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 2024), 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 dollars) 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:
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, bath 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.
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. 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). 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 body).
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.
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 paper).
In July 2022, Science published an article exposing the incident and the clear fraud that had occurred. Despite this, the researcher was allowed to remain in his position as a tenured medical school professor. It was not until June 2024 that the 2006 article was retracted at the request of the authors—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).
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.
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). The second then received a quiet backdoor approval (due to the immense controversy surrounding the first), and the third was partially approved a year and a half later.
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.”
• That drug was priced at $56,000 a year—making it sufficient to bankrupt Medicare, (which attracted a Congressional investigation).
• Brain swelling or brain bleeding was found in 41% of patients enrolled in its studies. 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 profile (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 trail (which for context, translated to a 0.45 reduction on a scale where a reduction of at least 1-2 points is needed to create an impact which is in anyway meaningful for a patient).
The third monoclonal (which targeted amyloid plaques thought to be more pathologic) 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.
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), while the other two have had very modest sales (e.g., 290 million for the most popular one).
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