Hepatoxicty: Fact or Fiction - AnabolicMinds.com

Hepatoxicty: Fact or Fiction

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    Cool Hepatoxicty: Fact or Fiction


    Do you guys believe this article. " I suggest that maximum dosages should be 500mg to 900mg per day. They should be cycled for perhaps 8 weeks at a time". Not sure if I'd bet my life on this.

    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 aa’s, never go beyond 50mg day, never go longer than 4 weeks, etc. All of this is crap! 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 AAS. 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 AAS, 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-AA 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 population 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 AAS, 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 participants 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.

    http://www.avantlabs.com/magmain.php...ID=8&pageID=84

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    I don't know what the long term possibilities are, but judging from bloodwork alone I would say that it's pretty obvious that prolonged use can really run a number on you. You would be ignorant to think that you wouldn't suffer SOME ramifications from extended, irresponsible usage...
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    grain of salt
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    The take home message is that long term use, with no protective supps can very well lead to fatty liver disease. Short term use of things like M1T in high doses can most certainly lead to choleostatic hepatotoxicity..we've seen that anecdotally.

    IMHO, the more immediate danger is in skewing lipid values..and yes, this relates directly to liver issues but more importantly there's some scarey heart and nervous system issue that need to be addressed.

    We need a protective drug or supplement that prevents choleostasis during a cycle..then all of these issues would be moot.
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    Quote Originally Posted by bioman
    The take home message is that long term use, with no protective supps can very well lead to fatty liver disease. Short term use of things like M1T in high doses can most certainly lead to choleostatic hepatotoxicity..we've seen that anecdotally.

    IMHO, the more immediate danger is in skewing lipid values..and yes, this relates directly to liver issues but more importantly there's some scarey heart and nervous system issue that need to be addressed.

    We need a protective drug or supplement that prevents choleostasis during a cycle..then all of these issues would be moot.
    I agree. I have always read and been taught that the liver is one of the most resilient organs in the body and it has the ability to repair itself from all but the most substantial of damage.

    My main concern with taking methylated products is damage to the lipids not the liver. This is my opinion for the most part: obviously there are compounds out there that are extremely toxic and should prolly just be avoided altogether.
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    I agree with you guys, I’d worry about other things more then the liver. But this guy’s article is crazy 500mg to 900mg a day of a mythel is terrible. This is a case of a bodybuilder not wanting to face the reality that mythel steriod can be very bad and we need to minimize the risks. Heck if this was true their would be no reason to inject, just run a good mythel for 8 weeks that would make awesome gains.
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    Imagine the sides from 500mg of SD or Ergo. Imagine the bloat from 500mg of of DBOL. Apparently high dose methyls also cause brain damage
  8. KD1
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    I relate using an oral steroid for 4 weeks to going on a month long alcohol binge. How many times a year would you subject your body to something like that? For me, once or twice tops.
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    So you spend 1-2 months per year binging on alcohol

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    Interesting article. It's true liver damage concerns are overblown, but that doesn't mean sucking down half a gram of dianabol a day is a good idea. Yes, you could probably survive it, but that's not exactly the point. Not to mention the cost and the fact that it's not necessary.
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    Quote Originally Posted by bioman
    We need a protective drug or supplement that prevents choleostasis during a cycle..then all of these issues would be moot.
    Didn't someone release one recently, one of the sponsors? I remember seeing something and wanting to look into it, but didn't get the chance and I've lost track of the post.
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    CEM brought out some liver enzyme that was supposed to stop choleostasis possibly but I haven't heard a peep. Perhaps he could gift some to a member who could promise to run a log with blood work throughout. IF it worked well CEM would be sitting on a hot product all of a sudden and we could be more liberal with the methyls.

    I'd volunteer but I am NOT running a harsh methyl for a long time. The physchiatric effects of the last SD cycle were way too much.
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    Quote Originally Posted by bioman
    I'd volunteer but I am NOT running a harsh methyl for a long time. The physchiatric effects of the last SD cycle were way too much.
    That's why I've stayed away from running any hormones for a while too.
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    Do you mean psychiatric? As in; mental state? If so how?
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    mental state hmmmmm...
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    Severe depression in the second week of SD. My theory is that for some like me, once your cholesterol values crash so do your serotonin levels. There are a few studies linking low cholesterol to depression, suicide and violent behavior...after my last cycle, I'm a believer.
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    Several studies... dating back to the late 80's early 90's...
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    Quote Originally Posted by Knowbull
    Do you mean psychiatric? As in; mental state? If so how?
    I'm already prone to mood swings, hormones obviously can make that worse, especially when discontinued. PCT crash is bad enough under normal circumstances, for the last couple years my work and life in general has been stressful and turbulant in and of itself. Aggravating that just doesn't seem like a good idea to me, so I lay off major 'supps' like the methyls and stick with more moderate things. Don't know about any cholesterol link to depression, sounds interesting though.
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    Abstracts found just at mercola.com, I'm sure PubMed has many more.

    "Results of a study conducted by Dutch researchers provide additional evidence for a link between low cholesterol levels and an increased risk of depression in men. Investigators measured serum cholesterol levels in some 30,000 men, as part of a large screening program.

    They compared the presence of depressive symptoms, anger, hostility, and impulsivity in these men, to men with cholesterol levels in the normal range. They found that men with chronically low cholesterol levels showed a consistently higher risk of having depressive symptoms.

    Cholesterol may affect the metabolism of serotonin, a substance known to be involved in the regulation of mood as the researchers have previously shown that serotonin levels are also reduced in men with low levels of cholesterol.

    Psychosomatic Medicine 2000;62."



    Despite the fact that most people are worried about having cholesterol levels that are too high, yet another study has found that low cholesterol is actually associated with adverse behavioral effects such as aggression and depression.

    While the medical establishment continues to push the suppression of cholesterol levels to abnormally low levels, it is not widely known that there is a significant amount of evidence linking low cholesterol to aggressive behavior and depression.

    According to researchers from Yale University School of Medicine, "The well-documented negative association between serum cholesterol and aggressive behavior has led Kaplan (Psychosom Med 1994 Nov-Dec;56:479-84) to propose a cholesterol-serotonin hypothesis of aggression.

    According to this hypothesis, low dietary cholesterol intake leads to depressed central serotonergic activity, which itself has been reported in numerous studies of violent individuals."




    "Researchers studied 25 violent psychiatric patients

    For 7 days, the patients wore signaling devices that emitted an average of seven signals a day.

    Following each signal, patients filled out a mood questionnaire.
    The authors found that "Total serum cholesterol (TSC) concentration was positively associated with measures of affect, cognitive efficiency, activation, and sociability, suggesting a link between low TSC and dysphoria."

    "These findings are consistent with the cholesterol-serotonin hypothesis and with the substantive literature linking both aggression and depression to depressed central serotonergic activity," they conclude.

    Journal of Behavioral Medicine, December 1, 2000; 23: 519-529"






    "Canadian investigators examined the relation between low serum total cholesterol and deaths from suicide. Adjusting for age and sex, they found that those in the lowest quarter of total cholesterol concentration had more than six times the risk of committing suicide as did those in the highest quarter.

    This effect persisted after the exclusion from the analysis of the first 5 years of follow-up and after the removal of those who were unemployed or who had been treated for depression.

    These data indicate that low serum total cholesterol level is associated with an increased risk of suicide.

    Epidemiology 2001 Mar;12:168-72"






    "Levels of cholesterol and other fatty molecules in the blood may have an impact on mood and aggression, according to a new study. Studies have shown that male psychiatric patients with low cholesterol (below160 mg/dl) are twice as likely to attempt suicide, and elderly men with low cholesterol are three times as likely to be depressed. And studies in animals have found that monkeys fed a diet low in fat and cholesterol are more aggressive than those fed a normal diet.

    The theory is that cholesterol level may influence serotonin, the neurotransmitter in the brain that has been linked to depression. However, it's not yet clear if the low cholesterol actually causes the depression or aggression, or if some other health factor is responsible for both low cholesterol and changes in mood swings.

    Psychiatric Services (1997;48:875-876)"





    "A study conducted by a Duke University researcher suggests that healthy women with very low cholesterol levels have higher depression and anxiety levels than women with higher cholesterol levels. Only about 10% to 15% of the US population has such low levels, defined as 160 micrograms per deciliter or below.

    The research suggests that women in their early 20s or late teens seem to be prone to depression and anxiety if they have very low cholesterol levels. These cholesterol levels are extremely low and occur naturally, not as a result of diet or lifestyle.

    Psychosomatic Medicine June1999;61."



    "A study conducted by a Duke University researcher suggests that healthy women with very low cholesterol levels have higher depression and anxiety levels than women with higher cholesterol levels. Only about 10% to 15% of the US population has such low levels, defined as 160 micrograms per deciliter or below.

    The research suggests that women in their early 20s or late teens seem to be prone to depression and anxiety if they have very low cholesterol levels. These cholesterol levels are extremely low and occur naturally, not as a result of diet or lifestyle.

    Psychosomatic Medicine June1999;61."


    and the real weiner...

    "Cholesterol in your brain is key to the cell connections needed for memory and learning.

    Past research has suggested that brain "support cells" known as glial cells produce a substance that allows the brain's nerve cells, or neurons, to communicate.

    Cholesterol levels in the blood do not determine the brain's supply, as blood cholesterol molecules are too large to cross the blood-brain barrier. The blood-brain barrier is a mechanism that strictly controls the type of molecule allowed to enter into the brain from blood vessels.

    Instead, glial cells appear to churn out their own cholesterol supply. The researchers zeroed in on cholesterol through experiments with cells in which the lipid triggered the formation of synapses -- the connections through which nerve cells communicate.

    Thus the availability of cholesterol appears to limit synapse development.

    In addition, the investigators found that, when cultured alone, neurons produced some cholesterol. But only when glial cells were present was there a cholesterol supply abundant enough for "massive" synapse formation.

    According to the researchers, these findings suggest that any "genetic or age-related defects" in the brain's cholesterol use may impair the circuitry behind mental functioning.

    Science November 9, 2001;294:1354-1357"



    Obviously, from a scientific standpoint I cannot stand up and state with 100% confidence that methyls that lower lipid values cause depression or mood disorders..BUT the evidence is a little more than just casual association here. It's more of a connect the dots kind of conclusion..but hey, it works for me because I lived it last cycle.
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    Sorry, one of those posted twice.
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    My trans test cycle made me feel strange, very sad at times for no reason.
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    Very informative post Bioman, thanks brother. So what's the best ancillary supp. for keeping cholesterol levels in the normal range?
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    That's the million dollar question. I don't think there is one that can stop methyl-induced choleostasis.
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    Thanks for the good posting, I must admit I have had minor crashing AFTER a long SD cycle but not during, as far as hepatoxicity, thats real and a relevant concern regarding anything ingested.
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    There is a typo in the first post. It was meant to say 500 to 900 mgs a week. If you read down about half way he says this. No where does it say you should be using 500 to 900 a day. I for one beleive this when it comes to the tried and true orals (with the exception of halotestin and cheque drops) but who knows with this new DMT and whatnot that they are putting in these OTC supps.
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