Most people want to live a long and happy life or at least avoid a short and miserable one. If youre in that majority, then youre in luck. Over the last decade,a quiet research revolutionhas occurred in our understanding of the biology of aging.
The challenge is to turn this knowledge into advice and treatments we can benefit from. Here we bust the myth that lengthening healthy life expectancy is science fiction, and show that it is instead scientific fact.
Theres plenty of evidence for the benefits of doing the boring stuff, such as eating right. Astudy of large groups of ordinary peopleshow that keeping the weight off, not smoking, restricting alcohol to moderate amounts and eating at least five servings of fruit and vegetable a day can increase your life expectancy by seven to 14 years compared with someone who smokes, drinks too much and is overweight.
Cutting down calories even more by about a third, so-called dietary restriction improves health and extends life in mice and monkeys, as long as they eat the right stuff, though thats a tough ask for people constantly exposed to food temptation. The less extreme versions oftime-restricted or intermittent fasting only eating during an eight-hour window each day, or fasting for two days every week is thought to reduce the risk of middle-aged people getting age-related diseases.
You cant outrun a bad diet, but that doesnt mean that exercise does not do good things. Globally, inactivity directly causes roughly 10% of all prematuredeaths from chronic diseases, such as coronary heart disease, Type 2 diabetes and various cancers. If everyone on Earth got enough exercise tomorrow, the effect would probably be to increase healthy human life expectancy by almost a year.
But how much exercise is optimal? Very high levels are actually bad for you, not simply in terms of torn muscles or sprained ligaments. It can suppress the immune system andincrease the riskof upper respiratory illness. Just over30 minutesa day of moderate to vigorous physical activity is enough for most people. Not only does that make you stronger and fitter, it has been shown toreduce harmful inflammationand even improve mood.
However fit you are and well you eat, your immune system will, unfortunately, get less effective as you get older. Poor responses to vaccination and an inability to fight infection are consequences of this immunosenescence. It all starts to go downhill in early adulthood when the thymus a bowtie-shaped organ in your throat starts to wither.
That sounds bad, but its even more alarming when you realize that the thymus is where immune agents called T cells learn to fight infections. Closing such a major education center for T cells means that theycant learn to recognizenew infections or fight off cancer effectively in older people.
You can help a bit by making sure you have enough key vitamins, especially A and D. A promising area of research is looking at signals that the body sends to help make more immune cells, particularly a molecule calledIL-7. We may soon be able to producedrugs that contain this molecule, potentially boosting the immune system in older people.
Another approach is to use the food supplement spermidine to trigger immune cells to clear out their internal garbage, such as damaged proteins, which improves the elderly immune system so muchthat its now being testedas a way of getting better responses to COVID vaccines in older people.
Senescence is a toxic state that cells enter into as we get older, wreaking havoc across the body and generating chronic low-grade inflammation and disease essentially causing biological aging. In 2009, scientists showed that middle-aged micelived longer and stayed healthierif they were given small amounts of a drug called rapamycin, which inhibits a key protein called mTOR that helps regulate cells response to nutrients, stress, hormones and damage.
In the lab, drugs like rapamycin (called mTOR inhibitors) make senescent (aged) human cellslook and behave like their younger selves. Though its too early to prescribe these drugs for general use, a new clinical trial has just been set up to test whether low-dose rapamycincan really slow down aging in people.
Discovered in the soil of Easter Island, Chile, rapamycin carries with it significant mystique and [has been hailed] in the popular press as a possible elixir of youth. It can evenimprove the memory of micewith dementia-like disease.
But all drugs come with pros and cons and as too much rapamycin suppresses the immune system, many doctors are averse to even consider it to stave off age-related diseases. However, the dose is critical and newer drugs such asRTB101that work in a similar way to rapamycin support the immune system in older people, and can evenreduce COVID infection ratesand severity.
Completely getting rid of senescent cells is another promising way forward. A growing number of lab studies in mice using drugs to kill senescent cells so-called senolytics show overall improvements in health, and as the mice arent dying of disease,they end up living longer too.
Removing senescent cells also helps people. In a small clinical trial, people with severe lung fibrosis reported better overall function, including how far and fast they could walk,after they had been treatedwith senolytic drugs.
But this is only the tip of the iceberg. Diabetes and obesity, as well as infection with some bacteria and viruses, can lead to more senescent cells forming. Senescent cells also make the lungs more susceptible to COVID infection, and COVIDmakes more cells become senescent. Importantly, getting rid of senescent cells in old micehelps them to survive COVID infection.
Aging and infection are a two-way street. Older people get more infectious diseases as their immune systems start to run out of steam, while infection drives faster aging through senescence. Since aging and senescence are inextricably linked with both chronic and infectious diseases in older people, treating senescence is likely to improve health across the board.
It is exciting that some of these new treatments are already looking good in clinical trials and may be available to us all soon.
Richard Faragher is a professor of biogerontology at the University of Brighton in England. Lynne Cox is an associate professor of biochemistry at the University of Oxford, also in England. This was first published by The Conversation Life extension: the five most promising methods sofar.
