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Originally Posted by Animalhouse The information on why too low estrogen is detrimental to recovery is here- http://www.mesomorphosis.com/article...production.htm
as well as this being taught to me by my gym owner a veteran competitor and steroid user.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
As it says current and recent history affects the concentration of Lhrh receptors in the pituitary. therefore very low estrogen during a cycle will have a detrimental effect on recovery-even in the presence of normal levels of Lhrh if receptors are down regulated you will not produce a normal level of Lh and therefore a normal level of testosterone after the cycle. Anti aromatose like femera and anastrozole{arimidex} can lower estrogen a great deal and each persons reaction to a given dosage varies. that is why without blood tests it is just an educated guess how a drug during the cycle is affecting you |
No offense...I'm not trying to start an argument, but just because someone says it, doesn't make it true. Receptor up and downregulation is a dynamic process, which is, in most cases, changing on a minute by minute basis in response to ligand concentrations. The idea that "past history" has any
significant impact on receptor concentrations in the present is pretty far-fetched. Too many generalizations are drawn from these 3rd party articles with no primary literature citations.
However, estrogen levels which are "too low" are not easy to come by while on a cycle containing
test. Even doses of AIs used clinically are not going to drop our estrogen levels below physiological levels in most cases, because we simply are introducing so much aromatizable substrate (
test) into our bodies.
I agree that individual variation in aromatase activity is high, but at doses of .25-.5mg/day of Adex with 10mg/day of
nolva, while someone is using
test at ~500mg/wk, nobody should have their estrogen levels dip below physiological levels.
Just another related tangent for all the high estrogen proponents out there:
J Clin Endocrinol Metab. 2000 Jul;85(7):2370-7. Related Articles, Links
Comment in:
J Clin Endocrinol Metab. 2001 Apr;86(4):1836-8.
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.
nmauras@nemours.org
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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