Daz-69
Bluelighter
- Joined
- Jun 10, 2014
- Messages
- 142
An interesting look at PCT:
As you approach the start of PCT, as your steroids dissipate you introduce an Aromatase Inhibitor. You do this to reduce the amount of estrogen conversion that takes place.
Your externally administered testosterone will drop to nothing and you will not be producing testosterone as you start PCT. So you want to make sure that you have reduced estrogen as well.
This is just going into PCT. You want to create a situation where both estrogen and testosterone will rise together. So the AI of your choice should be used in the last 2 weeks of the cycle and immediately discontinued at the start of PCT.
The choice of SERM and duration may vary but PCT should always start with Clomid. You do not need a huge dose in the first few days.
Here is what to do:
Addendum
Another thing I forgot to mention is don't wait for the steroid ester to completely clear before starting Clomid. Start w/ moderate dosed Clomid EOD or lower dose ED during the time wait for longer esters to clear.
This is relevant for something like Cypionate.... so during the 16 days it takes to clear dose Clomid.
Also HCG is sometimes used but only during the least two weeks before PCT starts. you may choose to dose 1000mcg EOD (5 dosings) for 10 days.
A SERM is not a SERM is not a SERM.
Clomid does more then act as an anti-estrogen in certain tissues. In the pituitary it acts as an estrogen, sensitizing pituitary cells to the actions of gonadotropin-releasing hormone (GnRH). This stimulates release of FSH & LH. Enclomid the active anti-estrogenic component of Clomid is as effective as Clomid in this regard.
Tamoxifen (an anti-estrogen) is completely ineffective.
Clomid mediates the positive effect at the estrogen receptor.
Both Clomid and tamoxifen are almost equally effective at binding to the pituitary estrogen receptor. As noted Tamoxifen has no estrogen mediated effect in terms of an ability to increase GnRH-stimulated release of FSH & LH. What it does is just occupy the receptors...or block them so that E2 or Clomid can not have a positive influence.
That isn't what we want in the first few weeks of PCT. That is why not to use Tamoxifen in those early weeks.
Here is one of several studies demonstrating what I refer to:
As you approach the start of PCT, as your steroids dissipate you introduce an Aromatase Inhibitor. You do this to reduce the amount of estrogen conversion that takes place.
Your externally administered testosterone will drop to nothing and you will not be producing testosterone as you start PCT. So you want to make sure that you have reduced estrogen as well.
This is just going into PCT. You want to create a situation where both estrogen and testosterone will rise together. So the AI of your choice should be used in the last 2 weeks of the cycle and immediately discontinued at the start of PCT.
The choice of SERM and duration may vary but PCT should always start with Clomid. You do not need a huge dose in the first few days.
Here is what to do:
Start with Clomid for three weeks and reduce the dosage and overlap it with Nolva in week four. Dose Nolva for 3 weeks thereafter.
In the first 3 weeks of PCT use insulin everyday or attempt to increase local IGF-1 w/ Mod GRF (1-29)/GHRPs or both. Use GHRH/GHRP everyday
After 7 weeks in the last day of Nolva introduce an AI and run that by itself for three or four days.
Then introduce some lower/moderate Nettle Root extract. What you want to do is slightly increase the free test by occupying just a little SHBG. You don't want to do anything but make a very slight impact. You want to be able to use the Nettle Root for 3 months and have it be effective this entire time AND do not want it to cause shedding! A prostate pinch is not a good sign either.
If your hair starts to shed you either messed up or it is time to stop. See when you increase free test more test will be converted to DHT.
After 3 months drop the nettle root extract. The slight increase in free test helps support strength ever so slightly.
Thats about it. PCTs as you can see are very long. But they are designed to recover from 6 month cycles. PCT is about as long as the cycle.
Then stay off and learn to be natural again for another 6 months or more.
In my opinion this approach can allowed you to fully recover after years of experimentation.
In the first 3 weeks of PCT use insulin everyday or attempt to increase local IGF-1 w/ Mod GRF (1-29)/GHRPs or both. Use GHRH/GHRP everyday
After 7 weeks in the last day of Nolva introduce an AI and run that by itself for three or four days.
Then introduce some lower/moderate Nettle Root extract. What you want to do is slightly increase the free test by occupying just a little SHBG. You don't want to do anything but make a very slight impact. You want to be able to use the Nettle Root for 3 months and have it be effective this entire time AND do not want it to cause shedding! A prostate pinch is not a good sign either.
If your hair starts to shed you either messed up or it is time to stop. See when you increase free test more test will be converted to DHT.
After 3 months drop the nettle root extract. The slight increase in free test helps support strength ever so slightly.
Thats about it. PCTs as you can see are very long. But they are designed to recover from 6 month cycles. PCT is about as long as the cycle.
Then stay off and learn to be natural again for another 6 months or more.
In my opinion this approach can allowed you to fully recover after years of experimentation.
Addendum
Another thing I forgot to mention is don't wait for the steroid ester to completely clear before starting Clomid. Start w/ moderate dosed Clomid EOD or lower dose ED during the time wait for longer esters to clear.
This is relevant for something like Cypionate.... so during the 16 days it takes to clear dose Clomid.
Also HCG is sometimes used but only during the least two weeks before PCT starts. you may choose to dose 1000mcg EOD (5 dosings) for 10 days.
A SERM is not a SERM is not a SERM.
Clomid does more then act as an anti-estrogen in certain tissues. In the pituitary it acts as an estrogen, sensitizing pituitary cells to the actions of gonadotropin-releasing hormone (GnRH). This stimulates release of FSH & LH. Enclomid the active anti-estrogenic component of Clomid is as effective as Clomid in this regard.
Tamoxifen (an anti-estrogen) is completely ineffective.
Clomid mediates the positive effect at the estrogen receptor.
Both Clomid and tamoxifen are almost equally effective at binding to the pituitary estrogen receptor. As noted Tamoxifen has no estrogen mediated effect in terms of an ability to increase GnRH-stimulated release of FSH & LH. What it does is just occupy the receptors...or block them so that E2 or Clomid can not have a positive influence.
That isn't what we want in the first few weeks of PCT. That is why not to use Tamoxifen in those early weeks.
Here is one of several studies demonstrating what I refer to:
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro, E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen, AJP - Endocrinology and Metabolism, Vol 240, Issue 2 125-E130
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M.
Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively.
Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M.
Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively.
Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin
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