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Why are you hurt?
This circumstance is associated with an increased incidence of oncological diseases, primarily liver cancer, with alcohol abuse.
Two stages of ethyl alcohol processing. Alcohol dehydrogenase converts alcohol into toxic acetaldehyde, causing hangover symptoms. Aldehyde dehydrogenase neutralizes acetaldehyde molecules by converting them to harmless acetic acid. It helps with headaches and nausea, but with a sense of shame for yesterday's will have to accept.
When we drink, alcohol is gradually processed into acetaldehyde, and he, fortunately, turns into acetic acid. But at the same time, the effects of alcohol consumption depend on the activity of the two enzymes involved in this process.
If the activity of both enzymes is equally high, then a person can drink a lot, almost without experiencing any intoxication or hangover. If the activity of the first link is low, then the person experiences a long time intoxicating from a small dose of alcohol and at the same time practically does not suffer from the abuse, because all the aldehyde formed is promptly processed into acetic acid. In fact, there is nothing good in these options, because if a person does not suffer because of the ingestion of large doses of alcohol, then he is more likely to begin to abuse it. In the long run, the third option is safest, when alcohol dehydrogenase produces aldehyde quickly, and aldehyde dehydrogenase processes it into acetic acid slowly. Yes, in this situation, a person practically does not feel pleasantly intoxicated, but instead quickly feels the unpleasant symptoms of a hangover — but such a person is unlikely to be able to bring himself to become an alcoholic. It is this effect that is reproduced during “stitching”: a person who wants to stop taking alcohol is implanted with a disulfiram capsule under the skin. This drug inhibits the activity of aldehyde dehydrogenase, so drinking alcohol becomes dangerous and very unpleasant: it turns into poisonous acetaldehyde, and this process stops.
Naturally, enzyme activity depends on genes. The most active form of alcohol dehydrogenase is called ADH2 * 2 - it processes ethyl alcohol into toxic acetaldehyde very quickly, so that people who inherit this version of the gene from at least one of the parents become alcoholics twice as rare as people with other enzyme variants. The second enzyme, aldehyde dehydrogenase, works the worst for carriers of the ALDH2 * 2 allele - their accumulated aldehyde is practically not converted into acetic acid, and they don’t like to drink either. O. Tikhodeev’s book, Fundamentals of Psychogenetics, says that only three people were found throughout the world who could still force themselves to become alcoholics, despite the fact that the genes of the disabled aldehyde dehydrogenase were inherited from both parents. Never has the phrase “mice cried, pricked, but continued to eat cactus” has not received such visual confirmation
The effect of alcohol on the brain, of course, also depends on individual genetic characteristics. So far, the data are mostly statistical: among the dozens of variants of genes encoding different subunits of the gamma-aminobutyric acid receptor, there are genes associated with alcoholism. Some genes involved in the control of the dopamine, serotonin, and endorphin systems also demonstrate a statistical relationship with alcohol dependence. There are a lot of all these genes9, their effects are extremely diverse, each of them is significantly influenced by other genes and the external environment, so there will most likely never be an absolutely accurate genetic test for predisposition to alcoholism. Even after analyzing fifty of your genes, not a single doctor decides to say: “One bottle of wine a week definitely will not lead you to addiction!” - there is always the risk that gene 42 of this set will change its activity after you enter under the rain, it will act on gene No. 38 and on the unrecorded gene No. 61, and the bottle of wine that follows will prove to be fatal for you.
Approximate genetic tests nevertheless already exist and are widely used. As a rule, laboratories first of all analyze the activity of enzymes and sometimes even three or four genes are randomly selected that are related to the effects of alcohol in the brain. For example, the Moscow Center for Molecular Genetics studies the DAT1 and ANKK1 genes associated with dopamine activity, and the OPRM1 gene, which encodes the mu receptor for opiates. This is quite logical: pathological dependence actually develops when alcohol is tightly embedded in the work of the reward system, which works on dopamine and endogenous opiates. The private American company 23andMe, the first in the world to introduce cheap genetic screening to identify predispositions to dozens of diseases at the same time, also analyzes the dopamine receptor and transporter genes, DAT1 and DRD2, and also draws attention to the rs7590720 segment on the long arm of the second chromosome; what it is for is not yet very clear, but a study of 3792 people showed that nucleotide substitution at this place increases the risk of developing alcoholism by 35%.
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Why are you hurt?
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