Evidence from in vitro studies is more convincing than no evidence, particularly in supporting general underlying principles. The direct interaction of DHT with aromatase and the estrogen receptor is basic biophysics, not overly subject to cross-species variation.
You mischaracterize what was said. This is about the relative activity of androgens and estrogens in men on TRT. While higher doses of testosterone do lead to higher levels of estradiol, the incremental increases can be attenuated with higher levels of DHT. At the same time, the estradiol is less effective when there's greater DHT interference at receptors. An additional mechanism is possible, in that work shows that "... DHT antagonism of estrogen ... appears to occur by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding." The sky's-the-limit crowd demonstrates the principle involved; symptoms of elevated estrogen are supposed to be addressed by raising the testosterone dose until resolution. Then there's the not-insignificant matter of the successful treatment of breast cancer with DHT and its derivatives, strongly contradicting the assertion that "serum levels do not have any physiological effect."
My places of education discouraged puerile ad hominem attacks as a means of persuasion. Yours?
