How do class II steroids cause shutdown?

[bmj]

So I've read that steroids are grouped into two categories: Class I's bind androgen receptors, Class II's exhibit their actions via other mechanisms. If the negative feedback that results in shutdown is caused by the drug binding to the androgen receptor in the hypothalamus, then how can a class II steroid cause shutdown?

Perhaps they DO have affinity for the androgen receptor (maybe higher for the hypothalamic receptors than those in muscle tissue), but the MAJORITY of their anabolic effect is due to a different mechanism? Still, a class II should be less suppressive than a class I, right?

I guess with something like dianabol, aromatization to estrogens can cause suppression. But what about something like superdrol (class II, right?) which is commonly branded as one of the most suppressive orals yet does not aromatize?

Any thoughts on this would be greatly appreciated. Thanks!

 

[gelin]

That classification represents a gross over-simplification of what is actually occurring. It's popular because it's easy for people to devise their stacks... warts and all. Brolore mixed with a lil' bit of science.

Yes, as you suggest, there are definitely androgenic properties to the so-called class II's, most likely because the activation of the AR's isn't quite as direct as with the class I's, but is still taking place nonetheless. You can google "indirect receptor activation steroid" if you want to kill time and hypothesize various mechanisms... co-factors, upregulation, transcriptional changes...

"Aromatization" is hardly a requisite for shutdown. All AAS can cause shutdown simply due to the fact that they mimic endogenous T to a close enough extent, and the body stops producing its own as a result. The hypothalamus responds to superdrol or whatever by shutting off FSH & GnRH production... leading the Leydig cells to stop producing T. The lethargy that is often associated with superdrol can probably be attributed to this decline in T.

When people talk of aromatization, they are usually concerned with gyno and getting bloated. But compounds that don't aromatize - such as epistane for example - can often still cause gyno. This can occur on cycle, perhaps through progestin-mediated effects, as well as after cycle as a result of poor PCT / badluck combined with T rebound.

In other words, there are almost always sides. Needless to say, oral, 17-methyls are all going to be pretty nasty on your liver while you're on cycle, unlike injectables.

Anyway, hope I more or less answered some of your questions. I hate writing in this little box & I've got to crash.

 

[sethroberts]

That classification system is bogus. All steroids have "on-target" and "off-target" effects. The so-called Class II steroids were observed in the literature to have fairly low binding affinity for the andrgoen receptor so it was assumed that they must be exerting their anabolic effect through a non-AR mechanism. Some more recent literature has shown that while the binding affinity is low for some steroids, they are still able to bind and transactivate the androgen receptor in part due to their long plasma half life (compared to the short half-life of free testosterone in plasma).

 

[bmj]

Thanks for the responses guys. Reps. The whole class I/II thing seems to be a pretty poor grouping system, I guess its just a way that people have tried to make sense out of how some compounds stack better with others.

Gelin, the reason I mentioned aromatization is because estrogen is supposed to have a greater suppressive effect on the hypothalamus than testosterone, so I was thinking that maybe the metabolites of some of the class II's might be more suppressive than the active compound itself.

As for superdrol, this is progestin based, right? Maybe that explains why people report so much shutdown when taking it?

Thanks again for your responses guys.