Results 1 to 13 of 13
  1. #1
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default What is a 17aa steroid?

    You've probably heard of "orals" or 17-alpha alkylated (17aa) steroids. Examples are winstrol, anavar/oxandrolone, dianabol, halotestin, etc. Examples that are NOT 17aa steroids are test propionate, NPP, test enanthate, equipoise, etc.

    These are generally known to be harsh to the liver. Generally speaking, guys are encouraged to NOT run all-oral cycles because of this - primarily because of the dosages men would require. They do use them in conjunction with other injectibles, but keeping the orals to short runs like 4-6 weeks and including liver support (milk thistle, or products like Tyler's Liver Support, LIV 52, etc). Women, on the other hand, very commonly use anavar or winstrol, because they are short esters and will clear quickly, are relatively mild in terms of sides, and do not require injection (i.e. they appear to be just a pill you pop and not a real steroid that requires needles. Less scary. Less "hardcore".) Also at low doses like 10 mg ED, they can be run for longer periods of time, producing nice, maintainable results.

    Here are some references about 17aa steroids:
    Note: as w/ all internet sources, please be intelligent about reading information and keep it context and relative to other things you read.

    http://en.diagnosispro.com/disease_information-for/clinical-manifestations-17-alkylated-steroids-administration-toxicity/10006-104.html

    http://www.usantidoping.org/athletes/cheating_health.html
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  2. #2
    OLYMPIAN Sistersteel's Avatar
    Join Date
    Feb 2009
    Location
    Strolling down Adrenaline Alley
    Posts
    2,836
    Rep Power
    5775

    Default

    Let me add that Alkylation is what makes oral steroids survive their first pass through the liver as well as what makes them hepatoxic.

    Oral Primo is the only 17 Beta Alkylated oral steroid which makes it relatively less harmful on the liver than the Alpha Alkylated steroids.

  3. #3
    RX MEMBER NPCKnight's Avatar
    Join Date
    Feb 2009
    Posts
    2,559
    Rep Power
    55890

    Default

    Alkalinization?

  4. #4
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default

    Quote Originally Posted by NPCKnight View Post
    Alkalinization?

    From wikipedia:

    Alkylation is the transfer of an alkyl group from one molecule to another. The alkyl group may be transferred as an alkyl carbocation , a free radical, a carbanion or a carbene (or their equivalents) [1]. Alkylating agents are widely used in chemistry because the alkyl group is probably the most common group encountered in organic molecules. Many biological target molecules or their synthetic precursors comprise of an alkyl chain, with specific functional groups in a specific order. Selective alkylation, or adding parts to the chain with the desired functional groups, is used, especially if there is no commonly available biological precursor.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  5. #5
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default

    http://www.mesomorphosis.com/article...e-steroids.htm



    How to Make Anabolic Steroids Orally-Active?

    by Patrick Arnold Pat is responsible for launching several major product and innovation in the prohormone industry through LPJ Research and Ergopharm, including the first to release androstenedione, 1-AD, 6-OXO, 4-androstenediol, and 19-norandrostenediol. In addition, he is responsible for bringing innovative delivery systems to the prohormone market including HPB cyclodextrin, bioadhesive technology for sustained release, and sustained release sprays.
    The subject of androgenic / anabolic steroids, and the different ways that have been found to make them orally active, has been tossed around lately on the internet mags. This is an interesting topic to the science minded out there, but beyond that, it also has potential utility to the prohormone supplements. The following is my take on the subject, including scientific references and conjecture on my part.
    The problem with natural androgens
    Testosterone is the primary androgen in the human, and is the golden standard by which all other steroids are compared. Unfortunately, testosterone has very poor activity when taken orally. This necessitates that testosterone be administered by extra-oral means such by injection, subcutaneous pellet implant, and transdermal gel or patch.
    17alpha alkylated steroids
    Scientists have developed several synthetic testosterone derivatives that have increased oral bioavailability. The first synthetic alteration that scientists utilized is known as 17 alpha alkylation. 17a alkylation involves the addition of an alkyl group (methyl or ethyl) to the alpha position of the 17 carbon of the steroid backbone. The alkylation at this position prevents the major route of androgen deactivaton oxidation to a 17-keto steroid - from taking place. This allows a large part of the steroid to avoid liver first pass metabolic degradation. Examples of 17a alkylated steroids are methyltestosterone and Norethandrolone (Nilevar)
    While 17a alkylation is a very effective means of rendering steroids orally active, it suffers from a serious drawback. These steroids are all to some extent toxic to the liver. Some are more toxic than others, but they all have been associated with this problem. Jaundice is not completely uncommon with the usage of this stuff, although this condition is generally confined to individuals who are predisposed to liver problems. Several cases of liver cancer have supposedly been linked to 17a alkylated steroids, however, nothing definitive has been established in this regard. On the other hand, it is somewhat common to observe increases in blood test indicators of liver stress such as BSP retention, and intrahepatic cholestasis (a condition where bile clogs up and stops flowing from the liver).
    While the dangers of 17a alkylated steroids are not trivial, they still comprise some of the most potent anabolic agents available, and therefore their use continues. Most smart bodybuilders are aware of the potential toxicities of these steroids, and therefore they are judicious with their use of them.
    Lipophilic steroid derivatives
    After ingestion, most steroids make their way to the intestines where they are absorbed into the portal circulation. The portal circulation carries the steroid directly to the liver, which is the workhouse of destructive metabolism and inactivation of drugs. As a result, if the steroid is not protected in some way, very little will make it through the liver and into the rest of the body where it can do its magic.
    In addition to the portal route, there is another route through which substances can be absorbed into the body from the intestine. If a substance is lipophilic (fat like) enough it will be absorbed in the same manner that dietary fat is. Dietary fat is incorportated into chylomicra, which are small fat globules composed of protein and fat. These chylomicra are absorbed into the lymphatic circulation, which by passes the liver. If you make a steroid lipophilic enough by altering its structure, then it too will incorportate into chylomicra and absorb into the lymphatic system. Once in the lymphatic system it can cross over into the general blood circulation, making it there without being subjected to the massive metabolic breakdown in the liver.
    Scientists have found that by adding lipophilic side chains to steroids, they will to some extent be absorbed into the lymphatic system. If the side chain is linked on in such a way that it can hydrolyze (break apart) easily after being absorbed, the steroid is essentially rendered orally active. Two side chains that have been utilized to increase the oral bioavailability of steroids through increased lymphatic absorption are long chain alkyl ester groups, such as is seen with testosterone undecanoate (andriol), and enyl ether groups, such as is seen with quinbolone (anabolicum vaster).
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  6. #6
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default

    The term "orally active" is of course a relative term. Lipophilically modified steroids are more orally active than the free parent steroids, however, they are no where near as active as the 17alpha-alkylated steroids. Testosterone undecanoate (TU) is probably the most commonly known lipophilically modified androgen, and it is not considered a very potent compound (its recommended daily dosage is about 240mg). In fact, one study found the oral administration of testosterone undecanoate led only to an absolute testosterone bioavailability of 6.83 +/- 3.32%. That is very slight, especially considering the fact that in the same study they found the bioavailability of straight testosterone to be 3.56 +/- 2.45% (Eur J Drug Metab Pharmacokinet 1986 Apr-Jun;11(2):145-9). That means TU is just a little less than twice as orally active as free testosterone, which is unimpressive to say the least.
    The other problem with lipophilic steroid preparations is the high variability in absorption from one person to another. In other words, one guy might absorb the stuff very well while the other guy might absorb very little. There is also high variation within individuals themselves, depending on their gastrointestinal condition when they take the stuff. In another study, ten post-menopausal women were given 40 mg of TU and their peak blood values were recorded. The values varied widely - more than ten fold (range: 5.8-64.0 nmol/L) - amongst the subjects (J Clin Endocrinol Metab 1998 Nov;83(11): 3920-4).
    There is no specific data I can find on the bioavailabilty of enyl ether compounds, but since their mode of action is identical to long chain alkyl ester compounds like TU, it is a fair assumption that they too are not outstandingly high in oral bioavailability, or in consistency of absorption. What I do know is that the one and only enyl ether oral steroid on the market today (quinbolone) is generally regarded by european bodybuilders / athletes as too weak to even bother taking.
    Ring A modified steroids
    There is one more class of anabolic / androgenic steroids that are orally active. These have unique structural modifications in the steroid A ring. What these modifications do is help preserve the steroids 17beta hydroxyl group, and minimize oxidation to the inactive 17-keto form.
    Androgens such as testosterone exist in the body in an equilibrium between their active 17beta hydroxyl form and the inactive 17-keto form.
    Normally, the equilibrium lies pretty far to the right (formation of inactive 17 keto steroid), however some steroids have certain modifications made in the A ring that alter this equilibrium by shifting it heavily to the left (towards the formation of active 17beta hydroxyl steroid).
    The most common A-ring modifications that shift the 17beta hydroxyl / 17-keto equilibrium to the left are methylation at the 1alpha position, and unsaturation (double bond) in the 1(2) position (Acta Endocr, 41, (1962) 494). Examples of orally active steroids that contain one or more these modifications include methenolone (Primobolan), mesterolone (Proviron), and 1-testosterone.
    You probably have heard of mesterolone and methenolone, but it is doubtful you have ever heard of 1-testosterone. 1-testosterone is a very interesting compound, not just because it is orally active but also because it is very anabolic. It has been reported to be over 7 times as anabolic as testosterone in a study funded by the pharmaceutical giant Searle (J Org Chem, 27 (1962) 248). Furthermore, being a 5alpha reduced steroid, it should not aromatize to estrogens.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  7. #7
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default

    Clipped from http://www.ironmagazine.com/anabolic_steroids.php


    Types of Steroids

    Below we've compiled a list of some anabolic steroids, including their relative potency and some other info. Sometimes, the names of steroids can be confusing to a newbie. This is because you have the chemical name, the various brand names, and the slang or street names for each product.

    For example, methandrostenolone is known to most people as Dianabol, but you probably hear it referred to as D-bol. Of course, you'll likely be using the veterinary version called Reforvit-B, whose street name is Reffie or Reffie-B. Got all that? Don't worry, the more you read the more you get used to all the terminology. To help you out, I've listed the chemical name as well as a few of the trade names for each 'roid.

    Fluoxymesterone (Halotestin, Stenox)

    This is a 17-alpha alkylated steroid. In other words, it's been altered in order to withstand the liver's "first pass" metabolism to a better degree, i.e., the liver doesn't inactivate the stuff before it can exert its effects. Without this alkylation, you'd need much higher concentrations to get results, as is the case with any 17-AA. Anyhow, this steroid appears to have a lower affinity for the AR, but can agonize the receptor at higher dosages.

    As far as "real world" effects, fluoxymesterone has a reputation for increasing strength to a large degree. However, gains in muscle mass on this steroid aren't very great. In clinical settings, dosages range from 2.5 mg to 40 mg a day in divided dosages. However, bodybuilders have been known to use from 30 to 80 mg per day. It has a half-life of approximately 9.2 to 10 hours. (I'll talk about why knowing about half-lives is important later.) Oh yeah, and it doesn't aromatize. This means it's not likely to convert to estrogen, the female hormone. In the real world, that means the risk getting gyno (bitch tits, i.e. breast tissue growth in males) is small to nonexistent.

    Methandrostenolone (Dianabol, Reforvit, Anabol)

    This 17-AA steroid was the first to be introduced to athletes in the 50s. Bodybuilders caught on soon after, no doubt. It's aromatizable, and therefore can increase estrogen levels. Since it doesn't bind very well to the AR, it's thought that it works by antagonizing the effects of catabolic glucocorticoids.

    D-bol has a great reputation for increasing both size and strength to a pretty good degree. While the half life isn't readily available in the literature, it can be assumed through deductive reasoning that it's around four to seven hours. Bodybuilders typically use around 25 to 100 mg per day depending on whether it's used alone or in conjunction with another steroid (a practice called stacking).

    Stanozolol (Winstrol)

    This steroid is also17-AA. It can't aromatize and doesn't bind very well to the AR. Consequently, it's likely to exert its anabolic effects in a similar fashion to that of methandrostenolone. In other words, it affects glucocorticoids in a beneficial manner.

    Another benefit may be its ability to antagonize or block progesterone from binding to receptors. Progesterone is one of the reasons why certain anabolics cause water retention.

    Stanozolol has a great reputation for increases in strength as well as moderate increases in muscle mass. Actually, these "moderate" gains are rather impressive, considering that this drug doesn't cause much water retention. In clinical settings, typical dosages are between 2 to 6 mg daily. In order to see desired effects, bodybuilders typically consume between 25 to 100 mg daily. While I can't locate any literature on its half-life, based on its molecular composition it would seem to have a slightly longer half-life than most of the other orals. I'd say it's likely to be in the range of 7 to15 hours.

    Oxandrolone (sold as oxandrolone powder or Oxandrolona)

    This is yet another 17-AA. It won't aromatize but appears as though it will bind to the AR as long as the dosages are high enough. It has a reputation for increasing strength gains, as well as having a "hardening" effect. This is supported somewhat, as oxandrolone was shown to reduce subcutaneous fat to a greater degree than Testosterone. Whether this is an inherent property of all 17-AA steroids or an effect that's unique to oxandrolone, I'm not sure.

    Oxandrolone, along with most of the other synthetic steroids, are thought to be equally (if not more) anabolic than Testosterone on a milligram per milligram basis, while minimizing androgenic side effects. Oxandrolone was shown to have approximately six times the anabolic effect of methyltestosterone in human subjects, following oral doses. Oxandrolone may also increase the number of skeletal muscle androgen receptors.

    In clinical settings, dosages have ranged from 1.25 to 80 mg per day. Bodybuilders may take anywhere from 25 to 160 mg per day. The half-life is approximately nine hours.

    Methenolone Acetate and Enanthate (Primobolan)

    This steroid doesn't aromatize and can either be ingested via the acetate version or injected via the enanthate. This steroid does bind rather well to the AR and is known for its mild gains in muscle mass. Still, considering that it'll cause next to zero water retention, these gains are rather good. (Note that some bodybuilders think certain steroids work better based solely on the weight they gain. In actuality, they could be just retaining a lot of water along with the muscle gains. These are the same guys who think they "lose" a lot of muscle after their cycle is completed, when they actually just lost much of the water they'd been holding.)

    Clinical dosages that are commonly seen with methenolone range from 10 to 20 mg daily, sometimes a little higher for the oral version. For the enanthate version, dosages are usually 100 mg every two to four weeks. Bodybuilders typically use 400 to 1000 mg a week. The half-life appears to be very similar to Deca, perhaps slightly shorter. So with this in mind, I'd say the half-life would be around five to seven days.

    Oxymetholone (Anadrol)

    This 17-AA steroid can't aromatize, but has been known to have progestenic properties and thus, can cause water retention. It has a great reputation for increasing muscle mass and strength to a large degree. It's also thought to have a very high anabolic/androgenic ratio.

    The typical dosage in clinical settings is one to five milligrams per kilogram of bodyweight per day. So, a 150 pound person would consume anywhere from 68 to 341 mg per day. However, the higher dosages aren't employed that often. Bodybuilders typically consume around 50 to 150 mg per day. While I can't find info on the half-life in the formal literature, it would seem it's similar to that of stanozolol. Obviously, this isn't a hard fact, but the half-life should be right in the neighborhood of 7 to15 hours. Only God and Bill Roberts know for sure.

    Testosterone Enanthate, Cypionate, Propionate, Suspension (commonly called "T")

    This steroid can aromatize and binds well to the AR. It's well known for its ability to produce great gains in muscle size and strength, provided that the dosages are high enough. It does cause quite a bit of water retention and has quite a few side effects when compared to the other anabolics.

    Clinical dosages vary, but cypionate and enanthate are both injected every two to three weeks at dosages of around 200 to 300 mg. Propionate and suspension aren't preferred as they don't provide that long of a sustained release. Bodybuilders typically use around 500 to 1,000 mg per week. The cypionate ester has a half-life of around eight days. Enanthate is just slightly shorter and propionate is quite a bit shorter. By the way, Testosterone in a suspension has a half-life of only 10 to 100 minutes.

    Nandrolone Decanoate and Laurate (usually referred to as Deca)

    This steroid binds very well to the AR and doesn't aromatize. It can produce moderate gains in muscle mass with little water retention. However, it, like oxymetholone, can be progestenic leading to water retention when higher dosages are used.

    In clinical settings, dosages are around 50 to 100 mg every three to four weeks. Bodybuilders use around 300 to 800 mg per week. The decanoate ester has a half-life of six to eight days and the laurate ester commonly seen in veterinary products has a slightly longer half-life.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  8. #8
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,629
    Rep Power
    2147958

    Default

    http://www.bodybuilding.com/fun/par19.htm

    By: Roy Harper

    NOTE: The opinions below are the author's only and may not represent the opinion of Bodybuilding.com. It is important for you to research all sides of an issue and consult your doctor before taking any medical advice.
    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:
    The Study
    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.
    This article appears courtesy of www.mindandmuscle.net
    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