Research into aging is sparsely funded in comparison to research into the biochemistry and treatment of any specific common age-related disease, such as atherosclerosis or Alzheimer’s disease. Yet these conditions are caused by aging. So we have the strange situation in which the past century of work on treating age-related conditions has produced only small gains, because the research and development communities have steadfastly refused to work on the root cause of these conditions – which is to say the mechanisms of aging, the accumulation of cell and tissue damage that causes degeneration and dysfunction.
This problematic and frustrating state of affairs is slowly changing, and more rapidly in the past few years, but the gains made by patient advocates and the small community of researchers who do work on aging are still incremental. The mechanisms of aging remain a small area of research in comparison to the rest of medicine. This is far out of line, given that age-related disease – the consequence of the mechanisms of aging – is the dominant form of human mortality, by far the greatest medical cost imposed upon individuals, and causes by far the most suffering. Year after year, the priorities for medical research and development remain distant from this reality.
Leonard Hayflick is a retired eminence in the field who happens to hold the completely incorrect view that aging is, in some meaningful way, a consequence of thermodynamics and entropy gain over time. This is easily dismissed: an aging cell or an aging individual is not a closed system, and therefore can certainly lose entropy over time given suitable circumstances. Most of what he has to say about the present poor allocation of resources and attention is quite right, however. Just substitute a focus on molecular damage and persistent metabolic waste after the SENS view of aging for Hayflick’s considerations of thermodynamics.
All major United States institutional advocates for research on the biology of aging and for the leading causes of death assert that aging is the greatest risk factor for these deaths. Nevertheless, all fail to support research on the etiology of aging despite having mechanisms to do so. Bordering on scandal, research on the cause of aging in life forms is not a major priority for any organization in this country with “Age” or “Aging” in its title. This neglect is inexplicable because the mantra believed by most physicians, geriatricians and biogerontologists is that “Aging is the greatest risk factor for the leading causes of death.” It does not require a great leap of intellect to ask: “Then, why is research on the etiology of the greatest risk factor that increases
vulnerability to cancer, cardiovascular disease, stroke, and Alzheimer’s disease (AD), ignored?”
The field of aging is the only area of biomedical research where causation is ignored. This inexplicable omission is compounded by the fact that aging is a universal human phenomenon for all who live long enough to experience it. Even for those in good health, that condition is merely the slowest rate of aging and dying. Today, like the former rich and powerful, their modern counterparts have the same goals in the form of funding hundreds of biotech startup companies. Plus ça change, plus c’est la meme chose. In these modern efforts there seems to be little understanding that there is an enormous difference between the molecular biology of what determines the longevity of life forms and what causes their aging. Longevity is determined by anabolic processes and addresses the question, “Why do life forms live as long as they do?” Aging is a catabolic process that addresses the question, “Why do longevity systems eventually fail?”
There is a general failure to understand that manipulating the genome or anabolic processes in living forms which may increase longevity, or cure a disease, tells us nothing about the dysfunctional or missing molecules that characterize the catabolic process of aging. Research on the biogerontology of aging is unique because of the common belief that the goal is to interfere or manipulate the process. The availability of funds for age-associated disease research is several orders of magnitude greater than what is available for research on the fundamental biology of their greatest risk factor. The resolution of any age-associated disease has not in the past, nor will it in the future, improve our understanding of the etiology of aging. A century ago, the leading cause of death in old age was pneumonia, often called “the old man’s friend” (with its sexist overtones). Pneumonia is no longer one of the leading causes of death in old age and its resolution did not advance our knowledge of the cause of aging. Nor will the resolution of any other age-associated pathology.