UDCA 250mg/capsule

UDCA 250mg/capsule. 60 Capsules.


UDCA (UDCA) is a chemical called a bile acid. It occurs naturally in bile and can be used to dissolve gallstones. The liver produces bile that is stored in the gall bladder. Bile is released by the gall bladder to aid the digestion of fats. It consists of cholesterol dissolved within bile salts. Gallstones occur in the gall bladder as a result of too much cholesterol, or too few bile salts within the bile. The imbalance causes excess cholesterol to separate out of the bile and form stones. UDCA causes gallstones to dissolve by a mechanism that is not fully understood. It is known to reduce the production of cholesterol by the liver and also to reduce the absorption of cholesterol from the gut. Both of these actions decrease the amount of cholesterol that passes into the bile. Also, since UDCA is a bile acid itself, it increases the level of bile acids within the bile. The combination of these two factors reverses the imbalance and stops the cholesterol separating out of the bile. The gallstones then begin to dissolve.


Besides existing in its natural form, UDCA has been synthesized, and all pharmaceutical formulations are synthetic. Besides dissolving gallstones, UDCA exerts other actions. Oral 17 alpha alkylated steroids often cause a condition called cholestasis. Cholestasis is any condition in which bile excretion from the liver is blocked, which can occur either in the liver where bile is formed, or in the bile ducts.

Extrahepatic cholestasis -- which occurs outside the liver -- can be caused by bile duct tumors, strictures, cysts, diverticula, and other damage. Other potential causes for this type include stones in the common bile duct, pancreatitis, pancreatic tumor or pseudocyst, primary sclerosing cholangitis, and compression due to a mass or tumor on a nearby organ.


It has been proposed in research settings that oral steroids interfere with the pump that exports bile out of liver cells. UDCA exerts a number of therapeutic effects which prevent and treat cholestasis. For instance, UDCA has been shown to stimulate enzymes that increase the density of these bile transporters within the bile pump, allowing bile to exit the liver more readily (2,3). UDCA also protects hepatocytes (liver cells) against bile induced apoptosis (programmed cell death) (2).


Whatever the primary mechanism is for AAS induced cholestasis, UDCA has proven effective in treating the condition. In one study, it was show in the research subject a marked improvement of severe cholestasis and acute renal failure through the administration of UDCA. (4)


UDCA has also been shown to lower both total cholesterol and LDL (bad) cholesterol via at least two different mechanisms. In one study (6) researchers observed that UDCA lowered the hepatic (liver) production of cholesterol by interfering with a key enzyme in cholesterol synthesis.


In another study, UDCA was administered to animals with moderately elevated cholesterol, here UDCA lowered plasma LDL by increasing the number of LDL binding sites on the liver, allowing for greater LDL uptake by the liver (7).


These studies suggest UDCA might be a worthwhile supplement to consider researching if a concern exists solely regarding cholesterol. When bile enters the digestive tract, a certain portion is reabsorbed, leading to cholesterol reuptake. UDCA seems to block a portion of this cholesterol reuptake, providing for yet another mechanism whereby UDCA lowers cholesterol (8).


One bottle of CuttingEdge Laboratories UDCA contains 60 Tablets, 250 MG's each tablet.


Intended for Research purposes only.


(1) Pertusi R, Dickerman RD, McConathy WJ Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis? J Am Osteopath Assoc. 2001 Jul;101(7):391-4.

(2) Paumgartner G, Beuers U. UDCA in cholestatic liver disease: mechanisms of action and therapeutic use revisited. Hepatology. 2002 Sep;36(3):525-31.

(3) Micheline D, Emmanuel J, Serge E. Effect of UDCA on the Expression of the Hepatocellular Bile Acid Transporters (Ntcp and bsep) in Rats With Estrogen-Induced Cholestasis. J Pediatr Gastroenterol Nutr. 2002 Aug;35(2):185-91.

(4) Habscheid W, Abele U, Dahm HH. Severe cholestasis with kidney failure from anabolic steroids in a body builder. Dtsch Med Wochenschr. 1999 Sep 10;124(36):1029-32.

(5) Velayudham LS, Farrell GC. Drug-induced cholestasis. Expert Opin Drug Saf. 2003 May;2(3):287-304.

(6) Miettinen TE, Tarpila S, Gylling H. The effects of UDCA on serum and biliary noncholesterol sterols in patients with gallstones. Hepatology. 1997 Mar;25(3):514-8

(7) Ceryak S, Bouscarel B, Malavolti M, Robins SJ, Caslow KL, Fromm H. Effect of UDCA on hepatic LDL binding and uptake in dietary hypercholesterolemic hamsters. Atherosclerosis. 2000 Nov;153(1):59-67

(8) Eusufzai S, Ericsson S, Cederlund T, Einarsson K, Angelin B. Effect of UDCA treatment on ileal absorption of bile acids in man as determined by the SeHCAT test. Gut. 1991 Sep;32(9):1044-8