New Gene Adds a Piece to the Puzzle of Human Aging

(April 3) -- The discovery of a gene thought to control longevity, immunity and the body's resistance to illness is reinvigorating scientific efforts to slow down or even stop the process of human aging.

It's a promising find, but far from definitive. In fact, the gene is only the latest in a long list of potential explanations for why, despite persistent scientific efforts, we're all still getting older.

The gene, dubbed DAF-16, was examined by researchers at the University of Birmingham in England. They compared the gene's activity among four species of worms. Those with the most active genes were likely to live longer, and be more able to fend off illness, than species with less DAF-16 activity.

Importantly, DAF-16 was active throughout the worm's cells, which indicates that aging may not have a specific locus, such as, for example, hormonal glands or the brain.

Humans and mammals also have the DAF-16 gene, and the research team suspects that relative DAF-16 activity might be an evolutionary adaptation.

Understanding it, however, could help scientists circumvent evolution and develop methods to lengthen human life and fortify us against illness.

If, that is, the gene has the same connection to aging and immunity in humans as it does in worms. And even if researchers find a link, it's still likely that DAF-16 is only part of an intricate aging puzzle that's been confounding scientists for centuries.

Biogerontology, the study of biological factors behind aging, is a relatively new science. But it has made rapid advances in the last three decades, with expert theories falling largely into two camps: programmed theories, which suggest that aging and lifespan are inherent to our DNA; and damage theories, which counter that damage accumulates in the body, eventually leading to death.

In all likelihood, researchers suspect, it's some combination of both. Here are a few of the top factors that could help explain aging and help scientists proffer a solution.

Free radicals: The tiny molecules, produced as byproducts whenever cells create energy, are known to cause wear and tear within the body. Antioxidants, which occur naturally in the body and in nutritious foods, fend off the damage wrought by free radicals. They're also in red wine, as part of an oft-touted compound called resveratrol.

Plenty of direct evidence suggests that free-radical accumulation damages the body. But the molecules have yet to be linked directly to aging and death. Likewise, antioxidants, the molecules that do away with them, haven't been proved to promote longevity in humans.

Hormones: New research suggests that one of the oldest theories of aging is perhaps not the best. Scientists have long been aware of a connection between old age and dwindling levels of hormones such as hGh (growth hormone). But efforts at prescribing hGh to stimulate longevity have largely been a failure.

Human studies concluded that hGh therapy hastens the spread of cancer. And studies on mice found that hGh actually increased energy levels but decreased lifespan, leading anti-aging expert Joao Pedro de Magalhaes to liken hGh to "cocaine for grandpa."

Mitochondria: Known as the power plants of the body's cells, mitochondria yield usable energy for life's every process. In 2004, researchers in Sweden managed to fast-forward old age by injecting the mitochondria of mice with a genetic defect. Within days, the mice were suffering from osteoporosis, hair and weight loss, and enlargement of the heart.

Their study, published in Nature, offered a cause-and-effect glimpse of how gradual mitochondrial mutations might promote aging and death. In a paper accompanying the work, University of Washington geneticist Dr. George Martin noted that "changes in the mitochondrial DNA may be among the more important processes of aging."

Telomeres: Thought to be the deciding factor in cells death, telomeres operate as protective strands of repetitive DNA at the ends of cell chromosomes. Each time a cell divides, telomeres shorten, until they become so short that the cell stops dividing and dies instead.

Several studies have demonstrated the link between telomere length and aging, and one company is even marketing a supplement to boost levels of telomerase, the enzyme that sustains telomere length. The caveat? Other organisms don't exhibit the same telomere shortening, so an animal study on telomerase-boosting is out of the question.