ExcelMale
Menu
Home
What's new
Latest activity
Forums
New posts
Search forums
What's new
New posts
Latest activity
Videos
Lab Tests
Doctor Finder
Buy Books
About Us
Men’s Health Coaching
Log in
Register
What's new
Search
Search
Search titles only
By:
New posts
Search forums
Menu
Log in
Register
Navigation
Install the app
Install
More options
Contact us
Close Menu
Forums
Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
Pituitary restart while on TRT: promising initial results with GnRH plus enclomiphene
JavaScript is disabled. For a better experience, please enable JavaScript in your browser before proceeding.
You are using an out of date browser. It may not display this or other websites correctly.
You should upgrade or use an
alternative browser
.
Reply to thread
Message
<blockquote data-quote="Cataceous" data-source="post: 213267" data-attributes="member: 38109"><p>I did try another experiment with reduced enclomiphene and minimal TRT dosing. Unfortunately the results are inconclusive. This was a three month period in which I injected 4.5 mg testosterone propionate daily, with no other ester. I reduced the enclomiphene dosing to 12.5 mg every four days. The GnRH regimen was unchanged. There were no problems with testicular discomfort this time. The subjective results were adequate, but lacking when compared to the <a href="https://www.peaktestosterone.com/forum/index.php?topic=16143.0" target="_blank">standard protocol</a> that uses an ester blend and EOD enclomiphene. With the standard protocol I've had libido, cognition, mood and sexual function be consistently good for months. In this experiment there was some unevenness in libido, mood and sexual function, and I felt that cognition was somewhat degraded.</p><p></p><p>There was an interesting correlation with pain sensitivity. Earlier this year I started taking some palmitolyethanolamide (PEA) to see if it would help with chronic pain from a damaged joint. Within weeks of starting the pain was substantially lessened, and remained that way until I tried this experiment. During the experiment I realized that the pain had returned to pre-PEA levels. I just assumed the joint had further degraded. But a few weeks after I ended the experiment and returned to the normal protocol the pain abruptly lessened. Is there a causal relationship? I don't know. There's substantial research linking estrogen and pain sensitivity—either as promoter or inhibitor, depending on the study. If the connection is real in this case then it could potentially be linked to enclomiphene's antagonism of estrogen receptors. The skeptic in me notes that it's only E4D versus EOD enclomiphene dosing—should that be enough to make such a pronounced difference? In any case, the hypothesis to test is that PEA and enclomiphene work synergistically to reduce pain sensitivity. This is not a trivial reduction—I'd put it at two to three points on a ten-point scale.</p><p></p><p>Before resuming my standard protocol I had lab work done at a pre-injection trough. At 430 ng/dL, total testosterone was much higher than expected. This was surprising and disappointing. Based on previous measurements with propionate the trough was expected to be in the 200s ng/dL. It was also the intent of the experiment to see if lower troughs would help to maintain HPTA activity. Given the high trough, it's less surprising that LH was undetectable. Another inexplicable anomaly was having total estradiol in the mid-40s, which yields the highest E2/T ratio I've ever seen.</p><p></p><p>If the subjective results had been better then I might have continued the experiment and tried to better understand things with additional testing. But I knew that my standard protocol was preferable, and thus I was not motivated to continue this line of research.</p></blockquote><p></p>
[QUOTE="Cataceous, post: 213267, member: 38109"] I did try another experiment with reduced enclomiphene and minimal TRT dosing. Unfortunately the results are inconclusive. This was a three month period in which I injected 4.5 mg testosterone propionate daily, with no other ester. I reduced the enclomiphene dosing to 12.5 mg every four days. The GnRH regimen was unchanged. There were no problems with testicular discomfort this time. The subjective results were adequate, but lacking when compared to the [URL='https://www.peaktestosterone.com/forum/index.php?topic=16143.0']standard protocol[/URL] that uses an ester blend and EOD enclomiphene. With the standard protocol I've had libido, cognition, mood and sexual function be consistently good for months. In this experiment there was some unevenness in libido, mood and sexual function, and I felt that cognition was somewhat degraded. There was an interesting correlation with pain sensitivity. Earlier this year I started taking some palmitolyethanolamide (PEA) to see if it would help with chronic pain from a damaged joint. Within weeks of starting the pain was substantially lessened, and remained that way until I tried this experiment. During the experiment I realized that the pain had returned to pre-PEA levels. I just assumed the joint had further degraded. But a few weeks after I ended the experiment and returned to the normal protocol the pain abruptly lessened. Is there a causal relationship? I don't know. There's substantial research linking estrogen and pain sensitivity—either as promoter or inhibitor, depending on the study. If the connection is real in this case then it could potentially be linked to enclomiphene's antagonism of estrogen receptors. The skeptic in me notes that it's only E4D versus EOD enclomiphene dosing—should that be enough to make such a pronounced difference? In any case, the hypothesis to test is that PEA and enclomiphene work synergistically to reduce pain sensitivity. This is not a trivial reduction—I'd put it at two to three points on a ten-point scale. Before resuming my standard protocol I had lab work done at a pre-injection trough. At 430 ng/dL, total testosterone was much higher than expected. This was surprising and disappointing. Based on previous measurements with propionate the trough was expected to be in the 200s ng/dL. It was also the intent of the experiment to see if lower troughs would help to maintain HPTA activity. Given the high trough, it's less surprising that LH was undetectable. Another inexplicable anomaly was having total estradiol in the mid-40s, which yields the highest E2/T ratio I've ever seen. If the subjective results had been better then I might have continued the experiment and tried to better understand things with additional testing. But I knew that my standard protocol was preferable, and thus I was not motivated to continue this line of research. [/QUOTE]
Insert quotes…
Verification
Post reply
Share this page
Facebook
Twitter
Reddit
Pinterest
Tumblr
WhatsApp
Email
Share
Link
Sponsors
Forums
Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
Pituitary restart while on TRT: promising initial results with GnRH plus enclomiphene
This site uses cookies to help personalise content, tailor your experience and to keep you logged in if you register.
By continuing to use this site, you are consenting to our use of cookies.
Accept
Learn more…
Top