T Nation

GH Use During PCT, Counterproductive?


Not sure where to put this, but it just occurred to me, and I'd like some of you guys to chime in...guess a new thread is as good as any place.

Would GH use during PCT inhibit pitiuitary recovery?

Let's think about this very briefly: goal during PCT is to bring back testes, pituitary, and hypothalamus each to functioning on their own. However, as they are all shut down after a cycle, I wonder if GH use during PCT--an idea that has been kicked around this forum--might not be detrimental to pituitary recovery.

We don't know yet if AAS use causes the pituitary to decrease GH secretion as part of its response to being suppressed by exogenous hormone use. I haven't seen any studies that measure that parameter at least, and we also know that exogenous GH use does suppress pituitary secretion of GH via at least one mechanism (somatostatin), and then some more (there's never only one 1 kind of response to biological stimuli) but I don't recall all the details right now...

Just thinking out load before I finally go to sleep for the "night". Hope to get some thoughts.

Want some thoughts from the science minded crowd.

Yes I know it will help keep cycle gains when used during cycle, and/or probably also during PCT. Does the benefit outweigh the other side?


The WHOLE pituitary is not 'deactivated' from negative feedback loops, just the secretion of certain neurochemicals and hormones.

So with T, it isn't the Pituitary that is important, it is the Hypothalamus. This secretes the GnRH which stimulates the secretion of LH and FSH from the Antior pituitary lobe. It does not simply 'turn on' the Pituitary to start making shit, as would have to be the case for inhibition of one hormone inhibiting all pituitary secreted hormones (or if the glands are removed physically or chemically of course).

With GH (my knowledge is not as deep), GHRH is released from the Hypothalamus which in turn signals the Ant. Pituitary to release Somatotrophin.

It isn't that the pituitary is totally inhibited from working, but that Somatostatin prevents or decreases the release of GH from that particular gland (in negative feedback at least).
This (AFAIK) has nothing to do with LH and FSH.


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BBB you are right. Dbol does increase IGF-1 secretion from the liver ( anadrol does it too). I think it had more to do with it's structure (17AA), which cause some kind of immediate compensatory reponse from the liver itself. I doubt it is pituitary/hypothalamus related. It is hard to say about negative feed back though, no human studies have been done in this area.


Yeah, I know the whole pituitary doesn't just "shut down" across the board Brook, same with the hypothalamus. That would be pretty much stupid. I am also aware that somatotropin ( lol, I said 'statin' in my OP) regulates GH release in feedback.

I'm aware that the pituitary continues secreting most other signals.... What I was idly wondering is do you think there may be any "pathway cross talk" from adding exogenous gh helping to keep GNRH, LH, FSH low during pct through other indirect mechanisms.

We know that androgens tend to help increase GH secretion---although I have no idea if that holds up all the way through with large exogenous doses of test, or if there's a point at which androgen levels actually "buckle" GH release. As meph noted dbol increases IGF-1 in the liver and we know that co-exposure to IGF-1 and 2 strongly inhibits the GH axis, while exposure to only one of them is slightly inhibitory. Also meph, one of the studies I linked in the GH thread implies that there may be a major hypothalamic regulation loop for IGF-1, although no one can say for certain yet.

So could there be any mechanism through which supra-natural levels of GH can affect androgen regulation (possibly through effects on LH, FSH, et al. )? I dunno, I am throwing it out there for the big wigs in here to mull over.

Alright, sorry for the confusion fellas. I was wondering out load and I didn't use very precise language.


Somatotropin is GH - it doesn't regulate GH. Somatostatin was correct in the context you used it.

No need for the attitude Aragorn - It was a fair response to your post. As i did say, the only way what you were asking could happen was IF the whole gland shut down or if they were chemically removed so something.

And you DID focus on the Pituitary's release of GH - without mentioning the Hypothalamus' input in that, so how am i supposed to know what you 'know' or not?


And this is where you get into trouble sometimes Brook. I'm not sure where you got that idea, but I made an effort to write in a way that I hoped insured that I didn't have an attitude in my response. I was trying to clear my question up because I know the time I generally get these random thoughts is the time I'm least equipped to articulate them properly (right before bed).

You DID have a fair response to my original post, which was precisely why I was trying to make everything a bit clearer in my second post. I knew I wasn't being clear and I tried to fix error (


You're very right about the statin/trophin of course!! I've been mixing too many science topics together in each day now, and combined with chronic sleep deprivation, I'm starting to lose my grip on vocab :). Bad mistake, but one to which I have always been prone :(. Should have just left that alone, because I made the confusion worse with my second post. Pardons gentlemen.

I'm not sure that the only way to affect things is by wholesale removal of the pituitary... we know that there are major hypothalamic feedback loops, and there is evidence to support the idea that at least IGF-1 is part of a large one that may be able to affect GH. It makes sense to me that there could be pathway cross-talk from directly GH involved pathways to other parts of the hypothalamus and pituitary (indirectly of course) involved in T production/regulation. Things that go one way in regulation (androgens modulating GH axis), generally speaking go the other way as well (GH axis ---> androgens), even if not quite as directly.

...but of course that's why I asked the question, because I didn't know and I wondered if it had occurred to anyone else's mind. I haven't done a lot of reading to date on it and I wanted to see.

I still think GH use during PCT is an effective way to use it. Just wondering out loud.

My apologies if you felt an attitude.


Define 'trouble'...

No problem mate - i did feel attitude, but nothing worth discussing :wink:

I agree - GH is very useful during PCT.

On deeper thought, i can see where the idea came from - as BBB mentioned with IGF stimulating negative feedback - and some orals increasing IGF..