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GGT normal, but AST and ALT elevated!!
- Thread starter Whacked
- Start date
[email protected]
New member
Have you been taking any pain medication? I was taking generic percocet one time and my ast level was well over 100. Acetaminophen and alcohol can raise liver values as well. I would use some Glucorel (it is R-ala) from the af store. R-ala is one of the best liver healers you can take.
Whacked
New member
[email protected] said:
Nope -- Just Test + Aromasin.
(I got off all orals --VAR--- about 5 weeks ago now).[email protected] said:
On it year-round
LoneTree said:
dogoftheday, his ALT and AST are off the chain....
Those are not even slightly elevated, they are extremely HIGH.
Whacked, whatever you are taking, it's definitely stressing your liver bigtime.
Typically those two are elevated from 17AA orals.
DIV
The levels show that there are high levels of those enzymes in your blood. Although the liver may be stressed it does not show you have "liver damage" per se, and probably don't with GGT being so low. Those same enzymes can come from muscle damage as well as liver damage. They can jump that high from your weight training if it's intense enough. GGT doesn't come from your muscle but would be elevated if your liver was damaged.
Unlike most studies, this was done on people just like you.
Clin J Sport Med. 1999 Jan;9(1):34-9.
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.
OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.
Unlike most studies, this was done on people just like you.
Clin J Sport Med. 1999 Jan;9(1):34-9.
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.
OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.
