The goal of Alzheimer’s prevention is to find and improve as many of them as possible, ideally long before symptoms show up. That’s still the goal after symptoms start or after an MCI diagnosis, but the longer you wait after a diagnosis, the lower your chances of cognitive improvement.

One of the not-so-simple contributors is how cholesterol behaves in the brain.

Just FYI: this post gets a little technical. I’ve kept it as plain as I can for anyone who wants to understand the process, but if you want the bottom line: Lowering brain cholesterol really isn’t “a thing” and would miss the real problem if it were, although we hear that high cholesterol in the brain is a dementia risk factor. It’s actually poor cholesterol transport in the brain, especially for APOE4 carriers, and we can do something about that.

Several things affect how well the brain handles its cholesterol:

• Your APOE genotype

• How well brain cells move extra cholesterol out

• How efficiently the brain gets rid of what it doesn’t need

• Insulin resistance

• Oxidative stress

• Inflammation

• Aging

• Plasmalogen levels

That last one, a group of fats called plasmalogens, is missing from most of the conversations I’ve heard, and it’s tied to most of the others on the list.

It matters for anyone working on prevention or helping someone with MCI or early dementia, and it matters most for people who carry a gene called APOE4.

What does APOE4 have to do with cholesterol?

If APOE4 is new to you, it’s the strongest known genetic risk factor for late-onset Alzheimer’s. About one in four people carry at least one copy. One copy raises the risk, and two copies raise it more.

The APOE gene makes a protein, also called APOE, that helps move cholesterol around the body. Because of the way the APOE4 version handles cholesterol, APOE4 carriers tend to have more of it in their blood.

That may or may not be a problem, depending on other factors, but it makes them more likely to be prescribed medication to lower it. Some are even told it will protect their brain.

Is lower cholesterol always better?

Cholesterol itself isn’t dangerous. Your cells depends on it.

• Every cell in your body uses it to build and maintain its outer layer.

• Your body uses it to make hormones like estrogen, progesterone, testosterone, and cortisol, along with vitamin D.

Your brain needs it. Your brain is about 2% of your body weight, but holds about 25% of your body’s cholesterol.

• Your brain uses cholesterol to build the connections between brain cells where memories get made.

• It uses cholesterol to make myelin, the protective coating that wraps the brain’s wiring so signals travel fast.

• It uses cholesterol to make its own hormones, including pregnenolone and its own estrogen and progesterone, which support memory, mood, and myelin repair.

Cholesterol becomes a problem when it gets damaged by oxidation, which is most often driven by high triglycerides, insulin resistance, and a few other things I’ll cover in a future post.

Low cholesterol carries its own risks. In older adults, higher total cholesterol has been linked with a lower risk of dementia, and low cholesterol has been linked with shrinkage in the brain’s memory centers.

In long-term studies, lower cholesterol showed up years before people were diagnosed. In the ReCODE protocol, we view total cholesterol under 150 as a serious risk factor.

Where does your brain get its cholesterol?

The cholesterol system in your brain is separate from the one in the rest of your body. Your brain makes its own cholesterol. A protective lining around the brain’s blood vessels, called the blood-brain barrier, keeps the cholesterol in your bloodstream out, along with other things that could harm the brain.

Keeping the two systems separate is how your brain stays in control of its own cholesterol supply.

A high cholesterol number on your blood test is telling you about your blood, not your brain. Cholesterol in the brain can become a dementia risk factor, but not because there’s too much of it.

The problem comes when it can’t be transported as well as it was when you were younger, and that’s especially true for people who carry the APOE4 gene.

What happens when cholesterol builds up in the brain?

When cholesterol isn’t transported well, it builds up in brain cells. Through a complicated process related to that buildup, the brain makes more amyloid-beta, the sticky protein that forms clumps and is used to help diagnose Alzheimer’s.

Your brain relies on a few key players to move extra cholesterol out of its cells.

• A pump in the outer layer of brain cells pushes extra cholesterol out.

• The APOE protein picks it up and carries it to where it’s needed. A building block in APOE called cysteine helps it do this job well, and the APOE4 version is missing it.

• Plasmalogens help cholesterol leave the cell so it can be carried away.

Plasmalogens are a special kind of fat built into the outer layer of your cells. Besides helping clear cholesterol, they make up a large share of myelin, which breaks down in Alzheimer’s.

Brain plasmalogens can’t be measured directly, but blood levels can, and low blood levels have been linked with Alzheimer’s and with how severe the dementia is.

Plasmalogen levels peak somewhere between 30 and 40, then decline, dropping significantly by around 70. Blood levels start falling years before memory problems appear, and the lower they go, the more severe the dementia tends to be.

Why are APOE4 carriers hit hardest?

Those of us who carry the APOE4 gene make a version of the APOE protein that’s missing the cysteine building block, so it doesn’t transport cholesterol as well. That doesn’t matter much when we’re young, because our bodies are making plenty of plasmalogens, which make up for it and keep cholesterol moving.

As we get into our 50s and beyond, our plasmalogen levels drop. APOE4 carriers tend to have even lower levels on top of that decline. In a study of about 6,300 people, blood plasmalogens were highest in APOE2 carriers, lower in APOE3, and lowest in APOE4.

Without enough plasmalogens to make up for the missing cysteine building block, cholesterol builds up, more amyloid-beta gets made, and the risk climbs.

Low plasmalogens can lead to cholesterol buildup with any APOE type, but APOE4 carriers are more vulnerable.

Low plasmalogen levels are treatable. It’s clear from the before/after test results that the right supplementation increases them. Eating plasmalogen-rich foods like scallops or taking a standard supplement doesn’t raise them enough.

It takes plasmalogen precursor supplements, like Prodrome’s N3 and N9, which make it through digestion and give your body what it needs to build plasmalogens, skipping the early steps of production that slow down with age.

Does a statin help your brain?

Some statins, including atorvastatin (Lipitor), simvastatin (Zocor), and lovastatin, are fat-soluble and cross into the brain, where they slow how much cholesterol it makes.

Over time, that can lower the amount in the brain somewhat. Some researchers suspect that’s part of why some people report memory problems on those statins, though the FDA’s review didn’t tie the reports to any particular type.

The brain’s problem isn’t that it’s making too much cholesterol. It’s that it isn’t clearing the extra. Making less doesn’t help clear what’s already built up, and it leaves the brain with less of the cholesterol it needs. Two large trials gave simvastatin or atorvastatin to people with mild to moderate Alzheimer’s, and neither slowed their decline.

Why haven’t you heard about plasmalogens?

Plasmalogens aren’t a trace lipid. They make up about 20% of the fats in the outer layer of the brain’s gray matter and more than 30% in white matter, and your heart, lungs, kidneys, and muscles depend on them too.

Researchers have been reporting low plasmalogens in Alzheimer’s brains since the 1990s, while most Alzheimer’s research spent the next 30 years focused on amyloid itself.

That may be starting to change. In 2026, John Hardy, one of the two scientists who first proposed the amyloid hypothesis, the idea that amyloid plaques cause Alzheimer’s, which has driven most drug research for 30 years, co-authored a study finding that APOE4 carries less plasmalogen than APOE3, even in people with no sign of Alzheimer’s.

His team concluded that low plasmalogens likely help cause Alzheimer’s and called for research on raising them as a treatment.

What does the research show for APOE4 carriers?

In 2019, researchers measured plasmalogen levels and APOE type in 1,205 older adults.

• Overall, APOE4 carriers were about twice as likely to have dementia as people with the common APOE3/3 type.

• APOE4 carriers with high plasmalogen levels had a dementia rate of 14.3%.

• People with APOE3/3 had a dementia rate of 14.0%.

Those last two numbers are basically the same, which is significant. It suggests that high plasmalogen levels put APOE4 carriers at about the same risk as people with APOE3/3. Suggesting that APOE4 carriers with high plasmalogens have about the same dementia risk as the APOE 3/3 carriers

This study didn’t prove that raising plasmalogens will prevent dementia. What it does tell APOE4 carriers is that the gene doesn’t decide everything on its own.

Plasmalogens can be measured, and if they’re low, they can be raised. And in this study, higher plasmalogens went along with less dementia for everyone, whatever their APOE type:

The results of these analyses indicate that the net effect of APOE genotype on cognition and the prevalence of dementia is dependent upon the plasmalogen status of the person.

The 2019 study came from Prodrome Sciences, the company behind the plasmalogen blood test, and I’m certified in their testing. The independent research I’ve shared in this post points in the same direction.

Plasmalogens aren’t a silver bullet because there isn’t one for Alzheimer’s. They’re part of the silver buckshot. The biology linking low plasmalogens, cholesterol buildup, and amyloid is strong enough that I consider plasmalogen levels as one of the targets worth testing and addressing, alongside everything else that person needs.

Next week, I’ll move from the brain to the body: what turns the cholesterol in your blood from something your cells need into something that damages your blood vessels, and why the same things that damage it also raise your risk for Alzheimer’s.

Knowing your plasmalogen level, or your loved one’s, is a good move toward reducing Alzheimer’s risk related to brain cholesterol.

I covered how to test, which supplements I use, and how to get started in the upgrade/paid section of Plasmalogens: The Brain’s Essential Fat. Paid subscribers have access to the full archive and my brain resources list as well as supplement discounts, including plasmalogen precursors.

As always, joining my Direct Access membership is where I see people successfully make sustainable lifestyle changes that support Alzheimer’s prevention. They have access to all the implementation info for the ReCODE protocol, but even more important is the connection with others on the same path. Direct Access for Q/A with me, what’s working, troubleshooting, and a monthly Zoom call to make it all so much more personal and create lasting relationships.

Email info@angelachapman.net chat for more info and/or a 3-day free pass!

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Today, what works and what doesn’t. Over the past decade, the great majority of people who have reached out to me have been wives. The story is close to the same every time. Her husband has been told he has mild cognitive impairment (MCI). He came home with a prescription and a follow-up appointment in six months, and she came home with a stack of questions.

By the time she finds me, she has usually spent several late nights reading everything she can find, and she has a strong feeling that something important is being missed.

She’s right. If you’re in that position right now, the most useful thing I can tell you is to start now, and I want to explain why.

“Mild” is a misleading word

When MCI is caused by Alzheimer’s, the disease has typically been developing in the brain for 15 to 20 years before the first symptoms appear. Amyloid builds up, tau tangles spread, inflammation rises, and the brain loses connections between nerve cells, all while a person is still working, driving, and paying the bills.

The Alzheimer’s Association’s revised criteria now define Alzheimer’s by these biological changes. Under that definition, someone with MCI whose biomarkers show amyloid and tau already has Alzheimer’s disease. What he doesn’t have yet is an Alzheimer’s dementia diagnosis, because his symptoms haven’t become severe enough to interfere with daily life.

Not every case of MCI comes from Alzheimer’s dementia. Sleep apnea, nutrient deficiencies, an underactive thyroid, certain medications, and other conditions can cause the same symptoms and should not be left unchecked.

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What the standard visit covers

A typical investigation usually includes a short memory test, an MRI to rule out a stroke or tumor, and a few basic labs. Sometimes, an appointment with a neuropsychologist. Then comes a prescription, usually donepezil (Aricept), which can ease symptoms, modestly for a while in some people, but does nothing to change the disease process. In a three-year trial of people with MCI, it did not reduce the number who went on to develop Alzheimer’s dementia.

Most people in a twenty-minute appointment don’t have the time, or even think to ask what’s really driving the decline in this particular man, or if they do, the answer is often “we don’t know”. So the six-month follow-up becomes a wait to see how much worse things get.

Waiting to see if things get worse is pretty risky.

The new infusions, and why they fall short

The newer option many families hear about is an anti-amyloid infusion, Leqembi or Kisunla, given by IV every two to four weeks. Both carry the FDA’s strongest warning for brain swelling and bleeding, a risk that rises sharply for anyone with the APOE4 gene.

People on the drugs still declined, a few months more slowly than people on placebo, and when they stopped treatment, their decline returned to the untreated pace. Eisai’s computer model projects that staying on Leqembi could delay dementia by nearly three years, but so far, no one has been treated long enough to know.

The drugs rest on the idea that amyloid is the problem, yet autopsy studies have found that roughly a third of people who died with normal memory had enough plaques and tangles in their brains to meet the criteria for Alzheimer’s.

Newer drugs on the horizon may eventually be effective, affordable, and safe for APOE4 carriers, and one could become a real asset combined with a program that addresses the full picture. Today’s drugs are a long way from that, and waiting for them costs the time Alzheimer’s disease doesn’t allow.

What it really takes

Cognitive decline is a much wider process than amyloid, and much of what drives it starts elsewhere in the body: blood sugar problems, damaged blood vessels, chronic inflammation, infections, toxins, poor sleep, and the loss of hormones and nutrients the brain depends on. In 2024, the Lancet Commission on dementia estimated that 45% of dementia cases are linked to 14 risk factors we can change, most of them involving the whole body.

Their list leaves out a lot, including sleep, diet, chronic infections, gum disease, toxins, and hormones. Dr. Bredesen compares Alzheimer’s to “a roof with 36 holes.” Patch one hole, however well, and the rain still pours in through the other 35. Problem not solved.

Patch enough of them, and the results can be meaningful and lasting. Judy Benjamin watched her mother live with Alzheimer’s for 20 years, and in 2011, at 67, she was diagnosed herself. She became Dr. Bredesen’s first patient and followed his protocol closely.

Fast forward to 2025, at age 80, she walked nearly 2,800 miles from San Diego to St. Augustine to raise awareness that Alzheimer’s isn’t a one-way street. This September, at 82, she finished a 550-mile walk across England, from Land’s End to London.

Fifteen years after her diagnosis of Alzheimer’s, her cognition is normal, she works as a brain health coach and travels the world telling her story.

After a decade of working with people across every stage of this disease, I’ve seen five things make the difference.

Starting as early as you can. Before you have symptoms is the best time, but Alzheimer’s is still considered a disease of old age, so prevention seems unnecessary to most.

The signs of “senior moments” are a warning sign that the brain needs attention.

At the MCI diagnosis stage, the brain still has reserve to work with.

The published cases of people who improved their scores, some of them back into the normal range, were intentionally people who started at MCI. The lower the cognitive score when someone begins, the harder the climb, and past a certain point the realistic goals shift.

A thorough investigation. Two people can walk into a doctor’s office with the same memory score for very different reasons. One may have insulin resistance and oxygen dropping every night from untreated sleep apnea. Another may have mold toxins from a slow leak behind a bathroom wall and a reactivated herpes virus.

Each needs something the other doesn’t, and the only way to know which “holes are in the roof” is to test for them. I organize these hidden contributors by systems and test accordingly: Immune, Gut, Metabolic, Detoxification, Nutrients, Neuro, Cardio. Each category has specific tests, most are not standard. Dr. Bredesen calls this comprehensive evaluation a cognoscopy.

A comprehensive program. Social media is full of lifestyle advice for brain health, and much of it is sound. For someone who has already progressed to MCI, though, those pieces have to come together in a comprehensive plan built around what the right testing shows. Dr. Bredesen’s group has built the evidence for this approach since 2014, most recently in a randomized control trial with people who have MCI or early dementia.

After nine months on a personalized program, participants’ overall cognitive scores rose from about the 30th percentile for their age to about the 65th, while the group receiving standard neurology care slipped downward.

Their spouses noticed it too: partners in the personalized group reported improvement, and partners in the standard care group reported decline. The paper is still in peer review, and the trial was funded by a nonprofit foundation, because there’s no drug to sell at the end of it.

Community. In that randomized trial, participants worked with coaches and were expected to exercise six days a week. Exercise is just one several lifestyle aspects. Coaching was not a side detail.

The core of this program is lifestyle change, and anyone who has made a New Year’s resolution knows how it tends to look by February.

There are thousands of excellent books on diet, exercise, sleep, and stress. Many of us have read a few of them, closed the cover, and found ourselves facing the same problem the next morning, because the change has to happen in the kitchen at 9 p.m. and in the decision to put on walking shoes at 7 a.m., long after the reading is done.

Age adds challenge. A 70-year-old man who has eaten the same breakfast for forty years and has a bad knee faces a steeper climb than a 55-year-old who already walks every morning.

For wives, there’s another layer. You’re often making these changes for two people, one of whom may not remember the plan, may not believe anything is wrong, or may push back on dietary changes. And you’re doing it surrounded by people who still see Alzheimer’s as a one-way street.

When the general belief is that nothing can be done, anything outside the standard prescription can look like snake oil to the friends and family offering opinions. Food is where this shows up most. “Oh, just let him eat what he wants” comes from love, from people who have no idea how much blood sugar, inflammation, and nutrition have to do with his brain.

Then there’s dinner out with friends, when suddenly the two of you are ordering differently from everyone else at the table.

I’ve heard more than one story from wives about the pressure that follows: the dessert passed his way, the teasing, the “one won’t hurt.”

The research on behavior change explains why this matters so much. It’s been documented that people who join a lifestyle program with like-minded peers and receive added educational support are far more likely to stick with it.

I see sustainable long-term lifestyle changes in my Direct Access members all the time.

Community is important. A place where people know your name. A place where you learn what you’re doing and why, so you can hold your ground without offending anyone at the dinner table or restaurant if needed. And when to let it go.

Where the constant questions you have in the beginning get answered by a certified practitioner, quickly and without scheduling an appointment or driving across town.

Where you can talk with and ask questions of others who have already been through what you’re just learning. And where you can get live, face-to-face connection with those same people, who understand, because all of us need that.

The wife of one of my first clients was instrumental in guiding the creation of my Direct Access community years ago. I have no idea how many questions she asked me as she began her journey, but it was clear that she literally needed direct access! : )

And so have all those since.

It truly would have been helpful in my own life when I realized my mom was on the same path as other female relatives. Any info would have been helpful back then, before we had all that has been building since 2016.

Staying with it. The people who wrote their stories in The First Survivors of Alzheimer’s, like Judy, have held their improvement for years by staying with the program. What they continue is a way of living that corrects many of the causes of their decline and improves their heart, blood sugar, sleep, and energy along the way, combined with tracking their data to eliminate the guesswork.

Here’s the good news

MCI is the stage where the most can still change. The contributors driving decline can be found with the right testing. Many of them can be corrected, and the research shows people improving rather than just declining more slowly. You don’t need to wait for a new drug or a worse score to begin. You can start now, with a personalized plan and people around you who understand what you’re doing and why.

It all starts in the Direct Access community, send an email to info@angelachapman.net requesting a link to more information.

Paid subscribers get my supplement discounts and my Brain Health Resources list, the tools and products I trust for exactly this work. See paid subscriber perks here.

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Even in 1940, nearly one in four Americans lived on a farm, eating mostly what they could grow, raise, catch, or hunt. Were they healthier? Not in every way. Families with too little, or too little variety, suffered deficiency diseases.

But when people had enough to eat, they ate whole food, and type 2 diabetes and obesity, two of the strongest drivers of Alzheimer’s and other chronic diseases today, were rare.

Nutrition is one of the most powerful factors in health, and in brain health especially.

Fast forward to today.

You can buy a steak that came out of a 3D-printer!

When I first read that 3D-printed steak was being sold in American grocery stores, I didn’t believe it. I assumed it was one of those stories that circulates online and falls apart when you look under the hood. So I fact-checked it.

It’s real! Last month, an Israeli food-tech company called Steakholder Foods started selling 3D-printed “plant-based” meat in Northeastern U.S. stores under the brand name Perfecta.

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Don’t let “plant-based” fool you: the plants in this case are soy flour and refined oils, held together with binders and starches, with little of the nutrition you’d get from actual plants.

The line includes a marbled steak, a filet mignon, chicken breast, salmon patties, and white fish patties. Nowhere on the package does it say the food came out of a printer.

Under U.S. labeling law, it doesn’t have to. Labels must list ingredients and allergens, but there’s no requirement to say how the food was made.

I had a hard time believing that was legal. Then I remembered that fake food has been legal for decades. Our grocery stores are full of products designed by food chemists to look, taste, and feel like something they aren’t. My great-grandmother wouldn’t even recognize them as food.

Perfecta is just one more ultra-processed product in a long line of them.

What makes it especially insidious is what it’s designed to replace. Beef, chicken, and fish provide essential nutrients the brain and body depend on, and a printed imitation looks like the real thing, even chews like the real thing, without supplying them.

Using supplements to make up the difference defeats their purpose, which is to be supplemental when needed. Replacing real food with supplements is not a good option for your health.

Most shoppers still trust that what’s sold as food is food. They’re busy, they’re feeding families, and they aren’t turning over every package. Even those who read the ingredient list aren’t likely to connect “rapeseed oil, methylcellulose, modified maize starch” to what happens in their brain down the road.

I don’t believe anyone would knowingly choose meat that came out of a 3D printer. The problem is, how would you know? And even if labeling is eventually required, the marketing pitch will be that it’s healthier than real meat, and vegans and vegetarians will be especially targeted.

It isn’t healthier for anyone: omnivore, herbivore, or carnivore.

No matter how advanced the technology becomes, or how similar they can make something taste, it can’t replace real food for the human body.

Here’s why as it relates to meat.

Three kinds of “meat” at the grocery store

When I talk about eating meat, and the many viewpoints on it, people picture the meat case at their grocery store. That’s where it gets complicated, because most of what’s there comes from animals raised far from the way they should naturally live.

Industrial agriculture took the first step decades ago. Cattle were moved off grass and into feedlots to be fattened on corn and soy. Chickens were moved into crowded barns with no sunlight. Salmon were moved into ocean pens and fed processed pellets. The animals got bigger and cheaper, and the meat lost much of what made it valuable to us.

Perfecta “meat” takes the next step and removes the animal entirely. That might sound appealing to a vegan or vegetarian, but it’s still an ultra-processed food, and it isn’t good for anyone.

So shoppers are choosing among three kinds of meat:

1. Printed imitations

2. Meat from industrially raised animals (most common today)

3. And meat from animals raised the way they naturally live - not as easy to find nowadays, but it’s out there when you know what you’re looking for.

I don’t eat the first two, ever. Here’s why each one matters for your brain.

What real meat and fish give your brain

Beef, chicken, and fish from well-raised animals provide a combination of nutrients the brain depends on. Many of them come only from animal foods, or are far more absorbable from them.

All nine essential amino acids. Your body can’t make these, so you have to eat them. Beef, chicken, and fish contain all nine in the proportions the human body uses.

From beef: vitamin B12, which plants don’t make and which the brain and nerves can’t function without. Heme iron, the form your body absorbs best, carries oxygen to a brain that uses about 20% of your body’s supply. Zinc is essential for communication between brain cells. Beef also provides creatine, which brain cells use for energy, and carnosine, an antioxidant concentrated in muscle and brain tissue.

From chicken: B6 and niacin, both needed to make neurotransmitters, plus selenium and choline. Choline is what your body uses to make acetylcholine, the neurotransmitter most depleted in Alzheimer’s.

From fish: DHA, the main structural fat in brain cell membranes. Low DHA levels are consistently linked to faster cognitive decline. Fish also provides EPA, an omega-3 that calms inflammation, along with iodine, selenium, and vitamin D. Fish and shellfish are also among the richest sources of taurine, which helps protect brain cells from overstimulation and oxidative damage. Taurine levels decline as we age.

Why Perfecta works against your brain

Perfecta is a premix of ingredients that is pushed through nozzles in thin layers, building up something that looks like beef, fish, or chicken.

Here’s the ingredient list for the marbled steak: water, soy flour, rapeseed oil, coconut oil, methylcellulose, natural flavoring, salt, beet root powder, modified maize starch, food coloring, caramel, xanthan gum, locust bean gum, and sunflower lecithin.

That’s fourteen ingredients.

A real steak is beef, a single whole food with B12, heme iron, zinc, creatine, and all nine essential amino acids naturally present.

Pefecta is missing what the brain counts on from meat and fish. There’s no B12, which the brain and nerves can’t function without, no DHA in the printed salmon, and no heme iron, creatine, or carnosine.

It has much less protein. The 9-ounce marbled steak has 26 grams of soy flour protein, while a real 9-ounce steak has more than 50, with all nine essential amino acids naturally present. The salmon patty, just under 2 ounces, has 4 grams. The same amount of real salmon has about 10.

Its fats promote inflammation. Refined canola oil is processed with high heat and chemical solvents that damage its fats. It adds to the omega-6 overload in the American diet, with no omega-3s to balance it, and chronic inflammation is one of the main drivers of Alzheimer’s.

Its binders and starches may disrupt your gut. Research suggests some of the texturizers and emulsifiers in processed foods can thin the gut’s protective lining and promote inflammation. Whatever affects the gut affects the brain.

It’s ultra-processed, and that pattern is the real risk. One analysis of the Perfecta steak classifies it as ultra-processed (NOVA 4), the most processed category. The research linking ultra-processed food to brain decline is consistent:

• In UK Biobank data, every 10% increase in ultra-processed food intake was associated with a 25% higher risk of dementia.

• A Brazilian study following over 10,000 adults found that people getting more than about 20% of their calories from ultra-processed foods had 28% faster cognitive decline.

• In 2024, a large U.S. study linked each 10% increase in ultra-processed food to a 16% higher risk of cognitive impairment.

The same eating pattern is linked to type 2 diabetes and insulin resistance, heart disease, stroke, obesity, depression, colorectal cancer, gut dysbiosis, and higher all-cause mortality.

These are Alzheimer’s risk factors themselves. Insulin resistance is so tightly linked to the disease that some researchers call Alzheimer’s “type 3 diabetes.”

Why industrial meat also falls short

For decades, red meat has been blamed for heart disease, cancer, and more. But the large studies behind that reputation relied on food questionnaires that often lumped hot dogs, bacon, and deli meat together with unprocessed beef.

Here’s one that separated it, Micha et al., Circulation, 2010. A meta-analysis of 20 studies covering over a million people. Processed meat was associated with a 42% higher risk of heart disease and 19% higher risk of type 2 diabetes. Unprocessed red meat showed no significant association with either.

Feedlot beef

Most beef in this country spends its last four to six months in a feedlot, also called a CAFO (concentrated animal feeding operation), confined and fattened on corn and soy.

The grain diet damages cattle’s digestive tracts and livers, so antibiotics go into their feed every day. The meat ends up with fewer omega-3s and antioxidants and more omega-6.

Routine antibiotic use in food animals is also a major driver of antibiotic-resistant bacteria, which affect all of us.

Confined chickens

Most chicken is raised in windowless barns holding thousands of birds, with no sunlight and no access to the outdoors. Chickens naturally forage for insects, worms, seeds, and greens.

Confined chickens eat only corn and soy, and they’re bred to reach market weight in six or seven weeks, fast enough to damage their own muscle tissue.

Farmed salmon

Farmed salmon are crowded into ocean pens and fed pellets made increasingly from soy and vegetable oils. Their omega-3 levels dropped by about half in less than a decade, and their pink color comes from a pigment added to the feed.

Taste

Chicken, beef and salmon taste different when raised in these conditions. It’s not subtle, and it’s not good.

You don’t know it because you have probably been eating it most or all of your life.

I remember grilling hamburgers when my mother-in-law was over many years ago. She couldn’t believe how good they tasted. She actually said “this tastes like the hamburger I had when I was a kid”. She was born in 1937.

What well-raised meat gives you

When cattle are raised regeneratively and finished on grass, moved frequently across pasture in a way that rebuilds the soil, the differences are measurable:

• The omega-6 to omega-3 ratio drops dramatically. In one major review, it was about 1.5 to 1 in grass-finished beef versus roughly 7.5 to 1 in grain-finished.

• CLA, vitamin E, and beta-carotene are higher. The yellow tint you sometimes see on grass-finished fat comes from the beta-carotene.

• Phytochemicals from the pasture plants show up in the meat. Grain-finished beef has far fewer of them.

• Antibiotics aren’t routinely needed, because the animals are eating what they’re meant to eat.

Saturated fat isn’t one thing.

It’s a family of fatty acids that behave differently in the body. Grass-finished beef tends to contain more stearic acid, a saturated fat with a neutral effect on LDL cholesterol, and less myristic and palmitic acid, the saturated fats most associated with raising LDL.

The total amount of saturated fat is about the same; what changes is which saturated fats you’re getting. Grass-finished beef also has less fat overall, and that fat comes with more omega-3s, CLA, and antioxidants. (Daley et al., Nutrition Journal, 2010)

Context matters too. Saturated fat eaten alongside sugar and refined carbohydrates is a different metabolic situation from saturated fat in a whole-food diet that keeps insulin in check.

If you eat plant-based

Many people buying products like Perfecta may be making a thoughtful choice for ethical, personal health, environmental, or religious reasons, and that choice deserves respect.

A whole-food plant-based diet built on lentils, beans, tempeh, tofu, nuts, seeds, and vegetables is real food, and it can be done well for the brain.

What concerns me is the growing category of processed imitations. They’re marketed as the healthy choice. Nutritionally, they belong on the same shelf as other ultra-processed foods.

A word about saturated fat and ApoE4

To be clear, I’m not telling you to eat more meat, or any meat at all. Just that if you do eat it, where it comes from matters a great deal for your brain.

I also know the question you may be asking if you carry the ApoE4 gene: doesn’t the saturated fat in meat raise cholesterol, and doesn’t that increase my risk for heart issues or dementia?

Dr. Bredesen’s answer for ApoE4 carriers is to limit saturated fat. E4 carriers tend to see a bigger rise in LDL cholesterol from saturated fat than people without the gene. He recommends getting most of your fat from olive oil, avocado, nuts, seeds, and wild fatty fish, and keeping red meat a smaller part of the plate, from grass-fed, well-raised animals, and that’s advice people using the ReCODE protocol should follow.

That said, E4 carriers and people in general can vary widely in how they respond, so he recommends that we rely on lab testing to guide each person rather than a single rule.

Of course, a basic cholesterol panel does not provide enough information.

Cholesterol deserves its own conversation, and I’ll be covering it in an upcoming post.

Here’s how to use what you now know:

• How to take the confusion out of the labels

• What I buy and where

• How I get the benefits of liver into my diet without tasting it (not a supplement)

• The 6 labs that tell you what your diet is doing

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With a long maternal history of Alzheimer’s, when a study says especially women and at risk, it’s talking about me. Maybe it’s talking about you too.

Ultimately, blood flow to the brain is important for everyone. So I dug in.

The study, in plain English

Rapamycin has been around for decades, mostly to keep transplant patients from rejecting a new organ. It works by blocking mTOR, a master switch inside cells that tell them to grow and build.

When mTOR stays switched on too much, as it tends to with age and possibly more so in APOE4 carriers, cells spend less time on repair and cleanup, including the cells that line your blood vessels.

Blocking it shifts them back toward maintenance, which is why longevity researchers are interested in rapamycin, and why Dr. Lin wanted to know whether it could restore blood flow to the brain.

Dr. Ai-Ling Lin at the University of Missouri spent years showing that rapamycin restored blood flow to the brain in mice carrying APOE4, the strongest genetic risk factor for Alzheimer’s.

Then she tested it in people. The full study was published in September 2026 in the Journal of Cerebral Blood Flow & Metabolism.

Twenty-three healthy adults, ages 45 to 65, took a low dose of rapamycin every day for four weeks. Nine of them carried APOE4. Those nine saw blood flow to the brain rise by more than 15%, and the gains came mostly from the women, whose blood flow rose by roughly 30% in the memory area and 35% across the whole brain. The men with APOE4 barely responded.

No one knows why yet, but women APOE4 carriers likely start with more room to improve, for reasons I'll explain below. The people without APOE4 saw no real change, likely because their blood flow had little room to improve. Both groups were considered healthy at the time of the study. Things change if you have insulin resistance, high blood pressure, or sleep apnea, which reduce blood flow with or without the gene.

The researchers hope that restoring blood flow early, years before symptoms, might delay or prevent Alzheimer's altogether.

My honest take

I’m glad this research exists, and I’m glad women carriers responded well, since we make up nearly two-thirds of everyone diagnosed.

But nine people. Four weeks. No placebo group. No measure of memory. And a drug that suppresses the immune system, with no long-term data on using it for prevention. The bigger trials are still years away.

Most of us don’t want to wait for the next study, the next drug, the next headline, especially when the thing this study is measuring can already be changing in the brain.

Why blood flow matters so much

Whether or not you carry APOE4, and whether you're a woman or a man, your brain needs optimal blood flow to work at its best. Every minute of every day, your blood carries oxygen and nutrients to your brain.

Glucose and ketones for fuel, B vitamins, omega-3s, amino acids your brain uses to make neurotransmitters, all of it arrives through your bloodstream. Your brain has almost no reserves of its own, so it relies on a constant, steady supply.

Oxygen shows just how much your brain depends on that supply. Your brain is about 2% of your body weight and uses roughly 20% of your oxygen, and blood flow is the only way oxygen reaches it.

This is also why supplements can only do so much on their own. You can take every brain-supporting supplement on your shelf, but if blood flow to your brain is impaired, less of what you’re taking reaches the cells that need it.

The most common reasons blood flow slows:

• High blood sugar and insulin resistance, which stiffen and damage blood vessels

• Blood pressure that runs too high, or too low

• Sitting most of the day

• Sleep apnea, which drops oxygen to your brain over and over through the night

Blood flow problems are among the earliest changes researchers can see on brain scans in Alzheimer's, often showing up before amyloid buildup or brain shrinkage.

The vessel lining that keeps your coronary arteries healthy also keeps the tiny vessels in your brain open, so damage to one tends to show up in the other. That's why heart disease, atrial fibrillation, and high blood pressure all raise the risk of dementia, and why Dr. Bredesen counts vascular problems as one of the core drivers of Alzheimer's.

There’s good news here.

Blood flow to your brain is one of the fastest things in your body to respond.

It can change in weeks, sometimes hours, and the same steps that improve it also protect the barrier. The most reliable ones are already within your control.

What actually gets more blood to your brain

Nitric Oxide. Your blood vessels make their own medicine. Nitric oxide is a gas your blood vessel lining makes, and it tells the muscle in your vessel walls to relax so the vessels widen and more blood flows through.

It also keeps the lining smooth, which helps prevent inflammation and clots. Your body breaks it down within seconds, so it has to keep making it all day long, and it makes less every decade, starting approximately in men in their 40s and women in their 50s.

Healthy blood vessel linings make plenty of nitric oxide, and nitric oxide keeps them healthy.

The following impair blood vessel lining health:

• High blood sugar and insulin resistance

• High blood pressure

• Chronic inflammation

• Oxidized LDL and high ApoB

• High homocysteine

• Air pollution

• Heavy metals like lead and cadmium

• Inactivity

• Poor sleep and sleep apnea

• Chronic stress

• Excess alcohol

• Loss of estrogen after menopause

• Aging

All of these and more come up as topics in my Direct Access community and on our group Zoom calls. Click to learn more.

A supplement that can help increase nitric oxide is N1O1, a lozenge developed by Dr. Nathan Bryan, who has spent over 25 years researching nitric oxide. It dissolves in your mouth and delivers nitric oxide’s building blocks directly, so it doesn’t depend on the bacteria in your mouth the way beets and greens do.

The human research comes from Dr. Bryan’s earlier lozenge formulation. In a placebo-controlled trial of adults over 40 with several cardiovascular risk factors, one month of the lozenge raised nitric oxide markers in the blood.

In another trial, a single lozenge lowered blood pressure within an hour in people with hypertension.

No one has measured brain blood flow with it yet, but early trials show it improves how your blood vessels behave, and your brain depends on those same vessels.

You should talk with your doctor before using it, because the effects can stack. The studies were done in people who weren’t on medication. Skip it if you take nitroglycerin or erectile dysfunction medication.

N101: https://n1o1.com/product/n1o1-nitric-oxide-lozenges/

N.O. Beetz: https://n1o1.com/product/n-o-beetz/

Now, on to the ways your lifestyle habits can improve your blood flow.

Walk outside every day. Exercise is the most proven way to increase blood flow to the brain, including the memory center area.

Do it outside when you can, since sunlight on your skin converts stored nitrogen compounds into nitric oxide, which moves into your bloodstream and helps relax blood vessels.. Twenty to thirty minutes of brisk walking, fast enough that your breathing picks up, gets you both. If you can do more, then do more.

Pickleball counts. Studies in middle-aged and older players show it reaches moderate intensity, with bursts of harder effort, which is the range that increases blood flow and nitric oxide production. It adds two things a solo walk doesn’t: quick decisions and hand-eye coordination, which challenge the brain, and social connection, which on its own is linked to lower dementia risk.

The trade-off is injury, so be careful out there.

Rethink your mouthwash. Some of the nitric oxide your body uses depends on bacteria living on your tongue. They convert the nitrates in leafy greens and beets into a form your body turns into nitric oxide.

Antiseptic mouthwash wipes those bacteria out. In one study, healthy adults who used an antiseptic mouthwash twice a day for a week saw their blood pressure rise, and larger studies have linked twice-daily use to a higher risk of high blood pressure and prediabetes.

I keep refusing the travel bottles of Listerine I’m offered twice a year after a dental cleaning. And I do so by saying: Thanks, but that will decrease my nitric oxide : ). I get a confused look, but never a question.

If you use one every day, switch to a gentle, non-antiseptic option, and keep your mouth healthy with brushing and flossing.

I like Dentalcidin Rinse, it’s good for your oral microbiome and won’t interfere with nitric oxide. If you’ve opted in for my Fullscript discount, the links above will take you to it when you are signed in. You’ll save $7 every time you purchase. The corresponding toothpaste is also available and excellent.

Most people are saving well over $40/month on their supplements, so opting in makes sense.

I'll write more about the oral microbiome soon. For now, it's enough to know it matters for your brain as much as your heart.

Eat a big salad of greens. Arugula is one of the richest nitrate sources there is, followed by spinach, Swiss chard, and celery, and your body turns those nitrates into nitric oxide.

The conversion depends on bacteria on your tongue, and daily antiseptic mouthwash kills them, so switch to a non-antiseptic option. Long-term acid-blocking medications can blunt the same pathway, which is worth raising with your doctor.

Check your blood pressure, high and low. High blood pressure in midlife damages the small vessels in your brain, and better control has been shown to lower the risk of mild cognitive impairment.

Low blood pressure is often ignored, even though it’s common in lean, active women. If you get lightheaded when you stand, your brain may be getting shortchanged several times a day.

Where I’d start this week, along with a couple of easy to self-order blood tests is next:

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Living a life you want to remember, doing what you enjoy, with people you enjoy, changes how your whole life feels, and your brain lives inside that life. So this week, a different kind of list that feeds your soul and your brain : )

Sunshine, a walk in the morning or early evening
There’s a softness to the light at those hours, and the world feels a little slower. Make a point of noticing something new each time: a bird you haven’t heard before, the way the shadows fall across a neighbor’s porch, a flower that opened overnight. Small beauty is everywhere once you start looking for it. And the morning light sets your circadian clock, so you sleep better, which is when your brain does its cleanup.

A long chat with an old friend
You know the one. No matter how much time passes, you pick up right where you left off, as if no time has gone by at all. She knows your history, your family, the version of you from thirty or forty years ago. I don’t get to talk to that friend often as I’d like, but when we do catch up, it feels good. The laughter, the memories, the ups and downs of lives lived separately, but with a history that brings them together. I hang up feeling more like myself. Conversations like that are good for us in many other ways. They exercise memory, language, and emotion all at once, and social connection is one of the strongest health protections we have.

Try something new once a month
Remember the thrill of being new at something? The nerves, the uncertainty, the small victory when it finally clicks. A pottery class, a sport, a new trail, a recipe from a cuisine you’ve never cooked. A small thing, a silly thing, anything. Let yourself be a beginner again. Every new skill builds fresh connections in your brain and adds to your cognitive reserve.

Let it go
Think about how much room that old irritation takes up. The comment someone made, the thing that didn’t go your way, the worry you’ve turned over a hundred times. Imagine setting it down and walking away lighter. Your hippocampus will thank you, since years of stress hormones take a real toll on memory.

Water
A cold glass of water on a hot afternoon, a pretty glass you keep by your chair, with lemon or cucumber if you like. Make it something you enjoy rather than a chore to check off. Thirst cues fade as we age, and even mild dehydration dulls focus and memory.

Join in on something
Say yes to the book club, the volunteer shift, a class at the gym, the pickleball group that’s been asking. There’s something about being part of a “we” that makes the week feel fuller, and people with a sense of belonging and purpose show lower rates of cognitive decline over time.

Say I love you every day
To your husband or wife, your kids, your sister, your friend, your pet. Say it at the end of a phone call, say it on the way out the door. Nobody ever regretted saying it too often. Hearing it back releases oxytocin, which settles your whole stress response.

Forgive someone
You probably already know who. Forgiving doesn’t mean what happened was okay, and it doesn’t mean you have to connect if you don’t want to. It means you stop carrying it. It’s heavy. Resentment keeps your body in a low-grade stress state for years, and letting it go frees up energy for everything else.

Buy yourself flowers
Pick the ones you love, even if they seem extravagant. Put them where you’ll see them first thing in the morning. There’s no reason to wait for someone else to think of it. A little beauty on the kitchen table lifts your mood every time you walk past.

Relax, release perfection
The house doesn’t have to be spotless before friends come over. The dinner doesn’t have to be perfect. The email can go out with a typo. Let good enough be good enough and enjoy the moment you’re in and the people you’re with. Perfectionism keeps your body braced, and your brain feels that constant tension.

Don’t let life bother you
The traffic, the rude cashier, the plans that fell through at the last minute. Even the scary things that happen. It’s all part of life. It just is. Try shrugging more often. Some of the happiest people I know have mastered the art of “oh well,” and their nervous systems are better for it.

Give someone a small gift
A jar of homemade jam, flowers, a book you loved, a handwritten note tucked into a card. Watching someone’s face light up is one of life’s simplest pleasures, and giving activates the brain’s reward centers as strongly as receiving does.

Pay a compliment to a stranger
The woman in line at the grocery store with the beautiful sweater, or young children she’s trying to manage. The young man who held the door. Tell them. It takes three seconds, and it might be the kindest thing anyone says to them all day. You’ll walk away smiling too, and those small moments of connection with people you’ll never see again add up to a warmer, less stressed life.

Nurture your artistic side
Watercolors, woodworking, photography, writing, singing in the car with the windows down. Whatever you’ve always wanted to do or loved but set aside when life got busy, do it now. You don’t have to be good at it. Creativity engages memory, focus, and fine motor skills all at the same time.

Everything on the list above is nurturing and pulls you outward. Toward a friend, a stranger, a forgotten passion, simple pleasures, new experiences, a canvas, the sky at seven in the morning.

When your attention is on the person in front of you or the thing you’re making or doing, there’s less room for the rumination and fear that keep stress hormones elevated, disrupt sleep, and feed the anxiety so many are carrying.

The physical effects are real and measurable. People with strong social ties live longer. Loneliness raises inflammatory markers and blood pressure.

Time outdoors lowers cortisol and heart rate. Laughter, touch, and affection calm the nervous system and support immune function. Purpose and belonging are linked to better sleep, better cardiovascular health, and slower cognitive decline.

Go ahead and pick something. Call the friend. Buy the flowers. Go on the trip. Smile at everyone who walks by. Take the walk and look for something you’ve never noticed before. It really is a beautiful world.

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Meet NF-kB (pronounced “N-F-kappa-B”), a protein complex that plays a central role in your immune system. While it's essential for fighting infections and repairing injuries, it becomes a problem when it's chronically activated, meaning it stays ramped up long after the threat is gone instead of settling back down to its normal, low baseline.

Inside the brain, it acts as the master switch for inflammation, and in the context of Alzheimer’s disease, its chronic overactivation is a primary driver of neurodegeneration and cognitive decline.

What triggers NF-kB?

• Chronic Stress: Both physical and emotional stress can flip this switch. I put this first on purpose because it so often gets ignored.

• Toxins: Heavy metals like mercury and lead, and mycotoxins from mold exposure, are major triggers. These toxins are particularly dangerous because they can persist in the body, keeping NF-kB stuck in the “on” position and creating chronic brain inflammation.

• Poor diet: Sugar, processed foods, and trans fats are known to activate it.

• Infections: Chronic, low-grade infections keep this pathway “on” even when it should be resting.

• Leaky gut: When the gut lining is compromised, bacterial fragments called LPS enter the bloodstream and activate NF-kB.

• Poor sleep: Poor sleep slows the brain’s overnight cleanup, and sleep apnea lowers oxygen to the brain. Both activate NF-kB.

Why is chronic activation dangerous?

When NF-kB stays active for too long, it creates a storm of inflammation in the brain. This inflammation damages neurons, disrupts communication between brain cells, and accelerates the processes that lead to dementia, including:

• Amyloid-beta plaque formation

• Oxidative stress (cellular damage from free radicals)

• Tau protein tangles (another hallmark of Alzheimer’s)

Here is how NF-kB plays its destructive role in the aging brain.

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1. The neuroinflammation loop

When the brain’s immune cells (microglia) detect cellular stress, metabolic waste, or amyloid-beta plaques, they flip NF-kB to “on,” triggering the production of inflammatory chemicals called cytokines. Inflammation activates NF-kB, and NF-kB produces more inflammation, locking the brain into chronic immune activation.

2. Damage to synapses and neurons

This constant flood of inflammatory chemicals damages neurons, degrades synapses (the bridges where memories are formed), and impairs blood flow. Over time, it accelerates the loss of brain volume in regions critical for memory, like the hippocampus.

3. Compromising the blood-brain barrier (BBB)

The blood-brain barrier is a protective lining that keeps harmful things in your bloodstream out of your brain. Toxins, LPS from a leaky gut, chronically high blood sugar, and chronic stress can loosen it, letting those troublemakers into brain tissue, where they switch NF-kB on.

NF-kB that’s already on inside the brain damages the lining from the inside. Either way, more gets in, NF-kB stays on, and the barrier gets leakier, pouring fuel on the fire.

Why shutting NF-kB off is not the goal. You need balance.

NF-kB has a good side. Inside neurons, it helps form memories and protects them from dying. In the brain’s immune cells, short bursts help fight infection, clear debris and amyloid, and repair damage. The harm comes when it stays switched on in those immune cells, releasing inflammatory chemicals that damage the very neurons NF-kB normally protects.

So the goal is downregulation and restoration of balance, bringing chronic over-activation back down to a healthy, well-regulated baseline.

NF-kB can’t be measured directly. An elevated GFAP (one of the Alzheimer’s early detction tests) is one sign it’s chronically activated in the brain, but GFAP can stay normal while NF-kB is already being pushed on, so a normal result isn’t a green light. The more reliable clues are the drivers that switch it on in the first place.

In the next section: targeting brain inflammation, protecting your brain, and a lesser-known type of curcumin I use along with my discount code for it.

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Things are beginning to change, and the diagnosis is now sometimes preceded by Alzheimer’s blood biomarker tests and/or imaging that help clarify whether Alzheimer’s is on the horizon. That’s a good thing, except that it typically ends with a prescription that won’t stop or improve the disease, and no investigation into the actual causes for each individual.

The word “mild” is a comparison. It puts MCI on the scale below dementia and tells you nothing about how long it’s been building or why.

To see what that word leaves out, it helps to know how late-onset Alzheimer’s disease unfolds.

Alzheimer’s takes more than one form, and the one most people mean when they say the word is late-onset Alzheimer’s, diagnosed after age 65. There are other forms that begin earlier and progress more rapidly, and I’ll write about those another time.

Late-onset is associated with age, but it is not a disease of old age. It moves slowly through three stages that can take 20-30 years before a diagnosis.

Stage 1: Presymptomatic. You have no symptoms and cognitive tests would be normal, but other types of tests like p-tau217 would already be abnormal, showing that the processes related to an Alzheimer’s diagnosis have started. This stage can last 10-20 years, which gives you a long runway to take action to reverse it.

Stage 2: Subjective Cognitive Impairment. You notice changes, but they look like normal aging. A word won’t come. You lose the thread of what you were saying. You’re writing down appointments you used to remember without prompts. You have to think about where you parked your car. You may wonder if it’s something more than “normal,” and you may also be inclined to assume it isn’t until it gets worse.

Stage 3: Mild Cognitive Impairment. By the time it bothers you enough to schedule a doctor’s appointment and you hear the words Mild Cognitive Impairment, things have been going wrong for a long time. MCI is the stage before dementia. There is still a meaningful window to act, and MCI has been improved.

The most recent evidence is a randomized controlled trial of the ReCODE protocol, led by Dr. Bredesen and colleagues, and now in preprint while it goes through peer review. A very brief summary: Seventy-three people with MCI or early dementia, with MoCA scores of 18 or higher, were randomly assigned to a personalized protocol or to standard of care and followed for nine months at six clinics.

Of the 70 people who had blood biomarker testing, 68 showed brain changes associated with Alzheimer's. The personalized group improved on every cognitive and symptom measure, while the standard of care group declined in overall cognitive function and memory.

The treatment effect size for overall cognitive function was calculated to be greater than previously published clinical trials, seven times the effect size of the lecanemab trial and four times the effect size of the donanemab trial.

You can read the full study with all the details here.

Stage 4: Alzheimer’s dementia diagnosis. The symptoms now interfere with daily life. Bills go unpaid, medications get missed, familiar routes become confusing, and tasks like cooking, driving, or keeping track of the day need help from someone else. While people have improved and even reversed their symptoms at this point, there are a lot of variables.

The First Survivors of Alzheimer’s: How Patients Recovered Life and Hope in Their Words is an encouraging book. There’s a complete Q/A section written by Dr. Bredesen in the second half.

Review those stages and think about how we handle cancer. Nobody suggests waiting for stage 4 to find out. We have mammograms and colonoscopies so it can be caught at stage 1, when there are the most options and the best outcomes. Alzheimer’s has a stage 1 too, and finding it there, before any symptoms, is a completely different situation from finding it at stage 4 with a dementia diagnosis.

Right now, most people find out at stage 3 or 4.

Waiting for an Alzheimer’s diagnosis is clearly not a good idea. Unfortunately, most people don’t have this information, so they never learn that there were opportunities to act long before it got to that point.

Recently, I was at a social event, and a woman asked what kind of work I do. I told her, and she looked at me, confused. Then she told me her sister had been diagnosed with Alzheimer’s. She had never heard any of what you just read. She had never heard of Dr. Bredesen or the ReCODE protocol. I didn’t go into details in that situation. She didn’t ask questions.

We only talked for a few minutes, but it reminded me again that what I’ve spent the last decade doing, which feels so normal to me now, is still not widely known.

Sharing this post or forwarding it to friends could help more people learn that there’s a whole new body of research related to Alzheimer’s that lights up a very different path forward than what has always been thought of as a one-way street.

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A few common symptoms in the Subjective Cognitive Impairment stage that are easy to dismiss as “normal aging”:

• Words that won’t come, replaced with “the thing” or “you know”

• Losing the thread mid-conversation

• Repeating stories and not realizing you had told them before, over and over again. People listen politely, not wanting to point it out. So you may not know if you’re doing this.

• Things put in places they don’t belong

• Missed appointments, or needing reminders for what used to be automatic

Mild Cognitive Impairment

Each year, about 15 percent of people with MCI progress to an Alzheimer’s diagnosis. Over several years, that adds up to a large share of the people who receive this label. I have more than a decade of experience working with people at every stage, and I have seen far more improvement at SCI and MCI than after an Alzheimer’s diagnosis.

Here’s a real-life example: He had an MCI diagnosis and elevated p-tau217. He had “cognoscopy” lab testing, a term coined by Dr. Bredesen reflecting a wide array of tests for underlying contributors, and a year of implementing his personalized plan. His wife explains his progress after a year of using the ReCODE protocol:

“I’d been noticing lots of confusion, he didn’t remember recent conversations, and quite often would give me a ‘blank stare’ — like nobody’s home. Our GP listened carefully to our issues and ordered a cognitive test for him. Thus, the result — somehow it’s quite daunting to see it written in black and white from a ‘clinical’ perspective. As of now, he is sharper mentally. He is a retired pastor, now in an interim position. His memory is better, his delivery is on point — with clarity — no stumbling or losing his place. Also, I — and other family members — have noticed that he doesn’t have the ‘blank look’ that he had a year ago.”

That’s real progress.

Aside from MCI, declining cognition as you age is common. That doesn’t mean it’s normal. It’s common because we accept it as part of aging, most people don’t know how to prevent it, and because our modern diet, lifestyles, infections, and an increasingly toxic world sit at the root of cognitive decline and of the escalating number of people being diagnosed with MCI and Alzheimer’s. For most people, it doesn’t have to happen or keep getting worse when you intentionally give the brain what it needs to drive brain plasticity in a positive direction. There are quite a few things that it requires.

An aging brain responds to how you treat it, what you feed it, novelty, stress, movement, heart and gut health, sleep, infections, and exposures. Whether or how much it declines with age depends on those inputs.

If you’re on a prevention path, noticing symptoms, or have a diagnosis, here are three things you can do right now, one each for diet, sleep, and your home, and what to do after that.

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But what if I told you that the health of your mitochondria is crucial not only for your longevity, but for the proper function of your brain as you age?

It seems like something we should understand and know how to take care of, doesn’t it?

And yet you may never have had a conversation about it, especially with your doctor. You may talk about cholesterol and blood pressure even with your friends, but what about your cellular health?

Actually, you have had those conversations. You might be talking about having less physical energy, forgetting why you walked into a room, the signs of aging on your face, your graying hair, or any number of things associated with aging.

What we think of as aging is the gradual “rusting” of our cells. That “rusting” is called oxidative stress. It causes dysfunction in our mitochondria as we age. While some of that is natural, it’s common in my work to see oxidative stress scores in someone in their early 70s that correlate with a person in their late 90s. Those people are suprised and alarmed, but there’s good news.

Even with accelerated aging, what goes up can come down. Not to the level of your youth, but when oxidative stress levels start coming down, and mitochondria start functioning better, people start feeling better and cognition often improves.

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Left unchecked, could accelerated aging eventually lead to a diagnosis of MCI and eventually Alzheimer’s? Yes, in some people it does—oxidative stress and inflamation are tightly linked and known to be drivers of Alzheimer’s disease. The mitochondrial dysfunction goes along with it.

Interestingly, a 2021 clinical trial demonstrated that targeting a specific part of the mitochondria in mice blocked neurodegeneration and protected against Alzheimer’s disease. The result: key symptoms of Alzheimer’s improved, such as brain cells communicating with each other and creating the synaptic activity necessary for forming memories.

While this mouse study offers important implications, you have to remember that if you give a mouse Alzheimer’s for an experiment –– we call that mouseheimers –– you know what caused it. The researcher intentionally impaired the mitochondria. That means the researcher caused the mitochondrial dysfunction. That makes it easy to reverse.

In humans it is more complicated. You have to find out what’s causing the mitochondrial dysfunction.

While they may be able to come up with a drug to improve this specific aspect of mitochondrial dysfunction, what happens if you don’t control what’s causing it in the first place? This is what the ReCODE protocol consistently comes back to and why it has worked for so many people.

The Good News Beyond the Drug Pipeline

In this trial, cell-to-cell communication in the brain improved, energy production increased, and neurodegeneration was blocked by reducing oxidative stress and inflammation—the major contributors to brain cell death in Alzheimer’s. Importantly, what this research does is validate a foundational truth:

Supporting the health of your mitochondria is an essential component of protecting and restoring cognitive function.

Alzheimer’s is a decades-long progressive network insufficiency. Because it develops slowly, symptoms appear much later in the disease process. However, you have a substantial window of time to influence the trajectory of your brain health if you make cellular health a priority.

Hidden Threats to Your Cellular Health

Alzheimer’s doesn’t have a single cause. Specific functional lab testing can uncover the underlying disruptors that include:

• High levels of mycotoxins, metals or environmental exposures that are neurotoxic

• Inflammatory markers consistent with Chronic Inflammatory Response Syndrome (CIRS), the underlying driver of Inhalational Alzheimer’s.

• Blood-brain barrier disruption and intestinal permeability (”leaky gut”)

• Early insulin resistance (with blood sugar still in “normal” range), elevated homocysteine, various infections and many other things.

You also can identify some of these threats on your own, in your environment and lifestyle, and take steps to reduce or avoid them.

The right lifestyle adjustments combined with targeted cellular support can address many of these root causes, optimizing both brain and body wellness. In the rest of this post, we're moving on to the the steps you can take and targeted support you can use to start improving your mitochondrial health

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She provided additional details, and I asked if I could share because this is part of the chronic immune activation story I’ve been writing about lately. As a reminder, chronic immune activation means the immune system stays switched on — actively signaling and producing inflammation — long after the trigger that provoked it should have been resolved. In my experience with Alzheimer’s prevention and improving cognitive decline, it's almost always more than one trigger keeping it that way.

Two things are tangled together in her description. One is a timing observation: his cognitive symptoms started not long after his vaccine. The other is a lab result that didn’t make sense to her: how can his antibody levels stay this high, tested repeatedly over a year, if he’s never had COVID? That second question is the key to the first.

There isn’t just one kind of COVID antibody test. He’s had spike antibody tests twice, in 2025 and again in 2026, both markedly elevated. Spike antibody tests measure your response to the spike protein, and both infection and vaccination cause that response — a high result doesn’t tell you which one caused it.

When I asked which test he had, it turned out he had both of the tests I asked about. The spike antibody test result was high twice. And he also had a nucleocapsid antibody test, ordered by accident, which turned out to be the additional test needed to provide the clarity she wanted.

This one only comes back positive with actual infection, since vaccines don’t trigger a response to that part of the virus. His came back negative. So there’s no evidence he was ever infected — his high antibody levels are coming from the vaccine, and his immune system hasn’t fully stood down in close to two years.

She also shared that he carries two copies of the APOE4 gene, the strongest known genetic risk factor for Alzheimer’s, and that he’s had elevated TGF-beta1 since 2024, even after mycotoxin-related treatment. She wondered whether his immune system had “gone overboard” on the vaccine because of his genetics.

That’s a smart question.

Why the APOE4 question matters

APOE4 isn’t just about how the body clears cholesterol and amyloid. It also shapes how the immune system responds to a threat in the first place. Some research suggests APOE4 carriers mount stronger, more prolonged inflammatory responses than people without the gene. If true for him, his immune system isn’t malfunctioning — it may be doing what an APOE4/4 immune system is more prone to do.

Ongoing immune activation produces inflammatory signals that circulate through the blood. The brain normally shields itself with the blood-brain barrier, but sustained signals can wear that barrier down, letting inflammation reach the brain's immune cells and keep them on alert.

His high and not declining antibodies suggest the immune system may still be responding to residual spike protein — in his case, from the vaccine, since there's no evidence of infection. That alone doesn't mean it's affecting his cognition. It just means his immune system is still responding to the spike protein, which isn't necessarily abnormal in immunology — though the data on long-term risk from persistent spike protein specifically isn't available yet.

What could still be provoking the immune response? A few possibilities:

• Persistent spike protein or vaccine-derived material in his body hasn’t fully cleared

• Bystander activation from an unrelated, ongoing immune stressor keeping his whole system alert

• Simple individual variation in how long antibody titers stay elevated after any exposure

There’s likely more than one thing going on.

The more things an immune system is activated against at once, the more likely that signaling reaches and affects the brain. A single elevated antibody by itself is one thing. Multiple simultaneous sources of activation are a different situation.

He’s had mold exposure, with remediation for his home in 2023, along with antifungal treatment for the internal mycotoxin burden. Continued elevated TGF-beta1 after treatment could mean re-exposure happened, or that treatment addressed the fungal component without addressing his actual mycotoxin body burden, which is a separate thing to measure.

If his immune system has also been under sustained pressure from mold this whole time, that’s a system already working overtime on a separate front for the same span his spike protein antibody levels have stayed elevated.

It would be interesting to see whether his spike antibody starts declining once his TGF-beta1 normalizes — if both move together, that could fit the bystander activation pattern listed above. If TGF-beta1 normalizes and the spike antibody doesn’t budge, that suggests they’re more independent than connected.

She’s right to keep tabs on this. Sustained high levels of spike protein antibodies are worth taking seriously, and she and her husband have already done a lot of work trying to improve his cognition —

mold remediation, pursuing fungal treatment for the mold, working with their doctor on his testing over time. It also happened to work out well that the test that finally clarified his antibodies was ordered by accident, and turned out to be the most revealing one they could have gotten relative to whether he had COVID or not.

Here’s their good news. He’s improved. The cognitive issues he was having previously, like trouble following TV shows and getting lost driving to familiar places, have gotten better. His current main difficulty is word-finding. He’s also physically active, which is one of the best things you can be for your cognition.

His spike protein antibody level, meanwhile, hasn’t moved across nearly two years of testing. The cognitive improvement appears to line up with the mold treatment, not with any change in his vaccine-related antibody.

Right now, for his cognition specifically, the mold-related piece looks like the active problem, and addressing it is what moved the needle.

The more things a chronically activated immune system is dealing with at once — mold, a latent virus, a vaccine response that hasn’t settled, a leaky gut, a genetic tendency to hold onto all of it — the harder it is for that system to stand down. Each contributor adds to the total load, and the total load determines whether the immune system can quiet itself.

Once you start correctly identifying and addressing what’s actually contributing, even one piece at a time, as this couple as done, things can genuinely get better. His case is proof of that.

What the research actually shows

Researchers reviewed medical records for over six million adults 65 and older and compared new Alzheimer’s diagnoses in the year after COVID-19 infection versus no infection. The numbers were small either way — 0.68% of the COVID group versus 0.35% of the non-COVID group — but that’s roughly double, even after adjusting for age and other risk factors. This doesn’t prove COVID causes Alzheimer’s, and it can’t tell you whether COVID was acting alone or lighting a fire under something already there. But it’s important information at a scale worth taking seriously.

Why persistent activation happens

COVID-19 and the vaccine both provoke a strong immune response that resolves in most people. In a meaningful subset, it doesn’t. Some people continue producing spike protein long after infection clears.

Researchers studying vaccinated people with unresolved symptoms describe a similar pattern of persistent spike protein and ongoing immune dysregulation, with no infection involved at all.

None of this research has isolated the vaccine or the virus as a sufficient cause on its own — none of it looked for other contributing factors. That’s typical: researchers usually look for a single variable, when in something as complex as Alzheimer’s, it’s usually a combination.

In my experience, chronic immune activation is not from one thing. Common overlapping contributors I see:

• Mold toxins, sometimes alongside a reactivated latent Lyme infection

• A leaky gut, which carries its own ongoing immune response until healed

• Elevated antibodies to other viruses, like EBV or HHV6, even without full reactivation

It’s not uncommon for all of those to be in play at the same time.

A chronically activated immune system produces a steady stream of inflammatory cytokines that circulate well beyond the original problem. As mentioned earlier, in the brain, they prime microglia into a persistent defensive state and can break down the blood-brain barrier — the structure meant to keep inflammation out of brain tissue.

Once that barrier is compromised, amyloid production increases, neurons come under sustained stress, and the slow damage that eventually shows up as cognitive decline begins to build.

The specific trigger matters far less than whether the immune system stays switched on long enough for this process to take hold.

It should be reversible if addressed properly, early enough.

If you’re recognizing pieces of your own experience, or your spouse’s, or someone else you love — the next questions I’m exploring in the rest of this post are how you’d actually find out what’s driving it, and what to do about it.

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When it comes to preventing Alzheimer’s or reversing symptoms of cognitive decline, testing for mycotoxins, metals, and other environmental toxins is an essential part of a personalized, root-cause approach. The lab tests I order for my clients often reveal a high toxic burden, usually dominated by mycotoxins. It happens so often, I’m not even surprised anymore.

While our bodies are able to detoxify and clear everyday exposures, chronic mycotoxin accumulation can eventually overwhelm those pathways—especially when specific genetic susceptibilities impair clearance. These toxins can cross the blood-brain barrier, provoke neuroinflammation, and disrupt cognitive function.

The inflammation that occurs in response to these toxic exposures can cause widespread health problems, including progressive neurodegeneration. Mycotoxins from molds in water-damaged buildings are among the most common contributors to Mild Cognitive Impairment (MCI) and Alzheimer’s disease that I see.

The majority of people have no idea they have been exposed, and well over half of my clients who are dealing with this type of cognitive decline do not have a family history of Alzheimer’s or the APOE4 gene. They do have another gene in common that makes them more susceptible to illness from mycotoxins. Sometimes they have both genes.

Toxins should be investigated for anyone diagnosed with MCI or Alzheimer’s, as well as for anyone with cognitive symptoms or who wants to protect their cognitive longevity before symptoms appear. Having a family history of Alzheimer’s is irrelevant.

I recently had symptoms that I was eventually able to connect to mycotoxins in my home. A home I had tested a year or so prior with no issues. It started with reactions to certain foods that caused facial flushing, like a severe sunburn. Something that’s commonly a result of mast cell activation. Each time it happened, it a took a full week to resolve. It was unusual for me to react to anything, and concerning.

Then I started experiencing issues with word finding and trouble completing sentences. I tested myself and my home.

About three days after I received the ERMI mycotoxin test results for my home, which included a very high HERTSMI score, I got myself – and my cat : ), out of the environment. Instead of Florida, I’m writing this post from North Carolina, where I’ve now been living and working for a month while communicating with an excellent mold inspector and reading remediation proposals.

My husband has handled scheduling and being home for the various appointments, while staying with a friend when he isn’t working. I’m just as serious about him not getting Alzheimer’s as I am myself! The test results convinced him not to stay in the house.

His father had Alzheimer’s, and his mother is currently in memory care. He does not have the APOE4 gene, but I can tell you for a fact that there was a high level of mycotoxins in his parents’ home.

I’m fortunate to have an alternative place to live while this issue is being addressed. Even if I didn’t, I would have found a way to get out because my number one priority is not getting Alzheimer’s. As you already know, my maternal history of the disease is daunting.

I’ve worked with far too many people who have been diagnosed with Mild Cognitive Impairment and Alzheimer’s disease, in whom test results revealed mycotoxins to be a major contributor, to stay in a toxic environment.

Removing yourself from the environment is the most critical first step, yet it is often the hardest to execute, either because an alternative location isn’t readily available or the threat is invisible and easy to discount as “not that bad”.

After a diagnosis of MCI or Alzheimer’s, people stay in a toxic environment because they don’t know it’s toxic. The standard medical approach doesn’t include a conversation about mycotoxins, let alone an investigation for them. Because a spouse living in the same environment is usually completely unaffected, the issue is easily dismissed, if it comes up at all.

Most of the time, the only symptom my older clients have related to mold is cognitive decline and eventually a diagnosis of MCI or Alzheimer’s. In clients under 65, they usually start having difficulty with calculating and/or reading comprehension; sometimes visual disturbances - that aren’t just near or far-sightedness. The majority do have a genetic susceptibility to mycotoxins and don’t have the APOE/4 gene. Some have both.

My symptoms are gone, and I’m in the midst of a detox that I’ll continue for 3 months before retesting. I’d really like to go home, but I won’t stay there again until remediation is complete and the test results after remediation are to my satisfaction. The process to get to the point of remediation has so far taken a month. We hope to have it scheduled in the next 2-3 weeks, and I hope to be back home in a month.

Here’s why investigating your toxic load is non-negotiable even if you don’t have symptoms, and especially if you do:

• Toxic Accumulation: Over time, our bodies store various toxins in tissues, where they can continuously disrupt cellular signaling and cognitive function.

• Chronic Neuroinflammation: Ongoing immune activation drives neuroinflammation, which damages synapses and accelerates processes that lead to cognitive decline.

• Oxidative Stress: Excessive free radicals damage brain cells.

• The Gut-Brain Axis: Toxins frequently compromise the intestinal barrier and alter the gut microbiome.

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The Alzheimer’s pathology connection: Amyloid and P-Tau

Mycotoxins breach the blood-brain barrier and trigger defensive amyloid-beta plaques, while simultaneously blocking cellular energy production, which starves neurons and causes tau proteins to misfold into tangles (p-tau).

Once that cascade begins, without intervention, the damage doesn't stay confined — over time, it spreads outward across the entire brain. As more cells break down, the neural networks that control everything begin to fail, resulting in a progressive and ultimately unstoppable loss of brain tissue and function.

Toxicology and neurodegeneration literature substantiates this pathway, confirming that environmental biotoxins, including mycotoxins, trigger oxidative stress, M1 microglial activation, and neuroinflammatory cascades that drive this progressive brain destruction.

It’s the total body burden—driven by both the magnitude and the duration of exposure—that is the critical tipping point that can lead to Alzheimer’s.

Other factors, such as increased intestinal permeability, can also play a less obvious but significant role.

Early action is your best friend. This has been stopped, and people have gotten better. But there are a lot of variables, and you need to get help with it as soon as possible.

Common symptoms of chronic biotoxin illness—from any source—are often dismissed or misattributed. They can include:

• Cognitive impairment and brain fog

• Anxiety and mood fluctuations

• Sleep disturbance and insomnia

• Fatigue and exercise intolerance

• Executive dysfunction (difficulty organizing, planning, or word-finding)

• Difficulty with reading comprehension, math, or spelling

• Visual disturbances

• Persistent digestive issues

A typical conventional doctor’s appointment for these symptoms usually results in separate diagnoses—MCI, chronic fatigue, insomnia, IBS, or anxiety—complete with corresponding management medications, but absolutely no investigation into toxins a potential root cause.

If toxins are driving the problem and are never discovered and addressed, true healing remains out of reach.

As a ReCODE-certified practitioner, our data-driven approach is designed to pinpoint precisely what to look for when assessing cognitive decline. Testing for toxins is always part of the protocol. For the client and the home. We also test for specific genetics related to biotoxins. All are listed, with links, below

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The foundation is how you live.

Diet, sleep, exercise — both physical and cognitive — stress reduction, optimizing gut health, meaningful social connection, and continuing to learn and experience new things. These are foundational pillars of an anti-Alzheimer’s lifestyle, and no supplement replaces any of them. If the foundation isn’t in place, supplements are filling a leaky bucket.

What supplements do is support and extend what lifestyle alone can’t fully accomplish — particularly as we age:

• Our ability to absorb certain nutrients declines

• Our bodies face increasing levels of oxidative stress

• And the specific biological vulnerabilities associated with Alzheimer’s risk require more targeted nutritional support than food alone can provide.

The brain has enormous nutrient requirements. It is the most metabolically active organ in the body, and it depends on a steady supply of specific vitamins, minerals, fatty acids, and antioxidants to function optimally. Many of these are depleted by chronic stress, poor sleep, gut dysfunction, medications, and the normal process of aging. Replenishing them isn’t optional — it’s maintenance.

But here’s what matters almost as much as which supplements you take: the quality of what you’re taking and whether you actually need it.

Why brand quality matters — and why I don’t buy supplements on Amazon

The supplement industry is largely unregulated. Unlike pharmaceuticals, supplements don’t require pre-market approval from the FDA. That means what’s on the label isn’t always what’s in the bottle — and in some cases, what’s in the bottle includes contaminants, fillers, or doses that don’t match what’s stated.

Third-party testing exists to address this, and reputable brands invest in it. They test for purity, potency, and the absence of contaminants including heavy metals. Many do not.

Amazon is a particular problem. Even well-known brands sold on Amazon are frequently counterfeited, stored improperly, or sold past their expiration date by third-party sellers. I’ve seen lab analyses of supplements purchased on Amazon that contained a fraction of the stated dose — or none of the active ingredient at all. This isn’t theoretical. It happens regularly.

I purchase and recommend supplements exclusively through Fullscript, a professional dispensary platform that works directly with high-quality brands and maintains proper storage and handling throughout the supply chain. It is a significantly safer and more reliable source than retail — including Amazon, grocery stores, and big box retailers.

Being targeted and intentional — why testing changes everything

Taking supplements without knowing what you actually need is guessing. Some guessing is reasonable — there are nutrients that most people are deficient in and that are broadly safe to supplement. But for a genuine prevention protocol, targeted testing is what separates a thoughtful approach from throwing money at bottles.

Three categories of testing are particularly valuable:

Advanced micronutrient testing — intracellular and serum.

Standard blood tests measure nutrients in the serum — the liquid part of your blood. But serum levels reflect what’s circulating, not what’s actually inside your cells where nutrients do their work. You can have a normal serum level of a nutrient and still be functionally deficient at the cellular level. Intracellular testing measures what’s actually available inside your cells, which is a fundamentally more accurate picture of your nutritional status.

I use this testing with clients regularly, and the results are consistently revealing. People who eat well and take supplements still show intracellular deficiencies in nutrients critical for brain health — B vitamins, magnesium, antioxidants, zinc. Knowing specifically what’s low means we can address it precisely rather than broadly.

Advanced cardiometabolic testing

As covered in previous posts, metabolic health and brain health are deeply connected. Insulin resistance, oxidative stress, vascular inflammation, and lipid dysfunction are all upstream contributors to Alzheimer’s disease. Advanced cardiometabolic testing — well beyond a standard cholesterol panel — gives us a clear picture of where metabolic dysfunction is occurring and which nutritional and lifestyle interventions are most needed. It also tells us which supplements are most relevant for your individual situation.

Plasmalogen testing

Plasmalogens are phospholipids that play important roles throughout the brain and body. Your body makes them, a lot of them, all your life. Although production declines, often sharply, with age.

In the brain, plasmalogengs play a key role in how your brain cells communicate. They also play a crucial role in cholesterol efflux in the brain, especially in APOE4 carriers.

The same test provides information about mitochrondria health, the methyltransferase system, peroxisomes, specific gastrointestinal tract acids, dietary fatty acids and more.

So while you can take a variety of supplements without any lab data at all….

…my goal is always to be intentional. Every supplement in a well-designed protocol is there for a reason, ideally supported by data.

In the rest of this post, I cover six foundational supplements most people benefit from, the specific brands I use and recommend to my clients, and how to access my Fullscript practitioner supplement dispensary for 15% off a variety of supplements every time you order, which more than offsets the upgrade.

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Today, we are looking at the “low-hanging fruit”—the straightforward, everyday adjustments that protect your neural network before symptoms ever start.

Three of the easiest wins involve a common medication swap, your senses, and your dental health.

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The Statin Swap

If you take a cholesterol-lowering medication, it pays to know which type is in your medicine cabinet. Certain statins are lipophilic (fat-soluble), which means they easily cross the blood-brain barrier and enter your central nervous system.

While keeping your cholesterol in a certain range is the doctor’s main goal, you actually do not want to deplete cholesterol inside the brain. The brain is the most cholesterol-rich organ in the body, holding about a quarter of your total supply.

Unlike the rest of your body, the brain manufactures its own cholesterol locally because it can’t use the cholesterol circulating in your bloodstream. Inside the brain, cholesterol is an absolute must: it builds and repairs neuronal membranes, forms and maintains synapses (the connections between brain cells), and produces myelin—the protective insulation that helps nerve signals fire rapidly and efficiently.

When a lipophilic statin crosses the blood-brain barrier, it can disrupt this delicate local supply. For susceptible individuals, that depletion can impair brain cell communication and manifest as brain fog, word-finding difficulties, memory issues, or a general sense of mental drag.

The fix is often as simple as a conversation with your physician. Asking about a hydrophilic (water-soluble) alternative—like pravastatin or rosuvastatin—keeps the medication focused on your liver for cholesterol lowering rather than your brain tissue.

Dental Hygiene

We tend to think of oral health as separate from brain health, but chronic gum disease is anything but local. When your gums are tender, swollen, or bleeding, it creates an open doorway for oral bacteria to slip directly into your bloodstream.

The most notorious offender is a bacterium called P. gingivalis. Once it enters the bloodstream, it can travel to the central nervous system. In fact, researchers have repeatedly identified P. gingivalis and its toxic enzymes directly inside the brains of Alzheimer’s patients. Once in the brain, this bacterium acts like a constant spark, fueling chronic inflammation, triggering immune alarms, and accelerating tissue damage.

The good news? Closing this entry point is completely within your control. Keeping up with professional cleanings twice a year—along with daily brushing, flossing, or using a water flosser—can prevent or heal inflamed gum tissues. Treating active gingivitis cuts off a major, continuous source of brain-bound inflammation at the root, all without needing a single prescription pill.

Vision and Hearing Correction

When your eyesight or hearing starts to fade, your brain has to work overtime just to decode basic sounds and sights. Straining to read fine print, discern contrast in low light, or piece together a muffled conversation eats up an enormous amount of brain energy—energy that should be going toward memory and focus.

Over time, the constant extra strain takes a heavy toll. Add in the fact that missing out on everyday sights and sounds means your neural pathways stop getting the stimulation they rely on, and you create an environment where cognitive function starts to slip faster than it should.

Updating your glasses, treating cataracts early, or getting a hearing evaluation that may indicate a need for hearing aids aren’t just quality-of-life upgrades so you can watch TV or chat with friends more easily. They’re some of the easiest, most practical ways to take the daily pressure off your brain and keep your neural pathways firing the way they should.

These everyday adjustments build a strong foundation, but protecting your brain also requires looking at the biochemistry happening underneath the surface.

In the section below, I explain a common metabolic driver of Alzheimer’s that has no symptoms but can be detected with a simple blood test—one that is rarely part of your routine panels, but could easily be added by your doctor.

We will cover why it matters so much for prevention, how you can self-order it if you want to, and the straightforward action steps to bring it down if your level is elevated.

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My mother had Alzheimer’s. So did her sister. So did their mother, and her mother before that. My cousin — my aunt’s daughter — died of it too, at sixty-four. Four generations of women in my direct maternal line, five diagnoses in all, the same disease finding its way down the same branch of the family tree — while the men in the family never got it at all.

As a ReCODE practitioner, I’ve seen a similar pattern in most of the women I’ve worked with.

If you’ve watched this happen in your own family — mother, grandmother, sister, maybe an aunt — you’ve probably felt the particular dread of maternal-line Alzheimer’s. It isn’t random.

There are real, identifiable reasons Alzheimer’s travels down through the women in a family more than it travels through the men, and understanding those reasons is the difference between feeling stalked by your genetics and understanding exactly what you’re working with.

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Why the Maternal Line Carries More Weight

It starts with your mitochondria — organelles inside your cells that produce the energy your brain and body run on. Every mitochondrion in your body came from your mother’s egg — none from your father.

Your mitochondria's DNA is inherited from your mother, generation after generation — passed to both sons and daughters, but only carried forward by the daughters. Any inherited weakness in cellular energy production travels that same maternal line.

Your brain is the most metabolically expensive organ you have. It uses roughly twenty percent of your body’s total energy despite being a fraction of your body weight, and when mitochondrial function is compromised, the brain is often the first place the deficit shows up.

This is one of the reasons Dr. Dale Bredesen, whose research underlies the ReCODE protocol I empower my clients to use for prevention, frames Alzheimer's as fundamentally a problem of energy supply not meeting energy demand in vulnerable neurons.

Then there’s the imaging research, which comes at this from two separate angles and lands on the same conclusion from different evidence.

Researchers have scanned the brains of healthy adults — people with no symptoms at all — and looked at how well different regions were using glucose, the brain's main fuel. In adults whose mother had Alzheimer's, certain regions showed the brain wasn't using glucose efficiently enough, in the exact areas the disease usually affects.

This can start as early as your thirties. Left unaddressed, it gradually worsens over many years and leads to cognitive impairment. It's just one of several reasons women with a maternal history are more likely to develop Alzheimer's — and fortunately, it's also one of the risk factors we can actually do something about.

A separate line of research, measuring amyloid plaque rather than glucose metabolism, found the same maternal skew: children of mothers with Alzheimer’s were more likely to test positive for amyloid-beta on imaging, years before any symptoms appeared, while a father’s history alone didn’t carry the same weight.

Amyloid-beta has long been blamed as the cause of Alzheimer's. But the drug companies most invested in that theory have run the trials themselves, and clearing amyloid from the brain has repeatedly failed to stop the disease. A growing body of research, including the ReCODE model, treats amyloid instead as a downstream response — which means there's a lot we can do about what's actually driving it.

Two distinct measures — impaired glucose metabolism and amyloid-beta accumulation — each independently show that maternal history carries more weight in the brain than paternal history does, in both men and women, years before diagnosis.

Add hormones. Estrogen plays a direct role in how the female brain generates and uses energy — it supports glucose metabolism in exactly the regions most vulnerable to Alzheimer’s. When estrogen drops sharply during perimenopause and menopause, some women experience what researchers have started calling a brain energy crisis: a measurable dip in glucose metabolism that can precede cognitive symptoms by years.

This is part of why women make up two out of every three Alzheimer’s diagnoses. It isn’t that women live longer. There’s a specific hormonal transition landing in brains already operating with less metabolic reserve, in a body that inherited its cellular energy machinery from a mother who was working with the same constraint.

The Risk Factors That Are Specific to You

APOE4 is the genetic variant most associated with Alzheimer’s risk, and it’s inherited from either parent — but several studies have found that APOE4 carriers whose mother had Alzheimer’s show a stronger risk signal than carriers whose father had it.

The gene is the same either way. Something about maternal transmission appears to compound it. Mitochondrial inheritance is one leading explanation, though it doesn't fully account for why the effect shows up so much more in daughters than sons, since sons inherit the same mitochondria.

That’s why researchers are also looking at the X chromosome. Recent studies have already identified specific Alzheimer's risk genes on the X chromosome, some of which only show up when researchers isolate APOE4 carriers, suggesting the two may be compounding each other rather than acting independently.

This research is only a couple of years old, and the specific mechanisms are still being mapped, but it's a real and active area of study — and the kind of thing that could help explain a pattern like the one in my own family better than APOE4 alone ever could.

Autoimmune and thyroid conditions, which run more heavily in women and often travel through generations of the same family, add another layer — chronic inflammation and thyroid dysfunction both interfere with the brain’s energy supply along a similar pathway. So does a history of insulin resistance, which shows up disproportionately in women with a family history of Alzheimer’s and which some researchers now refer to as “type 3 diabetes” when it affects the brain specifically.

Finally, but certainly not least important, chronic stress deserves its own place related to a woman's risk for Alzheimer's. The stress hormone cortisol, when it's ongoing rather than occasional, negatively impacts the hippocampus — the same brain region Alzheimer's targets first.

Women's bodies process stress differently than men's, and the downstream effects touch several other risk factors beyond what's already covered here — chronic stress disrupts sleep, drives blood sugar instability, raises inflammation, and strains the cardiovascular system, all of which feed directly back into brain metabolism.

None of this means inheritance is destiny. Many women with a maternal history of Alzheimer’s never develop Alzheimer’s.

What differs is what happens to the underlying biology across a lifetime — the inflammation, the toxin load, the blood sugar control, the hormone trajectory, the sleep, the chronic stress.

Why the ReCODE Protocol Matters Here

For prevention, it’s called PreCODE - Prevention of Cognitive Decline. This is exactly where Dr. Bredesen’s thirty years of research changed how I think about prevention. The research shows us that Alzheimer’s isn’t one disease with one cause — it’s a downstream result of dozens of possible imbalances across metabolic, inflammatory, hormonal, toxic, and mitochondrial systems, and no two people arrive at the same endpoint through the same combination of causes.

So the question isn’t will I get Alzheimer’s because of my family history. Genetics raise your risk, but that’s not the whole story. It’s “which of the specific, measurable, addressable issues that likely contributed to my mom’s Alzheimer’s are already present in me, right now, years or decades before any symptom would show up.”

That’s a fundamentally different question. Dysfunction precedes symptoms by a long runway. Alzheimer’s doesn’t arrive the day you notice you’re forgetting things — it’s been building in the biology for years, sometimes decades, before a diagnosis. That runway is where the real leverage is.

Those who came before us didn’t have this information; if they had, prevention would have been possible for them too.

We have the opposite problem now — so much information that it’s overwhelming to navigate alone. Diet and exercise matter, and changing them is a real step in the right direction, but they’re not everything.

Real change also means understanding what’s actually happening in your own biology, which takes functional lab testing most people still don’t have easy access to.

Below is where this moves from pattern to precision. Family history tells you there’s risk — it doesn’t tell you which imbalances are actually driving it in your body, right now. Lab testing does.

I’ll explain the kind of testing that’s needed to build a personalized protocol, how to get it and also how to actually implement – instead of just trying to follow a generic list of things you collect from the internet that’s hard to follow consistently.

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Once you understand what’s really happening to you because of chronic stress, you’re much more likely to recognize it, notice it more often, and reduce it.

The stress response was designed to save your life. When you perceive a threat — whether physical, emotional, or chemical — your brain activates the fight or flight system, flooding your body with stress hormones that:

• Sharpen your focus

• Increase your heart rate

• Prepare you to run, fight, or hide

Your digestive system shuts down. Your reproductive system shuts down. All available energy goes toward responding to the threat.

This is a brilliant system. It works exactly as it should — when the threat is short-term.

The problem is that the stress you’re most likely living with today is not short-term. It’s relentless. Financial pressure, caregiving responsibilities, work demands, family dynamics, health fears, and the low-grade anxiety that comes from simply watching the world — these don’t resolve in minutes the way a near-accident on the highway does. They stay.

And your body responds to that sustained perception of threat the same way it responds to any other.

Chronic stress is like living with one foot on the gas pedal and one foot on the brake at the same time, flooding your body with stress hormones.

When the stress response stays on, there is no time for repair. The systems responsible for your health cannot do their jobs when your body believes it is constantly under threat.

What makes this particularly relevant to Alzheimer’s is that chronically high cortisol, a stress hormone, negatively impacts the same areas of the brain that Alzheimer’s impacts. Over time it can cause the prefrontal cortex — the region responsible for memory, learning, planning, attention, and decision-making — to begin to shrink.

It affects the hippocampus, which is central to memory and emotional regulation and is also the area most affected early in Alzheimer’s disease. And it increases the size of the amygdala, which amplifies fear and anxiety.

Chronic stress also depletes BDNF — the brain’s growth factor — which is necessary for the birth and nourishment of new brain cells throughout your life. It depletes serotonin and dopamine. And it drives inflammation — the kind that can compromise the blood-brain barrier and accelerate the very processes we’re trying to prevent.

None of this causes Alzheimer’s in isolation. But chronic stress is a strong upstream contributor — and for many people, it may be where the metabolic unraveling begins.

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Why women are more vulnerable

Estrogen, which is neuroprotective in many ways, also amplifies the stress response in the short term. As estrogen declines during perimenopause and menopause, the regulation of that stress response becomes less stable, and the brain becomes more vulnerable to its effects.

Women also have a more reactive stress response system overall, which means cortisol is released more readily and in greater amounts in response to perceived threats.

Women also tend to ruminate more — to replay, rehearse, and worry.

Interestingly, you can turn on the stress response just by thinking about a current problem or one you anticipate in the future. Which means the stress is not always coming from outside circumstances — it’s being generated internally, by thought.

If you have a maternal history of Alzheimer’s, there’s an additional layer. Seeing your mother or grandmother decline with Alzheimer’s is itself a chronic stressor. The worry, the grief, the anticipatory fear — these are real stressors with real physiological effects.

And there’s a cruel irony in the fact that caring for someone with Alzheimer’s, which is one of the most emotionally and physically demanding things you can do, is also one of the most significant chronic stress exposures a brain can undergo.

Women are the primary caregivers for spouses and parents with Alzheimer’s. They are also, by a significant margin, the ones who develop the disease themselves. Two-thirds of all Alzheimer’s diagnoses are women.

The daughters who care for their mothers are often walking the same road their mothers walked — carrying the same stress, experiencing the same sleeplessness, putting themselves last in the same way, and ultimately facing the same risk.

That cycle is worth interrupting. The stress you are living with right now is relevant to the brain you will have in the future. Managing it is not a luxury or a self-indulgence. It is part of your Alzheimer’s prevention strategy.

In the rest of this email, I share specific, practical strategies for turning off the stress response — including one I use before going to sleep every night that also improves my ability to fall asleep.

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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?

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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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