Cy, there is a raging argument over at another board and the following statement was made: “17AA steroids upregulate the corticoid receptor…they increase the density of the corticoid receptor”. Therefore, the poster says, they produce gains which are hard to maintain post cycle. This coupled with the hepatoxicity issue is enough to make the poster proclaim, “they are just not worth the risk.”
Now, I can see where some 17AA steroids MIGHT upregulate the corticoid receptor–such as Dianabol–but all 17AA? Even my statement concerning Dianabol is merely conjecture however.
What’s your take on the poster’s statements? Specifically, is there any reason to believe that Oral Turinabol would “upregulate the corticoid receptor”?
Hi Crowbar. Oh boy, several things to clear up here.
First, an anti-glucocorticoid effect whether via competitive antagonism, repressed GR-transactivation, etc., is generally inherent to all androgens, 17 alpha-alkylated or not, at least to some degree. This can be easily located in the primary literature. Nandrolone, testosterone and DHT have all have well-demonstrated anti-glucocorticoid effects. In fact, prior to serious investigation into the effects upon the androgen receptor, the anti-glucocorticoid effect was a predominating proposed mechanism for anabolic steroids.
Now, as far which androgens which one would suspect would lead to an up-regulation of GR, those would likely be those that are good competitive antagonists, such as nandrolone and as you’ve noted, likely methandrostenolone.
Here’s the biggest problem of all, however and I see this misconception all over. An up-regulation or down-regulation of these receptors as a consequence (key word being consequence) of the presence and then withdrawal of these compounds is not something of concern. This is really a simple and very brief change we’re talking about. Simply put, in many cases where a given tissue is lacking a given hormone or the receptors are being antagonized, the next best thing is an up-regulation of those receptors in an attempt to increase tissue responsiveness to what little hormone is available. Once this deficit is no longer present or the antagonist is removed, again, you experience a brief down-regulation. I think the misconception is that these shifts in receptor expression continue long after the change in stimuli and that just isn’t true. Just as important, again, is the other misconception that the down-regulation of GR’s is a CAUSE of the net result, when in fact it’s simply an insignificant consequence of competitive antagonism. So, that hypothesis doesn’t hold up.
Hope that helps answer your question.