We measure what research truly links to health over time
There are markers that predict the risk of disease and mortality with solid, published evidence. These are what guide the method. Here we explain which they are, what the research says, and the limits with which we use them.
A predictor is not a cure
A predictive biomarker is a measure associated, in studies, with a higher or lower future risk. Knowing you are at risk lets you act earlier — but measuring a predictor is not the same as a treatment that has been shown to change the outcome. We keep the two things distinct, always.
That's why we speak of markers that measure and predict, not of therapies that cure or rejuvenate.
The markers that matter (and what the research says)
These are among the best-documented predictors in the literature. The evidence cited describes the state of the science: studies on large populations, not results obtained on our patients.
Cardiorespiratory fitness (VO₂max)
What it measures: the capacity of the heart and muscles to produce and use energy under effort. What the research says: it is among the most powerful predictors of all-cause mortality, with no known upper limit of benefit. (Mandsager et al., JAMA Network Open, 2018; n≈122,000)
ApoB — number of atherogenic particles
What it measures: the number of particles that can deposit in the arteries — information that classic LDL cholesterol does not fully capture. What the research says: it captures heart-attack risk better than LDL cholesterol alone. (Marston et al., JAMA Cardiology, 2022)
Lp(a) — lipoprotein(a)
What it measures: a lipid fraction largely determined by genetics. What the research says: it is a causal, inherited cardiovascular risk factor; it is typically measured once in a lifetime. (Kamstrup et al., JAMA, 2009; Clarke et al., NEJM, 2009)
Coronary artery calcium (CAC score)
What it measures: the amount of calcium in the coronary arteries — a direct "snapshot" of atherosclerosis already present. What the research says: a very high score is associated with a risk comparable to those who have already had a cardiovascular event. (Multi-Ethnic Study of Atherosclerosis — Peng et al., Circulation, 2021. Citation under verification.)
Grip strength
What it measures: overall muscular strength, with a simple in-office test. What the research says: it predicts all-cause mortality, with prognostic value documented in large populations. (Leong et al., PURE study, The Lancet, 2015; n≈140,000)
Chronic low-grade inflammation (hsCRP, IL-6)
What it measures: the background level of inflammation ("inflammaging"). What the research says: it is associated with higher mortality and is an actionable cardiovascular risk factor. (concept: Franceschi et al., 2000; CV risk: JUPITER trial — Ridker et al., NEJM, 2008)
Glycaemic control (HbA1c)
What it measures: the average blood sugar of the last few months. What the research says: it is associated with mortality across the whole spectrum, even below the diabetes threshold. (Khaw et al., Annals of Internal Medicine, 2004)
The citations are studies on large populations and describe the state of the science. They are not data collected by Longevilife. The first author and DOI of each citation are under editorial verification before publication.
Biological age: a monitoring tool, not a diagnosis
Chronological age is the one on your ID. Biological age estimates how "old" the body is at the molecular level. Epigenetic clocks estimate it by reading DNA methylation patterns. (Horvath, 2013; Hannum et al., 2013)
The more recent versions are associated with mortality and disease better than chronological age (PhenoAge — Levine et al., 2018; GrimAge — Lu et al., 2019; DunedinPACE — Belsky et al., 2022), and there are signals — yet to be consolidated — that lifestyle may influence them (CALERIE RCT — Waziry et al., Nature Aging, 2023).
We use biological age as a tool for monitoring over time, not as a diagnosis. Epigenetic clocks are not validated clinical endpoints or diagnostic tests (Bell et al., 2019). A single measurement can carry a margin of technical noise: what matters is the trend over time, not the isolated number. We do not say, and you cannot expect from us, that we "reverse" or "rejuvenate" your biological age by a precise number of years. It is the field longevity medicine is looking toward: if it enters our panel, we will say so explicitly.
What it means, in practice
We measure validated predictors in order to act earlier: to spot a risk while it is still modifiable and build a targeted path. Measuring well is the first step, not the guarantee of the result.
And we keep distinct what has strong evidence (the markers on this page) from what has weak or preliminary evidence. When a technology or therapy has limited proof, we say so — we do not present it as "longevity science".
On this page we discuss only markers with solid evidence. Some treatments often associated with "longevity" — infusions, oxygen therapy, regenerative therapies — have, to date, no proof of effect on longevity or mortality. That's why we don't present them here as science.