You also have the DHT all wrong. Why can it not be the Aromatase inhibitor being a medication with side effects that caused your problem? Why is it DHT? The DHT receptors at the tissue level are fully saturated at a fairly low testosterone level (250ng/dl in the prostate for example) What you are measuring in the serum is just excess. It has no effect on the tissues, because those receptors have been fully saturated.Good stuff. I didn’t read the entire JCEM paper, but it looks like a good design. Randomized and double-blinded. That said, the study population was hypogonadal, but not under treatment. So, like you pointed out, the findings may not translate in those with HPTA suppression.
The reason I asked in the first place was that while on cream, I used a (very small) dose of an AI a few times. A few days after my last AI dose, my resting heart rate skyrocketed and blood pressure spiked. I felt terrible. As I had been applying it for well over five half lives, I assumed that I should have already been at a relative steady state on the cream. So my theory was that the AI indirectly pushed an already high DHT even higher, amplifying the sympathetic nervous system effects. Don’t know. Just speculating, but that was the reason for the question.
I saw some benefit on the cream, and was applying to both the scrotum and shoulder. Many guys reference this paper that suggests that scrotal absorption is 8 times higher than abdominal absorption. Anecdotally, I have heard of guys with free T at extremely high levels with scrotal application and others that struggle to get their levels up no matter where they apply. I was really looking for anecdotes on non-scrotal success stories, as that is where I suspect I will find success.