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confused about liver enzymes
- Thread starter illuminat
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Its All Genetics
New member
high liver enzymes means ur liver is working harder than the normal range. this can be cause by sickness or by taking creatine or juice
Big_Joe
New member
Transaminase levels are indicators of liver cell damage. They can also be indicators of muscle cell damage, such as what happens from lifting heavy. Also transaminase levels are not liver function tests but indicators of inflammation of the liver. If you are doing heavy lifting you can drive your ALT level way up. Mine have been over 250 shortly after a heavy session. This is about 200 points above baseline. To tell if the elevated ALT is from muscle cell damage and not liver cell damage you need to also check GGT, gamma-glutamyltranspeptidase. If GGT and ALT are elevated then you have liver dysfunction. If only ALT, and ALT is only mildly elevated say below 500, you most likely have muscle cell damage contributing to the ALT score.
As for transaminase levels effecting the liver I would doubt it. If they did then when inflammation of the liver occurred the transaminases would increase the inflammation. This would lead to a circular event and death would be the end result.
As for transaminase levels effecting the liver I would doubt it. If they did then when inflammation of the liver occurred the transaminases would increase the inflammation. This would lead to a circular event and death would be the end result.
Whacked
New member
dexter_heaven
Banned
Dr. Caroline Becker, an endocrinologist with a large practice in Mt. Kisco, N.Y: She said: "Even with individuals with pre-existing liver disease I would have no compunction in giving them injectable testosterone."
The study that follows suggests anabolic steroid-induced liver toxicity may be exaggerated. The blood tests that are commonly thought to indicate liver toxicity, ALT (SGOT) and AST (SGPT) were elevated in both drug-free bodybuilders and drug-using bodybuilders.
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD; Pertusi RM; Zachariah NY; Dufour DR; McConathy WJ.
Clin J Sport Med, 9(1):34-9 1999 Jan.
Abstract 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.
PEACE
D_H
The study that follows suggests anabolic steroid-induced liver toxicity may be exaggerated. The blood tests that are commonly thought to indicate liver toxicity, ALT (SGOT) and AST (SGPT) were elevated in both drug-free bodybuilders and drug-using bodybuilders.
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD; Pertusi RM; Zachariah NY; Dufour DR; McConathy WJ.
Clin J Sport Med, 9(1):34-9 1999 Jan.
Abstract 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.
PEACE
D_H
