oral AAS and liver protection.

[trinitysurf]

Liv 52 interests me because it is a liver protective supplement that actually has been researched quite a bit. Granted, a lot of the research isn't US based and I personally have no idea if the parameters for these studies are standardized across the globe. Regardless, here are some links that may help add to the discussion further:

From Himalaya's site - links to 24 clinical papers on Liv 52: http://www.himalayahealthcare.com/research/liv52.htm

Some of the papers go back over 50yrs. Did Himalaya fund them all? Did they or counterparts create the journals they're published in? I don't know and it could always be a possibility (I've seen it before with the semi-bogus journals...) but a lot of guys have sworn by and/or used Liv 52 for decades.

As mentioned above, Liv 52 honestly sounds like it should be more of a post cycle treatment however. I read somewhere at one point (can't think of where) where it was that or known that these kinds of products can actually inhibit 17aa uptake via the liver when taken concurrently. For example, it's known that approximately 1/3 of an oxandrolone dose actually gets metabolized and the rest is excreted in urine (Llewellyn, Anabolics 10th ed) - do you want a liver protective supplement interfering with that tiny -and expensive!- amount of aas? Also as mentioned in the other posts, in the end, it's entirely up to the individual, their health and concern for their liver if they choose to use these or not.

 

[graniteman]

The thing that always comes to mind for me is are these supps in any way hindering the ability of the oral AAS to be absorbed or do they act directly on liver tissue only? The reason 17-aa drugs are so harsh is because they have to pass through the liver twice. And it's not like walking through someone's living room... it's more like walking down a dark alley knowing you're going to get in several fights along the way. I guess my question would be IF these supplements succeed in their efforts, do they strengthen the liver's ability to withstand an attack from these orals (thus lessening the bioavailability of the drug) or do they simply repair what has been damaged?

The amazing thing about the liver is it can actually re-generate itsself, grow new cells. Transplants are done with partial livers. I did see somewhere a few studies on sylmarin (milk thistle) but never saw the end results. They were done on patients with hepatitus c.

 

[Dirk Diggler]

I have a friend who is an ER doc and he told me that they use NAC for tylenol overdose patients for it's ability to prevent long term liver damage. I've not read any studies, but my friend is kind of a beliver in eastern medicine. Since this discussion, I take 1600-2000mg of NAC daily...and its cheap.

Something to think about

 

[dr jim]

Yes NAC is used for ACUTE APAP toxicity (AAS cycling would be considered a sub-acute or chronic exposure) to restore depleted glutathione which occurs as a consequence of acetaminophen metabolism. However since glutathione restoration prevents the use of a SECONDARY metabolic TOXIN PRODUCING pathway (which CAUSES of the hepatic injury) NAC is considered an antidote which I mentioned as a collective exception earlier.

Importantly, not only is NAC an antidote it's a very effective one indeed, since the mortality approaches ZERO provided NAC therapy begins within the first 8 hours of an ACUTE APAP OVERDOSE.

Importantly AAS associated hepatic injury has NOTHING to do with depleted glutathione or the use of an alternative pathway but is rather the consequence of de-methyizatiion (removal of the 17 positioned alkyl group). The exacting mechanism is unknown (glutathione stores are unaffected) and speculative mechanisms range from; free radicals, abnormal transporter proteins, subpar cofactor levels or enzymatic deficiencies.

Regardless the result from AAS hepatic toxicity is essentially identical to ALMOST ANY other drug related toxin. The net effect is the development of hepatic "drug induced cholestasis" with the inability of the liver to metabolize AND secrete bile into the biliary tree.

Importantly the accumulation of bile is also "toxic'' and is believed responsible, at least in part, for some of the hepatic insult. As a consequence A FEW hepatologists use Ursodiol (which enhances the metabolism of bile) to treat those patients with DIAGNOSED DRUG RELATED LIVER DISEASE.

Nonetheless there are no clinical trials on the efficacy of this therapy and it's unlikely to be beneficial since it does NOT treat the primary causation itself.

What to do?

Be smart and do NOT EXCEED moderately dosed AAS ORAL cycles and limit their duration to NO MORE than SIX weeks. Furthermore exposure to other hepatotoxins such as ALCOHOL is ill advised since this is likely to worsen the overall hepatic insult ESPECIALLY in those predisposed.

jim

 

[dr jim]

So in conclusion is there any evidence to support the use of SUPPLEMENTS to PREVENT hepatic injury from ORAL AAS?
NOT, or DOCTORS would be using them now for alcohol related hepatic injury, IMO!

JIM

 

[CBS]

Aside from the extra expense and lack of proven efficacy, one needs to keep in mind that oral AAS induced cholestasis typically takes about 4 weeks before onset, however, oral cycles are usually limited to 4 to 6 weeks in duration. As mentioned by Dr Jim, the most efficacious treatment for drug induced liver changes is discontinuation of the offending agent, and since oral cycles are so short, the use of liver supplements is pointless, even if they were beneficial (which they are not).

Regarding the suggestion that liver toxicity of oral AAS is overestimated, there is some evidence to back this up. The liver changes commonly seen only involve the transaminases and very rarely affect bilirubin or GGT's. Complications such as peliosis hepatitis or liver failure seem to be exceedingly rare.


The bottom line is the effect of oral AAS on the liver is largely dependant on the dose and duration. If you plan to run longer than the usual cycle or plan to run more than one oral simultaneously, periodic LFT's should be run throughout the cycle, but be aware that if abnormalities arise, discontinuation, NOT liver supplements, is the solution.

Regards

CBS



Anabolic steroid-induced hepatotoxicity: is it overstated? Clin J Sport Med 1999;9(1):34-9. Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ. Anabolic Steroid-Induced Hepatotoxicity: Is It Overstated? : Clinical Journal of Sport Medicine

OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders.

DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis.

PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls.

MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.

CONCLUSION: 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.

 

[Grumpyfit]

This is a good question. A little boy who has muscular dystrophy has been on an experimental oral aas for over 10 years with no breaks. I asked the parents if he was also taking any liver and/or organ protection and they stated no. They did state the steroid prolonged the onslought of paralisis and his life.

 

[oldnslow]

So, if one wanted to run a longer oral cycle, would monitoring the aforementioned values, CK, AST, ALT, be sufficient to signal a problem before damage is done? If so, at what intervals?

 

[jhotsauce7]

Dr Jim ursadiol...that is the same as ursodeoxycholic acid correct? That's the pharmaceutical name?

 

[Dirk Diggler]

Jim,

Thank you for that information on NAC! I still take plan on taking 1200mg of NAC every day....eventhough it seems like a waste of time/money.... It's cheap insuracne...what can I say

 

[dr jim]

Dr Jim ursadiol...that is the same as ursodeoxycholic acid correct? That's the pharmaceutical name?

Correct! Perhaps your thinking, well how about this drug? Nope!

The effects of Ursadiol on patients with primary biliary cirrhosis (these unfortunate patients develop "scaring" of the bile ducts which allows the bile to accumulate) while initially encouraging, because it DID improve transaminase levels, does NOT effect mortality!


Is the frequency of AAS associated liver disease any higher than that of alcohol, I suspect not. However what we do know FOR SURE is the longer someone drinks and the more extensive the exposure the greater the likelihood of developing evidence of hepatic injury as evidenced thru elevated transaminase enzyme levels.

More importantly much like the genetic basis for alcohol related cirrhosis, there are those whom appear predisposed to severe liver injury with CHRONIC AAS exposure (based on case reports) consequently the notion of running a continuous "multi drug oral cycle" especially absent periodic enzyme assays is asking for trouble and must be avoided.

However as CBS (who is this guy anyway?) mentioned the hepatic insult occurs (or may be identifiable by increased enzymes) after a latent period of several weeks. This occurrence is not at all unusual with most hepatic toxins and still provides enough time to discontinue AAS use once detected. As an aside, any significant increase of bilirubin above the precycle baseline warrants an IMMEDIATE cessation of the offending agent!!!

Finally as many VETS have already mentioned most of this discussion is much to do about nothing primarily because the liver is our toxic waste dump and has a truly REMARKABLE capacity to heal itself, which is just another reason why hepatic supplements only add cost to an already expensive endeavor.

Best
jim

 

[Casca]

^^^damn if that discussion didn't just open my eyes. Thx.