More on mTOR and Gender Longevity Differences

This paper comes from a group that considers aging to be a programmed process involving later-life overactivity of processes vital to early-life development rather than the result of stochastic accumulation of unrepaired cellular and molecular damage. I think that this view isn't well supported by the balance of evidence, but it does illustrate the complexity of aging that such divergent interpretations of the same data exist. The researchers' views don't diminish the data they produce from animal studies, but do mean that you have to read their interpretations of the data with that bias in mind:

One of the most long-standing mysteries of gerontology is that the females of most species live longer than the males. Not only most mammals but also women of different nations and at most historical periods live longer. Ironically, it may seem that males do not age faster but simply are weaker at any age. In fact, the mortality rate is higher in young males and teenagers too. Importantly, however, old males die from age-related diseases, whereas young males mostly die from risky behavior and physical competition with each other. While risky competition increases chances of mating and offspring, this simultaneously results in high accidental mortality (from fights) and males die young. There is no reason for them to be naturally selected for slower aging. Therefore, animals with a high accidental death rate tend to age faster. It is exceptionally important for such males early in life to be bigger and stronger (even on the cost of accelerated aging).

In brief, early in life, TOR drives growth, robustness and reproduction, while causing aging and age-related diseases later in life. This example of antagonistic pleotropy is in line with the evolutionary theory. We speculate that aging as a continuation of growth driven by the same mTOR pathway, leading to aging and diseases of aging culminating in organismal damage and death.

In sum, mTOR may drive both growth and aging, associated with hyper-functions coupled with signal-resistance and malfunction, loss of homeostasis, leading to development of deadly diseases of aging such as cardiovascular and metabolic diseases, neurodegeneration, cancer and organ atrophy or failure. We hypothesize that males have a higher levels of mTOR activity, providing advantage (and bigger size) for young males even though accelerated aging and early death might follow.



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