Category: Gastrointestinal

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Decades-old Puzzle Solved as Scientists Uncover Cause of IBD

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Scientists have identified the missing link between a long-known genetic signal in inflammatory bowel disease and a damaging immune response that switches off the body’s natural control of inflammation – opening the door to faster diagnosis and targeted treatment.

Interleukin-10.

Researchers at the Nuffield Department of Medicine, University of Oxford, together with Newcastle University’s Translational and Clinical Research Institute and the Department of Immunology at Cambridge University Hospitals NHS Foundation Trust, have identified an important driver of inflammatory bowel disease (IBD). This discovery reshapes understanding of IBD and opens the way to targeted approaches to diagnosis and treatment in a subset of patients. The findings suggest that inflammatory bowel disease is not a single condition, but a group of biologically distinct diseases driven by different underlying mechanisms.

In a study published in the New England Journal of Medicine, researchers analysed over 4900 patients with IBD and made two major discoveries: first, that a substantial subset of patients show autoimmune responses to one of the guardians of the immune system, interleukin-10 (IL-10), which leads to uncontrolled inflammation; and second, that this damaging immune response is the mechanism for one of the strongest known genetic risk factors for IBD.

Antibodies that block interleukin-10 (IL-10), a cell-to-cell messenger that normally acts as one of the body’s key controls on inflammation, effectively remove the immune system’s natural ‘brake’ on inflammation, allowing inflammatory responses to continue unchecked.

IBD, which includes Crohn’s disease and ulcerative colitis, affects around 500 000 people in the UK and millions worldwide. It is a lifelong condition that commonly begins in adolescence or early adulthood and can require repeated hospital treatment, long-term immunosuppressive medication and, in some cases, surgery. Despite advances in treatment, many patients cycle through multiple therapies without achieving lasting disease control – impacting their lives and costing the health care system millions.

The researchers found high levels of anti-IL10 neutralising autoantibodies in the blood of around 3.5% of IBD patients, both Crohn’s disease and ulcerative colitis, but not in healthy individuals. This could equate to 15 000-20 000 people with IBD in the UK carrying these autoantibodies.

The researchers also found that the presence of these antibodies was strongly linked to carriage of a particular genetic variant known as HLA-DRB1*01:03.

The link between HLA-DRB1*01:03 and a severe form of inflammatory bowel disease was first identified by Oxford researchers 30 years ago. The new findings show that people carrying this variant are far more likely to develop antibodies that block IL-10, helping explain how the gene contributes to disease.

The Oxford IL-10 Research GroupProfessor Holm Uhlig, a Paediatric Gastroenterologist and Director of the Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, and a senior author of the study, said: ‘We’ve suspected an important role of interleukin 10 in patients with inflammatory bowel disease for decades. The study now provides clear evidence and contributes the missing link between a well-known genetic variant that had been linked to severe inflammatory bowel disease in the past and the very recently discovered autoimmunity to interleukin 10. 

‘Understanding what drives the inflammation, provides a clear explanation for disease in this group of people and opens the door to new treatments that target the autoantibodies themselves or cells that produce those autoantibodies.’

The paper, ‘IL-10 Autoantibodies and HLA-DRB101:03 in Inflammatory Bowel Disease’, is published in the New England Journal of Medicine.

Source: University of Oxford

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Can Probiotics Help Treat Depression?

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Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health

In a pilot clinical trial published in the Journal of the American Geriatrics Society that included older adults with depression receiving standard care, adding probiotic therapy produced modest but meaningful reductions in depressive and anxiety symptoms compared with adding a placebo. However, both groups demonstrated substantial overall improvements during follow-up.

For the trial, 58 participants in India aged ≥ 60 years with moderate depression were randomised 1:1 to receive daily probiotics or a placebo for 12 weeks, alongside standard antidepressant care. They were followed up for another 12 weeks.

Based on validated psychological scores, biomarker (serum brain-derived neurotropic factor level), and faecal microbiota profiling, investigators found that probiotics helped improve patients’ symptoms but did not confer clear additional gains in quality of life compared with placebo.  The findings support probiotics as a safe, biologically plausible adjunct to standard care, but larger trials are needed.

“The results of our study are novel, and we are now planning a follow-up, larger-scale clinical trial due to the encouraging findings,” said co-corresponding author Dr. Saibal Das, MBBS, MD, DM, PhD, of the Indian Council of Medical Research – National Institute for Research in Bacterial Infections, Kolkata. “My vision is to develop affordable healthcare solutions and make them available to the larger population for meaningful public health impact,” added co–corresponding author Abhinaba Ghosh, MBBS, MSc, PhD, a physician-neuroscientist from Tata Medical Center, Kolkata.

Source: Wiley

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Cutting Out Sucrose from the Diet May Disrupt Gut Microbiome

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Photo by Sharon Mccutcheon on Unsplash

Eliminating sugar from your diet may be more detrimental than previously thought, according to an animal study being presented Saturday at ENDO 2026, the Endocrine Society’s annual meeting in Chicago, Ill.

“Completely removing sucrose from a low-fat diet may unexpectedly disrupt gut health and promote inflammation and metabolic dysfunction, highlighting that balanced nutrition is more important than simply eliminating sugar,” said Rasheed Ahmad, PhD, principal scientist and head of the Immunology & Microbiology Department at the Dasman Diabetes Institute, in Kuwait City, Kuwait. The institute was founded by Kuwait Foundation for the Advancement of Sciences. Researchers investigated the effects of a sucrose-free low-fat diet compared to a sucrose-containing low-fat control diet in two groups of mice for 16 weeks. 

They evaluated glucose tolerance, insulin sensitivity, circulating metabolic hormones, the gut microbiome and inflammation in the colon and liver.

Mice fed the sucrose-free diet developed impaired glucose control, insulin resistance, gut microbial imbalance, intestinal inflammation and fatty liver changes, despite having no significant differences in body weight compared with control mice. 

“The findings suggest that complete removal of sucrose from a low-fat diet may negatively affect gut microbiota and metabolic health,” Ahmad said. “The study highlights the importance of maintaining balanced dietary carbohydrates to support gut and immune homeostasis.” 

Until now, the consequences of restrictive diets that eliminate sugar from a low-fat diet were unknown.

“This research may influence future dietary recommendations by emphasizing the importance of maintaining a healthy gut microbiome rather than focusing only on sugar restriction,” Ahmad said. “In the long term, these findings could help improve strategies for preventing and managing metabolic disorders, fatty liver disease and chronic inflammatory conditions.”

“Studies such as this reflect our institute’s commitment to advancing evidence-based scientific discoveries that improve public health outcomes and deepen our understanding of metabolic disease,” said Faisal Hamed Al-Refaei, MD, Acting Director General of Dasman Diabetes Institute.

Source: Endocrine Society

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Why Midnight Eating Can Be a Gut Punch

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Study finds that intestinal circadian clocks become misaligned by off-schedule eating, causing gastrointestinal issues

A microscopic image shows enteric neurons (orange) and macrophages (green) in the muscularis externa of a mouse small intestine. Muscularis macrophages were among the intestinal cell types that glowed green when a key circadian clock gene called Per2 was active during UT Southwestern investigators’ research.

Eating when the body is normally asleep appears to desynchronise the circadian clocks of different cell types in the intestines, a UT Southwestern Medical Center study suggests. The findings, published in PNAS, could help explain why shift work, jet lag, and other environmental stressors that affect circadian rhythms are associated with irritable bowel syndrome, inflammatory bowel disease, constipation, and other gastrointestinal disorders.

“Understanding how intestinal circadian clocks become misaligned may ultimately guide strategies involving meal timing, circadian-based therapies, or dietary interventions to improve gastrointestinal and metabolic health,” said Yuuki Obata, PhD, Assistant Professor of Immunology and Neuroscience at UT Southwestern. Dr Obata co-led the study with Shin Yamazaki, PhD, Professor of Neuroscience.

Research in the 1990s and 2000s showed that a region of the brain known as the suprachiasmatic nucleus (SCN) acts as a master timekeeper for the body, setting various cellular processes to occur rhythmically on a 24-hour period based on cycles of light and darkness. However, in 2000, Dr Yamazaki and his colleagues showed that cells throughout the body have their own autonomous circadian clocks that are influenced both by signals from the SCN and environmental cues.

In line with this idea, research has shown that the intestines have their own rhythms that can be influenced by a variety of factors, such as timing of meals. These findings were made using whole intestinal tissue, Dr Obata explained, but the intestines contain a variety of cell types – including muscle, nerve, and immune cells. It’s been unclear whether each of these populations has its own circadian clock and if they run on the same schedule.

To find out, Drs Obata and Yamazaki monitored novel mice with set 12-hour cycles of light and dark. They were engineered by Joseph Takahashi, PhD, Chair and Professor of Neuroscience at UT Southwestern, and his colleagues in the Takahashi Lab. Five intestinal cell types – enteric neurons, enteric glial cells, interstitial cells of Cajal (ICCs), smooth muscle cells, and muscularis macrophages – glowed green when a key circadian clock gene called Per2 was active. Although food was available at all times, the mice ate about 80% of their meals at night due to their nocturnal nature.

After about a week in this environment, the researchers observed intestinal cells glowing green at approximately the same times, suggesting the different cell populations had their own autonomous circadian clocks that cycled in sync. But when the researchers made food available only for four hours in the daytime – forcing the mice to eat at abnormal times – Per2 activity shifted to match this new rhythm in every cell population except for the ICCs. These cells resisted changes to their circadian clock, staying out of sync with the other cell types for weeks.

Such asynchrony may also occur in people who eat outside the body’s usual circadian rhythms, such as night shift workers or those who fly to different time zones. Because ICCs play a key role in intestinal motility, their resistance to adapt to a changed circadian clock could affect digestive and metabolic function.

Finding a way to synchronise the different intestinal cell populations through diet, probiotics, or drugs could eventually help ease the gastrointestinal problems associated with altered circadian timing, the researchers said.

Source: UT Southwestern Medical Center

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Promising Molecule for Coeliac Targets Gluten in the Stomach

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Photo by Mariana Kurnyk

A research project led by the Institute for Research in Nutrition and Food Safety (INSA) and the Faculty of Pharmacy and Food Sciences at the University of Barcelona, together with the Molecular Biology Institute of Barcelona (IBMB) of the CSIC (which stands for Consejo Superior de Investigaciones Científicas), has successfully designed and tested a gluten-degrading molecule that is a promising ally in the management of coeliac disease, an autoimmune disease whose symptoms are triggered by the consumption of gluten and other prolamins found in cereals. At present, there is a complete lack of treatment options beyond a diet free from gluten, which is difficult to maintain in Western societies where diets rely heavily on wheat products.

The major breakthrough is that the molecule is effective at very low concentrations and at a pH of 2 (the pH of the stomach) a condition that none of the molecules currently available or under development had previously achieved with efficiency. Although some of them are marketed as nutritional supplements, they are not an effective alternative to gluten-free diets.

The study has been published in the journal EMBO Molecular Medicine ahead of the International Day of Coeliac Disease on 16 May and is led by researchers Francisco J. Pérez-Cano (INSA-UB), and F. Xavier Gomis-Rüth (IBMB-CSIC). The co-first authors are Marina Girbal-González and Arturo Rodríguez-Banqueri (INSA-UB and IBMB-CSIC, respectively). Teams from the Institute for Food Science Research (CSIC-UAM), the University of Salzburg (Austria) and the Technical University of Munich (Germany) have also participated.

Counteracting the ‘trigger’ of coeliac disease

The trigger for coeliac disease are the prolamins, proteins found in most common cereals in our diet, such as wheat gluten. When these are digested in the stomach, they break down into smaller fragments (peptides). Some of these can be toxic, such as the gluten immunogenic peptides (GIPs), which can withstand the stomach’s gastric acids and reach the small intestine. Among these, one of the most immunogenic is the the ‘33-mer’, a fragment of the α-gliadin in wheat gluten that is highly immunogenic.

This poses a problem for people with coeliac disease, because once in the small intestine, the 33-mer and other GIPs bind particularly easily to a receptor of the immune system (the human leukocyte antigen, or HLA), triggering the inflammatory autoimmune response that causes the characteristic symptoms of the disease.

The results demonstrate that celiacase, a molecule stable in the stomach environment, could be an adjunctive therapeutic candidate to support a gluten-free diet.

Four years ago, the Proteolysis Group at IBMB-CSIC, led by F. Xavier Gomis-Rüth, described in an article in Nature Communications that nephrosin – a molecule found naturally in the digestive juices of the carnivorous plant Nepenthes ventrata – was capable of cleaving GIPs, building on results from the group of David Schriemer from the University of Alberta in Canada. In collaboration with the Autoimmunity, Immunonutrition and Tolerance Group at the UB’s Faculty of Pharmacy and Food Sciences, led by Professor Francisco José Pérez-Cano, they demonstrated that nephrosin can degrade the 33-mer peptide and other GIPs before they reach the intestine, thereby potentially preventing this autoimmune inflammatory response.

Designed using molecular engineering

In this study, the team has designed and tested a molecule based on nephrosin. Named celiacase, this new molecule exhibits its maximum activity at the gastric pH of the stomach, where, in synergy with the pepsin in our digestive system, it breaks down the GIPs in cereals and the gliadin in wheat before they pass into the duodenum.

“There are other proteases, generically termed glutenases, which break down gluten, but they are not fully active at pH 2 – the pH of the stomach – but rather at pH 7 – the pH of the duodenum – when the bolus has already left the stomach,” explains Gomis-Rüth. “Therefore, it is necessary to increase the doses to levels that make them unviable for therapeutic use.”

The team has tested the molecule in vivo using a mouse model developed by the University of Chicago, which is currently the model that most accurately replicates coeliac disease. The results show that celiacase is effective at very low doses, being able to mitigate the symptoms of the disease in gluten-fed mice, even at high gluten intake levels. “Intestinal atrophy, inflammation, the antibody response and dysbiosis – that is, the alteration in the composition of the microbiota – were reduced,” says Pérez-Cano. “Furthermore, immunoregulatory markers were restored to normal levels, as were microbial metabolic pathways.”

Another advantage of celiacase is that it is no longer active once it reaches the duodenum. “Once it has accomplished its function, there is no need for it to remain active, so that it does not interfere with other proteins in the body,” adds Gomis-Rüth.

The molecule and its potential applications have been patented, and the team is taking the first steps towards setting up a spin-off company and taking the development to more advanced stages.

This study has been partially funded by programmes run by the Ministry of Science and Innovation, the Government of Catalonia’s Agency for Management of University and Grants (AGAUR) AGAUR, the Catalan Coeliac Association, and the CSIC’s Conexión Trigo network.

Video

Source: University of Barcelona

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Head Impacts Associated with Altered Gut Microbiome in Football Players

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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 symptoms – are 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

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Some Common IBS Treatments Linked to Higher Risk of Death

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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

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

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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

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The Gut’s Connection to Healing Traumatic Brain Injuries

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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 Biology, Houston 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

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

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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