The Nature Study: What It Actually Shows

The headline claim

Researchers analyzed data from nearly 470,000 participants and concluded that 72-93% of Alzheimer's cases are attributable to two common APOE variants (ε3 and ε4). The study reframes the common APOE ε3 variant, which most people carry, as "risk-increasing" rather than "neutral" by comparing it to the rare, protective APOE ε2 variant.

Why those numbers need context

The 93% figure comes from the Alzheimer's Disease Genetics Consortium (ADGC) dataset, which is specifically enriched for people with a family history of Alzheimer's. This makes it a highly selected population, not representative of the general public. The more population-representative datasets in the same study (UK Biobank and FinnGen) showed notably lower attributable fractions: 75.7% and 71.5% respectively.

Even more importantly, all of these datasets come from populations where there's a clear gene-environment interaction between APOE and Alzheimer's risk. In other words, APOE's effects vary depending on where you live and what other risk factors you're exposed to. The study's authors didn't account for this geographic and environmental variation in their analysis.

What this means:APOE clearly matters. It's the strongest common genetic risk factor we have for Alzheimer's. But saying "93% of Alzheimer's is due to APOE" is like saying "100% of Alzheimer's is linked to having a brain." It's technically true in a statistical sense but potentially misleading about causation and ignores the critical role of environment, lifestyle, and other modifiable factors.

The more accurate takeaway:APOE influences how vulnerable your brain is to Alzheimer's-related damage, but it doesn't operate in isolation. Your genes may load the gun, but environment and lifestyle pull the trigger. This is actually good news because it means that even if you carry higher-risk APOE variants, you're not destined to develop the disease.

The More Exciting Story: APOE as a Drug Target

Here's what we're most optimistic about from this research era: APOE is becoming an increasingly viable target for prevention and treatment. And targeted therapies could provide another tool in our prevention toolkit.

Enter Obicetrapib: Promising Results from a Cholesterol Drug

What is Obicetrapib? Obicetrapib is a CETP inhibitor originally developed to treat cardiovascular disease. It lowers LDL ("bad") cholesterol and raises HDL ("good") cholesterol. But recent data from the Phase 3 BROADWAY trial revealed something unexpected: notable effects on Alzheimer's biomarkers.

The BROADWAY trial results (presented at AAIC 2025): In a pre-specified analysis of 1,727 participants with cardiovascular disease, including 367 APOE4 carriers, treatment with obicetrapib 10 mg daily for 12 months showed:

• In the full study population: Statistically significant reduction in plasma p-tau217 (p=0.0019)
• In APOE4 carriers: Significant reductions (p=0.0215)
• In APOE4/4 carriers: 20.5% reduction in p-tau217 levels vs. placebo (p=0.010)

Additionally, favorable trends were observed across other Alzheimer's biomarkers including NFL, GFAP, p-tau181, and Aβ42/40 ratio, with the most pronounced effects in APOE4/4 carriers.

Why p-tau217 matters: P-tau217 is one of the earliest detectable blood biomarkers for Alzheimer's disease. It can begin rising more than 20 years before cognitive symptoms appear and shows high accuracy in predicting future cognitive decline. Slowing or reducing its progression could represent meaningful upstream intervention.

How it might work: APOE's primary function is transporting cholesterol and fats in the bloodstream and brain. APOE4 appears to be less efficient at this job, which may lead to:

• Impaired cholesterol clearance from brain cells
• Reduced amyloid-beta clearance
• Increased neuroinflammation
• Disrupted lipid metabolism in astrocytes and microglia

By inhibiting CETP, obicetrapib increases functional HDL particles and appears to improve cholesterol transport. In a small Phase 2a study in early Alzheimer's patients with APOE4, treatment reduced brain cholesterol metabolites (24- and 27-hydroxycholesterol) by 11-12% in cerebrospinal fluid, suggesting it may have direct brain effects.

Preclinical and genetic data support this potential mechanism: rodents lacking the CETP gene show resistance to Alzheimer's pathology, and genetic variants that reduce CETP activity are associated with lower Alzheimer's risk and maintained cognitive function in aging, particularly in APOE4 carriers.

Why we're optimistic about this: Unlike observational genetics research, this is an actual intervention showing measurable biomarker effects in humans. The drug is oral, once-daily, well-tolerated across multiple large trials, and already in late-stage development for cardiovascular indications. We're cautiously hopeful that these early signals could translate into meaningful prevention benefits.

Current status: Obicetrapib is in Phase 3 trials with cardiovascular outcomes expected in late 2026. Given these Alzheimer's biomarker findings, dedicated brain health prevention trials may be forthcoming.

What This Means For You

Should you know your APOE status?

We think so (generally). APOE testing reveals your genetic starting point and enables risk stratification, treatment personalization, clinical trial eligibility, and helps you prepare for emerging therapeutics like obicetrapib that may work differently by genotype. But it's a personal choice, and knowing your status doesn't determine your destiny.

What's actionable right now:

1. Cardiovascular health is brain health Manage blood pressure (<120/80), optimize lipids (apoB, LDL, HDL, triglycerides, Lp(a)), control blood sugar and insulin sensitivity, exercise regularly

2. Support healthy lipid metabolism Mediterranean-style diet rich in omega-3s and monounsaturated fats, minimize trans fats and excess saturated fat, adequate choline (eggs, fish, cruciferous vegetables), omega-3 supplementation (especially for APOE4 carriers)

3. Address inflammation systemically Prioritize sleep (7-9 hours), manage chronic stress, maintain oral and gut health

4. Don't over-focus on genetics Gene-environment interactions matter enormously. Populations with high APOE4 prevalence but low Alzheimer's rates demonstrate that genetic risk is highly modifiable by environment and lifestyle.

The Bottom Line

The Nature study's headline-grabbing statistics appear to overstate APOE's role by analyzing highly selected populations and not accounting for gene-environment interactions. But that doesn't diminish what really matters: APOE is a major, potentially modifiable risk factor, and we're finally developing tools to target it more directly.

The obicetrapib data represents something more tangible than population genetics: an actual drug showing measurable effects on Alzheimer's biomarkers in living humans. If these results hold up in dedicated prevention trials, we could be looking at one of the first pharmacologic interventions that meaningfully addresses genetic Alzheimer's risk.

The future of brain health isn't about accepting your genetic hand. It's about understanding it clearly (not through sensationalized headlines), addressing modifiable factors, and staying informed about emerging therapies that may help target genetic vulnerabilities.

FEATURED BIOMARKER

Omega-3 Index: What Your Blood Reveals About Your Brain

What it is: The Omega-3 Index measures the percentage of EPA and DHA in your red blood cell membranes. It reflects your omega-3 status over the past 2-3 months (similar to how HbA1c reflects blood sugar over time). An Omega-3 Index of 8% or higher is considered desirable for heart and brain health; most Americans fall between 4-5%.

Why it matters for your brain: DHA is one of the primary structural components of your brain's cell membranes, and EPA plays a powerful anti-inflammatory role. Together, they support everything from neurotransmission to neuroplasticity.

The research is compelling and continues to grow. A large meta-analysis of 48 longitudinal studies involving over 103,000 participants found that dietary omega-3 intake was associated with an approximately 20% lower risk of dementia and cognitive decline. In the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort, long-term omega-3 supplement users showed a 64% reduced risk of Alzheimer's disease. And a dose-response meta-analysis of 58 randomized controlled trials published in Scientific Reports found significant improvements in attention and processing speed with omega-3 supplementation.

The APOE4 connection: If you carry the APOE4 gene variant, omega-3s may be especially relevant for you. Research suggests that APOE4 carriers may have more difficulty transporting DHA into the brain, which means they may benefit from higher intake, ideally started before cognitive symptoms appear. 

How to improve it:

• Eat SMASH fish regularly. Salmon, Mackerel, Anchovies, Sardines, and Herring are the richest food sources of EPA and DHA. Aim for at least two servings per week. (Tilapia, shrimp, and clams are good protein sources but are not meaningful sources of omega-3s.)
• Supplement strategically. BetterBrain recommends fish oil with 1-2g of DHA daily, taken with food, from a reputable third-party tested brand. If you're vegetarian or vegan, algal oil supplements provide EPA and DHA directly from the original marine source.
• Monitor your levels. Your optimal dose depends on your starting point, your genetics, and your diet. Tracking your Omega-3 Index through blood testing takes the guesswork out of supplementation.

BetterBrain Tip: Low omega-3 levels are one of the most common findings among our members, and one of the most actionable. In fact, fish oil supplementation is one of the first techniques our coaches recommend. Many members see meaningful improvement in their omega-3 ratio within 90 days of starting a targeted protocol.

Check your omega-3 levels with BetterBrain →

BETTERBRAIN HACK

The SMASH Strategy: Making Omega-3 Rich Foods Easy

Getting enough omega-3s from food alone is absolutely possible, but it takes some intention. The acronym SMASH makes it simple to remember the best sources: Salmon, Mackerel, Anchovies, Sardines, and Herring.

The science: Not all fish are created equal when it comes to omega-3 content. A 3-ounce serving of wild salmon delivers roughly 1,500-2,000 mg of EPA and DHA combined. Sardines pack around 1,600 mg along with impressive amounts of protein (22g), vitamin D, B12, calcium, and selenium. Meanwhile, popular choices like tilapia or shrimp contain only a fraction of those levels.

Quick wins to try this week:

• Sardine lunch hack: Grab a tin of sardines packed in extra virgin olive oil. Pair with whole grain crackers and your favorite hot sauce. It's one of the easiest, most nutrient-dense lunches you can assemble in under two minutes.
• Salmon prep day: Bake a couple of salmon fillets on Sunday. Use them throughout the week in salads, grain bowls, or alongside roasted vegetables. If you're looking for a new recipe, here's an awesome from coach Erika that we featured in a previous newsletter. 
• Anchovy upgrade: Melt anchovies into pasta sauces, salad dressings, or olive oil for a savory umami boost. They dissolve completely, so even anchovy skeptics tend to enjoy them this way.
• Frozen is fine: Don't overlook frozen fish. Flash-frozen fish is often fresher than what's sold at the counter, and wild-caught frozen salmon is widely available and more affordable.

A note on mercury: You may wonder about heavy metals in fish. The SMASH fish are all smaller, shorter-lived species that accumulate far less mercury than large predatory fish like tuna and swordfish. Eating SMASH fish multiple times per week is both effective and safe.

BetterBrain Insight: Combining omega-3 intake with B vitamin supplementation may enhance the benefits. Research suggests that DHA supplementation works best when paired with adequate B vitamin levels, particularly for slowing brain atrophy. This is why BetterBrain looks at the full picture of your nutritional biomarkers, not just one nutrient in isolation.

If eating SMASH fish multiple times a week isn't realistic for your lifestyle, or if your Omega-3 Index is still below target after dietary changes, supplementation is a simple and effective next step. Our go-to pick is Carlson's The Very Finest Fish Oil, which delivers 1,600 mg of omega-3s per serving, is third-party tested for purity and potency, and comes in a natural lemon flavor that makes it easy to take daily.

Content Corner

The Form of Omega-3 May Matter for Your Brain

A clinical trial underway at the University of Cincinnati is investigating something fascinating: not just whether omega-3s help the brain, but which form of DHA is most effective at actually reaching it.

Bottom line: Standard fish oil supplements deliver DHA in a form called TAG-DHA (triglyceride-bound). But emerging evidence suggests that LPC-DHA (lysophosphatidylcholine-bound DHA), the form naturally found in fish, may be significantly more effective at crossing into the central nervous system. The trial is comparing the two head-to-head in 153 older adults with mild cognitive decline, measuring DHA levels directly in cerebrospinal fluid for the first time.

This research is still in progress, and we want to be clear that standard fish oil supplements remain well-supported by the existing evidence base. But it's an exciting example of how the field is moving beyond "do omega-3s help?" toward "how do we optimize their delivery to the brain?" We'll be watching this one closely and will share results when they're published.

Also worth noting: a December 2025 narrative review highlighted the particular importance of omega-3s for postmenopausal women, given the loss of estrogen's neuroprotective effects. The authors recommended monitoring omega-3 levels and integrating supplementation into public health strategies for women after menopause.

BetterBrain Takeaway

Omega-3 fatty acids are among the most studied nutrients in the world, with over 50,000 published research papers. The evidence consistently points in one direction: adequate EPA and DHA intake is associated with better cognitive outcomes and lower dementia risk. Yet the vast majority of us aren't getting enough. Testing your levels, eating SMASH fish regularly, and supplementing strategically are three concrete steps you can take today.

The Basics: What Is Cholesterol?

What Is Cholesterol?

Cholesterol is a fatty molecule that serves critical functions throughout your body. It forms the outer layer of every cell, helps produce hormones (including testosterone, estrogen, and cortisol), enables vitamin D synthesis, and supports nerve function. Without cholesterol, you simply couldn't survive.

But there's an important distinction to make: "cholesterol" isn't one thing.

When we talk about cholesterol in the blood versus cholesterol in the brain, we're really talking about two separate systems that operate differently.

Blood cholesterol: Cholesterol travels through your bloodstream inside particles called lipoproteins. These particles come in different types:

• LDL (low-density lipoprotein): Often called "bad" cholesterol, LDL particles deliver cholesterol to cells throughout your body
• HDL (high-density lipoprotein): Called "good" cholesterol, HDL particles help transport excess cholesterol back to the liver
• VLDL (very low-density lipoprotein): Primarily transports triglycerides but also carries some cholesterol
• IDL (intermediate-density lipoprotein): A transition form between VLDL and LDL

Brain cholesterol: Your brain makes its own cholesterol and keeps it completely separate from blood cholesterol. The blood-brain barrier prevents cholesterol in your bloodstream from entering your brain. This means the cholesterol circulating in your blood and the cholesterol in your brain are part of two entirely different pools.

The Heart Risk:

Why apoB Matters More Than LDL

What is apoB?

ApoB (apolipoprotein B) is a protein found on the surface of all atherogenic (plaque-forming) particles, including LDL, VLDL, IDL, and Lp(a). Each particle contains exactly one apoB molecule, making apoB a direct count of total potentially harmful particles.

Why apoB beats LDL cholesterol: Traditional LDL-C (LDL cholesterol) tells you how much cholesterol LDL carries, but not how many particles you have. Two people can have identical LDL-C but vastly different particle numbers and risk levels.

• Many small LDL particles (each carrying less cholesterol) = "normal" LDL-C but high particle count and high risk
• Fewer large LDL particles (each carrying more cholesterol) = higher LDL-C but fewer particles and potentially lower risk

ApoB counts every atherogenic particle regardless of size. This makes it the best single marker for cardiovascular risk.

The triglyceride connection: Elevated triglycerides (often from insulin resistance) fundamentally alter lipid metabolism:

• VLDL becomes triglyceride-enriched
• Particles get remodeled into small, dense LDL
• ApoB particle count increases
• You can have "normal" LDL-C but dangerously high apoB

This is why metabolic health is critical for cardiovascular risk.

The Brain Side:

Why Cholesterol Is Essential

While high apoB threatens your heart, brain cholesterol is absolutely essential.

Critical brain functions:

• Myelin formation: Insulates nerve fibers for rapid signal transmission
• Synapse formation: Creates and maintains neuron connections
• Cell membranes: Every neuron needs cholesterol-rich membranes
• Neurotransmitter release: Regulates how neurons communicate

How the brain gets cholesterol: Astrocytes (brain cells) produce cholesterol and package it into brain-specific lipoproteins containing apoE (apolipoprotein E) for delivery to neurons.

The APOE genetic factor:

• APOE ε2: Protective against Alzheimer's, better cholesterol handling
• APOE ε3: Most common, considered neutral
• APOE ε4: Increases Alzheimer's risk, disrupts brain cholesterol metabolism

Research from MIT shows APOE4 is associated with brain cells to accumulate cholesterol abnormally rather than using it to make healthy myelin. This isn't about too much or too little cholesterol but how effectively the brain uses it.

Cholesterol and Alzheimer's: Brain regions vulnerable to Alzheimer'sshow signatures of being 'super cholesterol-hungry,'as researchers describe it, constantly trying to produce and absorb cholesterol. When this system fails (especially with APOE4), neurodegeneration may follow.

The Paradox Resolved

In the bloodstream: High apoB drives atherosclerosis. Particles penetrate artery walls, oxidize, trigger inflammation, form plaques. Goal: Keep apoB low (<60-80 mg/dL) to prevent cardiovascular disease.

In the brain: The brain makes its own cholesterol independently. Blood cholesterol can't cross the blood-brain barrier. Goal: Support healthy brain cholesterol metabolism through metabolic health.

This separation means lowering blood cholesterol doesn't starve your brain. Your brain continues making what it needs regardless of apoB levels.

The Bottom Line

Cholesterol isn't inherently good or bad; context is everything. In your bloodstream, high apoB poses serious cardiovascular and cerebrovascular risks. In your brain, cholesterol is essential for structure and function.

The good news: these systems are separate. Lowering apoB to protect your heart doesn't harm your brain. In fact, protecting your cardiovascular system through better lipid management, metabolic health, and inflammation control also protects your brain.

Understanding which biomarkers matter empowers informed decisions. It's not about fearing cholesterol; it's about managing it intelligently.

Want to understand your complete lipid profile and genetic risk?

BetterBrain includes apoB, advanced lipid testing, metabolic biomarkers, and APOE genetic testing for a complete cardiovascular and brain health picture. 

 Still have questions? Schedule a free 15 minute consultation with a brain health coach today here.

Cholesterol gets a bad rap. For decades, we've heard that it clogs arteries and causes heart attacks. But here's what doesn't make headlines: your brain contains 25% of your body's total cholesterol despite making up only 2% of your body weight. As lipid expert Dr. Tom Dayspring puts it, "Cholesterol is almost certainly the most important molecule in the brain."

So how can cholesterol be both necessary for brain function and a major cardiovascular risk factor? The answer lies in understanding where cholesterol is, how it gets there, and what form it takes.

In this post, we're taking a deeper dive into cholesterol than usual. We'll break down what your cholesterol numbers actually mean, why the standard tests miss critical information, and how the cholesterol story connects cardiovascular health to brain health.

The Basics: What Is Cholesterol?

Cholesterol is a fatty molecule that serves critical functions throughout your body. It forms the outer layer of every cell, helps produce hormones (including testosterone, estrogen, and cortisol), enables vitamin D synthesis, and supports nerve function. Without cholesterol, you simply couldn't survive.

But there's an important distinction to make: "cholesterol" isn't one thing.

When we talk about cholesterol in the blood versus cholesterol in the brain, we're really talking about two separate systems that operate differently.

Blood cholesterol: Cholesterol travels through your bloodstream inside particles called lipoproteins. These particles come in different types:

• LDL (low-density lipoprotein): Often called "bad" cholesterol, LDL particles deliver cholesterol to cells throughout your body
• HDL (high-density lipoprotein): Called "good" cholesterol, HDL particles help transport excess cholesterol back to the liver
• VLDL (very low-density lipoprotein): Primarily transports triglycerides but also carries some cholesterol
• IDL (intermediate-density lipoprotein): A transition form between VLDL and LDL

Brain cholesterol: Your brain makes its own cholesterol and keeps it completely separate from blood cholesterol. The blood-brain barrier prevents cholesterol in your bloodstream from entering your brain. This means the cholesterol circulating in your blood and the cholesterol in your brain are part of two entirely different pools.

The Heart Risk: Why apoB Matters More Than LDL?

What is apoB?

ApoB (apolipoprotein B) is a protein found on the surface of all atherogenic (plaque-forming) particles, including LDL, VLDL, IDL, and Lp(a). Each particle contains exactly one apoB molecule, making apoB a direct count of total potentially harmful particles.

Why apoB beats LDL cholesterol?

Traditional LDL-C (LDL cholesterol) tells you how much cholesterol LDL carries, but not how many particles you have. Two people can have identical LDL-C but vastly different particle numbers and risk levels.

• Many small LDL particles (each carrying less cholesterol) = "normal" LDL-C but high particle count and high risk
• Fewer large LDL particles (each carrying more cholesterol) = higher LDL-C but fewer particles and potentially lower risk

ApoB counts every atherogenic particle regardless of size. This makes it the best single marker for cardiovascular risk.

What is the triglyceride connection?

Elevated triglycerides (often from insulin resistance) fundamentally alter lipid metabolism:

• VLDL becomes triglyceride-enriched
• Particles get remodeled into small, dense LDL
• ApoB particle count increases
• You can have "normal" LDL-C but dangerously high apoB

This is why metabolic health is critical for cardiovascular risk.

The Brain Side: Why Cholesterol Is Essential

While high apoB threatens your heart, brain cholesterol is absolutely essential.

Critical brain functions

• Myelin formation: Insulates nerve fibers for rapid signal transmission
• Synapse formation: Creates and maintains neuron connections
• Cell membranes: Every neuron needs cholesterol-rich membranes
• Neurotransmitter release: Regulates how neurons communicate

How the brain gets cholesterol

Astrocytes (brain cells) produce cholesterol and package it into brain-specific lipoproteins containing apoE (apolipoprotein E) for delivery to neurons.

The APOE genetic factor

• APOE ε2: Protective against Alzheimer's, better cholesterol handling
• APOE ε3: Most common, considered neutral
• APOE ε4: Increases Alzheimer's risk, disrupts brain cholesterol metabolism

Research from MIT shows APOE4 is associated with brain cells accumulating cholesterol abnormally rather than using it to make healthy myelin. This isn't about too much or too little cholesterol, but how effectively the brain uses it.

Cholesterol and Alzheimer's

Brain regions vulnerable to Alzheimer's show signatures of being "super cholesterol-hungry," as researchers describe it, constantly trying to produce and absorb cholesterol. When this system fails (especially with APOE4), neurodegeneration may follow.

The Paradox Resolved

In the bloodstream: High apoB drives atherosclerosis. Particles penetrate artery walls, oxidize, trigger inflammation, form plaques. Goal: Keep apoB low (<60-80 mg/dL) to prevent cardiovascular disease.

In the brain: The brain makes its own cholesterol independently. Blood cholesterol can't cross the blood-brain barrier. Goal: Support healthy brain cholesterol metabolism through metabolic health.

This separation means lowering blood cholesterol doesn't starve your brain. Your brain continues making what it needs regardless of apoB levels.

The Bottom Line

Cholesterol isn't inherently good or bad; context is everything. In your bloodstream, high apoB poses serious cardiovascular and cerebrovascular risks. In your brain, cholesterol is essential for structure and function.

The good news: these systems are separate. Lowering apoB to protect your heart doesn't harm your brain. In fact, protecting your cardiovascular system through better lipid management, metabolic health, and inflammation control also protects your brain.

Understanding which biomarkers matter empowers informed decisions. It's not about fearing cholesterol; it's about managing it intelligently.

Want to Understand Your Complete Lipid Profile and Genetic Risk?

BetterBrain includes apoB, advanced lipid testing, metabolic biomarkers, and APOE genetic testing for a complete cardiovascular and brain health picture.

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Meet Sarah Ferreira, MS, MPH, RD, IFNCP: Brain Health Coach

Sarah Ferreira, MS, MPH, RD, IFNCPis an integrative and functional dietitian with dual master's degrees in Nutrition and Public Health, plus additional training in applied neuroscience and brain health. Her clinical interests include dementia prevention, neurological conditions, thyroid and digestive health, and the psychology of eating behavior.

Sarah's career spans inpatient clinical nutrition, eating disorder treatment, community nutrition with WIC, and 1:1 and group work at the Cleveland Clinic Center for Functional Medicine. She's passionate about helping people build confidence through knowledge and celebrating strategic successes over time.

Outside of her professional life, Sarah can often be found with a stack of library books, at a flamenco dance class, or spending time outdoors with her young son. She believes the fullest life is best lived with strong black coffee, flavorful curries, and mango in just about any form.

Sarah's Top Recommendations

Her new favorite brain health technique:

"My new favorite brain health technique is supplementing with Magnesium L-Threonate, a form of magnesium with some evidence of the ability to cross the blood brain barrier more efficiently than other types. I love it because it supports clearer thinking, better focus, and a calmer nervous system without feeling sedating. It's become a simple daily ritual that I plan to keep!"

Here's one of our favorite magnesium picks.

A simple strategy that's been especially effective for clients:

"Sleep troubles are so frustrating, and make it much more difficult to focus, maintain healthy blood sugar, and keep energy levels up. A simple strategy I've been talking about with clients who struggle with sleep is lowering the room temperature at night.

As bedtime approaches, core body temperature should drop; a cooler environment reinforces this process and signals the brain that it's time to wind down. Sleeping in a cooler room, typically around 60 to 67°F, has been shown to promote deeper slow wave sleep and reduce nighttime awakenings. A cooler setting can also prevent overheating, which is a common disruptor of REM sleep. Altogether, adjusting the thermostat is a simple, evidence aligned way to improve both the depth and consistency of your sleep."

A mindset shift that makes a big difference:

"Shifting away from 'ideal or nothing' thinking can be incredibly freeing and supportive of long term success. When clients think in extremes like 'I need to be at the gym for 45 minutes in order to exercise,' or 'If I can't do this perfectly, it's pointless,' I encourage them to think about the next best step and adopt a mindset of purposeful experimentation as they try out new things.

Over time and with consistency, small wins accumulate and foster self compassion, shape our sense of self, increase motivation, and create a positive sense of control over our brain health."

Her go-to brain boosting ritual:

"My go to brain boosting ritual is early morning movement. In the winter, I notice the best benefits for mood and mental clarity with a challenging Pilates session, weight lifting, and indoor cycling. It feels like a major win if I can get it done before my toddler wakes up!"

What she's most excited about in brain health research:

"I'm really excited about the ongoing accumulation of evidence around nutrition and brain health. Studies increasingly show that long term, nutrient dense eating patterns can support memory, focus, and even slow age related cognitive decline. Key nutrients like omega 3 fatty acids, antioxidants, and choline appear to protect neurons, reduce inflammation, and support healthy brain signaling.

What I find especially uplifting is how practical and adaptable these findings are, both for personal habits and for guiding clients. Framing food as a tool for cognitive resilience makes healthy eating feel meaningful and empowering, rather than restrictive."

Content Corner

Huberman Lab: Nutrients For Brain Health & Performance

Bottom line: This Huberman Labs episode is a practical companion to what Sarah shared about nutrition and brain health. Dr. Andrew Huberman, Stanford neuroscientist, breaks down the specific nutrients proven to support brain function, both for immediate cognitive performance and long term brain health.

The episode covers ten science supported tools, starting with the fact that fat is the most important element for brain function because it provides the structural building blocks for neurons. Huberman explains that omega 3 fatty acids, particularly DHA, are essential for brain health, with foods like salmon, mackerel, and sardines being top sources. He recommends 1.5 to 2 grams of DHA daily for those not consuming enough fish.

Beyond omega 3s, he dives into choline (500mg to 1g daily), which supports focus by providing the substrate for acetylcholine, a key neurotransmitter. He also covers anthocyanins from blueberries (60 to 120 grams of fresh berries daily has been shown to enhance cognition in older adults), phosphatidylserine for reducing cognitive decline, and creatine for brain energy, particularly beneficial for those who don't eat meat.

The key insight? Huberman emphasizes that the goal is to get proper nutrients via food first, then use supplements as a backup. He also explores something fascinating: how we can actually rewire our food preferences toward healthier choices by understanding the gut brain connection and the psychology of taste. Our brains can learn to crave the foods that are good for us.

BetterBrain Takeaway:The nutrients Huberman highlights, omega 3s, choline, and antioxidants, are exactly the ones Sarah mentioned being excited about. Whether you're looking to optimize focus now or protect your brain for the long term, this episode offers specific, actionable guidance on what to eat and how much.

Featured Domain: Cognitive Reserve

What it is: Cognitive reserve refers to your brain's resilience to neuropathological damage. It's influenced by factors like education, occupation, and engagement in mentally stimulating activities. Individuals with higher cognitive reserve can better compensate for brain changes associated with aging and neurodegenerative diseases, delaying the onset of dementia symptoms.

The Science: A 2024 systematic review and meta analysis in Frontiers in Aging Neuroscience found that higher cognitive reserve across the lifespan is consistently associated with reduced dementia risk.

The key insight? It's never too late to start building reserve. Structured cognitive training combined with lifestyle modifications can enhance cognitive performance even in later life.

BetterBrain tracks multiple markers that contribute to cognitive reserve

Education: Higher educational attainment is associated with greater cognitive resilience. Studies show people with more years of formal education tend to be diagnosed with dementia later, even when their brains show similar pathology to those diagnosed earlier.

Stimulating Activities: Regular mental engagement builds neural networks. Activities like solving puzzles, reading, or learning new skills add to your brain's reserve. The brain operates on a "use it or lose it" basis.

Stimulating Vocation: Jobs requiring significant cognitive effort (problem solving, critical thinking, complex decision making) continually challenge the brain, strengthening neural networks and increasing cognitive reserve.

Languages: Multilingualism necessitates a complex neural network that improves the brain's ability to manage multiple tasks simultaneously. Research has shown that multilingual individuals tend to be diagnosed with Alzheimer's disease up to 4.5 years later compared to monolinguals. More on this below!

Hearing Sharpness: Hearing loss removes a major source of brain stimulation, causing language processing centers to weaken. Even mild hearing loss can double the risk of cognitive decline, while severe loss increases it up to 5x.

BetterBrain Tip: Your Health Profile in the BetterBrain Portal shows your Cognitive Reserve domain status alongside your other brain health domains. Check which of these markers might benefit from attention, and explore the relevant techniques we've suggested based on your results.

Technique Spotlight

Learn a New Language

Looking for a powerful intervention to build cognitive reserve? Language learning might be your perfect match.

The Science: One of the most fascinating findings in cognitive reserve research: speaking two languages proficiently can delay the onset of dementia symptoms by approximately 4 to 5 years compared to monolinguals.

A UCLA study of 253 Alzheimer's patients found that bilinguals were diagnosed 4.3 years later and reported symptoms 5.1 years later than monolingual patients. This effect holds regardless of education, immigration status, or the specific languages spoken.

How it works: Learning a new language creates dense neural networks through the constant mental exercise of switching between language systems, suppressing one language while using another, and building new vocabulary and grammatical structures. This cognitive "workout" strengthens executive function and working memory, capabilities typically compromised in Alzheimer's patients.

Getting Started: You don't need to become fluent to see benefits. Even basic language learning engages the brain's reserve building mechanisms.

Quick Wins:

• Download a language app like Duolingo and commit to 10 minutes daily
• Listen to podcasts or music in your target language during commutes
• Label items around your home in the new language
• Find a language exchange partner or conversation group
• Watch foreign films with subtitles, progressing from your language to the target language subtitles

BetterBrain Insight:If you currently only speak one language, consider this a high impact opportunity. Adding an additional language could reduce risks and improve your cognitive function in real time!

Content Corner

Tim Ferriss: How to Future-Proof Your Brain from Dementia with Dr. Tommy Wood

Bottom line: In this episode, Tim Ferriss sits down with BetterBrain's own Chief Science Officer Dr. Tommy Wood for a wide ranging conversation on dementia prevention. If you've been reading Grey Matters for a while, you'll recognize some familiar themes here, but hearing Tommy explain the "why" behind these strategies makes the science click in a new way.

Key takeaways: As we've emphasized many times, the Lancet Commission estimates somewhere between 45% and 70% of dementia cases are preventable through lifestyle factors. That stat bears repeating because it's genuinely hopeful: you can stack the deck massively in your favor.

On cognitive stimulation: Tommy digs into why cognitive stimulation works at a mechanistic level. The short version: your brain adapts when challenged beyond its current capabilities, much like muscles grow when trained to failure. It's not just about "using" your brain, it's about pushing it into that productive struggle zone. (This is exactly why language learning is so powerful, as we highlighted above.)

On exercise intensity: High intensity training appears to have outsized benefits for brain structure. One study found that participants doing intense interval training showed improvements in hippocampal function that persisted for five years after the intervention ended!

On sleep:You've heard us say sleep matters. Tommy adds a helpful reframe: don't catastrophize a bad night. Short term, your accuracy stays intact, it just takes a bit longer. Long term consistency is what counts.

The conversation also touches on topics close to our hearts: omega-3s and B vitamin synergy, oral health and dementia risk, and why addressing hearing or vision loss early really matters.

Still have questions about joining BetterBrain? Schedule a free 15-minute consultation with one of our brain health coaches here.