Please find below a summary of the topics we discussed in class on 8/28/12. The required readings for this week are 1, 2, and 3 listed below. Readings 4 and 5 are optional and well worth a look.
The topic for next week will be the microbiota and the evolution of damaging inflammation from diet. I have added the recently published QRB article that I published with colleagues Melissa Franklin and Chris Kuzawa. Read the Science Daily summary posted yesterday for an additional preview.
1. age-old-questionFlatt T and Promislow EL. 2007. Science (318) 1255-1256.
2. Evolution of the human menopause Evolution of the human menopause. Shanley DP and Kirkwood TB. 2001 Bioessays 23. 282-287.
3.Alcock_Franklin_Kuzawa Nutrient signaling: Evolutionary Origins of the immune modulating effects of dietary fat. Quarterly Review of Biology.Vol. 87, No. 3 (September 2012), pp. 187-223
4. Nesse and Dawkins. Evolution: Medicine’s most basic science. from The Oxford Textbook of Medicine, Modern Medicine: Foundations, Achievements, and Limitations, 2010.
5. Williams. Pleiotropy, Natural Selection, and the Evolution of Senescence. Evolution, 1957.
Due next week in hardcopy in class, no more than 1 single spaced page:
Writing project: Why do women cease to reproduce in middle age? How did menopause evolve in humans?
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 of women past 60 when most pre-historic women would be dead. So in the past reproductive aging would have been in sync with aging of the rest of the body. In this view menopause reflects the early mortality in pre-history and is a gene-environment mismatch. Argue for either the “grandmother hypothesis” or the “artificial lifespan prolongation” hypothesis.