Oral's liver toxicity - AnabolicMinds.com

Oral's liver toxicity

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    Question Oral's liver toxicity


    I mean i always hear how freaking toxic and dangerous orals are for the body and liver but i know guys that do 100 mgs of dbol for 8 weeks or so or bridge from epi to superdrol. Ive never even heard of one case of someone reporting back with liver issues. Could they really be that toxic?

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    yes
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    Lemme see studies
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    almost didnt recognize Rodja with his new avi
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    Quote Originally Posted by Borispili View Post
    almost didnt recognize Rodja with his new avi
    But do you recognize hepatotoxicity and its documented dangers now?
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    Those are only case studies, so they don't prove anything about the actual toxicity of Superdrol or other orals on the average person. Every single drug has people who react to it negatively, even drugs that most people do absolutely fine on.

    That being said, I don't deny the possibility that Superdrol can cause liver damage, however I am skeptical that the average person will experience any permanent liver damage on a typical cycle of Superdrol. I didn't even bother getting any bloods done when I used SD as a kicker for my last injectable cycle, but the first ever cycle I did was Epi at 40mg a day for 6 weeks. I got bloods done before my cycle and during the last week and my liver values were unchanged, still on the low end of the normal range.

    I plan on using Superdrol as a kicker @ 20 mg/day for my next cycle and may even just keep taking it the entire 12 wk cycle since I have a lot of it I got cheap before the ban, depends on if the sides are really bad or not. Of course I will be getting bloods done at maybe the 5 week mark, because there's no sense risking my liver to save $40, but like I said I am extremely skeptical I will have anything more than slightly elevated liver values. That being said, everyone's an individual and even if the average person can survive Superdrol just fine, that doesn't necessarily mean you will too. You may be the 1 guy out of 100 who's liver isn't quite healthy enough to handle it, so it's better to error on the side of caution and get blood tests done.
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    http://www.nature.com/ajg/journal/v1...g2006488a.html

    I also have the full study, and some others on different compounds.

    please dont make me look this shiit up, yes, it is very bad for you. if you dont believe it, you are an idiot. dont ask questions like this if you dont want to accept the obvious answer.
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    I appreciate the hard work, sadly, it seemed to be a waste of time for some hopefully it'll be of some use for others.
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    jbryand101b, I swear a while back you posted a study claiming the toxicity issue was overblown.

    I may have to dig it up, lol.
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    wasn't me, unless you're looking at post from like 08 when i was a newb.

    I think it is overblown, that doesn't mean it isn't a real issue.
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    Re: Oral's liver toxicity


    Hepatoxicity is overblown IMO

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    Quote Originally Posted by JudoJosh View Post
    Hepatoxicity is overblown IMO

    Sent from my Samsung Galaxy S™II using Tapatalk 2
    the samsung galaxy s II using tapatalk 2 is overblown.
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    Quote Originally Posted by jbryand101b View Post
    wasn't me, unless you're looking at post from like 08 when i was a newb.

    I think it is overblown, that doesn't mean it isn't a real issue.
    Sorry, it wasn't you, it was David Dunn.

    If anyone has time to read a massive wall of text, this is very interesting:

    Hepatoxicty: Fact or Fiction?
    by Roy Harper

    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 weak 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 not 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 livers 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. 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.
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    Re: Oral's liver toxicity


    Quote Originally Posted by jbryand101b View Post
    the samsung galaxy s II using tapatalk 2 is overblown.
    LMAO... I'm at work sitting at the front desk and literally busted out laughing when I read that.

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    Re: Oral's liver toxicity


    Anabolic steroid-induced hepatotoxicity: is it overstated?

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    Hepatoxicty: Fact or Fiction?


    Hepatoxicty: Fact or Fiction
    by Roy Harper

    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 weak 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 not 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 livers 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 50mg to 90mg 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? Dickerman 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.
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    Re: Oral's liver toxicity


    Quote Originally Posted by David Dunn View Post
    Hepatoxicty: Fact or Fiction
    by Roy Harper
    Did you miss post #14?
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    Here's my lab results from before and at the end of my 6 week 40mg Epi cycle. You can see that my liver values were actually slightly lower at the end of the cycle than when I started. I made plenty of strength gains and my test is shut down so it wasn't bunk Epi. This is just an n = 1 experience, obviously, but take it for whatever it's worth.

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    Quote Originally Posted by JudoJosh View Post
    Did you miss post #14?
    Clearly I did. Sorry
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    Edit for f** up on my part
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    Your post is OT. May want to start your won thread.
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    8 week epi--> superdrol bridge to much for my Liver ? Got liv 52
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    Quote Originally Posted by Borispili View Post
    8 week epi--> superdrol bridge to much for my Liver ? Got liv 52
    You being serious?
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    I think moderation is key. Most people have no problem popping a dozen ibuprofen a day or downing a 6 pack of beer but mention taking a Dbol pill and they're like "**** you better take it easy bro!"

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    Quote Originally Posted by Borispili View Post
    8 week epi--> superdrol bridge to much for my Liver ? Got liv 52
    If your liver does survive you will likely be left with devestated lipids. Oral steroids' liver toxicity produces a poor lipid profile as the liver regulates cholesterol.
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    Wht about tht dude with lab results who liver got barley hit
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    Quote Originally Posted by David Dunn View Post
    Your post is OT. May want to start your won thread.
    Sorry my bad thought I was posting in different thread stupid iPhone (I love blaming my iPhone)
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    Quote Originally Posted by thegodfather View Post
    I think moderation is key. Most people have no problem popping a dozen ibuprofen a day or downing a 6 pack of beer but mention taking a Dbol pill and they're like "**** you better take it easy bro!"

    Sent from my iPhone
    Ibuprofen has a LD50 of more than anyone can actually consume unless they basically made a Ibuprofen smoothy. Not even close to the same level in hepatoxicity.
    http://anabolicminds.com/forum/cycle-info/223429-abscent-minded-log.html
    Quote Originally Posted by csa2179 View Post
    Pin the kittens with the tren, then attack the judges with the kittens, uppity bastards
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    4 weeks on M1T, minimal liver support. Enzymes went from 20's to low 40's
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    Distilled h2o is tht good or bad idk wht those numbers mean
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    Quote Originally Posted by Borispili View Post
    Distilled h2o is tht good or bad idk wht those numbers mean
    Normal range is in the low 40's. doctors were not alarmed at the low 40's reading
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    If you don't want liver issues don't take orals..simple as that
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    Quote Originally Posted by JD261985 View Post
    If you don't want liver issues don't take orals..simple as that
    Very very true
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    Nutraplanet has the cheapest TUDCA I know of and they're having a clearance sale on some whey too. If you're really worried about it then go ahead and order some. It's cheaper than a blood test. IIRC the half life of TUDCA is pretty long compared to orals so you can just take it once a week, twice if you're really worried about it.
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    Quote Originally Posted by Gerbil View Post
    Ibuprofen has a LD50 of more than anyone can actually consume unless they basically made a Ibuprofen smoothy. Not even close to the same level in hepatoxicity.
    acetaminophen is hepatotoxic.
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    Re: Oral's liver toxicity


    Quote Originally Posted by Gerbil View Post
    Ibuprofen has a LD50 of more than anyone can actually consume unless they basically made a Ibuprofen smoothy. Not even close to the same level in hepatoxicity.
    Yeah but ibuprofen is hard on the kidneys..
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    Quote Originally Posted by R1187 View Post
    acetaminophen is hepatotoxic.
    I am not saying it is not but it takes chronic taking of it to acquire the level of liver damage. Most case studies I have read on its hepatoxicity have been over months and months of use. Comparing that to methyls is like saying, meth and caffeine are both stimulants.
    http://anabolicminds.com/forum/cycle-info/223429-abscent-minded-log.html
    Quote Originally Posted by csa2179 View Post
    Pin the kittens with the tren, then attack the judges with the kittens, uppity bastards
  

  
 

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