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Every row of the evidence table
One row per finding: what was tested, which way the result went, and how the study was built. The answer by area, and where the studies disagree, are on the main page.
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Showing 27 of 382 rows. One row per study per exposure: a study that tested two different things appears twice, once for each.
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| Exposure | Question | Direction | Outcome measured | Design | People | Effect size, as the source reported it | Source |
|---|---|---|---|---|---|---|---|
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Mixed
whyThe two measures moved in opposite directions over 2015-2021: standardised incidence fell from 3.5% to 2.8% per year while prevalence rose from 10.5% to 11.8%; gaps between Black or Hispanic and White beneficiaries narrowed. |
Age- and sex-standardised incidence and prevalence of diagnosed dementia among US Medicare fee-for-service beneficiaries, 2015-2021 | cohort study | not stated | The overall age and sex standardized incidence decreased between 2015 and 2021 from 3.5% to 2.8%. Prevalence increased during this time from 10.5% to 11.8% |
BMJ
2025 ✓ Peer-reviewed PMID 40393738 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Benefit
whyDirection is for more recent birth cohort: after controlling for age and period, later-born cohorts were less likely to have dementia in all three regions, more so among women; the point estimates for men in England were not significant. |
Age-specific dementia prevalence by birth cohort in the US, Europe and England | cross-sectional study | 62,437 | point estimate for 1944-1948 vs 1919-1923 cohorts: US, -0.55 [95% CI, -0.77 to -0.34] vs -0.18 [95% CI, -0.25 to -0.10]; Europe, -1.49 [95% CI, -1.72 to -1.27] vs -0.24 [95% CI, -0.35 to -0.13]; and England, -0.48 [95% CI, -0.89 to -0.08] vs -0.23 [95% CI, -0.38 to -0.07] |
JAMA Network Open
2025 ✓ Peer-reviewed PMID 40455442 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Benefit
whyDirection is for later birth cohort: each successive cohort had a significantly lower incident dementia rate, independent of sex, education and age. |
Incident dementia rate by decade of birth (1902-1941) | cohort study | 3,010 | Compared to the earliest birth cohort (1902-1911), each subsequent cohort had a significantly lower incident dementia rate (1912-1921: incidence rate ratio [IRR] = 0.655, 95% confidence interval [95% CI] = 0.477-0.899; 1922-1931: IRR = 0.387, 95% CI = 0.265-0.564; 1932-1941: IRR = 0.233, 95% CI = 0.121-0.449) |
The Journals of Gerontology: Series A (Biological Sciences and Medical Sciences)
2019 ✓ Peer-reviewed PMID 30312371 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Benefit
whyDirection is for the later survey year: prevalence fell from 11.6% to 8.8%, with rising education associated with some of the decline despite a worse cardiovascular risk profile. |
Dementia prevalence among US adults 65+, 2000 versus 2012 | cross-sectional study | 21,057 | Dementia prevalence among those 65 years or older decreased from 11.6% (95% CI, 10.7%-12.7%) in 2000 to 8.8% (95% CI, 8.2%-9.4%) (8.6% with age- and sex-standardization) in 2012 (P < .001) |
JAMA Internal Medicine
2017 ✓ Peer-reviewed PMID 27893041 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Benefit
whyDirection is for later calendar epoch: incidence fell 44% from the first to the fourth epoch, but only among people with at least a high school diploma. The authors could not fully explain the decline. |
5-year incidence of dementia across four epochs (late 1970s to early 2010s) | cohort study | 5,205 | The 5-year age- and sex-adjusted cumulative hazard rates for dementia were 3.6 per 100 persons during the first epoch (late 1970s and early 1980s), 2.8 per 100 persons during the second epoch (late 1980s and early 1990s), 2.2 per 100 persons during the third epoch (late 1990s and early 2000s), and 2.0 per 100 persons during the fourth epoch (late 2000s and early 2010s). Relative to the incidence during the first epoch, the incidence declined by 22%, 38%, and 44% during the second, third, and fourth epochs, respectively. This risk reduction was observed only among persons who had at least a high school diploma (hazard ratio, 0.77; 95% confidence interval, 0.67 to 0.88) |
New England Journal of Medicine
2016 ✓ Peer-reviewed PMID 26863354 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
Benefit
whyDirection is for the later-born population: prevalence was 6.5% against the 8.3% expected from the earlier study (odds ratio 0.7), which the authors read as a cohort effect. |
Dementia prevalence at age 65+ in three English areas, CFAS II (2008-11) versus CFAS I (1989-94) | cross-sectional study | 15,431 | Using CFAS I age and sex specific estimates of prevalence in individuals aged 65 years or older, standardised to the 2011 population, 8·3% (884,000) of this population would be expected to have dementia in 2011. However, CFAS II shows that the prevalence is lower (6·5%; 670,000), a decrease of 1·8% (odds ratio for CFAS II vs CFAS I 0·7, 95% CI 0·6-0·9, p=0·003) |
The Lancet
2013 ✓ Peer-reviewed PMID 23871492 |
| Birth cohort and calendar period (secular trend in dementia) All modifiable factors together | Prevention |
No effect
whyIncidence was consistently but non-significantly lower in the 2000 subcohort (rate ratio 0.75, 95% CI 0.56-1.02, borderline). The authors read the pattern, together with lower mortality and larger brain volumes, as suggesting a decline, but the primary comparison did not reach significance. |
Age-adjusted dementia incidence, 2000 subcohort versus 1990 subcohort | cohort study | 7,496 | Age-adjusted dementia incidence rates were consistently, yet nonsignificantly, lower in the 2000 subcohort in all strata, reaching borderline significance in the overall analysis (incidence rate ratio 0.75, 95% confidence interval [CI] 0.56-1.02). Mortality rates were also lower in the 2000 subcohort (rate ratio 0.63, 95% CI 0.52-0.77) |
Neurology
2012 ✓ Peer-reviewed PMID 22551732 |
| Mixed neuropathology at autopsy (LATE-NC, Lewy, vascular, ADNC) All modifiable factors together | Prevention |
Harm
whyDirection is for degenerative pathology profiles: more than 80% had mixed pathologies, and of five clustered profiles the LATE-NC/hippocampal sclerosis and the ADNC/amyloid angiopathy profiles showed the fastest cognitive decline. |
Latent neuropathologic profiles at autopsy and their associated cognitive trajectories over up to 30 years | cohort study | 1,633 | not established — pubmed abstract results gives profile sizes but no numeric estimate of the differences in cognitive decline. |
JAMA Network Open
2026 ✓ Peer-reviewed PMID 41543852 |
| Mixed neuropathology at autopsy (LATE-NC, Lewy, vascular, ADNC) All modifiable factors together | Prevention |
Harm
whyDirection is for LATE-NC: found in 64% of brains, stages 1a, 2 and 3 were associated with dementia and lower MMSE, it was among the strongest independent predictors of dementia, and its attributable risk (24.2%) exceeded that of Alzheimer's neuropathologic change (18.6%); it usually occurred alongside other pathologies. |
Frequency of LATE-NC at autopsy in people aged 85+, and its association with dementia and MMSE alongside other pathologies | cohort study | 295 | LATE-NC was found in 189 of 295 subjects (64.1%) ... When LATE-NC and ADNC were assessed in a multivariate model without other dementia-associated pathologies, the attributable risk was higher for LATE-NC than ADNC (24.2% versus 18.6%) |
Brain
2025 ✓ Peer-reviewed PMID 38938199 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors. The Danish estimate (37.8% across 16 factors) is lower than the Lancet Commission's global 45%. |
Population attributable fraction of dementia | cohort study | 1,753,515 | Overall population attributable fraction 37.8% (95% CI 35.6-40.0); infections 9.4%, depression 8.7%, CVD 7.6% |
The Lancet Public Health
2026 ✓ Peer-reviewed PMID 42425116 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors: depression, diabetes, low education, smoking, obesity, physical inactivity and alcohol overconsumption each independently raised the hazard of early-onset dementia, and most associations were stronger for early-onset than late-onset dementia. |
Incident early-onset dementia (before 65) and late-onset dementia over a median 13.7 years | cohort study | 544,442 | Black versus White race (1·61 [1·23-2·11]), grade school education or less (1·99 [1·67-2·38]), diabetes (2·45 [1·99-3·03]), depression (2·73 [2·34-3·20]), smoking (1·86 [1·56-2·22]), obesity (1·24 [1·04-1·48]), physical inactivity (1·33 [1·11-1·59]), and alcohol overconsumption (1·22 [1·01-1·47]) were independently associated with higher hazards of early-onset dementia |
The lancet. Healthy longevity
2026 ✓ Peer-reviewed PMID 41936382 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors. Which factor mattered most differed by APOE risk group, on 2,065 cases split across 11 factors and three genetic strata, so the subgroup estimates are imprecise. |
Incident all-cause dementia over 12.4 years | cohort study | 182,473 | Low social contact HR 3.86 (95% CI 2.08-7.17) in low APOE risk group; less education PAF 11.35% in high APOE risk group |
Annals of Neurology
2025 ✓ Peer-reviewed PMID 41085200 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying hypertension, diabetes or smoking. The attributable share rose with the age at which the factors were measured (22% at 45-54, 44% at 65-74), which is what you would expect if some of it is reverse causation rather than cause. |
Population attributable fraction of dementia by age 80 | cohort study | 12,274 | 22-44% of dementia by age 80 attributable to hypertension, diabetes or smoking |
JAMA Neurology
2025 ✓ Peer-reviewed PMID 40455489 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors: the Commission attributes 45% of cases to 14 modifiable factors, which is the same number read the other way as prevention potential. The Commission's own caveat is that "some associations might be only partly causal". |
Population attributable fraction of dementia | systematic review | not stated | "estimated that the PAF for all 14 risk factors was 45.3%" (Table 1: overall PAF 45.3%, rounded 45%); high LDL cholesterol unweighted PAF 18.7%, weighted 6.9%, rounded 7%; untreated vision loss unweighted 6.0%, weighted 2.2%, rounded 2% |
The Lancet
2024 ✓ Peer-reviewed PMID 39096926 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors. 39 candidate factors were screened against 485 cases, so individual estimates are imprecise. |
Incident young-onset dementia | cohort study | 356,052 | 485 incident young-onset dementia cases (16.8 per 100,000 person-years) among 356,052 participants; 39 candidate risk factors tested, most of the associated factors modifiable |
JAMA Neurology
2024 ✓ Peer-reviewed PMID 38147328 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the risk factors. The weighted combined estimate (32.0% for seven factors) is lower than the Lancet Commission's 45% for 14. |
Population attributable fraction of dementia | meta-analysis | not stated | Weighted combined PAF 32.0% (95% CI 26.6-37.5) for seven modifiable factors |
Lancet Healthy Longevity
2024 ✓ Peer-reviewed PMID 38824956 |
| Modifiable risk factors combined All modifiable factors together | Prevention |
Harm
whyFor the vascular risk factors: up to a quarter of the education-dementia association ran through hypertension, diabetes and related midlife factors, so carrying them accounted for part of the excess risk. |
Incident dementia | cohort study | 13,368 | 8-44% lower dementia risk with higher education vs grade school; up to 25% mediated by midlife vascular risk factors |
Annals of Neurology
2023 ✓ Peer-reviewed PMID 36966451 |
| Peripheral diseases combined (population attributable fraction) All modifiable factors together | Prevention |
Harm
whyDirection is for carrying the peripheral diseases: together they were related to about one-third of global dementia burden, led by periodontal disease, chronic liver disease, hearing loss, vision loss and type 2 diabetes. Attributable fractions assume the pooled associations are causal. |
Population attributable fraction of global dementia burden for 16 peripheral diseases | meta-analysis | not stated | Globally, these peripheral diseases collectively were related to a combined PAF of 33.18% (95% confidence interval (CI) 16.80-48.43) of dementia burden, corresponding to 18.8 million prevalent cases. The leading ten PAF contributors were periodontal diseases (6.10%, 95% CI 0.95-10.28), cirrhosis and other chronic liver diseases (5.51%, 95% CI 1.77-8.86), age-related and other hearing loss (4.70%, 95% CI 3.51-6.06), blindness and vision loss (4.30%, 95% CI 3.43-5.05), type 2 diabetes mellitus (3.80%, 95% CI 3.06-4.53) |
Nature human behaviour
2026 ✓ Peer-reviewed PMID 41559195 |
| Population burden (prevalence, incidence, lifetime risk) All modifiable factors together | Prevention |
No direction reported
whyA burden-of-disease decomposition: age-standardised rates rose slightly and population growth was the largest driver of the rise in cases. It compares no exposure, so no direction is recorded. |
Global prevalence, incidence, mortality and DALYs of young-onset dementia, 1990-2021 | modelling study | not stated | Global age standardized prevalence and incidence of dementia among people under 65 years increased from 93.39 and 16.24 per 100,000 persons in 1990 to 96.09 and 17.16 per 100,000 persons in 2021; mortality increased from 0.89 per 100,000 population to 0.91 per 100,000 population; and age standardized DALYs increased from 45.60 per 100,000 persons to 46.78 per 100,000 persons |
Translational Psychiatry
2025 ✓ Peer-reviewed PMID 39966345 |
| Population burden (prevalence, incidence, lifetime risk) All modifiable factors together | Prevention |
No direction reported
whyA lifetime-risk estimate (42% after age 55, higher in women, Black adults and APOE4 carriers) and a projection of new cases. It compares no exposure, so no direction is recorded. |
Lifetime risk of dementia from age 55, and projected annual US incident cases to 2060 | cohort study | 15,043 | The lifetime risk of dementia after age 55 years was 42% (95% confidence interval: 41-43). Rates were substantially higher in women, Black adults and APOE ε4 carriers, with lifetime risks ranging from approximately 45% to 60% in these populations. The number of US adults who will develop dementia each year was projected to increase from approximately 514,000 in 2020 to approximately 1 million in 2060 |
Nature Medicine
2025 ✓ Peer-reviewed PMID 39806070 |
| Population burden (prevalence, incidence, lifetime risk) All modifiable factors together | Prevention |
No direction reported
whyA pooled incidence and prevalence estimate with no exposure compared, so no direction is recorded. |
Pooled incidence and prevalence of frontotemporal dementia | meta-analysis | not stated | Pooled crude incidence for FTD was 2.28 (95% CI, 1.55-3.36) per 100 000 person-years and prevalence, 9.17 (95% CI, 3.59-23.42) per 100 000 people |
JAMA Neurology
2025 ✓ Peer-reviewed PMID 40920400 |
| Population burden (prevalence, incidence, lifetime risk) All modifiable factors together | Prevention |
No direction reported
whyA prevalence estimate and forecast: cases are projected to rise from 57.4 million to 152.8 million while age-standardised prevalence stays flat, with the rise attributed to population growth and ageing. It compares no exposure, so there is no direction to record. |
Number of people with dementia worldwide, 2019 and forecast to 2050 | modelling study | not stated | We estimated that the number of people with dementia would increase from 57·4 (95% uncertainty interval 50·4-65·1) million cases globally in 2019 to 152·8 (130·8-175·9) million cases in 2050. Despite large increases in the projected number of people living with dementia, age-standardised both-sex prevalence remained stable between 2019 and 2050 (global percentage change of 0·1% [-7·5 to 10·8]) |
The Lancet Public Health
2022 ✓ Peer-reviewed PMID 34998485 |
| Population burden (prevalence, incidence, lifetime risk) All modifiable factors together | Prevention |
No direction reported
whyA pooled prevalence estimate with no exposure compared, so there is no direction to record. |
Global prevalence of young-onset dementia (ages 30-64) | meta-analysis | 2,760,379 | Age-standardized prevalence estimates increased from 1.1 per 100 000 population in the group aged 30 to 34 years to 77.4 per 100 000 population in the group aged 60 to 64 years. This gives an overall global age-standardized prevalence of 119.0 per 100 000 population in the age range of 30 to 64 years, corresponding to 3.9 million people aged 30 to 64 years living with YOD in the world |
JAMA Neurology
2021 ✓ Peer-reviewed PMID 34279544 |
| Race and ethnicity (population comparison) All modifiable factors together | Prevention |
Harm
whyDirection is for being African-American or American Indian/Alaska Native relative to Asian-American members: incidence was highest in those groups (26.6 and 22.2 per 1000 person-years) and lowest in Asian-Americans (15.2). The authors present this as a benchmark for reducing disparities, not as a biological effect of race. |
Dementia incidence 2000-2013 and 25-year cumulative risk at age 65 | cohort study | 274,283 | Dementia incidence (n = 59,555) was highest for African-Americans (26.6/1000 person-years) and AIANs (22.2/1000 person-years); intermediate for Latinos (19.6/1000 person-years), Pacific Islanders (19.6/1000 person-years), and whites (19.3/1000 person-years) and lowest among Asian-Americans (15.2/1000 person-years). Risk was 65% greater for African-Americans (hazard ratio = 1.65; 95% confidence interval = 1.58-1.72) versus Asian-Americans |
Alzheimer's & Dementia
2016 ✓ Peer-reviewed PMID 26874595 |
| Sex and gender differences (research agenda) All modifiable factors together | Prevention |
No direction reported
whyA position paper from an expert network. It sets out 12 priority research areas on sex and gender in Alzheimer's disease and reports no effect estimate. |
None measured (research agenda) | None | not stated | not established — position paper; the abstract reports no effect estimate. |
Alzheimer's & Dementia
2018 ✓ Peer-reviewed PMID 29907423 |
| Sex differences (biological sex as exposure) All modifiable factors together | Prevention |
Harm
whyDirection is for female sex: at higher amyloid levels women had higher plasma p-tau217 than men, greater tau deposition and accumulation at a given p-tau217 level, and faster cognitive decline in two of the cohorts. |
Plasma p-tau217 by sex and amyloid load; tau PET accumulation and cognitive decline | cohort study | 1,292 | Compared with men, women had significantly higher baseline p-tau217 levels at higher aggregated Aβ Centiloid levels (β, -0.21 [95% CI, -0.37 to -0.05], P = .009; highest interaction was found in the Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease/Longitudinal Evaluation of Amyloid Risk and Neurodegeneration [A4/LEARN] cohort) |
JAMA neurology
2026 ✓ Peer-reviewed PMID 41697669 |
| Sex differences (biological sex as exposure) All modifiable factors together | Prevention |
Harm
whyDirection is for female sex: women had higher odds of a high neuritic plaque burden than men after adjustment, and were more likely to reach Braak stage V-VI. Black non-carriers and non-carriers of African ancestry were least likely to have high plaque burden, a protection weakened in ε4 carriers. |
Neuritic plaque burden (CERAD score) at autopsy by sex, and its interaction with APOE ε4, race and African ancestry | cross-sectional study | 2,268 | Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P < .001), and this association remained significant in adjusted models for sociodemographic and vascular factors and APOEε4 status (adjusted OR, 1.65; 95% CI, 1.33-2.20; P < .001). APOEε4 carriers of both sexes had an approximately 4-fold greater odds of plaques |
JAMA neurology
2026 ✓ Peer-reviewed PMID 41729539 |