What happens is that the brain becomes extremely vulnerable to neurodegeneration — and it's rarely caught early, though it can be. No medication touches it, because the problem isn't a chemical imbalance that a drug can correct. It's a shortage of an essential cellular lipid your body has been manufacturing your entire life, one that's barely made it into mainstream conversation despite years of clear research on how necessary it is for brain health.

This combination will strain any brain and increase Alzheimer’s risk, but an APOE4 brain has less protection against it.

I’m sharing a client example below.

Being proactive about brain health, you have likely spent plenty of time thinking about amyloid plaques, tau tangles, inflammation, insulin resistance, diet and exercise.

But there is a foundational cellular player missing —one that underpins everything from how your neurons talk to each other to how your brain handles oxidative stress.

It’s called plasmalogens. And if you want to protect your cognition as you age, it’s time to get familiar with them.

What the Heck Is a Plasmalogen?

Your brain runs on a type of structural fat called a lipid. It's what every neuron is made of.

A few specific lipids do most of the heavy lifting: cholesterol, DHA, myelin, and plasmalogens. All have a role in your cognition, but we're focused on plasmalogens today.

Plasmalogens are a specialized class of phospholipids (fatty molecules) that make up a massive percentage of your cell membranes—accounting for roughly 20% of the total lipid mass in your brain.

They are heavily concentrated in places throughout your body that demand high performance: your brain (both grey and white matter), your heart, your lungs, your immune cells, and even your eyes.

Think of plasmalogens as the ultimate multi-taskers of cellular health:

1. The antioxidant shield: Plasmalogens act as front-line defenders against oxidative stress. When free radicals or environmental toxins threaten the delicate fats in your brain, plasmalogens absorb the damage first, neutralizing the threat.

   1. The problem: Aging and high toxic burden significantly diminish plasmalogens.

2. The Memory Drivers: Your cholinergic neurons—which are critical for learning, focus, and memory—require sufficient plasmalogens to operate properly. Without them, communication between neurons falters, and cognition is impaired.

   1. Research shows that individuals suffering from cognitive decline and Alzheimer’s disease have significantly depleted levels of plasmalogens in their blood and brain tissue.

3. The Brain Cholesterol Manager: Plasmalogens help keep cholesterol moving smoothly in the brain. When they're too low to do that, cholesterol can build up in the brain. This buildup can eventually trigger amyloid-beta, a sticky, toxic protein fragment that can impair communication between neurons. This is a risk that is especially high for APOE4 carriers whose cholesterol transport proteins are structurally impaired.

   1. The cholesterol system in the brain is separate from the one in your body. Restoring plasmalogens improves cholesterol efflux in the brain.

4. Not Just for the Brain: While brain health gets the spotlight, plasmalogens are vital system-wide. They maintain heart muscle stability, support lung surfactant integrity, and high blood levels are strongly correlated with lower all-cause mortality and overall longevity.

Natural Production and the Aging Cliff

For most of your life, your body acts as a manufacturing plant, building its own plasmalogens inside cellular structures called peroxisomes. It makes a lot of them because they are so important.

However, we hit a turning point as we age. While natural production hums along for decades, levels peak in midlife and begin a distinct, progressive decline as we move past age 50 and into our 60s, leaving our cellular membranes increasingly vulnerable.

This decline is heavily accelerated by lifestyle and internal stressors even in younger people. Chronic oxidative stress, environmental toxins, metabolic dysfunction, and chronic immune activation –– read about that in my previous post –– burn through your plasmalogen reserves at an alarming rate.

As mentioned above, research shows that individuals suffering from cognitive decline and Alzheimer’s disease have significantly depleted levels of plasmalogens in their blood and brain tissue. As you age, your body isn’t going to start making more of them, although precursors can reliably raise them. It’s only recently been possible to test these levels, but the test is not widely available. I use it for all my clients, and I’m sharing it today.

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Why You Can’t Rely on Direct Plasmalogen Supplements

Given how crucial they are, you might wonder why you can’t simply buy a bottle of plasmalogen supplements at GNC—such as the popular version made from scallops—and fix the problem.

Here is the biological truth: Intact plasmalogens cannot be directly supplemented to great effect because they can’t survive the digestive process, cross into your bloodstream to support your cells.

To genuinely raise your cellular levels, you have to use specialized precursors that bypass digestion and supply your cells with the raw building blocks they need.

A Real-World Wake-Up Call: Why Proactive Testing Matters

To see how this plays out in a real person, take a recent client of mine whose goal is to prevent Alzheimer’s because of his family history and APOE4/4 gene. He wanted all the lab data that would help us develop a personalized prevention plan.

He had been proactive on his own in a number of ways, including using a scallop-derived plasmalogen supplement, assuming he was fully covered for plasmalogens.

When his lab results came back, his plasmalogen levels were extremely low—at the 12th percentile. That’s a real-life example showing that direct plasmalogen supplementation doesn’t raise plasmalogen levels.

Environmental toxins, elevated IgG viral antibodies, and several other factors were also uncovered that he was previously unaware of.

His proactive mindset is exactly what he needs for the best chance of preventing an Alzheimer’s diagnosis down the road. Uncovering these hidden contributors to Alzheimer’s that he couldn’t discover without the right tests now turns a ticking time bomb into a modifiable roadmap for prevention and a way to measure progress.

Ready to find out where your plasmalogen levels stand and start rebuilding?

In the rest of this email you’ll learn about

• The lab test used to measure plasmalogens that also provides a window into several biological systems that usually require attention.

• Specific plasmalogen precursors, a 25% discount, and how to know which one to start with.

• What I use for myself and why.

• An exclusive opportunity to gain access to the test along with a review to understand your results.

• and I’ve recorded a video for you showing before/after test results.

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As a proactive person who wants to prevent Alzheimer’s, you already know that the current system is failing us. The drug companies just keep doing the same thing over and over by trying to clear amyloid-beta—a short-sighted strategy that still hasn't stopped the disease.

To prevent or treat Alzheimer’s by solely attacking amyloid is like trying to put out a house fire by just turning off the smoke alarm, while the kitchen is still ablaze.

So, what is the actual problem? At the root, Alzheimer’s comes down to two things that aren’t as simple as they sound: chronic immune activation and metabolic dysfunction. If you’re following the research on prevention, then you are hopefully already addressing your metabolic health with proactive testing, diet and lifestyle adjustments.

But what about the chronic immune activation that is mostly silent? Today I’d like to share my personal experience with this; what it is, what led me to uncover it in myself, how I did that, and what I’m doing about it. Without this type of action, it will continue and could eventually lead to an Alzheimer’s diagnosis, regardless of my healthy lifestyle.

Alzheimer’s is not a single disease with a single cause. My underlying contributors may not mirror yours, but the point is to learn from the process of discovery and not assume everything is fine because you don’t have symptoms.

Connecting the dots between my functional lab results from several test panels gave me the clarity I needed. Now, I’m taking targeted action to resolve ongoing immune activation for Alzheimer’s prevention before I have symptoms.

Using my own data, I’m not guessing about what to do. I can measure my progress and adjust as needed.

Three powerful instigators of chronic immune activation, especially in combination:

• High levels of viral antibodies from past or current infections. Past infections represent dormant viruses that your immune system successfully keeps under wraps—unless something disrupts that balance.

• Antibody Activity from a Leaky Gut: When your gut lining becomes compromised, it lets undigested food, toxins, and microbes slip into your bloodstream. This includes wheat gluten and bacterial toxins called lipopolysaccharides (LPS). Because your immune system constantly detects these everyday invaders, it keeps firing and refuses to shut down—creating a state of endless inflammation.

• Mycotoxin (Mold) Antibodies: These show up when your body is constantly battling toxins from environmental mold exposure, creating a hidden, ongoing trigger that keeps your immune system active.

Why chronic immune activation is so dangerous:

Because it causes ongoing, low-grade inflammation.

When these triggers are left unaddressed, the immune system can get stuck in the “on” position indefinitely, sending out continuous inflammatory signals as it tries to neutralize the threats.

You might experience any combination of warning signs—such as brain fog, joint pain, gut issues, or insomnia—which are usually medicated as separate conditions while the underlying immune activation continues unchecked. Or, you might not have symptoms you feel concerned about.

Eventually, these circulating inflammatory signals can disrupt the blood-brain barrier. This can allow things to get into the brain that don't belong there, and can also allow brain-derived proteins to leak out into general blood circulation where the immune system reacts to them.

This is why chronic immune activation is so often at the root of Alzheimer's. It’s complicated, but it is one of the most active areas of research right now. You can click this link to read one of many related studies: Systemic inflammation as a central player in the initiation and development of Alzheimer’s

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Last week, I shared that my early detection tests showed an elevated p-tau217 (a key marker of tau damage). That result is what led me to test for chronic immune activation in myself.

The rest of this post explains:

• The tests I used

• Connecting the dots between results because it wasn’t straightforward

• The “triage protocol” I developed because I couldn’t do everything at the same time

• And what I almost missed that was directly connected to the immune activation revealed.

• I’m also sharing a checklist you can use to help determine if chronic immune activation could be affecting you.

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Not because I had symptoms. I wanted these tests because of my family history of Alzheimer’s. I’ve seen too many people affected by this disease, both personally and professionally, to let this slide.

I wanted to know what was happening in my brain right now, while I have plenty of time to do something about it.

Honestly, I expected my results to look pretty good. I’ve been living an anti-Alzheimer’s lifestyle consistently for about two decades. I’ve been a ReCODE practitioner since 2016. I’ve spent almost a third of my life learning about the brain, studying the underlying drivers of cognitive decline, and teaching people how to reduce their risk or reverse symptoms of Mild Cognitive Impairment.

So when one of my own markers came back elevated, it immediately had my attention because I understood exactly what that result meant.

It meant Alzheimer's-related processes were already happening in my brain, despite my proactive lifestyle and functional lab testing. And that meant I needed to investigate for reversal rather than prevention.

This is the part I wish more people understood: relying on symptoms before you take action is risky business, especially when it comes to Alzheimer's. You can do everything right and still get Alzheimer's — because the absence of symptoms doesn't mean your prevention is working.

In my case, early detection test results led me to use more specific lab testing to look even deeper for the hidden causes driving that number up. I wasn’t alarmed, I was grateful for the wake-up call.

Finding out you have an elevated Alzheimer’s biomarker before symptoms appear is like detecting cancer in stage 1 rather than finding it in stage 4. No one wants that news. You have it. But if you had to choose, you would absolutely want to catch it early — while you still have a really good chance to stop it.

The same is true for Alzheimer’s. Early detection tests provide the opportunity to act earlier, while the brain is still far more resilient and responsive. And they give us the sense of urgency that is so often missing from prevention without symptoms.

Had all my results been in the normal range, I would have continued with my prevention plan as usual. And here's a consideration that matters: if you have a family history of Alzheimer's and your early detection tests come back normal, celebrate that, but remember, the test didn't lower your risk. You still need to be on a prevention plan.

There are now two categories of testing that matter for Alzheimer’s prevention. The first is early detection — the newer blood tests that can reveal whether Alzheimer’s-related processes may already be developing in the brain years before symptoms. The second is what Dr. Dale Bredesen coined a cognoscopy — a deeper functional investigation designed to uncover the underlying hidden contributors driving those brain changes, or potentially leading to them in the future.

The fact that we can get this kind of information early is great news for anyone who wants to be proactive about Alzheimer’s in an effort to avoid symptoms and a diagnosis. I wish it had been available for my mom. I have no doubt she would have gotten on this train.

In the rest of this email, I cover the three biomarkers I consider most important, what each one measures, how to get them, what I did after receiving my results, and something critical to consider before you do.

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My grandmother started showing unmistakable signs not long after that. Then my aunt was diagnosed, not long after my grandmother died. By the time my mother was symptomatic, I didn’t need a genetic test to tell me what I already knew. I was at real risk.

Not some day risk. Now risk.

This was 2010. I went looking for something to do about it, and there was nothing. No formal program, no studies with good outcomes. Every doctor I asked told me the same thing — there’s nothing you can do, just wait and see. So, I waited and tried not to think about it.

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That’s not where we are anymore.

Today, we know everything is connected, and it’s not a one-way street with the brain running the whole show alone. The brain and body depend on each other to function properly.

We have Dr. Dale Bredesen’s thirty years of research into what actually drives this disease — and the research of many others that continues to validate his work. It’s not just one scientist, and there’s not just one cause.

Alzheimer’s is a convergence of metabolic, inflammatory, toxic, vascular, hormonal, and mitochondrial dysfunction, all of it building over time before a single cognitive symptom shows up.

That means we have an actual open door for prevention, and it’s a lot wider than most people assume when you start early. But here’s what I’ve watched happen, over and over, during a decade of doing this work: knowing an open door for prevention exists doesn’t mean anyone walks through it.

I understand why. A diagnosis is concrete — a date, a doctor, an appointment on the calendar, a name for symptoms, a concrete reason to take action.

Prevention asks you to act against something that hasn't happened yet, something you can't see, something a standard lab panel won't even flag. It requires you to take action even though nothing is telling you that you need to — no symptom, no test result, no doctor raising a flag.

You feel and function completely fine. Or even if you notice “senior moments”, it’s easier to turn them into a joke rather than answer the question that briefly pops up in your mind. Either way, you don’t feel like you have a reason to act strategically or urgently. And… you may not know what to do.

The mind does what minds do with a hypothetical threat — it waits. It waits for the cough before it quits smoking, the chest pain before it changes the diet, the diagnosis of mild cognitive impairment before it finally, finally moves toward action.

I will not tell you that’s fine. It isn’t. Alzheimer’s is rapidly becoming the third leading cause of death globally as the number of people diagnosed climbs year after year. Your life is what’s at stake, and so is what your diagnosis would mean for the people who’d carry it with you. Prevention is possible, but you have to refuse to let awareness be where this ends for you.

The problem with awareness and general advice is that they’re so general. Alzheimer’s is a multifactorial disease that’s not exactly the same in each person, although the results of it are eventually the same.

We hear a lot of general advice, all of it good: Mediterranean or Ketoflex 12/3 diet, exercise, sleep, socialize, reduce stress. And almost everyone I talk to about this is trying to follow that advice. They think they’re doing ok, doing all they can, and yet they aren’t very confident that it’s working.

Diet and lifestyle factors are definitely important for Alzheimer’s prevention. I’m diligent about mine because a strong foundation for brain-body wellness is critical. It’s also important that the standard blood tests your doctor orders are in optimal ranges and that you know what those are. A blood glucose of 96 is not optimal just because it’s less than 100.

But is that enough? Based on my experience, I have to say no. That’s because a lot can be happening in the brain and body that standard labs aren’t measuring and that don’t cause symptoms for a long time. And when they do, often those symptoms don’t seem brain-related.

By the time you’re asking the same question several times within an hour without realizing it, brain changes have been going in the wrong direction for a long time.

My own early detection tests revealed the very beginning of this, which caused me to take a much deeper dive into the reasons why. What I found makes a big difference in my Alzheimer’s prevention strategy.

It’s time to start asking better questions — even about advice that sounds definitive.

You probably remember the lithium study that got so much attention. My inbox was flooded with people forwarding it to me. It’s an important study, and it’s actionable, but it is not the cure for Alzheimer’s. Why not?

Clarifying questions matter. Questions that take your individual risk factors into account are crucial. Do you know what yours are? How would you find out? Questions lead you down a path toward discovery, and the answers can lead to actions you may not have known were necessary — or even known existed.

Instead of living with a looming threat you’re not quite sure about, trying not to think about it, wondering if every forgetful moment is “it” — you can open the gate to empowerment with knowledge. But knowledge isn’t the empowerment itself. The actions you take based on that knowledge are. And it isn’t a one-time event. It’s a process.

One of the most important life skills my dad taught me was to ask good questions. It’s served me well, and when it comes to preventing Alzheimer’s, it can serve you well too, if you’re willing to act on the answers.

I’ve been engaged in a proven protocol for prevention for over ten years, asking and answering questions that keep my data-driven, action-oriented plan alive. My cognition at 62 is better than ever.

But there was one question I hadn’t answered about my Alzheimer’s prevention strategy until about a year ago, and I had to answer it for myself before I could ask anyone else to answer it for themselves.

I was prompted to answer it after my 64-year-old first cousin died because of Alzheimer’s.

Am I really preventing this, or has it already started and I just don’t know it yet?

Are you asking the right questions? Do you know which questions to ask and how to get the answers? I just added a chat space for paid subscribers to help with that.

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The APOE gene comes in three common variants — E2, E3, and E4. Everyone inherits two copies, one from each parent:

• E2 is relatively rare and may offer some protective effect

• E3 is the most common, carrying baseline risk of about 10-15% by age 85

• E4 is the variant that raises your risk for Alzheimer’s more than just the risk that everyone has

Carrying one copy of APOE4 increases Alzheimer’s risk approximately three-fold. Carrying two copies—APOE4/4—increases risk up to twelve-fold and is associated with an earlier age of onset.

Approximately 25% of the population carries at least one copy, and nearly 40% of all Alzheimer’s diagnoses involve someone who carries it.

How APOE4 Actually Works

Knowing whether or not you have this gene can actually work in your favor because the gene is not your destiny. You’re not fighting against a “bad gene”—you’re managing the consequences of a protein made by the gene that’s structurally less equipped to do its job well. That’s actually good news, because there are multiple ways you can intervene for Alzheimer’s prevention, including:

• Supporting plasmalogens for the proper function of brain cells responsible for cognition.

• Preventing chronic inflammation or taking action to stop it

• Supporting mitochondrial function

• Supporting how efficiently your brain and body transport cholesterol and fats

• Decreasing toxic exposures and supporting detoxification

Ultimately, it all comes down to cellular health—removing the insults and providing the fuel and nutrients.

It helps to understand why having the APOE4 gene raises your Alzheimer’s risk, so let’s take a look at six ways it does that.

1. Brain inflammation

APOE4 disrupts the brain’s immune cells, causing them to overreact and release more inflammatory molecules than they should. Rather than responding to a threat and standing down, the inflammatory response in APOE4 carriers tends to be more intense and harder to resolve. This pattern shows up throughout the body as well, not just in the brain. Chronic low-grade inflammation is one of the most consistent contributors to Alzheimer’s disease, and APOE4 keeps a foot on the accelerator of that process.

2. Amyloid accumulation

One of the primary jobs of the APOE protein is to help clear amyloid from the brain. The E4 variant does this poorly. It doesn’t bind well to toxic amyloid, which means the brain’s clearance system is less efficient—and amyloid builds up faster and in greater amounts over time. This is one of the reasons APOE4 carriers tend to have higher amyloid burden at earlier ages.

3. Reduced brain energy

APOE4 carriers typically show lower brain energy production—called hypometabolism—in areas of the brain most affected by Alzheimer’s disease, usually decades before any symptoms appear. When the brain’s energy production falters, neurons become vulnerable.

This is particularly relevant if you’re a woman with a maternal history of Alzheimer’s. Research suggests that women are more likely than men to experience brain hypometabolism, and a maternal family history compounds that vulnerability further—meaning reduced brain energy is an especially significant factor for you specifically.

4. Vascular dysfunction

APOE4 reduces blood flow to the brain, limiting the delivery of oxygen and nutrients that neurons depend on. Reduced cerebral blood flow is both an early marker and an accelerating factor in Alzheimer’s disease—and one more reason why cardiovascular health and regular aerobic exercise are not optional for APOE4 carriers.

5. Cholesterol problems in the brain

The brain produces its own cholesterol and depends on proper transport and clearance of that cholesterol to function well. APOE4 disrupts this process—it is less efficient at facilitating cholesterol efflux from brain cells, meaning cholesterol builds up rather than being properly cleared. That buildup is directly linked to amyloid accumulation. Lowering cholesterol in the brain is not the solution because it’s a transport problem. The goal is to keep it moving properly, not to lower it.

6. A compromised blood-brain barrier

APOE4 can impair the integrity of the blood-brain barrier—the protective barrier that keeps pathogens, toxins, and inflammatory molecules out of the brain. When that barrier becomes permeable, the brain is exposed to substances it was never designed to encounter, and the immune response that follows contributes directly to neuroinflammation and neurodegeneration.

The Bottom Line

APOE4 risk factors don’t exist in isolation—they’re all connected and progressive. Prevention starts with the fundamentals: diet and lifestyle choices that matter for everyone and give you a strong foundation for brain-body wellness. But understanding your individual vulnerabilities through targeted testing gives you a personalized strategy based on your hidden risk factors before they start causing symptoms.

Combined with APOE4’s effects on inflammation, amyloid clearance, brain energy, vascular health, and cholesterol efflux—the picture becomes one that warrants real urgency about prevention.

Alzheimer’s isn’t inevitable. Your genes respond to your environment—both internal and external. The research is clear that lifestyle and targeted intervention using the right lab data can meaningfully change the trajectory for APOE4 carriers, especially when prevention begins before symptoms appear.

The information above helps you understand why the APOE4 gene is a serious risk factor for Alzheimer’s. The upgrade section provides practical interventions —the testing decision you may be pondering, and several supplements and lifestyle interventions that actually address the specific mechanisms we just covered. I’ve also shared a link to join my Fullscript dispensary for supplements, along with sharing my practitioner discount.

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Most people don’t ask that question when a prescription is written or an over-the-counter bottle gets tossed into the shopping cart. It helps a symptom, so you take it.

That’s a completely understandable path — it’s how most of us have been taught to think about medication. The unconscious assumption is that if it’s prescribed or sold on a shelf, it must be safe.

But some of the most commonly prescribed — and commonly purchased over the counter — medications have associations with cognitive decline and dementia that most people have never been told about.

For women with a maternal history of Alzheimer’s who are already working to reduce their risk, this information is especially worth having.

To be clear upfront:

• I am not suggesting you stop taking anything you’ve been prescribed

• That conversation belongs with your doctor

• What I am suggesting is that you know what you’re taking, understand what the research says about long-term use, and feel empowered to have a more informed conversation with your physician

Because here’s what I’ve observed over more than a decade of working in Alzheimer’s prevention: most people have never been told that certain medications they’ve been on for years carry a meaningful association with dementia.

And when they find out, they feel betrayed and wish they had been told.

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Proton pump inhibitors (PPIs)

PPIs are among the most widely prescribed drugs in the country. They’re used to treat acid reflux and indigestion, and many people take them daily for years.

Common names include:

• Omeprazole (Prilosec)

• Pantoprazole (Protonix)

• Esomeprazole (Nexium)

The problem with long-term PPI use goes beyond the stomach:

• They impair the absorption of B12, magnesium, and zinc — nutrients that are critical for optimal brain function

• They alter the gut microbiome in ways that have effects on brain health, given how directly the gut and brain communicate

• Long-term use has been associated in research with an increased risk of dementia

• Additional concerns include kidney problems, heart issues, and increased fracture risk

PPIs aren’t easy to stop once you’ve been on them for a long time — the acid rebound can be significant, and tapering needs to be done gradually with a doctor’s guidance. But stopping the medication without addressing why the acid problem developed in the first place leaves the root cause untouched. That means you need a plan that’s based on your specific lab results.

Anticholinergic medications

This category deserves particular attention. Anticholinergic drugs work by blocking the action of acetylcholine — a neurotransmitter that plays a central role in memory, learning, and attention.

In other words, these drugs interfere with the very brain chemistry involved in cognitive function.

What makes this especially concerning is how many common medications fall into this category — including some you can buy without a prescription.

The cumulative effect of blocking acetylcholine over months and years is not trivial. Research has shown that long-term anticholinergic use is associated with increased dementia risk, and the effect appears to be dose-dependent — meaning the longer and more consistently you take them, the greater the concern.

People with an existing dementia diagnosis should never be on these medications.

As a woman at risk for Alzheimer’s with a maternal history of the disease, I would never take one of these medications.

Common anticholinergic drugs include:

• Benadryl and other first-generation antihistamines (diphenhydramine, chlorpheniramine)

• Tricyclic antidepressants such as amitriptyline

• Bladder medications for overactive bladder such as oxybutynin

Benzodiazepines

Benzodiazepines are prescribed for anxiety, sleep, and muscle relaxation. Long-term use has been associated with an increased risk of Alzheimer’s disease — significantly enough that some researchers have called it a public health concern.

The mechanism matters here. Benzodiazepines suppress areas of the brain involved in transferring information from short-term to long-term memory.

That’s not a subtle side effect.

Common benzodiazepines include Xanax, Valium, Ativan, Klonopin, and Restoril. Used occasionally and short-term, the risk profile is different. Used consistently over months and years, the picture changes considerably.

The question worth asking isn’t just “is there a safer medication?” It’s “what can I do instead of what can I take?” That question opens a very different kind of conversation — a more productive one.

Upgrade to get the rest of this email, where I go deeper on each medication category, the functional testing that can help you address the root cause, and the lifestyle and supplement approaches that support your body in ways medication can’t.

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Not even close.

In the entire body of research on Alzheimer’s prevention, exercise stands alone as the single most consistently supported, most broadly effective, and most accessible tool we have.

And most people are either not doing it, not doing enough of it, or not getting the most out of it.

This isn’t about weight or appearance or cardiovascular fitness, though those matter too. This is specifically about what happens inside your brain when you exercise — and the list is remarkable.

For women with a maternal history of Alzheimer’s, or anyone who’s determined to protect their brain health, this is not optional information. This is the most powerful tool available to you.

What exercise actually does for your brain

• It grows new brain cells. Exercise is one of the most powerful stimulants of BDNF — brain-derived neurotrophic factor — a protein I sometimes describe as Miracle-Gro for the brain. Intensity matters more than modality: heavy lifting, high-intensity intervals, and aerobic exercise that elevates heart rate all drive BDNF production. It does three critical things: stimulates the growth of new brain cells, particularly in the hippocampus (memory center); strengthens connections between brain cells, supporting learning and memory; and protects existing neurons from degeneration and death.

• It reduces inflammation in the brain. The kind that progressively damages neurons over time and is one of the most consistent drivers of Alzheimer's disease.

• It improves insulin sensitivity in the brain. Brain insulin resistance — sometimes called Type 3 diabetes — is one of the most consistent metabolic contributors to Alzheimer’s disease. Exercise is one of the most effective interventions known for improving insulin sensitivity.

• It supports the blood-brain barrier. Regular physical activity helps maintain the integrity of the barrier that keeps toxins and pathogens out of your brain tissue.

• It improves sleep quality. Exercise is one of the most reliable ways to improve the depth and architecture of your sleep — during deep sleep the brain clears waste, consolidates memory, and repairs cellular damage.

• It supports energy production in brain cells. Exercise stimulates the growth of new mitochondria — the tiny “batteries” inside every cell — keeping neurons fueled and functioning.

• It lowers chronic stress hormones. Cortisol — your primary stress hormone — damages the brain's memory center when it stays elevated for too long. Regular exercise is one of the most effective ways to bring it back into a healthy range.

• It improves blood flow to the brain. Reduced blood flow is both an early sign and a contributor to Alzheimer's disease. Exercise keeps the brain's blood vessels healthy and ensures it receives the oxygen and nutrients it depends on.

The degree to which exercise protects the brain is so consistent across the research that some researchers have described a sedentary lifestyle as one of the single largest modifiable risk factors for Alzheimer’s disease. That’s a strong statement.

It's worth clarifying what sedentary actually means — because this is one of the most common misconceptions about exercise and brain health. You can exercise every morning, or play pickleball three times a week, and still have a sedentary lifestyle.

An hour of movement doesn't cancel out eight hours at a desk, an evening on the couch, and a day spent mostly sitting. Research shows that prolonged uninterrupted sitting has its own independent effects on metabolism, circulation, and brain health — separate from whether you meet exercise guidelines.

Breaking up sitting time throughout the day — standing, walking briefly, doing a few air squats or push-ups periodically, moving every hour or so — matters alongside structured exercise. Both count. Neither replaces the other.

For women with a maternal history of Alzheimer’s, you are already working against elevated risk. Exercise and moving throughout your day is one of the most direct and accessible ways to work back against it — start today if you haven’t already.

In the upgrade section of this post, I cover the most common obstacle to developing an exercise habit and how to overcome it, what types of exercise the research supports most strongly for brain health, what the research says specifically for women over 50, and how to build an exercise habit that’s sustainable — not just for overall fitness and your brain health.

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When they decline — and they all decline with age — your brain feels it. So does your body, your energy, your sleep, your mood, and your metabolism.

For both men and women, this hormonal decline is real and relevant to brain health. For women, the sex hormones decline dramatically during perimenopause — the transition leading up to menopause — and that's one factor that makes women more likely to get Alzheimer's than men.

And for women with a maternal history of Alzheimer’s, this hormonal withdrawal happens against a backdrop of already elevated risk — and the two converge in ways that standard medicine rarely addresses.

Women with a maternal history of Alzheimer’s are more likely to have inherited mitochondria that make the brain more dependent on hormonal support — and less resilient when that support is withdrawn. The same hormonal decline that affects other women presents a more significant inflection point for you.

This connection is almost never made in a regular doctor’s office.

Has your primary care doctor, gynecologist, or neurologist ever talked with you about your hormonal health related to your brain health?

In over a decade of working with clients, only one has ever said yes — and she was working with a functional medicine doctor.

I’ve been proactively managing and testing my own hormones for twenty years. What I’ve learned — from my own results, my own prescriptions, and working with clients — is that this is one of the most important and most overlooked pieces of Alzheimer’s prevention, especially for women. Tell your friends.

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The hormones your brain depends on:

Your brain has receptors for nearly every hormone in your body because it was designed to depend on them. When hormone levels decline — and they decline in everyone with age — those receptors are still there, waiting for signals that are no longer arriving at the same strength.

The brain loses regulatory inputs it counted on for energy production, inflammation control, and neuronal repair. That gap is one of the reasons hormonal decline is directly connected to Alzheimer's risk in both men and women — and one of the reasons addressing it matters for preventing the disease or improving early symtpoms of cognitive decline.

To understand why hormonal decline matters so much for brain health, it helps to see the full scope.

The list below isn’t exhaustive — it’s meant to show you several of the hormones your brain depends on, and what each one contributes to keeping it functioning well. If you skim it now, it is worth coming back to for a better understanding of the roles they play in your brain.

• Estrogen — supports memory formation, the chemical that drives learning and recall, the clearance of harmful proteins that accumulate in Alzheimer’s disease, and the energy production that keeps neurons alive. It also acts as a potent antioxidant that protects brain cells from oxidative damage.

• Progesterone — a calming hormone that improves your sleep quality, has direct anti-inflammatory effects in brain tissue, and supports myelin repair — the coating on the connections between brain cells that keeps communication clear.

• Testosterone — supports your cognitive function, mood, motivation, memory, and the long-term survival of brain cells.

• DHEA — supports the growth of new brain cells, memory consolidation, and protects the brain’s memory center from damage caused by chronically elevated stress hormones.

• Vitamin D — technically a hormone, not a vitamin. Vitamin D supports neuronal survival, reduces neuroinflammation, regulates immune function in the brain, and low levels are consistently associated with increased Alzheimer's risk.

• Thyroid hormones (T4 and T3) — regulate how efficiently your brain produces and uses energy, and support the connections between brain cells that make thinking, memory, and focus possible.

• Insulin — a hormone that regulates how your brain cells take in and use glucose for fuel.

• Cortisol — your primary stress hormone. In proper balance, it supports alertness. When it’s chronically elevated — as it is in many women — it damages the same areas of the brain that Alzheimer’s damages and depletes other protective hormones.

• Pregnenolone — your master precursor hormone that is made from cholesterol in your brain. Serves as the raw material from which many other hormones are made and supports memory, mood, and brain cell function.

• Melatonin — supports your sleep-wake cycle, helps your brain clear waste overnight, and has direct protective and antioxidant effects in brain tissue.

• Growth hormone — supports brain cell repair, brain metabolism, and your deep sleep architecture. Declines significantly after midlife, contributing to the progressive reduction in deep sleep many women notice in their 50s and beyond.

• IGF-1 (insulin-like growth factor 1) — supports brain cell survival, strengthens connections between neurons, and plays a direct role in clearing harmful proteins from the brain.

Twelve hormones that naturally decline with age. All of them relevant to your brain health.

Intentionally supporting your hormonal health helps maintain your brain health.

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The aging process does not render you powerless. Hormonal decline is real, but your response to it is a choice — and that choice is made one day at a time through how you eat, how you sleep, how you move, and how you manage stress. The right supplements can also be helpful for some of them.

You may have already noticed that none of that is easy to change : )

Research consistently shows that people who have support, accountability, and a positive community with the same goals are significantly more likely to make changes that last — and to sustain them over time. My Direct Access community offers all of this and more.

Send an email to info@angelachapman.net for more info to get a free 3-day pass to check it out.

This is not about stopping the clock. It’s about aging on purpose to extend your health span and giving your brain every advantage available to it for as long as possible. That is always within your reach.

Upgrade to paid for what I believe is the best test for assessing your hormonal health and how to get it, what I personally do to support my hormonal health, an honest look at BHRT and what to do if it’s not for you, and why supporting all of your hormones matters regardless of the path you choose.

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Her fasting glucose was 102. Technically just over the line into prediabetic range, the kind of number a doctor might mention briefly and suggest she watch her diet. Nothing urgent. Except it is.

Her triglycerides were 436. That’s not a subtle signal. It’s safe to assume it had been high for a long time. That’s a system in serious metabolic distress — the result of a diet high in carbohydrates and sugar, and a clear sign of the insulin resistance that diet had produced. High triglycerides interfere with the brain's ability to use glucose efficiently — which matters enormously for a brain already at risk for the energy deficits that drive Alzheimer's disease. Her mother, grandmother, and sister had all had the disease.

Her hs-CRP — a marker of systemic inflammation — was 3.16. Anything above 1.0 is considered elevated from a cardiovascular standpoint. Hers was more than three times that.

Her fasting insulin was 11.7. This is not a standard test — her doctor almost certainly never ran it. Combined with her fasting glucose of 102, that tells you her cells were already experiencing insulin resistance.

Her A1c was 5.4. Completely normal — and almost certainly the number that would have reassured everyone. But a normal A1c alongside elevated insulin isn’t a clean result. It means her pancreas was still working hard enough to keep blood sugar out of the diabetic diagnosis range, while the underlying system was already under serious strain.

Her HDL was low at 51. That means her triglyceride/HDL ratio was 8.5:1. That’s a powerful warning sign for insulin resistance—her cells had stopped responding normally to insulin, and her body had likely been compensating for years without any obvious symptoms.

This is the metabolic environment that should concern everyone related to their risk for Alzheimer’s.

Glucose, triglycerides, insulin, inflammation. These numbers told a metabolic story that had been shifting for years — within ranges that attracted no medical attention, while the disease was already well underway. We know Alzheimer’s begins a couple of decades before symptoms.

Her maternal history made it all track. Raising the very real issue of brain hypometabolism that you can read about by clicking this link. But her doctor may not have known about her maternal history of Alzheimer’s, or how these markers further elevated her risk.

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Even today, Alzheimer’s prevention isn’t the lens through which traditional doctors are viewing lab results.

These aren’t obscure markers. With the exception of fasting insulin — and usually A1c — they appear on the standard blood work your doctor orders every year.

Which means you can start using them to protect your metabolic health, whether your doctor flags them or not. The most powerful tools for protecting your brain aren’t prescriptions or procedures — they’re diet, movement, sleep, and targeted supplementation.

Things you control entirely on your own.

If fasting insulin isn’t already on your panel, ask your doctor to add it next time. Once you have both glucose and insulin results, you can calculate your HOMA-IR — a measure of insulin resistance — using a free online calculator.

A score below 1.0 is optimal. Above 1.9 suggests early insulin resistance is developing. Above 2.9 indicates it is already significant. My mom’s was 2.9.

Insulin resistance is so consistently linked to Alzheimer’s disease that some researchers have called it Type 3 diabetes. These are not numbers to leave unexamined. And this is not the only contributor.

Brain hypometabolism is when the brain’s ability to use glucose is impaired; an early risk factor for Alzheimer’s that begins decades before symptoms, especially if you have a maternal history of the disease.

Insulin and glucose have a close relationship in the body and the brain. Take these numbers seriously, along with your triglycerides. These are easy first steps for your Alzheimer’s prevention strategy. They aren’t the only ones, but they are important.

You actually have a lot of control over preventing Alzheimer’s – this is just the tip of the iceberg. But getting your metabolic health under control is foundational.

What follows for premium subscribers are the optimal ranges for several key markers found on standard lab panels you probably have results for — what to look for, what warrants attention, and what you can start doing about it today.

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By the time symptoms appear, the underlying biology has been moving in the wrong direction for a very long time.

One of my clients with a maternal history of Alzheimer’s came to me after receiving a diagnosis of mild cognitive impairment. She was prescribed a medication, told it might or might not help, and she would have to wait and see if things got worse.

The diagnosis was simply a diagnosis. There was no investigation into why her cognition was declining.

We got to work looking for the underlying contributors to her cognitive decline and were able to identify several.

Over the next several months, we focused on improving specific diet and lifestyle factors, along with reducing toxic exposures and inflammatory burden. Within about five months, her brain fog and memory problems improved dramatically. And the arthritis in her hand went away.

Last year, we measured her oxidative damage levels and they were high. The test estimated that her oxidative stress burden looked more like someone in their late 90s, than her current age of 72.

Even though her cognition had markedly improved, the oxidative stress damage was still significant and was specifically affecting the health of her cell membranes, her nitric oxide pathways, and her vascular health.

While oxidative stress damage is one of the foundational processes contributing to Alzheimer’s disease, the actual damage created by oxidative stress is what eventually drives dysfunction in the brain and body.

One simple urine test provided a significant amount of valuable information for her ongoing prevention plan .

She has now been working with me for five years, and after we incorporated the oxidative damage testing into her prevention plan a year and half ago, repeat test results show meaningful improvements in several of the markers.

Seeing improvement in her oxidative damage markers validated that the interventions were improving the cellular health connected to her brain-body wellness. It was proof that even in her 70s, she could make meaningful progress.

This is one reason I believe oxidative damage deserves far more attention in conversations about Alzheimer’s prevention and cognitive decline.

Most people have heard the term oxidative stress, but very few people really understand what it means. And because of that, there is very little urgency around it.

Oxidative stress is essentially a form of biological wear and tear. It develops when the body is producing more cellular damage than it can properly repair.

Over time, the body starts losing its ability to keep up with the damage because the insults causing the damage are ongoing. They continue day after day, year after year, eventually overwhelming the body’s ability to maintain and repair itself efficiently.

Most people do not connect oxidative damage to its symptoms because the symptoms are dismissed as “normal aging.”

And it is true that oxidative damage is part of the aging process. But what is “normal,” and what is excessive?

At what point does normal biological aging become accelerated aging that leads to disease?

The common symptoms are:

• lower energy

• brain fog

• poor recovery from stress

• worse sleep

• more aches and pains

• blood sugar problems

• declining exercise tolerance

• subtle memory lapses

The common assumption is those changes are simply unavoidable with age and therefore “normal.” But in many cases, they are signs that oxidative damage is accumulating faster than the body can efficiently repair it. If you take action early enough, you can improve it.

Doctors don’t always explain this kind of cellular damage to people. They may hear they need to “eat better and exercise,” or take a medication for symptoms, but never really understand the cellular implications.

What I’ve observed over many years working with people concerned about cognitive decline is that when people can actually see test results showing the biological damage affecting their body and brain, and when the information is explained in an understandable way, they become much more motivated to take consistent action.

The brain is especially vulnerable to oxidative stress.

As oxidative stress continues, inflammation inside the brain increases. Damaged proteins and cellular debris begin accumulating faster than the brain can clear them. Repair systems become less efficient.

This is where the process begins moving toward what may eventually be diagnosed as Alzheimer’s disease.

It is not unusual that oxidative damage levels can improve.

What is unusual is actually measuring it, connecting it to Alzheimer’s risk, and then using the data over time to see whether interventions are meaningfully changing biological health.

This information provides a useful high-level view of oxidative damage and inflammatory stress affecting biological health. We can, and do, gather more specific data to better understand what is driving those processes and contributing to Alzheimer’s risk when personalizing the PreCODE protocol for an individual.

In the upgraded section of this email, I’m sharing:

• the oxidative damage panel I use and how to self-order it

• what the biomarkers on the panel show us

• and what you can begin doing to lower it and support healthier brain-body aging

• An interview with the client referenced above, discussing her progress

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Researchers call this brain hypometabolism.

It means the brain is not using glucose efficiently for fuel, and it’s one of the earliest and most common things seen in Alzheimer’s disease. In fact, brain hypometabolism can often be seen on FDG-PET scans years — sometimes decades — before the first cognitive symptoms appear.

This is especially important for people with a maternal history of Alzheimer’s because several major Alzheimer’s risk factors are inherited more strongly through the mother’s side, particularly those involving mitochondria, inflammation, and brain hypometabolism.

Mitochondria are the energy-producing structures inside your cells, and they are inherited almost exclusively from your mother. Your brain uses an enormous amount of energy every day. When brain cells begin struggling to efficiently access and use fuel, they become more vulnerable and less resilient over time.

Researchers have shown that cognitively normal adults with a maternal history of Alzheimer’s often have lower glucose metabolism in Alzheimer’s-prone brain regions long before symptoms begin.

That matters because Alzheimer’s doesn’t suddenly appear the day someone receives a diagnosis. The processes in the brain begin developing years earlier.

And honestly, this changes how we should think about prevention.

If brain energy problems are already silently developing in our 40s, then prevention cannot simply start when we get older or after symptoms begin.

It has to start much earlier.

While an FDG-PET scan can reveal whether someone already has brain hypometabolism, I’ve simply assumed I have it because of my maternal family history.

I actually do have 5 good reasons to believe Alzheimer’s would eventually become very likely for me if I ignored this, and other hidden risk factors. Those 5 good reasons are the 5 women in my direct maternal line who have already had it.

The good news is that brain hypometabolism is modifiable. That’s the part I want more people to understand.

The women in my family who developed Alzheimer’s knew nothing about brain hypometabolism. They had no access to the information we have today. In their lifetime, and during most of mine, Alzheimer’s prevention and reversing early symptoms of cognitive decline were considered to be impossible.

Even though researchers first began identifying abnormal brain glucose metabolism in Alzheimer’s disease back in the late 1970s and early 1980s. Even now, most people, including many physicians, still don’t understand how important this concept is for prevention.

My female relatives developed symptoms in their mid-late 60s, but the metabolic dysfunction contributing to those symptoms began much earlier.

My cousin, especially. Her cognitive symptoms actually became obvious in her 50s, and she died at age 64 after progressing to late-stage Alzheimer’s disease. That means the underlying metabolic dysfunction in her brain could have started in her 30s or 40s.

Do I think hypometabolism was the only thing contributing to Alzheimer’s in my family?

No. Alzheimer’s is multifactorial. But I absolutely believe it was one of the factors affecting all of them.

Brain hypometabolism can exist for years before obvious cognitive decline appears As time passes, there may be symptoms that are easily dismissed as stress, aging, burnout, menopause, poor sleep, or simply “having too much going on.”

Because the brain is not producing and using energy efficiently, early signs of that can show up in subtle ways. Some people also describe a vague sense that their brain “doesn’t feel as resilient” as it used to, even though standard cognitive testing is still normal.

The exciting part is this: The brain has another fuel source called ketones.

Ketones are molecules your liver produces primarily from fat when your body is no longer getting a constant supply of glucose (sugar) from food.

This naturally happens overnight while you sleep, during exercise, or when meals contain fewer carbohydrates, and there’s a longer period of time between eating.

Unlike glucose, ketones can still provide energy to brain cells even when glucose metabolism in the brain has become impaired.

In other words, ketones can help provide fuel to brain cells that are running low on energy because of impaired glucose metabolism. This is one reason ketogenic strategies are being studied so heavily in Alzheimer’s prevention and early cognitive decline.

In the paid section below, I’m going to walk through a few practical ways to begin using this information to support your brain energy without becoming obsessive or feeling like you need to change everything overnight.

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