Mechanisms of malnutrition

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In virtually all disease states, the mechanisms of malnutrition fall under seven general categories (Table 3.1). These include decreased food intake, maldigestion, malabsorption, alterations in metabolism of nutrients, increased nutrient requirements, increased nutrient losses and drug-nutrient interactions. The effect of inflammatory bowel disease will be addressed with each of these causes individually (Table 3.2).

Decreased food intake is commonly encountered in IBD, especially in Crohn's disease. This frequently occurs because of anorexia and association of food intake with nausea, vomiting, diarrhea or pain, as well as the imposition of various restrictive diets by a variety of individuals and for a variety of reasons.

Table 3.1

Mechanisms of Malnutrition in Disease

Decreased food intake



Altered intermediary metabolism of nutrients Increased nutrient losses Increased nutrient requirements Drug: nutrient interactions

Table 3.2 Causes of Malnutrition in IBD





Nausea, vomiting Abdominal pain, diarrhea Restrictive diets



Increased requirements Losses from the gut

Altered intermediary metabolism Drug nutrient interactions

TNF-a; other pro-inflammatory cytokines Stricture, abscess Inflammation;

obstruction Recommendations from family, friend, physicians Sclerosing cholangitis, intestinal bacterial overgrowth I absorptive surface area

Absence of terminal ileum Inflammation, fever Inflammation

Bleeding TNFa, IL-ip and IL-6



I dietary intake

I dietary intake I variety & amount of food I dietary intake

I fat & fat soluble vitamin absorption

Vitamin & mineral deficiencies (Vitamin B12 not absorbed) Weight loss

Protein & mineral losses Iron deficiency anemia I albumin and other protein synthesis I calcium absorption, fmagnesuria, fmuscle wasting I folate absorption & reduction to tetrahydrofolate

Adapted from Jeejeebhoy KN: Management of nutritional problems of patients with Crohn's disease. CMAJ 2002;163:913-918. With permission.

Recent research efforts have investigated the possibility that proinflammatory cytokines may have a role in anorexia of IBD. An increased 5-hydroxytryptamine (5-HT) release from the hypothalamic paraventricular nucleus has been observed in a rat model of colitis by Ballinger et al. In these animals, dietary intake was decreased compared to healthy controls, and food intake was subsequently normalized when brain 5-HT was depleted with p-chlorophenylalanine injection into the hypothalamus [2].

Injection of interleukin-ip (IL-ip) had been shown more than a decade ago to increase hypothalamic release of 5-HT [3]. Leptins have also been identified to be elevated in inflammation and to be associated with suppression of food intake [4]. It is also well known that the proinflammatory cytokines, tumor necrosis factor alpha (TNF-a), IL-ip and interleukin 6 (IL-6) are increased in active Crohn's disease [5] and that they play a role in the pathogenesis of IBD [6]. These findings suggest a possible interrelationship of the pro-inflammatory cytokines and anorexia of IBD. Recent observations by Bannerman and coworkers [7] of subjective appetite parameters in a small number of patients with active and inactive Crohn's disease support the animal studies, in that hunger was significantly lower in those with active Crohn's compared with healthy subjects. Serum leptins were significantly associated with percentage of body fat and, when data were corrected for body composition, leptins showed a tendency to be higher in patients with active Crohn's disease.

In addition, food intake may be curtailed by symptoms that the patient associates with eating, such as nausea, pain, diarrhea and embarrassing incontinence. Furthermore, it is not unusual for the clinician to find that patients have restricted their food intake based on diets provided by not only the medical profession, but also a variety of sources such as well-meaning acquaintances, relatives or, more recently, the Internet. When a patient has had multiple suggestions of limiting a variety of foods, it is common to learn that entire food groups have been eliminated from the diet. Additionally, dietary beliefs of patients with IBD can significantly alter food patterns, and in particular have been shown to decrease the intake of calcium and folic acid [8]. These special dietary recommendations and beliefs can cause the food that is ingested to be deficient in various nutrients.

In Crohn's disease involving the small intestine, the diseased mucosa may cause maldigestion of nutrients. This can occur in proximal disease where mucosal disaccharidases are destroyed by mucosal injury, causing undigested carbohydrates to provide osmotic loads with resulting diarrhea and flatulence from metabolism by colonic flora. Additionally, ileal disease may result in decreased bile acid absorption, thus decreasing the bile acid pool. The result is that lipids are prevented from being solubilized, and thus they are poorly digested within the lumen of the proximal small bowel as a result of inadequate mixing of triglycerides with pancreatic enzymes. Furthermore, primary sclerosing cholangitis, a biliary complication of IBD, especially ulcerative colitis, may also result in decreased bile secretion and decreased digestion and absorption of fats and fat-soluble vitamins. Small intestinal bacterial overgrowth may also cause fat maldigestion as a result of deconju-gation of bile salts by bacteria. The effect of increased and altered flora in the small intestine is progressive damage to the mucosa with depletion of disaccharidases.

Malabsorption occurs as a result of inflammation of the intestinal mucosa, as well as intestinal resection causing decreased mucosal surface area available for absorption, especially Crohn's disease. Distal ileal resection affects absorption of bile acids, mentioned previously, and vitamin B12. Bacterial overgrowth also causes malabsorption of vitamin B12 as a result of the utilization of the vitamin B12 preferentially by the bacteria and depletion of the B12 supply available to the distal ileum. Malabsorption is less of an issue in ulcerative colitis.

Altered intermediary metabolism of nutrients by cytokines has become the topic of recent studies of Crohn's disease [1]. Inflammatory cytokines, including TNFa, IL-1^ and IL-6, are produced by activated monocytes/macrophages and lymphocytes in response to various stimuli and cause alteration of metabolism of protein, carbohydrate and lipid. In Crohn's disease these inflammatory cytokines are produced in excessive amounts in blood and intestinal mucosa [9, 10, 11, 12]. Reimund and colleagues found that univariate analysis of various anthropometric and biochemical measures of nutritional status in patients with Crohn's disease were significantly linked with inflammatory cytokine levels [13]. Specifically, mean arm circumference (MAC), triceps skinfold thickness (TSF), albumin and transthyretin were negatively correlated with TNFa levels, while IL-1^ was negatively correlated with body weight, body mass index, MAC and albumin. Furthermore, there was a negative correlation between the nutritional parameters, albumin and transthyretin, and inflammatory proteins, including erythrocyte sedimentation rate, C-reactive protein, fibrinogen and orosomucoid. Insulin-like growth factor (IGF-I) was positively associated with albumin, transthyretin, retinol-binding protein and vitamin A levels. These data, as well as knowledge of the role of TNF-a in switching amino acids toward acute-phase reactant synthesis and away from albumin synthesis [14], led to the suggestion that reduction of inflammation with associated correction of nutritional protein synthesis should be a goal of therapy in Crohn's disease [13].

Increased requirement of calories may result from fevers and sepsis in IBD. Increased basal metabolic rate in active IBD has been suggested to cause malnutrition [15], though in quiescent disease this probably does not occur [16]. Indeed in those with active disease, the increased basal energy requirements are likely offset by decreased requirements for activity, since those who are more ill are usually less active [15]. Al-Jaouni and coworkers identified that patients with active Crohn's disease had increased resting energy expenditures, enhanced lipid oxidation and decreased diet-induced thermogenesis compared to controls [17]. The effect of lipid peroxidation was directly related to disease activity. Yet, increased lipid oxidation was even seen in patients with inactive Crohn's disease [18]. Accelerated mucosal cell turnover may also increase nutrient requirements in IBD.

Increased nutrient losses occur in either Crohn's disease or ulcer-ative colitis as a result of inflammation and transudation of protein and fluid from the affected mucosa. Furthermore, mucosal hemorrhage causes loss of iron in both diseases. Fistulae, which most commonly occur in Crohn's disease, cause a loss of zinc, fluids and electrolytes. Unabsorbed fats, found primarily in Crohn's disease, bind calcium and magnesium within the intestinal lumen, causing wastage of both minerals.

Drug:nutrient interactions are an additional potential source of malnutrition in IBD. Sulfasalazine decreases absorption of folic acid and also decreases dihydrofolate reductase, so folic acid is not metabolized to its active form, tetrahydrofolate. Corticosteroids inhibit calcium absorption, cause magnesuria (thus magnesium wasting) and alter protein metabolism, causing muscle wasting. Antibiotics can decrease the vitamin K available from colonic bacterial metabolism. Cholestyramine binds bile acids, making them unavailable for adequate digestion of fat and fat soluble vitamins.

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