Category: News

  • Women with endometriosis face 46% higher risk of type 2 diabetes, study finds

    Women with endometriosis face 46% higher risk of type 2 diabetes, study finds

    Women with endometriosis have a 46% higher risk of developing type 2 diabetes than women without the condition, according to a new study led by researchers at the George Mason College of Public Health and collaborators.

    Following data from nearly 3 million women over 25 years, the study, published in Diabetologia, is the largest to date examining the relationship between endometriosis and type 2 diabetes. Maggie Fuzak Nunziato, a George Mason doctoral student in epidemiology, led the research with Anna Pollack, professor of Global and Community Health.

    Researchers found that diabetes risk varied across different forms of endometriosis, suggesting the condition may have broader long-term health implications than previously recognized. They believe the chronic inflammation associated with endometriosis may play a role in metabolic health, though more research is needed to understand the connection.

    “Previous studies largely evaluated endometriosis as a single condition and generally reported little or no overall association with type 2 diabetes,” said Fuzak Nunziato, the study’s lead author. “Our findings add to a growing understanding that endometriosis may affect more than reproductive health alone.”

    Notably, researchers found the association was strongest among premenopausal women and women without obesity—groups not traditionally considered at the highest risk for type 2 diabetes.

    Why it matters

    Endometriosis affects about 1 in 10 women of reproductive age. It occurs when tissue similar to the uterine lining grows outside the uterus, which can often cause chronic pelvic pain, infertility, and other complications.

    If the study’s findings are confirmed by future research, they could help clinicians identify women with endometriosis who may be at higher risk for type 2 diabetes and who could benefit from earlier screening or prevention efforts.

    More study details

    The study analyzed health records from nearly 3 million women in the Utah Population Database between 1996 and 2021, including nearly 100,000 diagnosed with endometriosis.

    Researchers found that some forms of endometriosis carried a much stronger association with diabetes than others. The link was greatest among women with extra-pelvic endometriosis, meaning the disease is found outside the pelvis.

    The researchers emphasize that the findings show an association, not proof that endometriosis can cause type 2 diabetes. They say more research is needed to better understand the biological mechanisms connecting the two conditions, and whether earlier metabolic screening could improve outcomes for women with endometriosis.

    The study also included collaborators from the University of Utah, the University of Arizona, Brigham and Women’s Hospital, and Intermountain Health.

    Journal Diabetologia

    DOI 10.1007/s00125-026-06828-w 

  • Essential vitamin B12 mined from exploded gut bacteria

    Essential vitamin B12 mined from exploded gut bacteria

    Vitamin B12 is biological gold.

    All living organisms need a little bit of it to form red blood cells and DNA, as well as to build and support brain and nerve cells. But it’s hard to come by: Humans don’t make it. Animals don’t make it. Plants don’t make it.

    In fact, this essential nutrient is made exclusively by certain bacteria and archaea.

    But we’ve got to have it, so we scavenge.

    Humans tap natural food sources such as meat, shellfish, fish, poultry, and dairy, as well as supplements, to get what we need.

    Scientists have a clear picture of how B12 is absorbed into the body. What is harder to understand is how and why those elite microbial B12 producers allow their precious stock to become available to the broader microbial community in the first place.

    In a paper published recently in the ISME Journal, Virginia Tech biologist Bryan Hsu and collaborators revealed the mechanism for B12 release: plundering by bacteria-eating viruses called bacteriophages, or phages.

    Phages are viruses that infect only bacteria. Although they are ecologically entrenched with bacteria, phages are harder to classify and more mysterious. Hsu, the Blackwood Junior Faculty Fellow in the College of Science, studies how phages shape the gut microbiome.

    Phages attack bacteria in a gruesome process called lysing. The virus attaches to a bacterial cell, injects its own DNA, and reprograms the host cell to manufacture more phages. When the bacterial cell eventually succumbs, it explodes into a flood of new phages. But there’s more than just new phages in the bacterial death gush.

    “It has all the DNA, the protein, sugars — all these things that the bacterial cell normally hoards so that it can continue to grow,” Hsu said.

    It also includes vitamin B12.

    In the paper, Hsu’s research team demonstrated that phage infection is a primary driver for releasing B12. David da Silva Barreira, the study’s first author and a former Virginia Tech postdoctoral associate, verified this by co-culturing a B12 producer with a B12 consumer that needs to scavenge for B12 from the environment.

    Without introducing the phage, the B12 user didn’t grow. It couldn’t get to the B12, and the nutrient remained trapped inside the intact producer cell.

    But then they unleashed the phages to lyse the producer, and the consumer began to thrive.

    “In a genetically well-defined system, we can demonstrate that phage is necessary,” said Hsu. “The B12 doesn’t just leak out.”

    To confirm that B12 specifically drove the growth boost — rather than other cellular contents — da Silva Barreira repeated the experiment with a producer strain genetically engineered to lack B12. When phages lysed the modified cell, the user failed to grow. The result proved that B12 was the essential component — a first for the field.

    To test whether the findings held up in a more complex environment, the researchers conducted similar experiments on major types of gut bacteria found in the human digestive tract. Microbes dependent on B12 grew only when a phage lysed a B12 producer.

    Taken together, these findings suggest that the brutal methods of bacteriophages play a critical role in distributing nutrients, promoting microbial diversity, and supporting microbiome gut health.

    Study collaborators include:
    Hannah Poole, an undergraduate student majoring in biological sciences
    Rogério A. Bataglioli, a postdoctoral associate in biological sciences

    Original study DOI: 10.1093/ismejo/wrag160

  • Mindfulness-Based Therapy for Opioid Misuse Offers Massive Return on Investment

    Mindfulness-Based Therapy for Opioid Misuse Offers Massive Return on Investment

    A new economic evaluation from the University of California San Diego School of Medicine has revealed that Mindfulness-Oriented Recovery Enhancement (MORE) — an innovative, evidence-based, neuroscience-informed therapy for opioid misuse and chronic pain — provides $12 in cost savings for every dollar spent, between two and six times more cost effective than other addiction treatments such as residential or intensive outpatient treatment. Over the course of a patient’s life, the analysis found that these savings came out to more than $324,000 per patient.

    Each dollar spent on a mindfulness-based opioid misuse treatment could yield $12 in economic benefit

    The results suggest that, if widely implemented, MORE could provide a potent, cost-effective solution for the opioid crisis, which currently costs the U.S. as much as $4 trillion per year in health care, criminal justice and lost productivity costs. The findings are published online in the journal Value in Health.

    “Opioid misuse is a major driver of overdose deaths, hospitalizations, homelessness and economic loss, so substantially reducing opioid misuse could have huge positive consequences for society,” said lead author Eric Garland, PhD, professor of psychiatry at UC San Diego School of Medicine and endowed professor at the Sanford Institute for Empathy and Compassion. “Our study suggests that MORE could be part of a scalable solution that improves outcomes for patients while also reducing burdens on the health care system and society at large.”

    MORE, developed by Garland, combines a unique sequence of mind-body techniques designed to address addiction, emotional distress and chronic pain at the same time. The intervention teaches mindfulness skills to regulate craving and pain, cognitive reappraisal skills to manage stress and negative emotions, and savoring techniques to help patients reconnect with naturally rewarding experiences.

    “Opioid addiction decreases the brain’s ability to experience natural healthy pleasure, driving increased cravings for the drug,” said Garland. “Our research shows that MORE helps restore this capacity in the brain, reducing cravings and preventing opioid misuse.”

    Previous publications from the MORE research team, based on a randomized clinical trial of 250 adults with chronic pain who were misusing prescribed opioids, found that the treatment reduced opioid misuse by 45% (tripling the effect of standard therapy), led to improvements in pain symptoms and opioid dosing, and strengthened the brain’s responses to positive experiences to reduce cravings. The new study, based on the trial data, sought to put this clinical success into an economic context, asking whether the treatment is cost-effective in addition to being clinically effective.

    The economic analysis found:

    • MORE had a benefit-to-cost ratio of 12-to-1, meaning the intervention was estimated to generate $12 in economic benefit for every $1 spent.
    • This is significantly greater than prior estimates for several other addiction treatment approaches, including comprehensive case management (1.8 to 1), residential treatment (between 2.0 to 1 and 4.8-to-1) and intensive outpatient treatment (5.1-to-1).
    • The lifetime cost savings per patient were $324,489.

    The researchers say the economic benefits of MORE likely stem from reductions across several major categories of harm associated with opioid misuse, including healthcare utilization, criminal justice involvement, lost productivity and overdose mortality.

    “At a relatively low cost, MORE has strong potential to reduce opioid misuse and generate substantial economic benefits for patients, health systems and society,” said Fernando Wilson, PhD, co-author on the study, professor of economics and population health sciences at the University of Utah, and director and endowed chair of the Matheson Center for Health Care Studies. “The cost of implementing MORE is small, and its potential payoff in averting misuse and risk of opioid use disorder is very large.”

    The new study builds on a broader body of evidence supporting the therapy. MORE has now been tested successfully in more than 16 randomized clinical trials involving over 2,500 participants, and has been taught to more than 1,200 clinicians in the United States and internationally. However, the researchers suggest that MORE could have an even larger impact if embedded more widely into health systems, which will require support and investment from healthcare organizations, insurers and policymakers.

    “My hope is that MORE can become a central part of the standard of care,” said Garland, “not only in addiction treatment settings, but also upstream in primary care, where we have a chance to intervene before opioid misuse progresses to more severe addiction.”

    Read the full paper: Economic Evaluation of Mindfulness-Oriented Recovery Enhancement for the Treatment of Opioid Misuse

    Watch the video: Promising Tool Against Opioid Use Disorder

    The study was funded, in part, by grants from the National Institutes of Health (R01DA058621, R01DA056537 and R01DA057631).

    Dr. Garland is Founder of the MORE Science Institute. The authors declare no other competing interests.

  • Different inflammatory processes tied to the same Alzheimer’s disease-related brain shrinkage and memory loss

    Different inflammatory processes tied to the same Alzheimer’s disease-related brain shrinkage and memory loss

    Alzheimer’s disease may look similar from one person to another even when different biological processes are driving the damage, according to a new study led by researchers at the University of California, Irvine.

    The researchers identified two distinct patterns involving inflammation in the brain. One was associated with damage to the brain’s small blood vessels, a marker known as white matter hyperintensities. The other was associated with the buildup of amyloid beta, considered a hallmark protein of Alzheimer’s disease.

    Although the two patterns differed by their connection to inflammatory markers, both were connected to higher levels of a blood marker associated with abnormal tau. They were also connected to shrinkage in brain regions that support memory and, ultimately, to poorer memory performance.

    The findings were published in Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring. They support the idea that Alzheimer’s is not driven by exactly the same process in every person. Different combinations of inflammation, blood vessel damage, amyloid buildup and other biological problems may produce similar patterns of brain damage and memory loss.

    The findings have potentially profound clinical impacts. They may lead to the design of more targeted therapies and provide one explanation for the failure of clinical trials in Alzheimer’s disease thus far.

    “We keep talking about Alzheimer’s as though it is one disease with one cause, but the biology is much messier than that,” said senior author Michael A. Yassa, PhD, professor and James L. McGaugh Endowed Chair in Neurobiology and Behavior and director of UC Irvine’s Center for the Neurobiology of Learning & Memory. “Different biological problems may push the brain toward the same damaged state. For treatment, the key may be figuring out which processes are doing the most harm in each person and how they interact.”

    Different markers point to different kinds of damage

    The researchers studied 126 adults aged 60 and older who did not have mild cognitive impairment or dementia. The participants were enrolled in Yassa’s NIH-funded Biomarker Exploration in Aging, Cognition, and Neurodegeneration, or BEACoN, study.

    The research team combined blood tests, magnetic resonance imaging, amyloid PET brain scans and memory assessments. The scientists then used a statistical model to understand the pathways that connected these markers to downstream memory loss.

    They focused on two proteins found in blood, YKL-40 and glial fibrillary acidic protein, or GFAP. Both are associated with the activity of support cells in the brain that respond to injury and disease, but the study found that the two markers were linked to different biological patterns. Higher YKL-40 levels were associated with more white matter hyperintensities. These appear as bright spots on MRI scans and often reflect damage caused by disease in the brain’s small blood vessels. Higher GFAP levels, by contrast, were associated with greater amyloid buildup measured with PET imaging.

    “The two markers were signaling different processes or pathways that ultimately connect to the visible signs of Alzheimer’s,” said first author Batool Rizvi, PhD, who conducted the work while a graduate student with Yassa and is now a postdoctoral fellow at UC Davis. “Our results suggest that inflammation in Alzheimer’s is not one single process and that different inflammation mechanisms may act in parallel and converge on the same downstream outcome of cell loss.”

    Different routes, similar outcomes

    Both the small blood vessel damage and amyloid buildup were independently associated with higher levels of phosphorylated tau 217, or p-tau217. This blood marker is commonly used to detect abnormal changes involving tau, another protein central to Alzheimer’s disease.

    Higher p-tau217 levels were associated with thinning of tissue in the medial temporal lobe and with a smaller hippocampus. These brain regions play major roles in learning and memory. Participants with smaller hippocampal volume also performed worse on a memory test that measured how well they retained previously learned information after being presented with new material.

    The results suggest that inflammation connected to blood vessel damage and inflammation connected to amyloid may represent separate biological routes that become associated with a common pattern of tau-related changes and damage in memory systems.

    “This may help explain why a treatment aimed at one target works for some people but has little effect on others,” Yassa said. “A person whose disease is driven largely by vascular injury may need a different treatment from someone whose dominant problem is amyloid-related inflammation. Many people will probably have a mixture of both, along with other processes that we did not measure here.”

    The researchers said that future blood tests could combine several markers to provide a clearer picture of the processes affecting an individual patient. That information could help researchers design better clinical trials and eventually match patients with treatments aimed at the biological drivers most important in their disease.

    “Amyloid and vascular injury should not necessarily be treated as competing explanations,” Rizvi said. “They may be different parts of the disease in different people, or they may occur together. Following these markers over time could help us understand which process becomes active first and which one is most closely tied to cognitive decline.”

    Alzheimer’s may be many biological problems with a common endpoint

    The study reflects a broader view of Alzheimer’s that Yassa described in a 2025 essay in The Transmitter, titled “Everything, everywhere, all at once: Inside the chaos of Alzheimer’s disease.”

    In the essay, Yassa argued that Alzheimer’s may appear to be one disease because several biological problems can eventually produce similar symptoms. Amyloid may be an important driver in some people, while inflammation, blood vessel injury, problems with glucose use or excessive brain activity may play larger roles in others. These processes can also interact with one another. Over time, they may push the brain into a damaged and unstable condition that persists even after the original trigger is reduced.

    The current study provides evidence for one part of that framework by showing that two distinguishable patterns involving inflammation were associated with a common set of downstream brain changes.

    “Alzheimer’s may be less like a single chain of events and more like several roads leading to the same place,” Yassa said. “That makes the disease harder to understand, but it also opens more opportunities for treatment. We need to identify the main biological drivers in each person instead of assuming that everyone should receive the same therapy.”

    Study limitations and next steps

    The researchers cautioned that the study provides a snapshot in time. It cannot determine which changes occurred first or prove that one biological factor caused another. The participants were cognitively unimpaired, and some blood measurements were available in only a subset of the study group. The sample was also predominantly White, which limits how broadly the results can be applied. Larger studies will need to follow more diverse groups of people over time. Future research should examine whether these patterns predict memory decline, whether they change as Alzheimer’s progresses and whether they can be used to select and inform treatments.

    The study was supported by the National Institute on Aging grant R01AG053555.

    About the Center for the Neurobiology of Learning & Memory: Established in 1983 by the UC Regents, with James L. McGaugh as its Founding Director, the CNLM is the first research institute in the world dedicated to the interdisciplinary study of the fundamental brain mechanisms of learning and memory. It is credited with numerous seminal discoveries about how memory works and is recognized as a global leader in the area. Led by Director Michael Yassa, the CNLM is home to more than 120 faculty scientists at UC Irvine and beyond. For more information, visit cnlm.uci.edu.

    About the University of California, Irvine: Founded in 1965, UC Irvine is a member of the prestigious Association of American Universities and is ranked among the nation’s top 10 public universities by U.S. News & World Report. The campus has produced five Nobel laureates and is known for its academic achievement, premier research, innovation and anteater mascot. Led by Chancellor Howard Gillman, UC Irvine has more than 36,000 students and offers 224 degree programs. It’s located in one of the world’s safest and most economically vibrant communities and is Orange County’s second-largest employer, contributing $7 billion annually to the local economy and $8 billion statewide. For more on UC Irvine, visit www.uci.edu.

  • Reducing protein intake could promote healthy aging

    Reducing protein intake could promote healthy aging

    Protein-fortified foods are popping up everywhere, from cereal and coffee to even protein water. But a new review covering over 350 papers on protein restriction and aging—publishing July 31 in the Cell Press journal Cell Press Blue—suggests that consuming less protein could have greater health benefits and could, in some cases, extend lifespan. The authors describe how protein restriction slows aging by improving metabolism, changing how cells respond to nutrients, reducing cellular damage, and preserving healthy cell function.

    “It’s absolutely crystal clear that there are benefits of protein to muscle growth and exercise response of active individuals,” says Dudley Lamming, the paper’s corresponding author, of the University of Wisconsin-Madison. “But because most people are relatively sedentary, many people are likely consuming more protein than they actually need, which probably has negative health consequences.”

    For decades, scientists have known that eating less calories can extend lifespan in many organisms and reduce the risk of age-related diseases like cancer. But maintaining a calorie-restricted diet is difficult for most people.

    Previous studies have found that eating less protein can extend the lifespan of flies and rodents without reducing their calorie consumption. Several recent clinical trials in humans have also shown that reducing protein intake can reduce weight and fat mass and improve fasting blood sugar in humans, even though protein-restricted individuals tend to eat more calories.

    But at the same time, some studies have found that eating more protein could promote weight loss and reduce age-related muscle loss in older adults when paired with exercise. Those findings prompted US authorities to update its dietary guidelines this year, recommending an increase in daily protein intake to 1.2–1.6 grams per kilogram of body weight (0.5–0.7 grams per pound), nearly doubling the previous recommendations.

    With Americans consuming more protein than ever and older adults encouraged to boost their intake, Lamming and his colleague set off to review decades of research on protein restriction and aging. Drawing on more than 350 papers, the team outlined potential mechanisms that consistently emerge across studies and may explain how protein-restricted diets could improve health and promote longevity. These mechanisms suggest that protein restriction slows aging by improving metabolism, changing how cells respond to nutrients, reducing cellular damage, and preserving healthy cell function.

    One of the key players is a hormone called fibroblast growth factor 21 (FGF21), which rises when protein intake is low. FGF21 can increase the body’s energy expenditure, improve blood sugar control, and reduce inflammation. Studies in mice have shown that animals with higher FGF21 levels lived longer than normal mice, and the benefit was more pronounced in male mice than female mice. Eating less protein raises FGF21 levels in humans as well.

    The review also highlights several amino acids, the building blocks of protein, that appear to drive many of these effects, including methionine, isoleucine, and valine. Studies show that consuming too much of these amino acids could trigger biological processes that promote growth, increasing the risk of obesity, inflammation, and other age-related diseases.

    “These studies show that the amount of protein sedentary people are eating today may have negative health consequences, at least at the population level,” Lamming says.

    He adds that while some people, like pregnant women and some older adults, have higher protein needs, for most sedentary adults, protein-fortified food may not provide the health benefits people expect.

    Lamming notes that athletes often consume large amounts of protein without developing metabolic diseases. He suspects that regular exercise, perhaps by using protein to build strong healthy muscles, helps protect them from the negative health effects associated with a protein-rich diet.

    “Recent recommendations have encouraged people to eat more protein, but they’ve also encouraged people to exercise more,” Lamming says. “We probably need to personalize protein recommendations based not just on age, but also on how physically active people are.”

    ###

    This work was supported by the National Institute on Aging, the Wisconsin Partnership Program, and the University of Wisconsin–Madison.

    Cell Press Blue, Knopf et al., “The hallmarks of protein and amino acid restriction in aging and longevity” https://www.cell.com/cell-press-blue/fulltext/S3051-3839(26)00077-0

  • For veterans with severe PTSD, psilocybin-assisted therapy may help

    For veterans with severe PTSD, psilocybin-assisted therapy may help

    The first U.S. clinical trial of psilocybin-assisted therapy in veterans with PTSD who got no relief from conventional treatments has established that the protocol is safe, causing no serious adverse events or increases in suicidal thinking or behavior.

    But the preliminary clinical results exceeded researchers’ expectations: In the pilot trial with 12 veterans, 75% of participants were in remission one month after the study’s end. Their symptoms no longer met the criteria for post-traumatic stress disorder.

    “For a population with severe treatment-resistant PTSD, these results are striking,” said Stacey Armstrong, first author of the new study, published today (July 30, 2026) in Communications Medicine.

    “While treatments do work for some veterans with PTSD, they’re falling short for many, leaving veterans to continue to search for solutions, which can lead to treatment dropout, long-term disability and elevated suicide risk,” said Armstrong, senior researcher and associate director of the Center for Psychedelic Drug Research and Education (CPDRE) in The Ohio State University College of Social Work.

    “It’s this unmet need that inspires us.”

    The 11-week trial period combined eight hours of psychotherapy followed by two doses, 15 milligrams and 25 milligrams, of synthetic psilocybin, the active ingredient in magic mushrooms. Six to eight more hours of integrative therapy followed the drug treatment.

    From baseline to one month after treatment was finished, there was an overall average drop of 27.5 points in clinician-rated PTSD symptoms among the group. Nine participants had a clinical response to treatment and were in remission. No severe adverse events occurred, with the most common side effect being a mild headache after taking psilocybin. Suicidal ideation scores did not significantly change from baseline to one month post-treatment.

    Future papers from this study will assess the treatment’s effectiveness up to six months after the trial, as well as biological changes and effects on other PTSD-related problems like sleep disorders and substance use, said Alan Davis, senior author of the study, director of the CPDRE and associate professor of social work at Ohio State.

    Anecdotal observations, and previous research showing that depression remission endured for five years after an earlier psilocybin trial that Davis co-led, suggest the combined therapies could have staying power for many people whose symptoms are not eased by traditional therapies.

    “It’s been an incredible honor to work with veterans in this study, many of whom have been suffering with PTSD for decades or longer,” said Davis, who also holds faculty appointments in psychology and internal medicine at Ohio State.

    “Some experiences we’ve seen in actual treatment sessions are extremely profound and meaningful. The ability for them to go back and to revisit really difficult events that happened to them and to find a new way of understanding them and a new way of moving forward in their life has really been exciting.”

    One participant’s experience
    To be eligible for the trial, veterans had to have severe PTSD that was considered treatment-resistant. The need for help in this population became quite evident as participant recruitment began: Over 3,600 applicants reached out to partake in online prescreening and 668 were assessed for eligibility. Though the initial goal was 15 participants, the final number was 12 – nine men and three women.

    Zachariah Collett, a U.S. Army veteran from Washington Court House, Ohio, considers himself one of the lucky ones who was selected to participate.

    Collett joined the Army in 2002 as an enlisted soldier and later became a military police corps paratrooper, serving a 28-month combat tour in Iraq. By age 25 he was medically retired. Among the diagnoses and service-connected disabilities that led to retirement was post-traumatic stress disorder.

    His symptoms included nightmares, a short temper, feeling constantly on guard and being angry virtually all the time – leading to behavior that had a negative effect on his family.

    “I was just absolutely tortured by the internal struggle, the internal dialogue, the noise inside my head and the inability even to just be still,” Collett said. Years of trying counseling and medications didn’t help.

    It was an intensive 41-day self-discovery experience combining a healthful diet with a series of integrative therapies that first put Collett on the path to healing. When he later learned about the psilocybin trial, he saw it as the perfect opportunity – and medicine – to take a “deeper dive.”

    Now three years out from the treatment, he said the psilocybin-assisted therapy had a profound effect on him, his family and his marriage.

    “For the first six months to a year, I felt like I had this fantastic set of training wheels while I’m relearning the way to act in situations,” he said. “That’s the great thing about this medicine. It’s gentle and it allowed me the space to rediscover, or discover, things I didn’t know I was capable of doing.

    “It allowed me the opportunity to create peace, and stillness, and acceptance, and forgiveness and grace – all those things opposite of resentment and anger and hatred. It’s rather beautiful.”

    Where the magic happens
    A rigorous psychotherapy schedule is a key part of the process, with evidence from the trial suggesting that PTSD symptoms were lowered even before the drug was administered.

    “There is this big question in the psychedelic therapy field right now about how much of this is a drug effect, how much of this is a therapy effect, and how much is a combination of the two,” Davis said.

    This study, the first to try to answer the question, found a drop in PTSD symptoms from baseline to the end of preparation therapy, with a much larger reduction after the psilocybin doses.

    “This treatment is more than just a drug,” Davis said. “The drug itself is a catalyst for the deep work that opens a window for people to perhaps access things they wouldn’t be able to access emotionally otherwise, and what that does is catalyze the therapeutic process after.

    “That’s where the magic actually happens. It happens in the therapy, and in the changes that people start to make in their lives after the treatment’s concluded.”

    The research team acknowledges that pilot studies with no control group tend to produce larger effect sizes than standard clinical trials. They hope to secure funding to follow up with a larger randomized, controlled clinical trial.

    “Recognizing the tools that we have don’t work so well and recognizing the significant burden of PTSD in the United States carried by our servicemen and women and veterans, this seemed like the right direction to go,” Armstrong said. “Too many veterans right now are suffering despite the treatments that we have, and that’s why we feel that this research is important.”

    Davis, who has been studying psychedelics as a component of mental health treatment for the past 16 years, said, “This is a very exciting time for psychedelic-assisted therapy research. These treatments are generally safe, well tolerated and showing a strong signal of efficacy.”

    This research was supported by Ohio State’s College of Social Work, The Center for Psychedelic Drug Research and Education, the Clinical Research Center/Center for Clinical Research Management of The Ohio State University Wexner Medical Center and Ohio State’s College of Medicine.

    Additional co-authors were Adam Levin, Nathan Sepeda, Hillary Shaub, Taweh Hunter, Angela Douglas and Rafaelle Lancelotta, all of Ohio State.

  • For mind and body: Community gathering places may counteract cognitive disability

    For mind and body: Community gathering places may counteract cognitive disability

    Community gathering places, where residents lead group activities, have been promoted across Japan as part of long-term care prevention efforts to extend healthy life expectancy. These often involve exercise and social interaction and are meant to help prevent cognitive decline. However, previous studies have reported inconsistent findings regarding their association with cognitive disability.

    Therefore, a research group, led by Associate Professor Kazuki Uemura at Osaka Metropolitan University’s Graduate School of Rehabilitation Science, investigated whether exercise habits influence the relationship between participation in community gathering places and cognitive disability. The researchers analyzed data from self-administered questionnaires and long-term care insurance records from 3,511 older adults in Habikino City, Osaka Prefecture, who had not been certified as requiring long-term care. After excluding invalid answers, 2,578 were included in the primary analysis. Participants and non-participants in city-supported weekly exercise groups were tracked for four years, and the risk of cognitive disability was examined using survival analysis.

    The study found that among older adults without regular exercise habits, those who participated in community gathering places had approximately half the risk of developing cognitive disability compared with non-participants. In contrast, no significant association was observed among older adults who already exercised regularly.

    “These findings support a growing direction in long-term care prevention policy, which creates opportunities for participation that are accessible to older adults who may find regular exercise difficult,” said Associate Professor Uemura.

    Furthermore, additional analyses focused on physical functional decline revealed similar benefits from community activities. As they are designed to accommodate frail older adults, the physical components provide additional health benefits for those without exercise habits.

    “We hope this evidence will help inform community-based initiatives that support a wide range of older adults and contribute to policies aimed at reducing health inequalities.”

    The findings were published in the Journal of the American Geriatrics Society.

    ###

    About OMU 

    Established in Osaka as one of the largest public universities in Japan, Osaka Metropolitan University is committed to shaping the future of society through the “Convergence of Knowledge” and the promotion of world-class research. For more research news, visit https://www.omu.ac.jp/en/ and follow us on social media: X, Instagram, LinkedIn.

  • New Study Shows Low-Dose Omega-3 Intake Does Not Raise Atrial Fibrillation Risk

    New Study Shows Low-Dose Omega-3 Intake Does Not Raise Atrial Fibrillation Risk

    A new meta-analysis led by researchers from the Fatty Acid Research Institute (FARI) provides the clearest picture to date of the relationship between omega-3 fatty acid supplementation and atrial fibrillation (AF), helping resolve years of confusion generated by earlier reports.

    Published in Circulation: Arrhythmia and Electrophysiology, the study, led by Dr. Nada Abuknesha, PhD, an Associate Scientist at FARI, analyzed data from 35 randomized controlled trials involving 114,592 participants—more than four times the number of studies included in previous meta-analyses. Researchers also incorporated unpublished trial data and previously unavailable safety information to provide the most comprehensive assessment of AF risk to date.

    The Key Finding

    The analysis found that low-dose omega-3 supplementation (less than 1,500 mg/day EPA+DHA) was not associated with an increased risk of AF, even among individuals at elevated cardiovascular risk.

    In contrast, only in the setting of high-dose omega-3 therapy (>1,500 mg/day, typically prescription-strength formulations) used in patients with established cardiovascular disease was AF risk modestly increased (i.e., the absolute risk increase was 0.8%).

    “Our findings show that the relationship between omega-3s and atrial fibrillation is much more nuanced than previous headlines suggested,” said William S. Harris, PhD, President of the Fatty Acid Research Institute (FARI) and senior author on the study. “For the vast majority of people taking nutritional doses of omega-3s, these data should provide reassurance that there is no meaningful increase in atrial fibrillation risk.”

    Addressing a Long-Standing Controversy

    In recent years, several meta-analyses suggested that omega-3 supplements may increase the risk of AF. However, those reports included no more than eight randomized trials, focused primarily on cardiovascular outcome studies, and did not account for many eligible trials where AF data were available but unpublished.

    The new FARI-led analysis expanded the evidence base substantially by:

    • Including 35 randomized controlled trials involving 114,592 participants
    • Incorporating 15 trials containing previously unpublished AF data
    • Including studies reporting zero AF events, reducing publication bias
    • Evaluating risk according to both omega-3 dose and underlying cardiovascular risk, providing a more clinically meaningful interpretation of the evidence.

    Putting the Findings Into Clinical Context

    Researchers emphasize that even among high-risk cardiovascular patients receiving prescription-level omega-3 doses, the observed increase in AF should be weighed against the well-established cardiovascular benefits demonstrated in major clinical trials.

    For example, previous studies of high-dose EPA have shown reductions in heart attacks, stroke, and other major cardiovascular events that substantially outweigh the small increase in atrial fibrillation risk.

    “The decision to take or discontinue omega-3 supplements should be a discussion between a patient and his/her healthcare provider,” said Harris. “What this study does is provide clinicians with better guidance on which patients may benefit from closer monitoring when using high-dose omega-3 therapies while reassuring consumers that it is safe to consume omega-3 fatty acids from foods and dietary supplements.”

    Implications for Consumers and Clinicians

    The findings reinforce an important distinction between:

    • Nutritional omega-3 supplementation (typically 500-1,500 mg/day), commonly used to support general health and cardiovascular wellness.
    • Pharmacological omega-3 therapy (typically 2-4 grams/day), prescribed for individuals with elevated triglycerides or established cardiovascular disease.

    The authors emphasize that AF risk profiles should be evaluated separately for each category, as nutritional doses do not carry the same clinical implications as higher pharmacological doses.

    About the Study

    The study, Effects of Omega-3 Fatty Acid Treatment on Risk for Atrial Fibrillation: An Updated Meta-Analysis of 35 Trials Including 114,592 Individuals, was led by researchers from the Fatty Acid Research Institute in collaboration with investigators from institutions worldwide. The systematic review included published and unpublished randomized clinical trial data and represents the largest analysis to date examining omega-3 supplementation and incident AF.

    Disclaimer: This publication from FARI was commissioned by the Global Organization for EPA and DHA Omega-3s (GOED). GOED did not have any input into the study design, data analysis or interpretation.

    About the Fatty Acid Research Institute (FARI)

    The Fatty Acid Research Institute (FARI) is a non-profit research and education foundation created by William S. Harris, PhD, FASN. Dr. Harris is also the founder of OmegaQuant Analytics. FARI was founded in order to accelerate discovery of the health effects of fatty acids, most notably, the long chain omega-3 fatty acids EPA and DHA. FARI researchers and scientists focus single-mindedly on publishing high-quality research studies on the multiple relationships between fatty acid levels and human (and animal) health outcomes. These studies will help improve the ability to predict risk for disease, and more importantly, suggest ways to reduce risk by changing diets and/or supplementation regimens. www.faresinst.org

    About Dr. Bill Harris:

    Dr. Harris has been a leading researcher in the omega-3 fatty acid field for more than 40 years. He has nearly 400 scientific papers on fatty acids and health, the vast majority on omega-3. He has been on the faculty of three medical schools (Universities of Kansas, Missouri (at Kansas City), and South Dakota) and has received 5 NIH grants to study omega-3. He was the co-author on three AHA statements on fatty acids and heart health. As the co-inventor of the Omega-3 Index (and other omega-3 blood tests) and founder of OmegaQuant Analytics, Dr. Harris has been ranked among the top 2% of scientists worldwide based on the impact of his research. Dr. Harris publications: https://www.ncbi.nlm.nih.gov/myncbi/1fAOCyhA-fcQV/bibliography/public/

  • Your gut may help your brain decide what to remember

    Your gut may help your brain decide what to remember

    The taste of a madeleine famously sent French writer Marcel Proust back into vivid memories of childhood. New research suggests that this kind of recollection may involve more than the brain alone. Signals from the digestive system may also help determine which food-related experiences become memories.

    The study, led by Scott Kanoski, professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences, indicates that the gut may contribute to memory formation, particularly when an experience involves finding and consuming food.

    Published in Nature Communications, the research examined the vagus nerve, one of the body’s main communication routes between the digestive system and the brain. The nerve is already known to influence digestion, appetite, and feelings of fullness. The new findings suggest that it may also carry information that helps the brain store memories.

    How Gut Signals Reach the Memory Center

    In experiments with rats, the researchers found that eating nutrient-rich foods increased the release of acetylcholine in neurons connected to the hippocampus. The hippocampus is a brain region that plays a central role in learning and memory.

    Acetylcholine is a neurotransmitter that helps the brain record new information and form memories. The increase depended on messages traveling from the gut through the vagus nerve.

    When the researchers disrupted communication along the vagus nerve, acetylcholine levels no longer rose after the animals ate. The rats also struggled more on tests that required them to remember where they had recently located food.

    Nutrients Matter More Than Sweetness

    The experiments also showed that the brain’s memory system responded to the nutritional content of food, not simply to how pleasant or sweet it tasted.

    Rats that consumed sugar or fat displayed strong activity in brain pathways involved in memory. By contrast, animals given low-calorie or noncaloric liquids that tasted sweet did not produce the same response.

    The results suggest that the brain distinguishes between flavor and actual nutritional value. A sweet taste alone was not enough to activate the memory-related pathway.

    “We think the mechanism likely evolved to help animals remember vital information about food sources,” says study first author Logan Lauer, a PhD student in Kanoski’s lab. Recalling where certain plants sprout first in the spring can help hungry animals find important nutrients. Signals from the gut tell the brain, “This meal provided valuable nutrients, so remember where and how you got it.”

    Why Food Location Memories Matter

    For animals in the wild, remembering the location of a reliable food source can be essential for survival. A meal that provides useful nutrients may trigger the gut to send a message that encourages the brain to store details about where the food was found and how it was obtained.

    This process could help explain why certain food experiences become especially memorable. The body may be designed to place greater importance on meals that deliver energy or valuable nutrients.

    Unhealthy Diets May Weaken the Pathway

    Although foods rich in sugar and fat produced strong short-term memory responses, frequent exposure to those foods had the opposite effect over time.

    Rats that ate high-fat and high-sugar diets early in life later showed weaker communication between the gut and the hippocampus. Their memory-related brain responses remained reduced even after they returned to a healthier diet.

    These animals also performed worse on tasks that tested their ability to remember where food had been located. The results suggest that prolonged consumption of unhealthy foods may interfere with the same gut-to-brain system that initially helps record food-related memories.

    Possible Links to Cognitive Decline

    The findings may have broader implications for human health. Obesity, poor nutrition, and metabolic conditions such as diabetes have already been linked to a higher risk of cognitive decline.

    This research points to one possible biological explanation. Repeated exposure to unhealthy foods may gradually damage or disrupt communication between the gut and the brain, making it harder for the memory system to function normally.

    The results could also offer clues about neurodegenerative diseases.

    “The disruption of acetylcholine signaling in the hippocampus is one of the earliest neurochemical changes in Alzheimer’s disease,” says Kanoski. “By revealing that this system is boosted by gut signaling from the vagus nerve, novel therapeutic targets could leverage this information to explore vagus nerve-based approaches, such as vagus nerve stimulation.”

    New Possibilities for Memory Treatments

    The discovery raises the possibility that future treatments could focus on strengthening communication between the digestive system and the brain.

    Approaches that stimulate the vagus nerve or improve gut health might eventually be investigated as ways to support memory and preserve cognitive function. Vagus nerve stimulation is already being studied for several neurological and psychiatric conditions, and the new findings suggest that memory could become another area of interest.

    The researchers caution that more work is needed to determine whether the same process occurs in humans. For now, the experiments provide further evidence that the gut and brain work together far more closely than once believed.

    About the Study

    In addition to Kanoski and Lauer, study authors include Anna Hayes, Andrea Suarez, Alexander Bashaw, Molly Klug, Alicia Kao, Robert Cheng, Jessica Rea, Keshav Subramanian, Anna Nourbash, Kristen Donohue, and Lindsey Schier of USC Dornsife; Kevin Myers of Bucknell University; and Léa Décarie-Spain of Université de Montréal.

    This work was supported by National Institute of Diabetes and Digestive and Kidney Diseases grants DK104897, DK123423, F31AG092136; Postdoctoral Ruth L. Kirschstein National Research Service Award from the National Institute on Aging grant F32AG077932; Quebec Research Funds postdoctoral fellowship 315201; and an Alzheimer’s Association Research Fellowship to Promote Diversity.

    Story Source: Materials provided by University of Southern California.

  • Ministry Of Ayush Partners With IndiaAI to Boost AI-Driven Innovation In Traditional Medicine

    Ministry Of Ayush Partners With IndiaAI to Boost AI-Driven Innovation In Traditional Medicine

    The Ministry of Ayush has signed a memorandum of understanding with IndiaAI, the Ministry of Electronics and Information Technology, to accelerate AI‑driven innovation in the Ayush sector, strengthen research, digital health and capacity building, an official statement has reported.

    Ministry of Ayush connects with AIKosh platform

    Further, the Ministry of Ayush will onboard the AIKosh platform for sharing eligible health research artefacts, including datasets, metadata, AI models, toolkits and relevant use cases.

    This integration is expected to facilitate greater collaboration, innovation and responsible development of AI solutions for the Ayush sector, the statement said.

    Kavita Jain, Joint Secretary & Chief Vigilance Officer, Ministry of Ayush underscored that the integration of Artificial Intelligence with Ayush will open new avenues for evidence-based research, knowledge management and innovation.

    She added that the collaboration with IndiaAI will help leverage advanced AI capabilities across areas such as research, medicinal plants, drug administration and capacity building, making the Ayush ecosystem more technology-driven and future-ready.

    Sudeep Srivastava, Joint Secretary, Ministry of Electronics and Information Technology (MeitY), highlighted the importance of integrating modern technology with India’s traditional knowledge systems.

    He said that the partnership will enrich AIKosh with traditional healthcare datasets and will empower researchers and practitioners of traditional medicinal sciences through AI-enabled innovation.

    Naman Goyal, OSD, Ayush Grid, noted that under its Emerging Technologies component, Ayush Grid is developing AI-driven platforms to accelerate the digital transformation of the Ayush sector.

    The collaboration marks an important step towards building a technology-enabled Ayush ecosystem by bringing together the strengths of traditional knowledge and modern AI capabilities, the statement noted.

    The partnership will focus on accelerating the adoption and application of AI across key Ayush domains, including research, capacity building, medicinal plants and drug administration.

    The MoU will help access to GPU-based and high-performance computing infrastructure through the IndiaAI initiative at subsidised rates, subject to defined service-level agreements.

    Access to advanced computing infrastructure is expected to help address critical infrastructure requirements and support the scaling of sophisticated AI research and applications in healthcare and traditional medicine.