They will absolutely lessen the effect of progesterone. They are PARTIAL AGONISTS. Testosterone is NOT a partial agonist, it is a full agonist
"Partial agonists (such as buspirone, aripiprazole, buprenorphine, or norclozapine) bind and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist. They may also be considered ligands which display both agonistic and antagonistic effects - when both a full agonist and partial agonist are present, the partial agonist actually acts as a competitive antagonist, competing with the full agonist for receptor occupancy and producing a net decrease in the receptor activation observed with the full agonist alone. Clinically partial agonists can activate receptors to give a desired submaximal response when inadequate amounts of the endogenous ligand are present, or they can reduce the overstimulation of receptors when excess amounts of the endogenous ligand are present."
Your test/deca/tren analogy makes absolutely no sense considering that both Deca and Tren are higher affinity steroids. So, test is a 100, deca 120 and tren a 400 any of these will work as an agonist. Deca has a lower activity level than progesterone so, with it binding it displaces progesterone therefore it will be a partial agonist. You'd have to take far higher doses to get the same activity level. Since testosterone is at 100% activity, it's not really a comparison with something with 30% activity. Think about it.
By the way, I didn't paraphrase, I took the QUOTE right from his presentation. I stand by my point that reducing hormone levels in healthy men below normal levels isn't a good idea. That was my point...
There is a ton that we don't know. However, I doubt messing with every hormone in your body at once is a good idea. The point is that for normal people to try and drop their prolactin levels is potentially harmful. If you have higher than normal, by all means...however, I keep reading these threads where guys are worried about reducing prolactin when there is no indication that they have high levels. By the way, my wife has hyper prolactemia and at the risk of TMI, she has no lactation, but somehow 100's of BRO's have this issue...
Clin Pharmacol Ther. 1995 Sep;58(3):354-9.
Restoration of normal sperm characteristics in hypoprolactinemic infertile men treated with metoclopramide and exogenous human prolactin.
Ufearo CS, Orisakwe OE.
Department of Physiology, Faculty of Medicine, Nnamdi Azikiwe University, Nigeria.
We investigated the effects of induced increase in prolactin levels on spermatogenesis in 20 infertile men with hypoprolactinemia using exogenous human prolactin (hPRL) and metoclopramide. The subjects were selected from a population of 175 infertile men in whom the prevalence of hypoprolactinemia was 33.14%. Mean basal plasma prolactin was 2.79 +/- 0.62 ng.ml-1 in the infertile men and 9.57 +/- 2.14 ng.ml-1 in the normal control subjects. At the sixteenth week, mean plasma prolactin was 9.41 +/- 1.3 ng.ml-1 in subjects treated with exogenous hPRL and 5.2 +/- 0.7 ng.ml-1 in subjects treated with metoclopramide. Mean basal sperm concentration was approximately 8.8 million per milliliter in the infertile men and 41.5 million per milliliter in the normal control subjects. Mean sperm concentration was approximately 37 million per milliliter in subjects treated with exogenous hPRL, whereas the peak mean value was 23 million per milliliter in subjects treated with metoclopramide for 16 weeks. At basal conditions, the mean percentages of abnormal sperm were 66.75% +/- 14.93% and 21.36% +/- 4.78% in infertile and normal subjects, respectively. In subjects treated with exogenous hPRL and metoclopramide, the mean percentage of abnormal sperm were 24.7% and 31%, respectively, at week 16. Mean plasma prolactin, mean sperm concentration and the mean percentage of abnormal sperm were 3.3 +/- 1.4 ng.ml-1, 7 million per milliliter, and 60.5, respectively, in the infertile subjects after drug withdrawal at week 14. In normal control subjects, there was no significant difference (p = 0.01) in the plecebo effect. We therefore conclude that the low prolactin levels in this group of infertile men may be one of the primary causes of their infertility.
J Androl. 1985 Jan-Feb;6(1):10-4.
Induced hypoprolactinemia and testicular steroidogenesis in man.
Suescun MO, Scorticati C, Chiauzzi VA, Chemes HE, Rivarola MA, Calandra RS.
The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.i.d.). Serum LH, prolactin (PRL), androst-4-ene-3,17 dione (androstenedione), testosterone, and 5 alpha-androstane-3 alpha, 17 beta-diol (5 alpha-Diol) levels, as well as intra-testicular testosterone, dihydrotestosterone (DHT), 5 alpha-Diol and zinc (Zn) concentrations, were determined. Daily administration of bromocriptine caused a marked suppression of serum PRL (mean +/- SEM, 23.8 +/- 2.5 vs. 6.4 +/- 1.0 ng/ml) without concomitant changes in serum LH levels (mean +/- SEM, 8.3 +/- 1.6 vs. 8.9 +/- 2.1 ng/ml). Hypoprolactinemia induced a significant decrease (P less than 0.05) in the mean peripheral testosterone levels; but 5 alpha-Diol and androstenedione remained unchanged. However, in testicular tissues, bromocriptine treatment resulted in significant increases in mean concentrations of total androgens (P less than 0.001), testosterone (P less than 0.001) and DHT (P less than 0.02). Testicular levels of 5 alpha-Diol were not significantly altered. There was no change in Zn levels in basal conditions and during bromocriptine administration. These results indicate that short-term suppression of serum PRL levels in man affects basal testicular function without altering serum LH. However, a direct action of bromocriptine on the human gonad cannot be excluded.
Andrologia. 1985 Mar-Apr;17(2):172-7.
Bromocriptine, a dopamine agonist, directly inhibits testosterone production by rat Leydig cells.
Chambon M, Grizard G, Boucher D.
We investigated the direct effects of bromocriptine (BR) on both basal and hCG-stimulated testosterone production by rat collagenase-dispersed Leydig cells. In a final volume of 2.2 ml, 2.10(6) Leydig cells were incubated at 33 degrees C for 3 h either alone or with various amounts of hCG (1. 10. 10(2). 10(3). 10(4) mUI/vial) and BR (1.5 10(-9), 1.5 10(-7), 1.5 10(-5) M); BR was dissolved in 20 microliters of ethanol. BR (1.5 10(-5) M) decreased significantly both basal and hCG-stimulated testosterone production whereas at lower doses, BR had no effect. These results suggest that the dopamine itself may regulate rat Leydig cell function and that there is room for criticism of BR-induced hypoprolactinemia as an experimental model to study the effect of prolactin on the androgenic function.
Fertil Steril. 1991 Feb;55(2):355-7.
Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.
Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.
Department of Medicine, Shimane Medical University, Japan.
To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.