The Great Alzheimer’s Scam and The Proven Cures They’ve Buried for Billions

What if… amyloid plaques in the brain were the body’s way of trying to PROTECT THE BRAIN… and not the cause of Alzheimer’s?

https://www.midwesterndoctor.com/p/the-great-alzheimers-scam-and-the

Some snippets:

“Dale Bredesen’s Discovery

Dale Bredesen is a creative neurologist with a background in functional medicine who spent several years examining the Alzheimer’s question. From it, as detailed in The End of Alzheimer’s, he reached a few pivotal conclusions:

•Amyloid protein is a protective mechanism the brain uses to protect itself from other stressors that endanger brain tissue.

•Rather than there being one type of Alzheimer’s, there are actually three with different symptoms, and it is essential to recognize which type someone has before initiating treatment.

•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, in turn, results from the loss of signals that sustain brain cells, and the dismantling of neural connections outweighing the formation of new ones, gradually compounding over the decades.

As such, his formula was fairly straightforward: identify the type of Alzheimer’s someone has, eliminate its causes, and gradually wait for the physiological momentum to shift from neurodegeneration to neurodevelopment.

Most importantly, as the previous chart showed, his model worked. Beginning with a 2018 report of 100 patients from numerous providers whose cognitive decline was reversed by this model, a pilot study (completed in 2022) was able to show these remarkable case reports could be replicated in a controlled manner:”

—-

“What Causes Alzheimer’s Disease?

This mirrors the three hats worn by the multitalented molecule, amyloid-beta, which is derived from APP. It is part of the inflammatory response and can function as an antimicrobial agent (thus it is part of your body’s ability to fight infections); it responds to inadequate levels of hormones, vitamins, nutrients, and other supportive (or trophic) factors by downsizing the more expendable synapses; it is part of the protective response to toxin exposure—for example, binding very tightly to metals such as mercury and copper [due to its negative charge].

In Bredesen’s model, there are multiple distinct types of Alzheimer’s disease, reflecting different underlying causes. The original three subtypes have since been expanded to at least five, each representing a different biological driver of cognitive decline. 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. This subtype often presents with classic Alzheimer’s memory loss and typically develops in the sixties to seventies. However, in individuals with substantial genetic risk (e.g., APOE4 carriers), it may appear earlier—in the late forties to fifties, or in the late fifties to sixties for those with a milder genetic predisposition.

• Type 1.5 – Glycotoxic: Sometimes referred to as a hybrid of Types 1 and 2, 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 and is especially common in individuals with prediabetes or metabolic syndrome.
Note: the enzyme the body uses to break down insulin (which is nearly always chronically elevated in those who have metabolic syndrome) is the same enzyme it uses to break down amyloid plaques. Likewise, because elevated insulin levels and metabolic dysfunction play such a key role in Alzheimer’s, this has led many to refer to it as “type 3 diabetes.”

• Type 2 – Atrophic: This type is caused by deficiencies in nutrients, hormones, and other factors that provide trophic (supportive) signals to brain cells. These include vitamin D, thyroid hormone, estrogen, progesterone, testosterone, and brain-derived neurotrophic factor (BDNF), among others. The resulting lack of neuronal support triggers a similar downsizing mechanism seen in Type 1. Type 2 tends to emerge about a decade later than Type 1 and may occur alongside it, particularly in individuals experiencing both inflammation and hormonal/nutritional decline.
Note: I believe that in many cases, functional nutritional deficiencies result not from a lack of nutrients, but rather from a lack of fluid circulation that prevents those nutrients from reaching the cells. For this reason, I find that better results are sometimes seen from improving fluid circulation rather than aggressively increasing supplemental nutrition.

• Type 3 – Toxic: This subtype results from exposure to toxic substances that directly damage neurons. Common culprits include biotoxins, such as mold-derived mycotoxins (from water-damaged buildings—which is a huge issue), chronic infections (including Lyme disease), heavy metals (like mercury and lead), and industrial or household chemicals.
Note: the exact infectious agents are a matter of debate. For example, we’ve found that Cytomegalovirus, and Human Herpesvirus 6, can periodically cause cognitive decline, and once an appropriate antiviral is administered, a significant improvement is observed. Likewise, many believe Lyme bacteria within the brain is one of the most common infectious causes of cognitive decline and frequently treat it to address the condition. Bredesen, in his work highlights the importance of Herpes simplex-1 virus, Lyme disease (a spirochete bacterium), P. gingivalis (an oral bacterium), and various fungal infections (mold toxins are notorious for causing cognitive impairment at all ages). Others also emphasize the importance of oral spirochete bacteria, which can travel into the brain.

Unlike Types 1 and 2, which involve more selective and adaptive brain responses, Type 3 causes widespread and often unpredictable neuronal death. It typically occurs earlier in life—often between the forties and sixties—and is less strongly associated with genetic risk factors, such as APOE4. 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. This type typically cannot be reversed unless the source of toxicity is identified and removed.

Note: I believe 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. Some of the most common problematic medications for brain health include certain high blood pressure medications (because they lower cerebral perfusion), statins (as they inhibit the production of compounds essential for brain function), acid reflux medications (which interfere with the absorption of vital brain nutrients—making it critical for everyone to have adequate stomach acid), antidepressants, antipsychotics, benzodiazepines, antihistamines (since, like many sleeping pills, they block restorative sleep), and anticholinergics (such as those prescribed for incontinence).

Additionally, after creating the initial list, he later created two more types:

• Type 4 – Vascular: In this form, chronic restriction of cerebral blood flow—due to factors such as hypertension, atherosclerosis, or small vessel disease—leads to gradual neuronal injury and cognitive decline. This vascular insufficiency deprives neurons of oxygen and glucose, impairing their function and survival. Type 4 often appears later in life (typically 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.
Note: conventionally (including within Breseden’s model) hypertension is typically viewed as a cause of arterial damage and impaired blood flow. Many believe the opposite (that the body raises blood pressure to ensure blood can still flow through damaged arteries) and that lowering blood pressure excessively can cause organs to not get the blood that they need (all of which is detailed here).

• Type 5 – Traumatic: This subtype is associated with a history of brain injury—either a single significant concussion or multiple smaller, repeated head traumas. It is especially common in athletes and military veterans (although we also see it in less concussion prone individuals). The trauma sets off a cascade of inflammation, tau accumulation, and blood-brain barrier disruption, leading to chronic cognitive and emotional dysfunction. Symptoms can emerge years or even decades after the injuries, and they often include impulsivity, emotional instability, and executive dysfunction—with the best example of this being the dementia frequently seen in professional football players (which for decades the NFL covered up).

Note: there are a variety of causes of dementia. While Alzheimer’s is the most common, other forms such as frontotemporal dementia and vascular dementia also frequently occur. In many cases, the exact type of dementia one is diagnosed with is not always correct. One study found 30.2%-56.7% of those diagnosed with AD did not have it, an autopsy study found 12-23% did not have it, and a study found 63% of those with Alzheimer’s also had another dementia causing disease process within their brain (an issue that increases with age, further increasing the difficulty of accurately diagnosing dementia). However, since each of these diseases shares a similar process that causes their formation, it should be understood that what is described here often applies to treating forms of dementia as well as Alzheimer’s.

I generally agree with this list, and hesitate to disagree with it as he has much more experience in this area than I do. However, over the years, I have met numerous gifted physicians who have had varying degrees of success in treating dementia, in many cases with protocols that showed significant improvement.

From that experience, while I have seen many compelling models provide results, I have concluded that the primary issue is poor fluid circulation to the brain and poor fluid drainage from it, as this essentially explains all the other datapoints I’ve come across and frequently yields the most direct results for patients.
Note: while nutrition is important, I believe that in many cases, functional nutritional deficiencies result from insufficient blood flow to transport the existing nutrients to the tissues. For this reason, in many cases, I find that improving circulation rather than loading up on nutrients is an ideal treatment strategy.

More importantly, I find the same pathological processes that are at work in dementia are commonly seen in many other challenging chronic illnesses, and hence view the epidemic of Alzheimer’s disease to be yet another manifestation of systemic issues giving birth to a wave of chronic disease in our society, rather than an independent isolated problem.”

Read rest here: https://www.midwesterndoctor.com/p/the-great-alzheimers-scam-and-the