Ulter,
I assume your using teslac abstracts as an example because you agree that all steroidal based aromatase inhibitors share the same properties. Fair enough.
I also assume that you know estrogen is not the only hormone involved in the negative feedback loop?
Both studies you refer to are using men with an abnormaly high estrogen level. I have no doubt that reducing super-physiological estrogen to normal levels will increase testosterone every time, but this could be achieved with any AI.
Unfortunately we are probably not dealing with obese men who have abnormal levels of estrogen. I presume that most members of this board are in fairly good shape and are probably using some kind of AI during a cycle, and therefore begining PCT with a semi-normal estrogen level.
If this is the case, less estrogen does not always mean more testosterone, and when you bring estrogen down to sub-physiological levels you begin to have problems with leydig responsiveness as well as direct androgen receptor suppression coming from a molecule that …. well…. acts like an androgen.
Aromatase inhibitors prevent granulosa cell differentiation: an obligatory role for estrogens in luteinizing hormone receptor expression
M Knecht, AM Brodie, and KJ Catt
Endocrinology, Sep 1985; 117: 1156.
Effect of an inhibitor of aromatization, 1,4,6 androstatriene-3,17-dione (ATD) on LH release and steroid binding in hypothalamus of adult female rats.
Exp Brain Res. 1986;64(3):407-10.
Slama A, Gogan F, Sarrieau A, Vial M, Rostene W, Kordon C.
Now, I know you have plenty of product testers and friends on this board who may say otherwise, but from the anecdotal reports Ive seen (including my own experiences), ATD kills sex drive, negatively influences cholesterol profiles and “dry’s” out your joints… all related to having sub-physiological estrogen levels from an overly powerful steroidal AI.
The studies with rats don’t show a positive result either. ATD hurts fertility and it even appears that it promotes homosexuality…..
Antifertility effects of an aromatase inhibitor, 1,4,6-androstatriene- 3, 17-dione
AM Brodie, JT Wu, DA Marsh, and HJ Brodie
Endocrinology, Jan 1979; 104: 118.
Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.
ME Kaplan and MY McGinnis
Horm Behav, Mar 1989; 23(1): 10-26.
Behavioral action of estrogen in male hamsters: effect of the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD).
E Steel and JB Hutchison
Horm Behav, Jun 1988; 22(2): 252-65.
Hormonal regulation of adult partner preference behavior in neonatally ATD-treated male rats.
J Bakker, T Brand, J van Ophemert, and AK Slob
Behav Neurosci, Jun 1993; 107(3): 480-7.
Lastly, I never said AI’s would suppress testosterone production. I merely expressed the idea that steroidal-based AI’s can have an inhibitory effect at a cellular level, therefore ATD would not be an optimal choice for hypogonanal man wishing to regain natural testosterone production, especially those whom already may have normal estrogen levels.
We could throw abstracts at each other all night long, but the bottom line remains. There is no sense in using an AI with potential fertility inhibitory problems if you can choose an AI that encourages fertility, such as the AI's weve included in Dermacrine.
Next please.
-Pp