Causes
Intolerance of fructose is caused by incomplete absorption (malabsorption) of fructose or chains of fructose linked together (fructose oligosaccharides, fructans, inulins) in the small intestine. Changes in the activity of the transport proteins underlying the absorption of fructose may be genetically determined, or due to inflammation or stress, but little is known about the exact triggers for the malabsorption, which often first appears in adulthood. The incompletely absorbed sugar consequently reaches the large intestine / colon, where it is metabolized by the colonic bacterial flora to various gases including methane and hydrogen, and other products, including some toxins. The role of increased intestinal permeability is unclear. Malabsorption leads to the symptoms of intolerance. This common and benign form of fructose intolerance must be distinguished from the rare and potentially dangerous hereditary fructose intolerance (HFI) (see Hereditary fructose intolerance).
Fructose or fructans are consumed as fruit, vegetables and grains in daily amounts of at least 20 to 60g, depending on the local diet and the consumption of high fructose corn syrup (HCFS) containing snacks or drinks. Some sports and fruit drinks contain up to 50g of fructose per 1000ml. Fructose consumption has increased markedly in the last decades and is implicated in the rapid increase in childhood obesity and the metabolic syndrome.
Frequency in population and natural history
- Approximately 30% of adults without major racial differences
- Up to 70% of patients with Irritable Bowel Syndrome
Commonly appears in adults and may be triggered by stress or inflammation.
Symptoms
These include bloating, abdominal cramps and pain, diarrhea and constipation, increased intestinal sounds and gas production, reflux (e.g. acid taste in mouth, heartburn) and nausea or vomiting. These symptoms resemble those of functional bowel disease and up to 70% of patients with Irritable Bowel Syndrome are fructose intolerant.
Depression may be more common in both adults and children with fructose malabsorption, and improves with strict dietary reduction in fructose intake. This may be due to lowered tryptophan levels in the blood.
Zinc and folic acid blood concentrations are decreased in a proportion of fructose intolerant.
Testing and diagnosis
See Tests.
In case of suspicion of severe fructose intolerance in children a careful history should be taken and specific genetic tests performed to exclude hereditary fructose intolerance (HFI) before performing the fructose breath test. This is recommended to prevent serious reactions to the ingested fructose.
Management
Reduction of the intake of fructose and fructans to individually tolerated levels will rapidly lead to symptom relief in most individuals. Best results are obtained if all dietary poorly absorbed, short-chain carbohydrates (FODMAPS) are reduced. The identification of fructose or fructan content is not intuitive and requires specialist advice to ensure adequate vitamin, fruit and vegetable intake. Generally the foods identified as ‘healthy’ contain fructose or fructans and replacement with other equally healthy alternatives or the addition of supplements constitute the dietician’s challenge. Sorbitol consumption should be reduced to a minimum, due to the high degree of concurrent intolerance and symptom exacerbation (see Sorbitol intolerance). As concurrent glucose consumption increases fructose absorption and hence tolerability, foods with high glucose content are better tolerated and glucose taken just before meals may reduce symptoms. Small amounts of fructose eaten after meals are better tolerated than a single dose on an empty stomach.
See Food tables for a listing of fructose and glucose food content.
Information nuggets
- Food allergies may co-exist.
- Lactose and fructose intolerance co-exist in approximately 20-30% of individuals
- Sorbitol and fructose intolerance very commonly co-exist and may exacerbate each other (see Sorbitol intolerance).
- Inulin-type fructans (chains of mainly fructose molecules) are interesting compounds to watch. They are natural components of food, including wheat, onion, banana, garlic, leek and chicory. They are non-digestible, fermented in the colon, and classified as dietary fiber and prebiotic. Animal and emerging human research have demonstrated the following effects: modification of composition and activities of the gut flora, improved stool production, enhanced absorption of calcium and other minerals, regulation of gastrointestinal endocrine peptides, increased immunity and resistance to infections, improved lipid homeostasis and the likelihood of reducing the risk of intestinal infections, functional bowel diseases, colon cancer, osteoporosis and obesity. Inulin-type fructans are thus functional food ingredients that are eligible for enhanced function claims, but, as more human data become available, risk reduction claims will become scientifically substantiated.
Links to literature
Shepherd S, Gibson. Fructose malabsorption and symptoms of Irritable Bowel Syndrome: Guidelines for effective dietary management. J Am Diet Assoc. 2006;106:1631-1639 (click to download pdf).
Hereditary fructose intolerance (HFI)
In distinction to the fructose malabsorption described above, HFI is a severe fructose intolerance due to genetic defects (aldolase B) mainly affecting children at the time of introduction of sugars, but also manifesting in adults. Besides the same symptoms as fructose malabsorption (above), metabolic disturbances, such as hypoglycemia, and permanent liver and kidney damage can ensue. In infants the disease may be lethal due to seizures and coma. There is even sensitivity to the fructose component of sucrose, household sugar, as well as to infusions containing fructose. All forms of sucrose and fructose, and probably also sorbitol, should be strictly avoided. A positive family history of sugar intolerance or an aversion against sweets / candies is a useful clue. Diagnosis is by careful history taking, blood sampling for metabolic, liver and kidney disease, and, specifically, genetic testing. At present not all forms of HFI can be identified using blood tests.
Links to literature:
http://www.bu.edu/aldolase/HFI/