Gynecomastia is a benign enlargement of the male breast resulting from a proliferation of the glandular component of the breast.Gynecomastia results from an altered estrogen-androgen balance, in favor of estrogen, or increased breast sensitivity to a normal plasma concentrations of circulating estrogen level.
The predominant androgen, testosterone, is synthesized in males mainly by the Leydig cells of the testes (95%) and, to a much lesser extent, by zona reticularis cells of the adrenal cortex (5%). Two thirds of the circulating testosterone is bound to sex hormone–binding globulin (SHBG). Testosterone is converted to dihydrotestosterone (DHT) in the target tissues (5-alpha reductase). DHT is often considered the active form of testosterone. Testosterone is under feedback regulation of luteinizing hormone (LH), secreted by the pituitary gland in the brain. Estrogen production in males is mainly from the peripheral conversion of androgens (ie, testosterone, androstenedione) through the action of the enzyme aromatase, mainly in muscle, skin, and adipose tissue.
The normal production ratio of testosterone to estrogen is approximately 100:1. The normal ratio of testosterone to estrogen in the circulation is approximately 300:1.
Generally, gynecomastia is a benign condition. Upon examination and medical evaluation, most patients are usually satisfied with a simple explanation of the condition and reassurance that the condition is benign, particularly if the enlargement is minimal. Surgical intervention is typically reserved for diagnostic purposes or for patients who request treatment. Most patients who visit a plastic surgeon request treatment for psychological reasons. These patients seek treatment because they find the condition embarrassing. They wear loose clothes and avoid exposure in showers and swimming pools, which greatly inhibits their activities of daily living.
Frequency: In the US: Gynecomastia is the most common cause for male breast evaluation. The frequency is highly variable based on the criteria used for defining the condition. In one study, a figure of 38% was reported in boys aged 10-16 years using a definition of breast tissue greater than 5 cm in diameter. In another series, gynecomastia was noted in approximately 10% of boys aged 12-17 years. In yet another report, gynecomastia was noted in 36% of young military recruits and in approximately 57% of men older than 50 years. Autopsy studies indicate a prevalence ranging from 4-40%.
Gynecomastia can be classified based on etiology. Idiopathic gynecomastia accounts for approximately 75% of cases. Physiologic gynecomastia occurs primarily in newborns and in adolescents at puberty. In the newborn, the neonatal breast results from the action of maternal estrogens, placental estrogens, or both in concert. The increased breast tissue usually disappears in a few weeks. Adolescent gynecomastia is common during puberty. The median age of onset is 14 years. Breast tissue growth is often asymmetrical, and the breasts are frequently tender. Adolescent gynecomastia usually regresses by age 20 years. However, residual gynecomastia may be present in one or both breasts.
Pathologic gynecomastia is due to testosterone deficiency, increased estrogen production, or increased conversion of androgens to estrogens. The pathological conditions associated with gynecomastia include congenital anorchia, Klinefelter syndrome, testicular feminization, hermaphroditism, adrenal carcinoma, liver disorders, and malnutrition.
Many pharmacological agents can cause gynecomastia. These drugs can be categorized by their mechanisms of action. The first type is drugs that act exactly like estrogens, such as diethylstilbestrol, birth control pills, digitalis, and estrogen-containing cosmetics. The second type is drugs that enhance endogenous estrogen formation, such as gonadotropins and clomiphene. The third type is drugs that inhibit testosterone synthesis and action, such as ketoconazole, metronidazole, and cimetidine. The final type is drugs that act by unknown mechanisms, such as isoniazid, methyldopa, captopril, tricyclic antidepressants, diazepam, and heroin.
From Wikipedia: Causes
Physiologic gynecomastia occurs in neonates, at puberty and with aging.
Potential pathologic causes of gynecomastia are: medications including hormones, increased serum estrogen, decreased testosterone production, androgen receptor defects, chronic kidney disease, chronic liver disease, HIV, and other chronic illness. Gynecomastia as a result of spinal cord injury and refeeding after starvation has been reported. In 25% of cases, the cause of the gynecomastia is not known.
Medications cause 10-20% of cases of gynecomastia. These include cimetidine, omeprazole, spironolactone, finasteride and certain antipsychotics. Some act directly on the breast tissue, while other lead to increased secretion of prolactin from the pituitary by blocking the actions of dopamine (prolactin-inhibiting factor/PIF) on the lactotrope cell groups in that organ. Androstenedione, used as a performance enhancing food supplement, can lead to breast enlargement by excess estrogen activity. Marijuana use is also thought by some to be a possible cause, but this is controversial.
Increased estrogen levels can also occur in certain testicular tumors, and in hyperthyroidism. Certain adrenal tumors cause elevated levels of androstenedione which is converted by the enzyme aromatase into estrone, a form of estrogen. Other tumors that secrete hCG can increase estrogen. A decrease in estrogen clearance can occur in liver disease, and this may be the mechanism of gynecomastia in liver cirrhosis. Obesity tends to increase estrogen levels.
Decreased testosterone production can occur in congenital or acquired testicular failure, for example in genetic disorders such as Klinefelter Syndrome. Diseases of the hypothalamus or pituitary can also lead to low testosterone. Abuse of anabolic steroids has a similar effect.
Although stopping these medications can lead to regression of the gynecomastia, surgery is sometimes necessary to eliminate the condition.
The condition usually can be diagnosed by examination by a physician. Occasionally, imaging by X-rays or ultrasound is needed to confirm the diagnosis. Blood tests are required to see if there is any underlying disease causing the gynecomastia.
Gynecomastia is not physically harmful, but in some cases can be an indicator of other more dangerous underlying conditions. Furthermore, it can frequently present social and psychological difficulties for the sufferer. Weight loss can alter the condition in cases where it is triggered by obesity, but for many it will not eliminate it as the breast tissue remains.
* Generally, no treatment is required for physiologic gynecomastia.
* In approximately 90% of patients, pubertal gynecomastia resolves spontaneously within several weeks to 3 years. Breasts greater than 4 cm in diameter may not completely regress.
* Identifying and managing an underlying primary disorder often alleviates breast enlargement.
* If hypogonadism (primary or secondary) is the cause, parenteral or transdermal testosterone replacement therapy is instituted.
* For patients with idiopathic gynecomastia or residual gynecomastia after treatment of the primary cause, medical or surgical treatment may be considered.
* Clomiphene, an antiestrogen, can be administered on a trial basis at a dose of 50-100 mg/d orally for up to 6 months. Approximately 50% of patients achieve partial reduction in breast size, and approximately 20% of patients note complete resolution. Outcomes vary with the type and duration of gynecomastia. Adverse effects are rare and include visual problems, rash, and nausea.
* Tamoxifen (Novladex), an estrogen antagonist, is effective for recent-onset and tender gynecomastia when used in doses of 10-20 mg orally twice daily. Up to 80% of patients report partial-to-complete resolution of gynecomastia within 3 months. Nausea and epigastric discomfort are the main adverse effects.
* Other drugs used less frequently include danazol and testolactone.
o Danazol, a synthetic derivative of testosterone, inhibits pituitary secretion of LH and FSH, which decreases estrogen synthesis from the testicles. The dose used for gynecomastia is 200 mg orally twice daily. Complete resolution of breast enlargement has been reported in 23% of cases. Adverse effects include weight gain, acne, muscle cramps, fluid retention, nausea, and abnormal liver function tests.
o Testolactone, a peripheral aromatase inhibitor, has been used with varying success rates (<40% decrease in size) in doses of 150 mg orally 3 times/d for 6 months. Nausea, vomiting, edema, and worsening of hypertension have been reported with its use.
Surgical Care: if the gyno doesn't resolve itself (adolescent gyno) naturally, nor later respond to *physican-ordered* pharmacological treatment.
* Reduction mammoplasty is considered for patients with macromastia or long-standing gynecomastia or in those in whom medical therapy failed. It is also considered for cosmetic reasons (and accompanying psychosocial reasons).
* If surgery is necessary for patients with lipomastia (ie, pseudogynecomastia), liposuction may suffice.
I found quite a bit of anecdotal evidence that turmeric (curcumin) extract is an effective herbal treatment for many men. I would do a google search and read up on this option.
It is beyond the ability of this forum to provide medical advice - that's the provence of medical professionals. See your doctor for examination, evaluation and technical advice or treatment for this condition.