Biological age: what the tests really measure, and what they don’t tell you
A blood draw or a saliva sample, and out comes a number: your biological age. Behind it lies serious research, but also estimates that disagree from one test to the next, and promises to “reverse” your age that the evidence does not back. What these tests measure, how much they are worth, and what to do with the result.
By Rubens Valcy
Founder of MyTwin
Published on
Contents
A blood draw or a saliva swab, and a number comes back: “biological age, 34”. Tests like these promise to tell you how fast you are aging, then help you bring that number down, sometimes by several years. The idea rests on serious research. What gets sold online often goes well beyond what that research shows.
This article looks at what these tests actually measure, how reliable they are and what they leave out. It follows on from our article on healthspan, which ranks longevity levers by strength of evidence.
Chronological vs biological age: an estimate, not a direct measurement
Your chronological age is on your passport. Biological age starts from a simple observation: two people born the same year do not age at the same pace. The US National Institute on Aging describes it as how old our cells, tissues and organ systems appear to be, based on their biochemistry.
Yet this age cannot be read off anywhere. It is calculated: a statistical model, developed on thousands of people, turns biological measurements into a number of years. The result depends on the model, the data it was built on and what it was trained to predict. “Biological age” is not one measurement but a family of estimates, and they do not all answer the same question.
Two families of tests: blood chemistry and DNA
Measures based on a blood test
The most studied is Phenotypic Age, or PhenoAge. A 2018 study in PLOS Medicine calculates it from chronological age and nine routine blood markers:
- albumin, creatinine and glucose;
- C-reactive protein (CRP), a marker of inflammation;
- lymphocyte percentage and white blood cell count;
- mean cell volume and red cell distribution width;
- alkaline phosphatase.
The result is expressed in years: the age that, in the reference population, matches the person’s estimated mortality risk. Among more than 11,000 US adults followed for about twelve years, each additional year of Phenotypic Age, at the same chronological age, was associated with a 9% higher risk of death from any cause. The association held in seemingly healthy participants, with no reported disease and a normal BMI. The authors point to the main limitation themselves: no repeated measurements over time, and the need to confirm the findings in other cohorts.
Each of these markers also means something on its own, and is read in the context of the sample: that is what our guide on how to read blood test results covers.
Epigenetic clocks
The second family reads DNA methylation: chemical tags on DNA that shift with age without changing the genetic code. In 2013, Steve Horvath built a clock from 8,000 samples, based on 353 sites in the DNA, that estimates the “DNA methylation age” of most tissues.
Later clocks were trained to predict something other than chronological age. GrimAge, published in 2019, combines DNA-based estimates of seven blood proteins and of smoking history; it is associated with time to death, coronary heart disease and cancer. DunedinPACE, published in 2022, gives a pace rather than an age. It comes from a New Zealand cohort followed over two decades on 19 indicators of organ function. A value of 1 means one year of biological aging per calendar year; above 1, aging is faster.
These clocks are also offered by companies that sell tests directly to consumers. According to a 2025 analysis in Epigenomics, such tests often use saliva or a cheek swab, which are easier to collect, whereas most clocks were trained on blood, whose methylation profile is different.
Blood chemistry
- What is analyzed
- Nine routine blood markers, plus chronological age.
- What the result estimates
- The age that, in the reference population, matches the estimated mortality risk.
- Example
- PhenoAge
- The limitation to keep in mind
- Validated on a population, without repeated measurements over time.
DNA
- What is analyzed
- DNA methylation, in blood; consumer tests often use saliva or a cheek swab.
- What the result estimates
- Depending on the clock: an age, a mortality-related risk or a pace of aging.
- Example
- Horvath’s clock, GrimAge, DunedinPACE
- The limitation to keep in mind
- Technical noise that can be large, and clocks that contradict each other.
How reliable is a single result?
A biological age test is first of all a lab measurement, with its share of noise. A 2022 study in Nature Aging measured the same sample twice: for six widely used epigenetic clocks, technical noise alone produced gaps of up to 9 years between the two results. The authors propose a way of computing the clocks that brings most of these gaps under 1.5 years. DunedinPACE, for its part, was built by leaving out the least reproducible DNA sites. Reliability therefore depends on the clock and on how it is computed.
The Epigenomics analysis goes further. Because they are trained on different aspects of aging, clocks often give conflicting estimates for the same sample. A recent illness, stress or a medical treatment can skew a reading; two labs that process the data differently can get different results; and there is no agreed cut-off at which a gap becomes clinically meaningful. The authors conclude that, as things stand, these clocks should not be used to make decisions about an individual.
The issue goes beyond epigenetics. Researchers from the Biomarkers of Aging Consortium, in a 2024 review in Nature Medicine, note that there is still no consensus on how biomarkers of aging should be validated before they are used in the clinic. With PhenoAge, the lab tests are routine, but the estimate remains a population statistic, validated without repeated measurements.
Can you lower your biological age?
“Turn back the clock by ten years”: the promise is everywhere. In humans, the evidence is thin. One example is the CALERIE randomized trial, whose analysis published in 2023 in Nature Aging looked at epigenetic clocks. In all, 220 adults without obesity were randomly assigned either to cut their calorie intake by 25% for two years or to keep eating as usual. In practice, the first group reduced its intake by about 12% on average. The authors note that earlier findings came mostly from small studies without a control group.
The result: a pace of aging, measured by DunedinPACE, slowed by 2 to 3%. The other clocks tested, including GrimAge, did not change significantly. The authors describe small effects, in an analysis carried out after the fact, among healthy volunteers who do not represent the general population. Above all, they point out that a conclusive answer will require long trials measuring the onset of chronic disease and mortality.
Moving a marker, in other words, is not proof of a longer life in good health. And the calorie restriction in the trial was prescribed and monitored in a research setting: it is not something to try on your own. The National Institute on Aging urges caution with anti-aging interventions, especially when they seem too good to be true.
What to do with your result
A biological age is not a target to hit. Used with some distance, it can open a conversation with a doctor: which markers drive the result, what do they say about your risk factors, what is worth keeping an eye on? More often than not, the answer leads back to levers you already know.
Those levers are the same whatever the number. The National Institute on Aging sums them up plainly: eat well, exercise, get enough sleep, cut back on unhealthy habits and stay socially connected. For fitness, our article on VO2 max and longevity goes through what is known. And if you see a doctor practicing longevity medicine, the same question applies to every test on offer: what evidence is it based on?
Finally, a single measurement says little; its trend, measured the same way, says more. Tracking your data over time to estimate a risk is the idea behind predictive health.
That is the approach behind MyTwin Longevity, an app built on MyTwin, the health digital twin: it estimates biological age with PhenoAge from a blood check-up, and has it reviewed with a doctor specialized in prevention and longevity. The full journey is described in the launch of MyTwin Longevity, told by the MyTwin Lab.
Frequently asked questions
It is an estimate of how old the body appears to be, calculated by a statistical model from biological measurements: blood markers, or DNA methylation in the case of epigenetic clocks. It is compared with chronological age, but it is not a diagnosis.
They give an estimate, not an exact measurement. For some epigenetic clocks, technical noise alone can produce gaps of up to 9 years on the same sample, and different clocks often give conflicting results. A single result should be read with caution, and two different tests cannot be compared.
Evidence in humans is still thin. In the CALERIE trial, two years of calorie restriction slowed the pace of aging measured by one epigenetic clock by 2 to 3%, with no significant effect on the other clocks tested. Nothing yet shows that lowering this number adds years of good health.
PhenoAge is calculated from chronological age and nine routine blood markers. Epigenetic clocks, such as GrimAge or DunedinPACE, analyze DNA methylation. They estimate different things, and their results are not interchangeable.
Sources
- National Institute on Aging, March 26, 2021, “The epigenetics of aging: What the body’s hands of time tell us”.
- Liu Z et al., 2018, “A new aging measure captures morbidity and mortality risk across diverse subpopulations from NHANES IV: A cohort study”, PLOS Medicine, 15(12):e1002718.
- Horvath S, 2013, “DNA methylation age of human tissues and cell types”, Genome Biology, 14(10):R115.
- Lu AT et al., 2019, “DNA methylation GrimAge strongly predicts lifespan and healthspan”, Aging, 11(2):303-327.
- Belsky DW et al., 2022, “DunedinPACE, a DNA methylation biomarker of the pace of aging”, eLife, 11:e73420.
- Apsley AT et al., 2025, “From population science to the clinic? Limits of epigenetic clocks as personal biomarkers”, Epigenomics, 17(18):1447-1461.
- Higgins-Chen AT et al., 2022, “A computational solution for bolstering reliability of epigenetic clocks: Implications for clinical trials and longitudinal tracking”, Nature Aging, 2(7):644-661.
- Moqri M et al., 2024, “Validation of biomarkers of aging”, Nature Medicine, 30(2):360-372.
- Waziry R et al., 2023, “Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial”, Nature Aging, 3(3):248-257.
This article is provided for information purposes only. It does not replace advice, diagnosis or treatment from a healthcare professional.
