In short
- The common mechanism is an imbalance between oestrogenic and androgenic activity, not a “rise in female hormones” and nothing more.
- There are three moments in life when it appears physiologically and usually resolves on its own: the newborn period, puberty and old age.
- Drugs account for between 10% and 25% of cases, and the list of those with a demonstrated association is a good deal shorter than the one that circulates on the internet.
- Anabolic steroids are a very common and very under-declared cause: in a prospective study, the real level of use was 39.2% against the 4.1% recorded before surgery.
- In adults, a proper assessment finds an underlying cause in 45-50% of cases. Looking for it is worth the trouble.
- No medication is stopped or changed on your own initiative: it is discussed with whoever prescribed it, who is the person who can weigh up alternatives.
- Hormonal treatments taken on your own initiative —oestrogen receptor modulators or aromatase inhibitors— are not generally justified according to the European guidelines.
Behind almost all gynaecomastia lies the same mechanism: a change in the proportion between the body’s oestrogenic and androgenic activity. Oestrogens do not have to rise; it is enough for the balance to tip. What differs from one case to another is what tipped it —a stage of life, a medication, a substance, an illness— and whether that can be put right.
The useful question, then, is not “why me”, but what is keeping it going. Something very specific depends on the answer: a good proportion of recent gynaecomastia resolves once the cause is removed, and that is why the assessment always begins by looking for it and not by booking a theatre.
This page sets out the causes section of the general guide to gynaecomastia. If what you want to know first is whether yours is gland or fat, start with how gland is told apart from fat.
The balance, explained without jargon
Breast tissue responds to two opposing signals: oestrogens stimulate it and androgens hold it back. While the proportion holds, a man’s gland stays as a minimal remnant behind the nipple. When that proportion is altered —because androgens fall, because oestrogens rise or because a drug blocks the receptor—, the gland proliferates: the ducts and the stroma around them increase. That is exactly how the reference review on gynaecomastia in adolescents describes it.
There is one detail worth understanding because it explains many apparently causeless cases: fatty tissue converts androgens into oestrogens. That is why excess weight not only adds fat to the chest: it also pushes the balance towards the side that stimulates the gland. Fat and gland are not separate compartments; they feed each other.
The three ages at which it appears on its own
Gynaecomastia has three physiological peaks over a man’s lifetime, and knowing that saves a lot of alarm:
- The newborn period. From maternal oestrogens crossing over. It resolves with nothing done.
- Puberty. It is the commonest and the one that worries families most. It is due to the transient imbalance between oestrogens and androgens during development, and most resolve on their own, although it can take from several months to a few years.
- Old age. From the gradual fall in testosterone and the rise in the proportion of fatty tissue.
On puberty, one figure is worth having because it orders expectations. A population study of 531,686 boys aged 12 to 15 found a diagnosed incidence of 1.08%, falling to 0.7% among those with a normal body mass index, and with 70% of the cases concentrated between the ages of 13 and 14. It is a far lower figure than the prevalences obtained by examining every teenager, and the difference is informative in itself: feeling some gland is one thing and having gynaecomastia that gets as far as being diagnosed is quite another.
Medication: which ones really
Here it is worth separating the wheat from the chaff, because endless lists circulate. An evidence-based review analysed every published association between drugs and gynaecomastia since 1940 and graded them by the quality of the proof. Its opening conclusion is the most useful of all: most of the associations described rest on poor-quality evidence, mainly isolated case reports.
With that filter applied, the drugs with a demonstrated association are:
- spironolactone;
- cimetidine;
- ketoconazole;
- growth hormone;
- oestrogens;
- chorionic gonadotrophin (hCG);
- antiandrogens;
- GnRH analogues;
- 5-alpha-reductase inhibitors.
And with a probable association: risperidone, verapamil, nifedipine, omeprazole, alkylating agents, HIV medication —efavirenz—, anabolic steroids, alcohol and opioids.
A second review, on the same subject, puts the proportion of cases attributable to drugs at around 20% and ranks how common they really are in practice: antiandrogens, protease inhibitors and nucleoside reverse transcriptase inhibitors are the commonest drug causes; first-generation antipsychotics, spironolactone, verapamil and cimetidine, less common.
🚨 And now the important part, which is not the list: if you are taking any of these drugs, do not stop or change it on your own initiative. Many of them treat problems more serious than gynaecomastia, and in several cases there are alternatives to be weighed up with whoever prescribed it. What is worth doing is taking the complete list of your medication to the consultation, including anything taken without a prescription.
Anabolic steroids: the figure that changes the conversation
This is the cause that appears least in medical records and most in operating theatres.
A three-year prospective study at a tertiary hospital asked about anabolic steroid use before surgery and again three months afterwards. Before surgery, it was recorded in 4.05% of patients. Afterwards, the real figure turned out to be 39.19%. Almost ten times as high.
There is no need to read it as a lie: it is a habit with little social acceptance, and that is why it is under-declared. But it has direct practical consequences:
- It changes the outlook. Gynaecomastia associated with anabolic steroids can resolve on stopping the cycle, particularly if it is recent. The authors themselves point out that surgery is not always indicated in these cases.
- It changes the risk of it coming back. Having surgery and carrying on using is the most direct route to the problem reappearing.
- It changes the technique. That same piece of work recommends meticulous haemostasis and careful glandular excision precisely in order to reduce recurrence and complications.
It also describes the profile that raises suspicion: a high body mass index, an athletic build and recent weight gain.
That is why the question is asked at the consultation, and asked without judgement. It is not an interrogation: it is the difference between planning the right operation and planning one that will come undone.
Alcohol and other substances
Alcohol is among the substances with a probable association, along with opioids. The mechanism is twofold: a direct effect on testicular function and, in chronic use, liver damage, which alters the metabolism of the sex hormones.
The European guidelines expressly include in the history the use or abuse of substances related to gynaecomastia, and recommend that, once they are stopped, the approach should be watchful waiting. That is: first you remove what is keeping it going and observe; you do not operate straight away.
When hormones have to be investigated, and what is asked for
Not all gynaecomastia needs blood tests, but the threshold is lower than people suppose, because in adults a proper assessment reveals an underlying condition in 45-50% of cases.
The European guidelines describe what a full assessment covers:
- A detailed history: when it appeared, how long it has lasted, sexual development and function, and use of associated substances or drugs.
- Physical examination of the breast and the genitals, including testicular ultrasound. This point is frequently overlooked and is one of those that most justifies the work-up.
- Blood tests, which may include testosterone, oestradiol, SHBG, LH, FSH, TSH, prolactin, chorionic gonadotrophin, alpha-fetoprotein and liver and kidney function tests.
- Breast imaging when the examination is inconclusive; and a direct biopsy if the lesion is suspicious, without persisting with further imaging.
It is worth stressing that this work-up is not requested by a plastic surgeon in order to operate: it is requested by any doctor in order to find out what is going on. Finding the cause can avoid surgery, and in the odd case it can pick up a problem that matters a good deal more than the chest.
What does not work, and what can prove costly
The idea of resolving gynaecomastia with tamoxifen, anastrozole or other drugs bought without a prescription circulates in gyms and on the internet. The European guidelines are explicit: the use of selective oestrogen receptor modulators, aromatase inhibitors and non-aromatisable androgens is not generally justified in the treatment of gynaecomastia. And testosterone is only indicated in men with a demonstrated deficiency, not as a cosmetic resource.
Self-medicating with these drugs is not harmless: they are medicines with real adverse effects, they are taken blind without knowing whether there is any deficiency and, on top of that, they muddy the later work-up, because they alter precisely the parameters that would then have to be measured.
And if the cause is removed, does it go away?
It depends above all on how long it has been there. Recent gynaecomastia is active glandular tissue, and it can regress when the stimulus that caused it disappears: that is why the guidelines recommend watchful waiting once the underlying illness has been treated or the substance involved has been stopped.
Over the months, however, that tissue becomes fibrous. And fibrous tissue no longer responds: it stays. It is the reason those same guidelines consider surgery the treatment of choice in long-standing gynaecomastia, and also the reason why it is as well not to let years go by hoping it will resolve on its own when it has already gone a long time without changing.
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Frequently asked questions
Do anabolic steroids cause gynaecomastia?
Yes, they are among the substances with a probable association and in surgical practice they are a very common cause: in a prospective study the real level of use was 39.2%, against the 4.1% recorded before surgery. If the gynaecomastia is recent and the cycle is stopped, it can resolve; if it is established, it will not.
I am taking a drug from the list — should I stop it?
Not on your own initiative. Discuss it with the doctor who prescribed it: in some cases there is an alternative and in others the treatment matters more than the gynaecomastia. What does help is taking the complete list of your medication to the consultation.
Could it be a serious hormonal problem?
It could, and that is why it is investigated. In adults, a proper assessment finds an underlying cause in 45-50% of cases, and the examination includes the genitals and a testicular ultrasound. Most of the time nothing worrying turns up, but it is a check worth making.
Is tamoxifen any use for getting rid of it?
The European guidelines do not generally justify the use of oestrogen receptor modulators or aromatase inhibitors to treat gynaecomastia. Buying them without a prescription adds risks of its own and, on top of that, alters the tests that would later have to be interpreted.
My teenage son has developed breast tissue — does anything have to be done?
The likeliest thing is that it is pubertal gynaecomastia, which resolves on its own, although it can take from months to a few years. That does not mean not seeking advice: an assessment rules out other causes, gives a sense of the timescale and spares the wear of waiting without knowing.
Why has it appeared if I do not take anything?
Because drugs account for only between 10% and 25% of cases. The rest is split between the physiological stages of life, excess weight —fatty tissue converts androgens into oestrogens—, liver, kidney, thyroid or testicular disease, and a group in which no specific cause is identified.
If I stop going to the gym and lose weight, will it go?
The fatty component will come down, and in pseudogynaecomastia that can resolve it. If there is a glandular disc, no: the gland does not respond to calorie balance, and once the fat that was disguising it is lost it usually shows even more.
Sources
- Deepinder F, Braunstein GD. Drug-induced gynecomastia: an evidence-based review. Expert Opin Drug Saf. 2012;11(5):779-795. PMID 22862307 — systematic review since 1940 with grading of the quality of the evidence: drugs cause 10 to 25% of cases, most of the published associations rest on poor-quality evidence, and the demonstrated and probable associations are listed.
- Bowman JD, Kim H, Bustamante JJ. Drug-induced gynecomastia. Pharmacotherapy. 2012;32(12):1123-1140. PMID 23165798 — it puts the cases attributable to drugs at around 20% and ranks the drug causes by how common they really are, headed by antiandrogens, protease inhibitors and nucleoside reverse transcriptase inhibitors.
- Beniwal M, Singh K, Singh P, Sharma A, Beniwal S. The Burden of Anabolic Androgenic Steroid-Induced Gynecomastia. Indian J Plast Surg. 2023;56(4):338-343. PMID 37705825 — three-year prospective study: the real level of anabolic steroid use was 39.19% against the 4.05% recorded before surgery; the authors point out that surgery is not always indicated in these cases and describe the profile that raises suspicion.
- Kanakis GA, Nordkap L, Bang AK, et al. EAA clinical practice guidelines—gynecomastia evaluation and management. Andrology. 2019;7(6):778-793. PMID 31099174 — an underlying condition in 45-50% of adults, the recommended battery of examination and blood tests, testicular ultrasound, watchful waiting once the cause has been removed, and the absence of general justification for oestrogen receptor modulators, aromatase inhibitors and non-aromatisable androgens.
- Metwalley KA, Farghaly HS. Gynecomastia in adolescent males: current understanding of its etiology, pathophysiology, diagnosis, and treatment. Ann Pediatr Endocrinol Metab. 2024;29(2):75-81. PMID 38712491 — pubertal gynaecomastia as the main cause in adolescence, from an imbalance between oestrogenic and androgenic activity, transient in character and with resolution that can take from months to years.
- Berger O, Hornik-Lurie T, Talisman R. Pubertal gynecomastia incidence among 530,000 boys: a cross sectional population based study. Front Pediatr. 2024;12:1367550. PMID 38510076 — 531,686 boys aged 12 to 15: a diagnosed incidence of 1.08%, of 0.7% among those with a normal body mass index, with 70% of the cases between the ages of 13 and 14.
Sources checked one by one against PubMed on 12 August 2026.
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Finding out the cause is what decides whether gynaecomastia has to be operated on or whether removing what is keeping it going is enough. At the Instituto de Cirugía Plástica del Mediterráneo, in Valencia, the first consultation sorts that part out: what can be felt, since when, what medication and what substances are involved, and what work-up is worth requesting before anything else is considered.
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Educational content reviewed by Dr Alessandro Thione, registration no. 46/4621959, and Dr Alberto Ruiz Cases, registration no. 46/4624050, specialists in Plastic, Aesthetic and Reconstructive Surgery. This page neither prescribes nor advises against any particular treatment: no medication should be stopped or changed without consulting the doctor who prescribed it.
Registration no. 46/4621959
Registration no. 46/4624050
Last reviewed: 6 September 2026. This content is for information only and does not replace an individual assessment by a healthcare professional.





