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Leonard Hayflick, Ph.D.

clinical manifestations are absolutely aging phenomena.

David: I would imagine that many people believe it largely because of their appearance. Children with progeria look uncannily like old men and women, with balding heads and wrinkled skin, and they appear to suffer from many of the symptoms of old age. The photographs that I’ve seen are particularly striking.

Dr. Hayflick: Yes, but you can find photographs of two different pathologies, with two different etiologies that look similar. I mean, if a person gets hit by a bus, and their legs are crippled, and they’re walking around on crutches, and I pull somebody else out of the wings who has suffered from polio who is also walking on crutches, you’re not going to tell me they’re caused by the same agency.

David: What do you think are the primary causes of aging?

Dr. Hayflick: It’s very simple. We know the cause of aging, despite it appearing to be a mystery to most people. First of all, let me tell you what aging is and then I think the cause will be implicit. In animals that reach a fixed size in adulthood, aging is the random systemic loss of molecular fidelity, that after reproductive maturity, accumulates to levels that eventually exceed repair, turnover, or maintenance capacity. That’s the definition. It’s the progressive loss of molecular fidelity that increases vulnerability to age-associated diseases. So that’s the answer.

David: What do you think causes that “random systemic loss of molecular fidelity?”

Dr. Hayflick: What causes that loss of fidelity is based on the fact that complex biological molecules are kept in a state of fidelity as a result of a variety of chemical forces and various chemical bonds–van der Waals forces and other well-known bonds that keep molecules together. It is also well known that the energetics–the energy that keeps those bonds in the state that they’re in, in molecules that are functioning–do not last forever. They last for varying periods of time–from as short as nanoseconds for ATP to years for collagen–so that there’s a spectrum of energy levels in biological molecules. We have elaborate maintenance, turnover, and repair systems to keep those molecules in their correct functional state.

However, after reproductive maturation molecular errors begin to accumulate and exceed repair capacity for a very simple reason. There’s no need to keep those molecules in a perfect state after reproductive maturity, because the animal possessing those molecules has already done what nature intends for it to do, and that is to reproduce. The proof of that statement is that for 99.99 percent of the time that we’ve been human we’ve had a life expectancy of less than twenty years. It’s only been within the blink of an eye, on an evolutionary time scale, that we’ve have had life expectations greater than that.

David: Do you think that aging is actually a process that evolved?

Dr. Hayflick: No, aging is something that was never intended for us to see in the first place. It is an artifact of civilization. Aging only occurs in humans, and in the animals that you and I choose to protect–like zoo animals, domesticated animals and pets. It does not happen in the wild. We were intended to die at the age of thirty, but we’ve learned how to deal with the causes of our death such that we have revealed, teleologically, a process that we were never intended to see in the first place. And now we’ve got to live with it.

David: Why do you think that researching the causes of aging is more important than directing biomedical research efforts to the study of disease?

Dr. Hayflick: Because the goal of aging research should not be–and I believe that it’s simply illogical to believe that it could be–to increase human longevity. That is, I should say, the goal of aging research should not be to intervene with the aging process and thereby increase longevity. The goal of biogerontological research should be to discover why an old cell is more vulnerable to pathology than is a young cell, and that key question is not being addressed by anybody on the planet at the moment. The reason it’s important should be obvious.

When every physician in the world (of course I’m exaggerating, but I’m not too far off the mark) wakes up in the morning, they say this to themselves: The greatest risk factor for the leading causes of death–that is cardiovascular disease, stroke, and cancer–is the aging process. There’s no physician on the planet who will dispute that. So I have a very simple-minded question: Why is the funding for research on the fundamentals of the biology of aging microscopic when compared to funding for research on the leading causes of death?

David: That’s a very good question.

Dr. Hayflick: It’s such a good question that whenever I show it on a slide [during a lecture] the physicians become slack-jawed and have no answer. But I think I know what the answer is.

David: What do you think it is?

Dr. Hayflick: Misunderstanding, greed, and power. Researchers in the fields of cardiovascular disease, stroke, and cancer require funding–after all this is one of our major industries. They don’t want to undermine that industry or change careers to become biogerontologists. Now they might not know this consciously, or realize consciously that that’s what’s happening, but it is. You can’t sell a senator or a representative on funding for the aging process. You can sell them on funding for cardiovascular disease, stroke, and cancer because either they or someone they know has one of them. They don’t know that the underlying process that makes them vulnerable to those leading causes of death is the aging process, because of a huge failure to educate them.

David:  I recently interviewed John Guerin, the director of the Ageless Animals Project. What do you think we can learn from studying animals that don’t appear to age, like rockfish and turtles?

Dr. Hayflick: Well, I would hope that we could learn what the longevity determining processes are at the molecular level, and how the energetics of key molecules are maintained for periods of time in those animals that are unattainable in mammals.

David: What do you think is some of the most important aging research that is currently going on?

Dr. Hayflick: I rather think that the most important aging research is not being done today. I think a lot of the research being done today is misleading, especially the large area of work being done with invertebrates, namely worms and flies. There’s almost a weekly announcement by one of the workers in the field that they discovered a new gene for aging, and I think that’s absolute nonsense. There are no genes for aging. Most people don’t understand the difference between aging and longevity determinants. Genes control development and indirectly longevity. They do not control aging. I would defend that position by another simple analogy, and that is to ask people who believe that genes cause aging to show me in the blueprints for their automobile where it is written, telling their automobile how to age. There are no such directions in blueprints. Why? Because the process is a spontaneous process. It requires no instructions, and the same is true in biological material. The only reason that animals of different species live longer than others is because of the differences in the longevity determinants. That is, the characteristics of molecules at the time of reproductive maturation including the level of repair turnover and maintenance systems to operate.

David: Do you think that maximum life span of human beings can be extended?

Dr. Hayflick: Oh yes. I think it has been, and it will continue to be on an evolutionary time scale. There’s every reason to believe that. We have fairly good evidence that the present human life span was established about a hundred thousand years ago, based on brain weight/body weight ratios. There’s no reason to believe that it’s not increasing, but we have no evidence for it, and in fact we have one amusing bit of evidence against it. The world’s oldest human being was a French lady named Jeanne Calment. She was born in 1875 and died in 1997. She was 122 and a half years old. The day that she died the world’s oldest person was, I think, 118, which means that in that instant human longevity dropped four years, right? Now we know that’s wrong because we’re dealing with exceptions to the enormous body of the population. So what the death of Jeanne Calment told us was that at the moment of her death human longevity dropped by four years, and this is the problem in making these kinds of determinations. So it’s really guesswork, but I think it’s safe to accept the fact that human longevity is increasing on an evolutionary time scale. This means that we’re not going to detect an increase, if it’s occurring–and if we keep proper records, which is doubtful–for the next 10,000 years or more.

David: But do you think that through own research, and our own medical advancement, that we’ll be able to intervene in the aging process and extend the maximum human life span?

Dr. Hayflick: No, I don’t. Let me tell you why. If you resolved all of the leading causes of death currently written on death certificates for older people–namely, cardiovascular disease, stroke, and cancer–you could not possibly add more than fifteen years on to human life expectation. So even if we put every hospital, medical center, and the NIH out of business, and drive every physician on to an unemployment line, the maximum increase in human life expectancy would be fifteen years. Period. That’s something that

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