticizing universal vaccination against the disease.

The two routine childhood shots that the committee will vote on this week are not new. The MMR vaccine was first licensed in 1971, and the MMRV vaccine, which adds chickenpox protection to the same shot, was approved in 2005. The hepatitis B vaccine has been recommended to newborns for over 30 years, starting in 1991.

Vaccination immediately after birth protects infants from contracting the virus from their mothers upon delivery. That's because the virus spreads through bodily fluids — including blood, saliva, menstrual, vaginal and seminal fluids — and can pass to babies in the birth canal.

Hepatitis B is a viral infection that can become chronic, especially for people who are infected as infants. It can easily go undetected, causing liver damage and raising the risk of liver cancer. Once chronic, it's a permanent infection that requires antivirals and shots to manage, and it can lead people to need liver transplants. Mothers are screened for the infection, but their cases sometimes go undetected and this puts babies at risk, Higgins said.

On Tuesday (Sept. 16), former CDC officials told KFF Health News that the ACIP is likely to recommend pushing out the vaccine to age 4.

"What you're going to hear tomorrow is an argument that we can identify these mothers who are positive and vaccinate their babies early and wait til the others get a little bit older before we vaccinate them," Schaffner said. "We tried that. It did not work."

"Those kids that fall through the gaps," he said, "they're now at risk for infection and subsequent liver damage, cancer and death."

Anti-vaccine advocates argue that the shot is not necessary for newborns because hepatitis B infections in adults often spread via intravenous drug use or sexual activity. But before newborn vaccination was introduced, there were about 18,000 cases of hepatitis B in children under 10 in the United States each year, Higgins said. In about half of those cases, the source of the infection was unknown. Kids can pick up the virus via contact with even tiny amounts of blood, such as from a scraped knee, a shared toothbrush exposed to bloody gums, or a toddler biting incident at daycare.

By comparison, in 1990, there were three new cases of hepatitis B for every 100,000 children and adolescents in the U.S., according to CDC data. By 2002, that number had dropped to 0.3 out of every 100,000. Today, it sits below 0.1 per 100,000.

The benefits carry on to adulthood: Because the vaccine induces long-lasting protection, rates of hepatitis B in people ages 30 to 39 years — the first to be vaccinated as infants — show a steep decline after 2015.

"The downside of this is minimal to none," Dr. Michelle Barron, senior medical director of infection prevention and control for the UCHealth hospital system in Colorado, told Live Science. "The vaccines are safe."

The MMRV vaccine

Per the current vaccination schedule, children get their first dose of either the MMRV, or the MMR along with the chickenpox vaccine, between the ages of 12 and 15 months. A second dose comes between 4 and 6 years old and typically provides lifelong immunity to the infection.

Within three years of the introduction of the MMRV shot, researchers noted an increased risk of febrile seizures, or seizures brought on by fever, in kids who got the MMRV vaccine rather than the MMR and chickenpox shots separately. According to the CDC, the risk of seizures is twice as high from MMRV than for the MMR in kids between the ages of 1 and 2, which translates to one additional febrile seizure per every 2,300 to 2,600 MMRV doses administered in this age group.

Related: Measles has long-term health consequences for kids. Vaccines can prevent all of them.

"We — and by 'we,' I mean pediatricians and vaccine experts and the ACIP — were appropriately concerned about this, and there was incredibly thoughtful deliberation about how recommendations should change," said Dr. David Higgins, an assistant professor of pediatrics at the University of Colorado Anschutz Medical Campus. The committee determined that it's preferred that children under 4 get the MMR and chickenpox vaccine as separate shots.

However, because the risk of febrile seizures tied to the vaccine is small, the committee left open the option for parents who wanted one less needle for their kids to opt for the MMRV after being informed of the risks and benefits.

In general, between 2% to 5% of children under 5 sometimes experience seizures in response to a fever (caused either by an infection or a vaccination), and about one-third of kids who have one febrile seizure will go on to experience more. While kids with a history of febrile seizures have a slightly higher chance of developing epilepsy later in life, in almost all cases, the fever-induced seizures cause no damage and go away as the child ages.

If the ACIP restricts patients' option to get the MMRV vaccine, clinics that use the shot will likely see supply problems, Higgins told Live Science.

Both the MMRV and MMR vaccines prevent measles, which can cause deadly pneumonia, brain swelling, immune memory loss, and sometimes a progressive and fatal neurological disorder called subacute sclerosing panencephalitis (SSPE). They also prevent mumps, a viral infection that can cause deafness and male infertility; and rubella, a viral infection that causes a fever and rash and that, in pregnant women, can result in abnormal heart and brain development for the fetus.

The chickenpox vaccine not only prevents the painfully itchy viral infection, but also reduces the risk of kids getting shingles, a blistering rash caused by the same virus that causes chickenpox reactivating in the nervous system long after the initial infection passes.

Creating a controversy

A 2017 policy statement from the American Academy of Pediatrics summarizes the safety data on the hepatitis B vaccine in Vaccine Safety Datalink, a huge vaccine-safety monitoring project started in 1990. Per those data, there is "no evidence of a causal association between receipt of hepatitis B vaccine and neonatal sepsis or death, rheumatoid arthritis, Bell’s palsy, autoimmune thyroid disease, hemolytic anemia in children, anaphylaxis, optic neuritis, Guillain-Barré syndrome, sudden-onset sensorineural hearing loss, or other chronic illnesses."

There's no sign of any new data that would change this conclusion. But bringing it up at the ACIP meeting will likely feed a lack of trust in vaccination, overall, Barron said.

"All of this is external noise to cause skepticism and to cause alarm around vaccines in general," Barron said. "This multifaceted attack against vaccines that have existed for 30 to 40 years, have been used safely and effectively during that time, without new studies, without new data — I really feel it's just another tactic to scare people."

The meeting may also be an opportunity to spread fears about the timing of the childhood vaccine schedule in general — a frequent point of attack by anti-vaccine advocates. While activists claim the safety of the schedule has not been studied, that's untrue.

"At each stage, it has been studied to see whether the new vaccine added to the schedule will cause noteworthy adverse effects," Schaffner said. "That's before the recommendation is made."

After the addition of a new vaccine to the schedule is made, there are multiple safety reporting systems in place to monitor for any side effects not caught in trials — like the one that caught the increased risk of febrile seizures in young kids with the MMRV vaccine. These systems enable long-term studies that look for any serious outcomes over time across the population, Higgins said. And "we have not seen any credible connections there."

America's Health Insurance Plans (AHIP), a trade group of private insurers, announced in a statement on Sept. 16 that insurers would continue to cover vaccines that were recommended as of Sept. 1, 2025, until at least the end of 2026. But half of U.S. kids get their vaccines through the federal Vaccines for Children program, and ACIP recommendations directly determine which vaccines are included in that program.

The program specifically serves uninsured and underinsured children; kids who are on or eligible for Medicaid; and American Indian or Alaska Native children who qualify under the Indian Health Care Improvement Act.

"While I love seeing the health insurers come out and say, 'We think vaccines are important; we are going to cover them,'" Higgins said, "I am really worried about the half of children in the U.S. who get vaccines through the Vaccines for Children Program."

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

Three scientists have won a $250,000 award for their contributions to developing a life-saving therapy for the genetic disease cystic fibrosis (CF).

The prize, called the Lasker-DeBakey Clinical Medical Research Award, went to Dr. Michael Welsh of the University of Iowa, Paul Negulescu of Vertex Therapeutics and Jesús (Tito) González of Integro Theranostics. It's one of this year's Lasker Awards — biomedical-research prizes established in 1945 that are often called the "American Nobels."

"It's super gratifying," said González, who was formerly the senior director of biology at Vertex Therapeutics. "It's very rare to actually have something [in medical research] that goes all the way to patients and is made widely available, and to have such a dramatic effect," he told Live Science.

The treatment, called Trikafta, extends the lifespans of people with CF by decades — and patients who start treatment in childhood or adolescence are expected to live near-average lifespans. By comparison, when the disease was first discovered in the 1930s, most patients died in early childhood. And even in the 2010s, before Trikafta's approval in 2019, about half of CF patients died before age 40.

"Today, the estimated median age of survival for persons with cystic fibrosis who were born between 2020 and 2024 and have access to treatment is 65 years," Dr. Eric Sorscher of Emory University wrote in an essay about the award, published in The New England Journal of Medicine. "Available projections suggest that health and longevity may increase further as modulators begin to be administered at younger ages."

The Lasker Award "also brings back a lot of great memories and it really warms your heart when you think of all the people you've worked with, and all the time and effort," González added. "I just hope people understand how difficult it is to go this far."

Related: Scientist who discovered body's 'fire alarm' against invading bacteria wins $250,000 Lasker prize

CF is an inherited disorder caused by mutations in a gene called CFTR. When functional, the gene enables cells to make tubes inside their membranes that charged particles called ions can flow through. That, in turn, lets water flow as it should through tissues and helps organs, like the lungs, intestines and pancreas, do their jobs properly.

But in CF, the CFTR gene malfunctions, causing thick, sticky mucus to clog the linings of these organs. The mucus gums up airways, raising the risk of dangerous infections and scarring in the lungs, and it can cause issues with digestion, the absorption of nutrients and insulin signaling.

Lab research conducted by Welsh in the 1980s and 1990s helped lay the groundwork for Trikafta, a drug that addresses the molecular cause of most types of CF. Working with cells from the airways of people with the disease, Welsh and colleagues unraveled the "physiological consequences" of the most common genetic error seen in people with CF, González explained.

Their work demonstrated that this defect in the CFTR gene — known as delta-f508 — makes it so that charged particles can't pass through the tubes in the cell membrane as easily. The mutation means that the tubes never actually reach the surface of the cell, so the ions get stuck. In various experiments that involved cooling down the cells as they grew in lab dishes, Welsh showed that the tube could be made to reach the cell surface and thus better transport ions.

Meanwhile, as a postdoctoral scholar in the lab of Nobel-winner Roger Tsien, González co-invented a system that could accurately track the flow of ions across cell membranes in real time. The initial inspiration behind the system was to study how the brain worked, as ions moving across membranes enable brain cells to fire, he said. But the system was also perfect for testing potential new CF drugs designed to fix the ion-transport issues.

"This allowed us to screen tens of thousands of compounds a day," González said. "While electrophysiology, the standard method at the time for studying ion channels in depth, was very slow, just a handful a day."

The researchers refined the process to hunt for CF drugs at biotech company Aurora Biosciences, which was later acquired by Vertex Pharmaceuticals.

Negulescu, also at Aurora and later Vertex, led the project of screening molecules to see how they affected ion transport. His team looked for "potentiators," which boost the flow of ions, and "correctors," which help move the tubes into the right position in the cell membrane. This effort led to the approval of several iterations of CF drugs — in 2012, 2015 and 2018 — before finally leading to Trikafta's approval in 2019.

When they started getting data back from the earliest human trials of their first-generation drug, González recalled "that was super exciting because that it became very real. It's like, 'Oh wow, this is not just theory; this is actually working in patients.'"

Trikafta combines three drugs to effectively treat most people with CF. Its use has reduced the number of lung transplants and hospitalizations for infection among people with the disease, and improved patients' quality of life, according to a statement from the Lasker Awards.

"Welsh, González, and Negulescu’s achievements are affording people with CF the chance to thrive now and to plan vibrant futures," the statement says.

Two additional Lasker Awards were awarded this year, including one for basic research and another for special achievements in medical science.

The former prize went to Dirk Görlich of the Max Planck Institute for Multidisciplinary Sciences in Germany and Steven McKnight of the University of Texas Southwestern Medical Center. These two researchers uncovered unsung roles for low-complexity domains — complex regions of protein sequences — which are key to how cells organize their innards, and also explored how that organization goes awry in disease.

The latter prize went to Lucy Shapiro of Stanford University to recognize her 55-year career in biomedical sciences, during which she has reshaped biologists' understanding of how bacterial cells divide and develop. In particular, her work highlighted the importance of spatial organization within bacterial cells, and how this relates to the way they work internally. She's also being recognized as the founding director of Stanford's Department of Developmental Biology, which was established in 1989, as well as a key consultant to global leaders on issues such as antibiotic resistance, emerging infectious diseases and biological warfare.

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

For almost 40 years, people who suspect they've been harmed by a vaccine have been able to turn to a little-known system called the Vaccine Injury Compensation Program — often simply called the vaccine court.

Health and Human Services Secretary Robert F. Kennedy Jr. has long been a critic of the vaccine court, calling it "biased" against compensating people, slow and unfair. He has said that he wants to "revolutionize" or "fix" this system.

I'm a scholar of law, health and medicine. I investigated the history, politics and debates about the Vaccine Injury Compensation Program in my book "Vaccine Court: The Law and Politics of Injury."

Although vaccines are extensively tested and monitored, and are both overwhelmingly safe for the vast majority of people and extremely cost-effective, some people will experience a harmful reaction to a vaccine. The vaccine court establishes a way to figure out who those people are and to provide justice to them.

Having studied the vaccine court for 15 years, I agree that it could use some fixing. But changing it dramatically will be difficult and potentially damaging to public health.

Deciphering vaccine injuries

The Vaccine Injury Compensation Program is essentially a process that enables doctors, lawyers, patients, parents and government officials to determine who deserves compensation for a legitimate vaccine injury.

It was established in 1986 by an act of Congress to solve a specific social problem: possible vaccine injuries to children from the whole-cell pertussis vaccine. That vaccine, which was discontinued in the U.S. in the 1990s, could cause alarming side effects like prolonged crying and convulsions. Parents sued vaccine manufacturers, and some stopped producing vaccines.

Congress was worried that lawsuits would collapse the country's vaccine supply, allowing diseases to make a comeback. The National Childhood Vaccine Injury Act of 1986 created the vaccine court process and shielded vaccine manufacturers from these lawsuits.

Here's how it works: A person who feels they have experienced a vaccine-related injury files a claim to be heard by a legal official called a special master in the U.S. Court of Federal Claims. The Health and Human Services secretary is named as the defendant and is represented by Department of Justice attorneys.

Doctors who work for HHS evaluate the medical records and make a recommendation about whether they think the vaccine caused the person's medical problem. Some agreed-upon vaccine injuries are listed for automatic compensation, while other outcomes that are scientifically contested go through a hearing to determine if the vaccine caused the problem.

Awards come from a trust fund, built up through a 75-cent excise tax on each dose of covered vaccine sold. Petitioners' attorneys who specialize in vaccine injury claims are paid by the trust fund, whether they win or lose.

Some updates are needed

Much has changed in the decades since Congress wrote the law, but Congress has not enacted updates to keep up.

For instance, the law supplies only eight special masters to hear all the cases, but the caseload has risen dramatically as more vaccines have been covered by the law. It set a damages cap of US$250,000 in 1986 but did not account for inflation. The statute of limitations for an injury is three years, but in my research, I found many people file too late and miss their chance.

When the law was written, it only covered vaccines recommended for children. In 2023, the program expanded to include vaccines for pregnant women. Vaccines just for adults, like shingles, are not covered. COVID-19 vaccine claims go to another system for emergency countermeasures vaccines that has been widely criticized. These vaccines could be added to the program, as lawyers who bring claims there have advocated.

These reform ideas are "friendly amendments" with bipartisan support. Kennedy has mentioned some of them, too.

A complex system is hard to revolutionize

Kennedy hasn't publicly stated enough details about his plan for the vaccine court to reveal the changes he intends to make. The first and least disruptive course of action would be to ask Congress to pass the bipartisan reforms noted above.

But some of his comments suggest he may seek to dismantle it, not fix it. None of his options are straightforward, however, and consequences are hard to predict.

Straight up changing the vaccine court's structure would probably be the most difficult path. It requires Congress to amend the 1986 law that set it up and President Donald Trump to sign the legislation. Passing the bill to dismantle it requires the same process. Either direction involves all the difficulties of getting a contentious bill through Congress. Even the "friendly amendments" are hard — a 2021 bill to fix the vaccine court was introduced but failed to advance.

However, there are several less direct possibilities.

Adding autism to the injuries list

Kennedy has long supported discredited claims about harms from vaccines, but the vaccine court has been a bulwark against claims that lack mainstream scientific support. For example, the vaccine court held a yearslong court process from 2002 to 2010 and found that autism was not a vaccine injury. The autism trials drew on 50 expert reports, 939 medical articles and 28 experts testifying on the record. The special masters deciding the cases found that none of the causation hypotheses put forward to connect autism and vaccines were reliable as medical or scientific theories.

Much of Kennedy's ire is directed at the special masters, who he claims "prioritize the solvency" of the system "over their duty to compensate victims." But the special masters do not work for him. Rather, they are appointed by a majority of the judges in the Court of Federal Claims for four-year terms — and those judges themselves have 15-year terms. Kennedy cannot legally remove any of them in the middle of their service to install new judges who share his views.

Given that, he may seek to put conditions like autism on the list of presumed vaccine injuries, in effect overturning the special masters' decisions. Revising the list of recognized injuries to add ones without medical evidence is within Kennedy's powers, but it would still be difficult. It requires a long administrative process with feedback from an advisory committee and the public. Such revisions have historically been controversial, and are usually linked to major scientific reviews of their validity.

Public health and medical groups are already mobilized against Kennedy's vaccine policy moves. If he failed to follow legally required procedures while adding new injuries to the list, he could be sued to stop the changes.

Targeting vaccine manufacturers

Kennedy could also lean on his newly reconstituted Advisory Committee on Immunization Practices to withdraw recommendations for certain vaccines, which would also remove them from eligibility in the vaccine compensation court. Lawsuits against manufacturers could then go straight to regular courts. On Aug. 14, 2025, the Department of Health and Human Services may have taken a step in this direction by announcing the revival of a childhood vaccine safety task force in response to a lawsuit by anti-vaccine activists.

Kennedy has also supported legislation that would allow claims currently heard in vaccine court to go to regular courts. These drastic reforms could essentially dismantle the vaccine court.

People claiming vaccine injuries could hope to win damages through personal injury lawsuits in the civil justice system instead of vaccine court, perhaps by convincing a jury or getting a settlement. These types of settlements were what prompted the creation of the vaccine court in the first place. But these lawsuits could be hard to win. There is a higher bar for scientific evidence in regular courts than in vaccine court, and plaintiffs would have to sue large corporations rather than file a government claim.

Raising the idea of reforming the vaccine court has provoked strong reactions across the many groups with a stake in the program. It is a complex system with multiple constituents, and Kennedy's approaches so far pull in different directions. The push to revolutionize it will test the strength of its complex design, but the vaccine court may yet hold up.

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

At a Sept. 4, 2025, hearing before the Senate Finance Committee, Health and Human Services Secretary Robert F. Kennedy Jr. faced heated questions from numerous senators about his vaccine policies, including his stance on COVID-19 vaccines and mRNA vaccine technology generally.

Although Kennedy agreed that Operation Warp Speed, President Donald Trump's signature initiative to produce COVID-19 vaccines in nine months, was a tremendous achievement, he also maintained that COVID-19 vaccines cause widespread and serious harm, including death, particularly in young people — a claim for which there is no evidence.

Some especially pointed questions came from Republican Sen. Bill Cassidy of Louisiana, a physician who provided the final vote needed for Kennedy's confirmation in February 2025 after Kennedy promised him that he would not change the Centers for Disease Control and Prevention's process for recommending vaccines. Cassidy pointed out that with the limitations and confusion caused by the CDC's new rules around COVID-19 vaccines, "I would say effectively we are denying people vaccines." To which Kennedy replied, "Well, you're wrong."

At the hearing, Kennedy stood by his decision to cut US$500 million in HHS funding for 22 research contracts on mRNA vaccine technology. HHS has said it will instead pour these funds into research on a traditional approach to designing vaccines that was first used more than 200 years ago. With such vaccines, called whole-virus vaccines, a person's immune system is presented with the whole virus, often in weakened or inactivated form. This switcheroo has puzzled many scientists.

A few days before the hearing, on Sept. 1, Trump demanded that pharmaceutical companies prove that COVID-19 mRNA vaccines work, saying that the CDC was "being ripped apart over this question." It was his first public acknowledgment of the chaos roiling the CDC amid the firing of its director, Susan Monarez, and subsequent resignations of four high-level agency officials.

Meanwhile, public health experts and HHS staffers are calling for Kennedy to be fired, and several senators at the hearing echoed that call.

As a vaccinologist who has studied and developed vaccines for over 35 years, I see that the science behind mRNA vaccine technology is being widely misstated. This incorrect information is shaping long-term health policy in the U.S. — which makes it urgent to correct the record.

Are mRNA vaccines less safe than whole-virus vaccines?

HHS defended its cancellation of mRNA vaccine research based, in part, on a nonpeer-reviewed compilation of selected publications called the COVID-19 mRNA "vaccine" harms research collection. This document lists about 750 articles claimed to describe harms caused by mRNA vaccines against COVID-19. However, the vast majority of these articles aren't about vaccines but about the harms of getting infected with SARS-CoV-2, the virus that causes COVID-19. And notably absent from it is the huge body of data showing mRNA vaccines actually prevent these harms.

For example, the document being used to justify RFK Jr.'s claims about mRNA vaccines highlights 375 studies reporting that the virus's spike protein alone, which is produced when the virus replicates, can cause excessive inflammation and tissue damage. This is true. But the document marshals this evidence to support the claim that mRNA vaccines, which are designed to produce spike proteins, cause the same harm — which is not accurate.

While viral replication results in uncontrolled production of a large amounts of the protein, the way it's produced by the mRNA vaccine is very different. The vaccine produces a small, controlled amount of spike protein inside a few cells — just enough to induce an immune response without causing damage. And by blocking the virus's replication, it reduces the amount of spike protein in circulation, actually having the opposite effect.

What about side effects like myocarditis?

Early reports flagged a type of heart swelling called myocarditis as a rare side effect of the mRNA vaccine, particularly for young men ages 18 to 25 after a booster dose. A 2024 review identified about 20 cases out of 1 million people who received the vaccine. However, that same study found that unvaccinated people had an elevenfold higher risk of getting myocarditis after a COVID-19 infection than vaccinated people.

What's more, another 2024 study showed that people who developed myocarditis after vaccination had fewer complications than those who developed the condition after getting infected with COVID-19.

Do mRNA vaccines make the SARS-CoV-2 virus resistant?

Another claim from the compilation of supposed mRNA vaccine harms that was cited as a reason for cutting funding for mRNA technology is that mRNA vaccines cause mutations in the SARS-CoV-2 virus that make them resistant or less susceptible to the vaccine.

When a virus replicates in its host, it produces millions of copies of its genetic material. Mutations are copying errors that occur naturally during the replication process. These acquired mutations produce new variants, which is why both the COVID-19 mRNA and the whole-virus flu vaccine get updated annually — to keep up with natural changes in the virus.

Slowing down viral replication decreases the rate at which a virus can acquire new mutations. Since both mRNA and whole-virus vaccines stop or slow the virus from replicating, both types of vaccines help reduce the emergence of resistant viruses.

Viruses can mutate to escape from antibodies, but the mRNA vaccines are not causing the emergence of more virulent strains, likely for at least two reasons. First, mRNA vaccines induce immune responses that can attack the virus at multiple spots, so it would have to come up with many mutations at once to escape the vaccine's defenses. Second, even if the virus could acquire all these mutations, they would likely weaken it, making it unable to cause or even transmit disease.

mRNA vaccines versus new SARS-CoV-2 variants

Kennedy, in announcing cuts to mRNA vaccine research on Aug. 5, 2025, claimed that mRNA vaccines don't work against respiratory viruses and that HHS was moving toward "safer, broader vaccine platforms that remain effective even as viruses mutate."

Both whole-virus vaccines and mRNA vaccines protected against COVID-19 and prevented hospitalization and death for millions of people worldwide between 2020 and 2024, but there's clear evidence that the mRNA-based vaccines provided significantly better protection than whole-virus vaccines. And for COVID-19, mRNA vaccines are more effective against new variants, which emerge as viruses mutate, than whole-virus vaccines.

The COVID-19 mRNA vaccines started with exceptionally high efficacy, exceeding 94%. When the SARS-CoV-2 delta and omicron variants emerged in the spring and fall of 2021, mRNA vaccines became less effective in preventing infections. However, they remained highly effective in preventing severe illness, whereas in unvaccinated people the rates of severe illness and hospitalization remained high.

This is because mRNA vaccines induce the immune system to make both antibodies and specialized immune cells called T cells. These elements can recognize multiple parts of the virus, including ones that don't change, enabling significant protection against new variants.

What's more, the mRNA vaccines have a superpower that no other type of vaccine can currently match: They can be quickly updated and manufactured within two to three months. To develop a whole-virus vaccine, researchers must first spend months isolating and propagating the virus. Conversely, making an mRNA vaccine requires just sequencing the virus's genetic code — a process that today takes just hours.

If a new pandemic began today, mRNA vaccines are currently the only type of vaccine that could be developed quickly enough to disrupt its spread.

The future of mRNA vaccine technologies

Thirty years ago, when scientists first started developing mRNA vaccine technology, they recognized its potential to overcome major limitations of whole-virus vaccines — namely, slow production time and more limited ability to protect from new viral variants. Today, mRNA vaccines are also being developed to prevent or treat diseases including HIV and cancer, as well as autoimmune and genetic diseases.

Of course, this technology can be further improved. New mRNA vaccine technologies are aimed, among other things, at making mRNA vaccines easier to store to allow for faster distribution and reduce their short-term side effects, eliminate the rare risk of myocarditis and more quickly block a respiratory infection.

The National Institutes of Health is funneling money away from new mRNA technologies toward a single project developing universal vaccines based on traditional whole-virus vaccine technology. Universal vaccines are urgently needed to provide broader protection against ever-changing respiratory viruses, such as influenza, that are major pandemic threats.

A 2022 study in mice and ferrets showed that a universal flu vaccine NIH plans to support has promise. However, multiple studies of potential universal flu vaccines based on mRNA technology show even more potential. Such vaccines could induce broader immunity than whole-virus vaccines by eliciting antibody and T-cell responses that target an even wider range of flu viruses.

It's hard to square those benefits with the fact that HHS and NIH have named the planned new universal vaccine platform "Generation Gold Standard," insisting that it represents a new standard in science and transparency. The effort seems more akin to eliminating all e-bike technology and telling everyone who seeks one to get by with a single brand of a 10-speed bike: Getting to the intended destination may still be possible, but it will be slower and harder.

And in the case of abandoning mRNA vaccine research, it may lead to lives needlessly lost, whether due to potential medicines untapped or to pandemic unpreparedness.

This article was updated to include details from Kennedy's Sept. 4, 2025, hearing.

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

A single dose of the psychedelic drug LSD may ease generalized anxiety disorder for months, a clinical trial has found.

The trial results, published Thursday (Sept. 4) in JAMA, include data from 194 people with moderate to severe anxiety across the U.S. The study compared these participants' responses to different doses of LSD against a placebo treatment. It found that the drug alleviated symptoms in many patients for at least three months after just one exposure.

That said, participants who were given low doses of LSD — either 25 or 50 micrograms — did not see a significant change in their symptoms. The effect kicked in only at higher doses — either 100 or 200 micrograms — and those given 100-microgram doses had the best results.

In fact, 12 weeks out from treatment, about 47% of the people who were given 100 micrograms were in remission, based on a standardized anxiety rating scale. And about 65% of the people in that group saw their scores on the scale fall by at least half. By comparison, only about 20% of the placebo group was in remission at the 12-week mark and about 30% saw their scores halved.

"This work has the potential to make significant contributions to the emerging field of psychedelic drug research," Dr. Claudio Soares, a professor of psychiatry at the Queen's University School of Medicine in Ontario, wrote in a commentary about the trial. It's the first study to examine how different doses of LSD compare with a placebo for relieving anxiety. In addition, the trial didn't explicitly incorporate psychotherapy into the treatment, meaning it could help pin down whether LSD in and of itself has an anti-anxiety effect, he added.

"Furthermore, the study highlighted an early response to treatment and positive effects on comorbid depressive symptoms, both of which are promising findings that should guide future trials," Soares said.

Related: 1 psychedelic psilocybin dose eases depression for years, study reveals

While there are approved anti-anxiety drugs, not all patients respond to them, the trial runners noted in their report. Estimates suggest about 50% of patients do not have an adequate response to first-line anxiety treatments, such as benzodiazepines or serotonin selective reuptake inhibitors (SSRIs, which are also used for depression).

As such, there's still a need for more effective, well-tolerated anti-anxiety medicines, the trial runners argue.

Enter LSD. The psychedelic is thought to trigger its mind-altering effects — such as visual hallucinations and a feeling of being high — in part by enabling communication between brain cells that don't normally interact. It's thought that this action might trigger a period of enhanced plasticity in the brain, during which a person with anxiety could break out of the harmful thought patterns that characterize the condition. But this mechanism is not fully understood and is still being studied.

Trials that have combined LSD with psychotherapy hinted that the drug can have a positive and sustained effect in treating anxiety. But because these trials were testing two interventions — LSD plus therapy — it's hard to know what LSD was contributing on its own.

The new trial aimed to investigate that question by including people who were not undergoing psychotherapy. In all, 18% of the participants were receiving external psychotherapy when they entered the study and continued receiving therapy during the study, the report noted.

At baseline, the 194 participants scored an average of 30 on an anxiety scale from 0 to 56, where the threshold for "severe" anxiety is 24. A score of 7 or less indicates remission. Patients given the 100-microgram dose saw, on average, a 21-point drop in their scores.

"A treatment effect emerged 1 day after the dosing day and persisted through week 12," the report authors noted.

The vast majority of side effects tied to the treatment were expected and resolved once the dosing of the drug concluded. These effects included visual perception changes, nausea, headache and euphoric mood. Notably, side effects were reported across all the study groups, including the placebo group, but occurred at the highest rates in the high-dose groups. For instance, more than 90% of the 100-microgram group reported hallucinations, as did 100% of the 200-microgram group.

Two people reported "feeling intoxicated" in the 50- and 100-microgram groups, respectively, but felt normal by the end of the dosing session.

Although the side effects were generally mild to moderate in severity, they did prompt a handful of people to drop out of the trial, so the LSD treatment may not be tolerable to all patients.

The trial does have some limitations, including the short follow-up time of only three months and the inclusion of some patients who still underwent therapy during the trial, Soares said. But in all, the trial provides crucial data that could help "further inform regulatory pathways for the use of psychedelic drugs as stand-alone treatments," he said.

Future research will be needed to evaluate how well the effects of the drug last over longer time frames, particularly after a single dose, he concluded.

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

Cannabis smoke can seem gentler than tobacco's, but that impression of marijuana may be deceptive. Deep in the lungs, the drug's chemistry is far from benign, recent research suggests. Some studies have even linked heavy cannabis use to a heightened risk of some cancers, including those of the head and neck.

So is there a clear link between cannabis and cancer, and if so, what causes it?

Each lungful of cannabis smoke is a brew of the high-inducing ingredient tetrahydrocannabinol (THC), fine particulates, and certain carcinogens that are also found in tobacco. But cannabinoids may bring their own twist by quietly rewiring the lungs' immune settings.

"The airway's protective lining weakens, antiviral signals falter, and inflammation flares," said Raphael Cuomo, a scientist working at the intersection of cancer prevention and addiction at the University of California, San Diego. In one study with mice, cannabis smoke dulled both tumor-fighting and infection defenses. In another, THC blunted the effects of immunotherapy, weakening tumor-killing immune cells in the body.

Cannabis also triggers other changes in the immune system, according to studies in humans, cells and lab mice. In the airways, levels of proteins tied to inflammation spike when cannabis is used consistently. A protein called MUC5AC, which lines and protects the respiratory tract, is made in excess in certain cells, hinting at early tissue changes. Cannabis smoke can skew the enzymes that maintain tissue and switch off genes that respond to toxins.

The responses of the lungs' patrol cells — alveolar macrophages — can be stunted. And in the blood, shifts in cellular messengers called cytokines and faint changes in epigenetics become a molecular diary of exposure.

Related: Could cannabis treat cancer someday? Here's what the science says so far

In summary, "cannabis smoke, from its toxic byproducts to THC, can irritate lungs and weaken immunity," Sayantan Bhattacharyya, a cancer systems biologist who will soon be a senior postdoctoral scientist at the University of Limerick in Ireland, told Live Science.

But immune disruption is only one factor that might raise cancer risk. Cannabis smoke may also tug on deeper levers inside cells — the molecular switches that cancers use to grow and spread.

Among these, few are as infamous as the epidermal growth factor receptor, or EGFR. In one of the few studies of its kind, Bhattacharyya examined 83 men with glottic cancer, which affects the voice box, and found that cannabis smokers in the group had markedly higher activation of EGFR and related cancer proteins than either tobacco smokers or nonsmokers.

"EGFR governs [cell] growth, repair, and survival," Bhattacharyya said. "In cannabis smokers, constant activation can fuel unchecked proliferation, speed genetic damage, and hasten the leap toward cancer — triggering earlier onset, faster spread, and treatment resistance." That said, Bhattacharyya's study included only 83 people with one type of cancer, so more work is needed to know if the results are broadly applicable.

Bhattacharyya sees two priorities for future research. One is to develop realistic lab models — such as "organoids," 3D-printed tumors and organ chips — to study how cannabis amplifies EGFR. The other is to probe potentially dangerous additives that might be lurking in unregulated cannabis products, he said.

For all the unsettling biology uncovered in laboratory studies, real-world studies of cannabis smokers tell a mixed story. Some research links heavy cannabis use to higher cancer risk, while others find no clear connection. Still, Cuomo maintains that long-term use of the drug may increase the odds of developing cancer, based on what we know so far.

For people who already have cancer, however, Cuomo has shown that cannabis use isn't linked to an earlier death — a puzzle researchers now call "Cuomo's paradox." In fact, studies have found that, in cancer patients, cannabis can boost appetite and curb chemotherapy-induced nausea, even as its smoke may potentially be planting the chemical and cellular seeds of disease.

The challenge going forward will be to accurately assess both the benefits and harms of cannabis in order to weigh them against one another.

Editor's note: This story was updated on Aug. 21, 2025, to note that Bhattacharyya will hold a position at University of Limerick.

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

Imagine this: You're at your doctor's office with a sore throat. The nurse asks, "Any allergies?" And without hesitation you reply, "Penicillin." It's something you've said for years — maybe since childhood, maybe because a parent told you so. The nurse nods, makes a note and moves on.

But here's the kicker: There's a good chance you're not actually allergic to penicillin. About 10% to 20% of Americans report that they have a penicillin allergy, yet fewer than 1% actually do.

I'm a clinical associate professor of pharmacy specializing in infectious disease. I study antibiotics and drug allergies, including ways to determine whether people have penicillin allergies.

I know from my research that incorrectly being labeled as allergic to penicillin can prevent you from getting the most appropriate, safest treatment for an infection. It can also put you at an increased risk of antimicrobial resistance, which is when an antibiotic no longer works against bacteria.

The good news? It's gotten a lot easier in recent years to pin down the truth of the matter. More and more clinicians now recognize that many penicillin allergy labels are incorrect — and there are safe, simple ways to find out your actual allergy status.

A steadfast lifesaver

Penicillin, the first antibiotic drug, was discovered in 1928 when a physician named Alexander Fleming extracted it from a type of mold called penicillium. It became widely used to treat infections in the 1940s. Penicillin and closely related antibiotics such as amoxicillin and amoxicillin/clavulanate, which goes by the brand name Augmentin, are frequently prescribed to treat common infections such as ear infections, strep throat, urinary tract infections, pneumonia and dental infections.

Related: Mold that led to penicillin discovery revived to fight superbugs

Penicillin antibiotics are a class of narrow-spectrum antibiotics, which means they target specific types of bacteria. People who report having a penicillin allergy are more likely to receive broad-spectrum antibiotics. Broad-spectrum antibiotics kill many types of bacteria, including helpful ones, making it easier for resistant bacteria to survive and spread. This overuse speeds up the development of antibiotic resistance. Broad-spectrum antibiotics can also be less effective and are often costlier.

Why the mismatch?

People often get labeled as allergic to antibiotics as children when they have a reaction such as a rash after taking one. But skin rashes frequently occur alongside infections in childhood, with many viruses and infections actually causing rashes. If a child is taking an antibiotic at the time, they may be labeled as allergic even though the rash may have been caused by the illness itself.

Some side effects such as nausea, diarrhea or headaches can happen with antibiotics, but they don't always mean you are allergic. These common reactions usually go away on their own or can be managed. A doctor or pharmacist can talk to you about ways to reduce these side effects.

People also often assume penicillin allergies run in families, but having a relative with an allergy doesn't mean you're allergic — it's not hereditary.

Finally, about 80% of patients with a true penicillin allergy will lose the allergy after about 10 years. That means even if you used to be allergic to this antibiotic, you might not be anymore, depending on the timing of your reaction.

Why does it matter if I have a penicillin allergy?

Believing you're allergic to penicillin when you're not can negatively affect your health. For one thing, you are more likely to receive stronger, broad-spectrum antibiotics that aren't always the best fit and can have more side effects. You may also be more likely to get an infection after surgery and to spend longer in the hospital when hospitalized for an infection. What's more, your medical bills could end up higher due to using more expensive drugs.

Penicillin and its close cousins are often the best tools doctors have to treat many infections. If you're not truly allergic, figuring that out can open the door to safer, more effective and more affordable treatment options.

How can I tell if I am really allergic to penicillin?

Start by talking to a health care professional such as a doctor or pharmacist. Allergy symptoms can range from a mild, self-limiting rash to severe facial swelling and trouble breathing. A health care professional may ask you several questions about your allergies, such as what happened, how soon after starting the antibiotic did the reaction occur, whether treatment was needed, and whether you've taken similar medications since then.

These questions can help distinguish between a true allergy and a nonallergic reaction. In many cases, this interview is enough to determine you aren't allergic. But sometimes, further testing may be recommended.

One way to find out whether you're really allergic to penicillin is through penicillin skin testing, which includes tiny skin pricks and small injections under the skin. These tests use components related to penicillin to safely check for a true allergy. If skin testing doesn't cause a reaction, the next step is usually to take a small dose of amoxicillin while being monitored at your doctor's office, just to be sure it's safe.

A study published in 2023 showed that in many cases, skipping the skin test and going straight to the small test dose can also be a safe way to check for a true allergy. In this method, patients take a low dose of amoxicillin and are observed for about 30 minutes to see whether any reaction occurs.

With the right questions, testing and expertise, many people can safely reclaim penicillin as an option for treating common infections.

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