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One of the mysteries of evolution is why aging occurs once we reach a stage where we can no longer reproduce. Recent research suggests that aging may be a consequence of our evolutionary adaptation to reproduction, shaped by natural selection over millions of years.
A study conducted on 276,406 participants from the UK Biobank analyzed their genetic data and found that individuals carrying gene variations that promote reproduction are less likely to survive into old age. This finding supports the antagonistic pleiotropy hypothesis, which proposes that mutations promoting reproduction are more likely to reduce lifespan.
The study revealed that people with genetic variations promoting reproduction had a higher likelihood of dying by the age of 76. Furthermore, it indicated that these genetic variations have increased over generations from 1940 to 1969, suggesting that humans are still evolving and strengthening this trait.
Despite our improved health compared to previous generations, the pattern of high reproduction and low survival, or vice versa, is still evident in modern humans. Our gene variants are the result of hundreds of thousands of years of evolution. This persistence of the pattern is surprising, according to Steven Austad, an expert in aging research at the University of Alabama at Birmingham.
Why does fertility decline with age?
The evolutionary origins of aging have long puzzled scientists, particularly the decline in reproductive performance with age. From an evolutionary perspective, it may seem advantageous to be more fertile in old age, allowing for more time to pass on our genes. However, the antagonistic pleiotropy hypothesis challenges this notion.
According to this hypothesis, the benefits of fertility in early life come at the cost of aging. Traits and genetic variants that are important for growth and fertility during youth can cause problems and lead to fragility and poor health in old age. This study provides robust evidence from a large sample of humans to support this idea.
For instance, menopause and the loss of fertility in women are examples of this trade-off. Eggs deplete over a woman’s lifetime, making her more fertile in young adulthood but resulting in infertility during menopause. Biologists believe that the advantages of regular reproductive cycles outweigh the cost of infertility in later life, although menopause accelerates the aging process.
Another example is a gene variant that enhances fertility, increasing the likelihood of having twins. While this may be advantageous in terms of leaving more copies of the variant, it also leads to increased wear and tear on the body, causing accelerated aging. Conversely, a gene variant that reduces fertility early in life may slow down the aging process.
The Impact of Environment on Aging
While the antagonistic pleiotropy hypothesis has its critics, it fails to consider the significant influence of the environment and socioeconomic changes on the aging process. This study also supports the notion that humans are living longer due to advancements in healthcare rather than genetic evolution. Zhang, a researcher involved in the study, highlights that “phenotypic changes are primarily driven by environmental shifts, including changes in lifestyles and technologies.”
A surprising finding of the study was the observable effect of reproductive genes on aging. Despite the importance of environmental factors, the study’s patterns remained visible, thanks to the large sample size. This research could have implications for understanding age-related diseases. By examining these genetic variants, scientists may be able to monitor and potentially prevent certain health problems that arise later in life.
The antagonistic pleiotropy hypothesis has long been supported by evidence, but primarily in non-human studies. However, this paper’s research on humans, with its extensive sample size, adds weight to the hypothesis. It may help explain the prevalence of genetic disorders throughout human evolutionary history. For example, sickle cell anemia, an inherited blood disorder, evolved as a protective mechanism against malaria.
Zhang also suggests that antagonistic pleiotropy could be at play in Huntington’s disease, a neurodegenerative disorder. Mutations causing Huntington’s disease have been found to increase fecundity, or the number of offspring produced. Additionally, these mutations have been hypothesized to lower rates of cancer.
The implications of this research extend to the field of anti-aging. In theory, manipulating antagonistically pleiotropic mutations could prolong life. However, this approach would come at the cost of reducing or delaying reproduction. Further studies in this area could contribute to advancements in the science of anti-aging.
