Your driver's license has one number. Your biology has another. Enter 9 standard lab markers below to calculate your Phenotypic Age, the peer-reviewed Levine 2018 biomarker of aging used in longevity research and validated against all-cause mortality.
The Levine Phenotypic Age formula calculates biological age from 9 standard lab markers: albumin, creatinine, glucose, CRP, lymphocyte %, MCV, RDW, alkaline phosphatase, and white blood cell count. A phenotypic age higher than chronological predicts increased all-cause mortality and disease risk independently of age. Lower biological age tracks with cardiometabolic and inflammatory health.
Source: Levine ME et al. Aging 2018 · UCLA Phenotypic Age formulaPhenotypic Age combines 9 routine biomarkers into one number that captures organ-level aging, inflammation, metabolic dysfunction, and immune resilience. Move the markers, you move the number.
Reflects protein status, liver synthesis, and chronic disease burden. Low albumin is one of the strongest mortality predictors in older adults.
A breakdown product of muscle. Both very high and very low are risk markers, high suggests kidney decline, low suggests sarcopenia.
Fasting glucose above ~100 mg/dL signals insulin resistance, the core engine of metabolic aging, cardiovascular disease, and cognitive decline.
"Inflammaging", low-grade chronic inflammation, is a root cause of nearly every age-related disease. CRP is the cheapest way to measure it.
Lower lymphocyte fractions correlate with immune senescence. Falling lymphocyte% with age is a hallmark of T-cell exhaustion.
Mean cell volume reflects B12, folate status, and bone marrow function. Drift in either direction is a quiet but reliable aging marker.
Red cell distribution width is one of the single most powerful biomarkers of mortality across all causes. High RDW = systemic stress.
Alkaline phosphatase rises with bone resorption, liver stress, and certain hormonal shifts. High-normal ALP is a subtle aging tell.
Chronically elevated white cells signal smoldering inflammation. Persistently high-normal WBC is associated with shorter lifespan in large cohort studies.
Phenotypic Age is dynamic, it responds to what you measure and change. Whether any protocol is appropriate for you is decided by a U.S.-licensed physician after reviewing your labs, history, and goals.
Take the 60-second quiz. A U.S.-licensed physician reviews your information and builds a plan around your goals. Membership includes the consultation, ongoing medical care, and a muscle-preservation guide when a weight-loss medication is prescribed.
Find my protocol Test then treatThis score runs on 9 lab markers. A comprehensive panel adds testosterone, free T, SHBG, lipids, and HbA1c so a clinician can see exactly which markers are moving your number, then track them over time.
See lab panelsPhenotypic age summarizes nine markers into one number. These tools let you peel apart the inputs, hormones, metabolism, and see where to intervene.
Hand-picked guides on biological age, longevity biomarkers, inflammation, and the science of aging, from our research library.
Your chronological age is the time since you were born. Your biological age is how much aging your body has actually accumulated, measured by molecular, cellular, and physiological markers that predict mortality, disease risk, and functional decline.
Two 50-year-olds can have biological ages of 38 and 62 depending on lifestyle, hormonal status, metabolic health, and inflammatory burden. The gap (sometimes called "Age Acceleration") is the actionable part, and it's modifiable.
Developed by Dr. Morgan Levine and colleagues at Yale, Phenotypic Age weighs 9 routine clinical biomarkers plus chronological age in a Gompertz mortality model. The output predicts all-cause mortality better than chronological age alone. Compared to expensive epigenetic clocks (Horvath, GrimAge, DunedinPACE), Phenotypic Age uses tests you can get on any standard CMP + CBC + CRP panel, making it the most practical longevity biomarker available today.
Excellent, you're aging more slowly than the population average. Keep doing what you're doing, recheck every 6-12 months, and stay alert to drift in any single marker (rising CRP or glucose are the early warning signs).
Don't panic, this is the most common result, and it's the most modifiable. The first step is a comprehensive lab panel (testosterone, free T, SHBG, lipids, HbA1c added to the 9 markers above) so a clinician can identify the specific drivers. From there, a physician-guided plan and targeted lifestyle changes can compress the gap measurably within 3-6 months.
The Levine Phenotypic Age formula is validated in NHANES III and IV (the U.S. national health survey) cohorts and predicts 10-year mortality with similar accuracy to the most expensive epigenetic clocks. It is the most widely cited and reproduced biological-age metric in peer-reviewed literature.
Yes, published studies have shown reductions of 1-3 biological years within 8-24 weeks of interventions including caloric restriction, omega-3 supplementation, and physician-guided medical optimization. The faster you measure → intervene → re-measure, the faster you compound progress.
Every 3-6 months when actively optimizing, then annually once stable. Most men see measurable shifts in CRP, glucose, and albumin within 8 weeks of starting a structured protocol.
The markers this score runs on, glucose, hs-CRP, albumin, and the rest, all respond to change, and published studies show the gap can compress within months. Whether any protocol is appropriate for you is decided by a U.S.-licensed physician after reviewing your labs, history, and goals.
This calculator uses the Phenotypic Age algorithm, a peer-reviewed biological-age measure built from nine routine blood markers. It is an educational estimate and does not diagnose any condition. It is not medical advice.
How this tool calculates
Biological age is estimated using published clinical-biomarker age-adjustment formulas. The methodology draws from the PhenoAge framework (Levine et al.) and supplemental published biological-age scoring methods. This is an educational estimate based on clinical biomarkers; it is not a DNA methylation test or a diagnostic instrument.
Peer-reviewed sources
Important. This tool is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment. The tool does not prescribe medication, recommend specific dosing, or substitute for clinical evaluation. Compounded medications referenced anywhere on this site are not FDA-approved; the FDA does not verify the safety, effectiveness, or quality of compounded drugs. Treatment decisions are made only by a licensed U.S. physician after individual patient evaluation.
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