Liver damage - AAS usage vs alcohol

[SIR-LOIN]

I wonder if there's any documented comparisons of the impact on the liver from AAS vs. alcohol? I have a good friend who has been a heavy drinker for prob 25 years (he's 43) at home now dying from cirrhosis, prob 1 - 2 weeks to live. Made me wonder if moderate to heavy chronic aas usage is worse.... Say blasting at least half the year with more than a gram a week, cruising at say 200mg / week? I know there are other factors such as orals or not, diet etc. But generally speaking, which is worse? I'm thinking alcohol is worse, dont hear much about bbers checking out due to liver probs.

 

[alpha6164]

I can probably guarantee that AAS usage would be worse and here is why. It takes approx. 20yrs of drinking a fifth of hard liquor every single day to develop liver cirrhosis. I also see patients that drink regularly (not alcoholic level) where their liver enzymes never go out of range. However, it is very common that just a few weeks of a high dosage AAS and your enzymes already start to go out of range (meaning liver damage) let alone if you did that for 20yrs. The fact that the liver enzymes bump up so quickly compared to alcohol would only mean the damage is much quicker and more severe.

 

[STORM SHADOW]

I can probably guarantee that AAS usage would be worse and here is why. It takes approx. 20yrs of drinking a fifth of hard liquor every single day to develop liver cirrhosis. I also see patients that drink regularly (not alcoholic level) where their liver enzymes never go out of range. However, it is very common that just a few weeks of a high dosage AAS and your enzymes already start to go out of range (meaning liver damage) let alone if you did that for 20yrs. The fact that the liver enzymes bump up so quickly compared to alcohol would only mean the damage is much quicker and more severe.

Ok... so of the MILLIONS of athletes using steroids for the past 30 years across America and Europe... MILLIONS of former athletes are getting new livers. I'm sorry.... I don't buy it for a sec. This would be so well known if true

 

[alpha6164]

Ok... so of the MILLIONS of athletes using steroids for the past 30 years across America and Europe... MILLIONS of former athletes are getting new livers. I'm sorry.... I don't buy it for a sec. This would be so well known if true

First these athletes are not taking steroids daily for 20yrs. The OP asked which of the two substances are more damaging. The response was that for you to damage your liver to failure (cirrhosis) it takes ~20yrs of drinking a fifth of hard liquor EVERY DAY. If you took 50mg A-bombs EVERY single day you will damage your liver way before 20yrs. If you compare the toxicity of two substances you have to compare them at the same frequency ingested. If you drank a fifth of liquor only six months out of the year and rested your liver for another six months, most likely you will never develop cirrhosis since the liver has such a high self repair ability.

It is a stupid comparison because no one takes AAS orally for 20yrs straight anyways. But if they did they cause way more damage than alcohol taken daily.

 

[STORM SHADOW]

No disrespect but you did say "The fact that the liver enzymes bump up so quickly compared to alcohol would only mean the damage is much quicker and more severe."

In the 80's everybody used Orals with injectables through their entire cycle... add to that the MASSIVE protein diet... they should be dead but they are not. Peeps now taking upwards of 1.5g per week of test and adding tren on top now add dbol or A bombs or my fav Halo... I should be dead... but I'm not. I knew guys that shot up 3 times a day! oh oh oh!~ now add lasix during contest prep! I'm sorry...I just don't see it and I've known guys on Tren A year round.

 

[Bolan]

Stick with injectables and get regular blood work done. :headbang:

 

[alpha6164]

No disrespect but you did say "The fact that the liver enzymes bump up so quickly compared to alcohol would only mean the damage is much quicker and more severe."

In the 80's everybody used Orals with injectables through their entire cycle... add to that the MASSIVE protein diet... they should be dead but they are not. Peeps now taking upwards of 1.5g per week of test and adding tren on top now add dbol or A bombs or my fav Halo... I should be dead... but I'm not. I knew guys that shot up 3 times a day! oh oh oh!~ now add lasix during contest prep! I'm sorry...I just don't see it and I've known guys on Tren A year round.

No disrespect taken. Yes, the fact that just a few week of orals bump up the enzymes exactly means that liver damage is already occurring. A few weeks of alcohol intake does not bump your enzymes. I am not sure if you understand what those enzymes really mean. AST and ALT for example are enzymes that live within the cells of your liver tissue. They just done float around in the blood. You have a natural turn over of cell death and when those liver cells die the AST and ALT get released into the serum and where we detect them.

So the only way your AST and ALT suddenly bump ACTUALLY means that you have increased in cell death and damage. That is it. No there way to interpret it than that. So if you drink a fifth of liquor every day for 3 months and your liver enzymes dont bump up but 3 months of Abombs bump your liver enzymes mean that A-bombs are more damaging. The reason people are not ending up on transplant lists with oral AAS is that they are just never taking it as long and with the frequency that alcoholics take alcohol.

Also talking about test E and tren is irrelevant since injectables do not have an effect on the liver. It is the methylated oral AAS that damage the liver and not injectables.

 

[STORM SHADOW]

Ok correct me if I'm wrong... the liver even breaks down injectables to the 19-keto steroid doesn't it?

 

[infinity1]

No disrespect taken. Yes, the fact that just a few week of orals bump up the enzymes exactly means that liver damage is already occurring. A few weeks of alcohol intake does not bump your enzymes. I am not sure if you understand what those enzymes really mean. AST and ALT for example are enzymes that live within the cells of your liver tissue. They just done float around in the blood. You have a natural turn over of cell death and when those liver cells die the AST and ALT get released into the serum and where we detect them.

So the only way your AST and ALT suddenly bump ACTUALLY means that you have increased in cell death and damage. That is it. No there way to interpret it than that. So if you drink a fifth of liquor every day for 3 months and your liver enzymes dont bump up but 3 months of Abombs bump your liver enzymes mean that A-bombs are more damaging. The reason people are not ending up on transplant lists with oral AAS is that they are just never taking it as long and with the frequency that alcoholics take alcohol.

Also talking about test E and tren is irrelevant since injectables do not have an effect on the liver. It is the methylated oral AAS that damage the liver and not injectables.

Alpha- the methylated orals are much less harsh on the liver than the 17aa orals. As far as injectable-the 17aa injectables are only slightly less toxic to the liver than the oral versions of the same drug. The problem with this thread is that there will only be conjecture as to which is worse for your liver (alcohol vs orals) as there will never be studies performed on humans with the orals as medicine has deemed testing humans with AAS unethical. We can only go on broscience at this point.

 

[Amazon Doll]

Alpha......you are a wealth of good information!

i'm glad you are here. :headbang:

 

[alpha6164]

Alpha......you are a wealth of good information!

i'm glad you are here. :headbang:

Thanks Doll



Infinity,

You are absolutely right that it would be unethical to do a trial to see which is worse. But i disagree that the speculation is "broscience" lol. It is a little more sophisticated than that. Its just not oral AAS, but many other oral medications including antibiotics for example. Just get on tetracycline 500mg four times a day for a month and your liver enzymes will be all messed up. It is what it is. We usually dont care cause we only prescribe tetracycline for 10-20 days. But no doubt when a substance is so toxic that it bumps your enzymes in matter of a few weeks that if you stayed on it for 20yrs that you would be pretty screwed. Believe it or not, alcohol is not such a bad molecule. You really have to abuse the shit out of it and i mean at the alcoholic level to cause permanent liver damage. There are far more damaging substances than alcohol. It is just that alcohol is addicting physiologically, and causes the addicts to take in large amounts and more importantly over long periods of time.

 

[SIR-LOIN]

Great info boys! Thanks a lot

 

[infinity1]

Thanks Doll



Infinity,

You are absolutely right that it would be unethical to do a trial to see which is worse. But i disagree that the speculation is "broscience" lol. It is a little more sophisticated than that. Its just not oral AAS, but many other oral medications including antibiotics for example. Just get on tetracycline 500mg four times a day for a month and your liver enzymes will be all messed up. It is what it is. We usually dont care cause we only prescribe tetracycline for 10-20 days. But no doubt when a substance is so toxic that it bumps your enzymes in matter of a few weeks that if you stayed on it for 20yrs that you would be pretty screwed. Believe it or not, alcohol is not such a bad molecule. You really have to abuse the shit out of it and i mean at the alcoholic level to cause permanent liver damage. There are far more damaging substances than alcohol. It is just that alcohol is addicting physiologically, and causes the addicts to take in large amounts and more importantly over long periods of time.

Alpha,

I thought you would get a kick out my "broscience". I agree. I think we can come up with theories based on the knowledge we have. I have had my enzymes checked while on cycle and on the tail end of 100mgs of a50 per day and my levels were only slightly out of range and upon a subsequent visit 3 weeks later completely back to normal. I can remember many years ago having bloodwork done for an insurance exam and my liver enzymes came back a little out of range because I had been on a 2 day bachelor party bender in the days before. Moral of the story is that all of these substances react differently in each person and elicit different test results as well. but for what its worth I think long term oral usage would be worse on your liver than alcohol use. People have been drinking alcohol for a lot longer that they have been taking aas. Im sure some will disagree but thats just my 2 cents.

 

[LK3]

so much of these conversations are purely speculation based upon taking all types of things out of context and not looking at all of the variables.

everyone love to use drol as an example of toxicity however there are plenty of studies on it where it is used within the medical dose ranges 1-5mg/kg on women, childeren and the very ill where liver values stya well within range and these people are on for 6 months to several years.

im in no way suggesting that people partake in potentially damaging behavior, however i also think this whole toxicity issue gets blown way out of proportion.

if you get regular blood work then pay atention to it. and stay on as many anti-ox as possible that protect the liver and things should be fine, also think, drinking or aas, tylenol or aas, how many different variables might people realy be playing wiht?

 

[Stewie]

Sorry to hear about your friend. 45 is too young.

 

[thatbloke]

i dont know about a documented study comparing the 2

but there are studies done on anadrol on anemia patients, and those studys showed highly eleveted liver values after 10 weeks of anadrol use, i might be able to dig it up if i can find it

although u can say that was 10 weeks, thats pretty dam short in comparisent to alcohol which takes on average years of abuse to have the same efect

from personal experience ive used 40mg of dbol daily for 4 weeks and my liver values never went up (way back on ym first cycle), while ive used 50mg an drol a day for 3 weeks and my liver values were double the normal range 8 weeks after i stopped the drol

Ok correct me if I'm wrong... the liver even breaks down injectables to the 19-keto steroid doesn't it?

yes it does, the liver breaks down everything that goes into the body whether it be food, water, drugs, chemicals etc, and breaks them down no matter how they are administered (oral, nasal, injected, even anal )

 

[thatbloke]

here ya guys go

this study showed 150mg drol daily increased liver values 5 fold within the first 4 weeks on 23% of patients

it also happen to be the study that showed 100mg fo drol gave almost identical weight gains as 150mg of drol

admitingly this doesnt compare alcohol, but i dotn think youll be able to find a study on alcohol that increased peoples liver values 5 fold

Double-blind, randomized, placebo-controlled phase III trial... : AIDS

1: AIDS. 2003 Mar 28;17(5):699-710. Links

Double-blind, randomized, placebo-controlled phase III trial of oxymetholone for the treatment of HIV wasting.

Hengge UR, Stocks K, Wiehler H, Faulkner S, Esser S, Lorenz C, Jentzen W, Hengge D, Goos M, Dudley RE, Ringham G.
STD-Unit, Department of Dermatology and Venerology, University of Essen, Germany. [email protected]
BACKGROUND: Despite highly active antiretroviral therapy (HAART), chronic involuntary weight loss still remains a serious problem in the care of HIV patients. Various alterations in energy metabolism and endocrine regulation have been found to cause loss of lean body mass (LBM) and body cell mass (BCM). Previous studies in HIV-positive men undergoing androgen replacement therapy or treatment with recombinant growth hormone (rGH) have shown partial restoration of LBM, but these treatments have largely been ineffective in eugonadal individuals. STUDY DESIGN: Double-blind, randomized, placebo-controlled trial of 89 HIV-positive women and men with wasting assigned to the anabolic steroid oxymetholone [50 mg twice (BID) or three times daily (TID)] or placebo for 16 weeks followed by open-label treatment. STUDY ENDPOINTS: Body weight, bioimpedance measurements, quality of life parameters and appetite. RESULTS: Oxymetholone led to a significant weight gain of 3.0 +/- 0.5 and 3.5 +/- 0.7 kg in the TID and BID groups, respectively (P < 0.05 for each treatment versus placebo), whereas individuals in the placebo group gained an average of 1.0 +/- 0.7 kg. Body cell mass increased in the oxymetholone BID group (3.8 +/- 0.4 kg; P < 0.0001) and in the oxymetholone TID group (2.1 +/- 0.6 kg; P < 0.005), corresponding to 12.4 and 7.4% of baseline BCM, respectively. Significant improvements were noted in appetite and food intake, increased well-being and reduced weakness by self-examination. The most important adverse event was liver-associated toxicity. Overall, 35% of patients in the TID, 27% of patients in the BID oxymetholone group and no patients in the placebo group had a greater than five times baseline increase for alanine aminotransferase during the double-blind phase of the study. CONCLUSIONS: Oxymetholone can be considered an effective anabolic steroid in eugonadal male and female patients with AIDS-associated wasting. The BID (100 mg/day) regimen appeared to be equally effective as the TID (150 mg/day) regimen in terms of weight gain, LBM and BCM and was associated with less, but still significant liver toxicity.

 

[MantusJohn]

It depends how much alcohol but for me 6 months of
a pint or 2 vodka/ED raised my liver enzymes 10X normal
and even 8 weeks 40mg DBol didn't have effect
on anything

I know guys running 50mg DBol/day for over a year with no problems

OK my bad here I said DBol and your asking about Drol

Drol gets a bad wrap from it being used for medical purposes
on 70yr old patients for over a year at ten times the amount
a pro BBer would use it at

 

[MantusJohn]

here ya guys go

this study showed 150mg drol daily increased liver values 5 fold within the first 4 weeks on 23% of patients

it also happen to be the study that showed 100mg fo drol gave almost identical weight gains as 150mg of drol

admitingly this doesnt compare alcohol, but i dotn think youll be able to find a study on alcohol that increased peoples liver values 5 fold

Double-blind, randomized, placebo-controlled phase III trial... : AIDS

1: AIDS. 2003 Mar 28;17(5):699-710. Links

Double-blind, randomized, placebo-controlled phase III trial of oxymetholone for the treatment of HIV wasting.

Hengge UR, Stocks K, Wiehler H, Faulkner S, Esser S, Lorenz C, Jentzen W, Hengge D, Goos M, Dudley RE, Ringham G.
STD-Unit, Department of Dermatology and Venerology, University of Essen, Germany. [email protected]
BACKGROUND: Despite highly active antiretroviral therapy (HAART), chronic involuntary weight loss still remains a serious problem in the care of HIV patients. Various alterations in energy metabolism and endocrine regulation have been found to cause loss of lean body mass (LBM) and body cell mass (BCM). Previous studies in HIV-positive men undergoing androgen replacement therapy or treatment with recombinant growth hormone (rGH) have shown partial restoration of LBM, but these treatments have largely been ineffective in eugonadal individuals. STUDY DESIGN: Double-blind, randomized, placebo-controlled trial of 89 HIV-positive women and men with wasting assigned to the anabolic steroid oxymetholone [50 mg twice (BID) or three times daily (TID)] or placebo for 16 weeks followed by open-label treatment. STUDY ENDPOINTS: Body weight, bioimpedance measurements, quality of life parameters and appetite. RESULTS: Oxymetholone led to a significant weight gain of 3.0 +/- 0.5 and 3.5 +/- 0.7 kg in the TID and BID groups, respectively (P < 0.05 for each treatment versus placebo), whereas individuals in the placebo group gained an average of 1.0 +/- 0.7 kg. Body cell mass increased in the oxymetholone BID group (3.8 +/- 0.4 kg; P < 0.0001) and in the oxymetholone TID group (2.1 +/- 0.6 kg; P < 0.005), corresponding to 12.4 and 7.4% of baseline BCM, respectively. Significant improvements were noted in appetite and food intake, increased well-being and reduced weakness by self-examination. The most important adverse event was liver-associated toxicity. Overall, 35% of patients in the TID, 27% of patients in the BID oxymetholone group and no patients in the placebo group had a greater than five times baseline increase for alanine aminotransferase during the double-blind phase of the study. CONCLUSIONS: Oxymetholone can be considered an effective anabolic steroid in eugonadal male and female patients with AIDS-associated wasting. The BID (100 mg/day) regimen appeared to be equally effective as the TID (150 mg/day) regimen in terms of weight gain, LBM and BCM and was associated with less, but still significant liver toxicity.

This is a study on HIV patients not healthy BBers.

I don't think that is what he is asking for

 

[discohornet]

Hepatoxicty
Fact or Fiction
By Roy Harper


This article was originally featured in issue #8 of Mind and Muscle Magazine. Be sure to also check out www.avantlabs.com for the full Avant Labs product line of groundbreaking supplements.

We all know that the alpha alkylated steroids are hepatotoxic, right... But, is there actually any truth to this? We’ve been told for years that if you take 17 alpha-alkylated steroids, you will eventually run into Liver problems. Never combine 17 alpha-alkylated's, never go beyond 50mg day, never go longer than 4 weeks, etc. All of this is ! As I we walk you through some studies, today, you’ll see 17 alpha-alkylated steroids can be hepatotoxic but not to the degree you would think.

To make a steroid hepatotoxic, you need only a small change to a steroid molecule; A strong bond that cannot readily be down broken by enzymes in the Liver. This may be a bond at the 17th position, or even at the 1st position (as in methenolone or proviron). Because the Liver cannot easily break the steroid down before it is released in to the blood stream, this also results in the steroid to becoming more orally bio-available.

We can see that the Liver has to work harder to break down these steroids. Enzymes in the blood and tissue easily metabolize other steroids such as testosterone. Commonly, this increase in Liver activity has been viewed as a harmful process, but as you will see, this increase is, in and of itself, irrelevant. The Liver is THE filter of the human body -- it can figure out what to do with just about anything. The only real problem comes in when one keeps their Liver at full blast for long periods of time.

Let’s look at some studies showing the Hepatotoxicity of steroids. Here's one of my favorites, a study published in 1979[1]. Essentially, researches did a study of deaths caused by hepatic angiosarcoma (a malignant tumor of vascular tissue in the Liver) between 1964 and 1974. Researchers found 131 reported cases of death from hepatic angiosarcoma. Out of the 131 cases, 3.1% (4 cases) were reported to be at all related to the use of androgenic-anabolic steroids. Keep in mind that these 4 people could have Liver complications before any steroids were used, aka a genetic disposition. In fact there is no proof, in this study at least, that the anabolic-androgenic steroids even caused the hepatic angiosarcoma.

This is the classic case of associating a cause with an effect, without any evidence, aside from both existing. Furthermore, based on the above numbers, there are only 0.4 cases of hepatic angiosarcoma reported each year, by those using anabolic steroids. Now consider the number of people on steroids at this time. Now factor in all the people that don’t know their ass from a hole in the ground when it comes to using anabolic steroids, properly. Clearly, this is very week evidence. Lastly there has not been a real increase in hepatic angiosarcoma since the early seventies. Meanwhile, there has been a huge, almost exponential, increase in steroid use during this period.

Another study, that somewhat supports the previous Hepatotoxicity case, showed the possibilities of hepatic adenomas(cysts in the Liver) caused by androgenic-anabolic steroids[2]. In this study, a Japanese girl was found to have multiple Liver lesions after the use of the drug oxymetholone (aka anadrol). Most everyone “knows” that anadrol is linked with Liver problems, but a closer inspection into this study shows more.

Apparently, this girl, starting at the age of 14, was diagnosed with aplastic anemia. She was prescribed oxymetholone at 30mg per day. This continued for 6 years until the lesions first appeared. Assuming that the girl was most likely around 100 lbs., this was a pretty heavy dosage. If you extrapolated this data out to a 200 - 250lbs. male, that would be taking approximately 60 - 90mg of anadrol per day for 6 years. Ouch!

The researchers also stated that there were only 17 other cases of hepatic adenomas, found in English literature between 1975 and 1998. They failed to mention the causes of these 17 cases, but there is no reason to believe they were all using 17 alpha-alkylated androgens and 17 is certainly miniscule compared to the number of people who have used them. The authors’ finish off the study by saying the following: "This report may be helpful in identifying the potion who is at risk of developing hepatic sex hormone-related tumors." So remember, if you're a small 14-year-old girl taking 30mg of anadrol per day for 6 years, you may be at risk!

Let's move on to some more useful studies. Take for example a 1995 study that showed the toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures[3]. In this study the researchers used the following drugs and dosages:

Steroid 1x10^-8M 1x10^-6M 1x10^-4M
19-nortestosterone 0.002744mg 0.2744mg 27.44mg
Fluoxymesterone 0.003365mg 0.3365mg 33.65mg
testosterone cypionate 0.004126mg 0.4126mg 41.26mg
Stanozolol 0.003285mg 0.3285mg 32.85mg
Danazol N/A N/A N/A
Oxymetholone 0.003325mg 0.3325mg 33.25mg
testosterone 0.002884mg 0.2884mg 28.84mg

Estradiol 0.0027424mg 0.2724mg 27.24mg
Methyltestosterone 0.003024mg 0.3024mg 30.24mg


As proof of the hepatoxicity they used Lactate dehydrogenase release, neutral red retention, and glutathione depletion to determine plasma membrane damage, cell viability, and possible oxidative injury, respectively.

What they showed was that the 17 alpha-alkylated steroids, methyltestosterone, stanozolol and oxymetholone, significantly increased Lactate dehydrogenase release and decreased neutral red retention at the 1x10^-4M dosage for 24h. Both methyltestosterone and oxymetholone also showed depleted glutathione at the 1x10^-4M dosage after 2h, 6h and 8h treatments. In other words they increased Liver activity. You may also note that the other, non-alkylated steroids showed no significant difference in any levels. All in all this not only shows that 17 alpha-alkylated steroids are directly “hepatotoxic”, but also non-alkylated steroids are note hepatotoxic at all. But is this a real measure of Hepatotoxicity? There is yet to be any correlation between the increase of the above-mentioned measurement and “Hepatotoxicity”. Obviously, high dosages of the 17 alpha-alkylated steroids are potentially dangerous, but upon closer inspection, the study reveals more.

Take a look, the researchers took cell cultures from the liversse of 60-day-old Sprague-Dawley rats. Not only are rat livers much smaller than human livers, but these were merely cultures. Furthermore, it was the 1x10^-4M concentrations that caused the most changes, but these are approximately 1 to a 1/3 of a full, daily human dosage -- at least for the 17 alpha-alkylated steroids. Even at the 1x10^-6M concentration, there were no significant changes observed. It's apparent that the levels of 17 alpha-alkylated steroids used were potentially toxic, but for a human to take the same amount would be insane. I'm guessing this could translate to maybe 4 grams every 24 hours or 28 grams a week if not more.

What is common so far is we can only prove that any steroid, that is believed to be hepatotoxic, only increases Liver activity. I’ll say it again, where is the correlation to Hepatotoxicity? We know that if the Liver is running at 100% for long periods this may cause complications, but this is akin to any other chemical, which is metabolized by the Liver. Ever noticed that Liver cancer due to alcoholism takes decades of constant alcohol abuse? It’s apparent that the possibility for Hepatotoxicity is there, but for the smart steroid user this is nearly an impossible task.

Another study done in 1999, attempted to show the acute and chronic effects of stanozolol on the Liver[4]. In acute treatments of stanozolol, dosages not mentioned, both cytochrome P456 and b5 (microsomal enzymes) levels dropped after 48 hours, and then at 72 hours, levels significant increased. On the other hand, with chronic treatments, time or dosage not mentioned, these microsomal enzymes showed a decrease in levels. Researchers showed that both acute and chronic treatments resulted in "slight to moderate inflammatory or degenerative lesions in centrilobular hepatocytes", but the authors did not note true Hepatotoxicity.

How about we look at the other side of the story, the good studies. For instance, in a 1999 study, which looked at the effects of an 8-week cycle of 17 alpha-alkylated steroids[5]. The researchers used fluoxymesterone, methylandrostanolone, or stanozolol on rats at 2mg/kg-body weight, five times a week for 8 weeks. That's 182mg per dosage, for a 200lb man, or 910mg per week. Half of the rats were sedentary and the other were trained on a treadmill.

Levels of NADH-cytochrome c reductase, succinate cytochrome c reductase, and cytochrome oxidase (showing Liver activity), increased in the steroid-administered rats, while citrate synthase showed no change. Comparatively, in vitro, the "cytochrome oxidase and citrate synthase activities were insensitive to the anabolic steroids, whereas NADH-cytochrome c reductase and succinate cytochrome c reductase activities were partly inhibited."

Furthermore, in vivo, each rat had Liver enzyme levels that were within normal range. From this, the researchers determined that the steroid-administered rats, trained or sedentary, did not show "...classical serum indicators of hepatic function". Extrapolating this, 910mg a week for 8 weeks could potentially have little to no effect on the Liver in humans.

As for human studies, in 1999 researchers tried to prove that the Hepatotoxicity of steroids is overstated[6]. In this study, 15 of the partints were bodybuilders using self-administered steroid dosages and 10 were non-steroid bodybuilders. Serum data was compared to 49 patients with viral hepatitis, and 592 exercising and non-exercising medical students. [

All of the bodybuilders showed increases in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) while gamma-glutamyltranspeptidase (GGT) levels were in the normal range. In comparison, hepatitis patients showed increased ALT, AST, and GGT levels while the control exercising medical students showed increased CK levels. From this, the researchers suggested that it is the correlation between AST, ALT and GGT that shows true Liver dysfunction. Keep in mind, we can only guess that the 15 steroid users were using 17 alpha-alkylated steroids, and we do not know what the dosages that were used., but common sense tells us the results are likely relevant.

Last but not least, a simple study done in 1996, showed the long term benefits after taking a 3 month break from steroids[7]. 16 bodybuilders using steroids were compared to 12 bodybuilders that were not. After a three-month drug withdrawal, the researchers showed that levels of Liver enzymes, types not mentioned, returned to the same as the non users. Again the dosages are left to the reader’s imagination and we can only guess that the 16 steroid users were using 17 alpha-alkylated steroids.

So what can we conclude from all of this? First off, 17 alpha-alkylated steroids are hepatotoxic in high dosages taken for a long time. On the other hand, short cycles and small dosages appear to be perfectly safe. I suggest that maximum dosages should be 500mg to 900mg per day. They should be cycled for perhaps 8 weeks at a time, and if needed a 3-month break from them should be used. Using the above-mentioned techniques, your Liver can be healthy for a long time. Simply put, the hysteria surrounding “Hepatoxic” steroids, is based mainly on folk lore.

References:

[1] Lancet 1979 Nov 24;2(8152):1120-3, Hepatic angiosarcoma associated with androgenic-anabolic steroids. Falk H, Thomas LB, Popper H, Ishak KG.

[2] J Gastroenterol 2000;35(7):557-62, Multiple hepatic adenomas caused by long-term administration of androgenic steroids for aplastic anemia in association with familial adenomatous polyposis. Nakao A, Sakagami K, Nakata Y, Komazawa K, Amimoto T, Nakashima K, Isozaki H, Takakura N, Tanaka N.

[3] J Pharmacol Toxicol Methods 1995 Aug;33(4):187-95, Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. Welder AA, Robertson JW, Melchert RB.

[4] Arch Toxicol 1999 Nov;73(8-9):465-72, Evaluation of acute and chronic hepatotoxic effects exerted by anabolic-androgenic steroid stanozolol in adult male rats. Boada LD, Zumbado M, Torres S, Lopez A, Diaz-Chico BN, Cabrera JJ, Luzardo OP.

[5] Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat Liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.

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

[7] Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and Liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.