Should be noted sampling bias is going to be heavily present within your TRT/hormone optimisation group. I lack clinical/field experience to make a perceived judgement regarding whether the use of an aromatase inhibitor ameliorates side effects associated with testosterone replacement. In the context of pure replacement there is little/on data regarding the concomitant use of aromatase inhibitors to combat side effects associated with the use of testosterone. Then again, the dosages/target testosterone concentrations aimed for by progressive doctors have little data regarding long term safety/efficacy in comparison to traditionally approved HRT/TRT dosages (generally aiming for around 500-700ng/dl, mid/high range FT).
At this point it’s a crapshoot, the use of an aromatase inhibitor alone doesn’t appear to significantly alter lipids and/or inflammatory markers.
You will find rodent models and/or perhaps a few in vitro studies using massive concentrations of the drug.
There is data indicating suppressing of endogenous oestrogen within healthy, eugonadal young men marginally decreases flow mediated dilation, though once again lipids, inflammatory markers etc remained stable. The unknown variable arises when we raise testosterone concentrations to borderline/flat out supra-therapeutic concentrations of which aren’t well studied over prolonged periods of time and the male notices adverse effects. Is the risk of stroke/myocardial infarction higher with high T + High E or High T + SLIGHTLY reduced E? Does the ratio make a difference? Rodent/in vitro models appear indicative aromatase inhibition in conjunction with a supra physiologic concentration of testosterone is associated with neurotoxicity. I’d have to find the study again, but it was interesting in that non-aromatizing/low aromatizing androgens were associated with in-vitro neurotoxicity (in-vitro models are flawed btw) even in low concentrations, the threshold for testosterone mediated neurotoxicity was comparably higher until aromatase inhibitors were introduced. Is this a byproduct of oestrogen eliciting a neuroprotective mechanism? Probably… We have enough data regarding this topic in particular. Granted is the risk/difference particularly significant within practical application? I’m not convinced either way.
Alcohol also impairs endothelial function, quite a large portion of the adult populace drinks. I read something recently that stated the average Australian drinks to excess thirty three days out of the year. The consumption of trans fats will induce endothelial dysfunction too as will living a sedentary lifestyle and more. Without adequate context, “endothelial dysfunction” doesn’t mean much. Excess testosterone/dihydrotestosterone will also induce endothelial dysfunction, sharply increase the risk of cardiovascular pathology down the line.