Role of Diet, Genes in Aging
Examined at AAAS Event

Extremely thin people (on nutritious diets) have a good chance of living longer, according to Richard Miller, senior researcher at the University of Michigan's Institute of Gerontology.

In a web-broadcast interview at AAAS this week during a SAGE (Science of Aging) Crossroads event, Miller answered questions on aging, and discussed the progress that science is making in slowing the process. SAGE Crossroads is the premier online forum for emerging policy issues related to research on human aging. Launched in March 2003 by the publishers of the journal Science and the Alliance for Aging Research, SAGE Crossroads provides policymakers, journalists and interested consumers with the opportunity to explore the impact of science and technology on aging.

Miller described laboratory experiments that extended the life span of mice by 50 percent, results obtained after reducing the animals' daily caloric intake by 40 percent. The change in diet also seemed to prevent deafness, breast cancer, cataracts, and other afflictions typically associated with aging.

"We can make a mouse live 3 years instead of 2," Miller said.

It's not a stretch to surmise that humans might also reap the benefits of a longer lifespan and healthier life by reducing the number of calories in their daily diet. For example, because obese people tend to be more susceptible to ill health, Miller suggests that losing weight could help humans avoid disease.

He noted, however, that comparable restrictions in the human diet would make a person excessively thin.

"A 5'10'' man like me would have to weigh 140 lbs," Miller said.

Genes and Aging

Modifying genes can lead to benefits similar to those of reduced caloric intake. Miller said that alterations in a number of mouse genes extend longevity (see sageke.sciencemag.org/resources/experimental/transgenic). By studying such genetically altered mice, researchers have been able to single out variances, such as hormone production levels, which might provide clues to the secrets of a longer lifespan.

While researchers know a great deal of what causes cells to die and stop dividing, there's little information on what turns a young person into an old one. Miller opened the discussion by defining aging as the process that turns young, healthy adults into older people who are more vulnerable to disease.

"It's important to distinguish this approach from the study of old people," he said. Aging is a scientific mystery; if we learn about aging and can intervene in the aging process, there will be a huge health impact.

One of the most important findings in recent years has had to do with mutations that affect lifespan found in worms (see sageke.sciencemag.org/cgi/content/full/sageke;2003/8/re2). A recent study revealed that certain mutations make worms resistant to all sorts of stresses, like extreme heat or oxidation; the same stresses that would cause non-mutated worms to expire.

This suggests that mutations in certain genes make cells that are stress resistant — mutations that, if characterized, could give scientists new ways to prevent diseases in humans.

Although the human lifespan has drastically increased within the last century because of advances in sanitation and in preventing and treating childhood diseases, science has yet to battle aging itself and the diseases associated with growing older, such as cancer and Alzheimer's.

"We must develop a way to slow aging down. It's not a matter of immortality, but a matter of slowing down the rate at which chronic diseases hit," Miller said.

It's also a matter of increasing public support for research on aging, he added. The public may endorse wholeheartedly the need for cardiovascular or cancer research, while being less enthusiastic about research on aging, even though it is essentially the same thing, according to Miller. He noted that research on the aging process would lead to better comprehension and, eventually, prevention of the diseases commonly associated with old-age.

A transcript of this Web cast is available on www.sagecrossroads.net.

—Carol Hoy

3 June 2003

See also,

sageke.sciencemag.org/cgi/content/full/sageke;2001/1/oa1
sageke.sciencemag.org/cgi/content/full/sageke;2003/8/re2
sageke.sciencemag.org/cgi/content/abstract/sageke;2001/9/nw31