what do you know about fructose malabsorption?

[perstephone]

It looks like that's the answer for my daughter, 2yo. She's still nursing, but we've been going round and round with GI symptoms- finally taking out all the high fructose fruits seems to be working. Quickly.
I suspected this a couple of months ago, when she clearly reacted to apples and pears but didn't think that it would really be fructose as she's been eating high fructose fruits for a long time.

My son has a salicylate intolerance, so we're no strangers to adjusting diet, just not thrilled about it. With my son, we supplement with some things to help his body handle the sals he does eat, and it helps his tolerance level.

What is there to do with fructose malabsorption? Is there something we can do to support the processing of fructose to get my daughter's body working closer to what it should be doing? The way I understand it, the fructose is getting all the way through to the large intestine and it should be removed way before that. If fructose is eaten with glucose, the glucose carries the fructose out where it belongs.

Any ideas? (besides forever avoiding onions, tomatoes, and the majority of fruit) Thanks a bunch!

[JaneS]

Disorders involving fructose metabolism
http://www.newworldencyclopedia.org/entry/Fructose

Fructose intolerance (Hereditary Fructose Intolerance or HFI) is caused by an inherited deficiency of the enzyme Fructose-1-phosphate aldolase-B. The absence of this enzyme prevents the breakdown of fructose beyond its intermediate fructose-1-phosphate. The resulting accumulation of fructose-1-phosphate and depletion of phosphates for ATP production in the liver blocks both the synthesis of glucose (gluconeogenesis) and the release of glucose through the breakdown of glycogen (glycogenolysis). If fructose is ingested, vomiting and hypoglycemia will result; long-term effects include a decline in liver function and possible kidney failure.

Fructosuria, in contrast, is caused by a genetic defect in the enzyme fructokinase. This benign disorder results in the excretion of fructose in the urine.

Fructose malabsorption (Dietary Fructose Intolerance or DFI) stems from a deficiency of a fructose transporter enzyme in the enterocytes (specialized cells found on the surface of the intestines). In fructose malabsorption, the small intestine fails to absorb fructose properly. In the large intestine, the unabsorbed fructose is metabolized by normal colonic bacteria to short-chain fatty acids and the gases hydrogen, carbon dioxide, and methane, which leads to symptoms of abdominal bloating, diarrhea, or constipation. Foods with high glucose content help sufferers to absorb fructose.

Whenever an enzyme deficiency is mentioned, I always think of magnesium deficiency. It would be interesting to uncover what nutrients support these enzymes. Like the PST enzyme which processes sals requires mag, sulfur, b6 and molybdenum.