Didn't hear one single reason from a performance standpoint, just a convenience standpoint, the WWB argument is bs, if you can't source good quality test is not a compound issue but a you issue, from a long term data standpoint test is actually safer to take than Enclomiphene, the "perfect levels" you claim from Enclomephine is misleading and overstating:
View attachment 50893
Hence why TRT is still the go to option for treating conditions like hypogonadism.
Mechanistical standpoint:
Enclomiphene stimulates your natural production via LH/FSH, RAD 140 strongly suppresses your HPTA axis, this problem is not real with exogenous testosterone as it bypasses your HPTA axis, also, important to mention all the strong data regarding Enclomephine is from hypogonadal men (which were not taking suppressive compounds), but it's safe to affirm that SARMs will leave you with test levels similar or even worse to hypogonadal men anyways.
Using a compound like Enclomephine that stimulates endogenous test production via LH/FSH while using a compound like RAD 140 that strongly suppresses your HPTA axis is stupid and would only contribute to a negative feedback loop. SERMs work by blocking estrogen receptors in the hypothalamus, signaling low E2, when you're taking SARMs they are usually resistant to metabolism and conversion from the aromatase enzyme, therefore making the mechanism a lot less convenient and supper sloppy.
Especially when the suppression is this strong:
View attachment 50902
We need to understand this is not a 1:1 extrapolation but can be used as a reference to understand how suppressive this compound is.
The "No risk of hyper responding or megadoses" is absolute bullshit, and it's once again overstating,
You would need to demonstrate this.
Extremely backwards, you are confusing the raw bioavailability of a direct hormone with the responsiveness of a multi organ system feedback loop, also, when you inject
100mg of test e, you are introducing a fixed unchanging chemical mass into your body, the way your body responds is a whole other topic, and this whole "overshoot" thing would be cause of crushed SHBG.
Another backwards statement, again, testosterone has a cleaner mechanism that bypasses the HPTA axis and doesn't rely on LH/FSH to endogenously create this response, therefore from a mechanism standpoint it has a cleaner and simpler mechanism, again, SERMs work by blocking estrogen receptors in the hypothalamus, signaling low E2, when you're taking SARMs they are usually resistant to metabolism and conversion from the aromatase enzyme, do i need to explain why this is suboptimal as a mechanism?
We don't need a specific study on RAD 140 with Enclomephine to know how the underlying mechanism works, we know how strongly RAD 140 binds to the AR, and we know how the hypothalamus responds to heavy androgenic signaling (which is the total shutdown of the GnRH).
@Nardicus @surgerymax