He emphasizes that all the advances in average life expectancy that have been derived from prevention and cures for diseases have not told us anything about the fundamental etiology of aging. "We do not know why cells age," Hayflick told me. And until we expand our knowledge of the fundamental cause of aging he does not foresee significantly extending average life expectancy; he is even less hopeful about extending human lifespan beyond the current limit.
Hayflick says that if cures are miraculously found for the leading causes of death, that will add about 13 years to average life expectancy. But, he points out, those cures will not increase the lifespan beyond the current limit. He warns: "People will continue to die as a result of aging." The explanation for why they are dying, he insists, will only be found by unraveling the mystery of the cause of molecular and cellular aging.
"How likely is that to happen?" I asked him. "Very unlikely," he admitted. Hayflick laments that two to three percent at most of the $1.27 billion that the National Institute of Aging (NIA) spends annually on aging research is allocated to fundamental biological research. That's why "little work is being done on the basic understanding of aging--not only in this country but worldwide."
According to Transparency Market Research, the anti-aging market is projected to reach $91.7 billion globally by 2019. Most of that money will be for anti-aging products and services with possibly only a tiny percentage for basic biological research.
Dr. Jan Vijg, Chair in Molecular Genetics at the Albert Einstein School of Medicine in New York City, and a lead researcher on the recent longevity study, confirmed in an interview on November 16, 2016, that a miniscule amount of funding goes to basic biological research, where many of the questions about aging are more likely to find answers. Vijg agrees with Hayflick on the dearth of knowledge about cellular aging. He says we know a lot about factors such as genomes (the DNA of genes) that affect cellular senescence but the question of why cells age remains largely unanswered.
On the positive side, Vijg notes that scientists in the field of aging are increasingly focusing on the biology of aging, not just the cure of diseases. He told me that he has recently applied for a large grant for the study of drugs that target aging rather than specific diseases. Hayflick, he acknowledges, "was the original defender of this position to study aging per se and now he's been proven correct."
If that direction is endorsed by a growing consensus of scientists, why the dearth of funding, I asked?
Dr. Vijg points to an entrenched establishment driven by the public, special interests, and lobbyists who want immediate results. People accept aging and death as natural facts of life, Vijg says, but they don't accept diseases as natural and thus they want cures for them. Basic research may seem abstract and remote. Few laypeople grasp that unraveling the underlying biology of aging could produce faster and more successful results.
Token funding for basic research on the biology of aging makes no sense, Hayflick argues, when it's clear that aging is the condition that increases vulnerability to age-associated diseases. Physicians and other experts on aging talk glibly, he says, about age-associated diseases such as cancer, cardiovascular, Alzheimer's, and other illnesses for which the elderly are at greater risk. And then they immediately utter the mantra that the greatest risk factor for age-associated diseases is aging. "But," he adds, "they never ask themselves why all these major causes of death are occurring in older people." If you try to answer that question logically, he continues, "you come to the conclusion that there must be something in old cells that provides the milieu or the opportunity for age-associated diseases that does not occur in young cells." Isn't it therefore highly probable, he conjectures, that "old cells may provide the condition that allows for the emergence of all age-associated diseases?"
If Hayflick's analysis is correct, shouldn't a significant part of the fifty percent of the NIA budget for aging research, which Hayflick says is designated for the treatment and cure of Alzheimer's (Vijg estimates an even higher percentage), be shifted to research on molecular and cellular aging, where a cure may be found?
Hayflick gets emotional in his frustration that researchers are not aggressively pursuing a strategy to understand why old cells are different from young cells: "Why in the hell aren't we studying the fundamental biology of aging if that is the major risk factor for age-associated diseases? Why are we ignoring it almost 100 percent?"
While unlocking the keys to cellular aging might enable vast numbers of people to live closer to the limit of life expectancy, Hayflick still cautions that it will not extend lifespan beyond its current limit. What then does he say about the limit? Is it fixed or can it be extended. And if it is possible to increase it, by how much?
Here Hayflick's analysis turns to an overarching law of nature. He explains that cells, like all things animate and inanimate, are subject to the second law of thermodynamics, which states that energy dissipates or spreads out when not constrained. Applied to aging, this means that entropy (energy dissipation) increases over time--and the increase in entropy forecasts the inevitability of death. Sounds pessimistic, but is that the end of the story? Maybe not.
Vijg acknowledges entropy as a limiting factor, but he believes it could be slowed if we had a better understanding of entropy at the cellular level. He also expresses great faith in science and therefore will not rule out future discoveries that could lead to a significant increase in human lifespan. Hayflick as well will not bet against science, but he adds this stern caveat: "First we must invest substantially in the study of the basic biology of aging."
(Article changed on January 14, 2017 at 17:21)