Dementia Risk Factors You Can Control: What Science Really Shows

Up to 45% of dementia cases worldwide may be preventable or delayable through actions people can take throughout their lives. This is the central finding from the 2024 Lancet Commission on Dementia Prevention, the most comprehensive scientific review of dementia risk factors ever conducted. The implications are profound: dementia is not simply a matter of bad luck or bad genes. Your daily choices—how you eat, move, sleep, and connect with others—genuinely matter for your brain's future.

This guide explains what science actually shows about reducing dementia risk, where the evidence is strong, where it's still emerging, and what you can realistically do with this information. We'll be honest about what we know and what we don't.

How scientific thinking about dementia has changed

Two decades ago, many doctors believed dementia was largely inevitable—something you either got or didn't based on your genes. Research has fundamentally changed this view.

The 2017 Lancet Commission identified nine modifiable risk factors accounting for 35% of dementia cases. The 2020 update added three more factors—excessive alcohol, traumatic brain injury, and air pollution—and raised the estimate to 40%. The 2024 update added two more factors, untreated vision loss and high LDL cholesterol, bringing the total to 14 modifiable factors and 45% of cases potentially preventable.

These aren't fringe findings. They represent the consensus of the world's leading dementia researchers, published in the Lancet, one of the most rigorous medical journals. The World Health Organization's 2019 guidelines on cognitive decline and dementia reached similar conclusions, recommending physical activity, tobacco cessation, healthy diet, and management of conditions like hypertension and diabetes.

The 14 modifiable risk factors organize by life stage, reflecting when they matter most. In early life (under 45 years), less education accounts for about 7% of potentially preventable cases—the single largest early-life factor. During midlife (45-65 years), hearing loss accounts for 7-8%, traumatic brain injury 3%, hypertension 2%, high LDL cholesterol, excessive alcohol 1%, and obesity 1%. In later life (over 65), smoking accounts for 5%, depression 4%, social isolation 4%, physical inactivity 2%, air pollution 2%, diabetes 1%, and vision loss.

These percentages represent "population attributable fractions"—estimates of what share of dementia cases might be prevented if each factor were eliminated entirely. They're theoretical maximums, not guarantees. But they tell us where to focus our attention.

Why movement matters more than most people realize

The evidence for exercise is among the strongest in dementia prevention research. A 2022 meta-analysis of 58 studies involving 257,983 participants found that high physical activity was associated with 20% lower risk of all-cause dementia, with even larger reductions for Alzheimer's disease (14-28%) and vascular dementia (21-32%).

The type of exercise matters less than many people think. Walking, swimming, dancing, gardening—any activity that gets you moving counts. The WHO and most major studies recommend 150 minutes per week of moderate-intensity activity, where you can talk but not sing. Recent research suggests even small amounts help: adding just five additional minutes of moderate-to-vigorous activity per day shows measurable benefits. One UK Biobank study found that concentrating exercise into one or two days per week—the "weekend warrior" pattern—appears as effective as spreading it throughout the week.

How does movement protect the brain? Multiple mechanisms work simultaneously. Exercise increases brain-derived neurotrophic factor (BDNF), a protein that supports neuron growth and survival. Physical activity improves cerebral blood flow and vascular health. Movement helps clear beta-amyloid, the protein that forms plaques in Alzheimer's disease. Exercise reduces inflammation throughout the body and brain. Regular activity improves sleep quality, which itself protects cognition.

The strongest evidence comes from studies of midlife activity. Exercise in your 40s and 50s appears more protective than exercise started later, though starting at any age shows benefits. One important caveat: some studies with very long follow-up periods (over 20 years) show smaller effects, possibly because people who will later develop dementia may reduce their activity years before diagnosis.

The truth about diet and brain health

No magic food or supplement will prevent dementia. But dietary patterns—the overall way you eat—show consistent benefits across research studies.

The Mediterranean diet, high in vegetables, fruits, whole grains, fish, legumes, and olive oil while low in red meat and processed foods, is associated with 11-30% lower dementia risk across multiple meta-analyses. The MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay) was specifically designed for brain health. It emphasizes leafy greens, berries, nuts, beans, whole grains, fish, poultry, and olive oil while limiting red meat, butter, cheese, pastries, and fried foods. Studies show 35-53% lower Alzheimer's risk with moderate-to-high adherence compared to low adherence.

Here's something that might surprise you: the WHO guidelines do not recommend vitamin supplements for dementia prevention in people without nutrient deficiencies. This is a strong recommendation based on moderate-quality evidence. Supplements like vitamins B, E, and omega-3 fatty acids have not been shown to reduce dementia risk in people who aren't deficient. Your money is better spent on whole foods.

The difficulty with diet research is separating food effects from lifestyle effects. People who eat Mediterranean-style diets often also exercise more, have higher education, and engage more socially. Researchers try to control for these factors, but they can't fully untangle them. Still, the consistency of findings across diverse populations suggests real protective effects.

Sleep's crucial role in brain maintenance

Sleep is when your brain clears metabolic waste, including beta-amyloid. During sleep, the space between brain cells expands by about 60%, allowing more efficient removal of these potentially toxic proteins. This biological reality helps explain why sleep problems are increasingly recognized as dementia risk factors.

The Whitehall II Study, following nearly 8,000 British civil servants for 25 years, found that persistent short sleep (six hours or less) at ages 50, 60, and 70 was associated with 30% higher dementia risk. Other studies show short sleep (six hours or less) increases risk by 22-46%, while long sleep (nine hours or more) increases risk by 74-120%—though long sleep may reflect early disease rather than cause it. The optimal duration appears to be approximately seven hours.

Sleep apnea deserves special attention. This condition, where breathing repeatedly stops during sleep, affects millions of people, many undiagnosed. Meta-analyses show 33-52% increased dementia risk in people with obstructive sleep apnea. Treatment with CPAP (continuous positive airway pressure) may help, though long-term prevention data is limited. If you snore loudly, wake up tired despite adequate sleep time, or your partner notices you stopping breathing at night, getting evaluated is worthwhile.

One honest caveat: sleep changes in later life may be early symptoms of dementia rather than causes. People often sleep worse as dementia develops, sometimes years before diagnosis. This makes it hard to know whether poor sleep causes dementia or the reverse. Midlife sleep problems are more clearly risk factors; late-life sleep changes may be warning signs.

Social connection isn't optional for brain health

Humans evolved as social creatures, and our brains reflect this. Social isolation and loneliness are now recognized as significant dementia risk factors, with the Lancet Commission estimating they account for 4% of potentially preventable cases.

A 2024 analysis synthesizing data from over 600,000 people across 21 cohorts found that loneliness increases dementia risk at a magnitude similar to physical inactivity or smoking. The research shows social isolation increases risk by 49-60%, loneliness increases risk by 23-31% for all-cause dementia and 39-72% for Alzheimer's disease specifically, and poor social networks increase risk by 59%.

Loneliness (the subjective feeling of being disconnected) and isolation (the objective lack of social contacts) both matter independently. You can feel lonely in a crowd or feel connected while living alone. Both the quantity and quality of relationships appear important.

The mechanisms likely include direct effects on stress hormones and inflammation, reduced cognitive stimulation, and fewer reasons to maintain health behaviors. Whatever the mechanisms, the message is clear: maintaining social connections isn't a luxury—it's a brain health necessity.

The hearing loss connection that surprised researchers

One of the most striking findings in recent dementia research involves hearing loss. The Lancet Commission identifies it as the largest single modifiable risk factor, accounting for 7-8% of potentially preventable dementia cases. Meta-analyses show hearing loss almost doubles dementia risk.

Why would hearing affect thinking? Several mechanisms are proposed. When hearing is impaired, the brain diverts more resources to understanding speech, leaving less capacity for memory and other functions—a phenomenon researchers call cognitive load. Hearing loss often leads people to withdraw from conversations and social activities, creating isolation. Reduced auditory input may cause changes in brain structure over time.

The crucial question: does treating hearing loss reduce risk? The ACHIEVE trial, a landmark randomized controlled trial with 977 participants, provides partial answers. Overall, hearing aids didn't significantly affect cognitive decline in the full study population. However, in a pre-specified subgroup of older adults at higher dementia risk, hearing intervention reduced three-year cognitive decline by 48%. Observational studies suggest hearing aid use before age 70 is associated with 61% lower dementia risk over 20 years.

This is a case where the science is still evolving. The evidence is strong that hearing loss is associated with dementia risk. The evidence that hearing aids prevent dementia is suggestive but not yet definitive. Given that hearing aids also improve quality of life and social function, addressing hearing loss makes sense regardless.

Why midlife cardiovascular health has lasting brain effects

What's good for your heart is good for your brain. High blood pressure, diabetes, obesity, and high cholesterol—the familiar cardiovascular risk factors—all increase dementia risk. But timing matters enormously: these factors are most dangerous in midlife (ages 45-65), not later life.

Hypertension in midlife increases dementia risk by approximately 60% according to meta-analyses. The SPRINT-MIND trial, the most rigorous test of blood pressure treatment for brain protection, randomized 9,361 hypertensive adults to intensive (below 120 mmHg) or standard (below 140 mmHg) blood pressure targets. While the primary dementia endpoint wasn't statistically significant (the trial ended early), intensive treatment reduced mild cognitive impairment by 19% and combined MCI/dementia by 17%. Follow-up studies show benefits persisting seven or more years after the trial ended.

Here's the paradox: in people over 75, higher blood pressure is sometimes associated with better cognition. This "reverse association" likely reflects that dropping blood pressure in late life can be an early sign of declining health, not a benefit of hypertension. The message: control blood pressure in midlife and maintain good control as you age.

Diabetes increases dementia risk by 50-100% across studies. The mechanisms are well-understood: insulin resistance in the brain, damage from high blood sugar, and accelerated vascular disease. Unfortunately, studies haven't clearly shown that tight blood sugar control prevents dementia—possibly because the damage accumulates over many years before diabetes is diagnosed, or because hypoglycemia (low blood sugar) from aggressive treatment may cause its own harm.

Obesity shows a fascinating pattern. Midlife obesity (BMI 30 or above) increases dementia risk by 33-91%. But late-life obesity appears protective—the "obesity paradox." This almost certainly reflects reverse causation: people often lose weight in the years before dementia diagnosis, so being heavier in old age may simply mark those who haven't yet started declining. The clear message: maintain healthy weight in midlife.

Depression and dementia have a complicated relationship

Depression approximately doubles dementia risk in most studies. But the relationship is complicated. Depression might be a genuine risk factor, an early symptom of developing dementia, or both—depending on when it occurs.

Studies with long follow-up help untangle this. Depression occurring more than 10 years before dementia diagnosis shows weaker associations than depression within the decade before diagnosis. The Swedish Twin Study found that depression within 10 years of dementia was associated with 3.9 times higher risk, while depression more than 10 years before showed no significant association. Research indicates depressive symptoms can emerge 15 years before formal dementia diagnosis.

This matters for interpretation: late-life depression may often be an early manifestation of brain changes rather than a separate risk factor. That said, depression at any age affects brain health through stress hormones, inflammation, and reduced engagement with protective activities. Treatment of depression improves cognitive function in people with Alzheimer's disease, though no study has proven that treating depression prevents dementia.

The practical takeaway: depression is bad for brain health regardless of whether it causes dementia directly. If you experience persistent sadness, loss of interest, or hopelessness, seeking treatment is important for many reasons, including protecting your cognitive future.

The evidence on smoking, alcohol, and brain injury

Smoking increases dementia risk by 30-40% for current smokers. The good news: quitting works. Former smokers show no increased risk compared to never-smokers, with risk normalizing approximately nine years after quitting. The message is unambiguous: quit at any age.

Alcohol has been more confusing. For years, studies suggested moderate drinking might protect against dementia—the "J-shaped curve" where moderate drinkers had lower risk than both abstainers and heavy drinkers. This view is changing dramatically.

A 2025 genetic analysis from Oxford, Yale, and Cambridge involving over 600,000 participants used Mendelian randomization (examining genetic variants that influence drinking) and found no protective effect at any level. Instead, dementia risk increased linearly with any amount of alcohol. The apparent protection in earlier studies likely reflected "sick quitter" bias (former heavy drinkers categorized as abstainers) and healthy user bias (moderate drinkers having healthier lifestyles overall).

Heavy drinking is unambiguously harmful—the Lancet Commission uses more than 21 UK units per week (about 12 US standard drinks) as the threshold for "excessive." For moderate drinking, the current evidence suggests it's probably not protective and may cause incremental harm. The safest approach: don't start drinking for health reasons, and if you drink, keep it minimal.

Traumatic brain injury increases dementia risk, particularly moderate-to-severe injuries (2.8-fold higher risk) and repeated mild injuries. Contact sports and military service are recognized risk factors for chronic traumatic encephalopathy (CTE), a distinct form of brain degeneration. Prevention—through seatbelts, helmets, fall prevention, and sports safety measures—is the only intervention.

Understanding cognitive reserve

The concept of cognitive reserve helps explain why some people tolerate more brain pathology than others before developing symptoms. First observed in autopsy studies where some people showed advanced Alzheimer's pathology despite having no symptoms during life, cognitive reserve represents the brain's ability to compensate for damage.

Dr. Yaakov Stern of Columbia University, who pioneered this field, demonstrated that Alzheimer's patients with higher education showed more extensive brain damage at the same level of clinical severity—their brains had found ways to keep functioning despite the pathology.

How is cognitive reserve built? Through education (especially in early life), occupationally complex and mentally demanding work, leisure activities like reading and puzzles and learning new skills, social engagement, physical exercise, and possibly bilingualism (though evidence is mixed on this last factor).

The reassuring news: cognitive reserve isn't fixed. While early-life education has particularly strong effects, activities throughout life contribute. The Lancet Commission emphasizes that "it is never too early or too late" to start building reserve.

However, there's a nuance often missed in popular accounts: cognitive reserve helps the brain cope with pathology, but it doesn't necessarily prevent pathology. People with high reserve maintain function longer, but once they do develop symptoms, they may decline faster—because by that point, the underlying damage is more advanced. Still, more years of healthy cognition is the goal, and reserve helps achieve it.

The trial that changed everything

Before 2015, no randomized trial had demonstrated that lifestyle interventions could improve cognitive outcomes. The FINGER trial (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability) changed that.

The study randomized 1,260 at-risk adults aged 60-77 to either a comprehensive intervention (nutritional guidance, physical exercise, cognitive training, and vascular risk monitoring) or general health advice. After two years, the intervention group showed 25% greater improvement in overall cognition, 83% greater improvement in executive function (planning, problem-solving), 150% greater improvement in processing speed, and 30% lower risk of cognitive impairment.

Effect sizes were modest but meaningful. Benefits extended beyond cognition to physical function, quality of life, and reduced risk of developing multiple chronic conditions.

Why did FINGER succeed where earlier trials failed? Several factors stand out. It targeted people at elevated dementia risk, not the general population. It addressed multiple risk factors simultaneously rather than focusing on just one. It included cognitive training, which trials focusing only on vascular factors often lacked. The intervention was intensive and structured rather than simple advice-giving.

The World-Wide FINGERS network, launched in 2017, now includes research teams in 71 countries adapting the FINGER model. The U.S. POINTER trial, published in JAMA in July 2025, confirmed the findings: both structured and self-guided interventions improved cognition, with structured intervention showing significantly greater benefits. Importantly, benefits were seen across all subgroups regardless of sex, ethnicity, or APOE-ε4 genetic status.

Not all multi-domain trials have succeeded. The PreDIVA trial in the Netherlands showed no overall effect, possibly because Dutch healthcare standards were already high, the population was older (70-78), and the intervention lacked cognitive training. The lesson: intensity, timing, and comprehensiveness all matter.

What the research cannot tell us

Scientific honesty requires acknowledging limitations. Here's what we don't know with certainty.

Most evidence comes from observational studies, where causation versus correlation remains uncertain. People who exercise more, eat better, and stay socially engaged also differ in countless other ways from those who don't. Statistical controls help but can't fully solve this problem. Mendelian randomization studies (using genetic variants as natural experiments) don't uniformly confirm causality for many risk factors.

Individual prediction is impossible. Population-level statistics don't translate to individual certainty. Someone with many risk factors might never develop dementia; someone with none might. We're dealing with probabilities, not destinies.

We don't know the "right" interventions with precision. We know general categories help (exercise, healthy diet, social connection) but can't specify exactly what type of puzzle, how many minutes of which exercise, or which specific foods matter most.

How risk factors combine—and whether addressing several together is better than addressing one intensively—remains unclear. Most research involves white populations in high-income countries. Risk profiles differ in other settings; the Lancet Commission estimates potentially preventable cases are actually higher in low- and middle-income countries (56% in Latin America, for example).

For some factors like depression, physical inactivity, and social withdrawal, we can't always determine whether they cause dementia or are early symptoms of developing dementia—or both. The FINGER trial and similar studies improved cognitive test scores. Whether this translates to fewer dementia diagnoses over decades isn't yet proven by randomized trials.

Putting this into practice

Given the evidence and its limitations, here are practical takeaways.

Move your body regularly. Aim for 150 minutes per week of moderate activity—walking counts. Some activity beats none; don't let perfect be the enemy of good. Midlife matters most, but starting at any age helps.

Eat a Mediterranean or MIND-style diet. Emphasize vegetables (especially leafy greens), fruits, whole grains, fish, nuts, legumes, and olive oil. Reduce red meat, processed foods, and sweets. Skip the supplements unless you have a documented deficiency.

Protect your sleep. Aim for seven hours. Address snoring or suspected sleep apnea—treatment may help cognition directly and certainly improves quality of life. Maintain consistent sleep schedules.

Stay socially connected. Nurture relationships. Join groups. Volunteer. Social connection isn't optional for brain health.

Manage cardiovascular risk factors, especially in midlife. Work with your doctor on blood pressure, cholesterol, and blood sugar. The targets that protect your heart protect your brain.

Address hearing and vision loss. Get regular screenings. Use hearing aids if needed. The evidence for direct dementia prevention is still developing, but treating sensory loss improves life quality and social engagement.

Never smoke, or quit if you do. Risk normalizes about nine years after quitting at any age.

Limit alcohol. Heavy drinking clearly harms the brain. Moderate drinking probably isn't protective despite what earlier studies suggested. Don't drink for "health benefits."

Keep learning. Formal education, new skills, mentally engaging hobbies—all contribute to cognitive reserve. This works throughout life, not just in youth.

Treat depression. Whether it's a cause or early symptom of dementia, depression is worth treating for many reasons. Don't minimize persistent mood changes.

Prevent head injuries. Wear seatbelts and helmets. Reduce fall risks. Take sports concussions seriously.

The honest bottom line

Dementia is not entirely within your control. Genetics matter. Age matters. Some people do everything "right" and still develop dementia; others take risks and don't. Life isn't fair.

But 45% is a large number. Nearly half of dementia cases may be preventable or delayable through actions across the lifespan. That's not a guarantee—it's a meaningful shift in odds. The earlier you start, the better, but it's never too late to benefit.

The FINGER trial and its successors show that structured interventions work. The population studies show that lifestyle patterns matter. The biology makes sense: what's good for your heart is good for your brain; what engages your brain builds reserve; what connects you to others protects cognitive function.

The science will keep evolving. New risk factors will be identified; some current associations may weaken with better studies. But the core message is unlikely to change: your brain isn't a passive recipient of fate. Through how you live—eating, moving, sleeping, connecting, learning—you're building or depleting your cognitive future. That knowledge is both a burden and a gift.

Sources:

Livingston G, et al. (2024). Dementia prevention, intervention, and care: 2024 report of the Lancet Commission. The Lancet.
Livingston G, et al. (2020). Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet, 396(10248), 413-446.
World Health Organization. (2019). Risk reduction of cognitive decline and dementia: WHO guidelines.
Ngandu T, et al. (2015). A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. The Lancet, 385(9984), 2255-2263.
Baker LD, et al. (2025). Effects of structured and self-guided physical activity interventions on cognition. JAMA.
SPRINT MIND Investigators for the SPRINT Research Group. (2019). Effect of intensive vs standard blood pressure control on probable dementia. JAMA, 321(6), 553-561.
Lin FR, et al. (2023). Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss in the USA (ACHIEVE). The Lancet, 402(10404), 786-797.
Sabia S, et al. (2021). Association of sleep duration in middle and old age with incidence of dementia. Nature Communications, 12, 2289.
Meng X & D'Arcy C. (2012). Education and dementia in the context of the cognitive reserve hypothesis: a systematic review with meta-analyses and qualitative analyses. PLoS ONE, 7(6), e38268.
Kivimäki M, et al. (2019). Physical inactivity, cardiometabolic disease, and risk of dementia: an individual-participant meta-analysis. BMJ, 365, l1495.