NO! As I said in the other thread:
QUOTE by Nandi: This sums its nice rather nice
"A cursory medline search will turn up a number of papers where the relationship between gynecomastia and progesterone is mentioned.
"What is being said is basically that progesterone can only cause or aggravate gyno in the presence of circulating estrogen."
Just a couple of quotes from studies I pulled up on medline:
"Plasma progesterone was raised in 36 of 50 (72%) men with liver disease compared with 20 healthy male control subjects. Plasma progesterone was significantly higher in men with non-alcoholic cirrhosis with gynaecomastia than those without, but no similar relationship was found in men with alcoholic fatty change and alcoholic cirrhosis. Hyperprolactinaemia was found in 14% of men with liver disease but levels were unrelated to the presence of gynaecomastia.. Increased circulating levels of progesterone and prolactin alone do not explain the development of gynaecomastia in patients with liver disease, but progesterone may be an additional factor acting in association with the known disturbances of other sex steroids. (1)
Progesterone enhances estrogen's stimulation of mammary gland growth, and our findings suggest that progesterone may play a role in the gynecomastia that occurs in men with hyperthyroidism. (2)
This is all we are saying: progesterone/progestins themselves are not capable of causing gyno (study 1), but enhance the action of estrogen, which is typically elevated in hyperthyroidism (study 2).
"True gynecomastia is a condition in which there is an enlargement of the male breast due to an increase in ductal tissue and periductal stroma.[13]"
http://www.medscape.com/viewarticle...LN3SJ1SStuTa53D|-3360746919023192434/184161393/6/7001/7001/7002/7002/7001/-1
Estrogen receptor knockout mice manifest significantly impaired ductal development, implying that estrogen is key to ductal development, and by definition (see phrase in quotes above) gynecomastia.
I've cited these references time and time again. This is truly flogging a dead horse. If others wish to continue the discussion please do so. I'm bowing out as everything that can be said has been said many times over.
(1) Gut. 1982 Apr;23(4):276-9.
Progesterone, prolactin, and gynaecomastia in men with liver disease.
Farthing MJ, Green JR, Edwards CR, Dawson AM.
(2) J Clin Endocrinol Metab. 1988 Jan;66(1):230-2.
High serum progesterone in hyperthyroid men with Graves' disease.
Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K.
Antiestrogenic properties of raloxifene.
Draper MW, Flowers DE, Neild JA, Huster WJ, Zerbe RL.
Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA.
This 21-day, open-label study evaluated the effects of raloxifene and tamoxifen on estrogen-induced changes in serum levels of anterior pituitary hormones (prolactin, luteinizing hormone, and follicle-stimulating hormone), sex steroids (testosterone, estradiol), and binding globulins [thyroid binding globulin (T3 resin uptake), transcortin, sex steroid binding globulin]. Seventeen healthy male volunteers completed the study after being randomized to one of three treatments: raloxifene, tamoxifen, or placebo. Six subjects received raloxifene (200 mg daily) for 10 days, 6 subjects received tamoxifen [20 mg twice a day (b.i.d.)] for 10 days, and 5 subjects received placebo for 10 days. All subjects received ethinyl estradiol (20 micrograms b.i.d.) for 7 days starting 3 days after initiation of study drug or placebo treatment. Results of the primary analysis of this study indicate that for six of the seven analyzable parameters of estrogen action (excluding luteinizing hormone) raloxifene blunted the estrogen response; this effect was significant only for T3 resin uptake. Tamoxifen administration significantly blunted or reversed the estrogen effect in all six of these parameters. Raloxifene, an effective antiestrogen in animal models, is also antiestrogenic in humans.
"Anyway, when ethinyl estradiol was given, prolactin increased by 2.96 ng/ml above baseline in the placebo group. Tamoxifen completely reversed this leading to a drop of 1.29 ng/ml below baseline. Raloxifene only blunted the increase: after raloxifene administration, prolactin remained elevated by 0.85 ng/ml."
Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation.
Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F.
A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers.The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine ..
As Nandi put it:
"So for those people worried about the (IMO non-existent) prolactin induced gyno, tamoxifen looks like it would be an effective treatment. Another reason to forget the foolish use of bromocriptine to treat gyno and just stick with the tried and true Nolvadex."
