Telomeres and Aging: The Hayflick Limit, Telomerase's Cancer Trade-Off

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Every time a human cell divides, the DNA copying machinery cannot finish the very tip of each chromosome, an issue called the end replication problem. DNA polymerase reads in only one direction and needs an RNA primer to start, so 50 to 100 base pairs are lost per division. Telomeres, thousands of repeats of the sequence TTAGGG, absorb that loss. In the 1970s Soviet biologist Alexey Olovnikov proposed that this shortening sets a ceiling on cell life, explaining Leonard Hayflick's finding that cultured human cells divide only about 50 to 70 times. Cells that hit the limit enter senescence and release inflammatory chemicals linked to aging.

The chromosome tip folds into a T-loop held by a six protein complex called shelterin, which stops repair enzymes from fusing chromosomes together. In 2009 Elizabeth Blackburn, Carol Greider, and Jack Szostak won the Nobel Prize for discovering telomerase, the enzyme that rebuilds telomeres. It is active in germ cells and some stem cells but switched off in most cells, because about 90 percent of tumors reactivate it to become immortal. Aging, the episode argues, may be the price of protection against cancer.

Oxidative stress from reactive oxygen species speeds telomere shortening
Links between psychological stress and short telomeres weaken once publication bias is considered
The four year VITAL trial reported that vitamin D3 and omega-3 slowed shortening by roughly three years' worth
Mice start with far longer telomeres than humans but lose them much faster
Leach's storm petrels appear to gain telomere length as they age, and most bacteria have none at all

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