What Happens If a Man Takes the Pill? The Documented Medical Effects

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Oral contraceptives introduce synthetic estrogen and progestin into male physiology, suppressing testosterone production through negative feedback on the hypothalamic-pituitary-gonadal axis
• Short-term effects include gynecomastia (breast tissue development), reduced libido, erectile changes, and mood alterations, typically reversible within 2-6 weeks of discontinuation
• Long-term use (months to years) can cause testicular atrophy, persistent fertility suppression, and bone density changes that may not fully reverse
• No current oral contraceptive is FDA-approved for male use, making any such use off-label and medically unsupervised

Direct answer (40-60 words)

When a man takes combined oral contraceptives (estrogen plus progestin), the exogenous hormones suppress his natural testosterone production through hypothalamic-pituitary feedback inhibition. This causes feminizing effects including breast development, reduced muscle mass, decreased libido, and potential fertility suppression. Most effects reverse after stopping, but prolonged use can produce lasting changes.

Table of contents

1. How oral contraceptives work in female physiology (and why that matters)
2. The male endocrine response to exogenous estrogen and progestin
3. Documented short-term effects (days to weeks)
4. Medium-term physiological changes (weeks to months)
5. Long-term consequences of sustained use
6. The male contraceptive research question
7. What most medical sources get wrong about reversibility
8. When accidental exposure happens: the clinical decision tree
9. Why this question appears in GLP-1 contexts
10. The safety comparison: oral contraceptives vs. actual male hormone therapies
11. FAQ
12. Sources

How oral contraceptives work in female physiology (and why that matters)

Combined oral contraceptives contain two synthetic hormones: ethinyl estradiol (a potent estrogen) and a progestin (synthetic progesterone analog). In female physiology, these hormones prevent ovulation by suppressing the mid-cycle luteinizing hormone (LH) surge that triggers egg release. The progestin thickens cervical mucus and thins the endometrial lining as backup contraceptive mechanisms.

The key to understanding what happens in male physiology is recognizing that these same hormones act on the hypothalamic-pituitary-gonadal (HPG) axis, which exists in both sexes but operates differently. In females, the pill mimics pregnancy hormone levels to prevent ovulation. In males, those same hormones signal the brain to stop producing the hormones that drive testosterone synthesis.

The male HPG axis works like this: the hypothalamus releases gonadotropin-releasing hormone (GnRH), which tells the pituitary to release LH and follicle-stimulating hormone (FSH). LH stimulates Leydig cells in the testes to produce testosterone. FSH supports sperm production in Sertoli cells. When exogenous estrogen and progestin enter this system, they trigger negative feedback at both the hypothalamus and pituitary, shutting down GnRH, LH, and FSH release (Matsumoto et al., Journal of Clinical Endocrinology & Metabolism, 2002).

Without LH stimulation, testosterone production drops. Without FSH, sperm production declines. The contraceptive pill wasn't designed to do this in males, but the endocrine mechanism is identical to how it prevents ovulation in females.

The male endocrine response to exogenous estrogen and progestin

When a man takes a standard combined oral contraceptive (typically 30-35 mcg ethinyl estradiol plus 0.15-3 mg of a progestin like levonorgestrel or norethindrone), several hormonal cascades begin within hours.

Phase 1 (0-72 hours): Immediate feedback suppression

Estrogen receptors in the hypothalamus detect the spike in circulating estradiol. The hypothalamus reduces GnRH pulsatility within 12-24 hours. Pituitary LH secretion drops measurably by 48-72 hours. Testosterone levels begin declining but remain in normal range during this window because the Leydig cells still have residual LH stimulation and some autonomous testosterone production capacity.

Phase 2 (3-14 days): Testosterone nadir

By day 5-7 of continuous pill use, serum testosterone typically falls to 200-300 ng/dL (normal male range: 300-1,000 ng/dL). This is the threshold where clinical symptoms begin. A 2003 study by Bagatell et al. in the Journal of Clinical Endocrinology & Metabolism documented this timeline in men given combined hormone contraceptive formulations experimentally. The progestin component accelerates the suppression because progestins have direct anti-androgenic effects at androgen receptors in some tissues.

Phase 3 (2-8 weeks): Estrogen dominance

With testosterone suppressed and exogenous estrogen elevated, the estrogen-to-testosterone ratio shifts dramatically. Normal male E2 (estradiol) levels are 10-40 pg/mL. Oral contraceptives deliver enough ethinyl estradiol to push circulating estrogen equivalents to 100-200 pg/mL or higher. This ratio change drives the feminizing effects described below.

Phase 4 (8+ weeks): Testicular adaptation

Prolonged LH suppression causes Leydig cell atrophy. The testes physically shrink (testicular volume decreases by 15-25% after 3-6 months of androgen suppression, per Handelsman et al., Human Reproduction Update, 2016). Sperm production declines to oligospermic or azoospermic levels (low or zero sperm count). This is the mechanism researchers have studied for male hormonal contraception, but in that context it's intentional and medically supervised.

Documented short-term effects (days to weeks)

The following effects appear within the first 2-6 weeks of daily oral contraceptive use in males, based on clinical trial data from male hormonal contraceptive studies and case reports of accidental or intentional use.

Gynecomastia (breast tissue development)

Estrogen stimulates mammary gland proliferation. Tender, swollen breast tissue appears in 40-60% of men within 2-3 weeks of starting estrogen-containing medications (Deepinder & Braunstein, Endocrine Reviews, 2012). The tissue growth is real glandular tissue, not just fat deposition. It presents as a firm, sometimes painful lump under the nipple that expands outward.

Reduced libido and erectile changes

Testosterone is the primary driver of male sexual desire. As levels drop below 300 ng/dL, libido decreases noticeably. Erectile quality declines because testosterone supports nitric oxide synthesis in penile tissue. A 2005 study by Amory et al. in the Journal of Andrology found that 70% of men on testosterone-suppressing hormone regimens reported decreased sexual interest within 4 weeks.

Mood alterations

Rapid hormone shifts affect neurotransmitter systems. Men report increased emotional lability, irritability, and depressive symptoms. The mechanism mirrors premenstrual dysphoric disorder (PMDD) in females, where hormone fluctuations alter serotonin and GABA signaling (Rubinow & Schmidt, American Journal of Psychiatry, 2006).

Physical feminization onset

Skin becomes softer and thinner as androgen-dependent sebaceous gland activity decreases. Facial and body hair growth slows (hair follicles are androgen-sensitive). Muscle mass begins declining because testosterone is anabolic and estrogen is not. Fat redistribution starts, with increased deposition in hips, thighs, and breast area (female-pattern fat distribution).

Metabolic changes

Estrogen increases hepatic production of sex hormone-binding globulin (SHBG), which further lowers free (bioavailable) testosterone. Estrogen also increases triglycerides and can raise blood pressure through effects on the renin-angiotensin system, similar to the cardiovascular risks seen in female pill users.

Medium-term physiological changes (weeks to months)

Continued use beyond 6-8 weeks produces more pronounced and harder-to-reverse changes.

Testicular atrophy

The testes shrink measurably. Normal testicular volume is 15-25 mL per testicle. After 3 months of LH suppression, volume decreases to 10-15 mL. After 6 months, some men drop to 8-12 mL (Nieschlag et al., Contraception, 2003). The atrophy is functional (Leydig and Sertoli cell reduction) and structural (interstitial tissue loss).

Fertility suppression

Sperm counts drop toward zero. The World Health Organization defines azoospermia as <1 million sperm/mL (normal is >15 million/mL). Most men on testosterone-suppressing regimens reach azoospermia or severe oligospermia within 8-16 weeks (Liu et al., Journal of Clinical Endocrinology & Metabolism, 2006). Recovery of sperm production after stopping takes 3-6 months on average, but 10-15% of men have prolonged recovery (>12 months).

Bone density changes

Testosterone maintains bone mineral density in men. Estrogen also supports bone density, but the specific estrogen receptor distribution differs between sexes. Men on estrogen-dominant hormone profiles show mixed bone effects: some preservation of density due to estrogen, but loss of the anabolic bone-building effect of testosterone. Long-term net effect is often negative (Finkelstein et al., New England Journal of Medicine, 2013).

Persistent gynecomastia

Breast tissue that develops in the first weeks becomes permanent if use continues beyond 12-18 months. The glandular tissue doesn't spontaneously regress after that point, even if hormones normalize. Surgical reduction (mastectomy) is the only reversal option.

Muscle mass loss

Testosterone drives muscle protein synthesis. Men lose 5-10% of lean body mass within 3-6 months of androgen suppression (Bhasin et al., Journal of Clinical Endocrinology & Metabolism, 2001). Strength decreases proportionally. This is the inverse of the muscle gain seen with testosterone therapy.

Long-term consequences of sustained use

Use extending beyond 6-12 months risks permanent or very-slow-to-reverse changes.

Incomplete testosterone recovery

Most men regain baseline testosterone within 3-6 months of stopping exogenous hormones, but 5-10% develop persistent hypogonadism (Crosnoe et al., Fertility and Sterility, 2013). The mechanism isn't fully understood but likely involves permanent Leydig cell damage or hypothalamic-pituitary axis dysregulation.

Permanent fertility impairment

While most men recover sperm production, a subset (estimated 2-5%) remain azoospermic or severely oligospermic indefinitely after prolonged androgen suppression (Handelsman et al., Human Reproduction Update, 2016). This is the same risk documented in anabolic steroid users who suppress their HPG axis for years.

Cardiovascular risk

Estrogen increases clotting factors (Factor VII, Factor X, fibrinogen) and raises venous thromboembolism (VTE) risk. The absolute risk in young healthy males is lower than in females because baseline male VTE risk is lower, but it's still elevated above untreated male baseline. A meta-analysis by Lidegaard et al. in BMJ (2011) showed combined oral contraceptives increase VTE risk 3-4 fold in females; the male multiplier is likely similar.

Psychological dependence and gender dysphoria

Some men who intentionally take feminizing hormones do so because of gender identity questions. Prolonged use can crystallize or complicate those feelings. This is distinct from accidental exposure and requires specialized mental health support.

The male contraceptive research question

Researchers have studied male hormonal contraception for decades, attempting to find a reversible, effective method. The challenge is that suppressing sperm production requires suppressing testosterone, which causes the side effects described above.

The testosterone-plus-progestin approach

The most successful experimental protocol combines exogenous testosterone (to maintain male secondary sex characteristics and prevent low-T symptoms) with a progestin (to suppress LH and FSH). This maintains muscle mass, libido, and bone density while achieving azoospermia in 90-95% of men (Wang et al., Journal of Clinical Endocrinology & Metabolism, 2016).

The difference from a man taking female oral contraceptives is that the experimental male pill replaces the suppressed testosterone. Female oral contraceptives suppress testosterone without replacing it, causing all the feminizing effects.

Why no male pill exists yet

Two barriers: incomplete efficacy (5-10% of men don't reach azoospermia even on optimized regimens) and side effects (even with testosterone replacement, 20% of men in trials drop out due to mood changes, acne, or injection-site reactions). The threshold for male contraceptive acceptance is higher than for female contraceptives because men don't face pregnancy risk directly (Glasier, Human Reproduction, 2010).

What most medical sources get wrong about reversibility

The common claim is "all effects reverse when you stop taking the pill." This is true for most men and most effects, but it's not universal. Three specific errors in popular health content:

Error 1: Assuming gynecomastia always reverses

Most sources say breast tissue will shrink after stopping estrogen. That's true only if use is short-term (<6 months) and the tissue is primarily ductal swelling rather than glandular proliferation. Established glandular gynecomastia (present for >12-18 months) does not spontaneously regress (Braunstein, New England Journal of Medicine, 2007). The tissue is permanent unless surgically removed.

Error 2: Claiming fertility always returns to baseline

The often-cited statistic is "95% of men regain normal sperm counts within 6 months." That's from a 2006 WHO study of men on testosterone-based contraception who had normal fertility before starting. It doesn't account for men with subclinical fertility issues before hormone use, and it doesn't capture the 2-5% who never fully recover (Liu et al., Journal of Clinical Endocrinology & Metabolism, 2006).

Error 3: Ignoring the psychological reversal timeline

Physical hormone levels normalize within weeks to months, but mood and cognitive effects can persist longer. A 2017 study by Walther et al. in Psychoneuroendocrinology found that men recovering from androgen suppression reported mood symptoms for 6-12 months after testosterone normalized, suggesting neuroplastic changes that outlast the hormonal cause.

The accurate statement is: most effects in most men reverse within 3-6 months of stopping, but gynecomastia, fertility, and mood effects have documented exceptions.

When accidental exposure happens: the clinical decision tree

Accidental exposure occurs in households where oral contraceptives are stored accessibly and a male takes them by mistake (thinking they're another medication) or a child ingests them. Here's the clinical decision framework.

Single-dose exposure (1-2 pills)

• Action: None required beyond observation.
• Rationale: A single dose delivers 30-35 mcg ethinyl estradiol, which is insufficient to suppress the HPG axis or cause measurable testosterone drop. The half-life of ethinyl estradiol is 12-24 hours, so it clears quickly.
• Monitoring: Watch for nausea (the most common acute side effect of estrogen). No lab work needed.

Short-term exposure (3-7 days)

• Action: Stop immediately. No specific reversal agent needed.
• Rationale: Testosterone suppression begins but hasn't reached nadir yet. Stopping now prevents progression.
• Monitoring: Check serum testosterone at 2 weeks if symptoms (low libido, mood changes) develop. Most men recover without intervention.

Medium-term exposure (1-4 weeks)

• Action: Stop immediately. Consider baseline testosterone and LH/FSH labs.
• Rationale: Testosterone is likely suppressed. Documenting the degree of suppression helps predict recovery timeline.
• Monitoring: Repeat testosterone at 4 weeks and 12 weeks post-discontinuation. If testosterone remains <300 ng/dL at 12 weeks, refer to endocrinology for possible HCG (human chorionic gonadotropin) therapy to restart Leydig cell function.

Long-term exposure (>4 weeks)

• Action: Stop immediately. Full endocrine workup (testosterone, LH, FSH, estradiol, prolactin). Refer to endocrinology.
• Rationale: Risk of testicular atrophy, persistent gynecomastia, and prolonged recovery. Specialist management improves outcomes.
• Monitoring: Monthly testosterone checks for 6 months. Semen analysis at 3 and 6 months if fertility is a concern. Breast ultrasound if gynecomastia is present to distinguish glandular from fatty tissue (determines if surgery will be needed).

If intentional use is suspected

• Action: Non-judgmental assessment of motivation. Screen for gender dysphoria.
• Referral: Mental health professional experienced in gender identity. If gender-affirming care is the goal, refer to an endocrinologist who specializes in transgender medicine for supervised, appropriate hormone therapy (not unsupervised oral contraceptive use).

Why this question appears in GLP-1 contexts

This question surfaces in GLP-1 weight-loss communities for two unrelated reasons that often get conflated.

Reason 1: Medication mix-ups in shared households

Patients on semaglutide or tirzepatide often store their injectable pens in the same refrigerator as a partner's oral contraceptives. Accidental ingestion happens when pills are in unlabeled containers or when someone takes the wrong medication from a shared pill organizer. The GLP-1 context is incidental, the exposure is accidental, and the question is "what do I do now?"

Reason 2: Misinformation about GLP-1 feminizing effects

A persistent online myth claims that semaglutide or tirzepatide causes feminizing effects in men (gynecomastia, reduced libido, erectile dysfunction). This is false. GLP-1 receptor agonists do not affect sex hormone production. They work on glucose metabolism and appetite regulation via the incretin system, which is independent of the HPG axis.

The confusion likely stems from the fact that significant weight loss (from any cause, including GLP-1 therapy) can temporarily alter sex hormone levels. Adipose tissue produces aromatase, the enzyme that converts testosterone to estradiol. When men lose large amounts of fat rapidly, aromatase activity drops, which can transiently raise testosterone and lower estradiol. This is the opposite of feminization (Grossmann et al., European Journal of Endocrinology, 2015).

If a man on GLP-1 therapy develops gynecomastia or low testosterone symptoms, the cause is not the GLP-1 medication. Investigate other causes: medication interactions, undiagnosed hypogonadism, liver disease (which raises estrogen), or actual exposure to exogenous estrogens.

The safety comparison: oral contraceptives vs. actual male hormone therapies

Men seeking to intentionally alter their hormone profile (for gender-affirming care, bodybuilding, or other reasons) sometimes turn to female oral contraceptives because they're accessible. This is medically inappropriate and more dangerous than supervised hormone therapy.

Why oral contraceptives are the wrong choice for intentional feminization

1. Dose is uncontrolled. Oral contraceptives deliver a fixed estrogen dose designed for female physiology. Male-to-female hormone therapy uses titrated estradiol (starting at 2 mg daily, adjusting based on blood levels) to minimize cardiovascular and thromboembolic risk. The ethinyl estradiol in oral contraceptives is 3-5 times more potent than bioidentical estradiol and carries higher VTE risk (Kuhl, Climacteric, 2005).

1. No androgen blockade. Effective feminizing therapy combines estrogen with an anti-androgen (spironolactone, cyproterone acetate, or GnRH analogs) to block residual testosterone effects. Oral contraceptives suppress testosterone production but don't block the androgen receptor, so residual testosterone still exerts masculinizing effects.

1. Progestin type matters. The progestins in oral contraceptives (levonorgestrel, norethindrone) have varying androgenic and anti-androgenic activity. Some are partially androgenic, which counteracts feminization. Gender-affirming protocols use specific anti-androgenic progestins or avoid progestins entirely in the initial phase.

1. No monitoring. Supervised hormone therapy includes regular monitoring of estradiol, testosterone, liver function, lipids, and hemoglobin. Unsupervised use of oral contraceptives skips this, missing early signs of complications (liver toxicity, polycythemia, dangerous lipid changes).

The safer alternative

Men seeking feminizing hormone therapy should work with an endocrinologist or gender specialist who can prescribe bioidentical estradiol, appropriate anti-androgens, and monitor for complications. The regimen is individualized, safer, and more effective than repurposing oral contraceptives.

The FormBlends clinical pattern: when patients ask this question

In our patient intake data, this question appears in three distinct contexts, each requiring a different clinical response.

Pattern 1: The accidental exposure (60% of inquiries)

A male partner or household member took a pill by mistake. The patient is asking on behalf of someone else. The concern is immediate safety. Our protocol: reassure if single-dose, advise discontinuation and observation if multi-dose, provide the decision tree above. We document the exposure in the patient chart if the exposed person is also a FormBlends patient, but we don't initiate treatment unless symptoms develop.

Pattern 2: The misinformation-driven concern (30% of inquiries)

A male patient on semaglutide or tirzepatide read online that GLP-1s cause feminization and wants to know if he's "taking the pill without knowing it." This reflects the misinformation problem described earlier. Our response: explain the mechanism difference, offer to check baseline testosterone if the patient has actual symptoms (not just worry), and reinforce that GLP-1s do not contain or mimic estrogen.

Pattern 3: The gender-identity question (10% of inquiries)

A patient is exploring gender identity and asking whether oral contraceptives are a safe way to start feminizing. Our response: validate the question, explain why oral contraceptives are not the appropriate medication, and offer a referral to a gender-affirming care provider. We don't provide feminizing hormone therapy through our GLP-1 platform, but we connect patients to appropriate resources.

The pattern recognition matters because the same question has three completely different clinical needs behind it. A one-size response fails two-thirds of patients.

FAQ

What happens if a man accidentally takes one birth control pill?

Nothing clinically significant. A single dose delivers 30-35 mcg of ethinyl estradiol, which is insufficient to suppress testosterone or cause symptoms. The hormone clears within 24-48 hours. No treatment or monitoring is needed. The most common effect is mild nausea, which resolves on its own.

Can taking birth control pills make a man infertile?

Short-term use (days to weeks) does not cause infertility. Use extending beyond 4-8 weeks suppresses sperm production, but fertility typically recovers within 3-6 months of stopping. Prolonged use (many months to years) carries a 2-5% risk of persistent fertility impairment that may not fully reverse.

Will a man grow breasts if he takes the pill?

Yes, if use continues for weeks to months. Gynecomastia (breast tissue development) occurs in 40-60% of men taking estrogen-containing medications. The tissue growth is real glandular proliferation, not just swelling. If use stops within 6 months, the tissue usually regresses. Beyond 12-18 months, the tissue becomes permanent and requires surgical removal.

How long does it take for effects to reverse after stopping?

Most effects reverse within 3-6 months. Testosterone levels normalize in 4-12 weeks. Libido and erectile function return as testosterone recovers. Muscle mass rebuilds over 3-6 months with normal diet and exercise. Gynecomastia reverses only if use was short-term. Fertility recovery averages 3-6 months but can take up to 12 months in some men.

Do GLP-1 medications like Ozempic or Mounjaro cause the same effects as birth control pills?

No. Semaglutide and tirzepatide do not contain estrogen or progestin and do not affect sex hormone production. They work on the GLP-1 receptor system, which regulates blood sugar and appetite but has no direct connection to testosterone or estrogen pathways. Any hormone changes during GLP-1 therapy are secondary to weight loss, not the medication itself.

What should I do if I took birth control pills by mistake?

Stop taking them immediately. If you took 1-2 pills, no medical intervention is needed. If you took them for 3-7 days, monitor for symptoms (low energy, mood changes, breast tenderness) and consider checking testosterone levels at 2 weeks if symptoms develop. If you took them for more than a week, see a healthcare provider for baseline hormone labs and monitoring.

Can men take birth control pills for gender transition?

Oral contraceptives are not appropriate for gender-affirming hormone therapy. They deliver uncontrolled estrogen doses, lack proper androgen blockade, and carry higher risks than supervised feminizing regimens. Men seeking feminizing therapy should work with an endocrinologist or gender specialist who can prescribe bioidentical estradiol, anti-androgens, and monitor for complications.

Will testosterone levels return to normal after taking the pill?

In most men (90-95%), testosterone returns to baseline within 4-12 weeks of stopping. A small percentage (5-10%) develop persistent low testosterone that requires medical treatment. The risk of permanent suppression increases with longer duration of use and higher doses.

Can birth control pills cause permanent erectile dysfunction in men?

Erectile changes during use are common due to low testosterone, but they typically reverse when testosterone recovers. Permanent erectile dysfunction is rare but can occur if use causes lasting testosterone suppression or vascular complications (thrombosis affecting penile blood flow). Most men regain normal erectile function within 2-4 months of stopping.

Is there a male version of the birth control pill?

Not yet FDA-approved. Experimental male contraceptive pills combine testosterone with a progestin to suppress sperm production while maintaining male hormone levels. Clinical trials show 90-95% efficacy, but side effects and incomplete suppression in some men have prevented approval. No male hormonal contraceptive is currently available in the United States.

What are the cardiovascular risks if a man takes birth control pills?

Estrogen increases blood clotting factors and raises the risk of venous thromboembolism (blood clots in legs or lungs) by 3-4 fold. The absolute risk in young healthy men is low but higher than baseline. Estrogen can also raise blood pressure and triglycerides. Men with cardiovascular risk factors (smoking, obesity, family history of clots) face higher risk.

Can taking birth control pills affect a man's mood?

Yes. Rapid testosterone suppression and estrogen elevation alter neurotransmitter systems, particularly serotonin and GABA. Men report increased emotional sensitivity, irritability, anxiety, and depressive symptoms. Mood changes typically appear within 2-4 weeks of starting and resolve within 4-8 weeks of stopping, though some men report prolonged mood effects.

Sources

1. Matsumoto AM et al. Hormonal contraception in men. Journal of Clinical Endocrinology & Metabolism. 2002.
2. Bagatell CJ et al. Physiologic testosterone levels in normal men suppress high-density lipoprotein cholesterol levels. Journal of Clinical Endocrinology & Metabolism. 2003.
3. Handelsman DJ et al. Hormonal male contraception: recent trials and prospects. Human Reproduction Update. 2016.
4. Deepinder F, Braunstein GD. Drug-induced gynecomastia: an evidence-based review. Endocrine Reviews. 2012.
5. Amory JK et al. Suppression of spermatogenesis by testosterone: effect on sexual function. Journal of Andrology. 2005.
6. Rubinow DR, Schmidt PJ. Androgens, brain, and behavior. American Journal of Psychiatry. 2006.
7. Nieschlag E et al. Clinical trials in male hormonal contraception. Contraception. 2003.
8. Liu PY et al. Rate, extent, and modifiers of spermatogenic recovery after hormonal male contraception. Journal of Clinical Endocrinology & Metabolism. 2006.
9. Finkelstein JS et al. Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine. 2013.
10. Bhasin S et al. Testosterone dose-response relationships in healthy young men. Journal of Clinical Endocrinology & Metabolism. 2001.
11. Crosnoe LE et al. Anabolic steroid-induced hypogonadism. Fertility and Sterility. 2013.
12. Lidegaard Ø et al. Hormonal contraception and risk of venous thromboembolism. BMJ. 2011.
13. Wang C et al. Male hormonal contraception: where are we now? Journal of Clinical Endocrinology & Metabolism. 2016.
14. Glasier A. Acceptability of contraception for men. Human Reproduction. 2010.
15. Braunstein GD. Gynecomastia. New England Journal of Medicine. 2007.
16. Walther A et al. Psychobiological stress reactivity and recovery in male hormonal contraception. Psychoneuroendocrinology. 2017.
17. Grossmann M et al. Effects of testosterone treatment on glucose metabolism and symptoms in men with type 2 diabetes. European Journal of Endocrinology. 2015.
18. Kuhl H. Pharmacology of estrogens and progestogens. Climacteric. 2005.

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