A Wrinkle in Time
A modest proposal to slow aging and extend healthy life.
While eliminating smallpox and curtailing cholera added decades of life to vast populations, cures for the chronic diseases of old age cannot have the same effect on life expectancy. A cure for cancer would be miraculous and welcome, but it would lead to only a three-year increase in life expectancy at birth. A cure for heart disease would be equally welcome, but we would gain only four-and-a-half years as a result. Gains in longevity from cures for diseases are much smaller today than one might expect because aging bodies face multiple lethal conditions—an effect known as competing causes. Competing causes in aging bodies means that those saved from dying from one condition will eventually face an elevated risk of dying from something else. Death is a zero sum game for which there is no cure.
While we can extend life in aging bodies through behavioral improvements and medical treatments, the time has arrived to acknowledge that our current model of reactive medicine, of trying to treat each separate disease of old age as it occurs, is reaching a point of diminishing returns.
For some people, disease reduction will add healthy months and years, but others will be inadvertently exposed to highly disabling conditions for a longer portion of their lifespan than would otherwise be the case. Let's say physicians replaced the heart valve in an 82-year-old woman who would die without treatment, and she lived another decade. Her life was successfully extended by modern medicine, but what if the last five years of her life involved Alzheimer's disease, requiring 24-hour care—a condition that would not have arisen had she died of heart disease a decade earlier? This is one of many negative trade-offs forthcoming if current efforts to attack diseases are successful in manufacturing survival time in the absence of decelerated aging.
In spite of considerable time and resources invested in the analysis, prevention, or cure of individual fatal and disabling chronic diseases, nearly all of the diseases and disorders experienced by middle-aged and older people still show a near exponential rise in the final one-third of life. That's because the essential cause of our troubles—aging—marches on unaltered by these interventions.
It's important to acknowledge the fundamental differences between disease and aging. Although age-associated changes in the body produce an increased risk of disease, the reverse is not true. That is, reducing the risk of disease has no influence on biological aging. Thus, if a population is preserved with increasing efficiency by advances in technology that reduce the risk of disease, those saved will live into increasingly later sections of the lifespan where aging takes a greater toll on body and mind. Life extension achieved in this way could extend old age by exposing survivors to the high-risk conditions of frailty that are common, and largely immutable, near the end of life—the very outcome that medicine and public health practitioners are trying to avoid.
Many scientists and geriatric physicians now suggest that the primary goal of medical technology should not exclusively be life extension but, rather, lengthening the period of youthful vigor. Although efforts to combat disease should continue, one way to protect against the unwanted prolongation of old age while simultaneously extending the period of healthy life is to pursue the means to modify the key risk factor that underlies almost everything that goes wrong with us as we grow older—aging itself. Those of us working toward this goal have referred to this shift in approach to public health as the "Pursuit of the Longevity Dividend."
The longevity dividend means a commitment to research that would attack aging at its roots and allow us to apply the findings in order to extend our healthy years. This is no longer science fiction—scientists have already extended life in the laboratory. For example, experiments have demonstrated that by manipulating certain genes, altering reproduction, reducing caloric intake, and changing the signaling pathways of specific physiological mechanisms, the duration of healthy life of both invertebrates and mammals can be extended. Meanwhile, in the laboratory of real life, there are already people living among us who have survived to extreme old age with healthy bodies and minds—implying that the genetic clues to decelerated aging are likely to be contained within our own genome. In other words, there is ample reason to be optimistic that decelerated aging can be achieved for humans.
Pursuing an aggressive research strategy to devise interventions against aging requires that it is a goal worth pursuing (it is), and that we have good leads to follow (we do), but it does not require that we know, in advance, which of the current ideas about mechanisms affecting the rate of aging are most likely to produce effective interventions.
S. Jay Olshansky is a professor in the School of Public Health at the University of Illinois at Chicago.