Aging
Navigate
Review|Volume 6, Issue 2|pp 84—91

Evolution of sexually dimorphic longevity in humans

David Gems1
  • 1Institute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK
Received: January 8, 2014Accepted: February 21, 2014Published: February 22, 2014

Copyright: © 2014 Gems et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Why do humans live longer than other higher primates? Why do women live longer than men? What is the significance of the menopause? Answers to these questions may be sought by reference to the mechanisms by which human aging might have evolved. Here, an evolutionary hypothesis is presented that could answer all three questions, based on the following suppositions. First, that the evolution of increased human longevity was driven by increased late-life reproduction by men in polygynous primordial societies. Second, that the lack of a corresponding increase in female reproductive lifespan reflects evolutionary constraint on late-life oocyte production. Third, that antagonistic pleiotropy acting on androgen-generated secondary sexual characteristics in men increased reproductive success earlier in life, but shortened lifespan. That the gender gap in aging is attributable to androgens appears more likely given a recent report of exceptional longevity in eunuchs. Yet androgen depletion therapy, now used to treat prostatic hyperplasia, appears to accelerate other aspects of aging (e.g. cardiovascular disease). One possibility is that low levels of androgens throughout life reduces aging rate, but late-life androgen depletion does not