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Leonard Hayflick, Ph.D.

surfaced in the mid-’70s. Then the first country to actually license vaccines produced in WI-38 was Yugoslavia, then Germany, Russia, England, and finally in 1972, the United States, during which time several people had died from working with monkeys and their kidneys. I also have to say that approximately ten million people in this country received the polio vaccine in the early ‘60s, and they received at no extra charge live SV40 virus, which of course we all knew caused human cells to transform into cancer cells, and produced tumors in baby hamsters. Well, it took roughly a decade to get my cells finally approved in this country, and as it stands today approximately one billion people on this planet have received vaccines produced in my cell strain WI-38, and I haven’t received a nickel from that.

David: That’s simply unbelievable.

Dr. Hayflick: It’s unbelievable also because it was not possible to patent WI-38 in 1962. We tried to patent it, but the patent office threw it out because it was impossible to patent a living thing at the time.
David: But you can do it now.

Dr. Hayflick: Yes, partially as a result of my lawsuit. My lawsuit played a key role in that. During the litigation that I conducted against the NIH, the FDA was defended by the Justice Department and during the litigation the ChakraBarty decision was made by the Supreme Court. The name of that decision derives from a worker at Monsanto Chemical Company, who, roughly around that period of time, discovered a species of bacteria that chewed up oil and spit out perfume or sugar, or something nice. So this bacteria could be used for bioremediation purposes–that is, oil spills. Well, if you’re a company, and you discovered a species of bacteria that’s going to chew up oil and produce Chanel No. 5, you got a winner. So they tried to patent it, and of course it was thrown out. But they had the bucks to appeal it to the Supreme Court, and in 1980 the Supreme Court ruled yes, you can patent living things, because by this time the pressure was mounting from the emerging biotech industry to have this happen. So that played into my lawsuit.

My lawsuit, by the way, established the fact that scientists–biologists in particular–have intellectual property rights, and that was established indirectly by my lawsuit. It was the first lawsuit in this country made in effort to establish the intellectual property rights of biologists. What happened was that many of the leaders of the biological community who branded me as a thief in public, then embraced this concept, and the thinking of the biological community turned around 180 degrees. Today, if you don’t have a commercial affiliation, or aren’t doing something to raise money by serving on a scientific advisory board, you’re a failure in biology. When I sold my WI-38 cells to Merck for fifty bucks to pay for postage and handling I was damned as a criminal. That’s the difference.

David: Things have really changed.

Dr. Hayflick: It’s absolutely mind-boggling. Just one last example. If an employee of NIH, about whom everything belongs to the government–perhaps with the exception of the oxygen that she/he’s breathing–ever sold anything made by them in a federal laboratory to make money in 1962 they wouldn’t only put him/her in Leavenworth, they’d lower Leavenworth on top of them. Today, workers at the NIH can earn up to a hundred thousand dollars a year extra, over their salaries, for discoveries that they make in their taxpayer owned government laboratories. The NIH even puts on an annual science fair trying to sell what they have discovered to companies nationwide, a practice that’s done also by every major research university in this country, and a practice that was unthinkable in the ‘60s. That gives you some idea of how the climate’s changed substantially as a result of my lawsuit which I eventually won. Emerging biotech companies offered amicus briefs in my defense knowing that had I lost the case the biotech industry could not have happened because the founders of those companies were taking biological material from their tax payer supported labs and opening up new companies.

David: Knowing what you know today, what sort of role do you think the limit on cell divisions that you discovered plays in the human aging process?

Dr. Hayflick: I think it plays an essential role. I think that the failure to understand its key role is based on the failure of most biogerontologists–and certainly most scientists–to understand the difference between aging and longevity determination, something that people should be aware of but they’re not.

You have to understand that distinction in order to understand my answer to your question, and it’s this. When you buy your Mercedes-Benz for a hundred thousand dollars, and drive it off the showroom floor you have a certain expectation about its longevity–namely, it damn well better drive well for eight or ten years without requiring major repairs, or you’ve been fleeced. When I drive my Yugo off of the showroom floor, and I paid five or ten thousand dollars for it, I have a completely different expectation about its longevity. I think you will intuitively understand why the longevity of your Merc and my Yugo are different–namely, different design, better workmanship, and better materials used in the Merc as opposed to the Yugo.

Now when those two machines are driven off the showroom floor the same process begins to occur, and that is the aging process, which means loss of molecular fidelity, or loss of molecular integrity over time. So the aging process is going to probably start earlier, and be more profound, in the Yugo than it will be in the Merc, because the longevity determinants are completely different in both kinds of cars. Now that concept lifts over to biology, and it’s just as true in biology as it is inanimate objects. This is key to understanding the answer to your question.

The finite lifetime of cultured, normal human and animal cells, is a reflection of the maximum capability of that cell lineage to replicate, which is rarely–and I would argue never–reached, in real life because the aging process will kill the individual well in advance of that maximum number of divisions. There’s ample evidence for that. There are literally hundreds and hundreds of papers in the scientific literature that describe the changes that occur in normal human cells as they approach their loss of replicative capacity, and many of those hundreds and hundreds of changes are similar to the changes that occur in humans as we age. So if you argue that the cells go through fifty doublings, the changes begin to appear at, let’s say, the fifteenth or twentieth doubling, and become more and more apparent or emphasized up to the fiftieth doubling. Those are age changes. But the limit on the cells’ capability of replication is a reflection of the longevity determining process.

David: Do you think that if we were able to stop the telomeres from growing shorter with each cell division that that might be a way of increasing human longevity?

Dr. Hayflick: No, I don’t. I think that’s an overly simplistic but widely held belief. First of all, cancer cells usually have telomeres that are shorter than normal cells, so the simple act of reducing the number of telomeres, or arresting them to become shorter, could be worse than not interfering with them at all. In other words, it could be that they might become cancer cells.

David: So you think that telomere loss only really becomes a problem when all the telomeres are gone, and the DNA starts to unravel?
Dr. Hayflick: Well, I don’t think we know that that’s happening. It’s a possibility. It’s speculative, but there’s no evidence for that occurring.

David: One of the people that I interviewed for this collection was Michael Fossel. When I spoke with him he told me that he thought that introducing telomerase into the cell nucleus (which would prevent the telomeres from growing shorter with each division) might play a key role in human longevity.

Dr. Hayflick: I know Mike very well. He’s promoted this idea for ten or fifteen years. He thought that telomere shortening and telomerase were the answer to aging and cancer, and that it would happen within a year. We’re now ten years later, and it still hasn’t happened. I don’t think it will happen, because he’s got a very overly simplistic belief.

David: One of the interesting things that Michael Fossel told me when I interviewed him was that people with progeria were born with shorter telomeres.

Dr. Hayflick: That could very well be true, but it’s got nothing to do with the issue.

David: Many people believe that individuals with progeria appear to suffer from a kind of accelerated aging process.

Dr. Hayflick: That’s the orthodox belief. It’s a knee-jerk reaction, and I don’t believe it’s true. I think that the best way to describe it is as biological McCarthyism–guilt by association.

David: What do you think is happening with progeric individuals?

Dr. Hayflick: I think that there’s ample evidence that it’s got a genetic basis. I think that features that make it look like accelerated aging are simply coincidental with some of the aging processes, but by no means all of them. There are many pathologies known in medicine that share similar clinical manifestations but have totally different etiologies.

There are many people, who like me are reluctant to believe the symptoms of progeria are accelerated aging phenomena. They might bear on longevity determinants. They probably do, but there’s no universal agreement that those

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