Fructose malabsorption

Fructose malabsorption, formerly named dietary fructose intolerance (DFI), is a digestive disorder in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose in the entire intestine. Intolerance to fructose was first identified and reported in 1956. Fructose malabsorption, formerly named dietary fructose intolerance (DFI), is a digestive disorder in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose in the entire intestine. Intolerance to fructose was first identified and reported in 1956. Occurrence in patients identified to be suffering symptoms of irritable bowel syndrome is not higher than occurrence in the normal population. However, due to the similarity in symptoms, patients with fructose malabsorption often fit the profile of those with irritable bowel syndrome. In some cases, fructose malabsorption may be caused by several diseases which cause intestinal damage, such as celiac disease. Fructose malabsorption is not to be confused with hereditary fructose intolerance, a potentially fatal condition in which the liver enzymes that break up fructose are deficient. Fructose malabsorption may cause gastrointestinal symptoms such as abdominal pain, bloating, flatulence or diarrhea. Fructose is absorbed in the small intestine without help of digestive enzymes. Even in healthy persons, however, only about 25–50 g of fructose per sitting can be properly absorbed. People with fructose malabsorption absorb less than 25 g per sitting. Simultaneous ingestion of fructose and sorbitol seems to increase malabsorption of fructose. Fructose that has not been adequately absorbed is fermented by intestinal bacteria producing hydrogen, carbon dioxide, methane and short-chain fatty acids. This abnormal increase in hydrogen may be detectable with the hydrogen breath test. The physiological consequences of fructose malabsorption include increased osmotic load, rapid bacterial fermentation, altered gastrointestinal motility, the formation of mucosal biofilm and altered profile of bacteria. These effects are additive with other short-chain poorly absorbed carbohydrates such as sorbitol. The clinical significance of these events depends upon the response of the bowel to such changes. Some effects of fructose malabsorption are decreased tryptophan, folic acid and zinc in the blood. Restricting dietary intake of free fructose and/or fructans may provide symptom relief in a high proportion of patients with functional gut disorders. The diagnostic test, when used, is similar to that used to diagnose lactose intolerance. It is called a hydrogen breath test and is the method currently used for a clinical diagnosis. Nevertheless, some authors argue this test is not an appropriate diagnostic tool, because a negative result does not exclude a positive response to fructose restriction, implying a lack of sensitivity. There is no known cure, but an appropriate diet and the enzyme xylose isomerase can help. The ingestion of glucose simultaneously with fructose improves fructose absorption and may prevent the development of symptoms. For example, people may tolerate fruits such as grapefruits or bananas, which contain similar amounts of fructose and glucose, but apples are not tolerated because they contain high levels of fructose and lower levels of glucose.