INTRODUCTION — Inflammatory bowel disease (IBD) is an inflammatory disorder of the gastrointestinal (GI) tract leading to symptoms of pain, nausea, fever, and diarrhea [1]. These symptoms can result in loss of appetite, reduced nutrient intake, altered nutrient metabolism, and ultimately impaired nutritional status. Loss of appetite is most likely the result of inflammation and the release of cytokines such as IL-1, IL-6, and tumor necrosis factor.
Dietary interventions in IBD focus on maximizing nutritional status, maintaining adequate intake, and avoiding foods that can exacerbate symptoms.
The prevalence of nutritional deficiencies and malnutrition has been well documented in IBD, especially in Crohn's disease (CD) [2]. It is important to identify patients who are malnourished in order to identify those patients who may require nutritional intervention. Optimizing nutritional status is important both to prevent long-term health consequences of malnutrition as well as to prevent relapses in patients with IBD.
This topic review will discuss nutrition and dietary interventions in adults with inflammatory bowel disease. Specific nutrient deficiencies in IBD, as well as growth failure and poor weight gain in children with IBD are discussed separately. Dietary risk factors for IBD are also discussed separately. (See "Nutrient deficiencies in inflammatory bowel disease" and "Growth failure and poor weight gain in children with inflammatory bowel disease" and "Definition of and risk factors for inflammatory bowel disease", section on 'Diet'.)
CAUSES OF MALNUTRITION — The factors that contribute to malnutrition and nutrient deficiencies in patients with inflammatory bowel disease, including reduced nutrient intake, malabsorption, and inflammation are discussed in detail elsewhere. (See "Growth failure and poor weight gain in children with inflammatory bowel disease", section on 'Malnutrition' and "Nutrient deficiencies in inflammatory bowel disease".)
NUTRITIONAL ASSESSMENT — The nutritional status of patients with IBD should be assessed to determine if dietary intervention is necessary. Measuring a patient's nutritional status involves a comprehensive assessment. This may include measuring body composition, dietary intake, energy expenditure, body function, and serum protein markers. (See "Dietary and nutritional assessment in adults".)
Relying exclusively on serum protein levels (eg, albumin and prealbumin) as definitive markers of nutrition is insufficient [3]. Albumin is a better predictor of a patient's clinical outcome in the hospital than of nutritional status [4]. Specific micronutrient (vitamin and mineral) deficiencies may also occur in patients with IBD depending upon their general nutritional status as well as the activity and location of their disease. These can be assessed by specific laboratory measures [5]. (See "Nutrient deficiencies in inflammatory bowel disease", section on 'Laboratory measures'.)
Global assessment tools should be used as part of standard nutrition screening to identify at-risk, malnourished patients. One of these tools is a subjective global assessment (SGA) analysis (figure 1) [6]. This global assessment tool takes into account multiple nutrition-related factors including functional status, dietary factors, multiple GI-related symptoms, weight loss, and a brief physical examination. (See "Dietary and nutritional assessment in adults".)
The SGA is a useful tool and has been used in conjunction with measuring body mass index, albumin, and trace elements in assessing the nutritional status of IBD patients. However, in one study, patients with IBD who were well nourished according to this standard nutrition screening were found to have a decrease in body cell mass (a measure of metabolically active tissues) as well as reduced handgrip strength compared with controls [7]. A separate study documented that patients with Crohn’s disease in remission often had a normal body mass index (BMI) (weight in kg/height in meters) but reduced handgrip muscle strength consistent with loss of protein muscle mass [8]. These observations suggest that IBD patients may look well or even exhibit excess weight while having alterations in body composition and body function and, as a result, may be candidates for nutritional supplementation as well. Therefore, it is prudent to ensure that all patients with IBD are assessed for adequacy of their nutritional status. (See "Growth failure and poor weight gain in children with inflammatory bowel disease", section on 'Nutritional assessment' and "Determining body composition in adults".)
CONSEQUENCES OF MALNUTRITION — Malnutrition in patients with IBD can lead to growth failure, weight loss, bone disease, and/or micronutrient deficiencies.
Growth failure — Chronic or intermittent growth failure, with associated pubertal delay, is common in children with Crohn’s disease (CD) and frequently reduces adult height. The evaluation and management of growth failure in children with IBD is discussed in a separate topic review. (See "Growth failure and poor weight gain in children with inflammatory bowel disease".)
Weight loss and reduced muscle mass — Weight loss and protein-calorie malnutrition have become less common among adults with IBD [5,9,10]. Historically, nutritional deficiencies or the inability to maintain ideal body weight occurred in 50 to 70 percent of adults with CD, and 18 to 62 percent of those with ulcerative colitis (UC) [11,12]. A 2009 study of 102 adults with IBD found 14 percent of those with CD and 5.7 percent of those with UC to be malnourished based upon body mass index (BMI) criteria [13]. However, muscle mass depletion was detected in more than half of the patients.
Muscle and fat mass depletion is associated with disease activity [13,14]. Adult patients with CD in remission usually have no differences in body composition compared with healthy controls [9,10].
The primary mediators of reduced muscle mass are inflammation (excessive catabolism, which accelerates protein breakdown), decreased physical activity, and/or glucocorticoid treatment [15]. Inadequate protein intake may also affect muscle mass, but this mechanism is not usually relevant in adults unless the deficiency is severe and prolonged (starvation). The protein intake of children with IBD is more likely to be insufficient because of their relatively high protein needs for growth. (See "Growth failure and poor weight gain in children with inflammatory bowel disease".)
Patients who have lost between 5 and 10 percent of their lean body mass usually have no clinical sequelae. However, loss of lean body mass beyond this threshold is associated with increased morbidity. As an example, reduced muscle mass is associated with poor wound healing and higher rates of infection after surgery [16,17].
Bone disease — Bone disease (osteoporosis and/or osteomalacia) is a common problem in IBD [18]. Its cause is probably multifactorial. Risk factors include glucocorticoid use and/or disease activity, age, pubertal delay, and deficiencies of calcium, vitamin D, and vitamin K [19]. Prevention and treatment of bone loss in IBD consists of attempting to reverse or minimize these factors. (See "Metabolic bone disease in inflammatory bowel disease".)
The evaluation and management of IBD-associated bone disease in children differs in several respects from that in adults, as discussed separately. (See "Growth failure and poor weight gain in children with inflammatory bowel disease", section on 'Bone disease'.)
Micronutrient deficiencies — Micronutrient deficiencies in patients with inflammatory bowel disease are discussed in detail elsewhere. (See "Nutrient deficiencies in inflammatory bowel disease".)
DIETARY INTERVENTIONS — Dietary interventions to improve nutrition and eliminate food triggers play a role in the treatment regimen in most patients with IBD. Clinical studies in this area are small in number, often not randomized or placebo-controlled, and contain small numbers of patients. Still, there are some conclusions we can draw from this body of literature.
Nutrition supplementation — Nutrition supplementation is the administration of commercially available supplements to increase calorie and protein intake. Oral ingestion is the preferred method of delivery, although tube feedings (nasogastric or nasoduodenal) are used when volitional oral intake is inadequate. Liquid nutritional supplementation may take the form of an elemental, semi-elemental, or polymeric diet. Each consists of liquid nutrients in an easily assimilated form, differing in their protein source; elemental (free amino acids), semi-elemental (oligopeptides), and polymeric (whole protein). The diet selected is usually based on individual preferences, individual tolerance, availability, and cost. (See "Nutrition support in critically ill patients: Enteral nutrition", section on 'Formulations' and "Nutrition support in critically ill patients: An overview", section on 'Enteral nutrition'.)
Enteral nutrition (liquid food delivered orally or via tube feeding) in addition to normal food is indicated in malnourished patients with IBD to improve nutritional status. In addition, enteral feeding has some efficacy in inducing remission in patients with active CD, although glucocorticoids appear to have superior efficacy. Prior to the approval of infliximab for induction of remission in fistulizing CD, the European Society for Clinical Nutrition and Metabolism guidelines recommended enteral nutrition be used as therapy in active CD, primarily when treatment with glucocorticoids is not feasible [20,21]. A systematic review showed that there was no difference in the induction of remission in CD when different formula compositions (elemental, semi-elemental, and polymeric) were compared [22]. A non-significant trend favoring very low fat and/or long chain triglyceride content was also found, but remains to be confirmed. Further analysis of six trials found that glucocorticoid therapy was more effective for inducing remission of active CD than was enteral nutrition.
Supplemental enteral therapy may also be effective in maintaining remission in CD, but this has not been definitively established. It is postulated that an oral supplement reduces exposure to the antigenic properties of normal food while boosting caloric intake [23]. A systematic review attempted to look at enteral nutrition for the maintenance of remission in Crohn’s disease [24]. Two randomized trials were identified that met inclusion criteria [25,26], but a pooled statistical analysis was not possible due to differences in the control interventions and outcome assessments.
The following studies describe the potential benefits of this treatment approach:
- In one study, patients who received a half elemental diet and a half normal diet had a lower relapse rate compared with patients who received a normal unrestricted diet [25].
- In another study, patients with Crohn’s disease who were taking in normal food were assigned to receive either elemental or polymeric nutritional supplements. Both approaches were equally effective for maintenance of remission and permitting steroid withdrawal [26].
- The benefit of oral supplements was also described in a third study in which normal table food was supplemented with a liquid formula [23]. Twenty-eight malnourished patients who received an oral supplement had improved well being, improved steroid withdrawal, decreased CD activity, and improved nutritional status.
- Finally, another study randomized 39 patients with CD to either normal food or normal food supplemented with an elemental diet [27]. At one year, remission rates were higher in those who received the supplemental elemental feeding (48 versus 22 percent).
Limited data exist on enteral nutritional therapy in patients with UC. One prospective randomized trial compared enteral nutrition with total parenteral nutrition as an adjunct therapy in severe UC patients on glucocorticoid therapy [28]. Remission rates were similar in the two groups.
Routine multivitamin supplementation with calcium is suggested in IBD in view of the nutrient deficiencies observed [5]. Patients may also require supplementation with specific micronutrients. It is also reasonable to suggest supplementation with folic acid based upon data suggesting that it might protect against the development of dysplasia [29]. (See "Nutrient deficiencies in inflammatory bowel disease" and "Vitamin supplementation in disease prevention", section on 'Folic acid'.)
Perioperative nutrition supplementation has not been demonstrated to improve outcome in surgical patients [30,31]. However, some severely malnourished patients might benefit from perioperative artificial feeding. (See "Nutritional issues in the surgical patient", section on 'Enteral feeding' and "Nutrition support in critically ill patients: An overview", section on 'Enteral nutrition'.)
Total parenteral nutrition — Total parenteral nutrition (TPN) consists of administering a nutritional formula intravenously when no food is given by any other route. The American Gastroenterological Association technical review of six trials concluded that TPN provided no benefit in the routine treatment of IBD and may be equivalent to enteral nutrition when treating patients with active CD of the small bowel [32]. However, TPN has a role in severe cases of active CD where enteral nutrition supplementation is not tolerated or standard drug treatment is not effective. TPN is also administered to correct nutritional deficiencies prior to surgery or as an in-home option for CD patients whose alternative is prolonged hospitalization or early surgery [33]. Home TPN may also be used for CD patients with multiple small bowel resections resulting in short bowel syndrome. (See "Nutrition support in critically ill patients: Parenteral nutrition" and "Management of the short bowel syndrome in adults" and "Nutrition support in critically ill patients: An overview", section on 'Parenteral nutrition'.)
Elimination diet — An elimination diet involves removing a food from the diet for a period of time and seeing whether symptoms resolve during that time. In patients receiving enteral nutrition, it involves introducing one new food at a time to identify foods that precipitate IBD symptoms. Many patients can identify foods that they believe may precipitate or worsen their disease and it is reasonable for them to avoid such foods. Using an elimination diet to identify at-risk foods may decrease the possibility of a "flare" of IBD.
Three studies provide support for this treatment approach.
- One trial compared the use of glucocorticoids versus an elimination diet in 78 patients who had achieved a remission of their IBD flare by the use of an elemental diet feeding [34]. Patients were instructed to introduce one new food group daily and to avoid foods that they knew previously resulted in precipitating their IBD symptoms. Relapse rates at two years were lower in the diet-treated than in the steroid-treated group (62 versus 79 percent). Food intolerances to cereals, lactose, and yeast products were common.
- Another study evaluated the use of an elimination diet versus an unrefined carbohydrate, fiber-rich diet in patients with CD who were currently in remission [35]. Relapse rates at six months were 100 percent in the unrefined carbohydrate, fiber-rich diet versus 30 percent on the elimination diet.
- In a longer-term study, 31 patients with CD who obtained clinical remission after four weeks of enteral feeding were followed for 36 months [36]. Twenty of the patients were placed on a defined dietary elimination protocol, while the remaining patients were continued on an unrestricted diet. Of the 14 patients who completed the elimination diet process, three relapsed. Of the 11 patients eating a regular diet, nine relapsed. Almost all of the relapses occurred in the first six months.
Lactose elimination can be particularly beneficial. Lactose intolerance is frequently noted in patients with ulcerative colitis. Patients with suggestive symptoms should undergo a lactose breath hydrogen test to confirm the diagnosis. Calcium supplementation should be maintained in patients with limited lactose intake to minimize the risk of bone loss. (See "Lactose intolerance".)
Low carbohydrate diet — There have been anecdotal reports of a low carbohydrate diet being helpful in preventing relapse in patients with inflammatory bowel disease. There is no recommendation from any major healthcare society supporting this intervention and there is little literature in this arena. One study randomized 204 patients with CD in remission to omega-3 fatty acids, a placebo, or a low carbohydrate diet. In an intent-to-treat analysis, neither the omega-3 fatty acid supplementation nor the low carbohydrate diet resulted in any improvement in relapse as compared to placebo [37].
The Specific Carbohydrate Diet (SCD) is a very restrictive low carbohydrate diet that has been promoted for multiple chronic and autoimmune diseases, including IBD, autism, and celiac disease [38]. The diet is built upon the premise that intestinal microbes that contribute to the development of IBD use carbohydrates as their primary energy source, leading to the production of acids and toxins that can injure the small intestine, further impairing carbohydrate digestion and absorption. (See "Immune and microbial mechanisms in the pathogenesis of inflammatory bowel disease", section on 'Role of microbes'.)
The SCD is grain-free, lactose-free, and sucrose-free [39]. It also limits the intake of some legumes and tubers and it does not allow for the intake of processed foods due to additives. The diet does allow for the intake of unprocessed meats, poultry, fish, eggs, honey, non-canned vegetables, some legumes, fruits, nuts, homemade yogurt, and some lower-lactose cheeses (eg, cheddar).
The data on the SCD are limited to a case report of two patients who improved on the diet [40] and many patients find the diet difficult to follow due to its restrictive nature. In addition, some clinicians express concern that it could lead to nutritional deficiencies [39]. Randomized trials examining the SCD are required before it can be recommended.
Probiotics — Probiotics are living, nonpathogenic micro-organisms (eg, yeast, lactobacilli) that, when ingested, are believed to have the potential to exert a positive influence on host health and physiology [41]. In UC patients following surgery, there appears to be a benefit to the use of the probiotic VSL-3 (CSL Milan, Italy) (3 to 6 g/day) for the prevention of recurrent pouchitis [42]. In addition, one study found that the use of the probiotic Escherichia coli Nissle 1917 (Mutaflor®, Ardeypharm Herdecke, Germany) was as effective for the treatment of relapse in UC patients as the drug mesalamine [43]. There have not been convincing data on the efficacy of various probiotics for the prevention of relapse in CD [44]. (See "Probiotics for gastrointestinal diseases" and "Pouchitis", section on 'Probiotics'.)
Other dietary interventions — Other dietary interventions have been considered; however, conflicting data exist regarding their use.
Fiber — The benefit of increasing dietary fiber in IBD patients remains controversial. Fiber has a beneficial effect on commensal gut bacteria. Some dietary fiber upon metabolism will form short-chain fatty acids, which have been shown to stimulate water and sodium absorption in the colon and to promote mucosal healing [45].
Dietary fiber may have a role in the maintenance of remission. In one study, for example, the consumption of Plantago ovata seeds (10 grams twice daily) was as effective as a maintenance dose of mesalamine (500 mg three times daily) in maintaining remission for up to 12 months in patients whose ulcerative colitis was in endoscopic and clinical remission at the start of therapy [46]. A retrospective study of 32 patients with CD reported a reduced rate of hospital admissions and surgeries in a fiber-supplemented group compared with 32 patients in a control food group [47]. However, other studies have failed to demonstrate improved clinical outcomes of CD patients eating a fiber-rich diet [35,48].
Omega-3 polyunsaturated fatty acids — The existing data do not support the use of fish oils for maintenance of remission in UC or CD [49-51].
Omega-3 polyunsaturated fatty acids (03PUFA) are potent immunomodulatory substances. They are usually obtained from fish oils and contain eicosapentaenoic acid and docosahexaenoic acid. The ability of O3PUFA to downregulate the inflammatory response has been shown in both animal models and in humans. A randomized controlled trial demonstrated that fish oil supplementation reduces the production of inflammatory cytokines [52] and fish oil supplementation has been shown to reduce inflammation and the dose of antiinflammatory drugs required to promote weight gain in patients with IBD [49].
However, two large placebo-controlled trials in CD [53] and systematic reviews of clinical trials in patients with UC and CD [49,50] found that oral ingested fish oil supplementation, while safe, is ineffective for inducing or maintaining remission in either UC or CD. (See "Approach to adults with steroid-refractory and steroid-dependent ulcerative colitis", section on 'Fish oil'.)
Antioxidants — The data regarding the use of antioxidants in IBD are not substantial enough to make a recommendation. Antioxidants are substances that neutralize oxygen free radicals, metabolic products that are increased during inflammatory states and result in significant tissue damage. One randomized controlled trial of 57 patients using a combination of antioxidants as an antiinflammatory supplement for four weeks found that treatment produced a reduction in measured indices of oxidative stress with no effect on disease activity [54].
SUMMARY AND RECOMMENDATIONS — The prevalence of nutritional deficiencies and malnutrition has been documented in IBD, especially in Crohn's disease. It is important to identify patients who are malnourished in order to identify those patients who may require nutritional intervention.
Searching for
