
Areas of Research
Lyme’s Disease
Infections
Diabetes (Blood Sugar)
Ovaries (PCOS)
Acne (Skin)
Diarrhea from Clostridia Difficile
Leaky Gut from Clostridia perfringens & paraputrificum
Reduction of M2 Microglial activation
Insulin Resistance and Glucose Balance
Berberine, a botanical alkaloid from goldenseal used to control blood glucose in type 2 diabetes was recently tested in a study, activity and action of the mechanism of berberine were investigated in vivo and in vitro. In this study, insulin resistance was decreased after a five week administration of berberine by 46% to 48% respectively. Intracellularly berberine was found to increase glucose consumption (lowered plasma glucose) The insulin-induced glucose uptake was enhanced by berberine as well. Berberine exhibited no cytotoxicity and even protected plasma membranes in the cell culture! These results suggest that berberine enhances glucose metabolism by stimulation of glycolysis, which is related to inhibition of glucose oxidation in mitochondria.
In addition to the metabolic activities, In 1980, the hypoglycemic effect of berberine was found when berberine was used to treat diarrhea in diabetic patients in China. Since then, berberine has been used as an anti-hyperglycemic agent by many physicians in China. Studies have indicated that berberine is an effective insulin sensitizer with comparable activity to common glucose lowering drugs.
Anti Microbial Action
Berberine has a well-established antimicrobial activity in the control of infection by bacteria, viruses, fungi and parasites.
Berberine’s Action on PCOS and Fertility
It has been widely known that women with insulin resistance go on to develop PCOS and men with the same condition will have lower circulating levels of testosterone followed by higher estrogen. Studies have indicated that berberine is an effective insulin sensitizer with comparable activity to common glucose lowering drugs. Reduced insulin sensitivity is reportedly a factor adversely affecting the outcome of IVF in patients with polycystic ovary syndrome (PCOS)
Compared with placebo, greater reductions in total testosterone, free androgen index, fasting glucose and fasting insulin were observed in the berberine and metformin groups. Three months of treatment with berberine or metformin before the IVF cycle increased the pregnancy rate and reduced the incidence of severe ovarian hyperstimulation syndrome. Treatment with berberine, in comparison with metformin, was associated with decreases in BMI, lipid parameters and total FSH requirement, and an increase in live birth rate with fewer gastrointestinal adverse events.Berberine and metformin treatments prior to IVF improved the pregnancy outcome by normalizing the clinical, endocrine and metabolic parameters in PCOS women. Berberine has a more pronounced therapeutic effect and achieved more live births with fewer side effects than metformin.
Berberine and the Gut
Several studies have shown that berberine may modulate the gut microbiota through enriching short-chain fatty acid (SCFA)-producing bacteria and reducing microbial diversity. This in turn inhibits dietary polysaccharide degradation and decreases caloric intake in the gut, which may improve energy metabolism and intestinal health; anti-inflammatory effects; and immune regulatory effects. Berberine has been also found to affect specific bacterial species both in vitro and in vivo, including Bifidobacterium longum, Bifidobacterium bifidum, Clostridium perfringens, and Clostridium paraputrificum. It may also improve colitis by inhibiting the growth of gram-negative intestinal bacteria, such as Escherichia coli, Klebsiella pneumoniae and Proteus mirabilis. Besides repressing or killing harmful gut bacteria, berberine has some positive effect on beneficial gut microbiota, such as Bifidobacterium adolescentis and Lactobacillus acidophilus
Benefits surrounding Clostridia
Berberine has been proven to be ground breakingl for treating different symptoms caused by Clostridia. It has been beneficial to diarrhea outbreaks and has reduced M2 microglial activation by increasing the production of butyrate. In Regards to neurotransmitter physiology, Clostridia toxins Inhibit dopamine B-Hydroxylase, which is the rate limiting factor in the conversion of dopamine to norepinephrine. These toxins increase dopamine in cytosol, toxic dopamine metabolites, and oxygen superoxide which in turn depletes the brain of glutathione and leads to oxidative damage. With the increase in toxic metabolites, brain mitochondria and neurofibrils are damaged and mitochondrial dysfunction occurs. This in turn damages neuronal Krebs cycle enzymes, neuronal mitochondria and neurofibrils resulting in increased damage to brain mitochondria.
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