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Rio 2001
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I recently reviewed an article I wrote some time ago, adding some new references, so here it is...
AAS and liver
Hepatic alterations are caused almost exclusively by the 17 alpha-alkylated AASs ( Blue JG 1999), this is primarily due to the pharmacokynetic effect caused by the addition of a alkyl group to the AAS .
Although it is already well established that 17 aa AAS are toxic to the liver, how that hepatotoxicity develops differs according to the 17 aa used.
Alterations in the structure of the hepatic cell probably happen as a result of lipidic perioxidation of the membrane, as observed experimentally with methyltestosterone, oximetholone and stanozolol, through the increase of plasmatic LDH (extravasated enzyme of the harmed cell) and decrease of the glutahione (antioxidant) (Welder et al, 1995).
Surprisingly, two studies done with Oxandrolone 80mg / day in the malnutrition treatment of alcoholic hepatitis showed IMPROVEMENT of hepatic function, six months survival and nutritional state (Mendelhall et al,1984/1993), however the author alerts for the potential risk of administering a 17aa for patients with established hepatic lesion and suggests new studies. In any way, that should be an indicative of the low hepatotoxicity of the oxandrolone and probably in this case the benefits of a nutritional status upgrade caused by oxandrolone outweighted the harm of it being an alkylated.
Bile retention in the biliary ducts happens mainly with oxymetholone, and no rare jaundice not accompanied by enzymatic alterations is observed . The most serious liver effect of oxymehtolone, hepatic peliosis and even tumors are reverted with discontinuity of use and an extensive revision done recently failed in proving the correlation between AAS and liver cancer (at least in therapeutic doses).
Regarding lab tests to screen liver stress during AAS use, two recent studys showed that 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( Dickerman RD, 1999/2001).
So, considering what is known , what would be indicated for liver “protection” ?
As for liver protection efficiency, it is proven that milk thistle improves recovery of acute hepatitis and hepatic enzymatic profile in alcoholic hepatitis (Flora et al, 1998) and reduces mortality in the fulminant hepatitis, being the only recommended herb for tratment of hepatic cirrhosis by the influential Blumenthal of Monographs in Herbal Medicine . Of course the use of antioxidants, reducing hepatocyte membrane lipidic perioxidation is also suitable, so glutathione, glutamine, selenium and more recently Alpha lipoic acid (ALA) assured their usage. Recently it was demonstrated that the use of the combination selenium / alpha lipoic acid / milk thistle was effective treating hepatitis C , normalizing the hepatic function and turning unnecessary the hepatic transplant in a significant number of patients (Berkson et al, 1999). Furthermore, ALA showed to be an efficient quelant( (substance that links to the other, usually inactivating it) for cadmium and iron, reducing its hepatotoxicity, and , to the similarity of the sylibum ( Milk thistle), it constitutes an effective antidote for intoxications by mushrooms of the type Amanita.
How, then, to optimize hepatic protection for a cycle that includes 17aa?
1)Alcoholic abstinence;
2)Previous vaccination against hepatitis (advisable for anybody, mainly for those that frequently manipulate needles; of course is for your own use, but a contamination of the injected liquid, in spite of rare, is possible; besides, the contamination with the virus A and/or B can happen with any one, and there are some cases of AAS users that developed serious liver lesions because they had used 17 aa AS and already had hepatitis);
3)Avoid the combination of 17aa, frequently seen in oral-only cycles;
4)Avoid hepatotoxic drugs and herbs, mainly during cycles with 17 aa ( avoid confrei, echynacea, valerian root, nicotinic acid, iron, Vit A more than 10.000UI/day, antibiotics like Clavulonate, azitromicin, tetracycline and erytromicine, isotretinoine (accutane), phenytoin, bupropione (Zyban), tryciclics. In general, check for hepatic side effects before using a drug in a cycle with 17aa.
5)Avoid ingestion of saturated fat;
6)Use ALA 100mg 3 caps 3x a day;
7)Use milk thistle 300mg/day;
8)Vit E/ C / selenium;
9) Water;
10) Taraxacum officinale ( dandelia), increases the bile excretion, dry extract 3g / day or tincture 50 drops 3x a day ( reduces chances of cholestatic jaundice during oxymetholone use)
The use of amino acids that are part of the hepatic metabolism, such as methyonine, inosine and choline, as well as Vit B 12 doesn't have scientific back up, being reserved for nutritional purposes.
Lab work is also a form of hepatic protection, because lab alterations frequently preceed symptoms and allow diagnosis and precocious therapy, which is fundamental in the preservation of our metabolic plant, the liver.
Rio 2001/Primo
AAS and liver
Hepatic alterations are caused almost exclusively by the 17 alpha-alkylated AASs ( Blue JG 1999), this is primarily due to the pharmacokynetic effect caused by the addition of a alkyl group to the AAS .
Although it is already well established that 17 aa AAS are toxic to the liver, how that hepatotoxicity develops differs according to the 17 aa used.
Alterations in the structure of the hepatic cell probably happen as a result of lipidic perioxidation of the membrane, as observed experimentally with methyltestosterone, oximetholone and stanozolol, through the increase of plasmatic LDH (extravasated enzyme of the harmed cell) and decrease of the glutahione (antioxidant) (Welder et al, 1995).
Surprisingly, two studies done with Oxandrolone 80mg / day in the malnutrition treatment of alcoholic hepatitis showed IMPROVEMENT of hepatic function, six months survival and nutritional state (Mendelhall et al,1984/1993), however the author alerts for the potential risk of administering a 17aa for patients with established hepatic lesion and suggests new studies. In any way, that should be an indicative of the low hepatotoxicity of the oxandrolone and probably in this case the benefits of a nutritional status upgrade caused by oxandrolone outweighted the harm of it being an alkylated.
Bile retention in the biliary ducts happens mainly with oxymetholone, and no rare jaundice not accompanied by enzymatic alterations is observed . The most serious liver effect of oxymehtolone, hepatic peliosis and even tumors are reverted with discontinuity of use and an extensive revision done recently failed in proving the correlation between AAS and liver cancer (at least in therapeutic doses).
Regarding lab tests to screen liver stress during AAS use, two recent studys showed that 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( Dickerman RD, 1999/2001).
So, considering what is known , what would be indicated for liver “protection” ?
As for liver protection efficiency, it is proven that milk thistle improves recovery of acute hepatitis and hepatic enzymatic profile in alcoholic hepatitis (Flora et al, 1998) and reduces mortality in the fulminant hepatitis, being the only recommended herb for tratment of hepatic cirrhosis by the influential Blumenthal of Monographs in Herbal Medicine . Of course the use of antioxidants, reducing hepatocyte membrane lipidic perioxidation is also suitable, so glutathione, glutamine, selenium and more recently Alpha lipoic acid (ALA) assured their usage. Recently it was demonstrated that the use of the combination selenium / alpha lipoic acid / milk thistle was effective treating hepatitis C , normalizing the hepatic function and turning unnecessary the hepatic transplant in a significant number of patients (Berkson et al, 1999). Furthermore, ALA showed to be an efficient quelant( (substance that links to the other, usually inactivating it) for cadmium and iron, reducing its hepatotoxicity, and , to the similarity of the sylibum ( Milk thistle), it constitutes an effective antidote for intoxications by mushrooms of the type Amanita.
How, then, to optimize hepatic protection for a cycle that includes 17aa?
1)Alcoholic abstinence;
2)Previous vaccination against hepatitis (advisable for anybody, mainly for those that frequently manipulate needles; of course is for your own use, but a contamination of the injected liquid, in spite of rare, is possible; besides, the contamination with the virus A and/or B can happen with any one, and there are some cases of AAS users that developed serious liver lesions because they had used 17 aa AS and already had hepatitis);
3)Avoid the combination of 17aa, frequently seen in oral-only cycles;
4)Avoid hepatotoxic drugs and herbs, mainly during cycles with 17 aa ( avoid confrei, echynacea, valerian root, nicotinic acid, iron, Vit A more than 10.000UI/day, antibiotics like Clavulonate, azitromicin, tetracycline and erytromicine, isotretinoine (accutane), phenytoin, bupropione (Zyban), tryciclics. In general, check for hepatic side effects before using a drug in a cycle with 17aa.
5)Avoid ingestion of saturated fat;
6)Use ALA 100mg 3 caps 3x a day;
7)Use milk thistle 300mg/day;
8)Vit E/ C / selenium;
9) Water;
10) Taraxacum officinale ( dandelia), increases the bile excretion, dry extract 3g / day or tincture 50 drops 3x a day ( reduces chances of cholestatic jaundice during oxymetholone use)
The use of amino acids that are part of the hepatic metabolism, such as methyonine, inosine and choline, as well as Vit B 12 doesn't have scientific back up, being reserved for nutritional purposes.
Lab work is also a form of hepatic protection, because lab alterations frequently preceed symptoms and allow diagnosis and precocious therapy, which is fundamental in the preservation of our metabolic plant, the liver.
Rio 2001/Primo
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