The Prevention and Treatment of Crohn’s Disease with a Vegetarian Diet


The physician will already know that Crohn’s disease is difficult to treat and can be frustrating for both the patient and their physician. Safer and more efficacious treatments are needed for this disease.

The current standard treatment for Crohn’s disease involves medication to manage symptoms and induce remission, and when necessary, bowel resection. Medications used in the treatment of Crohn’s disease include the following:

  • 5-Aminosalicylic acid derivative agents (eg. mesalamine rectal, mesalamine, balsalazide)
  • Corticosteroids (eg. prednisone, methylprednisolone, budesonide)
  • Immunosuppressive agents (eg. mercaptopurine, methotrexate, tacrolimus)
  • Monoclonal antibodies (eg. infliximab, adalimumab, certolizumab pegol, natalizumab, vedolizumab)
  • Antibiotics (eg. metronidazole, ciprofloxacin)
  • Antidiarrheal agents (eg. loperamide, diphenoxylate-atropine)
  • Bile acid sequestrants (eg. cholestyramine, colestipol)
  • Anticholinergic agents (eg. dicyclomine, hyoscyamine, propantheline)

These medications, though efficacious to a degree, all have significant adverse reactions. Many of these medications will also be contraindicated in a significant number of patients.

Most patients with Crohn’s disease require surgical intervention during their lifetime, as it plays an integral role in controlling the symptoms and treating the complications of Crohn’s disease, but operative resection is not curative. Because of the high rate of disease recurrence after segmental bowel resection, the guiding principle of surgical management of Crohn’s disease is preservation of intestinal length and function. (1)

Mean annual costs for Crohn’s disease are about $8265. 31% of costs were attributable to hospitalization, 33% to outpatient care, and 35% to pharmaceutical claims. The annual dollar cost for Crohn’s disease in the United States is $3.6 billion. (2) It can reasonably be concluded that Crohn’s is both difficult and expensive to treat.

Symptoms of Crohn’s disease may subside with total parenteral nutrition or total enteral nutrition. But Crohn’s disease is well known to flare up after the resumption of meals. Therefore, the food in patient’s meals are thought to be an etiologic factor in gut inflammation. (3)

While parenteral nutrition is possible, nutrition taken orally is to be preferred if it won’t cause a flare up, or even better, if it can prevent flare ups and induce remission. This is what a vegetarian diet seems to accomplish.


The etiology of Crohn’s disease is unknown. Genetic, microbial, immunologic, environmental, dietary, vascular, and psychosocial factors have been implicated, as have smoking and the use of oral contraceptives and nonsteroidal anti-inflammatory agents (NSAIDs).

Epidemiology shows that IBD is prevalent in wealthy nations (4, 5, 6) where dietary westernization inevitably occurs (7, 8). Dietary westernization is characterized by increased consumption of animal protein, animal fat, and sugar. Diets rich in animal protein and animal fat cause a decrease in beneficial bacteria in the intestine (9, 10).

However, the risk of Crohn’s disease was found to be reduced by 70% in females and 80% in males following a vegetarian diet. (11)


Treatment is aimed at inducing remission.  An important and well-designed study using a semi-vegetarian diet, achieved a 100% remission rate at 1 year and 92% at 2 years. (12)

Plant-based dietary patterns may promote a more favorable gut microbial profile. Such diets are high in dietary fiber and fermentable substrate (i.e. non digestible or undigested carbohydrates), which are sources of metabolic fuel for gut microbial fermentation and, in turn, result in end products that may be used by the host (i.e. short chain fatty acids such as butyrate). These end products may have direct or indirect effects on modulating the health of their host. (13)

The naturally occurring substances in plant foods having anti-inflammatory bowel actions include phytochemicals, antioxidants, microorganisms, dietary fibers, and lipids. The literature indicates that many of these natural products exert their beneficial action by altering cytokine production. Specifically, phytochemicals such as polyphenols or flavonoids are the most abundant, naturally occurring anti-inflammatory substances. The effects of lipids are primarily related to the n-3 polyunsaturated fatty acids. The effects of phytochemicals are associated with modulating the levels of tumor necrosis factor α (TNF-α), interleukin (IL)-1, IL-6, inducible nitric oxide synthase, and myeloperoxide. The anti-IBD effects of dietary fiber are mainly mediated via peroxisome proliferator-activated receptor-γ, TNF-α, nitric oxide, and IL-2, whereas the effects of lactic acid bacteria are reported to influence interferon-γ, IL-6, IL-12, TNF-α, and nuclear factor-κ light-chain enhancer of activated B cells. These results suggest that the anti-IBD effects exhibited by natural products are mainly caused by their ability to modulate cytokine production. (14)

Studies, conducted using in vivo and in vitro models, provide evidence that pure polyphenolic compounds and natural polyphenolic plant extracts can modulate intestinal inflammation. (15)  Polyphenols may thus be considered able to prevent or delay the progression of Crohn’s disease, especially because they reach higher concentrations in the gut than in other tissues. (16)

While not perfect, of all the laboratory markers, C-Reactive Protein (CRP) is the most studied and has been shown to have the best overall performance. CRP is an objective marker of inflammation and correlates well with disease activity in Crohn’s disease. (17)  It is produced as an acute phase reactant predominantly in the liver, in response to stimulation by interleukin (IL)-6, TNF-α and IL-1β, which are produced at the site of inflammation. (18)

Adipocytes in hypertrophied mesenteric adipose tissue produce and secrete significant amounts of adiponectin, which may be involved in the regulation of intestinal inflammation associated with Crohn’s disease. Furthermore, adiponectin concentrations in hypertrophied mesenteric adipose tissues of Crohn’s disease patients correlated inversely with serum CRP levels (r = −0.51, p = 0.015) (19)  There is a good correlation between CRP and other measures of inflammation such as the Crohn’s Disease Activity Index, radioactive labelled fecal granulocyte excretion and fecal calprotectin. (20, 21, 22)

Vegetarian diets have been shown to increase adiponectin in diabetics, and reduce CRP in both diabetics and patients with coronary artery disease, and may well be doing the same in Crohn’s disease patients. (23, 24, 25)  This improved profile of cytokines may be part of the therapeutic efficacy of vegetarian diets in Crohn’s disease.


To put the efficacy of a vegetarian diet into perspective one must compare it to standard treatments. Overall, despite the use of oral mesalamine treatment in the past, new evidence suggests that this approach is minimally effective as compared with a placebo, and less effective than budesonide or conventional corticosteroids.  Induction of remission was noted in 52% of Crohn’s disease patients.

Maintenance of remission was reported in 71% of Crohn’s disease patients on azathioprine over a 6-month to 2-year period. Induction and maintenance of remission was noted in 70% of Crohn’s disease patients on methotrexate over a 40-week period. Induction of remission was reported in 32%, 26%, and 20% of Crohn’s Disease patients on infliximab, adalimumab or certolizumab, respectively. Approximately one-fifth of Crohn’s disease patients treated with biologicals require intestinal resection after 2–5 years in referral-center studies. (26)  The adverse reactions of the above medications are well-known, as are the risks and complications of surgery.

The safety and efficacy of a vegetarian diet to treat Crohn’s disease would seem quite advantageous. It has no contraindications and no adverse reactions. Therefore, it may be safely combined with standard treatments.

Treatment with a vegetarian diet also reduces the risk of common diseases that the Crohn’s patient will face in common with all patients, such as coronary artery disease and type II diabetes mellitus.

Given the substantial advantages more study is warranted. However, given its safety the physician can institute therapy with a vegetarian diet immediately.

Finally, every physician should practice prevention. The decreased risk of Crohn’s disease obtained with a vegetarian diet is considerable. It is a safe prophylaxis, and should especially be prescribed for patients at risk because of family history or because of cigarette smoking.



Kornbluth A, Sachar D, Salomon P. Crohn’s disease. In: Feldman M, Scharschmidt B, Friedman L, Sleisenger M, eds. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/ Management 6th Edition. Vol 2. 6th ed. Philadelphia: WB Saunders Co.; 1998.


Kappelman M, Direct Health Care Costs of Crohn’s Disease and Ulcerative Colitis in US Children and Adults. Gastroenterology. Dec 2008;135(6):1907-1913.


Chiba M, Ohno H, Ishii H, Komatsu M. Plant-Based Diets in Crohn’s Disease. The Permanente Journal. Fall 2014;18(4):94.


Bernstein C, Shanahan F. Disorders of a modern lifestyle: reconciling the epidemiology of inflammatory bowel diseases. Gut. Sept 2008;57(9):1185-1191.


Whelan G. Inflammatory bowel disease: epidemiology. In: Haubrich W, Schaffner F, Berk J, eds. Bockus Gastroenterology. Vol 2. 5th ed. Philadelphia: WB Saunders; 1995.


Shivananda S, Lennard-Jones J, Logan R, Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD). Gut. Nov 1996;39(5):690-697.


US Dept of Health and Human Services. Report of the Working Group on Arteriosclerosis of the National Heart, Lung and Blood Institute. Arteriosclerosis. Vol 2. Philadelphia: WB Saunders; 1981.


Popkin B. The nutrition transition in low-income countries: an emerging crisis. Nutrition Reviews. Sept 1994;52(9):285-298.


Hentges D, Maier B, Burton G, Effect of a high-beef diet on the fecal bacterial flora of humans. Cancer Research. Feb 1977;37(2):568-571.


Benno Y, Suzuki K, Suzuki K, Comparison of the fecal microflora in rural Japanese and urban Canadians. Microbiology and Immunology. 1986;30(6):521-32.


D’Souza S, Levy E, Mack D, Dietary patterns and risk for Crohn’s disease in children. Inflammatory Bowel Diseases. Mar 2008;14(3):367-73.


Chiba M, Abe T, Tsuda H, Lifestyle-related disease in Crohn’s disease: Relapse prevention by a semi-vegetarian diet. World Journal of Gastroenterology. May 2010;16(20):2484–2495.


Wong J. Gut microbiota and cardiometabolic outcomes: influence of dietary patterns and their associated components. American Journal of Clinical Nutrition. Jul 2014;100(Suppl 1):369S-77S.


Hur S, Kang S, Jung H, Review of natural products actions on cytokines in inflammatory bowel disease. Nutrition Research. Nov 2012;32(11):801-16.


Romier B, Schneider Y, Larondelle Y, During A. Dietary polyphenols can modulate the intestinal inflammatory response. Nutrition Reviews. Jul 2009;67(7):363-78.


Biasi F, Astegiano M, Maina M, Polyphenol supplementation as a complementary medicinal approach to treating inflammatory bowel disease. Current Medicinal Chemistry. 2011;18(31):4851-65.


Vermeire S, Van Assche G, Rutgeerts P. Laboratory markers in IBD: useful, magic, or unnecessary toys? Gut. Mar 2006;55(3):426-431.


Vermeire S, Van Assche G, Rutgeerts P. C-reactive protein as a marker for inflammatory bowel disease. Inflammatory Bowel Diseases. Sept 2004;10(5):661-5.


Yamamoto K, Kiyohara T, Murayama Y, Production of adiponectin, an anti-inflammatory protein, in mesenteric adipose tissue in Crohn’s disease. Gut. Jun 2005;54(6):789-96.


Fagan E, Dyck R, Maton P, Serum levels of C-reactive protein in Crohn’s disease and ulcerative colitis. European Journal of Clinical Investigation. Aug 1982;12(4):351-9.


Saverymuttu S, Hodgson H, Chadwick V, Differing acute phase responses in Crohn’s disease and ulcerative colitis. Gut. Jul 1986;27(7):809–813.


Hammer H, Kvien T, Glennås A, Melby K. A longitudinal study of calprotectin as an inflammatory marker in patients with reactive arthritis. Clinical and Experimental Rheumatology. Jan-Feb 1995;13(1):59-64.


Kahleova H, Matoulek M, Malinska H, Vegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type 2 diabetes. Diabetic Medicine. May 2011;28(5):549-59.


Krajcovicova-Kudlackova M, Blazicek P. C-reactive protein and nutrition. Bratislavske Lekarske Listy. 2005;106(11):345-7.


Chen C, Lin Y, Lin T, Total cardiovascular risk profile of Taiwanese vegetarians. European Journal of Clinical Nutrition. Jan 2008;62(1):138-44.


Peyrin-Biroulet L, Lémann M. Review article: remission rates achievable by current therapies for inflammatory bowel disease. Alimentary Pharmacology and Therapeutics. Apr 2011;33(8):870-9.