MESO-Rx
Anabolic Steroids
Anabolic Steroids & Liver [GI]
- Thread starter Michael Scally MD
- Start date
johnnyBALLZ
Well-known Member
I can't read the whole thing but it says right on the front "alternative supplement". Looks like some crap you'd find at GNC. Also, it's supposed to be spelled dianabol..
TexasCreed
New Member
Wow, I'm love the intensity on this thread. My experience, on juice for about 6 years. Heavy drinker till about 2 year ago. Always watched levels. Been really watching levels in past few months. Decreased alcohol intake severely reduced ggt and Ast and Alt. They were never too out of range though. Just started tudca at 500mg a day to see results. So milk thistle at 695 a day
Riedl MA. Critical appraisal of androgen use in hereditary angioedema: A systematic review. Ann Allergy Asthma Immunol. http://www.annallergy.org/article/S1081-1206(15)00034-4/abstract
OBJECTIVE: To provide an objective basis for evaluating the risk-benefit ratio of long-term androgen use in patients with hereditary angioedema (HAE).
DATA SOURCES: PubMed was searched with no time limitations using the keywords hereditary angioedema or angio-oedema combined with danazol, stanozolol, and androgen.
STUDY SELECTION: Qualifying articles were English-language reports of androgen use in patients with HAE, with relevant safety and/or efficacy information. Reports were categorized according to level of evidence (LOE).
RESULTS: The search process identified 153 citations, 63 of which contained relevant information; 2 additional publications were identified while other citations were being reviewed. Fifteen LOE 2 studies and multiple LOE 4 reports provided efficacy data, confirming a high level of prophylactic efficacy for androgen therapy in HAE, with occasional reports of poor prophylactic response.
Common adverse events include weight gain, menstrual irregularities, virilization, headaches, myalgias or cramps, mood changes, and elevations in creatine phosphokinase level, liver function test results, and serum lipid level. The risk of adverse events is often correlated with dose and/or treatment duration.
Rare cases of hepatic adenomas and hepatocellular carcinoma associated with long-term androgen use often had no preceding changes in liver function test results.
CONCLUSION: Androgen therapy may be effective for most patients with HAE; however, potential risks and adverse effects must be carefully considered and discussed with patients when considering options for long-term HAE prophylaxis.
OBJECTIVE: To provide an objective basis for evaluating the risk-benefit ratio of long-term androgen use in patients with hereditary angioedema (HAE).
DATA SOURCES: PubMed was searched with no time limitations using the keywords hereditary angioedema or angio-oedema combined with danazol, stanozolol, and androgen.
STUDY SELECTION: Qualifying articles were English-language reports of androgen use in patients with HAE, with relevant safety and/or efficacy information. Reports were categorized according to level of evidence (LOE).
RESULTS: The search process identified 153 citations, 63 of which contained relevant information; 2 additional publications were identified while other citations were being reviewed. Fifteen LOE 2 studies and multiple LOE 4 reports provided efficacy data, confirming a high level of prophylactic efficacy for androgen therapy in HAE, with occasional reports of poor prophylactic response.
Common adverse events include weight gain, menstrual irregularities, virilization, headaches, myalgias or cramps, mood changes, and elevations in creatine phosphokinase level, liver function test results, and serum lipid level. The risk of adverse events is often correlated with dose and/or treatment duration.
Rare cases of hepatic adenomas and hepatocellular carcinoma associated with long-term androgen use often had no preceding changes in liver function test results.
CONCLUSION: Androgen therapy may be effective for most patients with HAE; however, potential risks and adverse effects must be carefully considered and discussed with patients when considering options for long-term HAE prophylaxis.
Seo NK, Koo HS, Haam JH, Kim HY, Kim MJ, et al. Levels of serum testosterone predict prevalent but not incident non-alcoholic fatty liver disease. J Gastroenterol Hepatol. http://onlinelibrary.wiley.com/doi/10.1111/jgh.12935/abstract
BACKGROUND & AIMS: The association between testosterone level and development of nonalcoholic fatty liver disease is not well known. We examined the relationship of total testosterone level with development and regression of nonalcoholic fatty liver disease.
METHODS: Among the men who had undergone repeated liver ultrasonography in 2 years or more at a health promotion center, subjects with available serum testosterone level at baseline were included in the study. Alcohol consumers (>20 g/day) were excluded from the study.
RESULTS: Among the 1,944 men, 44.3% of subjects were diagnosed with nonalcoholic fatty liver disease.
Higher level of testosterone significantly lowered the prevalence of fatty liver (odds ratios per SD increase, 0.686 and 0.795 at baseline and follow-up, respectively).
During the median 4.2 years follow-up, 22.4% of subjects in the normal group developed fatty liver and 21.0% of subjects in the nonalcoholic fatty liver disease group recovered at the follow-up.
In longitudinal analyses, higher level of testosterone was significantly associated with the development or regression of fatty liver, before adjustment for obesity and metabolic parameters. However, in the full-adjusted model, testosterone level did not influence the development or regression of fatty liver.
CONCLUSIONS: Although testosterone level was significantly low in the subjects with nonalcoholic fatty liver disease in cross-sectional analyses, baseline testosterone level did not independently influence the development or regression of fatty liver at the median 4.2 years follow-up. Obesity and metabolic parameters may play key roles in the link between testosterone level and nonalcoholic fatty liver disease.
BACKGROUND & AIMS: The association between testosterone level and development of nonalcoholic fatty liver disease is not well known. We examined the relationship of total testosterone level with development and regression of nonalcoholic fatty liver disease.
METHODS: Among the men who had undergone repeated liver ultrasonography in 2 years or more at a health promotion center, subjects with available serum testosterone level at baseline were included in the study. Alcohol consumers (>20 g/day) were excluded from the study.
RESULTS: Among the 1,944 men, 44.3% of subjects were diagnosed with nonalcoholic fatty liver disease.
Higher level of testosterone significantly lowered the prevalence of fatty liver (odds ratios per SD increase, 0.686 and 0.795 at baseline and follow-up, respectively).
During the median 4.2 years follow-up, 22.4% of subjects in the normal group developed fatty liver and 21.0% of subjects in the nonalcoholic fatty liver disease group recovered at the follow-up.
In longitudinal analyses, higher level of testosterone was significantly associated with the development or regression of fatty liver, before adjustment for obesity and metabolic parameters. However, in the full-adjusted model, testosterone level did not influence the development or regression of fatty liver.
CONCLUSIONS: Although testosterone level was significantly low in the subjects with nonalcoholic fatty liver disease in cross-sectional analyses, baseline testosterone level did not independently influence the development or regression of fatty liver at the median 4.2 years follow-up. Obesity and metabolic parameters may play key roles in the link between testosterone level and nonalcoholic fatty liver disease.
HumanHealther
New Member
Milk thistle certainly has been known to help out the liver.
I think it may act kind of like soy isoflavones in the sense that it promotes estrogen metabolism.
http://www.ncbi.nlm.nih.gov/pubmed/21234288
The key here is maintaining adequate glutathione levels. Glutathione are conjugation enzymes that rid steroid metabolites.
Thing is, you can't actually orally supplement with glutathione.
Most good whey includes:
Glatamine + Cystine + Glutamic acid = Basic amino acid buildings for Glutathione
If you feel the need to jump start your liver into recycling or replacing used up Glutathione enzymes then think about supplementing with Alpha lipoic acid and N-Acetyl cysteine.
N-Acetyl cysteine is used on the front lines of hospitals to prevent liver failure associated with overdoses.
The first part of the article linked bellow goes more into detail about mechanisms.
http://howtostopgynecomastia.com/get-the-most-out-of-your-gynecomastia-reduction/
Cheers
Thapar M, Grapp O, Fisher C. Management of Hepatic Adenomatosis. Curr Gastroenterol Rep. 2015;17(3):434. http://link.springer.com/article/10.1007/s11894-015-0434-4
Hepatic adenomatosis (HeAs) is a rare clinical entity defined by the presence of 10 or more hepatic adenomas (HA) within the background of an otherwise normal liver parenchyma, in the absence of glycogen storage disease or anabolic steroid use.
HA is a benign tumor associated with oral contraceptive use. Recent advances in pathogenesis and classification of HA have questioned the distinction between these two diseases.
HA are currently classified into four different subtypes with genotypic and phenotypic correlation:
HNF-1a inactivated HA,
B-catenin activated HA,
inflammatory HA, and
undetermined subtype.
The clinical presentation of HA depends on the lesion size and the subtype. MRI using hepatospecific contrast agents is helpful in diagnosing the most common subtypes.
When diagnosis is uncertain, biopsy with immunohistochemistry is used to diagnose and classify the lesions.
Management is governed by the molecular subtype and tumor size. Pregnancy is not routinely discouraged but management is individualized.
Hepatic adenomatosis (HeAs) is a rare clinical entity defined by the presence of 10 or more hepatic adenomas (HA) within the background of an otherwise normal liver parenchyma, in the absence of glycogen storage disease or anabolic steroid use.
HA is a benign tumor associated with oral contraceptive use. Recent advances in pathogenesis and classification of HA have questioned the distinction between these two diseases.
HA are currently classified into four different subtypes with genotypic and phenotypic correlation:
HNF-1a inactivated HA,
B-catenin activated HA,
inflammatory HA, and
undetermined subtype.
The clinical presentation of HA depends on the lesion size and the subtype. MRI using hepatospecific contrast agents is helpful in diagnosing the most common subtypes.
When diagnosis is uncertain, biopsy with immunohistochemistry is used to diagnose and classify the lesions.
Management is governed by the molecular subtype and tumor size. Pregnancy is not routinely discouraged but management is individualized.
TexasCreed
New Member
I'm almost done with my 30 day supply of tudca at 250 twice a day. Along with milk thistle too. Going to a couple weeks more and then get blood work. Heard and seen lots of medical results raving on tudca.
Yes my nads do this on a regular basis
New market for liver disease spawns race for better testing
http://in.reuters.com/article/2015/03/15/us-liver-diagnostics-insight-idINKBN0MB0HJ20150315
http://in.reuters.com/article/2015/03/15/us-liver-diagnostics-insight-idINKBN0MB0HJ20150315
xovert
New Member
I would not use any orals at all...everyones body will react in a different way..with the onset of peps it outdates the gear use as far as iam concerned...what price fame.
Hild SA, Attardi BJ, Koduri S, Till BA, Reel JR. Effects of Synthetic Androgens on Liver Function Using the Rabbit as a Model. J Androl:jandrol.109.009365. http://www.andrologyjournal.org/cgi/rapidpdf/jandrol.109.009365v1
The objective of this study was to determine if the rabbit was a suitable model to test new synthetic androgens for potential liver toxicity within a short dosing interval.
Adult male rabbits were dosed orally daily on days 0-13 with 17 {alpha}-methyltestosterone (MT), as a positive control, and testosterone (T), as a negative control, to validate this model. Synthetic androgens tested were: 7 {alpha}-methyl-19-nortestosterone (MENT), dimethandrolone-undecanoate (DMAU), and 11{beta}-methyl-19-nortestosterone-17{beta}-dodecylcarbonate (11{beta}-MNTDC).
Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transpeptidase (GGT), and sorbitol dehydrogenase (SDH), as well as clearance of intravenous injected bromsulfonphthalein (BSP) from serum on days 0, 7 and 14, were determined.
As expected, T (10 mg/kg/day) did not adversely affect BSP retention or serum liver enzymes. MT (10 mg/kg/day) increased BSP retention, and AST, ALT, GGT, and SDH levels indicating that this model could detect androgens known to be hepatotoxic. DMAU and MENT (10 mg/kg/day), increased BSP retention, and all 4 serum liver enzymes as well, but the effects were less than those observed with MT at the same dose.
All parameters returned to baseline 2 weeks after cessation of dosing. 11{beta}-MNTDC at 10 mg/kg/day did not have an effect on BSP retention or liver enzymes, but a slight increase in serum GGT levels was observed in rabbits treated with 25 mg/kg/day. For the androgens that exhibited liver toxicity at 10 mg/kg/day (MT, DMAU, and MENT), a no observed effect level (NOEL) of 1 mg/kg/day was established.
Overall ranking of the synthetic androgens from most to least hepatotoxic based on %BSP retention was: MT >> DMAU > MENT > 11{beta}-MNTDC. Hence, the rabbit appears to be a promising model for detection of potential liver toxicity by synthetic androgens using BSP clearance and serum liver enzyme levels as early indicators of injury.
The objective of this study was to determine if the rabbit was a suitable model to test new synthetic androgens for potential liver toxicity within a short dosing interval.
Adult male rabbits were dosed orally daily on days 0-13 with 17 {alpha}-methyltestosterone (MT), as a positive control, and testosterone (T), as a negative control, to validate this model. Synthetic androgens tested were: 7 {alpha}-methyl-19-nortestosterone (MENT), dimethandrolone-undecanoate (DMAU), and 11{beta}-methyl-19-nortestosterone-17{beta}-dodecylcarbonate (11{beta}-MNTDC).
Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transpeptidase (GGT), and sorbitol dehydrogenase (SDH), as well as clearance of intravenous injected bromsulfonphthalein (BSP) from serum on days 0, 7 and 14, were determined.
As expected, T (10 mg/kg/day) did not adversely affect BSP retention or serum liver enzymes. MT (10 mg/kg/day) increased BSP retention, and AST, ALT, GGT, and SDH levels indicating that this model could detect androgens known to be hepatotoxic. DMAU and MENT (10 mg/kg/day), increased BSP retention, and all 4 serum liver enzymes as well, but the effects were less than those observed with MT at the same dose.
All parameters returned to baseline 2 weeks after cessation of dosing. 11{beta}-MNTDC at 10 mg/kg/day did not have an effect on BSP retention or liver enzymes, but a slight increase in serum GGT levels was observed in rabbits treated with 25 mg/kg/day. For the androgens that exhibited liver toxicity at 10 mg/kg/day (MT, DMAU, and MENT), a no observed effect level (NOEL) of 1 mg/kg/day was established.
Overall ranking of the synthetic androgens from most to least hepatotoxic based on %BSP retention was: MT >> DMAU > MENT > 11{beta}-MNTDC. Hence, the rabbit appears to be a promising model for detection of potential liver toxicity by synthetic androgens using BSP clearance and serum liver enzyme levels as early indicators of injury.
Liver damage is my greatest fear when it comes to taking oral steroids. I have more orals and prohormones than I do with my two year supply of injectibles! My dilemma is what is the best course of action to use when I began to use them? A small amount to help me with the workout? Do a short cycle low dose? Or monitor my liver function and values through getting blood tested every 30-45 days? So injectibles are the way to go I see.
OK doc, what the hell am I going to do with $1,700.00 plus of oral steroids and prohormones? Throw them away!!! ???
OK doc, what the hell am I going to do with $1,700.00 plus of oral steroids and prohormones? Throw them away!!! ???
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Shocking transformation of ex-bodybuilder given just three weeks to live after being diagnosed with liver cancer which he blames on 10,000 calorie per day pizza and energy drink diet
http://www.dailymail.co.uk/news/art...live-says-ll-beat-disease-healthy-eating.html
· Dean Wharmby, 39, was told he had just three weeks to live in November
· A large tumour was found on his liver and it was too big to operate on
· He's fighting his illness using natural remedies and sticking to a strict diet
· Huge u-turn for a man who used to eat eight bacon butties for breakfast, a Quarter Pounder meal as a snack and pizza while he waited for dinner
· Washed 10,000 calories a day down with seven to eight energy drink cans
But he now believes the high-protein, fatty diet he lived on for four to five years may have led to his illness, first diagnosed in 2010.
'It was because I was trying to be as big as possible,' Mr Wharmby told MailOnline.
'I can't say it was the diet for sure, but things like the energy drinks could be contributing factors. Red meats - all things we have found out have so many impurities in them now.
'I think it was a combination of it all.'
Mr Wharmby had been a bodybuilder for 20 years before he became ill.
In the beginning, he admits to taking steroids for about a year to create his physique because 'everybody did it'.
But he soon turned his back on them, as he began to build his personal training business.
It was then his diet took a turn for the worse.
http://www.dailymail.co.uk/news/art...live-says-ll-beat-disease-healthy-eating.html
· Dean Wharmby, 39, was told he had just three weeks to live in November
· A large tumour was found on his liver and it was too big to operate on
· He's fighting his illness using natural remedies and sticking to a strict diet
· Huge u-turn for a man who used to eat eight bacon butties for breakfast, a Quarter Pounder meal as a snack and pizza while he waited for dinner
· Washed 10,000 calories a day down with seven to eight energy drink cans
But he now believes the high-protein, fatty diet he lived on for four to five years may have led to his illness, first diagnosed in 2010.
'It was because I was trying to be as big as possible,' Mr Wharmby told MailOnline.
'I can't say it was the diet for sure, but things like the energy drinks could be contributing factors. Red meats - all things we have found out have so many impurities in them now.
'I think it was a combination of it all.'
Mr Wharmby had been a bodybuilder for 20 years before he became ill.
In the beginning, he admits to taking steroids for about a year to create his physique because 'everybody did it'.
But he soon turned his back on them, as he began to build his personal training business.
It was then his diet took a turn for the worse.
FDA warns consumers not to use muscle growth product called Tri-Methyl Xtreme.
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm442494.htm
A dietary supplement marketed to body builders and purported to contain anabolic steroids is linked to serious liver injury, the FDA warned on Monday.
The agency has so far received three reports of adverse events associated with Tri-Methyl Xtreme, which is sold on the internet and in some retail stores and gyms.
Symptoms may include abdominal pain, back pain, discolored urine, or unexplained fatigue.
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm442494.htm
A dietary supplement marketed to body builders and purported to contain anabolic steroids is linked to serious liver injury, the FDA warned on Monday.
The agency has so far received three reports of adverse events associated with Tri-Methyl Xtreme, which is sold on the internet and in some retail stores and gyms.
Symptoms may include abdominal pain, back pain, discolored urine, or unexplained fatigue.
May I get a bit of help from the two docs here please.
I have done a cycle of test + Anavar.
the orals was taken for 5 weeks at 50-60mg day.
I then stopped because I felt sick and the toxicity was becoming to high.
I lost appetite for 1 week, heartburn were to strong, and my stool had a very yellow pale colour plus I could see a lot of fat in the water after taking a dump.
I know that these are all sign of choleostatis (something spelled like that, sorry for my english is not my native language).
So I stopped the orals, continued just the test and did blood test.
GOT 37 U/I
GPT 70 U/I
GGT 9 U/L
Bilirubin total 0,56 mg/dl
Bilirubin direct 0,10 mg/dl
After 8 weeks that I stopped the orals I have now:
GOT 59 U/I
GPT 72 U/I
GGT 7 U/L
Bilirubin Total 0.67 mg/dl
Bilirubin direct 0.30 mg/dl
I think the last test is a bit skewed by what I did in the 3 days before drawing blood.
I had a very heavy workout and took one pain killer plus drank a bit of alchool (i never drink alchool)
I'm gonna retest in 4 weeks to see if my liver values are better.
It's 3 weeks after PCT at the moment, I'm a bit worried about my liver in general, it has been my first cycle but I feel like I'm still recovering from the toxicity given from the 5 weeks of Anavar.
I feel ok right now, no more disgusting gas, my stool is fine, no heartburn, my digestion is back to normal, but the liver values are not as pre blood cycle:
got 20
gpt 23
ggt 6
Something is still not right, could I developed a fatty liver? or some permanent choleostatis? or someother pathology?
I have done a cycle of test + Anavar.
the orals was taken for 5 weeks at 50-60mg day.
I then stopped because I felt sick and the toxicity was becoming to high.
I lost appetite for 1 week, heartburn were to strong, and my stool had a very yellow pale colour plus I could see a lot of fat in the water after taking a dump.
I know that these are all sign of choleostatis (something spelled like that, sorry for my english is not my native language).
So I stopped the orals, continued just the test and did blood test.
GOT 37 U/I
GPT 70 U/I
GGT 9 U/L
Bilirubin total 0,56 mg/dl
Bilirubin direct 0,10 mg/dl
After 8 weeks that I stopped the orals I have now:
GOT 59 U/I
GPT 72 U/I
GGT 7 U/L
Bilirubin Total 0.67 mg/dl
Bilirubin direct 0.30 mg/dl
I think the last test is a bit skewed by what I did in the 3 days before drawing blood.
I had a very heavy workout and took one pain killer plus drank a bit of alchool (i never drink alchool)
I'm gonna retest in 4 weeks to see if my liver values are better.
It's 3 weeks after PCT at the moment, I'm a bit worried about my liver in general, it has been my first cycle but I feel like I'm still recovering from the toxicity given from the 5 weeks of Anavar.
I feel ok right now, no more disgusting gas, my stool is fine, no heartburn, my digestion is back to normal, but the liver values are not as pre blood cycle:
got 20
gpt 23
ggt 6
Something is still not right, could I developed a fatty liver? or some permanent choleostatis? or someother pathology?
GOT range: less then 40
GPT range: less then 41
GGT range: less then 55
Bilirubin total: less then 1.0
Bilirubin direct: less then 0.35
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