LPS induces a violent inflammatory response in humans—so violent that it’s also termed endotoxin, meaning a toxin that comes from within.17 It’s used experimentally in laboratory research to instantly create inflammation in animal models to study the full array of illnesses rooted in inflammation, from inflammatory bowel disorders, diabetes, lupus, rheumatoid arthritis, and multiple sclerosis to depression, Parkinson’s disease, Alzheimer’s disease, and even autism. In a healthy individual whose intestinal lining is intact, LPS cannot gain entrance into the bloodstream by those tight junctions. But when the cells lining the intestines (remember: the intestinal wall is only one cell thick) are damaged or become impaired and those junctions are compromised, LPS is able to pass into the systemic circulation, where it sets off an alarm and triggers inflammation. Levels of LPS in the blood are in fact indicative of both leaky gut and inflammation in general.
Researchers around the world are finally looking at LPS as playing a pivotal role in depression. After all, inflammatory markers correlate with depression, and LPS increases the production of these inflammatory chemicals. And here’s where the science really shouts out to me: LPS not only compromises the gut by making it more permeable, it can also trespass the blood-brain barrier, bringing the pro-inflammatory message there as well.18
In 2008, the same Belgian researchers I quoted above documented a significant increase in the level of antibodies in the blood against LPS in individuals with major depression. Interestingly, the authors commented how major depression is often accompanied by gastrointestinal symptoms. And it’s one of the most logical explanations given the latest science is the fallout from a disrupted gut community. This is why we must focus on gut permeability and the tribes within the gut that are supposed to be protecting that intestinal lining.
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