Gut permeability and Toxic Bile Theory
Quick overview of Toxic Bile Theory and a review of the things that negatively and positively affect gut permeability (leaky gut)
Review of Love Your Liver Livestream #121: #leakygut, #SIBO, & #toxicbiletheory!
What is Toxic Bile Theory?
Basically, it states that the root cause of chronic disease states is a dysfunction of toxic bile – either there is too much, which results in diarrhea and the “burning” of the inside of the the intestines, or too little because it is leaking out into places it’s not supposed to be – through the intestines themselves, directly into the blood stream from the liver, or through failing biliary ducts.
Click here to read my notes on the basics of Toxic Bile Theory.
Toxic bile related to liver damage and leaky gut
Toxicity of bile affects gut microbiome.
Most bile (95%) is reabsorbed and goes back to the liver. If the returning bile is toxic, it results in liver damage. The damaged liver then puts out even more toxic bile, which feeds a vicious cycle. Liver damage is driving chronic disease. SIBO = liver damage. And SIBO and intestinal permeability (leaky gut) go hand in hand.
Need to reduce toxic load and put the right nutrients into the body so the bile becomes less toxic. This helps to heal the microbiome.
Leaky gut is caused by toxic bile eating holes in your gut.
The Vitamin A connection
Serum (blood) vitamin A levels and vitamin A levels in the liver are NOT correlated at all.
Vitamin A accumulates in the cells of fatty liver tissue and creates damage.
Non-alcoholic fatty liver disease (NAFLD) is the manifestation of metabolic syndrome in the liver. Low circulating retinol in NAFLD may not reflect a true “vitamin A deficiency,” but instead a disturbed vitamin A metabolism.
Any retinol (vitamin A) transforms into retinoic acid. Retinoic acid (RA) = chemical peels. When the liver dumps bile full of retinoic acid into your gut, it dissolves the intestinal lining. It drives intestinal inflammation. It also suppresses intestinal mucus production (so the mucosal layer of your gut can’t be maintained).
Endotoxin levels were significantly higher in mice fed a high vitamin A diet. Mild vitamin A supplementation is associated with gut dysbiosis.
RA is made by the body when it needs to break down vitamin A. If you have too much RA, the body will signal to slow down the production of it. This may be why short-term observations of vitamin A shows positive effects, but longer-term observations could reveal a causal role for RA in autoimmune diseases. That’s why short term cell studies are usually positive for vitamin A, but longer term human or animal studies are negative.
High levels of vitamin A cause midline defects in developing babies.
The Copper connection
Copper and copper-related proteins were characteristic of cholestasis (cholestasis is the slowing or stalling of bile flow through your biliary system). Copper is all over the place in cholestatic livers.
Copper makes the gut bacteria more resistant to antibiotics and increase the rate of E.coli.
Copper alters the tight junction permeability in your gut.
Copper had a negative effect on intestinal inflammation-related metabolic pathways.
Copper exposure early in life induced liver damage, gut dysbiosis, and killed the metabolism of the cells in the gut.
Iron
Vitamin A toxicity and iron toxicity go hand in hand. Vitamin A increases iron absorption.
Leaking toxic bile is positively correlated to how much iron is stuck in the liver.
Excess iron accumulates in the intestinal tract, which can catalyze the formation of reactive oxygen species and cause intestinal damage. Iron overload can cause iron to deposit into the intestinal mucosa, which increases inflammation and premature cell death.
Iron reshapes gut microbiome and metabolism.
Supplements to help the disease state: Zinc, selenium, magnesium, potassium
Zinc supplementation tightens leaky gut. It also inhibits NAFLD liver damage and inflammation. Inflammatory cytokines were significantly increased in zinc deficiency. (Note: Insufficient protein is often the cause of zinc deficiency.)
Selenium deficiency can increase oxidative stress, inflammatory responses, and intestinal permeability (leaky gut). Selenium deficiency also decreases intestinal immune function and induces apoptosis (cell death) of the duodenal villi (celiac!). Selenium can alleviate intestinal diseases such as IBD.
Zinc and selenium are both copper antagonists. (Connection: Copper increases intestinal permeability and zinc/selenium decrease it.) They are also anti-microbial and anti-fungal.
Both low magnesium and low potassium lead to leaky gut.