Every row of the evidence table

Direction 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.

Direction 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.

A pooled incidence and prevalence estimate with no exposure compared, so no direction is recorded.

A pooled prevalence estimate with no exposure compared, so there is no direction to record.

Direction is for an older-than-chronological sleep EEG brain age: each 10-year increase in the index was associated with a 39% higher risk of incident dementia, consistent across sex and age groups.

Direction is for a healthier plant-based diet: higher overall and healthful plant-based diet scores were associated with lower dementia risk, while a higher unhealthful plant-based diet score was associated with higher risk (pooled HR 1.42).

Pooled observational studies only.

Observational. Points the opposite way to the randomised MIND diet trial.

Observational. Points the opposite way to the randomised MIND diet trial.

Pooled observational studies only.

Dietary intake and blood levels, pooled from observational cohorts. The much larger supplement estimate (HR 0.36) comes from one cohort's self-selected supplement users, not from a trial.

Heterogeneity was extreme (I-squared 97%), so the pooled figure hides large differences between the 10 studies.

Heterogeneity was high (I-squared 95%). Reaches a firmer conclusion than the earlier BMJ meta-analysis of largely the same literature.

The overall PM2.5 estimate includes no effect (HR 1.04, 95% CI 0.99-1.09). Only the studies that actively assessed everyone for dementia showed a clear effect (HR 1.42, 95% CI 1.00-2.02). Most studies were at high risk of bias.

High overall and leisure-time activity were associated with lower dementia risk, but occupational and commuting activity were associated with higher risk. Certainty of evidence was very low to low.

The authors call the association weak (RR 0.97), and it was absent beyond 10 years of follow-up.

Pooled across 29 cohorts. The association weakened to HR 0.85 after maximal confounder adjustment and was not significant for low-intensity activity.

The authors state the association held in longer follow-ups, which is their answer to the reverse-causation objection raised by the Whitehall II cohort.

Seven small trials; working memory did not improve (P=0.14).

Direction is for a high polygenic score (excluding APOE): people in the top decile had a twofold risk of Braak stage >4 tangles and of moderate-to-severe amyloid plaque pathology at death. 91 loci identified, 16 new; 18 further loci await validation.

Locus-discovery genome-wide association study: it reports which genetic regions reached significance and no effect estimate for any exposure, so no direction is recorded. The study reports 14 new loci for clinically diagnosed AD and two from AD-by-proxy.

Direction is for carrying a higher genetic risk score: risk of AD rose 1.6- to 1.9-fold from the lowest to the highest decile, over and above age and APOE4. The main output is 75 risk loci, 42 new.

Direction is for having the impairment. Dual sensory impairment carried the highest risk (HR 1.63 for all-cause dementia, 2.55 for Alzheimer's).

Mostly observational (25 of 31 studies), so people who take up hearing aids may differ from those who do not. The authors call for randomised trials — and ACHIEVE, the trial that followed, was null overall.

Against untreated cataract. People who had surgery ended up at about the same risk as controls who never had cataracts (HR 0.84, 95% CI 0.66-1.06), and there was no short-term gain in those already cognitively impaired.

Direction is for having a vision impairment. Single vision impairment raised all-cause dementia risk but not Alzheimer's specifically; having both hearing and vision impairment carried the highest risk.

Pooled observational studies, so open to the confounding the natural-experiment studies were designed to avoid.

Antihypertensive treatment improved cognitive scores by a small amount (SMD 0.06, moderate certainty) but the reduction in dementia incidence was not statistically significant (OR 0.89, low certainty). The drug-class rankings rest on one trial per class and are described as highly uncertain.

Antihypertensive use tracked lower Alzheimer's risk but not lower non-Alzheimer dementia risk, where treated and untreated hypertension looked the same. A single baseline blood pressure reading predicted neither.

Individual participant data from five double-blind placebo-controlled trials, which is the strongest design in this table for this exposure.

Consistent across 14 trials (I-squared 0%) but small in absolute terms: 0.39 percentage points over about 4 years.

Heterogeneity was near-total (I-squared 98.9%) and the estimate went to null in people newly diagnosed with diabetes (HR 1.01), which is where prevalent-user bias would be smallest.

The split inside this one paper is the finding: the 41 observational studies show large benefits (SGLT2i OR 0.56, GLP-1RA OR 0.58) while the 23 randomised trials show no difference. When design and result disagree this cleanly, the trials are the ones to believe.

Education and job complexity each contributed independently; about 28% of the education effect ran through occupation.

Effect held over and above measured Alzheimer's pathology, which is the point of the reserve idea.

Eight kinds of sleep disturbance were analysed; both short and long sleep carried higher risk, as did excessive daytime sleepiness and insomnia.

No significant association with vascular dementia, and none of the 11 studies used biomarkers to confirm the diagnoses.

Persisted after controlling for depression and social isolation.