@dbossa thanks for your reply. Would you be willing to share more about your p5p usage? When you started, dose, length of time used, and reasons for stopping, etc? While I’m still researching the whole “AI is poison” thing, I do appreciate your feedback.
As for e2 not causing gynecomastia, I don’t think I can say that it doesn’t contribute to gynecomastia. It is definitely one of the factors involved in creating the perfect storm for it:
“Prolactin has also been reported to decrease androgen receptors and increase estrogen and progesterone receptors in breast cells, which can lead to male gynecomastia. Prolactin itself stimulates milk production in breast tissue that has been primed by estrogen and progesterone, but it does not directly cause gynecomastia itself.”
What is the role of hyperprolactinemia in the etiology of gynecomastia?
Updated: Mar 22, 2018
Author: George Ansstas, MD; Chief
Dbossa if genuinely interested in helping guys, should be listening to our personal experiences on this forum.
Instead he is very divisive. Even well known doctors see things differently and treat their patient’s based on their knowledge, experience and interpretation of medical research.
He does not contribute well to this forum at all. He clogs them up with his stern one sided personal beliefs. Obsession, and is always promoting his YouTube channel and now Facebook page.
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.
@unreal24278 you are kind enough to have detailed responses for Dbossa.
It is clear that he does not care about any clinical evidence, studies or personal experiences that fit what he is preaching.
He is very closed minded and in this evolving trt world, that is bad for guys seeking information.
See I value other guys opinions, studies they bring forward, and for sure their personal experiences. He does not. It’s almost as if he has some type of biz agenda.
I can attest to having tried anastrazole out of curiosity within the past 6 months to see if it made a difference.
Only notable observation was a slight reduction in overall water retention and a notable increase in facial aesthetics. Though this could be (for me) achieved by a simple dose reduction down from 150mg/wk+ to 100-125mg/wk. I generally choose the latter.
No significant difference in libido, health parameters etc. Though this is following acute use and doesn’t equate to having any significance within the realm of data/literature (sample size too small, duration of use minute in duration).
My opinion doesn’t mean much, however a TT of 1200ng/dl + a FT of 45 isn’t “trt” either. It’s not a cycle, but it isn’t TRT in the traditional sense of replacement in the sense virtually no male will ever naturally produce this amount of testosterone (not even close).
Plenty of people want to feel better and thus use one variable as a crutch in order to colloquially gloss over other, at times pivotally important parameters. What’s more, all this talk of androgen resistance… You can test for androgen resistance (i.e long cag repeat lengths, srd5a2 analysis etc), it’s really not that common. As a matter of fact I’m getting testing for PAIS as there’s a chance I might have partial androgen insensitivity syndrome (long story, I won’t divulge intimate details publically).
Guys with PAIS legitimately do require vastly supraphysiologic doses of T/androgens to feel normal. I’ve spoken to one doctor in particular who has stated he/she needs to get some PAIS patients up around 3000ng/dl+ to feel normal. Keep in mind this is Australia, an extremely conservative country when it comes to TRT/HRT.
Talking about endothelial dysfunction/cardiovascular disease. I’d argue this year round ought to marginally/moderately increase risk of heart disease and sharply increase the risk of clotting/DVT/Stroke.
I’m also not a fan of ad hominem attacks, putting others down etc because they harbour a different body of thought to you. Such behaviour comes across as immature, at times arrogant and narcissistic depending on the context. This is a blanket statement about anyone.
I’m not one to talk about someone when they have the inability to respond, so I’ll stop here as dbossa can’t reply at the moment.
When I said I dropped the AI & the HCG and dropped my TRT to 140mg a week and still had a E of 95. He should have been interested. And then to know that he takes 250+ and has an E of 60. I’m like that goes to show that people are different. I’m wondering what the actual numbers are of all the guys on his channel.
Also, @unreal24278 is spot on, the sampling of people on his channel is going to be biased. Anyone not on board with the koolaid is going to leave the group. And you are left with just the patriots.
I’d like to be on T and nothing else. But that doesn’t seem to be the case for me. I’m open minded, some other people are only open minded to their own beliefs.
I was thinking this morning, or maybe yesterday that all these AI threads go the same. I even posted in one “wait until DB sees this”, and when he did it was on! I even know who else will chime in. Perhaps a separate AI section. The questions all seem to be the same as well as all the responses. Maybe the threads will go differently without DB and the yes man.
I didn’t go any lower, that was 140 split into 3 x week. So I didn’t think I would be spiking. It left me with DEAD dick, ZERO desire, and unable to cum if I could manage an erection. My prolactin also went over range. I didn’t and don’t want to relive that. That was several months of disappointment and embarrassment.
I remember at the beginning 90-100 a week was enough. Now 3 years later am at 140. 120 was good to but I think I feel better at 140. My prolactin has been just slightly above range all along.
I take daily cialis. Libido and erections all good. Orgasm feels good but the volume of a different story. Good thing my lady doesn’t like the taste.
But being orgasms feel great the volume I decided to leave it alone. Don’t want to screw anything up.
I mentioned trying lower cause many are inclined to think more is better when less could be better.
Agreed. You tried it, it worked for you… it works for the vast majority of people in my opinion, but… that doesn’t mean that’s what everyone has to believe in order to be “open minded”. It means they have to be open to trying that and seeing if it works… if not, try something else. That’s what you did originally, but it isn’t a 1 way street.
Open minded by definition means being open to different ideas and trying different things.
Does this mean I can now ask questions about adding micro amounts of ai’s and get more rounded responses that don’t turn into “you don’t need an ai, E2 doesn’t cause gyno etc etc arguments?”
@Chris_Colucci that was the right decision- nicely put too!
'll update my thread with next labs- but upper “in range” E2 for me is equalling tits and soft erections
Going without an AI worked for me. But that’s only part of it. I meant that when I opened my mind, I started to see why AIs are harmful to men on trt. Why taking an AI and stopping aromatase stops aromatase in the brain and heart WHERE IT IS NEEDED TO PROTECT THOSE ORGANS. This is not a “may work for me but not necessarily for you” deal. Stopping aromatase while on trt is harmful to all men, because you’re taking away the protection that it offers.
The interesting thing about his channel is the number of guys that claim to have dropped their AI and feel worse, then go to another forum and admit to adding the AI back in and feeling better. They’d never say that in his group for fear of being banned
I believe this is because the data hasn’t changed. There’s no new studies (aside from the Indian study testing libido in e2>50pg; that was May 2020). The no AI side has mounds of data that doesn’t always say what they think it does, or they extrapolate too much from small samples or take things out of context.
I’d really love for someone to get 100 guys on TRT, half control e2 let’s say 30-50pg and the other half control for higher, say 60-80pg, and see who’s 1) healthier 2) feels better
Every. Single. Post. In their group pretty much goes like that. The other day someone ask about his 60% HCT level and the advice from several was to drop the AI. He didn’t even say he was taking one lol
