Femara in PCT?

[liftr486]

can u use femara in a PCT that includes hcg, clomid, and nolvadex?...after my cycle, my estrogen levels have been slightly elevated and im looking to lower it...will the femara hinder my recovery?

Buy Femara

 

[DrJMW]

Yes, Femara, armidex, and aromasin will hinder recovery. You actually need to increase your estrogen levels back to normal. The clomid/nolvadex, in addition to stimulating LH production, will block estrogen receptors.

 

[Mr. Black]

You actually need to increase your estrogen levels back to normal. .

I was under the impression that most users had increased estrogen levels at the end of a cycle? Thus lowering e would actually help increase endogeneous test production. I know there has been a study posted (theres one around can't remember where) done with arimidex that proves this exact mechansim. it actually increased the test subjects testosterone aorund 50%

 

[Mr. Black]

Here it is...

Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback.

Hayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF Jr.

Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA. [email protected]

The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 microg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 +/- 10 to 52 +/-2 pmol/L, P < 0.005) and IHH men (118 +/- 23 to 60 +/- 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 +/- 6% in NL vs. 56 +/- 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 +/- 9 vs. 58 +/- 6% for LH, P = 0.07; and 85 +/- 6 vs. 41 +/- 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 +/- 0.9 to 14.0 +/- 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 +/- 0.7 to 8.4 +/- 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 +/- 2.4 vs. 70 +/- 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH.

 

[argent]

I thought arimidex was good during PCT along with the SERM's and HCG?

 

[DrJMW]

If you have used an aromatase inhibitor with your aromatizing AAS in a bulking cycle, you will find your estradiol levels rather low. I see this all the times on blood tests. When you stop the aromatizing AAS intake along with aromatase inhibitor, you switch to HCG/Nolvadex for PCT. As the exogenous Testos leaves the system, your natural Testos level will begin to raise. At this point, your estrogen levels will start to increase. The Nolvadex will not only stimulate LH release, but it will block the estrogen rebound. Your liver and kidneys will work to remove the excess estrogen created during your recovery phase. I believe that you want your estradiol levels to return to normal. Everybody needs some estrogen (although I am sure some will debate this). The important thing is the Testos:Estradiol ratio.

 

[argent]

So is estrogenn part of the feedack loop in the hpta? I thought it was just a product of aromitization.