Is the first person who will live to 150 alive today?
That’s the subject of a “$1 billion bet” between two leading scientists in the field of aging: S. Jay Olshansky, a professor of epidemiology and biostatistics in the School of Public Health at the University of Illinois at Chicago, and Steven N. Austad, a biologist at the University of Alabama at Birmingham.
Friends since the early 1990s, the two made their bet in 2000 after a newspaper article quoted Prof. Austad as saying that living to 150 will soon be within our grasp. Each has put $300 into an investment account that the two men hope will be worth more than $1 billion in 2150, when the bet comes due. But even Prof. Austad, the optimist, says, “It’s going to be our descendants who get to collect that money.”
By 2150, Prof. Austad says, advances in biomedical science and drugs that improve cellular function “would make living to 100 routine, with a few people reaching the age of 150 years—somewhat like people routinely live to age 80 today with a few people living to 110.”
Prof. Olshansky says in his view, the upper limits of life expectancy are in the mid- to high 80s. Under that scenario, he says, “many more people will live to see 100.” But 150? No way.
The Leap Will Come From Focusing on Aging Itself
By Steven N. Austad
People born in the 21st century—today’s college students, for instance—can expect to live a century or more because their health will be unlike anything seen before in human history. This new surge in life expectancy will not be due to doctors becoming better at diagnosing and treating the diseases that kill us today. It will be due to our new ability to prevent and delay most or all of the diseases and disabilities that plague later life.
During the 20th century, life expectancy in the U.S. surged some 63%, to 77 years from 48. That progress was driven by better hygiene, the development of vaccines and antibiotics, and, later on, better diagnosis and treatments of individual diseases. Similar progress in the 21st century will easily take us to a 100-year lifespan.
We’ll get there, but not by focusing as we have in the past on one disease at a time. Near the past century’s end, a new approach to health began to emerge, focused not on diseases themselves, but on the underlying processes of aging itself. Aging is the biggest factor in virtually everything that kills us today.
Beginning with tiny roundworms and fruit flies, researchers discovered that treating aging as if it were a disease was not difficult. We could do it by altering genes, modifying diets and, most surprisingly, with the use of some existing drugs developed for other purposes. These treatments worked not only in the simplest animals; they also worked in mice—mammals like ourselves.
Geroscientists—a new word for a new field—have found that treating aging has remarkably broad benefits. One drug, for instance, called rapamycin, has made mice live considerably longer. It has delayed some mouse cancers and completely eliminated others; it also has delayed mouse versions of Alzheimer’s disease, heart aging and the advance of forgetfulness of later life. And in a limited study involving humans, a drug closely related to rapamycin was seen to have benefits for people 65 and older in the form of improved protection from flu when used in combination with a flu vaccine.
Then came a truly unexpected discovery. Rapamycin had virtually the same health benefits whether started later in a mouse’s life—the mouse equivalent of 60-75 years old—or early.
It’s true that the biology of mice is different from that of humans. But, as mammals, we do share 98% of the same genes as mice, so there are undeniably many similarities. Meanwhile, another drug, metformin, for treating diabetes, shows promise similar to that of rapamycin in preventing or delaying the maladies of aging. Moreover, the drug has shown more promise in studies involving humans than it has in mouse studies. The many studies involving humans and metformin were observational—meaning they compared people taking metformin for diabetes with people not taking metformin, or taking another diabetes drug, and compared the rates of cancer, heart disease and dementia in those groups. The studies found less-frequent incidence of these illnesses in the groups taking metformin than in the groups not taking it.
Discoveries of this sort are emerging at a faster and faster pace.
It’s true, as critics say, that adding just one year of life expectancy is more difficult the older one gets. With 80 years behind you, for example, and all the likelihood of various age-related illnesses lining up before you, the odds of reaching 100 worsen. But we have to stop thinking about age-related diseases as independent entities. Diseases associated with aging have extensively overlapping causes, so that a treatment (like rapamycin) affects most or all such ailments. Treating aging itself thus can dramatically change the mortality rates currently seen in our later years. If we could freeze the age-induced mortality rate at age 50 so that one faces no increased odds of falling sick, life expectancy soars to more than 125 years. Hundreds of life-extending animal experiments show that what we previously thought of as “limits” can be burst through with the right treatment.
No one should rush to get prescriptions or try out aging-retarding therapies before they are properly evaluated for safety and efficacy in people. But such testing has started. Numerous human trials have begun or are about to begin.
We don’t know yet which of the various health-extending treatments for aging that work so unequivocally in mice will work in people too, but we will. And the early evidence suggests that those treatments, even if they aren’t available until midcentury or later, can still extend lives and health like nothing we have ever seen before.
Dr. Austad is distinguished professor and chair in the department of biology at the University of Alabama, where he is also director of the Nathan Shock Center of Excellence in the Basic Biology of Aging. He is also senior scientific director with the American Federation for Aging Research in New York. He can be reached at reports@wsj.com.
Blame It on Math, Science, Common Sense and Our Bodies
By S. Jay Olshansky
Predicting that children born in the U.S. from 2000 on will have a life expectancy of at least 100 is nothing short of radical—but not for the reasons you might think.
Our understanding of the biology of aging will advance; breakthroughs are on the horizon that will slow the effects of aging; the resulting extension of healthy life will soon transform what it means to grow old; and Nobel Prizes await the scientists who make this possible.
Life expectancy will inch up, to well short of 100—but the Holy Grail of what I call extended healthspan will finally be realized. Let’s stop striving for an unattainable goal of radical life extension, or, worse, claiming that it’s already arrived. Common sense dictates that we shift the focus of medicine and public health to extending that part of our later lives in which we enjoy good health.
The problem with the idea of living routinely to the age of 100 is that math, science, common sense and our inherited body “design” get in the way.
The first longevity revolution—the 30-year increase in life expectancy seen in the 20th century—occurred mostly because of declining early-age mortality thanks to advances in public health. This was boosted later in the century by reductions in death rates at middle and older ages as lifestyles improved, and because of new methods of detecting and treating aging-related diseases.
But look where we are today. Even ideal behavioral risk factors won’t transform a 70-year old into a supercentenarian. Conquering aging-related diseases one at a time would yield diminishing gains in life expectancy the older one gets. And Alzheimer’s disease and obesity in our society are growing worse, not better, suggesting that just attacking diseases without slowing aging could worsen the health of future cohorts of older people.
Perhaps the biggest reason why humans can’t expect to routinely live to 100 is this: Life expectancy is a population metric, and it gets harder to move the needle the older we get.
Adding one year to life expectancy when it is 80 is orders of magnitude more difficult to achieve than when it is 50. Attaining a life expectancy of 90 requires the equivalent of cures for cancer, all cardiovascular diseases, diabetes, infectious diseases and accidental deaths. Getting to 95 requires the elimination of all known causes of death short of aging. And getting to 100 requires not only that we slow aging, but that survival time would need to be added to the lives of people aged 70-plus at a rate faster than it was added to lives of children born at the start of the 20th century.
There can and should be some marginal gains in life expectancy for demographic subgroups; reducing disparities between the rich and poor, for example, is desperately needed. But a second longevity revolution on par with the first is highly unlikely for the general population, even when a method of slowing aging becomes available.
One more point on the mathematical argument: The law of averages requires that for 100 to be the new life expectancy, a significant proportion of the population routinely must survive beyond the current maximum lifespan limit of 122—an age known to have been reached by just one person. This alone is sufficient to cast doubt on claims that 100 is the new normal.
Scientists who nevertheless back such claims point to research in which aging has been slowed and lifespans increased in short-lived species. But humans don’t experience biological time at the same rate as those species. A doubling of the lifespan of a short-lived species will likely yield only a fraction of that gain in humans. Doubling the lifespan of a mouse from three to six years doesn’t mean the lifespan of humans will double from 80 to 160.
Keep in mind that aging interventions aren’t seeking to “cure” aging itself. That would be an unrealistic target with no evidence to support it. Aging isn’t a disease, any more than growth, development, puberty and menopause are. When aging interventions are eventually introduced, they will likely delay diseases, compress morbidity, extend healthspan and yield economic dividends to individuals and societies. In the final analysis, though, some diseases will recede in favor of others, and the game of disease Whac-A-Mole (referred to as “competing risks” in epidemiology) will continue.
A better goal than extending human lifespan is the extension of the periods in our lives in which we enjoy good health. Humans are no more capable of routinely living to 100 as a population than we are expected to all run a 4-minute mile, high-jump 8 feet, or dunk a basketball—at least not in these bodies with this body design.
Dr. Olshansky is a professor of epidemiology and biostatistics at the University of Illinois at Chicago’s School of Public Health. He is also chief scientist at Lapetus Solutions and a board member of the American Federation for Aging Research. He can be reached at reports@wsj.com.
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