#4. Anavar and Winstrol as a tie.........both need high doses to be effective and are 17aa. Winstrol is particularily bad for the lipid profile for some reason.
Nope.
Oxandrolone is the safest steroid by far and should never be compared to winny in terms of liver toxicity. You say that someone needs to use 50+ mg/day to build mass and I agree, but you actually need more than that to equal winny in building strength. The reason you need to take more is that 28% of the oxandrolone you take is excreted untouched by your liver. So you need to take at least 28% more Ox than Winny just have equal blood levels. But I don't agree that ox is dangerous to your liver at that dose.
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Here they used 80mg/day and saw liver values IMPROVE.
1: Am J Gastroenterol 1991 Sep;86(9):1200-8
A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. I. Short-term effects on liver function.
Bonkovsky HL, Fiellin DA, Smith GS, Slaker DP, Simon D, Galambos JT.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
The present studies were designed to provide careful measures of effects of oxandrolone, an anabolic steroid, intravenous nutritional supplementation, and the combination of these two treatments on liver functions, metabolic balances, nitrogen metabolism, and nutritional status in patients with moderate to severe alcoholic hepatitis. Of 43 patients originally recruited, 39 (19 men, 20 women) with typical clinical and laboratory features of alcoholic hepatitis (11 Child's-Pugh class B; 28 class C) were admitted to a metabolic unit and completed a 35-day three-phase protocol. Phase I was a 10-day baseline period of observation, during which routine and special quantitative tests of liver function (galactose and antipyrine metabolism), a 7-day elemental balance study, and a 15N, 13C-leucine metabolism study were done. Phase II was a 21-day treatment period during which patients were randomly assigned to receive one of four regimens: 1) standard therapy, consisting of abstinence, a balanced, nutritionally adequate diet, and multivitamins; 2) oxandrolone
(20 mg orally four times a day) plus standard therapy; 3) nutritional supplementation, consisting of 2 L daily of 3.5% crystalline amino acids (in 5% dextrose), given by peripheral vein; or 4) a combination of oxandrolone and nutritional supplementation, along with standard therapy. Metabolic balances were repeated during phase II. Phase III was 2 or 3 days posttreatment, during which special studies of liver functions and volumes and leucine metabolism were repeated. All patients who completed phase I of study and were randomly allocated to one of the four treatment groups completed the subsequent two phases. Overall, with time, patients showed highly significant improvements in most clinical and laboratory features. For most standard laboratory tests (e.g., serum albumin, transferrin, prothrombin time) improvements were more marked in patients treated with nutritional supplementation and/or oxandrolone than in those given standard therapy alone.
Liver volumes fell in all treatment groups, with greater improvement in those treated with nutritional supplementation. Improvements in galactose and antipyrine metabolism rates were significant only in those treated with nutritional supplementation or oxandrolone. Effects of treatments on metabolic balances, nitrogen metabolism, and measures of nutrition are described in this issue in a companion paper.
We conclude that the addition of nutritional supplementation and oxandrolone to standard therapy of moderately severe or severe alcoholic hepatitis is well tolerated, and leads to more rapid improvement in the laboratory parameters measured.
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Here a woman who had been taking winny developed winny hepatotoxcity complications. So they switched her to oxandrolone and her condition improved without complication.
September 2000 • Volume 43 • Number 3
Treatment of lipodermatosclerosis with oxandrolone in a patient with stanozolol-induced hepatotoxicity
Stanozolol is a synthetic testosterone derivative with primarily anabolic (and few androgenic) effects that also has potent fibrinolytic properties.2 Presumably, it is the latter property that explains its successful use in the treatment of lipodermatosclerosis.3 However, major systemic side effects of stanozolol include sodium retention, hepatotoxicity, and lipid profile abnormalities.4 We describe a patient with chronic lipodermatosclerosis whose symptoms abated after treatment with stanazolol, but hepatotoxicity developed and the patient required alternative therapy.
Her worsening pain and extension of the induration prompted a trial of stanozolol (2 mg daily), which resulted in marked alleviation of symptoms within 2 weeks of its initiation. Unfortunately, within 2 months her liver enzyme levels rose from normal baseline levels (alanine aminotransferase, 38 U/L; aspartate aminotransferase, 38 U/L) to 257 U/L (alanine aminotransferase) and 562 U/L (aspartate aminotransferase).
Although the patient did not exhibit signs or symptoms of hepatotoxicity, the stanozolol was immediately discontinued, with full resolution of the enzyme abnormalities. A newer anabolic steroid was then started, oxandrolone (10 mg twice daily), because it had been reported to be less hepatotoxic. Within 2 weeks, she experienced a reduction in pain (from a score of 7/10 to 3/10) as well as subjective softening of the skin. After 3 months of oxandrolone therapy, her symptoms had continued to abate, and she decided to discontinue the medication. No abnormalities in liver enzymes were noted. Incidentally, several months later she was diagnosed as having an idiopathic cardiomyopathy (a literature search failed to find any reports of oxandrolone-induced cardiomyopathy).
The newer anabolic steroid oxandrolone also has known fibrinolytic activity, but unlike the majority of oral anabolic steroids it undergoes limited hepatic metabolism and is associated with a lower incidence of hepatotoxicity. In our opinion, oxandrolone represents a therapeutic option for those patients with stanozolol-responsive lipodermatosclerosis in whom hepatic toxicity develops.
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