Book claims Tren shuts down Cortisol Receptors PERMANENTLY

[Zyglamail]

I think the major problem we have here is that people just dont realize receptors have half lives too and are constantly replaced. Look closely at the quote in the first post


"An interesting aspect of all Trenbolone products is their apparent unique ability to permanently shut down existing cortisol receptor-sites. This explains in part the exceptional post-cycle lean mass retention...."

Now, I havent done a lot of research on tren in some time so im not agreeing or disagreeing with the statement, however look at the word existing, this is where people are getting mixed up. If the statement is true then it only applies tothe CR's you allready have and as stated a couple times over now, they will have been replaced many times over by the time your HPTA recovers from the cycle itself.

 

[Andy13]

I think the major problem we have here is that people just dont realize receptors have half lives too and are constantly replaced. Look closely at the quote in the first post


"An interesting aspect of all Trenbolone products is their apparent unique ability to permanently shut down existing cortisol receptor-sites. This explains in part the exceptional post-cycle lean mass retention...."

Now, I havent done a lot of research on tren in some time so im not agreeing or disagreeing with the statement, however look at the word existing, this is where people are getting mixed up. If the statement is true then it only applies tothe CR's you allready have and as stated a couple times over now, they will have been replaced many times over by the time your HPTA recovers from the cycle itself.

That may very well be the case, Zyg.
What I'm saying is that even if this did occur to the extent the original auther would have you believe, I still don't think it contributes much, if at all to muscle building.

Andy

 

[georgie24]

thoughts?

 

[rjl296]

thoughts?

pretty much answered already orb

 

[ireekofawesomeness]

interesting stuff...could there be any way that the shutting down of the existing receptors would cause some sort of a negative rebound a few weeks (or whatever the receptor's half lives are) into post cycle when the new receptors would once again react to the cortisol?

 

[DIVISION]

I heard that protein is good for muscles or something too.

I've also heard that a clitoris will grow if given the right "stimulus"......

Is she a "grower" or a "shower" ?

 

[Jenetic]

however look at the word existing, this is where people are getting mixed up. If the statement is true then it only applies tothe CR's you allready have and as stated a couple times over now, they will have been replaced many times over by the time your HPTA recovers from the cycle itself.

Well said Zyglamail.

The concern should be emphasized on the adrenal cortex secretion of cortisol. Possible but highly unlikely. In order for this to be permanent, there would have to be a permanent surpression of corticotropin releasing hormone (CRH) and/or arginine vasopressin (AVP) which are the primary hypophysiotropic hormones affecting adrenocorticotropin hormone (ACTH) release. ACTH is the principal regulator of cortisol production by the adrenal cortex. Cortisol, the main endogenous glucocorticoid, is synthesized in the adrenal cortex under the exclusive regulation of ACTH. The adrenal cortex produces approximately 25 mg cortisol per day, 0.1 mg aldosterone and 10 mg of the adrenal androgen dehydroepiandrosterone (DHEA). ACTH is the principal regulator of cortisol production by the zona fasciculata while it is of secondary significance in aldosterone and adrenal androgen production.

ACTH stimulates cortisol synthesis and secretion by affecting several steps in the steroidogenesis pathway:

1. ACTH increases the number of low-density lipoprotein (LDL) receptors resulting in increased cholesterol uptake, the precursor for the biosynthesis of all steroid hormones. Indeed, while the adrenal cortex can synthesize cholesterol, almost 80% of the cholesterol used in steroid synthesis derives from sources outside the adrenals.

2. ACTH stimulates the cleavage of the side chain of cholesterol converting it to pregnenolone, the first and rate limiting step in cortisol production. The CYP11A1 gene encodes the cholesterol side-chain cleavage enzyme, cytochrome P450. Expression of CYP11A1 is controlled by ACTH and the steroidogenic factor 1 (SF-1).

3. ACTH hydroxylates pregnenolone to give to 17-OH-pregnenolone, which then travels to the endoplasmic reticulum for conversion to 11-deoxycortisol. 11-deoxycortisol moves back to mitochondria where another hydroxylation takes place at position 21 to produce the final product, cortisol.

Cortisol is not stored in the adrenal cortex but is secreted promptly. The adrenal cortex synthesizes cortisol to maintain its normal serum levels.

Jenetic

 

[georgie24]

damn bro your replies are hot off the fucking press! good shit man

 

[geoboy]

I've also heard that a clitoris will grow if given the right "stimulus"......

Is she a "grower" or a "shower" ?

thats a secret

 

[geoboy]

Well said Zyglamail.

The concern should be emphasized on the Adrenal Cortex secretion of cortisol. Possible but highly unlikely. In order for this to be permanent, there would have to be a permanent surpression of Corticotropin releasing hormone (CRH) and/or Arginine vasopressin (AVP) which are the primary Hypophysiotropic hormones affecting adrenocorticotropin hormone (ACTH) release. ACTH is the principal regulator of cortisol production by the adrenal cortex. Cortisol, the main endogenous glucocorticoid, is synthesized in the adrenal cortex under the exclusive regulation of ACTH. The adrenal cortex produces approximately 25 mg cortisol per day, 0.1 mg aldosterone and 10 mg of the adrenal androgen dehydroepiandrosterone (DHEA). ACTH is the principal regulator of cortisol production by the zona fasciculata while it is of secondary significance in aldosterone and adrenal androgen production. The mechanism of ACTH action follows the classical peptide hormone rules. Indeed, ACTH binds to its receptors located on adrenal cell membranes activating a Gs-protein resulting in an increase of intracellular cyclic adenosine monophosphate (cAMP). ACTH stimulates cortisol synthesis and secretion by affecting several steps in the steroidogenesis pathway: (a) ACTH increases the number of low-density lipoprotein (LDL) receptors resulting in increased cholesterol uptake, the precursor for the biosynthesis of all steroid hormones. Indeed, while the adrenal cortex can synthesize cholesterol, almost 80% of the cholesterol used in steroid synthesis derives from sources outside the adrenals. (b) ACTH stimulates the cleavage of the side chain of cholesterol converting it to pregnenolone, the first and rate limiting step in cortisol production. The CYP11A1 gene encodes the cholesterol side-chain cleavage enzyme, cytochrome P450. Expression of CYP11A1 is controlled by ACTH and the steroidogenic factor 1 (SF-1). (c) ACTH hydroxylates pregnenolone to give to 17-OH-pregnenolone, which then travels to the endoplasmic reticulum for conversion to 11-deoxycortisol. 11-deoxycortisol moves back to mitochondria where another hydroxylation takes place at position 21 to produce the final product, cortisol. Cortisol is not stored in the adrenal cortex but is secreted promptly. The adrenal cortex synthesizes cortisol to maintain its normal serum levels.
Jenetic

Everything that guy just said is Bullshit. Thank You.

J/K.

I couldn't resist a "My Cousin Vinnie" moment (Joe Pesci).

good stuff. so from above it seems that with regard to production (secretion), as well as utilization (receptors), the notion of permanent cortisol-related impairment is unlikely.