A Thread Devoted To Gynecomastia

[BBC3]

So I am thinking too much is understated here. I am currently realized the potential implications may be far more profound than a simple and temporary growth of breast related tissue. I have a great respect for Millard Baker and remain loyal to this site simply due to the fact that Meso approaches all aspects of "steroid" use openly, honestly, and as accurately as possible. He has maintained this approach through what I am sure has been a constant cascade of negative influence. This making Meso unique in my opinion as displayed in objectivity always attempted and ALWAYS displayed by Millard himself as proven in his every post, principle utilized, and stated intentions. So I salute you! Thanks Doc and Bill as well as I have no doubt Meso would be sorely lacking without....!

So on the surface Gyno would seem like something that happens to uneducates, the poorly prepared, as an unfortunate side effect, or just natural to some folks with a genetic propensity. Realistically I am starting to think that Gyno is a much more profound issue than acknowledged, and at a minimum would appear to be occuring naturally in ALL MEN at some rate even if miniscule and remaining on not physically detectible, but cellular levels. My guess is that gyno OFTEN occurs in men with basically undetectible physical manifestations, but to real, eventual and consequential degrees. It is my opinion than Male Breast Cancer is COMPLETELY UNDERSTATED as it relates to both athletic and medical steroid use, and that the implications can/should no longer be ignored. Consider that we are in the forefront of the "Low-T Male Condition", and then consider the implications to YOU as these waters of mass steroid administration are clearly uncharted. The conundrum appears to be another result of the social implications involved, and the lack thereof of a proper address by medical standards.

While "stickies" appear to be a thing of the past, thread content remains along with an apparent growing publification of this web sites data through mainstream and basic internet searches. While the lack of stickies may leave some feeling the efforts quantify and qualify date in concise presentations for the purpose of learning is now absent, clearly the goal is being accomplished through basic thread presentation. After all, stickies appeared to eventually become simple threads with a slight favoratism applied, yet they appeared to become perversions of the intended message regardless. The concept of the "top level" listing even seemed somewhat tivial as to those that were not asking they were nothing more that impedences to access, and to those searching they became too convoluted. Enough as I begin to meander...

I propose to incept a formal Gyno thread (not this one) thus trying to capture exactly what this phenomon is, really. Obviously the point will be to try to retain the focus and reduce the rhetoric, so perhaps WE need to create an article based on both scientific as well as anecdotal data to present as the opening post. The apparent problem and bottom line is that I do not find a whole lot of data readily available out there. Basic searches simply discuss some mino indications and resulting occurances. The task will be to actually find the data to incorporate.

I am on the fence and really just ranting for now, so I will be looking for approval and motivation. There is a wealth of data here alone considering the subject of athletic steroid use as an expedite of the physical indications noted. So perhaps a thread in both the steroid and Mens Health columns discussing the findings of users alike. The thread should detail potential known manifestations resulting from steroid use listed in yes/no question type census for those that wish to participate. A conglomeration of the tecnically documented data available will have to be sorted and qualified as it relates,,, and may not. One way or the other it seems like complete and total negligence not to fully investigate this concept when after all, it may very well be the most noteworthy side effect one could have listed on the perverbial "This is your brain on drugs" infomercial....!

I am thinking facts and anecdotes in a real and responsible address of the subject. You know it does not take a PHD to produce an article. Only enough sense to gather and interpret data. Thats what the media is. Actually, I am thinking what socitey lacks is exactly the "middle man". Some smart enough to review and understand data, yet dumb enought to bring new perspective to light. And perspective not even possible from current aspects of technical expertise due to the inherent limitations of the separation of priniciples. To accurately review and access bringing new and viable perspective thus furthering real progress in a new light. This is what the media is NOT... Consider the internet is a vehicle created and available in these new and unprecendented times. It is also the reason this new potential exists, where as never before.

So a new field is born here. CONCILIATOR actually got one thing right, a good name for it.

PMs from anyone interested in contributing are welcome. Consider no input invaluable. I am busy so I really dont even know what my proposed level of involvement would be yet. Just bouncing it off the wall...

And knocking on HARD WOOD......

 

[Michael Scally MD]

Re: Gynecomastia

Gynecomastia

Braunstein GD. Gynecomastia. N Engl J Med 2007;357(12):1229-37. MMS: Error

During an evaluation for low back pain, a 67-year-old man is found to have gynecomastia on the right side that is nontender on palpation. Other than a body-mass index (the weight in kilograms divided by the square of the height in meters) of 32, the physical examination is normal. His medical history is notable only for hyperlipidemia; his only medication is a statin. How should his gynecomastia be evaluated and managed?

THE CLINICAL PROBLEM

Asymptomatic gynecomastia, or enlargement of the glandular tissue of the breast, is common in older men; it is found on examination in one third to two thirds of men and at autopsy in 40 to 55% of men.1-7 The condition has usually been present for months or years when it is first discovered during a physical examination. Histologic examination of the breast tissue in this setting usually shows dilated ducts with periductal fibrosis, stromal hyalinization, and increased subareolar fat.6-9In contrast, patients who present with symptoms of pain and tenderness generally have gynecomastia of more recent onset, and pathological findings include hyperplasia of the ductal epithelium, infiltration of the periductal tissue with inflammatory cells, and increased subareolar fat.6-9

The pathophysiological process of gynecomastia involves an imbalance between free estrogen and free androgen actions in the breast tissue; this imbalance can occur through multiple mechanisms.10 During mid-to-late puberty, relatively more estrogen may be produced by the testes and peripheral tissues before testosterone secretion reaches adult levels, resulting in the gynecomastia that commonly occurs during this period. The testes may directly secrete too much estradiol from a Leydig-cell or Sertoli-cell tumor. They may also secrete estradiol indirectly through the stimulatory effects of a human chorionic gonadotropin (hCG)–secreting tumor of gonadal or extragonadal germ-cell origin (also called eutopic hCG production) or a tumor derived from a nontrophoblastic tissue, such as a large-cell carcinoma of the lung or some gastric or renal-cell carcinomas (also called ectopic hCG production). In addition, the testes may secrete too little testosterone; this occurs in primary or secondary hypogonadism. The prevalence of these conditions increases with advanced age, and one study indicated that 50% of men in their 70s have a low free testosterone concentration.11

Estradiol and Estrone, Displaced by Some Drugs, Resulting in an Increase in Free Estrogen.

An adrenal neoplasm may overproduce the weak androgen androstenedione and other androgen precursors such as dehydroepiandrosterone, which are converted into estrogens in peripheral tissues. An increase in aromatase activity has been reported in a number of patients with gynecomastia associated with a variety of disease processes, including thyrotoxicosis, Klinefelter's syndrome, and adrenal and testicular tumors.12 Aromatase activity increases both with age and with an increase in body fat. Since body fat also increases with age, it is likely that a physiologic increase in the activity of the aromatase enzyme complex with normal aging is responsible for many cases of asymptomatic gynecomastia in older men. Indeed, there is a progressive increase in the prevalence of gynecomastia with an increase of the body-mass index, probably reflecting the local paracrine effects of estradiol production in the subareolar fat on the breast glandular tissue.4,5

Since estradiol and estrone bind less avidly to sex hormone–binding globulin than does testosterone, drugs such as spironolactone may displace relatively more estrogen than testosterone from this protein, increasing the bioavailable fraction of estrogen to a greater extent than bioavailable androgen. Similarly, an increase in the sex hormone–binding globulin concentration, which occurs with hyperthyroidism and some forms of liver disease, may be associated with greater binding of testosterone relative to estrogen, leading to a decrease in free testosterone relative to free estrogen. Androgen-receptor abnormalities, either due to a genetic defect or blockade by an antagonist such as bicalutamide or due to stimulation of the estrogen receptor by medications or environmental estrogens, may also result in gynecomastia.

STRATEGIES AND EVIDENCE

Diagnosis

The first step in the clinical evaluation of patients is to determine whether the enlarged breast tissue or mass is gynecomastia. Pseudogynecomastia is characterized by increased subareolar fat without enlargement of the breast glandular component. The differentiation between gynecomastia and pseudogynecomastia is made on physical examination, as shown in Figure 2 The other important differentiation is between gynecomastia and breast carcinoma. The tissue in gynecomastia is soft, elastic, or firm but generally not hard, the affected area is concentric to the nipple–areolar complex, and it is clinically bilateral in approximately half of patients. Breast carcinoma is usually hard or firm, is located outside the nipple–areolar complex, and is most often unilateral. In addition, skin dimpling and nipple retraction are not present with gynecomastia, but they may be seen in patients with breast carcinoma. Tenderness may be present in gynecomastia of less than 6 months' duration, but it is unusual with breast carcinoma. Nipple bleeding or discharge is present in approximately 10% of men with breast cancer, but it is not expected with gynecomastia.13 If the differentiation between gynecomastia and breast carcinoma cannot be made on the basis of clinical findings alone, the patient should undergo diagnostic mammography, which has 90% sensitivity and specificity for distinguishing malignant from benign breast diseases.14

Differentiation of Gynecomastia from Pseudogynecomastia and Other Disorders by Physical Examination.

Evaluation

Once the diagnosis of gynecomastia is established, it is important to review all medications, including over-the-counter drugs such as herbal products, that may be associated with gynecomastia. Ingestion of sex steroid hormones or their precursors may cause gynecomastia through bioconversion to estrogens. Antiandrogens used for the treatment of prostate cancer, spironolactone, cimetidine, environmental estrogens or antiandrogens, and one or more components of highly active antiviral therapy used for human immunodeficiency virus infection (especially protease inhibitors) have been clearly shown to be associated with gynecomastia.15-25 Several cancer chemotherapeutic drugs, particularly alkylating agents, can damage the testes and result in primary hypogonadism. Other drugs, including phenytoin and metoclopramide, have also been associated with gynecomastia, but a cause-and-effect relationship has not been proved.15

An adolescent presenting with gynecomastia usually has physiologic pubertal gynecomastia, which generally appears at 13 or 14 years of age, lasts for 6 months or less, and then regresses. Less than 5% of affected boys have persistent gynecomastia, but this is the apparent cause in a large proportion of young men in their late teens or 20s presenting for evaluation. Other conditions to consider in adolescents and young adults with gynecomastia are Klinefelter's syndrome, familial or sporadic excessive aromatase activity, incomplete androgen insensitivity, feminizing testicular or adrenal tumors, and hyperthyroidism.26-28 Drug abuse, especially with anabolic steroids, but also with alcohol, marijuana, or opioids, also should be considered.29

If an adolescent or adult presents with unilateral or bilateral gynecomastia that is painful or tender, and if the patient's history and physical examination do not reveal the cause (Table 1) hCG, luteinizing hormone, testosterone, and estradiol should be measured (Figure 3).30 Many of the available measurements of testosterone have poor accuracy and precision, especially in men with testosterone levels at the low end of the normal range.31 Measurement of these levels in the morning is recommended, since testosterone and luteinizing hormone secretion have a circadian rhythm (with the highest levels in the morning) as well as secretory bursts throughout the day. If the total testosterone level is borderline or low, free or bioavailable testosterone should be measured or calculated to confirm hypogonadism. Although such laboratory evaluation is prudent, no abnormalities are detected in the majority of patients.

Signs and Symptoms of Pathologic Processes That Cause Gynecomastia.

Interpretation of Serum Hormone Levels and Recommendations for Further Evaluation of Patients with Gynecomastia.

Laboratory tests to determine the cause of asymptomatic gynecomastia in an adult without a history suggestive of an underlying pathologic cause, with an otherwise normal physical examination, are unlikely to be revealing, and the extent of hormonal evaluation that should be performed in such patients remains controversial. The likelihood of discovering a pathologic abnormality is low in patients with long-standing asymptomatic gynecomastia in the fibrotic stage, and the long duration of the condition without other evidence of disease is reassuring; thus, many clinicians take a minimalist approach to evaluation. Nevertheless, measurement of the morning testosterone level and free or bioavailable testosterone and luteinizing hormone levels, if the morning testosterone level is low, is reasonable to detect hypogonadism, which is increasingly common with advanced age.11 A finding of a low free or bioavailable testosterone level and an elevated luteinizing hormone level indicates primary testicular failure, whereas a low free or bioavailable testosterone level and a normal or low luteinizing hormone level may indicate secondary hypogonadism.

Treatment

If a specific cause of gynecomastia can be identified and treated during the painful proliferative phase, there may be regression of the breast enlargement. This regression most often occurs with discontinuation of an offending drug or after initiation of testosterone treatment for primary hypogonadism. If the gynecomastia is drug-induced, decreased tenderness and softening of the glandular tissue will usually be apparent within 1 month after discontinuation of the drug. However, if the gynecomastia has been present for more than 1 year, it is unlikely to regress substantially, either spontaneously or with medical therapy, because of the presence of fibrosis. In such circumstances, surgical subcutaneous mastectomy, ultrasound-assisted liposuction, and suction-assisted lipectomy are the best options for cosmetic improvement, as described in several case series.32,33

During the rapid, proliferative phase, manifested clinically as breast pain and tenderness, medical therapy may be attempted. Most studies of drugs — including testosterone (in patients without hypogonadism), dihydrotestosterone, danazol, clomiphene citrate, tamoxifen, and testolactone — have been uncontrolled and thus difficult to interpret because gynecomastia may resolve spontaneously.34,35 The few randomized, double-blind, placebo-controlled trials generally have been limited by small samples.

Although not approved for the treatment of gynecomastia, the selective estrogen-receptor modulator tamoxifen, administered orally at a dose of 20 mg daily for up to 3 months, has been shown to be effective in randomized and nonrandomized trials, resulting in partial regression of gynecomastia in approximately 80% of patients and complete regression in about 60%.36-45 Patients in whom tamoxifen is effective usually experience a decrease in pain and tenderness within 1 month. In a retrospective analysis of a series of patients with idiopathic gynecomastia, 78% of patients treated with tamoxifen had complete resolution of gynecomastia, as compared with only 40% of patients receiving danazol.42 In case series describing the use of tamoxifen for this condition in more than 225 patients, adverse events were uncommon; they included epigastric distress in 2 patients38 and a post-traumatic deep-vein thrombosis in 1 patient.43

The aromatase inhibitor anastrozole was not shown to be more effective than placebo in a randomized, double-blind, placebo-controlled trial in boys with pubertal gynecomastia.46 Although in an uncontrolled study of 10 patients with pubertal gynecomastia, the selective estrogen-receptor modulator raloxifene was shown to result in more than a 50% decrease in the size of the gynecomastia in the majority of the boys, there are insufficient data to recommend its use at this time.44

It has also been suggested that therapy with tamoxifen may prevent the development of gynecomastia in men receiving monotherapy with high doses of bicalutamide (Casodex) for prostate cancer. In a randomized, double-blind, controlled trial involving men receiving high-dose bicalutamide (150 mg per day),47 gynecomastia occurred in 10% of patients who received tamoxifen at a dose of 20 mg daily, but it occurred in 51% of those who received anastrozole at a dose of 1 mg daily and in 73% of those who received placebo, over a period of 48 weeks; mastalgia occurred in 6%, 27%, and 39% of these patients, respectively. In another trial48 involving 3 months of therapy, gynecomastia, mastalgia, or both occurred in 69.4% of patients receiving placebo, 11.8% receiving tamoxifen (P<0.001 for the comparison with placebo), and 63.9% receiving anastrozole (not significantly different from the rate in the placebo group). Another randomized trial showed efficacy of a 10-mg dose of tamoxifen as prophylaxis against gynecomastia. Among patients treated with bicalutamide alone, gynecomastia occurred in 68.6% and mastalgia occurred in 56.8%. These rates were significantly lower among patients receiving one 12-Gy fraction of radiation therapy to the breast on the first day of treatment with bicalutamide (34% and 30%, respectively), and they were further reduced among patients receiving bicalutamide and tamoxifen (8% and 6%, respectively).49Although it has been used in men treated for prostate cancer, tamoxifen is not approved by the Food and Drug Administration for this indication.

AREAS OF UNCERTAINTY

The high prevalence of asymptomatic gynecomastia among older men raises the question of whether it should be considered to be pathologic or a part of the normal process of aging. It is likely, but unproved, that many cases of asymptomatic gynecomastia are due to the enhanced aromatization of androgens in subareolar fat tissue, resulting in high local concentrations of estrogens, as well as to the age-related decline in testosterone production.11,12,50 Another possible cause is unrecognized exposure over time to unidentified environmental estrogens or antiandrogens.18,19,21

There is no uniformity of opinion regarding what biochemical evaluation, if any, should be performed in a patient with asymptomatic gynecomastia. The diagnostic tests for patients with symptomatic gynecomastia of recent onset for which no cause is discerned on the basis of the history or physical examination (Figure 3) have a low yield; however, a prospective cost–benefit analysis in this population has not been performed. In a retrospective study of 87 men with symptomatic gynecomastia, 16% had apparent liver or renal disease, 21% had drug-induced gynecomastia, and 2% had hyperthyroidism, whereas 61% were considered to have idiopathic gynecomastia. Forty-five of the 53 patients in the group with idiopathic gynecomastia underwent endocrine testing, of whom only 1 patient (2%) was found to have an endocrine abnormality — an occult Leydig-cell testicular tumor.51

Finally, since the excessive aromatization of androgens to estrogens has been shown to be present in many patients with gynecomastia, it is unclear why aromatase inhibitors have not been more successful in the treatment of these patients or in the prevention of the development of gynecomastia in patients with prostate cancer treated with antiandrogens.

GUIDELINES

No professional guidelines are available for the management of gynecomastia.

CONCLUSIONS AND RECOMMENDATIONS

Asymptomatic gynecomastia is a relatively common finding on physical examination, and a careful history taking and physical examination are usually sufficient to identify pubertal gynecomastia, drug-induced causes, or an underlying pathologic process, with the possible exception of mild hypogonadism. Pubertal gynecomastia resolves with time in the majority of adolescent boys, and reassurance and follow-up physical examination usually suffice. In adults who present with the acute onset of painful gynecomastia without an obvious cause, hormonal evaluation, including measurements of serum hCG, testosterone, luteinizing hormone, and estradiol levels, should be performed in order to rule out serious and treatable causes, although serious disease is unlikely in this setting. During the acute florid stage of gynecomastia, a trial of tamoxifen, at a dose of 20 mg per day for up to 3 months, may be attempted. If the gynecomastia has not regressed by 1 year, or in patients who present with long-standing gynecomastia who are troubled by their appearance, surgical removal of the breast glandular tissue and subareolar fat is an option that has a good cosmetic result in the majority of patients. For a patient such as the man in the vignette, who is asymptomatic, is not bothered by his gynecomastia, and does not have a suggestive history or physical examination, a more minimalist evaluation (i.e., measurements of testosterone and luteinizing hormone levels, although even the use of these tests might be debated52) is recommended, and treatment other than weight reduction is not warranted for the gynecomastia.

 

[Michael Scally MD]

Unilateral Gynecomastia in a Young Adult

Lin YN, Liang SJ. Unilateral gynecomastia in a young adult. Intern Med 2011;50(12):1355. http://www.jstage.jst.go.jp/article/internalmedicine/50/12/1355/_pdf [Pictures & References – see link]

A 28-year-old previously healthy male non-smoker presented with left breast pain for 6 days. He also reported left chest pain and cough for 3 weeks. Physical examination disclosed a tender, elastic subareolar mass concentric to the left nipple without skin dimpling, nipple retraction, or discharge. A chest radiography showed anterior mediastinal mass with multiple lung nodules and masses (Picture 1). A computed tomography revealed a 9 cm anterior mediastinal mass, enlarged left breast glandular tissue, and multiple peripheral pulmonary nodules and masses (Picture 2). Blood tests showed beta-hCG more than 200,000 mIU/mL, estradiol 230 pq/mL, testosterone 5.91 ng/mL, SCC 0.5 ng/mL, AFP 1.13 ng/mL, and CEA 2.06 ng/mL. An ultrasound-guided biopsy confirmed a diagnosis of primary mediastinal choriocarcinoma after testicular sonography showed normal. Within the period of study, the tumors progressed rapidly in size. He was transferred to the oncology department for scheduled chemotherapy with etoposide, bleomycin, and cisplatin.

Primary mediastinal germ cell tumors are rare, and choriocarcinoma arising in the mediastinum is exceedingly rare (1). Patients with mediastinal choriocarcinoma are generally young men. Gynecomastia and high beta-hCG are unique presentations (2). The prognosis of primary mediastinal choriocarcinoma is still very poor despite the introduction of combination chemotherapy including cisplatin.

 

[UFgrad777]

Re: Gynecomastia

Gynecomastia

Braunstein GD. Gynecomastia. N Engl J Med 2007;357(12):1229-37. MMS: Error

During an evaluation for low back pain, a 67-year-old man is found to have gynecomastia on the right side that is nontender on palpation. Other than a body-mass index (the weight in kilograms divided by the square of the height in meters) of 32, the physical examination is normal. His medical history is notable only for hyperlipidemia; his only medication is a statin. How should his gynecomastia be evaluated and managed?

THE CLINICAL PROBLEM

Asymptomatic gynecomastia, or enlargement of the glandular tissue of the breast, is common in older men; it is found on examination in one third to two thirds of men and at autopsy in 40 to 55% of men.1-7 The condition has usually been present for months or years when it is first discovered during a physical examination. Histologic examination of the breast tissue in this setting usually shows dilated ducts with periductal fibrosis, stromal hyalinization, and increased subareolar fat.6-9In contrast, patients who present with symptoms of pain and tenderness generally have gynecomastia of more recent onset, and pathological findings include hyperplasia of the ductal epithelium, infiltration of the periductal tissue with inflammatory cells, and increased subareolar fat.6-9

The pathophysiological process of gynecomastia involves an imbalance between free estrogen and free androgen actions in the breast tissue; this imbalance can occur through multiple mechanisms.10 During mid-to-late puberty, relatively more estrogen may be produced by the testes and peripheral tissues before testosterone secretion reaches adult levels, resulting in the gynecomastia that commonly occurs during this period. The testes may directly secrete too much estradiol from a Leydig-cell or Sertoli-cell tumor. They may also secrete estradiol indirectly through the stimulatory effects of a human chorionic gonadotropin (hCG)–secreting tumor of gonadal or extragonadal germ-cell origin (also called eutopic hCG production) or a tumor derived from a nontrophoblastic tissue, such as a large-cell carcinoma of the lung or some gastric or renal-cell carcinomas (also called ectopic hCG production). In addition, the testes may secrete too little testosterone; this occurs in primary or secondary hypogonadism. The prevalence of these conditions increases with advanced age, and one study indicated that 50% of men in their 70s have a low free testosterone concentration.11

Estradiol and Estrone, Displaced by Some Drugs, Resulting in an Increase in Free Estrogen.

An adrenal neoplasm may overproduce the weak androgen androstenedione and other androgen precursors such as dehydroepiandrosterone, which are converted into estrogens in peripheral tissues. An increase in aromatase activity has been reported in a number of patients with gynecomastia associated with a variety of disease processes, including thyrotoxicosis, Klinefelter's syndrome, and adrenal and testicular tumors.12 Aromatase activity increases both with age and with an increase in body fat. Since body fat also increases with age, it is likely that a physiologic increase in the activity of the aromatase enzyme complex with normal aging is responsible for many cases of asymptomatic gynecomastia in older men. Indeed, there is a progressive increase in the prevalence of gynecomastia with an increase of the body-mass index, probably reflecting the local paracrine effects of estradiol production in the subareolar fat on the breast glandular tissue.4,5

Since estradiol and estrone bind less avidly to sex hormone–binding globulin than does testosterone, drugs such as spironolactone may displace relatively more estrogen than testosterone from this protein, increasing the bioavailable fraction of estrogen to a greater extent than bioavailable androgen. Similarly, an increase in the sex hormone–binding globulin concentration, which occurs with hyperthyroidism and some forms of liver disease, may be associated with greater binding of testosterone relative to estrogen, leading to a decrease in free testosterone relative to free estrogen. Androgen-receptor abnormalities, either due to a genetic defect or blockade by an antagonist such as bicalutamide or due to stimulation of the estrogen receptor by medications or environmental estrogens, may also result in gynecomastia.

STRATEGIES AND EVIDENCE

Diagnosis

The first step in the clinical evaluation of patients is to determine whether the enlarged breast tissue or mass is gynecomastia. Pseudogynecomastia is characterized by increased subareolar fat without enlargement of the breast glandular component. The differentiation between gynecomastia and pseudogynecomastia is made on physical examination, as shown in Figure 2 The other important differentiation is between gynecomastia and breast carcinoma. The tissue in gynecomastia is soft, elastic, or firm but generally not hard, the affected area is concentric to the nipple–areolar complex, and it is clinically bilateral in approximately half of patients. Breast carcinoma is usually hard or firm, is located outside the nipple–areolar complex, and is most often unilateral. In addition, skin dimpling and nipple retraction are not present with gynecomastia, but they may be seen in patients with breast carcinoma. Tenderness may be present in gynecomastia of less than 6 months' duration, but it is unusual with breast carcinoma. Nipple bleeding or discharge is present in approximately 10% of men with breast cancer, but it is not expected with gynecomastia.13 If the differentiation between gynecomastia and breast carcinoma cannot be made on the basis of clinical findings alone, the patient should undergo diagnostic mammography, which has 90% sensitivity and specificity for distinguishing malignant from benign breast diseases.14

Differentiation of Gynecomastia from Pseudogynecomastia and Other Disorders by Physical Examination.

Evaluation

Once the diagnosis of gynecomastia is established, it is important to review all medications, including over-the-counter drugs such as herbal products, that may be associated with gynecomastia. Ingestion of sex steroid hormones or their precursors may cause gynecomastia through bioconversion to estrogens. Antiandrogens used for the treatment of prostate cancer, spironolactone, cimetidine, environmental estrogens or antiandrogens, and one or more components of highly active antiviral therapy used for human immunodeficiency virus infection (especially protease inhibitors) have been clearly shown to be associated with gynecomastia.15-25 Several cancer chemotherapeutic drugs, particularly alkylating agents, can damage the testes and result in primary hypogonadism. Other drugs, including phenytoin and metoclopramide, have also been associated with gynecomastia, but a cause-and-effect relationship has not been proved.15

An adolescent presenting with gynecomastia usually has physiologic pubertal gynecomastia, which generally appears at 13 or 14 years of age, lasts for 6 months or less, and then regresses. Less than 5% of affected boys have persistent gynecomastia, but this is the apparent cause in a large proportion of young men in their late teens or 20s presenting for evaluation. Other conditions to consider in adolescents and young adults with gynecomastia are Klinefelter's syndrome, familial or sporadic excessive aromatase activity, incomplete androgen insensitivity, feminizing testicular or adrenal tumors, and hyperthyroidism.26-28 Drug abuse, especially with anabolic steroids, but also with alcohol, marijuana, or opioids, also should be considered.29

If an adolescent or adult presents with unilateral or bilateral gynecomastia that is painful or tender, and if the patient's history and physical examination do not reveal the cause (Table 1) hCG, luteinizing hormone, testosterone, and estradiol should be measured (Figure 3).30 Many of the available measurements of testosterone have poor accuracy and precision, especially in men with testosterone levels at the low end of the normal range.31 Measurement of these levels in the morning is recommended, since testosterone and luteinizing hormone secretion have a circadian rhythm (with the highest levels in the morning) as well as secretory bursts throughout the day. If the total testosterone level is borderline or low, free or bioavailable testosterone should be measured or calculated to confirm hypogonadism. Although such laboratory evaluation is prudent, no abnormalities are detected in the majority of patients.

Signs and Symptoms of Pathologic Processes That Cause Gynecomastia.

Interpretation of Serum Hormone Levels and Recommendations for Further Evaluation of Patients with Gynecomastia.

Laboratory tests to determine the cause of asymptomatic gynecomastia in an adult without a history suggestive of an underlying pathologic cause, with an otherwise normal physical examination, are unlikely to be revealing, and the extent of hormonal evaluation that should be performed in such patients remains controversial. The likelihood of discovering a pathologic abnormality is low in patients with long-standing asymptomatic gynecomastia in the fibrotic stage, and the long duration of the condition without other evidence of disease is reassuring; thus, many clinicians take a minimalist approach to evaluation. Nevertheless, measurement of the morning testosterone level and free or bioavailable testosterone and luteinizing hormone levels, if the morning testosterone level is low, is reasonable to detect hypogonadism, which is increasingly common with advanced age.11 A finding of a low free or bioavailable testosterone level and an elevated luteinizing hormone level indicates primary testicular failure, whereas a low free or bioavailable testosterone level and a normal or low luteinizing hormone level may indicate secondary hypogonadism.

Treatment

If a specific cause of gynecomastia can be identified and treated during the painful proliferative phase, there may be regression of the breast enlargement. This regression most often occurs with discontinuation of an offending drug or after initiation of testosterone treatment for primary hypogonadism. If the gynecomastia is drug-induced, decreased tenderness and softening of the glandular tissue will usually be apparent within 1 month after discontinuation of the drug. However, if the gynecomastia has been present for more than 1 year, it is unlikely to regress substantially, either spontaneously or with medical therapy, because of the presence of fibrosis. In such circumstances, surgical subcutaneous mastectomy, ultrasound-assisted liposuction, and suction-assisted lipectomy are the best options for cosmetic improvement, as described in several case series.32,33

During the rapid, proliferative phase, manifested clinically as breast pain and tenderness, medical therapy may be attempted. Most studies of drugs — including testosterone (in patients without hypogonadism), dihydrotestosterone, danazol, clomiphene citrate, tamoxifen, and testolactone — have been uncontrolled and thus difficult to interpret because gynecomastia may resolve spontaneously.34,35 The few randomized, double-blind, placebo-controlled trials generally have been limited by small samples.

Although not approved for the treatment of gynecomastia, the selective estrogen-receptor modulator tamoxifen, administered orally at a dose of 20 mg daily for up to 3 months, has been shown to be effective in randomized and nonrandomized trials, resulting in partial regression of gynecomastia in approximately 80% of patients and complete regression in about 60%.36-45 Patients in whom tamoxifen is effective usually experience a decrease in pain and tenderness within 1 month. In a retrospective analysis of a series of patients with idiopathic gynecomastia, 78% of patients treated with tamoxifen had complete resolution of gynecomastia, as compared with only 40% of patients receiving danazol.42 In case series describing the use of tamoxifen for this condition in more than 225 patients, adverse events were uncommon; they included epigastric distress in 2 patients38 and a post-traumatic deep-vein thrombosis in 1 patient.43

The aromatase inhibitor anastrozole was not shown to be more effective than placebo in a randomized, double-blind, placebo-controlled trial in boys with pubertal gynecomastia.46 Although in an uncontrolled study of 10 patients with pubertal gynecomastia, the selective estrogen-receptor modulator raloxifene was shown to result in more than a 50% decrease in the size of the gynecomastia in the majority of the boys, there are insufficient data to recommend its use at this time.44

It has also been suggested that therapy with tamoxifen may prevent the development of gynecomastia in men receiving monotherapy with high doses of bicalutamide (Casodex) for prostate cancer. In a randomized, double-blind, controlled trial involving men receiving high-dose bicalutamide (150 mg per day),47 gynecomastia occurred in 10% of patients who received tamoxifen at a dose of 20 mg daily, but it occurred in 51% of those who received anastrozole at a dose of 1 mg daily and in 73% of those who received placebo, over a period of 48 weeks; mastalgia occurred in 6%, 27%, and 39% of these patients, respectively. In another trial48 involving 3 months of therapy, gynecomastia, mastalgia, or both occurred in 69.4% of patients receiving placebo, 11.8% receiving tamoxifen (P<0.001 for the comparison with placebo), and 63.9% receiving anastrozole (not significantly different from the rate in the placebo group). Another randomized trial showed efficacy of a 10-mg dose of tamoxifen as prophylaxis against gynecomastia. Among patients treated with bicalutamide alone, gynecomastia occurred in 68.6% and mastalgia occurred in 56.8%. These rates were significantly lower among patients receiving one 12-Gy fraction of radiation therapy to the breast on the first day of treatment with bicalutamide (34% and 30%, respectively), and they were further reduced among patients receiving bicalutamide and tamoxifen (8% and 6%, respectively).49Although it has been used in men treated for prostate cancer, tamoxifen is not approved by the Food and Drug Administration for this indication.

AREAS OF UNCERTAINTY

The high prevalence of asymptomatic gynecomastia among older men raises the question of whether it should be considered to be pathologic or a part of the normal process of aging. It is likely, but unproved, that many cases of asymptomatic gynecomastia are due to the enhanced aromatization of androgens in subareolar fat tissue, resulting in high local concentrations of estrogens, as well as to the age-related decline in testosterone production.11,12,50 Another possible cause is unrecognized exposure over time to unidentified environmental estrogens or antiandrogens.18,19,21

There is no uniformity of opinion regarding what biochemical evaluation, if any, should be performed in a patient with asymptomatic gynecomastia. The diagnostic tests for patients with symptomatic gynecomastia of recent onset for which no cause is discerned on the basis of the history or physical examination (Figure 3) have a low yield; however, a prospective cost–benefit analysis in this population has not been performed. In a retrospective study of 87 men with symptomatic gynecomastia, 16% had apparent liver or renal disease, 21% had drug-induced gynecomastia, and 2% had hyperthyroidism, whereas 61% were considered to have idiopathic gynecomastia. Forty-five of the 53 patients in the group with idiopathic gynecomastia underwent endocrine testing, of whom only 1 patient (2%) was found to have an endocrine abnormality — an occult Leydig-cell testicular tumor.51

Finally, since the excessive aromatization of androgens to estrogens has been shown to be present in many patients with gynecomastia, it is unclear why aromatase inhibitors have not been more successful in the treatment of these patients or in the prevention of the development of gynecomastia in patients with prostate cancer treated with antiandrogens.

GUIDELINES

No professional guidelines are available for the management of gynecomastia.

CONCLUSIONS AND RECOMMENDATIONS

Asymptomatic gynecomastia is a relatively common finding on physical examination, and a careful history taking and physical examination are usually sufficient to identify pubertal gynecomastia, drug-induced causes, or an underlying pathologic process, with the possible exception of mild hypogonadism. Pubertal gynecomastia resolves with time in the majority of adolescent boys, and reassurance and follow-up physical examination usually suffice. In adults who present with the acute onset of painful gynecomastia without an obvious cause, hormonal evaluation, including measurements of serum hCG, testosterone, luteinizing hormone, and estradiol levels, should be performed in order to rule out serious and treatable causes, although serious disease is unlikely in this setting. During the acute florid stage of gynecomastia, a trial of tamoxifen, at a dose of 20 mg per day for up to 3 months, may be attempted. If the gynecomastia has not regressed by 1 year, or in patients who present with long-standing gynecomastia who are troubled by their appearance, surgical removal of the breast glandular tissue and subareolar fat is an option that has a good cosmetic result in the majority of patients. For a patient such as the man in the vignette, who is asymptomatic, is not bothered by his gynecomastia, and does not have a suggestive history or physical examination, a more minimalist evaluation (i.e., measurements of testosterone and luteinizing hormone levels, although even the use of these tests might be debated52) is recommended, and treatment other than weight reduction is not warranted for the gynecomastia.

Dr. Scally,

Would testosterone therapy be warranted for someone who has recent gynecomastia and their all labwork consistently showed normal T, normal E2, high SHBG, and low Free T?

This would assume of course that every other test mentioned in the above article was unremarkable/

 

[fit4life10]

Can tamoxifen be purchased without a perscription? Basically, is it legal to have without a perscription?

 

[BBC3]

I will say that reviewing further I have another thought and as relates to the prostate. As my own suspicion that there are many receptors in the body that can accept either androgens or estrogens could apply. It could also mean that there is MUCH room for NEW receptor development throughout life and the imbalance observed in breast cancer or benign gyno patients is due to imbalanced receptor development based on preponderance of population as a site location. I really have some silly notions about "first come first serve", and also "he who gets there first controls the roost".

So I find it interesting that one of the treatments is direct androgen therapy. All though I am not sure how they define androgens (with ref. to other articles as well). If testosterone this would not work. So it would also explain why an AI or a SERM might "cure" "BBs" in minor early onset cases, which I am not sure if it really does. SO I AM WONDERING HOW ALL THIS RELATES TO THE PROSTATE AND CANCER as I suspect many of the same priciples are involved. An my uro did note a few years back that they were starting to consider SERMS as a treatment or preventative measure for PC.

The bottom line is that any one here using testosterone for any purpose is probably expediting the condition of gyno as an elderly or older person. The real question is what is the percentage of BC in these cases. IS IT HIGHER than women with NORMAL genetic breast tissue? I am guessing not and all a function of time the same. Every day as my wife ages her tits get bigger, I can help but wonder if this does not need to be controlled in real life application. WE JUST WEREN'T MEANT TO LIVE THIS LONG. But my one thought on gyno which would APPEAR to be different in womens breast development and function is the fact that gyno in young men appears to ellicit fluid production in many cases, whereas normal breast development in women does not. The development is clearly not the same, which could mean better, OR worse conditions..

To the last poster. Presciption Tamox is prescription. CEM MESO Store has a concoction available in liquid form as a bulk chemical sold that you can purchse. Take it for what its worth. It is suppsed to be the same thing.

 

[fit4life10]

The reason I ask because growing up I felt I had gyno when I had hit puberty and even to this day I feel I do. I'm a big guy 6' 270lbs but I carry my weight well. I've lifted weight and played football since I was 14. I've been on TRT for six months which has helped me to pack on some muscle. Muscle that I had worked so hard for but could not attain because my T was low. There are lots of guys who weigh as much as me but have do not have the appearance of puffiness around the nipple area. My Dr is a prime example. He's short and very portly but his chest is flat as a board.

All my life the appearance of my chest has bothered me. Swimming? Nope. And I hated when we had to play shirts and skins in gym. Hated it!

I mean I guess I could go to my Dr and have him take a look but if not I'd like to buy this liquid form and try the smallest dosage I can to get rid of this.

 

[UFgrad777]

I will say that reviewing further I have another thought and as relates to the prostate. As my own suspicion that there are many receptors in the body that can accept either androgens or estrogens could apply. It could also mean that there is MUCH room for NEW receptor development throughout life and the imbalance observed in breast cancer or benign gyno patients is due to imbalanced receptor development based on preponderance of population as a site location. I really have some silly notions about "first come first serve", and also "he who gets there first controls the roost".

So I find it interesting that one of the treatments is direct androgen therapy. All though I am not sure how they define androgens (with ref. to other articles as well). If testosterone this would not work. So it would also explain why an AI or a SERM might "cure" "BBs" in minor early onset cases, which I am not sure if it really does. SO I AM WONDERING HOW ALL THIS RELATES TO THE PROSTATE AND CANCER as I suspect many of the same priciples are involved. An my uro did note a few years back that they were starting to consider SERMS as a treatment or preventative measure for PC.

The bottom line is that any one here using testosterone for any purpose is probably expediting the condition of gyno as an elderly or older person. The real question is what is the percentage of BC in these cases. IS IT HIGHER than women with NORMAL genetic breast tissue? I am guessing not and all a function of time the same. Every day as my wife ages her tits get bigger, I can help but wonder if this does not need to be controlled in real life application. WE JUST WEREN'T MEANT TO LIVE THIS LONG. But my one thought on gyno which would APPEAR to be different in womens breast development and function is the fact that gyno in young men appears to ellicit fluid production in many cases, whereas normal breast development in women does not. The development is clearly not the same, which could mean better, OR worse conditions..

To the last poster. Presciption Tamox is prescription. CEM MESO Store has a concoction available in liquid form as a bulk chemical sold that you can purchse. Take it for what its worth. It is suppsed to be the same thing.

A well known gynecomastia plastic surgeon told me that he has seen cases in which patients who had low T and gynecomastia had got a partial if not complete regression of their gyno after beginning T replacement and thereby not requiring his services. He did not say what the average age of the patients were however.

 

[BBC3]

Thanks for the input. I think I have heard that before but never followed up. One thing I can guarantee you is that they were not FATTIES I bet...

Also I have heard the concept of folks preaching that GYNO sets in AFTER SUCCESSION of steroids. IN fact, this was ALWAYS the gospel I heard as fear mongering growing up. I THOUGHT I had debunked this as how could one possible get gyno post cycle as the hormone supply has been removed.?? Lately, I am questioning RECEPTOR SITE HORMONE PROFILES that result from steroid use. And is there a domination by precendence, or new receptors grown during hormone application? So I think those rumors may have been true, and this may be why.

POINT - CLOMID while ON CYCLE MAY TURN OUT TO BE CRITICAL in preventing any potential estrogen receptor develpment in the soon to be documented I am certain.

A well known gynecomastia plastic surgeon told me that he has seen cases in which patients who had low T and gynecomastia had got a partial if not complete regression of their gyno after beginning T replacement and thereby not requiring his services. He did not say what the average age of the patients were however.

 

[UFgrad777]

Thanks for the input. I think I have heard that before but never followed up. One thing I can guarantee you is that they were not FATTIES I bet...

Also I have heard the concept of folks preaching that GYNO sets in AFTER SUCCESSION of steroids. IN fact, this was ALWAYS the gospel I heard as fear mongering growing up. I THOUGHT I had debunked this as how could one possible get gyno post cycle as the hormone supply has been removed.?? Lately, I am questioning RECEPTOR SITE HORMONE PROFILES that result from steroid use. And is there a domination by precendence, or new receptors grown during hormone application? So I think those rumors may have been true, and this may be why.

POINT - CLOMID while ON CYCLE MAY TURN OUT TO BE CRITICAL in preventing any potential estrogen receptor develpment in the soon to be documented I am certain.

Are Clomid and Tamoxifen similar?

 

[BBC3]

Yes there is plenty of availability with the seach engine. But long and short is they are both SERMS. They are also both touted similar in action with regard to jumpstarting the HPTA. Clomid is the historically used drug, and Tamoxifen is more recent and some say has a slightly better response. This is anecdotal and speculation for the most part, as each individual will always differ. Their action is that the are both physically similar to the Estrogen molecule and therefore compete with natural estrogen at the receptor point. The question, and variation in SERMS, is WHICH ESTROGEN RECEPTORS ARE BEING AFFECTED AND HOW. This is somewhat unknown moreso in WHICH. They just know area that the seem to act for sure. The variance in action is that some SERMS are AGONIST at SOME receptors, and SOME are antagonists. Who knows if all receptors are effected one way or the other for sure. So you also have other SERMS that have made their way into mainstream hormone modulation, like Faraston, which I think gave poor indications for GNRH/HPTA stimulation in one of the manufactures writeups I read. So it also depends on your cause, Breast blockade, or HPTA stimulation.... They are all typically developed as breast cancer drugs.

Are Clomid and Tamoxifen similar?

 

[UFgrad777]

Yes there is plenty of availability with the seach engine. But long and short is they are both SERMS. They are also both touted similar in action with regard to jumpstarting the HPTA. Clomid is the historically used drug, and Tamoxifen is more recent and some say has a slightly better response. This is anecdotal and speculation for the most part, as each individual will always differ. Their action is that the are both physically similar to the Estrogen molecule and therefore compete with natural estrogen at the receptor point. The question, and variation in SERMS, is WHICH ESTROGEN RECEPTORS ARE BEING AFFECTED AND HOW. This is somewhat unknown moreso in WHICH. They just know area that the seem to act for sure. The variance in action is that some SERMS are AGONIST at SOME receptors, and SOME are antagonists. Who knows if all receptors are effected one way or the other for sure. So you also have other SERMS that have made their way into mainstream hormone modulation, like Faraston, which I think gave poor indications for GNRH/HPTA stimulation in one of the manufactures writeups I read. So it also depends on your cause, Breast blockade, or HPTA stimulation.... They are all typically developed as breast cancer drugs.

Thanks.

I started with tamoxifen to combat gyno. I then read some favorable research on raloxifene so my dr. switched me to it. I can't say if the ralox has prevented a bad situation from getting worse but I do know there has been no regression in size whatsoever . If anything it has increased in size slightly. I am considering going back to the tamox just for cost reasons.

Maybe clomid would work.

 

[BBC3]

I am considering the use of Tamox to combat minor gyno myself.

I think that one of the problems with gyno that goes understated is the fact that once gyno is developed, IT IS SOMEWHAT SELF-SUSTAINING EVEN AT NATURAL HORMONE LEVELS, as it within its self, is generating the hormone conversion. I believe MANY are unaware of this as they quit at the very beginning of "the BB" and thus it is small enough that when the lactation ceases, it resides to unnoticeable, but primarily it is still small enough in the growth cycle to take many more years to rear its head again naturally. HOWEVER, I think there is a threshold as it relates to the size of the "BB". I am speculating the "BB" should be classified as a "Croftsman" or Benjamin"[)]. Meaning once one has the Benjamin, or 22 caliber, its gonna go on its own. Thats IMO. I am pretty sure I will now be playing around with a SERM the rest of my life to control it.

Something that really shocked me recently is the response I had to Wellbutrin when trying to sessate tobacco use. And I have used it before no probs. However, this time my titties were acting like I was supplementing hormones and juicy as hell. I had not touched any testosterone for over 6 months at the time and was pretty much trouble free. The wellbutrin actually progressed development further! This is an understated side effect in women and I think a strict accross the board for them that speculated as understated for polical reasons.

So let us know how Tamox works for your situation or PM me in a few weeks as I am curious.

BACK TO THE GENERAL SUBJECT OF GYNO IN MEN. One thing I am finding curious is that it would seem that there is lactation activity in the majority of steroid related gyno regardless of size, and in those with lactate activity, IT SEEMS TO BE NON-STOP. This condition does not exist in women and worries the shit out of me. For others reading you say, "bullshit, my titties never went leaking down my shirt". Well, what I have noticed is that you will only REALIZE the lactation if you have impropery duct development, which in essence I believe to be the reason for the "BB". So what I noticed is that I could get precipitate from either side, however, the one with the "bb" seemed only to express from an area away from the "tit", but within the areola. And thats some serious squeezing mind you. I will also point out that while its hard to keep your hands off the little bastards, I dont think its a good idea. But the long and short is that the nipple with more "normal" breast type development makes the same amount of lactate I SPECULATE, its just not trapped. So why then the regular lactation in males with breast develpment? I speculate as our hormone profile is different than a womans, it has something to do with the elevated levels of testosterone AS A NATURAL STATE that are converting to the required hormones that exists in a pregnant woman. Whereas they simply do not have the levels required to lactate year round, we do! So the question is how does this affect our HEALTH long term? I am starting to speculate gyno may need to be removed in all cases on duct type develpment. I wonder. And I am also thinking easiest if nipped in the bud. I AM HOPING that the horror stories I have heard refer to serious puberty onset cases will extended development on all fronts, and that someone with a "BB" can just have it "cut out no prob". I still fear reading some of those posts as it may drive me to having surgery if I become obsessed with the notion of correcting it. So I will try Tamox soon and report myself.

Thanks.

I started with tamoxifen to combat gyno. I then read some favorable research on raloxifene so my dr. switched me to it. I can't say if the ralox has prevented a bad situation from getting worse but I do know there has been no regression in size whatsoever . If anything it has increased in size slightly. I am considering going back to the tamox just for cost reasons.

Maybe clomid would work.

 

[Bridger]

Thanks.

I started with tamoxifen to combat gyno. I then read some favorable research on raloxifene so my dr. switched me to it. I can't say if the ralox has prevented a bad situation from getting worse but I do know there has been no regression in size whatsoever . If anything it has increased in size slightly. I am considering going back to the tamox just for cost reasons.

Maybe clomid would work.

I tried raloxifene for gyno a while back. It seemed to help. My doc wrote the script for 30 60mg tablets a month. But Anecdotal internet sources said 120mg/day for a month or two was effective. I was only able to stockpile enough to run 90mg for 45 days. I saw or felt noticeable decrease in the size of the lumps. I would like to give it another shot a 120mg day for two months before i look into surgery.

 

[UFgrad777]

I tried raloxifene for gyno a while back. It seemed to help. My doc wrote the script for 30 60mg tablets a month. But Anecdotal internet sources said 120mg/day for a month or two was effective. I was only able to stockpile enough to run 90mg for 45 days. I saw or felt noticeable decrease in the size of the lumps. I would like to give it another shot a 120mg day for two months before i look into surgery.

Interesting. I did run ralox at 120 mg but only for a few weeks.

Guys, I know this question seems off topic but I will bring it into focus later as it relates to my gyno development. My question is does SHBG levels vary throughout the day as does ones natural Testosterone levels? Or is it assumed to stay level throughout the day?

 

[Cleyon]

Thanks for this great information! I still have smoke coming out of my ears from trying to understand everything Dr. Scally said, but this is an invaluable resource!

 

[Jimstigator]

I am no expert but have used a good bit of Tamox (Nolvadex).

Over the past 10 years or so, I have had a few hormone imbalances occur which, among other things, gave me gyno... tenderness, lump, puffy nipple, increase of breast tissue. All three times Nolva successfully restarted my pituitary, but so far, it has not stuck for more than 4 or so years.

First time (7 years ago) treated with 30mg Nolvadex for 30 days and it went away completely.

Second time (4 years ago) - Treated with 30mg Nolvadex for 30 days and again, it went away.

Third time (Jan 2010-current) - Back on Nolva at dose of 20-30 mg for past few months. Lump smaller but not gone. Very tender under shirts still. Any additional brest tissue did go away. Provides relief, but I believe estrogen can push its way through.

-Jim

 

[UFgrad777]

I am no expert but have used a good bit of Tamox (Nolvadex).

Over the past 10 years or so, I have had a few hormone imbalances occur which, among other things, gave me gyno... tenderness, lump, puffy nipple, increase of breast tissue. All three times Nolva successfully restarted my pituitary, but so far, it has not stuck for more than 4 or so years.

First time (7 years ago) treated with 30mg Nolvadex for 30 days and it went away completely.

Second time (4 years ago) - Treated with 30mg Nolvadex for 30 days and again, it went away.

Third time (Jan 2010-current) - Back on Nolva at dose of 20-30 mg for past few months. Lump smaller but not gone. Very tender under shirts still. Any additional brest tissue did go away. Provides relief, but I believe estrogen can push its way through.

-Jim

Jim,

Did you use brand or generic tamoxifen?

 

[Jimstigator]

1st time - Liquid "Research Chemicals"
2nd time - Prescribed, generic tamox
3rd time (current) - Prescribed, generic tamox. My pharmacy doesn't even stock the brand name stuff (Nolvadex).

-Jim

 

[BBC3]

You are posting a little confusing. I believe you said Nolva restarted your pituitary fine - and no further problems, HOWEVER the STOPPING of the Gyno is not taking more than 4 years? Right??

You have to understand that this is the issue and why the development of gyno is so understated as a risk. One you have developed the tissue, you have BOUGHT IT..!! Its not going anywhere - EVER.. Short of a scalple... It may recede as once you remove the hormones action on it, the assoiciated inflammation, or ACTIVITY will cease. You may also find fluid activity that will cease. But only for a while.

The factors that determine how successfully one SHUTS IT DOWN are probably up in the air. I suspect their is some influence by local tissue receptors (pecs, etc) that helps. Thats a hunch. But you really dont hear a lot of BBs complaining past the point of supping.

But the most important factor you are missing is that these "breast Tissues" a male develops as gynocomastia HACE THEIR OWN :RECEPTORS!! So its like a snowball rolling down a hill. The more breast tissue is built, the more likely to have further gyno. Soon even without supping I suspect, it will thrive on its own. BUT FINALLY, may now even be generating hormones that are disruptive to other tissues and more systemic as awhole....

Again, developing Gyno via steroid use is like accelerating the normal development in a avg male to the point of 70 years worth or more...

I am no expert but have used a good bit of Tamox (Nolvadex).

Over the past 10 years or so, I have had a few hormone imbalances occur which, among other things, gave me gyno... tenderness, lump, puffy nipple, increase of breast tissue. All three times Nolva successfully restarted my pituitary, but so far, it has not stuck for more than 4 or so years.

First time (7 years ago) treated with 30mg Nolvadex for 30 days and it went away completely.

Second time (4 years ago) - Treated with 30mg Nolvadex for 30 days and again, it went away.

Third time (Jan 2010-current) - Back on Nolva at dose of 20-30 mg for past few months. Lump smaller but not gone. Very tender under shirts still. Any additional brest tissue did go away. Provides relief, but I believe estrogen can push its way through.

-Jim