HormoneHuman chorionic gonadotropinhCG

HCG

Glycoprotein LH-analog hormone · FDA-approved (fertility) · prohibited in males (sport)

Human chorionic gonadotropin (HCG) is the hormone the placenta makes in pregnancy — the one home pregnancy tests detect. As a medicine it is either purified from urine (Pregnyl, Novarel) or made by recombinant DNA (Ovidrel). It is not a small "research peptide" but a glycoprotein: two protein chains stuck together and coated in sugar, weighing about 36,700 daltons. What makes it useful is that it closely mimics luteinizing hormone (LH), the pituitary signal that tells the gonads what to do. In women, a burst of HCG triggers a mature egg to be released, which is why it is the "trigger shot" in IVF. In men, it acts on the Leydig cells inside the testes to make testosterone right where sperm are produced — which drives its big off-label role: men on testosterone replacement therapy (TRT) shut down their own LH, so low-dose HCG keeps the testes "switched on," preserving fertility and testicular size, a use well supported by controlled trials. HCG also has a notorious wrong use: the 1950s "HCG diet," which paired the hormone with a near-starvation 500-calorie regimen. The science is old and clear — the weight loss comes entirely from the starvation, not the hormone, and the FDA and FTC pulled OTC homeopathic HCG weight-loss products in 2011.

The short version

Human chorionic gonadotropin (HCG) is a hormone the placenta makes in pregnancy — it is the hormone home pregnancy tests detect. As a medicine it is purified from urine (Pregnyl, Novarel) or made by recombinant DNA (Ovidrel). Chemically it is a glycoprotein: two protein chains stuck together and coated in sugar molecules, weighing about 36,700 daltons — far larger and more complex than the small research peptides it often gets lumped in with.

What makes HCG useful is that it closely mimics luteinizing hormone (LH) — the pituitary signal that tells the gonads what to do. In women, a burst of HCG triggers a mature egg to be released (ovulation), which is why it is used as the "trigger shot" in IVF and ovulation-induction cycles. In men, HCG acts on the Leydig cells (the testosterone-making cells inside the testes), ordering them to produce testosterone right where sperm are made. That last point drives its big off-label role: men on testosterone replacement therapy (TRT) shut down their own LH, so the testes shrink and stop making sperm — adding low-dose HCG keeps the testes switched on, preserving fertility and testicular size.

HCG also has a notorious wrong use: the "HCG diet," a 1950s fad pairing HCG shots with a near-starvation 500-calorie diet. The science is clear and old — the weight loss comes entirely from the starvation, not the hormone. This page covers the legitimate, evidence-backed uses honestly and flags the diet myth and the thinner post-cycle convention as such.

Molecular identity

Specs

CAS number: 9002-61-3 (chorionic gonadotrophin)

Structure / class: Glycoprotein hormone (gonadotropin family) — NOT a simple peptide; no single small-molecule formula or sequenceUniProt P01215 / P0DN87
Subunits: Heterodimer: shared α-subunit CGA (92 aa, UniProt P01215) + hCG-specific β-subunit CGB (145 aa, UniProt P0DN87), heavily glycosylatedUniProt P01215 / P0DN87
Molecular weight: ~36.7 kDa (intact glycosylated heterodimer)UniProt P01215 / P0DN87
Molecular target: LH/CG receptor (LHCGR) agonist — LH analog on gonadal Leydig/granulosa cellsOvidrel FDA label
Forms: Urinary (Pregnyl/Novarel; dosed IU, IM) · recombinant choriogonadotropin alfa (Ovidrel; dosed µg, SC; 250 µg ≈ 5,000–10,000 IU)Ovidrel FDA label
Half-life: ~24–36 h terminal (recombinant SC median 29.2 h)PMID 33982429; Ovidrel label (PK)Half-life curve →
Brand / approval: FDA-approved: Pregnyl, Novarel (urinary), Ovidrel (recombinant) — fertility / ovulation trigger / male hypogonadismOvidrel FDA label
Anti-doping status: Prohibited in males at all times (WADA S2.2.1, chorionic gonadotrophin); not prohibited in femalesWADA 2026

Plain English

Mechanism

HCG binds the LH/hCG receptor (LHCGR), a G-protein-coupled receptor (a cell-surface switch) on gonadal cells. It is structurally and functionally an LH analog — it does what the body's own LH does — but with a much longer half-life, so a single dose acts for days. That durability comes from heavy glycosylation, especially the β-subunit's C-terminal peptide, which slows the body's clearance of it.

In men, receptor activation on the testicular Leydig cells drives testosterone synthesis, producing high intratesticular testosterone — the local concentration (10–100× the level in blood) required for normal sperm production. This is why HCG preserves spermatogenesis and testis size when exogenous testosterone has suppressed the pituitary's own LH; it is demonstrated in controlled human trials. In women, HCG mimics the mid-cycle LH surge, triggering final egg maturation and rupture of the pre-ovulatory follicle — the basis of the IVF and ovulation-induction "trigger shot."

The honesty point sits in what the receptor biology does and does not support. The Leydig-cell and ovulatory actions are real, human, and trial-backed. There is no comparable receptor mechanism for fat loss — HCG does not act on fat metabolism, which is why the controlled weight-loss trials came back negative.

Sources:PMID 15713727 PMID 20484472 DailyMed (Ovidrel)

Why people reach for it

Potential benefits

HCG is a genuine, FDA-approved hormone that acts as a direct LH-mimic at the gonad — and the honest split between its real uses and its famous myth matters. Here's what people reach for it for.

Keep the testes working through TRT — Its biggest off-label draw. HCG acts directly on the Leydig cells as an LH analog, maintaining the high intratesticular testosterone that testosterone-alone shuts down — preserving fertility and testicular size, a use supported by controlled human trials.
Stimulate the gonad even when the pituitary is offline — Because it bypasses the pituitary and signals the testis or ovary directly, people reach for it where upstream signaling is suppressed — the classic post-cycle and TRT-adjunct rationale.
The ovulation "trigger shot" — In women it mimics the mid-cycle LH surge to trigger final egg maturation and release — the FDA-approved basis of its role in IVF and ovulation-induction cycles.
The bottom rung of an HPG-axis stack — As the direct LH signal at the gonad, it pairs logically with the upstream rungs — Gonadorelin at the pituitary and Kisspeptin-10 at the hypothalamus — for a full-axis approach, and with FSH or testosterone to cover what it doesn't.
The myth to set aside — the "HCG diet" — The famous HCG weight-loss diet is debunked: a randomized trial and a meta-analysis found no benefit beyond the near-starvation 500-calorie regimen it's paired with, and the FDA/FTC pulled OTC homeopathic HCG weight-loss products in 2011. HCG has no fat-loss receptor mechanism.

Sources:PMID 15713727 PMID 20484472 DailyMed (Ovidrel)PMID 8527285

What people reach for HCG for, drawn from what the research reports and how it's used — the fertility and intratesticular-testosterone uses are trial-backed and FDA-approved; the weight-loss diet is debunked. This is not a weight-loss or disease claim.

Implied timing

Best time to dose

Implied best time

Anytime (consistent, 2–3×/week)

HCG isn't time-of-day sensitive — what matters is consistency on its schedule (typically every other day or 2–3× per week for TRT-adjunct use).

Unlike short-acting peptides, HCG has a long action — a terminal half-life of roughly 24–36 hours — so a single dose works across days and the exact hour of injection carries little weight.
Because it acts for days, the lever is the schedule, not the clock: TRT-adjunct and post-cycle use run on an every-other-day or 2–3×-weekly cadence, and keeping that cadence steady is what maintains intratesticular testosterone.
Many users simply align the HCG injection with their existing testosterone dose for routine and adherence — a practical anchor, not a pharmacokinetic requirement.
The exceptions are use-specific, not time-of-day: the ovulation trigger is a single dose timed ~36 hours before egg retrieval (event-timed, not clock-timed), and fertility-induction dosing follows its own multi-month schedule.

No study establishes an ideal time of day for HCG — this is reasoned from its long half-life and how it's used. Where most peptides cluster in a midday-to-evening window, HCG is largely time-of-day-independent: consistency on an every-other-day / 2–3×-weekly schedule is the lever, with the ovulation trigger being an event-timed exception.

Sources:PMID 15713727 DailyMed (Ovidrel)

How to run it

Dosing & protocol

HCG is injected — subcutaneously (SC) or intramuscularly (IM) depending on the preparation — and is always dosed in international units (IU) for urinary forms (Pregnyl, Novarel). Recombinant Ovidrel uses micrograms (µg) and is SC only; 250 µg Ovidrel ≈ 5,000–10,000 IU urinary HCG — the two forms are not freely interchangeable by unit. The tiers below cover the three main use contexts. The on-page calculator is set up for a 5,000 IU research vial.

Ovulation trigger and male fertility induction are FDA-approved indications. TRT-adjunct micro-dosing has trial support for the principle (Coviello 2005, Roth 2010) but the exact combination regimen is off-label convention. Post-cycle (PCT) use has no RCT support — flagged as convention only. WADA prohibits HCG for male athletes at all times (S2.2.1); not prohibited in females.

Tiered dose ranges

HCG protocols split by purpose; the IU range varies substantially depending on whether the goal is ovulation, fertility restoration, or testicular preservation.

Ovulation / IVF trigger (women, on-label):: 5,000–10,000 IU IM of urinary HCG, or 250 µg Ovidrel SC — a single dose given ~36 hours before scheduled egg retrieval, after FSH-driven follicular development.
Male fertility induction (on-label):: 1,000–4,000 IU IM or SC, 2–3× per week, for months; typically titrated to a mid-normal morning testosterone, with FSH added when sperm output remains incomplete.
TRT-adjunct / testicular preservation (convention):: 250–500 IU SC every other day, or 2–3× per week, added alongside testosterone — the low-dose principle supported by controlled trials at doses as low as 125 IU every other day (Coviello 2005, Roth 2010).
Post-cycle therapy / axis restart (PCT, convention):: Commonly 1,000–2,000 IU IM or SC every other day for 2–3 weeks, then tapering — convention based on HPG-axis reasoning, not RCT data; flagged as such.

Administration — subcutaneous or intramuscular

Route depends on the HCG form and the goal; SC works for the low doses used in TRT and PCT.

SC injection site:: Abdomen (a couple of inches clear of the navel), outer thigh, or love-handle area. Rotate sites between doses to prevent local irritation. SC is standard for TRT-adjunct micro-doses (250–500 IU) and for recombinant Ovidrel.
IM injection site:: Gluteus medius (upper outer quadrant) or vastus lateralis (outer thigh) — conventional for urinary HCG trigger shots and the higher fertility-induction doses. IM delivers faster peak absorption for the large trigger doses.
Frequency:: TRT-adjunct: every other day or 2–3× weekly. Fertility induction: 2–3× weekly on a multi-month schedule. Trigger: single injection only.
Reconstitution note:: Urinary HCG (lyophilized powder) must be reconstituted before use — see the reconstitution card below for the mixing math. Ovidrel comes prefilled; no mixing required.

Cycle & washout

Duration tracks the use context; HCG is not typically pulsed the way small research peptides are.

TRT-adjunct:: Co-administered continuously alongside testosterone for as long as preserving intratesticular testosterone and fertility matters. Monitor LH, FSH, estradiol, and total testosterone periodically — rising estradiol signals too high a dose or too-frequent injection and warrants a dose reduction.
Fertility induction:: Multi-month cycles, often 3–6 months, with FSH added if sperm production is incomplete after the first few months on HCG alone.
PCT:: 2–4 weeks of HCG, often followed by a SERM (clomiphene or enclomiphene) for 4–6 more weeks. The goal is to normalize LH/FSH and testosterone before the SERM taper; recheck serum testosterone and gonadotropins at the end.
Estradiol monitoring:: Because HCG raises intratesticular testosterone, aromatization to estradiol follows. Bloating, nipple sensitivity, or mood changes mid-cycle are signals to reassess dose and frequency.

Reconstitution at a glance — mixing math only

For a 5,000 IU lyophilized vial (the standard research size); the on-page calculator handles any vial size live.

Mix:: 5,000 IU vial + 2 mL bacteriostatic water = 2,500 IU per mL. On a U-100 insulin syringe: 250 IU = 10 units · 500 IU = 20 units · 1,000 IU = 40 units.
Alternate dilution:: 5,000 IU + 5 mL bacteriostatic water = 1,000 IU per mL. On a U-100 syringe: 250 IU = 25 units · 500 IU = 50 units — more syringe travel for the small TRT-adjunct doses, which reduces measurement error.

Sources:PMID 15713727 PMID 20484472 DailyMed (Ovidrel)

Substrate the signal needs

Nutritional cofactor precision

HCG supplies the LH signal — it orders the Leydig cells to make testosterone — but the testes still need the raw materials to answer that order. So the useful cofactors feed the steroidogenesis pathway hCG drives, or support the systemic environment the HPG axis depends on. This is reasoning from steroidogenesis physiology and HPG-axis biology, not an hCG nutrition study. Applies to the LH-mimic endocrine use only — not the debunked weight-loss diet.

Reasoned from Leydig-cell steroidogenesis + HPG-axis biology — not an hCG cofactor study. Supplement doses are common evidence-based ranges, not hCG-specific findings.

Amplify the signal environment — energy, stress, and sleep

The HPG axis is energy-gated: chronically underfed, overtrained, or sleep-deprived, the body down-prioritizes testosterone production regardless of how strong the LH signal is.

Adequate calories:: The Leydig cells cannot synthesize testosterone if the body is in a severe energy deficit — this is the opposite of the starvation "HCG diet." Eat at or above maintenance; severe restriction blunts the very pathway hCG is activating.
Cortisol management:: Chronically elevated cortisol (from overtraining, poor sleep, or chronic stress) suppresses LH at the pituitary and impairs steroidogenesis in the testes. Addressing the upstream stressor lets hCG's downstream signal land cleanly.
Sleep (7–9 h):: The largest testosterone pulse occurs during sleep. Prioritize sleep duration and quality; disrupted sleep suppresses the HPG axis above and below the site where hCG acts.

Supply the steroid substrate — cholesterol and Leydig-cell cofactors

Every steroid hormone is built from cholesterol — that conversion is exactly the step hCG's LH-mimic signal initiates in the Leydig cell. The nutrients below are the known inputs that testosterone synthesis runs on.

Cholesterol (dietary fat):: The immediate precursor of all steroid hormones. Very-low-fat diets can blunt testosterone output because the substrate for conversion is short. No supplementation needed — adequate dietary fat (saturated + monounsaturated from whole foods) keeps the supply available.
Zinc — 15–30 mg/day:: Zinc is directly involved in Leydig-cell testosterone production; deficiency measurably suppresses output. Zinc picolinate or bisglycinate 15–30 mg daily (with food). If running 30 mg long-term, pair with 1–2 mg copper bisglycinate to prevent depletion.
Vitamin D — 2,000–5,000 IU/day:: Vitamin D receptor (VDR) is expressed in Leydig cells; low vitamin D tracks with lower testosterone in population studies, and correcting a deficiency tends to normalize output. Dose to blood level (50–80 ng/mL is a common clinical target). Take with a fatty meal for absorption.
Magnesium — 300–400 mg/day:: Magnesium deficiency is associated with lower testosterone. Magnesium glycinate or malate 300–400 mg at night — also supports sleep quality, which is independently relevant. Avoid oxide form (poor absorption).
Boron — 3–6 mg/day:: Boron supports free testosterone by reducing SHBG (sex hormone-binding globulin) and may assist vitamin D metabolism. 3–6 mg calcium fructoborate or sodium borate daily with food.

Leydig-cell antioxidant support

Steroid synthesis in the Leydig cell generates oxidative stress as a metabolic byproduct — the testis is relatively sensitive to oxidative damage, which over time can impair Leydig-cell function.

Vitamin C — 500–1,000 mg/day:: Testicular tissue has high vitamin C concentration; it scavenges reactive oxygen species generated during steroidogenesis. 500–1,000 mg ascorbic acid split across the day.
Vitamin E — 100–200 IU/day:: Fat-soluble antioxidant with evidence for Leydig-cell protection in oxidative-stress models. Mixed tocopherols 100–200 IU daily with a fatty meal.
Selenium — 100–200 mcg/day:: Selenoproteins (glutathione peroxidase) protect the testes from oxidative damage and support spermatogenesis. Selenomethionine 100–200 mcg daily; do not exceed 400 mcg/day.

Combinations + timing

Stacking notes + timing windows

HCG sits at the bottom rung of the HPG axis — it is the LH signal itself, acting directly on the gonads. Its natural partners are either one rung above (upstream signals that drive the whole axis), or complementary hormones that cover what hCG does not (FSH for sperm, testosterone for systemic levels). Combining two agents at the same rung (two LH analogs) is redundant and is not listed.

Clinical and fertility conventions plus HPG-axis reasoning — combinations clinicians and users actually run, not pairings studied head-to-head as named stacks. Covers the LH-mimic endocrine use; none applies to, or supports, the debunked weight-loss diet.

HCG + Testosterone (TRT-adjunct stack)

The most established hCG combination — testosterone suppresses the pituitary's LH signal, and hCG replaces it at the gonad to preserve what testosterone alone shuts down.

Why it works:: Exogenous testosterone suppresses LH via negative feedback at the pituitary, which drops intratesticular testosterone (ITT) to near-zero — causing testicular atrophy and stopping sperm production. hCG acts directly on the Leydig LHCGR receptor, bypassing the suppressed pituitary and maintaining the high ITT required for spermatogenesis. Complementary: one supplies systemic testosterone, the other keeps the testicular machinery running. Supported by controlled trials (Coviello 2005, Roth 2010).
The protocol:: Testosterone at the user's TRT dose (e.g. 100–200 mg testosterone cypionate/enanthate IM or SC weekly) + hCG 250–500 IU SC every other day or 3× per week. Monitor estradiol — rising estrogen signals too-high hCG dose; reduce frequency before dose.
Outcome:: Maintained testicular size and fertility potential during TRT; the combination clinicians reach for when patients on testosterone want to preserve future fertility or prevent testicular atrophy.

HCG + Gonadorelin (upstream vs downstream LH ladder)

Gonadorelin (GnRH) acts one rung above — on the pituitary — while hCG acts one rung below, directly on the gonad. Different positions on one axis, not the same lever.

Why it works:: Gonadorelin prompts the pituitary to release its own LH and FSH in a pulsatile pattern, preserving the pituitary end of the axis. hCG directly drives the Leydig cell regardless of pituitary status. Layering them means the pituitary is stimulated AND the gonad is directly driven — used in cases where preserving both ends of the axis matters (e.g. during TRT, where the pituitary is suppressed). Different rungs: GnRH agonist = top; hCG = bottom.
The protocol:: Gonadorelin typically 100 mcg SC pulsed 2–3× per week (to mimic the natural GnRH pulse, avoiding pituitary desensitization from continuous agonist exposure) + hCG 250–500 IU SC every other day or 3× weekly. Clinical convention; exact scheduling is provider-directed.
Outcome:: Preserved pituitary + gonadal function simultaneously; increasingly used in TRT protocols that aim for complete-axis preservation, and in fertility prep before testosterone cessation.

HCG + Kisspeptin-10 (furthest-upstream axis priming)

Kisspeptin-10 is the upstream gate — it primes the hypothalamus to release GnRH, which drives LH, which hCG directly mimics. Top and bottom rung of the same ladder.

Why it works:: Kisspeptin-10 triggers the hypothalamic GnRH pulse; hCG provides the direct Leydig-cell drive. Running the top rung (kisspeptin → GnRH → pituitary LH) alongside the bottom rung (hCG → Leydig cells directly) covers the whole axis simultaneously — and since the two act at completely different levels, they are not redundant. Used in research for axis mapping; emerging in clinical fertility contexts.
The protocol:: Kisspeptin-10 6.4 nmol/kg body weight SC (the dose used in published human studies) pulsed to stimulate a GnRH pulse, + hCG 250–500 IU SC on alternating days. Highly experimental; no standard clinical regimen established.
Outcome:: Whole-axis stimulation: hypothalamus → pituitary → gonad. Reached for in experimental fertility/hypogonadism research where restoring full endogenous pulsatility alongside gonadal drive is the goal.

HCG + PCT SERM (axis-restart stack — post-cycle convention)

After anabolic-steroid suppression, hCG "wakes up" the atrophied Leydig cells, then a SERM (selective estrogen receptor modulator) prompts the pituitary to resume its own LH output. Sequential, not simultaneous — two different tools on two different rungs.

Why it works:: Prolonged exogenous steroid use leaves Leydig cells dormant and the pituitary deeply suppressed. A brief hCG course directly stimulates the Leydig cells back to responsiveness; then a SERM (clomiphene or enclomiphene) blocks estrogen feedback at the pituitary and hypothalamus, causing LH and FSH output to rise, which hands off to the now-receptive Leydig cells. Sequential: hCG first to restore gonadal sensitivity, SERM second to restart pituitary drive.
The protocol:: hCG 1,000–2,000 IU SC or IM every other day for 2–3 weeks, then transition to a SERM (e.g. clomiphene 25–50 mg/day or enclomiphene 12.5–25 mg/day) for 4–6 weeks. Convention only — no RCT; flagged as such. Serum testosterone and gonadotropins should be checked at the end of the SERM phase.
Outcome:: Restoration of the natural HPG axis after anabolic suppression. Convention; the RCT evidence is absent. Some clinicians prefer Gonadorelin over hCG in this context due to more physiological LH pulsatility.

Sources:PMID 15713727 PMID 20484472 DailyMed (Ovidrel)

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0 mL
Doses per vial: 10000
Concentration: 2500 mg/mL

One vial lasts

Daily: 10000 days
Every other day: 20000 days
5×/week: 14000 days

Very small draw volume — measurement precision on an insulin syringe is limited at this size. Verify with a researcher experienced with this peptide.

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

In men, HCG raises testosterone by stimulating the Leydig cells, and the increased testosterone can aromatize to estrogen — so the characteristic effects are gynecomastia (breast tissue growth), fluid retention, acne, mood changes, and testicular discomfort. These are dose-related and manageable, which is part of why low-dose regimens are preferred for testicular preservation.

In women, the principal serious risk is ovarian hyperstimulation syndrome (OHSS) when HCG is used as a trigger after FSH stimulation — ovarian enlargement, fluid shifts, and in severe cases blood-clot risk — along with the multiple-pregnancy risk inherent to ovulation induction. Across both sexes, injection-site reactions (pain, redness, bruising), headache, fatigue, and irritability are common and mild.

Worth separating out: the harms attributed to the "HCG diet" come mainly from its dangerous 500-calorie-a-day regimen (gallstones, electrolyte imbalance, heart-rhythm disturbance), not from the hormone itself. The honest framing is that HCG is a well-characterized hormone with real, predictable endocrine effects — and that the diet's dangers are a property of the starvation it is paired with.

Sources:DailyMed (Ovidrel)FDA Consumer Update 2011

As reported in literature

Research dosing ranges

These are the doses studied in the published literature, shown separately so the trial evidence is never mistaken for a recommended regimen. HCG's evidence is unusually deep and largely human: controlled trials establish both the low-dose intratesticular-testosterone principle in men and the trigger-shot role in women — and, separately, a randomized trial and a meta-analysis that put the weight-loss myth to rest.

Dose	Route	Model	Outcome	Sources:
125 / 250 / 500 IU every other day ×3 wk (+ 200 mg testosterone/wk)	SC/IM	Human RCT — healthy men, n=29, suppressed gonadotropins	Intratesticular testosterone preserved dose-dependently; testosterone-alone dropped it ~94% — low-dose HCG kept it in normal range	PMID 15713727
15 / 60 / 125 IU every other day	SC	Human — men with experimental gonadotropin deficiency	Intratesticular testosterone rose dose-dependently even at very low doses — establishes the micro-dose principle	PMID 20484472
5,000 kJ/day diet + HCG vs placebo (6 wk)	IM	Human RCT — 40 obese women, double-blind	No advantage over placebo on any measured variable; "no rationale for the use of HCG injections in obesity"	PMID 2405506
Simeons protocol (HCG diet) — 24 trials pooled	IM	Human meta-analysis (criteria-based)	No evidence HCG is effective for obesity — no weight loss, fat redistribution, hunger reduction, or well-being benefit	PMID 8527285
250 µg recombinant vs 5,000 IU urinary IM	SC	Human — infertile women in ART	Single trigger dose induces final follicular maturation/ovulation; recombinant SC non-inferior to urinary IM	DailyMed (Ovidrel)

Quick answers

Frequently asked

Does the HCG diet actually work?

No. A randomized placebo-controlled trial and a meta-analysis of 24 trials both found no benefit beyond the starvation-level calorie restriction, and the FDA and FTC pulled OTC homeopathic HCG weight-loss products in 2011. Any weight loss is from the 500-calorie diet, not the hormone — and that diet carries its own risks.

HCG vs gonadorelin — what's the difference?

Gonadorelin (and GnRH agonists) act upstream on the pituitary to release the body's own LH and FSH; HCG acts downstream as a direct LH-mimic on the gonads themselves. HCG bypasses the pituitary, has a much longer half-life, and gives a stronger, steadier Leydig-cell or ovulatory drive — which is why it works even when the pituitary is suppressed.

Why do men on TRT add HCG?

Exogenous testosterone shuts off the pituitary's LH, which shrinks the testes and stops sperm production. Low-dose HCG keeps the testes producing intratesticular testosterone, preserving fertility and testis size — a principle supported by controlled human trials.

Is HCG FDA-approved?

Yes — for ovulation/IVF triggering, male hypogonadotropic hypogonadism and fertility, and cryptorchidism in boys. It is not approved for weight loss or for TRT-adjunct/post-cycle use; those are off-label.

What's the difference between Pregnyl/Novarel and Ovidrel?

Pregnyl and Novarel are urinary-derived, dosed in international units (IU), and usually given IM. Ovidrel is recombinant (choriogonadotropin alfa), dosed in micrograms (µg), and given SC; 250 µg ≈ 5,000–10,000 IU urinary HCG. They are not freely interchangeable on a unit basis.

Will HCG cause a positive pregnancy test?

Yes — exogenous HCG can produce positive pregnancy tests and can interfere with HCG-based laboratory monitoring, because pregnancy tests detect the same hormone.

Is HCG banned in sport?

It is prohibited at all times for male athletes under the 2026 WADA Prohibited List (S2.2.1, as a testosterone-stimulating peptide), and permitted for female athletes. Athletes should verify current status via GlobalDRO for their sport and date.

Primary sources

References

UniProt P01215UniProt P01215 — Glycoprotein hormones alpha chain (CGA), shared α-subunit (92 aa)
UniProt P0DN87UniProt P0DN87 — Choriogonadotropin subunit beta (CGB), 145 aa mature (legacy P01233 demerged)
PMID 15713727Coviello et al., J Clin Endocrinol Metab 2005 (low-dose hCG maintains intratesticular testosterone)
PMID 20484472Roth et al., J Clin Endocrinol Metab 2010 (dose-dependent ITT with very low-dose hCG)
PMID 2405506Bosch et al., S Afr Med J 1990 (HCG & weight loss — double-blind placebo-controlled RCT)
PMID 8527285Lijesen et al., Br J Clin Pharmacol 1995 (Simeons HCG therapy — criteria-based meta-analysis)
PMID 33982429Kyhl et al., Clin Transl Sci 2021 (first-in-human PK/PD of recombinant hCG)
DailyMed (Ovidrel)OVIDREL (choriogonadotropin alfa) FDA Prescribing Information
FDA Consumer Update 2011FDA/FTC action removing OTC homeopathic HCG weight-loss products (2011)
WADA 2026WADA 2026 Prohibited List, S2.2.1 — chorionic gonadotrophin prohibited in males

Research use only · Not medical advice · Updated 2026-06-01