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Alcohol on an Oral Cycle?

Alcohol on an Oral cycle is not recommended because it cuts the effect of the drug or because it melts your liver down

What about the traditional weekend beer?

Cheers

Melts your liver.

Liver toxicity is for the most part overstated.

But is most certainly real, I know people that have developed jaundice from blatant stupidity involving 17a orals and alcohol.

[quote]Mancador wrote:
Alcohol on an Oral cycle is not recommended because it cuts the effect of the drug or because it melts your liver down

What about the traditional weekend beer?

Cheers[/quote]

If you are as serious as someone should be if they are using AAS there shouldn’t be any “traditional weekend beer”.

You can do a search for the answer to your extremely basic question.

i certainly wouldnt attempt it even as inexperienced as i am, the pressures on your liver would be too risky especially with orals, im sure everything inmoderation is a god mantra to go by but considering what alchol does to your diet, sleeping patterns etc…might be worth limiting

  1. If you are serious enough touse AAS then alcohol should be reduced beyond the “traditional weekend beer”

  2. Oral AAS are liver toxic in varying levels - as is alcohol. And Paracetamol (APAP).

  3. Everyones liver is different - you can get one person who drinks regularly and runs 12 week 100mg dbol cycles and has beautiful liver values.
    You also get those who end up in hospital after one night out on a 30mg 4 week dbol cycle with jaundice and a damaged liver.

  4. Is it worth the risk? Well if you intend to drink even moderately on orals i would suggest you maybe re-assess your need for AAS, but get a liver function test before your cycle, during and 1 week after the oral portion.

Thats it. I dont think that the liver toxicity fears are overstated, it totally depends on the liver function and health of the person stating it!
As i mentioned, genetics can determine you have a liver that will fail at 35 with low abuse/use - using toxic drugs will bring the date of failure forward dramatically.
Genetics can also give you the liver of an ape that will long out live all other organs… even with a decent amount of toxic abuse to it throughout the lifetime.

Regular liver function tests are the way to go with orals, and while i have a healthy liver - i never get pissed when on an oral stint.

Brook

cant live without the liver…hence the name

just dont get trashed everynight, or u will really have ur liver bent over a barrell, with its ass stickin up just waiting to get polvurized the orals throbbing manhood.

[quote]Westclock wrote:
Liver toxicity is for the most part overstated.
[/quote]

I don’t doubt you, but would you post your sources of this info? Thanks

apologies for the hijack, but i guess in some ways this is related.
As many of you know, i am helping in part, a close friend with Ankylosing Spondylitis.
The nature of his condition require daily dosages of anti-inflammatory agents.
At the moment he is reduced right down to 120mg of etroxcib. This is a hepatoxic drug, albeit, to what degree is not stated anywhere i have looked.

I currently have him on a test only cycle and he is slowly but surely, making progress again in the gym, and in his life in general, so we are considering adding an oral, namely dianabol as he has a lot of powder on his hands.
Would the two co-exist peacefully or will it be a battle to the jaundice? Just wanted some opinions if thats ok.

Hijack over, my apologies to the O.P

[quote]postal88 wrote:
Westclock wrote:
Liver toxicity is for the most part overstated.

I don’t doubt you, but would you post your sources of this info? Thanks

[/quote]
To be clear, I don’t want this to be seen as me supporting on-cycle consumption of alcohol, but here’s something to back up Westclock.

Clin J Sport Med. 1999 Jan;9(1):34-9
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.

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.


(edit)
testanabol -

Your post wasn’t showing up when I posted. The obvious caveat that I’m not a doctor & not providing medical advice applies :slight_smile:

I did a quick search for levothyroxine & didn’t see hepatoxicity mentioned in the contraindications. Excretion is renal, so I imagine it only stresses the liver by first pass… As you obviously know, it’s not a compound to be taken lightly given its actions on the thyroid. I’d certainly err on the cautious side & try to get bloodwork done as frequently as possible.

If he can do frequent liver enzyme tests, then you should be able to keep a lid on any elevated readings by immediately discontinuing the dbol in the case og elevated readings.

Etoricoxib is the drug he is taking. Sorry, was my rushed spelling that has probably thrown some confusion into the works.
Etoricoxic is a NSAID - non-steroidal-anti-inflammatory-drug. All of which have many gastro-intestinal pitfalls, hepatoxicity is just not really discussed anywhere unless im being a fucktard and losing my ability to google properly lol.

Dynamo; i think frequent bloodwork is required for him, however getting his doctor to comply with this is difficult, silly as that sounds.

Thanks guys

^^ bah, my bad. Read the name a little too fast.

Wrt NSAIDs they typically aren’t very stressful on the liver, and aspirin can actually be beneficial (if I have the chance to dig up some of my references on this I’ll PM you). I don’t know about the one that you specifically mentioned, though, so there could certainly be a higher risk profile involved.

[quote]whotookmyname wrote:
Clin J Sport Med. 1999 Jan;9(1):34-9
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.

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.
[/quote]

This study doesn’t look to be specifically about oral steroids though. For all we know, most of the subjects could have been exclusively on injectables, so I wouldn’t expect them to have unusual liver values. (Note that the OP only mentions oral cycles.)

the liver is quite a robust organ.
it can handle a beating and if ones liver is healthy to begin with then it can handle an oral cycle and a few weekend beers.

now there are so many variables that will change this.
will you be fine if you drink moderatly on a light oral cycle, sure you may be ok.
on the other hand, will your liver turn black and say fuck you buddy im out?
sure, you may kill it, no one knows for sure.
I personally think you would be fine but why?
why not go out with your buddies and instead of having a few beers have a near beer or a diet soda?

drink some water and some sprite whatever, you can still go out and have fun and not risk your health, no mater how small the risk really is.

I personally drink on cycle, I dont get drink all the time I will get wasted once every couple weeks to the point I have no idea who I am laying next to.
but I am different, I know what im doing and I know the risks and I dont care.
then again it is the beer and the bad food choices that hold me back. so your better off doing as I say and not as I do type thing.