Fertility doctors frequently prescribe Clomid (a SERM), or hCG, or some combination of the two, for patients going off TRT and trying to have kids.
In a recent thread, KSman suggested that combining hCG and SERMs is a bad idea because it jacks up E2 levels. I have a couple questions:
1) Why does this combo of drugs tend to do this? 2) What purpose does a SERM serve for fertility or restoration of endogenous production that would not be accomplished by lowering E2 using an AI? 3) It seems like both SERMs and AIs have the potential to create an E2 rebound if you stop using it. Is this right? If one has more potential to create an E2 rebound, which one is it?
I think the answer to # 1 is: Because hCG because it mimics LH, produces Test, and this aromatizes to E2, especially in the Testes; and because the body cranks out more E2 when E2 receptors are blocked--but I'd like to be sure
Clomid seems to have a track record for restoring pituitary function--it's been used successfully to restart athletes suffering from exercise-induced hypogonadism ("Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate ").
1) The SERM should lead to higher levels of LH for most. The combo of LH and hCG will over load the LH receptors in the testes, with risk of degrading the LH receptors, exactly wrong for recovery.
2) SERMs increase LH and FSH which supports fertility. A normal AI dose cannot do that. High dose anastrozole can increase LH, FSH, T and E2 - IN NORMAL YOUNG MALES WITH FULLY FUNCTIONAL HPTA's. So that does not apply to guys with hypogonadism, and quite costly to. See my recent post on this in the estradiol sticky.
3) SERMs increase E2, AIs lower E2. Rebound shutdown is a real problem with SERMs. One should be using both at one point then cruising on 0.5mg/week anastrozole in EOD doses after PCT to support recovery. The process does not end with PCT! A very involved subject that you will not easily understand.
"cranks out more E2 when E2 receptors are blocked" That is true in the context of the hypothalamus when on a SERM. You need to qualify what you say to make any sense for readers.
Clomid has severe estrogenic side effect for some. There is nothing that clomid does that nolvadex cannot do. Clomid was the first SERM on the block and there was a lot of research done on the first born. That demonstrated the actions of a SERM. With the second born, there was no reason to repeat all of that and the interests of the researchers and grant money was directed somewhere else. Do not let the related traffic about clomid lead you to thinking that it is somehow special or unique.
One lobe of the hCG complex is exactly the same as LH. So mimic is perhaps misleading. Better to simply state that hCG activates LH receptors.
"restart athletes suffering from exercise-induced hypogonadism" -with otherwise youthful cells and viable HPTA's. Again, has little to do with what this forum addresses. Those problems with those who over train or induced starvation can be fixed with changes to routine, diet and calorie intake. SERMs not needed, but might be a useful bridge. Note that the problem can be from low cholesterol levels and other health issues.
Thanks, that's very helpful. So, if one were going off TRT for fertility purposes, would it look something like this?
Prior to going off, maintain testicular health with low-dose hCG and control E2 via anastrozole Stop testosterone while maintaining anastrozole (lower anastrozole eventually to account for lower T levels?) Stay on anastrozole solo for a certain period of time to deal with any lingering estradiol issues before introducing the SERM Start SERM. At this point would one continue dosing anastrozole or stop anastrozole altogether? Discontinue SERM and use AI to stabilize estradiol. Restart testosterone, adjusting AI as appropriate to manage estradiol.