That I do....
MESO-Rx
Anabolic Steroids
Fun adventures with E2
- Thread starter idmd
- Start date
That I do....
This is how I view it too. While it's always instructive to know what is/is not in the medical literature, at the end of the day I have clomid or HCG and/or T. My degrees of freedom are then limited to dose and frequency.
I'm just trying to do what WORKS.
I'LL give ya some more help. PROLACTIN is the magic number. The one everyone seems to omit around here. E2 have never hurt my wood... Ever...
MY TREE, LIKES E.....
MY TREE, LIKES E.....
foreveryoung
New Member
I'LL give ya some more help. PROLACTIN is the magic number. The one everyone seems to omit around here. E2 have never hurt my wood... Ever...
MY TREE, LIKES E.....
I respectfully disagree with you totally on this
foreveryoung
New Member
I should elaborate.... I've done many experiments with modifying prolactin, most recently with cabergoline, and none of that had anywhere near the improvement that I find with letrozole and this is repeatable over and over again
I hear you and of course your observation is greatly respected!!
But when you consider the POST Orgasm experience is touted as more so prolactin related, you have to wonder what its doing on a 24/7 basis.??!! I also wonder how estrogen levels may be interacting and potentially modulating the effects of Prolactin.?
I have vast experience with NE and dopamine surge I am constantly influxed as a result of my Adderall usage. To separate the two is the difficult part. But I understand it is the NE which creates the orgasmic experience which also happens to coincide with the inability to gain erection.
So I am somewhat UNFAIRLY crossing lines with that said. Whereas the reports of spontaneous orgasms from Caber use and Dopamine coincide I am unclear. Not even sure what dark corner of my mind got me even so focused on Dopamine for this one...
1. I just SUSPECT that Prolactin's involvement with erections is poorly understood. The proof being that BOTH too high E or Too Low is touted as problematic for solid wood, and with no seemingly solid explanation.
2. Clearly, there is some kind of poorly understood relationship that Dop and Prolactin have. Pehaps NE is the missing link?
3. I just see too many guys complaining of lost wood all of the sudden, and with no explanation they can attribute to the holy blood work sheets. But of course you know how I feel about blood serum snapshots...
4. The only thing that I can surely point a finger at in my regiment, other than cardio (which i consider first as ED culpret), is NE. NE appears to be correlated with the action of the drugs like caber, which are apparently used to mitigate prolactin. Dopamine never did anything for my orgasm. NE is more similar to having one or already having had.
5. I have had incredibly high estrogen counts on labs most of my life that I have documented, and they don't correlate with my ED, or not... At least I keep telling myself.. LOL
6. With regard to Prolacin, THERE MUST BE A FINE LINE WALKED. As the borderline between a great orgasm, and already have had one in yur pants and while just walking around exists. ( I think, or did I just unfairly tie these two together in my head)?? But I recall that Spontaneous orgasm IS associated with Caber Use. If that fine line exists, it may explain the poor response with the caber. Did you experience any of the reported earth shattering orgasms when taking the caber? Whats your take on that?
I may have something off there, I am spent.
But when you consider the POST Orgasm experience is touted as more so prolactin related, you have to wonder what its doing on a 24/7 basis.??!! I also wonder how estrogen levels may be interacting and potentially modulating the effects of Prolactin.?
I have vast experience with NE and dopamine surge I am constantly influxed as a result of my Adderall usage. To separate the two is the difficult part. But I understand it is the NE which creates the orgasmic experience which also happens to coincide with the inability to gain erection.
So I am somewhat UNFAIRLY crossing lines with that said. Whereas the reports of spontaneous orgasms from Caber use and Dopamine coincide I am unclear. Not even sure what dark corner of my mind got me even so focused on Dopamine for this one...
1. I just SUSPECT that Prolactin's involvement with erections is poorly understood. The proof being that BOTH too high E or Too Low is touted as problematic for solid wood, and with no seemingly solid explanation.
2. Clearly, there is some kind of poorly understood relationship that Dop and Prolactin have. Pehaps NE is the missing link?
3. I just see too many guys complaining of lost wood all of the sudden, and with no explanation they can attribute to the holy blood work sheets. But of course you know how I feel about blood serum snapshots...
4. The only thing that I can surely point a finger at in my regiment, other than cardio (which i consider first as ED culpret), is NE. NE appears to be correlated with the action of the drugs like caber, which are apparently used to mitigate prolactin. Dopamine never did anything for my orgasm. NE is more similar to having one or already having had.
5. I have had incredibly high estrogen counts on labs most of my life that I have documented, and they don't correlate with my ED, or not... At least I keep telling myself.. LOL
6. With regard to Prolacin, THERE MUST BE A FINE LINE WALKED. As the borderline between a great orgasm, and already have had one in yur pants and while just walking around exists. ( I think, or did I just unfairly tie these two together in my head)?? But I recall that Spontaneous orgasm IS associated with Caber Use. If that fine line exists, it may explain the poor response with the caber. Did you experience any of the reported earth shattering orgasms when taking the caber? Whats your take on that?
I may have something off there, I am spent.
Back on track with your thread Title as related to E2...
And Correct me as perhaps I am misunderstanding the conditions that are the basis of this thread...?
But you MUST consider. And you just discontinued TRT was the origin of these feelings, physical symptoms, and this thread? Right? While you are interpreting that you are low on testosterone, and correlating with low on androgens and high on E. Are you not truly LOW on E as a result of discontinuing the TRT??
If you have done all that training and leaned up to the extent you have, and now you have cut the supply of exogenous testosterone. Then I would speculate you are lower on Estrogen, Proportionately, than ever before.??
And Correct me as perhaps I am misunderstanding the conditions that are the basis of this thread...?
But you MUST consider. And you just discontinued TRT was the origin of these feelings, physical symptoms, and this thread? Right? While you are interpreting that you are low on testosterone, and correlating with low on androgens and high on E. Are you not truly LOW on E as a result of discontinuing the TRT??
If you have done all that training and leaned up to the extent you have, and now you have cut the supply of exogenous testosterone. Then I would speculate you are lower on Estrogen, Proportionately, than ever before.??
Last edited:
foreveryoung
New Member
bbc3 I have done a lot of experimenting with the "anti prolactins" over the years, and have always been disappointed, but I still wonder about them and might still do some experimenting..... they have been extremely far from the hyped claims about powerful multiple orgasms and such, that is for sure
side effects are strong on these drugs too, to the point that bad effects outweigh any subtle good effects, if any
I might need to do a combination experiment, where I have e2 low and run dostinex and see how that works, but will see....
in the past I found some effect from bromocriptine, but bad sides... dostinex, hydergine, selegeline, all gave sides without real benefits, for sure not consistent reliable benefits
that is not to say that it is possible that I didn't happen upon the magical protocol with everything else synergized, but it sure isn't a simple fix to anything for me
side effects are strong on these drugs too, to the point that bad effects outweigh any subtle good effects, if any
I might need to do a combination experiment, where I have e2 low and run dostinex and see how that works, but will see....
in the past I found some effect from bromocriptine, but bad sides... dostinex, hydergine, selegeline, all gave sides without real benefits, for sure not consistent reliable benefits
that is not to say that it is possible that I didn't happen upon the magical protocol with everything else synergized, but it sure isn't a simple fix to anything for me
What I find interesting....and I know this isn't supported in the literature is my history is HIGHLY suggestive of being E2 related.
Before starting TRT with a tT of 196 and E2 of 22 my erections were really good - let's say erections 85% and libido 10%.
I then tried AI mono-therapy for 3 months and my tT went to 500 and my E2 was undetectable. 100% of the time my erections were great at 100% but libido was still 10%.
For 6 months after that I was on TRT + AI with a tT of 700 and E2 around 10. Erections were 100% and libido still 10%.
Over the next 2 months I reduced my dose of AI. tT stayed around 700 and E2 rose to 30. Erections at 85% and libido 50%.
Added hCG last month with tT same as always but E2 into 40's. Erections now 50% and libido 80%. If I take an AI erections get better but still not back to 100%. I never anticipated adding hCG would effect my erection quality and only went for blood work after the SD issues started.
In summary - when my E2 is way low erections are good and libido low. When E2 is around 30 libido starts coming up but erections start getting worse. By the time E2 is in the 40's erections are bad and libido is good. These findings have been 100% consistent with E2 levels.
Questions:
1. Do AI's cross the blood-testicular barrier? Do they effect E2 made by the testes?
2. When my E2 was really low my SHBG became low too and my fT went top of range. Could this be SHBG related? E2 has come up and so too has SHBG and my fT has gone down? Presumably if this has happened (didn't test it with my latest blood work) my unbound E2 should be lower too - wouldn't the expectation be less E2 influence.
I've got no dog in this fight other than I like libido boost and full feeling testicles hCG provides - if I can figure out how to improve my erections I'd be 100% happy with my TRT.
Before starting TRT with a tT of 196 and E2 of 22 my erections were really good - let's say erections 85% and libido 10%.
I then tried AI mono-therapy for 3 months and my tT went to 500 and my E2 was undetectable. 100% of the time my erections were great at 100% but libido was still 10%.
For 6 months after that I was on TRT + AI with a tT of 700 and E2 around 10. Erections were 100% and libido still 10%.
Over the next 2 months I reduced my dose of AI. tT stayed around 700 and E2 rose to 30. Erections at 85% and libido 50%.
Added hCG last month with tT same as always but E2 into 40's. Erections now 50% and libido 80%. If I take an AI erections get better but still not back to 100%. I never anticipated adding hCG would effect my erection quality and only went for blood work after the SD issues started.
In summary - when my E2 is way low erections are good and libido low. When E2 is around 30 libido starts coming up but erections start getting worse. By the time E2 is in the 40's erections are bad and libido is good. These findings have been 100% consistent with E2 levels.
Questions:
1. Do AI's cross the blood-testicular barrier? Do they effect E2 made by the testes?
2. When my E2 was really low my SHBG became low too and my fT went top of range. Could this be SHBG related? E2 has come up and so too has SHBG and my fT has gone down? Presumably if this has happened (didn't test it with my latest blood work) my unbound E2 should be lower too - wouldn't the expectation be less E2 influence.
I've got no dog in this fight other than I like libido boost and full feeling testicles hCG provides - if I can figure out how to improve my erections I'd be 100% happy with my TRT.
Yes I have heard reports of heart issues with these so I WONT touch them
I was thinking that Dosinex IS Bromo... Or did I get that wrong? Still, I understand the Cabergoline is the one reported to have the most profound effect of sex type response hands down. And make no mistake if you are even dosing a small amount weekly, it takes less than a month to reach full plasma concentration as the half-life is pretty long. This "commitment" when experimenting with this type drug is my primary motivator for leaving them alone..
Am I getting any of that information mixed up??.
@ OP - Sorry ID, did not mean to "semi-jack"... So then you are still on TRT. Did you bail out the discontinuation, or did it never take place.??
One point I would like to make (since you are still supplementing testosterone) is that I believe you are dealing with 2 STAGES of estrogen with regard to E2 involvement. (1) The Principle and direct interaction with testosterone at the point of the initial converting receptor, and (2)the result of the E2 circulation and cellular interaction beyond the point of origin. It happens, else we would not be able to measure it in blood serum. Then you have to somehow SPALCULATE the involvement of E3 derivatives potentially hogging sites, as well as CLEARANCE potential issues.
You are discussing the involvement of AI's which also does not account for E1 to E2 conbobulation as a potential biological reponse to diminshed E availability, as we can assume that the enzyme the AI is involving with pertains to testosterone more so. Still you have to project the body will compensate with EXPERIENCE simply by producing MORE Aromatase enzymes thus effectively nullifying the AI regardless.
So are you tracking your results based on drug experience (time on) as well.? And how your scenarios might apply with this considered?
I was thinking that Dosinex IS Bromo... Or did I get that wrong? Still, I understand the Cabergoline is the one reported to have the most profound effect of sex type response hands down. And make no mistake if you are even dosing a small amount weekly, it takes less than a month to reach full plasma concentration as the half-life is pretty long. This "commitment" when experimenting with this type drug is my primary motivator for leaving them alone..
Am I getting any of that information mixed up??.
@ OP - Sorry ID, did not mean to "semi-jack"... So then you are still on TRT. Did you bail out the discontinuation, or did it never take place.??
One point I would like to make (since you are still supplementing testosterone) is that I believe you are dealing with 2 STAGES of estrogen with regard to E2 involvement. (1) The Principle and direct interaction with testosterone at the point of the initial converting receptor, and (2)the result of the E2 circulation and cellular interaction beyond the point of origin. It happens, else we would not be able to measure it in blood serum. Then you have to somehow SPALCULATE the involvement of E3 derivatives potentially hogging sites, as well as CLEARANCE potential issues.
You are discussing the involvement of AI's which also does not account for E1 to E2 conbobulation as a potential biological reponse to diminshed E availability, as we can assume that the enzyme the AI is involving with pertains to testosterone more so. Still you have to project the body will compensate with EXPERIENCE simply by producing MORE Aromatase enzymes thus effectively nullifying the AI regardless.
So are you tracking your results based on drug experience (time on) as well.? And how your scenarios might apply with this considered?
Last edited:
Qualitatively right, but quantitatively what is the NET result? If you still have erectile strength (ES) issues, then presumably the E2 influence is still dominant. Maybe in a given mix of key factors (SHBG, tT, etc) there is a critical level for E2 above which ES becomes an issue. This may also be the case with the addition of HCG to your protocol. It gives your tT a boost via your own production of T but it also increases your E2.
Oh with deference DOC, in this instance the the OP is IDster and from what I've observed he is not a BROster.
How many "bros" would go online, locate an applicable article, ascertain the articles relevance by READING IT, and finally post the citation on Meso for debate. Very few!
Although like yourself, I disagree with his conclusions, I applaud the effort little of which is characteristic of "bro speak" or science, IME.
Jimmy
It's mates l
How many "bros" would go online, locate an applicable article, ascertain the articles relevance by READING IT, and finally post the citation on Meso for debate. Very few!
Although like yourself, I disagree with his conclusions, I applaud the effort little of which is characteristic of "bro speak" or science, IME.
Jimmy
It's mates l
So what's your take on this study Dr. S? How bout you Dr. Jim?
Similar threads
