Your chronological age tells you how many birthdays you've had. DunedinPACE tells you something different and more useful: how quickly your body is wearing down right now, while you still have time to change the trajectory.
Built from chemical tags on DNA in your blood (called DNA methylation marks), DunedinPACE estimates years of biological aging per calendar year. A score of 1.0 means you're aging at the average rate. Higher means faster, lower means slower.
DunedinPACE (Pace of Aging Calculated from the Epigenome) is not a single protein, hormone, or metabolite. It's a composite score calculated from methylation patterns at 173 specific spots on your DNA in blood cells. The algorithm was trained on 20 years of changes in 19 different organ-system measurements, including cardiovascular, metabolic, kidney, immune, dental, and lung function markers, in a long-running New Zealand birth cohort.
Unlike older epigenetic clocks that estimate your biological age at one point in time, DunedinPACE estimates the rate of decline in your body's overall function. Think of it as the speedometer rather than the odometer. Two people with the same biological age could have very different paces of aging, and the pace is what predicts what comes next.
Because this is a research-grade biomarker without standardized clinical cutpoints, it's best used as a tool to track your own trajectory over time, not as a single pass-or-fail number. The science is strong on what faster pace means for health outcomes, but the test does not yet have formal guideline thresholds.
Faster DunedinPACE consistently shows up in people with worse cardiometabolic profiles. In studies of adults with obesity, those with faster pace of aging had higher insulin resistance, higher inflammation as measured by C-reactive protein (a marker of body-wide inflammation), and worse cholesterol patterns.
In a study of 4,419 women, those with faster DunedinPACE had higher rates of both existing and newly developing high blood pressure, even after standard treatment. A longitudinal twin study of 1,384 people found that worse blood sugar control tracked with faster DunedinPACE more clearly than with other epigenetic clocks. A 5,403-person Australian cohort found that DunedinPACE was linked to both existing and future type 2 diabetes.
In a Strong Heart Study analysis of 2,323 American Indian adults, faster epigenetic aging (including DunedinPACE) helped explain part of the link between long-term arsenic exposure and both cardiovascular disease and death from any cause.
This is one of the strongest signals in the evidence. In a replication study across three cohorts totaling 5,702 adults, people with faster DunedinPACE had smaller total brain volume, thinner cortex (the outer brain layer that handles thinking), and more white-matter microlesions (small areas of damage in the brain's wiring).
In a study of 2,913 older adults, faster DunedinPACE predicted future dementia. In the Framingham Heart Study Offspring Cohort of 2,296 participants, a faster pace of aging was linked to preclinical cognitive decline and explained roughly a quarter of dementia risk. A separate analysis of 2,366 older women found that faster DunedinPACE was linked to faster increases in plasma Alzheimer's biomarkers over time.
In a Swedish twin study of 524 people followed from midlife to old age, changes in DunedinPACE preceded changes in the frailty index. The pace of aging clock moved first, then physical decline followed. This makes it useful as an early warning system rather than a confirmation of damage already done.
In a separate study of 560 older Australians, higher DunedinPACE predicted both increasing frailty scores year over year and the development of new frailty over time.
In a national US cross-sectional study of 2,529 adults, a faster pace of biological aging was positively linked to cancer risk, with physical activity reducing this association, especially in less active people and those over 65.
Cancer treatment itself appears to accelerate biological aging. A study of 417 women found that breast cancer diagnosis and treatment, especially radiation, accelerated DunedinPACE. In 2,939 childhood cancer survivors, exposure to genotoxic treatments accelerated biological age, helping explain elevated cardiometabolic and cardiovascular disease risk decades later.
A study of 1,087 twins found higher DunedinPACE was associated with greater risk of fractures and osteoporosis. In 118 adults with chronic low back pain, accelerated epigenetic aging was common and tracked with greater pain severity and disability. Five case-control studies covering 3,565 people found that schizophrenia was linked to accelerated DunedinPACE by midlife, not explained by smoking or medication.
DunedinPACE responds to your environment, not just your DNA blueprint. Studies link faster pace to non-essential metal exposure, especially cadmium, arsenic, and tungsten, while higher selenium, zinc, and molybdenum link to slower pace. A 1,762-person study found that adverse childhood experiences were associated with accelerated epigenetic aging in midlife. In a 2,309-veteran study, female and non-Hispanic Black veterans showed faster DunedinPACE even after extensive adjustment, pointing to social and environmental influences.
This matters because it means the number is not fixed. Your pace of aging reflects ongoing biology that responds to what you do, eat, breathe, and experience.
DunedinPACE is dimensionless, scaled around 1.0 to represent average aging speed. The values come from research cohorts, not clinical guideline bodies, and your specific lab may use slightly different reference cohorts. Treat these as orientation, not as hard cutpoints.
These ranges come from the original Dunedin development cohort and validation studies in mostly White adults of European descent. Cross-population validity is still being established, and your lab may report somewhat different numbers.
| Tier | Approximate Score | What It Suggests |
|---|---|---|
| Slower than average | Below 1.0 | Aging more slowly than the cohort average; generally favorable cardiometabolic and antioxidant profile |
| Average | Around 1.0 | Aging at roughly the cohort average rate |
| Faster than average | Above 1.0 | Aging faster than the cohort average; associated with higher risk of frailty, dementia, hypertension, and cardiometabolic disease |
Compare your results within the same lab over time for the most meaningful trend. Different labs and different array versions can produce slightly different absolute numbers.
DunedinPACE has high test-retest reliability, but a single number is most useful as a baseline. The point of this test is to see your trajectory. A study of 899 generally healthy older adults followed over 2 years found that current epigenetic measures are stable and highly predictable in the short term, with limited sensitivity to short-term change. That means you should expect modest movement reading-to-reading and focus on the longer arc.
A reasonable cadence: get a baseline, retest in 6 to 12 months if you're making meaningful lifestyle or treatment changes, then at least annually. Watching the line over years is more informative than fixating on whether your number is 0.95 or 1.05 today.
A faster pace of aging is a signal, not a diagnosis. The next step is to look at the systems most likely to be driving it. Consider pairing your DunedinPACE with standard markers of cardiometabolic health (lipid panel, hs-CRP for inflammation, fasting insulin and HbA1c for blood sugar control), kidney function (creatinine, cystatin C), and inflammation.
If your DunedinPACE is elevated alongside abnormal cardiometabolic or inflammatory markers, that pattern is worth investigating with your physician, ideally one who works in preventive or longevity-focused care. If the rest of your labs look fine but your pace is high, that's still useful information: it points to systemic biology that conventional panels are not yet flagging, and it gives you a reason to be more aggressive about exercise, sleep, environmental exposures, and diet quality before something shows up on a standard test.
Cell composition matters. Different blood cell types carry different DunedinPACE values, with T cells appearing biologically younger and monocytes older. Variation in the proportion of cell types in your sample can shift your reading.
Recent intense exercise is a known general preanalytical confounder for many blood biomarkers. While direct evidence on short-term DunedinPACE shifts is limited, it's reasonable to avoid heavy exertion in the 24 to 48 hours before your draw.
Validation has been concentrated in mostly European-descent cohorts. If you are from an underrepresented population, the relative interpretation of your number may be less precise, although the directional signal (faster vs slower) still applies.
Evidence-backed interventions that affect your DunedinPACE level
DunedinPACE is best interpreted alongside these tests.