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  1. #1
    powerliftmike's Avatar
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    injectable c17aa and liver

    How much less stressful is injectable dianabol and winstrol depot than its oral counterparts? Some claim the first pass is the most stressful and injectables avoid this, while others say the stress is nearly the same on liver, tho injectables will have less GI stress. Just want some opinions and hopefully facts on this.

  2. #2
    symatech's Avatar
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    neither is anything to worry about. the hepatoxicity with 17aa roids is blow way out of proportion. I've run 3 orals at the same time and had bloodwork done and there was never any cause for alarm. I think drinking alcohol does more damage to your liver than eating winny.

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    Quote Originally Posted by symatech
    neither is anything to worry about. the hepatoxicity with 17aa roids is blow way out of proportion. I've run 3 orals at the same time and had bloodwork done and there was never any cause for alarm. I think drinking alcohol does more damage to your liver than eating winny.
    Well, my blood test showed elevated enzymes after dbol and winny but I dont think it was too dangerous tho. I will get exact numbers next time I go to doc, my doc just called me telling me she was concerned about the increase in values and dont take any tylenol or alcohol and come back in few months for another test.

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    did you run any liver detox? liv52 & milkthistle or anything?

  5. #5
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    here are some studies
    ---------------------


    Hepatic effects of 17 alpha-alkylated anaboli-androgenic steroids.

    [No authors listed]

    AIDS: Use of 17 alpha-alkylated anabolic -androgenic steroids (17alpha-AAS) has been connected to hepatotoxicity. These steroids are used clinically to treat anemia, to prevent weight loss, and to treat wasting syndrome. The most common types of 17alpha-AAS are Methyltestosterone , Oxandrolone, Oxymetholone and Stanozolol . Liver disease and the effects of some anti-HIV drugs may contribute to hepatic dysfunction. Signs of hepatic dysfunction are listed. For those experiencing jaundice and related malfunctions, discontinuing the drug enables patients to recover. In many cases those who did not exhibit jaundice may have developed a tolerance for the drugs. Side effects such as cholestatic jaundice only occurred in a small number of patients taking the recommended doses of 17alpha-AAS. Peliosis hepatitis, hepatic tumors, and hepatocellular adenomas are other reported side effects. Proper dosing and monitoring of anabolic steroids reduces the risk of hepatotoxicity.

    Publication Types:

    PMID: 11366381 [PubMed - indexed for MEDLINE]
    -not the best I've seen. There are a few I've seen discussing this I'll see if I can find them.



    Does the choice of alpha-AAS really make a difference?

    Mutzebaugh C.

    AIDS: A comparison of the four most common types of 17 alpha-alkylated anabolic-androgenic steroids (alpha-AAS) indicates that all are effective, all have some risk of liver toxicity, and each needs to be administered properly. Higher doses of 17alpha-AAS, together with other lifestyle and chemical factors, may produce a greater chance for liver toxicity, but overall the risk of adverse hepatic function is lower than believed. The use of alpha-AAS for treating AIDS Wasting Syndrome may be a viable option if appropriate dosing is used. Patients should be monitored and tested regularly.

    Publication Types:
    PMID: 11366379 [PubMed - indexed for MEDLINE]
    again not a great one but I'll look for the ones I wanted to post for you.

  6. #6
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    Quote Originally Posted by symatech
    neither is anything to worry about. the hepatoxicity with 17aa roids is blow way out of proportion. .
    I agree Symatech.I've ran drol for 10 weeks at a time and had my blood-work done 2 weeks after discontinuing the drol and values were uncannily normal.The liver is far more forgiving than most ppl on anabolic boards want you to believe.


    ~Pinnacle~

  7. #7
    symatech's Avatar
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    This is only a small excerpt from The Merck Manual sec. 4, chapter 43: Drugs and the liver.

    here is a link to where you can read that section (and rest of the book) online for free. http://www.merck.com/mrkshared/mmanu...pter43/43d.jsp

    Steroid-type cholestasis is a pure reaction with little or no hepatocellular inflammation. Gradual onset of cholestasis without systemic symptoms is usual. Alkaline phosphatase is elevated, but aminotransferase levels are usually unimpressive, and liver biopsy shows only centrizonal bile stasis with little portal reaction or hepatocellular disarray. Complete resolution follows drug withdrawal. This type of cholestasis is produced by oral contraceptives, methyltestosterone, and related drugs, most of which are C-17 alkylated steroids. About 1 to 2% of women taking oral contraceptives develop the syndrome; worldwide figures vary, possibly because of genetic factors. The reaction appears to be an exaggeration of the physiologic effect of sex hormones on bile formation, rather than an immunologic sensitivity or membrane cytotoxicity. Interference with canalicular water flow, microfilament dysfunction, and altered membrane fluidity may be responsible, but the exact mechanism of cholestasis is uncertain.
    Steroid -related cholestasis is closely related to cholestasis of pregnancy (see Hepatic Disorders in Ch. 251). Women with cholestasis of pregnancy may subsequently develop cholestasis with oral contraceptive use; likewise, women who develop cholestasis while taking oral contraceptives may subsequently develop cholestasis of pregnancy.

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