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An alternative to changing the way cells process nutrients is giving them less to process in the first place. Studies have shown that rats whose caloric intake is 30% lower than that of a control group tend to live 30% to 40% longer. In humans, that would translate to a spartan diet of just 1,400 calories a day in exchange for 30 extra years of life.
Just how this business of swapping food for time works is not entirely clear, but George Roth, molecular physiologist with the National Institute on Aging in Bethesda, Maryland, has some ideas. When animals are placed on caloric restriction, Roth explains, the first thing that happens is that their body temperature drops about 1[degree]C. Lower temperature means a less vigorous metabolism, which means less food is processed. "In order to compensate for the reduction in diet," Roth says, "the animals switch from a growth mode into what can be thought of as a survival mode. They get fewer calories, so they burn fewer.
Cold and hungry, of course, is no way to go through life, but the condition has its rewards. When metabolism slows down, all its attendant processes do too, including cell division. Since, as Hayflick discovered, the number of divisions is limited, animals that go through them slowly may be able to salt a few away for later in life.
Roth, who has already observed the life-extending effectiveness of caloric restriction in rodents, is conducting similar experiments with primates. Even if they succeed, however, trying to apply the treatment to humans could prove dicey. In a nation of consumers for whom caloric belt tightening can mean little more than a smaller serving of French fries with their bacon cheeseburgers, the belief that people would be willing to reduce what they eat by a full third is probably unrealistic.
Roth finds this frustrating. "I think caloric restriction could take us beyond a life-span of 80," he says, "maybe even 120. After all, you rarely see a fat centenarian." Given modern dietary habits, however, it may be more practical to find out what part of the metabolic system caloric restriction operates on and then imitate that effect pharmacologically. "Essentially," explains Roth, "we'd use a pill to trick a cell into thinking less food is coming in."
Even if Roth succeeds, however, the impact of his work may be limited. In the world of antiaging, caloric reduction is essentially maintenance work, little more than patching holes in a slowly sinking ship and hoping you can stay ahead of the water it's still taking on. What senescence researchers really want is a way to get down into the body's engine room--the genes themselves--and rebuild things from the boilers up. Remarkably, it appears there may be a way.
Although he made history when he discovered the limits on cell replication in the lab, Hayflick left a question unanswered: why the cells die. In the years following his work, biologists mapping human chromosomes looked for a gene that enforced cellular mortality, but found nothing. One thing that did catch their eyes, however, was a small area at the tip of chromosomes that had no discernible purpose. Dubbed a telomere, the sequence of nucleic acids did not appear to code for any traits. Instead it resembled nothing so much as the plastic cuff at the end of a shoelace that keeps the rest of the strand from unraveling.