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napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
Research Chemical SciencesUGFREAKeudomestic
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsResearch Chemical SciencesUGFREAKeudomestic

Arimidex Boosts Testosterone?

M.O.D

New member
Study Shows That Arimidex Boosts Testosterone



Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V [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12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at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.
 
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