By contrast, in normal cell differentiation, cells divide and become more specialized, and their ability to live indefinitely simultaneously declines. The Hayflick limit may be not so much an intrinsic limit on living cells as a limit on when cells begin to differentiate, as in development of the embryo. When cells approach a limiting point, a genetic program normally shuts down the capacity for further division. If the genetic program doesn’t work, the result is uncontrolled multiplication, or cancer. The Hayflick limit doesn’t keep all cells from dividing—after all, germ cells such as eggs and sperm continue to divide—but it may give a clue about why aging brings an increase in cancer and a weakening of the immune system.
Studying aging by examining cells in a test tube raises some questions. For instance, the nutrient medium in a cell culture does not contain all the nutrients and hormones that a cell would normally receive. In addition, cells in the body become differentiated tissues and organs and remain in equilibrium in ways quite different from the way cells replicate in a test tube.
Fundamentally, the cellular theory of aging sees aging as somehow programmed directly into the organism at the genetic level. In this view, it is just as natural for the body to grow old as it is for the embryo or the young organism to develop to maturity, as we see in annual plants or the Pacific salmon. Does the cellular program theory of aging therefore apply to higher organisms such as mammals and, specifically, human beings? Perhaps, but it does not apply as obviously as it does to organisms in which rapid aging is tied to reproduction.
One of the most intriguing points in favor of the cellular approach to aging is the discovery that tiny tips at the ends of chromosomes—structures known as telomeres—become shorter each time a cell divides. Telomeres, it seems, comprise a biological clock marking the unique age of a cell as it divides. Studies are under way to explore the link between aging at the cellular level and what we recognize as aging in complete organisms. Elizabeth Blackburn won the Nobel Prize in Medicine for discovering the role of telomeres, which evidently play a crucial role in cellular aging (Brady, 2009). Biologists now understand that the length of a telomere can serve as a biomarker, or measurement of biological age beyond chronological age alone. Studies are under way to see if specific interventions can slow down the process of biological aging.
Is Aging Inevitable?
The biological aging process may not be the result of a rigid genetic program; it may simply be the complex and indirect result of multiple traits in the organism tied to normal development. In other words, the body may not be preprogrammed to acquire gray hair, wrinkles, or diminished metabolic functions. Rather, these supposed signs of aging may simply be telltale side effects of activities of the organism.
Consider the analogy of an aging car. Suppose a distinctive “species” of automobile were designed to burn fuel at a fixed temperature with an efficient rate of combustion. That specific rate of combustion is required for appropriate acceleration, cruising speed, fuel mileage, and so on. But, alas, when the car performs this way, it also inevitably produces certain emission by-products. Over time, these by-products clog the cylinders, reduce efficiency, and lead to the breakdown and final collapse of the machine.
In the case of the human “car,” burning oxygen in normal metabolism generates harmful by-products—namely, free radicals that prove toxic to the organism. The trade-off is that oxygen is essential for life yet harmful to our long-term well-being. Although the human “car” is not intentionally designed to accumulate toxic emissions in order to collapse, it cannot function at optimum levels without creating destructive by-products.
Now suppose we could find some special fuel additive that eliminates toxic emissions. Would we then have an immortal car? Probably not. Changing the fuel in your car won’t prevent accidents, nor will any fuel additive prevent rusting or the wearing down of springs and shock absorbers.
The human car analogy has its limits because an organism, unlike a manufactured object, has a capacity for repair and self-regeneration, at least up to a certain point; unlike an automobile, human beings have consciousness and can make choices about how to live out their life span. Nevertheless, to find out how we might modify or slow down biological aging, we must find out why the capacity for self-repair seems unable to keep up with the damage rate—in short, why aging and death appear to be universal.
One response to the question “Is aging inevitable?” would be to find organisms that do not grow old at all. As it turns out, there are such species. One of these is the hydra, a freshwater animal similar to the jellyfish. Do hydras age at all, or are they, in principle, immortal? The rate of death for the hydra does not seem to increase with time. Hydra cells are continually dividing and replicating themselves, and their telomeres remain the same length as well. Some species of flatworms show similar capacity for regeneration without signs of aging.
Urban Legends of Aging
“Antiaging medicine today is making rapid progress.”
No progress is being made at all. No intervention has ever been shown to slow the biological process of aging, other than caloric restriction (eating drastically less), but recent findings, while promising, are far from conclusive. Herbal supplements sold in health food stores are totally unregulated, and many are dangerous. None, including antioxidants, has ever been proven effective in slowing aging.
Ways to Prolong the Life Span
Most theories of aging depict biological aging as an inevitable process, like a disease to which we must all eventually fall victim. Some theories look on the organism as succumbing to chance events, whereas others see it as driven by a built-in biological clock. Yet whether aging is thought to occur by chance or by fate, most theories seem to reach a pessimistic conclusion about the inevitability of aging.
But aging is not a disease; rather, it is a process of change, part of which may make us vulnerable to disease. Instead of being driven by a single primary process timed through a single biological clock, aging is driven by many different clocks, each on a different schedule and unfolding in parallel developmental patterns.
Biological theories of aging could have enormous importance for an aging society. For example, the compression-of-morbidity idea assumes that there is a definite human life span, roughly 85 years, with a broad range from 70 to 100 years. There are thousands who live beyond 100, but the maximum number of years any human being has lived is 122. An age around that level is often assumed to be the maximum life span possible. But today, basic research in the biology of aging is challenging assumptions about a fixed maximum life span and the inevitability of aging as a biological process. Two approaches have been found that could extend the maximum life span for a species: one based on environmental intervention through diet, the other on a genetic approach.
Biological aging is inevitable, but diet and exercise may promote healthier aging.
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Environmental Approach
For more than 60 years, scientists have known of only one environmental intervention—restricting food intake—that extends life span in mammals. Caloric restriction is defined as the reduction in calorie intake while maintaining adequate intake of essential nutriments. In the 1930s biologists discovered that caloric restriction can extend the longevity of relatively short-lived mammals, such as rodents in the laboratory. In fact, caloric restriction seems to work in a variety of species. The question was: Could caloric restriction also extend longevity in higher mammals such as humans? In recent years scientists have sought to answer this question.
Urban Legends of Aging