T Nation

Why Not SERM on Cycle (w/hcg)?


I got to thinking about this addressing a "coming off" question in the TRT forum today...

We recommend using HCG during cycle in order to keep the 'T' portion of the HPTA awake in order to make post cycle recovery easier...this is a good recommendation, but obviously you are still shutting down your pituitary...

Why not use a SERM in conjunction with the hcg to preserve both the pituitary and testicles during cycle? Would this not make recovery easier?

First Cycle Double Checking

Thank you for asking this. I lurk these forums and have always wondered this but dont watn to ask because i beleive i will be flamed way to hard.


AFAIK it's because SERMs can reduce your gains. Somebody a lot smarter than me could run an analysis and figure out whether an easier recovery outweighs the reduction in gains (muscle gained vs. muscle retained).


I have often wondered this myself.

Also there seems to be alot of speculation that higher serum E levels actually increase gains(?). Hopefully someone cough BBB cough could enlighten us on this matter.



Yeah, there's nothing wrong with the question or idea, but unfortunately it just doesn't work. We know that a generation of lifters used nolva on cycle before AI's were readily available to prevent gyno, and they ended up shutdown just like everyone else.

As to why, well I'm no expert but I'll give it a shot. SERMs aid in recovery by competing with E2 for binding to ERs, preventing E2-mediated negative feedback. (And from papers that I've read, nolva does this in the pituitary, while clomid does so in the hypothalamus, though I'm not convinced that the distinction between the two is a clean as some have suggested.) Now, would the use of a SERM be better than the use of an AI on cycle, in preventing E2 binding? I doubt it...E2 would be around in high doses when using aromatic compounds, and it would have the opportunity to bind. Competitive inhibition only gets you so far. Regardless, that's not the whole story because E2 isn't the only mechanism of negative feedback. High levels of exogenous AAS cause negative feedback at the hypothalamus, preventing GnRH release. The mechanism is a little more complicated so I won't try to unravel it here. There can also be negative feedback from progesterone, though obviously that may not be an issue, depending on the compound.

Hope that helped a bit. Perhaps others can chime in.


Total Newb to AAS but from a biological-medical standpoint, your body is trying to maintain homeostasis by increasing estrogen through production and aromatizing to maintain the natural balance that it's supposed to have.. You actually need SERMS when you discontinue AAS and your body's production is minimized so that there is not an excess of estrogen while you are re-gaining hpta function and natural test production. Minimizing estrogen on cycle is not as ideal as inhibiting the aromatization of valuable testosterone on-cycle because estrogen has countless benefits such as lubricating joints and maintaining healthy libido. AI's seem to have more advantages for those who aromatize more and experience estro related sides such as gyno and massive water retention. Thats what I've learned so far.. feel free to flame or correct me on this.


^^ I don't want to put words in VTB's mouth but I don't think he's trying to argue SERM vs AI during cycle. He's asking why we don't use a SERM to keep the pituitary pumping LH and FSH so it doesn't get shut down, sort of like HCG for the pituitary.


I was unaware serms did anything at all to maintain or stimulate LH or FSH.


Yes exactly...

Yes this is why they are used in PCT to help restore HPTA functionality...


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Thanks, still learning.


Yes, other androgens in addition to T will definitely cause that negative inhibition.

Nolva has definitely been shown to decrease IGF-1 levels. I don't know if other SERMs don't, or if they just haven't been examined as closely. Not sure if the IGF-1 decrease is systemic (liver produced) or if it's also mirrored in IGF production in skeletal muscles.

I know that GH and related peptides definitely help me greatly in PCT; whether it's due to countering the drop in IGF, or to other factors, I can only guess.


I recently read something similar and was debating running IGF-1 Lr3 in my post cycle. Any thoughts on this? I haven't found many who have done this but it seems like a great addition to pct.


HCG is an analogue for LH when used on cycle...so your hypothalamus is still "shut down" with respect to producing LH if you take the HCG concurrently. The idea of using HCG during cycle is to make sure the testes are still in good working order after the cycle...you are faced then with only the problem of restarting the hypothalamus machinery to produce LH. This is versus if you didn't take any HCG on cycle, then you have the dual problem of restarting both your testes AND your hypothalamus.

But I think taking HCG contributes to hypothalamus shutdown. As I see it, if there is ample testosterone and estrogen in the body, and ample "LH", there is no need for the hypothalamus to produce any more, as long as you are using anabolics OR HCG.


The hypothalmus actually doesn't produce LH, it secretes something (I can't remember what) that tells the pituitary to produce LH...but your point is noted

I'm now convinced that it is pointless to run a SERM while on an AAS cycle, but from a TRT context, I think there still may be some potential there to keep the pituitary functioning since the T levels will be more moderate...though I now realize it would be redundant to take HCG on top of that, unless for some reason you can only get so much LH out of the pituitary though this method...in that case, HCG MIGHT be a supplement to the less than optimal LH as far as the testes are concerned...

really just mental masturbation at this point...


You are right. It's the pituitary that releases LH; the hypothalamus releases LHRP which stimulates the pituitary to release LH. My mistake...nice catch!


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I hereby declare myself....corrected. Thankyou sir. And Happy New Year to you and all.