This article is copyrighted by GreenMedInfo LLC, 2023
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
Anecdotal reports claim coconut oil produces remarkable recoveries from Alzheimer’s disease, but is there research to support this? Now, one study published in the Journal of Alzheimer’s Disease shows that a mechanism for coconut oil’s brain rescuing properties does in fact exist
The internet loves a good “natural cure” recovery story. For instance, when Dr. Mary Newport, MD, dramatically reverses her husband’s symptoms of Alzheimer’s disease after just two weeks of adding coconut oil to his diet, thousands enthusiastically share the story. But despite their popularity, anecdotes rarely stand the test of time, nor the scrutiny of the medical community, at least not like experimental research published in peer-reviewed biomedical journals.
All the more reason to celebrate a promising study published in the Journal of Alzheimer’s Disease titled, “Coconut Oil Attenuates the Effects of Amyloid-β on Cortical Neurons In Vitro.”[i] The study lends fresh experimental support to an accumulating body of anecdotal reports that coconut oil may alleviate and/or regress cognitive deficits associated with aging and neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s.
Medical researchers from the Memorial University of Newfoundland, St. John’s, NL, Canada, undertook a pilot study to investigate the effects of coconut oil supplementation directly on cortical neurons treated with amyloid-β (Aβ) peptide in vitro. Aβ peptide is the main component of certain deposits found in the brains of patients with Alzheimer’s disease believed to contribute to the disease.
The researchers noted that a clinical trial, which we reported on in our article MCT Fats Found in Coconut Oil Boost Brain Function in Only One Dose, reported significant improvements in Alzheimer’s disease patients after 45 and 90 days of treatment with medium chain triglycerides from coconut oil. They pointed out that this trial led to the marketing of the FDA-approved ‘medical food’ caprylidene (trade name Axona), but that the public has shown greater interest in coconut oil itself as a potential therapy, owing to its far greater affordability and availability.
The researchers sought to test the hypothesis that coconut oil is beneficial for neurodegenerative conditions using a cell model. Live rat neurons were exposed to various combinations of Aβ peptide and coconut oil, with the result that Aβ peptide reduced survival of neurons and coconut protected against this Aβ-induced reduction in survival time. The researchers noted that coconut treated Aβ cultured neurons appeared “healthier,” and that coconut oil “rescued” Aβ-treated neurons from mitochondrial damage caused by their toxicity. The researchers observed coconut oil preventing Aβ-induced changes in mitochondrial size and circularity. These findings have great significance, as mitochondria function is often compromised in the brains of Alzheimer’s disease patients.
According to the researchers, “The rationale for using coconut oil as a potential AD [Alzheimer’s Disease] therapy is related to the possibility that it could be metabolized to ketone bodies that would provide an alternative energy source for neurons, and thus compensate for mitochondrial dysfunction.” The researchers proposed that ketone bodies formed as a byproduct of coconut oil metabolism may offset Aβ-induced impairment of mitochondrial function and thus energy metabolism. Considering that the medium chain triglyceride found in coconut known as caprylic acid does cross the blood-brain barrier, and has been found to have anti-convulsant, in addition to, ketogenic effects, coconut oil likely does have a neuroprotective effect.[ii]
The researchers concluded, “The results of this pilot study provide a basis for further investigation of the effects of coconut oil, or its constituents, on neuronal survival focusing on mechanisms that may be involved.”
Clearly, one of the ways that coconut oil can ‘rescue’ the brains of Alzheimer’s patients is by addressing the metabolic derangement in the brain associated with the condition, or what is known as “type 3 diabetes.” As the brain ages, it becomes increasingly resistant to insulin, and therefore incapable of using glucose efficiently to meet its significant energy needs — hence the metaphor “type 3 diabetes.” Thankfully, nature has devised an alternative fuel source for the brain that is independent of glucose utilization and the insulin signaling system, namely, the use of ketone bodies. Coconut oil provides the substrate for the immediate production of these ketone bodies, enabling significant quantities to be produced within a matter of only minutes following ingestion. This metabolic restoration of function may explain why remarkable recoveries in cognitive function and memory have been observed, anecdotally.
Putting the science aside for a moment, coconut, like walnuts, both obey the so-called ‘doctrine of signatures.’ Both foods are encased by a skull-like shell, and contain within a fatty acid-rich ‘meat,’ that feed the organ – the brain – they resemble. Could the poetry of our direct experience tell us something about the value this food has to our brain, or should we continue to play agnostic and exercise great caution incorporating a ‘food as medicine’ approach until the men in white coats, and powerful economic forces behind them willing to shell out millions, if not billions of dollars, to “prove” in randomized, double-blind, placebo-controlled fashion something we probably already know is true?
For additional research on the benefits of coconut oil visit our research page on the topic: coconut oil health benefits. Or, visit our neurodegenerative diseases page for dozens of natural substances studied that may help these conditions.
A nationwide study of 27.8 million older Americans found long-term exposure to fine particle air pollution (PM2.5) is linked to a higher risk of developing Alzheimer’s disease, showing that everyday air quality directly influences brain aging
Each increase in long-term pollution exposure corresponded with about an 8.5% higher risk, highlighting how cumulative daily exposure shapes future cognitive health
Researchers found most of the Alzheimer’s risk from pollution occurs through direct effects on the brain — including inflammation, oxidative stress, and blood vessel damage — rather than being explained primarily by other diseases
People with a history of stroke showed greater vulnerability to pollution-related Alzheimer’s risk, indicating underlying vascular injury amplifies the neurological impact of environmental exposure
Long-term exposure patterns — not short pollution spikes — drove the strongest associations, meaning consistent reductions in daily pollution exposure represent a practical strategy to protect brain health over time
Alzheimer’s disease is the most common form of dementia — a progressive erosion of memory, judgment, and independence that ultimately proves fatal. It already affects millions worldwide, and those numbers are expected to surge in the coming decades.
Against that backdrop, a recent study identifies air pollution as a direct driver of brain degeneration — not merely a bystander, but an active cause. Scientists from Emory University and collaborating institutions reported in PLOS Medicine that long-term exposure to fine particulate matter — PM2.5, microscopic particles small enough to enter your bloodstream and brain — correlates with higher Alzheimer’s risk in a nationwide analysis of 27.8 million Medicare beneficiaries.1
These particles are roughly 30 times smaller than the width of a human hair — so small that your lungs can’t filter them out. They pass directly through lung tissue into your blood, and from there they cross your blood-brain barrier. During follow-up, nearly 3 million individuals developed Alzheimer’s, giving the study enormous statistical power.
What makes this finding striking is the magnitude and consistency. The analysis showed that each increase in long-term PM2.5 exposure aligned with a measurable rise in Alzheimer’s risk, even after researchers adjusted for age, socioeconomic factors, and major health conditions.
Although stroke, depression, and high blood pressure all raised dementia risk, they explained only a small portion of the pollution effect, which indicates that pollution itself acts directly on your brain through mechanisms such as inflammation, oxidative stress, and vascular injury. Taken together, this evidence reframes Alzheimer’s as more than a disease of aging or genetics. Environmental exposure now emerges as a modifiable driver of brain decline that affects millions.
Massive Study Shows Pollution Directly Harms Brain Health
For the PLOS Medicine study, researchers aimed to determine if air pollution itself drives Alzheimer’s risk or if other diseases act as the main pathway.2 Participants represented older Americans across regions, socioeconomic backgrounds, and health profiles, with an average age around 76 and a median follow-up of about six years. The findings reflect everyday exposure, not rare scenarios or specialized clinical populations.
• Higher pollution exposure translated into measurable increases in Alzheimer’s risk — The analysis showed that as people’s average PM2.5 exposure over five years went up, so did their risk of developing Alzheimer’s. Specifically, moving from a lower to a moderately higher level of pollution exposure was linked to roughly an 8.5% increase in risk. Even after adjusting for age, income indicators, smoking patterns, and other factors, the relationship remained consistent.
• Stroke history increased vulnerability more than other conditions — When researchers separated participants by medical history, individuals who had experienced stroke showed a stronger pollution-Alzheimer’s link. High blood pressure and depression were linked to Alzheimer’s overall but didn’t meaningfully change how pollution affected risk. This distinction helps you identify personal risk factors that amplify environmental exposure.
• Most of the pollution effect occurred directly rather than through other diseases — The researchers used a technique called mediation analysis, which essentially asks: does pollution cause Alzheimer’s directly, or does it first cause other diseases (like stroke) that then cause Alzheimer’s? Only 1.6% of the association was explained by high blood pressure, 2.1% by depression, and 4.2% by stroke, which indicates the majority of risk comes from pollution acting on the brain itself.
The study confirmed that higher PM2.5 exposure correlated with greater incidence of high blood pressure, stroke, and depression, each independently associated with Alzheimer’s risk. That layered effect creates a compounding burden: pollution raises disease risk while also exerting direct neurological damage.
• Time-related exposure patterns reinforced the findings — Researchers calculated five-year moving averages of pollution before Alzheimer’s diagnosis, which captured long-term exposure rather than short spikes. This approach shows that sustained everyday exposure — not a single event — aligns with neurodegenerative risk. Put simply, the air you breathe today is shaping the brain you’ll have in a decade.
• Neuroinflammation and oxidative stress act as primary drivers — Mechanistic discussion in the paper highlights neuroinflammation, meaning your brain’s immune system stays activated and damages tissue over time. Oxidative stress — cellular damage caused by unstable molecules — also emerged as a central pathway linking airborne particles to neural injury.
Think of it as biological rusting — unstable molecules strip electrons from healthy cells, degrading them the way oxygen corrodes unprotected metal, except it’s happening inside your neurons. Vascular injury, which refers to damage to blood vessels that supply your brain, further explains why cognitive decline accelerates with exposure.
Evidence cited in the research also shows exposure to fine particles associates with earlier accumulation of amyloid-beta plaques, tau tangles and other abnormal proteins commonly observed in Alzheimer’s disease. These protein changes represent physical damage inside the brain rather than abstract statistical associations.
Reduce Pollution Exposure to Protect Your Brain
The encouraging takeaway from all of this: because the strongest associations came from sustained everyday exposure rather than acute spikes, the risk is modifiable. Reducing your daily pollution burden — even modestly — over years can meaningfully shift your trajectory.
Air pollution acts as a direct driver of brain damage, and once you understand this, the most effective strategy becomes clear — reduce your exposure while strengthening your body’s cellular energy defenses. This isn’t complicated, but it does require consistency. Think in terms of cumulative load.
Every breath you take is either adding to the oxidative burden on your brain or giving it a chance to recover. Most people don’t think about air quality the way they think about diet or exercise, but the research makes it undeniable — what you breathe matters as much as what you eat. Lowering that burden day after day shifts the entire trajectory of brain aging in your favor.
1. Track your daily air exposure the same way you track any other health metric — Many people monitor their steps, their sleep, their macros — but they have no idea what they are breathing. That needs to change. Start checking your local PM2.5 levels every single day. You can use free apps that give you real-time readings for your area.
If you walk outdoors, exercise outside, or sit in traffic during your commute, your exposure windows spike dramatically. Adjust your timing accordingly. Early morning hours and periods right after rainfall typically carry lower particle concentrations because rain literally washes particulates out of the air. When pollution levels climb, shift your outdoor activity or move it indoors.
Once you turn this into a daily habit — just like checking the weather — it builds a level of awareness that many people completely lack. You start making smarter decisions automatically, because this is one of the few environmental risks you can actually manage minute by minute.
2. Upgrade your indoor air first, because that is where you spend the vast majority of your time — Most Americans spend roughly 90% of their day indoors.3 That means your indoor home air quality determines the largest single portion of your total pollution exposure, and most people have never given it a second thought.
Start with your sleeping area, because that is where you spend six to eight continuous hours breathing the same air. Place a high-efficiency particulate air (HEPA) purifier in your bedroom and run it every night. Nighttime exposure is particularly insidious because it compounds hour after hour while your body is supposed to be repairing itself.
You’re essentially bathing your brain in inflammatory particles during the exact window when it needs clean conditions to clear metabolic waste through your glymphatic system — the brain’s built-in drainage network that activates during deep sleep to flush out toxic proteins, including the amyloid plaques linked to Alzheimer’s.
If you cook with gas, run proper ventilation. Gas stoves release nitrogen dioxide and fine particulates directly into your kitchen air, and those particles spread throughout your entire home within minutes. If you live near a busy road or highway, keep your windows closed during peak traffic periods, typically morning and evening rush hours. I know fresh air feels healthier, but opening windows next to heavy traffic is the opposite of what you want.
However, when outdoor air quality is good — check your PM2.5 readings first — opening your windows is actually one of the best things you can do. Indoor air often contains higher concentrations of toxins than outdoor air, from off-gassing furniture, cleaning products, cooking residues, and building materials.
Airing out your home when conditions are favorable flushes out those accumulated indoor pollutants and replaces them with cleaner air. The key is being strategic about it — let the air quality data guide when you open up and when you seal things off.
3. Strengthen your cellular energy production and eliminate the dietary factors that amplify pollution damage — Your body’s ability to withstand pollution damage depends entirely on how well your mitochondria are functioning — and that’s shaped largely by what you eat. If your mitochondria can’t produce adequate cellular energy, your brain loses its ability to defend itself against the very particles you’re breathing in.
Support your cellular energy foundations with adequate carbohydrate intake — about 250 grams a day — based on your individual microbiome tolerance. Start with whole fruit and white rice. As your tolerance improves, you can expand into well-cooked root vegetables, then non-starchy vegetables, starchy vegetables like sweet potatoes or squash, beans, legumes, and finally, minimally processed whole grains. If bloating, pain, or loose stools appear, back down and proceed gradually.
You need sufficient glucose to fuel mitochondrial respiration — low-carb approaches can actually impair this process for many people. Make sure you’re consuming enough protein, roughly 0.8 grams per pound of lean body mass per day, or 1.76 grams per kilogram, with approximately one-third of that coming from collagen-rich sources like bone broth, slow-cooked meats with connective tissue, or a quality collagen supplement.
Collagen provides the glycine your body requires for glutathione production, which is your primary intracellular antioxidant against pollution-driven oxidative damage. Here’s where many people go wrong — they continue consuming seed oils loaded with linoleic acid (LA) while wondering why their inflammation markers stay elevated. Excess LA directly disrupts mitochondrial membrane function and dramatically increases your vulnerability to oxidative injury.
When you combine high LA intake with daily pollution exposure, you’re essentially pouring gasoline on a fire inside your cells. Eliminate soybean oil, corn oil, canola oil, sunflower oil, and all processed foods that contain them. Cook with grass fed butter, ghee, or tallow instead. This single dietary change removes one of the biggest amplifiers of pollution-related brain damage.
4. Use strategic light exposure as a daily brain protection tool — This is an underappreciated strategy for countering environmental toxin damage, and it costs absolutely nothing. Sunlight does far more than regulate your circadian rhythm — it directly supports mitochondrial energy production and stimulates the production of melatonin inside your mitochondria, not just in your pineal gland.
This mitochondrial melatonin functions as one of the most potent antioxidants your body produces, and it works exactly where pollution does its worst damage — inside the mitochondria themselves. Prioritize consistent morning sunlight exposure, ideally within the first hour of waking, and build up your tolerance for broader sun exposure gradually over time.
One important caveat — if you’ve been consuming seed oils, be cautious with intense, midday sun exposure, because the oxidized LA in your skin makes you far more susceptible to sun damage. As you clean up your diet, your sun tolerance will improve naturally. Avoid sunlight during peak hours (typically 10 a.m. to 4 p.m.) until you’ve eliminated seed oils for at least six months.
5. Adopt a structured detox strategy that targets ultrafine particles and microplastics together — Pollution doesn’t exist in a vacuum. The ultrafine particles driving the Alzheimer’s risk you just read about overlap significantly with microplastics and a whole range of industrial toxins that accumulate in your tissues over years and decades. These aren’t separate problems. They’re different facets of the same environmental assault on your body, and they need to be addressed together.
I’m developing a detox solution designed to address both microplastics and ultrafine particles. This is a project I’m deeply committed to because I believe it represents one of the most urgent health needs of our time. I’m also working on a book in which I go deep into how microplastics and ultrafine particles affect virtually every organ system in your body. More importantly, I lay out practical, step-by-step detox strategies to address these health threats.
FAQs About Air Pollution and Alzheimer’s Disease
Q: How does air pollution increase Alzheimer’s risk?
A: Long-term exposure to PM2.5 is associated with a measurable rise in Alzheimer’s risk because these microscopic particles enter your bloodstream and brain, triggering neuroinflammation, oxidative stress, and vascular injury. A nationwide analysis of 27.8 million Medicare beneficiaries found roughly an 8.5% increase in Alzheimer’s risk with higher long-term PM2.5 exposure.4
Q: Does pollution affect Alzheimer’s risk directly, or through other diseases?
A: Most of the pollution effect appears to act directly on your brain rather than primarily through other conditions. The study estimated only a small portion of the association was explained by related diseases — about 1.6% through high blood pressure, 2.1% through depression, and 4.2% through stroke — indicating pollution itself drives neurological damage.
Q: Who may be most vulnerable to pollution-related cognitive decline?
A: Individuals with a history of stroke showed a stronger link between pollution exposure and Alzheimer’s risk. While high blood pressure and depression are independently associated with dementia, they didn’t significantly change how pollution influenced Alzheimer’s risk, suggesting environmental exposure adds risk across populations.
Q: Why does long-term exposure matter more than short spikes?
A: Researchers evaluated five-year moving averages of PM2.5 exposure, demonstrating that sustained everyday exposure — rather than isolated pollution events — aligns with neurodegenerative risk. This highlights cumulative environmental burden as a key driver of brain aging.
Q: What practical steps help reduce pollution-related brain risk?
A: Reducing exposure — such as monitoring daily PM2.5 levels, improving indoor air quality with HEPA filtration, adjusting outdoor activity timing, and addressing lifestyle factors that influence oxidative stress — help lower your cumulative burden. Americans spend about 90% of their time indoors, making indoor air quality a major determinant of total exposure.
Alzheimer’s disease is commonly thought to result from abnormal plaque buildup in the brain that gradually destroys brain tissue. Almost all Alzheimer’s research for decades has been directed toward eliminating amyloid, even after the basis for much of this work was shown to stem from fraudulent research
The billions spent on amyloid Alzheimer’s research have only produced three drugs, all of which offer minuscule benefits and severe side effects
In contrast, affordable and straightforward treatments that reduce dementia or the preceding cognitive impairment have been maligned and buried by the medical industry
DMSO for example, has incredible neuroprotective qualities that have spared many stroke and spinal cord injury victims from a life of “incurable” disability. Decades of forgotten research also show it treats cognitive impairment and dementia
This article will review the great amyloid scam and the simple therapies for cognitive decline we’re never told about
Medicine is strongly biased towards adopting biochemical models of disease as this facilitates costly therapeutics being developed for each disease and hence sustains the medical industry. Unfortunately, in many cases, the biochemical approach to disease, at best, can manage symptoms, and as a result, many conditions remain “incurable” while non-patentable natural therapies that can cure them languish in obscurity.
That’s why, despite spending an ever increasing amount of money on Alzheimer’s research (e.g., the NIH spent 2.9 billion in 2020 and 3.9 billion in 20241), we’ve still failed to make any real progress on the disease. This is particularly remarkable given the vast costs to the country (e.g., last year Alzheimer’s was estimated to cost the United States 360 billion dollars2) and the even greater social costs that accompany it.
The Amyloid Juggernaut
In 1906, plaques (of amyloid) in the brain were identified as the cause of Alzheimer’s disease. As the years have gone by, the majority of research for treating Alzheimer’s disease has been targeted at eliminating these plaques. Unfortunately, to quote a 2022 article:3
“Hundreds of clinical trials of amyloid-targeted therapies have yielded few glimmers of promise, however; only the underwhelming Aduhelm has gained FDA approval. Yet Aβ still dominates research and drug development. NIH spent about $1.6 billion on projects that mention amyloids in this fiscal year, about half its overall Alzheimer’s funding.
Scientists who advance other potential Alzheimer’s causes, such as immune dysfunction or inflammation, complain they have been sidelined by the ‘amyloid mafia.’ Forsayeth says the amyloid hypothesis became ‘the scientific equivalent of the Ptolemaic model of the Solar System,’ in which the Sun and planets rotate around Earth.”
Note: Frequently, when a faulty paradigm fails to explain the disease it claims to address, rather than admit the paradigm is flawed, its adherents will label each conflicting piece of evidence as a paradox (e.g., the French “paradox” disproves the notion cholesterol causes heart disease4) and dig deeper and deeper until they can find something to continue propping up their ideology (e.g., cholesterol reducing statins provide almost no benefit for heart disease while having significant side effects yet continue being pushed on patients).
The consistent failure of the amyloid model to cure Alzheimer’s gradually invited increasing skepticism towards it, which resulted in more and more scientists studying alternative models of the disease. Before long, they found other factors played a far more significant role in causing the disease (e.g., chronic inflammation), and by 2006, this perspective appeared poised to change the direction of Alzheimer’s research.
In response, the amyloid proponents pivoted to defending their failed hypothesis was due not to amyloid clumps, but rather toxic parts of it (oligomers) and a Nature 2006 paper appeared which identified a previously unknown toxic oligomer, Aβ*56, and provided proof that it caused dementia in rats.5
This paper cemented both the amyloid beta and toxic oligomer hypotheses (as it provided the proof many adherents to the theory had been waiting for) and rapidly became one of the most cited works in the field of Alzheimer’s research. Its authors rose to academic stardom, produced further papers validating their initial hypothesis, and billions more were invested by both the NIH and the pharmaceutical industry in research of the amyloid and toxic oligomer hypothesis.
It should be noted that some were skeptical of their findings and likewise were unable to replicate this data, but rarely had a voice in the debate:
“The spotty evidence that Aβ*56 plays a role in Alzheimer’s had [long] raised eyebrows.6 Wilcock has long doubted studies that claim to use ‘purified’ Aβ*56. Such oligomers are notoriously unstable, converting to other oligomer types spontaneously. Multiple types can be present in a sample even after purification efforts, making it hard to say any cognitive effects are due to Aβ*56 alone, she notes — assuming it exists.
In fact, Wilcock and others say, several labs have tried and failed to find Aβ*56, although few have published those findings. Journals are often uninterested in negative results, and researchers can be reluctant to contradict a famous investigator.”
The Amyloid Scandal
At the end of 2021, a neuroscientist physician was hired by investors to evaluate an experimental Alzheimer’s drug and discovered signs that its data consisted of doctored Western Blots (and therefore erroneous assessments of what oligomers were present within research subjects’ brains).7 As he explored the topic further, he discovered other papers within the Alzheimer’s literature had been flagged for containing doctored Western Blots.
Note: Western blots, used to test for proteins, are one of the few easily detectable forms of research fraud (e.g., we discovered Pfizer submitted fake Western blots to regulators to “prove” their vaccine worked). Regrettably, far more undetectable fraud exists throughout the scientific literature (e.g., independent researchers comparing regulatory submissions discovered Pfizer also submitted doctored data on where the COVID vaccine is distributed in the body8).
Before long, the neuroscientist noticed three of those suspect papers had been published by the same author and decided to investigate the author’s other publications. This led him to the seminal 2006 Alzheimer’s publication, which contained clear signs of fraud.9
As investigation then uncovered 20 doctored papers written by the author, 10 of which pertained to Aβ*56 (along with a co-researcher attesting to earlier scientific misconduct by the author).
The Amyloid Industry
One of the remarkable things about this monumental fraud was how little was done about it. For example, the NIH was notified in January 2022, yet in May 2022, beyond nothing being done, the NIH gave the suspect researcher a coveted $764,792 research grant (signed off by another one of the authors of the 2006 paper10).
In July 2022, Science published an article exposing the incident and the clear fraud that had occurred.11 Despite this, the researcher was allowed to remain in his position as a tenured medical school professor.12 It was not until June 2024 that the 2006 article was retracted at the request of the authors13 — all of whom denied being at fault and insisted the doctored images had not affected the article’s conclusions.
Eventually, on January 29, 2025, during his confirmation hearing, RFK cited the paper as an example of the institutional fraud and wasted tax dollars within the NIH, and a few days later, the suspect researcher announced his resignation from the medical school professorship (while still maintaining his innocence).14
This odd behavior (e.g., the medical field continues to insist the proven fraud has not disproven the Amyloid hypothesis) likely results from how much money is at stake — beyond the research dollars, roughly 7 million adults have Alzheimer’s — equating to hundreds of billions in potential (Medicare funded) sales each year.15
The Failed Amyloid Drugs
Recently, a monoclonal antibody that made immune cells target amyloid demonstrated limited success in treating Alzheimer’s — which was embraced as revolutionary by the medical community, the pharmaceutical industry, and drug regulators. In turn, the first new drug received accelerated approval (which the FDA proudly announced).16 The second then received a quiet backdoor approval (due to the immense controversy surrounding the first),17 and the third was partially approved a year and a half later.18
Each year, JP Morgan (Chase Bank) hosts a private conference for pharmaceutical investors that sets the tone for the entire industry. In 2023, its focus (covered in detail here) was on the incredible profitability of the new Alzheimer’s drugs and the GLP-1s like Ozempic (which the FDA has also relentlessly promoted). Most remarkably, the (widely viewed as corrupt) FDA commissioner was a keynote speaker, and a few days before the conference, had enacted the second backdoor approval.
However, despite the rosy pictures painted around the drugs (which each attacked different aspects of amyloids), they were highly controversial as:
• The FDA’s independent advisory panel, in a very unusual move, voted 10-0 (with one abstaining) against approving Aduhelm, the first amyloid drug (which targeted amyloid plaques), but the FDA approved it anyways. In a highly unprecedented move, three of the advisors then resigned, calling it “probably the worst drug approval decision in recent U.S. history.”19
• That drug was priced at $56,000 a year — making it sufficient to bankrupt Medicare, (which attracted a Congressional investigation).20
• Brain swelling or brain bleeding was found in 41% of patients enrolled in its studies.21 Additionally, headaches (including migraines and occipital neuralgia), falls, diarrhea, confusion, and delirium were also notably elevated compared to placebo.
• No improvement in Alzheimer’s was noted; rather one analysis found it slowed the progression of Alzheimer’s by 20% (although this could have been a protocol artifact rather than a real effect).
The second monoclonal antibody (which targeted amyloid precursors) had a somewhat better risk benefit profile22 (only 21% experienced brain bleeding and swelling due to reduced targeting of stable amyloid plaques), and 26.4% reduction in the progression of Alzheimer’s was detected in the trial (which for context, translated to a 0.45 reduction on a scale where a reduction of at least 1 to 2 points is needed to create an impact which is in any way meaningful for a patient).
The third monoclonal (which targeted amyloid plaques thought to be more pathologic)23 was also contested as it caused 36.8% of recipients to develop brain bleeding or swelling, like the other amyloid medications, frequently caused headaches and infusion reactions (e.g., nausea, vomiting, changes in blood pressure, hypersensitive reactions, or anaphylaxis) and there were reasons to suspect the trial had greatly overstated its minimal benefits.
Remarkably, despite widespread protest against the third drug, the FDA’s new advisory panel voted unanimously in favor of it, even though it had a very similar mechanism, efficacy, and toxicity to the previously unanimously rejected amyloid drug.
It should therefore come as no surprise that, when the British Medical Journal conducted an independent investigation, it found that, within publicly available databases, 9 out of 9 (assessable) members of the advisory committee had significant financial conflicts of interest.24
Fortunately, despite the aggressive promotion of amyloid drugs and the industry’s best attempts to promote the sector, the market somewhat recognized how bad they were. The first drug had its price halved (then was withdrawn as no one wanted it — making around 5 million dollars total),25 while the other two have had very modest sales (e.g., 290 million for the most popular one26).
What Amyloids Drugs Show Us
From this, four things stand out:
• These drugs consistently damage brain tissue, indicating that their mechanism of action was inherently dangerous (e.g., it creates brain swelling by causing immune cells attacking amyloid also to attack brain tissue, or it creates brain bleeding by removing amyloid plaque that patches vessel walls and stabilizes brain tissue). Remarkably, despite this issue being recognized, it has not deterred the usage of these class drugs.
• An absolutely absurd amount of money and time has been wasted on this endeavor due to the medical field’s need to find a patentable drug.
• The focus on these lucrative drugs has diverted attention from other (off-patent) treatments that are more likely to help Alzheimer’s patients.
For example, a randomized controlled trial which gave MCTs derived from coconut found that over 6 months,27 80% remained stable or improved — which for context, is better than what any of the amyloid drug trials showed, and more importantly, does not cause brain bleeds (and costs a lot less than the annual rough $30,000 cost for those drugs).
Note: Numerous readers have shared that coconut oil improved their relative’s dementia.
Likewise, very few are aware of a 2022 study that should have revolutionized the entire Alzheimer’s field:28
Dimethyl Sulfoxide (DMSO) is a naturally occurring compound that has a variety of unique healing properties that allow it to rescue tissues from dying and revive those damaged from previous injuries — best demonstrated by decades of evidence showing DMSO can heal strokes, brain bleeds, severe concussions, and spinal cord injuries and save patients from a lifetime of paralysis.
“My uncle’s wife has dementia and has been unable to speak for over a year. My mom recently visited them and told them about DMSO. He began to give his wife DMSO orally. After two weeks she began to talk again.29
I read the article and began giving it to my 93 year old mother in her juice every morning at the end of November. She has had some form of dementia for over 15 years. Since taking the DMSO, she no longer suffers with severe sundowners. She is more ‘with it’ and can communicate and laugh with us. Her personality is back. She is crossing her legs again and lifting her pinky finger when drinking her coffee. It’s a lot of little things that make a difference.
She is able to understand when I am asking her to use the bathroom. She is more cognitive and has started coloring in her coloring books again.30
I deeply appreciate your posts on DMSO. You helped bring spontaneous interaction back into the life of my father with Alzheimer’s.”31
Numerous studies support these experiences:
• When rats had their carotid arteries surgically modified to reduce the blood going to the brain, DMSO prevented both the neuronal damage and the significant loss of spatial memory and learning that otherwise occurred.32
• In a similar study, rats who developed persistent and severe memory impairment from reduced brain blood flow received DMSO and FDP for 7 days, which improved their memory by 54%, nearly reaching the cognitive function rats whose blood flow was never cut off.33,34
• In rats, daily DMSO counteracted memory impairment induced by intracerebroventricular STZ infusions,35 while in a similar study,36 DMSO and Ginkgo biloba improved learning and memory in rats given Alzheimer’s disease.
• Drinking minute amounts of DMSO prevented the visual degeneration otherwise seen in rats engineered to have early Alzheimer’s disease.37 In another study of those rats, it protected key brain cells from disappearing and enhanced both their spatial memory and smell (while decreasing their anxiety).38 Likewise, in rats bred to develop cerebellar disorders, DMSO prevented age-related deterioration of certain cognitive functions (e.g., memory and spatial learning).
These results have also been replicated in humans:
• In 18 patients with probable Alzheimer’s after three months, DMSO greatly improved memory, concentration, and communication, alongside a significant decrease in disorientation in time and space.39
• In 104 elderly adults with dementia due to cerebrovascular diseases, concussions, or Parkinson’s, DMSO combined with amino acids significantly improved their cognition and motor function.40
• In 100 patients with cerebrovascular diseases (many of whom had dementia),41 DMSO caused almost all to have their cardiovascular parameters improve and:
“Recovery from the general symptoms was positive; there were favorable changes which were reflected in a feeling of well being, the recovery of agility, changes of mood from depressed to gay, improvement of sleeping, and clearer speech. As regards the ‘focal’ results, accelerated recovery from hemiplegia and hemiparesia was registered. A speedier recovery of speech in cases of defined or indicated aphasia took place.”
Conclusion
The Alzheimer’s story illustrates how medical science’s relentless focus on commercializable products has failed the country. This must be replaced with prioritizing understanding the root causes of the chronic illnesses we face.
Fortunately, now that MAHA can set national health policy and independent media has broken the media’s monopoly over the truth due to the lies we saw throughout COVID-19, more and more are stepping outside the medical orthodoxy to pursue therapies that can actually heal them. An opportunity like this has never existed before, and it is critical each of us brings attention to the need for real medicine before the window to fundamentally change the practice of medicine closes.
Author’s Note: This is an abridged version of a longer article which discusses the actual causes and treatments for Alzheimer’s disease and the cognitive decline which precedes it. That article, along with additional links and references, can be read here. Additionally, a companion article on how DMSO treats neurological injuries (e.g., strokes, brain hemorrhages, traumatic brain injuries, spinal paralysis, and developmental delay) can be read here.
A Note from Dr. Mercola About the Author
A Midwestern Doctor (AMD) is a board-certified physician from the Midwest and a longtime reader of Mercola.com. I appreciate AMD’s exceptional insight on a wide range of topics and am grateful to share it. I also respect AMD’s desire to remain anonymous since AMD is still on the front lines treating patients. To find more of AMD’s work, be sure to check out The Forgotten Side of Medicine on Substack.
A study of over 10,800 Australians age 70 and older found that people who always listened to music had a 39% lower risk of dementia, while those who often played an instrument had about a 35% lower risk
Those who engaged in both listening and playing music had a 33% lower risk of dementia and a 22% lower risk of cognitive impairment
Music activates multiple brain regions at once, including those tied to memory, movement, and emotion, making it especially useful for supporting recovery and preserving connections in dementia care
Enjoying music at an appropriate volume encourages regular listening, helping you incorporate joyful routines into your daily life
Joining a choir or playing an instrument also builds focus, coordination, and social connection. These factors may help keep your brain strong as you age
In the U.S., approximately 7.2 million adults aged 65 and older are living with Alzheimer’s disease, the most common form of dementia.1 That number is expected to rise to nearly 14 million by 20602 if no breakthroughs emerge. Each new diagnosis means another family navigating memory loss, personality shifts, and the emotional and financial demands of caregiving.
Healthcare costs are enormous and are expected to reach $384 billion in 2025, with unpaid family care valued at over $400 billion.3 With no cure in sight, researchers are turning to lifestyle strategies that may help delay symptoms and protect brain health. One of the areas they’re recently focusing on is music.
How Does Playing an Instrument Influence Dementia Risk in Older Adults?
The connection between music and brain health is gaining scientific attention, and new evidence suggests it may be more powerful than previously thought. A study published in the International Journal of Geriatric Psychiatry,4 led by researchers at Monash University in Australia, explored whether listening to music or playing an instrument could help protect against dementia and cognitive decline in people aged 70 and older.
• Researchers studied 10,893 Australians age 70 and older — The researchers examined data from participants enrolled in the ASPREE (ASPirin in Reducing Events in the Elderly) study and the ALSOP (ASPREE Longitudinal Study of Older Persons) sub-study. These large Australian cohorts followed older adults over time to track health outcomes. The participants were dementia-free at enrollment.
The team collected information on the subjects’ music-related habits, particularly how often they listened to music or played an instrument, and tracked cognitive health for several years. The goal was to see if these habits predicted dementia, cognitive impairment no dementia (CIND), and changes in thinking skills over time.5
• Frequent music listening showed the strongest protection — Participants who always listened to music had a 39% lower risk of developing dementia and a 17% lower risk of CIND compared to those who rarely or sometimes listened.6 They also maintained higher scores in global cognition and memory, which are key for everyday tasks such as recalling events and making decisions. Other cognitive domains, such as attention and language, did not show improvement.
• Playing an instrument offered benefits — Older adults who often or always played an instrument had a 35% lower risk of dementia.7 However, this activity was not linked to reduced CIND risk or improvements in cognitive test scores over time. Researchers suggest that while playing music may help, listening appears to have a more consistent effect on brain health.8
• Combining listening and playing gave additive benefits — Those who engaged in both listening and playing music had a 33% lower risk of dementia and a 22% lower risk of CIND.9 Lead author Emma Jaffa, an honors student in the School of Public Health and Preventive Medicine at Monash University, explained:
“These findings suggest music activities may be an accessible strategy for maintaining cognitive health in older adults, though causation cannot be established.”10
• Education level influenced the impact of music — The protective effects of music were most potent in participants with 16 or more years of education, while results were mixed for those with 12 to 15 years.11 Researchers believe this may relate to cognitive reserves, the brain’s ability to compensate for aging, where higher education combined with music engagement offers greater protection.
• No improvement in perceived mental sharpness — Despite objective gains in memory and global cognition, participants did not report feeling mentally sharper. This highlights a gap between clinical measures and personal perception, suggesting that lifestyle habits can improve brain health even if people don’t notice the changes.12
“Evidence suggests that brain aging is not just based on age and genetics but can be influenced by one’s own environmental and lifestyle choices,” senior author Professor Joanne Ryan, head of the Healthy Ageing Research Program at Monash University, said. “Our study suggests that lifestyle-based interventions, such as listening and/or playing music, can promote cognitive health.”13
Here’s a quick overview of the study findings, showing how everyday music habits were linked to memory and dementia risk in older adults:
Music habit
Risk reduction (%)
What this means
Listening to music most days
39% lower risk of dementia, 17% lower risk of CIND
Regular listening lowered dementia risk and slowed cognitive decline
Playing a musical instrument often
35% lower risk of dementia
Playing an instrument may support brain health, but the benefits were limited
Listening to music and playing an instrument
33% lower risk of dementia, 22% lower risk of CIND
Combining both activities showed strong protection
Dementia Isn’t Just ‘Getting Older’
According to the Alzheimer’s Association, dementia is “a general term for loss of memory, language, problem-solving, and other thinking abilities that are severe enough to interfere with daily life.”14 It’s sometimes called “senility,” a term based on the outdated belief that serious mental decline is a regular part of aging. But in reality, dementia reflects disease-related changes in the brain, not aging itself.15
Although they’re often confused for each other, dementia is not the same as Alzheimer’s disease. Rather, dementia is the umbrella term for conditions that cause cognitive decline, and Alzheimer’s is the most common type.
• Alzheimer’s accounts for about 60% to 80% of dementia cases — The next most common cause is vascular dementia, which develops when blood flow to the brain is reduced due to damaged or blocked blood vessels.
Some people experience changes linked to more than one type of dementia at the same time, known as mixed dementia. Other health issues can cause memory and thinking problems that look like dementia but aren’t permanent, including thyroid disorders and vitamin deficiencies.16
• What happens in the brain when you have dementia — Dementia begins when nerve cells in the brain (neurons) and their connections start breaking down. In Alzheimer’s disease, this process is driven by the buildup of sticky protein deposits called plaques, as well as twisted fibers called tangles, which disrupt communication between neurons.17
Over time, these changes shrink brain tissue and damage areas responsible for memory, reasoning, and language. These changes occur gradually, often taking years before symptoms appear.
• Dementia progresses in stages — In the early stage, people can still manage most daily tasks but may need reminders for appointments. The confusion becomes worse during the middle stage, and managing finances or cooking becomes difficult; help with dressing or bathing may be needed as well. During the late stage, independence is diminished as individuals frequently need full-time assistance with eating, using the bathroom, and moving around.18
• Risk factors you should know — Age is the most substantial risk factor, with most cases developing after the age of 65. Family history also plays a role, especially if a parent or sibling has dementia. Heart health matters too, as high blood pressure, diabetes, and smoking damage blood vessels and increase risk. Lifestyle factors such as physical inactivity, poor diet, and social isolation further raise vulnerability.19
When you listen to music, your brain lights up in several areas at once,20 including the auditory cortex that processes sounds, the limbic system that handles emotions, and the motor cortex, which is involved with movement. This “whole-brain” activation is powerful because most therapies only stimulate one or two regions. This is why music is gaining ground in hospitals and clinics, where it’s used as a tool to not just help patients pass the time but also support healing.21
• People with brain conditions often benefit the most — In people with brain injuries or neurodegenerative diseases, music stimulates key brain regions tied to memory, emotion, movement, and speech. One powerful example comes from patients recovering from a stroke. Those who struggle to speak may be able to regain words by singing. Using melody and rhythm also helps retrain the brain’s speech pathways22 when regular speech therapy isn’t enough.
• Music quickly calms the body — Slow, steady music can help your body relax by syncing with its natural rhythms. This gentle pace signals your parasympathetic nervous system, the part responsible for the “rest and digest” state. When that kicks in, your heart rate slows, blood pressure drops, and tense muscles start to loosen.23
• Music may protect the brain in multiple ways — A study published in Aging & Mental Health found that musicians were 64% less likely to develop mild cognitive impairment or dementia.24 Another study published in BMC Neurology suggests this protection may come from several overlapping effects, including improved executive function and working memory, enhanced brain plasticity, sensorimotor repair, reduced stress and depression, and increased social engagement.25
• Music’s benefits are evident in people already living with dementia — A study published in International Psychogeriatrics found that 39 residents in long-term care facilities in Iowa who listened to individualized music playlists experienced a significant reduction in agitation, including shouting and irritability, both during and after listening sessions. These benefits were more pronounced compared to when residents listened to generic classical relaxation music.26
• The link between music and the prefrontal cortex — Located behind the forehead, the medial prefrontal cortex is one of the last brain regions to deteriorate in Alzheimer’s disease, and it is strongly activated by music. Petr Janata, Ph.D., from the UC Davis Center for Mind and Brain, mapped brain activity while people listened to familiar music and explained:27
“What seems to happen is that a piece of familiar music serves as a soundtrack for a mental movie that starts playing in our head. It calls back memories of a particular person or place, and you might all of a sudden see that person’s face in your mind’s eye. Now we can see the association between those two things — the music and the memories.”
• Music deserves a place in healthy aging strategies — Researchers from the University of Exeter believe music should be included in strategies to support healthy aging and reduce dementia risk. They recommend encouraging adults to sing, take part in community music groups, or return to instruments they played earlier in life.28
“Public health interventions to promote healthy aging and dementia risk reduction should consider including advice for adults on engaging with music … There is considerable evidence for the benefit of music group activities for individuals with dementia, and this approach could be extended as part of a healthy aging package to proactively reduce risk and promote brain health,” they concluded.
How to Start Building a Dementia-Friendly Music Routine
Making music part of the daily routine doesn’t have to be complicated. Whether you’re caring for someone with dementia or creating your own brain-supportive habits, these steps will help you build a simple, personalized music routine that fits into daily life and supports long-term well-being:
• Make time for music every day — This can be listening to your playlist, singing along, or playing a simple instrument. Start small and build up gradually. The goal is to make music a regular, enjoyable part of your routine so it feels familiar and comforting.29
• Build a personalized playlist of favorite songs — Start picking out favorite songs you would hum and dance to. Familiar music helps spark memories, reduce anxiety, and improve mood for people with dementia. These tunes create comfort and connection, making sessions more enjoyable and effective.30
• Keep the environment calm — Pick a quiet room with minimal distractions. Use a comfortable chair and the listening method that feels best, whether it’s speakers or headphones. A quiet setting lowers stress and helps you focus on the music.31
• Be considerate of the loudness — Keep the volume comfortable and avoid sudden changes in tempo or loudness. Pausing between songs can help prevent overstimulation, while gentle pacing ensures the experience remains soothing for you.32
• Get active, then get social — When listening becomes comfortable, start with simple activities such as tapping a beat, humming, or singing along. Participating in a local singing group can also foster social connections.
• Review weekly and make changes — At the end of each week, look at what worked best. Which songs felt good? Was the session too long or too short? Was the room comfortable? Keep the things that helped and remove anything that caused stress. This makes your routine easier to follow and more enjoyable.
6 steps to build a music routine
1. Make time for music you love
2. Curate a playlist of your favorite songs
3. Set the mood for easy listening
4. Don’t turn up the volume too much
5. Move while you listen, enjoy meeting people
6. Track what worked best for you
4 Ways to Bring More Music into Your Life
If you already listen to music regularly, you can make it an even bigger and more meaningful part of your daily routine with these four tips:
1. Play an instrument — If you’ve ever wanted to learn an instrument, this is a great time to begin. Don’t worry about getting it right on the first try. Start with a few chords, a simple rhythm, or a beginner keyboard app. Even simple strumming on a guitar or tapping a drum gives your brain a workout while offering a sense of accomplishment and joy.
2. Use music to connect — Join a choir, attend a drum circle, or simply sing with friends or family. Shared music sparks bonding hormones like oxytocin, easing feelings of isolation and boosting emotional resilience. Plus, it’s fun — and fun is healing. These moments of connection can be especially meaningful for caregivers and loved ones navigating cognitive changes together.
3. Practice mindful listening — Instead of letting music fade into the background, choose one song and give it your full attention. Close your eyes, breathe deeply, and let the sound wash over you. This focused listening activates brain circuits that reduce stress, restore balance, and help you feel more centered and calmer — a simple ritual that can transform your day.
4. Reset your rhythm when life feels off track — If your sleep or energy feels out of sync, try listening to steady, rhythmic music at the same time each day, such as right after waking or before bed. Rhythm helps your brain re-establish patterns, regulate your internal clock, and create a sense of predictability that feels comforting and grounding. Think of it as a gentle reset button for your mind and body.
Music isn’t about hitting every note perfectly or remembering every lyric. It can also be about laughing when you miss a beat, sharing a song with someone else, and finding comfort in familiar melodies that bring you back to yourself. These moments nourish your brain, lift your spirit, and strengthen bonds that no diagnosis can erase. If you want to learn more about music’s profound ability to heal, check out “Harnessing the Healing Power of Music.”
Frequently Asked Questions (FAQs) About Music and Dementia
Q: Does listening to music every day lower dementia risk?
A: Yes. In a large study of adults aged 70 and older, people who always listened to music had a 39% lower risk of dementia and a 17% lower risk of cognitive impairment compared to those who didn’t listen as frequently.
Q: Is playing a musical instrument protective against dementia?
A: Yes. Older adults who often played an instrument showed about a 35% lower risk of developing dementia, although the benefits for specific thinking skills were less consistent than with listening.
Q: What kind of music works best for people with Alzheimer’s disease?
A: There’s no single “best” genre. Music that feels familiar and emotionally meaningful tends to work best, especially songs from earlier life that can spark memories and create a sense of calm and comfort.
Q: How often should older adults listen to music for brain health?
A: The biggest benefits were seen in people who listened regularly instead of occasionally. Making music a daily habit appears more important than the length of each session.
Q: Can music help reduce agitation or sundowning in dementia?
A: Yes, it can. Studies described in the article show that personalized music listening reduced agitation, anxiety, and irritability in people with dementia, especially compared to generic background music.
Q: Does singing in a choir help memory in older adults?
A: Singing in a choir may be helpful because it combines music with social interaction, focus, and routine. Researchers highlight group music activities as a promising way to support healthy aging and cognitive resilience.
Q: Is it too late to start learning an instrument to help the brain?
A: No. Starting later in life can still be beneficial. Even simple instruments or beginner practice engage attention, coordination, and creativity, all of which support brain health.
Q: How does music affect memory centers in the brain?
A: Music activates several brain networks at once, including those tied to memory, emotion, and attention. Familiar music strongly stimulates the medial prefrontal cortex, a region that often remains active longer in Alzheimer’s disease.
Q: What’s the difference between music therapy and casual listening?
A: Casual listening is informal and self-guided, like enjoying a favorite playlist at home. Music therapy is more structured and intentional, often used in care settings to support mood, behavior, or neurological recovery.
Q: Are there any risks to using music for people with dementia?
A: The main concern is overstimulation. Keeping the volume low, choosing familiar songs, avoiding sudden changes, and stopping if distress appears helps make music a beneficial and soothing experience.
Obesity increases Alzheimer’s risk by altering how fat-derived vesicles communicate with the brain, causing amyloid proteins to misfold and form toxic plaques that damage neurons and impair cognition
Specific lipids from obese individuals, including sphingolipids and ceramides, create oxidative stress in brain cells, reduce mitochondrial energy production, and accelerate the formation of sticky amyloid aggregates
Excessive fat consumption promotes Alzheimer’s development, though balanced, controlled intake at lower concentrations helps inhibit amyloid aggregation and reduce disease risk
Leptin resistance from obesity prevents this protective hormone from reaching the brain, disabling the cleanup process that normally breaks down amyloid proteins while worsening inflammation and cognitive decline
Cellular health restoration requires eliminating four key factors — excess linoleic acid from vegetable oils, endocrine-disrupting chemicals, electromagnetic fields, and endotoxins in the gut
Despite advances in health care, the obesity epidemic in America continues to worsen. According to the latest data from the Centers for Disease Control and Prevention (CDC), 40.3% of adults are already obese,1 and nearly 7 out of 10 U.S. adults meet the criteria for obesity under a new, more comprehensive definition published in JAMA Network Open.2
The new standard — previously proposed by an international panel of experts in The Lancet Diabetes & Endocrinology3 — goes beyond body mass index (BMI) to include waist and hip measurements that reveal hidden fat conventional BMI misses.
The implications of these figures are serious, as excess body fat increases the risk of other health complications, such as diabetes and stroke.4
Now, new research shows that obesity is also a risk factor in the development of Alzheimer’s disease.5 Based on the findings, excess body fat alters how amyloid proteins fold, causing them to clump and eventually cause cognitive issues.6
Obesity Drives Brain Plaque Formation Through the Vesicles
In a study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, researchers investigated how fat tissue communicates with the brain through microscopic particles known as vesicles. These are tiny cellular packages inside or outside the cell, and they carry fats, proteins, and genetic material.
The study’s focus was on whether these vesicles, released from human fat cells, influence the buildup of amyloid plaques — sticky clusters of protein thought to play a role in the development of Alzheimer’s disease.7
The researchers analyzed vesicles from adults with varying body fat levels and looked at how the fat-derived particles affected the behavior of amyloid proteins. Amyloid proteins are normally harmless, but when they begin to clump together, they form plaques that interfere with neuron communication.
• Obesity is a risk factor for Alzheimer’s disease — The team found that vesicles taken from people with more body fat changed the way amyloid molecules are assembled. These altered vesicles made amyloid clump faster and form denser, more toxic structures that are harder for the brain to clear away.
What makes this finding important is that it shows how your body fat obstructs cellular communication. The study revealed that when fat cells are overloaded, they send distorted signals through your vesicles. These signals carry lipids that change how brain proteins behave. In this case, those changes accelerate Alzheimer’s disease.
• The specific lipids inside the vesicles were not random — Obese individuals had vesicles rich in certain sphingolipids and ceramides — types of fats that directly influence inflammation and cell death. These compounds act like biological irritants, creating oxidative stress in neurons. Over time, that environment makes it easier for amyloid to stick together.
• The researchers also explored how these vesicles affect brain cells in a controlled lab setting — When human neural cells were exposed to vesicles from obese individuals, they observed increased cellular stress and decreased mitochondrial activity.
As you know, mitochondria are the cell’s energy factories. When they slow down, neurons lose energy, and their ability to process and clear waste — like amyloid — drops sharply. This loss of cellular energy is the same foundational issue that drives many chronic diseases, from diabetes to neurodegeneration.
• The study uncovered that these vesicles alter how amyloid folds at the molecular level — Normal amyloid proteins are flexible, but once these lipid-filled vesicles interact with them, the proteins take on a rigid structure — an abnormal configuration known to trigger plaque formation. This misfolding is what makes amyloid sticky, causing it to glue together into toxic aggregates that choke neurons.
Essentially, the lipid content of your fat vesicles rewires the shape of a brain protein that determines whether your neurons stay healthy or die.
• Too much fat of any kind is harmful — Another notable observation made by the researchers is how both saturated fat and unsaturated fat, at high levels, drive Alzheimer’s disease. In other words, even if you think you’re getting healthy fat from your diet, too much of it will eventually cause a reaction similar to consuming unhealthy fat:8
“[T]he convergent finding is that both saturated and unsaturated fatty acids can promote Aβ fibrillization at relatively high concentrations approaching lipotoxic conditions.”
• Striking a balance in fat consumption is important — In relation to the point above, controlling your fat intake can lower the risk of Alzheimer’s disease. According to the researchers:9
“Crucially some lipids exhibit concentration-dependent biphasic effects — promoting aggregation at higher levels yet inhibiting it at lower doses — highlighting the need for nuanced control of lipid microenvironments when considering therapeutic interventions or interpreting disease mechanisms.”
Another Study Examines the Obesity Angle of Alzheimer’s Disease
In a paper published in the International Journal of Molecular Sciences, researchers analyzed how obesity-driven changes in leptin directly increase the risk of dementia and Alzheimer’s disease. For context, leptin is a hormone produced by your body’s fat tissue that signals when you have eaten enough. From there, they focused on a concept called leptin resistance, which “perpetuates diseases such as dementia.”10
• What happens to your body when it begins to resist leptin — The researchers noted that leptin is strongly linked to impaired memory, slower learning, and higher risk for brain degeneration. Normally, leptin travels through the bloodstream to the brain, where it interacts with neurons in areas responsible for memory and learning, such as the hippocampus.
In healthy individuals, leptin supports the formation of new connections between brain cells and protects neurons from stress. But in people with obesity, the brain ignores leptin. The result is a double whammy — hunger control worsens, leading to more weight gain, while the brain loses one of its key protective hormones.
• Leptin influences how brain cells handle amyloid-beta — In normal conditions, leptin helps reduce amyloid levels by activating a cleanup process that breaks the protein down. However, once leptin resistance sets in, that cleanup machinery stalls. Amyloid proteins then start clumping faster, disrupting neural communication and fueling inflammation throughout the brain.
• Your weight plays a role in the secretion of leptin — The researchers showed that leptin production is affected by fat mass, and once your body becomes resistant to it, your risk of Alzheimer’s disease increases:11
“It has been shown that leptin is secreted by adipocytes and circulates in plasma in proportion to fat mass, and changes in body weight are associated with the possibility of developing AD [Alzheimer’s disease]. Therefore, it is not surprising that different investigations try to relate dysfunctional levels in leptin signalling with AD.
Thus, in some studies, low plasma leptin levels in old age have been found to be associated with an increased risk of cognitive decline and AD development.”
• Inflammation drives leptin resistance — As found in another study, obesity creates low-grade inflammation throughout the body.12 With this in mind, the featured study noted that this chronic state prevents leptin from crossing the blood-brain barrier (BBB) and into the central nervous system (CNS):13
“Low-grade inflammation due to obesity drives human C-reactive protein (CRP) production by hepatocytes in vitro and in vivo in humans. It has been found that peripheral human CRP can reduce the amount of human leptin that enters the CNS, preventing its transport across the BBB and into the median eminence. Furthermore, once inside the CNS, it reduces the physiological function of human leptin.”
When it comes to managing obesity, the usual advice is to “eat less and move more.” However, this glosses over many important things that need to be addressed to help you lose weight effectively. The real issue runs deeper than restricting calories — it’s a cellular energy dysfunction. At its core, your mitochondria aren’t working efficiently, and that’s what drives stubborn fat, constant hunger, and low energy.
Fortunately, there’s hope to turn things around. You can rebuild your cellular health by targeting what’s interfering with it. As I discuss in my book “Your Guide to Cellular Health,” there are four major factors involved. I call them the Four E’s:
•Estrogen overload and endocrine-disrupting chemicals (EDCs)
•Electromagnetic fields (EMFs)
•Endotoxins from an unhealthy gut
Together, these elements act like toxins that suffocate your mitochondria and throw your metabolism into chaos. When you clear them out, your body’s natural energy systems start working again. Here’s how to do it, step-by-step.
1. Minimize vegetable oil intake — Seed oils are hiding everywhere, such as in restaurant meals, processed snacks, “healthy” dressings, and baked goods. These oils are loaded with LA, a toxin that damages your mitochondria when eaten excessively. Once your mitochondria are saturated with LA, your body can’t burn fuel efficiently, and fat begins to oxidize and impact cellular function. To start reversing the damage of LA:
•Eliminate industrial vegetable oils such as canola, soybean, sunflower, safflower, corn, and grapeseed from your pantry.
•Next, replace them with metabolically friendly fats like grass-fed butter, tallow, and ghee.
•Avoid conventionally grown chicken and pork, which are often high in LA due to their ultraprocessed feed.
•Cook your own food using healthy fats since most restaurants use vegetable oils.
•Check ingredient labels carefully — vegetable oils lurk in items like almond butter, hummus, and gluten-free chips.
Reducing LA intake is one of the fastest ways to improve mitochondrial efficiency and shift your metabolism from storing fat to burning it. I recommend keeping your overall consumption below 5 grams a day, but if you can keep it below 2 grams, that’s even better.
2. Cut back exposure on endocrine disruptors — Excess estrogen affects everyone. Too much of it interferes with thyroid function and suppresses mitochondrial activity. EDCs, which are synthetic chemicals that mimic estrogen, make the problem worse. They’re found in plastics, receipts, cosmetics, tap water, and even certain medications. You can reduce your exposure from EDCs by making a few key swaps:
•Use glass and/or stainless-steel containers instead of plastic. In addition, never heat your food in plastic.
•Choose natural personal care products without chemical fragrances or parabens.
•Limit exposure to synthetic estrogens found in birth control pills and hormone replacement therapies.
•Support hormonal balance by maintaining adequate progesterone levels — progesterone counteracts excess estrogen and promotes healthy metabolism.
3. Shield your cells from EMF damage — Electromagnetic fields emitted by cellphones, 5G towers, Wi-Fi routers, and Bluetooth devices interfere with how your cells handle calcium. Essentially, too much intracellular calcium triggers oxidative stress. You can protect yourself from EMFs with these lifestyle changes:
•Keep your phone in airplane mode when not in use, especially during your sleep.
•Turn off Wi-Fi at night and move electronics out of your bedroom.
•Choose wired internet connections whenever possible.
•Avoid Bluetooth earbuds that constantly bathe your brain in invisible radiation.
•Spend time grounding outdoors. This means walking barefoot on soil or sand to help discharge excess electrical stress naturally.
4. Repair your gut to reduce endotoxins —Gut health is an important pillar of optimal wellness, as it influences every aspect of your metabolism. When harmful bacteria overgrow, they release endotoxins — compounds that damage mitochondria and trigger inflammation throughout your body. This gut-driven toxicity slows metabolism and disrupts energy balance. To fix your gut, follow these recommendations:
•If you have gut problems, temporarily avoid high-fiber foods since fiber feeds bad bacteria in a damaged gut.
•Focus on simple, gentle carbohydrates like ripe fruit and white rice until symptoms calm down. Aim for 200 to 250 grams of healthy carbohydrates a day.
•Once your digestion stabilizes, gradually reintroduce cooked vegetables, roots, and starches. These feed beneficial bacteria that produce short-chain fatty acids like butyrate, which strengthen the gut lining and restore healthy immune balance.
Frequently Asked Questions (FAQs) About Obesity’s Influence on Alzheimer’s Disease
Q: How does obesity increase the risk of Alzheimer’s disease?
A: Obesity alters how the body communicates at the cellular level. Fat cells release vesicles, which are microscopic carriers of fats and proteins, that distort how brain proteins fold. These changes cause amyloid proteins to clump faster and form plaques in the brain, disrupting neuron communication and contributing to Alzheimer’s disease development.
Q: What role do vesicles and lipids play in Alzheimer’s disease?
A: Vesicles from obese individuals are high in harmful fats such as sphingolipids and ceramides, which promote inflammation and oxidative stress in the brain. These conditions make amyloid proteins more likely to stick together and form toxic plaques, accelerating neurodegeneration.
Q: How does leptin resistance connect obesity to dementia?
A: Leptin is a hormone that regulates hunger and supports brain health. In obesity, the brain becomes resistant to leptin, reducing its protective effects. This leads to impaired memory, slower learning, and an increased buildup of amyloid proteins, all of which heighten the risk for Alzheimer’s disease.
Q: What lifestyle factors can worsen or improve brain health related to obesity?
A: Excessive fat intake — whether from healthy or unhealthy sources — can promote harmful amyloid buildup. Balancing fat consumption and reducing obesity-related inflammation are key. Moreover, addressing cellular energy dysfunction through healthier mitochondrial function can protect both metabolic and brain health.
Q: What practical steps can help prevent obesity-related brain damage?
A: Addressing the four E’s will help manage obesity and restore optimal cellular health:
•Excess linoleic acid — Reduce intake to less than 5 grams per day.
•Endocrine disruptors (EDCs) — Products such as plastics hamper thyroid function.
•Electromagnetic field (EMF) exposure — Radiation emitted from these devices affects intracellular calcium, resulting in oxidative stress.
•Endotoxins — Harmful bacteria release these toxic byproducts, affecting mitochondrial function. Repair gut function to minimize production.
New research shows that people with Alzheimer’s have higher cortisol levels and a skewed cortisol-to-DHEA-S ratio, revealing that chronic stress drives early brain degeneration long before memory loss appears
Cortisol, your body’s main stress hormone, damages neurons and disrupts energy metabolism when it stays elevated, while DHEA-S acts as a protective neurosteroid that helps your brain resist inflammation and oxidative stress
Bioenergetic researcher Georgi Dinkov connected these findings to thyroid and metabolic health, showing that when your cells don’t produce enough energy, cortisol rises and accelerates cognitive decline
Tracking your cortisol-to-DHEA-S ratio offers a powerful early warning sign for chronic stress and neurodegeneration, allowing you to take preventive action years before symptoms develop
You can rebalance these hormones naturally by fueling your metabolism with adequate healthy carbohydrates, improving sleep and light exposure, reducing overtraining, practicing calming breathwork, and using natural progesterone to help quiet cortisol
Alzheimer’s disease doesn’t begin with memory loss — it begins years earlier with a slow, silent shift in your body’s stress chemistry. Long before neurons die, your brain’s hormonal balance starts to erode under constant pressure from everyday stress. The same hormones that once kept you alert and focused start working against you, wearing down your brain’s repair systems and disrupting the flow of energy your cells depend on.
Cortisol, the body’s main stress hormone, plays a central role in this process. When it stays high for too long, it drains your metabolic reserves and interferes with memory formation. Meanwhile, a second hormone called DHEA-S acts as cortisol’s natural counterbalance, helping protect neurons and stabilize brain function.
When the ratio between these two hormones tilts toward cortisol, your brain loses its resilience and becomes more vulnerable to aging and degeneration. This hormonal tug-of-war — shaped by stress, diet, and metabolism — has drawn new attention from researchers exploring why some people develop Alzheimer’s while others do not. The latest findings suggest that long-term hormonal imbalance, not just genetics or plaque buildup, could be one of the earliest warning signs of decline.
Understanding this relationship changes how you think about prevention. By strengthening your metabolism, restoring hormonal balance, and reducing chronic stress, you can support your brain’s ability to heal and adapt — long before symptoms appear. The new research provides a roadmap for how to start.
Stress Hormones Tip the Balance Toward Alzheimer’s
A clinical study published in Cureus examined 85 adults in Serbia — 45 with diagnosed Alzheimer’s disease and 40 healthy peers of similar age and sex — to determine how two hormones, cortisol and DHEA-S, relate to brain health.1 Cortisol is your body’s main stress hormone, while DHEA-S (dehydroepiandrosterone sulfate) acts as its built-in counterbalance — a neurosteroid that supports brain resilience and energy metabolism.
Unlike DHEA, which is the fast-acting, active form, DHEA-S is its sulfated storage form that circulates in your blood far longer and provides a more stable picture of long-term stress balance. By focusing on DHEA-S, the researchers could better gauge chronic stress effects on the brain rather than short-term fluctuations. The scientists wanted to know whether Alzheimer’s patients showed measurable differences in these hormones or in their ratio, which indicates how well your body manages prolonged stress.
• People with Alzheimer’s had higher cortisol levels but not lower DHEA-S — Those with Alzheimer’s showed cortisol levels averaging nearly 399 nanomoles per liter (nmol/L) — about 20% higher than healthy adults — yet their DHEA-S concentrations stayed roughly the same.
This imbalance means the stress response remains chronically activated without the brain’s natural protection. When cortisol dominates, neurons experience more inflammation and less regeneration. The study also noted that this skewed balance was strongest among participants aged 65 to 75, suggesting that middle-to-late adulthood is when stress hormones begin exerting their most damaging effects.
• The cortisol-to-DHEA-S ratio proved to be the real warning sign — Although each hormone alone tells part of the story, the researchers emphasized that their ratio — how much cortisol outweighs DHEA-S — offers a clearer window into chronic stress and brain decline.
In Alzheimer’s patients, that ratio climbed steeply, implying that the body’s defense system against cortisol’s toxicity was failing. This finding helps explain why some people with normal cortisol readings still experience cognitive decline: it’s the imbalance, not just the level, that matters.
• Men and women responded differently, revealing hormonal sensitivity — In healthy adults, men had significantly higher DHEA-S levels than women, meaning their brains could have greater protection from chronic stress. But that sex difference disappeared in those with Alzheimer’s.
The disease seemed to override normal hormonal patterns, flattening DHEA-S levels in both sexes. This means that once neurodegeneration begins, your brain’s ability to maintain hormonal balance — one of its self-defense tools — breaks down.
• Age changed the picture again, suggesting a nonlinear hormonal response — When researchers divided participants by age, they noticed that younger Alzheimer’s patients (60 to 65) had higher DHEA-S levels, which dropped sharply in the 66 to 75 group before rising again after age 75.
This unexpected curve points to a possible window of hormonal collapse, where midlife stress overwhelms the body’s compensatory systems. If you’re in this age range and facing chronic stress, that’s when intervention — stress reduction, adequate rest, and metabolic support — could be most protective for your brain.
Cortisol Acts Like an Overzealous Cleanup Crew That Damages What It’s Meant to Protect
Elevated cortisol increases inflammation and oxidative stress — chemical reactions that corrode neurons and disrupt communication between brain cells. It also suppresses the growth of new neurons in your hippocampus, the brain’s memory center, making it harder to store new information.
In contrast, DHEA-S supports neuronal survival, enhances energy metabolism, and shields brain tissue from the harmful effects of excessive cortisol. When cortisol wins this hormonal tug-of-war, brain networks lose their flexibility and begin to deteriorate.
• Why stress and memory loss are so tightly linked — Chronic cortisol elevation interferes with glucose uptake in brain cells, depriving them of the fuel needed to form memories. It also increases amyloid-beta and tau accumulation — the same proteins that define Alzheimer’s pathology.
Meanwhile, DHEA-S helps counter these effects by enhancing insulin sensitivity and calming overactive immune responses in your brain. In simple terms, one hormone burns your mental circuits, the other repairs them.
• A new biological marker for early intervention — Instead of waiting for memory loss or imaging changes, tracking your cortisol-to-DHEA-S ratio could signal early stress damage years before cognitive symptoms arise.
If your cortisol stays high while DHEA-S falls or stagnates, that’s a red flag. Supporting your metabolic health, prioritizing quality sleep, and restoring hormonal balance could help keep your brain’s internal environment stable long before Alzheimer’s develops.
Lowering Cortisol and Raising Metabolic Energy Could Reverse Brain Decline
In a commentary, bioenergetic researcher Georgi Dinkov analyzed the Cureus study showing that people with Alzheimer’s disease had significantly higher cortisol levels and a skewed cortisol-to-DHEA-S ratio compared to healthy adults.2 He explained that these results validate decades of bioenergetic research linking chronic stress, low metabolism, and neurodegeneration.
Dinkov emphasized that it’s not just elevated cortisol that drives decline — it’s the imbalance between cortisol and protective steroids such as DHEA, testosterone, and progesterone. When this ratio tips toward cortisol dominance, your body remains in a chronic “fight-or-flight” state that accelerates tissue breakdown and cognitive loss.
• Dinkov connected the findings to thyroid-driven metabolic stress — Building on the Cureus data, Dinkov explained that hypothyroidism — a sluggish thyroid that slows metabolic energy production — creates the same hormonal pattern seen in Alzheimer’s patients: high cortisol and suppressed DHEA–S.
When your metabolism slows, your body compensates by ramping up stress hormones to stay alert and energized. But this backfires over time, leading to chronic brain inflammation, poor glucose uptake, and reduced adenosine triphosphate (ATP) production — the energy currency your brain depends on.
• Your cortisol-to-DHEA-S ratio predicts long-term health better than any single hormone — According to Dinkov, this ratio — spotlighted by the Cureus research — is among the strongest predictors of all-cause mortality and neurodegenerative risk. Even when cortisol fluctuates throughout the day, the ratio reveals whether your stress and repair systems are balanced.
Dinkov suggested measuring cortisol and DHEA-S in hair or nails rather than blood, since these tissues reflect long-term hormonal patterns. For anyone trying to gauge chronic stress or cognitive risk, this offers a simple, objective biomarker that’s far more reliable than a one-time blood test.
• Natural compounds help restore hormonal balance and metabolic strength — Dinkov referenced several well-known substances — aspirin, niacinamide (vitamin B3), progesterone, pregnenolone, thyroid support, glycine, and emodin — that help correct the same imbalance observed in the Cureus study. These compounds work by lowering excess cortisol, improving mitochondrial energy output, and supporting the production of protective hormones.
Niacinamide, for instance, increases NAD+, which fuels cellular repair, while aspirin dampens inflammation and cortisol overproduction. Used together, these tools shift your body back into a “rest-and-repair” mode rather than the constant stress chemistry that drives brain aging.
• DHEA acts as a built-in cortisol regulator — Dinkov explained one of the key ways DHEA helps keep cortisol in check: it blocks the enzyme that turns inactive cortisol back “on” and boosts the one that clears excess cortisol from your body. This dual action makes DHEA a natural cortisol buffer that prevents the overactivation of stress pathways.
In other words, DHEA gives your brain a biochemical “cooling system,” stopping cortisol from overheating your neurons. Supporting DHEA through thyroid health, nutrition, and targeted supplementation helps restore this essential balance.
• Stress is a symptom of low energy, not just emotional strain — Dinkov described how the elevated cortisol levels observed in the Cureus Alzheimer’s cohort represent a deeper issue: energy failure. When your cells don’t make enough ATP — whether from poor thyroid output, nutrient deficiencies, or aging — they turn to cortisol to compensate.
The hormone breaks down tissue to release fuel, but that process worsens energy depletion over time. This self-reinforcing loop explains why chronic stress feels endless: it’s a metabolic, not psychological, trap. Dinkov concluded that maintaining a low cortisol-to-DHEA-S ratio protects more than memory — it sustains whole-body resilience.
People who keep this ratio balanced experience better sleep, stable mood, and slower biological aging. His message is practical: by restoring thyroid function, eating enough to prevent energy deficits, and lowering chronic inflammation, you directly influence the biochemical environment that determines whether your brain decays or endures.
Rebuild Your Energy System to Lower Cortisol and Protect Your Brain
If you wake up tired, crash midafternoon, or feel wired when you should be asleep, your body’s stress chemistry has taken over. The Cureus study3 and Dinkov’s review4 both point to the same conclusion: your brain suffers when your cells can’t make enough energy.
To fix that, you have to restore steady fuel, retrain your stress response, and help your body recognize that it’s no longer in survival mode. Here’s how to bring your hormones — and your energy — back into balance:
1. Feed your metabolism the fuel it’s been missing — Cutting carbs keeps your body trapped in a constant stress loop because cortisol spikes whenever blood sugar drops too low. Break that pattern by eating enough healthy carbohydrates — around 250 grams daily — to give your mitochondria a steady energy supply.
Start with gentle foods like fruit and white rice. When your digestion feels stable (no bloating or irregularity), add cooked root vegetables, then more vegetables, legumes, and well-tolerated whole grains. Once your body trusts it’s being fed regularly, cortisol naturally declines, and your energy and focus stabilize.
2. Move in ways that restore instead of deplete — Overdoing endurance exercise or high-intensity intervals keeps your body in fight-or-flight mode long after the workout ends. Cortisol stays elevated, recovery slows, and sleep suffers.
Replace long, punishing sessions with physical activities that build energy rather than drain it — strength training, walking outdoors, dancing, or swimming at an easy pace. Use how you feel afterward as your guide: if you finish feeling grounded and calm, you’ve helped your hormones, not hurt them.
3. Train your nervous system to shift out of stress — Your breath is the fastest lever you have to quiet cortisol and activate your parasympathetic, or “rest and digest,” system. Try rhythmic breathing patterns like 4-7-8 or 4-8 breathing — inhaling for four seconds, holding briefly, and exhaling slowly for seven to eight seconds.
The extended exhale stimulates your vagus nerve, lowering heart rate and cortisol while signaling safety to every organ. Practice before bed, after meals, or whenever tension rises. Over time, your body learns that it no longer needs to live in emergency mode.
4. Rebuild your circadian rhythm through light and sleep — Cortisol follows your light exposure, not your alarm clock. Get outside within an hour of waking to anchor your body’s circadian rhythm, and dim screens and overhead lighting at night so melatonin can rise naturally.
Keep your bedtime and wake-up times consistent — even on weekends — to lock in hormonal balance. Deep, regular sleep clears stress hormones, strengthens memory, and repairs brain tissue. If you’re dragging through the day, fix your light and sleep first instead of relying on caffeine.
5. Use natural progesterone to quiet the cortisol surge — Bioidentical progesterone acts as your body’s built-in cortisol brake, restoring calm where chronic stress has hijacked balance. Unlike synthetic versions, natural progesterone fits perfectly into your body’s own receptor system, lowering cortisol’s overstimulation and supporting deep rest.
FAQs About Cortisol and Alzheimer’s Disease
Q: What did the new Alzheimer’s study reveal about cortisol and DHEA-S?
A: Researchers found that people with Alzheimer’s disease had cortisol levels roughly 20% higher than healthy adults, while their DHEA-S levels stayed about the same. This created a skewed cortisol-to-DHEA-S ratio — meaning stress hormones were overpowering the brain’s natural defenses. That imbalance, not just genetics or amyloid buildup, appears to drive the early stages of brain decline.
Q: How are DHEA and DHEA-S different?
A: DHEA is the fast-acting form of the hormone, while DHEA-S is the stable, long-lasting form stored in your blood. Because DHEA-S changes slowly, it’s a better measure of long-term stress and brain resilience. It also acts as a neurosteroid, helping neurons resist inflammation and oxidative damage while buffering cortisol’s harmful effects.
Q: What did Georgi Dinkov’s analysis add to this research?
A: Dinkov explained that the Cureus study confirms a broader principle: high cortisol and low metabolic energy often go hand in hand. He connected these hormone shifts to thyroid sluggishness, nutrient depletion, and aging — all of which drain cellular energy and raise stress chemistry. He also noted that maintaining a low cortisol-to-DHEA-S ratio predicts not just better memory but longer life and greater overall resilience.
Q: What practical steps help lower cortisol and restore hormonal balance?
A: To calm your stress system, start by fueling your metabolism. Eat enough healthy carbohydrates — about 250 grams per day — to keep blood sugar stable. Cut back on overtraining, use rhythmic breathing to activate your vagus nerve, and rebuild your circadian rhythm by getting morning sunlight and sleeping on a consistent schedule. These changes lower cortisol naturally while improving energy and mental clarity.
Q: How does progesterone fit into this picture?
A: Natural progesterone acts as a built-in cortisol blocker. Your body recognizes it as a calming, balancing hormone that reduces overstimulation, helps you sleep deeply, and stabilizes mood. Natural progesterone effectively blocks cortisol by reducing blood concentrations, helping restore hormonal harmony, protecting your brain and body from the long-term effects of stress.
Due to Alzheimer’s research focusing on a symptom of it (amyloid plaques), rather than its actual cause, Alzheimer’s has remained “incurable” for decades
Rather than being a single disease, Alzheimer’s has multiple different subtypes (e.g., those due to insulin resistance, nutritional deficiencies, inflammation, infections, or concussions), each of which requires a different treatment
Impaired blood circulation to the brain and lymphatic drainage from the brain are often the primary trigger that initiates the degenerative process seen in Alzheimer’s disease. Factors which impair this circulation (e.g., poor sleep) hence roughly double the risk of dementia, while treatments which improve this circulation frequently produce remarkable improvements for cognitive decline and dementia
DMSO is an effective treatment for brain injuries like strokes, and well-suited to address many of the root causes of dementia and reverse the degenerative state that dying neurons get trapped in. Because of this, there are many reports of it reversing dementia and clinical trials in both humans and animals corroborating these improvements
This article will review the actual causes of dementias like Alzheimer’s and the forgotten therapies many have successfully used to cure them
Alzheimer’s dementia is one of the most significant medical challenges our country faces (e.g., it places an incredible burden upon society, e.g., last year it was estimated to cost the United States 360 billion dollars).1 Yet, despite spending billions for research each year, cures remain elusive, something many believe results from the flawed belief that eliminating the amyloid plaques associated with Alzheimer’s will fix it. In turn, as I showed here:
• Decades of amyloid therapies have never produced a beneficial treatment.
• The newest “breakthrough” amyloid-eliminating monoclonal antibodies, at best slightly slow the progression of Alzheimer’s while simultaneously causing a host of side effects, including brain bleeding and swelling in over a quarter of recipients.
• The entire amyloid industry rests upon a fraudulent study no one wanted to retract due to how much was invested in the amyloid hypothesis.
In short, the money behind this juggernaut has caused research into the real causes of Alzheimer’s to be suppressed. For example, here I highlighted how coconut oil MCTs (safely) do more than any of the costly amyloid drugs — yet virtually no one knows this.2
Dale Bredesen’s Discovery
Many are also unaware of a 2022 study that should have revolutionized the entire Alzheimer’s field:3
That protocol was based on Dale Bredesen’s insightful realizations that:4
• Amyloid protein is a protective mechanism the brain uses to protect itself from stressors that endanger brain tissue — making attempts to treat Alzheimer’s by eliminating it are doomed to fail.
• The brain is designed to be able to adapt to the needs of life, so it is always creating or pruning neural connections and brain cells. Alzheimer’s results from the loss of signals that sustain brain cells and the dismantling of neural connections, outweighing the formation of new neural connections, a process that gradually compounds over the decades.
• Rather than there being one type of Alzheimer’s, there are actually multiple types that each require different treatment approaches.
Note: Beyond the 2022 trial, which showed individually targeted therapies could shift the brain’s momentum from neurological degeneration to regrowth,5 a 2018 report of 100 patients from numerous providers also showed it treated Alzheimer’s,6 as did a 2024 case series of patients with remarkable results,7 and there are now neurologists around the country administering Bredesen’s protocol with success.
The 6 Types of Alzheimer’s Disease
As this understanding of Alzheimer’s has produced tangible results, this suggests the causes of Alzheimer’s that Bredesen identified indeed play a key role in the disease — particularly since many other datasets corroborate their contribution to Alzheimer’s. They are as follows:
• Type 1 — Inflammatory — This form is driven by excessive inflammation, often metabolic or infectious in nature. Chronic activation of the immune system — due to factors such as insulin resistance, a poor diet, a leaky gut, or latent infections — leads the brain to engage in protective downsizing by removing synapses and neurons that are less essential for immediate survival. It often presents with classic Alzheimer’s memory loss and typically develops in the sixties to seventies.
• Type 1.5 — Glycotoxic — This subtype arises from insulin resistance and chronically elevated blood sugar. It leads to both inflammatory and trophic deficiencies, and is driven by glycotoxicity and the accumulation of advanced glycation end products (AGEs), which impair cellular function and synaptic integrity. It typically appears in the late fifties to sixties.
Note: Chronically elevated insulin promotes amyloid formation, as the enzyme the body uses to break down insulin is the same enzyme it uses to break down amyloid plaques.8
• Type 2 — Atrophic — This type is caused by deficiencies in key nutrients, hormones, and other factors that provide trophic (supportive) signals to brain cells, which then triggers a similar downsizing mechanism seen in Type 1. Type 2 tends to emerge about a decade later than Type 1.
Note: We find these nutritional deficiencies can result from poor circulation reducing existing nutrients reaching brain tissue, and hence often focus on improving circulation rather than extended supplementation.
• Type 3 — Toxic — This subtype results from exposure to toxic substances that directly damage neurons. Common culprits include biotoxins, chronic infections, heavy metals, and industrial or household chemicals. Causative infections (discussed further here) include Cytomegalovirus, Human Herpesvirus 1 or 6, Lyme disease, dental bacteria that can travel to the brain (e.g., P. gingivalis), and various fungal infections (as mold toxins are notorious for causing cognitive impairment at all ages).
Type 3 uniquely causes widespread and often unpredictable neuronal death, occurs earlier in life — often between the forties and sixties — and is less strongly associated with genetic risk factors. Cognitive decline in this type is frequently accompanied by psychiatric symptoms, sensory changes, or executive dysfunction (e.g., difficulty with math, organization, executive tasks), rather than the more classic early Alzheimer’s memory loss.
Note: Some of the most important neurotoxins to avoid are pharmaceuticals, and when I meet elderly individuals who have preserved their mental clarity, many report having largely avoided pharmaceuticals throughout their lives.
• Type 4 — Vascular — In this form, chronic restriction of cerebral blood flow from existing vascular diseases leads to gradual neuronal injury and cognitive decline. Type 4 often appears in the seventies or beyond) and may overlap with other subtypes. It tends to affect processing speed, attention, and executive function rather than memory alone.
• Type 5 — Traumatic — Severe head traumas or repeated concussions (e.g., in professional football players)9 set off a cascade of chronic degenerative processes that cause cognitive and emotional dysfunction to appear years or decades after the injuries — making it critical to prevent these injuries and seek appropriate treatment when head traumas happen.
Note: There are a variety of causes of dementia, many of which are frequently (roughly half the time)10,11 misdiagnosed as Alzheimer’s. In many cases, these respond to the same treatments which reverse Alzheimer’s, but in other cases, require different treatments.
Many practitioners I know who’ve successfully treated dementia with a variety of methods (listed here) all concluded it resulted from impairments of blood flow to the brain and lymphatic or venous drainage from it. For example:
•Zeta potential provides the disperse force which keeps constituents within fluids from agglomerating and clogging the circulatory vessels (e.g., vaccines frequently trigger detectable microstrokes by causing blood cells to clump together).
In a myriad of illnesses, we find restoring the physiologic zeta potential (discussed here) is pivotal for restoring health — particularly those associated with aging, as zeta potential worsens with age (due to declining kidney function). In turn, one of the physicians who inspired my medical path did so because his practice revolved around treating zeta potential and he repeatedly achieved significant cognitive improvements for his aging patients.
• China recently developed a surgery (detailed here) to increase the lymphatic drainage from the brain. Due to its low cost, it is being rapidly adopted nationwide. In parallel, an American procedure was developed to increase venous drainage from the head and reported to greatly improve multiple sclerosis along with other chronic neuroimmune disorders (which distant colleagues witnessed).
Note: I have seen many other circulatory enhancing therapies (listed here) also improve cognitive decline and dementia.
Furthermore, beyond blood being vital for neuronal survival, the proper clearance of waste products from the brain is as well. Unfortunately, due to how limited space is for the brain within the skull, robust lymphatic vessels do not exist, and instead, lymphatic drainage is created by astrocytes creating temporary lymphatic vessels around blood vessels during deep sleep.
This system, in turn, is highly vulnerable to disruption, and numerous studies have now linked impaired glymphatic drainage to dementia12 (e.g., TBIs impair glymphatic drainage13 and adequate glymphatic drainage is required to eliminate amyloid from the brain)14 — which likely inspired the Chinese surgical procedure for dementia.
Due to the fragility of this system, disruptions are quite consequential (e.g., a poor zeta potential thickens and slows the drainage of glymphatic fluids). For example, as glymphatic drainage only occurs during deep sleep, inadequate sleep has been extensively linked to dementia15 (e.g., one study found sleep disruption increased dementia by 104%,16 another by 22% to 50%,17 and a third saw a 139% increase18 — along with another finding that sleep disruption caused a 71% increase in mild cognitive impairment).19
Likewise, disrupted sleep was recently shown to accelerate the accumulation of amyloid plaques,20 and in another study, to mitigate the cognitive impairment created by Alzheimer’s plaques.21 Unfortunately, the pathologic proteins in Alzheimer’s have been shown to directly disrupt restorative sleep22 and to take away the ability to recognize one is suffering from impaired sleep23 — demonstrating why it is so important to restore your healthy sleep before the momentum of dementia has entrenched itself.
Note: Sleeping pills block restorative sleep, and have a variety of issues (e.g., they make users 2 to 5 times as likely to die24,25). Regarding dementia, multiple studies have found that sleeping pills increase the risk of it by 17% to 84%.26,27,28,29
The Life of Cells and Neuroplasticity
One of the things I continually marvel at about nature is not only the ability of a species to genetically adapt to its environment, but the inherent adaptability each organism has within its own lifespan to adapt to its own environment. Within the human body, there are many systems that are designed to change based on the needs of one’s environment (e.g., this is why weight training creates larger muscles), and among the most adaptable is the nervous system.
So, at any given moment, neural circuits that support certain activities are reinforced, while other circuits are pruned and eventually disabled, a process that allows the nervous system to adapt to the complex needs of its environment. At the same time, many complex neurological and psychiatric disorders arise from a momentum being established where dysfunctional neurological circuits perpetually reinforce themselves.
For these disorders to be treated, momentum must instead be built around a healthy circuit (for those interested, this is the best book I have seen on the subject).30 This momentum is a key reason why it is so important to have healthy thought patterns and regularly actively exercise your brain (another core component of programs for preventing Alzheimer’s).
If you do the opposite (e.g., watch TV all day), dysfunctional patterns can become established habits, while neurological damage occurs as parts of the brain you need but under utilize are pruned away.
A key way the brain accomplishes this adaptability is by eliminating neurons that are no longer deemed essential. Bredesen’s theory of Alzheimer’s is that it results from the balance between preserving and eliminating neurons being shifted towards removing them,31 which inevitably will result in cognitive decline.
Within Bredesen’s model, the amyloid protein plays a key role in this process,32 as when it is initially formed as the amyloid precursor protein (APP), it can then be split into two or four parts. If it is divided into two parts, those parts protect the neurological function in the brain. In comparison, if it is divided into four parts, the neurological function of the brain is damaged, and brain cells are eliminated.
Interestingly, its splitting into four parts causes future APPs to be split into four parts as well (creating a downward spiral). As a result, Brenden’s approach focuses on regaining a healthy momentum towards the two-part splitting while also providing the signals cells within the body require to survive.
The Cell Danger Response
When cells are exposed to external stressors, they often enter a primitive defensive metabolic cycle where they partially or fully “turn off” (e.g., mitochondrial respiration and protein synthesis within the cell decline) to protect themselves. Many chronic diseases, in turn, result from cells being trapped in this degenerative cycle (which often leads to cell death) rather than exiting it and resuming their normal function. Likewise, many therapies in regenerative medicine work by removing cells from this frozen metabolic state.
Because of this, many complex illnesses (e.g., COVID vaccine injuries, fibromyalgia, or autism) can only be treated if the underlying trigger for the cell danger response is removed. Then a regenerative therapy is provided which signals cells to exit the CDR. Similarly:
“The principle that blocking protein synthesis prevents long-term memory storage was discovered many years ago. With age, there is a marked decline of protein synthesis in the brain that correlates with defects in proper protein folding. Accumulation of misfolded proteins can activate the integrated stress response (ISR), an evolutionary conserved pathway that decreases protein synthesis. In this way, the ISR may have a causative role in age-related cognitive decline.”
In turn, much as treatments for the CDR often facilitate dementia treatment, therapies that inhibit the ISR have been found to restore the structure and function of brain cells and improve a variety of age-related memory deficits.33,34
DMSO
Dimethyl sulfoxide has a variety of unique therapeutic properties that allow it to treat a variety of diseases (e.g., it is miraculous for strokes and brain injuries), and in the year since I began publicizing this forgotten therapy, I have received thousands of remarkable reports of it treating numerous “incurable illnesses.”
Much of this results from DMSO’s ability to restore normal circulation, protect cells from lethal stressors, and revive shocked cells trapped in the CDR. As such, since the start of the series, in addition to receiving many reports from readers who saved themselves or a loved one from a disabling stroke with DMSO, many have also shared stories like this:
“My uncle’s wife has dementia and has been unable to speak for over a year.35 My mom recently visited them and told them about DMSO. He began to give his wife DMSO orally. After two weeks she began to talk again.”
Numerous studies (detailed here) have corroborated DMSO’s ability to treat dementia. These include:
• When cerebral blood flow was permanently reduced in rats, one study found DMSO prevented the neuronal and memory loss that otherwise resulted,36 while another found DMSO given afterwards treated it.37,38 Similar benefits have also been seen after Alzheimer’s was induced by injecting toxins into the brain,39,40 Likewise, in mice (or nematodes) engineered to develop Alzheimer’s, DMSO has been repeatedly shown to prevent the expected neurological damage.41,42,43
• DMSO has also been shown44 to prevent the neuronal damage from experimentally induced Parkinson’s and preserve the cognitive function of mice bred to rapidly develop severe degeneration of the cerebellum and brainstem.45,46
Note: IV DMSO is one of the few therapies I have come across which can halt Parkinson’s. To some extent oral DMSO helps as well (e.g., see this reader’s comment).47
• DMSO has also been shown to treat scrapie (a neurodegenerative prion disease from abnormal protein aggregates) in hamsters,48 to increase the activity of ALP the intercellular enzyme which eliminates cellular waste (including misfolded proteins),49 and in a large number of studies, to treat amyloidosis (pathologic accumulations of pathologic proteins.
In humans:
• 18 patients with probable Alzheimer’s after three months, DMSO caused a significant improvement in memory, concentration, communication, and orientation to time and space.50
• In 104 elderly adults with organic brain disease from the common causes (e.g., strokes, atherosclerosis, Parkinson’s, or head injuries), DMSO greatly improved their psychic and somatic function.51
• In 100 patients with cerebrovascular diseases CVD, many of whom were senile, over 50 days DMSO caused almost all to have a significant improvement in their CVD, along with significant improvements in mood, mobility, and speech.52
Conclusion
Medicine revolves around finding unique molecular targets for which disease specific treatments can be patented. Unfortunately, this model frequently fails in chronic illnesses, leading to grotesque situations like the one described here, where natural therapies, which can address the actual causes of devastating illnesses are sidelined to protect each disease’s lucrative “treatment” market.
This needs to change, and for the first time in my lifetime, thanks to MAHA, the political will at last exists to begin addressing the real reasons why there continues to be so much chronic illness in our society. The opportunity to make cognitive decline no longer an inevitable aspect of aging is finally here — if we dare to seize it!
Author’s Note: This is an abridged version of a longer article which discusses the actual causes and treatments for Alzheimer’s disease and the cognitive decline which precedes it. That article, along with additional links and references, can be read here. Additionally, a companion article on how DMSO treats neurological injuries (e.g., strokes, brain hemorrhages, traumatic brain injuries, spinal paralysis, and developmental delay) can be read here.
A Note from Dr. Mercola About the Author
A Midwestern Doctor (AMD) is a board-certified physician from the Midwest and a longtime reader of Mercola.com. I appreciate AMD’s exceptional insight on a wide range of topics and am grateful to share it. I also respect AMD’s desire to remain anonymous since AMD is still on the front lines treating patients. To find more of AMD’s work, be sure to check out The Forgotten Side of Medicine on Substack.
Older adults who consumed between 1.2 and 1.6 milligrams of copper daily scored higher on memory and processing speed tests, with stroke survivors benefiting the most
Higher copper levels in specific brain regions were linked to slower cognitive decline and fewer Alzheimer’s-related changes
A high-fat diet combined with high copper intake more than doubled the rate of memory loss, especially in language and verbal recall skills
Copper regulates enzymes that protect brain cells from oxidative stress and helps shift brain immune cells into a healing state after injury
Whole foods like grass fed beef liver, bee pollen, and shiitake mushrooms support copper balance, while strategic supplementation with copper bisglycinate helps restore levels in those with deficiency
Your brain runs on a delicate balance of minerals — and copper is one of the most important. It’s easy to overlook, but this trace nutrient controls the very processes that keep your mind sharp: how your neurons fire, how your brain makes energy, and how it clears out damaging waste. Without enough, systems start breaking down. You don’t think as clearly. Your memory slips. And your brain begins to age faster than it should.
What makes copper unique is that it’s both necessary and dangerous in the wrong context. Too little leaves your brain vulnerable to oxidative stress. Too much, and it becomes part of the problem — fueling inflammation and structural damage. That tightrope makes copper one of the most powerful, yet high-stakes, nutrients in your diet.
Most people aren’t thinking about copper when they eat. But what you’re eating — or not eating — could be shifting your copper balance in a way that accelerates cognitive aging without you realizing it. That’s why I want to show you what scientists are now uncovering about copper’s impact on your brain, and how dialing it in — not too much, not too little — is one of the simplest ways to sharpen your memory and protect long-term brain health.
Better Brain Function Seen with Daily Copper
A study published in Scientific Reports analyzed data from 2,420 American adults over age 60 to evaluate how dietary copper influences cognitive function.1 Using data from the National Health and Nutrition Examination Survey (NHANES) between 2011 and 2014, researchers reviewed both diet and memory test scores. Their goal was to determine whether eating more copper-rich foods translated into better brain performance.
• Older adults who consumed more copper scored higher on multiple brain tests — Participants who consumed the most copper — around 1.2 to 1.6 milligrams (mg) per day — consistently scored better on tests measuring memory, language, and processing speed. The relationship held even after adjusting for confounding factors like age, education, calorie intake, and levels of other minerals such as zinc, iron, and selenium.
• The strongest cognitive gains occurred below a specific threshold — Results followed a clear non-linear pattern. When copper intake reached about 1.2 to 1.6 mg per day, cognitive scores improved. But beyond that point, the benefits leveled off.
• Cognitive benefits were greatest in stroke survivors — Among participants with a history of stroke, the effect of copper was even more pronounced. Those in the highest copper intake group had significantly higher global cognition scores than those with the lowest intake. This suggests that copper intake is especially important for neurological recovery and brain resilience after a vascular event.
• Copper’s role in brain recovery likely involves antioxidant and energy enzymes — The study explained that copper serves as a cofactor for key enzymes like superoxide dismutase (SOD1), which neutralizes reactive oxygen species in brain cells. This action helps prevent oxidative damage — one of the main drivers of neuron death in aging brains. When copper intake falls below the optimal range, SOD1 activity drops, and damage from free radicals increases.
• Copper impacts neuroinflammation and brain cell repair — Researchers also noted copper’s influence on immune cells in the brain. Specifically, copper appears to reduce inflammation after a stroke by shifting microglia — the brain’s immune cells — from a damaging “M1” mode to a healing “M2” state. This transition lowers inflammatory cytokines, while boosting anti-inflammatory molecules.
Higher Brain Copper Linked to Slower Memory Loss and Less Alzheimer’s Damage
Published in the journal Molecular Psychiatry, this community-based study followed 657 older adults for nearly seven years before death and analyzed copper levels in four brain regions during autopsy.2 Researchers wanted to know whether brain copper levels were linked to how quickly memory declined and how much Alzheimer’s disease damage was found after death. They also tracked participants’ dietary copper intake to see if it influenced copper levels in the brain or disease severity.
• Participants with more brain copper declined more slowly and had fewer signs of Alzheimer’s — Higher copper levels in specific areas of the brain, particularly the inferior temporal and mid-frontal regions, were strongly associated with slower loss of memory, attention, and thinking speed over time. Those in the top third for brain copper experienced the slowest decline in global cognition and key memory domains.
• Memory and processing speed were the most improved cognitive areas — The biggest differences were seen in global cognition, working memory, semantic memory (understanding words and meanings), and perceptual speed (how quickly the brain processes information). Participants in the top copper group declined 0.03 units per year more slowly than those in the lowest group — small differences that add up over time.
• Higher brain copper was linked to lower odds of advanced Alzheimer’s stage — Participants with the most brain copper had 40% lower odds of being in the most severe stage of Alzheimer’s pathology compared to those with the lowest copper.
• Copper plays a key role in maintaining healthy brain structure and function — Copper is used by enzymes that support brain energy metabolism, gene regulation, antioxidant defense, and neurotransmitter synthesis. These enzymes protect neurons from oxidative stress, regulate iron, and help with signal transmission between brain cells. A copper shortfall weakens these defenses, leaving neurons more vulnerable to damage.
Copper is essential for brain health, but having too much also leads to neurodegeneration and neurological disorders. In an analysis published in the American Journal of Epidemiology, researchers tracked 10,269 middle-aged adults over a 20-year period to examine how dietary copper intake — especially when combined with high levels of saturated fat — affected cognitive performance and dementia risk.3
• Copper wasn’t a risk factor until paired with high-fat diets — Among those who consumed the most saturated fat, higher copper intake was linked to significantly faster cognitive decline. In this group, high copper doubled the rate of memory loss. In contrast, people with low saturated fat intake showed no negative effect from copper, even at higher doses. This interaction highlights how nutrients don’t act in isolation. Your overall dietary pattern matters.
• Verbal memory suffered the most in those with high copper and fat intake — The largest decline was seen in language-related skills. Participants with high copper and high saturated fat diets had the steepest drop in word recall and verbal fluency. These are early warning signs of dementia, especially Alzheimer’s-type cognitive impairment.
• Supplements weren’t the issue — most copper came from food — The researchers confirmed that nearly all copper came from dietary sources. Supplement users made up a small minority and didn’t skew the data. This underscores the need to evaluate food combinations, not just isolated nutrient doses.
• Brain damage likely driven by copper-induced oxidation of fats — The study authors proposed that excess copper oxidizes saturated fats and cholesterol in the bloodstream, triggering inflammatory damage inside the brain. When fats are oxidized, they form harmful compounds called aldehydes, which are known to impair neurons and increase beta-amyloid buildup, a hallmark of Alzheimer’s disease. This damage appears to be especially aggressive in brain regions responsible for memory.
• Related study found participants with the highest copper and saturated/trans fat intake had the worst cognitive outcomes — A study published in Archives of Neurology found that in people with diets high in saturated and trans fats, higher copper intake was linked to a dramatic decline in mental function.4 Their rate of cognitive decline was equivalent to aging 19 years faster compared to participants with low copper and low fat intake.
That means a 65-year-old on a high copper, high-fat diet had the brain function of an 84-year-old. The study found no such effect among those with high copper but low fat intake, showing it was the combination — not copper alone — that accelerated damage.
How to Balance Copper and Protect Your Brain from Cognitive Decline
Copper is one of the most misunderstood minerals in your body. While the mainstream narrative often warns about copper excess, the reality is that most people are walking around copper-deficient — and that has far-reaching consequences for your brain. Copper is foundational for mitochondrial function, iron regulation, and energy production. When it’s low, iron builds up in places it shouldn’t, oxidative stress spikes, and your neurons suffer.
If you’re feeling mentally sluggish, forgetful, or easily fatigued, your copper status may be off. But rather than guessing, I recommend a strategic approach that supports your body’s ability to regulate copper naturally — using whole foods, metabolic support, and, if needed, supplementation. Here are five key steps to optimize your copper levels and protect your brain:
1. Add copper-rich whole foods to your diet — Foods like grass fed beef liver, shellfish, shiitake mushrooms, dark chocolate, and bee pollen are some of the best sources of bioavailable copper. These foods don’t just supply copper — they deliver it in a way your body knows how to handle. Retinol (preformed vitamin A), found in beef liver and organ meats, plays a direct role in copper metabolism. Without enough retinol, copper can’t get where it needs to go.
2. Shift your macronutrient balance — more carbs, less fat — A high-fat diet disrupts how your body burns glucose and instead forces it to rely on fat for energy. That imbalance drives chronic disease. I now recommend keeping fat intake between 30% and 40% of your daily calories.
That means prioritizing healthy, digestible carbs like whole fruit, cooked root vegetables, white rice, and small amounts of well-tolerated whole grains, as long as your gut is healthy and you tolerate them. For healthy fats, focus on grass fed butter, ghee and tallow, while minimizing the polyunsaturated fat linoleic acid in vegetable oil.
3. Supplement strategically with copper bisglycinate if needed — If your copper intake is low or you’ve been dealing with signs of deficiency, such as brain fog or unexplained fatigue, consider taking 3 to 4 mg of copper bisglycinate daily. This chelated form is highly absorbable and less likely to irritate your gut. But don’t supplement blindly — test your levels, track your progress and adjust your copper intake as needed.
Balanced copper levels aren’t just about brain performance — they’re about restoring the mineral harmony that drives every system in your body. When copper is where it’s supposed to be, your energy, memory, and clarity come back online.
FAQs About Copper and Your Brain
Q: What does copper do for your brain?
A: Copper is essential for your brain’s electrical activity, antioxidant defense, and energy production. It activates enzymes like superoxide dismutase, which neutralize free radicals and protect neurons from damage. Without enough copper, your brain cells can’t generate energy efficiently or repair oxidative injury, leading to memory problems and cognitive decline.
Q: Can eating more copper-rich foods really improve memory?
A: Yes. Research published in Scientific Reports found that adults over 60 who consumed about 1.2 to 1.6 mg of copper daily had better memory, language skills, and processing speed — especially those recovering from stroke.5 Another study in Molecular Psychiatry showed that higher copper levels in brain tissue were linked to slower cognitive decline and less Alzheimer’s pathology.6
Q: Is too much copper dangerous for your brain?
A: It can be. While copper is necessary, too much — especially when paired with a high-fat diet — fuels oxidative stress. A study in the American Journal of Epidemiology found that high copper intake doubled the rate of memory loss in people eating diets rich in saturated fat.7 The damage is likely caused by copper oxidizing fats in the blood, triggering brain inflammation and beta-amyloid buildup.
Q: What foods help regulate healthy copper levels?
A: Grass fed beef liver, shellfish, shiitake mushrooms, dark chocolate, and bee pollen are excellent sources. Retinol (vitamin A) from organ meats is also needed to direct copper into your cells and prevent accumulation in the wrong places.
Q: Should I take a copper supplement?
A: If your diet lacks copper or you’re showing signs of deficiency, such as fatigue or brain fog, it may help to take 3 to 4 mg of copper bisglycinate daily. This form is gentle on digestion and highly absorbable. However, food-based copper should typically come first.
More than 7 million Americans live with Alzheimer’s today, and researchers project that number will rise to 13 million by 2050, doubling the burden on families
Researchers at the Jackson Laboratory (JAX) discovered twisted, narrowed retinal vessels in mice carrying a common gene mutation, showing changes that resemble early Alzheimer’s signs years before memory decline begins
They also found disrupted protein activity in both brain and retina, weakening energy production and vessel support, creating the conditions for Alzheimer’s long before symptoms appear
Visual sensitivity testing in over 8,000 adults predicted dementia risk up to 12 years ahead, showing how everyday vision struggles may signal hidden brain changes
Regular eye exams, better sleep, balanced carbohydrates, healthy fats, sunlight exposure, and methylene blue support offer practical steps to strengthen vessel health and protect your brain
More than 7 million Americans are now living with Alzheimer’s disease, a condition characterized by progressive memory loss, confusion, and changes in behavior that worsen over time. Alzheimer’s is the most common form of dementia, and according to researchers, this number will reach 13 million by 2050, creating an enormous medical and social burden.1
However, emerging research provides a revolutionary shift in the early detection of Alzheimer’s — according to the studies, a simple eye exam might be able to provide the first visible evidence of this disease, long before traditional symptoms appear. This opens the door to a safer and more accessible screening method, as well as gives hope in better management of the condition.
The Blood Vessels in Your Retina May Reveal Alzheimer’s Risk
A recent animal study published in Alzheimer’s & Dementia journal explored if changes in the eye’s blood vessels could act as early warning signs of Alzheimer’s disease, allowing routine eye exams to reveal this disease years before symptoms set in.2
Conducted by researchers at the Jackson Laboratory (JAX), the research focused on the retina, the light-sensitive layer of tissue at the back of your eye, to determine if abnormal blood vessel patterns in the eye could serve as a clear biomarker for brain changes linked to dementia.3
“Most people over 50 have some kind of vision impairment and get checked annually for prescription changes,” Alaina Reagan, a neuroscientist and one of the study authors, explained. “Are they more at risk if they have these vascular changes, and is that a point when doctors could start mitigating brain changes? That could be 20 years before cognitive damage becomes noticeable to patients and their families.”
• The research was conducted on mice bred with a specific genetic mutation — Called MTHFR677C>T, this common mutation causes the mice to develop “twisted vessels, narrowed arteries, and reduced branching in the retina,” as early as 6 months of age. These conditions closely resemble the vascular abnormalities seen in human Alzheimer’s patients, and are strongly associated with impaired blood flow and cognitive decline.4 Up to 40% of people have this similar mutation.
• Researchers observed striking details in these retinal changes — Unlike the smooth, organized vascular networks typically found in healthy eyes, the altered vessels appeared tangled and distorted. Because the retina and brain share nearly identical tissue, changes in one mirror changes in the other.
“If you’re at an optometrist or ophthalmologist appointment, and they can see odd vascular changes in your retina, that could potentially represent something that is also happening in your brain, which could be very informative for early diagnostics,” Reagan said.
“Your retina is essentially your brain, but it’s much more accessible because your pupil is just a hole, and we can see tons of stuff. All the cells are very similar, all the neurons are quite similar, all the immune cells are quite similar, and they behave similarly under pressure if you’ve got a disease.”
• The problems in the eye went beyond twisted blood vessels — According to the researchers, there was disrupted protein activity in both the brain and retina, too. Proteins are the body’s workers — they manage energy production, clear out waste, and help maintain strong vessel structures.
So when their activity is disrupted, those systems break down, meaning your brain and eyes lose their ability to properly fuel cells, clear out harmful byproducts, and keep vessels strong — setting the stage for Alzheimer’s disease.
• The study also highlighted important differences between male and female mice — Females fared much worse than their male counterparts. By the age of 12 months — roughly middle age for mice — they had fewer blood vessel branches and lower vessel density in their retinas.
This detail is striking because it parallels what doctors already see in humans — women across the globe experience higher rates of dementia compared to men.5 Age was another factor that changed the picture, as the retinal disruptions grew more severe as the mice got older.
• The research team is now working to apply these animal findings to humans — They are partnering with Northern Light Acadia Hospital in Maine to test whether similar retinal changes show up in patients carrying the same gene mutation.6 If they succeed, it means an optometrist could one day spot Alzheimer’s risk with a simple retinal exam decades before symptoms surface.
This research transforms routine eye care into a powerful tool to protect your brain health. Having an early warning system built into something you’re already doing opens up a pathway to earlier treatment — and better outcomes become far more realistic.
Genetics Shape How Your Eyes Age and Reveal Brain Health Risks
The researchers of the featured study have also conducted previous research on how genetic differences affect the way eyes age and how those changes connect to brain health. Their findings, published in Molecular Neurodegeneration earlier this year, investigated whether the retina could show signs of aging that mirror what happens in the brain. Their goal was to determine if specific genetic backgrounds create distinct retinal changes that could predict neurological decline.7,8
• The study involved nine genetically diverse strains of mice — All mice showed some form of retinal aging, but the type and severity of changes differed dramatically between groups.
• The researchers found how varied retinal aging can be — In one strain called Watkins Star Line B (WSB), the mice developed signs of age-related macular degeneration and retinitis pigmentosa, both are serious eye diseases that damage vision over time. In another strain known as New Zealand Obese (NZO), which is prone to metabolic dysfunction, the animals developed diabetic retinopathy, a condition where high blood sugar damages blood vessels in the eye.
• These differences were not random — They were predictable. Molecular changes in the eye accurately forecast which type of degeneration would occur. According to Gareth Howell, a professor at JAX and the study’s lead author:
“There’s more to the eyes than just simply seeing you. By understanding how the healthy eye ages in different genetic contexts, we may be able to determine people’s risk of developing diseases like Alzheimer’s.”9
Visual Sensitivity Loss Can Signal Alzheimer’s Risk Years Ahead
These studies from the JAX team are not the first to look at the connection between eye health and dementia risk. In 2024, researchers from Loughborough University in the U.K. released a study on how vision testing could reveal Alzheimer’s risk — as early as 12 years before diagnosis.
The study, which was published in the Scientific Reports journal, focused on whether reduced visual sensitivity — the ability to detect fine details, contrast, or subtle changes in the environment — could act as a long-term predictor of dementia. Instead of relying only on brain scans or memory tests, the researchers suggested that eye-based assessments could be paired with standard psychological tests to strengthen early detection.10
• The study population included more than 8,000 adults who have participated in the EPIC-Norfolk Prospective Population Cohort Study — The participants’ eyesight was tested years before they developed symptoms of Alzheimer’s, via computerized visual sensitivity training, which involves assessing a person’s visual processing speed and reaction time. Ahmet Begde, Ph.D., a doctoral researcher at Loughborough University and one of the study researchers, said:
“Visual sensitivity refers to an individual’s ability to detect and process visual information accurately and efficiently. We decided to investigate visual sensitivity as a predictor of dementia because previous research has shown that individuals with dementia often experience visual processing deficits, even in the early stages of the condition.”11
• The details of the findings showed a strong predictive link — Participants with lower visual sensitivity were far more likely to develop Alzheimer’s within the following decade compared to those with normal visual processing.
“A loss of visual sensitivity can lead to various difficulties in perceiving and processing visual information, such as difficulty recognizing objects or faces, struggles with reading or navigating in familiar environments, and challenges in perceiving visual details or contrasts,” Begde explained. “For example, a person with reduced visual sensitivity may have difficulty reading street signs while driving.”12
But this isn’t just about needing glasses or having blurry vision — it was about how the brain interprets what your eyes see. It means struggles with reading, judging distances, driving safely, or distinguishing between colors could be more than just frustrating — they might signal changes in your brain long before memory problems begin.
• Specific improvements came from combining vision tests with traditional neuropsychological exams — Alone, each type of test gives useful information, but when paired, they created a much clearer picture of future dementia risk.
• So what’s the biological explanation for these findings? This is because when Alzheimer’s develops, beta-amyloid plaques — sticky protein clusters linked to cell damage — disrupt both the brain and the pathways that process vision. This disruption reduces the efficiency of visual signaling, which shows up as difficulty detecting fine details or contrasts.
Another mechanism involves how the brain clears waste proteins. Inefficient clearance allows buildup that clogs communication between cells, especially in areas tied to vision.
• These results are unsurprising — In a Medical News Today article, Dr. Alexander Solomon, a surgical neuro-ophthalmologist and strabismus surgeon from California, comments that the findings of this study are actually consistent with what he sees in his patients every day. “It isn’t hard to imagine that as the brain is compromised by a process like dementia, some portions that help process our vision are affected,” he said.13
Practical Steps to Protect Your Eyes and Brain from Alzheimer’s
If you are worried about Alzheimer’s, the most important thing to understand is that the root cause of the damage is not memory loss itself — it starts years earlier with broken-down energy systems in your cells, blocked protein clearance, and weakened blood vessels in both the brain and the eyes. When you address these causes head-on, you give yourself a fighting chance to slow down or even prevent the decline. That’s why what you do today matters. Here are five steps I recommend you start putting into practice.
1. Lower your risk from hidden vascular stress — If you have high blood pressure, diabetes, or a family history of stroke or dementia, your blood vessels are under extra pressure. These same vessels feed your retina and your brain, so keeping them strong is key.
Eliminate seed oils and processed foods from your diet, as they damage vessel walls, and replace them with tallow, ghee, or grass fed butter. I also recommend adding regular movement into your lifestyle, such as walking every day, to keep your circulation healthy and blood vessels flexible.
2. Balance your carbohydrates to protect energy production — Your brain and retina run on energy, and that energy depends on carbs. I recommend eating 250 to 300 grams of clean carbohydrates daily, unless you are very active and need more.
Start with fruit, fruit juice with pulp, or root vegetables before you try complex starches. If you have gut problems, sip dextrose water slowly throughout the day. This keeps your mitochondria producing energy smoothly, which is foundational for preventing the decline that shows up in Alzheimer’s.
3. Clear out protein waste before it builds up — To help your body clear out waste proteins, you need efficient sleep and strong circadian rhythms. Expose yourself to sunlight in the morning to reset your internal clock, and avoid blue light screens at night. If you sleep poorly, your brain doesn’t clear out the sticky amyloid that clogs your neurons. I recommend making high-quality sleep a priority because it’s when your brain takes out the trash.
4. Strengthen your retina with regular eye exams — If you are over 50, getting regular annual eye test is essential to help identify early warning signs of Alzheimer’s or dementia. Treat the exam as your early-warning radar, and keep track of results, just like you would monitor blood sugar or cholesterol.
5. Use sunlight and methylene blue to support cellular energy — Your retina and brain cells both rely on strong mitochondrial function to stay alive and sharp. Safe sun exposure helps your cells produce energy directly — however, you need to make sure to eliminate all seed oils from your diet for four to six months before going out during peak sunlight hours. Otherwise, the linoleic acid (LA) in these oils can become embedded in your skin and oxidize under UV rays, causing DNA damage.
Meanwhile, methylene blue, in its pharmaceutical-grade capsule form, has been shown to reduce reductive stress at doses as low as 5 mg once a day. If you spend time in the sun and use methylene blue safely, you give your cells a double advantage — more energy, less stress, and a stronger defense against the breakdowns that fuel Alzheimer’s progression. Read more about it in this article: “Methylene Blue Is Beneficial for Slowing Skeletal Aging and Treating Brain Disorders.”
Frequently Asked Questions (FAQs) About Eye Exams and Alzheimer’s Detection
Q: How are eye exams connected to Alzheimer’s disease?
A: Research shows that twisted, narrowed, or poorly branching vessels in the retina resemble the same abnormalities that occur in the brains of people with Alzheimer’s disease. Because the retina is essentially an extension of your central nervous system, changes in the eye strongly mirror changes in the brain. Detecting these abnormalities during a routine exam could provide an early warning sign of Alzheimer’s years — sometimes even decades — before memory loss or confusion begins.
Q: What role do genetics play in Alzheimer’s risk shown through the eyes?
A: Genetics play a powerful role in shaping how your eyes and brain age. One mutation in particular, called MTHFR677C>T, affects up to 40% of people and disrupts blood vessel health. Studies on mice carrying this mutation revealed twisted, narrowed vessels and reduced branching in the retina, which closely resemble the vascular damage seen in Alzheimer’s patients. These abnormalities impair blood flow, restrict oxygen delivery, and contribute to cognitive decline.
Q: Are women at greater risk for Alzheimer’s-related eye changes?
A: Yes, women tend to face higher risks both in the brain and in the eye. Research on mice carrying the Alzheimer’s-linked mutation showed that females developed much more severe retinal damage than males. By 12 months of age — roughly middle age for mice — females already had fewer blood vessel branches and significantly lower vessel density. This directly parallels what doctors see in humans: women worldwide develop dementia at higher rates than men.
Q: Can vision problems predict dementia before memory issues appear?
A: Yes, vision problems often signal brain changes years before memory loss begins. A large study from Loughborough University followed more than 8,000 adults and tested their visual sensitivity, which is the ability to detect fine details, contrasts, and subtle changes in the environment. Those with reduced visual sensitivity were much more likely to develop Alzheimer’s within the following decade.
Q: What practical steps support eye and brain health to reduce Alzheimer’s risk?
A: First, reduce vascular stress by eliminating seed oils and eating healthier fats like tallow or grass fed butter. Second, balance your carbohydrates — your brain and retina need 250 to 300 grams daily for steady energy. Third, clear protein waste by prioritizing high-quality sleep and getting morning sunlight to reset your circadian rhythm.
Fourth, schedule annual eye exams and ask your doctor to check vessel health, treating it as an early-warning system. Finally, strengthen your cellular energy with safe sun exposure and pharmaceutical-grade methylene blue at 5 mg daily, which helps reduce reductive stress. Together, these steps give you more control over your long-term health, turning routine habits into a defense strategy against Alzheimer’s progression.
More than 13.5 million people are now using GLP-1 injections like Ozempic, up from 450,000 in 2018 — a sharp rise linked to an equally sharp increase in side effects
Patients using Ozempic are reporting rapid tooth decay, bleeding gums, and dental infections — even in people with no history of oral disease or poor hygiene habits
Reduced saliva and increased stomach acid — two known side effects of GLP-1 drugs — set the stage for bacterial overgrowth, acid erosion, bad breath, and irreversible enamel loss
Weight loss from GLP-1 drugs often includes bone and muscle mass, not just fat — putting users at higher risk for fractures, osteoporosis, and long-term structural damage
The oral bacteria triggered by Ozempic use, such as P. gingivalis, are linked not just to gum disease but to heart disease, pneumonia, and even Alzheimer’s
Over 13.5 million people today are now taking GLP-1 drugs — an astounding surge from nearly 450,000 prescriptions in 2018.1 Once prescribed as a drug for managing Type 2 diabetes, these injections are now being used for weight loss, and sold under brand names like Ozempic, Wegovy, and Mounjaro.
It seems like there’s no stopping their popularity. Unfortunately, the same can be said for the side effects being linked to these drugs. Social media is now abuzz with the latest concern being linked to GLP-1 medications. Apparently, people who are using these drugs are now coming down with sudden dental issues.
This Shortcut to a Slimmer Waist Could Ruin Your Smile
A news report from Fox News highlights yet another rising concern about GLP-1 medications, particularly how these drugs are triggering tooth- and gum-related issues. According to the report, patients and doctors are now seeing a consistent pattern of dental problems linked to these medications.2
• Beware of “Ozempic teeth” — Much like the infamous “Ozempic face,” this refers to oral health symptoms, such as tooth decay, gum disease, oral infections, bad breath, and dental collapse, that are showing up in people who are taking these medications. Even those with no prior history of dental disease are experiencing these side effects.
• Dental professionals are reporting these effects — While there is still no scientific evidence linking GLP-1 use with dental issues, medical experts are now seeing a pattern.3 Dr. Ricky Marshall, an oral health practitioner based in Arizona, has noticed the increasing number of patients who are reporting similar symptoms. “Patients have reported dry mouth while on Ozempic in both dental practices I work in,” he said.
• Why does Ozempic cause dry mouth? Marshall believes that the dry mouth side effect is one of the main reasons for the dental problems linked to these weight loss drugs. But why does this occur in the first place? Apparently, semaglutide, the active ingredient in these injections, affects your salivary glands and reduces saliva production. According to an article in The Conversation:
“It isn’t exactly clear why semaglutide has this effect on the salivary glands. But in animal studies of the drug, it appears the drug makes saliva stickier. This means there’s less fluid to moisten the mouth, causing it to dry out.”4
Your Digestive and Dental Health Are Connected
Unfortunately, those who use these weight loss drugs are often unaware of the side effects, as many of them aren’t indicated on the drugs’ information leaflet. But, according to The Hearty Soul, even if there are no direct warnings about these side effects, there are signs. “For example, one of the common side effects that appears on the label is acid reflux. This increase in acid can start to erode your teeth over time.”5
• Ozempic slows down digestion — This is what causes your stomach to produce more acid. Having higher amounts of stomach acid then results in acid reflux (heartburn), and when the acid goes back up and reaches your teeth, it “will absolutely contribute” to tooth decay, Marshall said.6
• Another one of Ozempic’s major side effects is vomiting — Semaglutide delays digestion, which can cause bloating, nausea, and vomiting. When you repeatedly vomit, the hydrochloric acid in your vomit erodes your teeth’s enamel, the protective outer surface. In particular, the back surface of the teeth is more prone to being damaged.7
• Bad breath is another concern — The reduced saliva production in your mouth allows bacteria like Streptococcus mutans, Lactobacillus strains, and Porphyromonas gingivalis to thrive, which leads to foul odor. Lack of saliva means your tongue is not being cleaned properly, which further contributes to halitosis.8
• Ozempic alters how you taste food — Dr. Daniel Rosen, a New York-based obesity specialist, said that people who take the injection also change the way they view food — a phenomenon dubbed as “Ozempic tongue.” While this is mainly due to the different taste receptors on the tongue, the effect could be related to your brain, too.
“You have to remember that taste is not just in your tongue it is also in your brain. We know GLP-1s lessen the dopamine hit from food, making the experience less enjoyable, which could be why tastes start to shift. Think of seeing a photo of a juicy burger on a menu and that first bite with the explosion of flavor in your mouth and juices dripping down to your chin,” Rosen said.
“That is the pleasure system in the brain responding to food. If all of that is dampened or turned off in the brain because of the GLP-1 medications you can see why someone would say food tastes different or that things don’t taste the same. Patients might say everything tastes the same, or food tastes so bland.”9
• Your oral health is not an isolated concern — It reflects the state of your systemic well-being. For example, the bacteria P. gingivalis produced as a side effect of Ozempic use not only leads to periodontal disease, but also impairs your innate immune response and raises your risk of Type 2 diabetes, heart disease, pneumonia, autoimmune disease, and mental health issues.
These recent alarms about Ozempic are a clear indication of how it’s setting off a silent breakdown, and if you’re not paying attention, the damage could become irreversible. Read “Ozempic and Other Weight Loss Drugs Linked to 162 US Deaths” to learn more about the damaging effects of these drugs.
You Lose More Than Just Body Fat — You Lose Bone and Muscle, Too
Another striking yet underreported side effect of GLP-1 drugs? Rapid loss of bone and muscle mass. With every injection, you’re just not shedding body fat; you’re also shrinking your bones and lean muscles, which has severe health consequences. According to an article in LADBible, “Losing this muscle can impair someone’s strength and joint stability, while reduced bone density also raises the risk of osteoporosis, a condition which can cause brittle bones.”10
• Nearly half of your weight loss could be coming from your bones and muscles — In one clinical trial on semaglutide, 140 participants were tracked over 68 weeks to observe its effects on obese individuals. While the participants lost 23 pounds of fat, they also lost 15 pounds of lean muscle mass. That’s nearly 40% of their total weight loss coming from tissue the body actually needs to survive and thrive.11
• The elderly are more severely affected — According to a Daily Mail article, individuals already dealing with age-related degeneration — postmenopausal women, older adults, and those with low baseline muscle mass — are suffering the worst outcomes from these weight-loss injections. Professor Carl Heneghan, director of Oxford University’s Centre for Evidence-Based Medicine, said:12
“Any drug that reduces muscle mass and bone density is a bad idea for people who are frail and those vulnerable to fractures with osteoporosis. The evidence is clear — these drugs carry significant risks and the longer a patient stays on them, the greater the risk.”
• Alarmingly, young people are also affected — Ozempic’s effects on bone and muscle loss aren’t just seen in the elderly. The LADBible article highlights how Avery, a 30-year-old singer, developed full-blown osteoporosis and osteopenia after just one year on Ozempic, taking the weight loss drug without a prescription.13
Osteoporosis typically affects postmenopausal women or elderly adults. So seeing this disease emerge in a young adult with no prior history is a clear warning sign that something is very wrong. On her social media, the singer warned people not to make the same mistake she did. “It’s become very normalized, but it’s really dangerous. I just can’t believe I did that damage to myself,” Avery said.14
These findings show how these “miracle drugs” alter your physiology at a foundational level. And if you keep using these shortcuts, you could find yourself paying a steep price for that slimmer waistline.
Your Oral Health Affects Your Overall Health Far More Than You Think
As I’ve mentioned in my previous articles, your mouth serves as a window to your physical and mental health — it’s the first indicator that something is not functioning properly inside your body. What’s more, the damage that Ozempic causes to your oral health could pave the way for worse health issues, such as:
• Cardiovascular disease — A review published in the Journal of Endodontics analyzed data from 12 research papers and found that people who have already lost all their natural teeth or only have fewer than 10 natural teeth remaining were 1.66 times more likely to die from heart-related issues compared to those with more teeth.15
• Infections — Having gum disease means your gums are inflamed; when this happens, pathogenic bacteria and viruses can enter your body through the leaky nature of your blood vessels. Once inside, they can spread to various areas via the bloodstream. When these harmful microbes reach your organs, they lead to inflammation and trigger disease.
• Alzheimer’s disease — A 2023 study published in the Neurology journal found that periodontitis (gum infection) causes your hippocampus to shrink — a marker of this neurodegenerative disease.16
When multiple systems in your body are struggling, your gums are often the ones that break down first. This is because although the gum tissues regenerate quickly, they are also exposed to constant bacterial challenges. That makes them both vulnerable and valuable as an early warning system. For this reason, I recommend implementing strategies to protect your oral health.
In addition, if you’re using Ozempic and are experiencing the telltale oral symptoms, it’s a sign that something more sinister is going on inside your body. The best course of action is to simply stop using these drugs.
Strategies to Manage Your Weight Naturally
You don’t need to rely on GLP-1 drugs to bring your weight back to a healthy state. Instead, I recommend optimizing your cellular energy production through a multifaceted approach that involves various diet and lifestyle changes.
While it takes effort to implement, the results are safer, healthier, and long-term — something Ozempic and other weight loss drugs just can’t offer. Here are strategies that I recommend for healthy weight management:
1. Avoid Ozempic and other GLP-1 drugs — Don’t fall for the hype. Although these medications initially seem efficient in eliminating excess fat, their benefits are usually short-lived and the side effects are damaging.
2. Eliminate vegetable oils from your diet — If you regularly consume ultraprocessed foods, I recommend stopping right now and replacing them with real, whole foods. Processed foods contain linoleic acid (LA)-rich vegetable oils that disrupt your metabolic pathways and alter how your body stores fat. Instead, cook your meals using tallow, grass fed butter, or coconut oil.
I also recommend downloading my new Health Coach app, which will come out soon. It has Seed Oil Sleuth™, a unique feature that will help identify every hidden source of seed oils in your meals. It also calculates your daily intake to the nearest tenth of a gram. Just scan the QR code below to join the early-access list to the app.
3. Shift your carbohydrate sources gradually — Avoid making sudden dietary changes that will shock your system. If your gut is compromised, start by introducing easily digestible carbohydrates like whole fruit or white rice before incorporating more complex carbs. If you have severe gut issues, sip dextrose water to provide your cells with a steady source of easy-to-digest, healthy carbohydrates for energy. After a week or two, begin to transition over to whole fruit or white rice.
4. Consider your protein and collagen intake — I suggest aiming for 0.8 grams of protein per pound of your ideal body weight and balancing that amount so that about one-third comes from collagen. This will help support muscle maintenance, tissue repair, and hormone balance.
If you exercise frequently, you might need to slightly increase your intake. My suggestion is to take it slow and listen to how your body responds. Stable protein intake is foundational for regulating cravings and stabilizing energy.
5. Support your mitochondrial health with other healthy habits — Getting daily sun exposure is one example; however, if you’re still consuming vegetable oils, make sure to avoid intense midday sun for at least four to six months. The LA in these oils migrate to your skin and oxidize under sun exposure, causing skin damage. Read “The Role of Sun Exposure in Optimizing Your Cellular Health” for more information.
Get enough sleep at night, minimize your stress, and incorporate moderate-intensity movement, such as walking, in your lifestyle. These strategies will support your cellular energy production and aid in weight management.
Remember, the shortcut to optimal health — and healthy weight loss — does NOT exist. If you’re still tempted to start using weight loss medications, use caution; make sure to read the studies, familiarize yourself with the side effects, and make sure you understand the dangers of these drugs.
Frequently Asked Questions (FAQs) About Ozempic and Oral Health
Q: What are “Ozempic teeth,” and why are people talking about them?
A: “Ozempic teeth” refers to a cluster of dental issues — such as tooth decay, gum infections, dry mouth, and enamel erosion — reported by users of GLP-1 weight-loss drugs like Ozempic, Wegovy, and Mounjaro. These side effects are not listed on drug labels, but dentists and patients are seeing a consistent pattern of sudden, severe oral deterioration.
Q: How do GLP-1 drugs like Ozempic damage your teeth and gums?
A: These drugs reduce saliva production, which normally helps clean the mouth and protect teeth. They also slow digestion, increasing acid reflux and vomiting — both of which bathe the teeth in acid. This combination erodes enamel, inflames gums, and creates the perfect environment for bacteria to thrive.
Q: Who is most at risk for these oral and bone-related side effects?
A: People with already compromised dental health, dry mouth, or poor digestion are especially vulnerable. Older adults, postmenopausal women, and those with low muscle mass are also at higher risk for severe bone loss and fractures caused by the rapid loss of lean tissue on these drugs.
Q: What’s causing the bad breath and strange taste changes reported with Ozempic use?
A: Reduced saliva allows harmful bacteria to thrive, leading to bad breath. Some users also report “Ozempic tongue,” where food tastes bland or unappealing. This shift is likely due to how GLP-1 drugs affect dopamine and taste perception, altering how the brain processes food-related pleasure.
Q: What are safer, long-term alternatives to GLP-1 weight loss drugs like Ozempic?
A: Instead of relying on injections, focus on restoring your body’s ability to produce energy efficiently. Start by removing vegetable oils from your diet, gradually reintroduce healthy carbohydrates like fruit or white rice, especially if your gut is sensitive, and prioritize protein and collagen (0.8 grams per pound of ideal body weight, with one-third from collagen). Support your mitochondria with sun exposure, quality sleep, stress reduction, and consistent movement like walking.
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