Dementia Prevention

The Lancet Commission's 14 modifiable risk factors account for nearly half of all dementia cases. Hearing loss is the largest single midlife factor, hypertension is the most aggressively treatable, and the rest read like a cardiovascular health checklist — because that's what they are.

The 2024 Lancet Commission on Dementia Prevention identified 14 modifiable risk factors that together account for ~45% of dementia cases globally. Acting on these is the most impactful thing most adults can do for long-term cognitive health.

The Lancet Commission framework

The 2024 Lancet Commission update ranks modifiable risk factors by population attributable fraction (PAF) — the proportion of dementia cases that would not occur if the risk factor were eliminated.^[1]

Early life

Less education (PAF ~5%) — cognitive reserve

Midlife (40s–60s)

Hearing loss (PAF ~7%) — largest single midlife factor
High LDL cholesterol (newly added 2024, PAF ~7%)
Hypertension (PAF ~2%) — but high effect at the individual level
Obesity (PAF ~1%)
Excessive alcohol (PAF ~1%)
Traumatic brain injury (PAF ~3%)

Later life (60+)

Smoking (PAF ~2%)
Depression (PAF ~3%)
Social isolation (PAF ~5%)
Physical inactivity (PAF ~2%)
Diabetes (PAF ~2%)
Air pollution (PM2.5) (PAF ~3%)
Visual impairment (newly added 2024, PAF ~2%)

The PAFs sum to ~45%. The remaining ~55% is non-modifiable (genetics, age, female sex for Alzheimer's specifically) or as-yet unidentified.

The biggest individual levers

1. Treat hearing loss

The single largest modifiable midlife factor.
The ACHIEVE trial 2023 showed hearing aids reduced cognitive decline in high-risk older adults (those with cardiovascular risk factors).^[2]01406-X/fulltext)
A 2026 target trial emulation in the ASPREE cohort (n = 2,777, dementia-free at baseline, 7-year follow-up) found hearing aid prescription cut 7-year incident dementia from 7.5% to 5.0% (RR 0.67), with a clean dose-response by frequency of use.^[3]
Mechanisms: reduced cognitive load from auditory effort; preserved social engagement; reduced isolation.
Action: Get audiometry if any decline suspected. If you pass a standard audiogram but struggle in noise, ask for extended high-frequency (EHF) audiometry — it explains ~64% of age-related variance in real-world speech understanding vs. ~16% for the standard test. Hearing aids are not vanity, modern devices are small and effective, and the device that lives in a drawer doesn't count. See Hearing for the full picture.

2. Aggressively treat hypertension in midlife

SPRINT-MIND found intensive BP control (target <120 mmHg systolic) reduced incident MCI and dementia compared to standard control (<140).^[4]
The 2024 Commission specifically calls for systolic <130 in midlife.
Most effective: lifestyle (DASH, exercise, weight loss) + medication if needed.

3. Manage cardiometabolic health

Type 2 diabetes roughly doubles dementia risk. Well-controlled diabetes is much less damaging than uncontrolled.
Visceral obesity specifically — central adiposity correlates with dementia more than total weight.
High LDL — the 2024 addition reflects accumulating evidence that vascular contribution to dementia is larger than previously recognized.
Action: track HbA1c, lipid panel, BP, waist circumference. Treat aggressively in midlife.

4. Exercise — both modalities

Aerobic exercise increases hippocampal volume.^[5]
Resistance training has independent cognitive effects (Liu-Ambrose).
The FINGER trial — a multi-domain lifestyle intervention including exercise — improved cognition in high-risk older adults.^[6]
Dose: 150+ minutes aerobic + 2 resistance sessions/week (general exercise guidelines).
The other side of the coin: prolonged sitting accelerates hippocampal atrophy and white matter hyperintensities independent of structured exercise. Highly sedentary older adults show worse trajectories on episodic memory and processing speed even when they meet the exercise guidelines — the active-couch-potato pattern. ~7,000 daily steps is associated with 38% lower dementia incidence vs. 2,000 steps. See Sitting.

5. Sleep — quality, regularity, OSA screening

Slow-wave sleep clears beta-amyloid via the glymphatic system.
Chronic short sleep predicts dementia incidence.
Sleep regularity independently predicts cognitive trajectory.
Untreated OSA is a substantial risk; CPAP improves cognitive trajectory in some studies.
Excessive habitual daytime napping (>60–90 min, especially in the morning or with high day-to-day variability) is now considered a behavioural marker of underlying neurodegeneration — see Daytime naps. Long naps don't cause dementia, but they're often an early visible sign of fragmented night-time sleep architecture and beta-amyloid accumulation.
Action: 7–8 hours, regular schedule, screen for OSA if any indicator. If you've started napping noticeably more than you used to, treat it as a signal worth investigating.

6. MIND-pattern eating, and minimise ultra-processed food

Morris et al. 2015: highest tertile MIND adherence ~53% lower Alzheimer's risk.
The MIND-USDA RCT 2023 was less impressive but still favorable; the broader pattern matters.
A 2026 BMJ systematic review found ultra-processed food intake is associated with accelerated cognitive decline and higher dementia risk even after adjusting for adherence to a healthy dietary pattern — a processing-specific effect on the brain on top of nutrient quality.^[7]
See Dietary patterns and Ultra-processed food.

Strong cohort signal — frequent social contact, married/partnered status, larger social networks all associate with reduced dementia.
The "loneliness epidemic" is a measurable health problem; social isolation is comparable to other major risk factors in cohort data.
The depth of the network matters far more than the binary "lives alone" — complex measures of social integration carry mortality OR ~1.91 vs. ~1.19 for coresidence alone. See Purpose.
Action: maintain regular real-world relationships; volunteer; participate in groups; for older adults, structured social programs.

8. Stay cognitively engaged

Educational attainment in early life builds cognitive reserve.
Continued learning in adulthood — language acquisition, music, complex hobbies — has cohort signal.
The ACTIVE trial showed durable cognitive training effects 10 years later.^[8]
"Brain training" apps have small, narrow effects with limited transfer to general cognition.
Action: real-world complex learning (language, music, dancing, complex skills) > digital "brain training."

9. Defend purpose, especially in late midlife

The Wisconsin Longitudinal Study (n=4,632, 28-year follow-up) found high purpose-in-life maintained through ages 63–70 was associated with OR ≈ 0.85 for dementia at age 80 and better global cognition / verbal fluency. Steeper decline in purpose between ages 52 and 70 predicted clinical dementia at 80.
Earlier Boyle et al. work in the Rush Memory and Aging Project found high baseline purpose associated with ~2.4× lower risk of incident Alzheimer's over ~7 years.^[9]
Late midlife is the critical therapeutic window — the years where retirement, empty nest, role loss at work, and early widowhood erode purpose, with measurable cognitive cost a decade later.
Action: plan the next role before the current one ends; build at least one purpose source independent of paid work; maintain weekly contact with a small set of relationships of substance. See Purpose.

What about specific supplements / drugs?

Modest evidence

Omega-3 (DHA) — observational signal; RCTs in healthy or MCI populations are inconsistent. Reasonable as part of overall pattern.
Vitamin D — repletion if deficient; no clear additional cognitive benefit at higher doses.
B vitamins (B6, B12, folate) — VITACOG trial showed cognitive benefit specifically in those with elevated homocysteine; routine use in non-elevated populations not supported.
Creatine — once corrected meta-analyses are applied, the cognitive effect in well-rested young adults is small. The benefit concentrates in older adults, vegetarians, and people under metabolic stress (acute sleep deprivation, hypoxia). 10 g/day is the rough threshold for measurable brain bioenergetic effects; standard 3–5 g/day muscle doses are insufficient. See Creatine.

Weak / negative evidence

Ginkgo biloba — multiple RCTs (GEM, Petersen) negative.
Resveratrol — no convincing cognitive RCTs.
Curcumin — small studies suggestive; not robust.
Most "memory" formulas — unproven mixtures.

Pharmacological

Anti-amyloid antibodies (lecanemab, donanemab) — modest disease-slowing in early Alzheimer's; not for prevention in healthy adults.
GLP-1 agonists (semaglutide, tirzepatide) — observational signal for reduced dementia incidence in T2D, plus a 100k-cohort association with 44% lower depression and 38% lower anxiety risk. The dedicated phase 3 EVOKE / EVOKE+ trials in early Alzheimer's missed their primary cognitive endpoint but moved CSF biomarkers (pTau181, total tau, neurogranin) in the right direction. The honest read: pathology biology can be modulated, but established clinical disease isn't being rescued at 3 years; the prophylactic-decades-earlier hypothesis is still open. See GLP-1 receptor agonists.
Statins — cohort signal for reduced dementia in statin users; not RCT-confirmed for dementia-specific outcome.

What's overrated

"Brain training" apps for transferable cognition.
Mega-doses of B vitamins in non-deficient populations.
"Anti-inflammatory" supplement protocols without dietary pattern change.
Coconut oil for Alzheimer's — anecdotal claims, no robust RCT support.

A practical brain-health checklist

Get audiometry every 5 years from age 50, sooner if any concern.
Treat hypertension aggressively in midlife — target <130 systolic if tolerated.
Treat T2D, prediabetes, and metabolic syndrome. Maintain HbA1c <5.7%.
Reduce LDL through diet, exercise, and statins if indicated.
Don't smoke. Drink minimally.
150+ min aerobic + 2× resistance per week.
7–8 hours sleep, regular schedule, screen for OSA.
Mediterranean / MIND-pattern eating. Leafy greens daily, berries 2+ times/week, fish, nuts, olive oil, whole grains, beans, poultry. Limit red/processed meat, butter, fried foods, sweets.
Stay socially connected. Real-world relationships matter.
Continue learning. Real skills, ideally social and physical (dancing, music, sports, languages).
Wear seatbelts and helmets; avoid repeated head impacts.
Reduce air pollution exposure where feasible (HEPA filtration in homes near major roads). See Environmental toxins for the full air-filtration story.
Get vision corrected. Cataract surgery, glasses, regular eye exams. The signal scales with severity of impairment, not just AMD diagnosis — uncorrected functional vision loss is the modifiable variable. See Vision.
Treat depression. SSRIs, therapy, exercise.

Family history of Alzheimer's: what to do

Most familial risk is via APOE ε4 carrier status — genetic testing is available but not always recommended (the actionable advice is the same as above whether you're a carrier or not).
The same modifiable factors retain effect size in APOE ε4 carriers — possibly more impact in absolute terms because baseline risk is higher.
For specific genetic testing decisions, work with a genetic counselor.