When I interviewed Dr. Nir Barzilai, a pioneer in the biology of aging, I was particularly sympathetic with the topic because I’m 51 years old and would like the second half of my life to be as pleasant and healthful as the first. (Yes, I think individuals can do things to maximize the likelihood of living to 100 years or more.) I’m already engaged in the conventional ones: exercise (Barzilai recommends a lot of it), eating right, and so forth. He says these steps really will slow down aging; it’s science, not just common sense.

But Barzilai goes way beyond those recommendations. Among other activities, he is doing lab research to identify the genetic markers that distinguish centenarians (who he says were generally healthy as they passed through their older years) and the rest of us.

Barzilai, who founded the Institute for Aging Research at the Albert Einstein School of Medicine in New York, began by talking about “curing” aging in a way that is parallel to the search for a cure for cancer. Yet he does not mean that we can live as long as we want. The outer limit of human lifespan, he says, is around 115 years. Yet we die, on average, before 80. That leaves room for 35 more years of life, which has an upside and a downside.

If we’re talking about 35 extra years of misery, it’s all downside: the rest of society pays, and the elderly individual doesn’t benefit. But Barzilai is working to increase healthspan, not just lifespan – and this is almost all upside. Staying healthy for longer means more productivity, more enjoyment of life, fewer medical expenses (to be paid by you or the government) and, perhaps most importantly, a lesser burden on your kids. In fact, he reports that medical expenses in the last year of life are one-third as large if that year occurs when you’re 100 than if you’re 70. This is called the “centenarian compression of morbidity.”

Barzilai is a strong advocate of metformin, not just to bring down sugar levels in diabetics but to slow or reverse the effects of aging on cells. In fact, metformin was originally used in the 1920s to prevent malaria and flu and was only later found to treat Type 2 diabetes. Like many drugs it has multiple uses, often discovered serendipitously. People who take metformin who don’t have diabetes, Barzilai says, develop diabetes less often and have a lower incidence of cancers, Alzheimer’s, and other age-related diseases. Metformin doesn’t work by lowering glucose levels but in some other way.

I asked Dr. Barzilai when he had a single breakthrough moment. He said that it was when he found out that dwarf or small specimens in nature live longer. They either have less growth hormone, or their biochemical switch from growth to protection mode is more effective. This latter concept is new to most people so let’s dig deeper.

Barzilai explains that when you reproduce, which is something you do at a young age, you need as much growth power as you can get. When you age, you have to switch to protection. You are no longer trying to produce as many new cells as you can, and to nourish them lavishly; you’re trying to keep the ones you’ve got. And, at that older age, giving them ample nourishment is the wrong strategy. That is why caloric restriction, and in particular intermittent fasting where caloric intake is concentrated in one part of the day (usually the morning), is effective at lengthening life when few other things are. Based on my conversations with Dr. Barzilai, I’m experimenting with this myself.

A great deal of what Barzilai has found in this research on aging has to do with this switch of energy. Biological processes that help you when you’re young may hurt you when you’re old, so he and his colleagues are working on finding effective ways of switching cells from one mode to the other.

So, what does big data have to do with all this? His research depends on large populations, and each person in the population has a genome consisting of 6.4 billion base pairs. Human beings produce between 80,000 and 400,000 proteins. All of these data are relevant, and data on this scale can only be managed and studied using fairly recent advances in artificial intelligence and machine learning. An example is that Barzilai uses big data to calculate a person’s biological age, which is then compared to chronological age to determine how well or poorly that that person is aging.

Barzilai’s book, Age Later: Health Span, Life Span, and the New Science of Longevity, fills in the details of this story. After increasing dramatically in the nineteenth and twentieth centuries, growth in life expectancy has slowed. The reason is that much of the low-hanging fruit – sanitation, antibiotics, and more recently statins – has been picked. Dr. Barzilai’s research, while not about to “cure” aging (if it did, we would live forever, which would be a nightmare) has the potential to restart the trend toward increases in life expectancy and in the quality of life.

Living longer also means needing an income for longer. Many savers preparing for retirement do not realize how long they or their spouse might live, and switch to a conservative investment strategy around age 65. But some of their money may be needed 35 years later! They should invest using a more long-term, aggressive strategy with part of their money, the part that might fund consumption at age 100.

If a significant proportion of people start living well past 100, that issue will become even more pronounced, and investors will have to plan for a possibly very long time horizon even in their later years. If health span increases commensurately, they will also want money for travel and recreation, further affecting investment strategy.

Longer lives, and better health in old age, have profound implications for family and social arrangements, government, investments, and even the shapes of cities. They do not have to mean added expense and burden. If the extra years are enjoyed in good health, they will be a blessing and convey benefits to everyone.

Listen to our full conversation: Nir Barzilai: Can Data Cure Aging?

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