Can We Slow Aging? A Field Guide to Evidence, Hype, and Hard Questions

Your feed offers three routes to a longer life this week. A podcast guest swears by a transplant drug taken once a week. An online shop sells a powder that promises to “restore youthful cell energy.” A clinic advertises infusions of plasma from young donors. Each comes with a scientific-sounding story and at least one real study somewhere in the background. So which, if any, should you believe?

This field guide won’t tell you what to take—that’s a conversation for you and a clinician. What it will do is show you where the evidence actually sits for the most talked-about ideas in longevity science, and which questions are still wide open.

First, what would “slowing aging” even mean?

Scientists distinguish between lifespan, how long you live, and healthspan, how long you live in good health. Most serious researchers are chasing the second: postponing the heart disease, cancers, dementia and frailty that pile up with age, ideally all at once rather than one disease at a time.

That goal runs into a practical wall. Ageing unfolds over decades, so a trial that waits to see whether people live longer would take a very long time and cost a great deal. And there is currently no FDA-approved treatment for ageing itself. One project, the Targeting Aging with Metformin (TAME) trial, was designed partly to test whether regulators could come to treat ageing as something a drug might target—more on that below.

Plain English: Healthspan is the number of years you live in good health. An intervention that extends lifespan without extending healthspan would simply add years of illness—which is not what most people mean by “slowing aging.”

The unglamorous evidence base

Before the exotic options, it’s worth noting what the National Institute on Aging (NIA) points to when it discusses healthy ageing: balanced nutrition, regular physical activity, not smoking, limiting alcohol, staying socially engaged and getting enough sleep. None of these is a longevity “hack,” and none is a guarantee. But they are backed by far more human evidence than anything that follows.

In longevity science, the most exciting claims tend to have the thinnest human evidence—and the most boring advice has the thickest.

Hype vs. Evidence

Here are six of the most discussed ideas, each with the popular claim and what published evidence actually shows. Remember the distinction between preclinical evidence (cells and animals), clinical evidence (human trials) and approved treatments.

• Rapamycin. The claim: an anti-ageing drug proven to extend life. The evidence: In a landmark 2009 Nature study run at three independent research sites, genetically diverse mice fed rapamycin starting at 600 days of age—late middle age for a mouse—lived longer: by 14% for females and 9% for males, measured at the age when 90% of each group had died. That is strong preclinical evidence. Rapamycin is an approved drug for other purposes, including preventing organ-transplant rejection, and it suppresses parts of the immune system. It is not approved to treat ageing, and there is no comparable evidence that it extends human life.
• Metformin and the TAME trial. The claim: a cheap diabetes pill that slows ageing. The evidence: Metformin is a long-established treatment for type 2 diabetes. The American Federation for Aging Research (AFAR) says studies have shown it can delay ageing in animals, which is why it was chosen for TAME: a planned six-year trial of more than 3,000 people aged 65 to 79 across 14 institutions, testing whether metformin delays age-related diseases such as heart disease, cancer and dementia. According to AFAR, the organisers are still seeking funding to launch it. There are no TAME results—be wary of any site that claims otherwise.
• NAD+ precursors (such as NR and NMN). The claim: supplements that recharge your cells and reverse ageing. The evidence: NAD+ is a molecule cells use in energy metabolism. In a 2018 randomised, placebo-controlled crossover trial of 30 healthy adults aged 55 to 79 (24 completed it), nicotinamide riboside (NR) was well tolerated and raised NAD+ levels in blood cells by about 60%, but produced no significant improvements in exercise capacity or metabolic function. A 2025 review in Nature Metabolism concluded that human trials have so far shown limited efficacy and that rodent results do not translate straightforwardly to people.
• Senolytics. The claim: drugs that flush out “zombie cells” and rejuvenate the body. The evidence: Clearing senescent cells delays some age-related changes in mice. In people, the evidence is early: a 14-person pilot in lung fibrosis without a placebo group, and a 60-person Phase 2 randomised trial in older women that, according to the NIA, found no meaningful difference on its main bone measure. The NIA has cautioned against self-treatment outside trials. We go deeper in The Cell Health Frontier.
• Caloric restriction. The claim: eat less, live longer. The evidence: In rodents, worms and flies, eating fewer calories while still getting adequate nutrients often extended lifespan, though results were inconsistent and some mouse strains lived shorter lives. In the NIA-supported CALERIE trial, 218 adults cut their calorie intake by about 12% for two years and saw lower blood pressure and cholesterol, with slight declines in bone density and aerobic capacity. The NIA says there is insufficient evidence to recommend any calorie-restriction or fasting diet, and that long-term effects in people remain unknown.
• Young plasma. The claim: infusions of young blood reverse ageing. The evidence: In 2019, the FDA warned consumers that plasma infusions from young donors, marketed for everything from normal ageing to dementia, have no proven clinical benefit for those uses, and carry risks including allergic reactions, infection, lung injury and circulatory overload.

The hard questions nobody has answered yet

How would we know it’s working?

Waiting decades for outcomes is impractical, so researchers want reliable biomarkers—measurable signals, such as blood tests or “ageing clocks” based on chemical tags on DNA—that track biological ageing. None is yet accepted as a substitute for real health outcomes. Our Longevity Dashboard explains which measures are clinically useful and which remain experimental.

Who pays to test cheap drugs?

Many candidates, like metformin, are old, inexpensive and off-patent, which leaves little commercial incentive to fund large trials. TAME’s long search for funding illustrates the problem.

What risk is acceptable in healthy people?

A side effect that is tolerable in a patient with a serious disease looks very different in a healthy 50-year-old taking a drug for 30 years. Long-term safety data in healthy people are exactly what the field lacks.

Who gets access?

If effective interventions emerge, questions of cost and equity will follow—and in the meantime, unproven products sold at high prices can exploit hope.

How to read the next longevity headline

1. Was it in mice, or in people? If people, how many, and was there a control group?
2. Did it measure lifespan, healthspan, or a lab marker?
3. Is the product being sold by the people making the claim?
4. Has a regulator approved it—for this use?

For a fuller checklist, see our guide on how to read a biotech breakthrough, or test yourself with the interactive Breakthrough Reality Check.

The bottom line

Can we slow ageing? In some animals, under laboratory conditions, the answer appears to be yes. In humans, the honest answer is that we do not yet know—and that the science is finally organised enough to start finding out. That is a genuinely exciting place to be. It just isn’t the place the advertisements say we’ve reached.