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Review identifies patient-targeted dietary recommendations for IBD
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The recent, rapid increase in the incidence and prevalence of ulcerative colitis and Crohn’s disease suggests an environmental trigger for inflammatory bowel disease, one of which could potentially be dietary, according to a recently published review.
Researchers reviewed the limited evidence behind patient-targeted dietary information for IBD from Internet searches and popular defined diets and summarized the data supporting the rationale for dietary intervention and the recommendations of poorly evidenced, popular diets.
Diet’s effect on gut inflammation
Mechanisms of dietary influence on gut inflammation may include direct dietary antigens, changes in gut microbiota and increased gastrointestinal permeability, the researchers wrote. Studies that support these disease mechanisms have shown:
- IBD development is consistently associated with dietary fatty acid and protein composition.
- Dietary fiber has been associated with lower risk for CD but not UC (HR=0.59; 95% CI, 0.39-0.9).
- Recurrence of CD “inflammation after ileal resection is dependent on exposure of the neoterminal ileum to the fecal contents.”
- High-fat diets may increase bowel permeability through changes in the gut microbiome.
- UC relapse is associated with greater consumption of meat (especially red and processed), eggs, protein and alcohol, and UC endoscopic activity is associated with sulfite consumption.
- Exclusive enteral nutrition induces mucosal healing and prolonged clinical remission of CD but not UC
- Exclusion diets have improved disease activity and prolonged time to relapse.
Patient-targeted diet recommendations
The review did not advocate any particular diet, but compiled the details and theories behind three defined diets commonly supported in lay literature: the specific carbohydrate diet (SCD), the fermentable oligosaccharides, disaccharides and monosaccharides (FODMAP) diet, and the Paleolithic diet.
The SCD is based on the theory that disaccharide and polysaccharide carbohydrates are poorly absorbed by the GI tract, causing overgrowth of bacteria and yeast that lead to excess mucus and small bowel injury. The diet restricts all but simple carbohydrates, or the monosaccharides glucose, fructose and galactose.
The FODMAP diet also is based on the notion that poorly absorbed carbohydrates cause bacterial overgrowth, but unlike the SCD, it restricts many fruits and vegetables.
The Paleolithic diet is based on the hypothesis that foods that were not present when human beings evolved can lead to modern diseases due to the GI tract’s inability to handle foods resulting from modern agriculture. This diet emphasizes lean game meats and noncereal plant-based foods.
There are no formal studies published about SCD or Paleo, but small pilot studies have tested FODMAP in patients with IBD, one that showed improved IBD symptoms (P<.02).
How to advise patients
“There is scientific evidence that dietary factors may influence both the risk of developing IBD and intestinal mucosal inflammation,” the researchers concluded. “However, there is a lack of large prospective controlled trials to provide the dietary recommendations patients desire. Taken together, studies of exclusive enteral nutrition, exclusion diets, and semivegetarian diets suggest that minimizing exposure of the intestinal lumen to selected food items may prolong the remission state of patients with IBD. Even less evidence exists for the efficacy of the SCD, FODMAP, or Paleo diets.”
Disclosure: James Lewis reports having served as a consultant for Nestec.
Perspective
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Robert M. Genta, MD
If it is true that we are what we eat, then people with inflammatory bowel disease are at risk for becoming a very diverse group. Jason K. Hou, MD, a Houston-based expert in the use of natural language for the evaluation of records of IBD patients, and his colleagues at the University of Pennsylvania, have performed a clever study to determine whether there is any scientific evidence behind the myriad of dietary recommendations aimed at patients with IBD that can be found on the Internet. Their conclusions, shared a priori by any skeptical casual user, are discomforting. Based on the advice of a certain site, a patient will adhere to a diet rich in eggs and devoid of refined grains, while another patient, having consulted a different site, will avoid eggs and enjoy white bread, spaghetti, and corn flakes. Both patients will refrain from drinking alcohol and avoid broccoli and Brussels sprouts, but will happily feast on poultry.
Virtually none of the dietary advice for IBD patients found on the Internet lies on scientific foundations. This is largely because disease-support sites tend to rely more on anecdotal information and lifestyle doctrines entirely divorced from scientific evidence (yoga, veganism, paleo, etc.) than on the peer-reviewed literature. In the specific case of IBD diets, the anarchy is worsened by the dearth of conclusive published studies; the conflicting suggestions that we love to deride in amateurish Internet sites have their counterpart in the conflicting conclusions found in different well-conducted studies.
What is a patient to do? Evidence-based, effective restricted diets take a considerable toll on the quality of life of patients with certain conditions (eg, celiac disease and eosinophilic esophagitis), but these burdens are largely offset by the marked improvement or disappearance of the symptoms these patients experience. Internet diets are based on frivolous opinions and misconceptions rather than data: did cave dwellers really eat better than we do? Is it wise to imitate the lifestyle of people who died well before age 40? These diets are generally normative, restrictive, difficult to follow, often expensive, and strict adherence to them may be socially divisive. Their benefits are at best those of a placebo. While waiting for more conclusive controlled studies, as Hou and his colleagues sensibly conclude, a personalized approach developed jointly by patients and their physicians will remain the best strategy for symptom control.
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