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Big Ones Help You Live Longer: It’s Telomeres Again

scientists show that mutations in telomerase are a predictor for long life span

What’s the secret to living to be 100? Vegetarianism? Lots of exercise? Making sure you never watch a Sandra Bullock movie, thus ensuring your blood pressure isn’t raised by contemplating the unfairness of a world in which so little talent can take a person so far?

Well sure, all of those things can help. But a new study shows that it may be our genes, more than our actions, which give us the chance of seeing out a century.

We’re looking at work which has just appeared in the Proceedings of the National Academy of Sciences. The scientists  are based at Yeshiva University in New York, and the lead investigator on this paper was Yousin Suh.

They’ve looked at the effects on aging of having a mutant, hyperactive telomerase gene. This is the same area of research which recently won its founders the Nobel Prize in Medicine.

The boffins studied the sequence of the telomerase gene in a number of Ashkenazi Jews. This is a well-established way of looking for genetic determinants of disease, etc, as the Ashkenazis have historically married and reproduced only within their own communities. That means that they have limited amounts of the background genetic noise which exists in other, more outbred populations, allowing scientists to draw conclusions about the roles of specific gene mutations.

They report here that those members of the study who lived the longest, and their descendants, had telomeres (see below) which were longer than other members of the population. Furthermore, this increase in telomere length was indisputably linked to their possession of mutant telomerase genes, which produce proteins with increased activity.

The gene seems to reduce the severity of age-related conditions, such as cardiovascular disease and diabetes. Dr Suh describes where the work is headed:

We’re now trying to understand the mechanism by which these genetic variants of telomerase maintain telomere length in centenarians. Ultimately, it may be possible to develop drugs that mimic the telomerase that our centenarians have been blessed with.

Don’t Hold Your Breath, But This May Lead To: well, hopefully to the pharmacological intervention Dr Suh describes. But, we have a nagging fear that this kind of research into genetic determinants of disease – while vital – will increasingly be used by insurance companies and others to create a genetic underclass of people; those who happen to have a regular or faulty telomerase gene will be stung with higher premiums.

A quick note about the science behind this for those unfamiliar with it: your DNA is stored in chunks, called chromosomes. Each time a cell divides, a small piece of each chromosome’s end is lost. To stop this eating into the genes stored near those ends, they are protected by telomeres, and it is these which gradually get shortened the more times a cell divides. Once the telomeres get too short, the cell either stops dividing or even dies.

Telomerase is a protein which your cells make to add extra telomeres to chromosome ends, thus keeping the cell youthful. So, overactive telomerase (seen in these lucky Ashkenazis) keeps the body from aging as quickly as it otherwise would.

If you’d like to read about the surprisingly eventful life of Elizabeth Blackburn, one of the molecular biologists who won that Nobel for telomere research, here’s a link to her biography:

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And, if you’d like to learn more about molecular biology, including telomeres, here’s the appropriate book from the always wonderful Idiots’ Guide series:

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