is tren harsh on liver?

[sweet t]

Hey guys what's up? i'm 4 weeks away from finishing a tren/prop cycle. i also ran some dbol at beginning, but only a few weeks. anyway, i had some bloodwork done yesterday, and of course my doc is freaking because my enzyme count is extremely high. i believe it's supposed to be 37 and it was over 100. do u think the tren has caused such a jump or is tren no harsher than the others out there. either way i guess i need to stop for a while and let it come back down before getting on again. any thoughts?

[sweet t]

any thoughts?

[Dally]

same boat sorta ... bump for you mang

[scriptfactory]

Most steroids have an effect on your lipid profiles to a certain extent. I'm sure pre-existing liver problems affect this considerably.
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Serum lipids in power athletes self-administering testosterone and anabolic steroids.
Alen M, Rahkila P, Marniemi J.

The purpose of the present investigation was to study the effects of testosterone and anabolic steroids on serum lipids in power athletes. Altogether 11 national top-level adult athletes completed the study. Five of them volunteered for the study group and the rest for controls. The follow-up consisted of 9 months of a strength training period. During the first 6 months, the subjects in the study group self-administered androgenic steroids on an average of 57 +/- 24.9 mg/day. The most interesting observation was the extremely low high-density lipoprotein (HDL) and HDL2 cholesterol concentrations of the androgen users. After 8 weeks of training, the study group had significantly (P less than 0.05) lower HDL cholesterol concentrations than the control group (0.53 +/- 0.11 and 1.14 +/- 0.19 mmol/l, respectively). This difference remained significant from 8 to 32 weeks of training. No systematic changes were observed in the control group. The HDL2 cholesterol concentration decreased by about 80% (P less than 0.01) and HDL3 cholesterol by about 55% (P less than 0.01) from the onset values in the study group. A substantial decrease in HDL cholesterol to total cholesterol and in HDL2 cholesterol to HDL3 cholesterol ratios were also noticed under the influence of exogenous androgens. The results of this study suggest that the sustained use of testosterone and anabolic steroids have a marked unfavorable effect on the pattern of HDL cholesterol in the serum of male power athletes.

Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Hartgens F, Rietjens G, Keizer HA, Kuipers H, Wolffenbuttel BH.

OBJECTIVES: To investigate the effects of two different regimens of androgenic-anabolic steroid (AAS) administration on serum lipid and lipoproteins, and recovery of these variables after drug cessation, as indicators of the risk for cardiovascular disease in healthy male strength athletes. METHODS: In a non-blinded study (study 1) serum lipoproteins and lipids were assessed in 19 subjects who self administered AASs for eight or 14 weeks, and in 16 non-using volunteers. In a randomised double blind, placebo controlled design, the effects of intramuscular administration of nandrolone decanoate (200 mg/week) for eight weeks on the same variables in 16 bodybuilders were studied (study 2). Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C), HDL3-cholesterol (HDL3-C), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and lipoprotein (a) (Lp(a)) were determined. RESULTS: In study 1 AAS administration led to decreases in serum concentrations of HDL-C (from 1.08 (0.30) to 0.43 (0.22) mmol/l), HDL2-C (from 0.21 (0.18) to 0.05 (0.03) mmol/l), HDL3-C (from 0.87 (0.24) to 0.40 (0.20) mmol/l, and Apo-A1 (from 1.41 (0.27) to 0.71 (0.34) g/l), whereas Apo-B increased from 0.96 (0.13) to 1.32 (0.28) g/l. Serum Lp(a) declined from 189 (315) to 32 (63) U/l. Total cholesterol and triglycerides did not change significantly. Alterations after eight and 14 weeks of AAS administration were comparable. No changes occurred in the controls. Six weeks after AAS cessation, serum HDL-C, HDL2-C, Apo-A1, Apo-B, and Lp(a) had still not returned to baseline concentrations. Administration of AAS for 14 weeks was associated with slower recovery to pretreatment concentrations than administration for eight weeks. In study 2, nandrolone decanoate did not influence serum triglycerides, total cholesterol, HDL-C, HDL2-C, HDL3-C, Apo-A1, and Apo-B concentrations after four and eight weeks of intervention, nor six weeks after withdrawal. However, Lp(a) concentrations decreased significantly from 103 (68) to 65 (44) U/l in the nandrolone decanoate group, and in the placebo group a smaller reduction from 245 (245) to 201 (194) U/l was observed. Six weeks after the intervention period, Lp(a) concentrations had returned to baseline values in both groups. CONCLUSIONS: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp(a) concentration. The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp(a) concentrations. The effect of this on atherogenesis remains to be established.

Reversibility of the effects on blood cells, lipids, liver function and hormones in former anabolic-androgenic steroid abusers.
Urhausen A, Torsten A, Wilfried K.

BACKGROUND: In contrast to the acute effects of anabolic-androgenic steroid (AAS) abuse, the long-term risk profile of former long-term abusers (ExA) is less clear. METHODS: Blood parameters of 32 male bodybuilders and powerlifters were studied. Fifteen ExA had not been abusing AAS for at least 12-43 months on average (mean dosage 700 mg for 26 weeks per year over 9 years), 17 athletes (A) were still abusing AAS (750 mg for 33 weeks per 8 years). FINDINGS: Hemoglobin (+5%), leucocytes (+33%) and platelets (+38%) were significantly higher in A. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher, cholinesterase activity (CHE) lower in A (65+/-55, 38+/-27 and 3719+/-1528U/l) compared to ExA (24+/-10, 18+/-11 and 6345+/-975U/l; each P<0.001) with normal values for gamma-glutamyl transpeptidase (gamma-GT) and bilirubin. ALT, AST and CHE correlated significantly with the extent (duration and weekly dosage, expressed as a point score) of AAS abuse in A (r=0.68, 0.57 and -0.62; each P<0.01). Total and LDL-cholesterol were similar, HDL-cholesterol was distinctly lower in A than in ExA (17+/-11 and 43+/-11 mg/dl; P<0.001) and correlated negatively with the extent of AAS abuse (r=-0.50; P<0.05). Testosterone and estradiol were significantly higher, while LH, FSH and the sexual-hormone-binding (SHB) protein were lower in A than in ExA (each P<0.001). Two ExA had testosterone levels below the normal range. INTERPRETATION: The alterations in cell counts, HDL-cholesterol, liver function and most hormones of the pituitary-testicular axis induced by a long-term abuse of AAS were reversible after stopping the medication for over 1 year. In some ExA, an increased ALT activity and a depressed testosterone synthesis were found.