• Day 1-7: Sedation prominent (qHS dosing helps), nausea, headache. Often a "thicker" feeling than sertraline — partly sigma-1, partly histamine cross-talk debate.
• Week 2-4: Caffeine sensitivity becomes obvious — most users have to drop caffeine entirely. Initial OCD/anxiety response begins.
• Week 4-12: Class-typical SSRI emotional blunting; sexual dysfunction (anorgasmia, low libido) often emerges and persists. Y-BOCS responders see meaningful symptom drop.
• Discontinuation: Worse than fluoxetine (no long-tail metabolite). Flu-like, dizziness, electric-shock sensations common with abrupt stop. Slow taper required.

• Tolerance: Generally maintained; "poop-out" possible long-term.
• Cycling: Not cycled. Continuous use is the model.

Avoid stacking with

• MAOIs (phenelzine, tranylcypromine, selegiline, linezolid, methylene blue): serotonin syndrome — absolute contraindication, 14-day washout.
• Other serotonergics: tramadol, 5-HTP, MDMA, St John's wort, dextromethorphan (high dose), other SSRIs/SNRIs.
• CYP1A2 substrates: caffeine (effectively contraindicated at any meaningful intake), melatonin (~17× AUC), ramelteon (~190× AUC, FDA contraindication), agomelatine (~60× AUC, EU contraindication), theophylline (~3× — narrow therapeutic index), tizanidine (~33× AUC, FDA contraindication), clozapine, olanzapine, duloxetine.
• CYP2C19 substrates: clopidogrel (reduced antiplatelet effect — relevant post-stent), PPIs (modest exposure increase), warfarin (INR rise).
• QT-prolonging combinations at high cumulative load.

Synergistic

• CBT / Exposure and Response Prevention (ERP): First-line behavioral therapy for OCD; combination outperforms either alone.
• Low-dose atypical antipsychotic augmentation (risperidone, aripiprazole) for OCD-resistant cases.

Worst interaction profile in the SSRI class along with paroxetine — but for different reasons. Paroxetine = CYP2D6. Fluvoxamine = CYP1A2 + CYP2C19. The CYP1A2 inhibition is what drives the "fluvoxamine kills coffee" reputation in the nootropic community and what makes co-prescription with melatonergics, ramelteon, theophylline, and tizanidine clinically dangerous.

For the user archetype: the caffeine interaction alone is disqualifying for anyone who uses or might use caffeine as a cognitive lever. Reintroducing one cup of coffee on fluvoxamine ≈ several cups of coffee in PK terms.

• CYP2D6 metabolism contributes minor pathway for fluvoxamine itself.
• CYP1A2 genotype matters for substrate co-administration but not fluvoxamine clearance directly.
• Smoking status is the dominant CYP1A2 modifier — heavy smokers may have ~30-50% lower fluvoxamine exposure; smoking cessation can spike levels into toxicity range.

• Baseline: Y-BOCS (if OCD), PHQ-9, GAD-7, body weight, sexual function questionnaire (ASEX), sodium, LFTs, ECG if cardiac risk factors.
• During use (monthly first 3 months, then quarterly): Y-BOCS, mood scale, body weight, sexual function (specifically track libido, orgasm latency, anorgasmia), sleep quality (PSQI), CYP1A2 substrate timing log (caffeine, melatonin, OTCs).
• Specific CYP1A2 timing log (this user): Document caffeine intake before any fluvoxamine trial — establish that caffeine is fully avoided or precisely controlled. Same for melatonin, agomelatine, OTC sleep aids.
• Post-discontinuation: Symptom return at week 2, 4, 8.