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New Study Links Alzheimer’s to Bacterial Endotoxins from the Gut

Alzheimer’s disease (AD) is a progressive form of dementia that destroys memories and other cognitive functions. This chronic neurodegenerative disease is the 6th leading cause of death in the US, affecting over 5 million Americans.

Scientists believe that damage to the brain likely begins a decade or more before memory loss and other cognitive symptoms arise. During this preclinical stage of AD, abnormal deposits of proteins can form amyloid plaques and tangled fibers throughout the brain. Meanwhile, neurons begin to lose function and die.

The initial damage appears to take place in the hippocampus, where memories are formed. However, as more neurons die, the damage continues to spread to other parts of the brain, and the brain tissue begins to shrink.

While the underlying cause of AD is not fully understood, more and more research continues to highlight the important bi-directional connection between the gut microbiome and the brain.

One such study, published this month in the Frontiers in Immunology journal, found that pro-inflammatory lipopolysaccharide (LPS) from the human gastrointestinal tract was abundant in the neocortex and hippocampus of AD-affected brains.

Lipopolysaccharide, or LPS, is a structural component of gram-negative bacterial cell membranes that reside in the human GI tract. When these gram-negative bacteria die, they shed the LPS from their cell membrane, and it begins to float freely in the lumen of the intestine as a bacterial endotoxin.

Inside the intestinal lumen, LPS is harmless to humans. However, if there is damage to the intestinal lining, then LPS can enter into the bloodstream, where it can trigger low-grade inflammation. This condition is better known as metabolic endotoxemia.

The findings of this ground-breaking study suggest that metabolic endotoxemia is an important contributor in inflammatory neurodegenerative diseases like AD. LPS in the brain has also been linked to mood disorders like anxiety and depression.

Fortunately, MegaSporeBiotic was formulated to target inflammation caused by bacterial endotoxins. In fact, a double-blind, placebo-controlled human clinical trial, published in the World Journal of Gastrointestinal Pathophysiology, found that just 30 days of supplementation with MegaSporeBiotic was enough to reduce serum LPS levels by a whopping 43% in healthy college students without any additional interventions.

These findings suggest that the unique strains found in MegaSporeBiotic were able to strengthen the integrity of the intestinal lining to keep endotoxins like LPS out of the bloodstream and the brain.

For more information on these topics, visit the Practitioner’s Corner by logging into your online account. If you’d like to create an account with us, you can register at https://microbiomelabs.com/physician-register/.

References

Zhao Y, Cong L, Jaber V, Lukiw W. Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of the Alzheimer’s Disease Brain. Front Immunol. 2017;8:1064.

Boutagy NE, McMillan RP, Frisard MI, Hulver MW. Metabolic endotoxemia with obesity: Is it real and is it relevant? Biochimie. 2016;121:11-20.

Stevens BR, Goel R, Seungbum K, et al. Increased human intestinal barrier permeability plasma biomarkers zonulin and FABP2 correlated with plasma LPS and altered gut microbiome in anxiety or depression. Gut. 2017;pii:314759.

McFarlin BK, Henning AL, Bowman EM, et al. Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers. World J Gastrointest Pathophysiol. 2017;8(3):117-126.