Living To 100: Lessons In Living To Your Maximum Potential At Any Age by Thomas T. Perls;Margery Hutter Silver

Living To 100: Lessons In Living To Your Maximum Potential At Any Age by Thomas T. Perls;Margery Hutter Silver

Author:Thomas T. Perls;Margery Hutter Silver [Thomas T. Perls;Margery Hutter Silver]
Language: eng
Format: epub
Published: 2012-02-02T23:53:00+00:00


FAMILY SECRETS

However, as centenarians began to enter the study, another unexpected pattern appeared: Now and then we would enroll centenarians who had a centenarian brother or sister. Slightly more frequently, a centenarian would enter the study and tell us about a brother, sister, or cousin who was 90 or older, and still healthy. Family clustering of centenarians such as this was extremely surprising. Although we had been discouraged from looking for genetic factors for longevity, it was hard to deny what we were seeing. The idea that two siblings would inherit the same 8,000 genes so frequently seemed highly unlikely. If longevity were so securely bred in these centenarians and their siblings, it would have to be passed along in the form of a much smaller number of genes, perhaps less than 50; otherwise, the probability of two siblings sharing a significant portion of them was too small.

This observation radically changed our ideas about the genetic control over aging. If, as was commonly believed, there were thousands of genes involved in the process, the likelihood of any one person reaching 100 would be random. It was as though the plans necessary to build an extra-durable airplane included about 8,000 additional and unrelated modifications, all of which had to be communicated from one engineer to the next. Making sure that the new airplane followed all the design specifications of its predecessor would be very difficult.

But what if only 50 major modifications-or even responsible for making a more durable airplane? The longevity inheritance patterns we were seeing encouraged us to think that we might be able to identify genes that determine the rate of aging and susceptibility to diseases associated with aging. These were genes that could either protect people from or predispose them to a broad range of conditions. Such genes could represent very powerful tools for studying aging and illness. If indeed there were a very small number of genes responsible for allowing people to age slowly and avoid disease, we had to begin looking for them.

We consulted Brad Hyman, the neuropathologist with whom we had studied apo-E gene variants associated with Alzheimer's disease. He cautioned us that it would be difficult to mount such a study. The tools of genetics were designed to look at genes associated with diseases; no one had ever tried to identify genes that make people healthier, and it was not clear that the techniques existed to do so. Moreover, just to begin looking for a small number of genes that conferred longevity meant that we would have to locate at least 250 centenarian sibling pairs, a daunting challenge. The demographer James Vaupel had predicted that only one out of 400 centenarians would have a centenarian sibling. The typical centenarian lives less than a year after turning 100, often dying before one can find out whether any siblings will become centenarians. One of our frustrations was the more frequent case of nonagenarian siblings who were in excellent health and appeared well on their way to 100 but were too young to enroll.



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