Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Eat for Gut Health: Dietary patterns rich in fiber, fermented foods, omega-3 fats, and plant polyphenols are associated with better gut health and may help maintain UC remission, though diet is not a substitute for prescribed therapy. Ultra-processed and high-sugar foods are linked to higher IBD risk. During an active flare a temporary low-residue diet may ease symptoms, but over the long term dietary diversity supports the microbiome. NIDDK
Manage Stress Actively: Psychological stress is associated with UC flares through the gut-brain axis and stress-related immune and microbiome changes, though it is one of several contributors rather than a sole cause. Regular stress management - exercise, mindfulness, sleep, and therapy when needed - is linked to fewer flares and better quality of life. Frontiers in Immunology (PMC)
Support Gut Microbiome Health: People with UC tend to have reduced microbial diversity and fewer butyrate-producing bacteria, though it is not settled whether this is a cause or a consequence of inflammation. A diverse, plant-rich diet and avoiding unnecessary antibiotics support the microbiome. The probiotic E. coli Nissle 1917 has evidence for maintaining remission comparable to mesalazine; discuss any probiotic with your clinician before starting. PubMed
Be Cautious With Anti-Inflammatory Painkillers: Non-steroidal anti-inflammatory painkillers such as ibuprofen and naproxen are often suggested as something for people with UC to limit, since they may aggravate symptoms. The evidence is genuinely mixed, and a meta-analysis found no consistent association with flares, so this is worth discussing rather than assuming it applies to you. NIDDK
How much of this is genetic?
Genetics explains 50% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Grännö et al. 2026, J Crohns Colitis
Background and further reading
Ulcerative colitis (UC) is a chronic inflammatory bowel disease marked by continuous, superficial (mucosal) inflammation of the colon and rectum. It almost always begins at the rectum and extends proximally without skip lesions. This distinguishes it from Crohn's disease, which can affect any part of the gut in a patchy pattern and inflames the full thickness of the bowel wall. Typical symptoms are bloody diarrhea, urgency, tenesmus, abdominal pain, and fatigue. An estimated 5 million people live with UC worldwide, and incidence has risen with industrialization, with the highest burden in Western countries.[1] UC is not curable but is usually controlled with medication; for severe or refractory disease, removing the colon (colectomy) is a definitive surgical option.
Genetic Basis: UC is heritable but less so than Crohn's: twin studies estimate UC heritability of liability around 50-67% (with monozygotic-twin concordance near 15-19%), still below the figure for Crohn's, where heritability runs roughly 75%.[2] Large international IBD genome-wide association studies have mapped roughly 240 risk loci, most shared between UC and Crohn's, though some are disease-specific.[3][4] The HLA region on chromosome 6 carries the strongest single association for UC, far larger than any other locus.[3] UC-specific signals point to the epithelial barrier (HNF4A, the E-cadherin gene CDH1, and LAMB1), alongside shared immune pathways such as IL-23/Th17 and IL-10 anti-inflammatory signaling.[5] Common variants explain only a minority of UC risk, leaving a large role for environment and the gut microbiome.
Environmental Factors: UC has a striking and well-replicated link to smoking: current smokers have a lower risk of UC than non-smokers, the opposite of the pattern seen in Crohn's.[6] This is a biological observation, not a recommendation, the overall harms of smoking vastly outweigh any effect on UC. Appendectomy, particularly when done for true appendicitis at a young age, is likewise associated with lower UC risk.[7] Other associations include a Westernized, low-fiber diet, antibiotic exposure, and the gut microbiome, which in UC tends to show reduced bacterial diversity and depletion of butyrate-producing species such as Faecalibacterium prausnitzii and Roseburia. Because these are largely observational links, they describe correlations rather than proven causes, and UC's geographic distribution tracks closely with industrialization.
The published research behind your score, and the variants it draws on.
3 published scores from 2 studies
The ulcerative colitis score combines 3 polygenic scores drawn from 2 published studies.
Le Berre C, et al. Ulcerative colitis. The Lancet (2023)
These traits are influenced by some of the same genes and variants as this one
Crohn's Disease: Chronic inflammatory bowel disease affecting the digestive tract lining.
Content updated August 2026.
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