The Great Alzheimer’s Scam and the Proven Cures They’ve Buried for Billions
January 2, 2026 A Midwestern Doctor and Dr. Mercola 5
Freepik
Over 7 million Americans have Alzheimer’s — equating to hundreds of billions in potential (Medicare funded) sales each year. Almost all Alzheimer’s research for decades has been directed toward eliminating amyloid that destroys brain tissue, even after the basis for much of this work was shown to stem from fraudulent research. Chronic inflammation plays a much larger role in the disease.
Last year, Alzheimer’s was estimated to cost the United States 360 billion dollars! The billions spent on amyloid Alzheimer’s research have only produced three drugs, all of which offer minuscule benefits and severe side effects. Other affordable remedies are available. 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.
[Note: The Need To Know News does not give medical advice, but reports the news; please consult with your own health experts before using any treatment]
amyloid plaques
[Note: this article published by Dr. Mercola is a shortened version of an article originally posted by a Midwestern Doctor – links can be found at the end of this post]
Story at-a-glance
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.
Join the Coalition! Become an affiliate member today! Click Here!
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.
•Removing amyloid offers minimal benefit and may be counterproductive. In fact, one of the only protocols that has had proven success in treating Alzheimer’s instead views amyloid as a protective mechanism the brain uses to prevent further damage.
•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
change in cognitive performance
Save
Note: The RECODE protocol was based around identifying the underlying cause of a patient’s cognitive impairment (as five different things can cause dementia), and then providing appropriate natural therapies to address the applicable cause. Since then, many others have replicated its success in their patients.
DMSO and Dementia
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.
lance grindle dmso
As many of DMSO’s mechanisms directly counteract the processes that trigger dementia, I have received many accounts like these from readers:
“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. 7 million Americans have Alzheimer’s — equating to hundreds of billions in potential (Medicare funded) sales each year. Almost all Alzheimer’s research for decades has been directed toward eliminating amyloid that destroys brain tissue, even after the basis for much of this work was shown to stem from fraudulent research. Chronic inflammation plays a much larger role in the disease.
Last year, Alzheimer’s was estimated to cost the United States 360 billion dollars! The billions spent on amyloid Alzheimer’s research have only produced three drugs, all of which offer minuscule benefits and severe side effects. Other affordable remedies are available. 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.
[Note: The Need To Know News does not give medical advice, but reports the news; please consult with your own health experts before using any treatment]
.
[Note: this article published by Dr. Mercola is a shortened version of an article originally posted by a Midwestern Doctor – links can be found at the end of this post]
Story at-a-glance
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.
Join the Coalition! Become an affiliate member today! Click Here!
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.
Dr. Nathan Bryan is a nitric oxide biochemist who has researched nitric oxide, a hormone, for the past 18 years. Nitric oxide is a gas produced in the endothelial cells that line blood vessels. There is a steep decline in nitric oxide from age 30 onward. When endothelial cells can no longer make nitric oxide gas, they no longer dilate and the blood vessels become constricted, causing inflammation, stiff arteries and plaque deposition that starts cardiovascular disease. Nitric oxide deficiency can also cause diabetes and Alzheimer’s Disease. He told a story about his father who was a paraplegic and a diabetic and had wounds that would not heal for 4 years. But when Dr. Bryan gave him topical nitric oxide treatments, the wounds healed in 6 months. he says nitric oxide can kill infections.
He explained that to boost nitric oxide production, we must stop eating sugars and other foods that are high on the glycemic index because it binds to almost everything and acts as a toxin. It destroys the microbiome. He said that is why diabetics have a 10 times higher incidence of heart attack, stroke, all cause mortality, and more.
Most Americans are deficient in vitamin D that is necessary for the production of nitric oxide. Mouthwash, which is used by 2/3 of Americans, is very destructive and kills the oral microbiome that helps produce nitric oxide.
He recommends eating zero sugar, good high quality protein, good quality fats, and few carbs.
Note: Need To Know News reports the news and does not make any health claims. Please consult your own health care professional before taking any supplements or changing your diet..
Before memory and thinking problems become obvious, people with dementia may display changes in mood and behavior
In the early stages of the disease, irritability, anxiety or depression may occur
Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food off other people’s plates
Alzheimer’s disease is the result of poor mitochondrial function; to optimize your mitochondrial function, you need to limit your intake linoleic acid (LA) to 5 grams a day or less
To achieve this, you’ll need to eliminate all processed foods, fast foods and the majority of restaurant meals, which are frequently loaded with or prepared using seed oils high in LA
Worldwide, more than 55 million people are living with dementia, and each year nearly 10 million new cases occur.1 Dementia is not a disease in itself but rather a term used to describe a number of different brain illnesses that may affect your memory, thinking, behavior and ability to perform everyday activities. The most common type of dementia is Alzheimer’s disease, which accounts for up to 70% of cases.2
Many people associate dementia with memory loss — and this is a red flag — however, not all memory problems are due to Alzheimer’s (and some causes of dementia-like symptoms, including memory loss, can be reversed, such as those related to thyroid problems and vitamin deficiencies).3
If you’ve noticed yourself or a loved one becoming increasingly forgetful or experiencing changes in thinking abilities, you should see a health care provider right away. Oftentimes, however, the first symptoms are so subtle they may be easily missed — and they may manifest as changes in behavior and mood long before memory problems become apparent.
Fortunately, there are two crucial prevention strategies that remain largely underdiscussed yet are relatively simple to implement — reducing linoleic acid (LA) intake and limiting exposure to estrogen.
Pay Attention to Personality Changes — An Early Sign of Dementia
Before memory and thinking problems become obvious, people with dementia may display changes in mood and behavior, according to a team of neuropsychiatrists and Alzheimer’s experts, who say the latter symptoms may be among the earliest signs of dementia.
The team released a 34-question checklist they believe could help diagnosis a new condition called mild behavioral impairment (MBI).4 Similar to mild cognitive impairment (MCI), which is defined by a noticeable decline in cognitive abilities that does not yet interfere with most daily functions, MBI describes changes in behavior and mood that may occur prior to MCI and the cognitive changes associated with dementia.
The checklist is intended to identify patients at risk of dementia earlier, as according study author Dr. Zahinoor Ismail, a neuropsychiatrist at the University of Calgary, among people with MCI, those with mood and behavior changes will progress to full-blown dementia faster.5 Some have expressed concern that the checklist may lead to overdiagnosis or false diagnosis, putting some people through increased medical testing and worry unnecessarily.
In the case of MCI, for instance, not everyone diagnosed will go on to develop Alzheimer’s or other types of dementia. In fact, The New York Times reported, up to 20% of those with MCI later turn out to be cognitively normal.6
Still, others say keeping an eye out for unusual behavioral or personality changes can help people get help, at least symptom relief, faster. Sadly, there is currently no cure for Alzheimer’s disease and, as it progresses, the disease is devastating not only for those diagnosed but also their friends and family. Prevention remains the best option, and I detail steps that can help below.
Behavioral and Mood Changes to Watch Out For
Dementia manifests differently in everyone, which is why the most important changes to watch out for are those that are unusual for your loved one. A person may, for instance, stop doing something they’ve always loved to do, be it cooking a certain dish for your birthday or watching the evening news.
Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food off other people’s plates.7 The Alzheimer’s Association noted:8
“Individuals living with Alzheimer’s or other dementia may experience mood and personality changes. They can become confused, suspicious, depressed, fearful or anxious. They may be easily upset at home, with friends or when out of their comfort zone.”
In the early stages of the disease, irritability, anxiety or depression may occur. In fact, a study published in the journal Neurology not only found that people who eventually developed dementia were twice as likely to develop depression earlier on in their lives, but they also tended to display mood changes in a consistent pattern.9 Time reported:10
“The symptoms appeared in consistent phases: first, irritability, depression and nighttime behavior changes; followed by anxiety, appetite changes, agitation and apathy. The final phase was elation, motor disturbances, hallucinations, delusions and disinhibition.”
In order for early mood and/or behavioral changes to be considered MBI, the change in behavior must persist for at least six months.
Signs of Mild Cognitive Impairment
In some people, MCI may follow the earliest changes in mood and behavior. MCI is a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease, although it is by no means a guarantee. It’s estimated that up to 18% of people aged 60 and older are living with MCI.11
Simply misplacing your keys on occasion is not cause for alarm, however forgetting important information that you would have normally recalled, such as appointments, conversations or recent events, may be a sign. You may also have a harder time making sound decisions, figuring out the sequence of steps needed to complete a task or judging the time needed to do so.
If you’ve been diagnosed with MCI, be aware that some cases do not progress and may even improve. Regular exercise, proper diet — including reducing your intake of LA — and engaging in mentally and socially stimulating activities may help to boost your brainpower.
Dementia: When to Worry?
It can be difficult to gauge if a loved one is declining mentally. If you have suspicions but aren’t sure, try keeping a notebook to jot down instances that concern you. You may be able to identify a pattern of events that makes the picture clearer.
Agnes B. Juhasz, nurse, dementia care specialist and author of ‘The Dementia Whisperer: Scenes From the Frontline of Caring,’ suggested making note of anything out of ordinary for that particular person. She wrote in the [U.K.]’s Mirror news:12
“Naturally, there are a few typical signs and possible changes that are worth watching out for more closely. These include the level of forgetfulness; acute or permanent confusion about certain things; disorientation in time and place; significant changes in behavior and personality; decreased judgment; changes in speech or writing; and withdrawal from social interactions and activities.
But all these suggested signs ultimately lead us back to the essential, magical question we always have to ask before we can arrive at any further conclusions: ‘Is this abnormal for this individual, or is it part of who they have always been?’ When we notice that something is new and odd, that has never occurred in a person’s life before, as far as we have observed, that is the point when further help may be needed.”
Early Warning Signs of Alzheimer’s
While an absent-minded mistake, like putting a mug in the wrong cabinet, is not cause for alarm, feeling confused about day-to-day tasks is.
Losing interest in hobbies, repetitive behaviors (phrases, gestures or questions), mispronouncing words or stuttering can also be signs. And while occasional forgetfulness, like forgetting why you were walking into a room, is not typically reason to worry, more profound confusion, like the room itself feeling unfamiliar, may signal a problem.13
The Alzheimer’s Association also compiled differences between symptoms of dementia, including Alzheimer’s, and typical age-related changes:14
Signs of Alzheimer’s/dementia
Typical age-related changes
Poor judgment and decision-making
Making a bad decision once in a while
Inability to manage a budget
Missing a monthly payment
Losing track of the date or the season
Forgetting which day it is and remembering it later
Difficulty having a conversation
Sometimes forgetting which word to use
Misplacing things and being unable to retrace steps to find them
Losing things from time to time
Why Addressing Mitochondrial Dysfunction by Reducing LA Is Key
Work by the late Ray Peat, a biologist and “father” of bioenergetic medicine, suggests Alzheimer’s disease is the result of poor mitochondrial function, which results in reduced energy production.15,16
To optimize your mitochondrial function, you need to address your diet, as the foods you eat are the substrate from which cellular energy is produced. LA wreaks havoc with your cellular machinery, which is why it should be limited to 5 grams or less per day.
To achieve this, you’ll need to eliminate all processed foods, fast foods and the majority of restaurant meals, which are frequently loaded with or prepared using seed oils high in LA. Instead, prioritize whole and minimally processed foods.
In addition to limiting LA in your diet, carnosine, a dipeptide composed of two amino acids — beta-alanine and histidine — is a crucial aid for LA detoxification, as it binds to advanced lipoxidation endproducts (ALEs) that form from oxidized seed oils in your diet.
While your body will slowly eliminate stored LA over time, provided you reduce your intake, carnosine can help reduce the oxidative damage caused by LA while your body is cleaning itself out. I take liposomal carnosine every day before meals to help detoxify LA.
LA is highly susceptible to oxidation, and as the fat oxidizes it breaks down into harmful sub-components such as ALEs and oxidized LA metabolites (OXLAMs). These ALEs and OXLAMs are what cause most of the damage.
Carnosine binds to ALEs like a magnet and acts as a sacrificial sink. It’s basically a substitute target for these profoundly damaging molecules. In this way, carnosine allows your body to excrete the ALEs from your body before they damage your mitochondria, DNA or proteins.
As an added benefit, carnosine is protective against Alzheimer’s,17 due to its ability to scavenge 4-hydroxynonenal (4HNE), a biomarker of oxidative stress that may increase the harm caused by free radicals.
Elevated Serotonin Linked to Dementia
High serotonin levels are also linked to dementia.18 While often described as the “happy hormone,” serotonin, a chemical messenger in the brain, acts as an antimetabolite, hindering energy production in your mitochondria. A September 2023 study found that having low levels of serotonin transporter (SERT) is linked to problems with memory and thinking skills, which can eventually lead to dementia or Alzheimer’s disease.
SERT is like a “cleanup crew” in the brain, helping to remove excess serotonin. When there’s not enough SERT around to do its job, serotonin levels outside of brain cells can rise too high. This excess serotonin floating around can cause trouble and contribute to problems with memory and thinking.
Considering that high extracellular serotonin can contribute to dementia, you’d be wise to keep your serotonin level as low as possible. One way to do that is by increasing GABA, which is available as a supplement.
The Estrogen Connection
Alzheimer’s disease (AD) is more common in women than men,19 and prolonged estrogen exposure is also linked to Alzheimer’s severity in women.20 As bioenergetic researcher Georgi Dinkov explained, “The study can be summarized with the simple statement that estrogen is detrimental while progesterone and testosterone are protective against AD.”21
Avoiding estrogen replacement therapy and minimizing your exposure to the estrogenic compounds found in hundreds of consumer products is therefore an important step to protecting your brain health.
Taking natural progesterone is also important, but be aware that most formulations are not effective as they are oral or transdermal. Ideally, pure progesterone powder should be dissolved in a high-quality vitamin E with MCT oil and rubbed on your gums. Typical doses are 25 to 50 milligrams once or twice a day.
In my view, what mature women really need are progesterone and pregnenolone, not estrogen. In practical terms, you’ll want to make sure your levels of progesterone and pregnenolone are within healthy limits (the levels you’d have in your 20s), which is around 30 mg a day.
More Tips to Prevent Alzheimer’s Disease
In addition to optimizing your mitochondrial function, lowering your intake of LA and avoiding things that raise your serotonin and estrogen, other helpful Alzheimer’s prevention strategies include:
Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — Research shows that your blood-brain barrier is negatively affected by gluten. Gluten also makes your gut more permeable, which allows proteins to get into your bloodstream, where they don’t belong. That then sensitizes your immune system and promotes inflammation and autoimmunity, both of which play a role in the development of Alzheimer’s.
Optimize your gut flora by regularly eating fermented foods or taking a high potency and high-quality probiotic supplement.
Make sure you’re getting enough animal-based omega-3 fats, such as krill oil. High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression and lowering your risk of developing the disorder.
Optimize your vitamin D level with safe sun exposure — Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. In one 2023 study, vitamin D reduced dementia risk by 40%.
Keep your fasting insulin levels below 3.
Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day. Avoid supplements like folic acid, which is the inferior synthetic version of folate.
Avoid and eliminate mercury and aluminum from your body — Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity. Make sure you use a biological dentist to have your amalgams removed. Sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants.
Make sure your iron isn’t elevated and donate blood if it is — Studies show that iron accumulations in the brain tend to concentrate in areas most affected by Alzheimer’s, namely the frontal cortex and hippocampus. Magnetic resonance imaging tests have also revealed elevated iron in brains affected by Alzheimer’s.
Exercise regularly — It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,22 thus slowing down the onset and progression of Alzheimer’s. In one study, women with the highest cardiovascular fitness had an 88% lower risk of dementia than those with moderate fitness.
Eat blueberries and other antioxidant-rich foods — Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against neurological diseases.
Challenge your mind daily — Mental stimulation, especially learning something new, such as how to play an instrument or speak a new language, is associated with a decreased risk of Alzheimer’s.
Avoid anticholinergics and statin drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers.
Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of CoQ10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.
