Aging & Longevity

Frequently asked

Why does building muscle get harder as you get older?

Researchers have documented a phenomenon called "anabolic resistance": aging muscle mounts a smaller protein-building response to the same dose of protein or the same bout of exercise that triggers a larger response in younger muscle. Muscle mass loss appears to begin quietly from middle age, at roughly 1% of total mass per year, and can reach around 50% of total muscle mass lost by the 8th or 9th decade of life in severe cases. Reviews describe several candidate mechanisms — blunted anabolic signaling, reduced blood flow delivering amino acids to muscle, and amino acids being retained in the gut before reaching muscle — but no single confirmed cause, and no agreement on how much of the effect can be reversed.

Does resistance training still work after 60, or even in your 90s?

Yes. In one of the earliest controlled trials, ten nursing-home residents averaging 90 years old gained 174% in knee-extensor strength after just 8 weeks of high-intensity training, though muscle size grew far less than strength did. Later meta-analyses covering hundreds to over a thousand older adults confirm resistance training reliably increases strength and muscle mass in this age group. It isn't identical to training at 25, though — a lab study found the cellular signaling that converts a workout into new muscle protein activated in younger muscle after exercise but failed to activate on the same tests in older muscle, and not every functional outcome, like gait speed, improves as reliably as strength does.

Does creatine still work for muscle after age 50?

A 2025 meta-analysis of 69 trials and 1,937 participants found creatine plus resistance training significantly increased squat and bench-press strength overall — but when the results were split by age, those gains were statistically significant in younger adults and not in older adults. Some trials in older women found a benefit when training ran 24 weeks or longer, and a 32-week trial found creatine increased lean tissue mass more than placebo. But in frail or hospitalized older adults, and in a 2-year bone-density trial in 200 postmenopausal women, creatine added nothing measurable beyond resistance training or usual care.

What does grip strength actually predict?

In a study of 139,691 adults across 17 countries, every 5 kg drop in grip strength was linked to a 16% higher risk of death from any cause and a 17% higher risk of cardiovascular death — a stronger association than the study found for systolic blood pressure. A separate analysis of 502,293 UK Biobank participants found the same pattern extended to cancer and respiratory disease deaths. No trial has tested whether training grip strength itself changes any of these outcomes, so researchers note it may be better understood as a marker of overall health than a modifiable target on its own.

What is sarcopenia and how do doctors measure it?

Sarcopenia's clinical definition changed in 2019 to center on low muscle strength rather than muscle size, using low muscle mass to confirm a diagnosis and poor physical performance to mark severity. How common it looks depends heavily on which yardstick is used: a 2025 meta-analysis of 52 studies and 70,202 older adults found reported prevalence ranging from 5.2% to 50.0%, with a pooled estimate of 18.8%. Measurement tools disagree with each other too — in one Hong Kong cohort, switching from a DXA scan to a bioelectrical impedance device changed a person's measured muscle mass by nearly 3 kg/m² on average — but however it's defined, sarcopenia consistently tracks with a more than doubled risk of death.

What's known about longevity peptides like Epitalon, MOTS-c, and SS-31?

The three sit at very different evidence stages. Epitalon, the synthetic peptide sold today, has essentially no direct human trial data of its own — nearly all the human research trail actually leads to a different substance, Epithalamin, studied for decades by one Russian/Ukrainian research group whose mortality-reduction claims have not been independently replicated in a blinded, placebo-controlled trial. MOTS-c has never been given to a human in a verified clinical trial; the one registry listing that names it shares identifying details with other listings already documented elsewhere as fabricated. SS-31 (elamipretide) has the most extensive human trial program of the three — more than a decade of Phase 1 through Phase 3 studies across four diseases — but its primary endpoints have failed or been mixed almost everywhere they've been tested, even as some open-label extensions and subgroups report improvement.

New to this?

Start here for plain-English explanations of clinical trials, evidence levels, and how to read a study.