At Andractim clinical doses (125-250 mg/d transdermal, 6-24 month courses)

• Day 1-7: Establishing topical application technique. Subtle initial effects: morning erections may improve subtly; mood/drive shifts minimal at this stage.
• Week 1-4: First subjective signals — gradual erection quality improvement (the Kunelius 2002 signal at week 12 emerges around here), libido shifts subtle but present. Sebum / oily skin uptick in some users. Notable absence of the dopaminergic/E2-mediated hedonic surge characteristic of T-class compounds — DHT delivers AR signaling but not the "feel-good" neurochemical layer.
• Week 4-12: Peak effects: stable AR-mediated phenotype — modestly elevated drive, erection quality, lean tissue tone in low-BF states. Hair shedding may emerge in genetically predisposed users (visible scalp recession at temples/vertex over 8-12 weeks). Hematocrit rising — first lab check at week 8-12.
• Month 3-6: Full hematologic + lipid response. HDL drop typical (DHT-class non-aromatizing → no E2 HDL preservation, drops more than T at equivalent androgenic exposure). PSA stable in most studies (Idan 2010, Kunelius 2002 — no PSA elevation at 6-24 months). Alopecia progresses in susceptible users.
• Off-cycle: Gel washout fast — apparent serum t½ 24-48h means DHT clears within ~7 days of last application. HPG axis suppression usually milder than T-class (no E2 contribution to feedback) — recovery 4-8 weeks typical. Hair loss progression in predisposed users may be partially permanent.

Characteristic effects

• "Dry, vascular, lean" appearance in low-body-fat states (analogous to drostanolone, but raw DHT inactivated more rapidly in muscle tissue → less anabolic muscle effect)
• Modest libido shifts (initially up via SHBG displacement / free-T elevation, varied subsequent course)
• Erection quality improvement in hypogonadal contexts (Kunelius signal)
• Hair shedding / scalp thinning in genetically predisposed users (DHT is the proximate molecular driver; finasteride / dutasteride cannot rescue because exogenous DHT bypasses the conversion step they block)
• Acne / oily skin in susceptible users (sebaceous gland AR activation — DHT is the dominant androgen at sebaceous glands)
• Prostate effects: BPH driver dose-dependently; minimal at low doses + short duration (Idan 2010 showed no volume change at 24 mo at 70 mg/d — but caveat: dose moderate, healthy middle-aged cohort)
• Mild prostate / urinary symptoms in older users

What users do NOT report

• Strong muscle-building effect (3α-HSD inactivation in muscle limits anabolic potency vs DHT-derivative AAS)
• Significant strength gain
• Cognitive enhancement
• Recovery acceleration
• Fat loss beyond what diet produces
• Mood elevation comparable to T (E2 contribution absent → "drier" psychological profile)
• "Pump" or "fullness" beyond what training produces

• Tolerance buildup: AR receptor downregulation occurs with all sustained AR agonism. DHT-specific tolerance not well-characterized but follows standard AAS pattern.
• Recommended cycle (clinical, NOT bodybuilder): Per indication. Andractim courses typically 3-12 months for hypogonadism/gynecomastia/micropenis indications, with reassessment.
• Reset protocol: Off-course 8+ weeks; HPG recovery typically faster than T-class esters (no E2 contribution to feedback). Endogenous DHT recovers as endogenous T recovers (5αR activity is constitutive).

Synergistic with — none recommended for this user

• Endogenous DHT physiology functions as one component of the integrated androgen system; "stacking" exogenous DHT with anything else is rarely indicated outside niche EU clinical contexts.

Avoid stacking with

• Finasteride / dutasteride: Mechanistic opposites. Finasteride/dutasteride suppress endogenous DHT by blocking T → DHT conversion; exogenous DHT bypasses this entirely. Combining is conceptually nonsensical.
• Testosterone (TRT): Most TRT effects are AR-mediated (DHT downstream of T) or E2-mediated (aromatization). DHT delivers AR signaling alone. Stacking is rare; usually one or the other. Adding DHT to T compounds HPG suppression without proportional benefit.
• Anastrozole / letrozole (aromatase inhibitors): DHT cannot aromatize. AI on top of DHT has nothing to inhibit (other than residual endogenous T → E2). Crashes E2 too low → joint pain, mood issues, lipid worsening, libido collapse.
• DHT-derivative AAS (Masteron, Anavar, Primobolan, Winstrol): All DHT-derivatives stabilize against muscle 3α-HSD inactivation via various ring modifications. Stacking with raw DHT compounds androgenic side effects (hair, prostate, skin, lipids) without proportional muscle-building gain. Particularly bad for hair-loss-predisposed users.
• Oral 17α-alkylated AAS (methyltestosterone, oxymetholone): Hepatotoxic + redundant. Combining strictly dominated by transdermal-only.
• Hair-loss treatments (oral finasteride/dutasteride, topical RU58841, minoxidil): Conflicting goals. Using minoxidil to mitigate damage from a compound you're voluntarily taking is unusual.

Neutral / safe co-administration

• Most non-hormonal nootropics (modafinil, citicoline, NAC, magnesium, fish oil) — no direct interaction. Issue is not pharmacological collision but underlying inappropriateness of exogenous DHT in healthy young eugonadal male.

• Warfarin / DOACs: AAS class generally potentiates warfarin via decreased clotting factor synthesis → INR monitoring required, dose reduction often needed.
• Insulin / oral hypoglycemics: Modest insulin sensitivity changes possible; less pronounced with DHT than aromatizing T.
• CYP-mediated metabolism: DHT is metabolized via 3α/3β-HSD pathways and CYP enzymes; clinically significant CYP-mediated drug interactions not well-characterized for DHT specifically.
• Hepatotoxicity: Transdermal DHT (Andractim) avoids first-pass hepatic exposure → minimal hepatotoxicity vs oral 17α-alkylated AAS. This is a key advantage of the transdermal route.
• Detection (WADA): S1.1 prohibited. Detection via urine LC-MS/MS for parent + metabolites; IRMS (carbon isotope ratio) used to distinguish exogenous DHT from endogenous DHT (since DHT exists naturally). Detection window for transdermal Andractim ~1-2 weeks after last application.

• AR (androgen receptor) CAG repeat length: Shorter CAG repeats = stronger AR signaling per unit ligand. Users with shorter repeats experience more pronounced androgenic side effects (hair loss, prostate, skin) at any given dose. DHT is a potent peripheral androgen — for users with shorter CAG repeats and male-pattern baldness predisposition, exogenous DHT is among the most aggressive compound choices for accelerating hair loss.
• SRD5A1 / SRD5A2 variants: Polymorphisms affect endogenous T → DHT conversion rates; less relevant for exogenous DHT (which bypasses 5αR). Variants may modulate baseline endogenous DHT and tissue distribution.
• CYP19 (aromatase) polymorphisms: Irrelevant for exogenous DHT (which cannot aromatize). Relevant for understanding individual baseline T → E2 conversion rates and how that interacts with the rationale for choosing DHT over T.
• Practical note: No pharmacogenomic test changes the SKIP-FOR-NOW verdict. The user's June 2026 23andMe may include AR CAG / SRD5A1/2 SNPs but interpretation will not change the SKIP recommendation. AR CAG repeats may be informative for future hair-loss-risk assessment if DHT or DHT-derivative AAS is ever considered.

For this user

Sourcing is solvable but irrelevant — no clinical indication. Skip the compound, do not engage the sourcing question.

• Baseline (before starting): Total + free testosterone, SHBG, LH, FSH, E2 (sensitive assay), DHT (LC-MS/MS preferred), prolactin, full lipid panel (LDL, HDL, total cholesterol, triglycerides, ApoB, ideally Lp(a)), ALT, AST, GGT, alkaline phosphatase, total + direct bilirubin, CBC (hematocrit), HbA1c, fasting glucose, eGFR, blood pressure, PSA, semen analysis (if fertility-relevant), echocardiogram if multi-course intent, hair density photos (frontal hairline, temples, crown — baseline for tracking AAS-driven progression — particularly critical for DHT given proximate-driver role), prostate volume on ultrasound baseline if >40 yo or family history of prostate cancer.
• During use (week 4-8): ALT, AST, GGT (less critical with transdermal route), full lipid panel, blood pressure, hematocrit, hair photos. Flag if HDL drops >50%, BP >140/90, or visible hairline recession.
• End of course: Full HPG panel (T, LH, FSH, E2, DHT) to quantify suppression; lipids; hair photos for end-of-course baseline; PSA recheck.
• Post-cycle: HPG recovery check at week 4-8; full lipid recovery check at week 8-12; hair photos at 8-12 weeks (assess whether shedding has stabilized or progressed).
• Long-term (multi-course users): Annual lipid trends, periodic echocardiogram, formal CVD risk recalculation, ongoing hair density photos, PSA + prostate volume monitoring.

• testosterone — parent molecule of DHT; foundational AAS / HRT compound; SKIP-AT-20 absent documented hypogonadism. If exogenous androgen ever appropriate, conversation starts here.
• finasteride — Type 2 5αR inhibitor; ~70% serum DHT reduction; FDA-approved for MPB + BPH; mechanistic opposite of exogenous DHT.
• dutasteride — Dual Type 1+2 5αR inhibitor; ~95% serum DHT reduction; FDA-approved for BPH; off-label for MPB.
• masteron (drostanolone) / masteron-enanthate — 2α-methyl-DHT; 3α-HSD-stable; the canonical "DHT-class hardening" bodybuilding AAS.
• anavar (oxandrolone) — 17α-alkyl + 2-oxa DHT-derivative; FDA-approved for catabolic states; oral; 3α-HSD-stable.
• primobolan (methenolone) — 1-methyl DHT-derivative; "lean tissue" reputation; injectable + oral forms; 3α-HSD-stable.