Listen to this audio link by the Canadian born rapper Baba Brinkman: all the way to senescence (with lyrics):
Understanding age-related risk of death and age-related disease are the result of tradeoffs and occur because of evolved life history traits.
We are going to cover evolutionary hypotheses of senescence for next week’s class. These hypotheses include antagonistic pleiotropy, declining power of selection, and mutation accumulation.
Antagonistic pleiotropy is the concept that a gene for survival or a gene that promotes
reproduction early can be selected for even if it kills you at a later
age. So selection favors juvenile survival at the expense of old age survival. This hypothesis recognizes that most traits have both costs and benefits, and are tradeoffs. The tradeoff in antagonistic pleiotropy is improved health and fertility in the young, but disease and premature death in older individuals.
Haldane and Medawar proposed the declining power of selection hypothesis of aging. This proposes that genes for maintenance and repair of the body are selected for more strongly at early ages (pre-reproduction) than after reproductive age. For this: imagine a hypothetical gene that prevents cancer at age 10 and another gene that prevents cancer at age 100. The gene that prevents cancer at age 100 will not have any effect most of the time because most people are dead by age 100 (this remains true even if you take senescence out of the equation – random accidents will claim many lives). The gene that affects 10 year olds is more likely to be expressed and have a benefit simply because most people are alive at age 10. Therefore the old-age gene will be invisible to natural selection, the gene that affects 10 year old will be subject to positive selection.
Medawar extended his idea to include mutation accumulation. This idea posits that the body accumulates deleterious mutations that take effect at older ages. Because of the declining power of selection, these mutations are not selected against, and contribute to declining function that we see with aging. In wild populations, not enough organisms reach advanced age, so these mutations are invisible. If allowed to achieve advanced chronological age, these mutations exert damaging effects, reducing fitness and contributing to senescence.
The disposable soma hypothesis is another idea to explain aging. This hypothesis recognizes that the nonreproductive part of the body (the soma) exists only to support the reproductive part of the body. At any moment in time an adult can devote energy to the maintenance of the body or to reproduction. Put simply, after successful reproduction, the soma is “disposable”, and genes are passed on. This tradeoff is vividly illustrated in adult salmon, also in octopus, which appear to do all their aging at once, immediately after a single reproductive effort. In many animals, bearing offspring shortens lifespan. There is some evidence of this in humans too.
Menopause is a strange phenomenon, because it represents premature aging of the female reproductive organs, asynchronous with the rate of decline in function for the rest of the body. It is paradoxical because it would seem that natural selection would seem to favor maximal personal reproduction throughout a woman’s adult life. Given the fitness benefits of continued reproduction, why does the female reproductive organ – the ovary – quit working so early? Humans are nearly unique in having a menopause; although menopause is also reported in killer whales.
Some suggest that menopause evolved because grandmothers are more successful at passing on their genes by investing in grandchildren than in more babies of their own. Others argue that menopause is a consequence of modern medicine prolonging the lifespan. This artificial lifespan prolongation hypothesis proposes that most pre-historic women would be dead by 60 in the environment of evolutionary adaptedness (EEA). So for ancient women, reproductive aging might have been in sync with aging of the rest of the body. In this view menopause is a gene-environment mismatch.
Writing assignment: What best accounts for menopause in humans – the grandmother hypothesis, the artificial lifespan prolongation hypothesis, something else?
Readings for next week:
1. Still Pondering an Age-Old-Question. Flatt T and Promislow EL. 2007. Science (318) 1255-1256.
2. Fabian, D. & Flatt, T. (2011) The Evolution of Aging. Nature Education Knowledge 3(10):9
3. Why do we age? Kirkwood Austad Nature 2000 (focus on section on reproduction and menopause)
4. Hawkes K. Human longevity: the grandmother effect
This piece about the death habits of female octopus is also very cool and worth a read.