By S. Jay Olshansky, Leonard Hayflick and Bruce A. Carnes
Any discussion of aging should first clarify its terms. Various definitions have been proposed, but we think of aging as the accumulation of random damage to the building blocks of life—especially to DNA, certain proteins, carbohydrates and lipids (fats)—that begins early in life and eventually exceeds the body’s self-repair capabilities. This damage gradually impairs the functioning of cells, tissues, organs and organ systems, thereby increasing vulnerability to disease and giving rise to the characteristic manifestations of aging, such as a loss of muscle and bone mass, a decline in reaction time, compromised hearing and vision, and reduced elasticity of the skin.
This accretion of molecular damage comes from many sources, including, ironically, the life-sustaining processes involved in converting the food we eat into usable energy. As the energy generators of cells (mitochondria) operate, they emit destructive, oxidizing molecules known as free radicals. Most of the damage caused by these reactive molecules gets repaired, but not all. Biologists suspect that the oxidative assaults ultimately cause irreparable injury to the mitochondria, thereby impeding the cell’s ability to maintain the integrity of the countless molecules needed to keep the body operating properly. The free radicals may also disrupt other parts of cells directly.
Aging, in our view, makes us ever more susceptible to such ills as heart disease, Alzheimer’s disease, stroke and cancer, but these age-related conditions are superimposed on aging, not equivalent to it. Therefore, even if science could eliminate today’s leading killers of older individuals, aging would continue to occur, ensuring that different maladies would take their place. In addition, it would guarantee that one crucial body component or another—say, the cardiovascular system—would eventually experience a catastrophic failure. It is an inescapable biological reality that once the engine of life switches on, the body inevitably sows the seeds of its own destruction.
Men and women in the developed world typically live longer now (75 and 80 years, respectively) than they did throughout much of history (about 25 years) because human ingenuity—which brought us sanitation systems, vaccines, antibiotics and so on—has had phenomenal success in thwarting the infectious and parasitic diseases responsible for a great deal of premature death. We live longer now not because we have altered the way we age but because we have altered the way we live.
Though inevitable, aging is not, as some might think, a genetically programmed process, playing itself out on a rigidly predetermined time schedule. The way evolution works makes it impossible for us to possess genes that are specifically designed to cause physiological decline with age or to control how long we live. Just as an automobile does not have a built-in plan for decline written in its blueprints, we do not possess genetic instructions that tell our bodies how to age or when to die.
The logic behind this assertion goes basically like this: Genes perpetuate themselves by orchestrating the transformation of a fertilized egg into a sexually mature adult that produces offspring. Clearly, any genetic variant that compromises this developmental process would be self-eliminating. Conversely, evolution is totally blind to the consequences of gene action (whether good, bad or indifferent) after reproduction is achieved. Genes or genetic variants that prove detrimental in the postreproductive part of the life span can become commonplace, but only if they participate in important processes early on. For example, several genes that contribute to cancer in the later years are known to participate in growth and development early in life.
Without a doubt, a host of our genes influence aging, but they do so indirectly, as an inadvertent by-product of processes involved in growth, development, and the maintenance of health and vigor. The lack of a specific genetic program for aging and death means that there are no quick fixes that will permit us to treat aging as if it were a disease. A single genetic intervention in an organism as complex as a human being would have little chance of combating the probably vast array of genes and biological activities that play subtle, unpredictable parts in the timing of our ultimate demise. (From Scientific American Online, December 29, 2008)
Exercise 3. You are going to read an article about centenarians – people who are more than 100 years old. Before reading discuss the following questions:
1. Are there any biological limits to human life span?
2. Have people reached the upper limit of longevity?
3. How can average life expectancy be increased?
4. Would you like to live to be a hundred years old? Why? Why not?