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Crohn’s disease is an inflammatory bowel disease (IBD) that affects approximately 600,000 people in the US.

[i],[ii] People who have Crohn’s suffer from a serious inflammation or irritation of their digestive tract which can lead to sores or ulcers forming. Crohn’s can attack anywhere along the entire digestive tract, but most commonly affects the end of the small intestine (called the ileum). The small intestine is where critical nutrient absorption takes place, so people with Crohn’s often don’t digest and absorb nutrients well. This can result in malnutrition, anemia and malabsorption of key vitamins and minerals such as vitamin B12, vitamin A, vitamin D, Vitamin E, vitamin K, folate, zinc, calcium and iron.

People with Crohn’s often experience a variety of challenging and debilitating symptoms including:

  • Severe watery diarrhea – most common
  • Intense abdominal pain or cramping – most common
  • Bloating
  • Weight-loss
  • Fever
  • Fatigue
  • Fat malabsorption – floating stools

Other less common symptoms may include:

  • Constipation
  • Rectal bleeding
  • Anemia (iron malabsorption)
  • Joint pain
  • Inflammation or irritation of the eyes
  • Painful reddish tender bumps on the skin

Crohn’s disease may also lead to complications which include:

  • Scarring and bowel obstruction (most common) – Scarring may narrow parts of the intestine (the narrow areas are called strictures) leading to slowed motility (food moves too slowly through the intestine) or even bowel obstruction / blockage.
  • Ulcers – Inflammation from Crohn’s can lead to sores in any part of the digestive tract including the mouth and anus.
  • Gallstones
  • Fistulas – These abnormal connections can form between parts of the intestine and the skin, other organs of other parts of the intestine. Because they contain fecal material, they must be drained and treated typically by a combination of antibiotics and surgery.
  • Malnutrition and anemia and osteoporosis – Damage from Crohn’s makes the small intestine less efficient at absorbing adequate nutrition and minerals, including calcium and iron. Also, some people with Crohn’s don’t consume adequate nutrition due to symptom flares.

What causes Crohn’s disease? 

Despite extensive research, the exact cause of Crohn’s disease remains unknown. People with Crohn’s have various mutations (NOD2, ATG16L1, IL-23, IL12B, STAT3 and NKX2-3) in their genes that healthy people don’t have. Expression of the altered genes affects how bacteria interact with the intestinal surface and how our immune system interacts with these adherent bacteria.[iii] An imbalance in intestinal bacterial developing in response to the genetic abnormalities present in Crohn’s, may be the trigger for damaging inflammation characteristic of Crohn’s disease. One study showed that Crohn’s patients who had their fecal stream, that harbors gut microbes, diverted by surgery experienced disease improvement but relapsed when the fecal stream was restored.[iv] Antibiotics usage may further promote this imbalance and increase the risk of developing Crohn’s disease. [v],[vi]

Several attempts have been made to identify individual disease-causing bacteria that might be responsible for Crohn’s. These include a type of E. coli bacteria referred to as “adherent invasive E. coli, a bacterium called Mycobacterium avium ssp. paratuberculosis, or MAP for short, as well as Klebsiella pneumonia.[vii] In each case, there is a lack of conclusive evidence that these bacteria actually cause Crohn’s and may be bystanders that take advantage of the compromised health of Crohn’s patients.

Loss of Microbiota Diversity

One thing is clear – People with Crohn’s have an altered microbiome, suffering a 50% decrease in the diversity of gut microbes including the loss of bacterial species Bacteriodes, Eubacterium and Lactobacillus.[viii] A separate study also observed depletion of commensal bacteria, notably Firmicutes and Bacteroidetes bacterial types.[ix] A third study observed a decrease in Bacteroides bacteria and a decrease in bacterial end products. These studies point to a significant imbalance or gut microbes in people with Crohn’s disease. This imbalance may help explain the higher incidence of Clostridia difficile infection in people with inflammatory bowel disease.[x]

Conventional treatments for Crohn’s include drugs that reduce inflammation, anti-diarrheal drugs, nutritional  supplementation, surgery and antibiotics. Identifying effective dietary strategies to reduce inflammation and improve remission would reduce the dependency on drugs often associated with significant side effects and health risks.

Small intestinal bacterial overgrowth (SIBO) in Crohn’s

SIBO represents a frequently ignored complication in CD, often mimicking an acute flare. The symptoms of SIBO can be difficult to differentiate from those caused by the underlying disease. People with Crohn’s disease have a predisposition to SIBO mostly due to altered motility from strictures, fistulas or surgery. Altered immune reactions to gut microbes causing inflammation that damage the digestive process may also promote SIBO.

Several studies found that SIBO was present in 23 to 34% Crohn’s patients tested.[xi],[xii],[xiii], [xiv]In one of the studies, 96 % of patients with strictures (scarring) tested positive for SIBO. Only one of the four studies referenced above used the most sensitive lactulose hydrogen breath test suggesting that SIBO may be have been found more often if this test has been employed in the other studies. Regardless, SIBO is present almost universally in Crohn’s patients with strictures.

This overgrowth is very disruptive to the normal digestive process perpetuating the classic cycle of damage to the small intestinal surface, carbohydrate malabsorption and SIBO. One study that examined lactose malabsorption in Crohn’s disease showed that patients often exhibited lactose malabsorption even if their ethnic background indicated a low risk of lactose intolerance.[xv] The presence of SIBO helps explain, at least in part, the frequent finding of malabsorption in Crohn’s as well as many of the symptoms in Crohn’s such as diarrhea, cramping and bloating.

Treating Crohn’s with the Fast Tract Diet

The Fast Tract Diet was designed to control SIBO but the diet may provide additional benefits for people with Crohn’s including:

  • Reducing inflammation
  • Overall symptom improvement
  • Improving nutrition – especially critical for children with Crohn’s
  • Promoting healing of the intestinal lining (mucosa)
  • Reducing or eliminating the need for drugs (always consult your doctor on this one)
  • Extending time in remission

To understand how the Fast Tract Diet may help with Crohn’s and what, if any modifications might be needed, let’s talk about what is known about diet and Crohn’s. The most studied type of diet for Crohn’s is the elemental diet, a complete liquid diet which contains fats, proteins and carbohydrates which are predigested and most readily absorbed. Elemental diets are designed to meet the patient’s nutritional needs without eating any solid food. In Crohn’s patients where the disease targets the ilium (lower small intestine), consuming an elemental diet was effective in avoiding hospitalization,[xvi] maintaining remission,[xvii] and superior to treatment with drugs, with the possible exception of prednisone (which can’t be taken long term due to side effects).[xviii],[xix],[xx],[xxi] One big drawback besides cost, is the unpalatability of elemental diet formulations. Despite the addition of flavoring, many people aren’t able to tolerate these products long term.

Studies have shown that patients with Crohn’s have a high intake of total carbohydrates, starch and refined sugar.[xxii], [xxiii] Other than studies on the elemental diet, few scientific studies have been done on other diets for Crohn’s. A number of diets including the FODMAP approach,[xxiv] Specific carbohydrate  diet,[xxv] and low sugar diet[xxvi] which limit carbohydrates have been shown to improve the symptoms of  Crohn’s. A moderately low carbohydrate diet was also used to treat Crohn’s.[xxvii] While patients did gain benefit for as long as they maintained the diet, their relapse rate was similar the placebo group. The authors were unsure if noncompliance with the diet was a factor in relapse. Also, the diet included 84 grams of carbs per day and thus was not a truly low carb, ketogentic diet. Though not published in medical journals the book Life Without Bread by Christian B. Allan and Wolfgang Lutz describes Dr. Lutz’s clinical successful experience treating both Crohn’s and Ulcerative colitis patients with a very low carb diet over a period of many years. Another potential problem with low carb diets is they often contain a significant amount of fiber and sugar alcohols which can promote excessive fermentation by gut microbes.

The Fast Tract Diet is based on the same principle as the elemental diet in that it’s designed for easy absorption and limits the amount of undigested carbohydrates potentially feeding SIBO. The diet should benefit people with Crohn’s that either have SIBO or have difficulty digesting a normal diet. Dietary changes will not likely change the underlying Crohn’s disease mechanism which is not SIBO, but rather a complex immunological disease. Put another way, I’m suggesting that the Fast Tract Diet will be supportive for Crohn’s improving nutrient absorption, controlling SIBO and reducing symptoms even though it’s not a cure for Crohn’s disease.

Update July 9, 2015: 

Additional studies found there is a significant loss of microbiota diversity involving Bifidobacteria, Lactobacillus and particularly, Faecalibacterium prausnitzii, a member of the Firmicutes class / C. leptum group bacteria thought to have significant anti-inflammatory properties. [xxviii],[xxix],[xxx]

 [i] Kappelman MD, Moore KR, Allen JK, Cook SF. Recent trends in the prevalence of Crohn’s disease and ulcerative colitis in a commercially insured US population. Dig Dis Sci. 2013 Feb;58(2):519-25.

[ii] Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a population-based study. Gastroenterology. 2005 Sep;129(3):827-36. Tursi A, Giorgetti GM, Brandimarte G, Elisei W. High prevalence of celiac disease among patients affected by Crohn’s disease. Inflamm Bowel Dis. 2005 Jul;11(7):662-6.

[iii] Podolsky DK. Inflammatory bowel disease. N Engl J Med. 2002 Aug 8;347(6):417-29.

[iv] Rutgeerts P, Geboes K, Peeters M, et al. Effect of faecal stream diversion on recurrence of Crohn’s disease in the neoterminal ileum. Lancet 1991;338:771–4.

[v] Hviid A, Svanström H, Frisch M. Antibiotic use and inflammatory bowel diseases in childhood. Gut. 2011 Jan;60(1):49-54.

[vi] Shaw SY, Blanchard JF, Bernstein CN. Association between the use of antibiotics and new diagnoses of Crohn’s disease and ulcerative colitis. Am J Gastroenterol. 2011 Dec;106(12):2133-42.

[vii] Rashid T, Ebringer A, Tiwana H, Fielder M. Role of Klebsiella and collagens in Crohn’s disease: a new prospect in the use of low-starch diet. Eur J Gastroenterol Hepatol. 2009 Aug;21(8):843-9.

[viii] S J Ott, M Musfeldt, D F Wenderoth, J Hampe, O Brant, U R Fo¨lsch, K N Timmis, S Schreiber. Reduction in diversity of the colonic mucosa associated bacterial microflora in patients with active inflammatory bowel disease. Gut 2004;53:685–693.

[ix] Frank DN, St Amand AL, Feldman RA, Boedeker EC, Harpaz N, Pace NR. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A. 2007 Aug 21;104(34):13780-5.

[x] Navaneethan U, Venkatesh PG, Shen B. Clostridium difficile infection and inflammatory bowel disease: understanding the evolving relationship. World J Gastroenterol. 2010 Oct 21;16(39):4892-904.

[xi] Castiglione F, Del Vecchio Blanco G, Rispo A, Petrelli G, Amalfi G, Cozzolino A, Cuccaro I, Mazzacca G. Orocecal transit time and bacterial overgrowth in patients with Crohn’s disease. J Clin Gastroenterol. 2000 Jul;31(1):63-6.

[xii] Klaus J, Spaniol U, Adler G, Mason RA, Reinshagen M, von Tirpitz C C. Small intestinal bacterial overgrowth mimicking acute flare as a pitfall in patients with Crohn’s Disease. BMC Gastroenterol. 2009 Jul 30;9:61.

[xiii] Rutgeerts P, Ghoos Y, Vantrappen G, Eyssen H. Ileal dysfunction and bacterial overgrowth in patients with Crohn’s disease. Eur J Clin Invest. 1981 Jun;11(3):199-206.

[xiv] Mishkin D, Boston FM, Blank D, Yalovsky M, Mishkin S. The glucose breath test: a diagnostic test for small bowel stricture(s) in Crohn’s disease. Dig Dis Sci. 2002 Mar;47(3):489-94.

[xv] Mishkin B, Yalovsky M, Mishkin S. Increased prevalence of lactose malabsorption in Crohn’s disease patients at low risk for lactose malabsorption based on ethnic origin. Am J Gastroenterol. 1997 Jul;92(7):1148-53.

[xvi] Watanabe O, Ando T, Ishiguro K, Takahashi H, Ishikawa D, Miyake N, Kato T, Hibi S, Mimura S, Nakamura M, Miyahara R, Ohmiya N, Niwa Y, Goto H. Enteral nutrition decreases hospitalization rate in patients with Crohn’s disease. J Gastroenterol Hepatol. 2010 May;25 Suppl 1:S134-7.

[xvii] Wilschanski M, Sherman P, Pencharz P, Davis L, Corey M, Griffiths A. Supplementary enteral nutrition maintains remission in paediatric Crohn’s disease. Gut. 1996 Apr;38(4):543-8.

[xviii] Matsueda K, Shoda R, Takazoe M, Hiwatashi N, Bamba T, Kobayashi K, Saito T, Terano A, Yao T. Therapeutic efficacy of cyclic home elemental enteral alimentation in Crohn’s disease: Japanese cooperative Crohn’s disease study. J Gastroenterol. 1995 Nov;30 Suppl 8:91-4.

[xix] Riordan AM, Hunter JO, Cowan RE, Crampton JR, Davidson AR, Dickinson RJ, Dronfield MW, Fellows IW, Hishon S, Kerrigan GN, et al. Treatment of active Crohn’s disease by exclusion diet: East Anglian multicentre controlled trial. Lancet. 1993 Nov 6;342(8880):1131-4.

[xx] O’Moráin C, Segal AW, Levi AJ. Elemental diet as primary treatment of acute Crohn’s disease: a controlled trial. Br Med J (Clin Res Ed). 1984 Jun 23;288(6434):1859-62.

[xxi] Zachos M, Tondeur M, Griffiths AM. Enteral nutritional therapy for induction of remission in Crohn’s disease. Cochrane Database of Systematic Reviews 2007, Issue 1. Art. No.: CD000542.

[xxii] Tragnone A, Valpiani D, Miglio F, Elmi G, Bazzocchi G, Pipitone E, Lanfranchi GA. Dietary habits as risk factors for inflammatory bowel disease. Eur J Gastroenterol Hepatol. 1995 Jan;7(1):47-51.

[xxiii] Penny WJ, Mayberry JF, Aggett PJ, Gilbert JO, Newcombe RG, Rhodes J. Relationship between trace elements, sugar consumption, and taste in Crohn’s disease. Gut. 1983 Apr;24(4):288-92.

[xxiv] Gearry RB, Irving PM, Barrett JS, Nathan DM, Shepherd SJ, Gibson PR. Reduction of dietary poorly absorbed short-chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease-a pilot study. J Crohns Colitis. 2009 Feb;3(1):8-14.

[xxv] Suskind DL, Wahbeh G, Gregory N, Vendettuoli H, Christie D. Nutritional Therapy in Pediatric Crohn’s Disease: The Specific Carbohydrate Diet. J Pediatr Gastroenterol Nutr. 2013 Sep 16.

[xxvi] Brandes JW, Lorenz-Meyer H. Sugar free diet: a new perspective in the treatment of Crohn disease? Randomized, control study. Z Gastroenterol. 1981 Jan;19(1):1-12.

[xxvii] Lorenz-Meyer H, Bauer P, Nicolay C, Schulz B, Purrmann J, Fleig WE, Scheurlen C, Koop I, Pudel V, Carr L. Omega-3 fatty acids and low carbohydrate diet for maintenance of remission in Crohn’s disease. A randomized controlled multicenter trial. Study Group Members (German Crohn’s Disease Study Group). Scand J Gastroenterol. 1996 Aug;31(8):778-85.

[xxviii] Wang W1, Chen L, Zhou R, Wang X, Song L, Huang S, Wang G, Xia B. Increased proportions of Bifidobacterium and the Lactobacillus group and loss of butyrate-producing bacteria in inflammatory bowel disease. J Clin Microbiol. 2014 Feb;52(2):398-406.

[xxix] Fujimoto T1, Imaeda H, Takahashi K, Kasumi E, Bamba S, Fujiyama Y, Andoh A. Decreased abundance of Faecalibacterium prausnitzii in the gut microbiota of Crohn’s disease. J Gastroenterol Hepatol. 2013 Apr;28(4):613-9.

[xxx] Sokol H1, Pigneur B, Watterlot L, Lakhdari O, et.al. Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16731-6.