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Dying “Young” at an Old Age

Elderly woman exercises with dumbbells outdoors.

The “longevity dividend” is defined by economists, demographers and gerontologists as the cost savings obtained by delaying aging.

Since no one can “delay” getting older, what we’re talking about here is delaying the onset of major diseases that come with age, such as cancer, diabetes, Alzheimer’s and cardiovascular disease. The longevity dividend isn’t really about living longer; it’s about living healthier for a longer portion of life. Instead of living to 85 and struggling with chronic diseases for the last 5 to 10 years of life, wouldn’t it be better to live past 80, with less than a year involving major health problems, as seen in centenarians? Doing so would not only reduce medical expenses, but improve the quality of life.

For decades, research and treatment protocols for age-related conditions have been approached from a “disease-specific” perspective. Success has been real but limited. The problem is that if someone is successfully treated for one age-related disease—for example, heart disease—the likelihood is that the patient will simply be struck down by another age-related disease, such as cancer. This is just trading one age-related disease for another.

I propose that there is a better way to approach the problem: going after the root cause of all of them.

The provocative reality is that unless we can successfully delay aging itself we will not successfully prevent or significantly delay these age-related diseases.

Do we have enough scientific knowledge to achieve the goal of delaying the aging process? Studies are in early phases, but we know that already scientists have developed a significant amount of knowledge. Studies on worms, flies and rodents provide insights into the conserved mechanism for longevity. Several such experimental subjects that were treated with drugs or modulated genetically have lived significantly longer and healthier lives. For example, the drug rapamycin extends the life span of rodents. Some of the results of those studies have been validated by Einstein’s study of hundreds of centenarians and their families, and newly discovered human genes have been subjected to drug development. Researchers in our center and others have identified the cellular mechanism by which the wine extract resveratrol extends the life of metabolically challenged rodents.

We are greatly encouraged by research findings among healthy centenarians in the Einstein Longevity Genes Study, whose participants are between 96 and 112 years old. Based on our observation that many participants have exceptionally high HDL cholesterol (the good cholesterol) due to a specific variant in the CEPT gene, a pharmaceutical company has developed a CETP inhibitor, which may also prevent several age-related diseases.

And special kinds of proteins derived from the cellular organelles called mitochondria are being developed by a biotech company to prevent age-related diseases. These and other examples indicate that a nascent but expanding group of drugs for testing exists.

How can we make it happen? It will take political will and funding. The April 2013 announcement by the Obama administration of a $100 million brain-mapping initiative shows that funding biomedical research can be a national priority. A similar collaborative model that allows teams of scientists to work together on delaying aging is a worthwhile goal.

Drug development is always challenging. The nature of research into aging and related drug discoveries presents a vexing hurdle.

How do you reliably prove that a drug delays aging without the need to test it over several decades? There is no single answer, but progress already under way suggests a course to follow.

  • First, we must make sure that a drug delays aging in several relevant species (e.g., rodents, rabbits, pigs), and determine, with genetic studies, that the same pathway is relevant to human health and longevity.
  • Second, we must develop drugs replicating those pathways, a process that involves pharmacokinetics/dynamics, toxicology, drug stabilization and other processes.
  • Third, because animal models don’t always reliably predict what will happen in humans, we must perform phase 1 clinical studies for safety and tolerability and phase 2 studies for specific indications. At Einstein, my colleagues Jill Crandall, M.D., and Meredith Hawkins, M.D., are currently leading such a study—testing if resveratrol reverses glucose intolerance in seniors.
  • Finally, we must test outcomes by using the developed drugs in a relatively healthy elderly population to determine whether aging is delayed.

These steps should be taken with the drugs currently in development and those on the horizon. But in order for meaningful progress to be made, we must fight aging with the same passion and investment we have given to battling heart disease, cancer and other conditions. We cannot simply accept that aging—at least unhealthy and painful aging—is a given. If we change our approach we could help untold numbers of people achieve longer, healthier and more satisfying lives.

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Nir Barzilai, M.D.

Nir Barzilai, M.D.

Nir Barzilai, M.D. is the Ingeborg and Ira Leon Rennert Chair of Aging Research and director of the Institute for Aging Research at Albert Einstein College of Medicine and is attending physician at Montefiore Medical Center.

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