Something from Bill Roberts on the subject
Bill Roberts, then how could the potential toxicity be compared? How would you personally rate the toxic potential of D-bol to Winstrol on mg to mg basis, for example?
omnibus
Bill, see this statement: "All of the 17 alpha alkylated androgens carry warnings about hepatotoxicity, peliosis, and liver cell tumors. While the tumors are mostly benign, fatal malignant tumors have been reported. Withdrawal of the drug results in complete disappearance of the peliosis and regression or cessation of progression of benign tumors. It would appear that these complications occur to a lesser extent with oxandrolone than with other drugs in the class which are almost completely metabolized in the liver. In contrast, one third of oxandrolone is excreted unchanged in the urine and the rest undergoes considerably less metabolic transformation in the liver." So it seems the unmetabolized amount excreted IS in fact used to measure liver toxicity. Hope the link to this info is OK to put here:
www.hereditaryangioedema.com/ oxscott.htm
Bill Roberts
The fact that someone (or some group) used this logic doesn't mean that it's valid. The argument most likely originated from Biotechnology General, which sells the compound. At least that is where I first encountered it, and for that matter I made the mistake of propagating that reasoning myself. At first glance it sounds reasonable but on further thought I think it makes no sense.
I really don't think you could find anywhere, on any sort of general treatment of hepatoxicity, it being claimed as true that a substantial percentage not being metabolized by the liver is a strong evidence of lack of liver toxicity.
As for whether oxandrolone is or isn't, I don't know of specific evidence of cytotoxicity as has been demostrated for several other 17-alkylated androgens BUT oxandrolone was not included in such testing. There is at least one case in the literature of liver damage attributed to oxandrolone: Am J Gastroenterol 1984 Feb;79(2):150-1. Michael Mooney was convinced based on blood tests that it is. Now, I don't know the specifics: perhaps he was making the error of attributing some harmless enzyme elevations to damage but I do know that if he did, it would have had to be despite being advised about that particular sort of error. I do not know the specifics of Brock's statements that clinical trials found hepatoxicity either.
Basically, it was almost a "magical" claim that oxandrolone wouldn't have been liver toxic, and I think the burden of evidence is on the claim that it isn't. And that burden isn't met. Most likely the reason it was thought not to be is because doses were typically so low. But, Anadrol wouldn't be thought liver toxic either at 2.5 mg per day, either...
Last Q for Mr Roberts
I know it's hard to measure the toxicity between the different orals mg for mg but since I'm sure your in contact with lots of athletes and probably have seen lots of liver enzyme readings I'd still like to ask this: How would you estimate or guess 50mg of D-bol to compare to 50mg of Winstrol as far as being potentially hepatotoxic. The reason I ask is this: Especially since IP appeared on the scene the recommendation for oral winstrol has been 50-100mg per day and generally regarded as pretty safe from a liver standpoint when used for 6-8 weeks. However, it is commonly believed that Dbol is much more toxic and is often only recommended at a max of 50mg for 4-5 weeks only. Basically it is commonly run at half the dose for half the length of time, compared to Winstrol, due to liver concerns. Is this logical?
omnibus
Anyone who can comment on the relative toxicity of Winstrol compared to Dbol?
Bill Roberts
If there is a difference in per milligram liver toxicity due to 17-alkylation between Dianabol and Winstrol, I can't tell which direction it would be, and as you said that's from years of seeing results of each. There may be a difference but I doubt it's important and, again, I don't know which it would be. Where there is a difference is that if no aromatase inhibitor is used, high estrogen levels from Dianabol can increase risk of hepatic cholestasis where Winstrol does not have this issue. I don't at all believe that Dianabol is a particular problem at 100 mg/day for reasonable periods of time like 6 weeks. Dianabol has certainly been used safely for periods of 6 weeks at 100 mg/day, many many times. It's just that there doesn't seem to be particular benefit from increasing relative to 50 mg/day, provided the 50 mg/day is divided into several doses per day, e.g. 5 doses per day.
omnibus
Thanks for the reply. I'm wondering about this statement though: "...high estrogen levels from Dianabol can increase risk of hepatic cholestasis." Does this apply only to estrogen aromatised from orals or test injections as well? For example: will using winstrol with maybe a gram of test without an anti-aromatase increase the risk of hepatic cholestasis compared to Winstrol without the test?
Bill Roberts
Yes, excessively high estrogen from any source increases this risk. Still, it's not ordinarily encountered in cycles of reasonable length. I was just mentioning it for the sake of completeness -- a difference that does exist between Winstrol and Dianabol in toxicity.
Check this study!
A person with the online name of Nandi12 showed me this study: Gastroenterology 1991 Feb; Different hepatobiliary effects of oral and transdermal estradiol in postmenopausal women.Van Erpecum KJ, Van Berge Henegouwen GP, Verschoor L, Stoelwinder B, Willekens FL. Department of Gastroenterology, University Hospital Utrecht, The Netherlands. "...This study indicates that transdermal estradiol does not induce lithogenic bile. On the contrary, oral estradiol leads to lithogenic bile in a subgroup of women with strong increases in serum estrone levels during oral treatment." Bill,doesn't this indicate that the toxicity of estrogen is related to the oral route of adiministration ?
Bill Roberts
If it is at all a demonstration of it, it's one confounded by other variables, and it may be no demonstration at all.
I did not read the article, but only the abstract.
The oral dose was 2 mg/day, but the transdermal dose was 0.1 mg/day. So if an effect was seen orally but not transdermally, might it not be because more steroid was delivered to the liver?
Secondly, the oral dose gave much higher levels of estrone than the transdermal dose. I have no idea if that would make a difference but it could be another confounding factor.
Lastly, what lithogenic bile is, is bile that is prone to form gallstones. This is not the same thing as 17-alkylated toxicity. I do not know how lithogenicity was measured in this study. It was not by the measure of cholesterol crystals, it says, but what it was, one would have to read the article itself to find out. In any case, while liver damage can lead to lithogenic bile, lithogenic bile by no means necessarily indicates liver damage. So this entire thing could have nothing to do with liver damage whatsoever, and since I have never heard of oral estradiol at moderate dose being considered a source of liver damage, I suspect the lithogenic bile in this study is not a marker of liver damage.
SWALE
Just a couple of thoughts. I look at GGT levels for evidence of liver damage. I don't know what liver enzymes they used as markers of same in the aforementioned study, but I can tell you it's a common mistake for physicians to only get ALT and AST, then tell a steroid athlete they're smoking their liver based only on those two enzymes, even though ALT and AST are also elevated by a good, hard workout. Also, CK levels should be drawn, because it can rise from muscle damage as well, and therefore is useful in differentiating liver damage from hard training, but is elevated even in non-training subjects taking steroids due to steroids' effect on the permeability of the muscle cell membrane. I'm thinking oxandrolone's stated low toxicity AND metabolized (conjugated) and unmetabolized urinary excretion is more a coincidence than anything else. The bottom line, to me, ends with effctive dose. Why would I care to make a comparison of hepatotoxicity between two medications when one is not being tested at a dosage which is desirable in terms of increasing strength or size? Also, as we repeatedly see by the responses on this Board, some are simply more sensitive to various steroids (for whatever metabolic, or other, reasons), and have learned to make their cycle choices based upon their own experience. As always, every-body's different. Finally, oral contraceptives (estrogens) increase cholesterol in the bile and are in fact shown to double the chance a woman will suffer cholelithiasis (gallstones) and cholecyctitis (painfully inflamed gallbladder) who takes them. However, those who are sensitive to exogenous estrogens in this way are also predisposed to a condition called the "recurrent jaundice of pregnancy", so their hepatobiliary tree may just be set up for it from the start.
