DHT levels and ARIMIDEX.

[Stew Meat]

Abdominal fat storage or love handle fat storage is not from estrogen. Gender specific fat storage is due to higher concentrations of beta receptor adipocytes... Adipose tissue in the abs are not estrogen sensitive like legs and butt...


Someone correct me if I'm wrong... I am not 100% on this.


I don't think your fat storage is caused by increased estrogen and I STRONGLY suggest against using antiestrogens when you don't need them.

You CAN NOT reduce your body's natural estrogen levels. Your body is geneticly predisposed with feedback controls and various mechanisms for maintaining the proper testosterone to estrogen ratios. Depleting your body of its necessary concentration of estrogen by competitive inhibition of aromitase enzymes is a BAD idea.


-Stew

 

[Jon De]

Stew,

From my experience I’d have to agree with your comment about the body’s pre-programmed test-est ratio. I just checked my blood test results and noticed that my test level increased 56% while my E2 level increased 53%. So if I increase my T-level further, my E level will continue to rise proportionately. That sucks.

So without resorting to anti-E’s, are there any other options or am I just stuck with a lifetime of high estrogen levels?

-Jon

 

[Jon De]

Stew,

I just read the study on Arimidex in the post (Read! Arimidex!). In this case it looks like Arimidex was given to normal individuals without artificially high estrogen levels and only positive results were noticed. Does this information have any effect on the advice that gave earlier in this post?

Thanks,
-Jon

 

[wilson6]

arimidex

Stew:

Have you seen this article?

Estrogen suppression in males: metabolic effects.

JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM. vol. 85, no. 7 (2000 Jul): 2370-7.

Abstract
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 First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between.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.

I have to get the whole article and see if they measure DHT and also any period following treatment to see if there was a rebound. If you're theory regarding upregulation of aromatase mRNA and protein is correct, then E2 should come back to baseline at some point if the dose of arimidex is not altered and there should be a rebound effect for several weeks following arimidex treatment.

W6

 

[cockdezl]

STEW, do you have any evidence that aromatase will be upregulated when using Anti-estrogen's or aromatase-inhibitors? I would be interested. I have never heard, anecdotally, of any type of estrogenic rebound after the use of say, Tamoxifen or Clomiphene.

Also, where did you read that the body has a programmed Test/Estrogen ratio?

"From my experience I’d have to agree with your comment about the body’s pre-programmed test-est ratio. I just checked my blood test results and noticed that my test level increased 56% while my E2 level increased 53%. So if I increase my T-level further, my E level will continue to rise proportionately. That sucks."

JOHN, in males, testosterone is the precursor to estrogen, since estrogen is NECESSARY for health even in men (the cardiovascular protection that is seen with testosterone therapy is due to aromatization into estrogen). So, yes, if you increase testosterone concentrations, then you increase estrogen concentrations, unless you inhibit aromatase.