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Despite the fact that in the last 150 years, life expectancy, mainly that of women, has increased from 45 to 85 years, the time of reproductive senescence, which corresponds to the age of natural menopause, has remained relatively constant; around 50-52 years.
The genetic integrity of oocytes decreases with age
and fertility ceases about 10 years before menopause.
The
responsibility for the regulation or lengthening of reproductive life lies in a set of genes
, as an international research team has discovered in a work that delves into the genetic knowledge of the biological mechanisms that govern human ovarian aging and whose data is published in the latest
Nature
.
According to Ignasi Roig, professor in the Department of Cell Biology, Physiology and Immunology at the Autonomous University of Barcelona (UAB), and one of the co-authors of this research,
genes have been determined that lengthen, and more specifically regulate, ovarian function
based on when menopause appears. "We have observed about 300 gene variants that affect when menopause appears, either later or earlier than is considered normal: a population average that is around 50 years."
Clinically,
the study makes different contributions
, although they are considered in the long term. On the one hand, according to the researcher, knowing the gene variants has made it
possible to design a 'genetic predictor'
through which it is possible to know which women are at risk of presenting early menopause. "This fact can be known from the day they are born because it depends on the genome, not on environmental variants. In this way, a woman would know that she could have an early menopause and, therefore, if she wanted to be a mother, plan a pregnancy in a adequate ".
Another possibility would be "to
freeze eggs or embryos to be able to implant them later
", especially considering that, currently, more and more women choose to delay motherhood at older ages.
Thus, it is suggested that
the ovarian reserve can inform future therapeutic strategies
for the treatment of infertility and fertility.
What are the variants to prolong the fertile age?
Most of the gene variants analyzed have repercussions by advancing the onset of menopause but, according to the scientist, "
some have been found that delay its appearance in humans
." Thus, for example, the one studied in a mouse model, the CHEK2 protein, involved in the cell cycle that responds to DNA damage, also lengthens ovarian function.
These CHEK2 proteins also intervene and influence other cell cycles
. In fact, in the work it has been observed that a large part of the 300 gene variants detected are associated with processes of quality control and DNA repair. "CHEK2 is precisely one of the proteins that intervenes in the mechanisms that are triggered when DNA damage is detected and the processes to repair it are activated."
Regarding whether these variants can play a role in the ovarian infertility that some women present, Roig points out that
there is a small percentage of women - around 1% - who have a very early menopause, before the age of 40
, which is a reason for infertility. "Some of the variants studied are responsible for the origin of this menopause so early that, logically, it can lead to infertility problems in some women. The weight of the different proteins is similar, it can be multigenic, which determines when menopause can appear it is a balance of all the variants that it presents ".
Once the mechanisms that regulate this process are known, the next step, also in the animal model, of this international project would be to try to modify them, from a therapeutic point of view, to extend fertile life.
Thus, another clinical utility that emerges from the knowledge of these genes is to try, "
in the long term, to design therapeutic strategies that facilitate the response to 'in vitro' fertilization treatments
, for example, or to increase or lengthen the fertile life of women. women undergoing certain therapies ".
Advantages of a late menopause
The research highlights the fact that
a later menopause protects against alterations related to bone health
, specifically osteoporosis, as well as cardiovascular and related to type 2 diabetes. But, on the contrary, its effects can also increase the risk and the incidence of hormone-dependent tumors, mainly that of the breast.
So how could a balance be struck to maintain benefits while minimizing risks?
According to Roig, studies in animals in which the ovarian function or the fertile life of the animal has been extended, the global health presents better indicators, which seems that "
this extension of the ovarian function could have a positive impact on the health of the females
, at least in mice. But it is also true that the same extension can have adverse effects such as the possible higher incidence of estrogen-dependent cancers. The essential challenge is to try to establish an adequate balance ".
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