Posted July 19, 2013

By David Templeton, Pittsburgh Post-Gazette

Aging is a disease, or so claims William H. Andrews.

His company, Sierra Sciences, hopes to cure aging.

Big claim. Fountain-of-youth kind of stuff. He even acknowledges being characterized as a snake-oil salesman, one of those who historically have sold anti-aging potions to a more than willing public.

But the molecular biologist, who helped discover the enzyme he hopes to use to improve cellular age, said his Reno, Nev., company is on the fast track to reversing the aging process in pets. Harvard University already has done it with lab mice. A drug for humans requiring human clinical trials and U.S. Food and Drug Administration approval could be only a few years away.

Scientists raise caution about Mr. Andrews’ claim but don’t brush it aside.

The reason is the telomere (TEE-lo-meer), which scientists have known about for decades and are finding growing evidence of its impact on cell age and health.

Telomeres — DNA protein caps at the ends of chromosomes — have been compared with the plastic and metal sheaths, or aglets, at the ends of shoelaces. When aglets wear away, the shoestring frays. The same idea generally holds true with telomeres and chromosomes.

Telomeres shrink in a natural progression each time a cell divides. As a person ages, cell telomeres shorten, which eventually can shrink to a level where the cell becomes inactive or senescent. If the telomere disappears, the chromosome, like the shoestring, unravels and the cell dies. When telomeres disappear, they promote a type of immune response that can lead to cancer. Senescent cells also can spawn biological consequences promoting cancer.

Shortened telomeres increase the risk of cancer, heart disease and other chronic diseases. There’s still debate, but evidence is growing that their shrinking can cause disease, with the disease process also accelerating the shrinkage.

While age naturally causes telomeres to shorten, stress, depression, obesity, smoking and a bad diet, among other factors, hasten the shortening process.

“It’s possible that short telomeres are biomarkers of the cumulative stress on the body. The effects of stress can cause higher cell turnover, and oxidative stress can shorten the telomeres,” said Patricia Opresko, an assistant professor in the department of environmental and occupational health in the University of Pittsburgh Graduate School of Public Health.

She is studying how environmental factors such as sunlight, pollution and oxidative stress affect telomeres.

Research, she said, is figuring out whether telomere length serves as a useful biomarker of a person’s biological vs. chronological age and whether they can predict one’s risk of chronic disease.

While lifestyle changes remain the best way available to protect one’s telomeres, the topic hovering over the entire science is whether lengthening them can restore health and biological youthfulness.

How to lengthen a telomere

Mr. Andrews was involved in the 1990s in discovery of the enzyme, telomerase, which an activate gene produces. Telomerase (te-LAW-mer-ace), works to prevent telomeres from shortening and appears to lengthen them if enough of the enzyme is generated. It represents the source of scientific optimism that organ function and youthfulness could be re-established in animals and humans.

That already occurred in a 2010 Harvard University-based study in which old, dying mice, deficient in telomerase, were given the enzyme to lengthen their telomeres. The principal investigator, Ronald A. DePinho, now directs the M.D. Anderson Cancer Center, in Houston.

“Telomere loss and uncapping provokes progressive tissue atrophy, stem-cell depletion, organ-system failure and impaired tissue injury responses,” according to the study.

Reactivation of telomerase extended the telomeres in the old mice, reducing DNA damage and halting the degeneration of multiple organs, including the testes, spleen, intestines and even brain neurons. The old mice recovered their health, became sexually active and restored function of the senses including the ability to smell.

The evidence implicated damaged or shortened telomeres as causing “age-associated organ decline and disease risk,” all associated with the lack of telomerase. Reactivation of telomerase, in turn, caused a reversal of systemic degeneration in mouse organs.

“The aging world population has fueled interest in regenerative remedies that may stem declining organ function and maintain fitness,” the study states. Those results, it says, support “development of regenerative strategies designed to restore telomere integrity.”

With such studies and hopeful results from existing telomerase-activation supplements (not requiring FDA approval) — AT-65 and Product B — Mr. Andrews said the potential is obvious.

“They turned old mice into young mice,” he said of the Harvard study published in Nature. “I want to take this myself and give it to my 85-year-old parents.

“I’ve never been more optimistic.”

One long-standing concern is that cancer cells also activate the gene that produces telomerase, which helps cancer cells to proliferate. That’s one reason why science has raised caution against developing medications too quickly to boost telomerase. Drugs now are being developed to do the opposite — reduce telomerase production to fight cancer.

But while telomerase is involved in cancer growth, Mr. Andrews said activation of the enzyme in normal cells would not only improve health but also help to activate the immune system to improve the battle against cancer.

Young adults beware

Sheldon Cohen, the Carnegie Mellon University director of the Laboratory for the Study of Stress, Immunity and Disease, said recent research he led involving telomere length and the common cold found their shortening reveals impacts in adults as young as 23.

A recent study he led revealed that people with shorter telomeres, when exposed to a rhinovirus that causes the common cold, showed a higher risk of infection and symptoms than those with longer telomeres. There was no notable impact for people 18 to 22. But infections and symptoms began to elevate at age 23 onward, representing the first evidence of telomeres in early adulthood.

The study published last spring in the Journal of the American Medical Association, said telomere shortening in immune cells is associated with an inability of the cells to divide and with the production of an inflammatory response. Both can lead to disease when exposed to a virus. Shortened telomeres also are associated with aging-related morbidity and mortality from other conditions involving the immune system, including other infectious diseases, cancer and cardiovascular disease.

Elissa Epel, an associate professor in the University of California San Francisco department of psychiatry, an author of several published studies on the effects of stress on telomere length, said a long history of infections can shorten telomeres, reflecting a vicious cycle in which a more aged immune system becomes less efficient at fighting off future infections.

“Many studies have shown that short telomeres predict earlier onset of diseases of aging, including cancer and heart disease,” she said. “It’s a valuable risk factor, regardless of whether it’s causal or not.”

Because of the cancer concerns associated with telomerase, Ms. Epel raised caution about Mr. Andrews’ efforts to develop drugs to activate its production this early in the scientific process.

“We think the only safe way to increase telomerase is to boost your health,” she said.

The list of best candidates, she said, include vigorous exercise, sleep quality, omega-3 oils such as fish oil, stress reduction and meditation.

“There’s always hope for a pill,” she said, “But I’d never take a supplement that improves cell division capacity that is relatively untested and not regulated by the FDA.”

David Templeton: [email protected] or 412-263-1578 .

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