Recovering from androgen-induced suppression

This page reviews the published evidence on the drugs used to restart the hypothalamic-pituitary-gonadal axis. It is not a protocol. Every drug named here is unlicensed for this purpose.

What the evidence shows

Findings are grouped by what kind of evidence each one is. That ordering is the point: a sentence from an FDA label and a sentence from a forum are not the same claim, and this page will not present them as though they were.

Clinical trial evidence

• THE TESTIS REMAINS hCG-RESPONSIVE DURING ANDROGEN-INDUCED GONADOTROPIN SUPPRESSION. In healthy men made LH/FSH-suppressed by weekly testosterone enanthate, intratesticular testosterone rose in a dose-dependent, linear fashion with concurrent hCG, and 250 IU every other day held ITT within 7% of the men's own pre-suppression baseline while 500 IU EOD pushed it 26% above baseline. Leydig cells are not rendered unresponsive by suppression — they are simply unstimulated because LH is gone. Anything claiming the suppressed testis cannot respond to hCG is contradicted by direct intratesticular measurement. [1]

  Dose or parameter studied: hCG 125, 250 or 500 IU subcutaneously/by injection every other day for 3 weeks, each arm on a background of testosterone enanthate 200 mg weekly

  Studied in: 29 men with normal reproductive physiology (healthy volunteers, ages spanning adolescent to middle-aged), suppressed for only 3 weeks by supraphysiologic testosterone enanthate. GAP FOR THIS APP: these were men with normal testes suppressed for 3 weeks under supervision — not men who have run multi-compound cycles for months or years. Responsiveness after long, high-dose or 19-nor-heavy exposure has not been measured this way.

• SERUM TESTOSTERONE IS A BAD PROXY FOR WHAT IS HAPPENING INSIDE THE TESTIS. In the same trial, baseline serum testosterone was only 1.2% of intratesticular testosterone, and testosterone enanthate alone (no hCG) suppressed ITT by 94% while serum testosterone was of course supraphysiologic. A normal or high blood testosterone number during or after a cycle says nothing about the intratesticular environment that spermatogenesis depends on. [1]

  Dose or parameter studied: testosterone enanthate 200 mg weekly for 3 weeks with saline placebo (the comparator arm)

  Studied in: Same 29 healthy men with normal reproductive physiology; the suppression arm received testosterone enanthate 200 mg weekly plus saline for 3 weeks.

• SERUM 17-HYDROXYPROGESTERONE TRACKS INTRATESTICULAR TESTOSTERONE AND IS ORDERABLE WITHOUT A TESTICULAR ASPIRATION. In gonadotropin-suppressed men given graded hCG, 17-OHP fell with testosterone alone, rose with 500 IU hCG, and was independently associated with directly measured ITT by multivariate regression — unlike androstenedione or DHEA. This is the closest thing to a non-invasive read on whether an hCG dose is actually reaching the Leydig cell. [2]

  Dose or parameter studied: hCG 0, 125, 250 or 500 IU every other day for 3 weeks on a background of exogenous testosterone

  Studied in: 29 normal men, healthy volunteers in an academic research setting, suppressed with exogenous testosterone for 3 weeks. Not validated as a monitoring tool in AAS users, and no threshold value for 'adequate' 17-OHP has been established for that population.

• SPLITTING hCG INTO SMALL FREQUENT DOSES BEATS A SINGLE LARGE ONE — THE SAME TOTAL DOSE, TWICE THE TESTOSTERONE RESPONSE. 1,500 IU as one injection raised testosterone to only 2.1x baseline at 48 h and then drove it BELOW baseline (0.7x) by day 7, with a 4.4x estradiol spike; the identical 1,500 IU split as 300 IU daily for 5 days produced roughly double the testosterone AUC, sustained levels, and essentially no estradiol spike. This is the human evidence behind low-dose frequent hCG rather than large boluses — large single doses provoke steroidogenic desensitization and an estrogen surge. [3]

  Dose or parameter studied: hCG 1,500 IU as a single injection versus hCG 300 IU daily for 5 days (same 1,500 IU total)

  Studied in: 7 healthy men (single high-dose arm) with a comparison divided-dose protocol; healthy volunteers, not androgen-suppressed and not AAS users. The desensitization physiology is expected to carry over, but the experiment was never repeated in suppressed men or at the 2,500-5,000 IU boluses common in community protocols.

• THE BEST RECOVERY-TIMELINE DATA IN EXISTENCE: median 3.4 months to a sperm concentration of 20 million/mL after stopping, 67% recovered by 6 months, 90% by 12 months, 96% by 16 months, 100% by 24 months. Faster recovery was associated with older age, Asian origin, SHORTER treatment duration, shorter-acting testosterone preparations, higher baseline sperm concentration, faster initial suppression, and lower baseline LH. Longer courses and long-acting esters predict slower recovery. Crucially, covariables changed the RATE but not the EXTENT — in this dataset everyone eventually recovered. [6]

  Studied in: 1,549 healthy eugonadal men aged 18-51 in 30 published male hormonal contraceptive trials (965 white, 535 Asian, 49 other), 1,283.5 man-years of treatment. MAJOR GAP: these are supervised, single-agent-class, pharmaceutical-grade contraceptive regimens in men with normal baseline fertility and typically 12-24 month exposures — NOT multi-compound supraphysiologic AAS cycles, 19-nors, or years of continuous use. The 100%-by-24-months figure should not be promised to this app's readers.

• IN ACTUAL LONG-TERM AAS USERS, RECOVERY IS OFTEN NOT COMPLETE — men abstinent for 3 to 26 months still had smaller testes, lower testosterone (some below 200 ng/dL) and reduced sexual desire versus non-using weightlifters. Roughly a third of former users (7/24) had a major depressive episode during withdrawal, and for four of them it was the only depressive episode of their lives. Two of 24 never regained normal libido or erectile function even on adequate testosterone replacement. [7]

  Studied in: 24 male former long-term AAS users (19 untreated, 5 on testosterone replacement) versus 36 non-AAS-using weightlifters recruited by advertisement in Massachusetts. Cross-sectional and naturalistic — men who felt worse may have been more likely to volunteer, and the sample is small.

• MORE THAN A QUARTER OF FORMER AAS USERS WERE STILL BELOW THE TESTOSTERONE REFERENCE RANGE A MEAN OF 2.5 YEARS AFTER STOPPING, versus zero controls, with higher rates of depressive symptoms (24.2%), erectile dysfunction (27.3%) and reduced libido (40.1%). Current users showed severely suppressed inhibin B and AMH — markers of Sertoli cell and spermatogenic damage, not just axis shutdown. [8]

  Studied in: 37 current AAS abusers, 33 former abusers (mean 2.5 years since cessation) and 30 healthy controls, all male recreational strength-training athletes aged 18-50 in Denmark. Cross-sectional design: it shows association, not that AAS caused each individual's low testosterone, and there is no information on whether any of the former users had done PCT.

Off-label use of an approved drug

• hCG 500 IU EVERY OTHER DAY ALONGSIDE TESTOSTERONE PREVENTED AZOOSPERMIA ENTIRELY IN A CLINIC COHORT FOLLOWED OVER A YEAR. In 26 hypogonadal men on TRT (injectable or gel) plus intramuscular hCG 500 IU EOD, no man became azoospermic and semen parameters were unchanged over more than a year of follow-up; 9 of 26 contributed to a pregnancy. This is 'prevent the hole' rather than 'restart from the hole' — and it is retrospective, uncontrolled, and used a dose 6-fold lower than the restart protocols below. [4]

  Dose or parameter studied: hCG 500 IU intramuscularly every other day, concurrent with daily topical testosterone gel or weekly intramuscular testosterone

  Studied in: 26 hypogonadal men, mean age 35.9 years, on prescribed TRT in a tertiary fertility practice; mean follow-up 6.2 months. Retrospective chart review with no control group. NOT men using supraphysiologic multi-compound AAS cycles, and not a study of restart after suppression had already occurred.

• THE ONLY PUBLISHED RESTART SERIES IN TESTOSTERONE-INDUCED AZOOSPERMIA USED hCG 3,000 UNITS SUBCUTANEOUSLY EVERY OTHER DAY PLUS AN ADJUNCT, AND SAW SPERM RETURN IN 95.9% AT A MEAN OF 4.6 MONTHS. Adjuncts were clomiphene, tamoxifen, anastrozole or recombinant FSH chosen by physician preference; no adjunct outperformed another, and no man stopped for adverse events. Note this dose is six times the fertility-preservation dose above — there is no trial establishing which is right for restart. [5]

  Dose or parameter studied: hCG 3,000 units subcutaneously every other day, plus clomiphene citrate, tamoxifen, anastrozole or recombinant FSH (or a combination) at physician discretion

  Studied in: 49 men presenting to two tertiary infertility clinics with azoospermia or severe oligospermia (<1 million/mL) while taking exogenous testosterone. Retrospective chart review, no control arm, no comparison against simply stopping — so the 4.6-month figure cannot be read as faster than unaided withdrawal. The authors say so explicitly.

• WHAT PREDICTS A SLOW RESTART, MEASURED DIRECTLY IN AAS USERS DOING PCT: in 44 men (median age 29, median cycle length 6 months) who stopped and did a standardised post-cycle regimen, 79.5% had recovered LH and total testosterone at 3 months and 20.5% had not. Recovery correlated negatively and strongly with duration of use (r = -0.857), the number of compounds run simultaneously (r = -0.443), the dose (r = -0.783) and the type of AAS used (r = -0.698). Inhibin B correlated with testosterone recovery and is proposed as a marker of spermatogenic epithelium recovery. [9]

  Studied in: 44 male AAS users, median age 29 years, median AAS duration 6 months, in a single-centre uncontrolled prospective Russian cohort. No control group of men who stopped WITHOUT PCT, so the 79.5% figure cannot be attributed to the PCT. Only 3 months of follow-up. Published in Russian.

• THE MOST-CITED MALE CLOMIPHENE DOSE IS 25 mg EVERY OTHER DAY, TITRATED TO 50 mg EVERY OTHER DAY — not 50 mg daily. In 86 hypogonadal men followed a mean of 19 months, 70% remained on 25 mg every other day at last evaluation and the rest on 50 mg every other day, targeting a testosterone of 550 ± 50 ng/dL. Testosterone and both gonadotropins rose significantly and no major side effects were recorded. [10]

  Dose or parameter studied: clomiphene citrate 25 mg orally every other day, titrated to 50 mg every other day if needed; mean treatment duration 19 months

  Studied in: 86 men with two consecutive morning testosterone measurements <300 ng/dL, mean age 29 (range 22-37), presenting to a Memorial Sloan-Kettering male-health clinic; 64% sought treatment for infertility. Prospective but uncontrolled case series (Level of Evidence 4). NOT a post-cycle population — these were men with hypogonadism of unspecified cause, and prior AAS use is not reported.

• DOSE RANGES ACTUALLY USED IN POOLED SERM TRIALS: clomiphene citrate 12.5-50 mg daily and enclomiphene citrate 12.5-25 mg daily, given for 1.5-4 months, across 292 men. Both raised testosterone significantly (clomiphene +11.56 nmol/L; enclomiphene +7.50 nmol/L pooled mean difference). Note enclomiphene's pooled effect was smaller than clomiphene's — these were not head-to-head comparisons, and the trials were short. [11]

  Dose or parameter studied: clomiphene citrate 12.5-50 mg daily, or enclomiphene citrate 12.5-25 mg daily, for 1.5-4 months

  Studied in: 292 men with obesity-related functional androgen deficiency across 7 studies. This is a metabolic/obesity hypogonadism population, NOT men recovering from exogenous androgen suppression, and follow-up maxed out at 4 months. Whether these dose ranges are the right ones for restarting a suppressed axis has not been tested.

• CLOMIPHENE RAISES TESTOSTERONE IN MOST MEN WHO TAKE IT — 73% gained at least 200 ng/dL over baseline, mean rise 329 ng/dL — AND BASELINE GONADOTROPINS DID NOT PREDICT WHO WOULD RESPOND. Neither baseline LH nor FSH significantly predicted the testosterone response; only age was associated on univariable analysis. A normal or slightly elevated baseline LH does not rule out a clomiphene trial. [12]

  Studied in: 332 hypogonadal men, mean age 36.2 ± 8.2 years, treated at two high-volume fertility centres 2013-2018; median first follow-up 6 weeks. Retrospective. A fertility-clinic population, not specifically post-AAS.

• A CONFLICTING AND MORE RECENT PREDICTOR ANALYSIS FOUND HIGHER BASELINE LH DID PREDICT A WORSE CLOMIPHENE RESPONSE (OR 0.82 per mIU/mL, P = .008), as did prior androgen deprivation therapy (OR 0.11). Only 47% of 292 men met the response definition (testosterone ≥400 ng/dL plus a ≥200 ng/dL rise) within 12 weeks. Baseline testosterone and age were NOT predictive. Read alongside the Keihani result above: the two studies disagree on LH, and both are retrospective. [13]

  Dose or parameter studied: clomiphene citrate 25 mg orally every other day, escalated to 50 mg every other day if total testosterone remained <400 ng/dL; labs repeated every 4 weeks after each dose change

  Studied in: 292 men with low or borderline-low testosterone at Memorial Sloan Kettering, median age 60 (IQR 50-66) — an older, comorbid, oncology-weighted cohort (41% prior radical prostatectomy, 12% prostate radiotherapy, 4.5% prior ADT). The authors flag this: the population is "skewed older and less healthy than average." This is close to the opposite of this app's readership, and the prior-ADT signal is the closest available analogue to prolonged exogenous androgen suppression.

• ENCLOMIPHENE'S GAINS DISAPPEAR WHEN YOU STOP IT. In the phase IIB trial, enclomiphene raised testosterone, LH and FSH and lifted sperm concentrations into the 75-334 million/mL range in every man treated — but total testosterone fell back to pretreatment values within one month of stopping, in both the enclomiphene and the gel arm. A SERM is a stimulus that works while it is being taken; it is not proof the axis has been repaired underneath. [14]

  Studied in: 12 men with secondary hypogonadism previously treated with topical testosterone — a proof-of-principle, randomized, open-label, two-centre phase IIB study. Twelve men total, split across two arms; effectively 5-7 men per arm for the semen endpoints. This is a very small, unblinded study, and enclomiphene has no FDA approval.

• THE STRONGEST ENCLOMIPHENE EVIDENCE — TWO PHASE III TRIALS — SHOWED IT RAISES TESTOSTERONE LIKE A GEL DOES BUT, UNLIKE THE GEL, DRIVES LH AND FSH UP AND HOLDS SPERM CONCENTRATION IN THE NORMAL RANGE, while the testosterone gel arm showed marked suppression of spermatogenesis over the same 16 weeks. This is the clearest demonstration that 'restoration' and 'replacement' are not interchangeable. Despite these trials, enclomiphene was never approved by the FDA. [15]

  Dose or parameter studied: two enclomiphene citrate dose arms daily for 16 weeks, versus AndroGel 1.62% — the abstract does not name the milligram doses (they fall in the 12.5-25 mg/day range reported in PMID 36604313)

  Studied in: Overweight men aged 18-60 with secondary hypogonadism (morning total testosterone ≤300 ng/dL and low or normal LH <9.4 IU/L on two occasions) in trials ZA-304 and ZA-305. These are obesity-related functional hypogonadal men, NOT men recovering from AAS. Treatment was 16 weeks and there is no post-cessation follow-up in this report.

• THE BEST-QUALITY TAMOXIFEN DOSE IN MEN OUTSIDE ONCOLOGY IS 20 mg/DAY, from a 212-man randomized placebo-controlled trial in idiopathic oligozoospermia (given with testosterone undecanoate 120 mg/day). Total sperm count roughly doubled at 6 months and spontaneous pregnancy occurred in 33.9% versus 10.3% on placebo. Note this trial deliberately combined tamoxifen with an oral androgen — it is not a study of tamoxifen alone, and it is not a study of restarting a suppressed axis. [16]

  Dose or parameter studied: tamoxifen citrate 20 mg/day orally plus testosterone undecanoate 120 mg/day for 6 months

  Studied in: 212 men with idiopathic oligozoospermia and couple subfertility (106 active, 106 placebo), plus 82 normozoospermic controls, at a Greek tertiary hospital. Men with idiopathic low sperm counts and intact axes — NOT men suppressed by exogenous androgen. Couple counselling was part of the intervention in all arms.

• TAMOXIFEN'S SIDE-EFFECT PROFILE IN MEN IS POPULATION-DEPENDENT AND POORLY CHARACTERISED LONG-TERM. Fewer than 5% of men across all indications withdrew for toxicity, and adverse events were least frequent in the infertility and idiopathic-gynecomastia populations — closest to this app's readers. But the review's own conclusion is that long-term side-effect data in men do not exist. The thromboembolic and endometrial warnings on the label come from women; the male long-term picture is simply unmeasured. [17]

  Studied in: Men prescribed tamoxifen off-label for breast cancer, infertility, idiopathic gynecomastia, and gynecomastia prophylaxis during prostate cancer antiandrogen therapy, pooled from RCTs and non-RCTs. Reasons for withdrawal were frequently unspecified in the source studies.

What the regulator approved

Where a drug on this page has a US label, this is what it was approved for and at what dose. Anything else is off-label — which is not the same as unsafe, but does mean no regulator has reviewed it for that use.

What nobody knows

These are the questions the literature does not answer. They are listed because on this subject the gaps are load-bearing: most of what circulates as settled practice sits in one of them.

• THERE IS NO RANDOMIZED TRIAL OF ANY PCT PROTOCOL VERSUS SIMPLY STOPPING. Not one. The Wenker series (hCG 3,000 IU EOD + adjunct, 95.9% recovery at 4.6 months) had no control arm, and its own authors write that studies are needed to 'document the presumed improved tolerability and speed of recovery compared with unaided withdrawal of exogenous testosterone.' The 79.5%-at-3-months PCT figure from Lykhonosov likewise has no comparison group. Nobody knows whether PCT speeds recovery, or whether the men who recover would have recovered anyway.
• THE hCG DOSE FOR RESTART IS UNKNOWN AND THE PUBLISHED NUMBERS DIFFER SIX-FOLD. Coviello established 125-500 IU EOD MAINTAINS intratesticular testosterone during 3 weeks of suppression in men with normal testes; Hsieh used 500 IU EOD for fertility preservation on TRT; Wenker used 3,000 IU EOD to RESTART after azoospermia. No study compares these for restart. Maintaining a functioning testis and restarting a shut-down one are different problems and the maintenance dose data should not be quoted as a restart dose.
• HOW LONG THE hCG-RESPONSIVENESS FINDING HOLDS IS UNTESTED. Coviello's men were suppressed for 3 weeks. There is no equivalent intratesticular-testosterone experiment in men suppressed for months or years, in men using 19-nortestosterone compounds (nandrolone, trenbolone), or in men who have already developed testicular atrophy. The correct statement is 'the testis remained hCG-responsive under 3 weeks of suppression in healthy men' — extending that to a 5-year blast-and-cruise user is an extrapolation, not a finding.
• OPTIMAL DURATION OF ANY PCT COURSE IS UNDEFINED. No trial establishes how many weeks of clomiphene, enclomiphene or hCG a restart requires, when to stop, or whether tapering matters. The clomiphene duration data (Katz: mean 19 months; Huijben meta-analysis: 1.5-52 months) come from ongoing hypogonadism treatment, where the drug is the therapy — not from time-limited restart protocols.
• WHETHER hCG SHOULD BE RUN DURING A CYCLE, AFTER IT, OR NOT AT ALL IS UNRESOLVED. Hsieh supports concurrent low-dose hCG preventing azoospermia in prescribed TRT; nothing tests whether that translates to supraphysiologic multi-compound cycles, and nothing compares concurrent hCG against a post-cycle-only approach for either speed or completeness of recovery.
• THE TWO BEST PREDICTOR STUDIES FOR CLOMIPHENE RESPONSE DISAGREE. Keihani (n=332, fertility clinic, mean age 36) found baseline LH and FSH did not predict testosterone response. Kim (n=292, oncology-weighted cohort, median age 60) found higher baseline LH was a significant negative predictor. Both are retrospective and the populations are very different. Do not present baseline LH as a settled go/no-go criterion.
• ENCLOMIPHENE IS NOT AN APPROVED DRUG ANYWHERE IN THE US AND HAS NO LABEL. Despite two completed phase III trials, no FDA prescribing information exists (verified 2026-09-07 for 'enclomiphene', 'enclomiphene citrate' and 'Androxal'). That means no FDA-reviewed dose, no approved indication, no adverse-reaction table, and — most practically — no FDA-enforced identity or content standard on product sold under that name. Compounded and grey-market enclomiphene content is unverified.
• hCG PRODUCT AND ROUTE: the FDA label product is urine-derived and 'Intramuscular Use Only.' The subcutaneous route used almost universally in this community, and hCG obtained outside a pharmacy, sit entirely outside the labelled product. There is no published bioequivalence or contamination data for grey-market hCG, and counterfeit or underdosed product would be invisible to a user without a 17-OHP or testosterone response check.
• THE LIU RECOVERY CURVES DO NOT DESCRIBE AAS USERS. The 3.4-month median and 100%-by-24-months figures come from 1,549 healthy eugonadal men in supervised contraceptive trials using pharmaceutical testosterone (± a progestagen) for defined periods. Kanayama and Rasmussen show real-world AAS users faring materially worse — testosterone below the reference range in over a quarter of former users at a mean 2.5 years. There is no equivalent large multivariate recovery-timeline dataset for AAS users, and presenting the contraceptive curves as an AAS prognosis would overpromise.
• NO EVIDENCE THAT PCT PREVENTS THE PSYCHIATRIC MORBIDITY OF WITHDRAWAL. Kanayama found major depressive episodes in 7 of 24 former users during withdrawal, and for four this was the only depressive episode of their lives; Hyams flags mood disorders, anxiety and suicidality. No study tests whether any PCT regimen reduces this risk, and Hyams notes symptoms can persist for months to years despite normalised biochemistry. Restart protocols should not be presented as mood insurance.
• LONG-TERM SAFETY OF REPEATED SERM COURSES IN MEN IS UNCHARACTERISED. The clomiphene label's visual-toxicity warning is explicitly dose- and duration-dependent and notes disturbances 'may be irreversible' — but that warning derives from women on 5-day cycles, not men on months of daily dosing. Tamoxifen's thromboembolic and endometrial warnings are female-derived; Wibowo's review states plainly that long-term side-effect data in men are lacking. Bone density, lipid and VTE outcomes for men cycling SERMs repeatedly over years are unmeasured.
• SERUM TESTOSTERONE RECOVERY DOES NOT EQUAL FERTILITY RECOVERY. Coviello showed serum testosterone can be normal or high while intratesticular testosterone sits at 6% of baseline. A restart judged by a testosterone panel alone can look successful while spermatogenesis is still absent. Semen analysis, and possibly inhibin B (Lykhonosov) or 17-OHP (Amory), carry information a testosterone number does not — but no validated monitoring algorithm for this population exists.
• NO HEAD-TO-HEAD RANDOMIZED COMPARISON OF CLOMIPHENE VERSUS ENCLOMIPHENE VERSUS TAMOXIFEN VERSUS hCG FOR RESTART. Wenker found no significant difference in recovery by supplemental therapy, but that was retrospective, non-randomized, with physician-chosen adjuncts and no power to detect a difference. Any claim that one agent is superior for PCT is currently unsupported.
• NOTHING IS KNOWN ABOUT SPERM DNA FRAGMENTATION OR OFFSPRING OUTCOMES after AAS exposure and PCT-assisted recovery. Recovery of sperm concentration is the endpoint every study reports; sperm quality and downstream outcomes are unmeasured.
• TAPERING VERSUS ABRUPT CESSATION HAS NEVER BEEN COMPARED. Community protocols assume a taper helps; there is no published trial of taper versus stop for either speed of axis recovery or severity of withdrawal symptoms.

Sources

Every identifier below was checked to resolve to a real record before publication. Citations retrieved from PubMed and DailyMed.

1. The Journal of Clinical Endocrinology and Metabolism (2005) — PubMed 15713727 ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate t
2. Fertility and Sterility (2008) — PubMed 17462643 With T administration alone, serum 17OH-P decreased significantly and increased significantly when 500 IU hCG was administered. End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independent
3. The Journal of Clinical Endocrinology and Metabolism (1984) — PubMed 6693540 Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 +/- 0.2 (SEM) X the baseline value at 48 h. Thereafter plasma T decreased to below normal (0.7 +/- 0.1 X baseline) 7 days after th
4. The Journal of Urology (2013) — PubMed 23260550 Testosterone replacement consisted of daily topical gel or weekly intramuscular injection with intramuscular human chorionic gonadotropin (500 IU) every other day. ... No patient became azoospermic during concomitant testosterone replacement and human chorioni
5. The Journal of Sexual Medicine (2015) — PubMed 25904023 All were noted to have been placed on combination therapy, which included 3,000 units HCG subcutaneously every other day supplemented with clomiphene citrate, tamoxifen, anastrozole, or recombinant follicle-stimulating hormone (or combination) according to phy
6. The Lancet (2006) — PubMed 16650651 The median times for sperm to recover to thresholds of 20, 10, and 3 million per mL were 3.4 months (95% CI 3.2-3.5), 3.0 months (2.9-3.1), and 2.5 months (2.4-2.7), respectively. Multivariate Cox's analysis showed higher rates of recovery with older age, Asia
7. Addiction (2015) — PubMed 25598171 Compared with the 36 non-AAS-using weightlifters, the 19 untreated former AAS users displayed significantly smaller testicular volumes [estimated difference, 95% confidence interval (CI) = 2.3 (0.1, 4.5) ml; P = 0.042] and lower serum testosterone levels [esti
8. PLoS One (2016) — PubMed 27532478 Overall, 27.2% (13.3; 45.5) of former AAS abusers exhibited plasma total testosterone levels below the lower reference limit (12.1 nmol/l) whereas no control participants exhibited testosterone below this limit (P < 0.01). Gonadotropins were significantly supp
9. Problemy Endokrinologii (2020) — PubMed 33351319 A three-month refusal to use AAS with PCT led to the restoration of HPG axis a in 79.5% of the volunteers. In 20.5% of cases, recovery did not occur. The negative effect of the duration of use, the number of simultaneously administered drugs, their dose and ty
10. BJU International (2012) — PubMed 22044663 CC was commenced at 25 mg every other day and titrated to 50 mg every other day. The target testosterone level was 550 ± 50 ng/dL.
11. Andrology (2023) — PubMed 36604313 Seven studies met the inclusion criteria providing information on 292 men with obesity-related functional androgen deficiency treated with clomiphene citrate (12.5-50 mg daily) or enclomiphene citrate (12.5-25 mg daily) for 1.5-4 months.
12. Urology (2020) — PubMed 32353397 TT levels increased significantly on CC treatment (mean change: 329.2 ng/dL, 95% CI: 307.4-351.0) with 73% of men having at least 200 ng/dL increase over baseline TT levels. In univariable linear regression models, only age was significantly associated with TT
13. The Journal of Sexual Medicine (2026) — PubMed 42251758 Multivariable analysis identified baseline LH (increase per mIU/mL) (OR 0.82, CI = 0.71-0.95, P = .008) as a significant negative predictor for achieving treatment response. Likewise, prior ADT was predictive for poor response (OR 0.11, CI = 0.01-0.6, P = .039
14. The Journal of Sexual Medicine (2013) — PubMed 23530575 Enclomiphene citrate elevated sperm counts in seven out of seven men at 3 months and six out of six men at 6 months with sperm concentrations in the 75-334 × 10(6) /mL range. ... TT decreased one month posttreatment to pretreatment values.
15. BJU International (2016) — PubMed 26496621 TT levels increased between baseline and after 16 weeks of treatment in all the treatment groups. FSH and LH levels increased in the enclomiphene citrate groups and decreased in the testosterone gel group at 16 weeks. Enclomiphene citrate maintained sperm conc
16. Fertility and Sterility (2003) — PubMed 14556812 Oligozoospermic patients were randomly assigned to two treatment groups with tamoxifen citrate, 20 mg/d, and testosterone undecanoate, 120 mg/d (n = 106) or placebo treatment (n = 106) for 6 months. ... The incidence of spontaneous pregnancy was 33.9% in the a
17. Andrology (2016) — PubMed 27152880 Less than 5% of men withdrew from tamoxifen therapy because of toxicity. This suggests that for most men, tamoxifen is well-tolerated. ... Long-term studies that rigorously document the side-effect profile of tamoxifen in men are lacking.
18. Chorionic Gonadotropin for Injection (urine-derived hCG, 10,000 USP units/vial) — US Prescribing Information (DailyMed) Approved indication: Three indications only: (1) prepubertal cryptorchidism not due to anatomical obstruction; (2) "Selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in mal
19. Clomiphene citrate tablets, USP 50 mg — US Prescribing Information (DailyMed) Approved indication: "Clomiphene citrate is indicated for the treatment of ovulatory dysfunction in women desiring pregnancy." The label contains no male indication of any kind. Every use in men — hypogonadism, fertility,
20. Tamoxifen citrate tablets — US Prescribing Information (DailyMed) Approved indication: Metastatic breast cancer in women and men; adjuvant treatment of node-positive and node-negative breast cancer; DCIS; and reduction of breast cancer incidence in high-risk women. There is no approved

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