Letzte Aktualisierung am 5. September 2024 von Dr. Michael Zechmann-Khreis
Lactose intolerance refers to the inability of the body to properly digest milk sugar (lactose) and the associated occurrence of gastrointestinal complaints. Milk sugar is a disaccharide, i.e. it consists of two individual sugars. Lactose is found in almost all dairy products and is normally broken down into its two individual sugars in the small intestine by an enzyme, lactase. This enzyme is formed in the wall of the small intestine and splits the lactose into its two components galactose (mucus sugar) and glucose (grape sugar). These simple sugars can then be absorbed into the body via the intestinal mucosa with the help of transport proteins. In people with lactose intolerance, this enzyme is missing (or insufficiently present), which means that not all of the lactose is broken down. The unsplit lactose continues into the large intestine. Bacteria are located there which process the lactose and produce gases and short-chain fatty acids, which then lead to the typical symptoms of lactose intolerance.
Types of lactose intolerance
Primary lactose intolerance
There are three different forms of primary lactose intolerance.
Endemic or ethnic lactose intolerance
This is the most common form of lactose intolerance worldwide. Around 70-80% of the world’s population have this form. It is genetic and is not a disease, but a normal condition. It occurs more frequently in warmer, sunny regions. All mammals, including humans, have the ability to digest lactose. In all mammals, however, this ability decreases or disappears with increasing age. This is because, biologically speaking, adults do not drink milk. The north-south divide is striking: While only 2-5% of people in the far north have this form, it is 15-20% in the Dach region and up to 60% in the southern Mediterranean. In East Asia and Africa, it even occurs in up to 100% of the population.
In some European humans, a genetic variant has developed during evolution that can continue to digest milk as adults. The reason for the continuation of enzyme production is a mutation of a specific gene. Lactase continues to be produced, even in old age. You can find a more detailed explanation of this form of lactose intolerance in our article on the global distribution of lactose intolerance.
Please note: The genetic test for lactose intolerance is not conclusive as to whether you have symptoms or not. Please read the article on the diagnosis of lactose intolerance.
congenital lactase deficiency
This is an autosomal recessive genetic defect in which not even the smallest amount of lactase is produced. This form is extremely rare and affects newborns. This defect is particularly evident in Finland.1
Developmental lactose intolerance
This is a very rare lactose intolerance that is only seen in premature babies. From the 8th week of pregnancy, the embryo already produces lactase. This production increases until the 34th week in order to reach a maximum at birth. Premature babies born before 32 weeks are often unable to produce sufficient lactase, which is why they are lactose intolerant. This form of lactose intolerance is reversible and has no effect on lactose intolerance later in life.
Secondary lactose intolerance
Health-related lactose intolerance
There is no genetic basis for this form. It occurs because of a disease or impairment of the small intestinal mucosa. It can also occur as a side effect of certain medications. This form of lactose intolerance regresses once the mucous membrane has regenerated or the cause of the intolerance has been eliminated.
If, for example, the intestine is so damaged due to coeliac disease that lactase can no longer be produced, this is secondary lactose intolerance. If the intestine recovers on a gluten-free diet, this ability can return. Secondary lactose intolerance is thus “cured”.
Diet-related lactose intolerance
It can also happen that you experience symptoms of lactose intolerance because your diet is not ideal. This happens when too much lactose is ingested on an empty stomach, for example through mixed milk drinks and ready-made products with dried milk products. The intestine is flooded with more lactose than the lactase that is actually present can break down. If the transit time is also short, i.e. the food slurry is transported quickly through the digestive tract, then lactose reaches the large intestine and is processed by the bacteria.
The microbiome also plays a role. Depending on its composition, more or less gas is produced and therefore more or less symptoms.
Milk allergy or lactose intolerance?
Milk allergies ( casein allergy, cow’s milk allergy, lactoglobulin allergy, mold cheese allergy4) differ from lactose intolerance or lactose intolerance. These are not intolerances to lactose (a sugar), but genuine allergies to certain proteins in milk. In the case of allergies, the smallest amounts are enough to cause symptoms. In the case of lactose intolerance, small amounts are harmless.
Summary
Lactose intolerance is the inability to properly digest milk sugar (lactose), which leads to gastrointestinal symptoms. Lactose, a disaccharide, is normally broken down into galactose and glucose in the small intestine by the enzyme lactase. In lactose intolerance, this enzyme is absent or insufficient, so that unsplit lactose enters the large intestine, where bacteria process it and produce gases and short-chain fatty acids that cause symptoms.
The amount of lactose eaten plays a major role in the occurrence of symptoms, as does the composition of the diet in terms of fats, proteins, fiber or minerals. The time spent in the digestive tract also plays a role. This means that you cannot generally say that you can or cannot tolerate a certain amount of lactose, as it always depends on your daily condition. However, you can usually assess your own tolerance well. Please also read our article on treating lactose intolerance.
Sources and others
- Catanzaro, R., Sciuto, M. & Marotta, F. Lactose intolerance: An update on its pathogenesis, diagnosis, and treatment. Nutr. Res. 89, 23-34 (2021).
- Ledochowski M. (Editor), “Klinische Ernährungsmedizin”, Springer-Verlag, 2009
- Vogelreuter A., “Food intolerances”, Wissenschaftliche Verlagsgesellschaft Stuttgart, 2012Further links
- DocCheck, retrieved on 1.9.2024