Fructose malabsorption is a gastro-intestinal disorder, characterized by the inability to absorb fructose efficiently. As a consequence fructose reaches the colon where it is broken down by bacteria into short chain fatty acids, CO2, lactic acid, CH4 (methane) and H2 (hydrogen). This will usually induce bloating, cramps, osmotic diarrhea along with other symptoms of irritable bowel syndrome and can be seen in about 50% of fructose malabsorbers.
Forms of Fructose
Fructose is a naturally occurring monosaccharide, which is present in fruits and natural sweeteners. It is ingested in three forms:
- A pure monosaccharide (single/simple sugar)
- The disaccharide (two monosaccharides linked together), sucrose – this involves fructose being linked with glucose
- The polymerized oligosaccharides and polysaccharides (polymerization is the process of chaining together many simple molecules to form a more complex molecule with different physical properties). Polymerized forms are variably described as inulins, fructans and fructo-oligosaccharides (FOS).
Over the past 30 years, fructose in its many forms has created a lot of interest; from its possible role in the generation of symptoms in patients with irritable bowel syndrome (IBS), as a prebiotic (food for probiotics), as a contributor to the obesity crisis (particularly in the US), in the development of non-alcoholic fatty liver disease, influencing the glycemic index of foods and in the development of dental caries. This article aims to address only one aspect of this spectrum – the effects and clinical significance of its malabsorption in the intestine.
Possible Disorders of Fructose Absorption
Low expense, easy availability, and extreme sweetness have made high fructose corn syrup an almost certain ingredient in a majority of processed foods. The ever increasing use of fructose sweeteners has resulted in a sharp increase in mean daily fructose intake after weaning. Increased fructose intake combined with the identification of children with clinical evidence of isolated fructose malabsorption (IFM) has stimulated interest in possible disorders of fructose absorption.
Intestinal absorption of fructose is carried out by the “ facilitative hexose transporter”, also known as the GLUT5. One theory related to the cause of fructose malabsorption is a defect in this fructose-related GLUT5 transport system, which then inhibits the duodenal uptake of the fructose.
The inability to absorb ingested fructose in a sufficient way leads to large quantities reaching the colon. The fructose is then broken down by colonic bacteria to short chain fatty acids, CO2, lactic acid, CH4 and H2 (as stated above). The type and extent of gastrointestinal discomfort caused as a result of these largely depends on the kind of colonic bacterial activity.
Fructose Malabsorption Diagnosis
Fructose malabsorption can be diagnosed by measuring the hydrogen concentration in the exhaled breath after an oral load of fructose. Patients with symptoms of depression have also been shown to have abnormal profiles of breath hydrogen excretion after ingesting fructose (and other sugars). Eliminating fructose from the diet resulted in an improvement in depression. In addition, fructose malabsorption was accompanied by a reduction in plasma tryptophan.
Fructose malabsorption provides a substrate for rapid bacterial fermentation, resulting in changes in gastrointestinal motility, the mucosal biofilm, and the profile of the microbiota.
Further studies are needed to clarify the background of these associations.
- Ledochowski M, et al. Fructose malabsorption is associated with decreased plasma tryptophan. J Gastroenterol. 2001: 4; 367-371
- Ledochowski M, et al. Fructose- and sorbitol-reduced diet improves mood and gastrointestinal disturbances in fructose malabsorbers. Scand J Gastroenterol. 2000: 35; 1048-1052
- Ledochowski M, et al. Fructose malabsorption is associated with decreased plasma tryptophan. Scand J Gastroenterol. 2001: 36(4): 367-371
- Bercik P, Colllins S, The relationship between intestinal microbiota and the central nervous system in normal gastrointestinal function and disease. 2009: 136; 2003-2014