The link between chronic stress and a marker of old age is being disentangled
TELOMERES are to chromosomes what plastic caps are to shoelaces—they stop them fraying at the ends. Unlike shoelaces, though, chromosomes replicate themselves from time to time as the cells they are in divide. This shortens the telomere and, after 50-70 such divisions (a number known as the Hayflick limit, after its discoverer), a chromosome can grow no shorter and the cell it is in can divide no more.
That provides a backstop against cancer. The rapidly dividing cells in a tumour soon hit the Hayflick limit and the process is brought to a screeching halt. Which is a good thing. The bad thing is that reaching the limit is one of the markers of old age. You do not want it to happen too quickly, particularly in tissues that have to do a lot of dividing in order to work properly, such as those in the immune system.
It has been known for some time that chronic stress (caring for a child with a protracted illness, for example) causes premature shortening of the telomeres. What has not been clear is whether this is a one-way trip, with each stressful period turning the telomeric ratchet irreversibly. This week, though, at a meeting of the American Association for Cancer Research in Orlando, Florida, a group of researchers led by Edward Nelson of the University of California, Irvine, showed that it isn’t. Their research suggests that stress management not only stops telomeres from shortening, it actually promotes their repair.
没有评论:
发表评论