I was browsing for some med articles around and i came to find this very interesting article about some endocrine disease and it came to me that it could explain why we have the so called "progesteronic" gyno. My following thoughts were -

Tren is known to be simply the most anti-catabolic compound there is. I don´t really know whether it binds to the AR keeping cortisol floating around not binded to the AR or if it promotes cortisol secretion do diminish. I just know that tren plays a number with Cortisol levels. Maybe someone can explain it better than me.

There is this congenital syndrome called 17-hydroxylase (17-OH) deficiency. My guess is that trenbolone , nandrolone and oxymetholone (all known by "progesteronic agonists") all can cause a temporary similar condition.

It all happens outside the usual HTPA axis. All must remember that the testes are not the only place we manufacture steroids . There is the adrenal gland.

INSIDE THE ARTICLE

Normal adrenal steroid biosynthesis results in 3 products—mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (androstenedione). Cortisol production is regulated by feedback with adrenocorticotrophic hormone (ACTH). ACTH stimulates the enzyme P-450scc (20,22 desmolase), with subsequently increased production of all adrenal steroids.

Decreased serum cortisol levels stimulate adrenocorticotrophic hormone (ACTH) release via negative feedback. Increased ACTH secretion causes overproduction of adrenal steroids preceding the missing enzyme as well as those not requiring the missing enzyme. The example depicts a deficiency of 21-hydroxylase, resulting in deficient mineralocorticoid and glucocorticoid production and excessive androgen production.

C-17alpha-hydroxylase is necessary to convert pregnenolone to 17-hydroxypregnenolone (17-OH Preg) and progesterone to 17-hydroxyprogesterone (17-OH Prog). Absence of C-17alpha-hydroxylase impairs all sex steroid and cortisol production. Low levels of cortisol result in increased adrenocorticotrophic hormone (ACTH) stimulation of steroids prior to the 17-OH step, resulting in increased accumulation and secretion of 17-deoxysteroids by the zona fasciculata, including pregnenolone, progesterone, deoxycorticosterone (DOC), and corticosterone.

Decreased serum cortisol levels stimulate ACTH release via negative feedback. The adrenal glands undergo hypertrophy, apparently due to ACTH-stimulated production of insulinlike growth factor-2 (IGF-2). Increased ACTH secretion also results in overproduction of both the adrenal steroids preceding the missing enzyme and those not requiring the missing enzyme. Treatment with exogenous glucocorticoid decreases ACTH secretion and subsequent suppression of overproduced steroids.

The full article can be read at http://www.emedicine.com/ped/topic1046.htm (i guess you´ll have to register as a physician, you can do it quickly and for free though).

Now it came to me that some people defend that Stanozolol can block trenbolone, oxymetholone and nandrolone gyno. I come to think about it, and why is that stanozolol users report joint pain? Is it because it has some relation with cortisol build-up, hence the effect of blocking the whole ACTH problem?

And, why is that the aborption pill (RU-486) is known to block oxymetholone, trenbolone and nandrolone gyno? Because it is a synthetic progesterone that acts as an agonist on the some and/or breast tissue? Just like nolvadex and clomid does?

Now as for why tren users who get gyno and take prolactin agonists get better... Isn´t progesterone responsible for sensibilizing the breast tissue so that the normal amount of estrogen and slightly elevated prolactin (HPTA inhibition causes its elevation, another feedback mechanism) promotes gyno?

Is this why lowering prolactin and using nolva gets rid of both problems?

Come to think about it.. it all explains itself. The whole issue is progesterone getting high because of the cortisol abscense. No aromatization, no nothing. (By the way there is no aromatization from androgens, whatever they are, to progesterone). And estrogen alone does not always cause gyno, even if it is elevated. (Some can get away with 1 gram in test only cycles with no anti-es... And got gyno traces from fina alone, drol or deca .

If someone sees some truth in this theory, i would like to discuss, maybe it can be the explanation we have always looked for on fina, deca and drol gyno.

Of course, the way to get rid of progesterone elevation will make you all laugh.

Not stimulating the adrenal gland to produce it. How?

DON´T CALL ME NAMES! USING SMALL AMOUNTS OF HYDROCORTISONE (eg, prednisone, dexamethasone).

Remember they won´t attach to the AR and diminish our gains or destroy our muscles. The AR is already binded to some other more powerful steroid, an androgen in the case. Of course, AAS dosage would have to be generous to ensure that.

Tell me what you think.

No pain, no gain.
No roids, more pain.