Phenylethylamine Dosage Guide

## Overdose Profile (Without MAO Inhibition) Fatal overdose from oral PEA alone is essentially impossible under normal physiological conditions. MAO-B in the intestinal wall and liver destroys the overwhelming majority of ingested PEA before it reaches the systemic circulation. Even at very high oral doses (1000mg+), the amount of PEA that survives first-pass metabolism is insufficient to produce dangerous systemic effects in most individuals. ## Overdose Profile (With MAO Inhibition) The overdose risk changes fundamentally when PEA is combined with MAO inhibitors. Without the protective destruction by MAO-B, PEA's sympathomimetic effects accumulate and can produce a medical emergency: ### Hypertensive Crisis - Severe, acute blood pressure elevation (systolic >200 mmHg) - Intense, sudden headache ("thunderclap" quality) - Neck stiffness and pain - Visual disturbances (blurred vision, flashing lights) - Chest pain - Risk of intracranial hemorrhage, stroke, or myocardial infarction ### Cardiovascular Emergency - Severe tachycardia (heart rate >150 bpm) - Cardiac arrhythmias - Palpitations with awareness of irregular heartbeat - In severe cases: cardiac arrest ## Excessive Dose Symptoms (Without MAO Inhibition) At high oral doses without MAO inhibition, the following transient symptoms may occur: - Tachycardia (rapid heart rate) - Elevated blood pressure - Anxiety and agitation - Headache - Nausea - Tremor - Insomnia These symptoms are generally self-limiting and resolve within 30-60 minutes as PEA is metabolized. ## Treatment For PEA-induced hypertensive crisis (combination with MAO inhibitors): - **Immediate blood pressure reduction** with IV phentolamine (alpha-blocker) or IV nitroprusside - **Cardiac monitoring** and antiarrhythmic therapy as needed - **Benzodiazepines** for agitation and seizure prophylaxis - **Do NOT use beta-blockers alone** — risk of unopposed alpha-adrenergic vasoconstriction - **Supportive care**: IV fluids, temperature management if hyperthermic