This piece arises from Future Tense, a collaboration among Arizona State University, the New America Foundation, and Slate. A Future Tense conference on life extension will be held at the New America Foundation on Tuesday, Nov. 16. (For more information and to sign up for the event, please visit the NAF Web site.) Read more of Slate’s coverage on longevity.
We have grown accustomed to the wonders of clean water, indoor plumbing, laser surgery, genetic engineering, artificial joints, replacement body parts, and the much longer lives that accompany them. Yet we should remember that the vast majority of humans ever born died before the age of 10 from an infectious disease. Humanity responded to this high risk of early death with ingenious advances in public health and medical technology, the result of which was a dramatic 30-year boost in life expectancy in the 20th century. The longevity revolution that followed led to a trade-off for which the world was unprepared: the rise of an aged population suffering from multiple chronic degenerative diseases.
Older people may have always existed throughout history, but they were rare. Aging as we know it, and the diseases and disorders that accompany it, represent new phenomena—products of 20th century resourcefulness. When infectious diseases were largely vanquished in the developed world, few anticipated the extent to which chronic degenerative diseases would rise. We call them heart disease, cancer, stroke, arthritis, Alzheimer’s disease, and many more, but we might as well collectively use one word to describe them all—aging.
Aging may be defined 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 loss of muscle and bone mass, 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. Aging should most appropriately be thought of as an inadvertent byproduct of operating the machinery of life, which means that evolution could not have given rise to these processes directly. Because nature does not have a program for aging and death, this makes it possible to conceive of interventions that influence the length and quality of our lives, but more importantly, it means evolution has given humanity an entrée into manipulating the speed with which we age.
Aging bodies with chronic diseases are not the same as young bodies with independently acquired infectious diseases. Yet medicine continues to act as if the diseases of aging are separate from the consequences of aging itself. It’s true that modern medicine has produced miracle treatments for some chronic diseases, such as dialysis for kidney failure, stents and bypass surgery for coronary artery disease, and new diagnostic procedures for detecting and successfully treating disease early. And we are learning how modifying behavioral risk factors can postpone the onset and progression of chronic diseases, such as keeping cholesterol in check to help prevent heart disease, losing weight to help prevent Type II diabetes, and quitting smoking to lower the risk of cancer.
However, while the risk of many infectious diseases can theoretically be reduced to zero through human interventions, even a complete control of behavioral risk factors for chronic degenerative diseases still leaves a population vulnerable to the destructive biological processes of aging. Humanity is paying a heavy price for the privilege of living extended lives—a new and much more complicated relationship with disease.
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.
This work is essential because without it we are facing a demographic certainty that there will be millions more very old people in the coming decades with conditions of extreme frailty and disability—some of which will be inadvertently caused by successful efforts to extend life by attacking fatal diseases. Slowing the aging process by an achievable three to seven years would simultaneously postpone all fatal and nonfatal disabling diseases, produce gains in health and longevity equivalent to cures for major fatal diseases, and create scientific, medical, and economic windfalls for future generations that would be roughly equivalent in impact to the discovery of antibiotics in the 20th century.
Medical institutes and public health professionals across the globe are dedicated to combating the causes and consequences of heart disease, cancer, stroke, and a myriad of other fatal and disabling conditions that plague humanity, and many people are alive today because of their heroic efforts. These battles need to continue. But so too should we fight on a new front: aging itself. The cost to create the longevity dividend is estimated to be about 1 percent of the current Medicare budget—an estimated $3 billion annual investment for just a few years that would create such a savings to health care that it would more than pay for itself.
The underlying premise of the longevity dividend is controversial—our medical world is entrenched in a one-disease-at-a-time model. But we must recognize that this model will never prevent the predations of old age. Our battle with death will inevitably fail, but proponents of the longevity dividend contend that death is not where the battle lines should be drawn. Scientific evidence now strongly supports the idea that it’s time to invest in the future of humanity by encouraging the commensurate political will, public support, and resources required to slow aging, and to do so now, so that most people currently alive might benefit from the investment. Extending healthy life would be one of the most important gifts our generation can bestow upon the future.
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