PUFA and endotoxin cause Alzheimer’s disease, while tau and amyloid beta protect the brain

You may have heard that Alzheimer’s disease occurs when tau protein and amyloid beta protein accumulate in the brain. But new evidence suggests that these proteins may not be the root cause of the disease, but rather a protective response to the underlying problem.

A study published in Nature Neuroscience adds additional insight into the role of tau protein in brain health, challenging the long-held belief that it is linked to Alzheimer’s disease.¹ Studies have shown that tau protects brain cells from oxidative stress and toxic lipids.

Tau protein is essential for forming lipid droplets in glial cells (support cells that surround and protect neurons). These lipid droplets act as a defense mechanism and help neutralize harmful oxidized lipids that damage brain cells.

When researchers increased tau levels in glial cells, this protective process was disrupted, making the cells more vulnerable to toxic lipids produced by stressed neurons. In other words, the tau accumulation seen in Alzheimer’s disease may be the brain’s attempt to fight off ongoing damage rather than the culprit.

Tau’s positive role in brain health

The brain’s glial cells are important for maintaining cognitive health and have developed remarkable mechanisms to protect the brain from oxidative stress. When neurons experience high levels of reactive oxygen species (ROS), they produce and release toxic lipid peroxides (LPO) as a self-preservation strategy.

LPO is a phenomenon that occurs when PUFAs are damaged. Glial cells then come to the rescue, absorbing these dangerous lipids and storing them in lipid droplets.²

This process is like a cellular recycling program in which glial cells safely contain and break down toxic lipids that can harm neurons. Research has found that the tau protein is important for these protective mechanisms to function properly.

Without enough tau, glial cells have difficulty forming these protective lipid droplets, making neurons more susceptible to oxidative damage. This finding highlights the importance of maintaining the delicate balance of tau in the brain. Too little is just as problematic as too much.

Accumulation of amyloid beta is a protective mechanism

The prevailing theory of Alzheimer’s disease focuses on the accumulation of amyloid beta (Aβ) plaques as the primary cause of cognitive decline. However, accumulating research has shown that Aβ plays a protective role in the brain.³

A study published in Alzheimer’s & Dementia found that⁴ We found a correlation between Aβ accumulation and glucose metabolism in the brains of Alzheimer’s patients. Contrary to popular belief, regions with higher average glucose metabolism have been shown to have greater Aβ deposition. This suggests that Aβ may accumulate more easily in brain regions with high metabolic activity as a protective measure.

Think of Aβ as the brain’s attempt to protect itself from damage in the most active areas. However, this protection appears to have limits. Higher levels of Aβ in individual brain regions of Alzheimer’s patients have been shown to be associated with lower glucose metabolism, indicating that excessive Aβ accumulation may eventually impair normal brain function.

This dual nature of Aβ – initially protective but potentially harmful in excess – may explain why Alzheimer’s treatments aimed at eliminating Aβ have largely failed.⁵

Despite this, the U.S. Food and Drug Administration (FDA) continues to approve dangerous Alzheimer’s drugs, including Leqembi, which binds to amyloid beta in the brain. Relying on medications to reduce amyloid beta is at best misguided and at worst exposing patients to potentially life-threatening side effects without any benefit. Alzheimer’s disease is a complex disease that requires a holistic approach for prevention and treatment.

Tau protein and Aβ appear to be the brain’s response to underlying damage rather than being the primary cause of neurodegeneration. Tau, in particular, is involved in stabilizing microtubules in neurons and may play a role in protection against oxidative stress. Likewise, Aβ acts as an antioxidant and may help seal damaged blood vessels.

The brain produces these proteins as a defense mechanism, but if the underlying cause of damage persists, their buildup can become excessive and potentially harmful. This shift in perspective highlights the importance of addressing root causes, such as metabolic dysfunction and inflammation, rather than focusing on tau and Aβ clearance.

How Seed Oils and Endotoxins Cause Alzheimer’s Disease

A thriving gut ecosystem is essential for overall health, including brain function. This diverse microbial community plays an important role in protecting the body against a variety of diseases, including Alzheimer’s disease. However, a diet rich in polyunsaturated fats (PUFA), including linoleic acid found in seed oils, wreaks havoc on gut health, leading to a series of harmful effects. Bioenergetics researcher Georgi Dinkov explains:⁶

“(Natural Neuroscience) Research⁷ It has been argued that ROS seen in Alzheimer’s disease (AD) may be caused by excessive lipid accumulation (e.g. in diabetes) and that this accumulation (even when localized to the brain) can itself be easily caused by a low-carbohydrate/high-fat diet. “

Nurturing beneficial oxygen-intolerant bacteria in the gut, including important species such as Akkermansia, strengthens gut defenses and promotes overall health. These beneficial bacteria ferment dietary fiber to produce short-chain fatty acids (SCFA), especially butyrate.

In particular, butyrate-producing bacteria, such as Eubacterium and Eisenbergiella, have been linked to a lower risk of Alzheimer’s disease.⁸ Butyrate strengthens the intestinal barrier by nourishing colonic epithelial cells. SCFAs also stimulate mucus production, creating a protective barrier against harmful bacteria.

Risk of leaky gut and endotoxemia

A decrease in oxygen-intolerant bacteria leads to increased intestinal permeability or intestinal leakage. This can cause toxins, undigested food particles, and harmful microorganisms to enter the bloodstream, causing systemic inflammation and chronic health problems. This inflammation may contribute to underlying damage promoting protective accumulation of Aβ and tau in the brain. Oxygen-intolerant bacteria are essential for converting indigestible plant fibers into beneficial fats.

They thrive in oxygen-free environments and require adequate cellular energy to sustain them. However, factors such as seed oil consumption, endocrine disrupting chemicals (EDCs) from plastics, and exposure to electromagnetic fields (EMFs) can impair this energy production, making it difficult to maintain an ideal anaerobic intestinal environment.

Additionally, the toxic lipids that tau helps neutralize are often a byproduct of excessive consumption of PUFAs and exposure to endotoxins. These factors cause chronic inflammation and oxidative stress in the brain, leading to the cognitive decline associated with Alzheimer’s disease.

In my opinion, the leading cause of death is endotoxemia, which leads to septic shock. This occurs when facultative anaerobes, also known as oxygen-tolerant bacteria, secrete endotoxins that should not be in the intestines. These pathogenic bacteria produce a highly toxic form of endotoxin, or lipopolysaccharide (LPS), which causes inflammation when it crosses the damaged intestinal barrier and enters the systemic circulation.

I would like to introduce a new, easy term to our vocabulary to identify the concept of Mighty Shock. Mighty is an abbreviation for mitochondria and describes mitochondria, which are targets of endotoxins. The reason endotoxin release is so dangerous is because it poisons and shuts down the mitochondria. I’ll be discussing this topic a lot more in the future, so get ready for more articles on Mighty Shock.

This chronic low-grade inflammation contributes to metabolic dysfunction preceding Aβ accumulation in AD, as discussed in previous studies. Therefore, leaky gut or a disturbed microbiome is one of the fundamental causes of all diseases, including neurodegenerative diseases such as Alzheimer’s disease.

Improving mitochondrial function and maintaining a healthy gut ecosystem reduces the effects of harmful endotoxins while promoting the growth of beneficial bacteria. Rather than focusing on eliminating Aβ and tau proteins, this approach alleviates factors that contribute to dementia and other chronic diseases by addressing the root causes of inflammation and metabolic disorders.

A holistic approach to brain health

Understanding the protective role of Aβ and tau, along with the importance of gut health, opens new avenues for the prevention and treatment of Alzheimer’s. Instead of targeting these proteins directly, future treatments could focus on supporting the brain’s natural protective mechanisms while addressing the root causes of neurodegeneration.

This includes strategies to reduce inflammation and optimize brain metabolism through gut health interventions. By fostering a healthy gut microbiome and addressing factors that disrupt the balance of oxygen-intolerant and oxygen-tolerant bacteria, excessive accumulation can be prevented while maintaining the protective effects of Aβ and tau.

Armed with this new understanding, you can take proactive steps to support brain health and reduce your risk of Alzheimer’s disease. By adopting a holistic approach to brain health that addresses these underlying factors, you can support the brain’s natural protective mechanisms and maintain cognitive function as you age. In addition to optimizing mitochondrial function, the strategies below may help reduce your risk of Alzheimer’s disease.