Hepato-toxicity: Fact or Myth?
We all know that alpha-alkylated steroids are hepato-toxic, right? Well, is there any truth to this?
We have heard for many years that if someone takes a 17-alpha-alkylated steroid they will end up having liver problems at some point. We have also heard many recommendations such as '' Never combine two steroids 17-a-a's '', '' Do not exceed 50 mg / day with any of these substances '', '' Do not use any of these roids for more than 4 weeks '', etc.
Well, this is all bullshit! Now we'll take a look at several studies, and you'll find that while 17-alpha-alkylated steroids certainly stress the liver; they are by no means as toxic as is often thought.
To turn a steroid into a hepato-toxic substance, you only need to make a small change at the molecular level; specifically creating a strong bond that cannot be broken by liver enzymes. This must be in the seventeenth position of the substance; or the first (as with methenolone or Proviron). Because the liver cannot easily break that bond, steroids enter the bloodstream better; therefore they are more bio-available orally.
We can see that the liver has to work hard to "break down" those steroids. Enzymes in the blood and other tissues can easily metabolize other steroids such as testosterone. Commonly, this increase in liver activity is seen as a harmful process, but as you will discover, this increase is actually irrelevant. The liver is the FILTER of the human body - it can figure out what to do with almost any substance consumed. The only real problem appears when a person keeps his liver working at its best for long periods of time.
Let's take a look at some studies that show us the hepato-toxicity of steroids.
Here's one of my favorites. It is a study published in 1979 . Essentially, it investigates the number of deaths caused by hepatic angiosarcomas (a malignant tumor that appears in the vascular tissue of the liver) between 1964 and 1974. The researchers found 131 cases of deaths induced by this condition. Of the 131 cases, 3.1% (4 cases) were directly related to the use of anabolic-androgenic steroids. Also keep in mind that these 4 people could have had liver problems (genetically inherited, induced by another cause, etc.) before consuming these substances. In fact, there is no evidence in this study to show that the use of EAA's caused someone to have liver angiosarcoma.
It is the typical case of associating a cause with an effect without any type of proof apart from its mutual existence. In addition, based on the numbers above, we can deduce that there are only 0.4 annual cases of liver angiosarcomas that may be related to the use of EAA's (obviously coupled to the population used in the study; but moving to reality, the percentage is similar). Now let's consider the number of people who are using steroids right now.
And finally, let's think about all those people who use these substances without having a damn idea what they are doing. It is obvious that the evidence that steroids are hepato-toxic is very weak as we have just discovered. Furthermore, there has not been a notable increase in the number of people affected by liver angiosarcomas since the 1970s. However, the number of steroid users has grown exponentially since then.
Another study, which supports the conclusions of the previous one; informs us about the possibilities of developing a hepatic adenoma (cysts in the liver) due to the use of steroids . In this study, it was discovered that a Japanese girl had multiple lesions on her liver from the use of oxymetholone (Anadrol). We all know that Anadrol is very bad for the liver… right? Well, this study brings us closer to this topic.
Apparently this girl (on her 14th birthday) was diagnosed with aplastic anemia. She was prescribed oxymetholone at 30 mg daily. This treatment lasted for 6 years. After that time, liver problems began to appear. Considering the girl would weigh around 100 pounds, that was a pretty high dose. If you extrapolate this data to a man of about 200 or 250 pounds; he should take 60-90 mg of Anadrol daily for 6 years.
The researchers also pointed out that there were only 17 cases of liver adenomas in England between 1975 and 1988. They forgot to mention the cause of these, but there is no reason to think that they were all caused by the use of 17-a-a steroids. In addition, in the hypothetical case that the 17 had been caused by the consumption of these substances, it is a minuscule number with the number of people who used them.
The authors ended the study by saying '' This report may be helpful in identifying the population that is at risk of developing sex hormone-related liver tumors. '' From what you remember, if you are a 14 year old girl who takes 30mg of Anadrol every day, and you do it for more than 6 years, you may be in trouble!
Now let's move on to a few more useful studies. Take as an example one made in 1995 that showed the toxic effects of EAAs in rat liver cell cultures . In the study, the researchers used the following drugs and dosages:
19-nor-testosterona -- 27,44mg
Cipionato de testosterona-- 41,26mg
estanozolol -- 32,85mg
testosterone -- 0,28mg
Methyltestosterone -- 30,24mg
As proof of the hepato-toxicity of the substances, they focused on the release of lactate dehydrogenase, the retention of neutral red and the depletion of glutathione (to determine the damage of the plasma membrane, the viability of the cell and the possible oxidative lesions; respectively).
What they found was that 17-alpha-alkylated steroids (Methyltestosterone, Stanozolol, and Oxymetholone) significantly increased Lactate dehydrogenase release and reduced neutral red retention at 1x10mg doses for 24 hours. Also, both Methyltestosterone and oxymetholone were shown to affect glutathione depletion with doses of 1x10 mg after treatments of 2, 6 and 8 hours.
In other words, what they did is increase the activity of the liver. Also note that the other steroids (other than 17-a-a) were not shown to significantly affect any of the levels studied.
After all this it is not only shown that 17-aa steroids are directly '' Hepato-toxic '', but we also observe that EAAs that are not 17-aa are not toxic to the liver in any way, right? … But is this a real measure to determine the hepato-toxicity of a substance?
In reality, there is no real relationship between the increase in the aforementioned values and hepato-toxicity. Obviously, high doses of 17-a-a steroids are potentially dangerous, but the study reveals even more data regarding this matter.
Take a look at this; The researchers took liver cell cultures from Sprague-Dawley rats that had lived an average of 60 days. Not only is it remarkable that the livers of rats are vastly smaller than those of humans, but the cells in the sample were simply cultures.
On the other hand, the concentrations that caused the most changes were those of 10mg, which go to approximately 1 to 1/3 of the doses used in humans; at least for the 17 alpha-alkylated EAAs. At doses of concentration equal to 4x10mg, there were no significant changes. It is evident that the doses of 17-a-a steroids used were very toxic, being so high. For a human being, taking a similar amount would be a fool's errand (It would be the same to take more or less 4g of the substances a day, that is, 28 or more grams a week).
The only thing that is proven with this study is that any supposedly hepato-toxic steroid, the only thing that it does is increase the activity of the liver. And I will say again, what is the relationship of this with Hepato-toxicity? Because I don't see it. We know that if we make the liver work 100% for long periods of time we will have problems; but this happens with any other chemical that is metabolized in the liver.
Have you realized that alcohol-related liver cancer takes decades of alcohol abuse to develop? It is clear that the possibility of Hepato-toxicity is there, but for the common steroid user it is practically impossible to reach.
Another study conducted in 1999 attempted to demonstrate the effects of acute and chronic stanozolol treatments on the liver . In the acute stanozolol treatments (with doses not mentioned) the levels of cytochromes P456 and B5 (microsomal enzymes) were reduced after 48 hours; and at 72 hours, they increased significantly. On the other hand, in chronic treatments (time and dose not mentioned), these enzymes were reduced.
The researchers concluded that both acute and chronic treatments resulted in: '' Inflammation and degenerative lesions in centrilobular hepatocytes; in a mild-moderate degree ''; but they did not mention any hepato-toxicity.
What if we look, on the other hand, at the studies focused on the benefits of these substances? For example, we have a 1999 study that focused on the effects of an 8-week cycle with a 17-a-a steroid . The researchers used fluoxymesterone, methylandrostanolone, and stanozolol in rats at a dose of 2mg / kg of body weight, 5 times a week for 8 weeks.
That dose equates to 182 mg / day for a 200 lb bodyweight man (or 910 mg per week). Half of the rats were sedentary, and the other half trained on a treadmill.
The levels of C-reductase NADH-cytochrome, C-reductase succinate-cytochrome and cytochrome-oxidase (showing liver activity) were increased in the rats that consumed the EAAs; whereas citrate synthase did not appear to show changes. Comparatively, in vitro, '' the activity of cytochrome oxidase and citrate synthase was not affected by EAA's; while that of the C-reductase NADH-cytochrome and that of the C-reductase succinate-cytochrome were partially inhibited ''.
Furthermore, in vivo, the liver enzyme levels of each rat were in acceptable ranges (within normal). From this, the researchers concluded that the rats that consumed steroids, regardless of their level of physical activity (trained or sedentary), did not show "… the classic serum indicators of liver function …" ".
Extrapolating this to reality, 910 Mg / Sem of one of these substances for eight weeks would possibly have little or no effect on the liver of a human being.
Regarding human studies, in 1999 other researchers tried to prove that the hepato-toxicity of steroids is overrated . In this study, 15 of the participants were self-administered steroid bodybuilders and another 10 were natural bodybuilders. The serum data of these individuals were compared with those of 49 patients with viral hepatitis; and 592 medical students.
All bodybuilders showed increases in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK); while gamma-glutamyl-transpeptidase (GGT) levels remained within normal ranges. In comparison, hepatitis patients showed an increase in ALT in AST and GGT, while medical students showed an increase in CK levels.
From this, the researchers suggested that it is the correlation between AST, ALT, and GGT that shows true liver dysfunction. Note that we can only assume that the 15 steroid users were using 17-alpha-alkylated EAAs, and we do not know the doses they were consuming. In any case, common sense tells us that the result of the study is relevant.
Last but not least, we have a study carried out in 1996 that shows us the effects that occur in the body after three months without taking steroids (in users who did so obviously) . 16 bodybuilders who used steroids were compared to 12 who did not. After a total abstinence from drugs for three months;
Researchers found that liver enzyme levels (not to mention the type of these) returned to normal values (those of natural bodybuilders). Again, the doses used are not mentioned; and we can only assume that EAA's consumers used 17-alpha-alkylated substances.
So what can we get out of all this?
First of all, that 17-a-a steroids are hepato-toxic if used at high doses for a long time.
On the other hand, short cycles and moderate doses appear to be perfectly safe for the liver. I suppose that the maximum doses will be between 50 and 90 mg daily, better not to risk it by putting more. They can be cycled for 8 weeks in a row, but a three-month break after this period would possibly be correct.
Using the techniques mentioned above, the liver of any steroid user will be healthy for a long time.
In short, the hysteria surrounding the '' hepato-toxicity '' of steroids is largely based on myths and false beliefs. Don't get carried away by gossip.
 Lancet 1979 Nov 24;2(8152):1120-3, Hepatic angiosarcoma associated with androgenic-anabolic steroids. Falk H, Thomas LB, Popper H, Ishak KG.
 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.
 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.
 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.
 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.
 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.
 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.