I've posted this in several other threads but thought it relevant here:
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.
(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.
Lack of estrogenic potential of progesterone- or 19-nor-progesterone-derived progestins as opposed to testosterone or 19-nor-testosterone derivatives on endometrial Ishikawa cells.
Botella J, Duranti E, Viader V, Duc I, Delansorne R, Paris J.
Laboratoire Theramex, Preclinical Research and Development Department, Monaco, Monaco.
Estrogen receptors of human endometrial cancer Ishikawa cells were found to be present in moderate amounts (160-200 fmol/mg protein), and to specifically bind moxestrol (R2858) with a very high affinity characterized by a Kd around 60 pM, when measured under equilibrium conditions. The binding specificity respected a decreasing order as follows: estradiol (E2: 100%) > 4-hydroxy-tamoxifen (4OHTAM: 52.7%) > estriol (E3: 5.7%) > estrone (E1: 2.1%) > TAM (0.2%). The induction of alkaline phosphatase activity (APase) used as an estrogen-specific response, confirmed the intrinsic estrogenicity of progestins derived from 19-nor-testosterone (19NT): norethindrone (NOR), norethynodrel and levonorgestrel, at concentrations ranging from 10(-8) to 10(-6) M. The effect of NOR was partially blocked by the antiestrogen 4OHTAM, which was also partially agonistic in this model, but neither by the antiprogestin mifepristone (RU486) nor by the aromatase inhibitor aminoglutethimide. A simulatory effect was also detected at 10(-7) or 10(-6) M with ethindrone, the testosterone- (T) derived progestin homologous to NOR, and with both androgenic parent-compounds, i.e. T and 19NT themselves. In contrast, progesterone (P) derivatives like medroxyprogesterone acetate (MPA) and chlormadinone acetate (CMA) remained totally inactive, as well as 19-nor-progesterone (19NP) itself or its progestagenic derivatives: ORG 2058 and nomegestrol acetate (NOM). Structure-activity relationships deduced from these studies suggest that it is not the absence of the 19-methyl group which can account for the estrogenic potential of the so-called "19-norprogestins", but rather their steroid structure derived from T in a broad sense (including the 19NT derivatives), as opposed to the non-estrogenic therapeutic progestins derived from P like MPA or CMA, or from 19NP like NOM.
Tamoxifen inhibits prolactin signal transduction in ER - NOG-8 mammary epithelial cells.
Das R, Vonderhaar BK.
Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, MD 20892-1402,
[email protected]
Tamoxifen (TAM), an antiestrogen, also acts as an antilactogen in mammary cells. In the present study we analyze the effect of TAM on the signal transduction pathway for prolactin (Prl). TAM bound specifically to NOG-8, an estrogen receptor-negative mammary cell line. Within 5 min of Prl treatment, raf-1, MEK and MAP kinase were induced 2-3-fold over the control level. TAM completely inhibited this Prl-induced activation of kinases as well as Prl binding and cell growth. These results indicate the potential role of TAM as an antilactogen in Prl responsive systems.
(3)Fertil Steril 1995 Oct;64(4):818-24 Related Articles, Links
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 ..
Pseudogyno is NOT itchy at all, its just NON-nodular fat deposits. Like darius i got a slight of that when bulking.
