By Thomas O’Connor, MD 5/3/2016 
Anabolic/Androgenic steroid (AAS) use is associated with a host of side effects- some can be serious and cause medical disease, others are more of a nuisance and can lead to a poor quality-of-life and cosmetic issues like gynecomastia. Of all the known side-effects of AAS, gynecomastia has to be one of the most infamous for sure. On the “steroid boards”, there are literally millions of blog posts discussing this common medical issue. With so much variability on this subject across the boards, I decide to write this article as a primer on how I see AAS related gynecomastia.
Since the early days of AAS use, men have been suffering with Anabolic Steroid Induced Gynecomastia (ASIG). It’s no wonder why this entity is known as “Bitch Tits”! How ironic; men take these drugs to be big, strong and too enhance their masculine physiques, but soon after starting these agents many develop tender, puffy nipples that resemble a woman’s breast. As an expert physician regularly seeing patients on AAS, I can tell you that this issue is in the top 10 most common reasons why men come see me.
Let’s review the basic physiology of how AAS lead to increased or “superphysiologic” estrogen levels and therefore gynecomastia. It should be noted that not all AAS that cause gynecomastia do so by direct conversion to estrogen. Some can directly and or indirectly cause gynecomastia via other specific mechanism-of-actions (MOA), e.g., Anadrol and its relations to “inherent estrogenic activity” and AASs trenbolone and nandrolone are associated with developing gynecomastia via direct stimulation of breast progesterone receptors in addition to causing elevated levels of systemic prolactin.
This article will focus on the “classic” AASs that lead to increased systemic estrogen levels and estrogen- based-gynecomastia. The normal man has testosterone/estrogen ratio of about 100/1. Certain types of AAS distorted this ratio. The exact MOA of how this happens is unknown, but it is thought that the body tries to maintain balance by increasing systemic estrogen levels in an attempt to counter the elevated testosterone/androgen/ susceptible AAS levels and or that there is some other “substrate’ driven model where a man’s body converts testosterone/androgen/susceptible AAS to estrogen in a liner fashion; specific drug/dose and gene dependent- man-per-man. Like many other things in human physiology,
I believe this is a truly multifactorial model. We know that there are many “polymorphic” genes involved here and that some men can take over 1 gram of testosterone IM per week, in addition to other aromatizable AAS and have no signs of gynecomastia, while other men suffer with severe gynecomastia on a low dose physiologic testosterone regimen. Hence, this topic is very controversial- even for some of the most cerebral, brightest Bro-Scientist’s!
What we know:
The human body has an enzyme called aromatase that converts androgens into estrogens and is found in various tissues and cells including adipose, blood vessels, brain, bone and skin cells (J Am Ac ad Dermatol. 2001 Sep;45(3 Suppl):S116-24.). It is thought that when aromatizable steroids like, testosterone esters/suspension, Dianabol and methyltestosterone interact with aromatase, these AAS agents are converted to systemic estrogen. And as previously stated, the MOA in addition to the “degree of conversion” has not been fully elucidated.
One thing for sure is that men will know when they have reached the “threshold” for estrogen levels to be high enough to cause gynecomastia, as they start to feel uncomfortable symptoms such as breast –nipple warmth, soreness and tenderness to even the slightest touch of a light shirt! The physical changes that can happen to a man’s pec/breast area can cause cosmetic disfigurement and lead to significant embarrassment- making some men feel ashamed at what they have done.
What can be done:
It goes without saying that the only way to avoid gynecomastia is to not take AAS or even Pro-Hormones. As a physician, I have a duty to educate you on this subject and to tell you that like any other drug-related side effects, you need to think deeply before you start taking anabolic steroids! I really mean this! So many men come to me and say that they wished they would have done more research on AAS prior to starting to use them and that if they did, they either would not have used them or certainly would have used them in a more conservative manner. Again, this is from the lips of experienced AAS users that I have seen over many years and NOT medical advice from me!
As discussed above, there are AAS that are susceptible to aromatization and will convert into systemic estrogen leading to gynecomastia in a drug/dose/man-per-man fashion. The boards talk about two medications that can limit the systemic conversion of androgen/aromatizable AAS to estrogen and block the effects of estrogen at the breast tissue site, respectively: Aromatase-inhibitors (AIs) and Selective Estrogen Receptor Modulators-SERMS. These are medications mainly intended for breast cancer, treating infertility in women and men and postmenopausal osteoporosis. These medications are very powerful and do work well for what the AAS user is looking for. I am amazed of how the AAS using community has learned how to use these drugs without the guidance of a physician over the past 20 years!! My concern is for the side effects of these medications. Most experienced AAS users take a two tier approach to the utility of these drugs- They use AIs, mainly for “prevention” during a AAS cycle, to keep systemic estrogen down and SERMS for “on the spot-emergency” situations of gynecomastia symptoms.
For anyone who “does their homework” and uses AAS with these agents, as esoteric as these prescribing methodologies are, it seems that the symptoms of gynecomastia will be absent or at least limited. The problem is that these medications can lead to some serious medical issues. The AIs can definitely reduce systemic estrogen levels while on testosterone and aromatizable AAS and I have seen that most men that come to me on AAS with AIs, either from the streets or from Anti-aging Clinics, their estrogen levels are zero! Living with very low or “no” measurable estrogen is not sustainable with any quality of life and can pose great health risks. Yes, there is less water retention and it is thought that body fat accumulation will be reduced in a physiologic climate of a high androgen/“low estrogen state”. This may be true, but again is it sustainable and how safe is it?
The most worrisome things I see and try to educate regarding the use of AIs are the adverse effects on the cardiovascular system. Anyone who knows me and my medical practice knows that I am the Cardiac “Guru”! Everything I do is focused on heart protection!! After all, the rate limiting step in life will be your heart!!! AIs are devastating to the good cholesterol HDL!! The problem is that many men have a naturally low HDL level and this is thought to be one of the reasons why men have heart disease earlier then women. I have seen several men on AASs and AIs suffer with blocked arteries. Apart from the heart issues, I see men complain with sexual issues and depression in addition to erratic behavior from AIs. We need balanced estrogen in our brains to think straight and for optimal sex. Another side effect of the use of AIs, although it would be a long-term consequence is the possibility of medication-induced osteoporosis. I have not seen this in my medical practice, but any man who uses AIs chronically and has low or absent estrogen for years would be at risk for this.
The SERMS are a class of drugs that act on estrogen receptors. The specific MOA that makes these agents so unique is that they act as agonists (stimulating activity) in some tissues and antagonist in other tissue (blocking activity). The AAS using community classically likes to use Tamoxifen, which is used medically for breast cancer, for the treatment of osteoporosis and “experimentally” for the lipids. As stated earlier, this SERM is used to “block” or deactivate systemic estrogen that is circulating. Remember, AIs block the production of estrogen from the conversion of androgen to estrogen in the body, so when there is sufficient circulating estrogen, breast tissue may be effected and gynecomastia may ensue.
Tamoxifen appears to reduce acute symptoms of gynecomastia in anecdotal terms, but again, like the AIs, I worry about the dangerous side effects and sustainability of these drugs. Especially when used concomitantly with AAS. Because this drug does nothing to reduce systemic estrogen, there is an increase in intravascular fluid (water retention) that can lead to hypertension. Fat storage appears to increase as well with this class of medications. These side effects are trivial compared to the potential for DVT (blood clots in the lower legs) and PE pulmonary embolism (blood clots in the lungs that can lead to death) that have been associated with Tamoxifen. Cancer. 2009 Oct 1;115(19):4442-9. doi: 10.1002/cncr.24508.
There has been discussion over the years, mainly by “Guru” Bro- Scientists that Tamoxifen is some kind of panacea regarding the deleterious effects AAS have on lipids- specifically HDL. I can tell you that this notion has never panned out clinically and I would say that using Tamoxifen to protect against heart disease while on AAS is nothing more than NUTS!
Is there a role for these medications in the clinic?
Yes. Men who use AAS need to see an expert Internist or at least a mid-level practitioner who is experienced with AAS use and at least have laboratory studies done, a physical exam for breast, heart and prostate health in addition to vital signs, e.g. blood pressure monitored! No ethical physician will turn away a man asking to have his blood pressure taken, a physical exam and his labs drawn regarding risks associated with AAS.
Clomid is a SERM and works well for men with hypogonadism/testosterone replacement therapy (TRT)- both for men who wish to maintain fertility and for standard TRT. This medication is a classic part of Post Cycle Therapy (PCT). It has been shown more recently in the literature to be a useful agent to wean men off AAS World J Nephrol. 2015 May 6; 4(2): 245–253. Today, we are seeing many general physicians in America using Clomid and other ancillary agents like HCG to help reduce suffering and recover men diagnosed with anabolic steroid induced hypogonadism (ASIH). In addition to this, there is a place for AIs in the management of men on TRT. Some men who are on appropriate-dose physiologic testosterone replacement can manifest superphysiologic levels of estrogen, despite normal testosterone levels.
Remember as discussed above, testosterone/estrogen balance is a multifactorial issue and some men simply have genes for becoming “out of balance” on TRT. When used in a very cautious and limited fashion, in men who have low heart disease risks- specifically normal HDL levels, the addition of a low dose AI to TRT can lead to improvements in quality of life via balancing androgen/estrogen levels. When this is done by an expert physician and the qualified patient is observed closely, symptoms of gynecomastia are rare as are adverse issues related to mood and sexual complaints. It’s all about balance and vigilance! Another very important point regarding TRT and superphysiologic levels of estrogen is the potential for breast cancer! The good news is that there is no definitive data indicating that TRT associated elevations of estrogen lead to breast cancer in men. I can tell you that this is something that any expert physician Rxing Testosterone to men has to think about and better have on his radar screen!!
On a closing note, the truth is that some men who develop AAS induced gynecomastia, despite close attention to AAS selection and regular use of agents discussed in this article, it may be necessary to see a plastic surgeon and have excess breast tissue permanently removed.
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Dr Thomas O’Connor, MD
