Home Supplements That Start With G Gonadotropin: Uses for Fertility, Evidence-Based Dosing, Risks, and Side Effects

Gonadotropin: Uses for Fertility, Evidence-Based Dosing, Risks, and Side Effects

7

Gonadotropins are prescription hormones that directly stimulate the ovaries and testes. In women, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) drive follicle growth and ovulation. In men, human chorionic gonadotropin (hCG) acts like LH to raise intratesticular testosterone, and FSH supports Sertoli cells for sperm production. Clinically, gonadotropins are used to induce ovulation in anovulatory cycles, optimize oocyte yield in in-vitro fertilization (IVF), and restore spermatogenesis in men with hypogonadotropic hypogonadism. Their benefits are tangible—higher ovulation rates, controlled follicle development, and, in the right setting, improved pregnancy chances. Yet they require careful monitoring; dosing and timing determine both success and safety. This guide explains how these medicines work, who benefits, how clinicians dose them, common pitfalls, and what the evidence shows, so you can discuss options with your care team in an informed way.

Essential Insights

  • Induces ovulation (women) and supports spermatogenesis (men) when the pituitary–gonadal signal is insufficient.
  • Primary safety concern is ovarian hyperstimulation syndrome; careful monitoring lowers risk.
  • Typical dosing: FSH 37.5–150 IU/day for ovulation induction; IVF often 150–300 IU/day; hCG trigger 250 micrograms or 5,000–10,000 IU.
  • Avoid use with hormone-sensitive cancers, active thromboembolic disease, or primary gonadal failure.

Table of Contents

What are gonadotropins and how they work

Gonadotropins are peptide hormones that act on the gonads. The two native pituitary hormones—FSH and LH—control follicle development and ovulation in women and regulate spermatogenesis and testosterone production in men. In clinical practice, we use highly purified urinary preparations and recombinant versions:

  • FSH-only products (e.g., recombinant follitropin alfa/beta/delta; highly purified urinary FSH) primarily drive granulosa cell activity and follicle growth.
  • hMG (menotropins) contains both FSH and LH activity derived from human urine; LH activity often comes from hCG.
  • Recombinant LH (lutropin alfa) provides defined LH activity, typically as an add-on for women with profound LH deficiency.
  • hCG (urinary or recombinant choriogonadotropin alfa) mimics the LH surge to induce final oocyte maturation in women and stimulates Leydig cells in men.

Mechanism, simplified.
FSH raises aromatase and promotes follicular recruitment and maturation. LH (or hCG) triggers meiotic resumption and ovulation by activating LH/hCG receptors on theca and granulosa cells, culminating in progesterone production. In men, hCG binds LH receptors on Leydig cells to increase intratesticular testosterone—a prerequisite for spermatogenesis—while FSH acts on Sertoli cells to support germ cell development.

Formulations and routes.
Most modern products are given subcutaneously using pens or prefilled syringes. Recombinant preparations provide consistent bioactivity and allow precise dosing increments (e.g., 37.5–75 IU steps). Urinary products can be more cost-accessible and are clinically effective when used appropriately.

Why dosing must be individualized.
Response depends on ovarian reserve (AMH, antral follicle count), age, body mass index, prior response, and, in men, baseline testicular volume and the degree/duration of gonadotropin deficiency. Too much stimulation increases risks (e.g., ovarian hyperstimulation syndrome, multiple follicles), while too little fails to recruit a dominant follicle or restore spermatogenesis.

Where gonadotropins fit in care pathways.
For anovulatory infertility (often PCOS), oral agents like letrozole are first-line; gonadotropins are used when oral treatment fails or is contraindicated. In IVF, gonadotropins are essential to grow a cohort of follicles for oocyte retrieval. For men with hypogonadotropic hypogonadism, gonadotropins are a cornerstone to initiate or restore fertility because exogenous testosterone suppresses spermatogenesis and does not induce sperm production.

Back to top ↑

Do gonadotropins improve fertility outcomes?

Women—anovulation and IVF.
In anovulatory women who do not respond to oral ovulation induction, low-dose FSH regimens can achieve monofollicular ovulation while keeping multiple pregnancy risk low. In assisted reproduction, individualized gonadotropin stimulation reliably increases the number of mature oocytes available for fertilization. Contemporary guidelines emphasize tailoring starting dose to predicted response (using AMH or antral follicle count), preferring antagonist protocols for safety, and using evidence-based triggers for final oocyte maturation. When applied thoughtfully, these strategies improve the chance of obtaining high-quality oocytes and embryos while minimizing complications.

Triggering ovulation.
For final oocyte maturation in stimulated cycles, choriogonadotropin alfa 250 micrograms has demonstrated clinical equivalence to 5,000–10,000 IU urinary hCG for triggering ovulation. In high-risk patients, a GnRH agonist trigger within an antagonist protocol may be used to drastically lower ovarian hyperstimulation risk; some programs then support the luteal phase more intensively or plan a freeze-all strategy when indicated.

Men—hypogonadotropic hypogonadism.
In men with pituitary or hypothalamic deficiency, gonadotropin therapy restores the physiologic signals required for sperm production. Typical outcomes reported across centers show spermatogenesis in a majority of men after sequential or combined therapy (hCG to prime Leydig cells, then addition of FSH). Time to first ejaculated sperm generally ranges from 3 to 9 months, sometimes longer when baseline testicular volume is small or the deficiency is long-standing. Pregnancy can occur naturally or with assisted techniques (e.g., IUI/IVF/ICSI) once sperm counts improve.

Where they do not work well.
Gonadotropins cannot overcome primary ovarian insufficiency or primary testicular failure, where the gonads themselves cannot respond. In cryptorchidism (undescended testis) during childhood, routine hormonal therapy is not recommended; early surgery is favored to protect fertility potential and reduce cancer risk.

Bottom line.
When the clinical problem is lack of gonadotropin signal (women who require controlled ovarian stimulation; men with secondary hypogonadism), these medicines are highly effective—provided dosing is individualized and monitoring is rigorous.

Back to top ↑

Who should consider gonadotropin therapy?

Women

  • Anovulatory (WHO Group II) infertility after unsuccessful trials with first-line agents (e.g., letrozole). Low-dose step-up FSH can coax a single follicle while limiting multiples.
  • IVF/ICSI cycles, where a cohort of follicles is required; gonadotropins are non-negotiable here.
  • Profound LH deficiency (rare): may benefit from adding recombinant LH (e.g., 75 IU/day) to FSH.
  • Ovulation triggering after stimulation: hCG (urinary 5,000–10,000 IU or choriogonadotropin alfa 250 micrograms) when not using an agonist trigger.

Men

  • Hypogonadotropic hypogonadism (pituitary or hypothalamic origin) seeking fertility: hCG to raise intratesticular testosterone, then addition of FSH to initiate/maintain spermatogenesis.
  • Post-pubertal secondary hypogonadism after pituitary surgery, trauma, functional hypothalamic disorders, or medication-related suppression (after recovery), when fertility is desired.
  • Adolescent induction of puberty in selected cases (specialist care), though protocols vary and require pediatric endocrinology oversight.

Situations favoring alternatives first

  • PCOS with ovulatory dysfunction: start with letrozole due to efficacy and lower multiple gestation risk.
  • Unexplained infertility: intrauterine insemination (IUI) protocols sometimes use mild gonadotropins, but many programs prioritize oral agents or move to IVF depending on age and prognosis.

Who is unlikely to benefit

  • Primary gonadal failure (e.g., testicular failure with high FSH/LH; primary ovarian insufficiency).
  • Untreated endocrine disorders causing anovulation (e.g., uncorrected thyroid, prolactin).
  • Cryptorchidism in children: routine hCG or GnRH/LHRH is not recommended; orchiopexy is standard.

Decision factors

  • Reproductive goals and timeline.
  • Predicted ovarian response (AMH, AFC) and age.
  • Baseline semen parameters, testicular volume, and the etiology/duration of hypogonadism.
  • Access, cost, comfort with injections, and clinic monitoring capacity.
  • Thromboembolic risk and personal/family history of hormone-sensitive tumors.

Back to top ↑

How to use them: protocols and doses

Women: ovulation induction (non-IVF)

  • Low-dose step-up FSH: common starting doses 37.5–75 IU subcutaneously daily from cycle day 2–3, with increments of 37.5–50 IU no more often than every 5–7 days until one dominant follicle emerges. The goal is monofollicular ovulation to minimize multiples.
  • Trigger: when a leading follicle reaches ~17–18 mm with appropriate estradiol, administer hCG (urinary 5,000–10,000 IU IM/SC) or choriogonadotropin alfa 250 micrograms SC to induce ovulation 34–36 hours later. Timed intercourse or IUI follows accordingly.

Women: IVF/ICSI stimulation

  • Starting FSH dose often 150–300 IU/day (sometimes lower or higher) individualized by AMH, AFC, age, BMI, and prior response. Both recombinant FSH and highly purified urinary FSH/hMG are acceptable; antagonist protocols are widely used for safety.
  • LH add-on: considered at ~75 IU/day in documented severe LH deficiency or selected poor responders, based on clinician judgment.
  • Trigger options:
  • Choriogonadotropin alfa 250 micrograms or urinary 5,000–10,000 IU hCG for standard responders.
  • GnRH agonist trigger in antagonist cycles for patients at high risk of ovarian hyperstimulation; often combined with a freeze-all or intensive luteal support plan.

Men: hypogonadotropic hypogonadism (fertility induction)

  • Phase 1 (Leydig cell priming): hCG 1,500–2,000 IU SC/IM two to three times weekly to raise intratesticular testosterone; target normal serum testosterone and clinical signs (libido, testicular growth).
  • Phase 2 (add FSH): after ~3–6 months—or once testicular volume increases—add FSH 75–150 IU SC two to three times weekly (or comparable hMG) while continuing hCG.
  • Monitoring: semen analysis every 1–3 months; adjust doses to maintain progress; anticipate 3–9 months to first sperm in ejaculate, longer in long-standing or prepubertal-onset cases.

Practical tips

  • Administration: rotate injection sites; pens and prefilled syringes simplify home use.
  • Storage: many formulations require refrigeration before opening; check the specific product leaflet.
  • Dose adjustments: in women, titrate slowly to avoid multiple follicles; in men, titrate to physiologic testosterone with semen endpoints.
  • When to stop or pivot: lack of ovarian response despite careful escalation may suggest alternative diagnoses or the need for IVF; in men, absence of sperm after a sustained course may prompt adjuncts (e.g., pulsatile GnRH where available) or assisted reproductive techniques.

Units at a glance

  • IU (International Units) are standard for FSH/LH/hMG dosing.
  • Micrograms (mcg) are used for recombinant hCG (250 micrograms), which is clinically equivalent to traditional 5,000–10,000 IU urinary hCG for triggering.

Back to top ↑

Common mistakes, side effects, and cautions

Common mistakes

  • Escalating FSH too quickly in ovulation induction, leading to multi-follicular response and increased multiple pregnancy risk.
  • Using hCG to treat cryptorchidism in children; routine hormonal therapy is no longer recommended—earlier surgery is standard.
  • Assuming exogenous testosterone restores fertility in men; it suppresses gonadotropins and inhibits spermatogenesis.
  • Triggering despite signs of high risk (very high estradiol, numerous mid-size follicles) rather than switching to an agonist trigger or a freeze-all strategy.

Side effects—women

  • Ovarian hyperstimulation syndrome (OHSS): abdominal distension, nausea, rapid weight gain, hemoconcentration; severe cases can involve ascites or thrombosis. Risk rises with high response (e.g., many follicles, high AMH/PCOS). Prevention includes antagonist protocols, judicious dosing, agonist trigger when appropriate, and cycle segmentation (freeze-all).
  • Injection-site reactions, headache, mood changes, breast tenderness, mild pelvic discomfort as follicles grow.
  • Multiple gestation risk if multiple dominant follicles are present in non-IVF cycles.

Side effects—men

  • Gynecomastia and breast tenderness (from aromatization of testosterone to estradiol), acne, fluid retention, and mood changes.
  • Injection-site reactions; rarely polycythemia if testosterone becomes supraphysiologic.

Contraindications and cautions

  • Do not use in hormone-sensitive malignancies (ovary, breast, uterus), unexplained vaginal bleeding, active thromboembolic disease, or primary ovarian/testicular failure where response is unlikely.
  • Address first: uncontrolled thyroid disease, hyperprolactinemia, adrenal disorders, and untreated pituitary tumors.
  • Pregnancy: gonadotropins are not used during pregnancy.
  • Drug interactions: few direct pharmacologic interactions; the key risk is physiologic—stacking stimulatory agents or inadequate monitoring.

When to call your clinic urgently

  • Sudden severe abdominal pain or rapid weight gain.
  • Shortness of breath, chest pain, calf swelling (possible thrombosis).
  • Severe headache or visual changes.
  • In men, painful testicular swelling or signs of severe gynecomastia.

Back to top ↑

Evidence summary, alternatives, and FAQs

Evidence in women

  • Major reproductive societies recommend individualized dosing with either recombinant or urinary FSH and favor antagonist protocols for general IVF populations because efficacy is comparable and safety is improved. For patients at high risk of OHSS, preventive measures include agonist trigger and cycle segmentation.
  • For ovulation induction, chronic low-dose step-up FSH (starting 37.5–75 IU/day, small weekly increments) is the accepted strategy to maximize monofollicular ovulation and minimize multiple gestation.
  • For final oocyte maturation, choriogonadotropin alfa 250 micrograms is clinically equivalent to 5,000–10,000 IU urinary hCG. Product labeling and regulatory summaries clarify dose and indications.

Evidence in men

  • In hypogonadotropic hypogonadism, sequential hCG then FSH (or combined) can restore ejaculated sperm in many patients; timeframes vary with baseline testicular volume, etiology, and duration of deficiency. Guideline updates in male infertility support gonadotropin therapy for fertility induction when endogenous LH/FSH are deficient and conception is desired.

Alternatives, complements, and special cases

  • Letrozole or clomiphene remain first-line for many anovulatory women; gonadotropins are second-line or used when planning IVF.
  • Pulsatile GnRH therapy (where available) can be an alternative to exogenous gonadotropins in some men and women with hypothalamic deficiency; access and logistics limit use in many regions.
  • Lifestyle and metabolic care: weight optimization, insulin sensitization (for PCOS), and thyroid/prolactin correction often improve response to any fertility therapy.
  • Doping and misuse: hCG and other gonadotropins are prohibited in sport; non-medical use carries risks and legal consequences.

Quick answers

  • How long should a woman take FSH before triggering? Until one or more follicles reach mature size with appropriate estradiol; this may take 7–14 days or longer with low-dose regimens.
  • How long until sperm appears with hCG/FSH therapy in men? Commonly 3–9 months; longer if prepubertal onset or very small baseline testes.
  • Is recombinant better than urinary? Both are effective; choice depends on cost, availability, and clinician preference.
  • Can I store pens at room temperature? Many pens can be kept at room temperature for limited periods after first use; check your specific product leaflet for exact limits.

Back to top ↑

References

Disclaimer

This information is educational and does not substitute for personalized medical advice, diagnosis, or treatment. Fertility medicines require specialist supervision, individualized dosing, and careful monitoring. Always consult your healthcare professional before starting, stopping, or changing any medication. If you experience urgent symptoms (e.g., severe abdominal pain, shortness of breath, chest pain), seek emergency care.

If you found this article useful, please consider sharing it on Facebook, X (formerly Twitter), or your preferred platform, and follow us for future updates. Your support helps us keep creating accurate, people-first guides.

RELATED ARTICLESMORE FROM AUTHOR