An item in yesterday’s New York Times reported a somewhat dispiriting result on the anti-aging front. (This is a subject that seems to attract my attention more and more as time goes by, for some reason, and particularly so this week, when I feel as though I am aging about 48 hours each day, with about 90% of it happening at seven a.m. when the alarm goes off). Apparently a troika of researchers at the University of North Carolina, the University of Michigan (go blue!), and Harvard have found that a gene called p16-Ink4a, in acting to prevent cancer, might be contributing to our senescence.
Here’s the idea. The regeneration of tissues is achieved by way of adult stem cells, but it doesn’t take so much for the division of these cells to start to go wrong, leading to the uncontrolled cell growth we call cancer. The longer you go, the more chance there is that such an error will occur, so as we get older the body begins to suppress the production of the protein – Ink4 – that keeps the stem cells in the youthful dividing phase. So it seems there is an unpleasant tradeoff here: either keep those cells dividing, with a rising risk of cancer, or gradually put on the brakes, and drive the body into decrepitude.
I am still confident that medical ingenuity will triumph, perhaps in my own lifetime, over senescence (not that such a victory would be without its own troublesome consequences), but this seems to be a bit of a setback. Read the Times story here, or read this article in Science.