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 Can Arimidex raise your natruel testosterone level?
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| Author | Topic: Can Arimidex raise your natruel testosterone level? | ||
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Cool Novice 
Posts: 33 |
In theory, I think it should. Does it? We've been having a discussion on clomid https://www.elitefitness.com/ubb/Forum1/HTML/057072.html In which it was mentioned that the mechanism clomid works on is basically fooling the body into thinking there is no estrogen, so LHRH gets bumped up. So, since the male body has no way of manufacturing estrogen, only aromitizing it, wouldn't the hypothalamus take the same sort of action in the presence of arimidex? Since if the doses were high enough you would have damn near zero estrogen for the hypothalamus to detect. So I would think it would see this extreme reduction in estrogen and turn up LHRH to get more test to aromitize. Which in turn the arimidex would block the aromitization of. Just a theory. Any validity to it?     | ||
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Amateur Bodybuilder 
Posts: 121 |
I may be on the wrong track but I think I read a post on here not too long ago where eveidence was presented indicating that arimidex was directly inhibitory to LH. Although you are on the right track about your theory. Also, I think males to produce estrogen other than just aromatisation but not much. | ||
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Freak 
Posts: 2201 |
Yes it will lower your E and raise your T levels. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 Related Articles, Books, LinkOut Estrogen suppression in males: metabolic effects. Mauras N, O'Brien KO, Klein KO, Hayes V Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected] We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.
[This message has been edited by ulter (edited March 25, 2001).] | ||
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Elite Bodybuilder 
Posts: 1052 |
J Clin Endocrinol Metab 2000 Sep;85(9):3027-35 Related Articles, Books, LinkOut
Hayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF 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. | ||
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Cool Novice
Posts: 33 |
Awesome. So tell me if I'm wrong here, but couldn't you do a mild, long term cycle of non-steroids like these and have some fairly decent results? Like a cycle of arimidex, clomid, maybe some proviron, and some kind of anti-cortisol? Is this to goofy to work? How mild would the results be? Maybe a cutting cycle or something. [This message has been edited by Jafar (edited March 25, 2001).] | ||
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Elite Bodybuilder
Posts: 1052 |
Well, I don't know how it equates exactly, but if there is a 58% increase in serum test as per ulter's study, and one normally produces, say 70mg/week, that would equate to a level of about 110mg/wk. That would be a very weak IMO. Couple this with the fact that with the drop in estrogen you will also likely see a drop in GH and IGF-1 and perhaps a decrease in the number of androgen receptors and I doubt that it would work very well. But I'm all for someone trying this experiment | ||
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Cool Novice
Posts: 33 |
Bump. | ||
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Amateur Bodybuilder
Posts: 192 |
Good stuff here bros, bump. |
All times are ET (US) | |
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posted March 25, 2001 05:50 PM
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