T3 (Liothyronine/Cytomel) for Thyroid Hormone & Metabolic Enhancement — Weight & Metabolism
Active thyroid hormone. FDA-approved for hypothyroidism. Abused at supraphysiological doses for fat loss. Significant cardiac and catabolic risks.
Overview
Liothyronine sodium (T3, brand name Cytomel) is the synthetic form of triiodothyronine, the biologically active thyroid hormone responsible for regulating basal metabolic rate, protein synthesis, and thermogenesis. T3 is FDA-approved for the treatment of hypothyroidism, myxedema coma (IV formulation), and as a diagnostic agent in T3 suppression tests. In clinical use, typical replacement doses range from 25-75 mcg/day. T3 is approximately 4-5 times more potent than levothyroxine (T4) on a microgram-per-microgram basis and has a significantly shorter half-life of approximately 1 day compared to T4's 6-7 day half-life. Liothyronine exerts its effects by binding to thyroid hormone receptors (TRα and TRβ) in the cell nucleus, which are ligand-activated transcription factors that regulate the expression of hundreds of genes involved in metabolism, thermogenesis, and development. At physiological doses, T3 maintains normal metabolic homeostasis. At supraphysiological doses (commonly 50-100+ mcg/day in performance contexts), T3 dramatically increases basal metabolic rate by 15-20%, enhancing fat oxidation and caloric expenditure. However, supraphysiological T3 also increases muscle protein catabolism, potentially causing significant lean mass loss during caloric restriction — a major concern that leads many users to co-administer anabolic compounds to counteract this effect. Exogenous T3 administration suppresses endogenous thyroid function via negative feedback on the hypothalamic-pituitary-thyroid (HPT) axis, reducing TSH and T4 production. Abrupt discontinuation can result in transient hypothyroidism lasting weeks to months. Cardiac risks of supraphysiological T3 include tachycardia, atrial fibrillation, angina, increased myocardial oxygen demand, and potentially sudden cardiac death in susceptible individuals. Bone loss (osteoporosis) is a significant concern with chronic supraphysiological thyroid hormone exposure.
Indications
- FDA-approved: Hypothyroidism (all causes) — replacement therapy
- FDA-approved: Myxedema coma (IV formulation) — emergency treatment
- FDA-approved: T3 suppression test — thyroid diagnostic
- Off-label: Combined T4/T3 therapy for hypothyroidism (controversial)
- Abused: Supraphysiological doses for fat loss and metabolic enhancement
- Abused: Component of bodybuilding 'cutting' stacks
Mechanism of Action
Liothyronine is rapidly and nearly completely absorbed from the GI tract. Peak plasma levels within 2-4 hours. Shorter half-life (~1 day) compared to T4 (6-7 days) means faster onset and offset of metabolic effects
Dosing
| Compound | Dose | Frequency | Notes |
|---|---|---|---|
| Liothyronine (T3/Cytomel) | 25 mcg/day | Once daily or split | Low therapeutic replacement dose |
| Liothyronine (T3/Cytomel) | 50 mcg/day | Split twice daily | Moderate dose; beginning of supraphysiological range for enhanced metabolism |
| Liothyronine (T3/Cytomel) | 75-100 mcg/day | Split 2-3 times daily | Supraphysiological dose for fat loss; significant cardiac and catabolic risks |
| Liothyronine sodium | 25-50 mcg | Every 4-12 hours | Myxedema coma ONLY — ICU setting with continuous monitoring |
Evidence Grade
GRADE A
Safety & Contraindications
- Supraphysiological doses cause significant cardiac stimulation — tachycardia, arrhythmias
- Atrial fibrillation risk increased at doses >75 mcg/day
- Muscle catabolism at supraphysiological doses — lean mass loss during caloric deficit
- HPT axis suppression — exogenous T3 suppresses TSH and endogenous T3/T4 production
- Requires slow taper to avoid rebound hypothyroidism — never stop abruptly
- Bone mineral density loss with chronic supraphysiological exposure
- Increased myocardial oxygen demand — dangerous in coronary artery disease
- Anxiety, tremor, insomnia, and heat intolerance at supraphysiological doses
- Drug interactions: potentiates warfarin, sympathomimetics, insulin requirements
- Narrow therapeutic index — small dose changes produce large metabolic effects
- Contraindicated in uncorrected adrenal insufficiency (adrenal crisis risk)