Why wouldnt you just take test cyp daily to find a dose that doesnt drastically raise e2 then fill the void with mast or primo which even if e2 was slightly elevated the primo could help with that then there isnt much need for an AI. All it boils down to is drawing labs and experimenting, but in my mind that is the route to go.
MESO-Rx
Anabolic Steroids
Non-aromatising substitute for testosterone
- Thread starter HUGE McBIGLARGE
- Start date
HUGE McBIGLARGE
Member
It would certainly be easier to take the most testosterone I can tolerate without an AI then stuff a DHT derivative in and call it a day.
But as mast and primo don’t aromatise, and they exert some anti-estrogenic effects, what do I gain from them? An androgen that doesn’t act like testosterone or DHT, and an anti-estrogen that doesn’t act quite like an AI. To me, that sounds potentially more complicated to “dial in” than throwing letrozole at my e2.
I’ll probably try mast/primo again at some point and assess the feels and see how I get on. But fuck low e2. This shit is horrible.
I hear ya have you tried daily injections to see if there is any difference? I mean im not sure what your goal is whether to blast, cruise or trt..but I just think leveraging test and finding out what that is by doing daily injections and drawing labs to find out what that dose is while keeping your e2 in range then filling the rest of the anabolic void with primo or mast if necessary ideally to where u are running little to no AI.
HUGE McBIGLARGE
Member
Daily injections made no difference to my e2.
I’m looking for a high amount of androgenism. I was on 142mg testosterone per week prescribed by my doctor for 12 months when I first started, and my total testosterone was around 950ng/dl, e2 was 90pmol/l, and I felt pretty crappy. I switched to transdermal testosterone, my total testosterone nearly doubled, my DHT went sky high, and my e2 quadrupled and I felt a lot better for it.
I’ve tried having my testosterone in range a number of times and it kills my libido. All of the “want” for sex is there, but none of the “desire”. I look at my very feminine 2D4D ratio and suspect something has been wrong with me since a fetus.
Thanks for the reply.
Elektrobot
Member
I didn't find any mention of your shbg in the thread
Have you been checking it in your bloodwork?
HUGE McBIGLARGE
Member
It’s around 30-55nmol/l. Average being around 40nmol/l. So a little on the high side. I dont usually mention it as my total testosterone is usually capped out.
Elektrobot
Member
I had an e2 of 95 on 100mg cyp /week. High shbg
I switched to prop december 3rd and had bloodwork done today to see if a shorter ester makes any difference for me. I'll post back here with the result when I get it. It will be interesting to see if a shorter ester makes any difference.
I'm wondering if high shbg combined with longer esters cause higher levels for some people
bananafeet
Member
Does the choice of AI make a difference? I was started on aromasin/exemestane and never used another type of AI or SERM.
When I was a fatty and started TRT I was on 12.5mg of aromasin 2x per week for 175mg test E per week.
Never really fussed with my E2 that much. I was on 500mg Test E with 12.5mg 3x per week of exemestane. Now I'm on 1000mg test E and 12.5mg 4x per week of exemestane.
I've read anecdotes that arimadex and letrazole can cause rebound E2. I'm pretty sure it's quite difficult to nuke estrogen completely with aromasin.
Am I missing something?
When I was a fatty and started TRT I was on 12.5mg of aromasin 2x per week for 175mg test E per week.
Never really fussed with my E2 that much. I was on 500mg Test E with 12.5mg 3x per week of exemestane. Now I'm on 1000mg test E and 12.5mg 4x per week of exemestane.
I've read anecdotes that arimadex and letrazole can cause rebound E2. I'm pretty sure it's quite difficult to nuke estrogen completely with aromasin.
Am I missing something?
HUGE McBIGLARGE
Member
To my understanding, yes. If I recall correctly, letrozole can pass more easily into organs such as the brain, liver, and testes than anastrozole. And anastrozole does the same more easily than exemestane. Estradiol enters organs as well, so what this actually affects is debatable.
Exemestane is also meant to be the most lipid-friendly at equivalent doses to letrozole or anastrozole. But the magnitude to which this is true is probably small.
If I recall correctly, exemestane is “suicidal”, where it permanently binds to the aromatase enzyme and the body must produce more aromatase in order for aromatisation to rise.
Letrozole and anastrozole are not suicidal. Meaning they can unbind from the aromatase enzyme. The body may compensate when aromatase is low by producing more than it ordinarily would. By ceasing letro/anastrozole abruptly, you can free all of the bound aromatase, which when combined with the greater aromatase production can yield big e2 jumps. That’s the theory, anyway.
As for exemestane not crashing e2 I’m not sure. Maybe something to do with it not passing into peripheral tissues as easily as letro/anastrozole, meaning peripheral aromatisation is always somewhat retained.
