Puzzle of the Century
Is it the fresh air, the seafood, or genes? Why do so many hardy 100-year-olds live in yes, Nova Scotia?
- By Mary Duenwald
- Smithsonian magazine, January 2003, Subscribe
(Page 8 of 10)
He speculates that longevity-enabling genes may work via several possible mechanisms, such as protecting against chronic diseases and slowing down the aging process. Then again, those processes may amount to much the same thing. “If you slow down the rate of aging, you naturally decrease susceptibility to illnesses like Alzheimer’s, stroke, heart disease and various cancers,” he says.
Clues to how such genes might operate come from a centenarian study being conducted by Dr. Nir Barzilai, a gerontologist and endocrinologist at Albert Einstein College of Medicine in the Bronx. Barzilai has found that his research subjects—more than 200 Ashkenazi Jewish centenarians and their children—have abnormally high blood levels of highdensity lipoprotein, or HDL, a.k.a. the “good” cholesterol. The average woman has an HDL level of 55, he says, whereas the grown children of his centenarians have levels up to 140.
He believes that a gene or genes are responsible for the extremely high HDL levels, which may have helped the very old people in his studies maintain their sharp minds and clear memories. He says their high HDL levels, which are presumably controlled by genes, might protect them from heart disease; HDL clears fat from coronary arteries, among other things.
Other researchers say that longevity-enabling genes might protect people in much the same manner as caloric restriction, the only treatment or dietary strategy shown experimentally to extend life. Studies with laboratory rats have found that those fed an extremely low-calorie diet live at least 33 percent longer than rats that eat their fill. The restricted animals also seem to avoid ailments connected with aging, such as diabetes, hypertension, cataracts and cancer. Another possibility is that longevity-enabling genes limit the activities of free radicals—unpaired electrons known to corrode human tissue. Medical researchers have suggested that free radicals spur atherosclerosis and Alzheimer’s disease, for instance. “Free radicals are a key mechanism in aging,” Perls says. “I wouldn’t be surprised if something to do with freeradical damage pops up in our genetic studies.”
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