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  • Scientists find how “zombie” cells fuel inflammation as we age

    Scientists find how “zombie” cells fuel inflammation as we age

    Inflammation is one of the immune system’s most important defenses. When the body detects an infection or injury, it sends out alarm signals that recruit immune cells and other cells to eliminate the threat and begin repairing damaged tissue.

    This response is essential, but it is supposed to shut down once the danger has passed. As people age, however, certain cells accumulate that can keep inflammation active for much longer than necessary. This persistent inflammation has been associated with numerous diseases that become more common later in life.

    Researchers at Sanford Burnham Prebys Medical Discovery Institute, Mayo Clinic, and collaborating institutions have now uncovered a previously unknown connection between mitochondria, cell metabolism, and this chronic inflammation. Their findings, published in Nature, also showed that interfering with part of the process reduced inflammation and supported healthier aging in mice.

    How “Zombie” Cells Accumulate With Age

    Many cells in the body are capable of dividing, allowing us to grow and helping tissues repair themselves after injury. But as we get older, increasing numbers of cells enter a state known as senescence. These zombie-like senescent cells stop dividing, yet they remain alive and active.

    “Senescent cells are not completely inert,” said co-corresponding author Peter Adams, PhD, the Jeanne and Gary Herberger Leadership Chair in Cancer Research at Sanford Burnham Prebys. Adams also is director of and professor in the Cancer Genome and Epigenetics Program.

    “They remain metabolically active and have an inflammatory program causing them to secrete inflammatory molecules.”

    When senescent cells activate this inflammatory program, they are described as having the senescence-associated secretory phenotype (SASP). SASP has been linked to widespread inflammation associated with aging as well as a range of chronic diseases.

    The research team, led by the laboratory of senior and co-corresponding author João Passos, PhD, a professor of Physiology at Mayo Clinic, set out to identify the molecular processes that drive SASP. Their broader goal was to determine whether those processes might be interrupted or reduced.

    “It turns out that there is a convergence of at least two biological pathways related to mitochondria,” said Adams. “One alters how DNA is stored to promote areas related to SASP, and the other boosts the expression of the exposed SASP genes.”

    Mitochondria Help Unlock Inflammatory Genes

    Although senescent cells no longer divide, they continue using energy and carrying out metabolic activity. The researchers found that their mitochondria, the structures responsible for much of a cell’s energy production, behave differently from those in healthier cells.

    In particular, mitochondria in senescent cells produced increased amounts of acetyl-CoA, an important molecule involved in metabolism.

    Acetyl-CoA also interacts with histones, spool-like proteins around which DNA is wrapped. By altering these histones, acetyl-CoA can loosen the way DNA is packaged. This does not change the genetic code itself. Instead, it makes certain genes more accessible, including genes involved in the inflammatory SASP response.

    That metabolic change alone, however, was not enough to explain why senescent cells continuously release inflammatory molecules.

    Two Mitochondrial Signals Work Together

    A second process was also required.

    Damaged mitochondria can leak DNA and RNA into parts of the cell where those molecules normally should not be present. The immune system interprets this misplaced genetic material as a danger signal, triggering an inflammatory response.

    These immune signals activate transcription factors that help switch genes on. Those factors are then able to target the SASP genes that have already been made more accessible by elevated acetyl-CoA.

    In other words, the researchers found that two separate mitochondrial processes converge. One exposes inflammatory genes, while the other provides the immune signal needed to activate them.

    “After seeing how these two independent pathways intersect, we wanted to see if interrupting one could prevent their partnership in promoting SASP,” said Adams.

    Blocking the Metabolic Signal Reduced Inflammation

    To test that possibility, the researchers used a drug called CTPI-2. The drug blocks a transport protein responsible for carrying a component needed to produce acetyl-CoA.

    When CTPI-2 was tested in mice, it reduced inflammation throughout multiple tissues. The treatment also improved tissue function and healthspan during aging.

    Importantly, the immune signals caused by leaking mitochondrial DNA and RNA were still present. But by weakening the metabolic signal involving acetyl-CoA, the researchers made SASP genes more difficult to access and reduced their inflammatory effects.

    “Even though the immune signaling from leaky mitochondria was still present, disrupting the metabolic signal made SASP genes less accessible and produced functional benefits,” said Adams. “Using selective inhibitors such as CTPI-2 to reduce acetyl-CoA and, in turn, inflammation is a novel therapeutic strategy that should be explored.

    “Also, more broadly, this research shows that targeting metabolic signals that influence DNA accessibility may represent a new approach for mitigating age-associated inflammation and functional decline.”

    The findings suggest that changing the metabolic signals controlling access to inflammatory genes could offer a new strategy for addressing chronic inflammation and declining tissue function during aging.

    Hélène Martini, PharmD, PhD, a postdoctoral researcher in the Passos lab at Mayo Clinic, is first author of the publication.

    Additional authors include:

    • Aaron Havas, Rabi Murad, Xue Lei and Rebecca A. Porritt at Sanford Burnham Prebys
    • Anthony B. Lagnado, Nicholas Pirius, Ana Catarina Franco, Gung Lee, Yeaeun Han, Jennifer L. Rowsey, Stella Victorelli, Wazim Mohammed Ismail, Amelia Mazzone, Tianna M. Espe, Taro Hitosugi, Ya Li, Alexander M. Washington, Jair Machado Espindola-Netto, Dominik Saul, Sundeep Khosla, Diana Jurk, Enis Kostallari and Alexandre Gaspar-Maia at Mayo Clinic
    • Jodie Birch at Imperial College London
    • Francisco D. M. Marques at Albert Einstein College of Medicine
    • Oliver D. K. Maddocks at the University of Glasgow

    The study was supported by the National Institutes of Health, National Institute on Aging, National Cancer Institute, National Institute of Diabetes and Digestive and Kidney Diseases, Department of Defense Ovarian Cancer Research Program, Hevolution Foundation, The Glenn Foundation for Medical Research, Cancer Research UK, and Robert and Arlene Kogod Center on Aging.

  • AI uncovers hidden Ozempic side effects across 400,000 Reddit posts

    AI uncovers hidden Ozempic side effects across 400,000 Reddit posts

    Artificial intelligence is giving researchers a new way to listen to what patients are saying about popular GLP-1 drugs. After analyzing more than 400,000 Reddit posts, a University of Pennsylvania team identified several symptoms reported by people using semaglutide (Ozempic, Wegovy, and Rybelsus) and tirzepatide (Mounjaro and Zepbound) that may not be fully represented in clinical trials or official regulatory information.

    The study, published recently in Nature Health, examined more than five years of posts from nearly 70,000 Reddit users. Two categories stood out as particularly deserving of further investigation: reproductive symptoms, including changes in menstrual cycles, and problems involving body temperature, such as chills and hot flashes.

    The findings do not establish that the medications caused these symptoms. Instead, researchers say the massive collection of spontaneous patient reports may reveal signals worth examining more closely.

    “Some of the side effects we found, like nausea, are well known, and that shows that the method is picking up a real signal,” says Sharath Chandra Guntuku, Research Associate Professor in Computer and Information Science (CIS) at Penn Engineering and the study’s senior author. “The underreported symptoms are leads that came from patients themselves, unprompted, and clinicians could potentially pay attention to them.”

    What Patients Report Outside Clinical Trials

    Clinical trials are designed to determine whether treatments work and to identify important safety problems, but they cannot necessarily capture every symptom that matters to patients once a medication is being used by a much larger population.

    “Clinical trials generally identify the most dangerous side effects of drugs,” adds Lyle Ungar, Professor in CIS and a co-author on the study. “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.”

    The distinction is important. The study found associations in what people discussed online, not proof that GLP-1 drugs were responsible for those experiences.

    “We can’t say that GLP-1s are actually causing these symptoms,” notes Neil Sehgal, the study’s first author and a doctoral student in CIS advised by Guntuku and Ungar. “But nearly 4% of the Reddit users in our sample reported menstrual irregularities, which would be even higher in a female-only sample. We think that’s a signal worth investigating.”

    Using Social Media as an Early Health Signal

    The idea of mining online conversations for clues about drug safety predates today’s AI boom. In 2011, Ungar participated in one of the earliest efforts to use material created by internet users to identify possible adverse effects from medications.

    Social media can capture experiences that patients discuss with one another but may never formally report to a doctor, drug manufacturer, or regulator.

    “Online patient communities work a lot like a neighborhood grapevine,” says Ungar. “People who are living with these medications are swapping notes with each other in real time, sharing experiences that rarely make it into a doctor’s office visit or an official report.”

    Since then, online patient communities have expanded enormously. That has made social media a potentially valuable source for studying how medications affect people in everyday life, although gaining access to platform data has become more difficult.

    Traditional clinical research remains essential, the researchers emphasize, but online conversations can provide information far more quickly when millions of people begin using a drug.

    “Clinical trials are the gold standard, but by design, they are slow,” says Guntuku. “This is not a replacement for trials, but it can move much faster, and that speed matters when a drug goes from niche to mainstream almost overnight.”

    AI Makes Massive Social Media Analysis Possible

    One of the biggest obstacles has always been scale.

    Guntuku describes the approach as “computational social listening,” which uses computational methods to identify patterns in large collections of online conversations about health.

    Patients, however, rarely describe symptoms using standardized medical terminology. One person might describe feeling unusually cold, another might mention constant chills, while a clinician could categorize those experiences using a specific medical term.

    Researchers therefore need a way to translate everyday language into standardized categories. One important reference is the Medical Dictionary for Regulatory Activities (MedDRA), which provides terminology widely used to classify medical conditions, symptoms, and adverse events.

    Previously, connecting huge numbers of informal social media posts with standardized medical terminology required enormous amounts of work, limiting how much data researchers could realistically analyze.

    Large language models such as GPT and Gemini are changing that equation by allowing researchers to process and categorize vast amounts of text more consistently and quickly.

    “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,” says Sehgal.

    Unexpected Symptoms Emerge From 400,000 Posts

    The researchers stress that Reddit users do not represent the overall population of people taking GLP-1 drugs. Reddit users tend to be younger, are more likely to be male, and are disproportionately located in the United States.

    Even with that limitation, the analysis produced a reassuring sign that the approach was detecting genuine patterns. Many of the symptoms discussed by Reddit users closely matched already known effects of semaglutide and tirzepatide.

    About 44% of users included in the study described at least one side effect. Gastrointestinal problems were the most common, consistent with the nausea and other digestive issues already associated with these medications.

    More intriguing were symptoms that appeared frequently enough to attract the researchers’ attention but may not be as well represented in current drug labels or conventional adverse event reports.

    Nearly 4% of users who reported side effects described reproductive symptoms. These included changes in menstruation such as bleeding between periods, heavy bleeding, and irregular menstrual cycles.

    Users also described changes involving body temperature, including chills, feeling unusually cold, hot flashes, and symptoms resembling a fever.

    Fatigue was another notable finding. It was the second most frequently reported complaint in the Reddit data, even though relatively few clinical trials reported fatigue often enough for it to reach established reporting thresholds.

    Why Menstrual and Temperature Changes Are Interesting

    One possible reason these reports caught researchers’ attention involves the hypothalamus, a small but extremely important region of the brain. Among its many jobs, the hypothalamus helps regulate hunger, hormones, reproduction and body temperature.

    “These drugs are thought to work by engaging part of the brain called the hypothalamus, which helps regulate a wide variety of hormones,” says Jena Shaw Tronieri, Senior Research Investigator at Penn’s Center for Weight and Eating Disorders and a co-author of the study. “That doesn’t mean the medications are necessarily causing these symptoms, but it could suggest that reports of menstrual changes and body temperature fluctuations are worth studying more systematically.”

    The researchers are not proposing that this biological connection proves GLP-1 drugs are responsible. Instead, it offers another reason to test the patient-reported patterns more carefully through controlled research.

    Turning Online Conversations Into Research Leads

    For now, the team hopes the results encourage scientists and clinicians to pay closer attention to symptoms that patients repeatedly discuss online.

    “They’re clearly on patients’ minds, and that’s worth paying attention to,” says Sehgal.

    The researchers also want to broaden their analysis beyond Reddit and beyond English-language communities. Doing so could help determine whether the same patterns emerge among different groups of people and on different social media platforms.

    “We don’t really know yet whether what we’re seeing on Reddit reflects the experience of GLP-1 users globally, or whether it’s particular to the kind of person who posts on Reddit in the United States,” Ungar says.

    In the longer term, rapid AI analysis of online patient conversations could potentially become an early detection system for emerging health concerns involving drugs, supplements and wellness products.

    That could be particularly valuable for substances that become popular online faster than conventional research can keep up. Loosely regulated or unregulated products, including injectable peptides, can spread quickly through communities on Reddit, TikTok and other platforms. Discussions among users may therefore provide some of the earliest indications of unexpected effects.

    “The whole point of this kind of approach is that it can move quickly, and that’s exactly when it’s most valuable,” says Guntuku.

    This study was conducted at the University of Pennsylvania School of Engineering and Applied Science. The authors report no outside funding. Tronieri reports receiving an investigator-initiated grant, on behalf of the University of Pennsylvania, from Novo Nordisk and receiving consulting fees from Currax Pharmaceuticals, LLC. The other authors report no conflicts of interest.

  • Ozempic and Wegovy may raise hair loss risk in some men

    Ozempic and Wegovy may raise hair loss risk in some men

    Men who are already genetically predisposed to the most common type of hair loss may face an additional 7 percent risk of losing hair when using drugs such as Ozempic, Wegovy, and Zepbound for type 2 diabetes and obesity, according to a new study.

    Researchers at NYU Langone Health examined the GLP1R gene, which naturally influences levels of glucagon-like peptide-1 (GLP-1) receptor proteins in the body. They used activity involving this gene as an indicator of GLP-1 agonist activity. Greater GLP1R activity is associated with higher levels of GLP-1 receptor proteins.

    The team compared genetic patterns associated with GLP1R activity with genes found in men who have androgenetic alopecia, the inherited form of hair loss that typically affects the top and front of the scalp. Because male hair loss has been studied far more extensively than hair loss in women, the researchers were only able to investigate a possible causal connection in men.

    Hair Loss Has Already Been Reported by GLP-1 Users

    Hair thinning has been reported by both men and women taking GLP-1 drugs. Until now, researchers have generally attributed much of that shedding to rapid weight loss, since these medications lower blood sugar and reduce appetite.

    In many cases, people taking GLP-1 drugs have reported that their hair begins growing again several months after their weight stabilizes. However, scientists have also suspected that genetics might play a role in the hair loss associated with these medications.

    The new findings, published online Sept. 3 in the Journal of Investigative Dermatology, provide evidence supporting that possibility.

    Researchers found that genetic variants associated with naturally higher levels of GLP-1 receptor proteins were more common in men with androgenetic alopecia.

    The team then adjusted its analysis to account for hypertension, a known risk factor for hair loss. High blood pressure is thought to interfere with blood flow to the scalp, potentially damaging the ability of hair follicles to grow normally. Even after accounting for hypertension, the additional 7 percent risk remained.

    Other Hair Loss Risk Factors Did Not Explain the Link

    The researchers also examined whether other conditions might account for the association, including insulin resistance (a cause of type 2 diabetes) and reduced testosterone levels.

    Neither factor explained the result. The increased hair loss risk associated with GLP-1 activity remained at 7 percent.

    Because the study examined genetic activity related both to GLP-1 use and to hair loss, the researchers say the overlapping genetic risk suggests that the two may share an underlying biological connection.

    “Our study provides the first genetic link between GLP-1 use and an increased risk of male- pattern hair loss from androgenetic alopecia, an association long suspected but until now not shown scientifically,” said study senior investigator Lynn Petukhova, PhD, an assistant professor in the Ronald O. Perelman Department of Dermatology and the Department of Population Health at NYU Grossman School of Medicine.

    Genetic Screening Could Eventually Identify Higher Risk

    The findings could eventually help doctors identify people who may be especially vulnerable to hair loss before they begin taking GLP-1 medications.

    “Our findings suggest that, if future experiments prove successful, some men, and possibly women too, could be screened and benchmarked for their risk of hair loss before being prescribed GLP-1 medications,” said Dr. Petukhova. “We could also envision these findings leading to some GLP-1 users being prescribed combination treatments to prevent hair loss, such as minoxidil or some other drug.”

    Dr. Petukhova said more research will be necessary to determine exactly how GLP-1 activity might interfere with hair follicle growth. She also plans to investigate whether the same genetic connection found in men is present in women.

    Large Genetic Databases Provided the Evidence

    For the analysis, the researchers drew on large publicly available genetic databases. These included the eQTLGen database, which contains information from 31,684 mostly White men and women, and the Complex Traits Genetics group database, which includes 205,327 mostly White men.

    Androgenetic alopecia is estimated to affect about half of White American males over age 50. Nearly the same proportion of White American females over age 50 are affected, particularly those who are postmenopausal.

    GLP-1 medications have also become increasingly common. Surveys indicate that an estimated 12 percent of Americans have used GLP-1 drugs solely for weight loss, including one-fifth of women ages 50 to 64. Since the first GLP-1 drug (Ozempic) was approved by the Food and Drug Administration in 2020, prescriptions for the medication have more than tripled.

    Funding support for this study was provided by National Institutes of Health grants R01AR080796 and K01AR075111.

    Besides Dr. Petukhova, NYU Langone researchers involved in the study were co-investigators Jerry Shapiro, MD, and Kristen Lo Sicco, MD. Other study co-investigators were Derek Mass, MBA; Mary Casagrande, MPH; and Poppy Gould, PhD; and co-lead investigator Archie Spindler.

    Drs. Shapiro and Lo Sicco have in the past served as study investigators for hair loss drugs and devices manufactured by Pfizer and Regen Labs. Dr. Lo Sicco is a paid consultant for Pfizer, Lilly, Ro, Priovant, Veradermics, and Aquis. The terms and conditions of all these relationships are being managed in accordance with the policies of NYU Langone.

    Additional study authors are co-lead investigator Ravi Ramesur, MD, PhD, at the University of Pennsylvania and King’s College London, and co-investigator Atlas Khan, PhD, at Columbia University.

  • Scientists discover a hidden switch that shuts down inflammation

    Scientists discover a hidden switch that shuts down inflammation

    Researchers at University College London (UCL) have identified a biological mechanism that helps the body bring inflammation to an end, a finding that could eventually lead to new treatments for chronic inflammatory diseases affecting millions of people.

    Inflammation is one of the immune system’s most important defense responses. It helps the body fight infection and repair damaged tissue. But if that response remains active for too long, it can begin to harm healthy tissue and contribute to conditions including arthritis, heart disease, and diabetes.

    Scientists have long known a great deal about how inflammation begins. What has been less clear is how the body decides that the danger has passed and shifts from fighting a threat to repairing the damage.

    A Natural Brake on the Immune System

    The new study, published in Nature Communications, points to a group of small fat-derived molecules called epoxy-oxylipins as part of that shutdown process.

    According to the researchers, these molecules act like natural brakes on the immune system. They help prevent excessive growth of intermediate monocytes,* a type of white blood cell that can support healing in the short term but may contribute to chronic inflammation if too many accumulate or remain active for too long.

    To study the process directly in people, the researchers gave healthy volunteers a tiny injection of UV-killed E. coli bacteria in the forearm. Because the bacteria were no longer alive, they could not cause an infection, but they still triggered a temporary inflammatory response.

    That reaction produced the familiar signs of inflammation, including pain, redness, heat, and swelling, similar to what can happen after an injury or infection.

    The volunteers were divided into two groups: prophylactic arm and therapeutic arm.

    Researchers then gave participants a drug called GSK2256294 at different stages of the inflammatory response. The drug blocks an enzyme known as soluble epoxide hydrolase (sEH). Under normal conditions, sEH breaks down epoxy-oxylipins, so blocking the enzyme allows more of these protective molecules to remain in the body.

    • Prophylactic arm: Participants received the drug two hours before inflammation began, allowing researchers to test whether increasing epoxy-oxylipins early could prevent harmful immune changes. In this group, there were 24 volunteers — 12 were treated, 12 untreated (placebo).
    • Therapeutic arm: Participants received the drug four hours after inflammation started, better reflecting how a treatment might be used after symptoms have already appeared. In this group, there were 24 volunteers — 12 were treated, 12 untreated (placebo).

    Pain Resolved Faster and Harmful Immune Cells Fell

    Both approaches produced similar results.

    Blocking sEH increased epoxy-oxylipin levels, helped pain resolve more quickly, and sharply reduced the number of intermediate monocytes found in both the blood and tissue. These immune cells have been linked to persistent inflammation and the progression of inflammatory disease.

    The treatment did not, however, significantly change outward signs such as redness or swelling. That suggests the drug may have been altering deeper immune processes even when visible symptoms remained largely unchanged.

    The researchers then investigated how the effect worked at the molecular level.

    They found that one epoxy-oxylipin, 12,13-EpOME, appears to suppress a protein signaling pathway known as p38 MAPK. This pathway helps drive the transformation of monocytes into the intermediate form associated with prolonged inflammatory activity.

    The team confirmed the mechanism in laboratory experiments and in volunteers who received a drug that directly blocks p38.

    First author Dr. Olivia Bracken (UCL Department of Ageing, Rheumatology and Regenerative Medicine) said: “Our findings reveal a natural pathway that limits harmful immune cell expansion and helps calm inflammation more quickly.

    “Targeting this mechanism could lead to safer treatments that restore immune balance without suppressing overall immunity. With chronic inflammation ranked as a major global health threat, this discovery opens a promising avenue for new therapies.”

    A Possible Route to Safer Anti-Inflammatory Treatments

    Many existing treatments for inflammatory and autoimmune diseases work by suppressing parts of the immune system. While that can reduce inflammation, it can also interfere with the body’s ability to defend itself.

    The pathway identified in the new study may offer another strategy: strengthening a natural process the body already uses to bring inflammation under control.

    Corresponding author Professor Derek Gilroy (UCL Division of Medicine) said: “This is the first study to map epoxy-oxylipin activity in humans during inflammation.

    “By boosting these protective fat molecules, we could design safer treatments for diseases driven by chronic inflammation.”

    He added: “This was an entirely human-based study with direct relevance to autoimmune diseases, as we used a drug already suitable for human use — one that could be repurposed to treat flares in chronic inflammatory conditions, an area currently bereft of effective therapies.”

    Why Epoxy-Oxylipins Matter

    Researchers focused on epoxy-oxylipins because earlier animal studies had suggested that these molecules can reduce inflammation and pain.

    Their role in humans, however, had remained much less clear.

    Compared with better-known inflammatory substances such as histamine and cytokines, epoxy-oxylipins belong to a relatively underexplored signaling system. Scientists suspected that this pathway might help the immune system naturally transition from an active inflammatory state toward recovery.

    The new human study provides direct evidence supporting that idea.

    Next Steps

    The findings could pave the way for clinical trials testing sEH inhibitors in chronic inflammatory conditions, including rheumatoid arthritis and cardiovascular disease.

    Dr. Bracken said: “For instance, rheumatoid arthritis is a condition in which the immune system attacks the cells that line your joints. sEH inhibitors could be trialed alongside existing medications to investigate if they can help prevent or slow down joint damage incurred by the condition.”

    Rheumatoid arthritis is an autoimmune disease in which the immune system mistakenly attacks tissue around the joints, causing pain, swelling, stiffness, and potentially long-term damage.

    Dr. Caroline Aylott, Head of Research Delivery at Arthritis UK, said: “The pain of arthritis can affect how we move, think, sleep and feel, along with our ability to spend time with loved ones. Pain is incredibly complex and is affected by many different factors. We also know that everybody’s pain is different.

    “That is why it is important that we invest in research like this, that helps us understand what causes and influences people’s experience of pain.

    “We are excited to see the results of this study, which has found a natural process that could stop inflammation and pain. We hope in the future that this will lead to new pain management options for people with arthritis.”

    * Intermediate monocytes are white blood cells that help fight infection and repair tissue. In short bursts, they help coordinate the immune response and support recovery, but if they persist or grow in excess, they keep the immune system switched on, leading to chronic inflammation.

    The study was funded by Arthritis UK and involved researchers at UCL, King’s College London, University of Oxford, Queen Mary University of London, and National Institute of Environmental Health Sciences, USA.

  • Your next prescription could be treating a side effect from the last one

    Your next prescription could be treating a side effect from the last one

    A large study across Ontario has found that widely used medications, including statins and iron supplements, can sometimes trigger a chain of additional prescriptions in older adults. In these cases, a side effect from one drug may be mistaken for a new medical condition, prompting treatment with another medication.

    The research, published in BMJ, was led by Dr. Paula Rochon, Director of Research at the Weston and O’Born Center for Mature Women’s Health at Sinai Health in Toronto. The findings suggest that certain combinations of prescriptions represent a common but often overlooked source of drug-related harm across the population. They can also create avoidable costs for the healthcare system.

    When a Side Effect Leads to Another Prescription

    This pattern is known as a potentially inappropriate prescribing cascade (PIPC). It occurs when a side effect caused by one medication is interpreted as a separate health problem, leading to another prescription that may not have been necessary.

    One example identified by the researchers involves non-steroidal anti-inflammatory drugs (NSAIDs), which are commonly used for pain. These medications are associated with increases in blood pressure. If that change is treated as a new case of high blood pressure, a patient may receive another medication instead of having the original pain treatment reconsidered.

    Older adults are particularly susceptible because they are more likely to have multiple health conditions and take several medications at the same time. With many drugs involved, it can become difficult for both clinicians and patients to determine whether a new symptom is actually being caused by an existing prescription.

    “These sequences of events are common but often missed in clinical practice,” said Dr. Rochon, who holds the Barry J. Goldlist Chair in Aging and Health at Sinai Health and is also a professor of medicine at the University of Toronto. “Knowing what medications you are taking, when they were started, and for what indication is important in order to identify possible prescribing cascades that may be problematic.”

    Researchers Identify 24 Common Prescribing Cascades

    The project involved an interdisciplinary international group of experts in medication prescribing and geriatric medicine. Collaborators came from the United States, Belgium, Italy, Israel and Ireland. The Sinai Health team included Drs. Vasily Giannakeas, Nathan Stall and Christina Reppas-Rindlisbacher, along with research staff Wei Wu and Joyce Li.

    In earlier work, the researchers drew on the expertise of 12 international panelists specializing in internal medicine, geriatric medicine and clinical pharmacology to develop a list of 65 PIPCs.

    For the new analysis, that list was compared with population-level prescription data from ICES, Ontario’s health data institute, working with Lavina Matai and Zhiyin Li. The team evaluated each possible cascade using three measures: how frequently the first medication was prescribed, how often a second medication followed it, and how strongly the two prescriptions appeared to be connected.

    That process allowed the researchers to identify 24 potentially inappropriate prescribing cascades that were both commonly observed in the population and had the potential to cause harm.

    Seeing the Pattern Behind Every Prescription

    For Dr. Rochon, the results point to an important communication gap that can develop gradually as medications accumulate.

    “Our concern is that so often these conversations between the health care prescriber and the patient are being missed, so people don’t recognize the sequences of events and that they are connected to one another,” she said.

    Addressing the problem means looking beyond a simple list of the medications a patient is currently taking. Physicians also need to consider when each drug was introduced, why it was prescribed, and whether a newer medication was added to address a symptom that might actually have been caused by an earlier treatment.

    Mature Women May Face Greater Risk

    The findings may be especially important for mature women. Over the course of their lives, women tend to experience more chronic conditions than men, receive more drug therapies, and have more adverse drug events.

    Taking multiple medications increases the opportunity for a side effect to be misinterpreted as a separate diagnosis. As a result, another drug may be added instead of tracing the symptom back to the medication that caused it.

    Technology Could Help Catch Drug Cascades

    The researchers say technology could provide one way to reduce these potentially harmful prescribing patterns.

    Automated clinical decision support systems could be designed to recognize a possible prescribing cascade as it develops. Such systems might alert clinicians when a new medication appears to be treating a known side effect of an existing drug, giving them an opportunity to reconsider the treatment plan before adding another prescription.

    This information could be incorporated into several types of automated tools that alert clinicians to potentially inappropriate prescribing cascades at the point of care.

    Pharmacists Could Play a Larger Role

    The researchers also see an opportunity to make greater use of pharmacists as part of the healthcare team.

    More directly involving pharmacists in prescribing decisions alongside physicians could help uncover medication patterns that might otherwise go unnoticed. Their expertise could help identify potentially inappropriate prescribing cascades that warrant further evaluation.

  • Tiny nanolaser could cut computer energy use in half

    Tiny nanolaser could cut computer energy use in half

    The development of a nanolaser could mark an early step toward a future in which microchips communicate entirely with particles of light.

    Researchers at DTU have created a tiny nanolaser that could eventually help make computers, smartphones, and data centers faster while using much less energy. The breakthrough was published in the scientific journalScience Advances.

    In the future, thousands of these lasers could potentially be integrated onto a single microchip. Instead of moving information around a chip with electrical signals, devices could transmit data using photons, the particles that make up light.

    “The nanolaser opens up the possibility of creating a new generation of components that combine high performance with minimal size. This could be in information technology, for example, where ultra-small and energy-efficient lasers can reduce energy consumption in computers, or in the development of sensors for the healthcare sector, where the nanolaser’s extreme light concentration can deliver high-resolution images and ultrasensitive biosensors,” says DTU professor Jesper Mørk.

    Mørk co-authored the study with, among others, Drs. Meng Xiong and Yi Yu from DTU Electro.

    Using Light Inside Computer Chips

    Much of the internet already relies on light to carry information through fiber optic cables. Inside computers, however, data still moves through electronic circuits using electricity. That approach produces heat and can limit how quickly information can be transferred.

    Nanolasers could bring optical communication directly onto microchips. By generating light signals efficiently inside the chip, they could allow information to move with very little energy loss, potentially making future devices faster, cooler, and more energy efficient.

    Mørk estimates that using nanolasers in computers could reduce energy consumption by as much as half.

    The compact DTU nanolaser is an important step toward that goal. Future chips designed around light-based communication would likely require thousands of extremely small, efficient lasers working together to transmit information across the chip.

    Breaking the Size Limit for Lasers

    The new nanolaser was created in DTU’s clean room facility, DTU Nanolab. According to Mørk, the device pushes beyond the conventional limit for how small a laser can be made.

    At its core is a structure known as a nanocavity, which traps and concentrates light within an exceptionally tiny space. Until now, achieving such intense confinement at this scale had been considered extremely difficult.

    When researchers shine a beam of light onto the device, both photons and electrons become concentrated in the same microscopic region. This interaction allows the laser to function at room temperature while requiring unusually little energy.

    The light-trapping structure used in the nanolaser was originally developed by Professor Ole Sigmund’s group at DTU Construct.

    Faster Devices and Lower Energy Use

    The next major challenge is making the nanolaser operate using electrical power. If researchers can achieve that, the technology could have broad applications across computing, communications, and healthcare.

    Computers and smartphones could potentially deliver greater performance while consuming less electricity. Data centers, which require enormous amounts of power, could also see substantial reductions in energy use, potentially leading to significant climate benefits.

    In healthcare technology, the nanolaser’s ability to concentrate light into an extremely small area could support ultra-sensitive sensors and high-resolution imaging systems.

    Researchers estimate that the remaining technical challenges could be solved within the next 5-10 years.

  • Scientists just made quantum computer operations 1,000 times faster

    Scientists just made quantum computer operations 1,000 times faster

    Quantum computers remain highly vulnerable to errors and tiny disturbances from their surroundings. The longer a quantum operation takes to complete, the more time there is for those errors to build up. Researchers at Chalmers University of Technology in Sweden have now developed a method that can perform a broad range of advanced quantum operations more than a thousand times faster. The advance tackles a major obstacle in the field and could help move quantum computing closer to becoming fault-tolerant.

    Quantum computers could eventually transform areas such as drug discovery, energy technology, cryptography, artificial intelligence, and logistics. Before that can happen, however, these machines need to become much more dependable.

    Why Quantum Computers Are So Error-Prone

    A major challenge is that quantum computations can be disrupted by extremely small environmental effects. Electrical noise, cosmic radiation, and overheating can all introduce errors while information is being processed.

    Traditional computers can experience errors too, but decades of development have produced reliable error correction methods that can quickly detect and repair them. Quantum systems are much harder to protect because the information they use is extraordinarily delicate.

    “The fundamental building blocks of quantum computers, known as qubits, are so sensitive that even the smallest disturbance can cause the quantum state to deviate from the target, resulting in the loss of information. If too many errors accumulate before they can be corrected, the computation can fail,” says Lei Du, researcher in Applied Quantum Physics at Chalmers University of Technology in Sweden, and lead author of the theoretical study published in the journal Physical Review Letters.

    A Different Way to Protect Quantum Information

    To make quantum computing more resilient and eventually fault-tolerant, researchers are investigating new ways to shield quantum information from errors. One promising strategy uses so-called bosonic quantum codes*.

    Instead of assigning quantum information to individual qubits, this approach stores it in microwave fields inside superconducting circuits.

    “Rather than storing quantum information in individual qubits, bosonic codes encode information in the microwave fields found within superconducting circuits. This approach has been shown to provide stronger protection against certain types of errors,” explains Tangyou Huang, researcher in Quantum Technology at Chalmers and co-author of the study.

    Quantum Operations More Than 1,000 Times Faster

    Working with bosonic quantum codes is not simple. Creating and controlling the required quantum states has traditionally involved guiding a quantum system through thousands of repeated driving cycles.

    That process can take considerable time, and every additional cycle creates another opportunity for outside disturbances to interfere with the calculation. In quantum computing, speed is therefore closely tied to reliability.

    Chalmers researchers Lei Du and Tangyou Huang have now proposed a different strategy. Rather than constructing the desired quantum states one small piece at a time, their method can perform a wide variety of operations much faster.

    “Our method shows that a diverse range of quantum operations on bosonic states can be completed within a single driving cycle, rather than the several thousand cycles that have been required previously. This makes the operations both faster and more efficient, while reducing the risk that disturbances will corrupt the information before the process is finished. It represents an important step towards fault-tolerant quantum computers,” says Lei Du.

    Quantum Lattice Gates Provide a Shortcut

    The new approach is built around Quantum lattice gates, a recently proposed universal set of quantum gates developed by the same research team.

    These gates act somewhat like shortcuts. Instead of requiring a long sequence of repeated control steps, they can allow the intended quantum operation to be completed in just one driving cycle. That could make the process faster, simpler, and less vulnerable to errors.

    “You can think of it like building a large Lego castle. Instead of assembling it brick by brick and risking mistakes along the way, quantum lattice gates act like pre-built Lego modules that can be connected quickly and efficiently,” says Tangyou Huang.

    Designed for Superconducting Quantum Computers

    The technique is especially well suited to superconducting quantum computers, which are among the most prominent technologies being developed in the international push toward large-scale quantum computing.

    Chalmers University of Technology is also using superconducting technology as it develops a 100-qubit quantum computer.

    “A key advantage of our approach is that it can be implemented using existing superconducting quantum circuit platforms. We are already discussing possible experimental realizations with colleagues at Chalmers, and we hope to see a demonstration of the method in the near future,” says Tangyou Huang.

    The researchers say the work addresses a central problem facing the field: efficiently producing and controlling quantum states that are capable of helping correct errors.

    “Our results address one of the major bottlenecks in the field: how to quickly and reliably create and control the error-correcting quantum states that could play an important role in future quantum computers,” says Lei Du.

    More About Bosonic Codes, Quantum Lattice Gates and Floquet Control

    *Bosonic quantum codes store quantum information in the states of, for example, microwave or optical resonators rather than in individual qubits. They are considered a promising tool for quantum error correction because they can provide built-in protection against certain types of errors.

    Quantum operations are needed to process that stored information. Quantum lattice gates are a recently proposed collection of basic building blocks that can be used to control bosonic quantum states. By combining and designing these gates, researchers can carry out a wide range of more complicated quantum operations.

    One method for implementing these operations is known as Floquet control, which uses periodic control signals to drive a quantum system. Earlier Floquet-based techniques have generally depended on slower processes involving many repeated driving cycles. The approach developed at Chalmers can instead perform quantum lattice gates directly in a single driving cycle, making some operations more than a thousand times faster.

    More About the Research

    The scientific paper “Single-Period Floquet Control of Bosonic Codes with Quantum Lattice Gates” has been published in Physical Review Letters. The authors are Tangyou Huang, Lei Du, and Lingzhen Guo. The researchers are affiliated with Chalmers University of Technology in Sweden and Tianjin University in China.

    The research was funded by the National Natural Science Foundation of China (NSFC), the Wallenberg Centre for Quantum Technology (WACQT), and the Knut and Alice Wallenberg Foundation.

  • One sugary drink a day linked to more than double the risk of stomach cancer

    One sugary drink a day linked to more than double the risk of stomach cancer

    About 65% of U.S. adults report drinking at least one sugar-sweetened beverage each day. New research from the Mass General Brigham Cancer Institute suggests that this common habit may be associated with a higher risk of gastric cancer.

    The researchers found that people who consumed sugar-sweetened beverages every day were more likely to develop gastric cancer than those who rarely drank them. Artificially sweetened beverages, however, were not linked to an increased risk. The findings were published in the journal Gastro Hep Advances.

    A Long-Term Look at Sugary Drinks and Cancer

    Earlier research has connected sugar-sweetened beverages with higher risks of colorectal, breast, and liver cancers. Until now, however, relatively little was known about whether these drinks might also be associated with gastric cancer.

    To investigate, researchers examined data from 112,284 participants enrolled in the Nurses’ Health Study and Health Professionals Follow-Up Study. These long-running studies collected detailed information about participants’ diets, lifestyles, and health over several decades. During the follow-up period, which also extended across decades, 278 participants developed gastric cancer.

    “This is the first study to demonstrate an association between sugar-sweetened beverage intake and gastric cancer in a U.S. population,” said senior author Andrew T. Chan, MD, MPH, a gastroenterologist and epidemiologist with the Mass General Brigham Cancer Institute. “Gastric cancer is the fifth leading cause of cancer death worldwide, but we’ve known very little about how diet might contribute to this cancer.”

    Daily Sugary Drinks Linked to 2.45 Times Higher Risk

    After the researchers adjusted for other factors that could influence gastric cancer risk, they found a striking difference between frequent and infrequent consumers.

    Participants who drank at least one serving of a sugar-sweetened beverage each day had a 2.45 times higher risk of developing gastric cancer than participants who consumed less than one serving per month. The association appeared in both women and men.

    Higher overall fructose consumption (fructose is the main sweetener in these drinks) was also associated with a greater incidence of gastric cancer.

    Among women in the Nurses’ Health Study, for example, consuming more than one sugar-sweetened beverage per day was associated with a 3.04-fold higher risk of gastric cancer compared with women who very rarely consumed these beverages.

    The pattern was different for artificially sweetened drinks. After researchers accounted for other potential factors, greater consumption of artificially sweetened beverages was not associated with a higher incidence of gastric cancer.

    For the study, sugar-sweetened beverages included carbonated beverages, punch, lemonade and sports drinks. Artificially sweetened beverages were defined as low-calorie carbonated beverages.

    Researchers Examined H. pylori Infection

    The researchers also explored whether Helicobacter pylori (H. pylori) might help explain the findings. Infection with this bacterium is a known risk factor for gastric cancer.

    H. pylori status was available for a subset of 940 participants. Slightly more than one third showed evidence of infection, but the researchers found no association between sugar-sweetened beverage consumption and H. pylori infection.

    Why the Findings Do Not Prove Cause and Effect

    The researchers cautioned that the study was observational, meaning it can identify associations but cannot establish that sugar-sweetened beverages directly cause gastric cancer.

    Other factors could have contributed to the higher cancer rates seen among people who consumed more sugary beverages. The researchers also had limited information about participants’ H. pylori status and family histories of gastric cancer.

    Another limitation was the study population. Participants were predominantly white, making it difficult to determine whether the association differs across racial and ethnic groups.

    At the same time, the study included a large number of participants and drew on detailed health, diet, and lifestyle information collected over many years. This allowed researchers to account for many other possible risk factors for gastric cancer.

    Further research will be needed to confirm the results and determine why sugar-sweetened beverages might be associated with a greater risk of gastric cancer.

    Authorship: In addition to Chan, Mass General Brigham authors include Tae-Geun Gweon, Jane Ha, Hanseul Kim, Mengxi Du, and Mingyang Song.

    Funding: This work was supported by R35 CA253185, U01 CA261961, R01CA263776, and a Stand Up to Cancer Gastric Cancer Interception Dream Team award.

    Disclosures: Chan served as a consultant for Pfizer Inc. and Boehringer Ingelheim and received grant support from Freenome Holdings outside the submitted work.

  • Scientists discover a powerful new antivenom hidden in rattlesnake blood

    Scientists discover a powerful new antivenom hidden in rattlesnake blood

    University of Maryland researchers have identified a promising new way to treat venomous snakebites by borrowing from snakes’ own natural defenses. Their approach uses toxin-blocking proteins that western diamondback rattlesnakes evolved to protect themselves from venom.

    By combining specific proteins found in rattlesnake blood, the researchers achieved unusually strong protection against venom from several dangerous snake species.

    The study was led by Distinguished University Professor of BiologySean B. Carroll and published in the Proceedings of the National Academy of Sciences. The findings could help researchers develop more powerful antivenoms for deadly snakebites, which remain a major health threat in some regions of the world.

    “This is one of those great stories when nature has already solved a problem we’ve been grappling with for decades,” said Carroll, who also holds the Andrew and Mary Balo and Nicholas and Susan Simon Endowed Chair at UMD.

    The Global Challenge of Snakebites

    Snakebite is considered one of the world’s most neglected tropical diseases. According to the World Health Organization, venomous snakes kill an estimated 80,000 to 140,000 people annually, while hundreds of thousands of survivors are left with permanent disabilities. Many of those affected live in rural areas where effective antivenom can be difficult to obtain.

    Existing antivenoms save lives, but they also have major drawbacks. They are typically produced by exposing large animals to snake venom and then collecting the antibodies those animals generate. Manufacturing these treatments can be costly, their quality and effectiveness can vary, and they may not work equally well against the many different toxins found in venom from different snake species. They can also cause serious immune reactions.

    Those limitations have pushed scientists to search for better options. In this case, the researchers turned to snakes themselves for clues.

    “We’ve known from anecdotes for 100 years that vipers tend to be resistant to their own venom,” Carroll said. “But for a long time, nobody knew what exactly was circulating in their blood that protected them.”

    A Natural Defense Hidden in Rattlesnake Blood

    In 2022, Carroll’s laboratory found part of the answer: a protein called FETUA-3. The researchers discovered that it could block the activity of many metalloproteinase toxins found in western diamondback rattlesnake venom. It could also bind to and inhibit toxins from the venoms of several other rattlesnake species.

    “Here was evolution’s way for snakes to protect themselves from accidental self-envenomation,” he said, which prompted a follow-up question. “Why rely on horse antibodies when nature has packaged an effective antidote right there in the snake?”

    For the new research, co-authors including Elda Sánchez, director of the National Natural Toxins Research Center at Texas A&M University-Kingsville, examined what each FETUA protein contributes to venom resistance.

    The team found that individual proteins could counter certain effects of venom. One might reduce bleeding, for example, while another could interfere with enzyme activity. However, none of the FETUA proteins on its own was able to completely prevent death from a venomous bite.

    Protein Combinations Dramatically Boost Protection

    The results changed when researchers combined several FETUA proteins. These mixtures were far more effective at blocking the harmful effects of venom than the individual proteins alone.

    Finding the best combinations is complicated because snake venom is extraordinarily complex. A single venom can contain around 100 toxin proteins belonging to multiple protein families, and venom composition differs from one snake species to another.

    “The ingredients are there,” Carroll said. “We just have to keep testing various mixtures.”

    In laboratory experiments, optimized combinations of the proteins were about 10 times more potent than the current sheep-derived rattlesnake antivenom. The mixtures completely neutralized the lethal effects of rattlesnake venom and also provided broad protection against venom from multiple viper species, including species separated by millions of years of evolution.

    “The fact that parts of these inhibitors have been perfectly conserved over 50 million years of snake evolution tells you just how real a risk this is for these animals,” Carroll said, noting that how snakes envenomate themselves, whether through mouth tissue during a bite, by eating envenomated prey, through cannibalism or all of the above, isn’t well understood.

    Toward a New Generation of Antivenoms

    The present study concentrated on metalloproteinases, one important family of venom toxins. The researchers are now using the same general strategy to target other toxin families.

    “We’re getting remarkably close to having effective solutions for the three major toxin families in vipers,” Carroll said. “What we’ve learned here, together with research we’re doing now, gives us real confidence that nature-based recombinant [lab-produced] antivenoms are within reach.”

    Carroll expects that the first commercial applications of “nature’s antivenom” could be in veterinary medicine, with treatments for human snakebites potentially following later.

    He envisions future antivenoms that protect against a wider range of venoms while also being safer, less expensive and easier to manufacture on a large scale than many current treatments.

    “We could make train cars-worth of this stuff and help solve a massive global health problem,” Carroll said. “Many of our most important medicines have come from nature. I’m delighted that the components for a better-than-commercial antivenom were in these snakes all along.”

    Along with Carroll, the UMD co-authors included Department of Biology visiting faculty specialists Fiona Ukken and Yetunde Ayinuola.

    The research was funded by the Howard Hughes Medical Institute and the Viper Resource Center (Grant #P40OD01960-22). This article does not necessarily reflect the views of these organizations.

  • Early statin use linked to 15% lower dementia risk

    Early statin use linked to 15% lower dementia risk

    Starting statin treatment soon after a type 2 diabetes diagnosis was associated with a reduced risk of developing dementia, according to research presented at ESC Congress 2026 and published in The Lancet Regional Health – Europe.

    As populations age, the number of people living with dementia is expected to increase substantially. Because there are currently no effective treatments capable of preventing or reversing most forms of dementia, researchers are increasingly focused on identifying factors that could reduce the likelihood of developing the condition.

    According to the Lancet Commission, nearly half of dementia cases could theoretically be prevented by addressing 14 modifiable risk factors. One of those factors involves managing cholesterol beginning in midlife.

    “Detecting and treating high levels of low-density lipoprotein cholesterol (LDL-C) from midlife is one such highlighted risk factor,” explained presenter, Doctor Tummas Ternhamar from Copenhagen University Hospital, Denmark.

    This issue may be especially relevant for people with type 2 diabetes. High LDL-C is common among these patients, while diabetes itself is recognized as a risk factor for cognitive decline and dementia.

    “We hypothesized that early initiation of LDL-C-lowering statins following type 2 diabetes diagnosis could be associated with a lower risk of dementia,” said Doctor Ternhamar. “And we tested this in a large nationwide study using analysis methods to emulate a randomized trial and reduce some of the bias associated with observational studies,” he noted.

    Tracking More Than 132,000 People

    Using Danish national registers, researchers identified 132,585 people who had not previously taken statins and who developed type 2 diabetes between 2006 and 2019. Participants were followed through the end of 2021, and medical records were examined for diagnoses of all-cause dementia.

    The researchers used a clone-censor-weight design to compare dementia rates according to when statin therapy began. One group did not start statins within five years of receiving a diabetes diagnosis. A second group began statins early, within one year of diagnosis, while a third began treatment later, between one and five years after diagnosis.

    During a median follow-up period of 7.1 years, 2.7% of participants developed dementia.

    Earlier Statin Use Linked to Lower Risk

    Compared with people who did not begin statin therapy, those who started statins within the first year after being diagnosed with type 2 diabetes had a 15% lower relative risk of dementia over 10 years.

    Starting treatment later was also associated with a benefit, although the association was smaller. People who began statins between one and five years after diagnosis had a 10% lower relative risk of dementia over 10 years. Similar results were observed in women and men.

    Doctor Ternhamar concluded: “In individuals developing type 2 diabetes, statins were associated with a lower risk of dementia, most pronounced in those with early initiation. Statins seem to be underused in patients with type 2 diabetes, despite their protective effects against cardiovascular disease. Our findings suggest another potentially important reason to ensure that patients with type 2 diabetes and high LDL-C receive timely statin treatment.”

    Findings Cannot Prove Statins Prevent Dementia

    The results suggest that beginning statin therapy sooner after a type 2 diabetes diagnosis may have potential benefits beyond the drugs’ established role in protecting cardiovascular health. However, because the research was observational, it cannot establish that taking statins directly prevents dementia.

    Commenting on the findings, Professor Isabel Goncalves, Member of the ESC Communication Committee, said: “People with type 2 diabetes already have a higher risk of dementia and are advised to lower cholesterol to reduce their risk of heart attack and stroke. This study suggests that starting statins soon after a type 2 diabetes diagnosis may also be linked to a modest reduction in dementia risk, with greater benefit than delaying treatment. Because statins are widely available and inexpensive, the findings are potentially important. However, this was an observational study, so it cannot prove that statins prevent dementia. The results should therefore support further research and help inform discussions between patients and clinicians.”

    This work was supported by grants from the Danish Cardiovascular Academy, which is funded by the Novo Nordisk Foundation and The Danish Heart Foundation, Herlev and Gentofte Hospital, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsens Fond, Beckett fonden, Overlæge Johan Boserup og Lise Boserups legat and Direktør Jakob Madsens og Hustru Olga Madsens fond.