sexgod
16yo HTN Gymcel
- Joined
- Apr 12, 2023
- Posts
- 256
- Reputation
- 194
Context:
This is my first high-effort thread. Layout might be scuffed; I don’t know all the forum formatting tricks yet. If you’ve got better sources or want to help me prettify, drop it below. Also, feel free to prove me wrong and teach me something new.
Standard Test E blast (≈500 mg/wk, 12–20 wks). Goal = understand if PCT actually does anything vs doing nothing / only hCG. This thread will include studies also: (World Journal of Men’s Health; Subst Abuse Treat Prev Policy; clinical case reports; urology/andrology reviews).
TL;DR for retards:
Test E crushes LH/FSH → endogenous T and spermatogenesis stop. Even lower doses (≈200 mg/wk) pushed ~¾ of men to azoospermia in trials.
Some guys recover naturally, but timelines are wild (months to a year+), and the crash feels like death (low mood/libido/energy). A minority stay suppressed long-term.
Evidence quality is mixed (few RCTs), but weight of data + physiology favors:
(1) Prevent atrophy with low-dose hCG on-cycle.
(2) Use a SERM post-cycle to kick LH/FSH sooner.
Combo hCG+SERM shows fastest fertility recovery in clinic series.
“No PCT” can still work, but it’s rolling the dice on how long you’ll be hypogonadal (and how much size/drive you hemorrhage meanwhile).
What we know:
Suppression is not a debate. Exogenous T → near-zero LH/FSH → T production + sperm halt. Even modest T dosing shut most men’s sperm off within months (male contraception literature).
Natural rebound happens—eventually. Median timeframes are measured in months, not weeks. During that time, quality-of-life tanks and relapse risk (going back “on”) spikes (survey of 470 AAS users).
Long tail exists. Reviews document men with prolonged hypogonadism post-AAS. Not common, but very real.
SERM-based PCT (Clomiphene / Tamoxifen):
Mechanism: Block estrogen feedback at hypo/pit → ↑GnRH → ↑LH/FSH → testes re-start T + sperm.
Evidence for: In hypogonadal/infertile men (non-AAS), SERMs reliably raise T and improve sperm parameters—this is standard off-label endocrinology.
Case data in ex-AAS users: SERM alone accelerated sperm/T return vs historical natural timelines (months vs ~year).
Survey data: PCT users reported fewer/shorter withdrawal symptoms vs no PCT.
Evidence against/limits: Few randomized trials in steroid users.
Not everyone responds (if the testes are too “asleep,” pituitary drive alone is slow to translate).
hCG: on-cycle and post-cycle:
Mechanism: LH mimic → directly stimulates Leydig cells → intratesticular T up → preserves spermatogenesis machinery.
On-cycle (prevention):
Low-dose hCG with T maintained intratesticular T (vs ~-94% without).
Men on TRT + hCG EOD stayed non-azoospermic; multiple conceptions occurred while on treatment.
Translation: keep your balls functioning so there’s less to “startup” later. This is why fertility/urology clinics co-admin hCG with TRT when kids matter.
Post-cycle (kickstart):
hCG can rapidly raise T when LH/FSH are still zero → eases the deepest trough.
Best evidence for fastest spermatogenesis return comes from hCG + SERM combos in clinic series (≈96% regained sperm, ~4–5 months).
Caveat: hCG alone keeps pituitary suppressed (you’re replacing LH). It’s a bridge; not a full restart, unless you transition off it and let SERM-driven LH take over.
“No PCT”, SERM-only, hCG-only, Combo outcomes:
No PCT:
Works for many over time. But you buy months of low-T symptoms, higher relapse risk, slower sperm return, and a small risk of long-term funk. Cheap, yes; comfortable, no.
SERM-only:
Speeds pituitary rebound (LH/FSH) → T rises in weeks for many.
If testes are very deconditioned, initial response can be sluggish (you didn’t prevent atrophy).
hCG-only:
Great for immediate T and “re-inflating” the testes, bad for re-starting the axis if you never come off it. Needs either a stop or a hand-off to SERM.
Combo (hCG + SERM):
Best clinical outcomes for fertility/time-to-sperm in ex-AAS/TRT azoospermia. Two-pronged: wake testes and wake pituitary.
More moving parts (AI if E2 spikes; dosing discipline), but tolerability was good in series (no discontinuations for AEs).
Side-effect reality check (not fearmongering):
Clomiphene: rare visual symptoms (~1–2%), dose/duration related; mood variability; generally safe short-term in men per cohort data.
Tamoxifen: rare clot risk in young men short-term; sometimes GI, hot flashes; often friendlier mood-wise.
hCG: can raise E2 (watch gyno/water), and prolongs pituitary suppression while on it. Chronic high doses risk Leydig desensitization—keep doses/time sane and transition off.
If you truly don’t care about the crash length and can eat months of low T, no PCT can still end in recovery. Many do. Some don’t.
If you care about time out of the hole (hormones, mood, libido, fertility), the most defensible path from the literature is:
keep testes alive with low-dose hCG on-cycle, then hand off to a SERM post-cycle to re-ignite LH/FSH.
The gap isn’t ideology; it’s probabilities and timelines. PCT doesn’t guarantee perfection. It reliably shifts odds toward a quicker return to baseline.
Sources:
World Journal of Men’s Health — AAS hypogonadism reviews; hCG preserving intratesticular T; TRT+hCG fertility data; lack of RCTs acknowledged.
Subst Abuse Treat Prev Policy (2023) — 470 AAS users; PCT ↔ fewer withdrawal symptoms, relapse pressure.
Clinical case reports/series — rapid sperm recovery with Clomid; hCG+SERM protocols restoring sperm in ex-AAS/TRT men in ~4–5 months.
This is my first high-effort thread. Layout might be scuffed; I don’t know all the forum formatting tricks yet. If you’ve got better sources or want to help me prettify, drop it below. Also, feel free to prove me wrong and teach me something new.
Standard Test E blast (≈500 mg/wk, 12–20 wks). Goal = understand if PCT actually does anything vs doing nothing / only hCG. This thread will include studies also: (World Journal of Men’s Health; Subst Abuse Treat Prev Policy; clinical case reports; urology/andrology reviews).
TL;DR for retards:
Test E crushes LH/FSH → endogenous T and spermatogenesis stop. Even lower doses (≈200 mg/wk) pushed ~¾ of men to azoospermia in trials.
Some guys recover naturally, but timelines are wild (months to a year+), and the crash feels like death (low mood/libido/energy). A minority stay suppressed long-term.
Evidence quality is mixed (few RCTs), but weight of data + physiology favors:
(1) Prevent atrophy with low-dose hCG on-cycle.
(2) Use a SERM post-cycle to kick LH/FSH sooner.
Combo hCG+SERM shows fastest fertility recovery in clinic series.
“No PCT” can still work, but it’s rolling the dice on how long you’ll be hypogonadal (and how much size/drive you hemorrhage meanwhile).
What we know:
Suppression is not a debate. Exogenous T → near-zero LH/FSH → T production + sperm halt. Even modest T dosing shut most men’s sperm off within months (male contraception literature).
Natural rebound happens—eventually. Median timeframes are measured in months, not weeks. During that time, quality-of-life tanks and relapse risk (going back “on”) spikes (survey of 470 AAS users).
Long tail exists. Reviews document men with prolonged hypogonadism post-AAS. Not common, but very real.
SERM-based PCT (Clomiphene / Tamoxifen):
Mechanism: Block estrogen feedback at hypo/pit → ↑GnRH → ↑LH/FSH → testes re-start T + sperm.
Evidence for: In hypogonadal/infertile men (non-AAS), SERMs reliably raise T and improve sperm parameters—this is standard off-label endocrinology.
Case data in ex-AAS users: SERM alone accelerated sperm/T return vs historical natural timelines (months vs ~year).
Survey data: PCT users reported fewer/shorter withdrawal symptoms vs no PCT.
Evidence against/limits: Few randomized trials in steroid users.
Not everyone responds (if the testes are too “asleep,” pituitary drive alone is slow to translate).
hCG: on-cycle and post-cycle:
Mechanism: LH mimic → directly stimulates Leydig cells → intratesticular T up → preserves spermatogenesis machinery.
On-cycle (prevention):
Low-dose hCG with T maintained intratesticular T (vs ~-94% without).
Men on TRT + hCG EOD stayed non-azoospermic; multiple conceptions occurred while on treatment.
Translation: keep your balls functioning so there’s less to “startup” later. This is why fertility/urology clinics co-admin hCG with TRT when kids matter.
Post-cycle (kickstart):
hCG can rapidly raise T when LH/FSH are still zero → eases the deepest trough.
Best evidence for fastest spermatogenesis return comes from hCG + SERM combos in clinic series (≈96% regained sperm, ~4–5 months).
Caveat: hCG alone keeps pituitary suppressed (you’re replacing LH). It’s a bridge; not a full restart, unless you transition off it and let SERM-driven LH take over.
“No PCT”, SERM-only, hCG-only, Combo outcomes:
No PCT:
Works for many over time. But you buy months of low-T symptoms, higher relapse risk, slower sperm return, and a small risk of long-term funk. Cheap, yes; comfortable, no.
SERM-only:
Speeds pituitary rebound (LH/FSH) → T rises in weeks for many.
If testes are very deconditioned, initial response can be sluggish (you didn’t prevent atrophy).
hCG-only:
Great for immediate T and “re-inflating” the testes, bad for re-starting the axis if you never come off it. Needs either a stop or a hand-off to SERM.
Combo (hCG + SERM):
Best clinical outcomes for fertility/time-to-sperm in ex-AAS/TRT azoospermia. Two-pronged: wake testes and wake pituitary.
More moving parts (AI if E2 spikes; dosing discipline), but tolerability was good in series (no discontinuations for AEs).
Side-effect reality check (not fearmongering):
Clomiphene: rare visual symptoms (~1–2%), dose/duration related; mood variability; generally safe short-term in men per cohort data.
Tamoxifen: rare clot risk in young men short-term; sometimes GI, hot flashes; often friendlier mood-wise.
hCG: can raise E2 (watch gyno/water), and prolongs pituitary suppression while on it. Chronic high doses risk Leydig desensitization—keep doses/time sane and transition off.
Bottom line:
If you truly don’t care about the crash length and can eat months of low T, no PCT can still end in recovery. Many do. Some don’t.
If you care about time out of the hole (hormones, mood, libido, fertility), the most defensible path from the literature is:
keep testes alive with low-dose hCG on-cycle, then hand off to a SERM post-cycle to re-ignite LH/FSH.
The gap isn’t ideology; it’s probabilities and timelines. PCT doesn’t guarantee perfection. It reliably shifts odds toward a quicker return to baseline.
Sources:
World Journal of Men’s Health — AAS hypogonadism reviews; hCG preserving intratesticular T; TRT+hCG fertility data; lack of RCTs acknowledged.
Subst Abuse Treat Prev Policy (2023) — 470 AAS users; PCT ↔ fewer withdrawal symptoms, relapse pressure.
Clinical case reports/series — rapid sperm recovery with Clomid; hCG+SERM protocols restoring sperm in ex-AAS/TRT men in ~4–5 months.
