The science behind the assessment

Biological sex is one of the strongest determinants of lifespan. Across virtually every country with reliable data, women outlive men by 4–7 years on average. The gap is driven by a combination of hormonal differences (oestrogen has cardioprotective effects), X-chromosome redundancy reducing expression of deleterious mutations, and behavioural differences in risk-taking and healthcare utilisation.

Source: WHO Global Health Observatory, 2023 World Health Statistics; Austad & Bartke, Cell Metabolism 2015.

Age sets your actuarial baseline — the median remaining lifespan for someone of your sex and age in the general population. As you age, your conditional life expectancy (the expected age at death given that you have survived to your current age) increases, because you have already survived the risks that claim others. A 70-year-old has a higher predicted lifespan than you might expect because they have survived to 70.

Source: UK ONS National Life Tables 2020–2022; WHO Life Tables 2023.

Life expectancy varies by up to 30 years between the highest and lowest countries. The gradient within high-income countries is smaller but still meaningful — Japan and Switzerland average 84–85 years, the US averages 77. Key drivers are healthcare system quality, diet norms (Mediterranean vs. ultra-processed), air quality, road safety, and social safety nets.

Source: The Lancet, Global Burden of Disease Study 2019 (195 countries); GHO 2023 life expectancy by country.

Urban walkability and air quality independently affect mortality. Walkable cities structurally increase daily movement without conscious effort — a study of 15 US cities found residents of highly walkable neighbourhoods lived 1.5 years longer than car-dependent equivalents. Air pollution (PM2.5) at high-traffic urban levels reduces lifespan by an estimated 1–3 years through chronic cardiovascular and pulmonary inflammation.

Source: Lancet Planetary Health 2021 (walkability study); WHO Global Air Quality Guidelines 2021; GBD Air Pollution Collaborators, NEJM 2017.

Waist circumference is a stronger predictor of cardiovascular mortality than BMI because it directly measures visceral adiposity — fat surrounding the organs. The INTERHEART study (27,000 people across 52 countries) found that waist-to-hip ratio explained 24.3% of attributable risk for myocardial infarction. Men with waist >102cm and women >88cm face substantially elevated cardiometabolic risk independent of weight.

Source: INTERHEART study, Lancet 2004; Janssen et al., CMAJ 2002; WHO waist circumference guidelines.

Resting heart rate (RHR) reflects autonomic nervous system tone and cardiac efficiency. A large Copenhagen Male Study (2,800 men, 16-year follow-up) found each 10-beat increase in RHR raised mortality risk by 16%. People with RHR above 90 bpm have roughly twice the cardiovascular mortality of those below 60 bpm. RHR is highly modifiable through aerobic exercise.

Source: Jensen et al., Heart 2012; Cooney et al., European Heart Journal 2010; Framingham Heart Study data.

VO2 max is the single strongest modifiable predictor of all-cause mortality in the research literature. A landmark JAMA study of 122,007 patients found that low cardiorespiratory fitness carried higher mortality risk than smoking, hypertension, diabetes, or high cholesterol. Moving from the lowest fitness quartile to the second lowest reduces mortality risk by 50%. Each MET (metabolic equivalent) increase in fitness is associated with a 13% reduction in mortality.

Source: Mandsager et al., JAMA Network Open 2018 (122,007 patients); Blair et al., JAMA 1989; Ross et al., Mayo Clinic Proceedings 2016.

Grip strength is a proxy for overall musculoskeletal health and is one of the most consistently replicated predictors of longevity in gerontology research. The PURE study (139,691 adults across 17 countries) found grip strength predicted cardiovascular mortality and all-cause mortality more strongly than systolic blood pressure. A 5kg reduction in grip strength was associated with a 17% increase in cardiovascular mortality.

Source: Leong et al., Lancet 2015 (PURE study, 139,691 adults); Rantanen et al., JAMA 1999; Metter et al., Journals of Gerontology 2002.

A meta-analysis of 15 studies (47,471 adults) published in JAMA Internal Medicine found that taking 7,000–8,000 steps per day was associated with a 50–70% lower risk of mortality compared to taking fewer than 4,000 steps. Benefits plateaued around 10,000 steps, and the relationship was dose-dependent. Importantly, step intensity (cadence) provided additional benefit independent of volume.

Source: Paluch et al., JAMA Internal Medicine 2021 (47,471 adults); Saint-Maurice et al., JAMA 2020; Tudor-Locke et al., IJBNPA 2011.

Muscle mass declines ~3–5% per decade after 30 (sarcopenia), increasing falls risk, insulin resistance, and metabolic dysfunction. A NHANES longitudinal study found that adults who resistance-trained twice weekly had 46% lower all-cause mortality odds. Resistance training also independently improves insulin sensitivity, bone density, and cardiovascular risk markers.

Source: Kraschnewski et al., Preventive Medicine 2016 (NHANES); Ruiz et al., BMJ 2008; Liu et al., BJSM 2019.

Sleep duration follows a U-shaped mortality curve — both too little and too much sleep are associated with elevated mortality. A meta-analysis of 16 prospective studies (1.3 million people) found that both short sleep (<6 hrs) and long sleep (>9 hrs) were associated with a 12% and 30% higher mortality risk respectively. The optimal window is 7–8 hours. Chronic short sleep impairs immune function, elevates cortisol, and accelerates cognitive decline.

Source: Cappuccio et al., Sleep 2010 (1.3M people); Gallicchio & Kalesan, Journal of Sleep Research 2009; National Sleep Foundation guidelines.

Sleep quality — measured by fragmentation, restorative depth, and subjective restedness — predicts mortality independently of duration. Poor sleep quality is associated with elevated inflammatory markers (IL-6, CRP), insulin resistance, and a threefold higher risk of hypertension. Restorative slow-wave sleep is essential for glymphatic clearance of amyloid-beta, linking sleep quality to dementia risk.

Source: Cappuccio et al., European Heart Journal 2011; Xie et al., Science 2013 (glymphatic system); Calhoun & Harding, Chest 2010.

Ultra-processed foods (UPF) — industrial formulations with five or more ingredients including additives, emulsifiers, and artificial flavourings — are associated with significantly higher all-cause mortality. A BMJ prospective study of 104,980 adults found each 10% increase in UPF consumption was associated with a 14% higher cancer risk. UPFs displace whole foods, drive overconsumption through hyperpalatability, and contain emulsifiers that disrupt gut microbiome integrity.

Source: Fiolet et al., BMJ 2018 (104,980 adults); Monteiro et al., Public Health Nutrition 2019 (NOVA classification); Srour et al., BMJ 2019.

A large meta-analysis (2 million people, 95 studies) published in the International Journal of Epidemiology found that consuming 800g of fruit and vegetables per day (approximately 10 servings) was associated with a 31% reduction in cardiovascular disease and a 13% reduction in all-cause mortality. Benefits were strongest for green leafy vegetables, citrus, and cruciferous vegetables. Even modest increases from a low baseline yield meaningful risk reduction.

Source: Aune et al., International Journal of Epidemiology 2017 (2M people, 95 studies); Wang et al., Circulation 2021; WHO fruit and vegetable guidelines.

The previously claimed J-curve benefit of moderate alcohol has been substantially revised. The GBD 2016 Alcohol Collaborators study (28 million people, 195 countries) concluded that the safest level of alcohol consumption is zero, and that any cardiovascular benefit is offset by increased cancer risk. Risk rises linearly with consumption. Alcohol is a Group 1 carcinogen (IARC), linked to seven cancer types including breast, colorectal, and oesophageal.

Source: GBD 2016 Alcohol Collaborators, Lancet 2018 (28M people, 195 countries); Wood et al., Lancet 2018; IARC Monograph Vol. 100E.

Smoking is responsible for approximately 8 million deaths per year globally. The British Doctors Study — a 50-year prospective study of 34,439 male doctors — established that lifelong smokers lose an average of 10 years of life, while those who quit by age 30 recover almost all of that loss. Ex-smokers who quit by 40 recover approximately 9 of the 10 years. The benefit of quitting is substantial at any age.

Source: Doll et al., BMJ 2004 (British Doctors Study, 50-year follow-up); Jha et al., NEJM 2013 (Cancer Prevention Study II, 216,917 people).

Loneliness and social isolation are now considered public health crises. A meta-analysis of 148 studies (308,849 people) by Holt-Lunstad et al. found that adequate social relationships increased survival odds by 50%, while loneliness carried a mortality risk comparable to smoking 15 cigarettes per day. Isolation elevates cortisol chronically, impairs immune function, and doubles dementia risk in older adults.

Source: Holt-Lunstad et al., PLOS Medicine 2010 (308,849 people, 148 studies); Cacioppo & Hawkley, Neuroscience & Biobehavioral Reviews 2009; National Academies of Sciences 2020 report on social isolation.

Chronic psychological stress accelerates biological ageing through multiple pathways: HPA axis dysregulation, chronic cortisol elevation, telomere shortening, and systemic inflammation. A study of mothers caring for chronically ill children found that high-stress caregivers had telomeres equivalent to 9–17 additional years of ageing. Work-related stress specifically is associated with a 40% increased risk of cardiovascular disease.

Source: Epel et al., PNAS 2004 (telomere shortening and stress); Steptoe et al., European Heart Journal 2012; Chandola et al., European Heart Journal 2008.

A strong sense of purpose is consistently associated with reduced all-cause mortality and cardiovascular disease. The MIDUS study (6,800 Americans) found that high purpose in life was associated with a 15% reduction in all-cause mortality over 14 years. Purpose may operate through better health behaviours (people with purpose are more likely to exercise, sleep well, and attend medical appointments) and through direct psychoneuroimmunological pathways.

Source: Kim et al., Psychosomatic Medicine 2013 (MIDUS, 6,800 participants); Boyle et al., Archives of General Psychiatry 2009; Cohen et al., Psychological Science 2016.

Diagnosed chronic conditions are applied as direct actuarial adjustments based on meta-analyses of condition-specific life expectancy data. Type 2 diabetes reduces lifespan by approximately 6 years (UKPDS); cardiovascular disease by 7–10 years depending on severity (Framingham); hypertension by 5 years if untreated. The model reflects managed (treated) rather than untreated burden, as treatment significantly modifies outcomes.

Source: UK Prospective Diabetes Study (UKPDS); Framingham Heart Study 60-year data; GBD 2019 Disease Collaborators, Lancet 2020.

Hypertension is the single largest modifiable risk factor for cardiovascular disease globally, responsible for 10.4 million deaths annually (GBD 2019). The SPRINT trial demonstrated that intensive blood pressure control (target <120 mmHg systolic) reduced cardiovascular events by 25% and all-cause mortality by 27% compared to standard control. Each 10 mmHg reduction in systolic BP reduces major cardiovascular events by approximately 20%.

Source: SPRINT Research Group, NEJM 2015 (9,361 participants); Lewington et al., Lancet 2002 (meta-analysis, 1M adults); GBD 2019 Risk Factors Collaborators.

Parental longevity is a proxy for genetic predisposition. Heritability of lifespan is estimated at 25–33% (Hjelmborg et al., Human Genetics 2006 — the largest twin study of longevity to date, across four Scandinavian countries). Having both parents survive past 90 approximately doubles the odds of living to 90 yourself. However, the model applies parental longevity conservatively — genetic factors are largely already captured in other modifiable risk factors, which carry the majority of variance.

Source: Hjelmborg et al., Human Genetics 2006 (Scandinavian twin study); Sebastiani et al., Science 2010 (centenarian genome study); Perls et al., Journal of the American Geriatrics Society 2002.