Across the globe, more of us than ever are reaching old age, thanks to advances in public health. But this success comes at a cost: The surge in age-related chronic disease is burdening health-care systems and leading to human suffering we are unprepared for. The causes of aging, and the therapies that might alleviate its effects, are increasingly at the forefront of public interest and intrigue. Here are myths about aging that persist.
Biological aging can't be slowed.
Average life expectancy in the United States increased during the 20th century by a remarkable 31 years. Maximum human life span, on the other hand — marked by the 122 years achieved by Jeanne Calment — did not grow significantly. Recent work in Nature suggests that this is because humans have an upper limit on longevity set by biology and inevitable wear and tear. As Dan Rafael wrote on ESPN when boxing champion Floyd Mayweather came out of retirement for one last fight, “Everybody gets old.” It’s just a fact; “Father Time will always be undefeated.” Biodemographer Jay Olshansky put it this way in Nature: “You run into basic limitations imposed by body design.”
Yet a limit on what our bodies can currently achieve does not equate to the inevitability of aging. Aging is incredibly malleable. Though they have identical DNA, queen bees can live 10 times longer than worker bees. There are countless examples of animals that can live hundreds of years (clams and whales) and some that show little sign of a greater risk of death in older ages (hydra and naked mole rats). Fundamentally, these animals don’t differ from us; they use the same genetic code and damage-control mechanisms. Some humans also age exceptionally well: Centenarians live longer and better, compressing the usual end-of-life incapacity. The problem is that the science aimed at healthy aging lags behind advances that have generated more elderly people. The growing field of geroscience offers hope, showing that genetic alterations and drugs such as rapamycin can slow the rate at which animals age.
Live fast, die young.
In a 1927 article in the Baltimore Sun titled “Why Lazy People Live the Longest,” American biologist Raymond Pearl tied variation in longevity to metabolic rates — the “rate of living” — and stated that this explained the longevity of women as compared with men. One might have hoped for this myth (and misogyny) to die as fast as Pearl’s energetic fruit flies, but it lives on. President Trump, according to a biography by The Washington Post’s Marc Fisher and Michael Kranish, believes that the “human body was like a battery, with a finite amount of energy, which exercise only depleted.”
But the claim that longevity requires a slow metabolic rate was based upon only a handful of species, and now we know of many exceptions. Naked mole rats live 10 times longer than their mice cousins and never get cancer despite a comparable metabolism. Recent work shows that regular exercise helps slow key signs of aging, boosting immune function and curbing mental decline. If anything, conserving our batteries as isolated couch potatoes ages us faster; successful aging is enhanced by exercise, engagement with life, staying in the workplace and maintaining social connections. If Keith Richards, who says the Rolling Stones “defy gravity,” is anything to go by, perhaps we should all be speeding up, not slowing down.
Antioxidants slow aging.
Supposedly, oxidants — or “free radicals” — are running rampant in our cells, damaging all they touch. And we are told that antioxidants in superfoods and beauty products will mop up free radicals, protecting us from their aging effects and keeping us young and disease-free. From celebrity endorsers like Gwyneth Paltrow with her website, Goop, and Dr. Oz with blueberries and sweet potatoes, the message is clear: Antioxidants are the elixir of youth. It’s a viewpoint perpetuated by eternally youthful athletes like Tom Brady, whose TB12 diet supplements claim to combat these “destabilizing atoms that can contribute to aging and illness.”
Free radicals, a class of molecules in cells that have unpaired electrons, can indeed cause damage in cells, but they have captured the public imagination as a source of old age with little scientific evidence. There is in fact more negative data than positive examples. Growing evidence even suggests that genetic manipulations that slow aging in animals like the nematode worm cause a small burst of free radicals that induces “mitochondrial hormesis,” preparing the worm for a stress to come and helping increase life span — science’s way of saying that what doesn’t kill you makes you stronger. Free-radical damage may be linked to chronic diseases, but as for the idea that it’s a driving cause of aging, it’s the myth itself that seems immortal.
Fewer calories mean a longer life.
Calorie restriction has been shown to slow aging and the onset of disease in monkeys, and it might have beneficial effects in people. The CR Society offers books like “The CR Way,” full of low-calorie meal ideas that support the less-is-more approach to longevity.
In truth, we just don’t know that the benefit of strict diets lies solely in their calorie content. Increasingly, it seems that many of the positive effects of calorie restriction on aging may be unrelated to caloric intake. Hungry animals and people tend to eat faster, and as a result spend more of their day eating nothing. These extended periods of abstinence are enough to slow aging in mice, whether overall calorie intake is reduced or not. The science uncoupling the effects of fasting and calorie restriction on aging is in its infancy.
The same goes for our understanding of whether “a calorie is a calorie” when it comes to longevity. During our evolution, we were likely to die of infection, accidents or disease long before we reached old age; hazardous living masked any negative consequences diet might have had. So if a high-protein “paleo” diet made our ancestors lean and strong to help spread their genes to the next generation, any adverse effects it had on aging would have gone unseen. High protein activates a sensor in our cells called mTOR, which builds body mass and is loved by weightlifters. But for healthy aging, being catabolic (burning), not anabolic (building), seems key; suppressing mTOR prolongs life in animals. Among mice fed diets with identical amounts of calories, those that lived longest and aged best ate lower amounts of protein.
Short telomeres explain aging.
As our cells divide, the chromosomes within them that carry the recipe for all cellular functions progressively shorten, because the replication machinery cannot get right to their tips. To prevent loss of information, these tips have protective caps known as telomeres, often likened to the plastic tips at the ends of shoelaces. But they can do only so much. With age (or continuous cellular division in a petri dish), telomeres become too short to be protective, and cells go dormant. Because cells in older people have shorter telomeres, telomere length is cited as a predictor of good or bad aging and even the central cause of the aging process. Lifestyle advice including more sex, meditation and yoga proposes to protect or even lengthen telomeres. “This is no snake oil. This is no humbug,” says a review of the popular book “The Telomere Effect,” co-authored by Nobel Prize winner Elizabeth Blackburn, in Psychology Today.
Aging is not caused by one event, however, as compelling as fraying telomeres may be. Some of our cells do not divide at all, and they age without shortened telomeres. Many animals have telomeres much longer than ours, yet they age faster than we do. Shortening telomeres may even be useful, protecting against unchecked cell division, which is a hallmark of cancer.