Hardly a week goes by without a news story about a scientific breakthrough that slows aging (or at least claims to). Meanwhile, social media feeds burst with ads and influencers hawking supplements and diet plans that purport to help us live longer.<\/p>\n\n\n\n
Clearly, longevity is having a moment, but is it the next revolution in medical science or just another wellness fad destined to be ironically short-lived?<\/p>\n\n\n\n
The answer is probably both. History is filled with examples of charlatans selling eternal youth in the form of a pill or potion, and many of today\u2019s longevity entrepreneurs will likely join their ranks. But there\u2019s a reason that longevity has entered the zeitgeist: Scientists are making incredibly promising breakthroughs that could help us live longer, healthier lives.<\/p>\n\n\n\n
Older people are obviously more likely to die, but how much more likely is pretty shocking: A person\u2019s risk of death doubles every eight years. That means when you\u2019re in your 20s, you might have a 1 in 1,000 chance of dying in a given year, but by the time you reach your 90s, your risk can surpass 1 in 6 \u2014 life and death at the roll of a dice. <\/p>\n\n\n\n
The reason behind this rise is a similarly sharp increase as we age in the risk of developing diseases like cancer, heart disease, dementia, and so on. If we could figure out how to slow or even reverse the biological aging process, we could reduce our risk of developing these diseases.<\/p>\n\n\n\n The first longevity medicines could be approved in time for most people alive today \u2014 maybe even in the next five years.<\/p><\/blockquote><\/figure>\n\n\n\n It\u2019s hard to overstate the impact this could have on humanity. Researchers estimate that even a cure for cancer would only add two or three years<\/a> to average life expectancy, because those lucky enough to survive would die of a heart attack or dementia a few years later. Treating the underlying aging process, however, would slow the march of cancer, dementia, and other maladies simultaneously. We\u2019d be protecting ourselves against most of humanity\u2019s deadliest killers.<\/p>\n\n\n\n For decades, most scientists believed that slowing aging was impossible, which is historically why many researchers have ignored the field. This lack of attention and perceived credibility has led to a lack of funding \u2014 the National Institutes of Health invests nearly 20 times more money<\/a> into cancer research than aging biology. Slowing aging is also a huge challenge because trials to test interventions could take decades \u2014 humans can live for 80-plus years and perhaps even longer if a treatment works.\u00a0<\/p>\n\n\n\n Given these challenges, it might seem like the only hope of living longer involves hitting the genetic lottery or being lucky enough to take part in a multidecade clinical trial when an effective drug is finally tested in people. Yet the first longevity medicines could be approved in time for most people alive today \u2014 maybe even in the next five years, if we get serious about the science.<\/p>\n\n\n\n One technique makes a 114-year-old\u2019s cells almost indistinguishable from ones found in the first moments of life.<\/p>\n<\/blockquote>\n\n\n\n Over the last few decades, longevity research has made serious progress. In the 1990s, scientists learned that changing a single gene in a nematode worm\u2019s DNA could double<\/a> its lifespan. While this discovery wouldn\u2019t directly translate to humans (we\u2019re a little more complicated than worms), it taught the scientific community that aging isn\u2019t some impossibly complex process. At the same time, gene-editing technology was rapidly improving, meaning we had the tools we needed to exploit this discovery.<\/p>\n\n\n\n Since then, scientists have uncovered what are known as hallmarks of the aging process<\/a>, the fundamental cellular and molecular drivers behind why we get older. Ranging from the molecular (damage to our DNA or the proteins that make up our cells) to the systemic (hormonal changes and the gradual loss of efficiency of the immune system), we have a better idea than ever before of what drives everything from wrinkles and gray hair to cancer and dementia.<\/p>\n\n\n\n From a biomedical perspective, these developments are exciting. Once you know what drives something, you have a better chance of figuring out how to slow it down, and lab and animal testing have given us dozens of promising leads for slowing \u2014 and perhaps even reversing \u2014 aging in humans. These range from cutting back animals\u2019 calories<\/a> to dramatically extend their healthy life to a single-letter change to a worm\u2019s DNA that can extend its life tenfold<\/a>. We can even employ a technique called epigenetic reprogramming, which has been used to make cells from a 114-year-old person<\/a> almost indistinguishable from ones found in the first moments of life.<\/p>\n\n\n\n There\u2019s also an ever-growing clutch of promising drugs<\/a> \u2014 the current leader is a combination of two drugs called rapamycin and acarbose that can make mice live 30\u201340% longer. Meanwhile, mice given senolytics \u2014 drugs that kill aged cells \u2014 live longer<\/a>, get cancer less frequently, and have fewer heart problems. They can also run farther and faster, experience less cognitive decline<\/a>, and, frankly, just look fantastic<\/a>, with thicker fur and plumper skin. <\/p>\n\n\n\n Many treatments that work in mice are even effective if they\u2019re started in late middle age.<\/p><\/blockquote><\/figure>\n\n\n\n Researchers are also seeing promise in nonpharmaceutical aging interventions. We now know we can make mice live longer through different gene edits or by refreshing the stem cells in their bone marrow. Given the rapid progress in these treatments for serious illnesses in humans, it might not be long before some of these longevity-flavored options make it out of the lab and into human trials.<\/p>\n\n\n\n Many treatments that work in mice are even effective if they\u2019re started in late middle age \u2014 great news for the almost half a billion people worldwide who are over the age of 65. Scientists are also rapidly developing ways to measure \u201cbiological age,\u201d which could massively speed up trials. Rather than waiting years to see which trial participants die or get sick, we could imagine doing a trial over a few months with a before-and-after biological age measurement giving rapid feedback on whether a new treatment works.<\/p>\n\n\n\n Some of the drugs that slow aging in mice are already safely used by millions of people around the world, so there\u2019s a clear path to trialing these meds as longevity treatments in humans, should someone be willing to fund the trials.<\/p>\n\n\n\n Unfortunately, science takes time, and while researchers develop new treatments, many people are going to continue cashing in on the longevity revolution, packaging up supplements or health devices with promising lab data \u2014 but no proper human evidence \u2014 as the key to a longer, healthier life. That\u2019s why understanding longevity science is now more critical than ever \u2014 to avoid being fleeced by charlatans<\/a>, while at the same time having one eye on the real breakthroughs that could be with us soon. Longevity is in a paradoxical place at the moment, but I hope we\u2019ll look back on this time with amusement in a few decades \u2014 or maybe a few centuries.<\/p>\n\n\n\n\n