Gyno - Bitch-Tits - Gynecomastia

 Luckily "gyno", or in this case lipomastia, does not always look that bad. Oftentimes it is more subtle, yet still annoying a psychological burden for men suffering from it. This pictures alone should be reason enough to give all the 45+ contributing mentioned in this article a wide, wide berth

If you type "gynecomastia" into your favorite search engine, your chances to find one of the major fitness and bodybuilding forums among your first hits are about 99%. This indicates that gynecomastia, lipomastia, "bitch tits", "fat tits" and whatever else many people use to measure by the same yardstick is much more prevalent than you would think if you conducted a survey on the street. The reasons for that are manifold. Men, who frequent those bulletin boards are oftentimes more conscious about their looks than Mr. Average, they are also more prone to be exposed to exogenous hormonal agents that can contribute to the development of the aforementioned unaesthetic pathologies. Most importantly, though, gynecomastia is something you don't talk about. You have it, you suffer, but you don't talk publicly about it - after all, that would just make you even more unmanly! Right? No, false! Utterly false!

In fact, the widespread implicit understanding that the above statement was right is a damn good reason for me to do the opposite and talk, or rather write about causes  and ways to get rid of this humiliating condition .

Why does my chest look like that, god damnit?

According to the currently accepted scientific paradigm, gynecomastia is a result of hormonal imbalances; mostly an overabundance of estrogen, which stimulates the glandular tissue of the male breasts and thus contributes to its growth and, in some cases, cancerous degeneration. The underlying reasons for these imbalances, on the other hand, are manifold and only partly understood. And while we will have a closer look at numerous individual factors in the following paragraphs, exogenous estrogens and estrogen like substances, an increased metabolism of androgens and an inhibition of the degradation of estrogens in the liver are probably the worst offenders.

"Prolactin gyno" - does it exist? Although I suspect that >60% of the "prolactin gynos" you read about on the pertinent bulletin boards are in fact mediated by high estrogen levels, there is scientific evidence for the occurrence of abnormal tissue growth in patients with prolactin-secreting tumors (Giminez-Roqueplo. 1999) - it thusly appears possible that compounds which either interact directly with the respective receptors or the administration of which will produce abnormally high prolactin levels, could lead to the development of gynecomastia in men. In view of the antagonistic relationship of prolactin and dopamine and the complicated interactions between dopamine and testosterone levels, it is yet well possible that this is just another instance of hypogonadism, in this case as a result of elevated prolactin and suppressed dopamine production.

These imbalance do not inevitably lead to an actual increase in breast tissue, though. Minor imbalances or chronic low exposure to synthetic or natural estrogens / estrogen-like compounds will often produce a general often subtle feminization of the male body, which is accompanied by an increased deposition of body fat in the chest area. In more severe cases, this can be a very pronounced accumulation of dense adipose tissue right under and around the nipples. And while these pseudo-gynecomastias or lipomastias may be totally benign, the humiliating "chest fat" is oftentimes just a companion or forerunner of pathological changes in the neighboring breast tissue.

A necessarily incomplete overview of the worst offenders

In the following overview that does not make any claims of being complete, I will thus not even try to make predictions like "... is more likely to cause lipomastia" or "... will rather induce gynecomastia". Moreover, you should also keep in mind that all of the pathologies, drugs and supplements can contribute to the development of gynocomastia, lipomastia and plain "chest fat", yet none of them, not even those for which a causal relationship has been established, will inevitable lead to the growth of the highly unaesthetic and potentially hazardous tissue overgrowth in the chest area!

Pathologies / diseases that are commonly associated with abnormal fat deposition, lipomastia and gynecomastia in men:

* Hypogonadism - Often but not always characterized by increased FSH, LH and SHBG levels and decreased total and free testosterone, as well as DHEAS levels; one of the most common non-environmental / drug-related reasons is Klinefelter' syndrome, a condition in which men have an extra X chromosome and which is usually associated with hypogonadism and reduced fertility (Yazici. 2010)

* Obesity - Obesity can contribute to the development of gyno- and even more lipomastia. In that it is not certain whether it is just a corollary factor with hypogonadism as the common denominator, or contributes directly to the development of unaesthetic and/or pathological changes in the breast tissue through an increased aromatization of testosterone into estrogen in the abundant adipose tissue (Wake. 2007)

* Liver cirrhosis - A cirrhotic liver (either due to alcohol or NAFLD) cannot metabolize the sex steroids properly. This does often result in low free testosterone and high estrogen levels, which can cause increases in chest fat or an enlargement and / or cancerous growth of the breast tissue (Cavanaugh. 1990). Similar effects could by the way arise from the (over-)use of supplements, such as berberine, quercitin, naringine, piperine, schisandra etc., which mess with the cytochrome P450 cascade, an enzymatic cascade that is responsible for metabolizing drugs and hormones (e.g. Gurley. 2012; Guo. 2012; Ho. 2000).

While the former were more or less "organ-related" causes of gynecomastia, the following list contains a handful of drugs that have scientifical evidence to back their causal involvement in the etiology of gynecomastia:

Anabolic steroids & prohormones - Either due to increased estrogen levels on cycle, hormonal shut-down and hypogonadism or hormonal imbalances after the cycle, use of compounds that have the potential to induce gynecomastia in PCT (see "hormonal agents" in list below) or (possibly) direct or indirect effects on prolactin (see red box above)

Other endocrine agents - Bicalutamide, Diethylstilbestrol, Dutasteride, Ethinylestradiol, Finasteride, GnRH, Goserelin, Leuprorelin

Drugs for gastrointestinal disorders - Metoclopramide

Diuretics - Spironolactone

In view of the fact, that most people will be aware of the dangers, it yet questionable in how far the commonly overlooked / largely unknown drugs and other offenders with less, but still existend scientific evidence to bolster their involvement in the development of abnormal fat deposition, lipomastia and gynecomastia in men do not pose a much greater threat. You should thus better beware of these:

Statins - Roberto et al. report a significantly higher incidence in male gynecomastia among statin users (Roberto. 2012). Interestingly, the relative increase in risk correlated with the ability of the respective drug to inhibit HMG-CoA, or, if you will, it's potency. Intriguingly, gynecomastia is rarely mentioned as one of the myriad of potential side-effects of statin treatment, although the non-corrected incidence rate in the database records Roberto et al. analysed was 1/68 - with 25% of the US population in the 45+ age range being "on a statin", this would translate into roughly 1Mio! cases of statin unduced gynocomastia among the baby boomer generation, alone (this calculation assumes that there are ~70Mio babyboomers, which would be in accordance with data from census.gov). You should also keep in mind that if statins can do that supplements, like red yeast rice, which is actually nothing but a natural statin, are likely to be able to induce gynecomastia, as well.

Proton pump inhibitors - Omeprazole, Ranitidine & co.

Antineoplastic agents & Calcium channel blockers - Estramustine, Imatinib, Mandipine, Nicardipine, Nisoldipine, Nitrendipine

Antivirals & -mycotics - Didanosine, Efavirenz, HAART, Indinavir, Ketoconazole, Nevirapin,

Lipid modifying drugs - Bezafibrate

Diuretics - Eplenerone, Bumetanidine

Hormonal agents - Chlormadinone, Clomiphen, Cyproterone acetate, Follicle-stimulating hormone, HCG, Medroxyprogesterone acetate

Immunosuppressants - Cyclosporin

Psychoanaleptics & Psycholeptics - Fluoxetine, Haloperidol, Olanzapine, Risperidone, SSRIs, Sulpiride

Despite the fact that for many of these drugs the exact mechanisms have not yet been elucidated, it is likely that in most cases their "pro-gyno effect" is a downstream result of impairments of the HTPA (hypothalamic-thyroid-pituitary-axes), liver function or both and thus eventually mediated by the same fundamental hormonal imbalances that were discussed in the second paragraph of this article.

Prevention is #1, but sometimes treatment is inevitable

Even if you don't have a plenty of skeletons in your closet, no history of legal or illegal drug abuse, no diet-induced NAFLD, are lean, don't use truckloads of useless supplements etc., puberty and "bad genes" alone could have left you with a batch of unwanted tissue in a place where it certainly does not belong. In this case, avoiding all the 45+ aforementioned factors may help not to make things even worse, it will yet not make those ugly little bastards disappear over night; and I guess that alone should be reason enough to come back for part II of this series, in which we are going to take a look at potential treatment strategies - including, but not limited to classic surgical interventions.

 Is it what he eats, is it what he drinks or is it just  andropause? Whatever it may be, Jack does not have the "classic gyno".

In the last installment of this two-part series on gynecomastia, lipomastia and co. we have seen that the number of appellations this common, mostly benign enlargement of the male breast has been given, is easily outnumbered by the potential, mostly pharmacological, but also supplemental and/or dietary factors which have been implicated in its development. In a recent paper, Krysiak and Okopien estimate the incidence of mild proliferation of the glandular breast tissue to 30%-50% of the male population (Krysiak. 2012). Against that background, the universal ignorance towards the profound psychological effects, as well as the tacit acceptance that, breasts or no breasts, "men don't cry" are certainly uncalled-for.

If it's benign you got to live with it!

The idea, "if it's not cancerous", it won't hurt, is probably also the main reason for the lack of viable (N=5), let alone "proven" (N=1, surgery) treatment strategies. A couple of case-reports and small scale studies do yet suggest that its surgical removal, which is uncertainly the method of choice for non-benign or exuberantly proliferating tissue growth, is not the only option you may have to get rid of a condition of which I suspect that it has been bothering many of you for years now.

Whichever of the following strategies you may pick, your first step should always be to avoid / drop all of the 45+ offenders I mentioned in the last installment, and to avoid the 10 previously discussed anti-androgens like a plague. Yet while these "passive" treatments may suffice to stop your breasts from growing even further, it is unlikely that they will put a long lasting real gyno (not just normal fat!) in remission. If you are among these unfortunate, yet certainly not rare cases, you may have to resort to one or more of the following "alternative" (from the perspective of most MDs) but not mutual exclusive anti-gyno strategies.

Getting rid of "gyno" by losing body fat (not weight!)

This poor boy may not know it, but he is just lying the fat foundation for embarrassing female breasts

It should actually be obvious that losing excess body fat is the logical next step following aforementioned necessity to avoid anything that could precipitate gyno. Aside from the constant assault to xeno- (BPA & co=)and purportedly healthy phyto-estrogens (soy & co), the obesity epidemic is probably the main reason for the high prevalence of enlarged breast tissue in the male part of the population, anyways. Particularly during puberty, when the natural hormonal production overshoots the increased aromatase activity in the abundant adipose tissue of today's Playstation gambling couch potatoes can be hazardous.

Puberty and the spontaneous regression of pubertal gynecomastia can yet also serve as an encouraging example that an ample increase and stabilization in the androgen to estrogen ratio, as it should occur towards the end of puberty, can send mild cases of pubertal gynecomastia and lipomastia into remission. Similar effects can be seen in adults, when

you lose fat without starving yourself - Starvation would lead to decreased androgen production and could, if anything, help not to make things even worse; more often than not, it does yet make things worse. After all, large breasts on a skinny man look even worse than breasts of the same size on a slightly chubby guy.

you are gradually losing fat over a long period of time - It is more than likely that the chest fat is going to be the last to go; in fact, it may take a profound reduction in total body fat shift the androgen-to-estrogen ration into the normal range before you see any improvements

you don't resort to questionable fat burners - with herbs, tea or whatever extracts in them that will have either direct estrogenic or anti-androgenic side-effects or mess with the cytochrome P450 cascade of your liver (see previous installment)

Fat loss is a particularly good tool to get rid of "fat tits", i.e. an unbalanced deposition of regular fat tissue. It will take its time, though, and it won't help to combat "acute flare-ups" from the (obviously accidental) ingestion of certain "supplements". It is likewise unrealistic to assume that it would put a full-blown gynecomastia, i.e. the (over-)growth of glandular tissue, cancerous or not, into remission.

Getting rid of "gyno" with Tomaxifen, a selective estrogen receptor inhibitor

In view of its kinship with breast cancer, it should not surprise you that the single scientifically well-established anti-gyno agent is a selective estrogen receptor modulator, in short SERM. Tamoxifen, brand name Nolvadex, has been used in a couple of small scale trial with reasonable success (e.g. Parker. 1986; Algaratnam. 1987; McDermontt. 1990; Ting. 2000), the results of which Braunstein et al. summarize as follows (Braunstein. 2007):

[A]dministered orally at a dose of 20 mg daily for up to 3 months, has been shown to be effective in randomized and nonrandom-ized trials, resulting in partial regression of gynecomastia in approximately 80% of patients and complete regression in about 60%.

Despite the existent evidence that would support the use of Tamoxifen as the "anti-gyno" drug of choice, Daughty and Wilson, in their 2003 letter to the editor of the British Journal of Medicine, rightly state:

The evidence base for their conclusion is small (135 patients) and is certainly not derived from randomised controlled clinical trials. [...] until more evidence shows that tamoxifen is safe in this condition it should not be recommended as first line treatment, especially in pubertal boys.

If you add to that the potential hepatoxicity, as well as the two documented cases of epigastric distress and the one known case of  post-traumatic deep-vein thrombois, it is self evident that you and your medical practitioner should carefully monitor your liver as well as other health parameters if you decide to give Tamoxifen or alternatively Clomiphene (cf. Plourde. 1983) a try.

Getting rid of  "gyno"  with  aromatase inhibotors

There is also some evidence from case reports that would support the use of 2nd generation aromatase inhibitors (AI), Letrozole, in particular, to combat gynecomastia. As Braunstein et al. point out (Braunstein. 2007), their efficiency seems yet to be limited to cases, where over-aromatization of testosterone into estrogen is the underlying reason of the the problem. If this applies to you, talk to your medical practitioner about the use of a very low dose of letrozole, like 2x per week 2.5mg.

Note: In a 2004 randomized controlled trial by Plourde et al. the "standard AI", Anastrazol, was ineffective for patients with residual pubertal gynecomastia (Plourde. 2004). Similarly, Riepe et al. found no effects in pubertal boys other than a reduction in breast tenderness (Riepe. 2004). It is therefore, as Sarah L. Maidment points out not not just that "Anastrozole may not be more effective than placebo in decreasing the size or volume of breast tissue in persistent pubertal gynaecomastia", but also that "its long-term effects and safety are still unknown" (Maidment. 2010).

If the over-aromatization is related to an increased amount of body fat, this treatment strategy should be complemented by appropriate lifestyle changes (diet + exercise; follow the SuppVersity for daily tips on what works). The effectiveness of your weight loss efforts will be largely augmented by the restoration of a normal estrogen-to-androgen ratio and will hopefully allow you to maintain the latter once you seize taking the drug.

If you hesitate to use a "real" aromatase inhibitor you could also resort to melatonin, of which a dose as low as 3mg melatonin per day taken at 5pm for 6-month can shift the testosterone-to-estrogen ratio into the desired direction (Luboshitzky. 2002)

Getting rid of "gyno" with topical DHT cream

Largely unknown in the US, but a relatively common treatment strategy in Europe, in particular in France, is the use of topical DHT cream. The available literature on this issue is scarce. The results of one of the few well-documented trials by Kuhn et al. are yet promising and stand in line with the natural "anti-estrogenic" effects of dihydrotestosterone (Kuhn. 1983):

Local administration of DHT was followed by the complete disappearance of gynaecomastia in 10 patients, partial regression in 19 and no change in 11 patients after 4 to 20 weeks of percutaneous DHT (125 mg twice daily).

This is a 33% success rate in patients with idiopathic (meaning we don't know the underlying reason) gynecomastia. That is less effective than tamoxifen  and certainly neither what you would call a "tried and proven" method, but probably better than the bro-scientific use of DHT-precursors and pro-steroids with structural resemblance to DHT. Especially in the US, it may however difficult to find a medical practitioner who would be willing to prescribe and monitor this treatment, I guess.

Conclusion and the last resort: Surgery

 Assuming that you find a surgeon who knows what he is doing, surgery is unquestionably the best - diet and exercise aside, probably also the safest treatment strategy. In cases of non-benign gynecomastia it should be the go-to treatment, anyway.

If we take a final look at the meager amount of treatment options, it stands to reason that the avoidance of anything that could exasperate the condition, as well as the reduction of body fat should have priority over all other treatment strategies. If those fail, the next step should be a comprehensive hormonal panel, on the asis of which you and your medical practitioner should decide which route to go.

In case none of the pharmacological approaches works, you can still resort to to surgery (or radio-therapy, but I guess most of you will prefer the knife, right?), the "gold standard therapy for symptomatic gynecomastia in most patients" (Johson. 2011). Just make sure you do not spoil the ship for a ha'porth of tar - or put more simply, go and seek an expert!