This is one of the few studies that I have seen pointing directly at elevated endotoxin/LPS as a direct cause of Alzheimer Disease (AD). Just as importantly, the study suggests that eating sufficient amounts of insoluble fiber may be a viable approach to preventing/treating AD due to the known effect of said fiber in reducing both endotoxin/LPS production as well as its absorption into the blood from the gut. While the study did not mention it directly, other approaches to lowering the endotoxin/LPS burden such as activated charcoal or antibiotics, may also be viable approached to AD, with the added convenience of increased portability and very long shelf-life. Still, the naturalness of eating foods high in insoluble fiber such as a carrot salad (which Ray himself recommended widely, and recently even became viral on social media), as well as the added health benefits of foods such as carrots, probably make that a primary option/approach for most people.
https://doi.org/10.3389/fneur.2022.900048
“…At the heart of the discovery is a molecule teeming with a virulent microbial-generated neurotoxin. Named lipopolysaccharide (LPS) and sourced from the Gram-negative bacteria Bacteroides fragilis found in our gastrointestinal (GI) tract, the specific neurotoxin in question is identified as BF-LPS. Dr. Lukiw expounds, “LPSs, in a broader sense, rank amongst the most potent microbial-derived pro-inflammatory neurotoxic glycolipids we know of.” He continues, “Various laboratories around the globe, ours included, have pinpointed diverse LPS variants within neurons in the brains affected by Alzheimer’s.” To elucidate, the research meticulously maps out the journey of BF-LPS from the gut to the brain and its subsequent effects. The pathway is as follows: BF-LPS seeps out of the GI tract, bypasses the blood-brain barrier using the circulatory system, and then infiltrates various brain compartments.”
“…Its presence there induces inflammation within the brain cells and hinders the neurofilament light (NF-L) — a crucial protein that maintains cell stability. A depletion in NF-L can cause severe neuronal cell atrophy, resulting in eventual cell death, a phenomenon prominently seen in AD-affected neurons. However, all is not lost. The research also uncovers a glimmer of hope — the entire process can be potentially thwarted with sufficient dietary fiber intake. What sets this discovery apart are its three innovative aspects. Firstly, the AD-triggering pathway originates within our own bodies, specifically in our GI-tract microbiome, making it active and inherent throughout our existence. Secondly, the perilous neurotoxin, BF-LPS, is an organic outcome of our GI-tract’s microbial metabolic processes. Lastly, controlling the abundance of Bacteroides fragilis in our microbiome, the neurotoxin’s primary source, is achievable through our fiber intake. Lukiw simplifies this: “From a dietary standpoint, balancing the microbial inhabitants of our microbiome can effectively regulate AD-related microbes and their potential to release neurotoxins like BF-LPS.”
