Why have I not seen talk on this. I posted a case of a man taking dhea nd icnreasing his estradiol and reducing his adiolg by half. No one seems to care.
PURPOSE:
To evaluate androgen production and metabolism during controlled ovarian hyperstimulation.
METHODS:
Five women, aged 33-42, were studied. All participants were undergoing controlled ovarian hyperstimulation with gonadotropin-releasing hormone agonist and human menopausal gonadotropins. Serum estradiol, estrone, androstenedione, testosterone, 3 alpha-androstanediol glucuronide, and sex hormone-binding globulin levels were measured at 6 time points during the cycle.
RESULTS:
The levels of all steroids increased significantly from baseline during controlled ovarian hyperstimulation. Mean total testosterone levels increased from 0.29 +/- 0.05 ng/mL to 0.58 +/- 0.07 ng/mL after gonadotropin stimulation. Sex hormone-binding gonadotropin levels increased from 50 +/- 16 nM to 73 +/- 12 nM after gonadotropin stimulation. Estrone/androstenedione and estradiol/testosterone ratios, reflecting the aromatase pathway, increased whereas 3 alpha-androstanediol glucuronide/androstenedione and 3 alpha-androstanediol glucuronide/testosterone ratios, reflecting 5 alpha-reductase activity, decreased.
CONCLUSIONS:
Controlled ovarian hyperstimulation with human menopausal gonadotropins results in increased serum testosterone and androstenedione levels. Whereas there is an enhancement in androgen metabolism by aromatase, 5 alpha-reductase activity with regard to androgen metabolism is diminished.
Can someone else read this study. And add your input it is a little complex because of the many factors.
ncbi.nlm.nih.gov/pmc/article … 345279.pdf
Our data are consistent with the enhancement of
the aromatase pathway during controlled ovarian hyperstimulation, whereas the 5®-reductase pathway
was inhibited. This demonstrates that androgens are
preferentially metabolized via the aromatase pathway during controlled ovarian hyperstimulation. Although it is not surprising that the aromatase pathway
predominates, it is interesting that 5®-reductase activity is suppressed with regard to androgen metabolism.
This suggests that the actual conversion of A and T to
DHT is not solely substrate dependent. It is possible
that 5®-reductase activity is modulated by competitive inhibitors, such as progesterone (21). Krieg et al.
(22) investigated 5®-reductase in benign prostatic hyperplasia and found the mean inhibitor constants of
progesterone, E1, and E2, with regard to 5®-reductase
activity, to be 0.11, 15.5, and 5.1, respectively.
We conclude that although androgen levels increase during controlled ovarian hyperstimulation,
androgen metabolism engenders a less androgenic milieu. This is due to increased aromatase activity, and
increased SHBG levels, which decrease free T levels.
By contrast, androgen metabolism by 5®-reductase is
decreased, possibly as a result of the presence of high
levels of other steroids.