mass dosing dbol/fina ? - AnabolicMinds.com

mass dosing dbol/fina ?

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    mass dosing dbol/fina ?


    i often hear of bros doing high doses of test, eq, primo, deca etc. can anyone break down why tren of dbol at high doses is overkill?

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    Because the sides start to massivly outweigh the gains achieved, and with D-bol there is also the issue of liver toxicity.

    ManBeast
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    Dbol due to toxicity.

    Tren- possible toxicity and health problems. Side effects can get very bad at high dosages.
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    cool. i'm running fina at 200mg eod. was to add a50 but decided to go with dbol at 40mg ed. i was curious because i know a50 can be used up tp 150 mg ed and wondered about dbol being used the same. i am aware of the sides but i meant other than the sides issue?
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    I'd stay right where you are on the fina, and take the dbol no higher than 50mg ed, those are "above average" dosages on both products already. Are you using liver support (milk thistle, NAC, etc?)

    ManBeast
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    Anadrol is a MUCH weaker drug mg:mg compared to dbol. Hence lower dosages of dbol is all that is needed and higher dosages of anadrol. It would NOT be wise to use 150mg of dbol daily.
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    Originally posted by size
    Dbol due to toxicity.

    Clin J Sport Med. 1999 Jan;9(1):34-9.

    Anabolic steroid-induced hepatotoxicity: is it overstated?

    Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

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

    OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

    PMID: 10336050 [PubMed - indexed for MEDLINE]
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    Originally posted by ManBeast
    Are you using liver support (milk thistle,
    ManBeast
    Milk thistle for the treatment of liver disease: a systematic review and meta-analysis.

    Jacobs BP, Dennehy C, Ramirez G, Sapp J, Lawrence VA.

    Department of Medicine, University of California, San Francisco 94143, USA. jacobsb@ocim.ucsf.edu

    PURPOSE: Milk thistle, an herbal compound, is the dietary supplement taken most frequently by patients with chronic liver disease. We performed a systematic review of the literature to determine the efficacy and safety of this herb for the treatment of liver disease. METHODS: We searched English and non-English reports through July 1999 using thirteen databases and reference lists, and contacting manufacturers and technical experts. Reviewers independently screened all reports to identify randomized placebo-controlled trials that evaluated milk thistle for the treatment of liver disease. Outcomes of primary interest included mortality, histological findings on liver biopsy specimens, serum aminotransferase and albumin levels, and prothrombin times. RESULTS: Fourteen trials met inclusion criteria. Four trials reported outcomes for mortality among 433 participants. The overall summary odds ratio for mortality in the milk thistle group compared with placebo was 0.8 (95% confidence interval [CI]: 0.5 to 1.5; P = 0.6). Three trials assessed histology on liver biopsy; study quality was inversely associated with the likelihood of histological benefit for milk thistle compared with placebo. There were no differences in serum alanine aminotransferase, aspartate aminotransferase, or albumin levels, or prothrombin times, among participants assigned to milk thistle compared with those assigned to placebo. The only statistically significant difference was a greater reduction in alanine aminotransferase levels among patients with chronic liver disease assigned to milk thistle (-9 IU/L, 95% CI: -18 to -1 IU/L; P = 0.05), but this reduction was of negligible clinical importance and no longer statistically significant after limiting analyses to studies of longer duration or of higher quality. The frequency of adverse effects was low and, in clinical trials, indistinguishable from placebo. CONCLUSION: Treatment with milk thistle appears to be safe and well tolerated. We found no reduction in mortality, in improvements in histology at liver biopsy, or in biochemical markers of liver function among patients with chronic liver disease. Data are too limited to exclude a substantial benefit or harm of milk thistle on mortality, and also to support recommending this herbal compound for the treatment of liver disease.







    The use of silymarin in the treatment of liver diseases.

    Saller R, Meier R, Brignoli R.

    Abteilung Naturheilkunde, University Hospital Zurich, Switzerland.

    The high prevalence of liver diseases such as chronic hepatitis and cirrhosis underscores the need for efficient and cost-effective treatments. The potential benefit of silymarin (extracted from the seeds of Silybum marianum or milk thistle) in the treatment of liver diseases remains a controversial issue. Therefore, the objective of this review is to assess the clinical efficacy and safety of silymarin by application of systematic approach. 525 references were found in the databases, of which 84 papers were retained for closer examination and 36 were deemed suitable for detailed analysis. Silymarin has metabolic and cell-regulating effects at concentrations found in clinical conditions, namely carrier-mediated regulation of cell membrane permeability, inhibition of the 5-lipoxygenase pathway, scavenging of reactive oxygen species (ROS) of the R-OH type and action on DNA-expression, for example, via suppression of nuclear factor (NF)-kappaB. Pooled data from case record studies involving 452 patients with Amanita phalloides poisoning show a highly significant difference in mortality in favour of silibinin [the main isomer contained in silymarin] (mortality 9.8% vs 18.3% with standard treatment; p < 0.01). The available trials in patients with toxic (e.g. solvents) or iatrogenic (e.g. antispychotic or tacrine) liver diseases, which are mostly outdated and underpowered, do not enable any valid conclusions to be drawn on the value of silymarin. The exception is an improved clinical tolerance of tacrine. In spite of some positive results in patients with acute viral hepatitis, no formally valid conclusion can be drawn regarding the value of silymarin in the treatment of these infections. Although there were no clinical end-points in the four trials considered in patients with alcoholic liver disease, histological findings were reported as improved in two out of two trials, improvement of prothrombin time was significant (two trials pooled) and liver transaminase levels were consistently lower in the silymarin-treated groups. Therefore, silymarin may be of use as an adjuvant in the therapy of alcoholic liver disease. Analysis was performed on five trials with a total of 602 patients with liver cirrhosis. The evidence shows that, compared with placebo, silymarin produces a nonsignificant reduction of total mortality by -4.2% [odds ratio (OR) 0.75 (0.5 - 1.1)]; but that, on the other hand, the use of silymarin leads to a significant reduction in liver-related mortality of-7% [OR: 0.54 (0.3 - 0.9); p < 0.01]. An individual trial reported a reduction in the number of patients with encephalopathy of -8.7% (p = 0.06). In one study of patients with cirrhosis-related diabetes mellitus, the insulin requirement was reduced by -25% (p < 0.01). We conclude that available evidence suggests that silymarin may play a role in the therapy of (alcoholic) liver cirrhosis. Silymarin is has a good safety record and only rare case reports of gastrointestinal disturbances and allergic skin rashes have been published. This review does not aim to replace future prospective trials aiming to provide the 'final' evidence of the efficacy of silymarin.
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    [Liver toxicity of androgen therapy in aplastic anemia]

    [Article in French]

    Pecking A, Lejolly JM, Najean Y.

    In a prospective group study, 254 cases of aplastic anemia treated with a high dose of androgens were followed a minimum of 4 months and up to 8 years. Damage to the liver was evaluated by the appearance of jaundice or abnormal liver function tests; these parameters were evaluated at least every 3 months. Of these patients, 17.3% had overt jaundice and 18.2% abnormal hepatic function tets (total 35.5%). The anomalies appeared rapidly, before month 4 for 50% of the patients and before month 10 for 80%. They were more frequent in men than in women or children, but not linked with previous biological abnormalities. Nor did frequency depend on whether C17 methyl androgen or C17 ethyl androgen was used. Associated corticosteroids offered no protection. None of the patients showed severe jaundice or cirrhosis. If the treatment was stopped, readministration led to relapse of the jaundice in only one-third of the cases. Only two patients in this series revealed a nonmalignant tumor of the liver. Therefore, this complication does not seem to suggest restriction in the use of androgens at high dosage and for long periods, considering the severity of aplastic anemia.
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    4 Deaths in ten years, at a time when people could find very little information on dosing, and most likely these deaths included other hepatic complications.


    Hepatic angiosarcoma associated with androgenic-anabolic steroids.

    Falk H, Thomas LB, Popper H, Ishak KG.

    A retrospective epidemiological study of deaths from hepatic angiosarcoma (HAS) in the U.S. showed that during 1964--74 there were 168 such cases, of which 37 (22%) were associated with previously known causes (vinyl chloride, 'Thorotrast', and inorganic arsenic) and 4 (3.1%) of the remaining 131 cases with the use of androgenic-anabolic steroids. It is suggested that the long-term use of androgenic-anabolic steroids is the fourth cause of HAS, the majority of cases still being of unknown aetiology. Moreover, the presented cases serve as a link in a spectrum of hepatic disorders recently recognised to be caused by environmental agents such as vinyl chloride, arsenic, and thorotrast, and by contraceptive and anabolic steroids. Similar precursor stages, usually not recognised by clinical laboratory tests and consisting of areas of hyperplasia of hepatocytes and sinusoidal cells and sinusoidal dilatation, lead potentially to hepatic adenoma, carcinoma, peliosis, and angiosarcoma
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    I will not argue that liver toxicity of anabolics is overstated b/c I believe it is. In addtion, other problems can arise besides liver issues.


    However, to encourage one to use an extreme dosage is STUPID and irresponsible.
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    I have to agree with size on this one, the liver toxicity is over-rated, but it is very irresponsible to tell people to take very high dosages of compounds known to stress the liver (to any degree). And while milk thistle might not be "the best" way to help one's liver, I was merely pointing him in the direction of basic niver support.
    Thanks for all the studies EBE, they were a great read.

    ManBeast
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    *I am not a medical expert, my opinions are not professional, and I strongly suggest doing research of your own.*
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    great info but i didn't see where anyone was being encouraged to use high doses. i'll re;read the thread. i missed that. i was curious why it was ineffective at those doses. i did get the answers i was looking for as always from you bros.
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    Originally posted by organdoner
    great info but i didn't see where anyone was being encouraged to use high doses. i'll re;read the thread. i missed that. i was curious why it was ineffective at those doses. i did get the answers i was looking for as always from you bros.

    There was no encouragement of extreme dosages. However, one could misunderstand some information and assume that extreme dosges can be used without any negative consequences.

    There are other issues of toxicity besides liver damage when using products.
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    I'd say the reason for tren not going to high would be due to concerns of progesterone related gyno. As for the dbol you probably could go higher if you really wanted to but most wouldn't because you can just up your dose of testosterone which has no real concerns of liver damage. Another reason would be because alot of people don't see any better results after a certain point and for most it seems to be 50mgs on dbol. I remeber awhile back when a few people tried 100mgs of dbol ed and only one of then saw better results and a few said any more than 75mgs was a waste. By the way if your looking to get big and strong fast next time try the anadrol instead of dbol. I've ran anadrol/tren before and it made me stronger than any cycle I've ever ran. I will warn you though most would advise against this because it is beleived that both tren and anadrol cause progesterone related gyno.
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    Although anadrol wont cause gyno via progesterone, it can cause gyno fairly easily.

    I had great results on a tren/deca/test/drol cycle, no gyno, maybe Im lucky
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    Originally posted by ex_banana-eater


    Clin J Sport Med. 1999 Jan;9(1):34-9.

    Anabolic steroid-induced hepatotoxicity: is it overstated?

    Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

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

    OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

    PMID: 10336050 [PubMed - indexed for MEDLINE]
    Don't take this the wrong way, because I'm an AAS user and an advocate of AAS use when done so responsibly, but this study is in the minority when it comes to attempting to justify that AAS don't cause liver problems.
    I just finished writing a review of literature on AAS abuse on cardiac function in bodybuilders and power lifters. I reviewed 8 research studies for the written review it self, while reviewing numerous others that would potentially be beneficial to my review of literature. Many of the studies I reviewed, inlcuding the one that is quoted above, do not control for the doses the subjects are administering. Interviewing the subect and asking him for the doses he administers does nothing to control for the margin of era. Even taking blood work to verify that the subject is in fact using the drugs he says he is does nothing to control for the doses administered. It's self-administration so there is huge margin of era and in many situations, the info, even presented in a peer reviewed journal such as the Clinical Journal of Sports Medicine, needs to be taken with a grain of salt, until other research teams can present more data which backs up such findings. Dozens of research studies out there have presented statistically significant data to show that certain oral AAS can potentially cause liver issues.
    I would really like to see more studies like the one above conducted, as long as they attempt to control for extraneous variables that can completly throw off outcome data. Hopefully there will be more to come in the future, at least I really hope so!
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    Originally posted by jmul508


    Dozens of research studies out there have presented statistically significant data to show that certain oral AAS can potentially cause liver issues.
    I would really like to see more studies like the one above conducted, as long as they attempt to control for extraneous variables that can completly throw off outcome data. Hopefully there will be more to come in the future, at least I really hope so!
    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 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.


    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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