I'm trying to decide if I should run m1t or sd. Can't decide because I know how harsh m1t is but the gains from it are like nothing I've ever seen or felt before. Superdrol is also excellent but also less harsh on the liver. I'm not sure what either does to lipids so I can't decide. Thoughts?
Pristi1340
New member
Still never tried M1T but I will eventually. SD is drier but mg-for-mg M1T is stronger supposedly
Jozifp103
MuscleChemistry Registered Member
I like that mentality. Just keep that liver protection flowing, and drink tons of water.
Well it was my plan originally, then I was having second thoughts because of my age (40) and the health risks involved. I did get 120 caps of udca and nac to run with the m1t for protection. I just needed time to reassure myself that I'll be ok as long as I take the preventative measures I'm putting in place like taking my supps, drinking lots of h2o, and not eating shitty food while running it. And its real udca, not the inferior tudca. I also read studies on the udca dosages required to cure cholestasis and I'll be taking a little less than that during the entire cycle.
Another question though, I'll be running mc igf with it too. Should I run it along side the m1t or after it? Or both? I have 2 bottles. I want to take advantage of the hyperplasia from the igf along with the power of m1t for a killer run.
Pristi1340
New member
yelis, how much you plan on running ed? how long, 4 weeks?
Yeah prob 4 weeks. I was considering 6 weeks maybe but I dont know if I should push it that far. I don't have a dosage plan yet, can u recommend one?
Was thinking maybe 10/20/20/30
Pristi1340
New member
you won't even need 30mg if its quality M1T bro
Tudca is just an OTC supplement, where udca (ursodiol) is a prescription drug and is what is used by the hospitals for various liver disease treatments like gallstones and cholestasis. It can also be found at a few rc places for research purposes. I only know 2 places that carry it.
Just fyi cholestasis is a liver disease where the bile ducts get blocked up and the liver is unable to get the toxins out of itself. This is generally what happens to individuals who are admitted to the hospital with liver pains from taking methylated AAS. It is treated with udca (ursodiol), 13 - 15mg/ kg bodyweight. I will be using 5 mg/kg bodyweight for prevention of cholestasis during my run.
Ursodeoxycholic acid (UDCA) is a white or almost white powder. It is practically insoluble in water, readily soluble in alcohol, sparingly soluble in acetone, in chloroform and in ether. It melts at 200 - 204°C. The IUPAC chemical name of UDCA is 3a, 7***946;-dihydroxy-5-cholan-24-oic acid. Its CAS number is 128-13-2. Ursofalk Capsule contains ursodeoxycholic acid 250mg, maize starch, colloidal silicon dioxide, magnesium stearate, gelatin and titanium dioxide.
PHARMACOLOGY
Pharmacodynamic properties
The mechanism of action of UDCA in liver and cholestatic disorders has not yet been explained totally. However, UDCA alters bile acid composition, resulting in increases in the concentration of UDCA and decreases in the concentrations of the more hydrophobic and potentially toxic bile acids, cholic and chenodeoxycholic acids. UDCA also has a choleretic effect, resulting in increased bile acid output and bile flow. There is some evidence for immunological effects, including a reduction of abnormal expression of HLA Class I antigens on hepatocytes and a suppression of immunoglobulin and cytokine production.
Pharmacokinetic Properties
UDCA occurs naturally in the body. After oral administration of a single 500 mg dose of UDCA to healthy volunteers, peak plasma concentrations were 7 to 16 µM. Tmax occurs at 60 minutes and a second peak plasma concentration occurs at 180 minutes. After oral administration of 250 mg, 500 mg, 1000 mg and 2000 mg single doses, respective absorption rates were 60.3%, 47.7%, 30.7% and 20.7% based on recovery from bile within 24 hours in patients with external biliary drainage.
In plasma, protein binding is 96 - 98%.
First pass extraction of UDCA from the portal vein by the liver ranges from 50 - 70%. UDCA is conjugated to glycine and taurine and then excreted into bile and passes to the small bowel. In the intestine, some conjugates are deconjugated and reabsorbed in the terminal ileum. Conjugates may also be dehydroxylated to lithocholic acid, part of which is absorbed, sulphated by the liver and excreted by the biliary tract. In healthy volunteers given UDCA 500 mg with 14C tracer, 30 - 44% of the dose was excreted in faeces in the first three days as UDCA (2 - 4%), lithocholic acid (37%) and 7-ketolithocholic acid (5%).
The biological half-life of orally administered UDCA is 3.5 - 5.8 days.
In patients with severe liver disease, renal excretion becomes a major route for elimination of bile acids.
Clinical Trials
Primary Biliary Cirrhosis
Five pivotal randomised, double-blind control studies examined the efficacy of ursodeoxycholic acid in the treatment of primary biliary cirrhosis. All 5 trials were of at least 2 years follow-up. Four of the five studies used a dosage in the range of 10 - 15 mg/kg/day; the fifth trial used a significantly lower dose of 7.7 ± 0.2 mg/kg/day. Significant improvement in some or all biochemical tests of liver function was shown in subjects given UDCA during the treatment period. Symptom improvement or improvement in histology were not consistently reported with UDCA but longer survival without liver transplantation was reported in two long term studies. One of the studies reported that the efficacy of UDCA in patients with primary biliary cirrhosis was greater in patients with less advanced disease (entry bilirubin < 2mg/dL; histological stage I or II) compared to patients with more advanced disease.
Primary Sclerosing Cholangitis
Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterised by inflammation, fibrosis, and destruction of the large intra- and extra-hepatic bile ducts. One pivotal randomised, double-blind placebo-controlled study examines the efficacy of UDCA in the treatment of PSC in 105 patients over 2 years. The dosage used was in the range of 13 - 15 mg/kg/day. Irrespective of initial histological stage, UDCA had no effect on time to treatment failure and survival, without liver transplantation. Serum bilirubin, ALP and AST improved, but UDCA was not associated with a significant improvement in symptoms or histological score. In three smaller randomised, double-blind, placebo-controlled studies, UDCA similarly showed significant improvement in liver biochemistry (in 2 of the studies) when compared to placebo, but did not significantly improve symptom scores. One study found significant improvement in some liver histological features in the patients treated with UDCA. These trials used UDCA doses ranging from 10 - 15 mg/kg/day.
Cystic fibrosis-related cholestasis
Cystic fibrosis (CF) is a hereditary disease with multiorgan involvement. Clinical liver disease is rare although many patients may have biochemical evidence of cirrhosis.
One double-blind, placebo-controlled, study randomised 55 patients with CF to UDCA 900 mg/day or placebo for one year. In addition, taurine supplements or placebo were randomly assigned. Efficacy was assessed by improvements in clinically relevant and nutritional parameters, and liver biochemistry. After one year, the UDCA group had significant improvement in GGT and 5'-nucleosidase but not AST or ALT. However, there was a deterioration of overall clinical condition, as measured by the Shwachman-Kulcycki score in those receiving placebo compared to the UDCA group.
In a dose comparison study, UDCA 20 mg/kg/day for 12 months resulted in a more pronounced improvement in GGT and ALT compared to UDCA 10 mg/kg/day. Improvements in AST and ALP were comparable. Although this study suggested a possible benefit with higher drug doses in resolving liver biochemistry, whether UDCA improves quality of life, histology, or survival is unknown.
INDICATIONS
URSOFALK is indicated in the treatment of chronic cholestatic liver diseases.
CONTRAINDICATIONS
URSOFALK must not be used in the presence of acute inflammation of the gall bladder and bile ducts; and obstruction of the biliary tract (common bile duct).
PHARMACOLOGY
Pharmacodynamic properties
The mechanism of action of UDCA in liver and cholestatic disorders has not yet been explained totally. However, UDCA alters bile acid composition, resulting in increases in the concentration of UDCA and decreases in the concentrations of the more hydrophobic and potentially toxic bile acids, cholic and chenodeoxycholic acids. UDCA also has a choleretic effect, resulting in increased bile acid output and bile flow. There is some evidence for immunological effects, including a reduction of abnormal expression of HLA Class I antigens on hepatocytes and a suppression of immunoglobulin and cytokine production.
Pharmacokinetic Properties
UDCA occurs naturally in the body. After oral administration of a single 500 mg dose of UDCA to healthy volunteers, peak plasma concentrations were 7 to 16 µM. Tmax occurs at 60 minutes and a second peak plasma concentration occurs at 180 minutes. After oral administration of 250 mg, 500 mg, 1000 mg and 2000 mg single doses, respective absorption rates were 60.3%, 47.7%, 30.7% and 20.7% based on recovery from bile within 24 hours in patients with external biliary drainage.
In plasma, protein binding is 96 - 98%.
First pass extraction of UDCA from the portal vein by the liver ranges from 50 - 70%. UDCA is conjugated to glycine and taurine and then excreted into bile and passes to the small bowel. In the intestine, some conjugates are deconjugated and reabsorbed in the terminal ileum. Conjugates may also be dehydroxylated to lithocholic acid, part of which is absorbed, sulphated by the liver and excreted by the biliary tract. In healthy volunteers given UDCA 500 mg with 14C tracer, 30 - 44% of the dose was excreted in faeces in the first three days as UDCA (2 - 4%), lithocholic acid (37%) and 7-ketolithocholic acid (5%).
The biological half-life of orally administered UDCA is 3.5 - 5.8 days.
In patients with severe liver disease, renal excretion becomes a major route for elimination of bile acids.
Clinical Trials
Primary Biliary Cirrhosis
Five pivotal randomised, double-blind control studies examined the efficacy of ursodeoxycholic acid in the treatment of primary biliary cirrhosis. All 5 trials were of at least 2 years follow-up. Four of the five studies used a dosage in the range of 10 - 15 mg/kg/day; the fifth trial used a significantly lower dose of 7.7 ± 0.2 mg/kg/day. Significant improvement in some or all biochemical tests of liver function was shown in subjects given UDCA during the treatment period. Symptom improvement or improvement in histology were not consistently reported with UDCA but longer survival without liver transplantation was reported in two long term studies. One of the studies reported that the efficacy of UDCA in patients with primary biliary cirrhosis was greater in patients with less advanced disease (entry bilirubin < 2mg/dL; histological stage I or II) compared to patients with more advanced disease.
Primary Sclerosing Cholangitis
Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterised by inflammation, fibrosis, and destruction of the large intra- and extra-hepatic bile ducts. One pivotal randomised, double-blind placebo-controlled study examines the efficacy of UDCA in the treatment of PSC in 105 patients over 2 years. The dosage used was in the range of 13 - 15 mg/kg/day. Irrespective of initial histological stage, UDCA had no effect on time to treatment failure and survival, without liver transplantation. Serum bilirubin, ALP and AST improved, but UDCA was not associated with a significant improvement in symptoms or histological score. In three smaller randomised, double-blind, placebo-controlled studies, UDCA similarly showed significant improvement in liver biochemistry (in 2 of the studies) when compared to placebo, but did not significantly improve symptom scores. One study found significant improvement in some liver histological features in the patients treated with UDCA. These trials used UDCA doses ranging from 10 - 15 mg/kg/day.
Cystic fibrosis-related cholestasis
Cystic fibrosis (CF) is a hereditary disease with multiorgan involvement. Clinical liver disease is rare although many patients may have biochemical evidence of cirrhosis.
One double-blind, placebo-controlled, study randomised 55 patients with CF to UDCA 900 mg/day or placebo for one year. In addition, taurine supplements or placebo were randomly assigned. Efficacy was assessed by improvements in clinically relevant and nutritional parameters, and liver biochemistry. After one year, the UDCA group had significant improvement in GGT and 5'-nucleosidase but not AST or ALT. However, there was a deterioration of overall clinical condition, as measured by the Shwachman-Kulcycki score in those receiving placebo compared to the UDCA group.
In a dose comparison study, UDCA 20 mg/kg/day for 12 months resulted in a more pronounced improvement in GGT and ALT compared to UDCA 10 mg/kg/day. Improvements in AST and ALP were comparable. Although this study suggested a possible benefit with higher drug doses in resolving liver biochemistry, whether UDCA improves quality of life, histology, or survival is unknown.
INDICATIONS
URSOFALK is indicated in the treatment of chronic cholestatic liver diseases.
CONTRAINDICATIONS
URSOFALK must not be used in the presence of acute inflammation of the gall bladder and bile ducts; and obstruction of the biliary tract (common bile duct).
Ursodeoxycholic acid
Ursodeoxycholic acid (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. Ursodeoxycholic acid 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 ursodeoxycholic acid 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 of more interest to AAS using bodybuilders. 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.
Intrahepatic cholestasis -- which occurs inside the liver -- can be caused by sepsis (generalized infection), bacterial abscess, drugs, total parenteral nutrition (being fed intravenously), lymphoma, tuberculosis, sarcoidosis and amyloidosis. Other causes of this form of the disorder include primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis (A,B,C, etc.), alcoholic liver disease, pregnancy, Sjogren's syndrome and others.
-Symptoms include the following: -Itching -Jaundiced (yellow) skin or eyes -Inability to digest certain foods -Nausea, vomiting -Right upper quadrant abdominal pain -Organ failure in cases of sepsis (but not from cholestasis itself) -Rash or fever in some cases of drug-induced cholestasis -Clay-colored or white stools -Dark urine
Often times a panel of standard liver function tests will show cholestasis before the symptoms even manifest themselves, but in general laboratory tests have limited diagnostic value. Transaminase (ALT, AST), alkaline phosphate, and bilirubin levels are typically elevated in proportion to the severity of the disease. AST and ALT can be elevated by exercise, so those are not particularly helpful in diagnosing cholestasis (1).
It is intrahepatic cholestasis caused by drugs (i.e.oral 17 alpha alkylated anabolic steroids) that is of greatest concern to bodybuilders. It has been proposed 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, we mentioned the bile transport pump. UDCA has been shown to stimulate enzymes that increase the density of these bile transporters, 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. Quoting from one study,
"A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae...Liver biopsy was compatible with cholestasis induced by anabolic steroids...The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement. (4).
Interestingly, there seems to be a genetic disposition to the development of drug induced cholestasis (5). This may explain why only some oral AAS users develop the disease and others can endure heavy cycles of 17-alpha alkylated orals. Cholestasis as well as hepatitis caused by non 17-alpha alkylated injectable steroids has been reported, but is rare.
Cholestasis can be caused by estrogen as well, both synthetic and endogenous. It is not uncommon for cholestasis to develop during pregnancy, when estrogen levels are high. It’s possible the rare reported cases of testosterone induced cholestasis might be due to elevated estrogen levels in susceptible individuals.
It should be stressed that if one develops the symptoms of drug induced cholestasis, the first line of treatment is to immediately discontinue the drug, and begin treatment with UDCA. Although there are no studies showing UDCA exerts any prophylactic effects against AAS induced cholestasis, the proposed mechanism whereby it upregulates hepatic bile transporters suggests it may very well help prevent the disease by increasing bile flow out of the liver. Once the offending drug is withdrawn, and UDCA therapy begun, the disease typically resolves.
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, somewhat typical of what is seen in many people subsisting on high fat western diets (and typical of what is seen in oral AAS users). 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).
So we see an added health benefit to UDCA use, even in those AAS users who do not experience cholestasis. Most bodybuilders watch their fat intake, but on a high protein diet that includes red meat, UDCA might be a worthwhile supplement to consider if one is concerned about cholesterol (and who isn’t these days).
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).
Dosages of commercial brands of UDCA vary depending on the type and severity of liver disease. For preventative purposes 500 mg per day might be sufficient. Once liver disease has developed, one ought to see their doctor, but a typical recommended dose is 13 to 15 mg/kg/day which may be given in 2 divided doses, i.e. in the morning and at bedtime, with food. But again, if any of the symptoms listed above develop, or liver tests come out showing cholestasis or some other liver disorder, don’t self medicate; see your doctor, and lay off the orals.
Ursodeoxycholic acid (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. Ursodeoxycholic acid 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 ursodeoxycholic acid 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 of more interest to AAS using bodybuilders. 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.
Intrahepatic cholestasis -- which occurs inside the liver -- can be caused by sepsis (generalized infection), bacterial abscess, drugs, total parenteral nutrition (being fed intravenously), lymphoma, tuberculosis, sarcoidosis and amyloidosis. Other causes of this form of the disorder include primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis (A,B,C, etc.), alcoholic liver disease, pregnancy, Sjogren's syndrome and others.
-Symptoms include the following: -Itching -Jaundiced (yellow) skin or eyes -Inability to digest certain foods -Nausea, vomiting -Right upper quadrant abdominal pain -Organ failure in cases of sepsis (but not from cholestasis itself) -Rash or fever in some cases of drug-induced cholestasis -Clay-colored or white stools -Dark urine
Often times a panel of standard liver function tests will show cholestasis before the symptoms even manifest themselves, but in general laboratory tests have limited diagnostic value. Transaminase (ALT, AST), alkaline phosphate, and bilirubin levels are typically elevated in proportion to the severity of the disease. AST and ALT can be elevated by exercise, so those are not particularly helpful in diagnosing cholestasis (1).
It is intrahepatic cholestasis caused by drugs (i.e.oral 17 alpha alkylated anabolic steroids) that is of greatest concern to bodybuilders. It has been proposed 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, we mentioned the bile transport pump. UDCA has been shown to stimulate enzymes that increase the density of these bile transporters, 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. Quoting from one study,
"A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae...Liver biopsy was compatible with cholestasis induced by anabolic steroids...The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement. (4).
Interestingly, there seems to be a genetic disposition to the development of drug induced cholestasis (5). This may explain why only some oral AAS users develop the disease and others can endure heavy cycles of 17-alpha alkylated orals. Cholestasis as well as hepatitis caused by non 17-alpha alkylated injectable steroids has been reported, but is rare.
Cholestasis can be caused by estrogen as well, both synthetic and endogenous. It is not uncommon for cholestasis to develop during pregnancy, when estrogen levels are high. It’s possible the rare reported cases of testosterone induced cholestasis might be due to elevated estrogen levels in susceptible individuals.
It should be stressed that if one develops the symptoms of drug induced cholestasis, the first line of treatment is to immediately discontinue the drug, and begin treatment with UDCA. Although there are no studies showing UDCA exerts any prophylactic effects against AAS induced cholestasis, the proposed mechanism whereby it upregulates hepatic bile transporters suggests it may very well help prevent the disease by increasing bile flow out of the liver. Once the offending drug is withdrawn, and UDCA therapy begun, the disease typically resolves.
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, somewhat typical of what is seen in many people subsisting on high fat western diets (and typical of what is seen in oral AAS users). 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).
So we see an added health benefit to UDCA use, even in those AAS users who do not experience cholestasis. Most bodybuilders watch their fat intake, but on a high protein diet that includes red meat, UDCA might be a worthwhile supplement to consider if one is concerned about cholesterol (and who isn’t these days).
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).
Dosages of commercial brands of UDCA vary depending on the type and severity of liver disease. For preventative purposes 500 mg per day might be sufficient. Once liver disease has developed, one ought to see their doctor, but a typical recommended dose is 13 to 15 mg/kg/day which may be given in 2 divided doses, i.e. in the morning and at bedtime, with food. But again, if any of the symptoms listed above develop, or liver tests come out showing cholestasis or some other liver disorder, don’t self medicate; see your doctor, and lay off the orals.
Its from PSL so the quality is there. Maybe I'll run it 10/20/20/20 then. Or should I just run 20 ed the whole run?
You might be right beast. I found this info on tudca. Looks like tudca is the active of udca.
https://www.clinicaltrials.gov/ct2/show/NCT01829698
http://examine.com/supplements/Tauroursodeoxycholic+Acid/
- - - Updated - - -
Sorry folks, didn't mean to steer you in the wrong direction. I'm an idiot.
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