Is it tru that LETRO can be used in replacement of CLOMID during PCT? SOmeone said this too me, so I wanted verify!
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Is it tru that LETRO can be used in replacement of CLOMID during PCT? SOmeone said this too me, so I wanted verify!
it can be used, though ideally both an AI and a SERM should be usedQuote:
Originally Posted by santacruz05
Quote:
Originally Posted by macrophage69alpha
when did this come about? i thought letro was no good during pct:shrug:
i just been off the boards for awhile and want to know if this is something new....
its nothing new, AI's can effectively restore testosterone production.Quote:
Originally Posted by flabbywussy
Diabetes Obes Metab. 2005 May;7(3):211-5. Related Articles, Links
Letrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadism.
de Boer H, Verschoor L, Ruinemans-Koerts J, Jansen M.
Department of Internal Medicine, Ziekenhuis Rijnstate, Wagnerlaan 55, 6800 TA Arnhem, The Netherlands. [email protected]
BACKGROUND: Morbid obesity is associated with increased estradiol production as a result of aromatase-dependent conversion of testosterone to estradiol. The elevated serum estradiol levels may inhibit pituitary LH secretion to such extent that hypogonadotropic hypogonadism can result. Normalization of the disturbed estradiol-testosterone balance may be beneficial to reverse the adverse effects of hypogonadism. AIM: To examine whether aromatase inhibition with Letrozole can normalize serum testosterone levels in severely obese men with hypogonadotropic hypogonadism. PATIENTS AND METHODS: Ten severely obese men, mean age 48.2 +/- 2.3 (s.e.) years and body mass index 42.1 +/- 2.6 kg/m(2), were treated with Letrozole for 6 weeks in doses ranging from 7.5 to 17.5 mg per week. RESULTS: Six weeks of treatment decreased serum estradiol from 120 +/- 20 to 70 +/- 9 pmol/l (p = 0.006). None of the subjects developed an estradiol level of less than 40 pmol/l. LH increased from 4.5 +/- 0.8 to 14.8 +/- 2.3 U/l (p < 0.001). Total testosterone rose from 7.5 +/- 1.0 to 23.8 +/- 3.0 nmol/l (p < 0.001) without a concomitant change in sex hormone-binding globulin level. Those treated with Letrozole 17.5 mg per week had an excessive LH response. CONCLUSION: Short-term Letrozole treatment normalized serum testosterone levels in all obese men. The clinical significance of this intervention remains to be established in controlled, long-term studies
Clin Endocrinol Metab. 2000 Sep;85(9):3027-35. Related Articles, Links
Comment in:
J Clin Endocrinol Metab. 2000 Sep;85(9):3024-6.
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.
letro will kill your sex drive because of cancelling out all of the estrogen correct?
it can if taken to high a dose .....
I don't like using Letro durring PCT but do like L-dex......... and yes a SERM and AI durring PCT is the best way to restore HPTA functions.
L-dex and Letro both work by the same mechanism but I feel that Letro is too strong and could cause problems after PCT. JMO
To strong at even say .25-.50mg eod or even e3d?
not exactly. but by suppressing aromatase activity in the brain too heavily. (brain estrogen- not systemic estrogen)Quote:
Originally Posted by flabbywussy
anything but clomid for me, it messes up my vision to bad.
the more i learn about letro, the more i like it.
so what dose would you want to run letro at for PCT?
bump
i wouldn't even bother with it because it takes up to 6 weeks to reach stable blood levels. with me it took around 7 weeks!Quote:
Originally Posted by lil swoll
i forget what the half life is, but you'd have to time it perfect so it was out of ur system after pct too.
too much hassle if u ask me:shrug:
Quote:
Originally Posted by flabbywussy
im using letro now during my cycle
so anybody know what dose of letro to run during PCT?
same dose is fine, or you can lower it to as low as 1mg ED. taking a Serm with it will offset any oestrogen deprivation issues that you might otherwise have.Quote:
Originally Posted by lil swoll
Quote:
Originally Posted by macrophage69alpha
Do you man .1mg. Im only taking .5-.75mg ED on cycle.