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Michael Fossel, Ph.D., M.D.

Countdown to Telomerase Therapy:
An Interview with Dr. Michael Fossel

By David Jay Brown


Michael Fossel, Ph.D., M.D. is a clinical physician and neurobiologist with a strong interest in the human aging process. He is currently the Clinical Professor of Medicine at Michigan State University, and Attending Physician at St. Mary’s Hospital Emergency Department in Grand Rapids, Michigan. Dr. Fossel is the author of Reversing Human Aging, and the recently published Cells Aging, and Human Disease. He believes that we are only around a decade away from a truly remarkable form of anti-aging therapy that holds the promise of perpetually renewable youth.

Dr. Fossel has dedicated years to studying progeria and other accelerated aging syndromes. Children with the progeric disease Hutchinson-Gilford syndrome die at an average age of twelve or thirteen. They usually die of heart disease, strokes, cancer and other illnesses that often strike the elderly. Children with progeria look uncannily like old men and women, with balding heads and wrinkled skin, and appear to suffer from many of the symptoms of old age.

Dr. Fossel believes that the evidence from these diseases, (combined with the fact that germ cells and cancer cells do not age), indicates that aging is largely a regulated process; i.e., a function of gene expression. According to Dr. Fossel, the key to understanding, and possibly reversing, human aging lies at the tips of our chromosomes. He thinks that one of the best places to intervene in the genetically-wired clock that determines our biological age is in the intracellular process of telomere replication. 

Telomeres are the base pairs located at the end of our chromosomes that hold the DNA molecule together. With the exception of germ cells (sperm and eggs) and cancer cells, each time a human cell divides the telomeres become a little bit shorter. This is why, no matter how optimum a cell’s environment is, after a certain number of cell divisions, the telomeres become too short, gene expression changes, downregulating cell repair and maintenance, and the cells age. The progeric disease Hutchinson-Gilford syndrome is caused by having telomeres that are too short are birth, so it doesn’t take too many divisions before the cells begin to show early aging.

The reason that germ cells and cancer cells don’t age–and can potentially divide forever–is because they produce an enzyme called telomerase, which keeps the telomeres intact when the cell divides. Dr. Fossel predicts that telomerase therapy could extend human life indefinitely  by resetting the genetic clock in healthy somatic cells, and turning it off in runaway cancer cells. He imagines that very soon everyone will have the potential to live for centuries in a body that looks and functions like its about twenty years old. 

Dr. Fossel earned his master’s degree in psychology at Weseyan University. He then earned his Ph.D. in neurobiology, and an M.D., from Stanford University. In 1998 Dr. Fossel won the Achievement Award in Preventive Medicine from the American College for Advancement in Medicine. He was the founding editor of the Journal of Anti-Aging Medicine (now Rejuvenation Research), and served as its Editor-in-Chief for six years.  Dr. Fossel is a widely published author of dozens of scientific papers and articles, and a popular international lecturer. He has also appeared on numerous radio and television shows, and in many science documentaries.

I spoke with Michael on July 3, 2004. Michael speaks fast, yet somehow manages to say every word clearly and distinctly. He radiates a sense of warmth and humor. In a message that he sent me, he described himself by saying, “On the whole, I prefer data to fame, accuracy to eminence, and gardening to tenure.” I spoke with Michael about the what he’s learned from working with progeric children, how telomeres are related to human aging, and the possible medical, societal, and psychological consequences of telomerase therapy and biological age reversal.

David: How did you first become interested in medicine, and what lead you to study the human aging process?

Michael: I think that, to a degree, both of these questions have the same answer. All of us have certain bents to our personality. For me, I suppose you could say, there is need to help people–and I don’t mean that in a naive, puppy-dog sense. I just get a certain amount of pleasure out of having people around me feel better, work better, live better, and enjoy themselves more.

As an an example, I work clinically doing predominantly emergency medicine. The practice of emergency medicine, per se, does not have a lot of intellectual interest for me. Not none–just not a lot. On the other hand, I can derive enormous emotional benefit from it. The fact that I can leave a room, and have someone laughing, who a minute ago was terrified, is something that I need just as much I need to pay my mortgage. And I think that that personality bent is what lead me into both medicine, and in the long-run, to aging.

There’s a passage in the forward to my new textbook where I talk about how easy it is for people to understand the importance of treating children, and that we often forget that, or don’t understand that, when we’re talking about the importance of treating the elderly. For me, that’s almost self-evident. Again, I think it’s a part of my personality, and it’s sometimes hard for me to understand why other people don’t understand the importance of that. But it’s just me.

David: Can you talk a little about why you think that telomeres are so important in understanding, and possibly reversing, human aging?

Michael: That’s an interesting question, because it is usually asked incorrectly, and gets answered incorrectly. There are people who have said–and it’s simply not true–that I think telomeres cause aging. Not a bit. To me, there are two issues here. One is, what causes aging? And, frankly, I find that uninteresting, and I’ll come back to why I say it that way. Telomeres, per se, don’t cause aging. They’re a piece of the entire complex cascade and process of the aging organism. But the more important question for me is, where’s the most effective point of intervention? 

I’ll give you a couple of examples of this. I get residents who come in to work with me clinically, who feel that if they’ve made a diagnosis, they’re done. Not a bit. Patients don’t come in for a diagnosis. They come in to be made better. Now it’s true that usually making a diagnosis helps you make patients better. But a patient doesn’t come in for a name. If you came in with a funny melanotic spot on your arm, you don’t so much care whether it’s melanoma or not. You want to know if I can make it never come back and kill you, or not.

All right, now the fact is I usually have to establish whether it’s melanoma. But it’s not the name, per se, that holds your interest. It’s–will this kill me? Can you prevent it? That’s the critical issue. The same thing’s true for me in aging. The issue for me is not what causes aging, and how does the cascade work, but what can we do to intervene, to prevent age-related disease and suffering. 

Now there are an awful lot of people who will start discussions with me about whether or not aging is a disease. Frankly, I don’t think that’s an important issue. Whatever you want to define age-related diseases as, the important issue is, can we intervene in them? For me, aging may or may not be a disease, but it certainly increases your likelihood of having a disease. So the question is, where can we intervene? Given that, my answer usually is, the most effective point of intervention is probably the human telomere–not because it causes aging, but because it’s probably the most effective point of intervention.

If I’m looking at heart disease (actually, atherosclerosis, causing both strokes and heart attacks), which is the major killer worldwide, I ask myself not what causes it, but where can I intervene? There are literally dozens of critical points of intervention–everything from high blood pressure to cholesterol levels, to a number of genetic factors, to smoking, and behavioral effects. But again, while I can intervene in your risk of heart disease by lowering your cholesterol, with say Lipitor, it may be that a more effective and efficient point of intervention would be the telomere. So that’s my question. Now to answer that question you really have to understand some of the processes. But it’s not the process, per se, that interests me in an intellectual fashion. It’s a totally concrete interest.

David: Why did you start studying people with progeria, and what have you learned about the process of human aging from studying people with accelerated aging disorders?

Michael: I started studying progeria in basically the mid-1970’s. In graduate school I think I used to have the world’s literature on progeria under my bed. I found much more interest when I began to attend the annual progeric reunions for the Hutchinson-Gilford progerics. For me there are two interests here. One is, what can we do for these children? The answer

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