Aging in America - Lawrence R. Samuel

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       One of Nature’s Best-Kept Secrets

      While medical schools did not do an adequate job teaching students about the bodies and minds of older patients, some in medicine and the sciences continued to target aging as an exciting area of inquiry and research. Corporate and academic funding committees clearly recognized that unlocking “one of nature’s best-kept secrets,” as the Atlanta Constitution described it, would be quite a feather in their organization’s hat. (The financial payoff for achieving such a feat would also likely be enormous.) In 1972, for example, Morton Rothstein, a biologist at SUNY Buffalo, won a million-dollar, five-year grant from the National Institute of Child and Human Development (NICHD) to try to learn the causes of aging and, it was hoped, how to control the process. Rothstein was eager to find a cure for aging should there be one, admitting that his getting close to the age of fifty played a role in his ambitious project. The biologist was very much in the cellular theoretical camp, and he planned to study how nematodes (small worms) aged over their brief (twenty- to forty-day) lives. Unlike humans, nematodes retain the same cells throughout life, offering a comparative analysis of aging at the molecular level that could perhaps reveal the precise reason for why all organisms get older. Rothstein’s initial thinking was that “ineffective enzymes” were the culprit, these faulty molecules triggering a chemical reaction throughout the body, which led to the aging process.50

      The startling array of theories regarding aging was in part a result of the limitations placed on scientists. Besides the ethics involved, experiments on aging in humans were less than practical because of our long life spans. An eighty-year study was obviously not feasible, as subjects could very well outlive the researchers. (Alex Comfort quipped that mice were preferable to Ph.D. students as subjects because they died much more quickly.) With studies limited to laboratory animals, little persuasive data had yet to be collected on precisely why organisms aged, making researchers look in unusual places. One promising area was progeria, the rare and tragic disease that prematurely aged infants and usually caused death in the early teenage years. Scientists investigating the process of aging believed they could learn much from children with progeria, although thankfully there were precious few cases reported. (Fewer than sixty could be found in the medical literature up to the early 1970s.) A bit more common was Werner’s syndrome, which was similar in some ways to progeria, but it too did not offer many cases to study.51

      There was a busy parade of supposed causes of aging through the 1970s, each one briefly taken quite seriously. Almost as a rule, scientists were over-eager to conclude that their particular line of research was the pot of gold everyone was searching for, perhaps in order to receive additional funding to pursue their work. Glands were often suspected of being at the heart, so to speak, of aging. In 1973, for example, a team at the University of Texas claimed that thymosin, a hormone produced by the thymus gland, was a major factor in the aging process. Blood levels of the hormone decreased dramatically as a person got older, the biochemists reported, hindering the body’s immune system’s ability to combat disease.52 At the very same time, other scientists down the road in San Antonio pinpointed the prostate gland as the thing that explained the mechanics of the aging of the human body. It was the eventual inability of that gland to maintain its normal growth and development that served as the first evidence toward understanding the molecular basis of aging, a pair of researchers from the Southwest Foundation for Research and Education crowed, not addressing how this applied to women, who do not have a prostate.53 Meanwhile, Alexander Leaf, a Harvard internist, claimed that it was the protein amyloid that accounted for some people living so long. As some other researchers had done, Leaf traveled to remote parts of Ecuador, the Soviet Union, and Pakistan to study the relatively numerous centenarians that lived in these areas. High concentrations of amyloid were found in the century-plus locals, making him think that the mysterious substance was the main ingredient of longevity.54

      Virtually any and every part of the human body was responsible for aging, according to scientists in the 1970s. Some said that the hypothalamus at the base of the brain contained a central “pacemaker” that instructed the body to get older, one version of the popular “clock” theory of aging.55 That timer in the brain told the pituitary gland to release “death hormones,” an extension of this idea went, killing the body when it was automatically programmed to die.56 Linking specific body parts to aging was not only silly but reminiscent of ancient medical theories such Hippocrates’s belief that certain bodily fluids affected human personality. That any of them were judged to be real possibilities demonstrates how little was actually known about physical aging in the late twentieth century. In his 1976 book Prolongevity, Albert Rosenfield compiled many of the theories about aging and extending life that had surfaced over the preceding decade. (The book’s subtitle—A Report on the Scientific Discoveries Now Being Made About Aging and Dying, and Their Promise of an Extended Human Life Span—Without Old Age—hardly needed extending.) Theories ranged from the sublime to the ridiculous, making anyone with anything close to an objective viewpoint conclude that this field of research was not one of science’s better moments.57

      With concern over air pollution (often called “smog” at the time) and other ecological threats a significant part of the national conversation, it was not surprising that scientists included them on their list of potential causes of aging. It was, more specifically, heavy oxidant stresses on cells that led to premature aging and disease, scientists theorized, justification for identifying agents that could protect against such damage. One of them was vitamin E, which was discovered in 1923 but whose precise function remained uncertain. Most experts agreed, however, that the nutrient did serve as a cellular defense against oxidants such as nitrogen dioxide and ozone, atmospheric gases known to be elevated in areas with high air pollution. Studies done at Berkeley in 1974 confirmed as much, bringing more attention to vitamin E as a potential antiaging agent. (Vitamin C was also believed to help delay the aging process.) Scientists stopped short of recommending that individuals gobble up large quantities of vitamin E to combat oxidants and thus slow down the aging process, but there was a consensus that the substance might very well play a major role in halting the decay of human cells. If nothing else, this line of research proved that cells did not self-destruct because of some kind of predetermined biological mechanism, an important revelation.58

      Although a minority of scientists was interested only in lessening the effects of old age during a normal lifetime, most equated the battle of aging with extending life expectancy. Over the course of the first three-quarters of the twentieth century, life expectancy in the United States jumped by about twenty-five years, from about forty-seven (46.3 for men and 48.3 for women) to roughly seventy-two (68.8 for men and 76.6 for women), an amazing phenomenon by any measure.59 By the 1970s, however, this dramatic extension of Americans’ average life span was slowing down considerably, a source of frustration to scientists who saw no reason it should not continue at a rapid rate. (The biggest factor contributing to the increased life expectancy was the much higher survival rate of infants and children.) Only a greater understanding of the basic processes of aging could lead to another exponential leap in life expectancy, making what was seen as the “deterioration” of the human body one of the central questions of science. The best genes, nutrition, and environment could not prevent aging, and the finest health care in the world would not prevent death—each a biological annoyance that kept many a scientist up at night. The problem of aging was a main topic of conversation at the 1974 annual meeting of the American Association for the Advancement of Science, with both physicians and academics offering their respective takes on what to do about the disturbing situation. Even a cure for cancer or heart disease would yield just a few more years of life expectancy, one of the attendees pointed out, not nearly enough for what was believed to be very much achievable: a society full of centenarians.60

      Like many scientists working in the area at the time, Alan Richardson, a professor of chemistry and biology at Illinois State University, was fairly confident that the average human life span could be extended by a decade or two, or possibly much longer. The key question, he told colleagues at the 1976 meeting of the American Aging Association, was whether aging was genetically programmed, something his own research with rats suggested. Should our genes be responsible for making us get older (specifically by a decline in protein synthesis,

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