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THIS ARTICLE WAS TAKEN FROM 300KLEEN'S WEBSITE WITH THE INTENT TO HELP OTHERS WHO DON'T KNOW.
This should help clear up a couple myths about steroid receptors. To begin with, the human body only has one type of receptor that will bind with steroids, namely the androgen receptors (ARs). This means that no matter how many drugs you stack it all has to bind to the same receptors before you see any results.
I also see many people talking about "hitting" this receptor with this drug and hitting that receptor with that drug - that's a load of crap! Contrary to popular belief, different steroids do not hit [bind with] different receptors, i.e. Sustanon 250, Deca-Durabolin, and Winstrol bind to the same androgen receptors; they do not have special receptors for each one.
Simply put, steroid hormones work by interacting with a steroid-specific receptor in the cell. The receptor is a protein to which the steroid binds; the steroid fits into a pocket on the receptor that is designed to accept the hormone like a lock and key.
Steroid hormone receptors aren't active until the steroid hormone is bound, therefore, it is either on or off. By activating transcription of specific genes, hormones (through their receptors) can change the milieu of proteins within cells, and this can lead to major changes in the body such as building muscle or building breast tissue.
The first important question to ask is, "How many ARs do you have? Is the number small or large? Can it be changed?" Since these are, in effect, little machines which are either on or off, and their effect is greater as more are activated, we want as many of them switched on as possible.
There are far fewer ARs than most people realize. Some authors who are opposed to AAS doses beyond 200 mg/week say that only this amount will be accepted by the receptors in muscle, and everything past that will "spill over" and go into receptors in the skin and elsewhere. That theory has been shown to be bunk.
Typical doses of AAS are high enough that a high percentage of the ARs are bound to AAS, whether the dose is say 400 mg/week or 1000 mg/week. If similar percentages of ARs are active, then close to 100% will be activated.
The ideal steroid hormone would have anabolic, or muscle-building, activity without androgenic activity, since the androgenic activity is associated with undesirable side effects such as infertility, hair loss, acne, increased risk of prostate disease, and more toxic effects like cardiovascular or liver disease. Furthermore, the ideal steroid would have no estrogenic effects because, among the side effects, is gynecomastia. Unfortunately this ideal steroid does not exist, probably because anabolic and androgenic effects are both regulated by the androgen receptor.
This should help clear up a couple myths about steroid receptors. To begin with, the human body only has one type of receptor that will bind with steroids, namely the androgen receptors (ARs). This means that no matter how many drugs you stack it all has to bind to the same receptors before you see any results.
I also see many people talking about "hitting" this receptor with this drug and hitting that receptor with that drug - that's a load of crap! Contrary to popular belief, different steroids do not hit [bind with] different receptors, i.e. Sustanon 250, Deca-Durabolin, and Winstrol bind to the same androgen receptors; they do not have special receptors for each one.
Simply put, steroid hormones work by interacting with a steroid-specific receptor in the cell. The receptor is a protein to which the steroid binds; the steroid fits into a pocket on the receptor that is designed to accept the hormone like a lock and key.
Steroid hormone receptors aren't active until the steroid hormone is bound, therefore, it is either on or off. By activating transcription of specific genes, hormones (through their receptors) can change the milieu of proteins within cells, and this can lead to major changes in the body such as building muscle or building breast tissue.
The first important question to ask is, "How many ARs do you have? Is the number small or large? Can it be changed?" Since these are, in effect, little machines which are either on or off, and their effect is greater as more are activated, we want as many of them switched on as possible.
There are far fewer ARs than most people realize. Some authors who are opposed to AAS doses beyond 200 mg/week say that only this amount will be accepted by the receptors in muscle, and everything past that will "spill over" and go into receptors in the skin and elsewhere. That theory has been shown to be bunk.
Typical doses of AAS are high enough that a high percentage of the ARs are bound to AAS, whether the dose is say 400 mg/week or 1000 mg/week. If similar percentages of ARs are active, then close to 100% will be activated.
The ideal steroid hormone would have anabolic, or muscle-building, activity without androgenic activity, since the androgenic activity is associated with undesirable side effects such as infertility, hair loss, acne, increased risk of prostate disease, and more toxic effects like cardiovascular or liver disease. Furthermore, the ideal steroid would have no estrogenic effects because, among the side effects, is gynecomastia. Unfortunately this ideal steroid does not exist, probably because anabolic and androgenic effects are both regulated by the androgen receptor.
