Pat,
LH was not measured in the Incledon study unless they left it out of the full text.
I’ve never seen any convincing research that androst-4-ene-3,6,17-trione is an aromatase inhibitor in humans. Now that Ive seen the in-vivo research, I’m definitely not convinced. I guess if there is cross–reactivity happening the results would be hard to interpret either way. I suppose 6-oxo DHT could have cross reacted as well? IMO, an effective oral aromatase inhibitor would give results similar to the study seen below.
My original point is that 6-oxo would not be conducive to post cycle therapy. The effects on LH/FSH are certainly not positive enough to consider 6-oxo as a “natural” test booster, and whether or not 6-oxo is an aromatase inhibitor is probably a mute point anyway, especially if it converts to its own estrogenic metabolites. (which appear to negatively effect LH in the lower dosed group and FSH in the higher dosed group)
Im sure 6-oxo can be an effective product in and of itself as a performance enhancer, but I don’t believe it’s a good choice for PCT.
-Pp
Reversal of the hypogonadotropic hypogonadism of obese men by administration of the aromatase inhibitor testolactone.
Zumoff B, Miller LK, Strain GW.
Metabolism. 2003 Sep;52(9):1126-8.
Studies from this laboratory have shown that obese men have elevated serum estrogen levels and diminished levels of follicle-stimulating hormone (FSH - follicle stimulating hormone - ) and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and we have hypothesized that it results from feedback suppression of the pituitary by the elevated estrogen levels. We tested this hypothesis by lowering the serum estrogens of 6 health obese men (body mass index [BMI], 38 to 73) by administering the aromatase inhibitor testolactone (1 g daily for 6 weeks). Twenty-four-hour mean serum testosterone rose in every subject, from a mean of 290 +/- 165 ng/dL to a mean of 403 +/- 170 (P <.0003); 24-hour mean serum estradiol decreased in every subject, from a mean of 40 +/- 10.8 pg/mL to a mean of 29 +/- 6.7 (P <.004); and 24-hour mean serum luteinizing hormone (lh - leutenizing hormone - ) increased in every subject, from a mean of 14.3 +/- 4.1 mIU/mL to a mean of 19.3 +/- 5.1 (P <.004). The rise in mean LH was due to an increase in the amplitude of the individual secretory pulses, especially at night. Twenty-four-hour mean serum estrone decreased nonsignificantly, from 48 +/- 14 pg/mL to 39 +/- 6.4, and 24-hour mean serum FSH - follicle stimulating hormone - increased nonsignificantly, from 13.5 +/- 5.3 mIU/mL to 15.0 +/- 5.4. The results are in accordance with the hypothesis, in that inhibition of estrogen biosynthesis (through administration of the aromatase inhibitor testolactone) results in alleviation of the HHG of our obese male subjects.