Alanine Aminotransferase

When high

Supplements:

• TUDCA -- 500-1000mg/day (with meals), bile flow and hepatoprotection; most evidence-supported supplement for AAS-induced cholestatic pattern
• NAC -- 1200-1800mg/day (empty stomach, divided doses), glutathione precursor; supported by mechanistic and observational data in AAS hepatotoxicity
• Milk Thistle (Silymarin) -- 300-600mg/day; standard form OR Silymarin Phytosome (Siliphos) 200mg 2x/day for ~10x absorption vs standard silymarin
• Alpha-Lipoic Acid (ALA) -- 300-600mg/day

Compound/AAS adjustments (highest-leverage intervention):

• Switch oral AAS to injectable equivalents -- injectable Winstrol, injectable Primobolan, injectable Anavar preparations substantially reduce hepatic first-pass burden vs oral versions; this is the single most effective intervention for AAS-induced ALT elevation
• Drop 17-alpha-alkylated orals entirely (Dianabol, Anadrol, Winstrol, Anavar, Superdrol, Halotestin) if enzymes persistently >3x ULN or alongside rising bilirubin
• Note: Proviron (mesterolone) is NOT 17-alpha-alkylated; it is hepatically well-tolerated and does not stress liver enzymes meaningfully
• Reduce alcohol to zero during any oral AAS cycle; alcohol and oral AAS hepatotoxicity are synergistic

Pharmacological options (severe or cholestatic elevation):

• Ursodeoxycholic acid (UDCA / Actigall) -- 10-15mg/kg/day (typically 500mg 2x/day for 80kg adult); prescription bile acid; more potent than TUDCA for confirmed AAS-induced cholestasis; case reports show resolution of bilirubin >100 umol/L with UDCA
• Indication: ALT >5x ULN with rising bilirubin, or a confirmed cholestatic pattern on imaging/biopsy
• All require physician oversight

Lifestyle:

• Reduce or eliminate oral steroids if persistently elevated
• Avoid alcohol and hepatotoxic medications
• Allow 8-12 weeks off orals between cycles for enzyme normalisation