HEALTH

Public Health’s Newest Tool: the Fountain of Youth

Dodging Disease May Not Be the Expedient Path to Living Longer

Sometimes people get a bad reputation just for being a little ahead of their time. Take the explorer Juan Ponce de Leon. For having sought a fountain of youth, the guy earned a place in history as a frivolous narcissist. But was he really so off the mark? An amazing string of discoveries in recent years suggests that the concept of slowing and perhaps even reversing aspects of biological aging is not so ridiculous after all. Indeed, a growing cadre of scientists is today beating the drum for a significant shift in the way medical research dollars are spent. The idea is that researchers can accomplish more by learning how to slow the aging process than they can by making incremental gains against individual diseases of aging, such as cancer and heart disease.

Life expectancy has grown by leaps and bounds in the past century. And to be sure, that success story has been written not by exotic anti-aging creams or wrinkle removers but by hard-won victories over infectious diseases, primarily through public health advances and antibiotics. A century ago, only about 40 percent of babies born in countries where births and deaths were reliably counted could be expected to live past the age of 65. Today, almost 90 percent do so. That’s one reason why in the United States alone, the number of people older than 85 is projected to quadruple by 2050, to 18 million from today’s 4 million.

But how do we keep that progress going in developed countries, now that infectious diseases have largely been tamed? The current approach to extending life, which has garnered some modest success in the past decade or so, has been to focus on curing those chronic diseases of aging that have become the modern era’s major killers, such as heart disease, stroke, cancer, diabetes, and Alzheimer’s disease.

Yet most of these diseases have proven remarkably resistant to treatment. More important, a number of research models have concluded that even if scientists were to score a complete home run by finding a “cure” for any single chronic disease such as cancer or stroke, life spans in developing countries would hardly grow longer. That’s because the other chronic diseases of old age are right there, waiting to kill us anyway at about the same age. You’d have to find cures for virtually all of them, these models suggest, to make any real progress at this point.

That’s where the anti-aging approach comes in. As it turns out, scientists studying the aging process in a wide variety of organisms—from worms to flies to fish to monkeys and people—have been finding that certain genes common to virtually all kinds of life play key roles in the metabolic and genetic processes that together underlie most diseases of aging. Some of these genes are important for repairing DNA damage caused by sunlight, chemicals, or other environmental insults. Others affect the levels of vital hormones. As scientists figure out what these key genes do, it becomes possible to envision developing medicines that mimic their activity, which typically wanes late in life.

Complementing that cross-species work, a number of ongoing research projects promise to clarify some of the most important anti-aging genes in people. In one project, described in this week’s issue of Technology Review, researchers are comparing DNA from two populations: people 80 or older who have never had serious illnesses and those who died of age-related ailments before they hit 80.

Two analyses to be published in the July 19 issue of the British medical journal, BMJ, make the case that such efforts could have big payoffs. Unlike conventional advances in lifespan, which in many cases have added years of disability and suffering to the end of life, the anti-aging approach would add healthy years, according to Colin Farrelly of the University of Waterloo in Canada. “There is a credible scientific basis for believing that we could slow aging in the foreseeable future,” he concludes. “And the amount of public funding we invest into such research will determine the likelihood and timescale of success for aging interventions.”

Others writing in that journal—including Robert Butler (a former head of the federal National Institute on Aging), S. Jay Olshansky (a leader in the field at the University of Chicago), and Daniel Perry (of the Alliance for Aging Research in Washington)—argue that $3 billion, or one percent of the Medicare budget, would be a “prudent” investment in anti-aging research. They make a convincing case that such an investment could pay for itself many times over by delaying not only the fatal diseases of old age but also the many debilitating conditions such as osteoporosis, arthritis, cataracts, and cognitive decline that typically take a big toll on quality of life in people’s final decade or two.

They call that benefit “a longevity dividend,” and it looks to me to have a much higher probable rate of return than most of the other dividends I’ve been counting on for my retirement. Meanwhile, hang in there, ol’ Ponce. Your reputation, if not your bod, may get rehabilitated yet.

Rick Weiss is a Senior Fellow at the Center for American Progress and Science Progress.

Tags: genetics, public health

Comments on this article

You can skip to the end and leave a response. Pinging is currently not allowed.