Scientists have found out how the generation of “children of the 90s” differs at the genetic level

No matter who says that man has stopped evolving, this is not so. And the work of geneticists from the Institute of Cytology and Genetics SB RAS confirms this. Having studied the genes of a large number of Novosibirsk residents born in the late 80s, early 90s and early 2000s, they came to the conclusion that the generation born in the crisis 90s has a different set of gene variants compared to the previous one and followed by control groups. Among them there were more options that are associated with stress resistance.

– Svetlana Vladimirovna, tell us what influences the variability of the species in modern society?

– It is often argued whether human evolution has stopped? Arguments for stopping are the fall in child mortality in the world and the associated fall in the birth rate. Parents are no longer, as a century ago, focused on high mortality among children when planning the size of their family. As a result of this, even for absolutely healthy people and for people with some kind of chronic disease, the number of children is equally small. But does this mean that due to the declining proportion of offspring, humans as a species are no longer changing? It turned out that it is changing, in particular, this is due to the rapidly changing conditions of our life in the last century. And our work, which assesses the genetic characteristics of citizens born during the crisis, proves this.

– Tell us how the research was conducted, who participated in it?

– The work was carried out under the auspices of the Russian Science Foundation on the basis of a survey of adolescents, which is carried out every five years by the Research Institute of Therapy and Preventive Medicine of Novosibirsk (now a branch of our institute). If earlier, when studying the “crisis” generation of children, scientists paid attention to their weight, height, smoking prevalence, features of lipid metabolism associated with the quality of nutrition, but now we have for the first time conducted a population study of the genetic “imprint” of the socio-economic crisis of the 1990s.

For the analysis, we used the blood of three groups of adolescents born with an interval of 10 years and collected in one of the districts of Novosibirsk. We were most interested in the samples of 14-17 year old adolescents obtained in 2009; they, accordingly, belonged to those born in 1992-1995. We considered the control groups to be teenagers from the same area, from the same schools, separated in age from those studied by 10 years, that is, born in 1982-85 and 2002-2005.

– And what did you find out?

– Changes in the frequencies of certain genetic variants relative to two control groups, which, of course, are associated with parents who decided to have children in the early 90s.

We were interested in genes involved in the regulation of stress and determining temperament traits, since the crisis of the 90s in Russia was characterized by a high level of social stress among the population.

A total of 21 such options were analyzed. It turned out that three of them were found statistically significantly more often in the “crisis” sample.

Two of the identified genes – DRD4 and COMT – are well known as genes that are responsible for dopamine metabolism. Apparently, carriers of certain alleles (variants of the same gene – Author) of these genes adapted better to conditions of prolonged stress and to a lesser extent postponed the birth of planned children during this period. As a result, in the generation born during the crisis, these options are more common than usual. Another variant with different frequency was found in the estrogen receptor gene (ESR1). It has so far been little studied, and there is no data on the mechanism of its influence on the development of the stress reaction. However, it is known that after suffering stress, people with this variant in their genome are more likely to suffer from post-traumatic stress disorder, and, oddly enough, they have, on average, a larger number of children.

Thus, we have shown that prolonged social stress in the population has different effects on fertility depending on the genotype.

– It turns out that children were often born in the 90s to both stress-resistant individuals and anxious ones?

– Yes, it turns out that the children of the 90s are those who carry the genes of both stress-resistant and anxiety-prone parents. We don’t yet know how this can be explained, apparently there are several ways how prolonged social stress can affect a family’s decision to have a child or to postpone it “for later.” Last year, for example, reports emerged for the first time that the predisposition to a depressive disorder and to a person’s sense of satisfaction with the meaning of his own life (the so-called eudaimonic well-being – the desire for happiness) is determined by the same set of genes.

– Do genes always determine resistance to stress? Could epigenetic factors play a role?

– Epigenetic regulation is, of course, possible. It is known that if a mother experiences stress during pregnancy, the child may be born with a modification of certain DNA sections. The genetic sequence does not change, but the genes begin to be regulated differently.

By the way, the “alarming” variant of the ESR1 gene was initially noticed when military veterans in the United States were examined. A correlation (relationship) of this gene variant with post-traumatic stress disorder developing after the war was obtained.

– What conclusion can be drawn based on all this?

– In an urbanized society, where a person is in a more rigid social framework, changes similar to those described are likely to occur.

Populations will accumulate some genetic variants that determine how they respond to stress, but the prevalence of some other diseases may also change. For example, it was previously shown that variants of the DRD4 and COMT genes, which showed an increase in the “crisis” group, in addition to resistance to stress, increase the likelihood of developing attention deficit hyperactivity disorder in their carriers.