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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Crohn's disease risk factors

Introduction

Overview

Overview

Crohn’s disease (CD) develops in genetically susceptible individuals through the interaction of inherited risk, environmental exposures, and gut microbial dysbiosis. No single factor is necessary or sufficient to cause disease.[1][2][3] The strongest risk factor is a first-degree relative with CD. The most important modifiable risk factor is cigarette smoking.[1][4] Other established risk factors include childhood antibiotic exposure, appendectomy, urban residence, and an industrialized (“Western”) lifestyle and diet. Breastfeeding and physical activity are associated with lower risk.[5] Most environmental associations come from observational data, and causality has not been established for most of them.[5]

Risk Factors

Risk Factors

Nonmodifiable risk factors

  • Family history is the single strongest risk factor. Having a first-degree relative with CD carries an incidence rate ratio of about 7.8. The risk is higher in relatives of patients with childhood-onset disease (OR ~10.6). About 8–12% of patients report a positive family history.[1][6][7]
  • Twin concordance for CD is about 30–50% in monozygotic twins, compared with about 4% in dizygotic twins and about 15% in monozygotic twins for ulcerative colitis (UC). This reflects a substantial but incomplete genetic contribution.[8][6]
  • Polygenic susceptibility:
    • Genome-wide association studies have identified more than 200–240 susceptibility loci. Together these explain only about 13.6% of CD variance, and most loci carry modest effects (OR 1.1–1.2).[8][6]
    • Higher-impact genes include NOD2 (CARD15) and ATG16L1, which are CD-specific and impair bacterial sensing and autophagy. IL23R is shared with UC.[8][2]
    • Risk variants are ancestry-specific. NOD2, ATG16L1, and IL23R coding variants predominate in White populations and are essentially absent in East Asian cohorts, where TNFSF15 is the dominant CD locus.[8]
  • Age: incidence peaks at 15–25 years, although CD occurs at all ages.[4]
  • Geography and industrialization: CD is most common in industrialized countries. North American incidence is 6.3–23.8 per 100,000 person-years.[4] Incidence is rising rapidly in newly industrialized regions such as Brazil, Taiwan, and East and South Asia. Among immigrants to high-incidence countries, younger age at immigration is associated with higher risk.[3][7]

Modifiable environmental and lifestyle risk factors

Risk factor Estimated effect size
Cigarette smoking OR 1.76
Antibiotic exposure (especially in childhood) OR ~1.74
Appendectomy and tonsillectomy Increased risk
Urban residence OR ~1.42 (Western populations)
Ultra-processed food intake HR 1.82 for ≥5 servings/day
Western dietary pattern (high saturated or animal fat, sugar, soft drinks; low fiber) Soft drinks OR ~1.56
Oral contraceptives OR ~1.31 ( Western populations)
Cesarean delivery OR ~1.16 (Western cohorts)
Vitamin D deficiency Increased risk
Enterohepatic non-pylori Helicobacter and Campylobacter species Increased risk

Protective factors

  • The following exposures are associated with lower CD risk:[1][5][9]

Gut microbiome

  • Dysbiosis is a consistent correlate of CD. It includes reduced microbial diversity, depletion of Firmicutes such as Faecalibacterium prausnitzii, and expansion of Proteobacteria, including adherent-invasive Escherichia coli. No single causative organism has been identified.[2][10][11]
References

References

  1. ↑ 1.0 1.1 1.2 1.3 Dolinger M, Torres J, Vermeire S (2024). “Crohn’s disease”. Lancet. 403 (10432): 1177–1191. doi:10.1016/S0140-6736(23)02586-2.
  2. ↑ 2.0 2.1 2.2 Kennedy MS, Chang EB (2025). “Emerging concepts and shifting paradigms for understanding the microbial basis of inflammatory bowel diseases”. J Clin Invest. 135 (17): e193969. doi:10.1172/JCI193969.
  3. ↑ 3.0 3.1 Xue M, Leibovitzh H, Jingcheng S; et al. (2024). “Environmental factors associated with risk of Crohn’s disease development in the Crohn’s and Colitis Canada – Genetic, Environmental, Microbial Project”. Clin Gastroenterol Hepatol. 22 (9): 1889–1897.e12. doi:10.1016/j.cgh.2024.03.049.
  4. ↑ 4.0 4.1 4.2 Cushing K, Higgins PDR (2021). “Management of Crohn disease: a review”. JAMA. 325 (1): 69–80. doi:10.1001/jama.2020.18936.
  5. ↑ 5.0 5.1 5.2 Piovani D, Danese S, Peyrin-Biroulet L; et al. (2019). “Environmental risk factors for inflammatory bowel diseases: an umbrella review of meta-analyses”. Gastroenterology. 157 (3): 647–659.e4. doi:10.1053/j.gastro.2019.04.016.
  6. ↑ 6.0 6.1 6.2 Noble AJ, Nowak JK, Adams AT, Uhlig HH, Satsangi J (2023). “Defining interactions between the genome, epigenome, and the environment in inflammatory bowel disease: progress and prospects”. Gastroenterology. 165 (1): 44–60.e2. doi:10.1053/j.gastro.2023.03.238.
  7. ↑ 7.0 7.1 Tao Y, Li Y, Zhou T; et al. (2025). “Etiological mechanisms underlying the hazard factors and inflammatory bowel disease: a prospective cohort study”. Sci Rep. 15 (1): 23517. doi:10.1038/s41598-025-08744-2.
  8. ↑ 8.0 8.1 8.2 8.3 Roda G, Chien Ng S, Kotze PG; et al. (2020). “Crohn’s disease”. Nat Rev Dis Primers. 6 (1): 22. doi:10.1038/s41572-020-0156-2.
  9. ↑ Ananthakrishnan AN, Bernstein CN, Iliopoulos D; et al. (2018). “Environmental triggers in IBD: a review of progress and evidence”. Nat Rev Gastroenterol Hepatol. 15 (1): 39–49. doi:10.1038/nrgastro.2017.136.
  10. ↑ Adolph TE, Zhang J (2022). “Diet fuelling inflammatory bowel diseases: preclinical and clinical concepts”. Gut. 71 (12): 2574–2586. doi:10.1136/gutjnl-2021-326575.
  11. ↑ Godny L, Elial-Fatal S, Arrouasse J; et al. (2025). “Mechanistic implications of the Mediterranean diet in patients with newly diagnosed Crohn’s disease: multiomic results from a prospective cohort”. Gastroenterology. 168 (5): 952–964.e2. doi:10.1053/j.gastro.2024.12.031.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Fahad Hasan, M.D.[2] Aditya Ganti M.B.B.S. [3]