Gynaecomastia, the benign enlargement of male breast tissue, affects many men during adolescence and later life. Whilst low testosterone is a recognised cause, the relationship between testosterone treatment and gynaecomastia is complex and often misunderstood. Does testosterone treatment help with gynaecomastia? The answer depends critically on the underlying cause, duration of breast tissue changes, and individual patient factors. Testosterone therapy is not a first-line treatment and may paradoxically worsen the condition in some cases. This article examines the evidence, explores when testosterone replacement might be appropriate, and outlines current UK treatment approaches for this common condition.

What Is Gynaecomastia and What Causes It?

Gynaecomastia is the benign enlargement of male breast tissue, resulting from an imbalance between oestrogen and androgen activity in breast tissue. It affects a significant proportion of men at some point in their lives, with peaks during infancy, adolescence, and older age. The condition can be unilateral or bilateral and ranges from a small amount of extra tissue concentrated around the nipple to more prominent breast enlargement.

The underlying pathophysiology involves an increased ratio of oestrogen to androgen action at the breast tissue level. This can occur through several mechanisms: increased oestrogen production, decreased testosterone production, or conditions that alter the balance between these hormones. Physiological gynaecomastia is common during puberty (affecting many adolescent boys) and typically resolves spontaneously within two years. In older men, age-related decline in testosterone production combined with increased peripheral conversion of androgens to oestrogens contributes to higher prevalence rates.

Common causes include:

• Medications – spironolactone, cimetidine, finasteride, anabolic steroids, anti-androgens, and certain antipsychotics

• Endocrine disorders – hypogonadism, hyperthyroidism, tumours producing human chorionic gonadotrophin (hCG), Klinefelter syndrome

• Systemic conditions – chronic liver disease, chronic kidney disease, malnutrition

• Substance use – alcohol, possibly cannabis (though evidence is limited), heroin, amphetamines

• Idiopathic – no identifiable cause found in a significant proportion of cases

It is important to distinguish true gynaecomastia from pseudogynaecomastia (fat deposition without glandular proliferation) and from breast malignancy. While male breast cancer is rare, it requires prompt investigation if suspected, particularly in men with unilateral, hard breast masses or nipple changes.

The Link Between Testosterone Levels and Gynaecomastia

The relationship between testosterone levels and gynaecomastia is complex. Whilst low testosterone (hypogonadism) is a recognised cause of gynaecomastia, the condition fundamentally results from an altered oestrogen-to-androgen ratio rather than absolute testosterone deficiency alone. Understanding this distinction is crucial when considering treatment approaches.

In hypogonadal states, reduced testosterone production leads to decreased negative feedback on the hypothalamic-pituitary axis. In primary hypogonadism (testicular failure), this results in elevated luteinising hormone (LH) and follicle-stimulating hormone (FSH) levels. In secondary hypogonadism (pituitary/hypothalamic dysfunction), LH and FSH levels are low or inappropriately normal. Low testosterone levels reduce androgenic signalling, which normally has counter-regulatory effects on breast tissue growth.

The enzyme aromatase, present in adipose tissue, converts testosterone and androstenedione to oestradiol and oestrone respectively. In men with increased adiposity or conditions affecting aromatase activity, this conversion is enhanced, potentially leading to gynaecomastia.

Paradoxically, exogenous testosterone administration can also cause or worsen gynaecomastia through aromatisation to oestradiol, particularly when supraphysiological doses are used (as seen with anabolic steroid abuse). This explains why bodybuilders using anabolic steroids may develop gynaecomastia despite having elevated androgen levels.

Clinical assessment should include two early-morning measurements of total testosterone, oestradiol, LH, FSH, prolactin, thyroid function, liver function, and renal function. Sex hormone-binding globulin (SHBG) and calculated free testosterone may be helpful in borderline cases. When a hormone-secreting tumour is suspected, serum hCG and possibly alpha-fetoprotein (AFP) should be measured, and testicular examination and ultrasound considered. Hormone measurements may help identify underlying causes, but gynaecomastia itself is a clinical diagnosis based on physical examination.

Does Testosterone Treatment Help with Gynaecomastia?

The evidence regarding testosterone treatment for gynaecomastia is limited and nuanced. Testosterone therapy is not a first-line treatment for gynaecomastia and may paradoxically worsen the condition in some patients. The effectiveness depends critically on the underlying cause, duration of gynaecomastia, and individual patient factors.

In men with confirmed hypogonadism and recent-onset gynaecomastia (typically less than 12 months' duration), testosterone replacement therapy may help by restoring the oestrogen-to-androgen balance. Early-stage gynaecomastia involves ductal proliferation and inflammation, which may be reversible with hormonal manipulation. However, once the condition progresses beyond 12 months, fibrosis and hyalinisation of breast tissue occur, rendering it largely unresponsive to medical therapy, including testosterone.

A significant concern is that testosterone therapy can exacerbate gynaecomastia through peripheral aromatisation to oestradiol. This risk is higher in men with increased adiposity or older age. Gynaecomastia is listed as a known adverse reaction in the Summary of Product Characteristics (SmPC) for testosterone products, though frequency varies by formulation.

Current UK clinical guidance emphasises that testosterone therapy should only be prescribed for confirmed hypogonadism with associated symptoms, not specifically for gynaecomastia treatment. There is no official indication for testosterone therapy in eugonadal men with gynaecomastia. If testosterone replacement is clinically indicated for hypogonadism, patients should be counselled about the potential risk of developing or worsening gynaecomastia.

Patients receiving testosterone therapy should be monitored for breast changes alongside standard monitoring (haematocrit, PSA as appropriate). If gynaecomastia develops or worsens during treatment, options include dose adjustment, weight management, or in specialist settings, consideration of an aromatase inhibitor (off-label use). Any unilateral, firm, or rapidly growing breast tissue warrants urgent investigation to exclude malignancy.

Treatment Options for Gynaecomastia in the UK

Management of gynaecomastia in the UK follows a stepwise approach based on underlying aetiology, duration, severity, and patient distress. Initial assessment should identify and address reversible causes. This includes reviewing medications (discontinuing or substituting causative agents where possible), treating underlying endocrine disorders, and managing systemic conditions such as liver or kidney disease.

For physiological pubertal gynaecomastia, reassurance and observation are appropriate, as most cases resolve spontaneously within two years. Adolescents should be reviewed at 6-month intervals, with intervention considered only if the condition persists beyond two years, is severe, or causes significant psychological distress.

Medical therapy options include:

• Tamoxifen (selective oestrogen receptor modulator) – may be effective particularly when used early (within 4–6 months of onset). Typical dose: 10–20 mg daily for 3–6 months. This is an off-label use and should be initiated and monitored by specialists, particularly in adolescents.

• Aromatase inhibitors (anastrozole, letrozole) – have limited evidence of benefit and are not routinely recommended. These are off-label uses requiring specialist oversight.

• Danazol – rarely used due to side-effect profile and limited efficacy.

Medical therapy is generally ineffective for long-standing gynaecomastia (>12 months) due to tissue fibrosis. In these cases, or when medical management fails, surgical intervention may be appropriate.

Surgical options include:

• Liposuction – for predominantly fatty tissue (pseudogynaecomastia)

• Subcutaneous mastectomy – excision of glandular tissue, often combined with liposuction

• Surgical techniques vary based on tissue volume and skin excess

NHS funding for gynaecomastia surgery is limited and typically requires demonstration of significant psychological impact or functional impairment. Many Integrated Care Boards (ICBs) classify it as a procedure of limited clinical value. Private surgical treatment is available, with costs typically ranging from £3,000–6,000.

Patients should contact their GP if they experience:

• New or worsening breast enlargement

• Unilateral breast changes or discrete lumps

• Nipple discharge, particularly if blood-stained

• Skin changes or nipple retraction

• Associated symptoms suggesting endocrine disorders (fatigue, reduced libido, erectile dysfunction)

Referral to endocrinology is appropriate for suspected hormonal causes, whilst surgical referral may be considered for persistent, symptomatic gynaecomastia after medical optimisation. Urgent two-week-wait referral is indicated if breast cancer is suspected, particularly in men aged 50 or over with unilateral breast masses with or without nipple changes.

Patients experiencing side effects from any medication should report them through the MHRA Yellow Card scheme (yellowcard.mhra.gov.uk).

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