Battling Nature (Part 1): Genetic Possibilities

4 min read

Age spots were the last things Linda Walsh wanted to see developing on her feet and legs three years ago. Just 42 years old, her hair was also beginning to fall out, her joints were increasingly stiff and she was constantly fatigued.

Today the Southern California resident's skin is blemish-free, and her hair is as lustrous and full as it has ever been. She's healthy and active, running her growing business. Walsh said that she owes the turnaround to antioxidant supplements and the specialized skincare products she religiously lathers all over her face and body.

As more Americans such as Walsh join the ranks of the aging population, they're finding that staying forever young isn't always as simple as taking a few pills and smearing on special lotions. Geneticists say that's because the cause of aging goes much deeper, all the way into the core of the body's cells -- the genes -- the blueprint of human life, which dictates how people grow, develop and age.

With the Centers for Disease Control and Prevention this summer reporting that Americans are now living an average of 30 years longer than they did in 1900, the thought of increasing human life expectancy may no longer be a fantasy.

"There are lots and lots of genes that can make a difference in how we age and how long we live," said Dr. George Martin, adjunct professor of genetics at the University of Washington School of Medicine in Seattle.

For the last 10 years, Martin has been studying Werner's syndrome, a disease that causes people to develop symptoms of aging as early as age 20. Persons with the syndrome develop gray hair, osteoporosis, heart disease and diabetes, symptoms that mirror the health of an aging person.

In 1996, Martin and his colleagues in laboratories around the world isolated the cause: a gene they call recQ, mutated so that it no longer works to support the cell's gene-maintenance machinery. When the machine slows down, the person affected begins to display the signs of premature aging.

Martin points out that because an alteration in a gene causes symptoms of aging, physicians might someday be able to target certain genes to slow the aging process.

What's offering more clues, however, is the study of animals whose genes can be very similar to human genes. University of Colorado scientists have found several genes in roundworms, for example, that, when mutated, allow the worms to live twice as long.

One of these genes controls how much antioxidant the body produces, said lead researcher Thomas Johnson, professor of behavioral genetics at the university's Boulder campus. When the gene is mutated, more antioxidant is produced to fight free radicals, byproducts of the body's energy-making process that cause aging by damaging tissues and cells. Roundworms that have more of the antioxidant live twice as long as worms that have the normal amount of antioxidant.

However, while antioxidant supplements may have rid Walsh of age spots, the supplements, including vitamins A, E and C, don't necessarily increase the body's ability to fight free radicals, Johnson added, explaining that some studies are showing that the body produces less antioxidant if it's already supplied through the diet.

Information Johnson is collecting from research could potentially help increase the human lifespan. Johnson recently set up a company, Denver-based GenoPlex, that will try to develop drugs to interfere with the aging process on the genetic level.

"It's impossible to predict what can happen," he said. But "there's no formal reason why we couldn't manipulate genes... in humans using drug approaches that would disrupt genes in the same way."

Manipulating genes may be the way to go, agreed Helen Blau, professor and chairman of molecular pharmacology at Stanford University School of Medicine. She and her team of researchers have been developing genetically engineered muscle cells, which could stimulate the body to produce blood vessels. Reinvigorated blood vessels could prevent the development of heart disease and poor circulation, as well as delay the muscle atrophy and the difficulties in wound healing that afflict older people.

So far, the genetically engineered cells have been successful at stimulating blood-vessel growth in mice, Blau said. With this success, she will begin clinical trials in the near future to see if the cells can cause blood vessels to grow in people.

However, like most scientists, Blau insists the anti-aging therapies aren't going to happen today. Instead, she said that while scientists now know so much about the genetics of aging, actual genetic therapies are a thing of the future.

"It's tremendously exciting," Blau said. "But it's not ready for prime time yet."