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Methodology

Published study estimates are cited to their sources: studies that follow people over time, trials, or reviews that combine studies. The calculator's curves also contain constructed points, flat regions and assumptions. Values between published points are model values, not findings reported by a study. Below is how we grade evidence, how the model works, then the bibliography grouped by domain.

Page last reviewed 2026-10-08. Changes to the scoring model are dated in the changelog. Weights are below.

Want to see how everyday habits feed these markers? The habit map traces each connection to its studies.

Four walks

The first tranche. Past the bends, more of the same buys less. These are not a plan and not a save.

Walk to the step bend

Ding et al. 2025, 14 prospective cohorts, all-cause mortality: about 7,000 steps a day versus 2,000, point estimate HR 0.53. That comparison is not the on-screen step target. Paluch et al. 2022, 15 cohorts, all-cause mortality: the displayed target is 8,000 steps a day under age 60 and 6,000 from age 60. Age only selects that target. It does not change the step curve.

Two short lift days

None is the reference. Two days a week, counted here as 30 minutes a day, is where the line flattens. The row can only raise the score, and it overlaps steps and VO₂ max. Momma 2022.

Fiber floor from food

The displayed fiber target is IOM/NASEM adequate intake: a gram floor of 38, 30, 25, or 21 g by sex and age. Age and sex only select that floor. They do not change the fiber hazard curve, which is absolute grams per day from Reynolds et al. 2019, all-cause mortality. Reynolds’s categorical peak at 25–29 g is a different number.

Sleep window around seven hours

Both sides of about seven hours are associated with higher all-cause mortality. The long side is steeper. Yin 2017.

What your score means

Your score compares your eight numbers with a typical 45-year-old's. 50 means you match them on all eight. Above 50, your numbers look more like those of people with lower death rates in large studies; below 50, more like those with higher death rates. It's a comparison, not a prediction.

Not yet in the score: aerobic minutes, sitting time.

Because almost nobody is typical on all eight, a 50 already beats almost 2 in 3 people.

How much each metric counts

The eight scored metrics, each with its study and grade, are on The 8 metrics. Markers that do not move your number are on More markers.

The composite is a weighted index of associations from large observational studies. It has never been validated as a combined clinical predictor — no cohort has measured all eight markers on the same people and tracked what happened to them — and association in these studies is not proof that changing a marker changes your risk by the same amount.

Physical Capacity · 44% of the composite

Cardiorespiratory fitness, movement, & strength training

VO2 Max18% of score

10 cited sources — see the bibliography below

Daily Steps13% of score

7 cited sources — see the bibliography below

Resting Heart Rate8% of score

8 cited sources — see the bibliography below

Strength Training5% of score

10 cited sources — see the bibliography below

Cardiometabolic · 34% of the composite

Vascular & glycemic control

Blood Pressure18% of score

15 cited sources — see the bibliography below

HbA1c15% of score

8 cited sources — see the bibliography below

Lifestyle · 22% of the composite

Sleep & nutrition

Sleep Duration13% of score

6 cited sources — see the bibliography below

Dietary Fiber9% of score

6 cited sources — see the bibliography below

What happens if you leave a metric blank

Once you start entering values, any of the eight you leave untouched counts as typical (the median reference) in your score, so it neither helps nor hurts. The calculator still shows a placeholder value on that row, marked as an estimate, but the placeholder does not feed your score. A blank metric keeps its normal share of the composite; it is not dropped, and the other seven are not reweighted to cover for it. A score built from a few entered markers is a real but partial picture, not a confidence-adjusted estimate. Enter all eight for the most complete score.

How we grade evidence

Each chip grades one claim on one endpoint, not a marker as a whole. A marker can carry a B headline on home and A facts on its metric page; those A facts are real and they are not the home number.

  1. Grade ARCT or meta-analysis of RCTs on that endpoint

    Someone ran the experiment on that outcome. A trial that finds nothing is still A — the letter is how hard it was tested, not whether the result was flattering.

  2. Grade Bprospective cohort with dose-response, or Mendelian randomization

    Large groups followed for years — not trials. Dose-response in a cohort, or a genetic natural experiment.

  3. Grade Ccohort association only

    The numbers moved together in a group of people. That is not the same as one causing the other.

  4. Grade Dmechanistic reasoning only

    A plausible mechanism. No human outcome study for this claim.

  5. Grade Xno evidence for the claimed endpoint

    We looked. This protocol has not been tested against that outcome.

Some cards show METHOD instead of a letter — method notes, not claims.

Every Grade A fact on this site is a randomized trial. Most of them did not lower all-cause deaths, and none of the eight scores is built on one. What the trials found.

Per-metric hazard ratios

For measures on a sliding scale, the curve runs between anchor numbers taken from the studies, and the shape between those anchors is our own. It is smooth, so risk changes gradually instead of jumping at cutoffs.

Domain aggregation

Technical notes

Metrics are grouped into three domains; each collapses to a single number via a weighted geometric mean, then the three combine the same way. Weights sum to 1 at both levels, so this is a weighted average of log hazard ratios — one metric moves the result by exactly its own weight share, and nothing is double-counted.

Why the composite is an index, not a risk estimate

Because the weights average rather than accumulate, the composite ranks profiles against the population median (1.00) but does not compound risk across markers. Estimating combined risk honestly would need a jointly-fitted multivariable model, and no cohort has measured all 8 markers on the same people. So the composite is published as an index and is never expressed as a percentage change in risk. Per-metric hazard ratios are different: each is a single-marker claim backed by a single-marker study, which is exactly what the cited papers support.

Score & comparison range

The score stays on its fixed midlife scale: 50 matches the same reference profile on all eight markers at every age. Your modeled ranking compares with the same sex in ages 20-29, 30-39, 40-49, 50-59, 60-69 or 70+. Ages 18-19 use a newly pooled same-sex adults 20+ comparison. Rankings are ranges, rounded outward in five-point steps.

How the citations are checked

Every metric is backed by at least five primary studies, listed in full below. Each quoted number is checked against the sentence in the paper it comes from. If we cannot find that sentence, the number does not ship.

What it is not

This is a directional, educational estimate — not a validated clinical risk model or medical advice.

What the eight do not cover

The scored eight are not a lifestyle score. Most of them are readouts — numbers that describe accumulated physiology — not the exposures mortality studies rank when they ask which actions account for most deaths. A person can smoke, drink heavily, eat poorly, and carry high body weight and still look typical or better on all eight. That is a scope choice, not a finding that those exposures do not matter.

Most of the eight are readouts

VO2 max, resting heart rate, and HbA1c describe what the body is doing now. Steps and fiber are intakes, and strength training is a count of days you did it. Sleep is duration, not regularity or clock time. Blood pressure is the closest exception: it is both a reading and close to the pathway the Global Burden of Disease ranks. That ranking is of disease burden (years lost to death and disability), not a deaths table, and it is a population share, not your personal risk.

Smoking, alcohol, diet quality, and body weight are not in the score

They have no input. Joint lifestyle-score cohorts are built from never smoking, weight in a healthy range, activity, moderate alcohol, and diet quality — the usual core in this literature. Physical activity here is scored only as VO2 max, steps and days of strength training, not as minutes of aerobic exercise. Smoking is the largest single gap against both that core and the GBD ranking; it was considered and declined as a product input. The epidemiology is not in dispute.

GBD 2021 Risk Factors Collaborators (2024) — Lancet
Global burden and strength of evidence for 88 risk factors in 204 countries and 811 subnational locations, 1990–2021
Population-level ranking of modifiable risk. Headline list is DALYs, not deaths. High systolic pressure, smoking, and high fasting glucose sit in the top tier. Death-count tables from secondary write-ups are not used here.
View source
Li Y, Pan A, Wang DD, et al. (2018) — Circulation
Impact of Healthy Lifestyle Factors on Life Expectancies in the US Population
Nurses' Health Study and Health Professionals Follow-up Study. Five-factor lifestyle score: never smoking, BMI 18.5-24.9, activity, moderate alcohol, diet quality. Cited for the factor set, not as a MarkerScore output.
View source

The markers outside the eight are on More markers. The bibliography below covers the eight scored metrics.

Physical Capacity sources

VO2 Max

Milanović Z, Sporiš G, Weston M. (2015) — Sports Medicine
Effectiveness of High-Intensity Interval Training (HIT) and Continuous Endurance Training for VO2max Improvements: A Systematic Review and Meta-Analysis of Controlled Trials
Fitness intervention endpoint, not mortality. 28 controlled trials, 723 healthy adults aged 18–45, training duration at least 2 weeks. Endurance training improved VO2max by 4.9 mL/kg/min and HIT by 5.5 mL/kg/min, each versus no-exercise controls. Not an all-cause mortality estimate or a calculator curve anchor.
View source
Singh et al. (2024) — Journal of Sport and Health Science
Comparison of objectively measured and estimated cardiorespiratory fitness to predict all-cause and cardiovascular disease mortality in adults: A systematic review and meta-analysis of 42 studies representing 35 cohorts and 3.8 million observations
Supporting source (page meta, not the anchor point table). 42 studies / 35 cohorts / 3,813,484 observations (81% male), 362,771 all-cause mortality deaths. Per 1-MET (3.5 mL/kg/min) all-cause mortality RR 0.86 (0.83–0.88), I² 97.66%. Objectively measured 0.90; maximal exercise-estimated 0.85; submaximal 0.94; non-exercise-estimated 0.85 (0.80–0.89) — no statistically significant differences. Non-exercise = prediction equations (age/sex/BMI/PA/RHR), not a consumer watch. Single baseline CRF; authors could not examine whether improved CRF reduced death. The calculator’s smooth curve is constructed; HR=1.0 at 38 M / 31 F is an ACSM midpoint, not Singh.
View source
Lang et al. (2024) — British Journal of Sports Medicine
Cardiorespiratory fitness is a strong and consistent predictor of morbidity and mortality among adults: an overview of meta-analyses representing over 20.9 million observations from 199 unique cohort studies
Umbrella of 26 SRs / 199 cohorts / 20.9 million observations — not a new pooling. Headline high vs low all-cause mortality HR 0.47 (0.39–0.56) is Han 2022 extracted in Fig 2. Per-MET 11–17% is Laukkanen 0.89 through Qiu eCRF 0.83. GRADE very low-to-moderate (male-heavy). No absolute mL/kg/min all-cause mortality target.
View source
Mandsager et al. (2018) — JAMA Network Open
Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing
Competing number, wrong construct. Cleveland Clinic referred treadmill testers, n=122,007, 13,637 deaths. Age/sex percentile bins of peak estimated METs, not absolute mL/kg/min. Low vs elite adjusted all-cause mortality HR 5.04 (4.10–6.20). “No observed upper limit of benefit” — not a reason to print 5.04 on this curve. Curve low end is 1.6.
View source
Kodama et al. (2009) — JAMA
Cardiorespiratory fitness as a quantitative predictor of all-cause mortality and cardiovascular events in healthy men and women: a meta-analysis
33 studies; all-cause mortality 102,980 / 6,910. Per 1-MET RR 0.87 (0.84–0.90). Low vs high RR 1.70 (1.51–1.92). Bins: low <7.9 METs, high ≥10.9 — sex-blind MET cutoffs, not this calculator’s 38/31 zero and not a ≥45 mL/kg/min goal. Observational, not a training trial.
View source
Han et al. (2022) — British Journal of Sports Medicine
Cardiorespiratory fitness and mortality from all causes, cardiovascular disease and cancer: dose-response meta-analysis of cohort studies
The 0.47 Lang’s abstract leads with. 34 cohorts, exercise-test CRF, healthy. Per 1-MET all-cause mortality RR 0.88 (0.83–0.93); highest vs lowest 0.47 (0.39–0.56).
View source
Laukkanen et al. (2022) — Mayo Clinic Proceedings
Objectively Assessed Cardiorespiratory Fitness and All-Cause Mortality Risk: An Updated Meta-analysis of 37 Cohort Studies Involving 2,258,029 Participants
Largest exercise-test all-cause mortality meta in Lang Fig 2. 37 cohorts, 2,258,029 people, 108,613 deaths. Top vs bottom tertile RR 0.55 (0.50–0.61). Per 1-MET 0.89 (0.86–0.92).
View source
Qiu et al. (2021) — Atherosclerosis
Is estimated cardiorespiratory fitness an effective predictor for cardiovascular and all-cause mortality? A meta-analysis
eCRF (algorithm) all-cause mortality meta. 8 cohorts, >170,000. Per 1-MET HR 0.83 (0.78–0.88), linear. Same range as meta-analyses of exercise-test fitness (RR 0.87–0.89), though the measures differ; Singh 2024 found no significant difference between estimated and measured fitness. Not a consumer-watch estimate.
View source
Sloth et al. (2013) — Scandinavian Journal of Medicine & Science in Sports
Effects of sprint interval training on VO2max and aerobic exercise performance: A systematic review and meta-analysis
Meta-analysis of 13 studies (of 19 identified: 4 RCTs, 9 matched-controlled, 6 uncontrolled), 2-8 week SIT interventions in sedentary/recreationally active adults. Weighted effect size g = 0.63 (95% CI 0.39-0.87); VO2max increases 4.2-13.4%. Central adaptation evidence "limited and equivocal" per authors; peripheral (muscle oxidative) adaptations solid. The effect size is a Hedges g, not a hazard ratio.
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Wen et al. (2019) — Journal of Science and Medicine in Sport
Effects of different protocols of high intensity interval training for VO2max improvements in adults: A meta-analysis of randomised controlled trials
Meta-analysis of 53 RCTs, healthy/overweight/athletic adults. Short-interval (≤30s)/low-volume (≤5min)/short-term (≤4wk) HIIT beat no-exercise control (SMD 0.79-1.65) but was not among formats shown to beat MICT; only long-interval (≥2min)/high-volume (≥15min)/longer-duration (4-12wk) HIIT beat MICT (SMD 0.65-1.07). Used here as the direct counter-evidence for sprint-interval-training.
View source

Daily Steps

Ding et al. (2025) — The Lancet Public Health
Daily steps and health outcomes in adults: a systematic review and dose-response meta-analysis
Primary source. Systematic review of 57 studies / 35 cohorts; 31 studies / 24 cohorts entered meta-analyses. The all-cause mortality figure is a 14-study dose-response (not the 57-study review count): 7,000 vs 2,000 steps/day HR 0.53 (95% CI 0.46–0.60), I² 36.3%. Inverse non-linear all-cause mortality association with inflection around 5,000–7,000. Authors: 10,000 remains viable for more active people; 7,000 is a more realistic target for some. The 2,000-step reference is the lower bound of the normal range for older adults, not a typical adult. Erratum PMID 40883040.
View source
Paluch et al. (Steps for Health Collaborative) (2022) — The Lancet Public Health
Daily steps and all-cause mortality: a meta-analysis of 15 international cohorts
Harmonised individual-participant data meta of 15 cohorts (47,471 adults, 3,013 deaths). Age-stratified all-cause mortality plateaus: ≥60 y at 6,000–8,000 steps/day; <60 y at 8,000–10,000 (p interaction 0.012). Quartile HRs vs lowest quartile: 0.60, 0.55, 0.47. Ding 2025 lists lack of age-specific analysis as a limitation of its own paper — Paluch is still the age-band meta.
View source
Banach et al. (2023) — European Journal of Preventive Cardiology
The association between daily step count and all-cause and cardiovascular mortality: a meta-analysis
17 cohort studies (226,889 people): each additional 1,000 steps/day is associated with 15% lower all-cause mortality (HR 0.85, 95% CI 0.81–0.91). The abstract also reports that a 500-step increment was associated with a 7% decrease in CV mortality (HR 0.93, 95% CI 0.91–0.95). Reference-quartile median 3,867 steps/day (IQR 2,500–6,675). Restricted cubic splines found a nonlinear dose-response; the per-1,000-step HR is a summary increment, not a linear curve starting at 3,867. Same construct (device steps → all-cause mortality); it does not establish Ding’s specific 5,000–7,000 inflection.
View source
Del Pozo Cruz et al. (2025) — Annals of Internal Medicine
Step Accumulation Patterns and Risk for Cardiovascular Events and Mortality Among Suboptimally Active Adults
Walking in sustained bouts of ≥15 minutes yielded lower 9.5-year mortality (0.80% vs 4.36%) and CVD incidence (4.39% vs 13.03%) than brief sporadic bursts, independent of total step volume.
View source
Inoue et al. (2023) — JAMA Network Open
Association of Daily Step Patterns With Mortality in US Adults
NHANES 2005–06 (n=3,101). Not part of Ding’s 14-study pool. Hitting ≥8,000 steps 1–2 days/week vs 0 days: adjusted 10-year all-cause mortality risk difference −14.9 percentage points (95% CI −18.8 to −10.9), not an HR. Primary model also adjusts for mean daily step count. Protective association plateauing at 3 days a week (aRD −16.5). Pattern is not Ding’s daily-average curve.
View source
Del Pozo Cruz et al. (2022) — JAMA Internal Medicine
Prospective Associations of Daily Step Counts and Intensity With Cancer and Cardiovascular Disease Incidence and Mortality and All-Cause Mortality
78,500 UK Biobank adults, median ~7-year follow-up: more daily steps up to ~10,000/day is associated with lower all-cause mortality and lower cancer and cardiovascular incidence and mortality. The paper reports dose-response as change in log-HR per 2,000-step increment rather than as fixed percentage reductions.
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Saint-Maurice et al. (2020) — JAMA
Association of Daily Step Count and Step Intensity With Mortality Among US Adults
NHANES cohort of 4,840 adults: higher daily step counts strongly linked to lower all-cause mortality (8,000 vs 4,000 steps/day HR 0.49; 12,000 vs 4,000 HR 0.35), with no independent association for step intensity (cadence) after adjusting for total volume.
View source

Resting Heart Rate

Zhang et al. (2016) — CMAJ
Resting heart rate and all-cause and cardiovascular mortality in the general population: a meta-analysis
Primary source (page meta). General-population only; search to 1 Jan 2015. 46 studies. all-cause mortality: 1,246,203 people / 78,349 deaths. Multivariate RR 1.09 (1.07–1.12) per 10 bpm, I² 92.3%, n=35 — RR, not HR. Trim-and-fill 1.04 (1.02–1.06). Categorical vs lowest: 60–80 bpm RR 1.12; >80 bpm RR 1.45. all-cause mortality spline vs 45 bpm is linear (p nonlinearity = 0.1); 90 bpm is the CV-mortality threshold, not an all-cause mortality cliff. ECG subgroup 1.06 vs non-ECG 1.15 per 10 bpm. The calculator’s smooth curve (70=1.0; 40–50 floor 0.85; steepens above 80) is constructed.
View source
Aune et al. (2017) — Nutrition, Metabolism and Cardiovascular Diseases
Resting heart rate and the risk of cardiovascular disease, total cancer, and all-cause mortality – A systematic review and dose-response meta-analysis of prospective studies
Larger all-cause mortality meta (search to 29 Mar 2017). 87 studies overall; all-cause mortality n=48, RR 1.17 (1.14–1.19) per 10 bpm, I² 94.0%. Broader prospective mix than Zhang’s general-population-only pool. Webappendix high-vs-low all-cause mortality 1.69 (1.52–1.87).
View source
Raisi-Estabragh et al. (2020) — PLoS ONE
Age, sex and disease-specific associations between resting heart rate and cardiovascular mortality in the UK BIOBANK
Competing number, single cohort. UK Biobank n=502,534 (analysis 228,594 men / 272,737 women after 0.2% missing RHR), 7–12 y. Fully adjusted all-cause mortality per 10 bpm: men HR 1.22 (1.20–1.24), women 1.19 (1.16–1.22). Sitting Omron pulse, mean of two readings — closer to this slider than Zhang’s mixed ECG/non-ECG pool, and higher than Zhang’s 1.09. CVD mortality SHR 1.17 men / 1.14 women.
View source
He et al. (2022) — Public Health
Relationship of resting heart rate and blood pressure with all-cause and cardiovascular disease mortality
Retrospective cohort of 67,028 Chinese adults aged 60 and older, 361,975 person-years of follow-up, 9,326 deaths. Adults in the highest resting-heart-rate quartile had 25% higher all-cause mortality risk than those in the lowest quartile (HR 1.25, 95% CI 1.17-1.33).
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Okamura et al. (2004) — American Heart Journal
Resting heart rate and cause-specific death in a 16.5-year cohort study of the Japanese general population
Japanese general-population cohort of 8,800 adults (National Survey on Circulatory Disorders), followed 16.5 years. Middle-aged men (30-59y) in the highest resting-heart-rate quartile had 45% higher all-cause mortality (RR 1.45, 95% CI 1.06-2.00); associations were not significant in adults 60 and older.
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Custodis et al. (2016) — Clinical Research in Cardiology
Resting heart rate is an independent predictor of all-cause mortality in the middle aged general population
Heinz Nixdorf RECALL, n=4,091 without known CAD (3,348 free of rate-lowering meds), median 10.5 y, 398 deaths. Off meds, RHR ≥70 vs <70: all-cause mortality HR 1.68 (1.30–2.18); coronary events 1.20 (0.82–1.77), NS. Per 5 bpm all-cause mortality 1.13 (1.07–1.20); coronary 1.02 (0.94–1.11), NS. Authors: independent risk marker for all-cause mortality but not for coronary events. Marker, not a rate-lowering trial.
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Fox et al. (SIGNIFY) (2014) — New England Journal of Medicine
Ivabradine in stable coronary artery disease without clinical heart failure
RCT, 19,102 patients with stable coronary artery disease without clinical heart failure and a heart rate of 70 or more. Ivabradine was dosed to a target heart rate of 55 to 60 bpm; at 3 months mean heart rate was 60.7 vs 70.6 on placebo. Primary endpoint (cardiovascular death or nonfatal myocardial infarction): no significant difference, HR 1.08 (0.96–1.20). Higher primary-endpoint incidence with ivabradine in patients with activity-limiting angina (12,049 of 19,102). Lowering the rate with a drug did not improve outcomes. Heart patients, not the general population. All-cause death was a secondary endpoint, not the primary: HR 1.06 (0.94–1.21), no significant difference.
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Reimers et al. (2018) — Journal of Clinical Medicine
Effects of Exercise on the Resting Heart Rate: A Systematic Review and Meta-Analysis of Interventional Studies
Meta-analysis of controlled trials (most randomized, some not) in healthy people: 191 studies, 215 samples (121 endurance, 43 strength, 15 combined, 21 yoga, 5 school sport, 5 tai chi, 3 qigong, 2 unspecified). Endurance training and yoga clearly lowered resting heart rate; strength training alone showed no significant change overall, and the other types showed drops that did not reach significance. Drops were larger in groups that started with a higher resting rate and smaller at older ages. Resting heart rate is the endpoint, not death: it does not show that lowering the number changes deaths.
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Strength Training

Momma H, Kawakami R, Honda T, Sawada SS. (2022) — British Journal of Sports Medicine
Muscle-strengthening activities are associated with lower risk and mortality in major non-communicable diseases: a systematic review and meta-analysis of cohort studies
Primary source. 16 prospective cohorts of adults without severe illness, independent of aerobic activity. All-cause mortality, no vs any muscle-strengthening activity: RR 0.85 (95% CI 0.79–0.93), 7 studies, 42,133 cases in 263,058 people. Dose-response (6 studies, 37,178 cases): non-linear and J-shaped; the lowest RR was 0.83 (0.79–0.86) at 40 min/week, and the estimate stayed below 1.00 up to about 140 min/week. Maximum risk reduction about 10–20% at about 30–60 min/week. The authors state the effect of higher volume is unclear given the J-shape, and grade the all-cause mortality evidence very low certainty (GRADE). Figures confirmed against the full text (Europe PMC) 2026-09-29. The calculator converts days/week to minutes at an ASSUMED 30 min/session and holds the curve flat above 60 min/week; that plateau is a judgment, not a finding.
View source
Shailendra P, Baldock KL, Li LSK, Bennie JA, Boyle T. (2022) — American Journal of Preventive Medicine
Resistance Training and Mortality Risk: A Systematic Review and Meta-Analysis
Not independent of Momma 2022: all 6 studies in its any-vs-none pool are also in the Momma 7-study pool. 10 studies in the meta-analyses. Any resistance training vs none, all-cause mortality: RR 0.85 (95% CI 0.77–0.93), 6 studies; cardiovascular mortality RR 0.81 (0.66–1.00); cancer mortality RR 0.86 (0.78–0.95). Dose-response (4 studies) non-linear: maximum risk reduction of 27% at about 60 min/week (RR 0.74, 0.64–0.86); reductions diminished at higher volumes. Stronger at 60 min than the curve uses (0.80), which is a deliberate haircut for healthy-user bias.
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Patel AV, Hodge JM, Rees-Punia E, Teras LR, Campbell PT, Gapstur SM. (2020) — Preventing Chronic Disease
Relationship Between Muscle-Strengthening Activity and Cause-Specific Mortality in a Large US Cohort
Competing shape. Cancer Prevention Study-II Nutrition Cohort, 72,462 adults free of major chronic disease, 18,034 deaths over 13 years, Cox models controlling for aerobic activity. Versus no muscle-strengthening: more than 0 to under 1 h/week HR 0.88 (95% CI 0.82–0.94); 1 to under 2 h/week HR 0.90 (0.84–0.97); 2 or more h/week HR 1.01 (0.92–1.09), no reduction. The authors call the reason for no association at higher volume unclear. This is why the calculator’s flat plateau above 60 min/week is a judgment rather than a finding. Associations did not vary by amount of aerobic activity.
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Zhao M, Veeranki SP, Magnussen CG, Xi B. (2020) — BMJ
Recommended physical activity and all cause and cause specific mortality in US adults: prospective cohort study
Meeting both guidelines was linked to the lowest all-cause risk of the four groups. National Health Interview Survey 1997–2014, 479,856 adults, median follow-up 8.75 years, 59,819 deaths. Versus not meeting either guideline: muscle strengthening only HR 0.89 (95% CI 0.85–0.94); aerobic only 0.71 (0.69–0.72); both 0.60 (0.57–0.62). Leisure-time self-report.
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Stamatakis E, Lee IM, Bennie J, Freeston J, Hamer M, O’Donovan G, Ding D, Bauman A, Mavros Y. (2018) — American Journal of Epidemiology
Does Strength-Promoting Exercise Confer Unique Health Benefits? A Pooled Analysis of Data on 11 Population Cohorts With All-Cause, Cancer, and Cardiovascular Mortality Endpoints
Health Survey for England and Scottish Health Survey, 80,306 adults aged 30+, 5,763 deaths. Any strength-promoting exercise HR 0.77 (95% CI 0.69–0.87) for all-cause mortality. Meeting only the strength guideline (2 or more sessions/week) HR 0.79 (0.66–0.94); only the aerobic guideline 0.84 (0.78–0.90); both 0.71 (0.57–0.87).
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Saeidifard F, Medina-Inojosa JR, West CP, Olson TP, Somers VK, Bonikowske AR, Prokop LJ, Vinciguerra M, Lopez-Jimenez F. (2019) — European Journal of Preventive Cardiology
The association of resistance training with mortality: A systematic review and meta-analysis
11 studies (one randomized trial and 10 cohorts), 370,256 participants, mean follow-up 8.85 years. Resistance training vs no exercise, all-cause mortality: HR 0.79 (95% CI 0.69–0.91) alone and 0.60 (0.49–0.72) combined with aerobic exercise. Cardiovascular mortality HR 0.83 (0.67–1.03), borderline; no significant association with cancer mortality.
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Kraschnewski JL, Sciamanna CN, Poger JM, Rovniak LS, Lehman EB, Cooper AB, Ballentine NH, Ciccolo JT. (2016) — Preventive Medicine
Is strength training associated with mortality benefits? A 15year cohort study of US older adults
Weakest design here. National Health Interview Survey 1997–2001 linked to death records, adults 65 and older (N=30,162): guideline-concordant strength training (twice a week) had adjusted odds ratio 0.64 (95% CI 0.57–0.70) for all-cause mortality. An odds ratio, not a hazard ratio, in older adults only; 9.6% met the guideline.
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Garcia L, Pearce M, Abbas A, Mok A, Strain T, Ali S, Crippa A, Dempsey PC, Golubic R, Kelly P, Laird Y, McNamara E, Moore S, de Sa TH, Smith AD, Wijndaele K, Woodcock J, Brage S. (2023) — British Journal of Sports Medicine
Non-occupational physical activity and risk of cardiovascular disease, cancer and mortality outcomes: a dose-response meta-analysis of large prospective studies
Context for additivity, aerobic activity only. 196 articles, 94 cohorts, more than 30 million participants. All-cause mortality relative risk 0.69 (95% CI 0.65–0.73) at 8.75 marginal MET-hours/week (about 150 min/week of moderate-to-vigorous aerobic activity), with small added benefit above 17.5. Not a strength-training estimate; the strength curve here is built from aerobic-adjusted strength studies so the two are not counted twice.
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Celis-Morales CA, Lyall DM, Anderson J, Iliodromiti S, Fan Y, Ntuk UE, Mackay DF, Pell JP, Sattar N, Gill JMR. (2017) — European Heart Journal
The association between physical activity and risk of mortality is modulated by grip strength and cardiorespiratory fitness: evidence from 498 135 UK-Biobank participants
UK Biobank, 498,135 adults, 8,591 deaths over a median 4.9 years. The higher mortality hazard tied to low physical activity was greatest in the lowest grip-strength tertile (HR 1.11, 95% CI 1.09–1.14) and smallest in the highest (HR 1.04, 1.01–1.08). Grip strength modifies the activity–mortality link; no study puts strength-training days and grip strength in one model.
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Craig CL, Marshall AL, Sjöström M, Bauman AE, Booth ML, Ainsworth BE, Pratt M, Ekelund U, Yngve A, Sallis JF, Oja P. (2003) — Medicine & Science in Sports & Exercise
International physical activity questionnaire: 12-country reliability and validity
Measurement caveat. For the closest verified self-report activity instrument (IPAQ), test-retest Spearman rho clustered around 0.8, but criterion validity against an accelerometer had a median rho of about 0.30 for total activity. No strength-specific test-retest figure was found. A days-per-week count is simpler than a minutes estimate, but its reliability is an inference, not a measured figure.
View source

Cardiometabolic sources

Blood Pressure

Lewington et al. (Prospective Studies Collaboration) (2002) — The Lancet
Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies
Supporting source (page meta, not the joint rule). individual-participant data of 1 million adults, 61 prospective studies, no prior vascular disease. Findings quantify vascular death: ages 40–69, each 20 mmHg usual SBP (≈10 mmHg usual DBP) is associated with more than a twofold difference in stroke death and twofold differences in IHD and other vascular death. No threshold down to 115/75. Interpretation says “vascular (and overall) mortality”; abstract does not report an all-cause mortality relative-risk table. The calculator’s high-side max-penalty rule is constructed (LOW confidence); high-side 1.08 per 10 mmHg SBP is not Lewington’s ~2.0 per 20. Below 120/80 the curve is flat (no reward) as of 2026-09-10 — see Wang et al. 2026 below.
View source
Wang et al. (2026) — Journal of Hypertension
Association of blood pressure levels in the nonhypertensive range with mortality among people without traditional risk factors
Basis for removing the curve's low-end reward, 2026-09-10. UK Biobank, 80,730 adults screened free of traditional cardiovascular risk factors, restricted to the nonhypertensive range, 13.7-year median follow-up, 2,553 deaths, restricted cubic splines, endpoint all-cause mortality. The lowest SBP quintile (<114 mmHg) carried 16% higher all-cause mortality (HR 1.16, 95% CI 1.02–1.32) versus the third quintile (120–126 mmHg) — the opposite sign from the curve's old low-end bonus. Contrary evidence: Rapsomaniki et al. 2014 (below) reports no J-shape at low SBP, but for CVD incidence, not all-cause mortality.
View source
Bundy et al. (2017) — JAMA Cardiology
Systolic Blood Pressure Reduction and Risk of Cardiovascular Disease and Mortality: A Systematic Review and Network Meta-analysis
Nearest all-cause mortality pool — treatment achieved SBP, not usual-BP observational. 42 trials, 144,220 treated hypertensives. Lowest all-cause mortality at mean achieved 120–124 mmHg. all-cause mortality HR vs 130–134: 0.73 (0.58–0.93); vs 140–144: 0.59 (0.45–0.77); vs ≥160: 0.47 (0.32–0.67). No matching-construct usual office/home BP → all-cause mortality continuous general-pop meta-analysis is available.
View source
Brunström & Carlberg (2018) — JAMA Internal Medicine
Association of Blood Pressure Lowering With Mortality and Cardiovascular Disease Across Blood Pressure Levels: A Systematic Review and Meta-analysis
Competing treatment number. 74 trials, 306,273 people. Primary-prevention all-cause mortality: baseline SBP ≥160 RR 0.93 (0.87–1.00); 140–159 RR 0.87 (0.75–1.00); below 140 RR 0.98 (0.90–1.06) — neutral. Bundy’s 0.73 and Ettehad’s 0.87 do not show that treating below 140 lowers all-cause mortality.
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Jaeger et al. (2022) — JAMA Cardiology
Longer-Term All-Cause and Cardiovascular Mortality With Intensive Blood Pressure Control: A Secondary Analysis of a Randomized Clinical Trial
SPRINT extended: intervention-period all-cause mortality HR 0.83 (0.68–1.01); at median 8.8 y total follow-up, after intensity lapsed, all-cause mortality HR 1.08 (0.94–1.23). Outpatient SBP in the intensive arm rose 132.8 → 140.4 mmHg by year 10. Marker, not a one-time treatment effect.
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Ettehad et al. (2016) — The Lancet
Blood pressure lowering for prevention of cardiovascular disease and death: a systematic review and meta-analysis
Treatment-trial all-cause mortality companion, not the curve. 123 RCTs, 613,815 people. Every 10 mmHg SBP reduction: all-cause mortality RR 0.87 (0.84–0.91), I² 35%. Do not invert 0.87 into an observational usual-BP slope.
View source
SPRINT Research Group (Wright et al.) (2015) — New England Journal of Medicine
A Randomized Trial of Intensive versus Standard Blood-Pressure Control
One trial, not the curve. 9,361 high-risk adults without diabetes; SBP target <120 vs <140. Median 3.26 y, stopped early. all-cause mortality HR 0.73 (0.60–0.90). Jaeger is the same trial after intensity lapsed.
View source
Blood Pressure Lowering Treatment Trialists’ Collaboration (Rahimi et al.) (2021) — The Lancet
Pharmacological blood pressure lowering for primary and secondary prevention of cardiovascular disease across different levels of blood pressure: an individual participant-level data meta-analysis
Treatment individual-participant data, primary endpoint MACE not all-cause mortality. 48 trials, 344,716 people. Per 5 mmHg SBP: MACE overall HR 0.90 (0.88–0.92); all-cause mortality 0.98 (0.96–1.01); CV death 0.95 (0.92–0.99). Context line is stroke/HF/IHD/CV-death −13/−13/−8/−5%, not all-cause mortality.
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Rapsomaniki et al. (2014) — The Lancet
Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1.25 million people
CVD incidence, not all-cause mortality. CALIBER 1.25 million, 83,098 first CVD presentations. Lowest CVD risk at SBP 90–114 / DBP 60–74; hypertension lifetime CVD risk 63.3% vs 46.1%. Not the UI endpoint.
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Jones et al. (2025) — Journal of the American College of Cardiology
2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines
2025 clinical practice guideline replaces the 2017 guideline and updates guidance for clinicians managing high blood pressure. Its abstract does not state the category cutoffs or validate this food-swap schedule. Cutoffs are cited separately to the AHA Blood Pressure Categories chart.
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American Heart Association (blood pressure categories) (2025) — American Heart Association
Understanding Blood Pressure Readings
Blood Pressure Categories chart (reviewed August 14, 2025): normal is below 120 systolic AND below 80 diastolic; severe readings are above 180 systolic OR above 120 diastolic. The chart and emergency section advise calling 911 with very high readings and concerning symptoms. This engine conservatively routes equality too and withholds the schedule for any reported symptoms; these are product safety rules, not a diagnosis or prescribed BP goal.
View source
American Heart Association (home monitoring) (2025) — American Heart Association
Home Blood Pressure Monitoring
How to use a home blood pressure monitor (reviewed August 14, 2025): validated upper-arm cuff, quiet rest for at least 5 minutes, supported arm at heart level, two measurements 1 minute apart, preparation and immediate response to very high readings. Monitoring frequency follows clinician advice; the twice-weekly product schedule is not a guideline dose.
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Appel et al. (DASH Collaborative Research Group) (1997) — New England Journal of Medicine
A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group
Randomized feeding trial supports a fruit- and vegetable-rich dietary pattern, not a single-swap effect or this 90-day schedule.
View source
Sacks et al. (DASH-Sodium Collaborative Research Group) (2001) — New England Journal of Medicine
Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group
Randomized feeding trial supports lower-sodium choices within a dietary pattern, not a predicted result from these swaps.
View source
American Heart Association (potassium guidance) (2025) — American Heart Association
How Potassium Can Help Prevent or Treat High Blood Pressure
Potassium and your diet, Potassium-Based Salt Substitutes, and Can you have too much potassium? (reviewed August 14, 2025): potassium-rich foods and clinician advice for kidney disease or medicines affecting potassium. Restriction and prescribed-food-plan flags conservatively withhold this generic schedule.
View source

HbA1c

Zhong et al. (2016) — Scientific Reports
HbA1c and Risks of All-Cause and Cause-Specific Death in Subjects without Known Diabetes: A Dose-Response Meta-Analysis of Prospective Cohort Studies
Supporting source (page meta, not the anchor point table). 12 studies; all-cause mortality dose-response 113,526 people / 11,301 deaths. HR per 1% 1.03 (1.01–1.04), I² 28.9%. Non-linear: curves “relatively flat for HbA1c less than around 5.7%, and rose steeply thereafter.” After excluding undiagnosed diabetes (HbA1c ≥6.5%): all-cause mortality HR 1.01 (0.99–1.03). After also excluding prediabetes: all-cause mortality HR 1.01 (0.98–1.03), NS. Authors: the association “is driven by those with undiagnosed diabetes or prediabetes.” The calculator’s smooth curve is constructed (flat 1.00 to 5.6%; 6.0=1.15); 1.15 at 6.0 is not Zhong’s 1.03/1%.
View source
Schöttker et al. (2016) — BMC Medicine
HbA1c levels in non-diabetic older adults - No J-shaped associations with primary cardiovascular events, cardiovascular and all-cause mortality after adjustment for confounders in a meta-analysis of individual participant data from six cohort studies
Nearest individual-participant data all-cause mortality pool — non-diabetic ≥50, not the anchor point table. 6 European/US cohorts, 28,681 people, 6,769 deaths, mean 10.7 y. Increased (6.0–<6.5%) vs low (5.0–<5.5%) all-cause mortality HR 1.14 (1.03–1.27) after CV-risk adjustment (~50% of excess explained). Very-low (<5.0%) pooled NS. NHANES J lost significance after race/ethnicity, alcohol, BMI, iron-deficiency anemia and liver markers. Authors: small effects “do not support the notion of a J-shaped association.” Curve 6.0=1.15 is nearby; curve 6.5=1.35 is outside this paper.
View source
Cavero-Redondo et al. (2017) — BMJ Open
Glycated haemoglobin A1c as a risk factor of cardiovascular outcomes and all-cause mortality in diabetic and non-diabetic populations: a systematic review and meta-analysis
Competing number, categorical U, not this curve. 74 studies / 46 in the MA. Non-diabetic all-cause mortality >6.0% HR 1.74 (1.38–2.20); <5.0% HR 1.19 (1.04–1.36). Diabetic >9.0% 1.69 (1.09–2.66); <6.0% 1.57 (1.14–2.17). Authors: optimal 5.0–6.0% without diabetes, 6.0–8.0% with diabetes. 1.74 does not carry over to the curve’s 1.15 at 6.0%, nor 1.19 to the flat 1.00 below 5.6%.
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ACCORD Study Group (Gerstein et al.) (2008) — New England Journal of Medicine
Effects of Intensive Glucose Lowering in Type 2 Diabetes
High-risk T2D, intensive target <6.0% (median achieved 6.4%) vs standard 7.0–7.9% (median 7.5%). Primary MACE HR 0.90 (0.78–1.04), NS. all-cause mortality 257 vs 203, HR 1.22 (1.01–1.46), P=0.04. Targeting a number this calculator scores as 1.00–1.15 raised death in that trial. Marker, not a DIY treatment target. 2011 follow-up (PMID 21366473) 5-year all-cause mortality 1.19 (1.03–1.38).
View source
Aggarwal et al. (2012) — Diabetes Care
Low hemoglobin A1c in nondiabetic adults: an elevated risk state?
ARIC, n=13,288. HbA1c <5.0% vs 5.0–<5.7%: all-cause mortality HR 1.32 (1.13–1.55); cancer death 1.47 (1.16–1.84). Authors: “generalized marker of mortality risk,” a mix of healthy people and people in whom low HbA1c signals underlying illness. A 1.05–1.10 uptick below 5.0% was considered and not implemented.
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Khaw et al. (2001) — BMJ
Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of european prospective investigation of cancer and nutrition (EPIC-Norfolk)
EPIC-Norfolk, 4,662 men 45–79. Each 1% higher HbA1c: +28% all-cause mortality (P<0.002). After excluding known diabetes, HbA1c ≥7%, or prior MI/stroke: RR 1.46, P=0.05. 82% of excess population mortality at HbA1c 5.0–6.9%. Lowest rates below 5% — do not use Khaw backwards as a low-end-uptick paper.
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Cai et al. (2020) — BMJ
Association between prediabetes and risk of all cause mortality and cardiovascular disease: updated meta-analysis
129 studies, 10.07 million. General-population prediabetes all-cause mortality RR 1.13 (1.10–1.17). all-cause mortality was raised for HbA1c-IEC 6.0–6.4% (1.21, 1.06–1.38) and for IFG/IGT; not for “other definitions,” which includes HbA1c-ADA 5.7–6.4%. CVD was raised for HbA1c-ADA (1.17, 1.03–1.33). Binary prediabetes ≠ this continuous curve.
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Huang et al. (2025) — Frontiers in Endocrinology
Nonlinear association between glycated hemoglobin levels and mortality in elderly patients with non-diabetic chronic kidney disease: a national health and nutrition examination survey analysis
NHANES elderly non-diabetic CKD, n=1,931, mean age 73. Q1 3.7–5.3% all-cause mortality HR 1.48 (1.18–1.87) vs 5.7–5.8%. Wrong population for this calculator.
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Lifestyle sources

Sleep Duration

Yin et al. (2017) — Journal of the American Heart Association
Relationship of Sleep Duration With All-Cause Mortality and Cardiovascular Events: A Systematic Review and Dose-Response Meta-Analysis of Prospective Cohort Studies
Primary source. Prospective cohorts in generally healthy adults, search to December 2016. Nadir ≈7 h. Table 2 (nonlinear, 40 all-cause mortality risk estimates, reference 7 h): 8 h RR 1.04 (1.04–1.05), 9 h 1.15 (1.14–1.16), 10 h 1.32 (1.29–1.35). Linear short-sleep slope RR 1.06 (1.04–1.07) per hour below 7 h (P for nonlinearity on the short side = 0.12); linear long-sleep slope 1.13 (1.11–1.15) per extra hour. Extreme categorical pooling is 57 reports (shortest vs ref RR 1.13, longest 1.35) — not Table 2. The curve uses Table 2 on both sides, relative to 7 h: 4/5/6 h = RR 1.08/1.04/1.01 and 8/9/10 h = RR 1.04/1.15/1.32. The linear 1.06/h short-side extrapolation was retired on 2026-09-26.
View source
Ungvari et al. (2025) — GeroScience
Imbalanced sleep increases mortality risk by 14–34%: a meta-analysis
Newest categorical all-cause mortality pooling (search to October 2024): 79 cohort studies. Short sleep (<7 h vs 7–8 h) HR 1.14 (1.10–1.18); long sleep (≥9 h) HR 1.34 (1.26–1.42). Not a dose–response and not the curve. First author is editor-in-chief of the publishing journal.
View source
Kwok et al. (2018) — Journal of the American Heart Association
Self-Reported Sleep Duration and Quality and Cardiovascular Disease and Mortality: A Dose-Response Meta-Analysis
74-study review; the reported dose–response is 30 studies (>1 million people). Linear model: 9 h RR 1.14 (1.05–1.25), 10 h 1.30 (1.19–1.42), 11 h 1.47 (1.33–1.64). No significant increase below 7 h — that is the short-side disagreement with the curve’s Table 2 anchors (4/5/6 h = 1.08/1.04/1.01). Long side sits next to Yin Table 2.
View source
Shen et al. (2016) — Scientific Reports
Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies
35 articles. Nighttime Table 1 vs 7 h (36 results, 146,830 deaths / 1,526,609 people): 4 h RR 1.07 (1.03–1.13), 6 h 1.01, 11 h 1.55 (1.47–1.63). 24-hour sleep is a different column (11 h RR 1.84). The 4 h estimate, RR 1.07 versus 7 h, is close to the curve’s 1.08 at 4 h from Yin Table 2.
View source
Liu et al. (2016) — Sleep Medicine Reviews
Sleep duration and risk of all-cause mortality: A flexible, non-linear, meta-regression of 40 prospective cohort studies
PubMed abstract: 40 cohorts, 2,200,425 people, 271,507 deaths. J-shaped vs 7 h (24-hour sleep, n=29): 4 h RR 1.05 (1.02–1.07), 11 h 1.38 (1.33–1.44). Female short-sleep signal; male short sleep not significant in the subgroup. Not the primary source.
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Cappuccio et al. (2010) — Sleep
Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies
Foundational categorical pairing, not a dose–response: 16 studies / 27 cohorts, 1,382,999 people, 112,566 deaths. Short sleep RR 1.12 (1.06–1.18); long sleep RR 1.30 (1.22–1.38). This is the 1.12 / 1.30 pair the old page led with. Not the primary source and not a sleep-extension trial. Marker, not a treatment effect.
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Dietary Fiber

Institute of Medicine, Food and Nutrition Board (2002) — National Academies
Report Offers New Eating and Physical Activity Targets To Reduce Chronic Disease Risk
Nutritional advice only, not mortality evidence. The New Facts on Fiber section reports total fiber intake for adults 50 and younger: men 38 g/day, women 25 g/day; over 50: men 30 g/day, women 21 g/day. These IOM/NASEM adequate-intake values select the displayed floor; they do not change the hazard curve.
View source
Reynolds et al. (2019) — The Lancet
Carbohydrate quality and human health: a series of systematic reviews and meta-analyses
Primary source. WHO-commissioned series (185 prospective publications / 58 trials). All-cause mortality highest-vs-lowest is a 10-study observational pooling (not the 185-publication count): RR 0.85 (0.79–0.91), GRADE moderate, people without chronic disease. Fig 1A: assuming linearity, RR 0.93 (0.90–0.95) per 8 g more fibre/day (68,183 deaths). Greatest categorical benefit at 25–29 g/day (6 of 7 critical outcomes); dose-response linear with no plateau in the available data. REVISED 2026-09-10: the curve now uses the per-8g RR 0.93 directly, log-linear, anchored to HR 1.0 at 16 g/day (median reference intake), flat outside the ~5–35 g/day range Fig 2a modelled. The IOM/NASEM AI (38/30/25/21 g) is shown as an age/sex advice target only and no longer alters the score. Erratum PMID 30712898.
View source
Yao et al. (2023) — Frontiers in Nutrition
Dietary intake of total vegetable, fruit, cereal, soluble and insoluble fiber and risk of all-cause, cardiovascular, and cancer mortality: systematic review and dose-response meta-analysis of prospective cohort studies
Newer matching-construct all-cause mortality meta (search to August 2023). Highest vs lowest: 16 studies, RR 0.81 (0.77–0.86), I² 71.9%. Per 10 g/day: 14 studies, RR 0.90 (0.86–0.93), I² 86.1% — the full-text dose-response results and Table 2 specify this increment; the abstract does not state the unit. Non-linear (P=0.0096): steeper below 15 g/day, more gradual after. That inflection is Yao’s shape. The live curve has no 15 g kink: it is Reynolds’s per-8 g slope, log-linear, HR 1.0 at 16 g/day.
View source
Ramezani et al. (2024) — Clinical Nutrition
Dietary fiber intake and all-cause and cause-specific mortality: An updated systematic review and meta-analysis of prospective cohort studies
Largest pool: 64-study review, 3,512,828 people; all-cause mortality meta is 33 reports (not 64). Overall highest-vs-lowest all-cause mortality HR 0.77 (0.73–0.82), I² 67.9%. That headline mixes diseased cohorts. General-population subgroup (19 reports) HR 0.82 (0.77–0.86); non-general (cancer survivors, T2D, CKD, …) HR 0.67 (0.61–0.72). Highest-vs-lowest only — continuous estimates were dropped. Keep as the mixed-pool companion, not as the curve number.
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Mirrafiei et al. (2023) — Food & Function
Total and different dietary fiber subtypes and the risk of all-cause, cardiovascular, and cancer mortality: a dose-response meta-analysis of prospective cohort studies
28 prospective studies, 1,613,885 people, general population. Higher total and most subtypes (cereal, vegetable, legume, soluble, insoluble) associated with lower all-cause mortality; fruit fibre was not. Subtype HRs 0.77 (insoluble) to 0.93 (legume). The abstract’s dose-response meta-analyses suggested an inverse association between total fibre and all-cause, cardiovascular, and cancer mortality (GRADE moderate). It does not quote a per-gram slope, and it does not report a single total-fibre highest-vs-lowest HR. Calculator collects total grams, not subtype — moving the slider is not “eat fruit fibre.”
View source
Yang et al. (2015) — American Journal of Epidemiology
Association between dietary fiber and lower risk of all-cause mortality: a meta-analysis of cohort studies
Pre-Reynolds tertile pooling: 17 cohorts (982,411 people, 67,260 deaths). Top vs bottom tertile all-cause mortality RR 0.84 (0.80–0.87), I² 41.2%. Per 10 g/day RR 0.90 (0.86–0.94), I² 77.2%. Same per-10 g point estimate as Yao, older and smaller. Not the primary source.
View source

Model limitations

We correct calibration issues when we find them, and we disclose them here rather than waiting for someone else to find them first.

Calibration was corrected

Earlier versions anchored several curves’ "no added risk" point (HR = 1.0) at values well below what a typical adult actually does — the daily-steps curve, for example, treated 2,000 steps/day as the neutral baseline, when that is closer to the bottom of the range than the middle. The effect was that ordinary results looked better than they were. Scores are now expressed relative to a defined median reference profile for a 45-year-old US adult, so matching that profile on every marker scores exactly 50 — typical, not a test out of 100. See "Fifty isn’t the middle of the pack" below for why that is a higher bar than it sounds.

What the per-metric hazard ratios mean

Where a study reports a usable number at a named exposure, that anchor is the paper’s figure against that paper’s own comparator. Interiors of the PCHIP curves, and the constructions listed in the next card, are ours — direction from the papers, specific shape not. Recalibration of the composite left those per-metric numbers in place so the published anchors stay traceable. The composite score stays relative to the fixed median reference; the modeled comparison range uses the age and sex group.

More curve shapes are our own construction than three

Technical notes

Grip strength, VO2 max, and HRV are the three we previously named: Leong reports only a per-5kg slope (and, as of 2026-09-10, only on the below-optimal side — the above-optimal decline to a 0.7 floor was removed; the curve now holds flat at 0.8 at and above the 40/25 kg anchor because neither Leong nor Wu 2017 publishes a dose-response for getting stronger past it), Mandsager uses age/sex percentile bins, Jarczok compares quartiles (its HRV curve was rescaled 2026-08-29 to Jarczok’s covariate-adjusted estimate rather than the unadjusted one). Also constructed, and now named: the daily-steps PCHIP interiors (0 / 3k / 4k / 5k / 16k — 2,000 = 1.0, 7,000 = 0.53, 10,000 = 0.52, and 12,000 = 0.45 are all Ding 2025’s own reported figures as of 2026-09-10; Ding models 1000-step increments only up to 12,000/day, "due to scarce data past this point," so 16,000 stays flat at the 12,000 value — flat there is a data-scarcity cap, not a reported plateau); fibre’s curve was rebuilt 2026-09-10 to track Reynolds 2019’s all-cause-mortality dose-response directly — HR = 1.0 at 16 g/day (the median reference intake), moving log-linearly per that paper’s reported RR 0.93 per 8 g/day, over the roughly 5–35 g/day range Reynolds actually modelled (Figure 2a: “linear with no sign of a plateau within the available data”). Outside that range the curve is flat in both directions — below 5 g/day and above 35 g/day alike — because that is where the evidence stops, not because benefit stops or reverses. The age/sex fibre target (IOM/NASEM Adequate Intake, 38/30/25/21 g) is shown as advice only and no longer changes the score — Reynolds’s dose-response has no age or sex term, so scoring the same intake differently by age/sex bucket was never supported by the mortality evidence; sleep duration’s short-side PCHIP anchors (4 h = 1.08, 5 h = 1.04, 6 h = 1.01) are Yin 2017’s own Table 2 nonlinear estimates, same as the long side (8 / 9 / 10 h = 1.04 / 1.15 / 1.32) — changed 2026-09-26 from a steeper linear 1.06-per-hour extrapolation on the short side (1.19 / 1.12 / 1.06); gait speed’s 1.2 m/s recentre for a ~45-year-old (Studenski measured adults 65+); sleep-regularity’s log-linear fill between Windred’s 1.0 and 0.70 quintile endpoints (0.70 is the fully adjusted most-regular HR; 0.52 is the same contrast in the minimal model, not used; interiors 0.91 / 0.84 / 0.76 are ours, not Table 2); social’s three-level 0.85 / 1.0 / 1.25 (Strong / Average / Weak) is constructed around typical = 1.0 — not Wang 2023’s isolated-vs-not 1.32, and 0.85 is not 1/1.32 (isolation, loneliness, and living-alone are three separately pooled constructs); and the blood-pressure combination rule when systolic and diastolic disagree (the high-side shape and magnitude generally — the description previously overclaimed continuous interpolation from the Prospective Studies Collaboration; corrected 2026-09-10). Dental (poor HR 1.15, Wu 2021) and hearing (loss HR 1.13, Tan 2022) are directly-sourced figures, not constructed. Direction comes from the papers; those specific shapes are ours.

Three ranges we could not verify, and did not move

Three curve regions are not traceable to a cited continuous dose-response, and the underlying papers were paywalled (403) rather than confirmed or refuted when we checked — so the constants are disclosed here, not changed. HbA1c above 8% (anchors 8.0 → 1.95, 10.0 → 2.7): no cited source supplies a continuous dose-response reaching 10%; Schöttker’s population is non-diabetic (ceiling ~6.5%), and the other HbA1c citations are open-ended categorical bins — the 2.7 value is constructed. Would be settled by a diabetic-population continuous dose-response reaching 10% HbA1c. VO2 max’s top two knots (male 63/73, female 56/66 mL/kg/min): almost certainly beyond any cohort’s observed range; Singh 2024’s full text could not be opened to confirm its measured ceiling. Resting heart rate’s 40–50 bpm flat band (both pinned to 0.85): Zhang 2016’s own spline reads linear through that low zone (p nonlinearity = 0.1), arguing 40 and 50 should not score identically, but the range could not be confirmed from Zhang’s full text (cmaj.ca returned 403). None of these three constants were changed on inference alone.

Strength training can only raise your score

Strength training (days a week of exercise done to strengthen muscles) is scored at 5%, and the reference is zero days because most US adults do fewer than two a week. That makes it bonus-only: doing none scores as typical, never worse, and it is the one marker that cannot pull your score down. Each day counts as 30 minutes, an assumption with no source. The curve is flat above about an hour a week because the studies disagree there (one large cohort saw no benefit at two hours or more), so more is not scored as better. The evidence is observational and the pooled review grades it very low certainty, so confidence is LOW-MEDIUM. The zero-day reference comes from a secondary summary of a national survey, not a cited paper.

Balance is one clinic cohort, not the 2024 meta

Fail HR 1.84 is Araujo 2022 (CLINIMEX clinic volunteers, 10-second one-legged stance — the same test the calculator asks). Das et al. 2024 pooled 15 cohorts of mixed static-balance tests at HR 1.14 (1.07–1.21), I² 88%; that pool is not one-leg-only. Xie 2023 (CHARLS) is a 10-second semi-tandem stand, a different and easier test (1% failed vs Araujo’s 20%). The score uses Araujo’s figure.

The percentile comes from a simulation, not measured people

Age-band rankings preserve same-person survey measurements where available and draw the remaining markers from separate U.S. survey and exercise-testing data. The range covers proxy and assumed-dependence sensitivity runs plus core survey sampling uncertainty. It is not a fully validated population percentile or a medical result. Some inputs are indirect or older. Ages 70+ combine older survey cells and use the observed 70-79 exercise-testing median with a wider spread because direct 80+ values are missing. Fewer studies include people over 70, so this range is wider.

Fifty isn’t the middle of the pack

Score 50 matches the fixed midlife reference on all eight markers. It does not mean the middle of every age group. Only the modeled comparison changes with age and sex; the score, curves, weights and tier names stay fixed. Saved comparisons keep the age, sex, displayed range and distribution version from that assessment. Legacy saved results retain their old display.

The roadmap projects, it does not promise

Roadmap point gains are computed by re-running this same model with one input changed — so they can never drift away from your score — but they are arithmetic, not outcomes. They assume you hold every other metric where it is, that a change you make is genuine rather than a measurement artefact, and that the association the underlying study observed would apply to you. Observational cohorts show that people with better numbers die less often; they cannot prove that moving your number moves your risk by the amount shown.

Self-reported inputs carry real error

Grip strength, VO2 max, HRV, and sleep regularity in particular depend on the user’s equipment and technique, and are only as accurate as what the user measures and enters.

This is not a medical device

This is a general-wellness and educational tool. It is not a diagnostic device, it does not provide medical advice, and it must not be used to make treatment decisions. Discuss your results with a clinician.

Reference-profile changelog

Technical notes

2026-09-29 (strength training added; sitting reviewed). Strength training joined the composite as an eighth scored marker at 5% of the score. The other seven weights were scaled proportionally (each times 0.95), so their relative ratios are unchanged. Input is days a week (0 to 7), counted as 30 minutes a day; the curve (0, 30, 40, 60 minutes = 1.00, 0.87, 0.83, 0.80, then flat) is built from aerobic-adjusted studies (Momma 2022, PMID 35228201, figures confirmed against the full text; Shailendra 2022, PMID 35599175; Patel 2020, PMID 32762807). The reference is zero days, so the marker can only raise a score, and the reference profile still scores exactly 50. Confidence is LOW-MEDIUM. Sitting time was reviewed and kept out of the score because its effect is largely gone in active people and it cannot be framed as something to do; it is documented, unscored, on the sitting page. Score bands moved to 37/49/56/64/73, and the reference profile now reads ~p62 for men and ~p67 for women, almost 2 in 3.

Older entries

2026-09-29 (note on the percentiles below). The p75-range percentiles quoted in the older entries below are historical. After the 2026-09-26 distribution refresh the median reference profile (raw score 50) read ~p64 for men and ~p69 for women, about 2 in 3; the strength-training change above moved that to ~p62 and ~p67.

2026-09-19 (grip leaves the score). Grip strength was taken out of the composite, which then scored seven markers: steps, sleep, fiber, blood pressure, HbA1c, VO2 max, and resting heart rate. Grip is still published, unscored, on the more metrics page. Domain weights did not change; within Physical Capacity the remaining members are VO2 max 0.47, steps 0.33, and resting heart rate 0.20.

2026-09-10 (steps + grip + BP visualization). Two curve changes and four copy/rendering fixes, all following the same rule as the fibre rebuild: a curve tracks its source only as far as that source actually observed. Steps — Ding et al. 2025 (Lancet Public Health, PMID 40713949) models the all-cause-mortality dose-response in 1000-step increments from 2,000 up to 12,000 steps/day, capped there for data scarcity, not because the paper found a plateau. The curve had pinned 10,000 and 12,000 to an identical HR 0.51, discarding evidence inside Ding's own modelled range. Anchors moved to Ding's own reported figures vs the 2,000-step reference: 10,000 steps 0.51 → 0.52 (Ding: "48% ... in all-cause mortality"), 12,000 steps 0.51 → 0.45 (Ding: "the maximum risk reduction modelled ranged from 12% in cancer incidence to 55% in all-cause mortality"). 16,000 stays flat at the new 0.45 — above 12,000 Ding has no data, so flat is still correct there. Grip — the above-optimal decline (−0.005/kg to a 0.7 floor) is removed; the grip curve now holds flat at 0.8 at and above the 40 kg male / 25 kg female anchor, because neither Leong 2015 nor Wu 2017 publishes a dose-response for grip strength above that anchor, only a per-5kg-lower slope. The below-optimal side is unchanged. Blood pressure — the always-visible target band's start moved from 90 to 114 mmHg systolic (visualization only; the blood-pressure formula is untouched): Wang et al. 2026 (PMID 41411626, UK Biobank, n=80,730) reports the lowest systolic quintile (<114 mmHg) at 16% higher all-cause mortality vs 120–126, so painting all of 90–120 as uniformly "in the zone" contradicted the site's own cited source. Also fixed: the blood-pressure card's description no longer claims "continuous interpolation from the Prospective Studies Collaboration" (false — PSC/Lewington's endpoint is vascular death, not all-cause, and the high-side shape is hand-constructed); the steps habit-picker copy no longer calls 7,000/9,000 steps "at"/"past the plateau" (Ding shows continuing decline to 12,000); resting-heart-rate's 40–50 bpm flat band now has a disclosure symmetric to the existing above-80 one. Three further regions (HbA1c above 8%, VO2 max's top two knots, and the RHR 40–50 flat band itself) were reviewed and found not traceable to a cited dose-response, but were left unchanged — the source papers returned 403 and a mortality curve should not move on an unverified range. See "Three ranges we could not verify, and did not move" above. Re-deriving the distribution after the steps and grip changes moved the score-band cutoffs. Any score computed before this change is not directly comparable to one computed after it for profiles near 10,000–16,000 steps/day or above-optimal grip.

2026-09-10 (fibre curve). The fibre curve was rebuilt to depend only on absolute g/day, tracking Reynolds et al. 2019’s all-cause-mortality dose-response directly instead of the age/sex adequate-intake target. Before this change, a 30-year-old man and a 60-year-old woman each eating 30 g/day of fibre scored different hazard ratios (0.88 vs 0.81) purely because of their age/sex target bucket, with no mortality evidence behind the gap — Reynolds’s dose-response has no age or sex term. The new curve is anchored to HR = 1.0 at 16 g/day (the median reference intake) and moves log-linearly at Reynolds’s reported RR 0.93 per 8 g/day, over the roughly 5–35 g/day range the paper actually modelled (Figure 2a is "linear with no sign of a plateau within the available data" across that range). The curve is now flat outside 5–35 g/day in both directions — it no longer climbs to HR 1.225 for zero intake, and no longer keeps rewarding intake past target+20g the way the prior cap did. Flat means the evidence stops, not that benefit stops. The age/sex fibre target (IOM/NASEM Adequate Intake, 38/30/25/21 g) is unchanged and still shown as the advice line, but it no longer affects the score. Re-deriving the distribution after this change produced identical score-band cutoffs (35/45/52/59/67). Any score computed before this change is not directly comparable to one computed after it for profiles whose fibre intake was near the old age/sex target.

2026-09-10 (labels). The score-band labels were renamed — Below Typical / Typical / Above Typical / Strong / Exceptional / Elite — so the ladder reads monotonically in plain English; the old ladder put "Average" second from the bottom and landed the median person in "Fair." This is a naming change only. It is separate from, and did not cause, the percentile-cut moves logged below — those moved because the underlying model changed (dropping Recovery, then removing the blood-pressure low-end reward), not because the labels did.

2026-09-10. The blood-pressure low-end reward was removed. Below 120/80 the curve had been paying a bonus growing to a −10% floor at 100/68 and below; the best available all-cause-mortality evidence for that range (Wang et al. 2026, UK Biobank, 80,730 adults without traditional cardiovascular risk factors) found the opposite sign — the lowest systolic quintile carried 16% higher risk, not lower. The low side is now flattened to HR 1.0 — no reward, no penalty — below 120/80; the high side is untouched. This is the same change made for the HbA1c low-end reward on 2026-08-29, for the same reason: an unsourced bonus for an extreme value, in a direction the mortality evidence does not support. Re-deriving the distribution after dropping this reward moved the score-band cutoffs from 36/46/53/60/69 to 35/45/52/59/67; some profiles no longer get a below-120/80 bonus, so the whole population's raw scores shift down slightly. The median reference profile still scores exactly 50. Any score computed before this change is not directly comparable to one computed after it.

2026-08-29 (second pass). Separately from the reweight below, the scored stack was cut from 17 metrics to 8 keepers — the composite dropped the Recovery domain (HRV, hearing, dental) and now scores only steps, sleep, fiber, grip, blood pressure, HbA1c, VO2 max, and resting heart rate. Re-deriving the distribution for 8 keepers only moved the score-band cutoffs from 39/47/51/57/63 to 36/46/53/60/69. Any score computed before this change is not directly comparable to one computed after it.

2026-08-29. Four changes were made. Hearing-loss HR moved from an uncited 1.25 to Tan et al. 2022's pooled 1.13. Dental was redefined from a borrowed clinical-periodontitis HR (1.30) to a self-reported-tooth-loss HR of 1.15 (Wu et al. 2021, the only cited cohort using this app's own self-report modality) — the question itself changed from gum-disease status to natural tooth loss; the underlying 'good'/'poor' values and shareable-link encoding did not. HbA1c's low-end reward (HR 0.88 below 5.4%) was removed — Schöttker et al. 2016 and Zhong et al. 2016 found that association was inconsistent, non-significant, or driven by undiagnosed diabetes — so the curve is now flat (HR 1.0) up to 5.6% rather than U-shaped. HRV's 10ms endpoint moved from a constructed 1.40 (the curve never sat at Jarczok's unadjusted 1.56) to Jarczok et al. 2022's covariate-adjusted lowest-quartile estimate (~1.23); the other HRV anchors were pulled toward 1.0 at 33ms with per-point log-space factors of 0.587–0.652, not one uniform scale. HRV's weight within the Recovery domain fell from 0.5 to 0.3 (hearing and dental each rose from 0.25 to 0.35 to renormalize). Re-deriving the distribution after these changes moved the score-band cutoffs from 38/46/51/57/63 to 39/47/51/57/63, and the median reference profile's percentile from ~p75.4-75.8 down to ~p74.6-75.1 (male 74.636, female 75.058). Any score computed before this change is not directly comparable to one computed after it.

2026-07-29. The gait-speed addition below was revised after two problems turned up in the first version. First: the 1.2 m/s reference point is an unsourced judgment call, not a measured figure — Studenski et al. 2011 only measured adults 65+ (pooled mean 0.92 m/s); 1.2 m/s is this app's own recentring for a younger adult, now called out explicitly here, next to the gait-speed slider in the calculator, and in the source note below, rather than being folded silently into the model. Second, the weighting was fixed: the first version funded gaitSpeed's 0.15 weight in the Physical Capacity domain partly by cutting grip strength from 0.15 to 0.10 — grip strength has comparably strong, arguably more broadly-replicated all-cause-mortality evidence, so this read as favoring a newer, more speculative metric over an established one. Grip strength is restored to 0.15; the room for gaitSpeed now comes only from gaitSpeed's own initial allocation (0.15 → 0.10), leaving vo2max, steps, resting heart rate, and balance unchanged throughout. Re-deriving the distribution after this weight change moved the score-band cutoffs from 38/47/52/57/65 to 38/46/51/57/63 (close to the original pre-gait-speed 38/46/52/57/64), and the median reference profile's percentile from ~p73.7-74.1 back up to ~p75.4-75.8. Any score computed before this change is not directly comparable to one computed after it.

2026-07-29. Added usual gait speed (walked over a measured ~4-meter distance) as a 17th metric, in the Physical Capacity domain. Source: Studenski et al. 2011 (JAMA 305(1):50-58, PMID 21205966), a pooled analysis of 9 cohorts covering 34,485 community-dwelling adults 65 and older, one of the most validated all-cause-mortality predictors in geriatrics — age-adjusted HR for death of 0.88 (95% CI 0.87-0.90) per each 0.1 m/s higher gait speed. Because that cohort is older adults (mean age 73.5) and this app models a ~45-year-old reference population, the population median used for scoring (1.2 m/s) is a recentred judgment call rather than the source's own 0.92 m/s pooled mean. Adding a 17th metric shifted the simulated distribution slightly: score-band cutoffs moved from 38/46/52/57/64 to 38/47/52/57/65, and the median reference profile's percentile moved from ~p74.4-75.7 to ~p73.7-74.1. Any score computed before this change is not directly comparable to one computed after it.

2026-07-29. A check of the literature covered every ASSUMED spread parameter behind the simulated population used for percentiles and score bands. Most held up as the best defensible estimate and were left unchanged with stronger citations. One did not: VO2max's population SD was based on an inferred ACSM percentile-band width (6 mL/kg/min for both sexes); the FRIEND registry (Kaminsky et al. 2015, a large directly-measured cardiopulmonary exercise test cohort) reports the real figure as 9.6 (male) / 7.7 (female) — meaningfully wider. That widened the whole simulated distribution: the score-band cutoffs shifted (p80, previously 50, is now 52), and the median reference profile's percentile moved from ~p78.5-80.1 down to ~p74.4-75.7. Any score computed before 2026-07-29 is not directly comparable to one computed after it.

2026-07-27. The median reference profile behind every score was re-anchored on two markers. Daily steps moved from 5,500 steps/day (the same value for both sexes, which had no supporting source) to 8,500 (male) / 7,000 (female), based on NHANES accelerometer data and the All of Us Research Program. Grip strength moved from 42 kg (male) / 26 kg (female) to 41 kg / 29 kg, based on dominant-hand, best-of-trials norms from a NIH Toolbox study — and the model now states explicitly, for the first time, that it uses the dominant-hand convention throughout. VO2 max was reviewed against two disagreeing primary sources and deliberately left unchanged at 38 (male) / 31 (female), with the reasoning for that choice now written up in the model's source comments. Because the reference profile moved, the score-band cutoffs and the percentile shown next to a score also shifted slightly. Any score computed before 2026-07-27 is not directly comparable to one computed after it — re-run your numbers if you want an apples-to-apples comparison.

How much would the score move under different weights?

The weights above are one defensible allocation, not the uniquely correct one. To make that tradeoff inspectable rather than a single judgment call, we recompute the composite for a panel of 22 representative profiles (median-profile and single-metric deviations, both sexes) under four alternative weight sets: equal-weight across domains and members, cardiometabolic-heavy (50/30/20), physical-heavy (55/30/15), and one that swaps the sleep/fiber emphasis inside Lifestyle. The live model uses three domains and eight scored metrics.

The largest single swing observed, across every profile and every alternative weighting, is 12.0 points — a very-high-HbA1c profile scores 12 points lower under cardiometabolic-heavy weighting than under the current weights, because that alternative lifts the Cardiometabolic domain from its current 34% to 50% and HbA1c is the metric carrying that profile down. The next largest is 10.0 points: a very-high-VO2max profile scores 10 points lower under equal-weighting, which cuts VO2 max from its current 0.42 share of Physical Capacity to a uniform 0.25 and the domain itself from 44% to 33%. Averaged across all 22 profiles, the mean absolute swing is 2.2–3.5 points for the three domain-level alternatives. Swapping the sleep/fiber emphasis inside Lifestyle is by far the smallest — at most 1 point, 0.2 on average — since it reorders two members inside the lightest domain rather than touching the domain weights themselves.

This is presented as a bound on the current weights' influence, not a defense that they are uniquely correct: a handful of reasonable people could disagree on the weighting and move scores by about 2.2–3.5 points on average, or up to 12.0 points in the worst case we tested. Worth holding next to a fact from the roadmap — one realistic lifestyle change is typically worth 1–4 points. For the profiles at the extremes, the choice of weighting can matter more than the change you make.

Disclaimer. This tool is for educational purposes only and is not medical advice, diagnosis, or treatment. Consult a qualified healthcare professional about your own health. Read the full boundaries:What the score isn'tBack to the calculator →