Just two drinks a day may be far riskier than you think

 

Even alcohol consumption that many Americans would describe as moderate may carry significant health risks, including a greater likelihood of premature death, disability, cancer, and heart disease. That is the conclusion of a new study published in the Journal of Studies on Alcohol and Drugs, a journal published at Rutgers University.

The research, known as the Alcohol Intake and Health Study, was originally commissioned by the U.S. federal government to help shape updated national dietary recommendations. Researchers estimated that people who consume an average of 14 alcoholic drinks per week face a 1 in 25 lifetime risk of dying from alcohol-related causes. By comparison, consuming up to seven drinks weekly was linked to only small increases in risk for most health conditions.

"Even low levels of alcohol use come with health risks," says lead study author Kevin Shield, Ph.D., an associate professor at the University of Toronto and a senior scientist who leads the World Health Organization (WHO)/Pan American Health Organization (PAHO) Collaborating Centre in Addiction and Mental Health. "And that risk continues to increase the more someone drinks."

How Scientists Measured the Health Risks of Alcohol

To better understand the long-term consequences of drinking, Shield and his colleagues in the United States and Canada investigated how alcohol consumption over a lifetime contributes to disease and premature death among Americans.

Medical experts first examined more than 7,200 scientific publications covering illnesses and injuries associated with alcohol. Using this evidence, they estimated the risks for individual health conditions and combined those findings with large national health data sets. Statistical models then allowed the team to calculate how different levels of alcohol consumption affect the likelihood of developing serious health problems or dying prematurely.

The findings provide specific estimates that are missing from the latest U.S. Dietary Guidelines. The updated recommendations simply encourage Americans to "limit alcoholic beverages" without identifying a particular consumption threshold. Earlier versions advised men to drink no more than two alcoholic beverages per day and women no more than one.

"While the new U.S. Dietary Guidelines contain a useful 'less-is-best' message, they provide no quantitative framework. Our study was designed to do just that across the drinking spectrum," says study co-author Timothy Naimi, M.D., M.P.H., director of the University of Victoria's Canadian Institute for Substance Use Research and an adjunct professor at Boston University.

"It turns out that two drinks per day, which might be considered 'moderate' from a social standpoint, is associated with a substantially elevated risk of a premature death caused by alcohol," explains Naimi.

Moderate Drinking Offers No Significant Overall Health Benefits

The researchers looked beyond the risk of premature death to examine alcohol's connection to a wide range of immediate and long-term health problems. These included cancers (e.g., esophageal, oral, and breast), cardiovascular disease, liver disease, and injuries.

One of the study's most important findings challenges the longstanding belief that consuming small amounts of alcohol can improve health, particularly heart health.

"We did not observe a significant protective effect of alcohol on health at any level of consumption," says Shield. "At low levels, alcohol may be associated with a reduced risk of ischemic heart disease and stroke. But when you look across the full range of health outcomes, including cancer and other chronic diseases, those potential benefits are outweighed by the risks even at 7 drinks per week."

In other words, while some studies have suggested that light drinking may benefit certain aspects of cardiovascular health, those possible advantages do not translate into an overall health benefit once alcohol's links to cancer and other diseases are taken into account.

Why Individual Alcohol Risks Can Differ

Although the analysis drew on extensive scientific evidence, the researchers emphasize that its estimates describe risks across populations rather than predicting precisely what will happen to any particular person.

Shield says the statistical calculations relied on "the best possible data." However, he cautions that individual circumstances can substantially influence the results.

"However, we can't assume that means one person's individual health risk is the same as what is reported here -- that depends on other factors like lifestyle, genetics, drinking patterns, and other choices that differ person to person."

To estimate alcohol's overall impact, the researchers calculated risks for health conditions already known to be caused by alcohol and combined them into a broader assessment. However, scientists are continuing to investigate additional possible consequences of drinking, including emerging evidence connecting alcohol consumption to pancreatic cancer.

"Understanding those relationships, and how much alcohol contributes to those risks, is an area that still needs further work," says Shield.

What the Findings Mean for U.S. Drinking Guidelines

The results suggest that alcohol-related health risks become more pronounced when consumption exceeds one drink per day, regardless of whether the person is male or female. This provides a more specific reference point for people trying to understand how their drinking habits might affect their long-term health.

Rather than suggesting that any particular amount is completely safe, the findings show how risks increase with greater consumption and why drinking less generally reduces exposure to alcohol-related harm.

"Having a clearer threshold helps people better understand what level of drinking is associated with increased risk and make more informed decisions when drinking," says Shield.

The study has also raised questions about how scientific evidence was incorporated into federal dietary recommendations.

In an accompanying editorial, Robert M. Vincent, a former Associate Administrator for the U.S. Substance Abuse and Mental Health Services Administration, offers his perspective on the circumstances surrounding the research and its role in the development of national guidance.

"The Alcohol Intake and Health report was explicitly invited to inform alcohol guidance during development of the Dietary Guidelines for Americans, 2025-2030," he writes. "Despite the study's adherence to its mandate, its findings were sidelined."

Journal Reference:

1. Sinead George, Timothy S. Naimi, Katherine Keyes, Priscilla Martinez-Matyszczyk, Adam J. Milam, Jürgen Rehm, Alvaro Alonso, Steven Bell, Annie Britton, Laura Llamosas-Falcón, Erin Hobin, Suzanne E. Judd, Amy Justice, Christopher Kahler, Suthat Liangpunsakul, Stephanie K. Jones, Gregory Marcus, Katherine McGlynn, Derek Satre, Mingyang Song, Aaron Peter Thrift, Tomoko Udo, Ashley Wettlaufer, Zuo-Feng Zhang, Kevin Shield. Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week. Journal of Studies on Alcohol and Drugs, 2026; 87 (4): 621 DOI: 10.15288/jsad.25-00435

Cite This Page:

Journal of Studies on Alcohol and Drugs. "Just two drinks a day may be far riskier than you think." ScienceDaily. ScienceDaily, 25 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261024222030.htm>.

 

 

Scientists created a tiny device that can control your nerves to treat chronic pain

 

This tiny, wireless device could transform treatment for chronic pain and movement disorders by removing the need for surgery, batteries, or wires. Credit: NYU Abu Dhabi

A miniature medical device small enough to be delivered through a standard needle could change how doctors treat chronic pain and movement disorders. Developed by scientists at NYU Abu Dhabi in partnership with Cleveland Clinic Abu Dhabi, the technology can regulate nerve activity without surgical implantation, batteries, or connecting wires.

Roughly the size of a small seed, the device is injected into the body and positioned close to a specific nerve. Once in place, it sends carefully controlled electrical signals that alter the nerve's activity. Power is supplied wirelessly from outside the body, allowing doctors or patients to adjust the stimulation in real time.

The findings, published in Science Advances, describe a potentially less invasive way to deliver precise nerve stimulation. Rather than replacing existing treatments, which can include medications and surgically implanted devices, the technology could provide another option tailored to individual medical needs.

"This work represents a shift in how we think about treating nerve-related conditions," said Prof. Khalil Ramadi, Assistant Professor of Bioengineering at NYU Abu Dhabi and NYU Tandon and the study's senior author. "By creating a device that can be injected rather than surgically implanted, we are making these therapies simpler, safer, and more accessible, while still maintaining precise control over nerve activity."

Wireless Nerve Stimulation Without Surgery

One of the device's key advantages is that doctors can locate and monitor it using familiar imaging techniques, including ultrasound and computed tomography (CT) scans. These methods help guide placement near the intended nerve and allow the device's position to be checked afterward.

The implant also provides programmable electrical stimulation. This means the signals it delivers can be adjusted to suit a patient's needs, potentially giving healthcare providers greater flexibility in managing conditions that involve abnormal or unwanted nerve activity.

"This collaboration with NYU Abu Dhabi reflects our commitment to advancing innovative, clinically relevant research that translates into meaningful improvements in patient care," said Dr. Sawsan Abdel-Razig, Chief Academic Officer at Cleveland Clinic Abu Dhabi. "By bringing together multidisciplinary expertise, this work highlights how academic partnerships can accelerate the development of safer, less invasive therapies and expand access to advanced treatments for patients."

Promising Early Results for Chronic Pain Treatment

The researchers evaluated the technology through laboratory experiments and preclinical testing. Their results showed that the miniature device could deliver precise nerve stimulation while maintaining consistent performance under conditions designed to resemble real-world use.

The team also demonstrated that the device could successfully activate nerves in vivo, meaning within a living organism rather than only in an isolated laboratory setting. This finding represents an important early step toward determining whether the technology could eventually be used in medical care.

"This technology has the potential to bridge the gap between non-invasive therapies and traditional implants," said Dr. Mohamed Elsherif, Research Associate at NYU Abu Dhabi and first author of the study. "It opens the door to treatments that are both effective and easy to deliver, which could significantly improve patient care."

Although the device has demonstrated promising results in early testing, its ability to relieve chronic pain or improve movement disorders in human patients has not yet been established.

If further research confirms its safety and effectiveness, the technology could reduce the need for more invasive procedures while making advanced nerve stimulation treatments easier to deliver. Avoiding surgical implantation could also help decrease procedure-related risks and shorten recovery times, potentially expanding access to these therapies.

Additional contributors to the study from NYU Abu Dhabi were Salma Mansour, Zhansaya Makhambetova, Fotoon Aldhanhani, Batoul Khlaifat, Mahmoud Elbeh, Vega Pradana Rachim, and Sohmyung Ha. The Cleveland Clinic Abu Dhabi co-authors were Hicham Abada, Juan S. Barajas-Gamboa, and Carlos M. Abril Vega.

Journal Reference:

1. Mohamed Elsherif, Salma Mansour, Zhansaya Makhambetova, Fotoon Aldhanhani, Batoul Khlaifat, Mahmoud Elbeh, Vega Pradana Rachim, Sohmyung Ha, Hicham Abada, Juan S. Barajas-Gamboa, Carlos M. Abril Vega, Khalil B. Ramadi. An injectable, leadless bioelectronic interface for battery-free wireless peripheral neuromodulation. Science Advances, 2026; 12 (24) DOI: 10.1126/sciadv.aeg1437

Courtesy:

New York University. "Scientists created a tiny device that can control your nerves to treat chronic pain." ScienceDaily. ScienceDaily, 10 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261008005253.htm>.

 

 

Eating olive oil before carbs has a surprising effect on blood sugar

 

New findings suggest that meal order could become a practical tool for managing blood sugar, although human studies are still needed. Credit: Shutterstock

The order in which you eat different foods may have a surprising effect on blood sugar levels. Research in mice suggests that consuming fat before carbohydrates can reduce the sharp rise in blood sugar that typically follows a meal. The findings also reveal how hormones and nerve signals work together to influence this response.

Keeping blood sugar from rising too high after eating is an important part of diabetes management. Previous clinical studies have shown that eating vegetables, protein, or fat before carbohydrates can help limit these increases. This suggests that changing the sequence of foods during a meal could offer a practical, sustainable way to improve blood sugar control without eliminating entire food groups.

Scientists have generally explained this effect through two main mechanisms. The first is slower gastric emptying, which means food moves from the stomach into the small intestine more gradually. The second involves increased release of hormones called incretins, including GLP-1, which help the body regulate blood sugar.

However, researchers have not fully understood how hormones produced by the gut and pancreas interact with the nervous system to produce these effects. To investigate, an international research team examined how consuming fat before or after glucose influences blood sugar, hormone activity, and the speed at which the stomach empties.

"Our group has long been interested in practical dietary approaches that people can continue in everyday life," says corresponding author Daisuke Yabe of Kyoto University. "Meal-sequencing is appealing because it merely changes how a meal is eaten rather than requiring people to avoid entire food groups."

Testing How Olive Oil Changes Blood Sugar Levels

The researchers conducted a series of experiments in mice to determine whether the timing of fat consumption affected how the body processed glucose.

After an overnight fast, the mice were assigned to three groups. One group received water followed by glucose. A second group was given olive oil, followed 15 minutes later by glucose. The third group received glucose first, with olive oil administered 15 minutes afterward.

The scientists then measured blood glucose levels and several hormones involved in blood sugar regulation, including insulin, glucagon, GIP, and GLP-1. Glucagon is normally associated with increasing blood sugar, while GIP and GLP-1 help regulate glucose levels after eating.

To determine how quickly material was leaving the stomach, the researchers also administered acetaminophen, a common pain reliever. By measuring how much of the drug appeared in the bloodstream after oral administration, they could estimate the rate of gastric emptying.

The team extended the experiments to additional groups of mice, including animals with type 2 diabetes and others that lacked the receptor needed to respond to GLP-1.

They also performed experiments that blocked glucagon or GLP-1 signaling, surgically interrupted the vagus nerves below the diaphragm on both sides, and examined whether different dietary fats produced similar results. The vagus nerve is an important communication pathway between the brain and digestive system, helping coordinate functions such as digestion and hormone release.

Eating Fat First Slows Blood Sugar Spikes

The results showed a clear difference depending on when the mice received olive oil.

When olive oil was given before glucose, the initial rise in blood sugar was smaller than when the oil was administered afterward. The earlier fat intake also slowed gastric emptying, delaying the movement of glucose from the stomach into the intestine.

At the same time, consuming fat before glucose stimulated an early increase in several hormones, including glucagon, GIP, and GLP-1.

Importantly, these effects were also observed in mice with type 2 diabetes and severe insulin deficiency. This suggested that the response could still function even when normal insulin regulation was significantly impaired.

A Surprising Role for a Blood Sugar Hormone

One of the most unexpected findings involved glucagon, a hormone generally known for raising blood sugar by stimulating the liver to release stored glucose.

The researchers discovered that blocking glucagon signaling alone did not eliminate the blood sugar lowering effect of consuming olive oil before glucose. Blocking GLP-1 signaling by itself also failed to remove the benefit.

However, when both signaling pathways were blocked simultaneously, the beneficial effect was reduced.

This finding suggests that glucagon and GLP-1 work together as part of a more complex system that helps moderate blood sugar after fat is consumed before carbohydrates. It also reveals that glucagon, despite its familiar role in increasing blood sugar, can contribute to a response that ultimately limits the rise in glucose after eating.

The vagus nerve experiments provided another important clue. When the researchers interrupted these nerve pathways, the results suggested that communication through the vagus nerve also contributes to the body's response to nutrient order.

Together, these findings point to a coordinated interaction between digestive hormones, pancreatic signals, and the nervous system.

Could Changing Meal Order Help Manage Diabetes?

The findings offer a clearer biological explanation for why eating fat before carbohydrates may help reduce blood sugar spikes. Rather than relying on a single hormone or digestive process, the effect appears to involve multiple systems working together to control how quickly glucose enters the intestine.

This could have practical implications for diabetes management. Adjusting the order in which foods are eaten is relatively simple and may be easier to maintain than diets that require avoiding particular food groups.

However, the experiments were conducted in mice, and the same effects have not yet been established in humans through this research. Additional clinical studies will be needed to determine whether the mechanisms identified in the experiments can be used to improve blood sugar regulation in people with or without diabetes.

"Our findings suggest that the order in which nutrients reach the gut can engage a coordinated hormone-nerve response that changes how quickly the stomach delivers glucose to the intestine," says Yabe.

Journal Reference:

1. Yanyan Liu, Hiromi Tsuchida, Sodai Kubota, Saki Kubota-Okamoto, Takehiro Kato, Yukio Horikawa, Shin Tsunekawa, Hitoshi Kuwata, Yuuka Fujiwara, Yuji Yamazaki, Yuichiro Yamada, Hiroki Fujita, Katsumi Iizuka, Naoya Murao, Shinji Ueno, Yusuke Seino, Atsushi Suzuki, Yoshitaka Hayashi, Tsuyoshi Nakanishi, Daniel J. Drucker, Takahiko Shiina, Yasutake Shimizu, Yusaku Iwasaki, Toshihiko Yada, Yohei Seno, Yuya Takahashi, Toshinori Imaizumi, Takaaki Murakami, Michael Horowitz, Yutaka Seino, Daisuke Yabe. Olive Oil Before Oral Glucose Delays Gastric Emptying and Lowers Glycemia Through Partially Redundant Glucagon and GLP-1 Signaling in Mice. Diabetes, 2026; DOI: 10.2337/db26-0531

Courtesy:

Kyoto University. "Eating olive oil before carbs has a surprising effect on blood sugar." ScienceDaily. ScienceDaily, 11 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261008102700.htm>.

 

 

 

A plastic once thought harmless may be fueling fatty liver disease

 

Scientists have discovered that polyethylene, a plastic commonly found in food packaging and containers, may contribute to fatty liver disease and make its effects worse when combined with an unhealthy diet. Credit: Shutterstock

Microplastics have spread into nearly every corner of the environment. These tiny plastic particles have been found in ocean water, drinking water, and even inside the human body. Although their presence is well documented, scientists are still working to understand what prolonged exposure could mean for human health.

Researchers at the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) have now identified a potential health concern involving polyethylene, one of the most widely used plastics in the world. Their findings suggest that polyethylene microplastics may contribute to fatty liver disease, particularly when exposure occurs alongside an unhealthy diet.

Polyethylene accounts for approximately one-third of plastic production worldwide. It is used in numerous everyday products, including food wrappers, storage containers, plastic packaging, and the linings of beverage cups. Despite its widespread use, scientists have devoted relatively little attention to its potential effects on the liver compared with other types of microplastics.

"No studies have really looked into polyethylene's effect on liver health, and it's the most widely produced plastic," said Dr. Adi Joshi, associate professor in VMBS' Department of Veterinary Physiology and Pharmacology. "What we now know is that these microplastics, especially polyethylene, affect our liver's natural defense and repair mechanisms."

Common Microplastics May Contribute to Fatty Liver Disease

To investigate the possible health effects of polyethylene, Joshi and his colleagues examined whether exposure to this common plastic could promote fatty liver disease.

The condition develops when excessive fat accumulates inside liver cells. According to the American Liver Foundation, it affects approximately 25% of people worldwide, making it a major global health concern.

The researchers discovered that polyethylene exposure increased indicators of fatty liver disease even without the added influence of an unhealthy diet. When the plastic was combined with a diet rich in fat, fructose, and cholesterol, the signs of liver disease became more severe.

These results suggest that exposure to environmental pollutants and poor dietary habits may reinforce each other's harmful effects, potentially worsening liver damage.

"Those who have a more Western-style diet, including foods like burgers and sodas, may have a greater chance of progressing to fatty liver disease if they are also exposed to polyethylene," Joshi said.

The results were especially unexpected because polyethylene has traditionally been regarded as a relatively biologically inert material. In other words, scientists generally considered it less likely to interact with biological systems than more reactive substances.

However, the findings indicate that polyethylene may influence liver function in ways that were previously overlooked. Its effects appeared both independently and alongside dietary risk factors, raising important questions about how this common plastic interacts with the body's metabolism and protective mechanisms.

Scientists Pinpoint How Microplastics Affect the Liver

Understanding where and how polyethylene causes biological changes could help explain its potential role in liver disease.

To investigate these effects in greater detail, the Texas A&M team partnered with scientists at the University of Oklahoma and applied a powerful technique called spatial transcriptomics.

This technology allows researchers to study gene activity while preserving information about where individual cells are located within a tissue. Rather than simply measuring which genes are active, scientists can identify precisely where biological changes are occurring.

Using this approach, the team mapped areas of liver damage associated with polyethylene exposure and identified molecular pathways that may help explain the effects.

One important finding involved PPAR-alpha, a protein that helps regulate fat metabolism in the liver. The researchers found that polyethylene activated this protein, suggesting that it plays a significant role in the liver's response to microplastics.

They also identified ANXA2, a gene associated with tissue repair, as another possible contributor to the disease process.

Together, these discoveries provide a more detailed picture of how polyethylene may interfere with the liver's normal functions, including the mechanisms involved in protecting and repairing damaged tissue.

Joshi believes that understanding these biological pathways could eventually help researchers identify potential treatments that reduce the harmful effects of microplastic exposure.

Could Microplastics Contribute to More Serious Liver Damage?

Although the findings reveal a previously underexplored connection between polyethylene and fatty liver disease, several important questions remain unanswered.

The researchers plan to investigate whether polyethylene exposure could contribute to more advanced forms of liver disease, including fibrosis. This condition occurs when repeated or ongoing liver damage leads to the accumulation of scar tissue, which can interfere with the organ's ability to function properly.

The team also intends to examine other molecular processes involved in the liver's response to polyethylene. One particular focus will be determining whether targeting the PPAR-alpha pathway could help protect the liver against microplastic-related damage.

"This is the pioneering study showing that polyethylene can contribute to fatty liver disease and the use of spatial transcriptomics has determined exactly where the damage has happened within the liver," Joshi said. "The other microplastics might also be harmful to the liver, and we definitely need to look into other classes of microplastics."

The findings add to growing concerns about the possible health consequences of microplastics, although further research is needed to establish how these experimental observations translate to everyday human exposure.

For Joshi, the discovery highlights why scientists need to look beyond familiar risk factors such as diet when investigating chronic diseases. As research continues, understanding how common environmental pollutants interact with the body could reveal previously unrecognized contributors to long-term health problems.

Journal Reference:

1. Woncheol Jung, Hassan Abushukair, Nikhil Y. Patil, Felix Ampadu, Maryam Firouzi, Iulia Rus, Jinhyuk Choi, Sree Deepthi Muthukrishnan, Surendra Shukla, Stefano Tarantini, Anna Csiszar, Kamiya Mehla, Dongin Kim, Je-Hyun Yoon, Dowoon Kim, Juyang Kim, Jaehak Jung, Oxana Klementieva, Yatrik M. Shah, Eiji Yoshihara, Pankaj K. Singh, Aditya D. Joshi, Tae Gyu Oh. Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity. Science Advances, 2026; 12 (25) DOI: 10.1126/sciadv.aec8681

Courtesy:

Texas A&M University. "A plastic once thought harmless may be fueling fatty liver disease." ScienceDaily. ScienceDaily, 10 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261008102718.htm>.

 

 

This protective enzyme could help stop fatty liver disease from getting worse

 

A newly identified protective enzyme could offer scientists a new way to stop fatty liver disease before it causes serious liver damage. Credit: Shutterstock

Researchers co-led by Cedars-Sinai Health Sciences University have identified an enzyme that may help protect the liver from the damage that can occur as the most common form of liver disease becomes more severe. The findings, from a preclinical study published in Nature Metabolism, could eventually support new strategies for preventing serious liver injury and progression toward liver failure.

An estimated 100 million people in the U.S. have metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called nonalcoholic fatty liver disease, according to the American Liver Foundation. Roughly 20% to 25% of those affected go on to develop metabolic dysfunction-associated steatohepatitis (MASH), a more serious form of the condition in which excess liver fat is accompanied by inflammation, cell injury and scarring.

Why MASH Is Difficult to Treat

Current care mainly centers on lifestyle changes and efforts to limit additional liver damage. Although medications are available, treatment options are still limited, and there is currently no cure for MASH.

Earlier research has suggested that damaged mitochondria, the structures that produce energy for cells, may contribute to the development and progression of MASH. In the new multicenter study, Cedars-Sinai researchers found that levels of an enzyme called UBE2N decline in liver cells as the disease becomes more advanced.

"The UBE2N enzyme appears to protect the liver from the inflammation and damage associated with MASH by helping remove damaged mitochondria and supporting the breakdown of fat," said Ekihiro Seki, MD, PhD, professor of Medicine and Biomedical Sciences at Cedars-Sinai and co-corresponding author of the study. "When levels of the enzyme fell, we saw more damaged cells and injury to the liver."

Restoring UBE2N Reduced Liver Damage in Mice

The researchers then restored UBE2N to normal levels in the livers of laboratory mice. After doing so, they observed reductions in fat accumulation, inflammation and scarring.

Those results suggest that UBE2N could become a potential treatment target for preventing MASLD from advancing to MASH.

"The identification of this enzyme's role in regulating mitochondria in the liver is an important advance in understanding steatotic liver disease," said Shelly Lu, MD, the Women's Guild Chair in Gastroenterology and director of the Karsh Division of Gastroenterology and Hepatology at Cedars-Sinai. "Future studies can test whether enhancing this protective pathway can complement existing treatments, identify patients most likely to benefit and lead to new therapeutic approaches for preventing advanced disease."

Additional Cedars-Sinai authors include Michitaka Matsuda, So Yeon Kim, Takashi Tsuchiya and Yoon Seok Roh.

Additional authors include: Feng Wang, Jin Lee, Jeong-Su Park, Meizhou Huang, Hwan Ma, Guoyan Sui, Zixiong Zhou, Xufeng Wu, Haram Lee, Soohwan Oh, Hanseul Park, Key-Hwan Lim, Chun-Woong Park, Sang-Bae Han, Jin Tae Hong and Michael Karin.

Funding: This work was supported by the National Research Foundation of Korea (grant nos. RS-2025-02273102 and RS-2025-02603096), Regional Innovation System & Education (RISE) programme of Chungbuk (grant no. 2025-RISE-11-014-03), the Pinnacle Research Award of American Association for the Study of Liver Diseases (AASLD, to J.L.), the San Diego Digestive Diseases Research Center (SDDRC) Pilot/Feasibility Grant (NIDDK P30 DK120515, to J.L.), the National Institutes of Health (grant nos. R01DK085252, R01DK138591 and R01CA301632) and the National Natural Science Foundation of China (grant no. 82404726).

Journal Reference:

1. Feng Wang, Jin Lee, Jeong-Su Park, Meizhou Huang, Hwan Ma, Guoyan Sui, Zixiong Zhou, Michitaka Matsuda, So Yeon Kim, Takashi Tsuchiya, Xuefeng Wu, Haram Lee, Soohwan Oh, Hanseul Park, Key-Hwan Lim, Chun-Woong Park, Sang-Bae Han, Jin Tae Hong, Michael Karin, Yoon Seok Roh, Ekihiro Seki. UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis. Nature Metabolism, 2026; 8 (9): 1926 DOI: 10.1038/s42255-026-01590-0

Courtesy:

Cedars-Sinai. "This protective enzyme could help stop fatty liver disease from getting worse." ScienceDaily. ScienceDaily, 3 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261002080020.htm>.

 

 

Your gut may be making a molecule that raises Alzheimer’s risk

 

A compound made by gut bacteria may quietly raise Alzheimer’s risk and speed cognitive decline, giving scientists a promising new treatment target. Credit: Shutterstock

A molecule made by bacteria in the digestive system may increase the risk of Alzheimer's disease and accelerate cognitive decline in people with dementia, according to new research. The finding could point scientists toward a potential treatment strategy aimed at lowering Alzheimer's risk.

Nearly a decade ago, a research team led by University of Wisconsin-Madison professors Barbara Bendlin and Federico Rey found that the mix of microorganisms living in the intestines differs between people with Alzheimer's disease and healthy individuals.

"Since then, we've been trying to figure out how this difference in the gut perhaps leads to changes in the brain," says Bendlin, a professor of medicine in the UW School of Medicine and Public Health.

A Gut Molecule With Effects Beyond the Intestines

In a recent study published in the journal Nature Communications, Bendlin, Rey and their collaborators focused on imidazole propionate (ImP), a compound produced by certain bacteria in the gut. Their findings suggest that ImP may contribute to brain changes involved in Alzheimer's disease and related forms of dementia.

ImP production varies considerably from person to person. Some people appear to generate relatively large amounts, while others produce very little.

"ImP-producing bacteria are present in a large fraction of people, but they're not very abundant in most people," says Rey, a UW-Madison professor of bacteriology. "But something we have learned over the years is that a microbe doesn't have to be abundant to have an impact on the host."

Once produced in the gut, ImP can enter the circulation and reach other parts of the body. Previous research has linked the compound to type 2 diabetes and coronary artery disease.

The new study suggests that its effects may also extend to the brain. In mice, researchers found that ImP reaching the brain increased the accumulation of abnormal beta amyloid and tau proteins, two major hallmarks associated with Alzheimer's disease.

"That process eventually results in the death of neurons, and in humans is a key feature of Alzheimer's disease," Rey says.

Higher ImP Levels Linked to Faster Cognitive Decline

The researchers then examined blood samples from almost 1,200 people enrolled in the Wisconsin Registry for Alzheimer's Prevention and studies conducted through the Wisconsin Alzheimer's Disease Research Center.

Participants with higher concentrations of ImP in their blood were much more likely to show biological markers associated with abnormal proteins and impaired neuron function in dementia.

Because the volunteers had also completed cognitive testing over time, the researchers were able to compare ImP levels with changes in thinking and memory.

"And because we have the results of cognitive tests these volunteers took over time, we can see that the people with the highest ImP levels also experienced much faster cognitive decline," Rey says.

The team also discovered a genetic variation associated with substantially higher levels of ImP in the bloodstream. About 43% of the people in the study carried this variation.

Researchers suspect the genetic difference may influence how effectively the kidneys remove ImP from the blood, affecting how much of the compound remains in circulation.

"This genetic variation has been associated with increased Alzheimer's risk in large genetic studies before, and now we may understand why it's connected," Rey says.

A Potential New Target for Alzheimer's Prevention

One of the most important possibilities raised by the findings is that ImP itself could become a target for preventing or slowing Alzheimer's disease and related dementias.

However, reducing ImP through diet alone may not be straightforward. Gut bacteria produce the compound while generating energy from histidine, an amino acid that is essential for human health and found in many foods, particularly foods rich in protein.

"Generally improving your diet would probably help," Bendlin says. "But it's not as easy as saying, 'Stop eating eggs' or 'Don't eat so much red meat.' Because you need histidine, and it's all over the place."

Rather than trying to eliminate histidine from the diet, the researchers say the discovery could eventually lead to treatments that specifically reduce ImP levels in the bloodstream.

Identifying a particular molecule and a related genetic variation gives scientists a more precise target to investigate.

"It could be just like cholesterol, where people with elevated cholesterol take a drug, a statin, that reduces their risk for heart disease," Bendlin says. "If we can find an inhibitor that can help decrease the levels of ImP in the blood, that could hopefully reduce the risk of Alzheimer's and the speed of cognitive decline for a significant number of people."

Scientists from the University of California, Los Angeles and the University of Gothenburg also contributed to the study.

This research was supported in part by grants from the Wisconsin Partnership Program and the National Institutes of Health (R01AG070973, R01AG083883, R01AG092220, R21AG089348, R01HL168493, R01DK143650 and U54HL170326) and the U.S. Department of Agriculture (WIS03073).

Journal Reference:

1. Vaibhav Vemuganti, Jea Woo Kang, Qijun Zhang, Eric R. McGregor, James R. Hilser, Ruben Aquino-Martinez, Sandra Harding, Joseph Lawrence Harpt, Katharina R. Beck, Hailey Bussan, Jessamine F. Kuehn, Yuetiva Deming, Rachel Studer, Sterling C. Johnson, Sanjay Asthana, Henrik Zetterberg, Kaj Blennow, Corinne D. Engelman, Hooman Allayee, Rozalyn M. Anderson, Tyler K. Ulland, Fredrik Bäckhed, Barbara B. Bendlin, Federico E. Rey. Gut bacterial metabolite imidazole propionate potentiates Alzheimer’s disease pathology. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-74744-z

Courtesy:

University of Wisconsin-Madison. "Your gut may be making a molecule that raises Alzheimer’s risk." ScienceDaily. ScienceDaily, 3 October 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260930225459.htm>. 

 

Your gut bacteria may offer an early clue to how quickly your brain is aging

 

A UCLA study suggests that signs of faster brain aging may be connected to the bacteria and chemical compounds living in the gut, even in generally healthy adults. Credit: Shutterstock

A new UCLA study suggests that the pace of brain aging may be connected to bacteria in the gut and the chemical compounds they produce. The findings offer a new look at biological changes that may begin long before noticeable problems with memory or thinking appear.

Scientists have used brain scans for years to estimate a person's "brain age," which can differ from chronological age. Previous research has found that when the brain appears older than expected, that pattern can be associated with poorer memory, weaker thinking skills and changes in mood.

Most earlier studies, however, focused on older adults or people who already had neurological conditions. That left an important question unanswered: does an older looking brain also matter in younger, generally healthy adults?

Measuring How Old the Brain Appears

In a new study published in the journal eBioMedicine, UCLA Health researchers examined brain scans from nearly 1,500 adults divided across three separate groups.

The team used a scanning approach that measures how different areas of the brain communicate with one another while a person is at rest. Researchers then created a computer model that estimated each person's age based on those communication patterns.

They compared the estimated brain age with each participant's actual age. The difference between the two became what the researchers called the Brain Aging Index (BAI).

Older-Looking Brains Were Linked to Memory and Mood

Across all three groups, participants whose brains appeared older than their chronological age generally performed worse on tests of working memory and executive function. Those abilities help people hold information in mind, stay focused, plan, and organize.

People with a higher Brain Aging Index also reported more symptoms of depression. The patterns repeatedly involved brain regions associated with memory and self-referential thought, or the mental processes people use when thinking about themselves and their own experiences.

Gut Bacteria Offer Another Clue

For one of the study groups, the researchers also examined stool samples to see whether differences in brain aging were connected to changes in the gut.

They found that a higher Brain Aging Index was associated with specific gut bacteria and several metabolic byproducts. These included certain fat molecules, a cholesterol-related compound and lower levels of a hormone called estetrol.

The pathways connected with these biological signals involved the immune system, blood vessel function, communication between brain cells and the processes cells use to produce energy.

Signs of Brain Aging May Appear Decades Early

"Brain aging doesn't suddenly begin when we get older, but the biological signals may be detectable decades earlier," said the study's senior author Dr. Arpana Church, co-director of the Goodman-Luskin Microbiome Center at UCLA Health. "By linking these early brain changes with the gut microbiome and its metabolites, we are beginning to identify pathways that could ultimately help us understand who may be at risk and, importantly, where we might intervene to support healthier brain aging. This ultimately opens the door to exploring whether targeting gut health could one day support healthier brain aging."

Church said the findings may eventually help researchers identify people at greater risk of cognitive or mood-related decline earlier in life. They also raise the possibility that the gut could become a target for future strategies designed to support brain health and prevention earlier in life.

Journal Reference:

1. Kanhao Zhao, Gabriel A. Vignolle, Jennifer S. Labus, Emeran A. Mayer, Allison Vaughan, Marika Dy, Priten Vora, Ming W. Hung, Keith Vossel, Chris Gill, Daniele Del Rio, Catherine Stanton, R. Paul Ross, John F. Cryan, Rima Kaddurah-Daouk, Yu Zhang, Arpana Church. Brain-gut crosstalk associated with brain ageing in young and mid-life adults: a multicohort cross-sectional study. eBioMedicine, 2026; 132: 106468 DOI: 10.1016/j.ebiom.2026.106468

Courtesy:
University of California - Los Angeles Health Sciences. "Your gut bacteria may reveal how fast your brain is aging." ScienceDaily. ScienceDaily, 4 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261001214106.htm>.