My Healthspan Scorecard™

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SUFFICIENCY MARKERS (NOT SCORED)

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Tools

CONCEPT2 ERG · HAGERMAN REGRESSION

VO₂ Max Calculator

Estimate your maximal oxygen uptake (ml/kg/min) from an all-out 2,000 m rowing ergometer test. Based on Dr. Fritz Hagerman's validated regression equations derived from thousands of gas-exchange lab measurements at Ohio University.

TEST INPUTS

Biological Sex

Body Weight

RECOMMENDED DRAG FACTOR FOR YOUR 2K TEST

Training Background

Trained = competitive rower with structured aerobic base and rowing-specific conditioning.
General Fitness = recreational exerciser, gym-goer, or new to rowing.

2,000 m Time (Max Effort)

Enter the time from an all-out 2K piece on the Concept2 erg.

min

sec

tenth

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ML / KG / MIN

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Absolute VO₂ Max

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Relative VO₂ Max

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2K Avg Watts

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2K Avg Pace /500m

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Equation Used

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2K TEST PROTOCOL

Set drag factor via the PM5 menu (More Options → Display Drag Factor). Row a few strokes and adjust the damper lever until you hit your target. General guidance: 110–130 for most adults.

Warm up 8–10 min at light pressure (18–20 spm), then 3 × 10-stroke builds to race pace with 1 min easy between. Rest 3–5 min.

Set the monitor to 2,000 m (Select Workout → Standard → 2000m). Strap on a chest heart-rate monitor.

Row an all-out effort. Target even or slight negative splits. This must be a true maximal effort — the formula assumes you reach VO₂ max during the piece.

Record your finish time and enter it above. Cool down 5–10 min at light pressure.

Clinical Note: This is an estimate based on the Hagerman regression equations (Concept2 / Ohio University) derived from gas-exchange spirometry of 3,000+ subjects. Accuracy depends on true maximal effort, rowing technique proficiency, and altitude. Error margin is approximately ±5–10%. Gold-standard measurement requires indirect calorimetry (metabolic cart) during graded exercise to exhaustion. Enter your result into the Healthspan Scorecard VO₂ Max field above to see your age/sex tier classification.

INSULIN RESISTANCE INDEX · MATTHEWS ET AL.

HOMA-IR Calculator

Quantify your degree of insulin resistance using the Homeostatic Model Assessment. HOMA-IR reveals how hard your pancreas is working to maintain normal blood glucose — the earliest detectable signal of metabolic dysfunction.

FASTING BLOOD VALUES

Fasting Insulin

Drawn after 10–12 hour overnight fast. Units: μIU/mL (most North American labs).

Fasting Glucose

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HOMA-IR

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HOMA-IR Score

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Fasting Insulin

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Fasting Glucose

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Classification

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💎 < 1.0 — Insulin Sensitive

🟢 1.0–1.4 — Optimal

🏅 1.5–1.9 — Normal

🟡 2.0–2.9 — Early Resistance

🟠 ≥ 3.0 — Significant Resistance

Clinical Note: HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) was developed by Matthews et al. in 1985 (Diabetologia, 28:412–419; cited 25,000+ times) and validated against the euglycemic hyperinsulinemic clamp — the gold standard for measuring insulin resistance in vivo. The formula is: fasting insulin (μIU/mL) × fasting glucose (mg/dL) / 405. Values below 1.0 indicate high insulin sensitivity. Values of 2.0–2.9 suggest early insulin resistance, often preceding changes in HbA1c or fasting glucose by 5–10 years (Stern et al., Diabetes, 2002). Values ≥ 3.0 correlate strongly with metabolic syndrome criteria (Ascaso et al., Diabetes Care, 2003). Requires a 10–12 hour overnight fast for valid results. This calculator does not replace clinical interpretation.

Foundational Frameworks

The conceptual scaffolding the dashboard is built on.

Hallmarks of Aging. López-Otín, Blasco, Partridge, Serrano, Kroemer. Cell 153 (2013) 1194–1217. The original 9-hallmark framework.
Hallmarks of Aging: An Expanding Universe. López-Otín et al., Cell 186 (2023) 243–278. The expanded 12-hallmark framework: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem-cell exhaustion, altered intercellular communication, chronic inflammation, dysbiosis.
Hallmarks of Health. López-Otín & Kroemer, Cell 184 (2021) 33–63. The companion framework: spatial compartmentalization, maintenance of homeostasis, adequate stress response.
Pace of Aging. Belsky et al., PNAS 112 (2015) E4104. The original 18-biomarker pace-of-aging measure from the Dunedin Longitudinal Study.
DunedinPACE. Belsky et al., eLife 11 (2022) e73420. DNA-methylation biomarker of pace of aging; predicts morbidity, disability, mortality independent of GrimAge.
Nonlinear molecular waves of aging. Shen, Snyder et al., Nature Aging 4 (2024) 1619–1634. Multi-omics evidence of nonlinear biomolecular shifts at ages ~44 and ~60.

Marker Sources & Cutoffs

Evidence base for the tier thresholds used in scoring. Age- and sex-adjusted where applicable. Some markers are practitioner-set goals or test-vendor-specific scales, noted as such.

VO₂ Max

Age- and sex-adjusted percentile cutoffs from ACSM & Cooper Institute reference data. Mortality association: Mandsager et al., JAMA Network Open 1 (2018) e183605 — Elite cardiorespiratory fitness predicts ~80% lower all-cause mortality vs Below tier. Telomere correlation: Ryall & Denham, J Gerontol A 80 (2025) glaf068.

ApoB

Cutoffs aligned with European Atherosclerosis Society 2020 consensus. Mendelian randomization (Ference et al., JAMA 318 (2017) 947) supports ApoB as superior to LDL-C for atherosclerotic risk.

Blood Pressure (Systolic)

2017 ACC/AHA guideline thresholds. SPRINT trial (NEJM 373 (2015) 2103) supports targeting <120 mmHg in high-risk adults.

Fasting Insulin

Optimal range 2–6 µIU/mL per Kraft, Crofts, et al. work on hyperinsulinemia. Standard "normal" labs (<25) underdetect early metabolic dysfunction.

Grip Strength / BW

Sex-adjusted ratios anchored to NHANES and Fess hand-strength reference data. Mortality predictor: Leong et al., Lancet 386 (2015) 266 — every 5 kg drop in grip strength = 16% increase in all-cause mortality.

DunedinPACE

Cutoffs anchored to Dunedin cohort distribution: pace 1.0 = population mean, SD ≈ 0.08. Elite (<0.85) ≈ −1.9 SD (top ~3% of population). Belsky et al., eLife 11 (2022) e73420.

hsCRP

Age-adjusted. Base AHA/CDC cutoffs (<1 low risk, 1–3 average, >3 high). Older adults run ~30–50% higher at baseline; cutoffs adjusted accordingly. Elite cutoff tightened from prior <0.3 to <0.5–0.8 (age-tiered) — defensible physiological floor; lower values are not a recognized clinical optimum.

HbA1c

ADA standard cutoffs. Bachmann et al. (JAMA 311 (2014) 587) on subclinical glycation. <5.0% = ideal metabolic flexibility.

Resting Heart Rate

Cooper Clinic longitudinal data. Aune et al. Nutr Metab Cardiovasc Dis 27 (2017) 504 — RHR >80 bpm = 45% higher all-cause mortality vs <60 bpm.

Triglycerides

NCEP ATP III plus Reaven on TG/HDL ratio. Optimal <70 mg/dL aligns with metabolic-syndrome-free ranges.

Mitochondrial Age Δ

Practitioner-extrapolated metric. In-house formula cross-referencing Krebs-cycle metabolite ratios and fatty-acid oxidation efficiency, scaled to age-equivalent estimate, then subtracted from chronological age. Conceptually: Δ < −5 yrs (mitochondria functioning ~5+ years younger) is Elite; Δ > +5 yrs warrants attention. Not a validated clinical biomarker; useful for tracking response to mitochondrial interventions (Urolithin A, NAD precursors, exercise).

DEXA Body Fat

Sex-adjusted athletic/healthy/overweight thresholds from American Council on Exercise standards.

Cystatin-C

Age-adjusted. Standard adult range 0.5–1.0 mg/L. Kidney function declines ~1%/yr after age 30; cutoffs adjusted to avoid penalizing age-related drift. Ferguson et al. Am J Kidney Dis 65 (2015) 113.

Omega-3 Index

Harris & von Schacky framework. Target >8% (Elite >9%) = ~30% reduction in cardiac sudden death risk vs <4%.

AA:EPA Ratio

Inflammatory balance marker. Sears framework, Ferrucci et al. J Clin Endo 91 (2006) 439 on systemic inflammation correlation.

Sitting-Rising Test

Brito et al. Eur J Prev Cardiol 21 (2014) 892. Score <8/10 = 5–6× higher all-cause mortality vs perfect 10.

N3 Deep Sleep

Age-adjusted. N3 declines ~50% from young adulthood to 60s. Adjusted cutoffs reflect biological norms. Mander et al. Neuron 94 (2017) 19.

Homocysteine

Age-adjusted. Standard cutoffs (<10 desirable). Elite cutoff tightened from prior <5 (aggressive, clinically unestablished) to <7 — defensible physiological optimum supported by McCully and B-vitamin literature.

Awakening HRV

Age-adjusted. RMSSD declines ~3% per decade after age 30. Young-adult cutoffs unfair to older patients. Umetani et al. JACC 31 (1998) 593 baseline norms.

NLR (Neutrophil:Lymphocyte)

Inflammatory aging marker. Forget et al. BMC Res Notes 10 (2017) 12. Optimal <1.5; elevated >3 = elevated systemic inflammation.

Sleep Efficiency

AASM standards. >85% = clinically normal; >90% = excellent; >93% = elite consolidated sleep.

Lipoprotein(a)

Cardiovascular risk independent of LDL. Kamstrup et al. JAMA 301 (2009) 2331 — Lp(a) >50 mg/dL = ~2× CVD risk.

Peak Expiratory Flow

Cooper et al. on pulmonary function as longevity predictor. Pulmonary function was included in original Dunedin Pace of Aging biomarker panel.

Orthostatic HR Δ

Autonomic resilience proxy. Fedorowski et al. J Hypertens 28 (2010) 551 on orthostatic intolerance and CV risk.

Cortisol:DHEA-S Ratio

Practitioner-set; assay-dependent. Higher ratios suggest catabolic stress dominance. Optimal range varies by lab; cutoffs here represent practitioner-set targets, not consensus clinical thresholds.

Total Testosterone (M) / DHEA-S (F)

Age- and sex-adjusted reference data from Endocrine Society guidelines and Mayo Clinic Labs.

Sleep HRV (7-night)

Age-adjusted. Same biological pattern as awakening HRV; cutoffs scaled accordingly.

Iso Split Squat Hold

Functional strength endurance test. Age- and sex-adjusted seconds thresholds based on practitioner field-test norms; predictive of fall risk and lower-extremity sarcopenia.

Morning Glucose

Bergman & Reaven on continuous glucose insights. <85 mg/dL = optimal metabolic flexibility; >100 = pre-diabetic territory.

Gut Microbiome Index

Test-vendor scale. Calibrated to Zinzino Gut Health Test (metabolomic IPA, Tryptophan, IPA:KYN ratio composite). Other microbiome tests (Viome, ZOE, BiomeFx) use different scales — re-calibrate cutoffs if using a different vendor. Underlying biology: tryptophan-IPA pathway as marker of gut-bacterial functional output and metabolic flexibility.

Scoring Methodology

How the composite is calculated and what it represents.

Linear tier ladder. Below = 5 pts, Average = 10, Good = 15, Excellent = 20, Elite = 25. Maximum score = 30 markers × 25 = 750. Linear weighting is gamification-friendly but does not perfectly mirror mortality hazard ratios — for some markers (ApoB, hsCRP) actual risk reduction scales nonlinearly.
Composite-visualizer gate. The Composite Pace, Regenerative Divergence chart, Healthspan Extension, and Healthspan Score all require a minimum of 5 filled markers spanning at least 3 of the 8 biological domains (cardiovascular, metabolic, inflammatory, aerobic fitness, strength & function, hormonal, sleep & recovery, cellular & detox). Below this threshold, single-marker outliers would drive a meaningless "pace of aging" output — for example, an Elite hsCRP alone would project a Tier 7 Outlier score regardless of cardiovascular fitness, sleep, strength, or DunedinPACE. The gate exists to ensure the Composite represents genuine multi-system synthesis rather than statistical noise from a narrow input. Individual marker tiers continue to display normally below the gate.
Composite Pace formula. avgScore = totalPoints / (filledMarkers × 25). Pace = 1.0 + (0.60 − avgScore) × 0.75, clamped to 0.70–1.40. avgScore of 0.6 (all "Good") = pace 1.0; avgScore of 1.0 (all Elite) = pace 0.70.
Healthspan Score. Sum of points achieved on filled markers, with the denominator adjusting to "max possible given how many markers you've filled" (e.g. 16 filled markers → max 400). Tier label computed against percent-of-max, not absolute score, so partial fills are fairly tier-classified.
Regenerative Divergence chart. Visualizes the pace number as a trajectory diverging from a calendar baseline (slope = pace − 1.0). The interactive scrub tooltip shows the strict, conservative bio-age delta at any future year using the published-literature linear formula: Δ = (1.0 − pace) × yearsHeld. At pace 0.80 over 20 years: +4.0 bio-yr younger. This is the measurement layer — direct interpretation of pace as a rate multiplier, no amplification.
Healthspan Extension card. Translates the bio-age delta into lived-experience terms by applying a 1.4× morbidity-compression multiplier: healthy years = bio-age delta × 1.4. The multiplier reflects the well-documented phenomenon that slow-aging cohorts experience compressed late-life morbidity periods — each year of bio-age separation yields roughly 1.4 healthy functional years gained because the morbid phase shrinks alongside lifespan extension. The 1.4× value is a defensible mid-range estimate; published studies show morbidity compression amplification ranging 1.2× to 1.6× depending on cohort and definition. This card is the meaning layer — what the bio-age delta becomes in actual lived experience.
Why two layers? The chart's strict bio-age math is the number that survives clinical scrutiny. The card's adjusted number is what motivates behavior change. Each is honest at its altitude, neither overclaims, and the two together tell the full story.
Three Biggest Leverage Points. The three filled markers with the lowest tier scores are surfaced as the user's highest-leverage targets. When 2+ of the bottom three share a body system (e.g. all sleep markers), a "pattern detected" callout names the cluster — turning what looks like three separate problems into a single system to focus on. Pure read of the existing tier data; no new math. Note: The dashboard surfaces individual markers rather than averaged system tiers, because system-level averaging can mask isolated high-risk values (e.g. an alarming Lp(a) reading offset by good apoB and triglycerides). Surfacing the specific worst markers preserves the clinical signal that practitioner review depends on.
Snapshot tracking. Saves a timestamped snapshot of all current marker values to local storage (capped at the most recent 12 snapshots). Future snapshots produce small inline sparklines next to each marker showing trend direction across visits. Green = improving, gray = flat, burnt = trending worse. Click any sparkline to open a history popover showing the exact value, date, and tier label for every recorded data point. All snapshot data is local-only and never transmitted anywhere.

Rejuvenation Tier Framework

A public-facing tier indicator that translates the Composite Pace into a meaningful position relative to verified longevity practitioners. Anchored to: published DunedinPACE distribution data (mean 1.00, SD ~0.08), the Rejuvenation Olympics leaderboard (rejuvenationolympics.com), and verified self-reports from documented practitioners.

Tier 0 · Accelerated Aging · Pace ≥ 1.10 · ~15% of the population. Aging biology is moving faster than calendar time. Highest-leverage moment to change direction.
Tier 1 · Calendar-Pace Aging · Pace 1.00–1.10 · ~50% of the population. Aging at or near population baseline. No rejuvenation underway.
Tier 2 · Aware · Pace 0.95–1.00 · ~20% of the population. Health-conscious lifestyle producing mild slowing.
Tier 3 · Engaged · Pace 0.90–0.95 · ~8% of the population. Consistent biohacker territory — daily protocol, supplementation, training.
Tier 4 · Optimized · Pace 0.85–0.90 · ~3% of the population. MD oversight protocol commitment — bloodwork, hormone optimization, structured exercise.
Tier 5 · Elite · Pace 0.78–0.85 · ~0.5% of the population. Rare territory. Multi-year protocol with comprehensive testing and intervention.
Tier 6 · Exceptional · Pace 0.65–0.78 · ~0.05% of the population. Rejuvenation Olympics top-25 territory. Examples: Dave Pascoe (best 0.66, ~$15K/yr protocol), Julie Gibson Clark (low-cost protocol).
Tier 7 · Outlier · Pace < 0.65 · <0.005% of the population. Top-of-leaderboard territory. Currently exemplified primarily by Bryan Johnson (best 0.48, ~$2M/yr protocol).

Tiers are descriptive, not normative. A Tier 3 result is meaningful and uncommon — about 8% of the population. The framework exists to ground the user's pace in real-world reference points rather than a vague "lower is better" frame. Note that published pace data typically reflects acute (peak intervention) measurement; sustained 30-year average paces are likely 0.05–0.10 closer to baseline due to life events, regression, and protocol adherence variation.

Limitations & Honest Disclosures

This is a practitioner tool, not a validated clinical risk model. Not FDA-approved.
Cutoffs are anchored to literature where available, practitioner-set where the science is contested or assay-dependent (cortisol:DHEA, mito age Δ, microbiome index).
Functional markers (VO₂, grip, split squat, PEF) reflect cumulative cellular activity and respond to training in 4–6 weeks. Cellular markers (DunedinPACE, hsCRP) reflect more current state and shift on 6–12 month timescales. Both belong in the composite; they capture different time-windows of the same underlying biology.
The composite is a multi-timescale resilience score, not a pure pace-of-aging measurement. Use DunedinPACE alone if you want the strictest cellular pace metric.
Sufficiency markers (Vit D, thyroid, ferritin) are evaluated for in-range vs out-of-range, not tier-scored, since outside-range values represent insufficiency rather than rate-of-aging signal.

All data persists locally to your device only. Nothing is transmitted to any server.