A risk factor is something associated with a higher chance of an outcome across a population. A modifiable one is a factor that can, in principle, be changed — unlike age or genetics. In 2024, the Lancet standing Commission on dementia identified 14 modifiable risk factors and estimated that around 45% of dementia cases worldwide could theoretically be prevented or delayed if all 14 were eliminated at the population level. That is the Commission's population-level modelling estimate — it is not a prediction about any individual person, and addressing these factors is not a guarantee of any particular outcome for you. What follows describes what each factor is and why researchers link it to long-term cognitive health.

Fewer years of formal education early in life is associated with higher dementia risk. The leading explanation is "cognitive reserve" — more education is thought to build networks and habits that let the brain tolerate more change before difficulties become apparent. Ongoing learning at any age is studied as a contributor to that reserve.

Untreated hearing loss in midlife is one of the larger individual contributors in the Commission's model. Proposed explanations include increased cognitive load from straining to hear, reduced stimulation of brain regions that process sound, and the social withdrawal that hearing difficulty often causes.

Newly added in the 2024 report. Untreated vision impairment — much of it correctable, such as cataracts or uncorrected refractive error — is associated with higher dementia risk, likely through similar pathways to hearing loss: reduced sensory input, reduced engagement, and reduced activity.

Also newly added in 2024. Elevated LDL cholesterol in midlife is associated with higher later-life dementia risk. The brain depends heavily on healthy blood vessels, and the same vascular damage that drives heart disease also affects cerebral circulation.

High blood pressure in midlife is among the most consistently identified vascular contributors. Sustained high pressure damages small blood vessels in the brain over years, which is associated with white matter changes and vascular contributions to cognitive decline.

Type 2 diabetes is associated with higher dementia risk. Mechanisms studied include vascular damage from chronically elevated blood glucose and the effects of insulin resistance on brain metabolism.

Midlife obesity is associated with higher later-life dementia risk. It rarely acts alone — it clusters with hypertension, diabetes, high LDL, and inactivity, which is part of why the Commission treats these cardiometabolic factors as a related group rather than isolated items.

Low physical activity appears across the dementia literature as a risk factor. Regular activity affects vascular health, blood glucose regulation, sleep, and mood — all of which are themselves linked to cognitive outcomes.

Smoking is associated with higher dementia risk through vascular damage and oxidative stress. Research indicates risk associated with smoking declines after stopping, which is why it is classified as modifiable rather than fixed.

Heavy alcohol consumption — in the Commission's framing, more than roughly 21 units per week — is associated with higher dementia risk, including through direct neurotoxic effects and alcohol-related brain injury.

History of significant head injury, particularly repeated injury, is associated with higher dementia risk. This is why protective equipment, fall prevention, and taking concussion seriously appear in prevention discussions.

Depression is associated with higher dementia risk. The relationship is complex and likely runs in both directions — depression may contribute to risk, and it can also be an early feature of cognitive change rather than only a cause of it.

Low social contact is associated with higher dementia risk. Social interaction is cognitively demanding in a way researchers consider stimulating, and isolation also tends to travel with inactivity, depression, and reduced sensory engagement.

Long-term exposure to air pollution, particularly fine particulate matter, is associated with higher dementia risk in population studies. This is largely a policy and environment-level factor rather than an individual behaviour.

Most of the evidence above is observational — it shows associations, not proof that changing a factor changes the outcome. Randomized trials are what test that directly. U.S. POINTER was a large randomized trial in older adults at increased risk of cognitive decline. It compared a structured, supported multidomain lifestyle intervention — exercise, dietary guidance, cognitive and social engagement, and cardiometabolic health monitoring — against a self-guided version of similar goals. Both groups improved on the study's global cognition measure over two years, and the structured group improved modestly more. What this supports: lifestyle intervention produced a measurable cognitive difference in a randomized setting, and more structure was associated with a somewhat better result. What it does not establish: that any individual will avoid, delay, or be protected from dementia or any other diagnosis. The difference between groups was modest, and cognitive test scores are not the same thing as disease outcomes.

• 14 modifiable risk factors and the ~45% population estimate: Livingston et al., "Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission," The Lancet, 2024;404:572-628. • Multidomain lifestyle intervention trial: Baker et al., "Structured vs Self-Guided Multidomain Lifestyle Interventions for Global Cognitive Function: The U.S. POINTER Randomized Clinical Trial," JAMA, 2025. This is a summary of published research for general education. It is not a complete or exhaustive citation of the field.