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What is Crohn’s disease?

Crohn’s disease (CD) is a type of inflammatory bowel disease (IBD) characterized by patches of inflammation in the digestive tract surrounded by normal mucosa.1 Crohn’s disease can affect the entire gastrointestinal tract – from mouth to anus – though it is more commonly associated with the colon and terminal ileum. While another type of IBD, ulcerative colitis (UC), can also cause inflammation of the gastrointestinal tract, UC is always limited to the colon and rectum.

According to the Center for Disease Control and Prevention (CDC), three million American adults reported a diagnosis of IBD in 2015.2 CD prevalence is highest in Europe (322 per 100,000), Canada (319 per 100,000), and the USA (214 per 100,000).3

Crohn’s is a chronic (long-term) disease and commonly diagnosed in patients between 15 to 35 years old. Patients may have prolonged periods of asymptomatic remission. Though there is no way to predict when symptoms will reappear, well-controlled symptoms can allow a patient to live normally.4

In the gastrointestinal tract, mucosa refers to the innermost layer, directly surrounding the open space within the tube.

What are the common symptoms?

Symptoms of Crohn’s disease can fluctuate from mild to severe, and usually manifest gradually. When the disease is active, symptoms may include5:

  • Abdominal pain
  • Abscesses
  • Cramping
  • Diarrhea
  • Fatigue
  • Fever
  • Hair loss
  • Oral problems
  • Reduced appetite
  • Weight loss

Crohn’s disease does not necessarily manifest with all symptoms at once. Patients may have periods of active illness (known as “flares”) followed by periods of remission in which the symptoms decrease or even disappear.

 What are the causes?

The exact cause of Crohn’s disease is unknown, but it may be a type of autoimmune disease in which the human body’s immune system attacks the lining of its digestive tract, causing inflammation. Genetic, environmental, immunological, and bacterial factors may all affect the development of the disease.6,7

Prevalence of Crohn’s varies greatly by region, environment, and ethnic group. For example, the annual incidence in North America is reported to be 3.1–20.2 per 100,000, while in the Asia-Pacific region it is estimated to be around 0.54 per 100,000. Incidence of CD is also higher in Ashkenazi Jews, urban populations, and in people living at northern latitudes.8

Crohn’s disease may be associated with:

  • Antibiotic use during childhood, suggesting that the microbiota of the intestinal tract could help establish healthy immune system activity1
  • Changes to the gut microbiome5
  • Cigarette smoking8
  • Diet, such as a low-fiber, high-carbohydrate diet8
  • Disruptions to the intestinal mucosa5
  • Medications, such as non-steroidal anti-inflammatory drugs (NSAIDs)8
  • Family history5

In other words, Crohn’s is a complex disease without a clear cause, which may have a microbiome-related component in susceptible individuals.7

is a condition in which your immune system mistakenly attacks your own body. The basis is the immune system’s failure to distinguish self from non-self, often termed ‘loss of tolerance’.20

How does this topic relate to my microbiome?

The intestinal microbiota may play a significant role in the development of Crohn’s disease.9 Although the precise mechanisms through which bacteria contribute to the disease are not completely understood, we know that Crohn’s patients’ microbiomes fluctuate more than those of healthy individuals.10 Many patients with IBD show an imbalance in the bacterial population of their gut microbiota – characterized by a reduction in their diversity – and this difference is especially notable in patients with Crohn’s disease.7,11

Some microorganisms have been proposed as triggers in the development of Crohn’s disease. For example, adherent–invasive Escherichia coli (AIEC), has been suggested as a potential pathogen in IBD,7 and has been identified in 22% of patients with Crohn’s disease.12 Other bacteria, like Faecalibacterium prausnitzii, have been detected more frequently in healthy people than in IBD patients.7

The gut microbiota is the microbial community inhabiting the intestinal tract.

Adherent-invasive Escherichia coli (AIEC) is a variant of the commonly distributed pathogen E. coli, and is capable of colonizing the intestinal mucosa by adhering and invading intestinal epithelial cells.12

Which diseases/topics are related to Crohn’s disease?

Crohn’s disease is a systemic illness that has been associated with multiple extraintestinal complications. These include13,14,15,16:

  • Anxiety
  • Arthritis
  • Depression
  • Osteoporosis
  • Primary sclerosing cholangitis
  • Renal stones
  • Secondary amyloidosis
  • Skin disorders
  • Venous and arterial thromboembolism
  • Vitamin B12 deficiency

Primary sclerosing cholangitis is a chronic liver disease defined by a progressive obstruction of the normal flow of bile. It is associated with inflammation and fibrosis of the biliary ducts.21

Amyloidosis refers to a group of diseases in which an abnormal amount of protein accumulates in body tissues. Secondary amyloidosis occurs when amyloidosis results from inflammation.22

How can I take action?

If you are experiencing changes in your bowel habits or have symptoms of Crohn’s disease, it’s important to consult your doctor. Your doctor can then conduct tests to check for Crohn’s. CD diagnosis is based on medical history, physical examinations, and imaging examinations. Tests and procedures can be ordered, including:

  • Blood or stool tests
  • Endoscopy or colonoscopy
  • Imaging procedures

Once diagnosed, the activity, severity, and extent of CD should be evaluated to adequately manage progression, intervention, and remission. Treatment may include medications, changes in lifestyle, probiotics, intervention treatments, and pain management.17,18,19


1. Ni, J., Wu, G. D., Albenberg, L., & Tomov, V. T. (2017). Gut microbiota and IBD: causation or correlation? Nature Reviews Gastroenterology & Hepatology, 14(10), 573–584.

2. Dahlhamer, J. M., Zammitti, E. P., Ward, B. W., Wheaton, A. G., & Croft, J. B. (2016). Prevalence of Inflammatory Bowel Disease Among Adults Aged ≥18 Years — United States, 2015. Morbidity and Mortality Weekly Report, 65(42), 1166–1169.

3. Torres, J., Mehandru, S., Colombel, J.-F., & Peyrin-Biroulet, L. (2017). Crohn’s disease. The Lancet, 389(10080), 1741–1755.

4. Molodecky, N. A., et al. (2012). Increasing Incidence and Prevalence of the Inflammatory Bowel Diseases With Time, Based on Systematic Review. Gastroenterology, 142(1), 46–54.e42.

5. Feuerstein, J. D., & Cheifetz, A. S. (2017). Crohn Disease: Epidemiology, Diagnosis, and Management. Mayo Clinic Proceedings, 92(7), 1088–1103.

6. Zhang, Y.-Z., Li, Y.-Y (2014). Inflammatory bowel disease: Pathogenesis. World Journal of Gastroenterology, 20(1), 91–99.

7. Ananthakrishnan, A. N. (2015). Epidemiology and risk factors for IBD. Nature Reviews Gastroenterology & Hepatology, 12(4), 205–217.

8. Gajendran, M., Loganathan, P., Catinella, A. P., & Hashash, J. G. (2018). A comprehensive review and update on Crohn’s disease. Disease-a-Month, 64(2), 20–57.

9. Alhagamhmad, M. H., Day, A. S., Lemberg, D. A., & Leach, S. T. (2016). An overview of the bacterial contribution to Crohn disease pathogenesis. Journal of Medical Microbiology, 65(10), 1049–1059.

10. Halfvarson, J., et al. (2017). Dynamics of the human gut microbiome in inflammatory bowel disease. Nature Microbiology, 2(5), 17004.

11. Gevers, D., et al. (2014). The Treatment-Naive Microbiome in New-Onset Crohn’s Disease. Cell Host & Microbe, 15(3), 382–392.

12. Darfeuille-Michaud, A., et al. (2004). High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology, 127(2), 412–421.

13. Bähler, C., Schoepfer, A. M., Vavricka, S. R., Brüngger, B., & Reich, O. (2017). Chronic comorbidities associated with inflammatory bowel disease. European Journal of Gastroenterology & Hepatology, 29(8), 916–925.

14. López-San Román, A., & Muñoz, F. (2011). Comorbidity in inflammatory bowel disease. World Journal of Gastroenterology, 17(22), 2723–2733.

15. Cucino, C., & Sonnenberg, A. (2001). The comorbid occurrence of other diagnoses in patients with ulcerative colitis and Crohn’s disease. American Journal of Gastroenterology, 96(7), 2107–2112.

16. Headstrom, P. D., Rulyak, S. J., & Lee, S. D. (2008). Prevalence of and risk factors for vitamin B12 deficiency in patients with Crohnʼs disease. Inflammatory Bowel Diseases, 14(2), 217–223.

17. Matsuoka, K., et al. (2018). Evidence-based clinical practice guidelines for inflammatory bowel disease. Journal of Gastroenterology, 53(3), 305–353.

18. Carter, M. J. (2004). Guidelines for the management of inflammatory bowel disease in adults. Gut, 53(suppl_5), v1–v16.

19. Crohn’s & Colitis Foundation. Diagnosing and Managing IBD. (2011)

20. Wang, L., Wang, F.-S., & Gershwin, M. E. (2015). Human autoimmune diseases: a comprehensive update. Journal of Internal Medicine, 278(4), 369–395.

21. Hirschfield, G. M., Karlsen, T. H., Lindor, K. D., & Adams, D. H. (2013). Primary sclerosing cholangitis. The Lancet, 382(9904), 1587–1599.

22. Ebert, E. C., & Nagar, M. (2008). Gastrointestinal Manifestations of Amyloidosis. The American Journal of Gastroenterology, 103(3), 776–787.