This blog is intended to go along with Population: An Introduction to Concepts and Issues, by John R. Weeks, published by Cengage Learning. The latest edition is the 12th (it came out in 2015), but this blog is meant to complement any edition of the book by showing the way in which demographic issues are regularly in the news.

If you are a user of my textbook and would like to suggest a blog post idea, please email me at: john.weeks@sdsu.edu

Monday, November 7, 2011

Trying to Get a Grip on Aging

One of the more widely accepted theories of aging is that put forth by Leonard Hayflick suggesting that each cell has a biological time-clock limiting the number of times that cell will reproduce. This is thought to be an evolutionary adaptation that prevents any cell from multiplying over and over and thus becoming a cancer (note that the National Cancer Institute defines cancer as "diseases in which abnormal cells divide without control and are able to invade other tissues"). No one has figured out how to change this upper limit on cell division, but new research by Darren Baker of the Mayo Clinic, reported in Nature, and covered in this week's Economist, suggests that some aging cells have adverse effects not only on themselves but on nearby cells, and that destroying those bad boys can improve the health of the nearby cells. Baker notes that: 
Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan.
The key phrase here is "healthy lifespan." This is not the same as increasing lifespan, but only making the older years healthier than they would otherwise have been. The experiments on mice that led to the conclusion that this is possible are complex, and we are almost certainly a long way from having any application to humans, but as the Economist concludes:
Genetically engineering people in the way that Dr Baker engineered his mice is obviously out of the question for the foreseeable future. But if some other means of clearing cells rich in P16INK4A from the body could be found, it might have the desired effect. The wasting and weakening of the tissues that accompanies senescence would be a thing of the past, and old age could then truly become ripe.

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