^

Health

A
A
A

Insufficient digestion syndrome: causes

 
, medical expert
Last reviewed: 19.10.2021
 
Fact-checked
х

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.

We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.

If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.

The basis for the occurrence of digestive disorders is the genetically determined or acquired inadequate production of digestive enzymes in the small intestine. Moreover, there is either a lack of synthesis of one or several enzymes, or a decrease in their activity, or a change in biochemical reactions that affect enzymatic activity.

Among the congenital fermentopathies, insufficiency of disaccharidases (lactase, saccharase, isomaltase, etc.), peptidase (gluten enteropathy), enterokinase is most often found. Acquired enzymopathies are observed in diseases (chronic enteritis, Crohn's disease, diverticulosis with diverticulitis, etc.) and resection of the small intestine, diseases of other digestive organs (pancreatitis, hepatitis, cirrhosis) and organs of the endocrine system (diabetes, hyperthyroidism) taking some medications (antibiotics, cytostatics, etc.) and irradiation. From the obtained fermentopathies, the most frequent is alimentary enzymopathy, in which the disturbances in the production and activity of enzymes are related to the nature of the food. So, deficiency of protein, vitamins, microelements in the diet, unbalanced nutrition (amino acid imbalance, disbalance between fatty acids, water-soluble and fat-soluble vitamins, mineral salts) can lead to persistent digestive disorders. In addition, the inhibition of the activity and biosynthesis of enzymes and protein can be due to the toxic effects of some natural components of food or contaminating foreign contaminants. The individual food products (beans, cereals, rice, eggs, etc.) have been found thermostable specific protein inhibitors, which form stable complexes with proteinases of the gastrointestinal tract and cause inhibition of their activity. As a result, digestion and digestion of the food protein are disrupted. The biosynthesis of certain enzymes is disturbed by the insufficiency of coenzymes - water-soluble vitamins. This is due to the presence in food products of antivitamins, which destroy or replace vitamins in the structure of enzyme molecules, significantly reducing or completely suppressing the specific action of vitamins. Nicotinic acid antagonist is a low-molecular compound - niacitin and niacinogen isolated from corn, and pyridoxine - linatinum, contained in flax seeds. Freshwater fish contain enzyme thiaminase, which catalyzes hydrolytic cleavage of thiamine. Avidin, a protein found in raw eggs, forms a stable complex with biotin in the gastrointestinal tract.

Pollution of food products with salts of heavy metals (mercury, arsenic), pesticides, mycotoxins (aflatoxins, trichothecene mycotoxins, etc.), which react with sulfhydryl groups of protein molecules, suppresses protein biosynthesis, inhibits enzymatic activity.

There are several forms of the syndrome of insufficiency of digestion, manifested by the violation of predominantly cavity; parietal (membrane) and intracellular digestion. In addition, there are mixed forms of digestive failure. All these varieties of forms are accompanied by diarrhea, flatulence and other dyspeptic disorders. At the same time, each of them has its own pathogenetic peculiarities.

Violation of predominantly cavitary digestion (dyspepsia) occurs due to an uncompensated reduction in the secretory function of the stomach, intestines, pancreas, bile secretion. An essential role in its occurrence is played by the disruption of the motor function of the gastrointestinal tract: congestion of contents due to spasm, stenosis or compression of the gut, or accelerated passage of food chyme, caused by accelerated peristalsis. The appearance of dyspepsia is facilitated by the transferred intestinal infections, changes in the intestinal microflora, when the number of bifidobacteria and Escherichia coli decreases , the upper parts of the small intestine are populated with microorganisms, the pathogenic flora is activated, which causes fermentation and putrefaction in the large intestine. Dyspepsia leads to nutritional deficiencies: overeating, unbalanced nutrition with the use of excessive amounts of carbohydrates, proteins or fats, eating foods that are devoid of vitamins. Especially dangerous is the excessive nutritional load in combination with mental and physical overstrain, overheating, supercooling, i.e. With factors leading to inhibition of the secretory function of the digestive glands.

Dyspepsia is often observed with damage to the stomach, intestines and other organs of the digestive system. At present, the isolation of so-called functional dyspepsia is hardly justified, since it is proved that every "functional" disease has its morphological substrate.

In the pathogenesis of dyspepsia, an important role is played by insufficiently complete digestion of nutrients by digestive enzymes, accelerated or delayed passage of chyme along the gastrointestinal tract, and the emergence of dysbiosis. Bacteria that appear in the upper parts of the small intestine secrete enzymes and take an active part in the digestion of nutrients. As a result of this process, toxic products are formed, such as indole, ammonia, low-molecular fatty acids, which irritate the intestinal mucosa, enhance its motor activity and, as it absorbs, cause intoxication of the body. The increase in the enzymatic activity of microorganisms in the large intestine is accompanied by an increased formation of these toxic products and in the distal parts of the intestine.

Translation Disclaimer: For the convenience of users of the iLive portal this article has been translated into the current language, but has not yet been verified by a native speaker who has the necessary qualifications for this. In this regard, we warn you that the translation of this article may be incorrect, may contain lexical, syntactic and grammatical errors.

You are reporting a typo in the following text:
Simply click the "Send typo report" button to complete the report. You can also include a comment.