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What If Aging Could Be Slowed and Health Spans Extended? | A Q+A With Nir Barzilai, M.D.

Life Biosciences
Feb 19, 2019 · 5 min read

What if you could live to 115, and have those be productive, healthy and entirely enjoyable years? Nir Barzilai, M.D., a renowned longevity expert, says it just may be possible. Listen to what he has to say about that, “zombie cells,” and what may be the cause of Alzheimer’s.

By Adam Bluestein

Nir Barzilai, M.D., is probably the person to talk to if you’re interested in being around a long, long time. Consider a few of his titles to appreciate the depth of his knowledge: He’s the Director of the Institute for Aging Research at the Albert Einstein College of Medicine and the National Institute of Health’s Nathan Shock Centers of Excellence in the Basic Biology of Aging, and he’s been named Chief Medical Advisor to Life Biosciences.

Here, in an opinionated conversation, he shares his vision for unlocking our optimal healthspans so we all lead longer, healthier lives.

Q. Why has aging research been so slow to progress?

A: Unfortunately, we work in silos. Within the National Institutes of Health, only one division — the National Institute on Aging — is concerned with investigating health; the others are all concerned with sickness. But the biggest risk for cancer and heart disease is aging. Although 80 percent of diseases occur in people over age 65, aging research gets only about three percent of all funding!

Q. Do you think we’re looking at aging through the wrong lens?

A. Definitely. People don’t understand that aging can be treated, just like hypertension or high cholesterol. If you target the biology of aging — rather than the individual conditions that occur as people grow older — you are less likely to get those age-related diseases we are so afraid of! You know what they are — heart disease, cancer Alzheimer’s. I like to say we (meaning my lab and Life Biosciences) are disease-agnostic. If we combat aging, we in turn help end these illnesses.

Q. Let’s talk about your research. You’ve studied Super-Agers, or the very old. What have you learned that can help the rest of us?

A: Only one in 10,000 people live past 100 years. I have about 700 of these Super-Agers in my study, and not only do they live longer, they live more healthfully. At the end of their life, they are sick for a very short time — which is a good thing. We’ve also learned that their longevity may not be due to healthy behaviors but the protective effect of certain genes. Studying those genetic effects will unlock how to help others live longer.

Q. But what if you don’t have those genes? Aren’t you just out of luck?

A: No; one of the reasons I started to study aging is because I don’t have longevity in my family nor the genes associated with it, according to DNA tests. But we can develop a drug that does what the [longevity] genes do. All the pharmaceutical companies are being helped to deliver drugs based on such genetic alterations for specific diseases. We use it to design drugs that will protect against the effects of aging.

Q. You’re doing research on metformin and aging. Is this drug a silver bullet?

A: Possibly. Metformin, which is already approved to treat type-2 diabetes, hits several of the eight pathways of aging [You can learn more here]. Once metformin fixes the part of the cell that is aging, other functions improve, too!

Q. Do you think the FDA will approve a treatment for aging soon?

A: I think it’s possible that within five years we’ll see metformin approved by the FDA as a treatment that can prevent age associated disease.

Q. I heard you mention the role of “zombie cells” in aging — this sounds scary! What are these and can they be killed?

A: These are technically called senescent cells; they’re aging cells that don’t function properly but don’t die — hence the “zombie” term. One of our Life Biosciences companies, Senolytic Therapeutics, is working on this challenge, developing what’s intended to become a drug to treat aging and other diseases. We’re going to see if removing those cells in sick people prevents the deterioration caused by diseases of aging.

Q. Let’s talk about another frightening topic: Alzheimer’s. Is your research targeting that, too?

A: For Alzheimer’s, aging is the major risk factor. Even if you have the genes that predispose you to the disease, it still takes 40 to 50 years to develop it, as certain proteins accumulate in the cells and create damage. We believe that it may be linked to a decrease in autophagy, which is akin to the cells’ garbage-disposal capacity. If you increase that capacity, you may be able to treat Alzheimer’s. One of Life Biosciences’ Daughter companies, Selphagy Therapeutics, tackles this garbage-disposal problem.

Q. Will we ever have 200 candles on our birthday cakes?

A: Our lifespan as a species is probably about 115 years. Most of us currently die in the U.S. before the age of 80. Clearly, we’re not using our potential for longevity.

Q. Can people afford to live 30 years longer? Can our society afford it?

A: There will be a vast impact on our culture — how we deal with retirement age, volunteering, interactions with the family. But there’s also a huge longevity dividend to improving our healthspan — by living healthier and then dying rather than lingering with age-related diseases. The Centers for Disease Control and Prevention (CDC) has found that the medical cost of the last two years of life in someone who dies over the age of 100 is only a third of that of someone who doesn’t live as long, because they don’t have drawn-out illnesses. Currently, we are accumulating diseases and their treatments, and we can’t keep doing that. If we don’t do something dramatic about aging, it’s going to bankrupt us.

Adam Bluestein is a frequent contributor to such publications as Fast Company, Inc., Men’s Journal, and Proto.

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