Winstrol
Stanozolol · Winny · Stromba · Stanabol · Tevabolin · Menabol
Last updated
At a glance
320
Testosterone = 100
30
Testosterone = 100
Overview
Why Winstrol Earned Its Place#
Winstrol is the cutting-cycle finisher that built its reputation on one thing: it makes you look dry. Vascularity sharpens, skin tightens over muscle, and the flat-but-full look that defines the last four weeks of a prep snaps into focus. It's not a mass builder and never has been — stanozolol is what you run in the final stretch of a cut, a photoshoot block, or a contest prep when the goal is hardness, not size.
The mechanism is specific enough to explain the look. As a DHT derivative with a pyrazole A-ring, stanozolol can't aromatize and isn't meaningfully 5α-reduced — no estrogen, no water, no gyno pressure. More importantly, it's one of the most potent SHBG suppressors in the AAS catalog, which means whatever test or masteron you've paired it with suddenly has a much higher free fraction working.
"Stanozolol, a synthetic anabolic steroid, is among the most potent suppressors of serum SHBG and typically causes a 30–50% decrease in HDL cholesterol within several weeks of use." — Grant et al., Annals of the NY Academy of Sciences (2024)
That HDL crash is the honest trade. Winny hits lipids hard, it's hepatotoxic at physique doses, and the tendon-drying reputation is real enough that ruptures are documented in the literature. The upside is that all of it is manageable — short cycles (4–8 weeks), TUDCA and omega-3s through-cycle, a smart test base, and no ego PRs on heavy eccentrics. Below we'll cover oral vs. injectable dosing, the classic cutting and hardening stacks (test/mast/winny, test/tren/winny), full side-effect management, and the PCT protocol to bring HPTA back online after the run.
How Winstrol works
Stanozolol is a DHT-derived 17α-alkylated anabolic steroid with a pyrazole ring fused to the A-ring of the steroid nucleus. That structural quirk is the whole story — it's what makes winstrol behave differently from every other DHT derivative on the shelf, and it's why the compound has a reputation for "hardening" rather than mass.
Androgen Receptor Agonism#
Like all AAS, stanozolol works by binding the androgen receptor in muscle tissue, translocating it to the nucleus, and driving transcription of myogenic genes — IGF-1 splice variants, structural protein synthesis, satellite cell activation. Its AR binding affinity is modest compared to trenbolone or pure DHT, but the on-paper anabolic:androgenic ratio (320:30) reflects selective tissue expression: strong skeletal-muscle and bone signalling with relatively low androgenic activity in scalp and prostate compared to testosterone.
"Due to its structure, stanozolol cannot undergo aromatisation or 5α-reduction, but it induces gene transcription via the androgen receptor and is detected in urine for weeks due to long-lived metabolites." — Rane A, Ekström L. British Journal of Clinical Pharmacology, 2012
The practical payoff: lean-tissue preservation in a deficit, strength retention during prep, and no estrogenic bloat muddying the look.
SHBG Suppression — the Hidden Multiplier#
This is where stanozolol earns its slot in a stack. It is one of the most potent SHBG suppressors of any AAS — serum SHBG drops sharply within the first 1–2 weeks of use, liberating free testosterone and free masteron/primo from whatever base is running underneath.
"Stanozolol, a synthetic anabolic steroid, is among the most potent suppressors of serum SHBG and typically causes a 30–50% decrease in HDL cholesterol within several weeks of use." — Grant B et al. Annals of the New York Academy of Sciences, 2024
This is why winstrol layered onto a test + mast prep "hits harder" than the raw mg totals suggest — the free-fraction of every other androgen in the stack goes up. It's also why stanozolol is rarely run solo; it has nothing to liberate without a test base underneath it.
No Aromatization, No 5α-Reduction#
Because stanozolol is already a DHT derivative and the A-ring carries a pyrazole substitution, the molecule is structurally locked out of two metabolic pathways that define most other AAS:
- Cannot aromatize to estradiol → no gyno, no estrogenic water retention, no need for an AI.
- Essentially not a 5α-reductase substrate → the parent compound is the active androgenic species in scalp and skin, and finasteride / dutasteride will not blunt its androgenic sides. This is the same trap that catches masteron and anavar users — DHT-derivative scalp shedding cannot be rescued with a 5-AR inhibitor.
The flip side of no estrogen is no estrogen-mediated joint lubrication or glycogen storage, which is the mechanistic root of the "dry" look and the dry joints.
Collagen and Tendon Effects#
This is the mechanism most users underweight until they tear something. AAS including stanozolol shift tendon collagen synthesis toward disorganized, lower-tensile-strength fibril patterns and suppress MMP-driven remodelling at the tendon-bone interface. Muscle contractile force scales up on cycle faster than tendon tensile capacity adapts, and the mismatch is where ruptures live.
"Use of anabolic-androgenic steroids is associated with an increased risk of tendon rupture, particularly involving the upper extremity (triceps and pectoralis major)." — Kanayama G et al. American Journal of Sports Medicine, 2015
Translation for programming: this is why max singles on week 3–4 of a winny run are how lifters end up in an OR. Warm up longer, skip the ego 1RMs, and stack 15 g hydrolyzed collagen + 50 mg vitamin C pre-training to support tendon adaptation.
Hepatic Load#
The 17α-methyl group that makes stanozolol orally bioavailable is also what makes it hepatotoxic — it survives first-pass metabolism precisely because it stresses hepatocytes. Transaminase elevation is predictable within weeks of starting, and histopathological liver changes have been documented at physique-relevant doses.
"The administration of stanozolol resulted in a significant elevation of transaminases and histopathological liver damage, confirming a clear hepatotoxic potential within a matter of weeks." — Boada LD et al. Archives of Toxicology, 1999
Critically — the injectable suspension is the same molecule and carries the same hepatic load. The community myth that "injectable winny is liver-safe" is wrong; the 17α-methyl group doesn't care which side of the gut wall you crossed. Cap runs at 6–8 weeks, run TUDCA 500–1000 mg/day through-cycle, and do not stack with a second 17α-alkylated oral.
Protocol
| Level | Dose | Frequency | Notes |
|---|---|---|---|
| Low | 20–30 mg | Twice daily | Documented entry-level range |
| Mid | 40–50 mg | Twice daily | Most commonly studied range |
| High | 50–100 mg | Twice daily | Oral: split AM/PM given the ~9 h half-life to maintain steady blood levels. Injectable suspension: EOD to ED, many users run it daily to keep levels flat. Pre-workout timing (60–90 min before training) is popular among strength users for the CNS feel. |
Cycle length & outcomes
Documented cycle
4–8 weeks
Plateau after
8 wks
Cycle Length & Onset#
Winstrol is a short-pulse finisher, not a long-run compound. The ceiling isn't efficacy — it's liver enzymes, lipid damage, and tendon dryness, all of which degrade non-linearly past week 6. Most users feel the hardening shift within 10–14 days: tighter skin, flatter water, sharper vascularity, and a CNS "snap" on heavy sets. Strength typically peaks around week 3–4.
Dose Ladder by Goal#
| Goal | Cycle Length | Oral Dose | Injectable Dose |
|---|---|---|---|
| First Winstrol run (cut finisher) | 4–6 weeks | 20–30 mg/day | 50 mg EOD |
| Intermediate cut / recomp | 6 weeks | 40–50 mg/day | 50 mg ED |
| Contest prep / photoshoot dry-out | 4–6 weeks | 50 mg/day | 50 mg ED |
| Peak week hardening | 7–10 days | 75–100 mg/day split AM/PM | 100 mg ED |
| Female cut (hardening) | 4–6 weeks max | 5–10 mg/day | not recommended |
Never exceed 8 weeks. Most experienced users cap at 6. Duration is hepatotoxicity-limited, not efficacy-limited — returns on tissue hardness plateau around week 4 while liver and lipid damage keep accruing.
Daily Timing#
Split the oral AM/PM to match the ~9 h half-life and keep blood levels steady. Strength-focused users often front-load 60–90 minutes pre-training on heavy days for the CNS feel. Injectable aqueous suspension is run daily or EOD — the microcrystalline depot extends plasma levels but daily dosing keeps the profile flattest.
"Following intramuscular administration, stanozolol exhibited a terminal half-life of approximately 82 hours, indicating prolonged depot release from the injection site." — Soma et al., J Vet Pharmacol Ther (2007)
The injectable is the same molecule as the oral — 17α-alkylated, equally hepatotoxic. Community lore that "injectable Winny is liver-friendly" is wrong. Choose oral for convenience, injectable only if you want flatter plasma levels or prefer the depot dosing pattern. Expect post-injection flu ("Winstrol cough") from the suspension vehicle.
No Loading, No Tapering#
Stanozolol doesn't require a loading phase — steady-state is reached within 3–4 days on the oral. There's no need to taper off either; simply stop at the end of the run. The oral clears in days; the injectable suspension has a long detectable tail (weeks to months for WADA purposes) but pharmacologically inactive levels drop within 1–2 weeks.
"Stanozolol cannot undergo aromatisation or 5α-reduction, but it induces gene transcription via the androgen receptor and is detected in urine for weeks due to long-lived metabolites." — Rane & Ekström, Br J Clin Pharmacol (2012)
Tested athletes: assume a several-month washout minimum.
Bloodwork Cadence#
| Timepoint | Panel |
|---|---|
| Pre-cycle (baseline) | CBC, CMP (AST/ALT/GGT/bilirubin), full lipid panel, BP |
| Mid-cycle (week 3–4) | LFTs, lipids, BP |
| End of cycle | LFTs, lipids, BP |
| Post-PCT (~6 weeks off) | Full hormone panel + LFTs + lipids |
Expect ALT/AST 2–5× ULN mid-cycle and HDL crashed to 10–20 mg/dL. This is routine for stanozolol, not an emergency — but it's exactly why runs stay short.
"Stanozolol is among the most potent suppressors of serum SHBG and typically causes a 30–50% decrease in HDL cholesterol within several weeks of use." — Grant et al., Ann NY Acad Sci (2024)
"The administration of stanozolol resulted in a significant elevation of transaminases and histopathological liver damage, confirming a clear hepatotoxic potential within a matter of weeks." — Boada et al., Arch Toxicol (1999)
Run TUDCA 500–1000 mg/day and NAC 1200 mg/day through-cycle, citrus bergamot 1000 mg/day plus 3–4 g EPA+DHA for lipids, and skip alcohol entirely. No concurrent 17α-alkylated orals — stacking winny with dbol, anadrol, or superdrol multiplies the hepatic load.
Tendon Protocol#
The real week-3 trap isn't the liver — it's tendon rupture risk at the triceps, pec, and quad.
"Use of anabolic-androgenic steroids is associated with an increased risk of tendon rupture, particularly involving the upper extremity (triceps and pectoralis major)." — Kanayama et al., Am J Sports Med (2015)
Non-negotiables on a Winstrol run:
- 15 g hydrolyzed collagen + 50 mg vitamin C 60 min pre-training (Shaw/Baar protocol)
- Extended warm-ups, ramping sets, no cold PR attempts
- Keep a wet compound in the stack — test at 200+ mg/wk, or add nandrolone 200 mg/wk or EQ 400–600 mg/wk for joint comfort
- Avoid max singles in weeks 3–6 unless meet day demands it
PCT#
Stanozolol on its own clears fast, but you're almost certainly running it on a test base. PCT timing is dictated by the longest ester in the stack — typically test E/C, meaning PCT starts ~2 weeks after the final test injection.
Standard SERM protocol:
- Nolvadex 40/40/20/20 mg/day over 4 weeks, or
- Clomid 50/50/25/25 mg/day over 4 weeks
Stanozolol itself doesn't need to be "run out" — stop it at the end of the cycle and let the test ester clear before starting the SERM.
Body Transformation Preview
Lean Mass Gain
2.7 lbs
2.0–3.4 lbs range
Fat Loss
2.0 lbs
1.5–2.5 lbs range
Lean Gain by Week
Risks & mistakes
Common (most users)#
- Joint dryness / "crunchy" feel — stanozolol pulls water out of connective tissue and synovial fluid. Expect it within 2–3 weeks. Mitigation: keep a wet compound in the stack (test at 200+ mg/wk, nandrolone 200 mg/wk, or EQ 400+ mg/wk), 15 g hydrolyzed collagen + 50 mg vitamin C 60 min pre-training, fish oil 3–4 g EPA+DHA/day, and don't train max singles on heavy eccentrics.
- Elevated AST/ALT — mid-cycle LFTs commonly run 2–5× ULN. Normal for the compound, returns to baseline post-cycle in the absence of other insults. TUDCA 500–1000 mg/day and NAC 1200 mg/day through-cycle, zero alcohol, no other 17α-alkylated orals concurrent.
- HDL crash / LDL rise — stanozolol is one of the worst AAS for lipids; 30–50% HDL drops within weeks are typical.
"Stanozolol, a synthetic anabolic steroid, is among the most potent suppressors of serum SHBG and typically causes a 30–50% decrease in HDL cholesterol within several weeks of use." — Grant et al. 2024, Ann NY Acad Sci
Mitigation: citrus bergamot 1000 mg/day, omega-3 at 3–4 g/day, cardio 3–4×/week, keep runs ≤6 weeks, low-saturated-fat intake.
- Acne / oily skin / scalp shedding — predictable DHT-profile androgenic sides. Finasteride will not help (stanozolol is not a 5α-reductase substrate). Topical antiandrogens (RU58841, pyrilutamide) and nizoral 2% 3×/week are the tools that actually work here. Benzoyl peroxide 2.5% and a retinoid for back/shoulder acne.
- Post-injection pain / "Winstrol cough" (injectable suspension only) — the microcrystalline vehicle causes local irritation and a transient cough/flushing/chest-tightness right after injection as particulate hits the pulmonary circulation. Unpleasant, not dangerous. Use 21–23g to draw, 25g to inject, warm the vial, shake vigorously, and inject slowly.
- Modest BP elevation — smaller than tren or anadrol but real, especially alongside HDL crash. Home BP cuff, check 2×/week.
Uncommon (dose-dependent or individual)#
- LFTs above 5× ULN — more likely at 75–100 mg/day, past week 6, or with concurrent alcohol/NSAID use. Drop the dose or end the run early. Re-check at 2–3 weeks post-cycle; if not trending to baseline, hold off on further orals for a full quarter.
- Cholestasis (itching, dark urine, pale stool, RUQ discomfort) — stop immediately and get bilirubin + GGT + ALP checked. Documented with 17α-alkylated AAS including stanozolol.
"The administration of stanozolol resulted in a significant elevation of transaminases and histopathological liver damage, confirming a clear hepatotoxic potential within a matter of weeks." — Boada et al. 1999, Arch Toxicol
- Tendinopathy / partial tears — common enough to mention here rather than in "rare." The risk is real and specifically clustered at triceps, pec major, and quad insertions.
"Use of anabolic-androgenic steroids is associated with an increased risk of tendon rupture, particularly involving the upper extremity (triceps and pectoralis major)." — Kanayama et al. 2015, Am J Sports Med
Back off intensity immediately at the first sign of tendon pain — do not train through it.
- Significant BP rise (>140/90) — add or increase telmisartan 40–80 mg/day, cardio daily, cut sodium. If BP won't come down, end the run.
- Libido drop / erectile issues mid-cycle — usually a test/estrogen balance problem, not stanozolol itself. Stanozolol's SHBG crash can actually raise free test too high relative to a low aromatase baseline. Check E2; low-dose tadalafil 5 mg daily handles the symptom while you sort the ratio.
Rare but serious#
- Hepatic adenoma / peliosis hepatis — benign but vascular liver tumors documented with chronic 17α-alkylated AAS use including stanozolol. Presents as RUQ pain, palpable mass, or incidental finding on imaging. Stop immediately, get ultrasound + hepatology referral.
- Sub-massive hepatic necrosis — rare, reported in case literature with stanozolol misuse (high doses, long runs, stacked orals). Jaundice + rapidly rising bilirubin + clotting derangement is an ER visit, not a forum post.
- Tendon rupture — triceps, pec major, and quad tendons under a heavy load on a dry compound. Surgical repair, long rehab, not always a full recovery. This is why you don't PR during winstrol weeks.
- MI / stroke in predisposed users — combined HDL crash, BP rise, and hematocrit elevation from the wider stack. Family history of early cardiac events + stanozolol is a stack worth rethinking.
Hard contraindications#
- Pre-existing hepatitis or LFTs already elevated — do not run. Fix bloodwork first, verify with a repeat panel, then reassess.
- Concurrent 17α-alkylated orals (dianabol, anadrol, superdrol, M1T, epistane) — additive, potentially fatal hepatotoxicity. One oral at a time.
- Untreated hypertension or dyslipidemia — get BP under 130/85 and lipids in a workable range before adding a compound that worsens both.
- Pregnancy or attempting conception — teratogenic; virilizes female fetuses.
- History of tendon rupture or active tendinopathy — the compound targets exactly the tissue that is already compromised.
- Tested competition (IPF, WADA-code sports, NCAA, military) — metabolites detectable for months.
"Due to its structure, stanozolol cannot undergo aromatisation or 5α-reduction, but it induces gene transcription via the androgen receptor and is detected in urine for weeks due to long-lived metabolites." — Rane & Ekström 2012, Br J Clin Pharmacol
Gender-specific and PCT considerations#
Women: stanozolol is one of the more forgiving AAS for female users because it doesn't aromatize and the androgenic rating is relatively low on paper, but virilization still applies — voice deepening and clitoral hypertrophy are permanent if ignored. Stay at 5–10 mg/day oral, cap runs at 4–6 weeks, and stop at the first sign of voice change. Skip dosing during menses if cycle disruption appears.
PCT: when stanozolol is the finishing oral on a test base, standard SERM PCT applies — nolvadex 40/40/20/20 or clomid 50/50/25/25, starting after the long ester clears. Stanozolol itself clears fast (days for oral, 1–3 weeks for the aqueous suspension tail) and doesn't dictate PCT timing. Retest LFTs and lipids at 4 and 8 weeks post — both should be trending hard toward baseline. If they're not, the next oral waits.
Stack & combine
Multipliers applied when these compounds run together. Values > 1 indicate a bonus on that axis. Tap a partner to expand the mechanism.
| Partner | Type | Lean | Fat loss | Recovery |
|---|---|---|---|---|
| synergistic | ×1.00 | ×1.00 | ×1.15 |
FAQ — Winstrol
Research & citations
5 studies cited on this page.
Conclusion
Winstrol is a classic contest-prep finisher—powerful for adding hardness, vascularity, and that unmistakable 'dry' physique when run intelligently.
Key takeaways:
- Oral dose: 40–50 mg/day (split AM/PM), 4–6 weeks is the community sweet spot
- Injectable: 50 mg ED to EOD is equivalent, but not less hepatotoxic—pain and post-injection flu are common
- Women: 5–10 mg/day, max 4–6 weeks; monitor for virilization
- Requires test base: Never run solo—pair with 150–250 mg/wk testosterone minimum
- Stacking: Shines alongside test/mast/primo for a photo-ready, carved look; avoid other 17aa orals
- PCT: Standard SERM (nolvadex or clomid) after test ester clears
Expect dry gains, visible hardness, and a sharp, finished look—if you manage liver, lipids, and joint support. The blueprint: short cycles, aggressive cholesterol management, and never max out connective tissue while on. Winstrol delivers when cycled for what it does best.