The evidence behind every factor Halo asks about

Search and filter the primary research behind Halo's longevity model — what the evidence shows, how strong it is, and where its limits are — with a link to every original study.

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Strong evidence
Moderate evidence
Limited evidence

Evidence quality is graded per record, not for the library as a whole. Each card names the specific reliability or bias concerns that apply — self-report accuracy, reverse causation, confounding — next to the claim they qualify.

These summarise population-level associations. They describe patterns across large groups of people, not a prediction about you specifically.

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34 results
Cohort study
Never smoker = reference; current smoking ~2.18–2.81× mortality in large cohorts; former smokers can approach never-smoker risk after prolonged cessation
Causal status: Causal support strong; mortality evidence mostly prospective
Reliability / bias notes: Self-report; pack-years and cessation timing matter; reverse causation can affect recent quitters
Banks et al · BMC Med · 2015 · PMID 25857449
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Meta-analysis
Highest vs lowest GGT quartile associated with 56% higher all-cause mortality (pooled RR 1.56, 95% CI 1.34–1.83) across 7 prospective cohorts, 273,141 participants
Causal status: Associational; proposed independent of alcohol intake but mechanism as a general oxidative-stress/liver marker not fully causal
Reliability / bias notes: GGT is nonspecific (affected by alcohol, medications, fatty liver); Asian subgroup result not significant
Du et al · Prev Med · 2013 · PMID 23571185
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Observational study
Danish cohort: premature family CVD death IRR ~1.72 for any CVD, ~2.21 for IHD; multiple affected relatives much higher
Causal status: Association/genetic + shared environment
Reliability / bias notes: Family-history accuracy; incomplete pedigree; mixed genetic and shared behavioural pathways
Ranthe et al · JACC · 2012 · PMID 22917005
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Observational study
Front-seat seat-belt use reduces fatal/nonfatal injury risk by ~60%; trauma database mortality OR ~0.49 vs no restraint
Causal status: Strong causal/interventional evidence for crash injury prevention
Reliability / bias notes: Crash-conditioned evidence; risk-taking behaviours correlated with non-use
Cummins et al. · 2011 · PMID 21720604
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Meta-analysis
Each 3-fold (1-SD) higher log-CRP associated with 1.55x non-vascular mortality (95% CI 1.41–1.69) and similar magnitude for vascular mortality, in an individual-participant meta-analysis of 160,309 people across 54 studies
Causal status: Causal role debated; CRP likely partly a marker of underlying inflammation/disease rather than a direct cause
Reliability / bias notes: Association attenuates but persists after adjusting for conventional risk factors and fibrinogen; residual confounding by subclinical illness possible
Emerging Risk Factors Collaboration (Kaptoge et al) · Lancet · 2010 · PMID 20031199
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Observational study
In nondiabetic adults, glycated hemoglobin showed a J-shaped association with death from any cause, remaining significant after adjustment for fasting glucose, in the ARIC cohort (n=11,092)
Causal status: Causal support strong for diabetes/CVD risk; all-cause mortality relationship J-shaped, so causal direction less clear at low HbA1c
Reliability / bias notes: J-shaped curve means very low HbA1c also carries excess mortality risk, likely reflecting reverse causation/frailty; overlaps with the separate diagnosed-diabetes question, so effects are kept modest to avoid double-counting the same underlying condition
Selvin et al · N Engl J Med · 2010 · PMID 20200384
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Mobile phone use and motor vehicle crash risk / hospital attendance

Moderate for crash risk; limited for mortality
Observational study
Crash case-crossover OR 4.1 for phone use within 5 min before crash; culpability OR 1.70 in another study
Causal status: Strong causal plausibility for crash impairment; direct mortality estimate limited
Reliability / bias notes: Self-report/recall; exposure definition; no robust all-cause mortality coefficient
McEvoy et al. · 2007 · PMID 17920840
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Observational study
Adjusted death risk rose stepwise as eGFR fell below 60 mL/min/1.73m2, from HR 1.2 (eGFR 45–59) up to HR 5.9 (eGFR <15), in a cohort of 1.12 million adults
Causal status: Causal support strong; graded, dose-dependent association independent of comorbidities
Reliability / bias notes: Single-measurement creatinine-based eGFR; residual confounding by unmeasured comorbidity possible
Go et al · N Engl J Med · 2004 · PMID 15385656
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Cohort study
1-SD decrement in low-frequency HRV power associated with 1.70x greater all-cause mortality hazard (95% CI 1.37–2.09) over 4 years in an elderly community cohort
Causal status: Associational; reflects autonomic dysfunction, prognostic value shown independent of traditional risk factors
Reliability / bias notes: Older, smaller cohort (n=736, 74 deaths); short 2-hour ECG recording window; results in elderly may not generalize to younger adults
Tsuji et al · Circulation · 1994 · PMID 8044959
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Cohort study
Job strain meta-analysis: CHD RR ~1.26; multicohort mortality HR 1.68 in men with cardiometabolic disease
Causal status: Association
Reliability / bias notes: Construct heterogeneity; socioeconomic confounding; reverse causation
PMID 29884468
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