• A study suggests that middle-aged and older adults with stronger, more regular daily patterns of activity and rest showed signs of slower biological aging.
• Participants with clearer differences between daytime activity and nighttime rest, and less fragmented routines, had more ‘youthful’ physiological age scores.
• The associations remained significant even after researchers accounted for factors including chronological age, sex, education, and certain health conditions.
• The findings suggest that rest-activity rhythms could become targets for interventions, potentially using wearable devices or lifestyle changes, aimed at slowing the aging process.

Biological aging refers to how well the body functions as it ages, which may not always be the same as a person’s chronological age.

Some people may age more slowly and stay healthier for longer, while others may experience faster aging due to various factors, such as lifestyle habits.

It is possible to partly measure aging through epigenetic changes. This describes changes to genes without altering the DNA itself.

Using these patterns, an epigenetic clock can estimate a person’s biological age. If a person’s epigenetic age is older than their chronological age, it may suggest faster aging and a greater risk of age-related diseases.

Lifestyle habits can strongly influence epigenetic aging, with research highlighting regular exercise and healthy sleep habits as powerful tools to support healthy aging.

Notably, growing research is showing an association between aging and changes in circadian rest-activity rhythms. This refers to the natural, roughly 24-hour cycles in a person’s pattern of being awake and active versus resting and sleeping.

Now, a study published in JAMA Network Open adds to this evidence, suggesting that adults who maintain stronger and more consistent patterns of daily activity and rest may experience slower biological aging.

What did the study find?

The study included 207 middle-aged and older adults participating in the long-running Baltimore Epidemiologic Catchment Area (ECA) cohort study. Participants had an average chronological age of around 68 years.

To measure daily activity patterns, the research team, led by the Johns Hopkins Bloomberg School of Public Health, used wrist-worn actigraphy devices for approximately 7 consecutive days.

These devices tracked periods of activity, rest, sleep, and sedentary behavior. Participants also kept sleep and nap logs.

The investigators compared these activity patterns with 4 established epigenetic clocks that estimate biological age using epigenetic markers. The clocks used in the study were:

• Horvath clock
• Hannum clock
• PhenoAge
• GrimAge.

The findings suggest that individuals with stronger and less fragmented rest-activity rhythms had significantly lower biological age scores on the GrimAge and PhenoAge measures, indicating slower physiological aging.

The associations remained even after accounting for factors such as chronological age, sex, education level, and certain health conditions.

Co-senior author Brion Maher, PhD, MS, a professor in the Bloomberg School’s Department of Mental Health was not surprised by the strength of the associations.

He told Medical News Today “it is not entirely surprising since GrimAge and PhenoAge are newer-generation epigenetic clocks that were designed to capture aging-related health risks, including mortality risk, disease burden, and physiological decline.”

“Because rest-activity rhythms are closely related to overall health, it makes sense that their associations would be more apparent in epigenetic clocks that are associated with health and mortality than with clocks that are primarily designed to estimate chronological age.”

– Brion Maher, PhD, MS

Similar trends also appeared with the Horvath and Hannum clocks. However, those findings did not reach statistical significance.

Why do rest-activity rhythms matter?

Rest-activity rhythms reflect the body’s broader circadian system. This describes the internal biological processes that regulate sleep, activity, hormone release, metabolism, and other functions over a roughly 24-hour cycle.

As people age, these rhythms often weaken and become more irregular. Another recent study by the research team linked weaker and more fragmented rest-activity rhythms to shrinking of the brain in older adults.

Previous studies have also linked disrupted circadian rhythms with a range of health problems, including cognitive decline, psychiatric disorders, and some cancers.

Therefore, the researchers suggest that rest-activity rhythms could become a useful marker of aging, and may provide a more meaningful measure of health than chronological age alone. If supported by further research, they may also emerge as possible targets for interventions to slow the aging process.

The study’s lead author was Chunyu Liu, a PhD student supervised by Maher and the other co-senior author, Adam Spira, PhD, MA, also a professor in the Bloomberg School’s Department of Mental Health.

“I think rest-activity rhythms may be an observable window into circadian regulation, and circadian regulation is not just related to aging—it may be part of the aging process itself,” Liu told MNT.

“In addition, circadian regulation is closely connected with many biological processes involved in aging. Stronger circadian rhythmicity may help coordinate these processes, which could be reflected in lower epigenetic age acceleration.”
– Chunyu Liu

Spira explained to MNT how measuring wrist movement in the study may reflect fragmented rhythms.

“In this study, we did not directly measure circadian rhythms — we measured movement at the wrist over 24-hour periods, which is an indirect measure of circadian function. The resulting data also reflect an array of environmental influences, such as bright light exposure at certain times of day,” he detailed.

“Fragmented rhythms represent more frequent, rapid transitions between rest and activity within a day. Fragmented sleep could manifest as fragmented motor activity at night in these rest-activity rhythm metrics,” Spira added.

“In general, more continuous, consolidated sleep is thought to be one of the many consequences or manifestations of stronger, less fragmented circadian rhythms,” he told us.

Researchers caution study was exploratory

While the study highlights a clear distinction between daytime activity and nighttime rest and “younger” biological aging, the authors emphasize that the study was cross-sectional, meaning it examined activity rhythms and biological aging at roughly the same point in time.

As a result, the research cannot determine whether disrupted rhythms contribute to faster aging, or whether aging itself weakens circadian patterns. The researchers note that longer-term studies will be necessary to clarify the direction of the relationship.

They also add that the study population may have underestimated the true effect, as the participants were older adults healthy enough to take part, whereas those who experience more rapid aging may have been too unwell to participate.

Managing circadian rhythms

The researchers suggest that wearable technology could eventually help monitor physiological aging and other health risks in real time.

“I think this is feasible in the long term,” Liu said to MNT. “Wearable devices are very good at continuously capturing patterns of rest and activity over multiple days or weeks. Those data likely provide a more reliable picture of daily rhythms than the information a healthcare provider obtains from a patient during a short clinical visit.”

“However, physiological aging is complex and likely cannot currently be measured directly in real time by wearables alone,” she added.

“The more realistic near-term use is that wearable-derived rhythm measures could help identify people with disrupted daily patterns who may be at higher risk for adverse aging-related outcomes, and could guide earlier lifestyle or clinical interventions,” Liu pointed out.

The study authors add that they hope to conduct future clinical trials investigating whether strengthening daily rest-activity rhythms could help slow biological aging.

• A global expert panel has recently announced that the condition hitherto known as polycystic ovary syndrome (PCOS) will officially undergo a name change to polyendocrine metabolic ovarian syndrome (PMOS).
• The name change acknowledges the fact that this gynecological condition is not just characterized by the formation of cysts on the ovaries but actually impacts metabolic health more broadly, as well as other aspects of health.
• The experts hope that the name change will lead to more accurate diagnoses and timely treatment of the condition.

On Monday, May 12, 2026, an international panel of experts dubbed the Global Name Change Consortium announced — via a health policy paper published in The Lancet — the official name change of polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS).

Previously, doctors would diagnose the condition formerly known as PCOS based on the presence of fluid-filled cysts on a person’s ovaries.

This condition is also characterized by irregular periods and unusual hair growth due to hormonal imbalances.

By shifting the name of the condition to focus on its metabolic implications, rather than the presence of ovarian cysts, and through the health policy changes outlined in the Lancet paper, the global expert panel is now aiming to emphasize the true systemic impact of this condition.

Not just ovarian cysts but a complex endocrine condition

Getting from PCOS to PMOS took no less than 14 years involving multidisciplinary expert consultations as well as surveys conducted with a total of 14,360 participants who had received a diagnosis.

The new name will be adopted globally over a 3-year transition period, with experts expecting that this process will be completed in 2028.

Through this name change, experts acknowledge that this reproductive system condition does not always present as expected — that is, it does not always involve the formation of ovarian cysts — and it affects more than just the reproductive organs, as it can impact hormone production, weight, a person’s skin, their metabolic health, as well as mental health.

“What we now know is that there is actually no increase in abnormal cysts on the ovary, and the diverse features of the condition were often unappreciated,” said one of the lead experts involved in the name-change process, Helena Teede, FRCOG, FRANZCOG, MBBS, PhD, Director of the Monash Centre for Health Research & Implementation at Monash University in Australia, in a press release.

Speaking to Medical News Today, Sameena Rahman, MD, board-certified ob-gyn, sex-med gynecologist, and menopause specialist, who was not part of the name-change panel, said she was thrilled about this change.

“This name change has been a long time in the making,” Rahman told us. She explained that “the previous name, PCOS, was both misleading and incomplete because it focused narrowly on ovarian cysts, which are not present in every patient and are not the root cause of the condition.”

“The updated terminology better reflects the true scope of the syndrome as a whole-body condition driven by insulin resistance, hormonal imbalance, and inflammation. It also helps destigmatize the diagnosis and shifts the conversation beyond reproductive health alone, recognizing that this is a complex metabolic and endocrine condition that affects multiple systems throughout the body.”

– Sameena Rahman, MD

A step towards better care and faster diagnosis

The experts in charge of the name change are also hoping that by shifting the focus in such a way as to emphasize that PMOS is a complex health condition, there will be fewer delayed diagnoses in the future, as well as care that is fully personalized.

Historical data suggests that many have not received a diagnosis for their condition until they sought fertility treatment, as the complexity of symptoms has often led to misdiagnoses, or contradictory diagnoses from different healthcare professionals.

“It was heart-breaking to see the delayed diagnosis, limited awareness and inadequate care afforded those affected by this neglected condition,” Teede noted in the press release.

“The agreed principles of the new name included patient benefit, scientific accuracy, ease of communication, avoidance of stigma, cultural appropriateness and accompanying implementation. This change was driven with and for those affected by the condition and we are proud to have arrived at a new name that finally accurately reflects the complexity of the condition. Make no mistake, this is a landmark moment that will lead to desperately needed worldwide advancements in clinical practice and research.”

– Helena Teede, FRCOG, FRANZCOG, MBBS, PhD

Rahman shared this hope, and emphasized that, “importantly, the updated terminology encourages clinicians and patients to view this as a lifelong metabolic and inflammatory condition — not simply a gynecologic issue.”

“That broader understanding can lead to earlier intervention and a stronger focus on preventing long-term cardiometabolic complications [associated with this condition] such as heart disease, diabetes, and other chronic health conditions,” she told us.

• New research from the United Kingdom shows that people who engage in artistic pursuits of various kinds experience a slower pace of aging.
• The study even suggests that the positive effect of having an active cultural life is akin to that of regular exercise.
• While this study does not prove a causal relationship, the researchers believe that artistic and creative pursuits can have beneficial effects on many aspects of health, including lowering inflammation and protecting brain health.

Participating in creative pursuits and engaging with arts and culture is good for the soul but could it also help the body stay in shape? That seems to be what a new study from University College London (UCL) in the United Kingdom is suggesting.

The study — whose findings appear in the journal Innovation in Aging — has found an association between engagement with arts and culture and a slower pace of biological aging.

Other studies have connected creativity with better cognitive health. For instance, research published in Nature Communications in October 2025 found that activities such as dancing and engaging with the visual arts could help the brain stay younger for longer.

It may be, however, that creative and artistic interests and activities may help the entire body maintain its youthfulness in some respect.

Speaking to Medical News Today, one of the study authors, Feifei Bu, PhD, principal research fellow in statistics/epidemiology within the Social Biobehavioural Research Group in the Department of Behavioural Science and Health at UCL, said that the research team was keenly interested in exploring just how artistic interest can actually shape our health throughout our lives.

“Arts and cultural engagement is increasingly seen as a health behaviour,” Bu suggested. “Many studies have linked it to health outcomes such as better cognition, lower depressive symptoms, and improved physical health.”

“However, very little research has examined whether its benefits are biologically embedded — so that’s what we wanted to explore in this study,” she told MNT.

More frequent artistic engagement linked to slower aging

In their study, the UCL researchers assessed survey responses regarding their engagement in arts and culture, as well as blood test results provided by 3,556 participants with a mean age of about 52 years. A little more than half of the participants were female, and the rest male.

The data came came from the UK Household Longitudinal Study.

In brief, the researchers wanted to see how engagement in the arts and culture would correlate with epigenetic aging — changes to DNA that influence the rate of biological aging.

They used no fewer than 7 epigenetic clocks in their research, which are tools for assessing age-related DNA changes.

Two of the younger-generation epigenetic clocks used, in particular — called DunedinPoAm and DunedinPACE — help provide an estimate of the pace at which a person is aging. The faster the pace of aging, the more likely it is that a person also has a higher risk of developing age-related conditions.

Another epigenetic clock, called PhenoAge, helped the researchers estimate individuals’ biological ages.

Overall, tests conducted using the three next-gen epigenetic clocks suggested that the more people engaged in artistic and cultural activities, and the wider the breadth of their cultural-artistic interests, the slower their pace of aging, and the younger their estimated biological age.

According to DunedinPACE data, engaging in artistic pursuits at least 3 times a year was linked to a 2% slower aging pace, and engaging in creative pursuits on a monthly basis was linked to a 3% slower aging pace compared to engaging with arts less than 3 times a year.

Those who pursued cultural activities on a weekly had a 4% slower aging rate compared to those who pursued such activities less than 3 times a year.

Cultural engagement as beneficial as regular exercise

Notably, these positive associations appeared to be on a par with the beneficial effects of exercise on aging, as the researchers also found that individuals who exercised on a weekly basis had a similarly slower aging pace.

These associations persisted with regard to biological age: according to PhenoAge tests, participants who engaged in artistic pursuits on a weekly basis or more frequently were 1 year younger on average compared to those who rarely pursued creative or cultural activities.

The researchers noted a similar association between weekly or more frequent exercise and biological age.

These associations were strongest for participants 40 years of age or older, and persisted even after the researchers accounted for confounding factors including body mass index (BMI), smoking status, education, and income level.

The older epigenetic clocks did not reveal any associations between more frequent cultural engagement and slower aging pace, or between exercise and and aging pace. The study authors believe this may be because the older generation of epigenetic clocks are less sensitive predictors of age-related changes.

Commenting on this study, Şebnem Ünlüişler, Chief Longevity Officer and genetic engineer at the London Regenerative Institute, in the United Kingdom, who was not involved in the research, said she was heartened by the findings:

“The findings are really encouraging — it is particularly interesting that arts and cultural engagement showed a measurable association with slower biological ageing, highlighting the importance of emotional wellbeing, creativity and social connection in long-term health. While the study does not establish causation, it adds to the growing body of evidence suggesting that meaningful lifestyle experiences may positively influence ageing pathways.”

Likewise, Opel Baker, MBChB, DipOccMed, MRCGP, general practitioner at the Mayfield Clinic Brighton and Hove, U.K., who was also not involved in the research, noted that he found the paper “really interesting.”

“Studies like this are incredibly important because they remind us that health is not shaped by medicine alone, but by how we live, connect and engage with the world around us,” Baker told us.

He noted that in his own experience as a family doctor he has witnessed “the profound impact that artistic and creative pursuits can have on both mental and physical wellbeing.”

Does it matter what cultural activities you engage in?

According to Bu, it does not matter what artistic, creative, or cultural activities a person chooses, as long as they engage in plenty of such pursuits — the more diverse the better.

“The arts cover a wide range of activities, each offering a distinct set of ‘active ingredients’ — [such as] esthetics, sensory or physical stimulation, social interaction, and emotional evocation — that benefit health,” the researcher told us.

“Our research shows that both frequency and diversity matter. The ‘most useful’ way would depend on the individual — their interests, what’s available to them, and what they enjoy doing consistently.”
– Feifei Bu, PhD

“Whether it is painting, music, dance, theatre or simply engaging with culture more regularly, these activities provide emotional release, cognitive stimulation, stress reduction and often valuable social connection, all of which are strongly linked to healthier aging,” Baker also said.

In Ünlüişler’s opinion, “activities that combine multiple benefits simultaneously may be particularly impactful.” She offered dance as an example, noting that it “incorporates movement, coordination, music, and social interaction, supporting both physical and cognitive health.”

Another example she cited was “group singing [which] may also offer unique benefits through breath control, emotional expression, and social bonding.”

“However,” Ünlüişler emphasized, “the study suggests that regular and meaningful engagement may matter more than any single activity itself.”

How exactly might creative activities help slow aging processes?

Bu stressed that the current study is “an observational study, [and thus] shows an association, not causation.”

“Although these findings are promising, more research is needed to cross-validate these findings and to strengthen the evidence for causality,” she cautioned.

Still, the study author had some working hypotheses as to the potential biological mechanisms that might underlie the association between engagement in artistic and cultural pursuits and a slower rate of aging.

According to her, “a likely explanation is that arts engagement helps reduce stress, inflammation and cardiovascular risks, all of which have been shown to be linked to epigenetic aging.”

Ünlüişler hypothesized that one key mechanism mediating the association between regular cultural engagement and a slower pace of aging is stress reduction.

“Chronic stress can accelerate aging through increased cortisol levels, inflammation and nervous system dysregulation, whereas activities such as music, painting, or dance may promote relaxation and emotional regulation,” she explained.

“Arts engagement may also support brain health through cognitive stimulation and neuroplasticity,” which refers to the brain’s ability to build fresh connections between neurons, Ünlüişler continued.

“In addition, social and creative activities are associated with improved mood, reduced inflammation, and a stronger sense of purpose, all factors linked to healthier aging,” she pointed out.

Baker agreed, making similar points to Bu and Ünlüişler, emphasizing the importance of lowering stress levels and building a sense of community through artistic pursuits:

“Chronic stress and isolation are two of the biggest contributors to poor long-term health, inflammation and accelerated ageing. Artistic pursuits can counteract this by promoting relaxation, improving mood, supporting brain function and creating a sense of purpose and fulfilment. What is particularly encouraging about this research is that it reframes creativity not as a luxury, but as something that may genuinely support longevity and overall health outcomes.”

How else might cultural engagement benefit health?

The UCL research team is not stopping at this study. Going forward, they are planning to validate the current findings on different populations, and to expand the research to look at other possible health benefits of cultural engagement.

“We plan to cross-validate these findings across different countries and populations. We also want to look beyond epigenetic clocks and explore other biological outcomes related to arts and cultural engagement.”

– Feifei Bu, PhD

Baker and Ünlüişler both also wanted to see further research validating the findings of the current study.

“Epigenetic aging clocks are still a relatively young area of research, and while they are promising, they currently show correlation rather than direct causation. This means we cannot yet say definitively that arts engagement slows biological ageing, only that there appears to be an association that warrants further investigation,” Baker pointed out.

Ünlüişler “would like to see long-term interventional studies exploring whether arts engagement can actively slow biological aging over time and which mechanisms are most responsible, such as stress reduction, inflammation control, or neurological resilience.”

“Further research into brain health, dementia prevention and emotional wellbeing would also be especially valuable, as healthy aging is ultimately about maintaining quality of life as well as longevity,” she stressed.

Overall, though, all the experts’ takeaway message was the current positive findings ought to encourage us all to tap into our creative interests as much as possible.

“We are increasingly recognising that healthy aging must involve emotional wellbeing, cognitive resilience and quality of life alongside physical health. Creative engagement has the potential to support all of these areas in a meaningful and accessible way,” Baker concluded.

• Recent evidence suggests that a commonly practiced form of surgery for knee osteoarthritis may actually worsen the condition.
• This may be because the initial damage to the meniscus cartilage, which this surgery addresses, is not the only cause of pain and discomfort in knee osteoarthritis.
• Orthopedic experts explain what this may mean for the treatment of this chronic condition going forward.

A common knee surgery — the partial removal of meniscus cartilage — may provide little benefit to people with knee osteoarthritis and may actually worsen their prospects for long-term knee health, according to new research from Finland, whose findings are reported in a correspondence paper published in The New England Journal of Medicine.

Study participants who underwent surgeries to remove torn parts of meniscus cartilage in their knees faired more poorly over the next 10 years than those who had undergone sham surgeries in which no cartilage was removed.

People who received the sham surgery had less knee pain, had increased use of the knee, and experienced less later osteoarthritis compared to those who had had meniscectomies.

The meniscus is a piece of tough, C-shaped rubbery cartilage in the knee that provides shock absorption between the shin bone and the thigh bone. It can tear as the result of a sudden twist.

More commonly, however, tears occur with age, and commonly go hand-in-hand with osteoarthritis. Most older people who have arthritis in the knee also have meniscus tears, and most older people with meniscus tears have arthritis.

Meniscus tears: What is the main source of pain?

For many years, it was assumed that meniscus tears were the source of knee pain.

Cedars-Sinai LA orthopedic surgeon and sports medicine specialist Clint Soppe, MD, who was not involved in the recent research, told Medical News Today: ”I remember 20 years ago, 15 years ago, hearing doctors, some of my mentors, say like, ‘Oh, well, you know, that’s not arthritic pain. That’s meniscus pain.’ The problem is you can’t tell.”

The study’s senior investigator, Teppo L.N. Järvinen, MD, PhD, of the University of Helsinki, however, told us that: “There is now a substantial body of evidence suggesting that we may have been targeting the wrong problem. The meniscal tear is often a visible finding, but does not seem to be the (sole) cause of pain — at best.”

“In middle-aged and older individuals, meniscal tears are extremely common, including in people with no symptoms,” Järvinen added. “That makes it unlikely that the tear itself is usually the main driver of pain.”

“This study fits into a pattern seen across medicine: Widely used treatments can persist despite limited evidence, and when tested rigorously, may turn out to offer little benefit — or even cause harm.”

– Teppo L.N. Järvinen, MD, PhD

Paul Arciero, DPE, of the Health and Human Physiological Sciences Department at Skidmore College, who was not involved in the recent research, agreed, saying that: “Anecdotally, most individuals, both active and sedentary, who have undergone arthroscopic partial meniscectomy report worsening of their pain and mobility over time.”

In relation to this, Soppe cited the advances in our understanding of chronic pain conditions over the past few decades.

According to him, “all these different cell mediators that we didn’t know about or know much about 20, 30 years ago — interleukin inhibitors, cytokines, enzymes, TNF-alpha, metalloprotein — all these things that we know are associated with pain, and probably associated with meniscus-type pain.”

What are the alternatives to meniscus surgery?

“I think one of the most important measures is giving [knee pain] time,” said Soppe.

During that waiting period, he recommended “helping with symptoms using different modalities: anti-inflammatory pills, physical therapy, icing, [and] rest.“

“Cycling a lot of times is helpful, [as well as] injection treatments such as cortisone, hyaluronic acid, and PRP [platelet-rich plasma therapy],” Soppe suggested.

Soppe himself said he still performs meniscectomies but only under very specific circumstances, namely when a patient’s meniscus tear is displaced, out of position, and therefore potentially causing other issues, and only when the above methods, including giving it time time, have failed to help.

He also suggested that for some, osteoarthritis may be sufficiently advanced that full knee replacement is a more sensible option than meniscectomy.

Previous meniscectomy surgery is a known risk factor for successful knee replacement surgery.

Arciero noted that there may still be a place for meniscus repair, saying: “In certain cases of acute, traumatic injury to the knee joint, there remains the necessity to perform appropriate surgery to repair the meniscus. However, in the majority of routine meniscus tears/pain, the evidence shows alternative treatments are more effective long-term.”

‘Sham’ surgery may still provide relief

In the study, the investigators performed diagnostic arthroscopy for participants in the sham group, noted Soppe. That procedure typically involves injecting a saline solution into the knee, slightly inflating it to provide better visibility for the tiny cameras that are to be inserted into the joint.

“They flushed the knee with fluid, which we call lavage of the joint,” he pointed out. “To me, that is not sham surgery, [because] even though they’re not messing with the meniscus, they’re potentially removing these types of cell mediators, like cytokines, interleukens, TNF-alpha, that probably modulate the pain.”

“It’s not exactly sham surgery,” he said, raising the possibility that those participants might have received some unintended pain relief after all.

• On April 30, 2026, the U.S. FDA announced it is considering removing GLP-1 medications from the 503B bulks list. 
• FDA’s 503B bulks list identifies drug substances that outsourcing facilities can use to compound medications.
• Experts agree removing GLP-1s from the 503B bulks list will significantly lower the availability of compounded GLP-1s drugs. 
• Patients may still be able to receive compounded GLP-1s through 503A compounding pharmacies, and consider legitimate alternatives for weight loss. 

On April 30, 2026, the U.S. Food and Drug Administration (FDA) announced it is considering removing glucagon-like peptide-1 (GLP-1) receptor agonists from the 503B bulks list, as there is no current clinical need for pharmacies to be able to compound these medications. 

This could include drugs such as semaglutide (the active ingredient in Ozempic and Wegovy), tirzepatide (the active ingredient in Zepbound and Mounjaro), and liraglutide (the active ingredient in Victoza and Saxenda).

According to the FDA’s announcement, the organization is asking for submitted comments for or against this decision by the end of June 2026 before making their final determination.

Medical News Today spoke with 4 obesity experts to find out more about what the FDA’s 503B bulks list is, the potential future availability of compounded GLP-1 medications, and what alternatives may be available for users who may not be able to afford the brand name drugs. 

What is the FDA’s 503B bulks list? 

According to Douglas Ewing, MD, FACS, DABOM, a board-certified bariatric surgeon and medical director of the Center for Weight Loss and Metabolic Health at Hackensack University Medical Center, and associate professor of surgery at Hackensack Meridian School of Medicine in New Jersey, the FDA’s 503B bulks list identifies bulk drug substances that outsourcing facilities can use to compound medications. 

“These outsourcing facilities, regulated under section 503B of the Federal Food, Drug, and Cosmetic Act, can produce larger batches of compounded drugs than traditional 503A compounding pharmacies, which compound for individual patients with specific prescriptions,” Ewing explained to MNT. 

“The critical difference between a drug on the 503B list and an FDA-approved medication is the level of scrutiny,” he continued.

“FDA-approved drugs undergo a long and rigorous process of clinical trials to prove their safety, effectiveness, and quality before they can be marketed to the public.”

“Compounded drugs, even from 503B facilities, do not go through this same pre-market approval process. While 503B facilities are required to follow current Good Manufacturing Practices (cGMP), the compounded drugs themselves are not FDA-approved.”

Will compounded GLP-1s still be available? 

If semaglutide and tirzepatide are removed from the 503B bulks list, the availability of compounded GLP-1s would drop significantly, Michael Snyder, MD, FACS, FASMBS, DABOM, medical director of the Bariatric Surgery Center at Rose Medical Center, founder and director of the Denver Center for Bariatric Surgery Foundation, and in-house obesity specialist at FuturHealth, told MNT. 

“Most current compounded supply is produced through 503B outsourcing facilities, which would no longer be able to compound them in bulk,” Snyder said.

“There may still be limited use under 503A compounding rules, where a medication is prepared for an individual patient based on a specific clinical indication, but that pathway is much more restricted and not designed for widespread use.”

Jen Manne-Goehler, MD, ScD,assistant professor of medicine at Harvard Medical School, agreed. 

“There may be some forms of compounded GLP-1 drugs still available despite this decision,” Manne-Goehler told MNT.

”Specifically, the FDA’s decision not to include these GLP-1s on the bulk compounding list would not be expected to affect their use by 503A pharmacies. 503A compounding pharmacies compound according to specific patient prescriptions and are required by state boards of pharmacy to comply with standards.”

Because of the popularity and high demand of GLP-1 medications, Mir Ali, MD, bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, worried this may drive some people to purchase their medication through a potentially unsafe option.

“What I think will happen is people will try to get the medications from other sources outside the U.S., and that is a little riskier,” Ali told MNT.

“You could not be getting the medication you are buying, you may be getting something different or something maybe even unsafe. So it may increase some risk if people are going to go to sources outside of the U.S. to try to get these medications.” 

Are compounded GLP-1 medications safe?

When asked about the safety of compounded GLP-1 drugs, Ewing said that is a complex question without a simple “yes” or “no” answer. “The safety of compounded GLP-1s can vary significantly depending on the source,” he explained.

“There are legitimate compounding pharmacies that adhere to high-quality standards. However, the lack of FDA approval and oversight for the final compounded products introduces inherent risks.”

– Douglas Ewing, MD, FACS, DABOM

“Concerns have been raised about the potential for contamination, impurities, and incorrect dosages in some compounded products,” Ewing continued.

“There have also been instances of pharmacies using different salt forms of semaglutide, which have not been approved by the FDA and whose safety and efficacy are unknown.” 

Manne-Goehler said that many reports have suggested that the current compounded GLP-1s have a higher number of severe side effects. 

“For instance, one study showed that compounded GLP-1 RAs are associated with a greater risk of adverse events, safety concerns, and product quality issues compared to non-compounded products,” she detailed.

“This may be because lower quality compounding practices can result in issues with drug quality, contamination or differences in the amount of active ingredient. Several medical societies have recommended against the use of compounded GLP-1 therapies.” 

Are there any legitimate alternatives to GLP-1s? 

If compounded GLP-1s become less available, Snyder said there are still legitimate, evidence-based options for weight loss. 

“That includes other FDA-approved medications for weight management, as well as structured medical weight loss programs that combine nutrition, behavioral support, and ongoing clinical monitoring,” he continued.

“We also expect that over time these medications will become more affordable and coverage should expand over time. But, clearly, not soon.” 

Ali said there are other medications available that are maybe available in generic form because they have been around longer, but they do not work quite the same, or maybe not even quite as well as the GLP-1 medications. 

“So there are other options available, but they may be less effective,” he added. 

For those who may be worried about affording the name-brand GLP-1 medications, Ewing said it is always worthwhile to check with your insurance provider about their coverage for weight-loss medications, as formularies can change, and what was not covered before might be now.

“Many pharmaceutical companies offer copay cards and patient assistance programs that can significantly reduce the out-of-pocket cost of brand-name GLP-1s for eligible individuals,” he detailed. “Services like GoodRx can offer significant savings on brand-name GLP-1 medications for those paying out-of-pocket.” 

“It is essential for patients currently using compounded GLP-1s to have an open conversation with their healthcare provider to explore these alternatives and develop a safe and effective treatment plan moving forward,” Ewing added. 

• Researchers found that the narrowing of large arteries was unlikely to result in lacunar stroke, a common form of stroke.
• In contrast, the widening of arteries within the brain was associated with both lacunar stroke and a brain issue known as cerebral small vessel disease.
• The study authors suggest that treatment for lacunar stroke and cerebral small vessel disease should look beyond addressing narrowing arteries and blood clots.

A study has shed new light on what might cause one of the most common forms of stroke, which could have major implications for how doctors treat and prevent it.

The type of stroke under investigation was lacunar stroke, a form of ischemic stroke. Lacunar strokes are smaller in size than other strokes and occur deep within the subcortical areas of the brain.

Lacunar strokes can happen when small blood vessels in these areas become damaged, a process that is also known as cerebral small vessel disease (cSVD). It has been unclear what underlying mechanisms cause this damage in the first place, however.

“This study provides strong evidence that lacunar stroke is not caused by fatty blockage of larger arteries, but by disease of the small vessels within the brain itself,” said study author Joanna Wardlaw, CBE, FRCP, FRSE FMedSci, FRCR, Professor of Applied Neuroimaging at the University of Edinburgh in the United Kingdom in a press release.

“Recognizing this distinction is crucial, because it explains why conventional treatments like antiplatelet drugs are not as effective for this type of stroke and highlights the urgent need to develop new therapies that target the underlying microvascular damage,” Wardlaw explained.

Ischemic strokes occur due to blood vessels becoming blocked, reducing blood flow to the brain. Around 87% of all strokes are ischemic strokes. Roughly a quarter of these are lacunar strokes.

Doctors tend to treat lacunar stroke in the same way as other forms of ischemic stroke, and the typical methods for preventing ischemic stroke aim to stop arteries narrowing and becoming blocked by buildups of fat.

However, the use of medications like aspirin has appeared to be less effective at preventing lacunar stroke than other forms of the disease.

What did the researchers look at?

For the study, published in Circulation, the researchers examined data from a total of 229 stroke patients. Of these, 131 had experienced lacunar stroke with the rest having experienced a mild non-lacunar stroke.

These patients were recruits of the Mild Stroke Study 3, a group consisting of people who had recently experienced strokes in Edinburgh, U.K., between 2018 and 2021.

Each participant underwent a range of clinical assessments and MRI brain scanning at the time of their recruitment to the study. Clinicians then repeated these assessments a year later.

The researchers wanted to investigate how changes to the arteries related to the different types of stroke as well as the cardiovascular health of the participants over time.

They were particularly interested in the narrowing of large arteries, which clinicians have traditionally seen as a major risk factor for all ischemic strokes, as well as the widening and lengthening of smaller arteries within the brain itself.

Narrowing of large arteries not associated with lacunar stroke

The researchers found that the narrowing of large arteries was not associated with lacunar stroke or any markers of cSVD.

However, widening and elongation of the small arteries within the brain did have an association with lacunar stroke. In fact, the patients whose scans showed these changes were four times more likely to have had a lacunar stroke.

These changes in the small arteries within the brain were also strongly associated with nearly all the markers for cSVD that the researchers measured for, as well as a higher risk of having a new silent stroke in the year after the initial assessments.

A silent stroke is a small amount of brain tissue damage that can occur due to restricted blood supply to the area. The word “silent” comes from the fact that they often appear to be symptomless.

More than a quarter of the patients experienced these silent strokes, even after receiving standard treatments to prevent new strokes from occurring.

These treatments include antiplatelet drugs, medication to lower blood pressure, and drugs for controlling blood cholesterol levels.

The authors suggest that solely focusing on these conventional treatments might not be the best choice in every case:

“Although these approaches remain important and should not be discounted, accumulating evidence, consistent with our results, suggests that guideline-based secondary stroke prevention, including antiplatelet therapy and statins, has limited efficacy in preventing the progression of cSVD-related brain damage.”

Possible reasons and limitations for the findings

Ischemic strokes like lacunar strokes occur due to reduced blood flow to parts of the brain. As a result, it may seem strange for there to be an association between lacunar strokes and the widening of small arteries.

The study authors suggest some potential mechanisms behind their findings. One is that there may be a shared genetic link between artery widening, lacunar stroke, and cSVD.

Another possible reason is that the widening and lengthening of certain arteries could result in extra stress being placed on other blood vessels. This could disrupt the flow of blood in these areas as well as damaging them.

Wardlaw explained to Medical News Today how this might work:

“One might think that wider blood vessels would give better blood flow but it can also be that the widening, as here, indicates loss of normal supporting membranes in the blood vessel wall of the large arteries, which means that the blood vessels are ‘baggy’ and less able to control flow. We think this is also what is happening to the small arterioles in the brain.”

Wardlaw said that the team had seen elsewhere that widening “was associated with worse function of the small blood vessels in the brain, which we know is a problem in lacunar stroke and small vessel disease.

“Therefore we think the large artery widening seen in our paper mirrors what is happening in the small arterioles in the brain which become baggy and lose the ability to constrict and dilate to manage blood flow,” she noted.

The authors note that their research was limited by the fact that their patient data all came from the stroke services in one single city. For the results to be generalizable to a wider population, they suggest larger studies looking at patients from a number of different locations are needed.

Changing approaches to post-stroke treatment

The researchers write that treatment for patients with lacunar stroke should aim to improve the functioning of small blood vessels in the brain rather than focusing on the potential clogging and narrowing of arteries.

Following up this research, the LACunar Intervention Trial 3 (LACI-3) is investigating whether two cardiovascular drugs — cilostazol and isosorbide mononitrate — can help target cSVD damage.

“The LACI-3 trial is testing two existing drugs used in heart and peripheral vascular disease that we think can improve the function of the small blood vessels in the brain and thus improve control of blood supply better,” Wardlaw told MNT.

By doing so, the hope is that this will “help to prevent more lacunar strokes and cognitive decline and other bad effects of small vessel disease.”

The trial is currently in its first year of recruitment at 38 different centers across the U.K. The team is aiming to recruit 1,300 people with lacunar stroke receiving treatment for 18 months, with the main outcome to assess being the effect on cognitive decline.

This trial could go some way to supporting the findings of the study and potentially alter the approach of future stroke treatment plans.

• A rare hantavirus outbreak has affected a cruise ship carrying nearly 150 people who were travelling from Argentina on a long-haul Atlantic journey.
• With a few confirmed deaths so far, several countries have ordered tracking and self-isolation for people at risk of suspected infection.
• However, the WHO currently maintains that the risk of human-to-human transmission and global spread is ‘low’ and the outbreak is under monitoring.
• Medical News Today spoke to three experts to find out what symptoms to watch out for, when to seek care, and what to do if they suspect contact with the hantavirus.

With international contact tracing efforts underway to track the passengers who disembarked the Dutch-flagged cruise ship MV Hondius early, concerns among the public about a larger outbreak of hantavirus have been growing.

What began with the confirmed death of a 70-year-old Dutch male onboard the cruise ship has become a hantavirus outbreak that has now spread to several passengers, with multiple in critical condition. That death marked the “index case” of the hantavirus outbreak, currently unfolding.

The ship, operated by Oceanwide Expeditions, was initially held off the coast of Cape Verde, and later authorized to sail toward the Canary Islands in Spain for further investigation.

Medical News Today spoke to three medical experts to learn more about how this virus spreads, what people can do to protect themselves, and whether this outbreak has the potential to turn into a bigger epidemic, similar to SARS-CoV-2:

• William Schaffner, MD, professor of preventive medicine in the Department of Health Policy, and professor of medicine in the Division of Infectious Diseases at Vanderbilt University Medical Center
• Justin Chan, MD, infectious diseases specialist at NYU Langone Health and Director of Infection Prevention and Control at Bellevue Hospital Center
• and Monica Gandhi, MD, MPH, an infectious diseases specialist with the University of California, San Francisco.

What we know so far about how the outbreak started

The Dutch man who died on April 11, 2026 aboard the MV Hondius had started to exhibit symptoms on April 6. This was 5 days after the ship had departed from Ushuaia, Argentina.

The ship alerted the case to the World Health Organization (WHO) on May 2, 2026, which was later confirmed as hantavirus after laboratory tests in South Africa.

As of May 11, 2026, there are at least 7 reported cases of confirmed patients. Three people, including the wife of the first victim, have died. One person remains in critical care in South Africa.

Several passengers have also been reported to have been hospitalized, receiving care in France, South Africa, The Netherlands, Switzerland, Singapore, and Spain.

The cruise ship was allowed to dock at the port of Granadilla, Tenerife on the Canary Islands on May 10. As passengers and crew disembark, they continue to be considered high-risk, regardless of symptoms, and are being medically evacuated to their respective countries of origin via non-commercial flights.

The total number of people on board the ship were 147 people, including crew.

As some passengers quarantine and others fly back to their various home countries, international tracing efforts have gained traction.

The WHO has declared the global risk of spread remains “low” as the outbreak is still confined to a small group of travelers.

Meanwhile, the European Centre for Disease Prevention and Control (ECDC) has activated the Early Warning and Response System (EWRS) to alert public health authorities in Europe of the situation.

What is hantavirus?

The hantavirus refers to a group of zoonotic viruses that are carried by rodents who spread the virus via their saliva, urine or feces.

Health authorities have identified that passengers have been infected with the Andes strain of hantavirus (ANDV). Although hantaviruses rarely spread via human-to-human contact, this particular strain is known to have the ability to be transmitted from person to person.

For this virus to spread between humans, authorities say close, prolonged physical contact is needed.

The initial passengers are thought to have been exposed to infected rodents or droppings before they boarded the ship. This strain of the virus is endemic in South America, indicating that the virus maintains a predictable, low-level presence.

Hantaviruses have been linked to svere disease and death, and can cause a severe respiratory illness called hantavirus cardiopulmonary syndrome (HCPS), for which the case fatality rate is as high as 50%.

What are the main symptoms of infection with hantavirus?

Schaffner said that what makes it hard to identify infections with hantavirus is that it may go undetected for the first few days.

“Hantaviruses cause stealth infections. The initial phase of the illness seems rather mild, with fever, headache, feeling poorly, some muscle aches – it does not alarm the patient,” he said.

However, after initial exposure, the virus has a broad incubation period that can last anywhere from a few days to 1 to 8 weeks before the patient starts to feel the symptoms, according to the WHO and the CDC.

“This can go on for 2 to 4 days and then the patient crashes, becomes seriously ill with hantavirus cardiopulmonary syndrome in which breathing becomes difficult, blood pressure drops and the patient feels very weak and sick,” he explained.

Chan said the Andes hantavirus causes symptoms such as fever, muscle aches, back pain, abdominal pain, vomiting and diarrhea.

“Severe illness follows with respiratory distress, pneumonia and drops in blood pressure. Lab testing is required to confirm hantavirus as the cause of illness,” he said.

Gandhi explained that there were two main syndromes caused by hantavirus: the Hantavirus Pulmonary Syndrome (HPS) or Hemorrhagic Fever with Renal Syndrome (HFRS).

“The kidney (renal) syndrome usually occurs in Asia or Eastern Europe and can be marked by fever, low platelets, acute kidney injury where urine production is down. The infected person can go into shock and have bleeding in the severe phases,” she said.

“The Andes strain causes lung symptoms and is found in South America generally. This syndrome is hallmarked by fever, shortness of breath, fluid in the lungs and shock. The patient can proceed to severe oxygen deprivation, bleeding, renal failure and require intubation and strong supportive care,” she added.

What MV Hondius passengers are being told to do

The ECDC published new guidance on May 9 for managing passengers linked to the Andes hantavirus outbreak on MV Hondius.

For passengers who are feeling sick and showing symptoms, the ECDC recommends they get tested and seek medical care as soon as possible.

They will also have the option to either stay in isolation in Tenerife, Canary Islands where the ship is docked or be flown to their respective home countries on special medical flights. For those who test negative, the ECDC still recommends quarantining and monitoring for up to 6 weeks to stay safe.

Passengers who are currently not experiencing any symptoms are still being considered high-risk contacts, and hence, are only able to travel via specially arranged transport, not on commercial flights. Self-quarantine at home is also being recommended until they are cleared for risk.

Meanwhile, for staff and healthcare workers tending to passengers or those with suspected hantavirus infection, the ECDC recommends they wear protective gear, including gloves, FFP2 masks and eye protection, as well as proper ventilation and cleaning in treatment facilities.

Passengers are also advised to wear masks to help stop the spread of germs.

SARS-CoV-2 vs. hantavirus: Detecting the origins

But will identifying the origins of this hantavirus outbreak be as difficult as SARS-CoV-2, the virus that causes COVID-19?

“[H]antavirus is not a new virus to humans as SARS-CoV-2 was so at this point, we think there was exposure from rodents to a few people boarding the ship from activities (such as bird watching in places with rodents) performed beforehand and then there was person to person spread on the ship,” said Gandhi.

“The originator of the virus was still likely rodent waste but the concern here is that the strain that led to this outbreak is spread person to person from close contact,” she said.

Chan explained that the Andes hantavirus was first discovered in Argentina in 1995, and nowadays, most commonly found in Argentina and Chile.

“While public health investigations are ongoing, given this cruise ship itinerary started in Argentina, it is most probable that at least the initial case was due to exposure to infected rodents found in that region,” he said.

Schaffner, meanwhile, underscored the importance of global preparedness in the face of such public health threats.

“This outbreak is a reminder of how small the globe is, how interconnected we are and how important the WHO is to epidemic preparedness,” Schaffner said.

“Scientists already are working on identifying the specific virus causing the outbreak. Public health authorities have begun their investigation of how the outbreak started. This still is in its early stages, so stay tuned,” he said.

Schaffner also noted that as this event unfolds and more information surfaces, medical experts’ recommendations may change, and people exercise caution and diligence.

• Some existing research has suggested that egg consumption could benefit brain health as we age, with one recent study indicating that eating one egg per week was linked to lower Alzheimer’s risk.
• A new study now claims that eating eggs at least five times a week is linked to a lower likelihood of receiving an Alzheimer’s diagnosis.
• The study authors emphasize that moderate egg consumption is part of a balanced diet, which benefits health overall.
• However, some questions remain in place about whether or nor the relationship between egg intake and brain health is causal.

When it comes to health benefits, eggs have had a fluctuating reputation over time. For years, a belief persisted that their high content of dietary cholesterol might negatively affect cholesterol levels in the human body.

More recent studies, however, argue that dietary cholesterol from moderate egg consumption does not contribute to higher levels of “bad” cholesterol in the human body and thus does not heighten heart disease risk.

In fact, there is evidence to suggest that the high nutritive content of chicken eggs could bring several health benefits, including better protein synthesis in muscles, and increased satiety (the sensation of being full) that can aid weight management.

A study published in in The Journal of Nutrition in July 2024 even found a link between egg consumption and a lower risk of Alzheimer’s disease.

According to this study of 1,024 older adults, eating one egg per week was linked with a 47% lower risk of Alzheimer’s compared with having eggs less than once a month.

Now, new research from scientists at Loma Linda University Health in California — which also appears in The Journal of Nutrition — has drawn similar conclusions, offering further support to the notion that regular moderate egg consumption may help protect brain health and lower the risk of cognitive problems.

The research team acknowledges that “the analyses in this study were supported by an investigator-initiated grant from the American Egg Board.”

Might 1 egg per day keep Alzheimer’s at bay?

In the current study, the researchers analyzed data provided through the Adventist Health Study-2 (AHS-2), which was linked with Medicare claims data files.

AHS-2 totalled a cohort of more than 96,000 people; of these, a little over 39,400 met the selection criteria for the current study.

Looking at participants’ reported dietary habits and the Medicare claims linked to their health diagnoses, the researchers found that people who reported eating eggs at least five times a week had an up to 27% lower risk of receiving an Alzheimer’s diagnosis compared to those who reported no egg consumption.

Compared to no consumption, having eggs 1 to 3 times per month was linked to a 17% lower risk of Alzheimer’s, and having eggs 2 to 4 times per week was linked to a 20% lower Alzheimer’s risk.

Speaking to Medical News Today, first author Jisoo Oh, DrPH, MPH, Associate Professor of Epidemiology in the School of Public Health at Loma Linda University, said that she and her colleagues were keen to study this association because they wanted to gain a better, more granular understanding of the modifiable risk factors for Alzheimer’s disease.

“While there is substantial interest in how nutrition influences brain health, there is still a knowledge gap regarding specific foods, including eggs,” said Oh.

“Eggs are widely consumed and contain several nutrients relevant to brain function, yet the evidence linking egg intake to clinically diagnosed Alzheimer’s disease has been limited,” she added.

“Most prior studies relied on short-term cognitive outcomes or cross-sectional data. The Adventist Health Study-2 provided a unique opportunity to examine this question in a large, well-characterized cohort with long-term follow-up and linkage to Medicare data, allowing us to study incident Alzheimer’s disease more rigorously,” the researcher explained.

How might eggs help support brain health?

While this study hasn’t addressed causation, the researchers hypothesize that eggs may have a protective effect on brain health thanks to the specific nutrients they contain.

Oh mentioned:

• “choline, which is essential for producing acetylcholine, a neurotransmitter involved in memory
• lutein and zeaxanthin, which accumulate in the brain and may help reduce oxidative stress
• omega-3 fatty acids (including DHA), important for neuronal structure and function
• vitamin B12, which plays a role in reducing homocysteine levels and supporting neurological function
• high-quality protein and tryptophan, which are involved in neurotransmitter pathways.”

According to her, “these nutrients may contribute to maintaining synaptic integrity, reducing inflammation and oxidative stress, and supporting overall cognitive resilience.”

“While our study does not directly test mechanisms, the findings are consistent with these biologically plausible pathways,” she noted.

Speaking of whether or not people should up their egg intake in light of these study findings, Oh advised “moderation” and paying attention to context.

“Our findings suggest that including eggs as part of a balanced diet may be beneficial for brain health, but they should not be viewed in isolation or as a ‘silver bullet’,” she cautioned.

“For most people, moderate [egg] consumption, such as a few times per week, appears reasonable and potentially beneficial, especially when part of an overall healthy dietary pattern that includes fruits, vegetables, whole grains, and other nutrient-dense foods.”

– Jisoo Oh, DrPH, MPH

“It’s also important for individuals to consider their overall health profile and dietary needs, ideally in consultation with a healthcare provider,” the researcher added.

Are eggs the key to better brain health as we age?

Other experts also emphasized that we would be remiss to believe that the answer to better brain health as we age is to be found primarily in egg consumption.

After reviewing the study findings, Michelle Routhenstein, MS, RD, CDCES, CDN, a preventive cardiology dietitian at EntirelyNourished, who was not involved in this research, told MNT: “My first reaction was, well what else are [the people in this cohort] eating? That question matters more than most people realize.”

For Routhenstein, it is important to acknowledge that the group this study focused on is already characterized by better overall health thanks to consistently healthy lifestyle habits.

“This was an observational study done in a very specific population, Seventh-day Adventists, who as a group smoke less, drink less, eat more plants, and have lower baseline rates of obesity, diabetes, and cardiovascular disease than the average American,” the dietitian pointed out.

“So when we see that moderate egg intake was associated with lower Alzheimer’s diagnoses in this cohort, we’re looking at what happens when people add eggs to an already protective dietary pattern, not to the typical Western diet,” she maintained.

“Eggs do contain nutrients with real brain health relevance, but we need to assess the full dietary pattern, cardiometabolic health, labs, and individual metabolic markers before drawing any conclusions about what eggs mean for any one person.”

– Michelle Routhenstein, MS, RD, CDCES, CDN

“It is also important to recognize that some of the funding came from the American Egg Board and the headlines need to be in check with the details of the study, what the actual study looked at and found,” the dietitian cautioned.

What are some caveats about egg consumption?

Routhenstein also outlined some potential health drawbacks to upping egg consumption, while stressing that overall it’s not a bad idea to include eggs in our diets.

Whether or not a person should start eating more eggs is always a matter of personal health context, said the dietitian.

“Eggs aren’t a ‘free’ food, but they’re not automatically off-limits either,” she told us. “They do contribute saturated fat and dietary cholesterol, so whether adding an egg makes sense really comes down to what the rest of your diet looks like and whether it keeps you within your daily saturated fat target.”

“It’s also important to recognize that some people are more sensitive to dietary cholesterol than others, they are called ‘cholesterol hyper-responders’,” Routhenstein pointed out.

“In those individuals, egg yolks can raise LDL more significantly, and may need to be limited more carefully, especially if cardiovascular risk is already elevated,” she explained.

How to get brain-protective nutrients if you don’t eat eggs

There are also people who prefer a diet that mostly or completely excludes animal food products, including eggs. According to Routhenstein, there is no reason for them to worry, as long as they are making sure they’re following a nutritious diet overall.

Like Oh, Routhenstein explained that “eggs can support brain health because they contain several relevant brain protective nutrients —from choline [to] lutein, zeaxanthin, vitamin B12, selenium, [and] protein — all of which can play positive roles in memory, brain structure, and brain associated inflammation.”

“That said, the human data we have right now is mostly observational, which means we can see associations, but we can’t say eggs prevent Alzheimer’s disease,” she cautioned.

“And it’s worth knowing that most of these same nutrients can be found in other foods or through a well-planned plant-forward diet,” Routhenstein emphasized.

The dietitian advised that:

“Choline can come from foods like soy, kidney beans, quinoa, and Brussels sprouts. Omega-3s and B12 are worth supplementing, with dosing based on your labs, age, and individual needs. And lutein and zeaxanthin? Dark leafy greens have you covered.”

Eggs and brain health research: Where to from here on?

Concerning the current study, Oh outlined “several important” caveats, including that it was observational in nature, meaning that it cannot establish causation, and that “the study population is relatively health-conscious (Seventh-day Adventists), which may limit generalizability.”

She also noted that “diet was assessed at baseline only, and changes [to diet] over time were not captured” and there was “limited data on very high levels of egg consumption.”

“While the results are encouraging, they should be interpreted as part of a broader body of evidence,” Oh said.

Going forward, Oh noted she would like to see this research replicated in more diverse populations, as well as “studies examining egg consumption earlier in life and long-term cognitive outcomes, more detailed work on specific nutrients in eggs (e.g., choline, DHA) and their independent roles, research incorporating biomarkers and neuroimaging to better understand mechanisms,” and a rigorous exploration of potential causal relationships.

“Ultimately,” she shared, “we hope this work contributes to a more nuanced understanding of how specific foods fit into dietary patterns that support healthy brain aging.”

• Researchers at UC San Francisco conducted a study on the psychedelic psilocybin to find out what kind of long-term physiological impacts it can have on the brain. 
• They gave the participants their first-ever high dose of the psychedelic and compared brain scans taken before, during, and after the large dose.
• The scientists linked the psilocybin dose to changes in brain activity, structure, and mental well-being.

A new study suggests a single high dose of psilocybin may trigger brain changes that persist for weeks after the experience.

The exploratory study found that the psychedelic, which is found in “magic mushrooms,” may not only alter brain activity but may also improve mood, insight, and thinking flexibility over time. 

While the study was limited in its participant pool size, the findings add to research that examines how psilocybin could potentially support mental health.

The study is published in Nature Communications.

Exploring how psilocybin impacts the brain 

Recent research shows that psilocybin may be a treatment option for mental health conditions, such as depression, that are not responsive to standard treatments. Controlled use of psilocybin is legal in only three states, though.

The psychedelic is suspected to work by increasing brain flexibility and disrupting rigid thought patterns. However, scientists are unsure exactly how this occurs. 

In the new placebo-controlled study, researchers set out to better understand both the psychological effects of psilocybin and its potential impact on brain structure. They recruited 28 healthy adults with no prior psychedelic use.

They administered two doses of psilocybin one month apart. The scientists started with a low dose of 1 mg, which they used as a control, and then followed up with a much higher dose of 25 mg. 

The sessions took place in an environment that the study authors described as being “dimly lit, aesthetically pleasing.” The participants wore eye masks while resting on a bed and listening to music while being monitored. 

The researchers conducted EEG tests to measure brain activity during the experience and MRI scans to examine brain structure and connectivity before their psilocybin dose, as well as one month later. They also used diffusion tensor imaging (DTI) to look at the brain’s white matter pathways.

The participants also completed psychological assessments measuring insight, well-being, and cognitive flexibility multiple times after each session. 

Marked changes after one large psilocybin dose

When the researchers analyzed the data from the 1 mg dose of psilocybin, they did not note any significant changes. However, the 25 mg impacted the participants in all measured areas. 

The large psilocybin dose caused strong effects, and most of the participants described it as being the “single most unusual state of consciousness” of their lives.

During the experience, the researchers observed increased “brain entropy” on the EEG. According to the Journal of Neuroscience Methods, brain entropy is the “measure of the complexity of brain activity that has been linked to various cognitive abilities.”

This can lead to making it easier to break out of unhealthy thought patterns.

The participants with the biggest increases in brain entropy reported more psychological insight the next day and improved mental well-being at the 4-week point after taking the high dose of psilocybin.

Encouraging anatomical ‘neuroplasticity’

The researchers also found structural changes in brain pathways linked to decision-making and emotion. 

DTI scans showed changes in white matter pathways one month after the large dose of psilocybin. These shifts may reflect changed or more efficient brain connectivity.

The scientists say that if further studies confirm this, it will be the first time “anatomical ‘neuroplasticity’” was found in a psychedelic study in humans.

When speaking with Medical News Today, the senior study author Robin Carhart-Harris, PhD, a neurology professor at UCSF, touched on the psychological well-being aspect of the study.

“It will therefore be relevant to people with depression and anxiety who will typically be low in well-being,” said Carhart-Harris. “This study suggests psilocybin therapy can improve general mental health and suggests candidate brain and psychological mechanisms for how this happens.”

More research on psychedelics for mental health needed 

Zishan Khan, MD, a board-certified psychiatrist and Regional Medical Director with Mindpath Health, who was not involved in the study, spoke with MNT about the study findings.

Khan described the study as being “carefully conducted, but still early-stage,” noting that it helps link the “acute trip” to measurable brain and well-being changes over time. 

While Khan found the multimodal design a key strength, he pointed out that the small participant pool means the findings are “hypothesis-generating rather than clinically definitive.” 

Khan also said that the brain changes may reflect neuroplasticity, but interpretation remains “complex” and requires further study over a longer period of time. 

When asked about clinical use, Khan said the study adds to the growing credibility of using psilocybin as a psychiatric treatment, but the study alone does not “justify viewing psilocybin as ‘ready for primetime’ in routine psychiatric practice.”

Andrew Coop, PhD, professor and associate dean for students at the University of Maryland School of Pharmacy, who was not involved in the study, also spoke with MNT. 

“Psilocybin has the potential to be a mainstream treatment, and several Phase III clinical trials are currently ongoing,” shared Coop. “Studies such as this add to the evidence of how psilocybin works, that it is due to a combination of the physiological effects on neurons and the actual psychedelic experience.”

Coop also noted that the study gives further credibility to the new federal executive order relating to psilocybin. The order moves to accelerate psychedelic research for potential medical access for mental illness. 

“Such conditions are devastating for patients, and evidence of the mechanism of action enhances the progress of psilocybin to being able to legally and safely help patients,” said Coop.

• Perimenopause, the time of life when a menstruating person’s cycles become disrupted as that person enters menopause, can take people by surprise.
• While information and education about menopause and how it can manifest are becoming more widespread, the start of perimenopause can be harder to identify correctly.
• Board-certified obstetrician-gynecologist Sheryl Ross explains how to figure out whether or not perimenopause has started, and what to do to minimize its impact, including making different dietary and other lifestyle choices.

In perimenopause, the female body begins its transition into menopause, which signals the end of fertility and the beginning of a new stage of life.

Recently, there has been increased awareness of the symptoms of menopause, particularly hot flashes, mood changes, night sweats, vaginal dryness, and brain fog.

However, the start of perimenopause can be hard to pinpoint, though it is generally characterized by more irregular periods and changes in the blood flow at menstruation. Perimenopause can also cause symptoms like vaginal dryness and mood changes.

According to data cited by the Office on Women’s Health, typically, perimenopause occurs in a person’s 40s, and this stage lasts around 4 years, after which menopause fully sets in.

“Perimenopause happens when your ovaries stop functioning consistently, upsetting the normal hormonal rhythm. Symptoms and hormonal changes of this transitional phase usually happen within 10 years of menopause. The 40s can be a time of hormonal unrest and chaos,” Sheryl Ross, MD, board certified OB-GYN and Women’s Health Expert at Providence Saint John’s Health Center in Santa Monica, CA, told Medical News Today.

Ross shared her medical experience and top tips on how to figure out when perimenopause has started, and what lifestyle changes to adopt for a smooth transition into this next stage of life.

How do you know if perimenopause has started?

Because of this, “it can be challenging to know the difference between these two normal hormonal cycles —perimenopause and menopause,” Ross told us.

According to her, the first step is to be aware of the symptoms associated with it, which are caused by fluctuations in estrogen levels.

These can include:

• irregular, erratic, and heavy periods
• night sweats and hot flashes
• sleep disturbances
• sudden changes in mood with depression and anxiety symptoms
• short-term memory loss and trouble focusing
• vaginal dryness
• low sex drive (low libido).

“Hot flashes and night sweats are known as ‘vasomotor’ symptoms and occur as a result of fluctuating estrogen levels,” Ross told us. “They can occur with the same vengeance and disruption in both perimenopause and menopause.”

According to her, “having hot flashes and night sweats only suggests fluctuating or declining estrogen levels and does not differentiate between perimenopause and menopause.”

Still, she said, “the conversation starts with knowing your symptoms and getting blood tests, including your FSH [follicle-stimulating hormone] and estradiol levels.”

What’s the best diet for perimenopause?

Ross emphasized that perimenopause symptoms can be disruptive and that they can seriously impact a person’s quality of life on a day-to-day basis.

Still, she noted that “simple lifestyle modifications, medications specifically treating each symptom, and hormone therapy” can all help keep any bothersome symptoms in check.

First and foremost, “consulting with a healthcare provider who treats perimenopause and menopause is recommended to be given personalized care and safe treatment options,” she advised.

At the same time, she said: “A healthy lifestyle goes a long way at any time in your life, but especially in this later chapter of life. […] There are simple adjustments you can start to make as soon as you notice hormonal changes in perimenopause.”

According to Ross, dietary changes can be key to staying at the top of one’s game during perimenopause:

“A diet focused on fresh fruits, vegetables, whole grains and fish, with limited alcohol intake and little red meat — similar to the Mediterranean diet — not only benefits your heart, it improves cognitive function. The Mediterranean diet is associated with the highest life expectancy and lowest heart disease rate and is proven to help perimenopausal symptoms.”

On the same note, she emphasized, this is the time to “ditch the fast food,” explaining that “the saturated fats and excessive sodium in fast food give you no ‘value’ whatsoever; in fact, depression is more common in those who eat fast food regularly.”

“Within weeks of removing this food, you will show a decrease in cholesterol levels and even a decrease in weight gain,” Ross suggested.

She also advised that: “Removing or decreasing sweets in your diet will not only limit your calorie intake; it will often reduce your intake of fat. A reduction of sugary foods will immediately reduce blood sugar, which will help in decreasing the bloating and water retention so common in perimenopausal women.”

• Current treatments for inflammatory bowel disease (IBD) focus on reducing inflammation and relieving symptoms through therapies such as medications.
• However, some people with IBD, which includes ulcerative colitis and Crohn’s disease, don’t respond to any type of therapy.
• Two new studies found that a combination of two medications may offer better results in treating IBD than using each drug individually, especially in people where other therapies had previously failed. 

Researchers estimate that more than 4.9 million people globally are living with inflammatory bowel disease (IBD) — an umbrella term for two conditions, ulcerative colitis (UC) and Crohn’s disease, that negatively impact the body’s digestive system.

There is currently no cure for IBD. Current treatments focus on lowering inflammation and symptom relief through the use of medications, lifestyle changes, and surgery, in the hopes of achieving remission.

Unfortunately, not all medications work for everyone with IBD. Past studies show that between one-third to one-half of people with IBD don’t respond to any type of therapy.

Now, two new studies recently presented at Digestive Disease Week® (DDW) 2026 report that a combination of two medications may offer better results in treating IBD than using each drug individually, especially in people where other therapies had previously failed. 

The findings of these studies have yet to be published in a peer-reviewed scientific journal.

Two parallel clinical trials study duo drug

Scientists conducted two Phase 2b clinical trials sponsored by Johnson & Johnson in tandem — DUET-Crohn’s and DUET-UC — which examined the use of a combination fixed-dose co-antibody therapy known as JNJ-4804 that combined the medications anti-IL-23 therapy guselkumab and an anti-TNF antibody called golimumab.  

“We’ve seen an explosion of new kinds of treatments over the last 25 years to treat IBD,” Bruce E. Sands, MD, MS, Dr. Burrill B. Crohn Professor of Medicine at the Icahn School of Medicine, and chief of the Division of the Dr. Henry D. Janowitz Division of Gastroenterology at Mount Sinai Health System, and lead author of the Crohn’s disease study, told Medical News Today.

“But unfortunately, while many of these drugs are quite effective, we’re seeing a plateauing of efficacy over time. We need to keep finding new therapies that work better and hopefully are more durable and also have good safety,” he said.

Studying two-drugs-in-one

“Crohn’s disease and ulcerative colitis are very complex immunologic diseases, and there are a lot of different pathways by which the disease occurs. So we think that if we block more than one of these pathways at the same time, we might get [more] additive benefit. So the DUET studies, both Crohn’s and UC, were designed to explore this by comparing a combination of two therapies to either one of those therapies alone.” 
— Bruce E. Sands, MD, MS

“Importantly, the study only allowed patients to come into the study that had already been on [at] least one previous advanced systemic therapy mechanism,” added Maria T. Abreu, MD, executive director of the F. Widjaja IBD Institute at Cedars-Sinai, and lead author of the ulcerative colitis study. “So, for example, they could have been previously on anti-TNF, they could have previously been on anti-IL-23, [a]nd they could have been on a multiple of these.” 

“Usually the low hanging fruit is to treat patients that have been on nothing,” Abreu explained to MNT. “If they’ve been on nothing, the world is your oyster. Most things help people who have been on nothing. But those patients that have been on previous medications and that medication either lost its mojo, lost its effect, or never had an effect, are more refractory to treatment.” 

“It’s actually possible that the immune system changes because now if you suppress only one thing, the immune system tries to find a way around it to continue this inflammatory response,” she said. “And so they were essentially asking for patients to be enrolled that were the most difficult to treat patients.”

Combo therapy significantly increases clinical, endoscopic response 

Researchers recruited 693 participants for the Crohn’s study and 572 for the UC study. Participants randomly received either a placebo, just golimumab, just guselkumab, or the combination therapy JNJ-4804.

At the conclusion of the UC clinical trial, researchers discovered that for study participants who had previously tried and failed one or more therapies, JNJ-4804 showed improved outcomes when compared with golimumab, as well as similar efficacy to guselkumab across key measures of remission and endoscopic improvement at 48 weeks. While in the CD trial, the highest dose of JNJ-4804 outperformed both individual drugs.

“For patients that have failed two or more mechanisms of action, which we’re getting more and more as we expand our armamentarium, it makes a lot of sense that we’re going to be using combinations of therapy,” Abreu explained.

“Ideally, they will be rational, meaning that the therapies will be complementary in their mechanisms of action and have some thought behind them. And this is really the first foray into that, is using this combination. So I think we’ll be reserving our combination therapies, at least for now, for the patients that are the neediest patients,” she said. 

When will this therapy be available to patients?

Although the results from these trials are promising, people with IBD may have to wait longer before this therapy becomes readily available as standard treatment.

“I think the significance of these studies is not only the direct results that show that this particular combination of anti-TNF and anti-IL-23, golimumab and guselkumab, is more effective than either one alone in the patients who have failed two or more classes of therapies. It speaks more broadly to the idea that combination therapies are a promising direction for the treatment of people with IBD in general.”
— Bruce E. Sands, MD, MS

“And very importantly, at least for this combination, we hope that in future combinations, there’s no increase in safety events, so there’s no more risk to the combination,” Sands said. 

“These were phase 2B studies, so to get approved, this combination will have to enter into phase 3 studies, which are considered the registrational studies that would lead to approval of the drug,” he explained.

“And because they will be large studies and will take a while to conduct, I imagine that we wouldn’t see these approved earlier than two-and-a-half or perhaps three years. But in the meantime, there’s a lot of excitement about that,” he added. 

People with IBD may need to be treated differently

Alyssa Parian, MD, director of the Center for Inflammatory Bowel Disease (CIBD), a comprehensive program offering specialized care for patients with IBD and related colorectal conditions, who was not involved in the study, spoke to MNT about these studies.

“We are already frequently using dual advanced therapy in our practice for patients with severe refractory disease,” Parian said. “These controlled trials help solidify what we are seeing clinically, that these patients have improved response to dual therapy and provide long-term safety data.” 

“The concept of a ‘co-antibody’ therapy that targets two inflammatory pathways at once is a significant step forward. Seeing that this approach may be able to ‘outsmart’ the immune system, as Dr. Abreu mentioned, is very exciting. The fact that the combination therapy shows additive efficacy without increasing safety risks is a critical finding.”
— Alyssa Parian, MD

“Long-term monitoring for durability will be critical as there may be concerns that the immune system may continue to find ways around even dual therapies,” Parian added. 

MNT also spoke with Ashkan Farhadi, MD, a board certified gastroenterologist at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, about these two clinical trials. 

Farhadi said it’s very important for researchers to continue to find new treatments for IBD, especially for those people for whom current treatments may not be working. He explained that many times, people with IBD are considered to be a heterogeneous group under one umbrella, but this tells us that maybe they are not one disease. 

“They are different diseases that they present very similar, and we call them all the same,” Farhadi continued. “And this is maybe why some of those patients respond beautifully to one medication and the other one does not.”

Some IBD patients don’t respond to treatments

“In general, over the board, we’re having something in a range of 30-50% or sometimes 58% response rates in all these medications. And then you put them in the context that you’re having 20-30% placebo response over the board, we’re having almost 40% of people who are not responding to particular medicine.”
— Ashkan Farhadi, MD

“And if you even switch (their medication), you may not get a response,” he added. “So it’s kind of natural to think that if you just use two medications, you can get a better response. So it’s not that out of touch, if you want to think about it.” 

• Novo Nordisk announced its rebranded oral semaglutide pill, Rybelsus, will soon be available as the ‘Ozempic pill’ following a formulation change.
• The smaller, reformulated pill will be available in different dosages than the Rybelsus pill, with Novo Nordisk stating it provides the same efficacy and safety profile as the original formulation.
• The healthcare company also states that the Ozempic pill will be available nationwide through pharmacies, telehealth, and mail-order services.
• Pricing is expected to vary by coverage, with insured patients potentially paying $25 for up to 3 months, while self-pay options are estimated between $149 and $299 per month depending on dose.

Semaglutide is a glucagon-like peptide 1 (GLP-1) receptor agonist that mimics a hormone to increase insulin secretion, slow gastric emptying, and reduce appetite.

The medication has Food and Drug Administration (FDA) approval for helping with long-term weight management and treating type 2 diabetes.

For many people, semaglutide is better known as the injectable drug Ozempic. However, many may not be aware that semaglutide has been available in oral form since it was approved by the FDA in 2019.

After previously announcing a rebrand and reformulation to Rybelsus in February 2026 to make the treatment more easily recognizable and bioavailable, Novo Nordisk announced that the “Ozempic pill” will be available for adults with type 2 diabetes in the United States starting Monday, May 4, 2026.

Highlighting that the oral pill can help improve blood glucose control alongside diet and exercise, while also reducing major cardiovascular events in adults with type 2 diabetes at increased risk, the pharmaceutical company adds that the pill will be available through 70,000+ U.S. pharmacies nationwide and select telehealth providers.

Rebrand and reformulation

Novo Nordisk’s Rybelsus was the first oral GLP-1 receptor agonist product approved by the FDA for the treatment of type 2 diabetes. It was available in 3 milligram (mg), 7 mg, and 14 mg tablets.

The oral pill was designed to help improve blood glucose control alongside diet and exercise, while also offering additional cardiometabolic benefits in certain high risk patients.

Now rebranded as the Ozempic pill, the updated formulation is available in different strengths of 1.5 mg, 4 mg, and 9 mg. In the press release, Novo Nordisk states that the Ozempic pill formulation is more bioavailable and works similarly to the Rybelsus tablets, offering the same efficacy and safety profile as the original formulation, but in a smaller pill.

The pharmaceutical company adds that people should take the new formulation the same way as before, so that people who were taking 3 mg should now take 1.5 mg, and so on.

While both injectable Ozempic and oral Rybelsus contain semaglutide and have approval for type 2 diabetes, Novo Nordisk suggest the brand name Ozempic is more synonymous with GLP-1 medications, hence the rename.

“While the oral form of semaglutide has been available for years as Rybelsus, the Ozempic branding is more widely recognized, which may lead to increased patient requests,” Mir Ali, MD, bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, told Medical News Today.

“Additionally, because the oral form has a longer shelf life, it may offer logistical advantages for certain prescribing patterns,” Ali explained.

Oral or injectable?

The choice between oral and injectable formulations is typically down to individual factors and preferences. It is advisable for a person to discuss options with their healthcare professional.

Generally, research suggests that injectable semaglutide achieves significantly greater HbA1c reductions compared to oral forms in those with type 2 diabetes.

Additionally, while the daily oral form may be preferable to weekly injections, research suggests that adverse events occur more frequently with oral semaglutide.

Speaking to MNT, Ali noted the potential advantages and disadvantages of oral GLP-1 medications:

“The primary advantages of oral GLP-1 medications are that they are easier to take, transport, and store. They are also typically less expensive to manufacture, which could lead to lower costs for patients. The disadvantages are that they are slightly less effective than injections and require daily instead of weekly administration.”

Pricing and access plans

Novo Nordisk also outlined pricing arrangements they suggest will improve access to the Ozempic pill. For insured individuals, the medication may be available for $25 for up to a 3-month supply.

Self-pay options, available through Novo Nordisk’s pharmacy and select telehealth providers, are expected to range from approximately $149 to $299 per month, depending on dose strength, defining a month’s supply as one bottle of 30 pills.

This may offer a cheaper alternative to injectable Ozempic, as while a 3-month supply may also be available for $25, self-pay patients can expect to pay $349 per month for doses up to 1 mg and $499 for the 2 mg dose.

“Pricing and insurance coverage are significant factors in medication adherence,” Ali told MNT.

“High out-of-pocket expenses make patients less likely to seek or maintain treatment. Consequently, if costs remain high, individuals in lower socioeconomic areas with limited health coverage will face significant barriers to accessing these medications,” he added.

A shift toward oral GLP-1 treatments?

The rebrand of the Ozempic pill may reflect a broader shift in diabetes care toward GLP-1–based therapies, with the FDA approving Foundayo, an oral GLP-1 receptor agonist from Eli Lily, in April 2026.

While GLP-1-based therapies have traditionally been administered via injection, the oral formulations aim to provide a more convenient alternative for those who prefer not to use injectable medications.

Novo Nordisk adds that the pill is manufactured end-to-end in the U.S. and will be widely distributed through established pharmacy networks. They also note that this is the first time oral semaglutide for type 2 diabetes is being offered through their direct-to-patient service.

“Accessibility is critical, especially as these medications are in high demand and have faced shortages,” Ali highlights. “Lack of access often leads patients to switch to less effective alternatives or discontinue treatment entirely.”

Beyond blood sugar control, Novo Nordisk also states that the Ozempic pill is also approved for reducing the risk of major cardiovascular events, including heart attack, stroke, or death, in adults with type 2 diabetes who are at elevated risk.

“Real-world cardiovascular benefits are linked to weight loss, improved blood pressure, and reduced inflammation,” Ali notes. “Some studies have shown a reduction in major adverse cardiovascular events by 18-20%. Patients with diabetes, obesity, and existing atherosclerotic cardiovascular disease stand to benefit the most.”

• A person’s brain health is affected by their physical and psychological health, experiences from infancy throughout their lifetime, and some environmental factors.
• Healthy lifestyle habits, such as eating a healthy diet, not smoking, not drinking to excess, getting adequate exercise and sleep, and avoiding stress, can all help improve brain health.
• In a statement published last week, the American Heart Association outlined how promoting healthy lifestyle behaviors, improving environmental conditions, and expanding access to health, social, and mental health care can protect brain health and reduce the risk of stroke and dementia.

Worldwide, the number of people ages 65 and over is expected to exceed 1.5 billion by 2050. And the goal is to remain healthy for as many of those years past 65 as possible. With cases of dementia rising, a key part of healthy aging is maintaining cognitive function and a healthy brain.

Last week, the American Heart Association (AHA) published a scientific statement outlining how experiences throughout a person’s life can affect brain health and how a person can improve their brain health.

The statement, which focuses on physical and psychological variables throughout life, highlights strategies that can help a person maintain brain resilience into older age.

“The main takeaway is that brain health is not determined only by age or genetics. It is shaped across the entire lifespan by a combination of physical health, mental health, sleep, lifestyle, social support, environment, and access to care. The American Heart Association statement is important because it reframes brain health as something we can influence much earlier and more broadly than we used to think.”

— Dung Trinh, MD, internist, of MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA

Experiences throughout life affect brain health

It has long been known that keeping your heart and blood vessels healthy is key to brain function, but this statement also focuses on other factors that affect brain health.

The statement highlights 10 factors that can adversely impact the health of a person’s brain:

• Early life infections
• Adverse childhood experiences
• Socioeconomic factors
• Chronic medical conditions
• Stress
• Anxiety and Depression
• Pollution and environmental exposures
• Chronic inflammation
• Disruption of the gut microbiome (dysbiosis)
• Poor sleep quality

These factors can affect the body in several ways, in turn affecting brain health.

“Many of the habits we think of as ‘heart healthy’ turn out to be ‘brain healthy’ too. This statement reinforces that idea, while also highlighting factors that do not always get enough attention in research or in everyday clinical care. One of the most important messages is that brain health is shaped across our entire lives and not just in old age. Experiences and choices made early in life can have a real impact decades later,” Melinda (Mindy) Patterson, PsyD, an Assistant Professor of Neurology with the University of Rochester Medicine, told Medical News Today. 

“That also means there is good news: no matter what stage of life you are in, there are steps you can take to lower your risk of stroke and cognitive decline,” she added.

Protecting brain health not just up to individuals

“The AHA statement also reminds us that brain health is not just an individual responsibility. Environment, education, food access, health care access, housing, pollution exposure, and social support all matter. So the future of dementia prevention is both clinical and public health oriented.”
— Dung Trinh, MD

The statement says governments should enforce policies to control air pollution and improve air quality, as pollution from sources such as pesticides and microplastics can lead to neuroinflammation, oxidative stress, and neurodegeneration. It also advocates adherence to routine vaccination schedules to help people avoid infections that can damage brain health.

It highlights that a multifaceted approach to address socioeconomic factors (eg, geographic location, race) and systemic inequalities to promote equitable access to resources and opportunities (eg, safe housing, healthy foods, education, healthcare, and mental health services) is needed to ensure that these social determinants of health do not adversely affect brain health.

How to protect brain health: Sleep, diet, exercise, and more tips

The AHA advises that straightforward lifestyle changes can positively impact brain health, and that both individuals and clinicians play a role.

Trinh echoed Patterson in advising that what is good for the heart is generally also good for the brain.

“First,” he told us, “control vascular risk factors. High blood pressure, diabetes, high cholesterol, obesity, and smoking are major threats to long-term brain health. Blood pressure control is one of the most important modifiable steps we have.”

“Second, prioritize sleep. Poor sleep and untreated sleep apnea can affect memory, attention, mood, inflammation, and vascular health. Sleep should be treated as a brain-health intervention, not as a luxury.”

Both Trinh and Patterson advocated regular physical exercise, with Patterson calling it: “The most important factor in preventing dementia and supporting brain health in the long term.” 

Trinh explained why exercise is so beneficial: “Physical activity improves blood flow, metabolic health, mood, sleep, and cognitive resilience. Even walking consistently can be meaningful.”

Diet is equally important. Trinh noted that the AHA statement highlights the emerging role of gut health and the gut-brain connection, telling MNT that people should “eat in a brain-healthy pattern. I generally recommend a Mediterranean-style diet: vegetables, fruits, legumes, whole grains, nuts, olive oil, fish, and fewer ultra-processed foods and added sugars.”

And he emphasized that people should protect their mental health and social connections.

“Chronic stress, depression, anxiety, and loneliness are not separate from brain health. They are part of the biology of aging. Social engagement, purpose, stress reduction, and treatment of mood disorders should be considered part of dementia-risk reduction,” Trinh added.

“Finally,” he told MNT, “avoid smoking, heavy alcohol use, and substance misuse, all of which can accelerate vascular and neurologic injury.”

Do I have to make these lifestyle changes all at once?

This may seem like an awful lot to think about, but Patterson advised that people do not have to make lots of changes all at once to help protect their brains as they age:

“For many people, reading about all the things that can lower the risk of dementia feels overwhelming. When I work with patients, I encourage them to pick one or two things to focus on and start there. People are much more likely to succeed at making healthy changes when they set small, realistic goals.”

“Instead of trying to change your entire diet at once, try adding one extra serving of vegetables each day, or cut back on sugary foods. Instead of going from no exercise to working out every day, try adding just one active day to your week. Once you hit those smaller goals, you start to build confidence and momentum — and from there, making even more changes becomes much easier,” she told us.

“It’s never too early, and it’s never too late, to start protecting your brain.”
— Melinda (Mindy) Patterson, PsyD

.

• A new study examined the impact of alcohol consumption in healthy adults who did not report drinking more than the accepted ‘low-risk’ alcohol limits. 
• Using MRI scans, the researchers found a correlation between higher alcohol intake and lower brain blood flow.
• Additionally, they saw that this effect was more pronounced in older adults.

Whether someone is grocery shopping or dining out, alcohol is almost everywhere. While moderate alcohol use is considered “low-risk,” more research is coming out that shows there may truly be no safe amount of alcohol.

A new study focused on healthy adults who consume alcohol moderately. The research team wanted to see if drinking has any neurological impact on adults who consume alcohol in a relatively “safe” way.

The findings are published in the journal Alcohol.

Challenging the idea of ‘low-risk’ alcohol intake

Alcohol consumption is common in the United States. According to the National Institutes on Alcohol Abuse and Alcoholism, around 85% of adults 21 and older reported drinking alcohol at least once. 

The Centers for Disease Control and Prevention (CDC) advise limiting alcohol use and says that people who do drink should do so moderately. They recommend that women limit themselves to 1 drink per day and men to 2 drinks per day.

Older, outdated research found that moderate alcohol use could have some health benefits, such as positive psychological benefits and a reduction in heart disease, but newer research is moving away from those hypotheses.

More recent research shows that moderate alcohol use can contribute to DNA damage and may even raise the risk of developing certain types of cancer.  

The researchers in the new study wanted to expand research on the potential impacts moderate alcohol use may have on the brain. 

They studied 45 healthy participants between the ages of 22 and 70 who did not have a history of alcohol use disorder. 

The researchers administered a series of questionnaires to determine the participants’ lifetime alcohol use and to also screen out factors that could impact brain health, such as neurological disorders, psychiatric conditions, and recent substance use.

Next, the researchers used MRI scans to measure cortical thickness, brain volume, and blood flow, also known as perfusion. 

The scientists next analyzed how alcohol consumption related to these brain measurements, including the combined effect of age and total lifetime drinking. 

Reduced brain blood flow, especially in older adults

The analysis of the MRIs and the participants’ self-reported alcohol use showed that moderate alcohol consumption may not be safe. 

The results showed that low levels of alcohol consumption were associated with reduced brain blood flow, which is important for delivering oxygen to the brain.

Also, people who reported higher monthly averages of alcohol consumption showed a greater reduction in blood flow compared to people with lower monthly averages of alcohol consumption. 

Reduced blood flow in the frontal and temporal lobes is significant because these areas control thinking, memory, and language. Over time, this reduced blood flow could contribute to cognitive decline. 

The scientists also found that these effects were amplified in older adults. The combination of getting older and having a higher lifetime alcohol intake was linked to widespread lower blood flow across most regions of the brain.

They also noted that older adults who had a higher average lifetime alcohol intake had thinner brain cortices. A thinner cortex in older adults may increase the risk of cognitive decline or dementia.

The study authors think that oxidative stress is a potential explanation for these findings. Oxidative stress causes cellular damage and is linked to aging and inflammation. 

Lead study author Timothy C. Durazzo, PhD, a professor at Stanford, spoke with Medical News Today and explained what is next for this research.

“[The] next steps are to investigate the associations of low-level drinking with measures of balance, coordination, and dexterity, in a larger group of participants, which are currently underway,” said Durazzo. 

He explained that a much larger study is needed to confirm the study findings: “The number of participants in our study, particularly for the blood flow measures, was very modest […] and requires replication, in a much larger group of participants, to verify the findings of our study.”

Durazzo also told MNT that the findings would not impact current guidelines due to the smaller participant pool.

Findings are a ‘warning signal’

Dung Trinh, MD, internist of MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic, spoke with MNT about the study.

“For many years, the public message was that light or moderate drinking may be harmless, or even beneficial in some cases,” said Trinh. “This study challenges that older idea by suggesting that even alcohol intake within traditional ‘low-risk’ ranges may be associated with measurable brain changes.”

Trinh mentioned that the study was “especially interesting” since its participants were healthy and had no history of alcohol abuse. 

However, he emphasized that the study is “small and observational” and would not impact alcohol intake guidelines at this point.

“It should be viewed as a credible warning signal rather than proof that low-level alcohol directly causes brain damage. The main takeaway is that ‘low risk’ does not mean ‘no risk‘.”

– Dung Trinh, MD

Trinh would like to see further research in this area, including expanding the study to include a larger population and more diverse groups.

• We’ve rounded up the latest research from this past month on the health benefits of vitamin D supplements.
• Among the studies we’ve covered as of late is one on a genetic link between vitamin D supplementation and reduced risk of type 2 diabetes.
• Another study examines the link between higher vitamin D levels and biomarkers of Alzheimer’s disease.
• And lastly, a study examines the effects of vitamin D on the immune system in the context of inflammatory bowel disease (IBD).

Vitamin D, also known as the sunshine vitamin, is often touted as a cure-all, but does its hype live up to the evidence?

Past research has shown that vitamin D, which, in a technical sense, is actually a hormone or prohormone, can benefit health in multiple ways, most notably bone and dental health, the immune system, and cardiovascular health.

However, very high doses of vitamin D have also been linked to health risks such as nausea, vomiting, and weakness, which underscores the importance of seeking medical supervision before taking such supplements.

Medical News Today has compiled three of the latest pieces of research investigating the benefits of Vitamin D and summarized their key findings.

Can vitamin D help prevent diabetes?

Published in the journal JAMA Network Open in April 2026, this study highlighted how vitamin D supplements can affect health outcomes depending on an individual’s genetics.

What did the researchers find?

The researchers found that high dose vitamin D supplementation reduced the risk of type 2 diabetes for some people, but had no significant effect for others.

Particularly, people with the AC or CC variants of the vitamin D receptor gene had a 19% decrease in their risk of prediabetes developing into type 2 diabetes when taking 4,000 IU/day.

However, the researchers and medical experts Medical News Today spoke to underscored the dangers of taking too much vitamin D, while reiterating that these findings would need to be replicated in larger trials.

Diabetes is also a complex condition, where nutrition, genetics, exercise, weight, sleep, and many factors play a role in its development and progression, so a supplement alone is likely to do little in terms of prevention.

Why is this study important?

This study adds to growing evidence that healthcare is evolving toward individualized solutions and precision medicine.

Though genetic testing is not a widespread practice and remains costly, the study makes a case for identifying patients who will benefit the most from a preventive solution or treatment

Vitamin D is also inexpensive and generally safe as a supplement, which could be valuable in efforts to reduce rising rates of type 2 diabetes.

“It’s promising, and my reaction is cautious optimism. The study suggests that vitamin D administration, in high risk individuals with certain genetic types, may be beneficial in preventing diabetes. It shows that in the future, we may be doing genetic testing to help determine if certain therapies can be used,” Jennifer Cheng, DO, chief of endocrinology at Hackensack Meridian Jersey Shore University Medical Center in New Jersey, who wasn’t involved in the study, told MNT.

Can vitamin D help protect against Alzheimer’s?

Published in Neurology Open Access, an official journal of the American Academy of Neurology, in April 2026, this study found that higher vitamin D levels were associated with lower tau protein levels, a key biomarker for Alzheimer’s disease, years later.

What did the researchers find?

Researchers from the University of Galway found that people with higher vitamin D levels in early middle age had lower tau protein levels on brain scans conducted an average of 16 years later.

However, they found no such link between beta-amyloid, another major biomarker for Alzheimer’s, and vitamin D levels in the blood.

Why is this study important?

This study serves as a reminder that modifiable risk factors are crucial in prevention or slowing down disease progression in Alzheimer’s and related dementias. If vitamin D deficiency can be addressed and treated earlier, the researchers hypothesize that this could reduce future dementia risk.

However, the study sample was small and homogeneous, participants had their vitamin D levels checked only once at the beginning of the study, and many other factors, such as lifestyle, may have affected the outcomes.

Steve Allder, MD, a consultant neurologist at Re:Cognition Health in London, the United Kingdom, who was not involved with the study, explained to MNT:

“Higher vitamin D levels may simply be a marker of overall better health rather than the driver of reduced tau pathology. For example, individuals with higher vitamin D are often more physically active, spend more time outdoors, and may have healthier diets, all of which are independently linked to better brain health.”

Can vitamin D help treat IBD?

Published in the journal Cell Reports Medicine, this study suggested vitamin D supplements may benefit those with inflammatory bowel disease (IBD) by helping ‘reset’ the gut’s immune system.

What did the researchers find?

Researchers monitored 48 adults with Crohn’s disease or ulcerative colitis, both of which fall under the umbrella of IBD, for 12 weeks and found that vitamin D helped reduce gut inflammation while promoting a more balanced immune response.

Vitamin D increased levels of the antibodies IgA and decreased levels of IgG, which helped the body recognize good gut bacteria while simultaneously preventing it from launching unnecessary attacks, as is what happens with an overactive immune system.

Why is this study important?

Although exploratory due to its scale and scope, this study could help change how we approach the treatment of inflammatory bowel disease (IBD), adding to the evidence that vitamin D could be an adjunct therapy.

In contrast to traditional treatments, which are based on suppressing the immune system, this study promotes “immune tolerance,” retraining the gut and immune system to coexist peacefully with gut bacteria.

John Mark Gubatan, MD, study author, and gastroenterologist at Mayo Clinic in Jacksonville, Florida, explained to MNT:

“Our exploratory study highlights [that] there could be potential benefits with vitamin D in controlling the interactions between the immune system and gut microbiome in patients with IBD and that further work is needed to understand the exact vitamin D levels and vitamin D supplementation strategies to support this in patients with IBD and other chronic inflammatory diseases.”

If you’d like to read more about our previous coverage on vitamin D, including the link between second heart attacks and vitamin D3 supplements, how vitamin D deficiencies can affect respiratory infection risk, and how vitamin D2 supplements compare to D3, check out our health news hub.

• The use of GLP-1 medications for weight loss continues to rise. 
• One drawback associated with GLP-1 medications is that weight loss not only includes fat loss, but muscle loss as well. 
• A new study found that over time, the majority of weight loss from GLP-1 medication was from fat loss, and not muscle loss.

The use of glucagon-like peptide-1 (GLP-1) receptor agonists for weight loss, like Zepbound and Wegovy, continue to rise. Recent polls report that one out of every eight Americans are currently taking a GLP-1 medication to either help lose weight or treat a chronic disease.

And with the recent approval by the Food and Drug Administration (FDA) of the Wegovy pill for weight loss, researchers expect GLP-1 medication usage to continue to grow. 

One potential drawback associated with GLP-1 medications is that weight loss not only includes fat loss, but muscle loss as well, with some studies finding that about 30% of the weight loss from GLP-1s may be contributed to loss of lean mass, or muscle mass.

Now, a new study published in the International Journal of Obesity has found that, over time, the majority of weight loss from GLP-1 medication was from fat loss, and not muscle loss.

Lean body mass loss lower than fat body mass after 12 months

For this study, researchers analyzed findings and data from 36 previously-conducted studies. The selected studies examined the impact of GLP-1 and dual GLP-1/GIP agonists on weight loss and body composition changes in adults who were overweight or obese, and who may or may not have type 2 diabetes.

Upon analysis, scientists found that after using the medications for 3 months, participants experienced a loss of about 9% of their starting weight.

This weight loss included noticeable decreases in visceral adipose tissue — or abdominal fat — as well as fat body mass, waist circumference, and their body mass index (BMI). 

However, after 3 months, researchers discovered only a modest loss in lean body mass. 

Then after 12 months of GLP-1 usage, researchers reported that participants experienced major reductions in visceral adipose tissue and fat body mass.

And while there was apparent lean body mass loss, scientists found it was relatively modest when compared to the amount of body mass loss.

Not the first study to question GLP-1s and muscle loss

Medical News Today spoke with Mir Ali, MD, a bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, about this study. 

Ali commented that this study’s findings align with his clinical experiences.

“Patients primarily lose fat when using these medications,” he explained. ”While some muscle loss may occur, the majority of the weight loss is fat loss.” 

This is not the first study to show that weight loss from the use of GLP-1 medications may be lower than we think. 

A study published in August 2025 found that lean muscle mass loss via a mouse model was less than previous studies had reported, and also found that a good portion of the lean muscle mass decrease came from other tissues, such as the liver, rather than from skeletal muscles.

And research presented at the European Congress on Obesity (ECO 2025) reported that adults taking GLP-1 drugs were able to retain muscle while losing weight by strength training and eating enough protein.

Crucial importance for more studies on GLP-1s and body composition

MNT also had the opportunity to speak with Douglas R. Ewing, MD, FACS, DABOM, medical director of the Center for Weight Loss and Metabolic Health at Hackensack University Medical Center in New Jersey, about this study. 

Ewing commented that as a doctor who treats patients who may be taking a GLP-1 medication, his first reaction to the study’s results was one of measured approval.

“It provides a robust meta-analysis that confirms what many of us have been observing in clinical practice: GLP-1 receptor agonists are effective for weight loss and, importantly, this weight loss appears to be of ‘high quality,” he explained. “This means patients are losing more fat mass than lean body mass, which is a critical factor for long-term health.”

Ewing said it’s crucial for researchers to continue examining how GLP-1 medications impact a person’s body composition for several reasons. He detailed:

“Muscle is more metabolically active than fat. A significant loss of muscle mass can lower a person’s metabolic rate, making it more challenging to maintain weight loss in the long run. Preserving muscle mass is essential for maintaining strength, mobility, and overall physical function. This is particularly important for older adults, who are already at a higher risk of falls and frailty.”

“Rapid weight loss can sometimes lead to sarcopenia, a condition characterized by the loss of muscle mass and function,” Ewing continued. “Continued research can help identify strategies to mitigate this risk, especially in vulnerable populations.“

“If a person loses a significant amount of muscle while on a GLP-1 and then stops taking the medication, they may be more prone to regaining weight, and this regained weight may be primarily fat,” noted Ewing.

How can you retain muscle while on GLP-1 medication?

For readers who may be taking a GLP-1 medication or considering taking one, Ewing offered these tips on how you can help retain muscle while still losing weight:

• prioritize protein: “Protein is the building block of muscle — I recommend patients should eat at least 1.0-1.2 grams of protein per kilogram of their ideal body weight,” Ewing said. Good sources of protein include lean meats, fish, eggs, dairy, tofu, and legumes.
• incorporate resistance training: Ewing said this is non-negotiable. “Strength training at least two to three times per week is vital for stimulating muscle growth and preserving lean body mass,” he explained. “This can include lifting weights, using resistance bands, or doing bodyweight exercises like squats and lunges.”
• don’t neglect aerobic exercise: Aim for at least 150 minutes of moderate-intensity aerobic activity each week, such as brisk walking, Ewing advised. “This is not only good for cardiovascular health but also helps with overall energy levels and can make it easier to stay consistent with workouts,” he added. 
• get adequate sleep: Quality sleep is essential for muscle repair and growth, Ewing said.
• work with a team: “I encourage my patients to work with a registered dietitian to create a personalized nutrition plan and a physical therapist or certified trainer to develop a safe and effective exercise routine,” Ewing added. 

• Worldwide, the number of people with obesity has more than doubled since 1990, with at least 16% of all adults now having the condition.
• Many health conditions are linked to obesity, among them cardiovascular issues, breathing problems, type 2 diabetes, and impaired mobility.
• A new study has found that for people with severe obesity and heart failure, losing weight can reverse some of the damage to the heart muscle.
• This, together with the results of another study that found impaired lung function in people with obesity, suggests that losing weight could help people with obesity to improve both their heart and lung health.

The number of people with obesity — having excessive fat deposits and a body mass index (BMI) greater than 30 — continues to increase around the world. Now, more than 16% of all adults worldwide are living with the condition. In the United States, the National Institutes of Health reports that 42.4% (2 in 5) of all adults have obesity.

Heart failure — where the heart does not circulate blood efficiently — is more common in people with obesity than those of a healthy weight. One study found that obesity doubled the risk of heart failure; another that obesity is a factor that causes both heart failure and death from heart failure. 

Heart failure with preserved ejection fraction (HFpEF) — a condition where the heart pumps normally, but does not fill properly because the heart muscle stiffens — accounts for around half of all cases of heart failure, and is more common in people with obesity than other types of heart failure.

Now, a study has found that losing weight can help reverse the effects of HFpEF and improve the contraction ability of heart muscle cells.

In the study, published in Science, researchers found that in people with severe obesity and HFpEF, those who lost more than 2kg/m² of BMI with GLP-1 agonist treatment saw improvements in heart muscle contraction.

Chemical changes in heart muscle tissue due to obesity

The researchers analyzed heart muscle cells (myocytes) taken by biopsy from 80 patients with obesity and HFpEF. They divided them into 2 groups — group 1 was cells from patients with a lower BMI (30 people), and group 2 was those from patients with more severe obesity (50 people).

As well as having substantially higher BMIs, people in group 2 had a greater incidence of other co-morbidities, including insulin resistance and sleep apnea.

Heart muscle cells from patients with HFpEF and severe obesity had a greatly reduced ability to increase force, which affects the ability of the muscle to contract. Cells from those with less severe obesity and HFpEF, and those without heart failure were more able to increase force.

The researchers found that cells from those with HFpEF and severe obesity showed similar changes to cells from people in end-stage heart failure, who were awaiting heart transplants.

The key change researchers discovered was in a protein, troponin-I, that is vital for contraction and relaxation of muscle in people with severe obesity and HFpEF. People who were more obese had greater phosphorylation of troponin-I, which the researchers showed weakened the force of the muscle cells.

David Kass, MD, the Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine, and corresponding author on the study, said that no drugs that might reverse this change had yet been approved by the FDA:

“There have been some efforts along this line, and some drugs worked quite well in cells — even human heart HFpEF cells — but failed in clinical testing where the drug appeared to have no effects at all. More work is needed, both academic and from industry around finding such drugs,” he told Medical News Today.

Linking obesity, heart failure, and impaired lung function

So why does obesity increase risk of heart failure, particularly HFpEF? Naveed Sattar, Professor of Cardiometabolic Medicine at the University of Glasgow, UK, explained to MNT:

“Obesity impacts blood volume, blood pressure, and so the pressures the heart has to work against. It also impacts how much tissue needs to be perfused [provided with blood] and it impacts kidney and inflammation pathways and some aspects of heart function in the left atrium, so that all the collective effects of obesity can lead to signs and symptoms of heart failure even if the main pump — the left ventricle — remains in good order in HFpEF.”

Kass explained how the prevalence of HFpEF has changed:

“When HFpEF was mostly found in older individuals who had poorly controlled chronic high blood pressures and ventricular hypertrophy that formed in response to this, obesity was much less common. Over the past 20 years, we have treated these comorbidities better, while obesity and severe obesity are increasing in prevalence substantially.”

But he reassured that, although the epidemiological association between severe obesity and HFpEF is well established, only around 5% of people with severe obesity in the United States have HFpEF.  

Heart function is not the only thing affected by obesity. A study presented last week at the American Physiology Summit in Minneapolis highlighted that, in older adults, obesity adversely affects lung function. The results of the study have yet to be published in a peer-reviewed scientific journal.

In their study, researchers reported that not only did those with obesity have significantly lower lung capacity, which limits the amount of air that can be inhaled, but they also were unable to fully empty their lungs when exhaling. These issues can cause chronic shortness of breath, wheezing and inefficient breathing, symptoms that are also seen in people with HFpEF.

Losing weight can reduce issues with heart and lung function

In the heart study, a subset of 16 patients, with a mean BMI of 39, undertook a 1.5 year course of weight-loss therapy, using GLP-1 receptor agonists (GLP-1RAs), injectable treatments used to treat both obesity and type 2 diabetes.

Their muscle cells regained contraction abilities and, in those who lost 10% or more of their body weight, their cells recovered to almost normal peak muscle cell force.

Kass suggested why this might have happened: “One possibility [is] that the change in the muscle protein — troponin I — that we highlight in [our study], that increased in tandem with BMI in the HFpEF patients, was reversed in those that lost weight.”

“We also show that in HFpEF patients, the capacity of of the heart muscle to contract to calcium declined in direct relation to the BMI increase; so we are in a way then reversing that same association — lower BMI [led to] greater calcium-tension response,” he added.

However, he cautioned that: “Much still needs to be done to confirm the exact biological changes that occur with the GLP1-RA treatments that are involved.”

Cheng-Han Chen, MD, board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, concurred: 

“Recent research does suggest that GLP-1 receptor agonists may have direct effects on the health and function of heart muscle cells. However, more research is necessary to determine whether these direct effects are responsible for the beneficial effects of GLP-1 RAs, rather than their effects on weight loss.”

“It’s become clear that large scale weight loss is already something many heart failure experts wish for their patients living with obesity with HFpEF, given such meaningful symptom and functional benefits, never mind the potentially many other comorbidity benefits. We now view obesity as a major target in HFpEF management.” 
— Prof. Naveed Sattar

• A study suggests that a 10-minute daily exercise program that a person performs lying down could significantly help to improve balance, agility, and trunk flexibility.
• The researchers suggest the improvements may be driven by changes in neuromuscular coordination, or how the brain and muscles work together, rather than increases in muscle strength or power.
• While the study involved healthy young adults, with the exercises being low intensity and performed in a stable, lying position, it may offer a safe and practical option for fall prevention and early stage rehabilitation.

Maintaining balance in humans is more complex than it may seem and requires proper alignment, whether standing still or moving.

The body coordinates a lot of information to support balance, allowing people to move more easily and put less strain on joints and muscles. However, with poor balance, even simple tasks can feel hard and the risk of falling or experiencing joint disorders increases.

The body’s center of gravity sits relatively high, and much of its mass is concentrated in the head and trunk. To stay upright and move efficiently, these heavier segments must be carefully aligned and supported by coordinated movements of the legs.

This relationship requires that the trunk and lower limbs work together seamlessly. When this coordination is disrupted, it can contribute to low back pain, inefficient movement, and reduced stability.

While many exercise programs target either core strength or leg strength separately, fewer strategies focus on integrating the two systems.

Now, a study published in PLOS One suggests that just 10 minutes of brief, low intensity exercise performed lying down, or in a supine position, that promotes coordination of these two systems could lead to measurable improvements in balance and agility.

A simple program, done lying down

To address this gap, a team led by researchers at Tokyo University of Agriculture and Technology developed a short exercise routine performed entirely in a supine position.

Performing these exercises lying down provides a wider base of support and reduces the effects of gravity, making it biomechanically stable and potentially safer for those in rehabilitation or with balancing difficulties.

The program mainly focuses on muscle control to build coordination between the core and limbs, facilitating easier, safer movement when standing.

The exercises include an abdominal press, to activate core muscles by pressing and tightening, a small bridge, to connect the abs, lower back, and hips so they work together, a leg slide and press, to train the legs to move smoothly and stay controlled, and playing ‘rock-paper-scissors’ with the toes to improve control and strength.

Study author Yoriko Atomi, PhD, Professor Emeritus at The University of Tokyo and Specially Appointed Professor at the Center for Neuroscience and Biomedical Engineering, The University of Electro-Communications, helped develop the exercise program to relieve her own joint pain.

In a background document prepared by Atomi, she emphasizes that maintaining good balance is key to staying independent and avoiding injury.

She suggests that practicing exercises can help maintain or improve balance, and reduce the risk of falls and joint pain, even as the body ages.

“I would like to share that by performing this supine exercise every day of the year as soon as I wake up, I have been able to manage issues such as knee and lower back pain,” Atomi disclosed in the background document.

Key findings of the study

The study involved healthy young adults completing a daily 10-minute session for 2 weeks, and used both randomized crossover and pre–post trial designs.

In the randomized crossover trial, 17 healthy young males completed both an exercise phase and a control phase. The researchers assessed physical fitness, including flexibility, agility, and strength, as well as static balance.

The pre-post study involved 22 males and females performing the program for 2 weeks. Researchers analyzed dynamic balance using motion sensors placed on the body during a side-step agility task.

The results across both experiments were consistent and showed improvements in balance, agility, and flexibility.

Participants showed reduced body sway during standing tasks, especially in more challenging positions with a narrow base of support. Additionally, performance in a side-step test, a measure of quick lateral movement, increased significantly and they improved in sitting trunk flexion, indicating a greater range of motion.

The researchers also found no change in strength or power, as measures such as grip strength, jumping distance, and sprint speed remained unchanged.

Speaking to Medical News Today, Atomi discussed who could benefit the most from this exercise program.

“Based on our healthy young study, we should also be cautious about directly generalizing these findings beyond the different backgrounds we studied,” she told us.

“However, because the exercises are low-load and involve relatively low physical risk, this type of program may also have potential for individuals with reduced physical function, including older adults, sedentary individuals, or those in rehabilitation settings. These groups will need to be studied directly in future research.”
– Yoriko Atomi, PhD

Why the supine position may help

Atomi highlights that the supine position frees the core from its primary function of supporting the body while standing. This makes it easier to study and train how the core and legs work together, because the body is under less strain.

“We chose the supine position because lying down reduces the postural demands placed on antigravity muscles, such as those in the back and lower limbs. This creates a simpler mechanical environment where participants may be better able to focus on coordinating the core muscles of the trunk with lower limb movement,” Atomi told MNT.

“The advantage is that this approach is low-load, relatively safe, and accessible, while still targeting important movement-control strategies that may transfer to standing posture and dynamic tasks.”

“The advantage is that this approach is low-load, relatively safe, and accessible, while still targeting important movement-control strategies that may transfer to standing posture and dynamic tasks.”
– Yoriko Atomi, PhD

The researchers add that the benefits of the exercise program are unlikely due to muscle growth, and instead suggest neuromuscular adaptations, or how well the nervous system coordinates the body and distributes weight efficiently.

“In simple terms, neuromuscular adaptation means that the body becomes better at using the muscles it already has, rather than simply building bigger muscles,” Atomi explained to MNT.

“Over a short period of time, the nervous system can improve how different body segments — such as the trunk and lower limbs — work together, making movement more efficient and coordinated.”

“In this study, we believe participants may have improved how they controlled their relatively heavy trunk and coordinated it with lower limb movement, which may have helped improve balance, flexibility, and agility even without major gains in strength or muscle size,” she added.

The supine position may not only allow the body to focus more on coordination and control, but may also lower physical strain, reduce injury risk, and also make the exercises more accessible to a wider range of people.

Interestingly, motion analysis also showed that after the program, participants stabilized their head and upper body more effectively during movement, suggesting improved central control of balance.

Potential applications

Although the study involved healthy young adults, the findings suggest broader possibilities.

A short, safe, and simple routine like this could be useful for fall prevention programs, early stage rehabilitation, or individuals with limited mobility or balance issues.

“Because the program is low-load, relatively safe, and designed to improve postural control and movement coordination, it may be particularly relevant for fall prevention or rehabilitation,” Atomi said.

“Our current findings are an early step, and future research will focus on testing its effectiveness in older adults and clinical rehabilitation populations to understand better how it can be applied in those settings,” she suggested.

While the findings are preliminary, they suggest that a brief daily exercise routine performed lying down may offer a practical and low risk way to improve balance, flexibility, and movement coordination, without the need for intense training.

The exercise program may also offer an accessible option that people can implement into their daily routine at home.

“Based on practical experience, people may gain at least some benefit from written instructions or illustrated guides alone. However, exercises involving trunk control and coordinated lower limb movement may vary in difficulty depending on the individual,” Atomi told MNT.

“Ideally, the best approach would be initial in-person instruction, along with periodic follow-up to ensure correct technique. If face-to-face supervision is difficult, video-based instruction or online guidance may also be valuable ways to improve understanding and support consistent practice,” she advised.

• For many years, we have heard about the potential health benefits of fish oil due in part to their high concentration of omega-3 fatty acids.
• Past studies have linked the consumption of fish oil to possible protection against several health concerns, including brain diseases like dementia and Alzheimer’s disease.
• A new study has found that fish oil supplements may not be beneficial for people who have experienced repeated mild traumatic brain injuries.
• Researchers believe the build-up of a specific omega-3 fatty acid could potentially disrupt brain healing and assist with the accumulation of the protein tau in the brain, via both human cell and mouse trials.

For many years, we’ve heard about the potential health benefits of fish oil due in part to their high concentration of omega-3 fatty acids.

Past studies have linked the consumption of omega-3 fatty acids or fish oil — either through oily fish or fish oil supplements — to possible protection against several health concerns, including cardiovascular disease, type 2 diabetes, rheumatoid arthritis, depression, and neurodegenerative conditions such as Parkinson’s disease, Alzheimer’s disease, and other forms of dementia.

Now, a new study published in the journal Cell Reports has found that fish oil supplements may not be beneficial for people who have experienced repeated mild traumatic brain injuries (TBI).

Instead, the build-up of a specific omega-3 fatty acid in fish oil could potentially disrupt brain healing and assist with the accumulation of the protein tau in the brain, which is considered to be a hallmark of Alzheimer’s disease, via both human cell and mouse trials.

Fish oil and repeated mild traumatic brain injuriess

For this study, researchers used a combination of models, including one with mice and another with human brain microvascular endothelial cells, to examine how long-term fish oil use might impact the brain. 

“This project developed over several years and was motivated by a broader question,” Onder Albayram, PhD, associate professor in the Department of Pathology and Laboratory Medicine within the Department of Neuroscience at the Medical University of South Carolina, and lead author of this study, told Medical News Today.

“Fish oil is widely used and generally considered beneficial, yet there are also observations in other areas of medicine suggesting that its effects may vary depending on the biological context, particularly during periods of tissue repair,” Albayram explained.

“We wanted to understand whether similar context dependent effects might exist in the brain,” he detailed. “To do this, we needed a model where the brain is actively engaged in recovery over time. Repeated mild head injury provided a useful framework, because it involves a prolonged and often subtle repair process, with elements of resilience and vulnerability.”

“In that sense, the model allowed us to study how dietary factors such as fish oil interact with the brain’s recovery mechanisms,” he continued. “The study evolved step by step, with the findings guiding the next questions.”

EPA linked to reduced brain repair capacity

At the study’s conclusion, researchers found that one specific omega-3 fatty acid in fish oil, eicosapentaenoic acid (EPA), was associated with a reduced repair capacity in the brain, potentially interfering with healing after a brain injury. 

“This was one of the most important parts of the study because it helped us move from observation to mechanism,” Albayram said.

“In the mouse model, several findings pointed toward the neurovascular unit, especially the cerebrovascular endothelial cells, as a vulnerable site after repeated mild brain injury. These cells form the inner lining of the brain’s blood vessels and help regulate blood flow, metabolic exchange, barrier function, and tissue repair. The human brain has an enormous vascular network, so even subtle changes in endothelial function can have meaningful consequences over time.”

– Onder Albayram, PhD

“Based on the mouse data, we developed an in vitro model using human brain microvascular endothelial cells to ask a more focused question: could EPA directly affect the repair capacity of these cells under conditions that allow fatty acid use?,” he continued

“What we found was that EPA, but not DHA, reduced endothelial repair responses, including vascular network formation and wound healing capacity. That was significant because it mirrored the direction of the mouse findings and suggested that EPA may act directly on the vascular repair machinery, rather than being only a secondary marker of injury,” said Albayram.

Long-term fish oil supplementation linked to tau buildup

Additionally, Albayram and his team also correlated long-term fish oil supplementation to vascular-associated accumulation of the protein tau in the cortex, as well as lower neurological and spatial learning. 

“We observed vascular associated tau accumulation in the cortex, which is a recognized but still not fully understood feature in conditions such as chronic traumatic encephalopathy,” Albayram explained.

“In human postmortem studies, tau often accumulates around blood vessels, but it is difficult to determine how this develops over time or whether the vasculature plays an active role in shaping this pathology. Our findings suggest that the cerebrovascular system, including endothelial cells, may be more directly involved than previously appreciated,” he told us.

“Importantly, these vascular changes were accompanied by neurovascular uncoupling, meaning a disruption in the coordination between neuronal activity and blood flow,” he continued. “This was observed alongside deficits in spatial learning and memory, indicating that the vascular and metabolic changes were functionally relevant. Ultrastructural analyses further supported this, showing disruption within the neurovascular unit.”

“Together, these results suggest that under certain conditions, dietary factors may influence how the brain’s vascular system adapts to injury, and that this can be linked to both pathological features, such as tau accumulation, and measurable changes in cognitive function,” Albayram added.

Moving beyond one-size-fits-all health advice

MNT had the opportunity to speak with Dung Trinh, MD, internist for the MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, about this research.

Trinh, who was not involved in the study, commented that its findings do not mean that fish oil is broadly harmful, but they do challenge the assumption that all omega-3 supplements are automatically brain-protective. 

“For patients with repeated mild head injuries, especially athletes, veterans, or people with recurrent falls, the finding that EPA may interfere with brain vascular repair is clinically important and worth paying attention to,” Trinh explained.

“Brain health is complex, and cognitive decline can come from many causes, including Alzheimer’s disease, vascular disease, traumatic brain injury, sleep problems, mood disorders, medications, and metabolic conditions. We need continued research so we can move beyond one-size-fits-all advice and develop more personalized strategies to protect memory, thinking, and long-term brain function,” he added.

Trinh advised readers not to panic about this study’s findings, and not to abruptly stop anything recommended by their physician. 

“This study does not prove that fish oil causes brain damage in the general population,” he continued. “But if someone has a history of repeated concussions or head trauma, they should talk with their doctor about why they are taking fish oil, what dose they are taking, and whether their supplement is EPA-heavy.”

How to follow a brain-healthy diet not dependent on fish oil

Meridan Zerner, MS, RDN, CSSD, LD, CHWC, founder of Meridan Zerner Nutrition in Dallas, TX, offered her top tips on how to follow a brain-healthy diet that is rich in whole foods, without relying on supplements. 

“First, I would gently and respectfully encourage people to pump the brakes a bit and have a deeper conversation with their healthcare provider,” Zerner said.

“This study does not overturn the previous broader recommendations and research. We do know that omega-3s (preferably from food) support the brain’s foundation, but repair is far more complex. It’s not one nutrient — it’s the whole environment: nutrition, sleep, blood flow, and recovery,” she emphasized. 

Zerner offered these starter recommendations for eating a brain-healthy diet focused on whole foods: 

• Eat fatty fish 2–3 times per week. Salmon, sardines, mackerel, herring, and trout are naturally rich in both EPA and DHA in a food matrix that the body may process differently than a concentrated supplement.
• Load up on colorful produce. Berries, leafy greens, beets, and cruciferous vegetables provide antioxidants and polyphenols that support the brain’s vascular health and help to reduce neuroinflammation.
• Include walnuts, flaxseeds, and chia seeds. This is small, but meaningful in that these foods provide ALA, a plant-based omega-3. While the conversion to EPA and DHA is very limited, they contribute to overall anti-inflammatory eating patterns.
• Follow a Mediterranean or MIND diet pattern. Both are supported by strong evidence for cognitive health. They emphasize olive oil, beans, whole grains, nuts, fish, fruits, and veggies which supply the brain with multiple protective nutrients.
• Stay well-hydrated and limit ultra-processed foods. The brain is roughly 73% water, and ultra-processed foods drive inflammation — the opposite of what we want for brain repair.

“This study […] is a smaller mouse study, which for most health scientists means that it raises excellent questions and definitely validates the need for actual human studies,” Zerner said.

“But again, the findings depend a lot on context — this is a rodent study, the effects observed are not universal across all omega-3 fatty acids, the dose of EPA that would create an equivalent dose in human beings is unclear, the number and severity of TBIs isn’t clear and all the mice were male,” she cautioned. 

“I would also defer to the lead researcher himself who said this is not a call for the public to abandon fish oil supplements, emphasizing that ‘biology is context-dependent’,” she added. “However, if you are an athlete in a contact sport, a military service member, or anyone at elevated risk for repetitive mild TBIs, this research does give us reason to pause and ask more questions.”

• Past research has discovered numerous health benefits of music, including improving mood, cardiovascular health, and cognitive function.
• A new study found that scientifically designed music may provide better immediate relief from anxiety than pink noise.
• When paired with auditory beat stimulation (ABS), the researchers saw that those who listened to music for as little as 24 minutes showed significantly reduced anxiety symptoms.

Many people nowadays choose to listen to pink noise, which is background sounds similar to rain or static, to relax, fall asleep, or drown out unwanted sounds such as traffic or neighbors.

But when it comes to easing anxiety, a new study, published in the journal PLOS Mental Health, shows that it may not be the best tool.

To test this, scientists explored how music, particularly music embedded with auditory beat stimulation (ABS), affected anxiety symptoms.

ABS is a technique that uses steady, rhythmic pulses of sound to shift the brain’s rhythm, switching it from a “stressed” to a “relaxed” speed/state.

As part of this study, researchers from Goldsmiths, University of London, and the University of Roehampton in the United Kingdom, and experts from Toronto Metropolitan University and the digital health company LUCID in Canada, examined whether spending more time listening to “meditative” music with embedded ABS led to greater relief in anxiety.

The researchers randomly assigned 144 adult participants, who were already taking anti-anxiety medication, to one of the following four groups:

• control group (24 minutes of pink noise): 36 participants
• 12 minutes of music + ABS group: 41 participants
• 24 minutes of music + ABS group: 33 participants
• 36 minutes of music + ABS group: 34 participants.

They used pink noise as a control group to see if music embedded with ABS actually had an effect on anxiety levels.

The researchers measured the participants’ anxiety and mood before and after the sessions using standardized clinical scales to track the immediate (acute) changes.

Longer listening leads to less anxiety

The researchers found a “dose-response” link between the amount of time people listened to music and their mood.

Participants who listened to music with ABS for 24 minutes experienced the strongest overall reduction in anxiety. People who listened to music for 36 minutes showed a “peak” effect and saw similar improvements in mood and a larger reduction in negative feelings. Those who listened for only 12 minutes did not see as great an improvement.

Participants didn’t only experience lowered anxiety, either. They also reported a general reduction in feelings like irritability, jitteriness, and distress, and felt more emotionally balanced overall.

The fact that all participants were already taking medication for anxiety and that they experienced relief with ABS and music shows that such tools may be a good complementary therapy to already existing treatments.

Medical News Today spoke to four experts — Peter Vernig, PhD, MBA, VP of Mental Health Services at Recovery Centers of America, Michael S. Valdez, MD, physician with a background in neurology and addiction medicine, Connie McReynolds, PhD, licensed psychologist specializing in ADHD, anxiety, and trauma, and Tessa Jesus, MT-BC, board certified music therapist and music integration manager at Youth Villages, to see how this intervention works.

How music helps calm anxiety

Previous research has found that music can benefit cardiovascular health and cognitive health. The effects of music on the brain and mood have also been documented by numerous studies.

“[N]euroscience has studied that music is processed in multiple areas of the brain because not only are we hearing the sounds, but we are processing the words, connecting to memories associated with that song, and potentially experiencing an emotional reaction. The activation in the brain only increases when someone is playing an instrument, singing, or even watching someone play music. We know music changes the brain,” said Jesus.

However, music embedded with ABS operates differently. To achieve this effect, first, the music starts playing at a speed that matches the person’s current heart rate, which is likely elevated due to stress/anxiety.

Then, the music slows to encourage the mood to shift into a calmer state, a phenomenon the researchers called the Iso-Principle. Thanks to the hidden pulses of ABS, the brainwaves then slowly sync up with the slower, more relaxed frequency.

What the study cannot answer yet

The study has a few limitations regarding the longevity of effects and its effectiveness as a standalone therapy.

“The study showed that, under controlled conditions, listening to 24 minutes of ABS music can help shift the brain into a calmer state. Notably, participants in the study were already on medication to treat their anxiety,” Vernig pointed out.

“The harder question [here] is durability. Does the effect last, and for whom?” said Valdez.

“What the study does not examine is the long-term effects of this kind of intervention. Although ABS music may be a helpful tool to cope with spikes in anxiety, it should probably only be used as an adjunct to other established treatments. Think of this like a rescue inhaler for asthma: it reduces acute symptoms, but does not address their underlying cause,” Vernig said.

Another limitation is whether these effects can be attributed to ABS alone or to the music.

“[I]t is important to note that utilizing headphones with good sound quality versus listening from a phone or computer will all have varying effects on the auditory beat stimulation part of this study. It is hard to differentiate whether their results are from the ABS or the music, or both, since a control group with just ABS was not utilized,” said Jesus.

McReynolds pointed out that the sample size could affect the generalizability of the results and that follow-up studies are needed.

“[T]he sample is narrow, consisting of adults with moderate anxiety who were on medication and were recruited online. Including medication dosages would have strengthened the findings, since drugs like SSRIs can cause emotional blunting that may have shaped the results. Like all promising early research, these findings will grow stronger as more independent studies build on them,” she said.

“Future studies could be strengthened by extending beyond self-report to include brain scans or physiological measures to confirm any changes that occurred in the brain,” she added.

• Vitamin D, which is mainly obtained from sunlight exposure, followed by dietary sources such as oily fish and dairy, plays an important role in our overall health.
• Previous studies have linked vitamin D deficiency to a higher risk for certain diseases, including type 2 diabetes.  
• A new study found that vitamin D supplements may help delay or prevent disease progression in those with prediabetes who also have specific variations in their vitamin D receptor gene. 

Vitamin D, obtained through exposure to sunlight and eating certain foods like fatty fish and egg yolks, plays an important role in our overall health. 

Past research shows that vitamin D is important for bone health, including keeping bones strong and helping prevent musculoskeletal issues like weak muscles, and supports the body’s immune system.

Previous studies have linked vitamin D deficiency to a higher risk for certain diseases, including cardiovascular disease, certain cancers, multiple sclerosis, dementia, and type 2 diabetes.  

Now, a new study published in the journal JAMA Network Open reports that vitamin D supplementation may help delay or prevent disease progression in those with prediabetes who also have specific variants in their vitamin D receptor gene. 

Previous research leading to the latest vitamin D study

For this study, researchers analyzed healthcare data from participants of the previous D2d study, which examined the potential effects of vitamin D supplementation on the prevention of type 2 diabetes. 

During the original study, researchers concluded that a 4000 IU daily vitamin D supplement did not result in a significantly lower risk of type 2 diabetes when compared to a placebo. 

However, researchers reportedly still wanted to know whether vitamin D supplementation could help anyone with prediabetes, which led to this study. 

In another D2d-related study, scientists discovered that blood levels of 40 to 50 ng/mL of 25-hydroxyvitamin (OH) D or higher were correlated with a substantial lowering in participants’ diabetes development risk. 

“A number of observational studies had reported an inverse association between the circulating 25(OH)D level and diabetes risk,” Bess Dawson-Hughes, MD, a senior scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, and lead author of this study, told Medical News Today.

“This was plausible because there are known vitamin D receptors in the beta cells in the pancreas, which secrete insulin. The observational data needed to be tested in a randomized controlled vitamin D intervention trial in order to establish that vitamin D actually influenced diabetes risk.” 

Vitamin D lowers diabetes risk in 2 specific gene variants

For this latest study, Dawson-Hughes and her team analyzed genetic data from about 2,000 participants of the original D2d study. 

At the study’s conclusion, researchers found that participants with the AA variant of the Apal vitamin D receptor gene didn’t respond to a daily high dose of vitamin D compared with placebo. 

However, study participants with the AC or CC gene variants did respond, experiencing a 19% lower risk of developing type 2 diabetes when taking a high daily dose of vitamin D.

“If confirmed, this finding defines an effective strategy to lower the risk of type 2 diabetes in adults with prediabetes,” Dawson-Hughes said. “Taking a single vitamin D capsule daily requires relatively little time and effort, is inexpensive, and is generally safe.” 

She also noted that these findings may aid future precision medicine for type 2 diabetes. 

“Our finding, if confirmed, would allow high dose vitamin D to be targeted to individuals with prediabetes who have the genetic potential to benefit,” Dawson-Hughes explained.

“Apart from the concept of genetic responders and non-responders, it appears from work by our lab and others that the relatively high 25(OH)D levels needed to reduce type 2 diabetes risk may, in fact, increase risk of falling in older adults. This underscores the need for clinicians to weigh the potential risk and benefit of treatment with 4000 IU per day of vitamin D in individual patients.” 
— Bess Dawson-Hughes, MD

Promise of potentially more personalized medicine

MNT spoke with Jennifer Cheng, DO, chief of endocrinology at Hackensack Meridian Jersey Shore University Medical Center in New Jersey, about this study, who commented that it’s an interesting study that highlights the importance of having a personalized approach to treating our patients. 

“It’s promising, and my reaction is cautious optimism. The study suggests that vitamin D administration, in high risk individuals with certain genetic types, may be beneficial in preventing diabetes. It shows that in the future, we may be doing genetic testing to help determine if certain therapies can be used.” 
— Jennifer Cheng, DO

“This is promising to have potentially more personalized medicine where genetic types can be analyzed to help determine if certain therapies are recommended or not,” Cheng said. “More research is needed to see if there are other factors that are associated with risk reduction.” 

Cheng said the next areas for research should be additional studies to see how different genetic factors and other factors impact the risk for the development of diabetes. 

“The development of diabetes is so multifactorial and associated with other genetic factors that we are not able to elucidate,” she continued. “Further, research and evaluation should be done to determine what are all the factors associated with increased risk of developing diabetes, to help mitigate those risk factors in high risk individuals.” 

Taking too much vitamin D may come with risks

MNT also spoke with Pouya Shafipour, MD, a board certified family and obesity medicine physician at Providence Saint John’s Health Center in Santa Monica, CA, who said that it’s important for researchers to continue to find new ways to help people potentially lower their type 2 diabetes risk because it is such a complex condition. 

“And it’s so on the rise that anything we can find to lower it, reverse it, control it, then we can control or reduce heart disease risk, we can reduce cancer, dementia, blindness, (and) nerve pain,” Shafipour detailed.

“[Type 2 diabetes is] a disease that impacts the entire body, so if we can use anything from diet, lifestyle supplements, vitamins, medications, weight loss, improving sleep, to reverse this, we can impact one’s entire life and significantly improve the quality of their life, longevity, and a lot of other disease reversal.”
— Pouya Shafipour, MD

Shafipour also said this study’s findings should be taken with a grain of salt because vitamin D supplementation helps only certain populations with this genetic variant. 

“So people shouldn’t rely on this study and then start taking high doses of vitamin D because mega doses of vitamin D can cause kidney stones, can cause toxicity, especially in people that [have obesity], as it’s a fat-soluble vitamin,” he explained.

“This is where precision medicine comes in, that they should talk to their provider about it, have their levels checked, and really see if it’s something that benefits them particularly, or do they need to take vitamin D for other reasons,” he added. 

• Research suggests the investigational drug asundexian could reduce the risk of recurrent ischemic stroke in those who have recently experienced a stroke or high risk transient ischemic attack (TIA).
• Unlike many existing anti-clotting treatments, it did not increase major or intracranial bleeding, addressing a major limitation of current therapies.
• The drug works by inhibiting Factor XIa, a clotting protein involved in harmful clot formation but less critical for normal bleeding control.
• Findings from a large Phase 3 trial suggest it could represent a new, safer approach to long-term stroke prevention.

Nearly 1 in 4 people who have previously had a stroke will experience a recurrent stroke. To help reduce this risk, clinicians will typically recommend antiplatelet or anticoagulant therapy, in addition to making lifestyle changes.

Prescribing blood thinners can help to prevent future clots and reduce the risk of recurrent, often severe, strokes. They can be particularly crucial for those with atrial fibrillation, or other high risk cardioembolic causes, with research suggesting they can reduce stroke risk by 64%.

However, while these medications are generally safe and can significantly reduce the risk of recurrent strokes, they carry an increased risk of bleeding. In particular, the most dangerous complication of anticoagulant therapy can result in bleeding in or around the brain, known as a hemorrhagic stroke.

Now, a study suggests that a new investigational medication could offer protection without the heightened bleeding risk associated with current treatments.

Published in The New England Journal of Medicine, the findings indicate that asundexian reduced the risk of a second stroke by 26% in people who had recently experienced a clot-related stroke or TIA, without increasing bleeding risk.

A long-standing challenge in stroke prevention

Preventing a second stroke remains a major clinical priority. However, current strategies can create a difficult balance, by aiming to reduce clot formation without exposing individuals to dangerous bleeding complications.

Various proteins, known as clotting factors, play a role in the formation of blood clots. The process of stopping bleeding, known as hemostasis, involves multiple interlinked steps. Therefore, targeting specific proteins may offer a viable option for reducing clot formation without complications.

Asundexian is an oral anticoagulant that inhibits the activity of clotting factor XIa. This protein is mainly involved in the formation of harmful blood clots.

As factor XIa plays a limited role in normal bleeding control, blocking its action may provide a viable option to safely prevent dangerous blood clots while preserving the body’s ability to stop bleeding after injury.

“Asundexian selectively inhibits factor XIa (FXIa), targeting a component of the coagulation cascade that is increasingly recognized as more important for pathologic thrombosis than for physiologic hemostasis,” said Ashkan Shoamanesh, MD, co‑principal investigator of the study and Population Health Research Institute (PHRI) senior scientist, when speaking to Medical News Today.

“This contrasts with existing anticoagulants—such as factor Xa inhibitors—which interrupt core steps required for both thrombus formation and hemostasis,” he said.

“FXI occupies a unique position within the intrinsic pathway, functioning primarily as an amplifier of thrombin generation. In the setting of vascular injury, exposure of abundant tissue factor activates the extrinsic pathway and generates a robust thrombin burst sufficient to achieve hemostasis, with only a limited contribution from FXI,” he continued.

“In contrast, in pathologic states such as atherosclerotic plaque disruption, tissue factor exposure is more modest, and sustained thrombin generation relies more heavily on FXIa-mediated amplification. In this context, FXIa promotes clot propagation and stability, contributing to vaso-occlusive and thromboembolic events,” he further explained.

“This biological distinction allows FXIa inhibition to uncouple pathologic thrombosis from hemostasis,” he added.

Trial results and what this means for stroke treatment

The findings come from the large, international OCEANIC-STROKE Phase 3 trial, which included more than 12,300 participants across 37 countries.

The average age of those in the study was 68 years, with a quarter over 75, and 33% were female. Roughly 95% of participants had recently experienced a non-cardioembolic stroke (a stroke not caused by a heart condition), with the remaining experiencing high-risk TIA.

They were randomly assigned to receive either 50 milligrams (mg) Asundexian plus standard antiplatelet therapy, or a placebo plus standard therapy.

Over the follow-up period, the researchers observed a 26% reduction in recurrent ischemic stroke in those taking Asundexian. Additionally, fewer people experienced major cardiovascular events, disabling or fatal strokes, no increase in intracranial bleeding, or a rise in serious side effects.

“Ischemic strokes account for approximately 87% of the roughly 800,000 strokes occurring in the U.S. each year,” Mike Sharma, MD, MSc, FRCPC, co-principal investigator of the study and a senior scientist at the PHRI, told MNT.

“Despite guideline-recommended therapy, these patients remain at substantial risk of recurrence, with approximately 1 in 10 experiencing another stroke within the first year. In this context, we observed a significant 26% relative reduction in the hazard of ischemic stroke with asundexian. This corresponded to an absolute risk reduction of 1.9% and a number needed to treat of 54 at one year,” he said.

“Notably, this represents a meaningful incremental benefit on top of contemporary secondary stroke prevention strategies. We also observed a 31% reduction in the risk of disabling or fatal strokes. Importantly, these benefits were achieved without an associated increase in bleeding risk.” 
— Mike Sharma, MD, MSc, FRCPC

These benefits were consistent regardless of age, sex, stroke severity, or underlying cause.

The researchers suggest that Asundexian’s ability to reduce stroke risk without increasing bleeding risk may offer a new paradigm in stroke prevention. Commenting on the key clinical takeaways, Shoamanesh told MNT:

“For one, OCEANIC-STROKE demonstrates that meaningful breakthroughs in secondary stroke prevention—with substantial treatment effects—remain achievable on top of existing guideline-recommended therapies.”

“Second, FXIa inhibitors represent a novel class of antithrombotic agents capable of reducing stroke risk without increasing bleeding, thereby providing a substantial net clinical benefit,” he continued. 

“For about 50 years the mainstay of secondary stroke prevention has been aspirin monotherapy. This represents the first significant improvement for most ischemic strokes apart from short term use of dual antiplatelet therapy.”
— Ashkan Shoamanesh, MD

Similarly, Christopher Yi, MD, board certified vascular surgeon at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, who was not involved in the study, suggests it may represent a new strategy for secondary prevention after non-cardioembolic ischemic stroke or high risk TIA.

“It should not replace aggressive risk-factor control, statins, blood pressure management, smoking cessation, diabetes control, and appropriate antiplatelet therapy, but it may eventually become an additional tool for selected high-risk patients,” he said.

When will this medication be approved for use?

However, despite the promising results, the study authors caution that Asundexian remains investigational and is not yet approved for clinical use. Further evaluation, regulatory review, and real-world data will be necessary before it becomes widely available.

Additionally, although the trial was large and diverse, certain patient groups, such as those with more severe strokes, were less represented, which may limit how broadly the findings apply.

If approved, Asundexian could provide a safer long-term option for preventing recurrent strokes, particularly for those at high risk of bleeding or unable to tolerate existing therapies.

“Within the framework of trial eligibility, there was no evidence of heterogeneity in treatment effect according to pre-specified subgroups,” Sharma said to MNT.

“For instance, patients benefited similarly irrespective of age, race, sex,  index event type (ischemic stroke versus TIA), history or vascular imaging evidence of atherosclerosis, acute lacunar versus non-lacunar infarction on brain imaging, or ischemic stroke subtype. We expect the results to apply to the majority of patients with non-cardioembolic ischemic stroke.”
— Mike Sharma, MD, MSc, FRCPC

“Taken together, these findings support the broad generalizability of the trial results to the majority of patients with non-cardioembolic ischemic stroke or high-risk TIA encountered in clinical practice,” Sharma said.

“This is further strengthened by the inclusion of patients with moderate-severe stroke severity up to an NIHSS of 15 and those who received acute revascularization therapies, including intravenous thrombolysis or endovascular thrombectomy,” he added.

Yi also suggests that Asundexian is likely to benefit are those with recent non-cardioembolic ischemic stroke or high risk TIA who remain at elevated risk for recurrence despite standard antiplatelet therapy.

“This may include patients with atherosclerotic disease, multiple vascular risk factors, or other markers of high recurrent stroke risk,” Yi told MNT. “It would not necessarily apply to patients with cardioembolic stroke from atrial fibrillation, where established anticoagulation strategies remain the standard of care.”

For now, the findings provide cautious optimism that effective stroke prevention without added bleeding risk may be within reach.

• A new study suggests that regularly drinking four cups of coffee a day could have a positive impact on mood and stress levels.
• Changes in mood and stress were also associated with changes in gut bacteria and the levels of certain metabolites.
• Most of the mood and gut changes occurred alongside drinking both caffeinated and decaffeinated coffee.

Coffee doesn’t just impact your energy levels first thing in the morning; it also influences the makeup of the gut microbiota, which in turn could influence mood and stress levels.

This is according to new research from APC Microbiome Ireland, a research center based at University College Cork, in Ireland. The study is published in Nature Communications.

“Coffee is more than just caffeine,” said study author John Cryan, PhD, Principal Investigator at APC Microbiome Ireland, in a press release. “It’s a complex dietary factor that interacts with our gut microbes, our metabolism, and even our emotional well-being.”

The term gut microbiota refers to all the different micro-organisms such as bacteria that live inside the digestive tract. They are a vital part of the gut microbiome, which refers not only to the microbes but also the environment they live in.

Research has already established that there is a two-way relationship between the gut and the brain, known as the gut-brain axis. This means that changes in the brain can lead to changes in the gut, and vice versa.

Gut microbiota play a key role within this relationship.

“Public interest in gut health has risen hugely,” said Cryan. “The relationship between digestive and mental health is also increasingly being better understood, but the mechanisms behind coffee’s effects on this gut-brain axis have remained unclear.”

Other research has suggested that gut microbes react to coffee, as well as associating different levels of coffee consumption with certain health outcomes. These include reduced risks of some chronic diseases, lower rates of all-cause mortality, and a lower risk of depression.

Researchers have not investigated the effects of coffee drinking and withdrawal over time on drinkers as well as their gut microbiota in depth up until now.

How did the study assess the effects of coffee intake?

The study began with a comparison of one group of 31 non-coffee drinkers with 31 coffee drinkers. Coffee drinkers were people who regularly consumed between 3 and 5 cups of coffee a day.

With each participant, the researchers assessed several parameters with a range of tests, questionnaires, self reports, and stool and urine samples. These included:

• cognitive function
• stress levels
• physical health
• mood
• immune function
• diet
• gut microbiome composition.

After these baseline tests, the non-coffee drinker group played no further part in the study.

The coffee-drinking group then stopped drinking coffee for 14 days, while also abstaining from other sources of caffeine, such as sodas and dark chocolate.

After this time, they reintroduced coffee to their diets. However, half of them (15 people) reintroduced decaffeinated coffee while the other half (16 people) reintroduced caffeinated coffee.

The participants then drank whichever type of coffee the researchers had blindly assigned to them for 21 days. Their instructions were to drink four sachets of instant coffee each day.

The researchers carried out further assessments on this group of participants throughout their period of abstinence from coffee and then again during the 3-week intervention phase.

How coffee reshapes the gut

The researchers found that when participants returned to drinking coffee after the 14-day abstinence period, both caffeinated and decaffeinated coffee were associated with improvements in mood.

The participants’ questionnaires revealed lower levels of stress, depression, and impulsivity after returning to either type of coffee.

Caffeinated coffee alone was associated with reduced anxiety and improved vigilance, attention, and blood pressure. In contrast, decaffeinated coffee was associated with improvements in learning, memory, physical activity, and sleep.

Interestingly, the researchers did not note any differences between the coffee drinkers and the non-coffee drinkers at the start of the study and after the abstinence period when it came to many of these factors. This included blood pressure, stress, anxiety, depression, sleep quality, and physical activity.

Alongside the changes in mood and cognition, the researchers also observed several changes in the guts of the participants.

During the 2-week abstinence period, they noted changes in levels of certain metabolites, which are small molecules that are produced during the process of metabolism.

These levels largely returned after the participants started drinking coffee again, although levels of metabolites closely associated with caffeine did not rise for those drinking decaffeinated coffee.

Overall, the researchers identified nine key metabolites that were closely associated with coffee drinking. These included theophylline, caffeine, and selected phenolic acids, and were “strongly linked to microbial species and cognitive measures.”

There were also clear differences between the gut microbiomes of coffee drinkers compared with nondrinkers. There were higher levels of specific species of bacteria associated with positive health effects in the guts of the coffee drinkers.

These included:

• Cryptobacterium curtum, which is associated with oral health
• Eggertella sp. CAG:209, which is associated with bile acid synthesis
• Firmicutes CAG:94, which is associated with positive emotions in females.

“Our findings suggest that coffee, whether caffeinated or decaffeinated, can influence health in distinct but complementary ways,” said Cryan in the press release.

Only caffeinated coffee linked to lower anxiety

“Our findings reveal the microbiome and neurological responses to coffee, as well as their potential long-term benefits for a healthier microbiome,” said Cryan in the press release. “Coffee may modify what microbes do collectively, and what metabolites they use.”

Medical News Today asked Cryan if it was possible that the coffee drinkers had less stress and depression after drinking coffee again due to the psychological impact of being able to return to a habitual behaviour rather than this being driven by the coffee itself.

Cryan told us that the return to a habitual behaviour can itself have psychological benefits, including reduced stress and improved mood, but that they designed the study to address this.

“We included both caffeinated and decaffeinated coffee, and both groups showed improvements in stress and depression. This suggests that non-caffeine factors, including psychological or behavioural effects, may play a role,” he said.

“However, only caffeinated coffee reduced anxiety and psychological distress, indicating that caffeine-specific biological effects are also involved,“ he added.

“Taken together, the findings suggest that the observed benefits are likely due to a combination of factors, biological effects of coffee compounds — including caffeine and (poly)phenols — microbiome-mediated mechanisms, and psychological effects linked to routine and expectation.”

– John Cryan, PhD

While these early results are of interest, it is important to note that the study was a relatively small one, with only data from 62 participants. The researchers also did not analyze differences due to ethnicity due to the majority of the participants being Caucasian.

The study also only investigated the effects of instant coffee. MNT asked Cryan whether different coffee types or preparation methods might provide different results.

“Different coffee types and preparation methods can significantly influence the chemical composition of the final drink,” he said. “The brew method affects levels of caffeine, (poly)phenols, and other bioactive compounds such as diterpenes and chlorogenic acids.

“In our study, we focused on controlled interventions using standardized caffeinated and decaffeinated coffee to isolate biological effects. However, instant coffee may differ from freshly brewed coffee in its polyphenol profile and processing-related compounds, which could influence how it interacts with the gut microbiome and metabolism,” Cryan explained.

“While we would expect broadly similar directional effects across coffee types, the magnitude and specific microbial or metabolic responses may vary depending on preparation method,” he continued. “This is an important area for future research, particularly in the context of personalized nutrition and microbiome responses.”

For now though, this study provides additional insight into the mysteries of the gut microbiome and the role that one of the world’s favorite drinks may have to play in health.

• New research in mice suggests that higher levels of serotonin might worsen the symptoms of tinnitus, a condition where a person hears constant buzzing or ringing in one or both ears.
• Tinnitus can severely impact mental well-being, causing or exacerbating symptoms of depression and anxiety.
• Since psychiatrists often treat clinical depression and anxiety with serotonin-increasing medication, the study finding is posing an important question about how best to manage tinnitus when it co-occurs with mental health conditions.
• Practicing psychiatrists and tinnitus experts, however, advise that the finding ought to be treated with caution.

According to the latest available estimates, 14% of adults around the world experience tinnitus, a condition characterized by the perception of constant ringing or buzzing in one or both ears.

Due to its nature, this condition can severely impact quality of life, including mental health, and it may cause symptoms of anxiety and depression.

There is also anecdotal evidence that tinnitus is fairly common in attention deficit hyperactivity disorder (ADHD), exacerbating problems with focus as well as anxiety.

Given all of this, the findings of a study on tinnitus conducted by researchers from Oregon Health & Science University (OHSU) in the United States and Anhui University in China, and recently published in PNAS may not spell good news.

The study, conducted in mice, found that higher levels of serotonin, a neurotransmitter or chemical messenger that plays key roles in emotional regulation, appeared to exacerbate behavioral responses associated with worsening tinnitus symptoms, such as becoming more easily startled by noises.

If confirmed in humans, this finding may pose certain problems for the treatment and management of anxiety and depression in people who also experience tinnitus.

This is because treatment plans for these two mental health conditions often involve taking selective serotonin reuptake inhibitors (SSRIs), a form of medication that aims to boost serotonin levels.

Higher serotonin levels may trigger hypersensitivity to perceived sound

This is study follows up on previous research from the scientific team, published in Cell Reports in 2017. In their previous study, the scientists examined the dorsal cochlear nuclei of mice brains.

This area of the brain is associated with the experience of sound, in general, as well as the specific and persistent noise experienced in tinnitus.

Through this, the researchers found that a specific type of neurons from that brain area became overactive and hypersensitive to sound when exposed to an influx of serotonin.

This finding led them to conduct the recent follow-up study, in which they employed an optogenetic approach, using a special type of light beams to trigger serotonergic neurons, or serotonin-producing brain cells. This made the mice hypersensitive to sounds, and more easily startled by noises.

“When you stimulate these serotonergic neurons, we can see that it stimulates activity in the auditory region in the brain. We also saw that animals then behaved as if they were hearing tinnitus,” co-senior author Laurence Trussell, PhD, professor of otolaryngology in the OHSU School of Medicine, explained in a press release.

“In other words, it’s producing symptoms that we would expect to be experienced as tinnitus in humans,” Trussell said.

Should people with both tinnitus and depression, anxiety avoid SSRIs?

According to the study authors, these findings may have important implications for people with co-occurring tinnitus and mental health conditions, particularly those treated with SSRIs.

“People with tinnitus should work with their prescribing physician to find a drug regimen that gives them a balance between relief of psychiatric symptoms like depression and anxiety, while minimizing the experience of tinnitus,” Trussell advised in the press release.

He also emphasized that “this study highlights the importance of clinicians recognizing and validating patient reports of medication-associated increases in tinnitus.”

Other experts, however, urged extreme caution in bringing these findings based on preliminary research to the doctor’s office.

Speaking to Medical News Today, Hamid Djalilian, MD, Chief Medical Advisor at the NeuroMed Tinnitus Clinic and professor of otolaryngology at University of California Irvine, who was not involved in the current study, stressed that he was surprised by its findings.

“This is completely the opposite of what we see in clinical practice,” Djalilian told us. He noted that adverse reactions to SSRIs involving worsening tinnitus symptoms are exceedingly rare:

“We very commonly treat tinnitus patients in our clinic with medications that increase serotonin levels in the brain, and the majority of patients have relief from this treatment, especially when combined with some lifestyle modifications. There are rare patients who are serotonin sensitive and get worse with medications that increase serotonin levels in the brain, but in our experience that is less than 5% of patients with tinnitus.”

Likewise, Sylvia Baker, MRCpsych, consultant psychiatrist at Re:Cognition Health, who was also not involved in this study, said that “these findings should be interpreted cautiously when considering human patients.”

Baker explained that, while “the new research identifies a plausible biological link between serotonin signalling and tinnitus-related activity, […] it does not show that SSRIs reliably worsen tinnitus in people.”

“Tinnitus is multifactorial and is often influenced by hearing changes, sleep, anxiety, depression, attention and general health. Some patients do report tinnitus changes while taking SSRIs, but the overall clinical evidence remains mixed and does not establish a clear causal effect,” she also noted.

What to do if tinnitus does worsen with SSRIs

While the likelihood of experiencing worsening tinnitus symptoms when taking SSRIs for the treatment of depression or anxiety is small, all the experts who spoke to MNT agreed that, for the few people who do find themselves in this situation, an individualised care plan is key.

Moreover, healthcare practitioners should take into account the possibility that mental and emotional distress may themselves be at the root cause of worsening tinnitus.

“If tinnitus changes occur during SSRI treatment, the response should be individualised rather than assuming the medication is definitely responsible,” Baker told us.

She advised that:

“Clinicians should assess both mental health symptoms and tinnitus severity, as anxiety and depression can themselves increase tinnitus distress. If a medication contribution seems possible, options may include slower titration, dose adjustment, or considering an alternative treatment, but patients should not stop SSRIs abruptly or without medical advice. Psychological approaches such as CBT [cognitive behavioral therapy], sleep support, and tinnitus-focused coping strategies can also be helpful.”

Speaking to MNT, Steven Allder, MD, consultant neurologist at Re:Cognition Health, likewise not involved in the recent study, said that, going forward, “there is also a need for pharmacovigilance and stratification work to identify which patients may be more susceptible to SSRI-associated tinnitus worsening, and whether this risk is influenced by dose, receptor profile or tinnitus subtype.”

What is the link between ADHD and tinnitus?

What about people with ADHD who experience tinnitus? Should they worry about the recent findings?

Baker stressed that, in the context of the current study, “the implications are more indirect.”

“There is limited evidence suggesting that attentional difficulties and sensory processing differences may influence how intrusive tinnitus feels, but there is no strong evidence that ADHD itself routinely causes tinnitus,” she told MNT.

“In practice, tinnitus in someone with ADHD should be assessed in the wider context of attention, sleep, anxiety, sensory sensitivity and medication timing, rather than being attributed too quickly to a single cause. Careful baseline assessment and avoiding multiple medication changes at once can help clarify whether symptoms are coincidental or treatment-related.”

— Sylvia Baker, MRCpsych

“The overlap between tinnitus and ADHD are through shared brain network dysfunction involving attention and sensory filtering,” Djalilian explained. 

“Impaired sensory gating in the brain’s salience center (the area that regulates attention) leads to ADHD and is the primary area of dysfunction that leads to bothersome tinnitus,” he continued.

Thus, he noted, “treatment is most effective for ADHD and tinnitus when it targets the neurological drivers of this attentional dysregulation.”

Mice can’t tell us if they experience tinnitus

For Djalilian, the fact that the recent findings come from an animal study means that they ought to be understood in the context of early research, and thus not extended to clinical practice just yet.

“Animal studies of tinnitus have been controversial. While the method used to detect tinnitus in animals (gap detection test) has been used for a long time, we are making an educated guess on the presence of tinnitus [when using],” he told us.

“We can’t objectively verify that the animal has tinnitus or ask them. The gap detection test is a behavioral test when a sound with a gap is presented to the animals. It is performed only at certain frequencies and if the animal potentially has tinnitus at a frequency other than those tested, it wouldn’t be detected. Also, if the gap detection test is positive, we still can’t be 100% sure if the animal is experiencing tinnitus. There have been a number of animal studies on tinnitus that never materialized when performed in humans.”

— Hamid Djalilian, MD

Going forward, Djalilian said he “would like to see this study performed in humans with serotoninergic medications.”

Allder suggested that the current study may be “best viewed as a mechanistic bridge: It strengthens the biological plausibility that serotonergic modulation can influence tinnitus, but it does not yet establish clinical causality in humans or explain the full heterogeneity of the condition.”

He also emphasized the necessity of confirming its findings in humans, and added that “further mechanistic research should focus on receptor-level specificity, particularly which serotonin receptor subtypes are involved in modulating auditory gain, as this could inform the development of more targeted therapies.”

“Causal intervention studies will be important to test whether selective modulation of serotonergic signalling can preserve antidepressant benefits while reducing auditory side effects,” Allder concluded.

• About 590 million people worldwide have diabetes, with more than 90% living with type 2 diabetes. 
• Although there is currently no cure for type 2 diabetes, it is possible to go into remission by making healthy lifestyle choices, such as eating a healthy diet. 
• A new study found that people with type 2 diabetes following the keto diet may have a better chance of reversing their diabetes than those just following a low-fat diet.

Researchers estimate that about 590 million people globally live with diabetes, with more than 90% having type 2 diabetes. 

Although there is currently no cure for type 2 diabetes, it is possible to go into remission, which is primarily accomplished through weight loss, regular exercise, and following a healthy diet that is usually low-calorie and low–carbohydrates. 

Now a new study published in the Journal of the Endocrine Society has found that people with type 2 diabetes following the keto diet, which is high-fat and low-carb, may have a better chance of reversing their diabetes than those just following a low-fat diet.

Keto vs low-fat diet for beta-cell function

For this study, researchers recruited 51 adults between the ages of 55 and 62 with type 2 diabetes. Participants followed either the keto diet or a low-fat diet for 12 weeks. 

Scientists focused on how both diets impacted participants’ proinsulin to C-peptide ratio, which shows how well the beta cells in the pancreas are functioning. 

“Carbohydrate-restricted diets have been shown to elicit several beneficial effects in patients with type 2 diabetes, including lowering HbA1c, systolic blood pressure, and triglycerides,” Marian Yurchishin, MS, pre-doctoral training fellow in the Department of Nutrition Sciences at the University of Alabama at Birmingham and lead author of this study, told Medical News Today.

“By identifying its therapeutic effects, we want to show that a ketogenic diet could serve as a complementary aspect of lifestyle therapy which could contribute to better glycemic control as a result of improved beta-cell function,” Yurchishin explained.

“Other than bariatric surgery or large-volume intentional weight loss, interventions for improving beta-cell function in type 2 diabetes, particularly in the absence of weight loss, do not currently exist. Further, these therapies may not be feasible or sustainable for most individuals. While the potential to restore beta-cell function is possible in early disease states, effective therapies and useful markers for gauging effectiveness of treatments are not known.”

– Marian Yurchishin, MS

Following keto diet helps improve beta-cell function

At the study’s conclusion, researchers found that while study participants both lost weight following either the keto or low-fat diet, those following keto experienced a decrease in the proportion of proinsulin secreted to a greater extent, a change that was associated with an improvement in beta-cell function. 

“The pancreas has to go through several steps to make insulin,” Yurchishin explained. “When beta cells are under significant stress, as seen in type 2 diabetes, they secrete a lot of proinsulin.”

”Proinsulin is a precursor to insulin, so elevated proinsulin levels indicate that beta-cells are overwhelmed and secreting ‘unfinished’ molecules as an attempt to keep up with the body’s increasing demands for insulin,” she continued. ”A larger decrease in proinsulin suggests that the ketogenic diet reduced this stress and allowed beta-cells to work more efficiently,  as evidenced by the improvements in beta-cell function.”

What might it be about the keto diet that would allow it to help improve beta-cell function? 

“One process that may contribute to beta-cell failure is their loss of glucose sensing and glucose responsiveness, which is thought to result from the beta-cells’ chronic exposure to glucose (e.g. glucose toxicity),” Yurchishin told us.

“Removal of this exposure via a carbohydrate restricted diet may therefore provide an environment for beta-cells to repair their secretory mechanisms, but more research is needed to identify the specific mechanisms behind this effect,” she noted.

“As beta-cells are responsible for secreting insulin in response to increases in blood glucose, restoration of their function allows these cells to produce adequate insulin to sustain adequate blood sugar levels,” she added. 

Research next steps: Longer study duration, specify type of keto

MNT had the opportunity to speak with Pouya Shafipour, MD, a board-certified family and obesity medicine physician at Providence Saint John’s Health Center in Santa Monica, CA, about this study, who commented he was not surprised by its findings. 

“For early cases of diabetes, keto can do miracles if people adhere to it well, and if they’re doing Mediterranean, higher fiber keto,” Shafipour, who was not involved in this research, said.

“But the biggest challenge with keto is that a lot of people do carnivore keto. They don’t necessarily eat the right type of fat and protein, and also adhere to it. This study […] is 12 weeks, and in 12 weeks it’s easier to adhere to it,” he pointed out.

According to him, another big challenge is that “people go on keto for 2, 3 months, get results, and then they start getting bored of it”.

“We’re living in a world that’s just flooded with carbohydrates, and once you get out of it, it’s hard to get back into a ketogenic state. It requires a lot of discipline, a lot of saying no to a lot of temptations. So keto is fantastic and miraculous, it’s just that adherence is a little bit challenging,” said Shafipour.

For the next steps in this research, Shafipour told us he would like to see a bit longer study duration and what type of specific keto diet participants are following. 

“Because keto to one person might mean just like the old school Atkins [diet], that you’re eating a lot of bacon and cheese,” he explained. “But now we found out that those inflammatory fats are not necessarily healthy, even though they cause weight loss, but they can increase tumor markers and inflammatory markers in the blood.”  

“[With] longer study adherence — you follow patients six months to a year to see how much they can adhere, and then you measure their C-peptides, A1C, and pancreatic cell function. We want to make sure with diabetes management, we’re not just managing the blood sugar, but we’re preserving pancreatic cell function and we’re actually reducing the IL6, the TNF alpha, all these inflammatory markers that are in the background destroying the body in a diabetic person.” 

– Pouya Shafipour, MD

Tips for following the keto diet

For those who may want to give following the keto diet a shot, Monique Richard, MS, RDN, LDN, a registered dietitian nutritionist and owner of Nutrition-In-Sight, offered some expert tips. 

“It is most important to prioritize a way to look beyond initial outcomes and consider sustainability, access, nutritional adequacy, and impact on overall health, especially cardiovascular health, which is closely tied to, or increased, in those with type 2 diabetes,” Richard said.

“The research established so far conveys that while low-carb and ketogenic diets may improve glycemic control in the short term, they may not be consistently superior over time compared to other balanced dietary patterns, or, not without their own side effects and shortfalls — i.e. gallbladder health, arterial inflammation, impact on liver function,” she advised.

While lowering carbs can help blood sugar levels, Richard said that how this is done and what they are replaced with matters just as much, if not more.

Some general recommendations for those interested in exploring the keto diet include: 

• Focusing on food quality, not just macros: Not all keto diets are created equal, Richard said. Replacing carbohydrates with highly processed meats, ultra-processed foods marketed as “keto-friendly,” and saturated fats may negatively impact heart health, while emphasizing unsaturated fats (olive oil, nuts, seeds, avocado) and non-starchy vegetables supports better outcomes.  
• Be strategic and mindful: It’s not about restriction, elimination, or excess of one or more particular food groups or macros. 
• Consider moderate carbohydrate reduction rather than extreme restriction: Even decreasing the frequency of refined carbohydrates, or portions consumed, in addition to the amount of added sugars can significantly improve glycemic control, Richard said.
• Keep the variety, hold the towering fat and protein stack: A double bacon cheese burger with extra bacon sans the bun is a lot for the digestive system to process, in addition to the excess sodium, preservatives, and lack of beneficial nutrients this combo contains, Richard explained. Restrictive and imbalanced diets can limit fiber, phytonutrients, and gut microbiome diversity which are all important for metabolic health.

“The best nutrition plan is the one that works for your biology and your life,” Richard added.

“As with most things in nutrition, there is no one-size-fits-all approach. The goal isn’t just to lower blood sugar — it’s also to support long-term health, quality of life, and sustainable habits. If someone is considering a ketogenic approach, I always emphasize doing so with guidance from a registered dietitian nutritionist (RDN) and healthcare team, especially because medications often need to be adjusted,” she advised.

• A new study suggests that gut health may be linked to Parkinson’s disease.
• Researchers found that changes in the gut microbiome may appear years before symptoms develop.
• The scientists say this could help identify people at higher risk earlier and be used to advise prevention strategies.

Gut health has become an area of increasing interest to researchers over the years. So far, scientists have linked it to digestion, inflammation, and even mental health.

More research is coming out that suggests there is a strong connection between gut health and the brain. Researchers from University College London examined the connection between gut health and Parkinson’s disease.

They found an association between the gut microbiome and Parkinson’s disease risk. While more research is needed, the findings suggest that shifts in gut bacteria may be an important early signal to watch in understanding and identifying the disease.

The study is published in Nature Medicine. 

Gut health and Parkinson’s: What’s the link?

Parkinson’s disease is a neurological condition that affects around 1.1 million people in the U.S. The neurodegenerative disease affects movement and can cause dementia. 

While treatments are available to help manage symptoms, there is no cure, and the disease progresses over time. As a result, many researchers are focusing on identifying early warning signs and new preventative approaches.

The researchers analyzed gut microbiome data from three categories of participants: 

• people diagnosed with Parkinson’s (271)
• people with a genetic risk factor GBA1 without symptoms (43)
• healthy controls (150)

They collected stool samples to identify different microbes in the gut and also measured the levels of these microbes to understand how common or rare they are in each person. This helped with understanding overall gut balance and finding patterns linked to disease risk or progression.

The researchers also assessed participants’ motor and non-motor symptoms, cognitive functioning, diet, and other health factors. 

Gut changes may indicate risk of disease

By combining clinical information with microbiome analysis, the researchers identified patterns associated with disease risk and progression. 

The scientists found distinct differences in the gut microbiomes of individuals with Parkinson’s disease compared to healthy individuals.

The researchers said around 25% of the gut microbiome showed significant changes when comparing the group with Parkinson’s to the control group. 

The scientists noted that the extent of microbiome changes was linked to disease severity in people with Parkinson’s. People with more advanced Parkinson’s had greater disruptions in their gut bacteria.

Based on non-motor symptoms (such as autonomic dysfunction and REM Sleep Behavior Disorder), the researchers classified part of the GBA1 group as “prodromal,” which is the pre-diagnostic phase of Parkinson’s. 

They also found this subgroup had an “abundance” of these microbe species compared to the healthy group and to people in the GBA1 group who did not have non-motor symptoms. 

These findings led the researchers to think that gut changes may begin years before symptoms begin. They think these patterns could eventually serve as an early marker of the disease. 

Overall, the study may serve as a step towards finding a way to detect Parkinson’s disease sooner and implement both preventative and treatment strategies. 

Will this change how Parkinson’s is treated?

Julie Pilitsis, MD, PhD, Chair of Neurosurgery at the University of Arizona Tucson and Physician Executive in the Functional Neurosurgery program at Banner University Medical Center, spoke with Medical News Today about the findings. Pilitsis touched on the strength of the study. 

“A major strength of this study is that these patterns held up across the globe,” said Pilitsis. “The researchers checked their findings against data from studies in the United States, South Korea, and Turkey and found similar bacterial shifts in Parkinson’s patients everywhere.”

Pilitsis said it is possible that the findings could create unneeded anxiety in people with the Parkinson’s genetic risk factor. 

“Only 10% of patients with GBA1 variants develop [Parkinson’s disease] by age 60 and 19% by age 80, meaning that the majority of people do not develop Parkinson’s,” she said.

Pilitsis said that the findings will not impact current medical management and that “more research is needed before these findings can be used in patient care for Parkinson’s disease, especially long-term research.”

• A new study suggests that environmental and lifestyle exposures, such as diet, smoking, and chemical exposure, may contribute to early-onset colorectal cancer.
• The study confirmed known risk factors, like tobacco use and diet, while also identifying a new association with the agricultural herbicide picloram.
• Regions with higher picloram use showed higher rates of early-onset colorectal cancer, suggesting a possible environmental link, though not proving causation.
• The findings highlight how cumulative lifetime exposures, known as the ‘exposome’, may help explain rising cancer rates in younger adults and could inform future prevention strategies.

Early onset colorectal cancer describes a diagnosis of colorectal cancer in adults under 50. Previously considered a disease of older age, colorectal cancer is rising globally at an alarming rate in younger adults, with a 1.4% annual increase in incidence reported.

Evidence suggests that in many areas colorectal cancer is increasing in younger adults faster than older adults, and roughly 1 in 5 diagnoses occurs in someone under the age of 55. Research also highlights that colorectal cancer is now the leading cause of cancer-related death among males and females under age 50.

While the incidence of early onset colorectal cancer rises, the drivers of this trend remain poorly understood. Previous research has suggested the potential role of the exposome. This term refers to all the exposures a person experiences throughout their life and how those exposures affect their health.

Now, a new study published in Nature Medicine, suggests that epigenetic changes, or ‘molecular footprints’, associated with dietary patterns, smoking, and pesticide exposure may help explain the rising incidence of early onset colorectal cancer.

Key findings of the study

Researchers from the Vall d’Hebron Institute of Oncology (VHIO) focused on the possible association between the exposome and colorectal cancer. However, rather than measuring exposures directly, the team examined epigenetic changes, specifically DNA methylation.

These are chemical modifications that influence gene expression without altering the DNA sequence itself. Experts often compare epigenetic marks to annotations in a book; they do not change the text but influence how it is read.

The study analyzed DNA methylation patterns in those diagnosed with colorectal cancer before and after age 50. The researchers then created epigenetic risk scores reflecting exposure to various environmental factors.

They found distinct epigenetic signatures linked to dietary patterns, tobacco use, and environmental exposures.

Lead study author José Seoane, PhD, Head of the VHIO Computational Biology Group, explained to Medical News Today how epigenetic signatures and risk scores make a useful tool for studying the exposome.

“Epidemiologists have been studying how our methylation is changed by the environment for quite a while. We have a lot of EWAS (epigenetic wide association studies) that identifies methylation locus associated with an exposure,” Seoane explained.

“We get this information and build signatures of how this signal is changing in tumor tissues, therefore we are able to retrieve a sort of ‘history’ of exposure from the methylation data,” he said.

The study confirmed known risk factors and notably found a new association with a widely used agricultural herbicide.

“In this study we identify an association between early onset colorectal cancer and some environmental exposures, studying their epigenetic profiles,” Seoane told MNT.

“We identify that smoking, diet and a pesticide named picloram are associated with early onset colorectal cancer.”
— José Seoane, PhD

Using U.S. population data, the researchers observed that counties with higher picloram use also had higher rates of early onset colorectal cancer, even after accounting for socioeconomic factors and other pesticides.

A possible new risk factor for colorectal cancer

Further analysis revealed that tumors linked to higher picloram exposure showed different molecular characteristics. This included fewer variations in the APC gene, a key gene involved in colorectal cancer development.

This suggests that environmental exposures could contribute to cancer development through mechanisms beyond traditional genetic alterations.

However, the researchers emphasize that these findings show an association, not proof of causation. As such, more studies are necessary to confirm whether picloram directly contributes to early onset colorectal cancer development.

“As the link between smoking and diet and early onset colorectal cancer has been already established by epidemiological studies, we were expecting to have it in our hits,” Seoane told MNT.

The pesticide with the strongest link

“Picloram was a surprise because it was never associated with cancer. In order to validate this, we correlate a database of incidence of early onset colorectal cancer in U.S. counties with a database of pesticide use in the same counties, and picloram was again the most significant hit, showing strongest association that other pesticides, for example glyphosate.”
— José Seoane, PhD

“Of course, we should be cautious, because both analyses are observational, so further research should be done to establish causal links,” he added.

Why this study matters

While further research is still needed, this study highlights the possibly larger role that environmental and lifestyle factors may play in cancer risk than was previously understood, particularly for younger individuals.

The findings also demonstrate the potential role of epigenetics as a tool for tracking lifetime exposures and identifying modifiable risk factors. MNT asked Seoane if there are modifiable risk factors that people should be more aware of.

“Of course, and I think this is one of the most important messages of this work: People are aware that diet is associated with cardiovascular diseases and smoking is associated with lung cancer,” Seoane said.

“Here we identify also that both diet and smoking are associated with early onset colorectal cancer. So it is reasonable to say that better diet and quitting smoking should lower the risk of colorectal cancer. Picloram is more complex, because if causal analysis confirms our results, very likely this should be regulated by governments.”
— José Seoane, PhD

The study authors also suggest that their findings could support improved prevention strategies, public health policies targeting environmental exposures, and earlier identification of individuals at higher risk.

By linking epigenetic changes to real-world factors, this study may offer a new framework to help explain the rising burden of colorectal cancer in younger populations.

• A new study highlights that older adults tend to nap more often, for longer, and earlier in the day as they aged.
• Notably, the study links increases in nap duration and frequency over time to a higher risk of death.
• While the association does not prove causation, it suggests that changes to nap patterns may reflect underlying health decline or disrupted body rhythms.
• Monitoring shifts in daytime napping could serve as a simple early warning sign to identify older adults who may need further medical evaluation.

Napping is a fairly common practice among U.S. adults, with estimates suggesting that roughly half of middle- and older-aged Americans report regular daytime napping. Other studies consistently report that napping is more common in older adults than in other age groups.

Like most adults, older individuals require about 8 hours of sleep for optimal health. However, multiple factors, such as age-related changes in circadian rhythm and sleep patterns, health conditions, medications, cultural beliefs, and lifestyle changes, can make sleep difficult and may contribute to a higher prevalence of napping.

Napping may relate to multiple health outcomes in older adults and could offer a modifiable behavioral factor that impacts health. However, research on napping in older adults has yielded mixed results, with some suggesting that infrequent short naps may be beneficial, while others suggest that frequent longer naps may be detrimental.

Now, a new long-term study published in JAMA Network Open, suggests that changes in daytime napping habits among older adults could serve as an early indicator of underlying health issues or increased risk of death.

Tracking naps over time

In this study, researchers from Mass General Brigham and Rush University Medical Center followed 1,338 participants for up to 19 years, monitoring both the duration and frequency of their naps.

Their findings suggest that with age, naps tended to become longer, more frequent, and more likely to occur earlier in the day.

The researchers found that individuals who took longer or more frequent naps, particularly in the morning, had a higher risk of death compared with those whose napping habits remained stable.

Notably, each additional hour of daytime napping was associated with a 13% increase in mortality risk. Likewise, each additional nap per day corresponded to roughly a 7% higher risk.

People who napped in the morning had a 30% higher mortality risk than those who napped in the afternoon. The study suggests that inconsistent napping patterns were not associated with an increased risk of mortality.

While the study does not prove that napping itself causes poorer outcomes, it highlights a strong potential association between evolving nap patterns and declining health.

Paying attention to napping patterns

The study authors suggest that increased napping may reflect underlying biological changes, such as disruptions in the body’s circadian rhythms or the early stages of chronic illness.

Lead author Chenlu Gao, PhD, an investigator in the Department of Anesthesiology in the Mass General Brigham, who is also an affiliated research fellow in the Division of Sleep and Circadian Disorders in the Department of Medicine, spoke to Medical News Today about the key findings from this study:

“For clinicians, the key message is that daytime napping patterns may be worth asking about as part of routine health monitoring in older adults. Clinicians tend to focus on nighttime sleep, but our findings suggest that what’s happening during the day is also informative.”

“Importantly, the associations between daytime napping and mortality remained significant even after accounting for nighttime sleep duration and fragmentation, which tells us that daytime napping carries independent information about health status,” Gao explained. 

“For the general public, the takeaway is to pay attention to daytime napping patterns. Excessive daytime sleepiness, especially if it’s becoming more frequent or predominantly occur in the morning hours, may be a signal of an underlying condition.”
— Chenlu Gao, PhD

A potential early warning sign

These findings suggest that napping could act as an easily observable marker of health status in older adults.

Through wearable devices or simple observation, it is possible to track sleeping patterns noninvasively. This may provide clinicians and caregivers with a practical way to monitor changes in napping behavior and help identify those who could benefit from further medical evaluation.

“Caregivers are often well-positioned to notice changes in daytime napping patterns,” Gao told MNT.

Signs to watch out for

“Signs worth paying attention to include: a loved one napping much more than they used to, falling asleep frequently and having trouble staying awake during the day, or regularly feeling drowsy in the morning hours despite having slept overnight. Snoring, gasping during sleep, or frequently waking during the night are also worth paying attention to, as these are potentially symptoms of sleep disorders that drive daytime sleepiness.”
— Chenlu Gao, PhD

Gao also noted to MNT that wearable technology could play a role in potentially identifying risk earlier.

“We think this is a promising direction. In our study, wrist-worn actigraphy was used to objectively capture habitual napping patterns, rather than relying on self-report, which can be unreliable,” she said.

“However, consumer wearable devices vary a lot in how accurately they assess sleep. Validating these devices and establishing which changes in nap patterns are most predictive of health decline will be important next steps. If we can identify reliable wearable-based markers, there is real potential to integrate them into routine care,” she added.

Is occasional napping a concern?

However, the researchers emphasize that it is not occasional napping that is concerning, but rather progressive increases in napping duration and frequency over time.

“Unfortunately, our study did not look at specific thresholds. Napping is indeed very common among older adults. In our study, 99% of the participants napped at least once during the monitoring period, so napping itself is not a red flag,” Gao said to MNT.

“What is concerning is a pattern of long and frequent naps, especially in the morning hours, when a healthy adult should feel refreshed after a night of rest.”
– Chenlu Gao, PhD

“In addition, a noticeable change from one’s usual nap patterns, such as napping much more than they used to, is also worth paying attention to. Future studies are needed to establish specific guidelines on napping behaviors to promote health,” she said.

While further research is still necessary to understand the association between increased napping and higher mortality risk, this study adds to a growing body of evidence linking sleep regularity with overall health and longevity.

For now, the researchers suggest that clinicians consider changes in napping habits as a potential red flag in aging populations, which may warrant closer attention and possibly earlier intervention.

MNT also spoke with Opel Baker, MBChB, DipOccMed, MRCGP, a general practitioner from the Mayfield Clinic in Brighton, United Kingdom, who was not involved with the study.

Prevention tips for excessive napping

Napping is a common behavior in older adults, and while it can have a restorative effect, it is advisable to limit naps to shorter durations. Setting alarms can be an effective way to help manage nap duration.

Evidence suggests that up to 30 minutes of napping may have the most benefit, while napping for more than 1 hour can lead to sleep inertia, a temporary state of disorientation upon waking. Additionally, longer or more frequent naps are also more likely to disrupt sleeping patterns at night.

Speaking to MNT, Gao highlights that addressing underlying conditions may help to reduce excessive daytime napping:

“If someone regularly experiences daytime sleepiness and needs to take naps, the first important step is to figure out why. If it is driven by conditions like obstructive sleep apnea or medical conditions that cause fatigue and frailty, then diagnosis and targeted treatments will be needed.”

Additionally, she adds that certain lifestyle changes can also be beneficial.

“If the excessive daytime sleepiness is driven by poor nighttime sleep, then improving sleep hygiene may help. Tips include: maintaining a consistent sleep schedule, limiting caffeine and alcohol especially in evening, avoid using electronic devices before bedtime, and staying outside of the bed when not intending to sleep,” Gao said.

MNT also spoke with Steve Allder, MD, a consultant neurologist at Re:Cognition Health in London, U.K., who was not involved with the study.

He emphasized that persistent excessive sleepiness should be medically evaluated rather than managed with lifestyle changes alone. He adds that the goal is to improve sleep at night and stay more alert during the day.

Allder concludes that reducing excessive napping is less about restriction and more about identifying and correcting the underlying drivers, whether neurological, behavioural or systemic. He suggests the following tips:

• Anemia is a common blood condition characterized by a lack of healthy red blood cells in the body. 
• A recent study examined how anemia may relate to dementia risk. 
• The study results indicated that having anemia was associated with greater levels of blood biomarkers for Alzheimer’s disease and with an increased risk for dementia over time. 

Anemia occurs when there is a low level of healthy red blood cells, and it has been linked to a number of chronic illnesses such as kidney failure, autoimmune diseases (rheumatoid arthritis and lupus), and inflammatory bowel disease like Crohn’s. Recently, scientists wanted to see if anemia had a link to dementia.

In a study published in JAMA Network Open, researchers examined data from over 2,200 adults and found that those with anemia had more biomarkers for Alzheimer’s disease.

In the long term, they observed that having anemia was associated with a higher risk of developing dementia. The participants who had the highest risk for dementia were those who had both anemia and higher levels of Alzheimer’s disease biomarkers.

The complex relationship between anemia and dementia

To conduct this study, researchers used information from participants who were part of the Swedish National Study on Aging and Care in Kungsholmen. Participants were all at least sixty years old and did not have dementia at baseline. In all, researchers analyzed data from 2,282 participants. 

Researchers looked at a number of blood biomarkers of Alzheimer’s disease from the blood samples of participants. They also evaluated participants for anemia, using criteria from the World Health Organization.

To do this, they looked at blood hemoglobin levels and saw if they were below a certain level. Hemoglobin is a protein in red blood cells that helps supply the body with oxygen. They also had data on diagnoses of dementia and mild cognitive impairment and information on several covariates. 

Among participants, 8.7% had baseline anemia. Participants with anemia were more likely to be male, have more chronic diseases, have a lower education level, and be older. Participants with anemia had higher levels of Alzheimer’s disease biomarkers. Two particular biomarkers were more elevated in men than in women.

There were 16 years of follow-up, and the average follow-up time was 9.3 years. Throughout the follow-up, 15.9% of participants developed dementia.

Overall, researchers found that anemia was associated with a higher risk of developing dementia. Participants with anemia had a 66% higher chance of developing dementia than participants who had normal hemoglobin levels.

They found that a higher risk for dementia remained true even after excluding participants who had mild cognitive impairment and who were diagnosed with dementia within six years of follow-up.

However, they found that anemia was not associated with higher dementia risk among participants who were carriers of APOE ε4, a gene that increases risk for Alzheimer’s disease. 

Do men and women have different risks?

The researchers also found the relationship between hemoglobin and higher dementia risk plateaued when hemoglobin levels reached a certain level, slightly above the definitions for anemia.  When looking at sex, they found this nonlinear association was significant for men but not for women. 

Finally, researchers found that the risk for dementia increased as levels of Alzheimer’s disease biomarkers increased and hemoglobin levels decreased. In contrast, participants who had low levels of the biomarkers and normal hemoglobin had the lowest risk for dementia.

One particular biomarker stood out: NfL. When combined with anemia, having an elevated level of this biomarker showed a risk for dementia that indicated an additive interaction. APOE-ε4 status also appeared to affect some results.  

The researchers also found that anemia appeared to increase risk for dementia and be linked to higher Alzheimer’s disease blood biomarkers more in men than in women, though researchers encourage caution with sex-specific findings. 

Courtney Kloske, PhD, Director, Scientific Engagement for the Alzheimer’s Association, who was not involved in the study, noted the following about the study’s findings:

“While previous research has linked anemia to an increased risk of dementia, this study adds new insight by examining that relationship with Alzheimer ’s-related blood biomarkers.”

“The research team found that people in the study with anemia, higher levels of pTau217, and a marker of brain cell death called neurofilament light chain (NfL) had an elevated dementia risk. The results also showed that study participants who did not have anemia and had lower levels of an Alzheimer ’s-related blood biomarker had the lowest dementia risk.”
— Courtney Kloske, PhD

What the study may be missing

This research provides valuable information, but also has a number of limitations. There is a risk for errors, such as in dementia diagnoses or in information that was self-reported by participants. 

The hemoglobin levels of participants fell within a particular range, and over 90% of participants who had anemia still had normal-sized red blood cells. Thus, they had a limited ability to explore more extreme anemia cases or those with abnormally sized red blood cells. Researchers further note that they looked at Alzheimer’s disease biomarkers in the serum instead of in the plasma, and the biomarkers’ concentration tends to be lower in serum. 

They also struggled with participants having missing data on hemoglobin levels and biomarkers, and these participants tended to have more comorbidities and be older than the participants they were able to include who had complete data. The authors note that these excluded participants were likely to be at a higher risk for dementia and anemia, and “their exclusion may have led to an underestimation of the associations.” 

There was also only baseline data on blood biomarkers, so researchers couldn’t explore how hemoglobin related to the Alzheimer’s disease biomarkers in the long term. 

Researchers were also limited because of the cohort they chose to use: individuals from a specific area of Sweden who were already enrolled in a long-term study. Most participants were also white. There should be caution when it comes to generalizing the results to other groups. Findings were also different between men and women, which is also an area that future research may be able to explore. Three of the study authors disclosed conflicts of interest. 

Finally, it’s important to note that this research doesn’t establish a causal relationship.

Dung Trinh, MD, internist, of MemorialCare Medical Group and Chief Medical Officer of Healthy Brain Clinic in Irvine, CA, who was also not involved in the study, noted that “anemia may not just be a background health issue in older adults, but part of the biologic context that makes the brain more vulnerable to neurodegenerative disease. At the same time, this is an observational study, so it shows a strong association, not proof that anemia causes Alzheimer’s disease or dementia.”

Could treating anemia help prevent dementia?

The research suggests that addressing anemia could potentially help with dementia prevention. Martina Valletta, MD, PhD candidate at Karolinska Institutet, and first author of the study, explained the following to MNT: 

“Our findings suggest that anemia is a relevant risk factor for dementia. Because anemia is relatively easy to detect with routine blood tests and, in many cases, treatable, it could represent a potentially modifiable target in dementia prevention strategies.”

“However, our study is observational, so we cannot conclude that treating anemia will directly prevent dementia. This remains an open question for future research,” Valletta said.

More broadly, it suggests the importance of evaluating anemia and not ignoring it.

“The main clinical implication is that anemia may deserve more attention in cognitive assessment, especially in older adults presenting with memory concerns. This study suggests low hemoglobin could be a meaningful risk marker that helps identify patients who may need closer monitoring or more complete evaluation.,” Trinh noted.

“It also raises the possibility that anemia could influence how clinicians interpret Alzheimer’s blood-based biomarkers in practice,” he added.

Why anemia alone is not a sign of dementia

“However, the findings do not mean that anemia is diagnostic of Alzheimer’s disease, nor do they prove that treating anemia will prevent dementia. For now, the practical takeaway is that anemia should not be dismissed as incidental in patients at risk for cognitive decline; it may be a clinically relevant signal that adds to the overall picture.”
— Dung Trinh, MD

The following text is a full, minimally edited transcript of the MNT In Conversation podcast episode titled: “ADHD in women: Breaking the stereotypes.”

Research has shown that women with attention deficit hyperactivity disorder, or ADHD for short, are likely to receive their diagnosis later in life. On average, women with ADHD receive their diagnosis 5 years later than their male peers.

Often they receive a misdiagnosis, such as anxiety or other mental health conditions, before a specialist accurately identifies ADHD. Many women with ADHD are missed altogether. Why exactly is that? And how can we improve our understanding of this often misrepresented condition?

I am Maria Cohut, Features Editor at Medical News Today.

And I am Yasemin Nicola Sakay, Global News Editor at Medical News Today.

Today we will delve into these and other questions around the difficulty of receiving an ADHD diagnosis as a woman on our latest podcast episode In Conversation.

You can listen to this episode in full below or on your preferred streaming platform.

Why it’s important to better understand ADHD in women

Yasemin Sakay: So Maria, I know this is a topic you’ve been very keen to tackle on the podcast. Do you feel comfortable sharing why that is?

Maria Cohut: Yeah, that’s basically because to be completely honest, full disclosure, I’m one of the many women who received an ADHD identification as adults.

Yasemin Sakay: Did that come as a surprise to you?

Maria Cohut: Not really. I think I’d always realized that my way of being in the world of interacting with things was a little bit different. Plus, I’ve had people make comments about the way in which I do things that have really struck me. For instance, working in an office, we had this little snack table and I remember, I very specifically remember this moment when I got up from my desk carrying my laptop with one hand, typing with another, walking towards the snack table and talking to one of my colleagues.

And my colleague was like, how can you do that? I was like, do what? How can you do five things at the same time? How can you walk and type and talk at the same time? To me, I realized that is just how my brain works. That is just how I function normally.

Yasemin Sakay: So why would you say you only received your diagnosis so late in life?

Maria Cohut: Well, first of all, think when I was growing up, say ADHD or neurodiversity wasn’t really a thing. People weren’t very aware of what that might be and how it might manifest. And on top of that, I had this image of being a quiet, a shy kid. I did very well in school.

Insofar as the people around me were concerned, I guess I didn’t really fit that hyperactive jumping off the wall profile that people might expect with something like ADHD or that would catch somebody’s eye. That’s why probably because I didn’t fit the template. People weren’t necessarily aware of the hyperactivity that was going on inside my brain.

Yasemin Sakay: Interesting. So do you feel like you learned to hide this very early on?

Maria Cohut: For sure I did, because I think really early on I managed to get an understanding of what was deemed socially acceptable and what wasn’t socially acceptable, or what would get me in trouble, for instance.

So I wouldn’t, I was a daydreamer, I was struggling to pay attention in class, but I would never own up to that, right? Because I figured out that people would just think that I’m being a bad student. I would like perform focus, which is a very weird thing to say, but that’s what I did.

Yasemin Sakay: Yeah, and they will present differently. So on that note, I think it’s time to welcome our special guest who will help us unpick some of these issues further.

Joining us today In Conversation is Professor Davida Hartman, Chartered Educational and Child Psychologist with the Psychological Society of Ireland, Adjunct Professor in the University College Dublin School of Psychology, as well as Clinical Director at The Adult Autism and ADHD Practice, and Co-director and Principal Psychologist at The Children’s Clinic.

Davida, welcome!

Prof. Davida Hartman: Thank you so much!

Maria Cohut: Do you mind if we start by asking you what got you interested in specializing in ADHD in the first place? Is it okay if you talk to us a little bit about that?

Prof. Davida Hartman: You know, it’s very interesting. It’s just, I often talk to a lot of my friends and colleagues who are working in this area and a lot of us that are currently working in this area have now discovered our own neurodivergence, have partners who are neurodivergent and children who are neurodivergent but when we started off at the beginning of our careers that wasn’t the case. None of us knew we were neurodivergent or had children at that stage.

And it really was just honestly, it started off by chance in that one of the jobs that I got was with, was supporting autistic children. Well, now I would know they were autistic and ADHD in schools and I really loved the work and then it flowed from there that I loved that work and then I sought out more experience in that area and then I focused on that in my college years. So it led on to that.

But what I would say is I think for a lot of us, what we realized was, well: Why were we drawn to that area? Why were we drawn to those children? And I always found that I really enjoyed their company. It never occurred to me at the time that I might be ADHD myself, but really enjoyed their company and I really enjoyed the, what I would say, the honesty in the interactions. And now I think, because what you see, I mean, what you see with neurodivergent people is, you know, they flock together, you know, once you see.

You know, there’ll be groups of friends and they’re all neurodivergent and neurodivergent people marry each other and all of this kind of thing. So I don’t think it was coincidence, but that’s how it happened. It was mostly my early career was very much in the area of autism and autistic children and then later autistic adults with the Adult Autism and ADHD Practice.

For years I’ve been working with ADHD children, but without realizing it because a huge amount of the kids that I look back now, I wouldn’t even know. And that’s part of one of the issues around ADHD experience and people not being identified as ADHD is that we don’t recognize it, we’re not identifying it enough as professionals. Like it wasn’t even until 2013 that you could be recognized officially as both autistic and ADHD, which really isn’t that. It’s so, so recent history. So ADHD is relatively new for me.

I mean, I was late identified as ADHD myself maybe 4 or 5 years ago. So I think my real interest started then. And also just seeing because my work was so much in the area of autism or autistic experience, more and more realizing that these kind of binaries between autism, ADHD and various different types of neurodivergence are so unhelpful.

It’s helpful to recognize these things as individuals so that people can understand themselves. But actually, there’s massive overlap between all these things and realising that, you know what, this is something I actually really need to understand both personally and professionally.

Why it takes so long for ADHD to be identified in women

Maria Cohut: That makes a lot of sense and we’ll come back to some of what you said just now as well. But I also just wanted to say, first of all, you took the words right out of my mouth with the birds of a feather flock together. And I’m so glad you said it because that’s also been my experience. And I’m also somebody who got a late diagnosis of ADHD. In fact, mine came last year. I’m not going to give you my age.

Prof. Davida Hartman: Congratulations!

Maria Cohut: Thank you! But it came last year and it took me… literal decades to obtain a, well, first of all, I guess, to think about asking for a diagnosis and then again, to obtain a diagnosis. And so that brings me to, I guess, the topic at hand. And I find it very striking that it takes so long for people to get a diagnosis of ADHD in adulthood and particularly for women, a diagnosis of ADHD. And my question to you is, why do you think, or why would you say, based on your experience, that is, why does it take so long for women to receive a correct diagnosis of ADHD?

Prof. Davida Hartman: You know, I think that there’s so many factors going on there from the very, very broad that our systems are medical systems, because unfortunately, I mean, we see like in our practice, we see ADHD as we’re neurodiversity affirmative. So we don’t see it as a disorder. We see it as a natural brain variation part of neurodivergence, not that it comes without its difficulties, of course, like every different neurology does.

But what I would say is that, unfortunately, ADHD is kind of housed and owned within this very medicalized, very medical model, disease disorder that was developed by white middle-aged cis men. And the DSM [Diagnostic Statistical Manual of Mental Disorders] and the ICD-11 [International Classification of Diseases 11th Revision] are based on white cisgendered children, young boys.

And so it looks at this very small, narrow way of being ADHD, which doesn’t encapsulate all the different ways that people can be ADHD and that people assigned female at birth and nonbinary people can experience being ADHD.

So we have this system that only thinks that’s hyperactive boys who can’t stay in their seat. And so there’s these kind of perceptions of being ADHD that didn’t fit how many people, not just women but many people were presenting and experiencing life. So people just literally weren’t thinking of it. Professionals weren’t thinking of it and women and girls weren’t thinking of it.

There’s also a huge amount of, I mean, listen, this is a whole other podcast, but there’s a huge amount of misogyny and distrust of women’s experiences. And so within the medical system, not just around ADHD, with anything, so that when women bring certain things to doctors or psychologists or any of that kind of thing, that their experiences would have been invalidated as, you know, and a lot of stuff would have put down to, you know, women issues and anxiety and all that kind of stuff.

And we see that across the board, not just with ADHD. So, but I think that the reason that it took decades, but I’m not sure that starting from now, it’s going to take decades because now, because the good part, I mean, there’s so many negatives about social media, but now with social media, there’s so many people talking out about their experiences.

There’s a lot more research from a personal perspective of this is me, I’m ADHD, this is how I experience the world. And so women are seeing that and are seeing other people and they’re recognising themselves, I experienced that, maybe I’m ADHD. And we’re talking more vocally, we’re going to the professionals and we’re saying, no, I think that I might be this, I want this looked at.

Does ADHD present differently in women vs men?

Yasemin Sakay: Yeah, no, you’ve touched on a great point there. You were about to come to how it presents differently maybe in women and girls. And I thought, how about let’s talk about the symptom differences? Like how does ADHD present in girls and women versus boys and men?

Prof. Davida Hartman: So the way that we approach ADHD, we come out from a neurodiversity-affirmative a perspective. So we don’t actually use the language of symptoms. Now I know everybody does. ADHD is very much owned by most of the researchers coming from the medical community. So it’s very much symptoms, diagnosis, all that kind of thing. But we don’t actually use symptoms because if you think about it, symptoms is the language of disorder and disease. So we use traits instead. And it’s a really helpful way of, yeah, it’s really helpful.

We don’t even use diagnosis. If you hear me saying identified and that I’m formally identified because diagnosis again we diagnose disease and disorder and look the thing is we are like officially you know people are like well you are diagnosing you are making a formal identification but you know language matters and we’re trying to shape the future and all that kind of thing.

But anyway so what I would say about the I know I talked about how it can present differently but actually I don’t know personally that it does actually present differently because I think that what we’re getting into there is, and people would have said that about being autistic also as well as ADHD, that it’s kind of buying into this idea that there are two different ways, that there is one way of being ADHD, but actually ADHD can look so, different whether, depending on where you live, depending on your culture, depending on your personality, depending on what’s going on in your life.

And I don’t necessarily think that there is, I don’t think ADHD itself presents differently in men and women. I think that men and women can be different and see we have to take into account nonbinary people as well of course and trans people and how does that fit then if you’re trans or nonbinary into that. So I think that notion that it can look different stops people from receiving the correct identification if you know what mean because I think there’s lots of women that do actually present in that how people would say a typical boys presentation but that it’s just not picked up because we’re not expecting it to be ADHD.

And then also you can’t get away from the societal expectations put on women to be good and to sit and be nice and to not say what we’re thinking and to manage everybody’s feelings and all that kind of stuff. And so we don’t even know how much of that cultural conditioning is going on in terms of how much. Possibly because of cultural conditioning it can look different.

Yasemin Sakay: You touched on a great point again, speaking of cultural conditioning and hiding. So a term that I’ve come across is masking. So do you think people who have lived with ADHD for longer, but they haven’t known it, do they learn to mask this better? And does this kind of further impact the likelihood of them seeking out medical help or like a diagnosis?

Prof. Davida Hartman: There is emerging research around masking, but a lot of is it within the autistic community, not as much within the ADHD community, because there’s a much more organized autistic community that are doing a lot more advocacy work in this area, whereas the ADHD advocacy community is smaller. It’s getting bigger, but it’s smaller and a bit less vocal around stuff like language and things like that, whereas with the autistic community, it’s a lot stronger. But again, it’s because ADHD is so significantly linked to medication. And so again, it’s housed within the medical community.

Okay, so masking is a huge issue. So for example, an example might be talking less, for example, you know, and again, there’ll be some situations, I mean, as you can tell already, I am a talker, so, you know, an example of me masking would be in some situations where I would have to really be working on talking less, you know, not saying every thought that came into my head, all of that kind of stuff.

And in some situations that’s actually helpful and I need to do that. But in other situations where someone might do that in social situations, so they might be around friends, like it’s supposed to be a situation where they’re enjoying themselves and getting support from their community of friends, but instead they’re working really hard on acting a certain way, communicating in a certain way, and actually that just causes significant stress on the person.

And also that leads to feelings of shame because usually they get it wrong or they might say things, blurt out and then they’re going home and they’re thinking about the things that they said and they wish they hadn’t said that. But there’s a lot of emerging research that masking is really significantly negatively impacts people’s mental health. And it gets to a kind of breaking point where people don’t even really know themselves because some masking is conscious and a lot of masking is unconscious. Like we were talking about how women learn to be nice and manage feelings and all that kind of stuff. A lot of that is unconscious.

I think that sometimes it just gets harder as we get older and then if we’re talking about women here, when perimenopause hits and when the demands increase, that it becomes harder and harder for people to mask and that’s when they start to think, okay, this is actually becoming a little bit untenable and what’s going on here.

Does perimenopause influence how ADHD presents?

Maria Cohut: Hold that thought, let’s come back to that because we have some questions about that as well. I just wanted to be very vulnerable here and interject and say this is genuinely bringing tears to my eyes. I think that is so true, the emotional and mental health toll that forcing yourself to fit a certain image when that is not the way in which you naturally interact with people and I think you know there’s obviously value in being a socially conscious person and knowing when to take space and when to give somebody else space to talk and talk about their experiences and whatnot.

If it crosses a certain line where you feel like you’re constantly holding back, that’s when it becomes really hard on the individual. I love what you said about how people assigned female at birth or people who, you know, have an experience of girlhood like me perhaps learn how to mask really early on because thinking very far back into my past, to my childhood, I am very aware that I was very conscious very early on that there were certain things I shouldn’t do and I shouldn’t say because people expected me to behave a certain way.

And so I learned very quickly not to do and not to say those things. But you mentioned perimenopause, making it harder to mask, to pretend that you don’t have these traits and this way of interacting with the world. I’m going to start broad and then maybe zoom in a little bit.

When you’re thinking of perhaps women who seek a diagnosis later in their adulthood, in their thirties, in their forties, maybe later, why do you think that is? And obviously perimenopause appears to be a factor. So how does that specifically affect how ADHD presents and how we’re able to manage it? And are there, you think, other factors, maybe?

Prof. Davida Hartman: There’s a bit of emerging research, again, we’re very early days in terms of research in this area, there’s very small studies, and very small studies in perimenopause as well as ADHD, you know, a lot of the research into ADHD is very deficit-focused and not focusing on women also.

There is research that’s kind of indicating that it’s possible that ADHD people, experience perimenopause earlier and certainly have more significant perimenopausal symptoms than people who are not ADHD. And I also think on top of that, and even anecdotally, what I would say is anecdotally and from a personal perspective, for me, I am ADHD, it did affect me. I didn’t realize. Looking back, it was very clear, but I had very scaffolded… So I think this is also the thing.

People who are very supported in earlier life, who have supportive parents, they’re able to manage that because ADHD, while it’s described at the moment in the DSM as this very deficit-based problem with attention, what we know is that there’s no… ADHD people have loads of attention. It’s just a difference in the way that we attend. So it’s very much based on novelty and it’s based on interest and it’s based on all of those kind of things. So there’s this abundance of attention that we can give to things. And creativity.

I had friends. I did fine in school. But it was only later in life when I had children. And then really it was when perimenopause hit that I thought, actually, I can see, I actually received my identification before I went through perimenopause. But that was only because colleagues of mine, friends and colleagues would say to me, you know, you’re very ADHD. And then I went to a psychiatrist and did the assessment and he was like, yeah, you’re ADHD.

And honestly, I was surprised at the time. I didn’t even, I had worked in the area for years. I was like, really? I am. Oh, okay. And again, not to go too broad with this, but where we are in society at the moment in terms of we’re losing our communities. We’re talking about women here, but middle-aged women previously would have had a community of support and even and would have been able, a lot of women would have been able for example to not be working two jobs now with the state of the economy.

Yasemin Sakay: So what I’ve kind of understood from what you’ve been telling me basically perimenopause dialed up a lot of your ADHD traits or made them more apparent. Is that correct?

Prof. Davida Hartman: Did it dial up or was it, do know what, was more, I don’t think, no, I don’t think that they dialed up, but it was more the difficult, because as I said, there’s massive strengths to being ADHD. And I wouldn’t say that my strengths are dialed up as in I don’t think I talk more than I used to, or I don’t think when I hyper focus, I hyper focus more than I used to.

But I would say in terms of my forgetfulness and in terms of say executive functioning, it’s just too many tasks. I think with perimenopause, as well your emotions are all over the place. It’s more your emotional reaction, your kind of emotional bandwidth to handle stress I would say gets harder.

Yasemin Sakay: So yeah, okay, so I’m gonna draw on something else you said. So you were talking about executive dysfunction and I’m thinking of brain fog, for instance. These perimenopause symptoms can look a lot like ADHD. How can we actually tell them apart if they’re perimenopause symptoms or ADHD?

Prof. Davida Hartman: Oh yeah, they’re very similar. But the thing is that to be ADHD, you have to have shown traits before the age of 12. To do an assessment, it has to be a really rigorous, in-depth assessment. And I know that there’s a lot of talk on social media, oh, everybody’s being diagnosed as ADHD and… ADHD and private companies.

Every so often there’ll be something about private companies and they’re just… handing out ADHD diagnosis willy nilly you know but actually it’s so not the case you have to go through a very rigorous assessment process where there has to be signs before you were 12 there has to be an impact on functioning and all this kind of things.

How do you confirm ADHD was present since childhood?

Maria Cohut: First of all, let me just confirm everything you said about how rigorous the assessment is. It really goes into a lot of details about just your life’s history and all of that. I find it very difficult to believe that people are just handing out these diagnoses or identifications like that.

But the difficulty that I have also found, and I think other people have also found with this has to have been present in your life before the age of 12 is that there are people who don’t have somebody in their lives who was present during their childhood, for instance.

Or maybe they do, but they are one of those people who are like, what, what’s ADHD? It’s not real. Everybody’s got ADHD these days. That’s just normal. Why are you, why do you think, why do you think you’re ADHD? I wonder how we can square up and deal with that difficulty. I don’t know there’s an answer to that question.

Prof. Davida Hartman: No, yeah, it’s really hard and we, like in the Adult Autism and ADHD Practice, we gather information and sometimes, because a lot of the time people remember, you know, again, it goes back to this mistrust of people. I really hate that culture not trusting people to talk about their own experiences. I really trust people.

So if they’re talking about their early experiences, and they’re saying, I struggled with this is what happened in school, this was me when I was younger. That’s all really valid and sometimes it just happens that the person can’t remember, there’s nobody there that does remember or the person that does remember as you say, because obviously this is all massively genetic and so if you’re ADHD it’s exceptionally likely at least one of your parents is ADHD as well. Of course they’re like, it’s all not… ah sure everybody, that was completely normal. Everything was, you know, normal in inverted commas. And it was normal and isn’t that great? I mean, at the same time, it’s wonderful because it means that…

So unfortunately that can happen though, because there are professional standards. So we really support self-identification. Like there’s no reason why, you know, if somebody wants to investigate the traits of ADHD or various neurodivergences, they can’t self-identify because we can have this conversation with somebody who comes into us. Okay, there’s no evidence from before the age of 12. However, from all the information you provided to us, it’s really looking likely.

You know, you have all these traits, your friends are all ADHD, your children have been identified ADHD, let’s face it, you know, you’re most likely ADHD even if we don’t have this evidence. And I have seen very good psychiatrists do situations where, okay, we don’t have that evidence, but we can still, with the psychiatrist’s support, we can still trial medication and see if it’s supportive.

You’re not going to get that everywhere because there’s a lot of bad practice out there. But yes, it is an issue.

Does everyone with ADHD need medication?

Yasemin Sakay: Does everybody that has ADHD need medication?

Prof. Davida Hartman: No, it’s so individual. It’s so individual. I think that you see, it’s a funny one because we come from a neurodiversity affirmative framework where we reject a medical model of disorder. But yes, we’re still within a system where people genuinely do get benefit from medication.

And I do know a lot of people that have come through us have really been very well supported by stimulant medication. But a lot of people aren’t. And I think what’s really unfortunate is there’s a lot of people who really pin their hopes on… I’m going to get this ADHD identification and then I’m going to get medication and my life is going to be perfect because they see all these people online.

There’s a lot of videos online, people saying, I took the ADHD meds and my mind suddenly went quiet and I didn’t hear voices and I was able to get everything done. But it doesn’t work for everybody. It doesn’t suit everybody. It’s very individual about whether a medication is going to support or suit somebody or whether they like it or whether they want it. So it’s certainly not to be all and end all.

But loads of people find it very helpful. And you know, it’s something that I’ve had to learn, you know, like, it’s one of the areas where, what we always talk about this as a team, that we need to remain open and curious and not kind of stake a flag in this is what we believe right now. Because earlier on in my career, I would have been very anti-medication. And now I think back and go, I really didn’t have a clue. Because I’ve seen now the benefit that it can have, and I’m just more knowledgeable about the area. But I think it’s really individual to the person.

What are the biggest obstacles to receiving an ADHD identification?

Maria Cohut: What you just said makes a lot of sense to me because there’s no one size fits all approach, right? For this kind of stuff, everybody needs to find what suits them best for the life that they live and who they are as a person. But I was just going to go briefly back to this notion of obstacles.

So we’ve talked about why people might choose to seek identification later in life. But I was going to ask what obstacles, what are some obstacles that women in particular face when it comes to accessing identification?

Prof. Davida Hartman: Well I think there’s obstacles for everybody at the moment in terms of the waiting lists are absolutely huge. know even if you know that you want an assessment and you’re trying to get one, the waiting lists are absolutely enormous and then to go privately obviously costs money. We did talk about it before but people seeing and professionals seeing this you know that ADHD is one specific way and that maybe a lot of women don’t necessarily come in presenting in that one specific way.

I think that a lot of professionals don’t really realize that ADHD can look so different for different people and can be so much about internal experiences. And a lot of professionals don’t realize, for example, that you can be successful in some areas. A lot of people that come through our practice are doctors, psychiatrists, and also artists and people that are employed and people who find it very difficult to hold down a job. But there’s also, you know, it’s such a wide variation of people. And I think that there really needs to be more education around what ADHD can actually look like.

Also I think that the fact is that because usually at that stage there is mental health issues, for example depression, anxiety are all linked and so everything gets this kind of that overshadowing where people think well they’re anxious and depressed. And that’s why all of these things are happening.

And it’s literally people, think the professionals just literally aren’t thinking about the possibility that this woman might be ADHD. I mean, I personally think that in all mental health services, there needs to be screening for neurodivergence, ADHD and autism across the board, even just to get professionals starting to think that this might be a possibility. I think that’s the biggest obstacle probably.

Maria Cohut: It makes a lot of sense to me again because I suppose a lot of the time, the longer that you’ve gone through life without identifying your specific flavor of neurodivergence, that can cause a lot of anxiety, a lot of depression-like symptoms, that can cause a lot of mental health and emotional struggles because you might not know why it is or like you might struggle again to fit this mold that people around you have created for you.

Prof. Davida Hartman: And it’s so important because in order to support anxiety and depression in all those different areas, we have to have an understanding of ourselves. that, for me, that’s the most important. And then it gives this permission to be yourself.

And that’s not to say that anxiety and depression goes away. Of course, it doesn’t. But it’s the start of, I think, people living much more authentic, happy lives is to truly understand themselves and why they do things in a certain way. And that’s the biggest benefit I would see of a of an identification, formal identification.

How should we reframe our thinking around ADHD?

Yasemin Sakay: So, Davida, what would you say is a constructive way for us to think about ADHD or neurodiversity?

Prof. Davida Hartman: Well, in terms of ADHD, I think that the really constructive way is to think about it not as a deficit of attention, like I said, but a variability, just a different type of attention. We talk about biodiversity in the natural world. To think about neurodiversity as there’s just different types of brains.

Each type of brain has different strengths and different challenges. And that ADHD can be seen as this variable attention, different types of attention, because in the world that we live in, in kind of Western civilization, let’s say, there’s a real emphasis on behaving neurotypically and what I call selective attention. Andso, which is basically being able to pay attention to one thing and one thing only.

So, you know, in school, for example, stop fidgeting because they’re not paying attention. Whereas with ADHD, there’s this variability of attention. So there’s an ability to pay attention to loads of different things at the same time. And there is very much interest based so if I’m really interested in that, I can pay attention to that so well. If I’m completely uninterested, then we’re going to see problems, then I’m going to really struggle. And that’s the case for me. It’s the case for like it’s one of the core kind of basis of ADHD.

But if you think about it, there’s nothing in itself wrong with that. We need lots of different brains. We need people who pay attention in different ways. And again, there’s going to be challenges with that because obviously in life there’s going to be, we’re going to have to do boring things sometimes. And so there’s going to be challenges there.

But then if you think about say a neurotypical brain that’s very good at selective attention but maybe isn’t so great in a crisis or maybe isn’t going to sit and really hyperfocus to the extent that they become absolute, you know, professional, like a lot of professional athletes, for example, are ADHD. Or if you read, like any time that you read about where there’s been massive discoveries made, for example, of our inventors, they’re often, when you read the stories about them, they’re clearly neurodivergent, like they’re clearly autistic or ADHD or usually both.

With neurodiversity, we really need to move to a place where we’re not saying this is the best way to be is the person that can sit down in a classroom or in a work place, in a work office and do their work. We need all those different types of brains in order to progress as a society.

How to support women with ADHD

Yasemin Sakay: On that note, I want to know as a person with lots of neurodivergent friends, what can I and what can we do to better support people, especially women in our lives who have or suspect they have a form of ADHD?

Prof. Davida Hartman: I think the most important thing is really just accepting people how they are. If you’re friends with someone, not getting angry with them for things like not texting or being late or forgetting your birthday. If you know they love you, you know that they care about you and they’re showing up for you in all these other ways, those are the things that people can feel really ashamed about.

Like what kind of a friend, because there’s this expectation if you forget somebody’s birthday, they don’t really care about you. If they haven’t texted you in two weeks, they don’t care about you, they don’t want to talk to you about it. And often it’s times it’s really not the case. It’s just issues with time perception and executive functioning and all those kind of things.

Because it’s something that they’ve done in the past they feel shame about, then they go into a shame spiral and then they don’t text at all. So I think as a friend, if you’re just kind to people and don’t take those things as signs that they don’t like you or care about you, that it’s just their neurodivergence and that, you know, that we show up to our friends in different ways. I think that it’s around that acceptance and normalization and not shaming that’s the most important thing from friends.

Maria Cohut: Once again, you’ve brought tears to my eyes, I have to say, because I recognize myself in some of the things that you described, and I have a huge problem with remembering dates, and particularly birthdays. And I have a list that I’ve written down of the birthdays of every single important person in my life, family, friends, chosen family, if you like. But the problem is I have to remember to look at it, which I sometimes don’t if I’ve had a bad day.

And then I remember the next day and I’m like, oh no, and I feel so bad about it because it’s actually important to me to remember and to make those people feel loved and to demonstrate that I care. And sometimes it just doesn’t work out that way. And it’s what you’re talking about, the shame spiral that really gets to you in the end.

Prof. Davida Hartman: It’s so important because people do hold such shame about it and it’s really not. It’s like expecting somebody in a wheelchair to walk at all. You know, it really is a difference in their… I forget people’s names. Sometimes I forget my friends’ children’s names. And these are people I care about. I care about so much. You know, I meet people I’ve forgotten their names and I know that society sees that as a sign of that I didn’t care about them or I didn’t like them or I weren’t interested in them. And it’s so not the case.

So, and I think that it’s really helpful when you are ADHD to be able to say that to your friends. Look, I know that I forgot your birthday, but you know, it’s not me, it’s my ADHD. But then we have bit of a laugh about it. But I do try and I, you know, I put in, I put it, but I think it’s going easy on yourself. You know, us going easier on our friends helps them be easier on themselves as well.

Maria Cohut: Thank you. And I’m going to be very annoying now. have, before I say goodbye, I have one final question and I think it’s going to be an annoying question because we just discussed how there’s no one size fits all approach for people. But based on your experience, professional and personal, if you like, if you had to give ADHD women, some tips or advice on how to manage themselves better, how to manage those aspects of ADHD that show up for them that interfere with their quality of life, what would you suggest?

Prof. Davida Hartman: I think that women, I think we take on a lot. I think, you know what, I think it depends on the life setup of the person. So what I would say is for women who are in relationships with children, with men, in straight relationships with men, with children, what I would say is to really work on not taking on everything.

I think that we’re kind of culturally conditioned and also we’re just very caring but we take on a lot and we do a lot and there’s a lot of expectations around we have to do the tea morning in the school and we have to do all the costumes for Book Day and we have to, I suppose actually it’s broader actually I think that’s a broader point it’s not just about women in straight relationships there’s a broader point around we don’t actually have to do everything, you know.

We don’t have to bake the cupcakes and we don’t have to sew all the things and we don’t have to do all the school activities. I think it’s moving away from these societal expectations of how we’re supposed to show up and how we’re supposed to look perfect and be on time and figuring out what’s too much because there is that idea of the mask, the oxygen mask on the airplane that we can’t if we’re not looking after ourselves and our health and getting exercise and doing the things that give us energy that it’s impossible for us to keep going. So we need to also think about ourselves, not just be caring for everybody else and looking after everybody else.

Maria Cohut: Thank you so much, Davida. This has been such a fabulous discussion, so important. I feel like we’re going to come back to it in the future. If you’re happy to rejoin us on the podcast in the future, I’m making this official right now, live on air. We would love to welcome you back because there’s just so many follow-up questions that I now have. But thank you so much. This has been absolutely fantastic. Really appreciate it.

• GLP-1 receptor agonists such as Ozempic, Zepbound, or Mounjaro are used to treat type 2 diabetes and obesity, however, they may also have positive effects on other health conditions.
• Researchers have been examining other potential uses for GLP-1 drugs outside of managing diabetes and weight loss, including treating rheumatic diseases. 
• A new study has discovered small amounts of the body’s natural GLP-1 hormone in the body’s synovial fluid, or joint fluid.
• Scientists believe this finding may potentially open up a new treatment option for various forms of arthritis, such as osteoarthritis and rheumatoid arthritis. 

There’s no denying the fact that the use of glucagon-like peptide-1 (GLP-1) medications has been steadily increasing. Recent studies found that about one in every eight Americans and about one in 10 people in Great Britain are taking a GLP-1 medication like Ozempic, Zepbound, or Mounjaro for weight loss or type 2 diabetes treatment. 

Over the last year, researchers have been examining potential uses for GLP-1 drugs outside of diabetes treatment and weight loss. For instance, past studies show that GLP-1s may also aid in treating cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), and rheumatic diseases, such as rheumatoid arthritis and osteoarthritis.

Now, a new study published in the journal The Lancet Rheumatology has discovered small amounts of the body’s natural GLP-1 hormone in the body’s synovial fluid, or joint fluid, potentially opening up a new treatment option for arthritis. 

Why focus on GLP-1s? 

For this study, researchers analyzed blood and joint fluid samples from participants of the Inflammation in Arthritis (INART) biobank at Aarhus University Hospital in Denmark. Study participants either had rheumatoid arthritis or spondyloarthritis.

“Arthritis comprises a range of diseases that cause joint pain, inflammation, and reduced quality of life,” Tue Wenzel Kragstrup, MD, PhD, associate professor in the department of biomedicine at Aarhus University, medical specialist in the Department of Molecular Medicine (MOMA) at Aarhus University Hospital in Denmark, and lead author of this study, told Medical News Today.

“While effective treatments exist for some forms [of arthritis], many patients still experience insufficient disease control or side effects. There is therefore a continued need to explore new biological pathways that could lead to improved or complementary treatment strategies,” Kragstrup continued.

Kragstrup said he and his team became interested in GLP-1-based therapies because experimental studies suggest that they may have direct anti-inflammatory and tissue-protective effects in joint disease. 

“At the same time, recent clinical studies have reported beneficial effects in conditions such as osteoarthritis and psoriatic arthritis,” he said. “However, from clinical studies alone, it is difficult to know how much of the benefit is due to direct effects in the joint and how much may be explained by weight loss or broader metabolic changes.”

“That is why we wanted to address a basic mechanistic question first: whether GLP-1 is actually present in the joint environment. If GLP-1 is detectable in synovial fluid, that supports the biological plausibility that GLP-1-based therapies could potentially act directly in the joint as well as systemically.” 
— Tue Wenzel Kragstrup, MD, PhD

Natural GLP-1 detected in joint fluid

After comparing participants’ blood and joint fluid samples to those from healthy volunteers, researchers detected small amounts of the body’s natural GLP-1 hormone in joint fluid. 

“The key finding is that GLP-1 can be detected in synovial fluid,” Kragstrup said. “This suggests that the joint is exposed to circulating GLP-1, but only to a limited extent under physiological conditions. This provides a biological basis for considering whether pharmacological GLP-1 therapies, which achieve much higher systemic levels, could also reach the joint and potentially have local effects.”

Additionally, scientists found that the level of GLP-1 hormone in the synovial fluid is directly tied to the levels in the blood of arthritis patients.

“We observed a clear correlation between GLP-1 levels in blood and in synovial fluid. This suggests that joint levels largely reflect systemic levels, likely through passive distribution from the circulation. This is important because it indicates that any increase in systemic GLP-1 levels (for example through medication) could potentially influence the amount that reaches the joint.”
— Tue Wenzel Kragstrup, MD, PhD

“The next step (in this research) is to find out whether GLP-1-based drugs reach the joints in high enough concentrations to have biological effects there,” Kragstrup continued.

“In collaboration with Steno Diabetes Center, we also plan to analyze blood samples from patients who have either received GLP-1-based treatment or undergone bariatric surgery, to see whether one of these approaches has a stronger effect on inflammation more broadly. This may help us separate effects related to the drug itself from effects related to weight loss and improved metabolism,” he added.

Be cautious of ‘over-interpreting’ findings

MNT spoke with Jeffrey Zarin, MD, an orthopedic surgeon specializing in joint replacement surgery at Cedars-Sinai Orthopaedics in Los Angeles, CA, about this study, who commented that his first reaction was to be cautious about “over-interpreting” its findings.  

“There are many studies that appear in the literature that identify new ideas or pathways for common problems such as arthritis, but often they represent very early stages of research to establish an understanding of the condition,” Zarin explained.

“‘Over-interpretation’ means that people may take this early information and interpret the findings in a way that suggests a treatment plan or improved technology that is not correctly derived from the study findings or outcome,” he told MNT.

“For example, in this study it establishes that GLP-1 and its derivatives have been able to be measured in synovial fluid,” he continued.

“It would be incorrect to conclude that because these proteins are present in joint fluid, that using a medication that affects their levels or efficacy will change the nature of arthritis. In fact, this study shows that the levels of these molecules are significantly lower in joint fluid than in the blood/plasma and may be incidental to the function of the joints.”
— Jeffrey Zarin, MD

“Also, there did not seem to be a difference between patients that had arthritis and those that did not, so conclusions about the effect of GLP-1 on arthritis should also be interpreted cautiously,” Zarin added. 

Zarin said it would be appropriate to follow the authors’ suggestion that the next step in their research should be to perform studies to assess whether GLP-1 levels in the joint fluid are correlated with the arthritic condition.  

“If there is a correlation, then further studies that assess interventions which can affect the GLP-1 levels and their effects on the symptoms and conditions of arthritis could lead to novel interventions for patients with arthritis utilizing the findings of the studies,” he said. 

• More than 55 million people worldwide are living with Alzheimer’s disease, estimates suggest.
• Treatment for Alzheimer’s disease currently includes medications, such as anti-amyloid drugs that work to remove amyloid-beta plaques from the brain of those with early Alzheimer’s disease.  
• A new study says that anti-amyloid medications may not have any clinically meaningful positive effects, and may increase the risk of swelling and bleeding in the brain.

Scientists believe there are more than 55 million people globally living with a type of dementia called Alzheimer’s disease.

While researchers are still unclear as to the actual cause of the condition, the current theories include a build-up of two proteins in the brain that form beta-amyloid plaques and tau tangles. 

There is currently no cure for Alzheimer’s disease. The disease is treated through a multifactorial approach that includes lifestyle changes, therapies, and medications that may help slow progression of the condition and manage its symptoms.

Some of these medications include anti-amyloid drugs, which work to remove amyloid-beta plaques from the brain of those with early Alzheimer’s disease.  

Now, a paper recently published in the Cochrane Database of Systematic Reviews has concluded that anti-amyloid medications may not have any clinically meaningful positive effects, and may actually increase the risk of swelling and bleeding in the brain.

Anti-amyloid meds may make little to no difference to dementia symptom severity

For this review, researchers analyzed data from 17 clinical trials, encompassing a total of more than 20,000 study participants with average ages between 70 and 74.

All the studies used were researching the use of anti-amyloid medications to treat participants with mild cognitive impairment (MCI) or mild dementia due to Alzheimer’s disease. 

At the study’s conclusion, the researchers found that, after 18 months, anti-amyloid medications may make little to no difference to dementia symptom severity and probably make little to no difference in the decline of memory or thinking ability. 

“Unfortunately, the evidence suggests that these drugs make no meaningful difference to patients,” Francesco Nonino, MD, a neurologist and epidemiologist at the IRCCS Institute of Neurological Sciences of Bologna, Italy, and lead author of this study said in a press release.

According to Nonino, “there is now a convincing body of evidence converging on the conclusion that there is no clinically meaningful effect.“

“While early trials showed results that were statistically significant, it is important to distinguish between this and clinical relevance. It is common for trials to find statistically significant results that do not translate into a meaningful clinical difference for patients,” he pointed out.

Additionally, researchers reported that the use of anti-amyloid medications likely increased the risk of swelling and bleeding in the brain. 

Does this mean anti-amyloid drugs are better left behind?

Medical News Today had the opportunity to speak with Megan Glenn, PsyD, a clinical neuropsychologist at the Center for Memory and Healthy Aging at the Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Center in New Jersey, about this review.

Glenn, who was not involved in the research, commented that while this review provides a valuable, high-level summary of the evidence to date, we must nevertheless be very careful in how we interpret its conclusions. 

“It’s crucial to understand that this review pools data from 17 different trials spanning many years, the majority of which involved older, unsuccessful drugs,” Glenn explained.

“Only two of the trials studied the recently approved treatments, lecanemab and donanemab. While the review’s overall conclusion finds no average clinically meaningful effect across all these drugs, it doesn’t erase the specific findings from the pivotal trials for the newer medications,” she emphasized.

“Those individual trials for lecanemab and donanemab did show a small, statistically significant slowing of cognitive and functional decline. This review reinforces the central question we as clinicians have been grappling with all along: Is that small effect — for instance, a 1-to-2-point change on a 90-point cognitive scale — truly meaningful in a patient’s daily life? When you weigh this modest benefit against the very real and frequent risks of brain swelling and bleeding, the risk-benefit calculation remains a serious conversation that every patient and family must have with their doctor.”

– Megan Glenn, PsyD

Understanding the importance of continued research

Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, a part of Baptist Health, told MNT that when it comes to Alzheimer’s disease research, it is crucial for scientists to assess both successful and unsuccessful medications. 

“When a drug or drug class shows no clinical benefit, it prompts a reassessment of the disease mechanisms, drug properties, and fundamental hypotheses,” Gliebus, who was not involved in the current review, explained.

“Understanding why some drugs fail can offer valuable insights into drug delivery, blood-brain barrier crossing, dosing strategies, patient selection, and trial design,” he continued.

While Gliebus reiterated that “the review emphasizes that removing amyloid from the brain doesn’t always lead to clinical improvement,” he also outlined why it is important to stay hopeful, noting that:

“Learning from failures is vital for scientific advancement, helping to refine research questions, prevent repeated mistakes, and develop more effective, targeted treatments. By considering both successful and unsuccessful approaches, the field stays dynamic, self-corrects, and remains receptive to new ideas.”

Review results do not change real-life clinical practice

MNT also spoke with Paul Monroe Butler, MD, PhD, an assistant professor in neurology at Harvard Medical School and neurologist at Mass General Brigham, about the recent review.

Butler, who was likewise not involved in this research, said his first reaction was that this review does not change what occurs in real clinical practice with the FDA-approved therapies lecanemab and donanemab. 

“The study pools successful and unsuccessful anti-amyloid drugs together, so it is not surprising that the average class effect looks modest,” he pointed out.

However, he added: “I wouldn’t accept the premise that anti-amyloid therapy has no clinical viability. At Mass General Brigham, one of the largest treatment programs in the world, we are seeing that these therapies can be delivered safely and can meaningfully slow progression for many patients with early-stage Alzheimer’s disease.“

“The real future is building on that foundation — combining amyloid-lowering with next-generation treatments that target tau, inflammation, and neurodegeneration,” Butler stressed.

He also noted that: “Alzheimer’s is not a single-pathway disease, and no one mechanism will be the whole answer. Each study — whether it succeeds or fails — sharpens our understanding of the biology, helps us identify which patients benefit, and guides us toward more effective and precise treatments. That iterative process is exactly how we move from early, modest therapies to increasingly transformative ones.”

What other treatment options might work for Alzheimer’s disease? 

If the anti-amyloid medication approach has no clinical viability, then what other treatment options are there that might work? 

Glenn said the focus on amyloid has been important, but we know Alzheimer’s is a complex disease. 

“In practice, we often see a mix of issues in the brain beyond just amyloid plaques,” she explained. “This is why the future of treatment must look at other targets.”

Glenn said several promising strategies are being pursued, including: 

• Targeting tau: “Another protein called tau forms toxic tangles inside brain cells, and the amount of tangles is closely linked to memory loss. Researchers are developing therapies to stop these tangles from forming and spreading.”
• Improving overall brain health which includes reducing chronic inflammation and supporting the brain’s energy supply: “This is the ‘heart-brain connection’ you hear about — the idea that managing blood pressure and diabetes, along with lifestyle choices like a heart-healthy diet and exercise, can help protect the brain,” she added. 

“The future [of Alzheimer’s treatment] likely isn’t one single magic bullet,” Glenn said. “The most effective approach will probably be a combination therapy, where treatments are personalized to address the specific mix of issues — whether it’s amyloid, tau, or vascular problems — in an individual patient.” 

• People with attention deficit hyperactivity disorder (ADHD) may struggle with maintaining focus for long periods of time, overall energy levels, and persistent anxiety.
• One strategy that may help adults with ADHD manage these aspects involves making healthier dietary choices and opting for foods linked to better brain health, energy boosts, and emotional regulation.
• Cardiology dietitian Michelle Routhenstein shares what a nutrition expert would eat in a day to help with ADHD.

Attention deficit hyperactivity disorder (ADHD) presents differently in every individual. However, some common aspects of ADHD include difficulty maintaining focus, recurring anxiety, and low energy levels.

Adults with ADHD may choose to take medication, undergo therapy, and incorporate various lifestyle changes in order to minimize the impact of some of these aspects.

One easier-to-achieve lifestyle change centers on diet, as many foods can support brain health, emotional regulation, and energy levels.

Michelle Routhenstein, MS, RD, CDCES, CDN, a preventive cardiology dietitian at EntirelyNourished, shares her top expert advice on what to eat as an adult with ADHD that will help you feel your best self.

Why keto may not help with ADHD

“Restrictive approaches like ketogenic diets are frequently promoted online for ADHD, but there is currently no direct clinical evidence supporting keto for primary ADHD,” Routhenstein told Medical News Today.

For one, she said, “blood sugar stability is particularly important in ADHD because the brain is more sensitive to fluctuations in blood glucose, which affects the consistency of energy supply to the brain.”

“With blood sugar swings and rapid drops, it can cause irritability, fatigue, brain fog, and increase anxiety,” she explained.

“While it may seem like a low-carbohydrate diet [like keto] would ‘fix’ this, stable energy actually depends on the right balance and proportions of carbohydrates, protein, fiber, and healthy fats to slow digestion, support glucose regulation, and provide the nutrients needed for efficient energy utilization.”
— Michelle Routhenstein, MS, RD, CDCES, CDN

A hidden danger in ADHD: Heart health risks

Beyond the obvious challenges that certain ADHD traits may pose on a day-to-day basis, there are also many hidden risks.

Recent research has suggested that people with ADHD are at a heightened risk of a wide range of chronic conditions, including cardiovascular diseases, which Routhenstein also pointed out.

“It is important to recognize that adults with ADHD also appear to have substantially higher rates of cardiovascular disease than adults without ADHD, with large population studies and meta-analyses suggesting roughly a 1.7–2.0 times higher risk,” she emphasized.

“A keto diet may increase risk of cardiovascular disease, and as a preventive cardiology dietitan, I would strongly advise against it,” she continued.

What is the best diet for ADHD?

So then, what works?

“While there is no single ADHD diet, research shows that a personalized plant-forward, nutrient-adequate Mediterranean-style diet pattern can help with focus, anxiety, cravings, and stable energy levels throughout the day,” Routhenstein told us.

She said that “the strongest evidence” yet indicates that prioritizing the consumption of fresh vegetables, fruits, whole grains, legumes, nuts, seeds, and fatty fish can boost brain health and help people feel well-rested for longer.

At the same time, she noted that it is best to avoid ultra-processed foods, products high in added sugars, and refined carbohydrates, all of which have been tied to negative impacts on the brain and health.

For example, a study from 2024 found that ultra-processed foods are linked to a heightened risk of cognitive decline, and a 2023 review of the existing evidence found a similar link with added sugars.

Refined carbohydrates, as in many types of white bread, pasta, and store-bought pastries, have likewise been linked to poorer cognitive performance.

What about ARFID?

One thing to keep in mind is that some people with ADHD have a strong aversion to certain flavors, smells, and food textures. For some, not all, this can be a sign of another condition, called avoidant/restrictive food intake disorder (ARFID).

“I have many clients who were diagnosed with ADHD in adulthood, and they often share what they call ‘picky eating’,” Routhenstein told us.

In such cases, people can work with a dietitian to identify foods they can enjoy and that provide the best nutritional profile.

“These ‘picky eating’ tendencies are usually sensory-based, where a person needs certain textures to comfortably eat foods, and may have strong aversions to others. When I help bridge the gap by achieving nutrient adequacy within their texture preferences, it supports their heart health goals and helps improve their overall energy, reduce anxiety, and decrease intense cravings.”

— Michelle Routhenstein, MS, RD, CDCES, CDN

• As we age, our bodies and our busy lives may make it harder to stick to an exercise routine but there are some ways to overcome the obstacles, experts say.
• Moreover, recent research suggests that matching the timing of exercise to a person’s chronotype may be the most beneficial to health but how can one achieve that?
• A sports medicine expert offers tips on how to find the best time to exercise, how to overcome tiredness and stick to your sports routine, and how to maintain motivation to work out.

Exercise benefits all aspects of human health, and public health experts all agree that an exercise routine is a must.

The World Health Organization (WHO), for instance, recommends “at least 150 minutes of moderate-intensity physical activity throughout the week, or do at least 75 minutes of vigorous-intensity physical activity, or an equivalent combination of both” for all adults.

As people grow older and their lives become busier, however, the fast pace of daily responsibilities, and the accumulated fatigue, may make it harder to find time and energy to exercise.

One recent study, published in the Open Heart journal, suggested that matching one’s exercise window to the time in the day when a person feels most awake and alert may be the most beneficial for cardiometabolic health.

But how can a person figure out the best timing, how do they overcome tiredness to stick to their exercise routine when necessary, and how do they maintain motivation to keep up with the workouts?

Medical News Today spoke to Mark Kovacs, PhD, a specialist in exercise physiology, to obtain expert advice on how to find an exercise routine that works best on an individual basis.

• A new study from USC researchers found an association between healthier diets containing fruits, vegetables, and whole grains and higher rates of early onset (or young-onset) lung cancer in nonsmokers.
• The researchers believe that pesticide residue may be a possible explanation for this association, and not healthy foods themselves, and plan to investigate it further.
• They also found a similar association with women who take oral contraceptives. 

While lung cancer mortality in the United States has declined significantly since 1990, incidence trends have been more nuanced. New lung cancer cases have fallen in men since the mid-1980s and in women since the mid-2000s, declining annually by 3.0% and 1.4%, respectively, from 2012 to 2021.

However, while overall incidence has gone down, researchers are concerned about a different trend: increasing lung cancer rates in younger nonsmokers, especially women. 

Researchers in the new study utilized data from the Epidemiology of Young Lung Cancer case study to examine this trend more closely. They found a surprising association between healthier eating patterns and early onset lung cancer among nonsmokers.

This finding is only an association, however, and does not prove that eating vegetables, fruits, or whole grains causes cancer. The authors suspect environmental factors may contribute to this. 

The researchers presented the study findings at the American Association for Cancer Research annual meeting.

The results of the study are yet to be published in a peer-reviewed scientific journal.

Exploring young-onset lung cancer

While lung cancer typically affects older adults who have a background of smoking, it can still affect younger adults, including nonsmokers. 

The average age of receiving a lung cancer diagnosis is 70, and when someone receives a diagnosis before the age of 50, it is referred to as “young-onset lung cancer.”

Newer studies found an increase in young-onset lung cancer incidence among nonsmokers, which prompted the researchers of the new study to further examine what may be behind this. 

The researchers analyzed data from the Epidemiology of Young Lung Cancer study, which is a nationwide observational study that examines factors linked to cancer mutations.

The study group included 187 patients with young-onset lung cancer, and women accounted for 78% of the cohort.  

The scientists grouped the participants based on the biological pathways driving their tumors:

• the EGFR pathway group (73)
• the fusion-positive group (82)
• the mixed mutations group (32)

Next, the researchers gathered epidemiological survey data covering the year before diagnosis. This included information such as smoking history, oral contraceptive use, and demographics. 

They also reviewed dietary habits, which were assessed using food-frequency questionnaires. The researchers assessed overall diet quality using the Healthy Eating Index (HEI); higher scores indicated healthier diets. 

Could pesticides explain the link between fruit, vegetables, and cancer?

The researchers reported that the majority of the participants of each group had never smoked. Prior smokers accounted for 32.9% of the EGFR pathway group, 13.4% of the fusion-positive group, and 21.9% of the mixed group. 

Of the nonsmokers with young-onset lung cancer, the researchers found a surprising association between dietary choices and risk. 

Using the HEI, researchers found that the EGFR and fusion-positive groups had higher-than-average food scores, around 65% for each group. Compared to the average U.S. adult’s HEI of 57, this is roughly a 13% difference. 

All groups also consumed more servings of dark green vegetables, legumes, and whole grains compared to the average adult. 

While this association is surprising, it should not be interpreted to mean that healthy foods cause cancer. The researchers say this points to the need to learn more about the environmental factors involved in growing the food. 

Jorge Nieva, MD, a medical oncologist and lung cancer specialist with USC Norris Comprehensive Cancer Center and lead author of the study, spoke with Medical News Today about the findings.

“There is a lot of work to be done, from measuring pesticide metabolites in lung cancer patients, to looking at different geographies and relative uses of different specific chemical substances,” said Nieva. 

Nieva pointed out that since all pesticides are not the same, they will need to understand the biological effects of each one. 

Contraceptives may explain lung cancer risk

Another interesting finding was that oral contraceptive use was notably higher than average among female participants in two groups. 

Around 11.4% of women ages 15 to 49 in the U.S. report using oral contraceptives, which is significantly lower than the rate of the female study participants who took oral contraceptives. 

The EGFR and mixed mutation groups stood out, as around 77% of the women in these groups reported ever taking oral contraceptives. Around 65% of the fusion-positive group reported taking them.

As with the healthy eating pattern association, this does not show that oral contraceptives cause lung cancer, but it does open the door to another pathway to explore to figure out why young-onset lung cancer cases are increasing, particularly in women. 

Nieva also touched on why women seemed more affected. He said that the mutations that contribute to young-onset lung cancer are more common in females. Notably, the “most common subtype, EGFR, more commonly expresses estrogen receptors, particularly in women.” 

Nieva further talked about how chemicals that disrupt the endocrine system are used in pesticides. 

“In our study and for the U.S. on average, women seem to have much healthier diets than men, and this might mean greater relative exposure to any contaminants that may be in whole grains, fruits and vegetables,” Nieva explained.

Proceed with care in interpreting these findings

David Yashar, MD, a hematologist-medical oncologist at MemorialCare Cancer Institute at Long Beach Medical Center, spoke with MNT about the study findings.

“In general, these are fascinating findings; however, I think we must be careful in the way we analyze the data,” said Yashar.

Yashar said results do not suggest that fruits, vegetables, or whole grains alone increase lung cancer risk. 

“It may be the link between pesticides that they use in growing the produce and whole grains that is the cause for increased rates of lung cancer in non-smoking females,” Yashar theorized.

Yashar also pointed out that even if someone is concerned about the findings, practicing healthy eating habits is still crucial to overall health. 

“We know that a poorer diet leads to obesity, and this also has a negative impact not only on one’s health, but also on the development of other cancers, such as breast cancer,” shared Yashar.

• A person’s circadian rhythm plays an important role in their overall health. 
• Past research shows that an unhealthy circadian rhythm may increase a person’s risk for several health conditions, including dementia, such as Alzheimer’s disease. 
• A new study found that older adults with a more fragmented circadian rest-activity rhythm experienced more shrinking of the brain in areas typically affected by Alzheimer’s disease. 

A person’s circadian rhythm — or natural sleep-wake cycle — plays an important role in their overall health. A healthy circadian rhythm helps ensure you get enough sleep each night, keeps your immune system strong, balances hormones, and regulates your metabolism. 

Past research shows that a disrupted circadian rhythm may increase a person’s risk for several health conditions, including cardiovascular disease, metabolic syndrome, obesity, type 2 diabetes, and dementia, including Alzheimer’s disease. 

A new study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association has found that older adults with a more fragmented circadian rest-activity rhythm may lead to shrinking of the brain, or brain atrophy, in areas associated with memory and emotion that are typically affected by Alzheimer’s disease. 

What is a fragmented rest-activity rhythm?

For this study, researchers analyzed health data from 344 adult participants with an average age of 73 with no signs of cognitive impairment who participated in the Baltimore Longitudinal Study of Aging. 

Study participants were asked to wear a wrist accelerometer for up to a week to measure their 24-hour rest/activity rhythms, including movement and inactivity, and also had MRI scans taken of three areas of the brain generally affected by Alzheimer’s disease — the parahippocampal gyrus, hippocampus, and amygdala.

“While disturbed sleep has been linked to poor brain health outcomes, much less is known about how rest-activity rhythms are related to changes in brain structure over time,” Adam Spira, PhD, professor in the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University, and senior author of this study, told Medical News Today.

“We wanted to better understand these associations using MRI measures of brain volume,” said Spira.

Data from the wrist accelerometers allowed scientists to measure how fragmented each participant’s daily rest-activity rhythm was. 

“Fragmented rhythms refer to how often a person switches between activity and rest throughout the day,” Marc Kaizi-Lutu, a doctoral researcher in the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University, and co-first author of this study, explained to MNT.

“Someone with more fragmented rhythms tends to more frequently shift between being active and inactive, while someone with less fragmentation has longer, more sustained periods of activity or rest,” Kaizi-Lutu continued.

Less fragmented daily rhythm leads to larger brain volume

At the study’s conclusion, researchers found that study participants with less fragmented daily rest-activity rhythms had larger volumes in the memory-associated brain areas the hippocampus and parahippocampus, and less shrinkage of the amygdala, which is vital for emotion. 

“These brain regions are particularly vulnerable in Alzheimer’s disease,” Daniel Callow, PhD, assistant professor in the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins University School of Medicine, and co-first author of this study, told MNT.

“Our findings show that individuals with less fragmented and more consistent rest-activity rhythms tend to have larger volumes in these areas and experience less shrinkage of the amygdala over time. Importantly, the longitudinal findings suggest that disrupted rhythms may precede change in brain structure, raising the possibility that more fragmented or less consistent RARs contribute to neurodegeneration.”

– Daniel Callow, PhD

Additionally, scientists observed a correlation between a more fragmented rest-activity rhythm with a quicker increase in the volume of brain ventricles. 

“Brain ventricles are fluid-filled spaces that often expand as surrounding brain tissue is lost,” Callow said. “Thus, our finding suggests that more fragmented rest-activity rhythms are associated with faster increases in ventricular size over time, which suggests a link between disrupted daily rhythms and more widespread brain atrophy.” 

Moving towards actively supporting healthier brain aging

MNT had the opportunity to speak with Dung Trinh, MD, an internist with MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, about this study.

Trinh, who was not involved in the research, said that this is an important finding because it strengthens the link between circadian rhythm disruption and brain health in aging. 

“What stood out most was that more fragmented rest-activity rhythms were associated with smaller volumes in brain regions involved in memory and emotion, and with faster brain atrophy over time, particularly in the oldest adults,” Trinh continued.

“Preserving brain volume is closely tied to preserving memory, independence, emotional well-being, and overall quality of life as people age,“ he explained.

“If researchers can identify modifiable factors that help protect brain structure, it creates opportunities to intervene earlier, before major cognitive symptoms appear. This kind of work helps move the field beyond simply diagnosing decline and toward actively supporting healthier brain aging,” Trinh noted.

“At the same time, I would interpret the study carefully: it shows a strong association, but it does not prove that fragmented circadian rhythms directly cause brain shrinkage,” he added. 

How to achieve a less fragmented rest-activity rhythm during the day

For those who may want to potentially help their brain health as they age by having a less fragmented daily rest-activity rhythm, Trinh said his best advice is to aim for regularity by:

• waking up at about the same time every day
• getting bright light exposure in the morning
• staying physically active during the day
• keeping meals and bedtime consistent
• limiting long or late naps
• avoiding caffeine or alcohol too close to bedtime.

“It is also important to talk with a clinician about issues like sleep apnea, insomnia, depression, or medications that can disrupt sleep and daytime alertness,” he added. “The key message is that a stronger, more consistent day-night pattern is generally healthier, even though this study does not prove that improving rhythm regularity will definitely prevent brain atrophy.”

• Exercise is part of a healthy lifestyle and a critical component of protecting heart health. 
• Some people are naturally alert at certain times, which is mostly determined by circadian rhythm ( our internal 24-hour clock) and chronotype.
• One study suggests that aligning exercise times with natural alertness in the morning or evening could offer health benefits, such as improved blood pressure and heart rate variability. 

Exercise offers many health benefits, such as helping people maintain a healthy weight, lowering blood pressure, and reducing the risk of a heart attack. But does the timing of exercise affect the possible health benefits?

One study published in Open Heart explored how aligning exercise timing with participants’ natural morning or evening tendencies affected a number of outcomes, including blood pressure, “bad” cholesterol, and sleep quality.

The results showed that participants who exercised during their natural alertness had better outcomes than those who did the opposite, particularly the greater decrease in blood pressure.

All participants were sedentary adults with at least one cardiovascular disease risk factor, yet the results suggest that individualized exercise timing could improve cardiometabolic health.

Exercising during natural alertness

This randomized controlled clinical trial enrolled 150 participants, of whom 134 completed the study. Participants were adults in Lahore, Pakistan, between the ages of 40-60 years.

All participants were sedentary and had at least one risk factor for cardiovascular disease. These included factors like blood pressure within a certain range or having a family history of premature cardiovascular disease. However, they excluded individuals who already had certain confirmed conditions, like coronary artery disease, as well as those taking certain medications. 

Researchers considered participants’ chronotypes, which are their natural tendencies toward being a morning or an evening person. They explain that “individuals differ not only in their preferred sleep and wake times but also in the timing of optimal physical performance and cardiovascular response to exercise.” They used a questionnaire to determine each participant’s chronotype, which was then confirmed by evaluating body temperature. 

Next, participants underwent the exercise intervention for 12 weeks. Participants did moderate-intensity aerobic training sessions. These included using a treadmill or walking briskly for 30 minutes and 5-minute warm-ups and cool-downs. Participants did these sessions at the University of Lahore teaching hospital, five days a week. 

Participants performed the exercise intervention within a certain range in the morning or evening. Some participants performed exercise interventions in line with their chronotype, while others exercised at the opposite time, such as a morning person exercising in the evening, as assigned in their group. 

Researchers measured participants’ blood pressure, heart rate variability, peak oxygen consumption, sleep quality, fasting blood sugar, and “bad” cholesterol levels at baseline and then again after the exercise intervention ended. 

Improved health outcomes from following natural body clock

The group that exercised at a time that aligned with their natural rhythms, such as morning or evening types, had better outcomes for blood pressure and heart rate variability. They also appeared to have better performance and exercise capacity outcomes. Finally, they also had better cholesterol, fasting glucose, and sleep quality outcomes. 

The observed improvements were better for the aligned group when it came to all outcomes. For example, the aligned group saw systolic blood pressure drop by almost 11 mmHg while the misaligned group only saw a 5.5 mmHg decrease. Similarly, “bad” cholesterol levels dropped by 13.7 mg/dL in the aligned group and only by 7.6 mg/dL in the misaligned group. 

Additional analysis found that participants who already had high blood pressure at baseline saw the greatest reduction in blood pressure when exercise was chronotype-aligned.

They also found that chronotype-aligned exercise was the greatest independent predictor of change in systolic blood pressure, suggesting that this exercise timing consideration could be particularly helpful for blood pressure.

Cheng-Han Chen, MD, board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, who was not involved in the study, commented the following: 

“This study characterized individuals by their chronotype (whether they were ‘early birds’ or ‘night owls’), and found that the participants [who] were assigned to exercise during their ‘preferred’ time actually underwent greater improvements to various cardiometabolic factors (such as blood pressure, cholesterol, and glucose values) compared to those exercising at ‘non-preferred’ times.”

“These results add to our understanding of how aligning exercise with someone’s internal circadian clock can potentially improve health outcomes and suggest a strategy to help us optimize the beneficial effects of exercise.”
— Cheng-Han Chen, MD

The researchers also found that morning-type participants in both aligned and misaligned groups saw better improvement than evening-type participants.

They explained that “the magnitude of improvement appeared descriptively greater in morning-type participants for several cardiovascular, autonomic and fitness-related measures.” However, the authors note that this data gives speculative insights. 

What the study may be missing

This study was fairly small, and the exercise intervention lasted for a fairly short time. Researchers note that it “does not provide insight into long-term outcomes or sustainability.” 

It also focused on a specific population already at risk of cardiovascular disease. The authors note that this data was from government hospitals in Lahore and that most participants had “middle- or lower- income backgrounds.” Additionally, they chose to exclude individuals with intermediate chronotypes, so those who didn’t quite fit into the morning or evening types. 

Thus, it’s unclear whether the results would be the same in other groups, such as those not at risk for cardiovascular disease, and the generalizability is limited. 

Full blinding in this type of study wasn’t possible either, so there is some risk of bias. Adherence to the exercise intervention was also higher in the aligned group. Participant dropout also could have affected the results. It’s also possible that participants’ evaluations of themselves as morning or evening types were inaccurate. Exercise adherence partially relied on participant reporting, which could also be inaccurate. Assessment of sleep quality also relied on participant reporting. 

Researchers chose to estimate peak oxygen consumption, which may not be as precise. Finally, researchers note that although they included only participants on stable medications, it’s still possible that these medications influenced the outcomes. 

The specific reasons for the observed results could be an aspect of future research. 

Danielle El Haddad, MD, cardiovascular medicine, UTMB, who was also not involved in the study, noted the following: 

“Several limitations should be considered when interpreting these findings. The study population was small and demographically restricted to middle-aged individuals (40–60 years) from a low- to middle-income Pakistani cohort, limiting external validity.”

“In addition, the exclusion of patients receiving commonly prescribed cardiovascular medications—specifically beta blockers and calcium channel blockers—reduces applicability to routine clinical practice, where such therapies are prevalent. The lack of blinding further introduces the potential for bias, particularly in subjective or effort-dependent outcomes such as exercise performance and adherence,” El Haddad added.

Should exercise timing be personal?

The research suggests a simple way to improve blood pressure and other outcomes through a more individualized approach, though more research is required. 

Afaq Motiwala, MD, assistant professor for interventional cardiology at the University of Texas Medical Branch, who was also not involved in the study, noted the following to Medical News Today: 

“This study supports a shift toward personalized lifestyle medicine, where exercise recommendations consider not only type, intensity, and frequency, but also timing of exercise. Aligning exercise with an individual’s circadian biology may maximize its clinical benefits, and also improve adherence, as patients are more likely to maintain routines that fit their natural energy patterns.”

People can discuss their options for exercise programs with their doctors, as well as how timing may impact outcomes.

It’s important to note that even in this study, both groups saw benefits. Exercise is still important overall, regardless of getting the timing perfect.

“We know that any exercise is better than none. We are just beginning to learn how the timing of exercise during the day can make it even more effective,” Chen said. 

• Over the past few years, GLP-1 receptor agonists have been growing in popularity for weight loss. 
• While many people lose between 5-15% of their starting body weight while on a GLP-1, as much as 20% of people may not respond to the drug. 
• Recent research has found that a person’s genetic makeup may explain why some people do not respond to GLP-1 drugs.
• A new review suggests that taking both a GLP-1 medication, and a medication that combines both naltrexone and bupropion into one pill, may be helpful for those who are not responding to GLP-1s alone.

Over the last few years, glucagon-like peptide-1 (GLP-1) receptor agonists have been growing in popularity for not only treating type 2 diabetes but also for weight loss. 

Recent surveys show that about one in every eight adults in the United States — or 12% — are currently taking a GLP-1 medication like Wegovy or Zepbound for weight loss or treatment of a chronic condition.  

Past research shows that most people taking a GLP-1 drug can expect to lose between 5% to 15% of their starting body weight over 1 year. 

However, there is a percentage, as much as 20% of people taking GLP-1s, who may not respond to the drug. According to a study recently published in Nature, a person’s genetic makeup may dictate to what extent they respond to GLP-1 treatment.

Another recent paper, a review published in the journal Obesity Science and Practice, says that taking both a GLP-1 drug, and a medication that combines both naltrexone and bupropion into one pill, may be helpful for those who are not responding to GLP-1s alone. 

What is Contrave? 

In this review, researchers provided an overview of how gut hormone analogs like GLP-1 medications and Contrave — a fixed‐dose, extended‐release combination of naltrexone and bupropion (NB‐ER) — impact eating behavior and the gut-brain axis. 

“Contrave is a medication that acts to alter [the] brain signal (dopamine pathway) in the part of the brain (hypothalamus) responsible for controlling how hungry we feel and how much energy we burn, as well as in the part of the brain (mesolimbic system) that controls how much pleasure we feel while eating certain foods and how compulsive we feel in repeatedly seeking the same pleasure,” Muzamil Hussain, PhD, a clinical research fellow diabetes and obesity at Ulster University in the United Kingdom, and co-author of this study, told Medical News Today.

“By altering these signals in the brain, cumulatively, Contrave promotes fullness, and reduces food cravings, hence causing weight loss,” Hussain argued.

“For example, some patients may crave fatty or sugary foods because their brain associates these with pleasure,” he continued. “Contrave dampens this brain signal and makes eating fatty food or sugary food less satisfying (less pleasurable) and reduces the urge to ‘comfort eat’ or crave these foods.” 

A multi-pronged approach to treating obesity

Through this study, researchers make the case for a combined approach, using both gut hormone analogs like GLP-1s, and NB-ER at the same time, to treat obesity 

“Combining NB-ER with GLP-1 makes mechanistic sense because GLP-1 primarily makes a person feel full faster and decreases hunger, while NB-ER reduces food cravings,” Hussain explained.

“Hence, this combination can potentially help patients who struggle with binge eating/impulsive (hedonic) eating or food cravings. It can also be useful for those who did not achieve at least 5% weight loss with (a) GLP-1 alone.” 

“A significant number of patients have suboptimal responses to GLP-1 therapies. This means that these patients did not achieve enough weight loss to provide them benefit in risk reduction for obesity associated conditions like diabetes and heart disease, while using [a] GLP-1 therapy alone. This is reason enough for the scientific community to keep investigating ways of finding alternative and adjunctive treatments to cater to the medical needs of this patient population.” 

– Muzamil Hussain, PhD

“Obesity treatment is not a one size fits all; we need to come up with a multi-pronged approach targeting multiple pathways to bring meaningful health benefits specially for those patients with sub-optimal response to GLP1s alone,” Hussain added. “NB-ER and GLP-1 combination therapy can be one of the potential options in this approach.”

There is no single obesity therapy that works for everyone

MNT had the opportunity to speak with Mir Ali, MD, a bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, about the recent review. 

Ali, who was not involved in the research, commented that the review’s conclusion reaffirms what he has seen in his own practice: Patients on combination medication therapy tend to see better results.

“Obesity is a chronic, pervasive health concern, and there is no single therapy that works for every patient,” he explained. “Due to the variability in response and other factors, finding new, more effective interventions is always a worthwhile effort.”

Jennifer Cheng, DO, chief of endocrinology at Hackensack Meridian Jersey Shore University Medical Center in New Jersey, agreed that obesity and weight loss are multifactorial, and there is still research needed to help determine who will be successful in weight loss and who will not respond.  

“As someone who treats these people regularly, I have personally seen the struggles that patients have in trying to lose weight,” Cheng, who was likewise not involved in the review, told MNT.

“There is a high degree of frustration when people are taking the time to administer medication and are not able to achieve the results they are expecting. Certain people are poor responders, and it is not always possible to predict who will, and who will not, respond appropriately,” she added. 

“It makes sense that adding on secondary therapy or a combination of therapies could assist certain patients with a personalized approach to weight loss,” Cheng continued. “People should work with their doctors to determine the best plan of care.” 

Cheng said it is also important to determine the reasons why there could be poor response to a medication, so that further weight loss can be achieved for these patients.  

“It is also important to identify these factors so that people can use alternatives or combined therapies immediately,” she explained. “Targeted and personalized medical therapy should be initiated sooner to help patients achieve results.” 

• A study suggests that a blood test measuring the biomarker pTau217 can detect early signs of Alzheimer’s disease years before symptoms or signs appear on brain scans.
• Higher pTau217 levels in cognitively healthy adults were linked to faster buildup of amyloid and tau proteins, as well as future cognitive decline.
• Changes in pTau217 often occurred before positive scans, suggesting it may be a more sensitive early detection tool.
• Low pTau217 levels were associated with a lower likelihood of developing significant Alzheimer’s-related brain changes over many years.

Estimates suggest that more than 7 million American adults are living with Alzheimer’s disease. Receiving a timely diagnosis can provide many benefits, such as helping to reduce cognitive and functional decline and allowing an individual to prioritize their health.

At present, diagnosis typically involves a combination of medical history, cognitive tests, neurological exams, and brain imaging. However, growing evidence is highlighting the possible role of certain proteins in diagnosing Alzheimer’s disease.

The accumulation of these proteins can begin years before clinical symptoms and may serve as measurable, specific biomarkers of underlying neuropathology. As such, they may allow for earlier and more accurate diagnosis than current methods.

Now, a study published in Nature Communications, suggests that measuring blood for phosphorylated tau 217 (pTau217) could reveal the earliest signs of disease progression in otherwise healthy older adults.

Blood biomarker may detect Alzheimer’s earlier than scans

Traditionally, clinicians have used brain imaging techniques, such as amyloid PET scans, to help detect early changes linked to Alzheimer’s disease. These scans can be effective at identifying early, even preclinical, signs of Alzheimer’s disease by detecting proteins in the brain, often before significant cognitive decline begins.

However, measuring for blood-based biomarkers may offer even earlier detection.

“We used to think that PET scan detection was the earliest sign of Alzheimer’s disease progression, revealing amyloid accumulation in the brain 10 to 20 years before symptoms appear,” said lead author Hyun-Sik Yang, MD, in a press release. “But now we are seeing that pTau217 can be detected years earlier, well before clear abnormalities appear on amyloid PET scans.”

The results build on recent momentum in the field, including the decision by the Food and Drug Administration to clear the first blood test for Alzheimer’s disease in 2025.

“For researchers, our results suggest that plasma pTau217 levels might be one of the earliest predictors of future Alzheimer’s disease progression and could be used to screen clinical study participants to identify individuals at risk of developing Alzheimer’s disease pathology and symptoms,” Yang told Medical News Today.

“For clinicians, I would not recommend using plasma pTau217 to screen cognitively unimpaired older adults,” he added. “Whether intervening in [Alzheimer’s] pathology at this early stage is beneficial remains unknown, so the clinical benefit of early screening strategies is unclear.”

“However, this study adds further evidence that plasma pTau217 performs robustly in detecting [Alzheimer’s] pathology, and, as many other studies suggest, plasma biomarker testing is an option to consider when evaluating patients with cognitive impairment.”
— Hyun-Sik Yang, MD

Higher pTau217, faster Alzheimer’s progression

Led by a team from Mass General Brigham, the research followed 317 cognitively healthy adults enrolled in the Harvard Aging Brain Study for an average of 8 years.

Participants ranged in age from 50 to 90 and underwent regular blood testing, brain imaging, and cognitive assessments.

The team examined whether initial levels and changes over time of pTau217 could help predict amyloid buildup in the brain, tau protein accumulation, and cognitive decline.

They found that individuals with higher pTau217 levels typically experienced faster progression of Alzheimer’s-related brain changes.

Notably, increases in pTau217 often occurred before amyloid PET scans turned positive, suggesting the biomarker could detect disease activity at an earlier stage.

“We were surprised to see it predict future amyloid-β accumulation even in those with low amyloid-β PET signals, i.e., in the “negative” range, because we had thought that brain amyloid-β accumulation is an initial event and that plasma pTau217 elevation would follow it,” Yang explained to MNT.

“We suspect our observation was driven by the relative sensitivity of the tests (i.e., plasma pTau217 might be more sensitive than amyloid-β PET in very early stages) rather than pTau217 driving amyloid-β accumulation. Nonetheless, our results have significant implications for clinical study design and biomarker panel selection,” he continued. 

The findings also show that those with low baseline pTau217 levels were less likely to develop significant amyloid buildup over many years.

“Personally, I think this finding may have the greatest practical utility for clinical study design and, once effective [Alzheimer’s] prevention strategies become available, for [Alzheimer’s] risk stratification in the clinic.”
— Hyun-Sik Yang, MD

“We observed that cognitive-unimpaired older adults with very low baseline pTau217 rarely became amyloid-positive (elevated amyloid-β on PET) during the PET scan follow-up period, which was on average about 6 years,” Yang said to MNT.

“This means that those with very low pTau217 levels are at a low risk of [Alzheimer’s] progression, and [Alzheimer’s] prevention trials might want to consider excluding this subgroup of people to optimally power their studies,” he added. 

Implications for early Alzheimer’s detection and prevention

Although the findings could have important implications for clinical trials and future screening strategies, the researchers caution that it is too soon to recommend routine pTau217 testing for the general population.

“There are already 2 FDA-approved pTau217 blood tests in clinical use. As more data accumulate, blood tests—especially pTau217—appear to be as good as, or even better than, cerebrospinal fluid testing and show excellent concordance with amyloid-β PET,” Yang told MNT.

“Given their greater accessibility, blood-based biomarkers are poised to replace more invasive or expensive tests in the near future, at least for diagnostic purposes,” he said.

“Nonetheless, given the prolonged preclinical phase of Alzheimer’s disease, clinical judgment cannot be fully replaced by biomarker testing, because elevated pTau217 or Aβ signals do not necessarily mean that [Alzheimer’s] pathology is the main driver of the patient’s symptoms; this part still requires clinicians’ judgment.” 
— Hyun-Sik Yang, MD

“I would also emphasize that plasma pTau217 measurements are not currently recommended for screening in cognitively unimpaired individuals. The clinical benefits of broader screening remain unclear, and pTau217 screening is appropriate only in research settings,” Yang concluded.

Co-senior author Jasmeer Chhatwal, MD, PhD, notes that the goal is to identify individuals at risk earlier, when preventive treatments may be more effective.

“By anticipating who’s going to turn amyloid-positive in the future, we are trying to push back the clock to enable earlier Alzheimer’s disease prediction,” Chhatwal said in a press release.

As research continues, blood-based biomarkers like pTau217 could become part of routine health checks, offering a more accessible and affordable alternative to current diagnostic methods.

These tests could play a central role in shifting Alzheimer’s care toward earlier diagnosis, targeted prevention, and more personalized treatment strategies.

• Ultra-processed foods are popular, but experts are interested in understanding all the possible risks. 
• One analysis found that eating higher amounts of ultra-processed foods was linked to higher fat accumulation in thigh muscles. 
• The results suggest the possible damage ultra-processed foods may pose to the muscles and indicate another reason to limit their intake. 

A study published in Radiology reports on a cross-sectional secondary analysis, which found that higher intake of ultra-processed foods was associated with a greater buildup of fat in thigh muscles, based on MRI scan data.

This research specifically included over 600 participants who were at risk for knee osteoarthritis.

The data reveals another factor that may affect the muscles and adds to knowledge of the possible dangers of eating higher amounts of ultra-processed foods. 

Ultra-processed foods and more fat in muscles

As noted in this research, ultra-processed foods contain additives as well as high levels of sugar and salt. How ultra-processed foods relate to muscle quality hasn’t been a major focus of research. 

This analysis was a cross-sectional secondary analysis that used baseline information from a long-term study called the Osteoarthritis Initiative.

For the current analysis, participants were at risk for knee osteoarthritis, a condition where there can also be muscle problems.

Participants did not have hip or knee osteoarthritis, or other conditions like rheumatoid arthritis or diabetes. However, some participants had radiographic data that could indicate early osteoarthritis. 

The average age of participants was just under 60, and researchers included 615 participants. Almost two-thirds of participants had overweight, and just under one-fourth had obesity, based on body mass index (BMI) data. 

Researchers looked at participants’ reports about their diets and evaluated the consumption of ultra-processed foods. They looked at thigh MRIs to assess fat infiltration into the muscle, focusing on 10 different muscles in the thigh. 

Researchers found that overall, higher intake of ultra-processed food was associated with higher levels of fat infiltration in the thigh muscles. 

Speaking to Medical News Today, study author Zehra Akkaya, MD, associate professor of radiology at Ankara University Faculty of Medicine, in Turkey, and researcher, consultant, and former Fulbright Scholar at the UCSF Department of Radiology and Biomedical Imaging, Clinical & Translational Musculoskeletal Imaging Research Group, summarized the main findings this way: 

“In a study of over 600 adults at risk of developing knee osteoarthritis, we found that diet quality plays an important role in muscle health. Specifically, independent of total calorie intake or overall fat consumption, a higher intake of ultra-processed foods was associated with greater fat accumulation within the thigh muscles, as seen on MRI scans.” 

When looking at individual muscle groups, those with the strongest relationship to ultra-processed food consumption were the adductor muscles in the model that adjusted for abdominal circumference.

Overall, women had greater levels of fat infiltration into the thigh muscles than men. However, the relationship between ultra-processed foods and fat infiltration into the thigh muscles did not appear to be affected by sex. 

Sensitivity analyses adjusting for dietary fat intake still found a significant relationship between ultra-processed food consumption and fat infiltration for all thigh muscles as well as the adductor and flexor muscle groups.

The findings for the extensor muscles remained significant in the model that adjusted for abdominal circumference.

Additionally, the relationship between eating ultra-processed foods and fat infiltration into muscle was stronger for participants who had worse damage on knee images. 

Study limitations and continued research

This research specifically focused on an older population already at risk for knee osteoarthritis, which limits generalizability to other groups.

Researchers also note that people in this group may have a greater risk for frailty and disability. In their paper, they conclude that “the findings may not be fully generalizable to populations outside the age range and characteristics of the OAI [Osteoarthritis Initiative] participants.”

They also acknowledge that there could be confounders that they missed. 

Additionally, most participants were non-Hispanic and white. The research also focused on fat infiltration in thigh muscles, so it is unclear if the results would be the same in other muscle groups. 

Furthermore, some of the data — for instance, regarding diet — was self-reported, which can lead to errors.

The study authors also emphasized that the percentage of the annual diet made up of ultra-processed foods is increasing and is even higher in the modern American diet than it was in their research.

Finally, this research did not evaluate long-term data. Akkaya told MNT:

“We would also like to note that this study was cross-sectional in design, which means we cannot draw conclusions about cause and effect. Future research should therefore use longitudinal approaches to better understand potential causal relationships, particularly across different age groups and diverse populations, given how widespread ultra-processed foods have become.”

Future research could further explore how diet affects individuals who already have osteoarthritis, based on the differences observed here between participants who had worse radiographic images and those who had normal ones.

It could also look at how the use of glucagon peptide-1 receptor agonists (GLP-1s), such as semaglutide medication, may affect outcomes in this area of research. 

What are the clinical implications?

Though this is only the beginning of research in this area, these findings indicate another component to possibly target when it comes to muscle health.

Patrick Kee, MD, PhD, a cardiologist at Vital Heart & Vein, who was not involved in this research, commented on the finidngs for MNT.

“Since muscle quality is essential for joint stability, the UPF [ultra-processed food]-induced fatty degeneration in thigh muscles may accelerate the onset and progression of knee osteoarthritis, a leading cause of global disability,“ Kee told us.

According to him, “these findings suggest that clinical management of musculoskeletal and metabolic health must go beyond simple caloric restriction and weight loss.“

“Instead,“ he emphasized, “it requires targeted public health and clinical interventions that emphasize dietary quality, specifically reducing the consumption of ultra-processed foods and favoring minimally processed options. This approach aims to preserve skeletal muscle integrity and mitigate ectopic visceral adiposity.”

The study results also more broadly point to another possible reason to limit consumption of ultra-processed foods. Ultra-processed foods are also linked to other health concerns, such as a higher risk of death related to cardiovascular disease and all-cause mortality.

Mir Ali, MD, a bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, likewise not involved in the recent study, told MNT that “these findings provide further evidence to advise patients to reduce their intake of ultra-processed foods.“

“While it is not yet clear from this specific study if increased thigh muscle fat accelerates joint damage, numerous studies have established that ultra-processed foods increase the risk of diabetes, heart disease, and cancer. Limiting these foods is essential for improving overall health,” Ali concluded.

• An artificial intelligence (AI) analysis of over 400,000 Reddit posts found that people taking GLP-1 medications frequently report side effects not fully captured in clinical trials or drug labels.
• Two notable categories of underreported symptoms include reproductive issues, such as irregular menstrual cycles, and temperature-related complaints, including chills and hot flashes.
• Additionally, fatigue was commonly discussed online, despite being less prominent in clinical trial data, while known side effects like nausea were also widely reported.
• Researchers stress the findings do not prove causation but suggest that AI analysis of social media could help identify patient concerns earlier and guide future clinical research.

GLP-1 receptor agonists are popular weight loss drugs that help manage obesity and type 2 diabetes. There is a growing demand for GLP-1–based therapies, with research suggesting roughly 1 in 8 U.S. adults report having ever used GLP-1 medication, with 6% currently using such drugs.

Common side effects of GLP-1 drugs are those of a gastrointestinal nature, such as nausea, vomiting, diarrhea, and constipation. Research suggests these adverse events may occur in 40 to 85% of people. Health experts advise that people can make dietary adjustments to help reduce these side effects.

Although many of these side effects are mild to moderate in severity and generally resolve shortly, adverse events remain a common cause of discontinuing the drug.

While these side effects are well-documented, many people also often report anecdotal adverse events while using GLP-1 drugs.

Now, a new study published in Nature Health used AI to analyze social media posts and uncovered patient-reported side effects linked to these medications that may not yet be fully captured in clinical trials.

Key GLP-1 findings from social media data

Led by researchers from the University of Pennsylvania, the study examined more than 400,000 Reddit posts from nearly 70,000 users discussing GLP-1 receptor agonists, including semaglutide and tirzepatide.

The analysis identified two main symptom categories that may warrant further investigation. These included reproductive symptoms, including irregular menstrual cycles and unexpected bleeding, and temperature-related issues, such as chills, hot flashes, and feeling unusually cold.

Additionally, fatigue emerged as a frequently discussed symptom, despite being less prominent in clinical trial data.

Commonly recognized side effects, such as gastrointestinal symptoms, were also widely reported, lending credibility to the approach.

“Some of the side effects we found, like nausea, are well known, and that shows the method is picking up a real signal,” said senior author Sharath Chandra Guntuku in a press release. “The underreported symptoms are leads that came from patients themselves, unprompted, and clinicians could potentially pay attention to them.”

The study highlights a growing field, sometimes referred to as computational social listening, where AI tools analyze large volumes of online content to identify health trends.

Historically, this approach has been limited by the difficulty of interpreting how individuals describe symptoms in their own words.

Mapping these descriptions to standardized medical terminology can be time consuming. However, recent advances in large language models make it possible to process such data at scale, enabling researchers to analyze patterns across hundreds of thousands of posts more efficiently and consistently.

Surprising GLP-1 side effects

Commenting on which newly identified symptoms were the most surprising, Neil Sehgal, ME, MS, the study’s first author and a doctoral student advised by Guntuku and Lyle Ungar, PhD, told Medical News Today:\

“There were a few interesting findings. The reproductive symptoms are one of the most interesting signals. Nearly 4% of users who reported side effects mentioned menstrual changes,  things like irregular cycles, heavy bleeding, or intermenstrual bleeding, and these symptoms aren’t prominently featured in the current prescribing information.”

“When you consider that we’re looking at a mixed-gender sample on Reddit, and that Reddit skews male, the true rate among women taking these medications could potentially be higher,” Sehgal said.

“Fatigue was also the second most commonly reported symptom overall, but has met relatively few reporting thresholds in existing trials. This gap between what patients are self-reporting online and what gets captured in trials is really what motivated this whole line of work,” he added.

Why clinical trials may miss some symptoms

Clinical trials remain the gold standard for identifying drug safety issues. However, they may not always capture the full range of patient experiences.

Typically, trials are designed to detect the most serious or common adverse effects. As such, they may overlook symptoms that individuals find bothersome but less dangerous, or that occur less frequently.

“Clinical trials generally identify the most dangerous side effects of drugs,” adds co-author Ungar. “But they can fail to find what symptoms patients are most concerned about; even though social media is not necessarily representative, a large collection of posts may reflect additional concerns.”

Still, the researchers emphasize that these findings do not prove causation. They highlight that the study only shows that users reported these symptoms while taking the medications, not that the GLP-1 drugs directly caused them.

The research team suggests there may be plausible biological reasons behind some of the reported symptoms.

GLP-1 drugs are thought to act on the hypothalamus, a region of the brain that regulates hormones, body temperature, and energy balance. Therefore, this could potentially explain reports of menstrual problems and temperature fluctuations.

However, more rigorous, controlled studies are necessary to determine whether GLP-1 medications are truly responsible.

Why negative Reddit posts don’t paint the whole picture

The study authors caution that Reddit users are not representative of the general population. The platform tends to skew younger, more male, and more U.S.-based than the broader population of people taking GLP-1 medications. As a result, the findings may not reflect the experiences of all individuals.

“The most important challenge is understanding what we’ve actually found. There are a few things that make that tricky,” Sehgal told MNT.

“First, Reddit users are not a representative sample of everyone taking these medications. If you had a good experience, you’re less likely to be writing about it online. So we’re almost certainly capturing a skewed slice of the full picture.”
— Neil Sehgal, ME, MS

“Second, we can’t say anything about causality. When someone reports a menstrual irregularity while taking one of these drugs, we don’t know if the drug caused it,” Sehgal continued.

“The way I’d summarize all of this is that our findings are best thought of as signals worth investigating further, not conclusions. We’re pointing in directions that we think deserve more rigorous follow-up, not closing the case on anything,” he concluded.

Additionally, one of the study authors reports receiving an investigator-initiated grant, on behalf of the University of Pennsylvania, from Novo Nordisk and receiving consulting fees from Currax Pharmaceuticals, LLC.

Social media could help monitor drug safety

The research team hopes their findings will encourage clinicians and regulators to pay closer attention to patient-reported experiences shared online. They also hope to expand future studies beyond Reddit to include other platforms and more diverse populations, as well as non-English-language data.

The researchers conclude that AI-driven analysis of social media could serve as an early warning system, especially for medications or health products that gain widespread use quickly.

“Prior research had already established that social media can be a useful tool for drug safety monitoring,” Sehgal adds.

“Ungar actually did a study back in 2011 looking at how to identify adverse events from breast cancer drugs on online message boards, so in some ways this work builds on a tradition that goes back a long time.”
— Neil Sehgal, ME, MS

“What’s changed is the technology. Large language models have made it possible to do this kind of analysis much faster with a level of standardization that could be difficult to achieve before,” Sehgal said.

For now, it is advisable for individuals taking GLP-1 medications, such as semaglutide or tirzepatide, to discuss any new or unusual symptoms with a healthcare professional.

• Researchers have been looking at already-used vaccines to potentially help lower risk for Alzheimer’s disease and other types of dementia. 
• One such vaccine is the influenza vaccine, which previous studies show may help lower a person’s dementia risk. 
• A new study found that older adults who receive a high-dose influenza vaccine may lower their Alzheimer’s disease risk more than those receiving a standard vaccine dose.

As researchers continue to find new ways of helping to reduce a person’s risk for Alzheimer’s disease and other types of dementia, some are examining vaccines that are already being used to lower risk for other diseases. 

For example, a study published in December 2025 found that the shingles vaccine might help lower a person’s risk for dementia, as well as slow disease progression. 

Other published research shows that vaccines like the tetanus and diphtheria (Tdap/Td) vaccine, pneumococcal vaccine for pneumonia, and influenza vaccine for the flu might also help reduce a person’s Alzheimer’s disease and dementia risk. 

Now a new study published in the journal Neurology reports that older adults who receive a high-dose influenza vaccine may lower their Alzheimer’s disease risk more than those receiving a standard vaccine dose.

Low-dose vs high-dose flu vaccine: How does it affect Alzheimer’s risk?

Paul Schulz, MD, professor and neurologist at UTHealth Houston, and lead author of this study, explained to Medical News Today that this new study continues previous research, including a study he and his colleagues published in 2022.

The 2022 study found that the influenza vaccination may help reduce the risk of Alzheimer’s disease by up to 40%, with six annual vaccinations.

“The nagging question after these studies was whether we had a true finding versus a spurious one due to ‘the healthy survivor effect,’ also called ‘the healthy vaccinee effect’,” Schulz told MNT.

“That means that folks who get vaccinated may generally have a healthier lifestyle: Just like they get vaccinated, they also exercise, take their blood pressure and cholesterol medications, see their doctors regularly, eat healthier, etc.” 

– Paul Schulz, MD

“Serendipitously, I gave a talk at the Houston Public Health Department, and they asked whether there was a dose-dependent effect,” he continued. “I wasn’t aware that folks over age 65 get a vaccine that is four times the strength of the standard vaccine due to our immune systems being less responsive as we get older.“

“But, it turns out that not everyone over age 65 gets the high dose influenza vaccine. The health department and pharmacies can run out of the high dose, etc,” said Schulz. 

“That led to the paper [where] the goal was to test whether, when we enrolled only people who were vaccinated [whether with a high or low dose], there was still a protective effect of vaccination on reducing Alzheimer’s disease risk,” he added. 

High-dose protective effect stronger in women

After analyzing health data from about 200,000 participants ages 65 and older, researchers found that those who received the high-dose influenza vaccine lowered their Alzheimer’s disease risk by about 55%, compared to 40% with those who received the standard vaccine dose.

Additionally, scientists reported finding the protective effect of the high-dose flu vaccine was stronger in women than men. 

“We don’t know why that is, but we do know that women and men’s immune systems are very different,” Schulz said.

“Men tend to have a stronger innate immune response (recognizing pathogens as foreign the first time we see them) and women tend to have a stronger antibody-mediated response. The antibody response is how vaccines work, of course, by having us make antibodies that are ready to attach to pathogens to which we are exposed,” he continued.

“So, our hypothesis is that women may have a more vigorous immune response. And, immune activity is involved in how brain cells are lost in Alzheimer’s disease. So, a more vigorous immune response to vaccines could translate into a greater effect of vaccines in women.” 

– Paul Schulz, MD

How might the flu vaccine help lower Alzheimer’s risk? 

Questions remain as to how a vaccine for the flu might help lower a person’s risk for Alzheimer’s disease. 

Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, told MNT there are a few biologically plausible possibilities.

“First, high-dose influenza vaccines generate a stronger immune response than standard-dose vaccines in older adults, and that may reduce the likelihood or severity of influenza infection and the systemic inflammation that comes with it,” Trinh, who was not involved in the recent study, explained.

“Since chronic inflammation and neuroinflammation are thought to play a role in Alzheimer’s disease, reducing inflammatory stress over time could be one pathway,” he hypothesized.

“Second, there is growing interest in the idea that some vaccines may ‘train’ or modulate the immune system in ways that influence brain health more broadly, although that remains theoretical,” he continued.

“The important point is that this study does not prove the mechanism; it raises a credible hypothesis that stronger protection against infection, stronger immune stimulation, or both could contribute to lower risk of Alzheimer’s.” Trinh said.

Promising findings with more research needed

MNT had the opportunity to speak with Rehan Aziz, MD, DFAPA, vice chair of education, psychiatry at Hackensack Meridian Jersey Shore University Medical Center, and associate professor of psychiatry and neurology at Hackensack Meridian School of Medicine in New Jersey, who commented he was excited about the study’s findings. 

“We already have compelling data suggesting that the shingles vaccine may reduce the risk of Alzheimer’s dementia, and this new study indicates that the flu vaccine could offer a similar protective benefit,” Aziz, who was likewise not involved in this study, explained.

“In my practice, I already recommend the shingles vaccine to older adults not only for its primary purpose but also for this potential cognitive benefit. Now, we can extend that same reasoning to the annual flu shot,” he told us.

“Furthermore, this study provides a strong clinical rationale for recommending the high-dose flu vaccine specifically, as it demonstrated a greater reduction in Alzheimer’s risk compared to the standard-dose version,” he added. 

MNT also spoke with Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, a part of Baptist Health South Florida, who said he found this research promising. 

“However, the study’s limitations, such as a short follow-up period and reliance on claims data, mean the findings should be interpreted with caution,” Gliebus, who was also not involved in the study, said. “More research is needed to confirm these results and understand the mechanisms involved.”

“Future research should include longer follow-up studies, randomized controlled trials, and investigations into the biological mechanisms behind the protective effects of high-dose influenza vaccines,” he detailed. “Studies should also focus on diverse populations, incorporate biomarker data, and explore the vaccine’s impact on cognitive decline progression.”

• Past studies show that eating a healthy, nutritious diet — such as a plant-based diet — may help in lowering a person’s risk of developing Alzheimer’s disease. 
• While a plant-based diet can be healthy with whole grains, legumes, and vegetables, it can also be unhealthy if it contains ultra-processed foods, fried foods, or foods high in sugars and salt. 
• A new study found that consuming an unhealthful plant-based diet may actually increase a person’s risk for Alzheimer’s disease and other types of dementia. 

Past studies show that eating a healthy, nutritious diet may help in lowering a person’s risk of developing Alzheimer’s disease or other types of dementia. 

One such diet is a plant-based diet, which emphasizes eating whole foods like vegetables, fruits, whole grains, legumes, nuts, and seeds, with little or no animal-based protein.

While a plant-based diet can be healthy, it can also be unhealthy if you choose ultra-processed foods, fried foods, or foods high in sugars and salt. 

Now, a new study published in Neurology, the medical journal of the American Academy of Neurology, has found that consuming an unhealthful plant-based diet may actually increase your risk for Alzheimer’s disease and other types of dementia. 

Healthy vs. unhealthy plant-based diet

For this study, researchers recruited almost 93,000 adults with an average age of 59. The study participant pool included people from several different ethnic groups, including Caucasian, African American, Japanese American, Native Hawaiian, and Latino. 

Study participants were asked to fill out food questionnaires at the start of the study to measure the types of healthy and unhealthy foods they consumed, and were given scores based on how closely they followed a healthy or unhealthy plant-based diet. 

“Plant foods have long been associated with broad health benefits, and plant-based diets have gained interest for environmental and other reasons,” Song-Yi Park, PhD, associate professor of population sciences in the Pacific Program at the University of Hawaii Cancer Center in Honolulu, Hawaii, and corresponding author of this study, told Medical News Today. “However, an earlier study by another group suggested that healthful and unhealthful plant foods may carry opposing effects on dementia risk.” 

“We adopted the indices they developed to distinguish the good and poor quality plant foods and examined their relationship with ADRD (Alzheimer’s Disease and Related Dementias) risk in our Multiethnic Cohort Study,” Park explained.

“Since this cohort has followed a large number of people from five racial and ethnic groups for (about) 30 years, we hoped to find out whether different quality plant foods are related to the subsequent ADRD risk differently. Especially, we wanted to see what happens to the related ADRD risk after people change their plant-diet quality over time,” she said. 

Eating more unhealthy plant-based foods raises dementia risk

Study participants were followed for an average of 11 years, and ranked into five subgroups based on their plant-based diet scores. 

During that time, researchers found that participants in the best subgroup who ate the most plant foods had a 12% lower risk of dementia, compared to participants in the lowest subgroup. 

When examining participants’ scores based on how healthy their plant-based diet was, the top subgroup lowered their dementia risk by 7%, while the lowest subgroup that consumed the most unhealthy plant-based foods increased their dementia risk by 6%. 

“This finding confirmed the overall hypothesis that people consuming more plant foods and more healthful plant foods were less likely to develop dementia later on,” Park said. 

Healthy diet changes reduce dementia risk even at older age

Additionally, Park and her team analyzed a subset of their participant pool, who were followed for 10 years, to look at how participants’ diets changed over time.

Researchers discovered that the participants whose diets changed to a more unhealthy plant-based diet increased their dementia risk by 25%. And those who moved away from an unhealthy plant-based diet lowered their dementia risk by 11%.

“This finding was more interesting, more indicative of potential benefits from individual changes,” Park said.

“The fact that we found the strongest dementia relationship from changes in unhealthful plant foods, rather than all plant foods or even healthful plant foods, seems helpful to understand what changes we can start with. And these relationship patterns were similar in people who were younger or older than age 60 at baseline, suggesting it’s not (too) late to make the change at an older age.”   
— Song-Yi Park, PhD

Diet quality matters for brain health

MNT spoke with Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, about this study, who commented that its results add meaningful evidence to something many clinicians have suspected for a long time: diet quality appears to matter for brain health, not just heart health. 

“What stood out to me is that this was a very large, multiethnic cohort followed over many years, and the findings were not simply about ‘eating more plants,’ but about the difference between healthier and less healthy plant-based eating patterns,” Trinh explained.

“Just as important, the study found that changes in diet over time were linked to dementia risk, suggesting that improving eating habits later in life may still be worthwhile,” he said.

“At the same time, I would be careful not to overstate the results, because this was an observational study, so it shows an association rather than proving cause and effect,” he added. 

As next steps for this research, Trinh said he would like to see intervention studies that test whether improving diet quality can directly reduce cognitive decline or dementia risk, rather than only being associated with it. 

“I would also like researchers to better understand which specific dietary changes drive the greatest benefit, how diet interacts with other risk factors such as diabetes, hypertension, and genetics, and whether some populations benefit more than others,” he added. 

Tips for eating a healthy plant-based diet

MNT also spoke with Monique Richard, MS, RDN, LDN, a registered dietitian nutritionist and owner of Nutrition-In-Sight, about this research, who said that one of the most important distinctions to make is that while a plant-based diet can be healthy, much of its health benefits depend on the types of food they select. 

“A plant-based diet can be incredibly health-promoting or it can also be highly processed and low in essential nutrients if convenient, manufactured food-like items are prioritized, or the only products available,” Richard detailed.

“Dietary patterns for an individual need to be adequate, varied, balanced, high in quality, nutrient-rich, and based on whole, real food curated by Mother Nature,” she continued. 

“Research consistently shows that whole, minimally processed plant foods such as vegetables, fruits, legumes, whole grains, nuts, and seeds, are associated with better cognitive and cardiometabolic outcomes. In contrast, plant-based diets high in refined grains, added sugars, and ultra-processed foods may not offer the same protection and can even contribute to inflammation, metabolic dysfunction, and systemic deterioration.” 
— Monique Richard, MS, RDN, LDN

• Diagnosing dementia at its earliest stages is important for granting people earlier access to treatments. 
• Over the last few years, researchers have been focused on finding new ways, such as blood tests, to help doctors diagnose dementia as early as possible.
• Researchers of a new study have developed the basis for a new blood test for the early diagnosis of dementia based on changes occurring in their gut microbiome. 

Over the last few years, researchers have been focused on finding new ways to help doctors diagnose dementia as early as possible. 

Diagnosing dementia at its earliest stages can help ensure people get access to treatments earlier, which can help with symptom management and quality of life. 

Some of these methods for diagnosing dementia at its earliest stages are blood tests searching for specific biomarkers that can be signs of dementia. 

Now, researchers from the University of East Anglia in the United Kingdom have developed the basis for a new blood test for the early diagnosis of dementia based on changes occurring in their gut microbiome.

Their research was recently published in the journal Gut Microbes. 

Metabolites help classify MCI vs. healthy brain

For this study, researchers analyzed blood and stool samples from 150 adults ages 50 and over. Recruited study participants ranged from no signs of cognitive impairment, to those with mild cognitive impairment (MCI) — which can be an early sign of dementia — and participants with subjective cognitive impairment (SCI), which is a self-reported decline in cognitive abilities like memory.

Through the blood and stool samples, scientists identified 33 key molecules produced by the gut microbiome and diet, as well as the bacteria living in their gut, called microbe-derived metabolites.

Using AI-powered machine learning, researchers examined different combinations of these chemicals to see how different combinations could help them identify healthy participants from those with MCI or SCI.

Scientists reported that even in study participants who had only started to notice mild memory changes, there were clear modifications to their gut bacteria and the metabolites they release into the bloodstream. 

Using just six of the discovered metabolites, the AI model was able to classify participants into the study’s three defined participant groups with 79% accuracy, and could tell healthy adults from those with MCI with more than 80% accuracy. 

“This adds weight to growing evidence that the so‑called gut–brain axis — the communication network between our digestive system and the brain — may play an important role in cognitive aging,” David Vauzour, PhD, associate professor in molecular nutrition in Norwich Medical School at the University of East Anglia, and lead author of this study, says in a press release.

“If particular gut bacteria or the chemicals they produce contribute to early cognitive decline, treatments involving diet, probiotics, microbiome‑based therapies, or personalized nutrition could one day form part of dementia prevention strategies.” 
— David Vauzour, PhD

Understanding the gut-brain link

So how could what’s going on in our digestive systems impact our brain health?

“The gut and brain are connected through what is known as the microbiota-gut-brain axis,” Manisha Parulekar, M.D., FACP, AGSF, CMD, director of the Division of Geriatrics at Hackensack University Medical Center and co-director of the Center for Memory Loss and Brain Health at Hackensack University Medical Center in New Jersey, explained to Medical News Today.

“The bacteria in our gut produce various compounds, or metabolites, from the food we eat. These metabolites can enter the bloodstream and influence brain health,” she said. 

“Analyzing metabolites and gut microbiome changes offers a chance to spot early signs of cognitive decline, as emerging evidence shows that the gut microbiome is important for brain health through the microbiota–gut–brain axis, which involves metabolic, immune, and neural signaling pathways,” said Peter Gliebus, MD, chief of neurology and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, part of Baptist Health South Florida.

“Dysbiosis in the gut can cause neuroinflammation, blood-brain barrier issues, and neuronal damage, all linked to cognitive decline and dementia. Metabolites such as indoxyl sulfate, choline, and tryptophan-derived compounds participate in important processes such as neurotransmitter production, oxidative stress regulation, and inflammation. Changes in their levels may indicate early disease processes before symptoms appear.”
— Peter Gliebus, MD

“Additionally, metabolite profiling and microbiome analysis can be performed using blood and stool samples, making these approaches less invasive and more accessible than traditional methods such as brain scans or spinal fluid tests,” Gliebus added. 

Research in larger, more diverse populations needed

MNT also spoke with Dung Trinh, MD, internist for the MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, about this study, who commented his first reaction was that this is a promising and biologically interesting study, but still early-stage research. 

Correlation, not causation

“It suggests that a small panel of blood metabolites linked to diet and the gut microbiome may help identify people with very early cognitive changes, which is exciting because we need less invasive ways to detect risk sooner. At the same time, this was a relatively small, cross-sectional study, so it shows association rather than proving that these markers can reliably predict who will go on to develop dementia.”
— Dung Trinh, MD

Trinh said the next step in this research is to test these findings in larger, more diverse groups of patients followed over time, so we can see whether these metabolite patterns truly predict future cognitive decline rather than simply reflecting differences already present. 

“I would also want to see the results replicated across different populations and compared directly with established Alzheimer’s blood biomarkers to understand whether they add meaningful value,” he added. “Ultimately, the field should move toward intervention studies to determine whether targeting diet, metabolism, or the gut microbiome could actually help delay or prevent decline.” 

• Everyone knows that making healthy lifestyle choices can help lower a person’s risk for many medical conditions, including dementia. 
• A new study found getting both the recommended amount of physical activity and sleep may be key to helping reduce a person’s dementia risk. 
• Researchers determined that getting either too little or too much sleep may increase dementia risk. 

Making healthy lifestyle choices, such as eating a healthy diet, not smoking, getting enough physical activity and proper sleep, can help lower a person’s risk for many medical conditions. 

One such condition is dementia — a condition that negatively impacts a person’s thinking and memory skills. 

“Dementia affects more than 55 million people worldwide, and despite decades of research, there is still no cure,” Akinkunle Oye-Somefun, PhD, from the School of Kinesiology and Health Science at York University in Canada, explained to Medical News Today.

“The treatments that exist can slow progression in some people, but they do not stop the disease. That is why identifying modifiable risk factors — behaviors people can change — remains a critical research priority. Behaviors like how much people move, how long they sit, and how long they sleep are among the most promising targets,” he explained.

Oye-Somefun is the first author of a new study published in the journal PLOS One that found getting both the recommended amount of physical activity and sleep may be key to helping reduce a person’s dementia risk. 

Regular physical activity lowers dementia risk by 25%

For this study, researchers analyzed data from adult participants ages 35 and older of 69 previously-conducted studies. Of these studies, 49 focused on participants’ physical activity, 17 on sleep duration, and three on sedentary behavior. 

“These three behaviors are all part of the same daily routine,” Oye-Somefun explained. “They shape each other, and all three can be changed. There has been growing evidence linking each one to brain health, and I felt it was important to ask: what does the full picture look like when the best available evidence is pooled across millions of people? The answer is that all three are important, because it means there is more than one lever people can pull.” 

At the study’s conclusion, researchers found that participating in regular physical activity was correlated with an average 25% lower risk of dementia. 

“Physical activity is one of the most important drivers of brain health,” Oye-Somefun said.

“What makes this particularly meaningful from a public health standpoint is that the association held up across 49 studies. It also held up in middle-aged and older adults, which tells us that it is not too late, and the window for benefit is not closed by the time people are in their 50s or 60s and older.” 
— Akinkunle Oye-Somefun, PhD

Sitting 8+ hours a day increases dementia risk by 27%

When it came to sleep, scientists discovered that getting too little sleep — less than seven hours a night — was linked to an 18% higher risk of developing dementia. And sleeping too much — more than eight hours a night — increased dementia risk by 28%. 

“This finding matters because both short and long sleep durations were linked to higher risk,” Oye-Somefun said. “Consistently sleeping outside the seven-to-eight-hour range, in either direction, may carry long-term implications for brain health — implications that are easy to overlook because they accumulate silently over decades.” 

Additionally, Oye-Somefun and his team found that study participants who sat for more than eight hours a day increased their dementia risk by 27%. 

“Sitting for long stretches is its own risk factor, and many adults spend much of the day sitting — often without knowing it,”Oye-Somefun said.

Breaking up sitting time is important

“Sitting at a desk for eight hours is quite common, and our findings suggest that kind of long, unbroken sitting is associated with brain health on its own. It is not just about adding movement to the day — breaking up time spent sitting also matters. Prolonged sitting may carry its own risk, even for people who are otherwise active.”  
— Akinkunle Oye-Somefun, PhD

“I do want to be transparent that this finding is based on fewer studies than the physical activity evidence, so we need more research before calling it settled,” he added. “But the signal is consistent given what we already know about prolonged sitting and cardiovascular disease, and it would be surprising if the brain were somehow unaffected.”

Low-risk strategies for overall cognitive health

MNT spoke with Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of the Healthy Brain Clinic in Irvine, CA, about this study, who commented its findings add meaningful support to something many clinicians already believe: that everyday habits like staying physically active, getting adequate sleep, and avoiding too much sedentary time may play an important role in brain health. 

“What makes it especially notable is the very large amount of data it brings together, which strengthens confidence that these associations are real and relevant,” Trinh continued.

“That said, this is still observational research, so it does not prove that these behaviors directly prevent dementia, but it does reinforce that they are sensible, low-risk strategies that fit well with what we already recommend for overall cardiovascular and cognitive health.” 
— Dung Trinh, MD

Trinh said the next steps in this research should move beyond association and better understand causation by doing more long-term intervention studies that test whether changing these habits can truly reduce dementia risk over time. 

“I would also like to see researchers use more objective tools, such as wearable devices, to measure physical activity, sitting time, and sleep more accurately, since much of the current evidence relies on self-report,” he detailed.

“Future research should examine how these behaviors work together, because in real life exercise, sleep, and sedentary time are interconnected, and understanding that interaction could help us give more precise, personalized prevention advice,” he added. 

• The Food and Drug Administration (FDA) has approved Eli Lilly’s Foundayo (orforglipron), a once-daily oral glucagon-like peptide-1 (GLP-1) receptor agonist, which offers a noninjectable option for weight management.
• Clinical data suggests the drug supports meaningful weight loss and can be taken without strict food or timing requirements, potentially improving ease of use and adherence.
• The approval was expedited through the FDA’s National Priority Voucher program, a new initiative designed to speed up access to treatments addressing major public health needs.
• Orforglipron’s approval highlights both the growing role of GLP-1 therapies in weight loss and the potential for faster regulatory pathways, bringing new treatments to patients sooner.

The Food and Drug Administration (FDA) has approved Eli Lilly’s once-daily oral GLP-1 receptor agonist, orforglipron, for adults with obesity, or overweight with weight-related medical problems.

This approval makes Eli Lilly’s oral GLP-1 receptor agonist, to be marketed as Foundayo, the second GLP-1 drug available in pill form, after Wegovy, which gained approval in December 2025.

In March 2026, a phase 3 clinical trial for oral orforglipron suggests it can lower blood sugar levels at least as well as, and in some cases better than, oral semaglutide.

Foundayo is notable not only for its oral formulation but also for being among the first medications approved under the FDA’s new Commissioner’s National Priority Voucher (CNPV) program, an initiative designed to accelerate access to treatments that address major public health needs.

A new option beyond injections

GLP-1 receptor agonists have transformed the management of obesity and type 2 diabetes in recent years. Evidence suggests roughly one in eight U.S. adults report having ever used GLP-1 medication, with 6% currently using such drugs.

Obesity remains a major global health concern, affecting hundreds of millions of people. It also increases the risk of conditions such as type 2 diabetes, cardiovascular disease, and certain cancers.

Thus, there is a growing demand for GLP-1–based therapies, which have demonstrated substantial benefits in weight reduction and metabolic health.

However, most currently available therapies are administered via injection. Research notes that many people report a preference for oral medication over injections, and injectable drugs can act as a barrier for initiating treatment.

“There is no single path that works for everyone living with overweight or obesity,” said Joe Nadglowski, president and CEO of the Obesity Action Coalition, in a press release.

“New treatment options expand choice and help more people find care that fits their lives, their goals and where they are in their journey – whether they’re just starting to explore treatment or looking for a different long-term approach,” noted Nadglowski.

Expanding access to treatment

Oral formulations may expand access to treatment, particularly for those reluctant to use injectable medications. They may also offer greater convenience and may be easier to scale and distribute than injectable alternatives.

After approving oral Wegovy in December 2025, the FDA has now also approved Foundayo. Similar to other GLP-1 drugs, the once-daily pill mimics the GLP-1 hormone, which helps regulate appetite and food intake.

Clinical trial data shows that participants taking Foundayo achieved meaningful weight loss compared with placebo, reinforcing its potential as an effective treatment option.

Richard Frank, MD, MHSA, Chief Medical Officer at Vida Health, spoke to Medical News Today about how orforglipron may expand access to GLP-1s: “The choice between a pill and an injectable comes down to patient preference and potency.”

“The injectables are clearly more potent but require a weekly injection. Whereas pills do not require a needle, which is appealing to a lot of patients,” added Frank.

He explained that:

“The Wegovy pill has to be taken in the morning on an empty stomach with a time delay before consuming any food or drink. Whereas Orforglipron can be taken any time during the day with or without food. While this makes Orforglipron more convenient, it is also less potent.”

As noted above, unlike some existing oral GLP-1 therapies, Foundayo can be taken any time of day without restrictions on food and water intake, which may improve adherence for some individuals.

“People living with obesity need treatment options that meet them where they are – and for many, a once-daily pill that can be taken with no food or water restrictions can offer them greater flexibility in how they approach their treatment,” said Deborah Horn, DO, director of the Center for Obesity Medicine at McGovern Medical School
 at UTHealth Houston, in a press release.

“With Foundayo, we now have an oral option that delivered an average of 12.4% weight loss at the highest dose in clinical trials – addressing both the clinical realities of obesity and the practical challenges patients face every day,” Horn noted.

Fast-tracked through a new FDA program

Notably, a key feature of this approval is its link to the FDA’s National Priority Voucher (CNPV) program.

Announced in June 2025, the CNPV program aims to expedite the review of drugs that address unmet medical needs, improve affordability, or support public health priorities.

Under this scheme, selected medicines may receive a significantly shortened review timeline. In some cases, it could take as little as 1 to 2 months compared with the typical 10 to 12 months.

Orforglipron was granted one of these vouchers, enabling a rapid regulatory decision and making it one of the first therapies to be approved through the program.

The FDA has stated that the initiative is intended to pioneer “new ways of bringing these cures and meaningful treatments to the market faster,” particularly in areas of high public health need.

Looking ahead

The approval of orforglipron signals both a shift toward more accessible obesity treatments and a test case for the FDA’s new accelerated review pathway. The CNPV program may play an increasingly important role in speeding up access to therapies that address urgent health challenges.

If widely adopted, oral GLP-1 therapies could reshape obesity treatment, making effective medications easier to use, distribute, and integrate into long-term care.

“Treating obesity with behavior change, generic anti-obesity medications, and GLP-1 seems to reduce the risk profile associated with all of these [cardiometabolic] diseases,” Frank added.

According to him, “Tracking, monitoring, and optimizing this risk reduction is critical to reducing the complications of cardiovascular-kidney-metabolic disease.” 

However, as with other GLP-1 receptor agonists, orforglipron carries safety considerations. Potential side effects may include gastrointestinal symptoms such as nausea, vomiting, and constipation.

Additionally, the drug label includes a boxed warning related to a potential risk of thyroid tumors. Therefore, it is advisable for people to discuss the potential risk and benefits of GLP-1 medications with their healthcare providers.

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• A new study examined the association between sleep habits and heart disease. 
• After getting 7 days of sleep data from the participants, the researchers used the following 10 years of health data to examine the impact sleep habits can have on heart disease.  
• They found that adults who did not keep a consistent sleep schedule and got under 8 hours of sleep had a higher risk of a major cardiovascular event (MACE).

Maintaining a regular sleep schedule is an important part of overall health. Prior research suggests that chronic sleep problems may contribute to developing diabetes, obesity, and mental health disorders.

Researchers from the University of Oulu in Finland took a closer look at the relationship between sleep and heart health in a long-term study of middle-aged adults.

They found that people who had both an irregular sleep schedule and got under 8 hours of sleep per night had the highest MACE risk.

The study is published in BMC Cardiovascular Disorders.

Observing 10 years of sleep patterns

The Centers for Disease Control and Prevention (CDC) recommends that adults get a minimum of 7 hours of sleep per night. Many adults in the U.S. struggle with getting enough sleep, with CDC research reporting that about one-third of adults get less than 7 hours of sleep each night.

Lack of regular sleep can contribute to a number of both physical and mental health issues, including affecting the heart. 

Poor sleep affects the body’s circadian rhythm, which helps regulate blood pressure and heart rate. Not getting enough sleep can affect blood pressure and cause it to stay elevated for a longer period of time instead of dropping at night during sleep.

With this in mind, the researchers in the current study wanted to learn more about the impact of sleep habits on heart health. They were interested in the participants’ bedtimes, sleep midpoints, wake-up times, and sleep duration.

The scientists used data from 3,231 adults in the Northern Finland Birth Cohort 1966. The participants wore activity monitors on their wrists for up to 2 weeks, and the researchers used the first 7 consecutive nights of sleep data for their analysis. 

They grouped sleep characteristics into the following categories: 

• regular
• fairly regular
• irregular 

The participants also completed health and lifestyle questionnaires that covered smoking and alcohol use. They underwent clinical testing for blood pressure, BMI, cholesterol, and blood sugar. 

The researchers used national health records during the 10 following years to track cardiac events such as heart attack, stroke, and cardiovascular-related death.

Double the heart event risk with poor sleep

The researchers found that sleep health may be about more than just the total number of hours slept per night. 

They found that participants with irregular bedtimes who also slept for less than 8 hours per night had a higher risk of cardiovascular events, including heart attack and stroke, over the following decade. 

These participants had nearly double the MACE risk compared to participants with more consistent sleep schedules.

The researchers also found a similar increase in risk among people with highly irregular sleep midpoints. Sleep midpoint, the halfway point between falling asleep and waking up, is considered an important marker of circadian rhythm stability.

Sarathi Bhattacharyya, MD, a pulmonologist, sleep medicine specialist, and medical director of MemorialCare Sleep Disorders Center at Long Beach Medical Center, who was not involved in the study, spoke with Medical News Today and explained the significance of this finding. 

He noted that when circadian rhythm is disrupted, “the body’s period for recovery and hormone signaling gets disrupted…chronic sleep deprivation can increase stress hormones and contribute to adverse cardiovascular risk.”

The researchers did not find that irregular wake-up time alone was associated with increased cardiovascular risk. 

Sleep consistency crucial for heart health

The researchers said the findings suggest sleep consistency may be an important public health focus, a point also emphasized by the experts who spoke with MNT.

“A two-fold increase in MACE is a significant difference and reiterates the importance of addressing sleep quality and duration issues in patients who may already have other risk factors for cardiac disease,” shared Bhattacharyya.

Brian Zachariah, MD, a board-certified psychiatrist with Mindpath Health, said the findings are clinically meaningful.

“The hazard ratio of approximately 2.0 is significant considering other traditional cardiovascular risk factors (like smoking vs non-smoking, diabetes vs no diabetes),” shared Zachariah.

What stood out most to Zachariah was that irregular bedtimes, rather than wake-up times, were linked to higher heart risk. He said this may reflect broader behavioral instability and circadian disruption. 

“Irregular sleep timing/circadian disruption plays a role in metabolic and inflammatory dysregulation. It can cause insulin resistance, increase systemic inflammation, which in turn can elevate atherosclerosis and thrombosis.”
— Brian Zachariah, MD

Cheng-Han Chen, MD, a board-certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center, also shared his thoughts with MNT.

“These findings add to our current understanding of how important sleep quality is to maintain heart health,” said Chen. 

Chen also pointed out that disruptions in the circadian rhythm can cause cortisol and adrenaline to fluctuate, which can contribute to higher blood pressure and obesity. 

“Heart disease is already the leading cause of death in the United States, and a two-fold increase in cardiovascular risk as noted by this study would be quite a significant and meaningful difference,” shared Chen.

• Researchers have noted an association between high vitamin D levels and low levels of tau protein on brain scans after several years.
• Tau protein is a biomarker for Alzheimer’s disease, the leading cause of dementia.
• There was no association between vitamin D and levels of amyloid-beta, another Alzheimer’s biomarker.

The authors of a new study have reported that having higher levels of vitamin D was associated with lower levels of tau protein — a biomarker for Alzheimer’s disease — several years later.

“These results suggest that higher vitamin D levels in midlife may offer protection against developing these tau deposits in the brain,” said study author Martin David Mulligan, MB BCh BAO, of the University of Galway in Ireland in a press release.

“Low vitamin D levels could potentially be a risk factor that could be modified and treated to reduce the risk of dementia.”

Vitamin D is a fat-soluble vitamin that the body produces when sunlight touches the skin. Most people can obtain what they need through sun exposure, but during winter months, when there is less sunlight, people can get it from supplements and some foods.

This vitamin is important for keeping bones, muscles, and teeth healthy by regulating the amount of calcium and phosphorus in the body. It can also play a role in reducing inflammation, supporting the immune system, and managing glucose levels.

What did the researchers measure?

For the study, published in Neurology Open Access, an official journal of the American Academy of Neurology, the researchers looked at 793 participants who did not have dementia. The participants had an average age of 39 at the start of the study.

At the beginning of the study, researchers measured the levels of vitamin D that participants had using blood tests.

The researchers defined high levels of vitamin D as being greater than 30 nanograms per milliliter (ng/mL). They defined anything less than this amount as being a low level of vitamin D.

At this stage, around 34% of the participants had low levels of vitamin D, with 5% taking a vitamin D supplement.

After an average of 16 years, brain scans then measured the amounts of tau and amyloid beta proteins present in the brains of the participants.

Buildups of these two proteins in the brain are associated with the development of Alzheimer’s disease, the most common cause of dementia.

After adjusting for factors that could affect the levels of tau, such as age, sex, and depression, the researchers found that having higher levels of vitamin D was associated with lower levels of tau protein.

There was no association between vitamin D and amyloid-beta levels, however. Medical News Today asked Mulligan why he thought this might have been the case.

“Accumulation of tau in some areas of the brain may occur earlier than the build up of amyloid,” he said.

“The participants in our study were relatively young when blood samples were obtained, and so an association between vitamin D and tau, compared to amyloid protein, may be more likely to be detected in a younger population.”

How promising are these findings?

“These results are promising, as they suggest an association between higher vitamin D levels in early middle-age and lower tau burden on average 16 years later,” said Mulligan in the press release.

“Mid-life is a time where risk factor modification can have a greater impact.”

This study has a number of limitations, however, which means people should be careful with how much importance they place on these findings for now.

A key limitation is that the researchers only had one measurement of vitamin D from the beginning of the study. Over the years that passed before the brain scans, the participants’ vitamin D levels may have changed significantly.

The way that the researchers measured vitamin D levels was also quite limited, defining a participant’s levels as either high or low with no middle ground.

Labelling levels above 30 ng/mL as high meant that someone with a level of 30 ng/mL would fall into the low level group. Experts define levels of 20 ng/mL and above as being adequate for overall health.

The researchers opted for this cutoff point rather than 20 ng/mL as this measurement had previously featured in previous studies with older groups of participants. In contrast, there was a relatively small number of people with levels lower than 20 ng/mL in this study’s sample.

Could other factors explain the findings?

Higher vitamin D levels may not have been the reason for the relatively lower tau levels.

MNT spoke with Steve Allder, MD, a consultant neurologist at Re:Cognition Health in London in the United Kingdom, who was not involved with the study. He explained what other factors may have been at work.

“Higher vitamin D levels may simply be a marker of overall better health rather than the driver of reduced tau pathology. For example, individuals with higher vitamin D are often more physically active, spend more time outdoors, and may have healthier diets, all of which are independently linked to better brain health.”
– Steve Allder, MD

“Socioeconomic status, access to healthcare, and lower rates of chronic disease could also play a role,” he added.

“Of course, these results need to be further tested with additional studies,” said Mulligan in the press release.

Are there other ways to reduce the risk of Alzheimer’s?

Getting sufficient amounts of vitamin D is important for overall health, but there are clearer steps people can take to reduce their risk of Alzheimer’s disease and dementia.

While people cannot control some risk factors for Alzheimer’s, such as age and genetics, people can adjust other factors associated with the disease.

Some steps that could help to reduce the risk of Alzheimer’s include:

• maintaining a healthy weight
• following a healthy diet
• exercising regularly
• managing blood sugar
• managing blood pressure
• keeping mentally active
• getting enough sleep
• limiting alcohol consumption
• not smoking

MNT also asked Dung Trinh, MD, internist for MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, about Alzheimer’s risk reduction.

“The strongest evidence still supports a multifactorial prevention approach, not a single nutrient or intervention,” Trinh said.

“Vitamin D may play a role in overall health, but it should be viewed as one small piece of a much larger prevention strategy — not a standalone solution.”

• Having a heart attack can raise a person’s risk for other cardiovascular conditions. 
• Following a heart attack, doctors typically prescribe a combination of therapies, including medications like beta-blockers. 
• A new study found that people who have had a heart attack, but who are considered low risk for other cardiovascular complications, may be able to safely discontinue beta-blocker use after at least one year. 

Researchers estimate that over 17.9 million people globally die each year from cardiovascular diseases, such as myocardial infarction, also known as a heart attack. 

Having a heart attack can increase a person’s risk for having other cardiovascular issues, including another heart attack, heart failure, arrhythmia, stroke, and peripheral artery disease.

To help lower your risk for these heart conditions, after a heart attack doctors normally prescribe a combination of lifestyle changes, such as eating a heart-healthy diet and quitting smoking, along with cardiac rehabilitation and certain medications, such as beta-blockers. 

Now, a new study presented at the American College of Cardiology’s Annual Scientific Session (ACC.26) reports that people who have had a heart attack, but who are considered low risk for other cardiovascular complications, may be able to safely discontinue beta-blocker use after at least one year. 

The results of the study were also published in The New England Journal of Medicine.

Continuing beta-blockers may not be needed in low-risk patients

For this study, researchers analyzed medical data from more than 2,500 participants with an average age of 63 in South Korea who, between 2021 and 2024, had no additional cardiac issues after taking beta-blockers for at least one year following a heart attack. 

Beta-blockers are a type of medication that help reduce heart rate and blood pressure by lowering the effects of stress hormones like epinephrine (adrenaline) on the body’s beta receptors. This can help improve blood flow and help manage future heart attacks, angina, and heart failure. 

At the study’s conclusion, researchers found that after a median of 3.1 years of follow-up, the study’s primary endpoint — including all-cause death, recurrent heart attack, or heart failure hospitalization — occurred in 7.2% of study participants who stopped taking beta-blockers, compared to 9% in those who continued to take them. 

“In appropriately selected patients who survived a heart attack and do not have heart failure or left ventricular systolic dysfunction, routine continuation of beta-blockers indefinitely may not be necessary,” Joo-Yong Hahn, MD, a cardiologist at Samsung Medical Center in South Korea, and senior author of this study, said in a press release.

“In practice, for stable patients who are several years out from a heart attack, discontinuation can be considered through shared decision-making and with monitoring of blood pressure and heart rate,” he said. 

Challenging a decades-long heart attack treatment practice

Medical News Today spoke with Cheng-Han Chen, MD, a board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, about this study. 

“Beta-blockers have been for decades a mainstay of medical therapy for patients who suffer a heart attack,” Chen commented. “These study results add to more recent research that beta-blockers may be less necessary in today’s age of newer and more efficacious medications and certainly make me re-examine their necessity in my patients who take them.” 

“Future research should examine whether these findings apply in a more diverse population and determine the categories of patients who may still benefit from beta-blocker therapy,” he added. 

MNT also spoke with Craig Basman, MD, a  cardiologist at Hackensack University Medical Center, who commented that this study is an important and welcome piece of research because it challenges a practice that has been in place for decades.

“It reinforces the direction we’ve been moving in cardiology: using evidence-based therapy to guide management,” Basman explained. “It’s not a green light for everyone to stop their medication, but it does open the door for a new conversation with the right patients about what is truly necessary for their long-term health.” 

Why would people want to stop using beta-blockers? 

For people who have experienced a heart attack and are on beta-blockers, the benefits of discontinuing them, for the appropriate patient, are primarily about improving their quality of life, Basman said. 

“While these drugs are important treatments for many conditions, they can have side effects for some individuals, such as fatigue, dizziness, depression, or exercise intolerance,” he detailed. “Being able to safely stop a medication means potentially alleviating these side effects, which can make a big difference in a person’s daily energy and well-being. It also reduces the number of pills a patient needs to take every day, which can be a significant relief.” 

Rigved Tadwalkar, MD, FACC, consultative cardiologist and director of Digital Transformation Pacific Heart Institute in Santa Monica, CA, agreed. 

“Beta-blockers are very effective medications, but they’re not always easy to live with long term. Many patients experience fatigue, reduced exercise tolerance, dizziness, sexual dysfunction, or just a general sense of being ‘slowed down.’ For someone who has otherwise recovered well and is trying to get back to a normal, active life, those side effects can be limiting.” 
— Rigved Tadwalkar, MD, FACC

“There’s also a broader principle here around minimizing unnecessary long-term therapy,” Tadwalkar continued.

“Every medication adds complexity, including a greater potential for interactions or side effects over time. In patients who no longer have a clear ongoing indication, in this case no heart failure, no ongoing angina or arrhythmia, being able to step back from a medication is good cardiology practice,” he explained. 

“The next step (for this research) is really about confirming and extending these findings across broader patient populations,” Tadwalkar added. “This was a well-done study, but it was conducted in a relatively specific group of patients, so it will be important to see similar results reproduced in more diverse populations, including more women and patients from different healthcare systems. That helps ensure the findings apply widely in everyday clinical practice.” 

• Inflammatory bowel disease is a chronic condition where the body’s immune system attacks the intestines.  
• Research is ongoing on the best ways to manage inflammatory bowel disease, including through medication and lifestyle changes.  
• Results from a small study suggest that taking vitamin D may be helpful for people with inflammatory bowel disease and may help the body avoid attacking itself.

Inflammatory bowel disease (IBD) is a condition that “triggers the body’s immune system to mistakenly attack healthy bowel cells,” leading to symptoms such as persistent fatigue, abdominal pain, chronic diarrhea, and unexplained weight loss, according to the Centers for Disease Control and Prevention.

IBD includes the subtypes of ulcerative colitis and Crohn’s disease, and people with IBD can experience flare-ups of such symptoms intermittently.

A recent study published in Cell Reports Medicine examined how vitamin D supplementation may affect people with IBD, and found that increasing vitamin D levels may help the body’s immune system tolerate gut bacteria.    

Vitamin D and how the body responds to gut bacteria 

This study involved 48 adult participants who either had ulcerative colitis or Crohn’s disease and also had low vitamin D levels. Researchers collected blood and stool samples from participants at baseline and then again at the end of twelve weeks. Over these 12 weeks, participants received weekly doses of vitamin D.  

Researchers evaluated a number of components, including disease activity, quality of life, and C-reactive protein in blood and stool samples. C-reactive protein can help with measuring inflammation in the body.  

Researchers also focused on looking at two critical types of immunoglobins: IgA and IgG. Immunoglobulins are specific proteins produced by certain white blood cells. IgA performs several helpful functions in the digestive system, including regulating gut bacteria.     

Researchers found that vitamin D had several positive effects on participants. They saw that vitamin D helped “reset” and “rebalance” the immune system’s communication with the gut microbiome. The researchers described this as promoting immune tolerance, rather than just suppressing inflammation.

Vitamin D supplementation also helped increase IgA levels, which are linked to a more stable immune response, and lower Immunoglobulin G (IgG) levels, which are linked to pro-inflammatory responses in the gut.

After 12 weeks, participants also had lower disease activity scores, meaning they felt better overall and clinically had fewer or less severe symptoms. The researchers also observed a decrease in stool-based markers of inflammation.

How does vitamin D achieve this effect?

“The study showed that vitamin D supplementation for 12 weeks resulted in improvement of the patients as measured by disease activity scores as well as markers of inflammation. Supplementation with vitamin D resulted in significant changes in the intestinal microbial composition that were likely beneficial as well as in the gut immune system,” Steven Cohn, MD, PhD, AGAF, FACG, chief of the Division of Gastroenterology and Hepatology at the University of Texas Medical Branch, who was not involved in the study, said.

Cristiano Pagnini, MD, PhD, consultant gastroenterologist and researcher at San Giovanni Addolorata Hospital in Rome, Italy, who was also not involved in the study, explained that the findings suggest that vitamin D may influence how the immune system interacts with the gut microbiome in IBD.

“By combining microbiome and immune profiling, the authors suggest that vitamin D supplementation could shift the balance from a more inflammatory IgG-driven response toward a more tolerogenic IgA-mediated one. This is an appealing concept, as it frames IBD not just as excessive inflammation, but as a failure of immune tolerance to gut bacteria,” he told Medical News Today.

Pagnini added that the study sheds light on mechanisms of potential interactions between the vitamin D pathway and microbiota composition, which aligns with recent hypotheses of a reciprocal, synergistic effect between vitamin D supplements and probiotics.  

Study limitations and what’s next in research 

This study was relatively small and did not provide long-term data; thus, larger, longer-term studies will likely be helpful as research moves forward.   

The researchers also acknowledge that giving vitamin D wasn’t based on a randomized process or compared to a placebo.  

Pagnini underscored that caution was warranted and that the study’s clinical endpoints were exploratory.

“Only serum vitamin D level is considered, while Vitamin D receptor (VDR) expression and activation are not investigated,” he said.

Pagnini also pointed out that the findings may be optimistically overinterpreted and that larger, controlled studies are needed.

“While the biological signals are strong, they do not yet translate into clear evidence of clinical benefit. As is often the case with sophisticated multi-omics research, there is a risk that mechanistic insights may be overinterpreted when applied to patient care,” he said.

John Mark Gubatan, M.D., study author, and gastroenterologist at Mayo Clinic in Jacksonville, Florida said the next steps in research would need to explain the biological mechanism behind how vitamin D behaves in the GI tract, as well as address questions such as how much vitamin D IBD patients need.

“Our exploratory study highlights [that] there could be potential benefits with vitamin D in controlling the interactions between the immune system and gut microbiome in patients with IBD and that further work is needed to understand the exact vitamin D levels and vitamin D supplementation strategies to support this in patients with IBD and other chronic inflammatory diseases,” he said.

“As a next step, we are hoping to better understand if some of the gut bacteria promoted by vitamin D could be used to directly to improve IBD and understand how this works from an immune landscape standpoint,” he continued.

“Furthermore, we hope to better understand how some of the B and T regulatory cells (immune cells that control inflammation) that migrate to the gastrointestinal tract increased by vitamin D in this study are helpful in patients with IBD,” he added. 

Should I take vitamin D if I have IBD?

This study suggests potential benefits of vitamin D supplementation for people with IBD.

“The implications of this study for care of patients with IBD are significant. The study suggests that vitamin D supplementation may have a role as a beneficial adjunct to current advanced therapy for this group of inflammatory bowel diseases,” Cohn said.

Cohn also noted that more research is needed before making widespread recommendations.

“Further studies of vitamin D supplementation on different disease subgroups and its interaction with specific therapeutic agents are needed to help clarify where supplementation with Vitamin D fits into current therapeutic approaches to treating patients with IBD,” he said. 

Gubatan noted that current guidelines on vitamin D supplementation were based on bone health and calcium metabolism.

“Patients with chronic inflammation may have different vitamin D needs. Patients who are vitamin D-deficient should discuss supplementation with their providers and have levels rechecked as per current guidelines. It’s too early to recommend measuring gut microbiome or immune markers to test vitamin D efficacy.”
— John Mark Gubatan, MD

“In practice, these findings support what clinicians are already doing: identifying and correcting vitamin D deficiency in patients with IBD. However, it would be premature to consider vitamin D as a stand-alone therapeutic strategy,” Pagnini added.