Nelson Vergel
Founder, ExcelMale.com
Highest prevalence of gynecomastia was observed between 21 and 30 years (n = 74; 31.2%). The most common presenting complaints were aesthetic concerns (62.8%) and breast pain (51.2%). 25.3% of the subjects had a history of pubertal gynecomastia. 56.5% had bilateral gynecomastia. 39.9% were overweight and 22.8% were obese. The etiology could not be identified in 45.1% of the cases; the most frequent identified causes were anabolic steroids consumption (13.9%), hypogonadism (11.1%), and use of pharmaceutical drugs (7.8%). Patients with bilateral gynecomastia had a longer history of disease, higher BMI, and lower testosterone levels.
The hormones involved in breast tissue physiology may be stimulatory (as estradiol and progesterone) or inhibitory (as testosterone), acting directly through their specific receptors at this level [6, 7]. Receptors for insulin-like growth factor 1 (IGF-1), IGF-2 [8], luteinizing hormone, and human chorionic gonadotropin have also been detected in breast tissue [7, 8]. Estrogens and progesterone apparently require the presence of growth hormone and IGF-1 to exert their stimulatory action on the breast [9]. Hyperprolactinemia may indirectly cause gynecomastia by suppressing gonadotropin-releasing hormone (GnRH) release, resulting in central hypogonadism, although prolactin receptors have also been detected in benign and malignant breast tissue. At breast level, prolactin might modulate progesterone and androgen receptors expression (increasing the former and reducing the latter) [10]. Furthermore, prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobuloalveolar differentiation only with concomitant progesterone [7].
Gynecomastia may result from an excess of estrogens (obesity, tumors, and exogenous sources) [11] with androgen deficiency (hypogonadism), hormone resistance [12], or altered ratio of estrogens to androgens (refeeding, liver disease, and renal failure) [13].
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The hormones involved in breast tissue physiology may be stimulatory (as estradiol and progesterone) or inhibitory (as testosterone), acting directly through their specific receptors at this level [6, 7]. Receptors for insulin-like growth factor 1 (IGF-1), IGF-2 [8], luteinizing hormone, and human chorionic gonadotropin have also been detected in breast tissue [7, 8]. Estrogens and progesterone apparently require the presence of growth hormone and IGF-1 to exert their stimulatory action on the breast [9]. Hyperprolactinemia may indirectly cause gynecomastia by suppressing gonadotropin-releasing hormone (GnRH) release, resulting in central hypogonadism, although prolactin receptors have also been detected in benign and malignant breast tissue. At breast level, prolactin might modulate progesterone and androgen receptors expression (increasing the former and reducing the latter) [10]. Furthermore, prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobuloalveolar differentiation only with concomitant progesterone [7].
Gynecomastia may result from an excess of estrogens (obesity, tumors, and exogenous sources) [11] with androgen deficiency (hypogonadism), hormone resistance [12], or altered ratio of estrogens to androgens (refeeding, liver disease, and renal failure) [13].
Full paper
