Licensed books on medicine
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“But I quit easily!”
So far, doctors can only estimate approximately whether the level of addiction will be increased or decreased compared with other people. In modern commercial tests, only one single gene is often tested - the one for which the connection with nicotine addiction is firmly proven and well studied.
This gene is called CHRNA3. It determines the structure of the alpha-3 subunit, one of the proteins in the composition of nicotinic acetylcholine receptors. The gene has an area rs1051730 in which people often have a mutation - replacing one of the letters of the genetic code (normally, cytosine should be present at this place, and during mutation it changes to thymine). This replacement is devoted to hundreds of studies conducted on tens of thousands of participants, and everywhere there is an undoubted statistical connection with the intensity of nicotine addiction. This is extremely mysterious, because in general, this particular nucleotide substitution in this region cannot affect the amino acid sequence of the protein and, accordingly, its structure and performance. Maybe it somehow changes the stacking of RNA, making the production of proteins themselves less effective. Or perhaps this nucleotide substitution was simply accidentally discovered first, but in fact it is associated with some other mutation that still changes the receptor's activity (if the previous few sentences sounded monstrous, but you still want to figure it out, then I remind you that the end of the book has a biological cheat sheet). As for the CHRNA3 gene, in any case, it is still being studied, because no one doubts the statistical relationship between its mutations and dependence.
In 2012, scientists from the University of Copenhagen published a paper in which the CHRNA3 gene was studied in as many as 57,657 people (of which 34,592 people had ever smoked). They found that among the inhabitants of Denmark, 11% possess two mutant copies of the CHRNA3 gene (that is, inherited them from both mother and father), 44% are heterozygotes, that is, carriers of one mutant and one standard variant, and the remaining 45% have two normal copies of the gene. It turned out that smoking with approximately the same frequency is found in all groups, but people with mutations in the CHRNA3 gene smoked significantly more cigarettes, and when trying to quit smoking, they needed nicotine replacement therapy more often and longer than people with the usual genotype. They are also more likely to develop chronic obstructive pulmonary disease, as well as lung cancer - however, this apparently follows directly from the higher intensity of smoking, because for non-smokers there is no connection between this gene and lung diseases.
In addition to the CHRNA3 gene, which for some reason turned out to be the most fashionable topic for research, there are, of course, other genes associated with the development of nicotine addiction. Another fragment of the acetylcholine receptor, the alpha-5 subunit, is encoded, as is easy to guess, by the CHRNA5 gene. It is a mutation in which amino acid number 398 in the protein changes: instead of aspartic acid, which is present in all animals, some people in this place appear asparagine. This mutation, apparently, originated in Europe, because there its prevalence reaches 37%, and among Africans, Asians and American Indians, it practically does not occur. Experiments on cell cultures have shown that a mutation impairs the receptor's performance - and this may mean that people are especially susceptible to the possibility of spurring his work with nicotine. And indeed, 43% of the carriers of this mutation reported in the polls that the first cigarette in life caused an intense high and emotional uplift. Among smokers with the usual version of this gene, the first cigarette so much liked only 10%.
Magnetic resonance imaging also demonstrates the differences between smokers with different variants of the CHRNA5 gene, and the mutation is associated with a smaller surge of excitement when you see a photograph of a smoking person (perhaps cigarettes do not act so much on smokers and this causes them to smoke again and again? ).
There are several dozens of genes for which a more or less pronounced statistical association with smoking has been established. In addition to the genes encoding acetylcholine receptors, enzyme genes responsible for the speed of nicotine processing and many genes associated with the work of dopamine and serotonin in the brain contribute to the formation of dependence. Many of these genes are associated with several addictions at once, for example, alcohol and nicotine.
Very simplifying and coarsening, we can say that in our brain there are metabolic pathways necessary to experience a feeling of pleasure. If they all work well in a person, then, in general, it is not necessary to smoke (although many still start and sit down). But on the other hand, if a person has some mutations that reduce the ability of his brain to experience a sense of pleasure, then the very first teenage cigarette produces an absolutely stunning impression on him, because it stimulates the work of the necessary receptors and activates the reward system to unprecedented heights. This experience, naturally, I want to repeat again and again. But, alas, with constant smoking, the system does not work that way, because the sensitivity of acetylcholine receptors gradually decreases. As a result, a person finds himself in a terrible vicious circle, in which he smokes more and more, so as not to be unhappy, and the receptors become less and less sensitive to nicotine (and to his own acetylcholine at the same time), and one has to smoke even more, and the sensitivity is further reduced, and stop getting harder.
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“But I quit easily!”
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