Letzte Aktualisierung am 11. December 2023 von Dr. Michael Zechmann-Khreis
There are basically two forms of fructose intolerance. However, these two forms have nothing to do with each other and are very different from a medical point of view. Hereditary fructose intolerance is a hereditary disease characterized by a congenital deficiency of the enzyme fructose-1-phosphate aldolase. The fructose is absorbed into the body via the intestine without any problems, but cannot be broken down properly in the liver. This form is extremely rare and leads to liver damage, kidney damage and hypoglycemia even in childhood. This serious illness occurs from the first complementary feeding. A healthy adult can no longer develop this disease. The term hereditary means “hereditary, inherited”.
Intestinal fructose intolerance(fructose malabsorption, fructose intolerance), on the other hand, is an acquired disease that is probably due to a defective and reduced transport system (GLUT-5 or GLUT-7) in the small intestine, i.e. fructose cannot be sufficiently absorbed into the body. However, once it has made it into the body, it can be broken down without any problems. This form affects about 15-30% of the population. The term intestinal means “belonging to the intestine”.
The simplified term“fructose intolerance” is used in public almost exclusively for intestinal fructose intolerance. We therefore also use this term here on the nmi portal. However, hereditary fructose intolerance is never meant (unless explicitly mentioned)!
Another difference: intolerance or malabsorption?
Maldigestion: means “poor digestion” – the The substance in question is not broken down properly in the stomach or small intestine and therefore cannot be digested properly
Malabsorption: means “poor absorption” – the The substance in question can only be transferred poorly or not at all via the digestive system and absorbed into the body
Intolerance: the malabsorbed substance causes symptoms
The difference between these terms lies in the detail and is not normally relevant for those affected. This is why the terms are usually used interchangeably. This means that fructose malabsorption is intestinal fructose intolerance. The same applies to the German term for intolerance. Fructose malabsorption is therefore also a fructose intolerance. The same applies to lactose intolerance, a lactose maldigestion is a lactose intolerance . From a medical point of view, things are different. For an exact diagnosis, the terms must of course be separated. Maldigestion can lead to malabsorption, which in turn can – but does not necessarily have to – lead to intolerance.
This means that there may be patients who have fructose malabsorption, but since they do not describe any noticeable symptoms, they do not suffer from intolerance. In medical practice, however, this will rarely occur, as patients usually come because of symptoms, i.e. they already have an intolerance. Malabsorption should also be treated, as this will also lead to problems in the future, even if the patient is unaware of it. This should certainly be taken into account in the case of multiple intolerances or patients with impaired self-perception!
In the diagnosis, the terms should therefore be broken down correctly wherever possible, but clear definitions used in the non-medical field should be used in communication with the patient. The diagnosis should be broken down even more clearly than stated here.
When do we start talking about fructose intolerance?
It is currently assumed that if less than 25g of fructose leads to symptoms in the H2 breath test, you are suffering from fructose intolerance. Normally, a person can absorb up to 50g of fructose without any problems. Does a healthy person eat more than these 50g, or is he influenced by medication or e.g. sugar alcohols, he may also experience temporary symptoms (temporary fructose intolerance).
Intestinal fructose intolerance: what happens in the body
It is not yet known exactly how fructose intolerance works, i.e. what does not work in the intestine. This is also because we do not know exactly how the absorption of sugars actually works. It is assumed that sugars are absorbed in the intestine with the help of transport proteins (GLUT, SGLT). The GLUT-5 transporter is responsible for fructose, but it can also be absorbed via GLUT-2 and GLUT-7 (5 ). These transporters bring the fructose from the intestine into the small intestinal cell, some of these transporters then bring the sugars out of the cell on the other side, into the blood. However, such transporters also react to other substances. Some sugar alcohols such as sorbitol, for example, block the GLUT-5 transporter, while glucose (glucose) may stimulate its activity. However, glucose has another effect. If there is a lot of it in the intestine, the GLUT-2 transporters migrate to the intestinal cell wall. As they also absorb fructose, more fructose can be digested. It used to be said: “Each molecule of glucose enables one molecule of fructose to be absorbed.” This sentence is probably not physiologically correct, but in practice this mnemonic still works.
This is why people with fructose malabsorption should avoid most sugar alcohols such as sorbitol, mannitol, isomalt, etc. and can eat glucose if they need to consume a lot of fructose (after the elimination period). But be careful: you shouldn’t do this too often and certainly not permanently, otherwise you run the risk of developing insulin resistance.
It is not yet clear why some people develop fructose intolerance.
Sources
(1) Rainer Klinke, Hans-Christian Pape, Stefan Silbernagl (eds.): “Lehrbuch der Physiologie”, 5th edition. Thieme, Stuttgart 2005
(2) Ledochowski M, Widner B, Fuchs D. “Fructose malabsorption”. J Ernährungsmed 2000; 2: 10-14
(3) Born Peter, World J Gastroenterol 2007 November 21;13(43): 5687-5691 “Carbohydrate malabsorption in patients with non-specific abdominal complaints”
(4) Manir Ali, Peter Rellos, Timothy M Cox, ItMed Genet 1998;35:353-365, “Hereditary fructose intolerance”
(5) Li Q, Manolescu A, Ritzel M, Yao S, Slugoski M, Young JD, Chen XZ, Cheeseman CI. Cloning and functional characterization of the human GLUT7 isoform SLC2A7 from the small intestine. Am J Physiol Gastrointest Liver Physiol 2004; 287: G236-G242
(6): Clinical Dictionary Pschyrembel, 261st edition, 2007; Verlag Walter de Gruyter
(7): H2 breath tests, M. Ledochowski, Ledochowski publishing house, 2008
(8): Ernährungsmedizin, K.Widhalm (ed.), Verlagshaus der Ärzte, 3rd edition, 2009
