For how we live.
Failing mitochondria are one of ageing's core hallmarks, and human trials of mitochondria-targeted compounds show flickers of benefit — but the strongest endpoints keep coming back null.
A prominent hypothesis holds that ageing is lost epigenetic information that can be reset. The mouse experiments behind it are striking, but no human study shows resetting the epigenome extends life.
Cellular senescence is a well-evidenced driver of ageing in animals. The first human trials of senolytic drugs that clear these cells are real but tiny, early, and nowhere near proving longer healthy life.
Mouse studies claimed one circulating protein reversed ageing of the heart, muscle and brain. A second team found the muscle effect ran the opposite way — and no human trial has ever tested it.
In 2,292 older adults, weak quadriceps tracked with higher mortality — but muscle size, measured by CT and DXA, did not. The finding reshaped how sarcopenia is defined and moved the target from bulk to strength.
A widely cited cohort found people with diabetes on metformin outlived matched non-diabetic controls. It fuelled the TAME anti-ageing trial — but the human signal is observational, and TAME is not running.
The idea that anti-ageing advances will soon add more than a year of life for every year that passes is popular in longevity circles. National death records point the other way.
A protein named after a Greek fate slows ageing in mice and sharpens memory in old monkeys. In people the evidence is a gene variant you are born with, not a treatment.
Sugars bond to proteins to form advanced glycation end products that accumulate with age and stiffen tissue. Low-AGE diets nudge metabolic markers, but no trial shows they slow ageing.
Immunosenescence, the age-related decline of immunity, is real: the thymus shrinks and the T-cell repertoire narrows. The proven counter is not a supplement but vaccines engineered to force a response.
The idea that a little stress makes the body stronger is sound biology, and the best-evidenced example is ordinary exercise. Stretched to cold, fasting and antioxidant pills, the human evidence thins fast.
Autophagy is the cell's self-clearing recycling process, and it wanes with age. Fasting, spermidine and rapamycin switch it on in lab animals — whether that extends human life is unproven.
The rise in chronic, low-grade inflammation with age is genuine, and researchers built a clock from it. The one large trial that lowered inflammation for a hard outcome treated heart disease, not ageing.
The DO-HEALTH sub-study is the first randomised evidence that a supplement can nudge DNA-methylation ageing clocks. The effect was tiny, and the parent trial found no benefit on health outcomes that matter.
The signalling that builds muscle in youth appears to speed ageing and cancer. People with lifelong GH deficiency avoid both — and GH given to healthy older adults raises harms without extending life.
Epigenetic clocks estimate a 'biological age' from DNA methylation. A 2022 study found technical noise alone could shift the result by up to 9 years between replicates of the same sample.
Dietary spermidine tracks with markedly lower mortality in one population study. The first year-long randomised trial of a spermidine supplement found no effect on memory.
Infusing plasma from young donors is sold as rejuvenation. The mouse work suggests diluting old blood may matter more than adding young blood — and regulators warn the paid infusions have no proven benefit.
A 2013 paper named nine hallmarks of aging; a 2023 update made it twelve. The framework is the field's shared map — but critics argue it describes ageing without explaining it.
The NAD+ precursors sold to slow ageing reliably raise NAD+ and are well tolerated. What the randomised trials do not show is a benefit to muscle, metabolism or how old you are.
It extends life in yeast, worms and flies, and in mice on a high-fat diet. In people it fails to reliably switch on the enzyme it targets, and higher intake tracks no drop in death, cancer or heart disease.
The length of your chromosome caps is a noisy population-level marker, not a personal verdict — and genetically longer telomeres raise the risk of several cancers, not lower it.
Twenty-one years of cancer follow-up, multimorbidity data to 2021, and a randomised trial in frail older adults. In each, metformin did not beat placebo. Lifestyle change did.
Consumer clocks report an age, an age gap or a pace of ageing. Expert panels agree no single biomarker is sufficient — and clocks have failed to move when an intervention demonstrably worked.
A $12 million gift will test whether low-dose rapamycin changes the transition to frailty in adults over 65 — the first study of the drug designed around an outcome rather than a biomarker.
The longest human trial of low-dose rapamycin for healthy ageing found no change in visceral fat, its own primary outcome. The positive findings it is quoted for rest on eight women.
A 2025 review walked through every study of low-dose rapamycin in healthy adults. The immune findings are real, the outcome data do not exist, and the review's own worked example does not add up.
A phase 2 trial of dasatinib plus quercetin missed its bone endpoint. A senolytic injected into the eye produced a 5.6-letter vision gain whose confidence interval crosses zero.
In 2023 declining taurine was proposed as a driver of ageing. Two years later the same journal published human, monkey and mouse data in which taurine rose or stayed flat.
A 2026 meta-analysis pooled every randomised human trial of the gut-derived supplement for muscle health. Only one outcome, from two trials, could be combined — and it missed significance.
Longevity trials want a measurement that moves in months instead of decades. A Berlin study ranked the candidates, and a four-week diet trial showed what a clock does when nothing much happens.