The Longevity Baseline.

Fitness and function: distinguish association from intervention

Cardiorespiratory fitness, often expressed as VO₂ max, is a measure of capacity. Observational differences can reflect prior health as well as training. Randomized evidence asks a narrower question: does an intervention preserve useful function? In LIFE, structured physical activity reduced major mobility disability from 35.5% to 30.1% over a mean 2.6 years in older adults at risk. That is 5.4 percentage points for this endpoint, not extra years of life. Study and population →

Strength and muscle are related but not interchangeable. Resistance-training trials support improvements in strength and function; a larger lean-mass reading alone cannot establish a survival effect. Read the trial synthesis →

Smoking exposure: a different order of magnitude

A large US observational analysis found more than ten years shorter life expectancy among current smokers compared with never-smokers. Cessation was associated with substantial recovery of survival. These are population estimates, not a forecast for an individual; nevertheless, they illustrate why a weak supplement signal should not displace a major established risk factor. Jha et al., 2013 →

Blood pressure: randomized clinical outcomes, with trade-offs

SPRINT randomized 9,361 adults at increased cardiovascular risk without diabetes. Intensive versus standard treatment reduced the primary cardiovascular composite from 2.19% to 1.65% per year over a median 3.26 years. All-cause mortality was lower (hazard ratio 0.73); some serious adverse events were more frequent. This demonstrates the value of studying clinical benefit and harm together. It is not a universal treatment target. SPRINT, 2015 →

Atherosclerotic risk: particles, exposure and events

ApoB and LDL cholesterol measure related aspects of atherogenic lipoproteins; neither is an ageing clock. A meta-analysis of 26 randomized statin trials found roughly 22% fewer major vascular events per 1 mmol/L LDL-cholesterol reduction. Absolute benefit depends on starting risk and follow-up. This treatment evidence should not be recast as proof that any isolated change in any lipid marker has the same effect. Cholesterol Treatment Trialists, 2010 →

Metabolic health: specify the treatment and the population

Obesity, glucose regulation and cardiovascular risk overlap, but improvement in one measure does not prove maximum-lifespan extension. SELECT studied adults with established cardiovascular disease and overweight or obesity without diabetes. Semaglutide reduced the primary cardiovascular composite from 8.0% to 6.5% during trial follow-up. That result belongs to this intervention and population; it cannot be assigned to every weight-loss method. Read the SELECT dossier →

Sleep and deficiencies: avoid a category error

Sleep regularity has observational links with mortality; prediction alone does not demonstrate that altering a schedule changes survival. Duration and regularity also describe different exposures. See the causal gap →

Correcting a clinically identified deficiency and supplementing an unselected population are different questions. VITAL did not demonstrate lower invasive-cancer or major-cardiovascular-event incidence with vitamin D in its primary analyses. This does not answer treatment of deficiency; it does challenge the idea that more supplementation automatically improves longevity. VITAL, 2019 →

Read the scale before the headline

These are different outcome classes, not guaranteed steps along one path. Compare absolute effects only when the outcome, population and duration are comparable. None of the percentages above can be added together or converted into a personal lifespan prediction.

The frontier matters precisely because established approaches leave so much unresolved. Compare the experimental evidence against that baseline, then ask what a future repair technology would have to demonstrate.