- A new study notes that higher levels of a routine stool test marker of gut inflammation is strongly associated with an increased risk of inflammatory bowel disease (IBD) flares, even when people were symptom-free.
- Elevated levels of this marker could predict both symptom-based and clinically confirmed IBD flares up to 2 years before they occurred, highlighting its potential value as an early warning tool.
- Additionally, the findings linked dietary meat intake to a higher risk of ulcerative colitis flares, an association not seen in Crohn’s disease.
- However, other dietary factors were not consistently associated with flare risk, challenging some common assumptions about diet and IBD.
Inflammatory bowel disease (IBD) describes a group of chronic, long-term conditions involving inflammation of the gastrointestinal tract, primarily comprising Crohn’s disease and ulcerative colitis.
The prevalence of IBD is rising, and current estimates suggest it affects between
An IBD flare occurs when symptoms develop due to active bowel inflammation. However, people may experience an increase in symptoms without necessarily having inflammation. Thus, the condition involves unpredictable periods of remission and debilitating symptom flares.
Research into the role diet plays in IBD flares is complex and strong evidence linking dietary patterns to flare risk has been limited.
Stool tests offer a noninvasive option to help diagnose IBD. Typically, they measure a protein known as calprotectin to indicate gut inflammation and help distinguish from noninflammatory conditions. Levels of this protein can also help monitor disease activity or treatment effectiveness
A new study, published in Gut, suggests that combining stool tests with dietary information could help forecast disease flares months before symptoms appear.
Led by scientists at the University of Edinburgh’s Institute of Genetics and Cancer, the findings offer fresh insights into how biomarkers and lifestyle factors could be used to personalise IBD care.
The study, known as PREdiCCt, involved more than 2,600 people with IBD. Participants were recruited from 47 National Health Service (NHS) centres across the UK between 2016 and 2020 while in remission.
At the outset, participants completed detailed food frequency questionnaires and provided clinical data including blood tests and a stool sample for fecal calprotectin.
The researchers followed the group for a median of 4 years, documenting both self-reported symptom flares and “objective” flares confirmed by clinical tests and treatment escalation.
The findings revealed that higher baselines of fecal calprotectin, even in the absence of symptoms, were strongly linked to future disease flares.
Among those with ulcerative colitis, individuals with elevated calprotectin levels had an objective flare risk of roughly 34% within 2 years, compared with approximately 11% for those with low levels.
Elena Rolt, MSc, DipION, IFMCP, nutritional therapist at health.miro, told Medical News Today that these results could push IBD care further toward proactive, biomarker‑guided management rather than waiting for symptoms to worsen.
Rolt, who was not involved in the research, added that this study could help to develop a tool to stratify individuals into different risk groups depending on their fecal calprotectin levels.
“The paper already combines fecal calprotectin with habitual diet, notably meat intake in [ulcerative colitis], and clinical characteristics to model flare risk, which is a step toward a formal risk calculator […] In practice, this could look like an online or app‑based calculator embedded in hospital systems, giving both patient and clinician a visual risk ‘score’ and a personalised plan.”
– Elena Rolt, MSc, DipION, IFMCP
Beyond biomarkers, the researchers also explored habitual dietary patterns.
They found that individuals with ulcerative colitis who ranked in the highest group for meat consumption had nearly double the risk of an objective flare compared with those who ate the least amount of meat.
However, this association was not observed in participants with Crohn’s disease.
Additionally, the researchers found no consistent links between flare risk and intake of fiber, ultra-processed foods, polyunsturated fats, or alcohol.
Charlie Lees, PhD, a gastroenterologist at the University of Edinburgh and senior author of the study, noted in a press release that:
“This major study is the first of its kind to properly track the relationship between habitual diet and disease flares in such a large, prospective way. It has been a massive team effort over the past decade to recruit and follow more than 2,600 people living with IBD across the UK.”
However, it is important to caution that this was an observational study. This means that the researchers cannot establish that eating meat directly causes disease flares.
Rolt also noted that these findings are likely to hold in other countries, even where diet and healthcare organisations may differ. However, the absolute risk and influence of diet and treatment may shift.
“[T]he main message — ‘raised FC in remission predicts trouble ahead’ –—is probably broadly generalizable, but specific risk percentages and meat‑related findings may need local validation in non‑U.K. cohorts before being fully adopted into practice elsewhere,” she told us.
Nevertheless, the results support future clinical trials to investigate whether dietary changes, alongside routine biomarker monitoring, may help to prevent flares, particularly in ulcerative colitis.
Tracking the relationship between habitual dietary patterns and disease flares could help to provide a new framework for IBD management.
In a press release, Lees added:
“Our results provide a new framework for management: using objective biomarkers to catch subclinical inflammation early and identifying specific dietary factors that may help prevent debilitating relapses. This is exactly the kind of personalised evidence-base we need to improve the lives of people living with Crohn’s and colitis.”
Using the objective biomarkers to catch subclinical inflammation early, and identifying specific dietary factors could help to prevent debilitating relapses.
Rolt further noted that it is important for clinicians to communicate that these findings support a nuanced, collaborative framework, rather than following a rigid rule.
“Because diet responses are individual, we would use this as a reason to experiment with lowering meat – especially processed and red meat – and watching your symptoms and calprotectin over time, rather than imposing a one‑size‑fits‑all ban,” she advised.
