Health & Fitness

Two preeminent aging experts are on opposing sides of a bet that someone living today will be alive in 2150.

“But we could only achieve that once,” he says. “Once you’ve used it up, you’re done. You then have to focus in on what happens at older ages. At the older ages, it’s no longer diphtheria and tuberculosis. You’ve got aging. You can treat diphtheria and tuberculosis. You can’t treat aging—yet.”

As we grow older, our bodies change. Our skin wrinkles, our backs stoop, our brains fill with plaque, and our blood vessels stiffen. Changes take place within our cells as well, including damage from environmental toxins and oxygen free radicals, the shortening of telomeres (the tips of chromosomes) as cells divide, and other things that scientists still don’t fully understand. All these changes raise our odds of dying, if not of one disease, then of another. Those odds double every seven years or so. That pace is the same from one culture to the next, Olshansky and his colleagues have found, and from one period of history to another. “No matter where we looked, it’s the same,” he says. Aging, in other words, is deeply etched in our biology. In fact, the same pattern turned up when Olshansky looked at other species. Dogs, for example, live only 10 years on average. But if you draw a dog curve and a human curve on the same scale, they are practically identical.


While the odds of dying have dropped dramatically for babies, they have dropped far less for the elderly. The maximum life span of humans has barely budged over the decades, even as the average life expectancy has soared. Simply attacking this or that disease won’t extend the human life span any further, says Olshansky. “Eliminating cancer would only get about three and a half extra years,” he says. If tomorrow no one ever died of a heart attack again, three years. In fact, the mortality curve suggests that ordinary medical advances would be unlikely to push the average life span of Americans past 85 years. A tiny fraction will live beyond 100.

In the seven years since the bet, obesity has exploded into a nationwide epidemic. Obesity can lead to heart disease, diabetes, and other potentially fatal disorders. Olshansky and his colleagues have built demographic models to project the effect obesity will have on the average life expectancy in the United States. The picture is grim. “We’re losing between two and five years within the next 50 years,” he says, “which is huge.”

Steven Austad, now 60 years old, still has the stocky body of a college wrestler, and there are creases on his face from field seasons in the sun. Although the malaria he contracted in Papua New Guinea still flares up, he rarely finds himself in the jungle these days. He has traded traps and radio collars for microscopes and centrifuges. In fact, he has brought the field to his lab near San Antonio: There’s a colony of naked mole rats in the basement. He and his colleague are now searching for the molecular differences between species that die young and others that live long.

In the years since the bet, Austad has grown even more certain that he’s right. Scientists now have a much more detailed understanding of how shutting down certain genes and restricting calories slow aging.

Scientist Edward Masoro, at the University of Texas, pioneered research in the 1990s that showed that calorie restriction in animals leads to a longer, healthier life span. It turns out that a low-calorie diet switches on a key gene called SIRT1, which controls a network of dozens of other genes. They create an army of proteins that protect a cell from damage. Related versions of SIRT1 trigger the same response in mammals, insects, and even yeast. Scientists in laboratories across the country were performing similar experiments on spiders, mice, and worms. For example, researchers at the University of California shut down a gene called daf-2 in a microscopic worm known as Caenorhabditis elegans and it lived twice as long. The scientists weren’t sure what daf-2 actually did, but the results were undeniable. Researchers at Brown University found that manipulating a gene known as IGF-1 had a similar effect on flies.

Discovering genes like SIRT1, daf-2, and IGF-1 opens up a new way to fight aging. After all, human biology isn’t all that different from the biology of mice or worms. We share many genes, such as daf-2, and they do similar things for us. So if scientists are already figuring out how to slow aging in animals, it might be possible to do the same for people. Instead of going hungry for the rest of your life, you might be able to take a pill containing molecules that are able to switch on SIRT1 in your cells. In recent years, scientists have launched a large-scale search for those molecules. One molecule that switches on SIRT1, known as resveratrol, is produced by grapes and other plants. Harvard University’s David Sinclair, PhD, and his colleagues have found that, as predicted, resveratrol shows signs of slowing aging. They fed resveratrol to 1-year-old mice that ate a high-fat diet that would normally cause them to drop dead after about a year. But with regular doses of resveratrol, the badly fed mice enjoyed a mortality rate as low as mice on a normal diet—three years.