Bile acid digests not only dietary fat but also body fat

Bile acid for fat loss?

Bile acid, that green or yellowish brown fluid secreted by your gall bladder can actually improve your health and speed up fat loss.

Bile is produced by the liver from cholesterol. Humans make around 500mg of bile daily, which consists of about 97% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids, and lecithin), amino acids, steroids, enzymes, porphyrins, vitamins, and heavy metals, as well as exogenous drugs, xenobiotics and environmental toxins.

Bile synthesis is an energy-dependent process (requires ATP), and a sluggish metabolism with low energy production will greatly reduce bile production. Cholic acid and chenodeoxycholic acid (CDCA) are the primary bile salts and each can be conjugated at the side chain with either taurine or glycine.

Bile is secreted to:

  • excrete many toxins, such as heavy metals (arsenic, copper, manganese, lead, mercury, selenium, silver, zinc, etc), drugs, other potentially harmful exogenous lipophilic substances as well as other endogenous substrates such as bilirubin, excess fat-soluble vitamins, etc.
  • aid in the digestion and absorption of fats and nutrients such as the fat-soluble vitamins.
  • excrete excess cholesterol.
  • protect the organism from enteric infections by excreting immune globulin A (IgA), inflammatory cytokines, and stimulating the innate immune system in the intestine.
  • promote cholehepatic and enterohepatic circulation.
  • detox many hormones (estrogen, prolactin, insulin, etc.) and pheromones.

Once secreted, gut bacteria can convert the primary bile acids into secondary bile acids, namely deoxycholic acid (DCA) and lithocholic acid (LCA). Intriguingly, microbial enzymes have the potential to create dozens of different bile acid-derived molecules. For instance, Ruminococcus gnavus is a novel ursodeoxycholic acid (UDCA)-producer (a beneficial secondary bile acid), which has anti-inflammatory properties that have been used in hepatitis and bile acid reflux conditions and represents about 3% of total secondary bile acids (R).

Patients with cirrhosis (chronic liver damage) have a decreased conversion of primary to secondary bile acids, because of a decreased abundance of gram-positive bacteria such as Lachnospiraceae, Ruminococcaceae, and Blautia. People with IBS-D have significantly elevated Escherichia coli and a significant decrease of leptum and bifidobacterium, which leads to an increase in fecal primary bile acid excretion and low secondary bile acid formation (R).

Secondary bile is very much needed, as it:

  • keeps excessive gut bacteria under control
  • activate receptors in the body that promote health and fat loss once reabsorbed
  • are chronobiological regulators of host circadian gene expression (R)

But, excess secondary bile is detrimental to the small intestine and colon, as it promotes DNA damage and inflammation, enhances tumor formation and is involved in colorectal cancer and diabetes.

Low bile acid secretion allows gram-negative bacteria to proliferate (which promotes inflammation and endotoxins), whereas high levels of bile allow gram-positive bacteria to proliferate, which is also bad in excess.

A diet high in polyunsaturated fats inhibit the growth of certain beneficial bacteria, such as Bacteroidetes and Firmicutes, and increases the growth of the bad microbe, Clostridia, which leads to an increase in deoxycholic acid (DCA) production. DCA in excess is toxic and increases the risk of cancer.

To recap quickly, bile is produced in the liver, secreted by the gallbladder during a meal, of which some are converted to secondary bile in the intestine by gut bacteria.

About 95% of the bile that is in the intestine is then reabsorbed in the distal ileum (end part of small intestine) and transported back to the liver to be reused. The remaining 5% is then excreted in the feces. The reabsorbed bile binds to two receptors, namely FXR and TGR5, to promote many functions, including fat loss.

Farnesoid X receptor (FXR)

FXR is expressed in several tissues, including the liver, intestine, adipose tissue, vascular wall, pancreas and kidney.

Conjugated and unconjugated bile acids are the natural ligands that activate FXRα, with CDCA (chenodeoxycholic acid; a primary bile acid) and its conjugated forms being the most potent natural agonists.

Insulin resistance and DNA overmethylation decrease FXR levels.

When FXR is activated, it:

  • Inhibits lipogenesis and increases beta-oxidation, cellular sensitivity to catecholamine and UCP1 expression, resulting in greater energy expenditure and thermogenesis (R).
  • Lowers serum lactate levels, which indicates that body-wide energy metabolism is shifted toward a more oxidative state.
  • Keeps gut bacteria under control, by activating AMP-activated protein kinase (AMPK), which increases extracellular signal-regulated kinase 1/2 (ERK½) (R). ERK½, in turn, activates the vitamin D receptor (VDR), which increases cathelicidin, which is a very potent anti-microbial peptide.
  • Reversing liver fibrosis and even assisting in liver regeneration after ischemia/necrosis (R).
  • Has an anti-inflammatory and anti-fibrotic effect in the kidney, with the resulting potential use of FXRα agonists to treat diabetic nephropathy and other fibrotic renal diseases (R).
  • Improves inflammatory bowel diseases (IBD), by alleviating inflammation, preserves the integrity of the intestinal epithelial barrier, preventing bacterial translocation in the intestinal tract, inhibiting bacterial outgrowth and endotoxemia (R, R).
  • Increases detoxifying enzymes, by activating C/EBPβ.
  • Improves ED (erectile dysfunction), as it greatly upregulates eNOS expression where it matters if you get what I’m saying (R).
  • Lowers the risk of and protects against atherosclerosis via decreasing lipogenesis, lowering elevated serum cholesterol, HDL and triglyceride levels and excessive accumulation of fat in the liver (R).
  • Improves insulin sensitivity, by reducing hyperglycemia (inhibits gluconeogenesis), TG, increasing liver glycogen (via increasing glycogen synthase kinase 3) and inhibiting lipogenesis. This will also contribute to a reduction in body fat.
  • Protects against intestinal tumorigenesis (R)
  • Speeds up mitochondrial recovery and promotes insulin sensitivity by increasing FGF19 (R).
  • Reduces circulating glucose (lowers high blood sugar) levels through suppression of the hypothalamus–pituitary–adrenal axis (R).

Cafestol (found in coffee) (R), androsterone (found in pine pollen) (R), green tea (epigallocatechin-3-gallate) (R) and forskolin (R) also activated the FXR receptor.

Guggulsterone (found in some fat burners) (R), ursodeoxycholate (UDCA) (R) and metformin (R) are FXR antagonists.

G protein-coupled bile acid receptor 1 (GPBAR1) a.k.a TGR5

TGR5 receptors are ubiquitously expressed, but its expression levels vary between different tissues, with high expression in the gallbladder and lower expression levels in brown adipose tissue (BAT), liver, intestine and selected areas of the central nervous system.

Secondary bile acid lithocholic acid (LCA) and it taurine conjugate, taurolithocholic acid (TLCA), which are created from CDCA, are the most potent endogenous ligands for TGR5.

When TGR5 is activated, it:

  • Increases mitochondrial activity and uncoupling by promoting deiodinase type 2 (which converts thyroid hormone T4 to T3) and PGC1α activity.
  • Lowers inflammatory cytokines such as NFκB, TNFα, IL-1β, IL-6, etc.
  • Protects against the development of cholesterol gallstones
  • Regulates energy metabolism in brown adipose tissue (BAT) (R). As little as 40-50 g of BAT could, if maximally stimulated, account for 20% of daily energy expenditure (R).
  • Relaxes and refills the gallbladder
  • Promotes the secretion of glucagon-like peptide-1 (GLP-1). GLP1 promotes satiety, stimulates lipolysis and improves insulin sensitivity. It has cardioprotective effects, in terms of inhibiting triglyceride-rich chylomicron formation, attenuation of atherogenic plaque inflammation and modulation of cardiomyocyte function (R).

Allopregnanolone (produced from pregnenolone -> progesterone -> 5alpha-dihydroprogesterone -> allopregnanolone) (R) and betulinic acid (found in rosemary) (R) are also a TGR5 agonists.

Promotors of bile secretion

  • ATPribose, inosine, methylene blue, pentadecanoic acid, succinic acid, etc, promote ATP production.
  • cAMPcaffeine, forskolin, Butea Superba promote cAMP.
  • Fats (olive oil increases the enzyme that produces bile and also promotes its secretion (R)) – Even small amount of fat, as low as 7g can promote complete gall bladder emptying. Even 2g of fat is able to increase bile secretion and change gall bladder volume by 27% (R).
  • Taurine (R)
  • Thyroid (R)
  • Caffeine (R)
  • Curcumin (R)

Decreases toxic secondary bile

An excess of bad gut bacteria produces too much toxic secondary bile, such as lithocholic acid and deoxycholic acid. Here are a few ways to lower them.

A diet high in fruits and vegetables increases the production of good bacteria and lowers the bad bacteria. Pre-biotic foods, such as banana, garlic, onions, artichoke, asparagus, leeks, cocoa, etc., if well tolerated, could be very beneficial to increase the production of the good gut bacteria.

Coconut oil helps to improve the gut microbe.

Vitamin B6 significantly reduced the production of a fecal secondary bile acid, lithocholic acid (the most toxic secondary bile acid and a risk factor for colon cancer), and markedly reduced the ratio of lithocholic acid to deoxycholic acid (a less toxic secondary bile acid) in feces (R).

Dietary curcumin and caffeic acid significantly reduced the fecal concentration of deoxycholic acid (DCA). Dietary caffeic acid, catechin, rutin, and ellagic acid significantly reduced fecal lithocholic acid (R).

Calcium bind to secondary bile and excretes it. Calcium may reduce the toxicity of high fat diets to the colon and reduce the colonic cancer risk associated with high fat diets (R). The hyperproliferative effect of dietary fat is inversely related to the amount of calcium in the diet (R).

About the author:

Hans Ambachtsheer enjoys crushing weight training, calisthenics and gymnastic workouts when he isn’t writing top content on nutrition, hormones and training that will help you surpass your goals and dreams. You can check his products and courses today for a very comprehensive and detailed, yet very simplistic and practical guide on how to sculpt the body you want.

4 thoughts on “Bile acid digests not only dietary fat but also body fat”

  1. I talked with someone who said they had their gallbladder removed because they had lost so much weight (-100 lbs.). I had never ran across in my reading on weight loss or health that weight loss could cause such a problem. How could this happen if you don’t mind? Also, so I can pass it on, would might the be the consequences to not having enough a gallbladder and not enough bile acid without one to produce it? Thanks.

    • Hey Jay,
      Someone lost weight due to a deficit and then had their gallbladder removed? I’m not sure I understand the context. Bile is necessary for disinfecting the bowels and can prevent SIBO. Bile also helps with the absorption of fat-soluble vitamins.

  2. I have trouble with my gallbladder. I have gall stones and IB-D after meals if I don’t take digestive enzymes with bile in them. Stools are pale as well. Do you know how I could potentially fix this or what could be causing the gallbladder issues.


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