Intestinal fructose intolerance

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Classification according to ICD-10
E74.3 Other disorders of intestinal carbohydrate absorption
ICD-10 online (WHO version 2019)

Intestinal fructose intolerance is the most common type of fructose intolerance, that is, intolerance to fruit sugar ( fructose ). If a larger proportion of consumed fructose gets into the large intestine due to incomplete absorption in the small intestine, it is called fructose malabsorption . Intestinal fructose intolerance is when the malabsorbed fructose also leads to symptoms such as diarrhea , flatulence and pain.

The importance of intestinal fructose intolerance has increased in the past as the amount of fructose in food has increased significantly in recent years due to industrially provided sweeteners.

The usual daily intake of fructose with food in various countries is 11–54 g per person.

terminology

The distinction between fructose malabsorption (FM) and intestinal fructose intolerance (= fructose malabsorption, which leads to symptoms and makes fructose intolerant, IFI for short) is still relatively new. In the older literature, both terms are almost always equated. However, it is overlooked that fructose malabsorption usually does not lead to fructose being intolerable.

The distinction between the two terms is similar (but not analogous) to the distinction in the case of lactase deficiency, where over the years the terms lactose intolerance for lactose intolerance due to symptoms and lactose malodigestion in the absence of symptoms have been established.

A designation proposed by Hoekstra in 1999, diminished fructose tolerance , has not been able to gain acceptance: This designation should create a clearer distinction for those people who show symptoms due to fructose malabsorption from other people, who are much rarer and more dangerous have hereditary fructose intolerance .

distribution

Scientific studies in various countries show that when given 25 g of fructose, around a third of people have fructose malabsorption , and of these around a third have symptoms caused by the malabsorbed fructose, i.e. H. intestinal fructose intolerance.

root cause

The cause of intestinal fructose intolerance (IFI) is the combined occurrence of fructose malabsorption (FM) and an additional functional bowel disorder. With fructose malabsorption, not enough fructose is extracted from the chyme in the small intestine , so that a larger part of this fructose reaches the large intestine . The functional intestinal disorder then results in the fructose entering the large intestine causing unpleasant symptoms such as diarrhea, gas or pain, i.e. H. makes this part of the fructose incompatible.

It is still unknown whether the below-average function of the fructose transport proteins is a normal frequency distribution within the population or a pathological change. In the latest literature review (2007), Gibson concludes that the proportion of fructose malabsorbers in the population is similar to that of patients with functional intestinal disorders, but symptoms after fructose malabsorption are significantly less common in the population, and that it can be assumed that fructose malabsorption is "normal" and so the reaction of the intestine to the malabsorbed fructose (ie the additional functional intestinal disorder) is actually responsible for the intolerance. Caspary writes in line with this theory that in a “normal” person about 20–30 g of fermentable carbohydrates reach the large intestine daily and the load limit is probably 20–50 g. Smith even estimated that the intestinal flora received around 70 g of carbohydrates per day. Rumessen concludes from its own hydrogen breath tests on 10 healthy people (5 out of 10 of these malabsorbed 25 g fructose, none with symptoms; maximum fructose intake ranged from 5 to> 50 g) that fructose malabsorption is a normal phenomenon in healthy people, and determines that in healthy people 30– 40 g of fructose can be malabsorbed without significant symptoms. Hoekstra concludes u. a. From the frequent coincidence of intestinal fructose intolerance and lactose intolerance, a general disturbance of the intestine with regard to movement or fermentation processes is more likely than a primary transport defect.

Gibson concludes that the reasons that the concept of fructose malabsorption has been poorly understood in gastroenterology may be in large part to be found in the following two points:

  • So far, fructose malabsorption has been regarded as a disease or abnormality.
  • It was not taken into account that non-absorbable fructans in the small intestine lead to the same symptoms as malabsorbed fructose.

Emergence

Fructose Malabsorption (FM)

GLUT-5 is a transport protein in the wall of the small intestine, with the help of which fructose can be selectively absorbed from the intestinal lumen along a concentration gradient; with increasing amounts of sucrose and fructose added, more GLUT-5 is formed.

In principle, fructose malabsorption (FM) can have various causes:

  • below average number of GLUT-5 in the wall of the small intestine
  • below average performance of GLUT-5 in the wall of the small intestine
  • too fast passage of the chyme through the small intestine, d. H. a short orozecal transit time.

A general distinction is made between two types of FM:

  • in primary FM, GLUT-5 or small intestine transit work poorly by nature,
  • in the secondary FM malabsorption is caused by damage to the intestinal mucosa by other diseases, such as celiac disease , acute gastrointestinal inflammation, Crohn's disease or medication.

Additional functional bowel disorder

So far nothing conclusive is known about the functional bowel disorder, which must be present in addition to FM so that symptoms occur when fructose enters the large intestine.

It is known that small molecules that enter the large intestine increase the osmotic pressure there , i.e. H. can lead to osmotic diarrhea and, on the other hand, can lead to rapid bacterial fermentation through the colon flora , producing substances that can also be osmotically active (e.g. short-chain fatty acids) or are gaseous and can thus cause flatulence ( carbon dioxide , methane , hydrogen , ...). However, a higher intake of unabsorbed carbohydrates adapts - e.g. B. after small intestine operations - the colon flora quickly. Studies show that about a third of the population has FM after ingesting 25 g of fructose, but only 1/3 of this third also experience symptoms.

The following possible causes are discussed in the specialist literature as possible reasons why symptoms only occur in less than half of the fructose malabsorbers after fructose ingestion:

  • Composition of the bacterial colon flora or its performance or its breakdown products
  • Problems with the transport and / or drainage of the intestinal contents or the absorption capacity for short-chain fatty acids in the large intestine
  • Problems converting information from the intestines (e.g. pressure or sugar levels) into the body's correct response
  • Problems with the transmission of information in the body ( feedback mechanisms)
  • Speed ​​of gastric emptying

Individual cases

Individual cases are known in which intestinal fructose intolerance first appeared after a stomach or intestinal infection, after taking antibiotics, after pregnancy, in the event of hormone fluctuations or during prolonged stressful situations. However, it is not known whether these events caused the fructose malabsorption and / or the additional functional intestinal disorder. But it also happens that the onset of the disease occurs insidiously without any particular trigger or recognizable cause.

Frequently, intestinal fructose intolerance occurs temporarily in childhood when people begin to consume fruit or large quantities of fruit juice.

Clinical manifestations

Symptoms

The main symptoms of fructose malabsorption are gas , diarrhea , nausea, and abdominal pain . In those affected who continue to eat fructose, the intestinal flora and thus the absorption capacity in the small and large intestines can deteriorate further. Other symptoms such as irritable stomach or irritable bowel syndrome can occur. The symptoms are mainly caused by the resulting carbon dioxide (flatulence) and the short-chain fatty acids (osmotic diarrhea).

Primary symptoms

The following symptoms occur after a single consumption of food containing fructose:
  • Abdominal pain, cramps, and colic (due to fermentation in the small and large intestines)
  • Flatulence (often foul smelling due to fermentation)
  • Mushy stool (often smelly due to fermentation)
  • Diarrhea (partly watery diarrhea due to osmotic effects)
  • Bloating
  • constipation

Secondary symptoms

Further symptoms can occur in those affected after frequent or regular intake of fructose. Most of these are linked to a further absorption disorder caused by fructose malabsorption, such as the essential amino acid tryptophan , folic acid or zinc .
  • Irritable bowel syndrome
  • Depression as a result of absorption disorders in the large and small intestines can also contain other substances, e.g. B. essential amino acids are not absorbed. Because of lack of tryptophan occur serotonin deficient symptoms on.
  • fatigue
  • a headache
  • nausea
  • Reflux (chronic heartburn)

A long list of other possible symptoms can be found at Bair.

Deficiency symptoms

The blood concentrations of tryptophan , folic acid and zinc are often low.

Investigation methods

Fructose malabsorption

Fructose hydrogen breath test

Using a hydrogen breath test , the diagnosis may fructose malabsorption be relatively easily made. In this test, the concentration of hydrogen (H 2 ) in the exhaled air is measured: After at least 12 hours without food, the exhaled air is examined for H 2 . Then the test person is administered orally fructose (usually 25 g of fructose in 250 g of water). If the hydrogen content rises significantly (usually 10-20 ppm , in individual cases ) during subsequent measurements at intervals of 15 to 30 minutes after a period of time corresponding to the passage through the small intestine (approx. 40–110 min) 3–6 ppm), then there is fructose malabsorption or small intestine colonization, as the human body itself does not produce hydrogen and this is therefore due to the ingested fructose.

Background : After ingestion of carbohydrates such as fructose, these enter the small intestine. The fructose is ideally completely or only partially absorbed in the small intestine; the reason is fructose malabsorption or small intestine overgrowth. This remaining fructose enters the large intestine undesirably. In the large intestine, certain bacteria convert carbohydrates into hydrogen, among other things. The hydrogen enters the lungs via the bloodstream and is exhaled. Lactulose is always indigestible for humans, therefore it always reaches the large intestine completely and can therefore be used as a control substance if the test is ambiguous. The ratio of exhaled hydrogen to fructose or lactulose that has arrived in the large intestine varies from person to person and depends in particular on the nature of the intestinal flora. People to whom this (almost) does not happen at all are called non-responders. The proportion of non-responders is up to 27%.

For example, intestinal lavage (for a colonoscopy) and certain antibiotics can flush out or kill the bacteria in question. How much breath hydrogen is produced per mass of carbohydrate that gets into the large intestine can be roughly determined by integrating the breath hydrogen concentrations after lactulose consumption over the small intestine passage time; With this result, it is then possible to use the rule of three in a correspondingly carried out and evaluated fructose-hydrogen breath test to calculate the amount of orally administered fructose that has reached the large intestine.

A lactulose-hydrogen breath test is therefore used to verify a negative fructose-hydrogen breath test and determine the orozecal transit time and the degree of malabsorption.

Measurement of the fructose plasma level

The attempt to diagnose fructose malabsorption on the basis of blood sugar values ​​or fructose serum concentrations after oral administration of fructose contradicts scientific knowledge, which is why this procedure is not used in the specialist literature.

Truswell (1988) showed with experiments on 103 people that the method is unusable because the change in the fructose serum concentration does not correlate with the malabsorption. There was even a tendency for higher fructose serum concentrations in malabsorbents than in non-malabsorbents.

Macdonald (1978) previously examined the temporal change in 8 blood serum values ​​(glucose = blood sugar, insulin, fructose, triglycerides, lactate, pyruvate, glycerol and uric acid) after oral administration of various amounts of fructose (0.25, 0.5) in only 9 healthy people , 0.75 and 1 g fructose per kg body weight). It was found that only the blood fructose concentration shows an increase, and this is proportional to the amount of fructose administered. Among other things, due to the extremely small number of test persons and because malabsorbents were not examined, this examination does not meet scientific standards.

In contrast to the lactose blood sugar test (where lactose is converted into glucose in the small intestine), a diagnosis of fructose malabsorption by measuring the blood sugar level (glucose) is not possible, since the fructose ingested is so slowly converted into glucose in the liver that a rise in blood sugar is not significant would. The attempt to make a diagnosis on the basis of a change in the glucose and fructose concentration in the blood due to fructose absorbed in the small intestine contradicts Truswell's knowledge that possible changes do not follow sufficient statistical regularity.

Intestinal fructose intolerance

In the event that one of the above If sufficient hydrogen excretion is detected in the fructose stress test and symptoms occur (which do not result directly from an overgrowth in the small intestine, but from fructose malabsorption), intestinal fructose intolerance is present.

Join one of the above If the fructose stress test shows symptoms (which do not result directly from an over-colonization of the small intestine, but from fructose malabsorption), no “normal result” (“healthy”) is to be issued even if there is no measurable hydrogen concentration, since in this case a non-responder and an intestinal one Fructose intolerance due to fructose malabsorption is expected.

Differential diagnoses

Hereditary fructose intolerance (HFI)

Before a fructose stress test, the extremely rare hereditary fructose intolerance ( HFI ) must e.g. B. be absolutely excluded by genetic testing, since the fructose stress test in this case can be life-threatening, as the enzyme deficiency in the liver in HFI would lead to the ingested fructose not being broken down and the glucose, the blood sugar , being displaced in the blood resulting in hypoglycaemia and possibly shock .

Overgrowth of the small intestine

  • Difficulties with positive fructose hydrogen breath tests are the distinction between fructose malabsorption and an overgrowth in the small intestine, especially since both often occur together. If the small intestine is incorrectly colonized, there are an unnatural number of bacteria in the small intestine which, after receiving fructose, can also produce hydrogen, so that in this case the excreted hydrogen no longer indicates absorption disorders. The distinction can often be made on the basis of the evolution of hydrogen elimination over time during the test. So speak z. B. an extremely early hydrogen excretion or a double peak for a small intestine overgrowth.
  • Nucera showed that after one week of antibiotics in irritable bowel patients with suspected small bowel colonization due to a lactulose hydrogen breath test, fructose, lactose and sorbitol malabsorption also disappeared in most cases. Nucera offers two explanations: One is that an existing overgrowth in the small intestine can falsely simulate malabsorption or that the overgrowth weakens the mucous membrane of the small intestine and thus leads to secondary malabsorption. From the high number of incorrect colonizations, Nucera recommends first ruling out incorrect colonizations before addressing malabsorption or elimination diets.

pathology

In the intestinal fructose intolerance is a functional bowel disorder, d. H. no pathological findings have been reported so far .

Treatment, therapy

  • To cure the functional bowel disorder that is present in addition to the FM and is responsible for the symptoms, no approaches have been validated due to a lack of knowledge of the exact cause.
  • In secondary FM , the elimination of the disease that causes the weakening of the small intestinal mucosa (e.g. antibiotic treatment of an overgrowth of the small intestine) by definition leads to the cure of the FM and thus also to the cure of the IFI .
  • With one exception, the therapies practiced up to now are limited to attempts to reduce symptoms by avoiding special foods and have practically no success with regard to healing, i.e. H. the subsequent possibility of being able to eat all food again without symptoms.

Avoid fructose and FODMAP

The symptoms of IFIs can be avoided by limiting the intake of fructose and high-fiber, flatulent foods as individually as necessary; an understandable nutritional therapy was published by Bair. More recent studies focus even more on the fact that in the case of intestinal fructose intolerance , other carbohydrates that reach the large intestine ( FODMAP = fermentable oligosaccharide, disaccharides, monosaccharides, and polyols) often cause the same symptoms, so it may be necessary to avoid them as well . These are z. B. to

  • Oligofructose (and inulin = polymeric oligofructose), as often found in fruits or food supplements such as prebiotics,
  • Stachyose, raffinose, verbascose, as found in legumes, beans, onions and leeks,
  • Lactulose (laxative),
  • Sorbitol, xylitol, mannitol, maltitol, palatinit (“isomalt”) and other sugar alcohols, as used in diet products.

In particular, the fructose alcohol sorbitol should be avoided , as it worsens the absorption of fructose in the small intestine when fructose is taken at the same time: The simultaneous administration of fructose and sorbitol led to far higher amounts of hydrogen in the air in 10 healthy people than the sum of the amounts of hydrogen from the individual tests the individual quantities. When fructose is administered alone, the amount of unabsorbed fructose (determined as the area “H 2 -ppm × time”) is proportional to the total amount administered. Furthermore, the amount of sorbitol in which malabsorption does not occur is only about 1/5 of the amount of fructose in which malabsorption does not occur.

Various food supplements containing xylose isomerase (an enzyme used in the food industry ) are said to convert the fructose in the intestine into glucose.

Glucose improves the absorption of fructose

GLUT-2 is a second transport protein in the wall of the small intestine, with the help of which not only glucose and galactose but also fructose can be absorbed from the intestinal lumen along a concentration gradient. GLUT-2 is quickly and reversibly incorporated into the wall of the small intestine as soon as the transport protein SGLT1 transports glucose. Since the absorption of fructose in the intestine is improved by glucose independently of GLUT-5 , an uptake in a 1: 1 ratio of fructose: glucose is not critical for FM in moderation. This also enables the absorption of household sugar (sucrose), which is broken down into glucose and fructose in the small intestine, independently of GLUT-5. Various studies on the absorption of sucrose then always yielded negative hydrogen breath tests with the administration of sucrose or 1: 1 (glucose or galactose or maltose): fructose.

Hoekstra (1999) suspects that the reason for this is that the simultaneous addition of glucose to fructose, sorbitol or xylose improves the absorption of the latter, entrainment effects for them through the water, which is also absorbed by the absorption of glucose (“solvent drag”). He also explains that amino acids significantly improve the absorption of fructose.

The German Nutrition Society advises against fructose malabsorption from a fruitless or fructose-free permanent diet. At IFIs, foods with a one-sided, high fructose concentration must be avoided in particular, as the glucose: fructose balance does not work here.

There are lists of foods with their glucose and fructose content (see section Web Links / Additional Material ).

Due to the above-mentioned improved fructose absorption through glucose, it is often recommended that foods containing fructose should be taken together with pure grape sugar in order to prevent indigestion. However, this tip should be viewed with caution. The supportive effect was only investigated with sugar solutions in sober study participants and does not take into account the different digestive speed of glucose powder and complete meals, nor the digestive problems caused by other poorly absorbable food components (e.g. sorbitol or fructans).

Other related intolerances

If the symptoms do not completely disappear even with a low-fructose diet (see above), there may be another intolerance; around 80% of lactose intolerant patients also suffer from fructose malabsorption.

No low fat diet

Cohen reports that in five children aged 12-25 months, the permanent switch to low-fat foods such as low-fat milk, e. Sometimes in connection with the administration of fruit juices and dietary fiber, it led to permanent diarrhea lasting several months, which disappeared within 5–28 days after switching to a higher-fat diet and reappeared with a reduced-fat diet. He concludes that the previously known effects of higher fat diets such as slower gastric emptying and increased oral transit time are responsible. In another study, Cohen shows that in 97% of children with persistent diarrhea (often caused by a previous stomach inflammation), the diarrhea disappears when they eat a higher fat diet and returns when they switch to a reduced-fat diet. He points out that if you are lactose intolerant, the usual 3.5% fat in milk is automatically omitted as a source of fat. See also the Prevention / Childhood section .

prevention

In childhood

It is known that foul-smelling watery diarrhea often occurs between the ages of 1 and 5 when fruits are ingested in the diet and larger amounts of fruit juice (especially apple juice) are consumed. Hoekstra questioned at an important role of fructose malabsorption here and recommends to its own investigations, a "normalization" of eating habits in terms of the "four F": fat, fiber ( fiber ), liquid and fruit juice which i. d. Usually leads to success after a few days:

  • Dietary fiber is known to hold water; The removal of fiber from naturally cloudy apple juice by means of enzymes to obtain clear apple juice means that clear apple juice is often no longer tolerated
  • The milk consumption, which decreases with age, and the energy supply via fruit juices lowers the amount of fat supplied and thus the time it spends in the gastrointestinal tract; Hoekstra recommends that 35–40% of food energy is obtained from fat
  • Fruit juice consumption should only take place with meals
  • Further fluid consumption should not exceed a normal level

If FM is diagnosed with no symptoms

If FM is diagnosed without symptoms, some of the fructose from food will get into the colon and change the intestinal flora there. The assumption that this can lead to intestinal fructose intolerance over a longer period of time has not been proven . A preventive measure against IFIs could be to avoid large amounts of fructose and sorbitol if FM is diagnosed with no symptoms.

Prospect of healing

Improvement of the GLUT

There is no known specialist literature in which a permanent improvement in the function of the glucose transporter GLUT-5 or GLUT-2 with regard to fructose transport is reported.

Avoid fructose

There is no known literature to show that a diet that avoided fructose has restored the intestinal flora, thereby eliminating intestinal fructose intolerance. However, it is known that the expression of GLUT-5 decreases with decreasing amount of fructose in the chyme and, in rats, that even a 3-day fructose-rich diet dramatically increases the fructose absorption capacity of the small intestine, so that with a low-fructose diet this is definitely a counterproductive effect is achieved.

Intestinal lavage

This article or the following section is not adequately provided with supporting documents ( e.g. individual evidence ). Information without sufficient evidence could be removed soon. Please help Wikipedia by researching the information and including good evidence.

There have been isolated reports that intestinal fructose intolerance disappeared at least temporarily after intestinal lavage in preparation for a colonoscopy.

Antibiotics

This article or the following section is not adequately provided with supporting documents ( e.g. individual evidence ). Information without sufficient evidence could be removed soon. Please help Wikipedia by researching the information and including good evidence.

There have been isolated reports that intestinal fructose intolerance has disappeared after taking special antibiotics (e.g. metronidazole ). However, it is unclear about these reports:

  • whether only a small intestine overgrowth has been eliminated that can produce similar symptoms and diagnostic results,
  • whether the colon flora has been modified in such a way that symptoms no longer occur if FM is still present, although fructose continues to enter the colon.
  • Giardia group of small intestine parasites (such as Giardia intestinalis ) can trigger FM and lactose malabsorption. Antibiotic treatment can also make the intolerance and digestive problems go away.

history

Irritable bowel syndrome

Before the so-called fructose malabsorption became known i. d. Usually the diagnosis of irritable bowel syndrome is made, since IFIs do not show any organic changes and thus a functional bowel disorder is present.

First work on fructose malabsorption

The first study on fructose malabsorption was reported in 1978: 4 patients who were without problems after several years of a fructose-free diet (F group) are compared to a control group of 11 patients with intestinal complaints who did not improve on a fructose-free diet (diagnosis: mostly LI or irritable bowel syndrome). The subjects of the F group and 30% of the control group complained of pain after administration of 100 g of fructose, the F group also of diarrhea. In terms of blood values, only the fructose concentration in the F group differed from the control group (0.4 instead of 0.5 mmol / l for 30–120 min). After administration of 50 g of fructose with 14 C marking, the F group exhaled a significantly lower amount of 14 CO 2 with the same total amount of CO 2 within the first 60 minutes , which the authors attribute to the fact that fructose is malabsorbed in the small intestine could be present. The authors refer to similar results from others in 14 C-lactose tests.

In 1983, Barnes found in a 12-year-old girl with permanent diarrhea by means of a breath test that even the small amount of 1 g fructose led to an increase of 10 ppm in the hydrogen concentration.

Statistics in specialist articles

Many technical articles on fructose malabsorption followed, most of which contained statistically useful material on the incidence of fructose malabsorption and intestinal fructose intolerance in different groups using hydrogen breath tests , but no publication information regarding healing of IFI due to primary FM .

Here is some information about the statistically usable material:

  • The higher the amount of carbohydrate administered in the tolerance tests, the more likely malabsorption / maldigestion is. The following table provides a self-made overview of malabsorption rates in approx. 1000 healthy and intestinal patients from the Gibson literature sources. The percentage of malabsorbers averaged over the number of publications is shown in brackets.
Test carbohydrate Amount, g % Malabsorbers in healthy people % Malabsorbers in intestinal patients
Fructose 20-25 19-47 (36) 31-54 (47)
Fructose 50 38-81 (64) not a single test
Sorbitol 5 50-57 (53) 58-68 (63)
Sorbitol 10 59-71 (65) not a single test
Sorbitol 20-25 84-86 (85) not a single test
Sucrose 50 (*) 0 0
(*) 4 different publications from 3 different research groups with a total of 53 people, of which at least 11 were intestinal patients (presumably FI).
  • A review of the literature shows that the dose of 1 g / kg body weight in children provides approximately similar malabsorption rates (44%) as the dose of 25 g in adults and 2 g / kg in 85% malabsorbents. If no more than 50% of those tested are to be classified as malabsorbers using the breath test, the dose for adults is 25 g and for children 1 g / kg (however, a maximum of 25 g).
  • The proportion of malabsorbents in men and women seems to be similarly high.
  • The proportion of malabsorbers in the healthy population seems to be similarly high as in intestinal patients (see also the table above).

Works by Born, Ledochowski and Gibson

In 1995 Born showed for the first time what origins the occurrence of symptoms in fructose malabsorption could have. He suspects from growth experiments with stool samples, which can be stopped with metronidazole in carbohydrate intolerants, that bacteroides strains could possibly be responsible.

Gibson started using the FODMAP diet described above for individuals with IFIs in 2006, which is the latest research on IFIs. His review from 2007 comprehensively summarizes the current status with regard to IFI / FM.

Ledochowski is the first to introduce the clear distinction between fructose malabsorption (= positive fructose hydrogen breath test) and intestinal fructose intolerance (= fructose malabsorption with symptoms), after mostly fructose malabsorption and (intestinal) fructose intolerance have been equated over the years.

Cultural aspects

In contrast to studies on lactose intolerance , the published studies on fructose malabsorption and intestinal fructose intolerance have not yet confirmed that the frequency of occurrence in the population differs greatly between different countries.

literature

  • Eating and drinking in case of fructose malabsorption . German Nutrition Society, ISBN 978-3-88749-211-3 .
  • H. Kasper: Nutritional medicine and dietetics . With the collaboration of Walter Burghardt - with access to the Elsevier portal. Elsevier Verlag, 2009, ISBN 978-3-437-42012-2 .
  • As controller, C. regulator, H. Braunewell: food intolerances in children . Trias-Verlag, 2010, ISBN 978-3-8304-3528-0 .
  • D. Reinhardt: treatment of diseases in childhood and adolescence . Springer Verlag, 2009, ISBN 978-3-540-71898-7 .
  • M. Sacherl: Hereditary fructose intolerance and fructose malabsorption: A manual with background knowledge from those affected for those affected . Wiedemann Verlag, 2007, ISBN 978-3-00-021754-8 .

Web links

Individual evidence

  1. ↑ a b c d e f g h i j k l m n o p q r P.R. Gibson, E. Newnham, JS Barrett, SJ Shepherd, JG Muir: Review article: fructose malabsorption and the bigger picture . In: Aliment Pharmacol Ther . 25, 2007, pp. 349-363.
  2. ↑ a b c A. Eisenmann, A. Amann, M. Said, B. Datta, M. Ledochowski: Implementation and interpretation of hydrogen breath tests . (PDF, 192 kB) In: J. Breath Res. . 2, 2008, pp. 1-9.
  3. ↑ a b c d e M. Ledochowski: H2-Atemteste , Verlag Ledochowski, 2008, ISBN 978-3-9502468-0-3 .
  4. ↑ a b H.-J. Thon, G. Bünnagel, M. Neuhausen: Does fructose malabsorption belong to the spectrum of causes in patients with diarrhea-dominant irritable bowel syndrome (IBS)? . (PDF; 58 kB) In: special med . August.
  5. ↑ a b c C.P. Corpe, CF Burant, JH Hoekstra: Intestinal Fructose Absorption: Clinical and Molecular Aspects (HTML full text) . In: Journal of Pediatric Gastroenterology and Nutrition . 28, 1999, pp. 364-374.
  6. ↑ a b c d e J.J. Rumessen, E. Gudmand-Hoyer: Absorption capacity of fructose in healthy adults. Comparison with sucrose and is constituent monosaccharides . In: Good . 27, 1986, pp. 1161-1168.
  7. ↑ a b c A.S. Truswell, JM Seach, AW Thorburn: Incomplete absorption of pure fructose in healthy subjects and the facilitating effect of glucose . (PDF; 1.7 MB) In: Am J Clin Nutr . 48, 1988, pp. 1424-1430.
  8. ↑ a b c d e P. Born, J. Zech, H. Lehn, M. Classe, R. Lorenz: Colonic Bacterial Activity Determines The Symptoms In People With Fructose Malabsorption . In: Hepato-Gastroenterology . 42, 1995, pp. 778-785. PMID 8847022 .
  9. ↑ a b c d P. Born: DD of unspecific abdominal complaints: the carbohydrate malabsorption . In: Münch. Med. Wschr. . 139, No. 29, 1997, pp. 32 / 436-36 / 440.
  10. ↑ a b c d e f W.F. Caspary: Diarrhea Associated with Carbohydrate Malabsorption . In: Clinics in Gastroenterology . 15, No. 3, 1986, pp. 631-655.
  11. ^ CJ Smith MP Bryant: Introduction to metabolic activities of intestinal bacteria . (PDF) In: Am J Clin Nutr . 32, 1979, pp. 149-157.
  12. ↑ a b G. Nucera, M. Gabrielli, A. Lupascu, EC Lauritano, A. Santoliquido, F. Cremonini, G. Cammarota, P. tondi, Pola P., G. Gasbarrini, A. Gasbarrini: Abnormal breath tests to lactose, fructose and sorbitol in irritable bowel syndrome may be explained by small intestinal bacterial overgrowth . In: Aliment Pharmacol Ther . 21, 2005, pp. 1391-1395. doi : 10.1111 / j.1365-2036.2005.02493.x . PMID 15932370 .
  13. ↑ JH Bond, BE Currier, H. Buchwald, MD Levitt: Colonic Conservation of Malabsorbed Carbohydrate . In: Gastroenterology . 78, 1980, pp. 444-447.
  14. ^ P. Born, C. Bauch, J. Zech, R. Lorenz, M. Classen: Carbohydrate malabsorption - the role of colon bacteria in the development of symptoms . In: Digestive Diseases . 15, No. 5, 1997, pp. 205-208.
  15. ↑ a b c F. Fernandez-Banares, M. Esteve-Pardo, R. de Leon, P. Humbert, E. Cabre, JM Llovet, MA Gassull: Sugar Malabsorption in Functional Bowel Disease: Clinical Implications . In: Am. J. Gastroenerol . 88, No. 12, 1993, pp. 2044-2050.
  16. ↑ a b c d e f g H. Bair: Fructose malabsorption . In: Nutrition News . Sept./Oct. 2003, 2003, pp. 11-14.
  17. ^ TR Fenton, JT Harries, PJ Milla: Disordered small intestinal motility: a rational basis for toddlers' diarrhea . In: Good . 24, 1983, pp. 897-903.
  18. ↑ D. Reinhardt: Therapy of Diseases in Childhood and Adolescence. 8th edition. Springer, 2007, ISBN 978-3-540-71898-7 .
  19. ↑ a b M. Ledochowski, D. Fuchs, B. Widner: Fructose malabsorption . In: Journal for Nutritional Medicine (edition for Switzerland) . 3, No. 1, 2001, pp. 15-19. M. Ledochowski, D. Fuchs, B. Widner: Fructose malabsorption . (PDF; 444 kB) In: Journal for Nutritional Medicine (edition for Austria) . 2, No. 3, 2000, pp. 10-14.
  20. ↑ a b c d e f g P. Born: Carbohydrate malabsorption - symptoms, diagnostics, therapy . In: Biological Medicine . 6, No. December 1990, 1990, pp. 356-361.
  21. ↑ a b c W.L. Dills: Protein fructosylation: fructose and the Maillard reaction . (PDF) In: Am J Clin Nutr . 58-Suppl., 1993, pp. 779S-787S.
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  34. ^ Enzyme isomerase in fructose malabsorption
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  37. ^ German Society for Nutrition : Fructose Malabsorption. DGEInfo 12/2005 - Consulting Practice, December 1, 2005
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