Can You Lower Your Risk of Alzheimer’s? What Actually Matters

Few health concerns carry the emotional weight of Alzheimer’s disease.

Maybe you watched a parent gradually stop remembering names. Maybe a grandparent became someone you barely recognized. Maybe you have caught yourself forgetting a word or walking into a room without remembering why, and a quiet question appeared:

Is this how it starts?

For a long time, conversations about Alzheimer’s offered very little sense of agency. Age mattered. Family history mattered. Genetics mattered. And for many people, that translated into the feeling that the future had already been written.

That picture is changing.

There is still no lifestyle program that can guarantee prevention of Alzheimer’s disease. But research increasingly suggests that brain aging is influenced by many of the same systems we spend decades affecting through cardiovascular health, metabolism, movement, sleep, sensory health, nutrition, social connection, and the environments in which we live.¹

Your genes may influence the landscape. They do not write every chapter that follows.

First, Alzheimer’s Disease and Dementia Are Not the Same Thing

Dementia is an umbrella term. It describes a decline in memory, thinking, reasoning, or other cognitive abilities severe enough to interfere with everyday function.

Alzheimer’s disease is a specific neurodegenerative disease and the most common cause of dementia. Other causes include vascular dementia, Lewy body dementia, frontotemporal dementia, and combinations of more than one disease process.

Alzheimer’s is associated with characteristic changes in the brain, including accumulation of beta-amyloid plaques, abnormal tau proteins, loss of connections between neurons, and eventually death of brain cells.²

But even that description is not the whole story.

The brain carrying those plaques and tangles also has blood vessels. It depends on glucose and oxygen. It communicates with the immune system. It responds to hormones. It changes with sleep. It receives sensory information. It exists inside a person who moves, eats, connects with other people, experiences stress, and accumulates decades of metabolic and environmental exposures.

That wider perspective is where the conversation becomes much more hopeful.

The Most Hopeful Part: Risk Is Not Completely Fixed

In 2024, the Lancet Commission on dementia prevention reviewed the evidence across the lifespan and identified 14 potentially modifiable risk factors associated with dementia.¹

They include:

• lower educational attainment;
• hearing loss;
• high LDL cholesterol;
• depression;
• traumatic brain injury;
• physical inactivity;
• diabetes;
• smoking;
• high blood pressure;
• obesity;
• excessive alcohol use;
• social isolation;
• air pollution;
• and untreated vision loss.

The Commission estimated that, at a population level, addressing these factors could theoretically prevent or delay a substantial proportion of dementia cases—approximately 45%.¹

That number needs context.

It does not mean an individual can follow a checklist and reduce their personal Alzheimer’s risk by exactly 45%. Population-attributable estimates are mathematical models built from associations across large groups of people.

But the larger message is hard to ignore:

A significant part of dementia risk appears to exist in areas that are potentially influenceable.

That is very different from being powerless.

Your Brain Does Not Age Alone

We often talk about “brain health” as though the brain occupies its own category.

It does not.

The brain receives roughly continuous support from the cardiovascular system, respiratory system, endocrine system, immune system, digestive system, and metabolic environment. It depends on adequate blood flow, energy availability, sleep, sensory input, physical activity, and social and cognitive engagement.

That is why our Brain & Cognitive Health approach looks beyond memory tests alone.

The useful question is not simply:

“What supplement is good for the brain?”

It is:

What kind of biological environment has this brain been living in—and which parts of that environment can we improve?

Genetics Matter. They Are Not a Verdict.

One of the best-known genetic influences on late-onset Alzheimer’s disease is the APOE gene.

Everyone inherits two APOE variants, one from each biological parent. The APOE ε4 variant is associated with increased Alzheimer’s risk and, in some populations, earlier disease onset. Having two copies generally carries more risk than having one.³

But APOE ε4 is a risk gene, not a guarantee.

Some people who carry APOE ε4 never develop Alzheimer’s disease. Others develop Alzheimer’s without carrying ε4 at all. The amount of risk associated with APOE also differs across genetic ancestry and populations.³

That is an important distinction for anyone who learns they carry a risk variant.

Your genotype is information.

It is not a countdown clock.

In fact, the 2025 U.S. POINTER randomized trial found that the cognitive benefit of its structured multidomain lifestyle intervention was similar in APOE ε4 carriers and noncarriers.⁴

That does not prove lifestyle eliminates genetic risk.

It does reinforce a powerful idea:

genetic risk does not make the rest of your physiology irrelevant.

The Most Exciting Research Is Not About One Supplement

For years, much of the prevention conversation focused on individual variables.

Does exercise help?

Does this diet help?

Does cognitive training help?

Does lowering blood pressure help?

Those are worthwhile questions, but real life does not happen one variable at a time.

The newer generation of Alzheimer’s-prevention research is increasingly asking a more Functional Medicine-style question:

What happens when we improve several parts of the system together?

U.S. POINTER Gave Us a Major Piece of That Answer

In 2025, researchers published results from U.S. POINTER, a large randomized clinical trial involving 2,111 adults ages 60 to 79 who were cognitively intact but at increased risk for cognitive decline.⁴

Participants followed one of two programs. Both addressed several areas at once:

• physical activity;
• nutrition;
• cognitive challenge;
• social engagement;
• and cardiovascular health monitoring.

One program was more structured, with prescribed goals, regular meetings, coaching, and greater accountability. The other provided a more flexible, self-guided approach.

After two years, cognitive scores improved in both groups—but improvement was statistically greater in the more structured group.⁴

That does not mean the program was proven to prevent Alzheimer’s disease. The trial measured cognitive performance over two years, not who eventually developed dementia decades later.

But it is still an important result.

Older adults at increased risk were not simply observed while cognition declined. Their cognitive performance was responsive to a multidomain intervention.

That is worth being excited about.

Then the Result Showed Up Again Across 11 Countries

In 2026, the LatAm-FINGERS trial extended the concept across 11 Latin American countries.

Researchers randomized 1,065 adults ages 60 to 77 at increased risk for cognitive decline to either a structured multidomain lifestyle program or a more flexible lifestyle program.⁵

The structured intervention again combined multiple domains rather than hunting for one magic lever.

After two years, both groups improved, but the structured group showed significantly greater improvement in overall cognition, with additional benefits in memory, executive function, and processing speed.⁵

Different countries.

Different cultures.

Different food traditions.

Same larger lesson.

Brain health may respond best when we stop asking for one perfect intervention and start improving the environment around the brain.

Your Arteries Are Brain Infrastructure

The brain is extraordinarily dependent on circulation.

That makes cardiovascular health neurological health too.

High blood pressure, elevated LDL cholesterol, stroke, vascular disease, smoking, and other cardiovascular risks are repeatedly associated with later cognitive decline and dementia.¹

This is not just an observational story.

The SPRINT MIND trial randomized adults with hypertension and increased cardiovascular risk to different blood-pressure targets. Longer-term follow-up published in 2025 found that intensive blood-pressure treatment was associated with lower rates of mild cognitive impairment and the combined outcome of mild cognitive impairment or probable dementia, although the result for probable dementia alone remained statistically inconclusive.⁶

That makes blood pressure a lot more interesting than a number on a cuff.

The same vessels supplying your heart are part of the vascular network supplying your brain.

Our Cardiovascular Health approach looks at blood pressure, lipids, metabolic health, inflammation, lifestyle, and other cardiovascular contributors with that bigger picture in mind.

Metabolic Health Reaches the Brain Too

Blood sugar is another example of something we tend to label as a separate “body” problem.

But diabetes is one of the modifiable dementia risk factors identified by the Lancet Commission, and metabolic dysfunction often travels with hypertension, obesity, vascular disease, sleep apnea, inflammation, and abnormal lipids.¹

The brain sits downstream of that entire metabolic environment.

That does not mean Alzheimer’s disease is simply “type 3 diabetes,” a phrase that is sometimes used far too casually.

Alzheimer’s is much more complicated than insulin resistance alone.

But insulin signaling, glucose metabolism, vascular health, and systemic metabolic function are legitimate parts of the brain-aging conversation.

If glucose or insulin regulation is already becoming abnormal in midlife, that is not something we want to wait until age 75 to care about.

Our Blood Sugar Health approach looks at those patterns before the conversation is reduced to one fasting glucose number.

Movement Is About More Than Burning Calories

Physical activity appears repeatedly in brain-aging research.

Large observational analyses have associated greater leisure-time physical activity with lower rates of dementia and Alzheimer’s disease, although observational research cannot prove that exercise alone caused the difference.⁷

Randomized trials of exercise by itself have produced more mixed cognitive results.

And that is actually consistent with the larger story.

Movement influences cardiovascular fitness, blood pressure, glucose regulation, body composition, mood, sleep, mobility, and the ability to remain socially engaged. It may therefore help the brain through several pathways rather than acting like a single neurological treatment.

The most compelling multidomain trials did not ask people to exercise and ignore everything else.

They combined movement with nutrition, vascular risk management, cognitive challenge, and social engagement.⁴⁵

That is a systems approach in action.

Sleep Is Not Lost Time

Sleep is sometimes treated as the part of the day when nothing is happening.

Neurologically, that could not be further from the truth.

Sleep participates in memory consolidation, metabolic regulation, autonomic function, immune regulation, and many other processes important to a healthy brain.

Research has also linked sleep-disordered breathing with cognitive decline. A 2024 meta-analysis of cohort studies involving more than five million participants found that sleep apnea was associated with higher rates of all-cause dementia and Alzheimer’s disease, although much of the underlying evidence remains observational.⁸

That means someone who snores heavily, gasps during sleep, wakes with headaches, or spends eight hours in bed but remains exhausted may have a brain-health reason—along with many other health reasons—to investigate sleep quality.

Our Sleep Health approach looks beyond the number of hours in bed to the quality, timing, breathing, recovery, and physiology occurring during those hours.

Hearing Loss May Be One of the Most Underappreciated Brain-Health Factors

This is one that surprises people.

Hearing loss is consistently associated with dementia risk and is included among the Lancet Commission's modifiable factors.¹

The ACHIEVE randomized trial took the question further by testing whether treating hearing loss could actually alter cognitive trajectories.

Across the trial population as a whole, hearing intervention did not significantly change three-year cognitive decline. But among the subgroup of participants who entered the study with greater risk for cognitive decline, hearing intervention appeared to meaningfully slow cognitive change.⁹

Why might hearing matter?

Several pathways are possible. Hearing loss may increase the cognitive effort required to understand conversation, reduce social participation, change sensory input, or coexist with other processes related to brain aging.

We do not need to know the entire mechanism before recognizing the practical point:

Protect your hearing. And if hearing is declining, do not treat it as an irrelevant inconvenience of aging.

Vision Belongs in the Conversation Too

Untreated vision loss was added as a modifiable dementia risk factor in the 2024 Lancet Commission.¹

Again, this reminds us that the brain does not exist independently of the sensory world around it.

Vision affects reading, mobility, exercise, driving, social interaction, independence, and access to cognitively stimulating activities.

Preserving sensory function helps preserve participation.

And participation itself appears to matter.

Connection Is Part of Brain Health

Humans are social organisms.

Social isolation is included among the Lancet Commission's potentially modifiable dementia risk factors, and a large meta-analysis involving more than 600,000 people found loneliness associated with higher subsequent rates of all-cause dementia and Alzheimer’s disease.¹⁰

Again, association is not destiny.

Loneliness may interact with depression, illness, mobility, socioeconomic circumstances, sleep, health behaviors, and early cognitive changes themselves.

But social life creates something neurologically interesting.

Conversation requires attention.

Relationships require memory.

Group activities require navigation, timing, movement, emotional processing, and adaptation.

People also influence whether we exercise, seek medical care, eat well, leave the house, and remain engaged with the world.

Our article Your Health Is Social, Too explores why connection belongs in a serious healthspan conversation rather than being treated as an optional extra.

Nutrition Matters—But There Is No Alzheimer’s-Proof Diet

This is where it is tempting to make the article much more exciting than the evidence allows.

Blueberries.

Omega-3s.

Turmeric.

Olive oil.

Ketones.

Resveratrol.

There is interesting research around all kinds of foods and compounds.

But no individual food has been proven to prevent Alzheimer’s disease, and no vitamin or supplement is currently established as an Alzheimer’s-prevention treatment.¹¹

That does not make nutrition unimportant.

It makes the story bigger than one ingredient.

Mediterranean- and MIND-style dietary patterns have repeatedly been associated with better cognitive outcomes and, in some observational studies, fewer Alzheimer’s-related brain changes. However, randomized dietary trials have produced more modest and mixed results.¹¹

From a Functional Medicine perspective, we are interested in what nutrition does to the larger terrain:

• blood sugar and insulin regulation;
• blood pressure;
• lipids;
• vascular health;
• body composition;
• nutrient status;
• gut function;
• and inflammatory signaling.

That is why our Personalized Nutrition approach focuses less on naming one perfect diet and more on matching nutrition to the person and the physiology we are trying to influence.

Plant Compounds Are Interesting for a Reason

Polyphenol-rich foods—berries, colorful plants, herbs, spices, tea, cocoa, olive oil, nuts, and others—frequently appear in brain-health research.

It is easy to reduce that story to “antioxidants protect the brain,” but the biology is more complicated.

Polyphenols are metabolized extensively, interact with cellular signaling pathways, and can be transformed by the gut microbiome. Different people may therefore process the same compounds differently.

Our article on polyphenols goes deeper into why eating a diverse range of plant compounds may be more useful than chasing one supposed brain-protective superfood.

The Gut-Brain Connection Is Real. The Alzheimer’s Application Is Still Emerging.

This is one of the areas where Functional Medicine has been interested for years and conventional Alzheimer’s research is now investigating much more seriously.

The gut and brain communicate through neural, immune, endocrine, and metabolic pathways. Gut microbes produce metabolites capable of interacting with the immune system and circulation, and researchers have identified differences in microbial communities among some people with mild cognitive impairment or Alzheimer’s disease.

A 2026 systematic review of human studies found alterations in microbial community structure across Alzheimer’s and mild cognitive impairment research, but results were heterogeneous and common diversity measures did not reliably distinguish Alzheimer’s from healthy aging.¹²

That tells us two things.

First, the microbiome-brain relationship is biologically plausible and absolutely worth investigating.

Second, we are not at the point where a stool test can tell us who will develop Alzheimer’s or where “fixing dysbiosis” can be claimed to prevent the disease.

The gut may be part of the brain-aging story without being the entire story.

For someone who already has significant digestive dysfunction, our Gut Health approach can address that physiology on its own merits while the research continues to clarify how much it influences long-term cognitive health.

Environmental Exposures Deserve a Place—Without Turning Everything Into “Detox”

The environment around us also enters the brain-health conversation.

Air pollution is now included among the Lancet Commission's potentially modifiable dementia risk factors.¹

Research continues into particulate matter, metals, pesticides, occupational exposures, endocrine-disrupting chemicals, and other environmental factors that may interact with neurological aging.

This is an area where precision matters.

We do not want to jump from:

“Some environmental exposures are associated with neurological risk”

to:

“Everyone needs a detox protocol to prevent Alzheimer’s.”

The useful approach is exposure-specific.

What are you actually exposed to?

How meaningful is the exposure?

Can it be reduced?

Is there a validated reason to test for it?

Our Environmental Toxins approach focuses on identifying and reducing meaningful exposures rather than treating “toxic burden” as an explanation for every symptom.

Protecting the Brain Also Means Protecting It From Injury

Traumatic brain injury is another potentially modifiable dementia risk factor.¹

This is a reminder that brain-health prevention is not always biochemical.

Seat belts matter.

Helmets matter when the activity calls for them.

Fall prevention matters.

Strength and balance matter with age.

Reducing repeated head injury matters.

Sometimes protecting long-term neurological health looks remarkably ordinary.

What About “Using Your Brain”?

Cognitive activity is another area that often gets reduced to crossword puzzles.

There is nothing wrong with crossword puzzles if you enjoy them.

But a cognitively engaged life is much bigger than one game.

Learn something difficult.

Read.

Teach someone.

Travel somewhere unfamiliar.

Learn an instrument.

Build something.

Navigate new technology.

Participate socially.

Practice a language.

Take on tasks that require attention, memory, planning, and adaptation.

The U.S. POINTER and FINGER-style interventions deliberately included cognitive and social challenge alongside physical and cardiovascular interventions rather than treating “brain training” as a standalone cure.⁴⁵

Again, the pattern is multidomain.

This Is Why Midlife Matters So Much

People tend to become interested in Alzheimer’s prevention when they reach older age.

But many of the factors associated with later dementia accumulate much earlier.

Blood pressure in your 40s and 50s matters.

Metabolic health matters.

Smoking history matters.

Movement habits matter.

Hearing matters.

Cardiovascular health matters.

The Lancet Commission deliberately organizes risk across the lifespan because dementia prevention is not something that begins when someone turns 75.¹

That may be one of the most empowering ideas in this entire article.

You do not have to wait for memory loss to start caring for the systems your future brain will depend on.

And If You Are Already Older, It Is Not “Too Late”

The opposite mistake is assuming that once someone reaches 65 or 70, the opportunity has passed.

That is not what recent trials suggest.

U.S. POINTER enrolled adults between 60 and 79.⁴

LatAm-FINGERS enrolled adults between 60 and 77.⁵

Both trials showed that cognitive performance remained responsive to multidomain lifestyle intervention in later adulthood.

We should not translate that into a guarantee of dementia prevention.

But we should absolutely allow it to challenge the idea that brain aging is simply something we watch happen.

What About Supplements?

There is no shortage of products marketed as memory protection.

Omega-3s.

Ginkgo.

Curcumin.

Resveratrol.

Phosphatidylserine.

Multivitamins.

Nootropics.

Some compounds have interesting research, and targeted supplementation can make sense depending on nutrient status, dietary intake, medications, health conditions, genetics, and the goal of the intervention.

But no supplement has been proven to prevent Alzheimer’s disease.¹¹

That does not mean supplements are useless.

It means they belong downstream of a better question:

What are we trying to change?

Correcting a deficiency is different from taking a product because its label contains a picture of a brain.

Do Not Let Biomarkers Become Fortune-Telling

Alzheimer’s biomarker science is moving rapidly.

Researchers and clinicians can increasingly measure biological changes related to amyloid and tau through imaging, cerebrospinal fluid, and newer blood-based testing.

Those advances are changing diagnosis and research.

But a risk marker is not the same thing as destiny.

The same principle applies to genetics.

A biomarker should answer a meaningful clinical question and be interpreted in the context of age, symptoms, history, and appropriate neurological evaluation—not used as a reason to tell an asymptomatic person that their future is inevitable.

Memory Changes Deserve an Evaluation, Not Just a Wellness Protocol

Risk reduction and diagnosis are different conversations.

If someone is developing progressive memory loss, getting lost in familiar places, repeatedly asking the same questions, struggling with finances or medications, losing previously familiar abilities, or experiencing other meaningful cognitive changes, the answer should not simply be:

“Let's work on your gut and inflammation.”

There are many causes of memory and cognitive symptoms, some of which may be treatable or reversible.

Medication effects.

Sleep disorders.

Depression.

Thyroid dysfunction.

Vitamin deficiencies.

Neurological disease.

Vascular disease.

And others.

Appropriate medical and neurological evaluation matters.

A Functional Medicine approach can work alongside that process by addressing metabolic, vascular, nutritional, sleep, digestive, and lifestyle contributors. It should not replace a necessary neurological diagnosis or disease-specific medical care.

The Functional Medicine Opportunity Is Not to Claim One Root Cause

Alzheimer’s is exactly the kind of condition that exposes the weakness in using “root cause” too simplistically.

There may not be one root.

There may be genetics interacting with decades of vascular health.

Metabolic dysfunction layered onto poor sleep.

Hearing loss reducing social engagement.

A sedentary lifestyle interacting with hypertension.

Nutrition influencing several of those variables at once.

Environmental exposures adding another layer of risk.

And biological processes we still do not completely understand.

That does not make the Functional Medicine lens less useful.

It makes systems thinking more important.

The goal is not to find the one hidden cause of Alzheimer’s. It is to identify which parts of the person's biological environment are working against long-term brain health—and which ones we can realistically change.

Start With the Factors That Pay You Back More Than Once

One of the best things about brain-health prevention is that most of the major targets are not brain-specific.

Improving blood pressure helps cardiovascular health too.

Improving insulin sensitivity helps metabolic health too.

Exercise supports muscle, bone, glucose regulation, cardiovascular fitness, mood, and mobility.

Better sleep affects nearly every physiological system.

Treating hearing loss can improve communication and participation even if dementia never enters the picture.

Building relationships makes life better now, not only decades from now.

Eating a nutrient-dense diet does not need Alzheimer’s prevention as its only justification.

That changes the risk-benefit calculation dramatically.

You are not sacrificing your present life to insure against one future disease.

You are improving systems that matter today while potentially building a more resilient brain for tomorrow.

Think in Decades, Not Detoxes

Alzheimer’s prevention does not need another seven-day cleanse.

It does not need a $300 bottle of supplements.

It does not need fear every time you forget somebody's name.

The emerging evidence points toward something both less glamorous and much more powerful:

protect the systems the brain relies on, repeatedly, over time.

Know your blood pressure.

Pay attention to blood sugar and metabolic health.

Move your body.

Protect your hearing and vision.

Take sleep seriously.

Stay connected.

Keep learning.

Build a diet around real food and individual needs.

Stop smoking.

Reduce meaningful environmental exposures where possible.

And do not wait until cognition has significantly declined before deciding that brain health matters.

The Future Is More Interesting Than “There’s Nothing You Can Do”

We still have enormous amounts to learn about Alzheimer’s disease.

We do not yet know why one person with substantial amyloid pathology remains cognitively resilient while another declines.

We do not know exactly how genetics, vascular biology, metabolism, immunity, the microbiome, environmental exposures, sleep, and other systems combine in every individual.

And we should be deeply skeptical of anyone who claims they can guarantee Alzheimer’s prevention.

But uncertainty is not the same thing as helplessness.

The 2024 Lancet Commission tells us that meaningful dementia risk exists in potentially modifiable domains.¹

U.S. POINTER showed that a structured, multidomain intervention can improve cognitive trajectories in older adults at increased risk.⁴

LatAm-FINGERS showed that a similar concept can work across countries and cultures.⁵

Those are not promises of prevention.

They are something better than false certainty:

evidence that there are actions worth taking.

You cannot choose your age or rewrite the genes you inherited. But you can influence the biological environment in which those genes and that aging brain have to operate.

That is the perspective behind our Longevity & Healthy Aging approach: the goal is not simply adding years, but protecting the capacity to think, move, connect, and participate in those years.

And if you want to understand which metabolic, cardiovascular, nutritional, sleep, digestive, hormonal, or lifestyle factors may be most relevant to your own long-term brain health, our Functional Medicine approach is designed to look at those systems together rather than waiting for one isolated marker to tell the entire story.