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Gynocomastia in Anabolic Steroid Users
Gynaecomastia in Anabolic Steroid Users

copyright Peter Van Mol 2009

Gynaecomastia is the development of breast tissue in males. It’s a side-effect often associated with anabolic androgenic steroid use/abuse, although it’s not all that prevalent in healthy males. One study with low-dose testosterone (200 mg/week of an ester amounting to roughly 140 mg of actual testosterone) showed a prevalence of roughly 8% (1) and likely in athletes and people using steroids for aesthetic purposes the incidence is significantly lower for various reasons including lower body-fat (adipose tissue is a primary source of aromatase, the enzyme that converts testosterone to estrogen) and the use of higher doses. Higher doses lead to higher circulation of androgens for an equal amount of aromatase that converts testosterone to estrogen. Androgens are capable of inhibiting the estrogen-induced proliferation of mammary epithelial cells and abolish estrogen-induced augmentation of ER- expression (2). They also further promote pro-apoptotic (cell-killing) effects in a wide variety of breast cancer cell lines (3).

To have this discussion we need to understand what gynaecomastia (gyno for short) is exactly. It is merely defined, as stated above, as the growth of breast tissue in males. An itchy or painful nipple is neither a symptom of gyno or the onset thereof, a distinction I wanted to make clear before going any further because all too often in this community users report these unrelated symptoms as being gyno or signs thereof, one of the primary reasons for the overconsumption of treatments (valid or otherwise) against the problem. The development is influenced by a number of factors including estrogens, progestins, GH, IGF’s and prolactin whose interaction isn’t always clear and sometimes ambiguous. This will make it essential to focus on what we know, since its often the uncertainties that are cited by pseudo-scientists as a cause or reason for various mechanisms. Before going deeper into the science and evidence in this regard, its perhaps interesting to look at the clinical history of gyno and its treatment. A distinction is usually made on the basis of size, and this is used a measure to gauge the level of permanent fibrosis. Fibrosis is often referred to as the point of no return and is invariably treated with surgery to remove the breast tissue. Only a biopsy can give absolute facts on fibrosis, and likely a number of conditions diagnosed as type 2 based on size are still perfectly treatable by other means, but not so much vice versa. If the tissue is over 3-4 cm it is considered type 2, before that it is considered type1. Gyno is prevalent in pre-pubescent boys (incidences of 70% are reported in some literature) and then disappears during puberty when androgens (testosterone/DHT) increase nearly 30-fold and estrogens increase only 3-fold. When gyno occurs during post-pubescent periods it’s almost invariably treated with anti-estrogens. Postpubertal men have significant levels of circulating estradiol, but their effects on mammary tissue are prevented by the simultaneous presence of high levels of testosterone (4).The notable exclusions are cases of hypogonadism (which are treated with androgen therapy of all things, the very thing so many people blame for rampant gyno) and hyperprolactinaemia due to tumors. Mild hyperprolactinaemia is usually caused by excess estrogen (5) and also treated with anti-estrogen therapy. It is of note that endocrinologists are quite content with this treatment, as there is no search for improved therapy for gyno. In short the authorities in the matter agree that a decreased androgen:estrogen ratio is the basis for the development of gyno in all of the above cases except prolactinoma. This is just a brief sketch and only pertains to naturally occurring cases of gyno and those AAS-users that are smart enough to seek diagnosis and council from a medical professional.

Cases where estrogen is the obvious cause

In most cases there is no argument that the cause of AAS-induced gyno is a decreased A:E ratio, caused by aromatization of an androgen to an estrogen, predominantly through the aromatase enzyme. Popular steroids like testosterone and methandienone operate in this manner. The prevalence is low in athletes and people who use for aesthetic reasons. This is because usually the doses administered invariably cause a higher androgen level than the amount of estrogen created from aromatization. Of great importance here is understanding what increased risk factors are for developing AAS induced gyno. First and foremost a tendency to develop gyno when not using AAS is a huge risk factor. If this is the case for you, you should get to the bottom of the cause first. If it is caused by hypogonadism, odds are using AAS may actually be a treatment for you. But in most other cases it’s an unusual level of estrogen formation. In those cases it’s important to decide whether you really want to pursue AAS use, and if so, to take precautions. Reducing the amount of aromatizable steroids to the strictly necessary amount (200 mg/week of testosterone) and combining them with non-estrogenic androgens is one method, preventive use of anti-estrogens is another. Preference is usually given to aromatase inhibitors when used for prolonged periods of time, but use of SERMS is also acceptable, we will go into the mechanism of these drugs later in this article. A higher body-fat percentage, as was alluded to earlier, is also a known risk factor since adipose tissue produces aromatase. Higher body-fat can also make the condition seem more drastic than it is, since fat deposits around the nipples will usually be larger. They can both obscure gyno or make it look worse than it is. Adressing this issue prior to AAS use, or concomitantly with AAS use will also be of huge benefit in later diagnosis. Lastly a low level of 5alpha-reductase can play a role. This enzyme converts testosterone to dihydrotestosterone (DHT). DHT has clear roles in controlling A:E ratio (it’s the reason we speak of A:E ratio and not T:E ratio). It can block aromatase (6), may competitively inhibit the estrogen receptor (7) and converts to the estrogen receptor beta specific 3alpha-androstanediol. We’ll explain the role of the latter when we discuss SERMS. Its not easy to diagnose a low 5AR level if it isn’t giving your problems, but some people will use 5AR inhibitors to stop androgenic side-effects and these form a huge risk for gyno. I highly advise against the use of such compounds. If you are unsure, or have no valid reason to believe you are at more risk, I would however advise to start on moderate testosterone only (400-500 mg a week – something I advise regardless since testosterone is by and large the most studied androgen, best for health and gains and the reference for all other AAS) and see what happens. If you think you are developing gyno, I would first and foremost get the opinion of a medical professional that it is in fact gyno.
If he does not advise treatment, the best way to treat it acutely is with a SERM (Selective estrogen receptor modulator), tamoxifen being the most used and best studied. Tamoxifen will block the Estrogen receptor alpha in breast tissue, the receptor that plays the most important role in breast cell proliferation (replication) (8). Because it stops the actions of circulating estrogens at the receptor its effect will be somewhat faster than those of aromatase inhibitors, which will take some time to reduce circulating estrogen and start having an effect. If we would look at the blood levels of estradiol when using an AI or a SERM we’d see very different things. The AI will reduce the level of estrogens, whereas a SERM will increase it (short term only), because the SERM is keeping the estrogens from binding the receptor. The end result with regards to estrogen receptor alpha is the same however : no estrogens are activating this receptor, so proliferation is halted. The reason we prefer tamoxifen however is because there is a second estrogen receptor, estrogen receptor beta. Both are stimulated similarly by estradiol (the primary estrogen) but have different roles. Estradiol shows a slightly higher affinity for the alpha receptor. This is actually how estrogenic effects are regulated. The alpha receptor causes proliferation of cells, the beta receptor inhibits proliferation and increases differentiation, or the maturing process into a fully functioning cell. So when estrogen increases proliferation starts, and when it reaches a certain threshold more binds to the more abundant beta receptor slowing proliferation and increasing differentiation. This is relevant because though tamoxifen also binds the beta receptor it does so with less affinity than estradiol and its unclear as to whether it activates or blocks the beta receptor. The net result is that proliferation is halted by tamoxifen’s negative effect on the alpha receptor, but estradiol is left in circulation to activate the beta receptor. The beta receptor offers us several benefits I may choose to address in an addendum later on, but here specifically it will further inhibit proliferation (tissue growth) and increase differentiation. Terminal differentiation aborts the proliferative capacity of a cell. So each cell that terminally differentiates is one more cell that won’t be replicating. These cells now await apoptosis (cell death) at the hand of androgen-mediated action (2,3,10,15,17,18,25,…). On top of that it reduces the risk of breast cancer and if breast cancer should ensue, it at least increases chances of it being benign (growth of tumor cells is dependent on uncontrollable proliferation). It seems that tamoxifen may impart the same benefit in the prostate (9). Aforementioned metabolite of DHT, 3alpha-androstanediol, is also a beta receptor specific estrogen (9) that promotes protective effects in breast and prostate tissue and can help stop and reduce breast growth. Another key reason why 5-alpha-reductase levels are a critical factor in determining risk for gyno.

One thing I do want to impart on people is that tamoxifen treatment must continue for some time to be effective. Too often tamoxifen is reported to be ineffective for acute treatment because it isn’t used sufficiently long. Tamoxifen inhibits the growth of breast tissue, but does not reduce it on its own. This is mediated by your androgen levels as a male and an AAS user. These cells do not dissolve, they are ultimately destroyed by genomic signals. This takes some time. On top of that early cessation risks rebound effects. Tamoxifen does not address circulating estradiol so early cessation will only lead to estradiol immediately binding ERalpha again, and barring any changes, starting problems all over again. Longer treatment with tamoxifen reduces ERalpha density (2), which only further promotes the beta-receptor mediated positive effects. It’s perfectly possible for tamoxifens effect to become visible after cessation, no doubt this is one primary reasons why treatments prescribed by quacks are sometimes deemed effective : they are administered at the time the cells are being destroyed, so that to a lay person it may seem that the medication is actually reducing his gyno. If ACTUAL tissue shrinks within days, its probably not what you are on right now, so if you took something because you thought tamoxifen did not work, and “it cleared up in three days” (I’m not kidding, I hear this stuff every day) its likely it was the tamoxifen and not the other drug.
If it turns out you are prone to gyno (early onset of gyno with testosterone only at moderate doses) you can always opt to make the needed changes in the future (preventive treatment with an AI or a SERM).

When estrogen is the cause but it’s not obvious

With some drugs estrogenic problems like gyno will occur, when its not seemingly possible. A prime example of this is the drug oxymetholone. This is a DHT-derived androgen, that does not possess the structural capacity to be aromatized. But it still caused notable estrogenic effects. Here too wild theories were thrown around about mediation by the progesterone receptor and what not, even though evidence was available that it showed no appreciable binding to that receptor (11). In these cases its likely that the effect is mediated by either the steroid binding directly to the estrogen receptor (it has been postulated for oxymetholone, but isn’t likely to be the primary cause because steric properties make it unlikely to be a potent estrogen if it is one) or the cause of metabolization to a compound that can bind and activate the estrogen receptor. With most steroids we can exclude these mechanisms because affinity for the ER is well documented for most compounds, and the metabolites are well characterized. Usually those metabolites are the standard hydroxylated ones, primarily at the 3-keto moiety, but also at various other positions on the steroid backbone depending on enzymatic affinity. Hydroxylation generally reduces activity at class I nuclear receptors, and form the key to glucoronidation, the process the body uses to attach long hydrophilic molecules to steroids to make them water-soluble so they can be excreted in urine. Oxymetholone however metabolizes in so many different ways, and many of its metabolites fall outside of the realm of known compounds (12). So its not a far fetch that one of these metabolites is directly estrogenic.

In these cases treatment is fairly limited to SERMs, both short term and long term, because aromatase inhibitors will have no effect. Obviously if you are prone to gyno, the primary solution is to stay away from overly estrogenic compounds like oxymetholone.

When none of the above fits

That’s when the shit hits the fan and the pseudo-science guru’s come crawling out of the woodwork with “theories”. I parenthesize the word because theory in the scientific context implies a plausible ground to base the theory on, when most of these “theories” go against conventional wisdom and even established fact.

Progestagenic action is often cited as a cause. Not so much as it used to (primarily because it’s been refuted and the guru’s have moved on to newer things that allow them to sell stuff, like prolactin – progesterone problems aren’t as easily treated). Progestagenic action is the ability for an androgen to bind and activate the progesterone receptor. Progesterone is often referred to as the other female hormone and is known to play a role in breast development, and can aggravate estrogenic action on breast in rodents , but doesn’t seem to share this effect in primates (2). This is often the case for androgens in the 19-nor line (missing the 19th carbon of the steroid structure of natural androgens) which are known progestins. The problem with this postulation is two-fold however. The first is that progesterone is not known to cause gyno in the absence of estrogen (14), and the second is the fact that androgens reduce the expression of the progesterone receptor (15). Combine that with the fact that the androgenic potential for this line of androgens (trenbolone and nandrolone most notably) far exceeds their progestagenic potential (based on RBA for AR and PR –16) which implies that the level of PR reduction is greater (more androgen binds to the AR causing the reduction) than the level of PR activation. It would also imply that if this was an issue, it would resolve itself over time as PR expression would continue to decline. PR activity also has no effect on androgenic potential to decrease breast tissue and progestins themselves show a distinct ability to decrease breast tissue (3). Note : The above may not apply for drugs with an equal or greater progestagenic RBA as androgenic RBA. This includes designer steroids like THG and supplements containing dienolone precursors like Tren extreme. Fact of the matter is that while these drugs do possess a decent (in the case of THG excellent) anabolic activity, they are all really better classified as progestins than progestagenic androgens. Their use is tantamount to chemical castration, and problems ensuing from poor recovery and hypogonadal conditions is frankly to be expected. With dienolone, potent estrogenic action in similar fashion to nandrolone, is also not to be excluded. I can see why an athlete would resort to a designer steroid, but anyone else that does is a blatant idiot and frankly deserves what he gets.

The thing is that gyno occurs quite frequently with nandrolone, whereas I’ve yet to witness a confirmed case of trenbolone gyno. This despite the fact that both the progestagenic capacity is greater and the difference between AR and PR activation is smaller than for nandrolone. With nandrolone however we’ve been able to elucidate the mechanism of its effect. Whereas tren clearly shows the effects of a progestin in its action, nandrolone seems to exert none of the typical progestagenic effects. In fact it seems to perfectly fit the bill of an estrogenic steroid, something that was widely believed and accepted before people had access to medline. Nandrolone does aromatize, but to a much lesser degree (19). It’s also been shown to bind the estrogen receptor, but doesn’t seem to activate it unless at micromolar doses in vitro (20), something that would take massive consumption to mimic in vivo. One study however did estimate nandrolone’s estrogenic potential at 60% that of estradiol (21). With those figures a higher prevalence of gyno with this steroid than with testosterone isn’t that hard to imagine, especially when you know that the same enzyme that converts testosterone to DHT (5-alpha-reductase), the metabolite with the most profound effect on estrogen inhibition in the breast also converts nandrolone to DHN, which is a significantly WEAKER androgen (thus causing a massive A:E imbalance). But where does the estrogenic action come from ? Researchers already established (22) that aromatase, PR and ER did not play a role because the co-administration of inhibitors for each compound had no significant effect on the estrogenic potential. The elucidation of its mechanism came through a study on the synthetic steroid estren, a direct precursor to nandrolone (23). It showed that estren was able to mediate estrogenic effects by binding the AR and activating Estrogen Response Elements (ERE’s) in the DNA. Consider ERE’s like little signs that say “hey estrogen receptor, bind here and do your thing”. Apparently estren cause the AR to confuse itself with an ER. Estren however is a highly unstable metabolite, which rapidly converts to nandrolone under physiological circumstances. The time-frame of estrens effect (increased ERE activation while it is increasingly metabolized to nandrolone) and estrens low RBA to the AR compared to nandrolone clearly shows that this effect is mediated by nandrolone. So nandrolone causes estrogenic effects by binding the androgen receptor.

This causes a huge problem in treatment, since the only way to stop this effect is to block the AR, and with it the anabolic effect of nandrolone. Technically there is some evidence that ERE’s can be blocked using piperedinediones (24) but I’m not aware of any formulations containing such products, nor is there any data on their safety. This is crucial : THE ONLY WAY TO STOP NANDROLONE’S ESTROGENIC EFFECT IS TO NOT USE IT. While I would think its logical that if a certain compound gives you more problems, or harder to treat problems, that you cease use of that product, especially since there are plenty of other products available that offer the same benefits, I would stress this extra for nandrolone. It’s easily replaced with a drug like boldenone, which is completely different, but produces the same outward results, probably a little leaner. But it’s easy to see why this compound would be great food for all the alternate “theory” guru’s, and their primary proof for “estrogen-management doesn’t work in every case”. Fact is it does, but in this case the only way to manage it is not to take it.

What about trenbolone ?

One could propose a similar mechanism for trenbolone, but it absolutely doesn’t have the characteristics of a highly estrogenic drug. It doesn’t aromatize, has no appreciable binding to the ER (16). It produces none of the typical things one associates with an estrogenic drug. I have to honestly say that while gyno is more common with nandrolone than aromatizable steroids, I’ve yet to see a single confirmed report of tren gyno. But any stimulatory activity of trenbolone on the breast in the absence of estrogen is highly questionable to say the least, especially since the literature demonstrates that trenbolone “counteracts the mammary stimulus of estrogens showing ultrastructural images of cell autolysis and necrosis” (25). This is in accordance with previously listed studies demonstrating the negative effect of androgens on estrogen-mediated breast proliferation (2,10).

The fact that trenbolone has some binding affinity for the PR often lays at the basis of these claims, but the truth is that while we know that trenbolone binds the PR, we have no idea whether it is an agonist or antagonist, something some people want to bend into their own view, suggesting mixed agonist/antagonist gene expression profiles to fit their theories. We currently assume it’s a progestin because of its effect on erectile dysfunction and the fact that a great many steroids in the 19-Nor line are known progestins. But progesterone is also used to treat erectile dysfunction, meaning antagonism can cause erectile dysfynction as well. So it’s really up in the air. What people seem to forget is that its largely irrelevant, because in vivo research in ovariectomized primates (2) has shown no effect of Progesterone, a pure PR agonist, on breast proliferation. So if lack of PR stimulation, as well as pure PR stimulation don’t affect breast proliferation, then no degree of agonism or antagonism will have a different effect. The fact that it was in vivo research also largely excludes trenbolone acting through PR to mediate upregulation of other hormones or receptors that could affect breast proliferation, like the latest prolactin theories.

Though it’s practically impossible this problem even really exists, I don’t want to exclude it entirely, and still offer some suggestions. Again I would like to state that if this compound is giving you some form of unexplicable, or worse, untreatable gyno, YOU SHOULDN’T BE USING IT. I really don’t see what the big problem is here. I can see a reluctance to stop using AAS altogether, but don’t really see the point in sticking to one particular drug that is giving you more problems than you care for. If use has to be continued I would argue for preventive use of an AI here over a SERM. I’m usually not a fan, but since if this problem exists it is yet to be elucidated, its best to take estrogen completely out of the equation. Anecdotal reports of such incidences frequently report pain and such, or freak lactation. Genotoxic effects cannot be excluded here and an endocrinologist should be consulted, and you should inform him of your use of this particular drug, and if so, of any failure of anti-estrogenic drugs to work over prolonged periods of time. Keep in mind previous notes made in this article on the correct and sufficiently long use of anti-estrogenic drugs.

The prolactin theory

Prolactin is the latest theory and pet peeve of the pseudo-scientists, most likely because progesterone was getting old, disproven (2) and was hard to make money off of since common anti-progestins are heavily regulated and hard to get a hold off, and the fact that PR inhibition has been linked with the occurance of gyno more than its treatment (26). In my quest to find out what gave rise to this theory I actually found the man that claims to have started it, and even he failed to provide even one single reason to assume this is anything more than a hoax. It doesn’t help that this person has a monetary stake in the sale of dopamine agonist drugs typically used to lower prolactin in patients irresponsive to standard treatments like androgen administration or anti-estrogen treatment, nor does his long standing reputation of making money off of people in these fraudulent manners.

Research conducted on androgen-insensitive mammals who have been ovariectomized, castrated and/or adrenalectomized (27) demonstrate a drastic decrease in prolactin because of the removal of estrogen-producing organs, while treatment in primates with an anti-androgen (18) seems to increase prolactin. This is consistent with the known regulation of prolactin by sex steroids, showing that estrogens are needed to increase and maintain increased prolactin, and that androgens inhibit this action in vivo (28). The theory is predominantly used to explain the action of the typical progestagenic androgens like nandrolone and trenbolone, showing that protagonists of the prolactin theory hold some (frequently expressed) belief that the PR plays a role in the prolactin increase, but progesterone too attenuates the estrogen-mediated increase in prolactin (28,35, ref), and repressed the downstream signaling cascade of prolactin (13,35) in the breast specifically. This ties into the known method of lactogenic induction in post-partum women, which is accompanied by a drastic drop in progesterone. Furthermore blood panels of users of anabolic androgenic steroids, including trenbolone and nandrolone, have been shown to have a slight decrease in circulating prolactin if anything, as one would expect with high androgen treatment. The one case where we do know gyno with lactation develops is in the use of low dose testosterone (29,30) and there we do in fact see a rise serum prolactin mediated by the imbalance in A:E ratio. It is also plausible to see this with improper post-cycle therapy after the use of heavily HPTA suppressing androgens (such as for example trenbolone) after cessation of the drug for some time, also linked to an imbalanced A:E ratio.

I’ve had this discussion at length on several message boards, including with the “inventor” of the theory and his disciples (regrettably at the expense of my leisure time, sleep and family life) in the hope of finding at least one morsel of evidence that suggests this theory holds ground, or is even stooled on a plausibility. When I pointed out that their theory goes against the grain and 40+ years of scientific research, they quickly turned the discussion to paracrine secretion of prolactin in the mammary gland and upregulation of the prolactin receptor. Before we delve into that subject, I want to explain my main beef with this postulation : It’s hard to completely disprove due to lack of specific research, but that also entails there is no research demonstrating this does occur, hence no reason to “assume” this theory in the first place. Especially since it forces you to accept that autocrine/paracrine regulation is linearly opposed to the systemic regulation of prolactin.

What we do know about autocrine/paracrine secretion and effects of prolactin doesn’t really bode well for the theory either however. There are two things we need to address here. The first is the activity of prolactin in benign breast tissue in males, and the second is the ability of prolactin to stimulate or cause gyno. We know that prolactin exerts its effects through the membrane bound prolactin receptor (PRLR), which then activates the Jak/stat kinase pathway in the cell leading to increased expression of target genes and that this receptor is required for the activity of prolactin (31,32). However studies done specifically in men with gynaecomastia demonstrate that only 20% of cases are PRLR positive (33), allowing us to simply state that at least 80% of gyno cases aren’t even susceptible to the effect of prolactin. This argument was frequently countered with the postulation that progestagenic effects upregulate PRLR, but it is widely documented (33,34) that there is no correlation between progesterone/PR expression and prolactin/PRLR expression and that progestins have no effect on breast proliferation in primates in vivo (2), excluding any downstream mediators that do affect it.

Having established that, we haven’t even addressed whether or not prolactin can cause gyno on its own. We’ve already demonstrated that it has no correlation with the progesterone receptor and that androgen mediation attenuates the activity of estrogen on prolactin. There is however also evidence that there is no correlation between gyno and prolactin, with plenty of cases of hyperprolactinaemia showing no signs of gynaecomastia, and vice versa, plenty of gyno cases showing no elevation in prolactin or prolactin activity. It has been suggested several times in fact that prolactin has no real effect in breast development in the absence of estrogens (5,34), further establishing anti-estrogen treatment as the primary treatment for gyno, with or without prolactin. Taken together the probability of PRLR positive gyno that isn’t responsive to estrogen management is extremely small. Combine that with the aforementioned unique dispersal of these occurrences to the places frequented by charismatic pseudo-scientists and you get the picture of a typical hoax.


Gynaecomastia is a condition that is quite rare in users of high dose androgens, such as athletes and people who use AAS for aesthetic reasons, and there are distinct factors that predict sensitivity to the condition. AAS-induced gynaecomastia, since its emergence, has been solely and successfully treated with estrogen management by laymen and medical professionals alike. Successful acute and preventive treatments for estrogenic side-effects have been established anecdotally in the community at large, and are widely supported by the existing literature. One should recognize that a certain amount of circulating estrogen has positive effects on health and well-being , as well as fat loss and possibly muscle and strength gains. For this reason it is wise to adhere to common sense and not self-administer additional pharmaceuticals for problems that aren’t there.

When problems do arise, and you have reason to believe that you are getting gynaecomastia, go see a medical professional about the condition first and foremost. The smart thing to do at this point is also to cease use of the likely causative agent, and start proper PCT to let yourself recover. Getting this condition while on high dose androgens could indicate underlying problems that pose severe threats to your health. Oftentimes your doctor will do no more than observe the condition at first. Most likely a preliminary blood test will already identify absolute estrogen or relative estrogen values as the culprit and treatment will be given accordingly. If your doctor refuses to treat, anti-estrogenic drugs are widely available, but if you do choose to self-administer these drugs, make sure you understand them and their correct use. If you are the person who is likely to believe aforementioned pseudo-scientists, this is especially relevant. For acute treatment the SERMs are widely documented to be effective, most notably clomiphene, tamoxifen and raloxifene.

If risk factors are in play, or if you have suffered gynaecomastia during past AAS use, especially if it came on early, preventive treatment with aromatase inhibitors may be wiser. Keep in mind however that this will not address estrogenic problems caused by drugs that do not aromatize to estrogens but are still estrogenic in nature, such as nandrolone and oxymetholone. One should take care to avoid these drugs. Long term treatment with SERMs is acceptable as well, but usually more costly.

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