Irritable Bowel Syndrome Message Boards

There are two type of fructose problems: hereditary fructose intolerance and fructose malabsorption. There is no such thing as fructose intolerance. It is a misnomer usually used to mean fructose malabsorption.

Hereditary fructose intolerance is a hereditary condition caused by a deficiency of liver enzymes that metabolise fructose. This condition is usually detected in childhood. It requires the elimination of all foods containing fructose including table sugar (sucrose). This disease can be fatal if not managed properly.

Fructose malabsorption is the inability of the small intestine to absorb excess fructose. Excess fructose means foods that contain more fructose than glucose. Table sugar has no excess fructose because it contains precisely equal amounts of glucose and fructose. Honey on the other hand, has about 5 grams of excess fructose because it contains about 41 grams of fructose and 36 grams of glucose per 100 grams.

Fructose that is accompanied with an equal amount of glucose as in the case of table sugar is absorbed in the small intestine by a different pathway (GLUT2 transporter) than free fructose (GLUT5 transporter). Fructose is well absorbed in the presence of amounts of glucose in the proximal small intestine whereas free fructose is slowly absorbed and along the length of the small intestine. Fructose malabsorption will occur when the activity of GLUT5 is impaired or when small intestinal bacteria are able to ferment the fructose before it can be absorbed. Fructose malabsorption, is defined by the appearance of hydrogen in the breath after an oral load of 25 grams of fructose. Individuals with fructose malabsorption have no problems with table sugar (sucrose) but foods with excess fructose can trigger IBS symptoms. However, the amount of excess fructose required to produce symptoms can range from very little to up to 25 grams. I am PI-IBS-D with fructose malabsorber and I cannot handle foods with more than 1 or 2 grams of excess fructose.

Fructose belongs to a broader class of poorly absorbed, short-chain carbohydrates or FODMAPs (Fermentable Oligo-, Di- and Mono-saccharides And Polyols) which includes such things as sorbitol, HFCS, raffinose, FOS, inulin, lactose and fructans. Many FODMAPs are identified as IBS triggers in the EFI.

The likely regions of the gut that generate most symptoms from FODMAPs are the distal small intestine and proximal colon. The volume of liquid in this region is dependent upon the osmotic load in that segment of bowel. Osmolality is kept within strict limits. Thus, small molecules in the diet that are poorly absorbed are candidates for changing the osmolality. Intraluminal gas is largely produced by fermentation of carbohydrates by bacteria. Their rapid production from FODMAP fermentation may cause increased luminal pressure and distension potentially triggering IBS symptoms. Also, fermentation of FODMAPs may produce methane gas in individuals whose colonic flora contain methogens. An increased concentration of methane gas in the colon is known to increase constipation.

Fructans which are long chains of fructose molecules sometimes trigger IBS symptoms although they are not as likely to as much as free fructose. Fructans are found in high concentrations in wheat. They are also found in foods like onions, leeks, garlic, shallots and asparagus. Most fructose malabsorbers can handle about 0.5 grams/serving of fructans or the equivalent to about one thin slice of bread. Many IBSers who are not celiac positive but feel they have gluten intolerance because wheat gives them problems may in fact be experiencing fructan malabsorption problems which may trigger IBS symptoms.

In summary, this latest research suggested that a FODMAP restricted version of the EFI diet may help up to 50% of IBSers of all subtypes. A personal dietary management strategy might initially included removal of foods like apples, applesauce, pears, honey, melons, grapes, etc and reduced consumption of wheat products. Later small amounts of these foods can be introduced until the individual finds the amounts of these foods they can handle or finds they have no problems with them at all.

My apologies for the long explanation. The notions are a bit complicated but worthwhile knowing if one wishes to design an optimum personal IBS dietary management strategy.

I hope this makes my comments a bit clearer as to why fructose malabsorption can be a problem for all IBS subtypes and why Prof. Whorwell's team might have prescribe the dietary regime Julieb is on

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STABLE: ♂, IBS-D 50+ years - Science of IBS

The FODMAP Approach to Managing IBS Symptoms
Evidence-based Dietary Management of Functional GI Symptoms: The FODMAP Approach
FODMAP Chart & Cheatsheet
The Role of Food & Dietary Intervention in IBS

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