Should You Pair an AI With Enclomiphene? (The Mechanism Explained)

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Should You Pair an AI With Enclomiphene?

In almost every case, no. The two drugs are doing overlapping work on the same signal, and stacking them does not double the effect, it just crushes your estradiol while you are already telling your brain estradiol is low.

Is there a situation where it would make sense to use an AI paired with enclomiphene? To answer that you have to see the whole loop first, because the loop is what both drugs are reaching into.

Your hypothalamus releases a signal that tells the pituitary to release LH, LH tells the testes to make testosterone, and some of that testosterone gets converted into estradiol, which is the messenger that travels back up and tells the hypothalamus to ease off, acting the same way a thermostat would cycle a furnace on and off.

The way that enclomiphene works, so what we're doing is we are basically blocking the signaling of estradiol so that your body thinks that it has low E2.

And when your body thinks it has low E2, it's gonna amp up the signal of testosterone production at the pituitary to basically tell your body to produce more.

But because the feedback that comes back to the hypothalamus to tell you to stop producing testosterone comes from the estrogen signal, if we block that, then basically what's happening is our body thinks it needs to make more.

So the testosterone rise you get from enclomiphene is not the drug adding anything. It is your own axis running hotter because the brake line got clamped.

Now what happens if we were to pair that with an aromatase inhibitor? What an AI is doing is it's actually going to the cells that convert testosterone into estradiol. Those enzymes are called aromatase, and a lot of them sit in adipose tissue, which is part of why body fat changes how much estradiol a given dose of testosterone produces.

So effectively the way an AI works is similar to what a CIRM would do, except in the case of a CIRM, what we're doing is we're just locking up the receptors that detect the presence of the E2, and the estradiol still gets produced normally, it is only the reading of that signal at the brain that gets jammed.

One drug stops the message from being written, while the other leaves the message sitting there and simply blocks the hypothalamus from ever opening it. Either way the hypothalamus gets the same blank page.

That is why these two are not complementary. They are redundant, and the redundancy has a cost, because estradiol is doing real work in bone, in joints, in libido, in lipids, and in how you actually feel. Blocking receptors at the brain while also shutting down production body-wide gets you low estradiol everywhere, not just where you wanted the signal quiet.

In my mind, it wouldn't make sense to pair any type of AI with a CIRM, and this is typically why when you see a post-cycle therapy protocol where we have guys coming off of testosterone cycles or steroid cycles, they bridge with a CIRM while they phase off of the aromatase inhibitor while they're on cycle to basically give their body that kick that it needs to turn its natural production back on.

Everything about this comes down to order. The AI was there for a problem that existed while exogenous testosterone was high. The CIRM is there for the problem that starts once it is gone.

If there's an overlap of the AI and the CIRM, it's very short, and the only reason we would do that would just be to account for the remaining half-life of the testosterone dose that we were previously on that was far above baseline levels, AKA steroid cycle doses, to hopefully bring ourselves back down into a TRT-level dose or completely off of the gear.