With lactose intolerance , lactose intolerance or lactose intolerance of ingested is milk sugar as a result of missing or reduced production of digestive enzyme lactase not digested or incomplete; this can result in an intolerance to milk and milk products. Lactose intolerance is very rare in children under the age of five. Usually it only develops in adolescence and adulthood. Lactose intolerance is very common worldwide, although there are significant differences depending on the region and population. Around 5 to 15% of Europeans cannot tolerate lactose. Lactose intolerance is rarest in Northern Europe. In Africa or East Asia, on the other hand, 65 to over 90% of adults are affected. The evolutionary advantage of the Northern Europeans, known as lactase persistence , arose from a gene mutation about 7000 years ago in the course of the increasingly important dairy farming.
All (healthy) newborn mammals form the enzyme lactase during suckling ( infants during breastfeeding ) , which splits the unabsorbed disaccharide lactose into the usable simple sugars D - galactose and D - glucose . For this purpose, lactase is formed in the thin intestinal mucosa (especially in the jejunum ) and is a component of intestinal juice ; it enables the newborn to use the lactose-rich breast milk as the main source of energy.
In the course of natural weaning from breast milk, lactase activity drops to around 5–10% of the activity at birth. This applies to humans and all other mammals. Only in populations that have been dairy farmers for a long time has a mutation prevailed which means that sufficient lactase is still produced in adulthood; this is known as lactase persistence. This is probably due to the fact that the higher lactase activity offered a selection advantage (minerals, nutritional value) for these groups.
In the case of insufficient lactase activity, unsplit lactose reaches the large intestine in humans, where it is absorbed and fermented by intestinal bacteria . Lactate (the salt of lactic acid ) and the gases carbon dioxide (CO 2 ), methane (CH 4 ) and hydrogen (H 2 ) are usually formed as fermentation products shortly after consumption . The gases lead, among other things, to a feeling of fullness, pelvic pain, flatulence and the short-chain fatty acids which are also formed, to nausea and vomiting. The osmotically active lactic acid causes water to flow into the intestine with diarrhea (osmotic diarrhea ). In Asia and Africa, the lack of lactase persistence affects most of the adult population (90% or more), in Western Europe, Australia and North America it is 5–15% (in fair-skinned people).
Lactose intolerance can have several causes:
- Congenital lactase deficiency (absolute lactose intolerance ): Due to a genetic defect , lactase production is severely restricted or no enzyme can be produced at all (so-called alactasia ). Inheritance is autosomal - recessive . It is a rare hereditary disease that can be identified by diarrhea in the first few days after birth.
- Some infants diagnosed with congenital lactose intolerance may have a rare disorder in which undigested lactose is absorbed by the stomach, enters the bloodstream ( lactosemia ) and is excreted in the urine ( lactosuria ). Since undigested lactose is harmful in the blood, the disorder can lead to symptoms of intoxication with cataracts and liver and brain damage undetected .
- Primary (natural) lactase deficiency : This digestive enzyme is usually produced in sufficient quantities in infants. After a few years, however, the amount of lactase produced decreases differently depending on the population. For example, a large part of the adult Central and South Asian population no longer tolerates dairy products , in northern areas (for most of the inhabitants of Europe and the Middle East or people of European and Middle Eastern descent and the Siberian and Mongolian ethnic groups), lactose intake usually continues well into old age no problem. The reason for the drying up of enzyme production in adulthood is a gene on the long arm of chromosome 2 (2q21) in the promoter area of the lactase gene: CC genotype of the C / T-13910 polymorphism or GG genotype of G / A-22018- Polymorphism.
Secondary (acquired or temporary) lactose intolerance (according to Leiß 2005), e.g. B. by the following causes:
- Diseases of the digestive system can damage so that the temporary lactase production is impaired, especially during childhood, lactase-producing cells in the small intestine; after curing, this deficiency usually disappears completely. In rare cases, the lactase-producing tissues are so damaged that they can no longer recover, leading to chronic lactose intolerance.
- bacterial or viral gastroenteritis
- chronic bowel disease
- Celiac disease / sprue
- intestinal lymphoma
- partial or total gastrectomy
- Short bowel syndrome
- Blind sac syndrome / large duodenal diverticulum
- Chemotherapy / radiation therapy
- chronic alcohol abuse
- Small intestinal parasites from the Giardia group (such as Giardia intestinalis )
A self-diagnosis of lactose intolerance can be carried out with a test sequence:
- Diet test: A consistent diet for several days without lactose, especially without milk, cream and "hidden" lactose (many finished products contain milk sugar or milk components). If there are no more symptoms during this time, lactose intolerance is possible.
- Exposure test: After a few days without lactose, a glass of water with 50 to 100 g of dissolved milk sugar is drunk. If the typical symptoms appear within a few hours, you are probably lactose intolerant.
The diagnosis is often ambiguous because there is only incomplete intolerance. In the usual form, the intolerance increases in the course of life, not so with the congenital lactase deficiency.
The following tests are more complex:
- H 2 breath test : This method is based on the detection of hydrogen (H 2 ) in the exhaled air. It is an indirect proof of lactase deficiency. In addition to lactic acid , acetic acid and carbon dioxide ,the bacterial processing of lactose in the large intestine also producesgaseous hydrogen . This reaches the lungs via the blood and is exhaled. Since there is normally no hydrogen in the exhaled air, a positive result indicates a possible lactose intolerance. This test measures the hydrogen concentration before and after the oral administration of a defined amount of lactose (milk sugar). The result is considered positive if the measurement result before and after the lactose administration shows a difference of 20 ppm hydrogen. However, this test leads to a negative result for every fifth lactose intolerant: These patients have certain (harmless) bacteria in their intestinal florathat produce methane , which means that it is not possible to detect hydrogen.
- Blood sugar test: This procedure is based on the measurement of the glucose content in the blood ( venous blood or capillary blood ), the lactase activity is determined by an increase in the concentration of glucose in the blood. Since lactose is normally broken down into galactose and glucose , the glucose value ( blood sugar value ) should rise if lactose is ingested. If this is not the case, a lactose intolerance is suspected. In this test, too, the patient consumes a defined amount of lactose (usually 50 grams dissolved in half a liter of still water) on an empty stomach. A blood sample is taken before ingestion and every 30 minutes after ingestion for two hours and the blood sugar level is measured. An increase of more than 20 mg / dl (1.11 mmol / l) glucose in venous blood or 25 mg / dl in capillary blood is normal. An increase of less than 10 mg / dl in venous blood is pathological. False negative results are possible in patients with latent or manifest diabetes mellitus .
- Genetic test: A genetic test for the LCT genotype has recently been carried out if lactose intolerance is suspected . A simple blood sample is used as the test material.
- Biopsy: In rare cases, a tissue sample must be taken from the small intestine and examined. Here the lactase activity in the small intestinal tissue is examined.
Lactose malodigestion does not necessarily lead to lactose intolerance
Clinical studies have shown that the primary lactase deficiency (non-persistence) and the resulting digestive weakness for milk sugar (lactose malodigestion) do not necessarily lead to the known symptoms of lactose intolerance. Most people with primary lactase deficiency can tolerate up to 12 g of lactose without symptoms, which is roughly equivalent to a glass of milk (200 ml). Of lactase deficiency test persons with significantly increased breath hydrogen after ingesting 25 g of lactose, about half tolerated this amount without symptoms. There are also people who digest lactose well but still show symptoms of intolerance, as well as people with a lactase deficiency whose symptoms persist even with lactose-free milk. Although the activity of intestinal lactase is not increased by continuously ingesting milk sugar, it can reduce both the breath hydrogen and the gastrointestinal symptoms. Adjustments in colon functions ( motility , transit and pH value) and an associated reduced perception of symptoms, also as a result of an altered metabolism of the colon flora , offer a likely explanation. Various probiotic, but above all live, conventional yoghurt cultures support lactose digestion and reduce the occurrence of gastrointestinal symptoms.
The effects of the lactase deficiency can e.g. B. can be reduced to a minimum by changing the diet to low or lactose-free foods. There are alternatives in the form of various milk substitute drinks , some of which are also enriched with additional vitamins and calcium . In addition to soy milk , grain or almond milk is available. There are also lactose-reduced dairy products, including milk, but also cheese, yoghurt, cream, quark and more. Another possibility is to supply the enzyme lactase from the outside in the form of chewable tablets or capsules through appropriate pharmaceutical products from the drugstore or pharmacy. However, the effectiveness of these supplements has not been proven beyond doubt.
Milk sugar, on the other hand, is added to many food products, such as breads, cereal bars, ready meals, seasonings, sausages, marinated meats, doughs, candies, ice cream, chocolate and instant products such as sachet soups. One reason for this is the “mouthfeel” desired by the food designer , which has a positive effect on the taste. Most of those affected, however, can tolerate smaller amounts of lactose with almost no symptoms, so that it is not necessary to avoid it completely. Since November 25, 2005, new regulations for the labeling of allergenic food ingredients have been in effect ( Federal Law Gazette I p. 2896 ). The labeling requirement also includes milk and milk components including lactose. Also, functional food and drugs , including birth control pills may contain lactose as an excipient, but in an absolutely negligible quantity.
Fermented milk products, including all sour milk products , cheese and quark, contain z. T. the enzyme lactase by nature, so that only very small amounts of milk sugar remain. This is mainly related to the production process, in particular the amount of bacteria added to the milk, which produce the enzyme lactase and thereby break down the milk sugar, as well as the maturation process and the duration of cheeses and yoghurts. In the case of cheese, the following generally applies: the longer the ripening process, the lower the lactose content.
It often happens that those affected strictly avoid milk and dairy products as a result. Whether or not there is a critical level of calcium deficiency depends on the balance of the other food. Some sources report that lactose intolerants are exposed to an increased risk of osteoporosis . The reason given is the lower consumption of foods containing calcium. With an overall balanced diet, a calcium deficiency is hardly to be expected.
From a 2007 study of the Mainz anthropologist Joachim Burger shows that lactose intolerance adult people a phylogenetically 's original property of the people that that is the ability to digest, even as an adult lactose problems, a relatively recent genetic innovation is. Together with British colleagues, Burger had examined nine European skeletons from the Neolithic and Mesolithic (7800 to 7200 years old) and, while analyzing their genes, discovered that none of these individuals was able to digest milk. On the other hand , a 1500 year old skeleton from the Merovingian period analyzed for control has the genetic modification so that this individual was able to digest lactose. A DNA analysis of the glacier mummy known as Ötzi also revealed that the man, who died around 5000 years ago, was lactose intolerant. The ability of adults to digest milk in Europe only spread in parallel with the expansion of agriculture and after the introduction of animal breeding, which has been taking place here for around 8,000 years. In the genome analysis of 18 skeletons from a medieval cemetery in Dalheim , published in 2013, 13 of them (72 percent) had the genotype for lactase persistence, which corresponds to today's level in Germany and Austria. In October 2014 a study of the prehistoric inhabitants of the Pannonian Plain was published ; with the result that the adjustment process took many thousands of years.
|Region or ethnicity||Lactose intolerance%|
|South East Asia||98|
|South of france||65|
|Tutsi ( Rwanda )||20th|
|Whites in the United States||12|
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