A brief summary I put together of recent papers on gynaecomastia in males:
What does medical science tell us about gyno:
Gynecomastia is characterised by proliferation and hyperplasia of ductal epithelium and edema of surrounding stromal and connective tissue and is due in part to increased sensitivity to circulating estrogen.. Stromal fibrosis becomes predominant feature during later stages of the condition and this feature is unlikely to respond to medical treatment..
Patients with symptoms of <1 year show greater prognosis for successful outcome..
Estrogen, along with GH and IGF-1, is required for breast growth in males. Since a balance exists between estrogen and androgens in males, any disease state or medication that can increase circulating estrogen or decrease circulating androgen, causing an elevation in the estrogen to androgen ratio, can induce gynecomastia...
Estrogen and progesterone act in an integrative fashion to stimulate normal adult breast development. Estrogen, acting through its ER receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development..
Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones. Thus, neither estrogen alone, nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1...
The GH effects on ductal growth are mediated through stimulation of IGF-1...
GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development ..
Furthermore, other data indicates that estrogen promotes GH secretion and increases GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development...
Breast development requires the presence of estrogen. Androgens, on the other hand oppose the estrogenic effects. Thus, equilibrium exists between estrogen and androgens in the adult male to prevent growth of breast tissue, whereby either an increase in estrogen or a decrease in androgen can tip the balance toward gynecomastia...
SHBG binds androgens more avidly than estrogen. Thus, any condition or drug that can displace steroids from SHBG, will more easily displace estrogen, allowing for higher circulating levels of estrogen...
Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells..
Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone..
Overexpression of aromatase in males caused increased mammary growth and histological changes similar to gynecomastia, an increase in estrogen and progesterone receptors and an increase in downstream growth factors such as TGF-beta and bFGF..
Gynecomastia may partly result from increased aromatase activity in adipose tissue, causing increased conversion of androgens to estrogens..
EDIT: Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development..
Selective estrogen receptor modulators are preferable as their antagonist effect is only on breast tissue, raloxifene is estrogenic on metaphyseal cells, it has an antiestrogenic effect on epiphyseal cells in vitro..
Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia
Sarah E. Lawrence, MD, FRCP(C) K. Arnold Faught, MD, FRCP(C), Jennifer Vethamuthu, MD, Margaret L. Lawson, MD, MSc, FRCP(C)
From the Department of Pediatrics, University of Ottawa, Ontario, Canada
Franz A, Wilson J: Williams Textbook of Endocrinology ninth edition, 877-885, 1998.
Santen R: Endocrinology fourth edition vol. 3: 2335-2341, 2001.
Bocchinfuso WP, Korach KS: Mammary Gland Development and Tumorigenesis in Estrogen Receptor Knockout Mice. Journal of Mammary Gland Biology and Neoplasia 90: 323-334, 1997.
Lubahn, DB, Moyer JS, Golding TS: Alteration of Reproductive Function but not Prenatal Sexual Development after Insertional Disruption of the Mouse Estrogen Receptor Gene. Proc Soc Natl Acad Sci Global 90:11162-11166, 1993..
Edman DC, Hemsell DL, Brenner PF: Extraglandular Estrogen Formation in Subjects with Cirrhosis. Gastroenterology 69: 819, 1975.
Kleinberg DL, Feldman M, Ruan W: IGF-1: An Essential Factor in Terminal End Bud Formation and Ductal Morphogenesis. Journal of Mammary Gland Biology and Neoplasia 5(1):7-17, 2000.
Ruan W, Kleinberg DL: Insulin-like Growth Factor I is Essential for Terminal End Bud Formation and Ductal Morphogenesis during Mammary Development. Endocrinology 140(11): 5075-81, 1999.
Walden PD, Ruan W, Feldman M, Kleinberg DL: Evidence that the Mammary Fat Pad Mediated the Action of Growth Hormone in Mammary Gland Development, Endocrinology 139 (2): 659-62, 1998.