Category: Gastrointestinal

Head Impacts Associated with Altered Gut Microbiome in Football Players

Non-concussive head impacts correlated with changes to the gut microbiome on following days, in pilot study tracking six US collegiate football players over one season

Image credit: Rich Barnes / Colgate Athletics, CC-BY 4.0 (https://creativecommons.org/licenses/by/4.0/)

Non-concussive head impacts – hits to the head that don’t cause clinically detectable symptomsare correlated with subsequent changes to the gut microbiome in a small sample of US collegiate football players, according to a new study published May 6, 2026, in the open-access journal PLOS One by Ahmet Ay and Kenneth Douglas Belanger of Colgate University, USA, and colleagues.

Non-concussive head impacts are common in American football, with players experiencing between 100 and 1000 across a season. While research has shown that full concussions can disrupt the gut microbiome – which regulates inflammation and the neuroimmune system – whether sub-concussive hits might produce similar effects had not been investigated.

In the new study, researchers tracked six NCAA Division I American football players across a competition season, beginning during preseason training. Their on-field activity profiles were monitored using GPS units and head impacts were tracked using a helmet-based sensor system; 226 faecal samples were analysed for their microbiome composition; and participants completed lifestyle questionnaires after each sample collection.

The researchers found that microbial diversity changed within two to three days after a substantial head impact. Specifically, certain bacteria – including the order Coriobacteriales, the family Prevotellaceae, and the genus Prevotella – tended to decrease in abundance while the genus Ruminococcus increased. In previous studies, these changes have correlated with brain injury and inflammation.

The athletes’ gut microbiomes also changed significantly over the course of the season, with mathematical modelling suggesting that the cumulative effects of non-concussive head impacts was likely associated with this shift, even after accounting for 15 potentially confounding factors including diet changes, exercise intensity, sleep, and stress.

The study is limited by its small sample size and lack of a control group, with its design meaning findings could only establish correlation but not causation. However, the authors conclude that even sub-symptomatic head impacts might affect the gut microbiome, both in the immediate aftermath of injury and over a longer time course in athletes who experience multiple impacts. 

Ken Belanger adds: “As far as we are aware, this is the first study to examine connections between head impacts and the composition of the gut microbiome – the complex community of bacteria and other organisms within the digestive system.”

“Our results provide evidence that even head impacts that do not result in a concussion or other reported symptoms may influence the microbes present within the gut, both in the short- and longer-term. Determining what causes these changes and whether they have a positive or negative influence on recovery from head injury will require further investigation.”

“Our research highlights the importance of thinking integratively about the interactions between the gut and the brain. We are only beginning to scratch the surface in our understanding of how these complex organs and organ systems communicate with and affect each other.”

Aziz Zafar adds: “After having only heard of the complicated interplay between neuronal inflammation and the gut microbiome, I found it to be such an exciting scientific experience to explore that interplay in the context of head impacts.”

Zachary Pelland adds: “It has been an amazing privilege to work so deeply on a personally and scientifically meaningful project which could not have happened without immeasurable support across academic departments, athletics, administration, and alumni at Colgate University.” 

Provided by PLOS

Some Common IBS Treatments Linked to Higher Risk of Death

Photo by Towfiqu Barbhuiya on Unsplash

A large, long-term study led by Cedars-Sinai Health Sciences University investigators suggests that some medications commonly prescribed to treat irritable bowel syndrome (IBS) – including antidepressants – may be associated with a small but measurable increase in the risk of death.

The findings, published in Communications Medicine, are based on nearly two decades of electronic health records from more than 650 000 US adults with IBS, making it the largest real-world study to examine the long-term safety of IBS treatments.

IBS is a chronic gastrointestinal condition which has no cure, but dietary modifications, behavioural therapy and medications can help manage symptoms.

“Many patients are diagnosed with IBS at a young age and may remain on medications for years,” said Ali Rezaie, MD, medical director of the GI Motility Program at Cedars-Sinai and senior author of the study. “However, most clinical trials of these medications last less than a year, so we know very little about their long-term safety. This study begins to address that gap.”

Researchers assessed patients taking Food and Drug Administration-approved IBS medications, as well as antidepressants, antispasmodics and opioid-based antidiarrhoeal drugs, such as loperamide and diphenoxylate – widely used and recommended in IBS care. They found that long-term antidepressant use was associated with a 35% higher risk of death, and that loperamide and diphenoxylate use were associated with roughly double the risk of death.

The study does not establish that these medications directly cause death; rather, the observed associations may reflect higher rates of adverse outcomes, such as cardiovascular events, falls and stroke, which were more frequent among exposed patients.

Although antidepressants are not FDA-approved for IBS, they are commonly prescribed for IBS patients to help reduce pain, calm symptoms and make the condition easier to manage. The study found that other recommended treatments, including FDA-approved medications and antispasmodics, were not associated with increased mortality risk.

Researchers emphasised that while the increase in risk is significant and may sound concerning, the overall risk to any individual patient is small.

“IBS patients should not panic, but they do need to understand and weigh the small but meaningful risks when considering long-term treatments,” said Rezaie, the director of Bioinformatics at the Medically Associated Science and Technology (MAST) Program at Cedars-Sinai. “Patients should speak with their healthcare provider about the safest and most effective options for managing their symptoms.”

Rezaie said more research is needed to confirm these findings and identify which patients may be at greatest risk. He also called for future treatment guidelines to better address the long-term safety of medications commonly used to manage IBS.

In the meantime, he emphasized a more personalised approach to IBS patient care.

“Treatment for IBS patients should focus on identifying the underlying causes and using the safest, evidence-based options available rather than relying on a single class of medications for long-term management,” Rezaie said.

By Kristin Reynolds

Source: Cedars-Sinai Medical Center

A New Treatment Protocol Targets the Deadliest Cases of C. difficile Infection

Clostridioides difficile. Credit: CDC

A new study from the University of Minnesota Medical School demonstrated that faecal microbiota transplantation (FMT) can rapidly reverse systemic inflammation and improve survival in patients with fulminant Clostridioides difficile (C. difficile) infection – a life-threatening condition characterised by a sepsis-like state. The findings were published in Clinical Gastroenterology and Hepatology.

C. difficile infection is the most common cause of healthcare-acquired diarrhoeal illnesses. Most of the mortality, estimated at 15 000 people annually in the United States alone, is associated with the severe and fulminant forms of the disease. C. difficile is listed as one of the most urgent infectious disease threats by the Centers for Disease Control and Prevention. The infection occurs in people with disrupted microbial communities in the gut, most commonly by antibiotic medications. 

In this study, investigators implemented a standardised FMT protocol developed at the University of Minnesota specifically for critically ill patients who were deteriorating despite intensive antibiotic therapies and were often too unstable for surgery. Among 18 patients treated, FMT was associated with rapid declines in inflammatory markers and achieved a 78% 30-day survival. 

“There is an important caveat to our findings – the window for the FMT intervention is very narrow because these patients are generally extremely sick,” said Alexander Khoruts, MD, professor at the University of Minnesota Medical School, director of the UMN Microbiota Therapeutics Program and a gastroenterologist with M Health Fairview. “Therefore, the FMT formulation needs to be easily accessible. We are in a unique position at the University because we have a facility in our institution where our FMT products are manufactured in accordance with pharmaceutical standards, and treatment units are always on hand in our cryobank.”

The University of Minnesota Microbiota Therapeutics program is the leading program in the world in developing microbiome-targeted therapies with live microbial communities. As a result of the team’s work, M Health Fairview recently implemented a dedicated system that alerts providers to hospitalized patients at risk of developing severe C. difficile infection so that they can get access to the optimal treatments earlier. 

Importantly, the findings also suggest an entirely novel mechanism by which FMT can modulate systemic inflammation in severe C. difficile infection. This is a topic of ongoing research. The team is also currently working to make this FMT treatment option more widely available to patients across the United States.

By Alex Smith

Source: University of Minnesota Medical School

The Gut’s Connection to Healing Traumatic Brain Injuries

Houston Methodist researchers find antibiotics aid recovery from traumatic brain injury

Coup and contrecoup brain injury. Credit: Scientific Animations CC4.0

In a new study published in Nature Communications BiologyHouston Methodist researchers led by Sonia Villapol, PhD, found that short-term antibiotic treatment significantly reduced neuroinflammation and neurodegeneration following traumatic brain injury (TBI) by altering the gut microbiome in animal models. 

“We found that antibiotic treatment following TBI can reduce harmful gut bacteria, decrease lesion size and limit cell death,” said Villapol, an associate professor in the Department of Neurosurgery at Houston Methodist. “Our results support a gut–brain mechanism in which microbiome changes influence peripheral immunity and, in turn, neuroinflammation after TBI.”

Administering antibiotics cleans the gut of harmful bacteria, allowing beneficial bacteria to flourish. The study found that two helpful bacteria, Parasutterella excrementihominis and Lactobacillus johnsonii, are key to driving cell repair. According to Villapol, they could also be major regulators for peripheral inflammation in the body.

Notably, 70% of immune system regulation is generated by the gut microbiome. During gut imbalance, the bidirectional nature of the brain-gut axis can wreak havoc throughout the entire body. 

“Our brains are constantly sending signals to the rest of our bodies. Following a traumatic brain event, those signals can get scrambled and disrupt other organs, including our digestive system,” Villapol said. “If the gut stays out of balance, the brain may have a harder time healing.”

There are an estimated 4 million traumatic brain injuries a year in the U.S. Recent studies indicate that TBI-induced gut microbiome imbalance may even contribute to the development of neurodegenerative diseases like Parkinson’s, Alzheimer’s and dementia. 

Villapol’s lab is focused on investigating and developing new neuroprotective treatments to fight inflammation linked with neurodegenerative disease. “If we can break neuroinflammation in the acute or chronic stage, we can reduce the risk of developing Alzheimer’s or dementia,” said Villapol. 

The next phase of the research will focus on bioengineering Parasutterella excrementihominis and Lactobacillus johnsonii to further develop precision therapies to reduce neuroinflammation.

Source: Houston Methodist

Trace Levels of Food Pathogen Aren’t Always a Health Risk, Study Finds

Photo by Andrea Piacquadio on Pexels

Ultra-sensitive food safety tests may drive food waste and unavailability with limited public health benefit, according to a Frontiers in Science study.

These food safety measures and ultra-sensitive tests may drive edible food being thrown away, excessive packaging, and extra costs for consumers.

The international team of researchers make it clear that food safety is an important concern, as foodborne pathogens account for approximately 420 000 deaths and 600 million cases of illness each year. However, the authors argue that food systems will be more sustainable, while continuing to protect public health, if “zero-detection” expectations are replaced with evidence-based targets for “sufficiently safe” food.

Their new article sets out how regulators might find trade-offs with other important factors, such as food supply security, sustainability, and nutritional health.

“Although the public expects food to be completely safe, there will always be some risk of foodborne illness. Zero risk doesn’t exist, and we shouldn’t be aiming for that either. Just as we don’t limit highway speeds to 10 miles per hour to minimize road deaths, we need to take a balanced approach that considers possible negative consequences of extreme food safety measures,” said lead author Prof Martin Wiedmann from Cornell University.


Read and download the article


Impact of aiming for zero risk

The study’s authors highlight several situations where excessive caution can cause harm.

Many rules and purchasing standards rely heavily on detecting a pathogen, sometimes treating any detection as unacceptable without fully considering dose, exposure, the food’s ability to support microbial growth, or who is most at risk.

For example, a food product might be considered contaminated if it tests positive for the bacterium Listeria monocytogenes, regardless of levels.

These alarms can result from ultra-sensitive tests detecting small amounts of microbes unlikely to cause disease in humans. In some cases, the concerns may come from bacteria that are not harmful themselves, but are an indirect indicator of contamination.

Throwing away such food reduces the available food supply and wastes resources. Similarly, recalling food products from consumers can damage consumer trust, pushing people away from otherwise healthy products.

Other protective measures, such as storage temperatures, packaging, and heat treatment, can waste energy, increase costs, and reduce nutritional content. While these are all important safety measures, they should only be applied if needed and associated trade-offs should be considered.

“A tremendous amount of food is wasted that would have been sufficiently safe to eat. Too often, trade-offs such as environmental or economic costs are only considered after a traditional microbial risk assessment. We cannot afford to carry on like this at a time when we desperately need to reduce our impact on the planet and assure not only food safety but food security,” said co-author Prof Sophia Johler at Ludwig Maximilian University of Munich, Germany.

Focus on risk rather than hazard

The current situation is driven by an emphasis on hazard-based assessments, according to the authors, where regulations focus on detecting pathogens, regardless of the threat to consumers. The researchers argue that the food system should move towards more flexible risk-based approaches, which assess the probabilities of harms and adjust the safety measures accordingly.

Regulations that overemphasize stringent corrective actions (such as recalls) when swab samples from a food-processing facility test positive for an indicator, for example, could lead to undue corrective actions in areas that are unlikely to contaminate the food. The authors explain that this could be an opportunity cost that diverts resources away from more effective interventions and control strategies in high-risk areas.

“There’s well-established evidence that focusing on end-product testing is generally ineffective to ensure safety. Overemphasis on end-product testing may distract from other food safety measures (e.g., applying validated and verified process controls), which can provide greater public health benefits,” said co-author Dr Sriya Sunil at Cornell University.

Better tools to assess priorities

Computational tools that incorporate vast amounts of information across the food production system could help with establishing acceptable risks.

One challenge is how to prioritize different hazards. For example, in the US, norovirus causes thousands of times more cases than Listeria monocytogenes, yet Listeria monocytogenes causes more deaths per year.

While there are trade advantages to having consistent international food safety standards, the balance between competing interests may vary between regions. This can become even more complex when factoring in the health and environmental implications of greenhouse gas emissions.

“Specialists across social sciences, economics, and life sciences must work together to establish values that align with consumers’ priorities. Together with advanced models that build on geographic information, AI, and genomics, we can assess, manage, and communicate risks far more accurately,” said Wiedmann.

Source: Frontiers

Gut Bacteria Regulate the Four Sections of the Colon

Source: CC0

The gut microbiome drives a process vital for protecting the colon against tissue injury, according to the findings of a study co-led by Cedars-Sinai Health Sciences University investigators. The discovery, published in Cell, has important implications for understanding how a wide variety of intestinal disorders may develop.

“Our research opens the door to treatments that focus on restoring key molecular signals in vulnerable regions of the colon,” said Ophir Klein, MD, PhD, executive director of Cedars-Sinai Guerin Children’s, executive vice dean of Children’s Health, and the David and Meredith Kaplan Distinguished Chair in Children’s Health. Klein is the senior author of the study.

Prior research has shown that the four sections of the colon – ascending, transverse, descending and sigmoid – have different functions and risks for disease, but it wasn’t clear why these variations exist.

In this study, the investigators showed that the identity of distinct regions of the colon are regulated by the gut microbiome. They identified nicotinic acid, a molecule produced by certain bacteria in the gut microbiome, as a main driver of these regional differences in the colon’s sections. Nicotinic acid, also known as niacin, part of the vitamin B3 family, helps the body convert food into energy and supports the health of cells.

The researchers compared laboratory mice with and without a microbiome. They found that production of nicotinic acid by bacteria in the upper colon activates a protective mechanism in colon cells. In mice without a microbiome, minimal nicotinic acid was produced, and cells in the upper colon became more vulnerable to damage and disease.

Investigators also studied human colon tissue samples. They found that the different sections of the human colon showed regional characteristics similar to patterns observed in mice. And in samples from human patients with the autoimmune disorder Crohn’s disease, this protective mechanism was reduced.

“Our work highlights the importance of studying host microbiome interactions with careful attention to specific colon regions, rather than treating the colon as a uniform organ,” said Jeremie Rispal, PhD, a postdoctoral scholar at the University of California, San Francisco, and the first author of the study. “We learned that the microbiome controls regional differences and tissue protection.”

Further study will be needed to confirm the precise mechanisms behind this protective effect and to determine how these findings might be used in new therapies for intestinal disorders.

Source: Cedars-Sinai Medical Center

Scientists Discover a Gut Bacterium Linked to Muscle Strength

Photo by Jonathan Borba on Unsplash

Ageing naturally weakens our muscles, but a new study published in the journal Gut have found a gut bacterium that may help turn the tide. The researchers Leiden University Medical Center and the Universities of Granada and Almería, found that Roseburia inulinivorans is linked to stronger muscles in both people and mice. The discovery hints at the potential for new probiotics to support muscle strength and healthy ageing.

While exercise and good nutrition remain important for maintaining muscle strength, scientists are now turning their attention to a lesser‑known player: the gut. “The bacteria living in our intestines help us process nutrients, regulate inflammation and manage energy,” Patrick Rensen, professor at the division of Endocrinology, notes. “All of these processes are essential for keeping our muscles healthy as we age.”

A gut bacterium linked to stronger muscles

In their new work, the researchers identified one particular gut bacterium, Roseburia inulinivorans, that appears to be linked to stronger muscles across the lifespan. “When we compared young adults aged 18 to 25 with older adults aged 65 and above, we noticed clear differences,” postdoc Borja Martínez-Téllez says. “Older adults who carried this bacterium had 29 percent stronger handgrip strength than those who didn’t.” In young adults, higher levels of Roseburia inulinivorans were associated with stronger muscles and better overall fitness. “It was remarkable to see the same pattern in both age groups,” Martínez-Téllez adds.

Testing the bacterium in mice

To find out whether this link was more than coincidence, the researchers carried out a series of experiments in mice. “We wanted to understand whether this bacterium actually causes improvements in muscle strength,” Rensen explains. After clearing the mice’s gut bacteria using antibiotics, they introduced human strains of Roseburia inulinivorans for eight weeks.

“The results were striking,” Rensen says. “The mice became 30 percent stronger, developed larger muscle fibres and produced more fast‑twitch fibres.”

The team also found that the bacterium changed how the muscles used certain building blocks and activated energy‑related pathways inside the muscle. “These metabolic changes may help explain why the muscles grew stronger,” according to Martínez-Téllez.

From discovery to potential probiotic treatment

Another key observation is that levels of Roseburia inulinivorans naturally decline with age. “This could partly explain why muscle strength drops as we get older,” Martínez-Téllez says. “If this bacterium supports muscle metabolism, then restoring it might one day help preserve muscle function later in life.”

Together, the findings suggest that Roseburia inulinivorans could become a future probiotic, developed into a safe, supplement‑like product aimed at preventing age‑related muscle‑wasting conditions. “A nutraceutical approach – using food‑based or naturally derived products – could offer a gentle and non‑invasive way to support healthy ageing,” Martínez-Téllez explains.

The researchers however caution that considerable work needs to be done before these findings can be turned into a treatment for humans.

Source: Leiden University Medical Center

Harnessing Gut Bacteria to Heal Traumatic Brain Injury

Houston Methodist researchers find antibiotics aid recovery from traumatic brain injury

Source: CC0

What if healing the brain after traumatic injury starts in the gut? In a new study published in Nature Communications BiologyHouston Methodist researchers led by Sonia Villapol, PhD, found that short-term antibiotic treatment significantly reduced neuroinflammation and neurodegeneration following traumatic brain injury (TBI) by altering the gut microbiome in animal models. 

“We found that antibiotic treatment following TBI can reduce harmful gut bacteria, decrease lesion size and limit cell death,” said Villapol, an associate professor in the Department of Neurosurgery at Houston Methodist. “Our results support a gut–brain mechanism in which microbiome changes influence peripheral immunity and, in turn, neuroinflammation after TBI.¨

Administering antibiotics cleans the gut of harmful bacteria, allowing beneficial bacteria to flourish. The study found that two helpful bacteria, Parasutterella excrementihominis and Lactobacillus johnsonii, are key to driving cell repair. According to Villapol, they could also be major regulators for peripheral inflammation in the body.

Notably, 70% of immune system regulation is generated by the gut microbiome. During gut imbalance, the bidirectional nature of the brain-gut axis can wreak havoc throughout the entire body. 

“Our brains are constantly sending signals to the rest of our bodies. Following a traumatic brain event, those signals can get scrambled and disrupt other organs, including our digestive system,” Villapol said. “If the gut stays out of balance, the brain may have a harder time healing.”

Recent studies indicate that TBI-induced gut microbiome imbalance may even contribute to the development of neurodegenerative diseases like Parkinson’s, Alzheimer’s and dementia. 

Villapol’s lab is focused on investigating and developing new neuroprotective treatments to fight inflammation linked with neurodegenerative disease. “If we can break neuroinflammation in the acute or chronic stage, we can reduce the risk of developing Alzheimer’s or dementia,” said Villapol. 

The next phase of the research will focus on bioengineering P. excrementihominis and L. johnsonii to further develop precision therapies to reduce neuroinflammation.

Source: Houston Methodist

Scientists Discover a Form of Constipation Caused by Gut-drying Bacteria

Two bacteria working together to break down intestinal mucus are identified as a contributing factor to chronic constipation

Scientists at Nagoya University in Japan have found two gut bacteria working together that contribute to chronic constipation. The duo, Akkermansia muciniphila and Bacteroides thetaiotaomicron, destroy the intestinal mucus coating essential for keeping the colon lubricated and faeces hydrated. Their excess degradation leaves patients with dry, immobile stool. This discovery, published in Gut Microbes, finally explains why standard treatments often fail for millions of people with chronic constipation.

Notably, the study shows that Parkinson’s disease patients, who suffer from constipation decades before developing tremors, have higher levels of these mucus-degrading bacteria. While constipation in Parkinson’s disease has traditionally been attributed to nerve degradation, these findings suggest that bacterial activity also plays a crucial role in the development of their symptoms.

Why mucin matters for digestion

Constipation is a very common digestive problem. Doctors have assumed it happens because of slow gut movement when our intestines are not moving food along fast enough. However, this explanation does not work for everyone.

Some people have constipation with no identifiable cause, referred to as chronic idiopathic constipation (CIC). Parkinson’s disease patients also face severe, treatment-resistant constipation, though it is clinically categorized separately from CIC. Many struggle with severe constipation for 20 or 30 years before they develop tremors and movement problems, but researchers did not know why until now.

Instead of focusing on nerve and muscle movement in the gut, the researchers examined the protective gel-like coating called colonic mucin, a substance in the large intestine that lines the intestinal walls and is found within stool. Colonic mucin keeps stool moist, helps it move smoothly through our digestive tract, and protects the intestinal wall from bacteria.

They found that two gut bacteria work in sequence to break down this mucin. B. thetaiotaomicron uses enzymes to remove protective sulfate groups from the mucin, and A. muciniphila then breaks down and consumes the exposed mucin.

Sulfate groups attached to colonic mucin molecules normally prevent bacteria from degrading them. When too much mucin is destroyed, stool loses moisture and becomes hard and dry, causing constipation. Because the problem is mucin loss, not slow gut movement, standard laxatives and gut motility drugs are often ineffective.

Researchers have identified a two-step bacterial process driving a new type of constipation: one bacterium removes protective sulfate groups while another consumes the exposed colonic mucin. Credit: Tomonari Hamaguchi, Nagoya University

A new frontier for gut health treatment

“We genetically modified B. thetaiotaomicron so it could no longer activate the enzyme sulfatase that removes sulfate groups from mucin,” Tomonari Hamaguchi, lead author and lecturer from the Academic Research & Industry-Academia-Government Collaboration Office at Nagoya University explained.

“We put these modified bacteria into germ-free mice together with Akkermansia muciniphila, and surprisingly the mice did not develop constipation; the mucin stayed protected and intact.”

The experiment proved that blocking the sulfatase enzyme prevents the bacteria from degrading mucin. Therefore, drugs that block sulfatase could treat bacterial constipation in humans.

For millions of patients with treatment-resistant constipation, including those with Parkinson’s disease, this discovery offers hope for new therapies that address the root microbial causes of their condition.

Source: Nagoya University

Crohn’s Disease Cut Activity by 40% in Study of Time-restricted Fasting

Irritable bowel syndrome. Credit: Scientific Animations CC4.0

A new randomised controlled study funded by the Crohn’s & Colitis Foundation found that time-restricted feeding, a form of intermittent fasting, significantly reduced symptomatic disease activity and systematic inflammation in adults with Crohn’s disease and overweight or obesity. The University of Calgary-led trial is the first to show that eating only within an 8-hour window can reduce Crohn’s disease activity by 40% and abdominal discomfort by 50% in just 12 weeks, compared to a standard eating schedule.

Participants practicing intermittent fasting not only lost about 2.5kg while controls gained approximately 1.7kg, but also showed notable improvements in blood markers of inflammation and immune health, including lower levels of leptin and PAI-1 – all without cutting calories.

Results of the study were published in Gastroenterology. People with IBD should talk with their healthcare team before changing their eating schedule to determine whether intermittent fasting is appropriate for them.

Time-restricted feeding (TRF) involves eating all meals within a set 8-hour window each day, followed by fasting for the remaining 16 hours.  This 12-week randomised trial included 35 adults with Crohn’s disease and living with obesity or overweight, with 20 assigned to TRF and 15 to their regular diet. Researchers measured disease activity, inflammation, and body composition at the start and end of the study.​​

“This study shows that while weight loss is an important outcome in people with overweight and Crohn’s disease, time-restricted feeding offers additional benefits beyond just the scale,” said Maitreyi Raman, MD, Associate Professor of Medicine at the University of Calgary, the study’s senior author. “We saw meaningful improvements in disease symptoms, reduced abdominal discomfort, favourable shifts in metabolism and inflammation, and promising changes in gut bacteria – all suggesting that intermittent fasting may help patients maintain lasting remission from Crohn’s disease.”​

The research was supported by the Crohn’s & Colitis Foundation’s Litwin IBD Pioneers program. “Time-restricted feeding is showing real promise as a new way to help people with Crohn’s disease manage not only their symptoms but also their overall health,” said Andres Lorenzo Hurtado, PhD, Senior Vice President of Translational Research & IBD Ventures at the Crohn’s & Colitis Foundation. “This research suggests that changing when we eat – not just what we eat – can improve metabolism, help the immune system work better, and support long-term remission from Crohn’s disease. We are excited to support studies like this that put patients at the centre of new solutions and encourage more research to make these benefits last for everyone living with IBD.”

“People with Crohn’s disease often look for practical tools to support their health alongside medication,” said Natasha Haskey, PhD, RD, Research Associate at the University of British Columbia and lead investigator in the study. “Our research suggests time-restricted eating may be a sustainable option grounded in biology, offering patients more ways to manage their own wellness.”

In addition to reducing Crohn’s disease activity, the study found a marked decrease in harmful visceral fat and key inflammatory signals in the blood of those who practiced intermittent fasting. The changes were not simply due to diet quality or calorie restriction, as both groups ate similar foods and amounts—indicating the timing of meals themselves may play a unique role in supporting digestive and immune health.​

Researchers note that, while these results are promising, larger trials are needed to confirm the long-term safety and effectiveness of this approach for broader groups of patients with IBD.

By Rachel Peifer

Source: Crohn’s and Colitis Foundation of America