People with genes linked to early childbearing are more likely to die before their 76th birthday.
People who have a genetic predisposition to have children earlier in life are less likely to reach the age of 76. This follows from an analysis of the DNA of more than 270,000 people.
Why we decline as we age is one of the greatest evolutionary mysteries. You would think that natural selection would ensure that genes that lead to a longer life are passed on more often. After all, a longer life gives you more time to reproduce, and therefore more time to transfer your genes – which are apparently beneficial for living longer. However, there is no evidence that natural selection prevents aging.
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Multiple properties
The fact that natural selection does not directly lead to less deterioration may be due to so-called antagonistic pleiotropy. Pleiotropy means that one gene is responsible for multiple traits. In antagonistic pleiotropy, at least one of those traits provides extra fitness early in life, while another trait is less beneficial later in life. It could therefore be that there are genetic mutations that, on the one hand, make people reproduce earlier, but on the other hand also lead to a shorter lifespan.
“These mutations that are beneficial for reproduction, but may later be harmful, are still passed on to the next generation,” says evolutionary biologist Jianzhi Zhang from the University of Michigan. ‘That is because reproduction is especially important in natural selection.’
To investigate this theory, Zhang and a geneticist conducted Erping Long of the Chinese Academy of Medical Sciences in Beijing has conducted a major study into the genetic link between reproduction and lifespan. Of that workrecently published in the scientific journal Sciencethey have found more convincing evidence for the principle of antagonistic pleiotropy.
Score
The pair analyzed the DNA of 276,406 people from the UK Biobank, a long-term health study in the United Kingdom. All participants in this study were born between 1940 and 1969, and had European ancestors.
The researchers calculated a so-called polygenic score for each person. That score indicates the extent to which a person’s combination of genes is associated with better reproductive health at a young age. The higher someone’s score is, the more likely that person is to be fertile for a longer period of time.
The researchers also collected information about the lifespan of the participants. They looked at how old someone had become or, if they were still alive, at how old their parents had become.
Passed on genes
Comparing the polygenic scores with the longevity data, the duo found that people with higher polygenic reproductive health scores were less likely to live to age 76 or older. There was no specific reason to use this age as a cutoff, says Zhang, “our results strongly support the antagonistic pleiotropy hypothesis.”
A possible mechanism is that some gene variants that promote reproduction can lead to diseases later in life. One of those variants, rs12203592for example, has been linked to some forms of cancer.
The team now hopes to collect more data from more diverse populations to see if this trend holds there too. ‘We don’t know yet whether our results also apply to African or Asian people, but I think we can expect this pattern.’
Environmental factors
It is important to mention that external factors, such as medical advances, have led to people living longer and having fewer children on average. “These changes in environmental factors have so much influence that genetic changes are very small in comparison,” says Zhang.
‘This is the first strong evidence for antagonistic pleiotropy in humans. It supports an important pillar of the evolutionary theory of aging,” says evolutionary biologist Steven Austad from the University of Alabama at Birmingham in the US, who was not involved in the study. ‘There is already a lot of evidence in laboratory animals, but it is important to extend this to humans to find out whether antagonistic pleiotropy applies more broadly.’
2023-12-17 13:12:46
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