Environment and heredity – ending

Alexandra Bruter, <url> 

We continue to talk about the extent to which a person's individual qualities – his character traits, inclinations, diseases - are biologically predetermined from birth.

Earlier we described how the reduced activity of the enzyme monoamine oxidase A (MAOA), caused by a certain mutation, can lead to a person's tendency to aggression and antisocial behavior. There are other mutations of the gene encoding this enzyme, which, on the contrary, increase the activity of MAOA.

Variants of MAOA with high activity instead of low are associated, on the contrary, with depression and anxiety. Not all studies agree that MAOA mutations that increase activity lead to depression (there are both confirmatory and refuting data). With a certain degree of confidence, we can only say that depression, in which highly active variants of MAOA are detected, is much worse treated with placebo. MAOA inhibitors are generally often and effectively used as medications against depression.

The antidepressant efficacy of MAOA inhibitors is easy to explain. The transmission of nerve impulses from neuron to neuron occurs due to the fact that the transmitting neuron releases a neurotransmitter substance into the space where the neurons touch. This neurotransmitter triggers the corresponding processes in the receiving neuron, and the signal goes on. The role of neurotransmitters is often played by the same monoamines: adrenaline, norepinephrine, serotonin and dopamine, which are destroyed by MAOA. The faster the neurotransmitter is destroyed, the less time it spends in the space between the neurons. The less time it spends, the weaker the transmitted signal. Therefore, with inactive MAOA, any irritation in the brain increases and causes a desire to attack immediately, and with too active, the sharpness of emotions is not enough to motivate action and a sense of fullness of life.

We have already mentioned above that placebo acts differently on people with different variants of the MAOA gene in the treatment of depression. This is not the only case when the genotype affects the susceptibility to the placebo effect. Other examples can be found in the essay "On whom the placebo works". It is clearly seen that the difference is observed in three cases: 

The fact that a genetic predisposition to it has already been detected in quite different situations makes one think that as the study proceeds, the same predisposition can be detected for the effects studied to date worse. And if your genes determine your psychological reaction, then where is the place for free will?

In the cases described above, there is a greater tendency to aggressive or depressive behavior and a different susceptibility to the placebo effect, the molecular mechanisms are, in principle, known. However, for example, in the case of IQ, it is statistically possible to detect the role of heredity, but it is not possible to understand the mechanism. There is a similar situation with the genetic nature of homosexuality. Mathematical models indicate that there are one or more genes that increase the likelihood that his or their male owner will turn out to be a homosexual. Probably, the fact that their female owners are more fertile helped to preserve the gene in the population. At the same time, it is unclear what kind of gene it is and what protein it encodes, but the fact of its existence indicates that the tendency to homosexuality is innate, and cannot be the result of propaganda. Also, homosexuality can hardly be considered a free choice of a person.

The hormone oxytocin controls many aspects of human behavior. First of all, those that relate to the manifestations of maternal care, but not only. Some time ago it was shown, and we wrote about it in the essay "Maternal Love Hormone", that oxytocin disinhibits the neurons of the auditory cortex of the brain, and makes the squeak of newborn mice audible to females. At the same time, the introduction of oxytocin into the brain of females who had never given birth made them caring mothers.

The question immediately arises about what will happen if mutations occur in the genes encoding oxytocin or the enzymes responsible for its metabolism. Most likely, a mutation that completely inactivates oxytocin would be quickly eliminated by selection, but would greatly affect the behavior of its few carriers. Caring for offspring is not the only aspect of behavior controlled by oxytocin. Research results show that oxytocin makes people's behavior more social and, for example, makes them more trusting. That is, again, trusting a person or not is not only your informed decision, but also the concentration of oxytocin in the body.

It has recently been shown that, at least in some cases, oxytocin deficiency is associated with autism and autism spectrum disorders. Actually, no one knows the exact cause of the development of diseases of this group, but it seems that they have a hereditary component. Screening genetic studies are trying to detect the genes responsible for autism, but they find a lot of candidate genes. Such a wide variety of candidate genes makes it impossible to build a simple and understandable model. One of these genes is the CNTNAP2 gene, the product of which is involved in the formation of contacts between neurons. It turned out that in mice with Cntnap2 turned off, the oxytocin content in the brain decreases, and difficulties arise with social behavior. The introduction of oxytocin for several weeks in the first days of life solves this problem, and then the animals develop normally.

Clinical trials of oxytocin as a cure for autism have been underway for some time, with rather varying success. Probably, success would be less variable if it were possible to select only those cases that are reliably associated with oxytocin deficiency (as in the case of a mutation in CNTNAP2), and guess the "therapeutic window" (oxytocin helped mice only if it was administered in the first weeks of life, and did not help in adulthood). But it is difficult to get into the therapeutic window in a person if genotyping is not carried out immediately after birth: the symptoms of autism rarely become noticeable in the first year of life. Genotyping also can't help much: a lot of candidate genes have been identified, mutations in which of them lead to oxytocin deficiency are mostly unknown.

However, oxytocin is a registered drug and its safety has been proven. Therefore, some parents whose children have been diagnosed do not wait for the results of clinical trials, but use oxytocin on their own.

In this essay, examples were given that social and antisocial behavior, intelligence and suggestibility, and possibly other properties of our psyche depend on the genes we inherited at the time of fertilization. In addition, the idea that the structure of the future personality is completely laid down in childhood is quite popular in society. There may be an idea that all this partially removes responsibility from an adult for his behavior and decisions. But even the American court defined it "partially" – as an opportunity to replace the death penalty with a 32-year prison sentence, and no more.

A set of mental traits and behavioral reactions inherited at birth and in early childhood should not be perceived as a prison in which to spend the rest of your life. Rather, they should be perceived as an apartment in a new building, which can be re-planned and furnished to your own taste. And, if cleanliness and order inside is a personal matter for everyone, then it is still the responsibility of the owners not to flood the neighbors and not to forget to turn off the gas when going on vacation.

Portal "Eternal youth" http://vechnayamolodost.ru

06.07.2015