Cienciaes.com: Abuse, genes and aggressiveness.

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Twenty years ago, in September 2002, I addressed this complex question when talking about a genetic and biochemical discovery that affected the aggressiveness of people according to the family or educational environment in which they had lived. I must say that the aggressiveness of animals and people was an aspect of behavior that had always fascinated me. When the discovery that I am going to talk about came about, he had already written a novel, entitled Chained Circumstances, in which he narrated the misadventures of a character who was unable, for genetic reasons, to control his aggressiveness in a normal environment, although he could control it in controlled environments. The protagonist himself discovers his condition on his own, which leads him to make decisions about his life that I am not going to tell you about. However, it is not that with this I want to induce or recommend you to read the novel, which, although it is not completely badly written, is very crude and hard, and is not suitable for delicate palates, nor for tender ages, as very judiciously warns one of his readers in a comment on Amazon.

But today we have not come to talk about my book, so let’s see what it had to say about aggression and what had been discovered about it two decades ago.

This is what he wrote then:

Now that the school year has just started, I remember that, as a child, I divided people into two types: those who, after being mistreated in some way by an older classmate, swore that when they were older they would find out about it. Whose little ones were they, and those who swore that when they grew up they would never mistreat the little ones. I did not know why I was already at such a young age, but a recent scientific study has come to confirm my suspicions, so early, that, indeed, people can well be divided into these two types.
It is well known to psychologists and psychiatrists that childhood maltreatment is a major risk factor for antisocial behavior. Children who experience physical abuse, or excessive rigidity or educational inconsistencies from their parents or peers, are at greater risk of becoming violent, and even criminal. In addition, the probability of becoming violent increases as the age at which children experience maltreatment for the first time decreases.
However, it is also well known that there are huge differences in the way different children respond to abuse. Fortunately, most abused children do not become delinquent or violent by the time they reach adulthood. As expected, the scientists assumed that these differences could be due to genetic factors of susceptibility, since when the environment is similar, the differences between individuals are usually due to genetic causes.
But what gene or genes might be responsible for these differences? An international group of British, American and New Zealand researchers set out to find out. The results of their studies are published in the journal Science at the beginning of last August.
The researchers studied the differences that children, mistreated or not, presented in the monoamine oxidase gene, or MOA for friends. This gene makes a protein that participates in the metabolism of important neurotransmitter molecules, such as serotonin and dopamine, among others, rendering them useless. It is known that the variation in the brain in the amount of these neurotransmitters, essential for certain types of interneuronal communication, may have to do with depressive states and aggressiveness. It was already known to the researchers that mice in which the gene for the MOA They were more aggressive than normal. In addition, it was also known that if these mice were reintroduced with the gene for the MOAHis aggressiveness decreased. Therefore, at least in mice, this gene influenced aggression.
The story of the gene does not end there MOA. This gene, in humans, is located on the X chromosome. This means that men have one copy and women have two. Thus, it is easier than defects in the gene of the MOA consequences in males than in females, who can compensate for a defective gene on one chromosome with a healthy copy on their second X chromosome. This is precisely what was observed in a Dutch family whose male members had inherited a gene for the MOA that didn’t work. These individuals exhibited antisocial and aggressive behavior. So all these facts suggested that the gene for MOA is important to control aggression, not only in mice, but also in humans, and that individuals who possess a gene for the MOA that doesn’t work, they are more aggressive.
But a gene can not only have defects that prevent it from working, it can also have defects, or modifications, that result in less protein production. In this case, the effects would be more subtle than in the case of the complete absence of the gene, and perhaps individuals who possess a gene that produces protein in less than adequate quantity are more susceptible to becoming aggressive individuals, especially if they live in a also aggressive environment. This was the hypothesis with which the researchers worked, a hypothesis that was also based on other studies and on the knowledge that the gene for MOAin effect, has two normal variants present in the human population, one variant that produces a lot of MOA and another variant that produces less.
What the researchers found is that, in the absence of child maltreatment, whether there is a lot or a little MOA produced by the variants of this gene has no influence on aggression as adults. That is, if children are treated with respect and consideration by adults and peers, they are not at increased risk of becoming violent, even if they have a variant of the gene that produces little MOA.
Things change when there is mistreatment and abuse. In this case, children with a variant that produces little MOA they are much more likely to become violent adults. However, those who possess a variant that produces a lot of MOA they are protected from the harmful effects of the abuse on their future personality and do not usually become violent.
The conclusions of this study, in this case, confirm that we can escape the influence of our genes if we control the environment in which we live well. An educational environment without violence, in which respect and kindness are encouraged, will be an environment that generates responsible, respectful and cooperative adults with others, regardless of the gene variant. MOA that is possessed Unfortunately, in our country, in addition to suffering from political violence, not enough is done to prevent daily violence, and above all, to encourage respect among children, who in many schools are allowed to insult and bully each other. humiliate them as if that behavior didn’t matter and was only for children. It seems to be more important that children learn mathematics and language than that they learn to respect their peers, but studies like this suggest, on the contrary, that to fix many serious social problems it is perhaps not necessary to use large material, educational or other resources. , but only foster an environment of respect among all, starting from the earliest childhood.

Thus ended the article I wrote in September 2002. What has happened since then?

The studies referred to in the article seem to have received additional evidence since they were published twenty years ago, and today it seems clear that the activity of the MOA It is related to both adaptive and pathological aggressive behavior.

The relationship between the activity of the MOA and aggressiveness is nonetheless complex. Both the environment and the period of life in which the partial or total deficiency of the activity of the brain seems to exert important effects on the final result. MOAsuch as the effects of other genes or enzymes and metabolic pathways and hormones. Among these, testosterone also seems to interact with the levels of MOA.

deficiency of MOA It can also generate anatomical changes in certain areas of the brain and affect the neural structures that regulate emotions, empathy, and aggressive behavior. This is therefore modified in a practically irreversible way if the deficiency of MOA occurs from birth, rather than as a result of any drug treatment later in life that may affect the activity of the MOAas is the case of treatments used for anxiety, depression or Parkinson’s disease, which collaterally affect the activity of the MOA without thereby increasing the apparent aggressiveness of patients receiving these drugs.

Regarding the way in which the deficiency in MOA can affect aggressiveness, there is still speculation today with the idea that the activity of the MOA It can affect the so-called flight or fight response, that is, the decision we must make in the face of a threat as to whether it is possible to avoid it by taking to our heels or it is too late to flee and we must face it.

The intensity of operation of the gene of the MOA depends on several factors. The first of these is the structure of the gene itself, which, as we have said, can vary from person to person. Some people have a region of ADN in the gene that enhances its functioning, while other people only have a variant of this region that only allows a lower intensity function.

In addition, the so-called epigenetic factors can also participate, that is, they literally act on the ADN and chemically modify it, which affects not the information it contains, but the intensity with which it is manifested.

As if this were not enough, more recently a gene has been discovered that is involved in regulating the amount of MOA produced from the gene regardless of whether it works a lot or a little. It’s all about the gene A DAYdiscovered in 2020. This gene does not produce a protein but a ARN long non-coding, that is, it is not translated into protein. This ARN interacts with him ARN produced by the gene MOA and decreases the levels of this that can be used to generate the protein. Not surprisingly, the gene A DAY It can have several variants and its operation can be subject to different factors that will also indirectly affect the levels of MOA from each person. Research on this gene has only just begun.

Jorge Laborda (09/11/2022)

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