Gynecomastia in Bodybuilding: Just a Benign Condition?

Gynecomastia may be a cosmetic nuisance for bodybuilders taking anabolic/androgenic steroids (AAS), but some interesting reports have been published recently which indicate associated and unrecognized long-term health risks. One has to separate the causes of gynecomastia in the general population from those relating to gynecomastia in the bodybuilding population. While some overlap may exist, clearly most gynecomastia in bodybuilders is the result of self-administration of steroids. Numerous articles in the bodybuilding literature have dealt with the causes and prevention of gynecomastia. The purpose of this article is not to revisit those discus-ions. Suffice to say that all gynecomastia ? the result of hormonal imbalance between the ratios of estrogen and testosterone. In gynecomastia you get stimulation of e same kinds of tissue in the male breast that form milk glands and ducts in the female breast. This stimulation results in the development of glandular and ductal tissue behind the male nipple but can track into the region of the armpit. When hormonally stimulated, the tissue in these regions may become swollen and painful. As long as lumps have not formed, use of anti estrogen drugs can have a moderate degree of success in suppressing the hormonal stimulation.

The most commonly employed anti estrogens include tamoxifen (Nolvadex), clomiphene (Clomid), testalactone (Teslac), mesterolone (Proviron), and anastrozole (Arimidex). For any bodybuilder with persistent gynecomastia lasting longer than 12 months or in whom actual lumps have formed, surgery becomes the only corrective option.

Most cases of gynecomastia in bodybuilders occur from the use of anabolic/androgenic steroids, but that does not mean all cases arise in this manner. In a small percentage gynecomastia may represent an early warning sign of a tumor hidden somewhere in the body, most commonly located in the testes, adrenal glands, liver or lungs. Cancers in those regions can actually secrete estrogen or in the case of testicular cancer, both estrogen and HCG. These testicular tumors may produce gynecomastia before they can even be felt on physical examination. The peak incidence of testicular cancer matches the age group of bodybuilders most frequently using AAS, early 20s to late 30s, pointing out the need for a thorough physical examination of any bodybuilder having gynecomastia.

After periods of starvation a phenomenon termed "refeeding gynecomastia" has been recognized for some time. Starvation seems to produce testicular suppression during restricted calorie intake, possibly as a result of depressed levels of folic acid. This situation is analogous to the low-carb/calorie precontest diet bodybuilders use to achieve the defined and ultra ripped look necessary to win at higher-level competitive bodybuilding. When the restriction ends and the body is exposed to a relative superabundance of calories (the post contest feeding frenzy), increased testosterone production occurs along with increased conversion of testosterone to estrogen. Once the competition has ended, most bodybuilders cycle down their AAS use and supplement with HCG. Both of these measures can also result in increased estrogen conversion, and therefore a competitive bodybuilder using AAS is most susceptible to the development of gynecomastia in the period immediately after cessation of the AAS cycle. He should maximize any use of anti estrogen drugs during this time.

So why the concern over what has in the past been considered a cosmetic problem?

Even medical therapy is not without side effects. Doctors have used tamoxifen in the treatment of male patients with breast cancer, and up to 30 percent of those patients reported decreased sex drive, mood swings, weight gain and depression - not exactly the mental attitude and physical changes desired by bodybuilders. Coupled with the well-documented psychological effects of AAS, the percentage of psychological changes is probably significantly higher.

Neither is cosmetic surgery risk-free. Fatalities have occurred related to the local anesthetic agent gaining access to the blood stream and causing abnormal heart rhythms. Without proper attention to the ultimate cosmetic goal, some bodybuilders have been left with deformed pectoral contours In addition, because stimulated breast tissue can extend toward the armpit, if any of this estrogen-sensitive tissue is left behind, gynecomastia unfortunately can recur.

Most important, however, recent reports in the medical literature have found there is a change in the cellular architecture in the male breast which may in turn suggest gynecomastia actually represents a precancerous condition. Previous literature had well documented that no cause-and-effect relationship existed between gynecomastia and male breast cancer, even though up to 40 percent of patients with male breast cancer also have gynecomastia. Established risk factors for male breast cancer include undescended or injured testes, liver disease, occupational or medical exposure to x-rays or magnetic fields, and family history of breast cancer. Undescended and/or injured testes produce inadequate amounts of testosterone, resulting in a change in the ratio of testosterone to estrogen. Diseases of the liver also alter the ratio as the liver is the site where some conversion of testosterone to estrogen takes place. Atomic-bomb survivors have demonstrated radiation of any kind can produce chromosomal changes in cells, and clearly the most important areas for this subject are testicular and breast cells.

Approximately 300 men will die each year from breast cancer with roughly 1500 new cancers discovered annually in the United States. Breast cancer in males is usually detected at a later stage than in females, and overall survival rates are there-fore lower. This is not to say that male breast cancer is common. In fact, it represents less than 1 percent of all cancers in men. Recent studies demonstrated that changes can occur in hormonally stimulated male breast tissue.

Such changes make the cells in that tissue susceptible to cancerous transformation - in other words, a precancerous state.

One report found an abnormal condition called apocrine metaplasia that, when it occurs in association with gynecomastia is indicative of AAS use. This form of metaplasia (the development of cells in a part of the body where they are not normally found) in any patient with gynecomastia should prompt questioning regarding AAS use. While this phenomenon is not a cancerous condition itself, changes that occur in metaplastic cells can also be seen in cancer cells, again suggesting a precancerous state.

Finally, a recent paper from Brazil reported that alterations in hormone levels can induce chromosome changes in the cells of male breast tissue. This finding is frightening as it suggests a direct causal link between elevated estrogen levels and male breast cancer. Researchers based the hypothesis of a cause-and-effect relationship on a small number of patients. Their conclusion will have to be confirmed on a more widespread clinical basis, but it may represent a new and significant side effect of AAS use. The findings of precancerous and chromosomal changes clearly indicate that gynecomastia is neither a cosmetic nor a benign condition and it needs to receive appropriate medical attention.