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Why are you hounding?
It is this circumstance that is associated with an increased incidence of cancer, especially liver cancer, with alcohol abuse.
Two stages of processing of ethyl alcohol. Alcohol Dehydrogenase turns alcohol into a toxic acetic aldehyde that causes hangover symptoms. Aldehyde dehydrogenase detoxifies the molecules of acetic aldehyde, converting them into harmless acetic acid. It helps with headaches and nausea, but with shame for yesterday, you have to accept.
When we drink, alcohol is gradually processed into acetic aldehyde, and it, fortunately, turns into acetic acid. But the consequences of alcohol intake depend on the activity of the two enzymes participating in this process.
If the activity of both enzymes is equally high, then a person can drink a lot, almost without experiencing alcoholic intoxication, or a hangover. If the activity of the first link is low, then a person longly experiences a pleasant intoxication from a small dose of alcohol and, at the same time, has almost no suffering due to abuse, because all the resulting aldehyde is promptly processed into acetic acid. In fact, there is nothing good in these options, because if a person does not suffer from taking large doses of alcohol, he is more likely to abuse it. In the long term, the third option is more safe, when alcohol dehydrogenase produces aldehyde quickly, and aldehyde dehydrogenase processes it into acetic acid slowly. Yes, in this situation, a person practically does not experience a pleasant intoxication, and instead quickly feels unpleasant hangover symptoms - but such a person is unlikely to be able to force himself to become an alcoholic. It is this effect that is reproduced when "sewing": a person who wants to give up alcohol is implanted under the skin with a capsule with disulfiram. This drug suppresses the activity of aldehyde dehydrogenase, so that drinking alcohol becomes dangerous and very unpleasant: it turns into poisonous acetic aldehyde, and the process stops there.
Naturally, the activity of enzymes depends on the genes. The most active form of alcohol dehydrogenase is called ADH2 * 2 - it processes ethyl alcohol into poisonous vinegar aldehyde very quickly, so people who inherited such a variant of the gene from at least one of the parents become alcoholics twice less often than people with other variants of the enzyme. The second enzyme, aldehyde dehydrogenase, works poorly in ALDH2 * 2 allele carriers - they do not practically store the accumulated aldehyde in acetic acid, and they also do not like drinking. In O. N. Tikhodeev's book "The Basics of Psychogenetics," it is said that only three people were found all over the world who still managed to force themselves to become alcoholics, despite the fact that they inherited the genes of non-functioning aldehyde dehydrogenase from both parents. Never before a phrase "mice cried, pricked, but continued to eat a cactus" did not receive so evident confirmation.
The impact of alcohol on the brain, of course, also depends on individual genetic characteristics. So far, the data are mostly statistical: among dozens of variants of genes encoding different subunits of the receptor for gamma-aminobutyric acid, there are genes associated with alcoholism. Some genes involved in the control of the dopamine, serotonin and endorphin systems also show a statistical relationship with alcohol dependence. All these genes are very numerous, 9 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 exact genetic test for predisposition to alcoholism. Even after analyzing fifty of your genes, no doctor decides to say: "One bottle of wine a week will not exactly lead you to addiction!" - there is always a risk that gene No. 42 from this set will change its activity after you get under the rain, will affect the gene number 38 and the unrequited gene number 61, and the following bottle of wine will still be fatal for you.
Approximate genetic tests nevertheless already exist and are widely used. As a rule, laboratories analyze enzymes activity primarily and sometimes randomly choose three or four genes related to the action of alcohol in the brain. For example, the Moscow Center for Molecular Genetics is researching the DAT1 and ANKK1 genes associated with dopamine activity, and the OPRM1 gene that codes for the mu receptor for opiates. This is quite logical: pathological dependence really develops when alcohol is tightly integrated into the work of a remuneration system that works on dopamine and endogenous opiates. Private American company 23andMe, the first in the world to introduce cheap genetic screening to identify predispositions to dozens of diseases simultaneously, also analyzes the genes of dopamine receptors and transporters, DAT1 and DRD2, and also draws attention to the site rs7590720 on the long arm of the second chromosome; for which it is needed, it is not yet very clear, but a study of 3792 people showed that the nucleotide replacement in this place increases the risk of alcoholism by 35%.
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Why are you hounding?
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