What Is Gastrointestinal Dysbiosis?
Gastrointestinal Dysbiosis is an imbalance of the intestinal microbiome, the billions of bacteria in our intestine. While antibiotics are sometimes necessary, antibiotics destroy God’s intended bacteria, the “normal flora” that are supposed to live in our intestines.
Destruction of Lactobacillus, a lactic acid-producing bacterium, results in a more alkaline intestinal pH. When the intestinal pH rises, pathogenic Candida and pathogenic Bacteria, which normally cannot reproduce in an acidic intestine, overgrow in the colon and small intestine.
Candida overgrowth causes Taurine deficiency, and three specific pathogenic bacteria, Klebsiella, Proteus, and Enterobacteracia, cause Serotonin deficiency when they overgrow the small intestine. SIBO is the medical term for Small Intestinal Bacterial Overgrowth.
Antibiotic-Induced Intestinal Dysbiosis Causes Neurotoxicity in the Brain White Matter
Patients suffering from intestinal Dysbiosis have excessive yeast mycotoxins and bacterial endotoxins that migrate from the gut to the brain. These toxins are lipophilic, fatty in molecular structure, and deposited in the fattiest organ, our brain, which is 60 percent fat. These neurotoxins inflame the brain’s white matter, the insulation on brain neurons called myelin, adding to the cumulative level of neurotoxicity.
Antibiotic-induced neurotoxicity causes further suppression of the immune system by “shutting down” the electrical current in the brain. This is problematic because the brain’s electrical activity stimulates cytokine activity.
Cytokines are the chemical messengers that activate our natural killer cells. When neurotoxins inflame the myelin sheath of brain neurons, they change the electromagnetic field surrounding the neuron, slowing the electrical impulse's speed. By this mechanism, neurotoxins essentially suppress the brain’s electrical activity.
In a healthy brain, the electrical current rapidly jumps over the myelin on brain neurons. However, when the myelin sheath becomes infiltrated with fatty neurotoxins from the gut and toxins from the Lyme spirochete, it fails to modulate immune function effectively.
After Chronic Lyme disease, patients develop antibiotic-induced gut toxicity, yeast mycotoxins and bacterial endotoxins migrate from the gut to the brain. These toxins are fatty in structure and deposit in the fattiest organ, our brain, which is 60 percent fat.
These neurotoxins inflame the brain’s white matter, the insulation on brain neurons called myelin, adding to the cumulative level of neurotoxicity, which is already significant from an accumulation of Lyme toxins in Lyme patients.
Antibiotic-induced neurotoxicity causes further suppression of the immune system by “shutting down” the electrical current in the brain. This is problematic because the brain’s electrical activity stimulates cytokine activity. Cytokines are the chemical messengers that activate our natural killer cells.
When neurotoxins inflame the myelin sheath of brain neurons, they change the electromagnetic field surrounding the neuron, slowing the speed of the electrical impulse. By this mechanism, neurotoxins essentially suppress the brain’s electrical activity. In a healthy brain, the electrical current rapidly jumps over the myelin on brain neurons.
However, it fails to modulate immune function effectively when the myelin sheath infiltrates fatty neurotoxins from the gut and toxins from the Lyme disease spirochete.
Lyme disease patients often become more debilitated after months of aggressive antibiotic therapy. Furthermore, prolonged antibiotic therapy suppresses the immune system in Chronic Lyme disease patients.
Lyme disease treatment consisting solely of antibiotic therapy can ultimately destroy the intestinal lining (where 70 percent of our immune system is located). Intestinal dysbiosis is the term used to describe an imbalance of intestinal organisms.
Prolonged antibiotic therapy ultimately kills our good intestinal bacteria. Lactobacillus is a healthy intestinal bacterium that produces lactic acid. Lactobacillus ensures that the ph of our intestine remains more acidic, disallowing the overgrowth of foreign invaders.
After prolonged antibiotic therapy, the intestinal ph becomes more alkaline, allowing excessive overgrowth of pathogenic yeast and the following toxic bacterium: Klebsiella, Proteus, and Enterobacteriaceae. When Candida mycotoxins and bacterial endotoxins destroy the intestinal lining, they also destroy our antibody factory, the Peyer’s patch in our intestinal lining.
Destruction of the intestinal lining also causes severe malnutrition. Several of the essential amino acids are utilized to make natural killer cells. Thus the production of killer lymphocytes suffers from a malnourished state. With enough antibiotic-induced destruction of the intestinal lining, Lyme disease patients develop severe Leaky Gut Syndrome. Once Lyme patients develop significant Leaky Gut Syndrome, their Immune System will waste resources attacking undigested food particles that “leak” across the damaged intestinal lining into the bloodstream. Typically, these food particles are too large to cross over from the gut into the bloodstream.
We have correlated abnormal brain chemistry patterns with Lyme bio-marker CD 57 levels and the abnormalities seen on the brain scans of our Lyme patients. Our Chronic Lyme disease research has proven that antibiotic-induced changes in brain chemistry cause excessive electrical activity in two specific brain regions.
How Gastrointestinal Dysbiosis Affects The Brain
My brain chemistry research correlating biomarkers with aberrations in brain scan activity has proven that antibiotic-induced changes in brain chemistry cause excessive electrical activity in two specific brain regions, as seen in the PET Scan to the side.
When these brain regions become severely overactive, patients develop depression and a “worry-worry” type of anxiety. When Chronic Lyme disease patients develop an overactive deep limbic center, they suffer from depression, moodiness, negativity, irritability, hopelessness, excessive guilt, and social anxiety, and they become more easily offended.
When Chronic Lyme Disease patients develop an overactive anterior cingulate, they become more argumentative, more stubborn, and hyper-focused on the negative, and they develop obsessive-compulsive worry.
