Drveejay11
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From Majutsu
A primer on anabolic steroid chemistry
This is some introductory material on steroid biochemistry, addressing some common questions, as well as basic terms and concepts for understanding a little bit about anabolics.
A Primer on Anabolic Steroid Chemistry for Newbies
What are anabolic steroids?
All anabolic steroids are chemical derivatives of the male sex hormone, testosterone. Due to testosterone's short biological half-life, which makes it last only a very short time in the human body, pharmacological use requires that the steroid be modified to slow metabolism by the liver. Typically, oral steroids are modified primarily by alkylation (replacing an H with a CH3 group), whereas injectable steroids are modified by esterification of the hydroxyl group. This leads to the creation of drugs that administer testosterone over time and may be taken orally or injected.
How do steroids work?
Anabolic steroids work by binding with the cytoplasmic androgen receptor (cytoplasmic meaning floating free within the cell as opposed to bound to the surface of the cell). The androgen
receptor is the body's "landing pod" for testosterone and other anabolics (which mimic testosterone). Once a steroid binds to an androgen receptor a new entity called the steroid-receptor complex is formed. The unoccupied steroid receptor is a 8S receptor, but when the anabolic binds it becomes a new 4-5S steroid-receptor complex. (Biochem Int. 1983 Nov; 7(5): 541-8.) The steroid-receptor complex is then like a ship that sails into the nucleus with the anabolic as its captain at the helm. The complex is translocated (in scientific terms) into the nucleus and binds to DNA. Once in the nucleus via the steroid-receptor complex, the steroid appears to enhance transcription of specific genes. The resulting mRNA is processed and sent out of the nucleus, resulting in increased protein synthesis and bigger muscles. There are three classes of steroid receptors, androgen, estrogen and glucocorticoid. Androgens we care about; estrogen is well known; glucocorticoids are used in medicine for things like severe asthma, etc. (Int J Sports Med. 1984 Jun; 5(3): 130-6.) To avoid confusion we call the testosterone receptor the androgen receptor(AR), versus the "steroid receptor" to avoid confusion with the other classes of steroids. Catabolic inhibition (as well as anabolic activity) may also occur in the nucleus if the complex inhibits the transcription of certain catabolic enzymes. BTW anabolic means getting bigger, catabolic means wasting away or muscle loss.
Where are androgen receptors located?
The presence of the androgen receptor indicates a tissue is androgen sensitive, and it's concentration gives an indication of how sensitive. The receptor is present in a number of organs, including skeletal muscle. Skeletal muscle typically contains 0.5-3 femto (1E-12) moles per milligram of protein, while other androgen sensitive organs, like the prostate gland, may have up to 25 times more receptors. This is key to understand. Androgen receptors are in the skeletal muscle, where they are anabolic when occupied. Androgen receptors are also in the prostate, skin, and scalp, causing prostatic hypertrophy, acne, and hair loss respectively. So there are two important compartments of androgen receptors: 1) Those in the muscles. 2) Those NOT in the muscles which cause good erection, energy and all the sides. Testosterone's effects are generally broken into two classes: anabolic and androgenic. Both appear to result from the same signalling pathway (in other words, the same receptor) as there are no proteins with anabolic effects independent of androgenic effects (meaning that protein juice sucked out of a skeletal muscle covered with test, when injected into skin, creates acne). The outcome is simply the effect of where the androgen receptor is located, not a different chemistry, receptor or anything else.
Why are some Anabolic Androgenic Steroids (AAS) considered more anabolic than others?
If the anabolic steroid binds to the androgen more strongly or more efficiently than another, it will sail that receptor-steroid complex into the nucleus more, resulting in more anabolic results. Usually they radiolabel (or color or dye in some way) the different anabolic steroids and let them compete for the receptor, like musical chairs with different teams. When several anabolic steroids were tested as competitors , Metribolone/Trenbolone was stronger than deca stronger than primo stronger than test. Winstrol (winny), halotestin and dianabol did not bind the androgen receptor much at all! (Endocrinology. 1984 Jun; 114(6): 2100-6.) Their anabolic activity is considered to occur through a non-AR pathway. In the old-school, it was thought best to mix an AR steroid with a non-AR steroid to cover all the bases: such as primo and dbol --arnold's supposed fave. Or the deca and dbol many bodies were built upon.
What is aromitization or conversion?
A final observation about feedback in biological systems: in a perfect example of biological control, a byproduct of testosterone metabolism is estradiol, which enhances catabolism. Thus, overadministration of testosterone-analog steroids can feed-back and minimize results. Unfortunately, the same circulating estrogen that is a byproduct of testosterone metabolism can cause water retention, fat deposits, and gyno -- some nasty sides. This is why some guys block the action of estrogen with nolvadex or the formation of estrogen with arimidex, or both.
Deca nandrolone also converts to progesterone. Trenbolone converts to a very progesterone-like metabolite equally well as deca. This may cause a progesterone gyno, LH hormone problems and terrific shutdown. This is why some never use tren and deca. But for those that can handle it, they are the strongest!
Why are some steroids more androgenic than others? The story of test and deca . . .
Testosterone, the principal androgen secreted by Leydig cells, exerts a wide range of actions including growth of the male reproductive tract (androgenic effects) and growth of non-reproductive tissues such as muscle, kidney, liver, and salivary gland (anabolic effects). As androgenic steroids were discovered some were found to have relatively more anabolic than androgenic activity. These differences result,in part, from the differential metabolism of the steroids in individual tissues and the varied activities of the individual metabolites. In the accessory sex organs (e.g. the prostate) testosterone is 5 alpha-reduced to dihydrotestosterone (DHT). DHT is even stronger at the androgen receptor than test! -- like super-test. However, this 5-alpha enzyme does NOT exist in skeletal muscle. So we get this super-test, super-strong effect everywhere we DON'T want it, the hair, skin, prostate, etc. In contrast, when 19-nortestosterone (NT or "deca") is 5 alpha-reduced, its affinity for androgen receptor DECREASES, resulting in a decrease in its androgenic potency, forming "weak shit". However, their anabolic potency remains unchanged since significant 5 alpha-reduction of the steroids does not occur in the muscle. In other words, deca turns itself into "weak shit" outside the muscles, which is everywhere we DON'T want androgenic potency. (J Steroid Biochem Mol Biol. 1995 Jun; 53(1-6): 253-7.) I always thought this was really, really clever. Primo is very similar, as is boldenone. They are mostly-clean anabolics. In fact, the only place people tend to miss androgenic activity is in the penis, with soft or problematic erections/libido. Some people take proviron, viagra/cialis, or just very low-dose test/HRT as needed for this reason while on their "really clean" anabolics.
How much can you push the AR button anyway?
At some point every bodybuilder asks this. Studies of dose response usually look only at testosterone at this point. But numerous studies suggest no leveling off or plateau of effect up to 600ew test. (Am J Physiol Endocrinol Metab. 2003 May; 284(5): E1009-17. Epub 2003 Jan 07; Am J Physiol Endocrinol Metab. 2001 Dec; 281(6): E1172-81.) This would indicate test at 2g ew would probably start to saturate or maximize the benefit of stimulating the AR. Of course, the other anabolics that are stronger, like tren, primo or deca would cut this down to a gram or less. Tren and deca both convert to progesterone at too high doses, but at 400-500ew could be stacked with primo (or possibly eq) at 400 or so, for a 1g anabolic stack. If affordable, 1g primo ew should maximize that avenue completely with no estrogen, progesterone, and less shutdown than the others. Although primo is slightly more androgenic than deca, and some notice worse skin or hair on primo. Mixing this with Winstrol (winny), halo, or dbol would cover the non-AR pathways for full anabolic coverage. All things said and done, 1g primo + dbol in spurts would seem to be a "perfect stack."
A primer on anabolic steroid chemistry
This is some introductory material on steroid biochemistry, addressing some common questions, as well as basic terms and concepts for understanding a little bit about anabolics.
A Primer on Anabolic Steroid Chemistry for Newbies
What are anabolic steroids?
All anabolic steroids are chemical derivatives of the male sex hormone, testosterone. Due to testosterone's short biological half-life, which makes it last only a very short time in the human body, pharmacological use requires that the steroid be modified to slow metabolism by the liver. Typically, oral steroids are modified primarily by alkylation (replacing an H with a CH3 group), whereas injectable steroids are modified by esterification of the hydroxyl group. This leads to the creation of drugs that administer testosterone over time and may be taken orally or injected.
How do steroids work?
Anabolic steroids work by binding with the cytoplasmic androgen receptor (cytoplasmic meaning floating free within the cell as opposed to bound to the surface of the cell). The androgen
receptor is the body's "landing pod" for testosterone and other anabolics (which mimic testosterone). Once a steroid binds to an androgen receptor a new entity called the steroid-receptor complex is formed. The unoccupied steroid receptor is a 8S receptor, but when the anabolic binds it becomes a new 4-5S steroid-receptor complex. (Biochem Int. 1983 Nov; 7(5): 541-8.) The steroid-receptor complex is then like a ship that sails into the nucleus with the anabolic as its captain at the helm. The complex is translocated (in scientific terms) into the nucleus and binds to DNA. Once in the nucleus via the steroid-receptor complex, the steroid appears to enhance transcription of specific genes. The resulting mRNA is processed and sent out of the nucleus, resulting in increased protein synthesis and bigger muscles. There are three classes of steroid receptors, androgen, estrogen and glucocorticoid. Androgens we care about; estrogen is well known; glucocorticoids are used in medicine for things like severe asthma, etc. (Int J Sports Med. 1984 Jun; 5(3): 130-6.) To avoid confusion we call the testosterone receptor the androgen receptor(AR), versus the "steroid receptor" to avoid confusion with the other classes of steroids. Catabolic inhibition (as well as anabolic activity) may also occur in the nucleus if the complex inhibits the transcription of certain catabolic enzymes. BTW anabolic means getting bigger, catabolic means wasting away or muscle loss.
Where are androgen receptors located?
The presence of the androgen receptor indicates a tissue is androgen sensitive, and it's concentration gives an indication of how sensitive. The receptor is present in a number of organs, including skeletal muscle. Skeletal muscle typically contains 0.5-3 femto (1E-12) moles per milligram of protein, while other androgen sensitive organs, like the prostate gland, may have up to 25 times more receptors. This is key to understand. Androgen receptors are in the skeletal muscle, where they are anabolic when occupied. Androgen receptors are also in the prostate, skin, and scalp, causing prostatic hypertrophy, acne, and hair loss respectively. So there are two important compartments of androgen receptors: 1) Those in the muscles. 2) Those NOT in the muscles which cause good erection, energy and all the sides. Testosterone's effects are generally broken into two classes: anabolic and androgenic. Both appear to result from the same signalling pathway (in other words, the same receptor) as there are no proteins with anabolic effects independent of androgenic effects (meaning that protein juice sucked out of a skeletal muscle covered with test, when injected into skin, creates acne). The outcome is simply the effect of where the androgen receptor is located, not a different chemistry, receptor or anything else.
Why are some Anabolic Androgenic Steroids (AAS) considered more anabolic than others?
If the anabolic steroid binds to the androgen more strongly or more efficiently than another, it will sail that receptor-steroid complex into the nucleus more, resulting in more anabolic results. Usually they radiolabel (or color or dye in some way) the different anabolic steroids and let them compete for the receptor, like musical chairs with different teams. When several anabolic steroids were tested as competitors , Metribolone/Trenbolone was stronger than deca stronger than primo stronger than test. Winstrol (winny), halotestin and dianabol did not bind the androgen receptor much at all! (Endocrinology. 1984 Jun; 114(6): 2100-6.) Their anabolic activity is considered to occur through a non-AR pathway. In the old-school, it was thought best to mix an AR steroid with a non-AR steroid to cover all the bases: such as primo and dbol --arnold's supposed fave. Or the deca and dbol many bodies were built upon.
What is aromitization or conversion?
A final observation about feedback in biological systems: in a perfect example of biological control, a byproduct of testosterone metabolism is estradiol, which enhances catabolism. Thus, overadministration of testosterone-analog steroids can feed-back and minimize results. Unfortunately, the same circulating estrogen that is a byproduct of testosterone metabolism can cause water retention, fat deposits, and gyno -- some nasty sides. This is why some guys block the action of estrogen with nolvadex or the formation of estrogen with arimidex, or both.
Deca nandrolone also converts to progesterone. Trenbolone converts to a very progesterone-like metabolite equally well as deca. This may cause a progesterone gyno, LH hormone problems and terrific shutdown. This is why some never use tren and deca. But for those that can handle it, they are the strongest!
Why are some steroids more androgenic than others? The story of test and deca . . .
Testosterone, the principal androgen secreted by Leydig cells, exerts a wide range of actions including growth of the male reproductive tract (androgenic effects) and growth of non-reproductive tissues such as muscle, kidney, liver, and salivary gland (anabolic effects). As androgenic steroids were discovered some were found to have relatively more anabolic than androgenic activity. These differences result,in part, from the differential metabolism of the steroids in individual tissues and the varied activities of the individual metabolites. In the accessory sex organs (e.g. the prostate) testosterone is 5 alpha-reduced to dihydrotestosterone (DHT). DHT is even stronger at the androgen receptor than test! -- like super-test. However, this 5-alpha enzyme does NOT exist in skeletal muscle. So we get this super-test, super-strong effect everywhere we DON'T want it, the hair, skin, prostate, etc. In contrast, when 19-nortestosterone (NT or "deca") is 5 alpha-reduced, its affinity for androgen receptor DECREASES, resulting in a decrease in its androgenic potency, forming "weak shit". However, their anabolic potency remains unchanged since significant 5 alpha-reduction of the steroids does not occur in the muscle. In other words, deca turns itself into "weak shit" outside the muscles, which is everywhere we DON'T want androgenic potency. (J Steroid Biochem Mol Biol. 1995 Jun; 53(1-6): 253-7.) I always thought this was really, really clever. Primo is very similar, as is boldenone. They are mostly-clean anabolics. In fact, the only place people tend to miss androgenic activity is in the penis, with soft or problematic erections/libido. Some people take proviron, viagra/cialis, or just very low-dose test/HRT as needed for this reason while on their "really clean" anabolics.
How much can you push the AR button anyway?
At some point every bodybuilder asks this. Studies of dose response usually look only at testosterone at this point. But numerous studies suggest no leveling off or plateau of effect up to 600ew test. (Am J Physiol Endocrinol Metab. 2003 May; 284(5): E1009-17. Epub 2003 Jan 07; Am J Physiol Endocrinol Metab. 2001 Dec; 281(6): E1172-81.) This would indicate test at 2g ew would probably start to saturate or maximize the benefit of stimulating the AR. Of course, the other anabolics that are stronger, like tren, primo or deca would cut this down to a gram or less. Tren and deca both convert to progesterone at too high doses, but at 400-500ew could be stacked with primo (or possibly eq) at 400 or so, for a 1g anabolic stack. If affordable, 1g primo ew should maximize that avenue completely with no estrogen, progesterone, and less shutdown than the others. Although primo is slightly more androgenic than deca, and some notice worse skin or hair on primo. Mixing this with Winstrol (winny), halo, or dbol would cover the non-AR pathways for full anabolic coverage. All things said and done, 1g primo + dbol in spurts would seem to be a "perfect stack."
great read
