AI needed in 1/6 men on clomid

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Nelson Vergel

Founder, ExcelMale.com
COMBINATION THERAPY WITH AN AROMATASE INHIBITOR IS NEEDED IN ONE OUT OF SIX HYPOGONADAL MEN TREATED WITH CLOMIPHENE CITRATE


Introduction and Objectives
Clomiphene citrate (CC) is a selective estrogen receptor modulator used off label to stimulate endogenous testosterone production in hypogonadal men. In some patients, CC leads to elevated estradiol levels, necessitating combination therapy with an aromatase inhibitor, such as anastrozole (AZ). The objectives of this project were to (1) determine the previously unreported rate of conversion from CC monotherapy to combination therapy with CC+AZ in hypogonadal men, and (2) test the hypothesis that men needing combination therapy with CC+AZ would have higher body mass index (BMI) compared to men maintained on CC monotherapy.

Methods
We obtained institutional review board approval and performed a retrospective chart review of hypogonadal men treated with CC by a single urologist at our institution between 2006 and 2013. Response to CC therapy was monitored with serum hormones; when estradiol became elevated above the reference range, AZ therapy was added.

Results
We identified 271 hypogonadal men treated with CC and followed for an average of 28 months (SD = 19). Following initiation of CC therapy, 46 (17%) patients required combination therapy with CC+AZ due to elevated estradiol levels. While age and race were similar between groups, the average BMI of patients who converted to CC+AZ combination therapy was significantly higher than those patients who remained on CC monotherapy (Table 1, p < 0.001).

Conclusions
Following initiation of therapy with CC, 17% of hypogonadal men developed elevated estradiol levels, necessitating combination therapy with an aromatase inhibitor. Men requiring the addition of AZ were obese (BMI > 30 kg/m2), implicating increased peripheral aromatization of androgens to estrogens as a contributor to elevated estradiol levels in these men during CC therapy.

The Journal of Urology
Volume 191, Issue 4, Supplement, April 2014, Pages e528–e529

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DHM

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Ive been on Clomid/Anastrazole for almost 2 years. Clomid keeps me from falling asleep at the dinner table, anastrazole keeps the bloating down.

Labs are optimal (600-900 Total T with good E2 ratio to Free T, normal SHBG) 12.5 mg clomid/4mg AI weekly.

I feel mediocre on this regimen and need to supplement in Bronkaid and Nuvigil daily to feel bright eyed.

Two or three things Ive considered:

- Clomid bio-product and its binding properties: Big numbers but I feel shitty, does Clomid cause contamination of the assay in some way? The rebuttal being "Well my nuts are big so they're still working". LH and other labs report increase as well, so not likely.

- Endogenous T not binding receptors optimally: Think of the type II diabetes concept, lots of clomid induced T being measured, what's going on?

- Endogenous T efficiency decreased, especially dopamine/brain T pathways: I feel regular with a combined therapy of SERMS, AI, and NOOtropics. If my reports are about the same as exogenous T users (TD or Inj) does exogenous T carry different binding properties/ efficiencies that ultimately produce a new dopamine response?


Im rambling while getting my health back, its been a long road. I use to be an 8 day/week athlete, now I just read about it! Never thought I'd be out of shape or let my health go ever in my life.
 
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