Liothyronine sodium is a synthetic form of triiodothyronine (T3), the most active thyroid hormone. It has been sold in the US as Cytomel since 1956 and is used to treat hypothyroidism (an underactive thyroid), to suppress thyroid-stimulating hormone (TSH) in thyroid cancer care, and in a diagnostic suppression test. An intravenous form is approved for myxedema coma, a life-threatening complication of severe hypothyroidism.
Outside medicine, T3 is taken by some bodybuilders and athletes to speed fat loss before competitions. The single most important fact for that context sits at the top of the FDA label: a boxed warning that thyroid hormones should not be used for obesity or weight loss, because normal doses do not work for that purpose in people with normal thyroid function and larger doses can cause serious or life-threatening toxicity (Cytomel label).
This page summarizes what the FDA labels, clinical studies and thyroid guidelines report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Thyroid hormone (synthetic L-triiodothyronine, sodium salt) |
| Brands / approval | Cytomel (Pfizer), first US approval 1956; generic tablets; IV liothyronine for myxedema coma |
| Route | Oral tablet; intravenous injection (hospital use) |
| Strengths | Tablets 5, 25 and 50 mcg; injection 10 mcg/mL |
| Labeled adult dose (hypothyroidism) | Start 25 mcg once daily; usual maintenance 25–75 mcg/day |
| Half-life | ≈22–23 h in blood in modern PK studies; ≈1 day in euthyroid people (isotope study); label lists a “biological half-life” of about 2.5 days |
| Potency vs T4 | 25 mcg liothyronine ≈ 100 mcg levothyroxine in euthyroid patients (injection label) |
| Boxed warning | Not for treatment of obesity or for weight loss |
| US status | Prescription-only; not listed among the Schedule III anabolic steroids |
| WADA status | Thyroid hormones are not named on the 2026 Prohibited List |
What it is
The thyroid gland makes two hormones built from the amino acid tyrosine and iodine: thyroxine (T4, four iodine atoms) and triiodothyronine (T3, three iodine atoms). T4 is largely a prohormone. About 80% of the T3 circulating in the blood is made outside the thyroid by enzymes (deiodinases) that remove one iodine from T4 (Cytomel label). T3 was first identified in human plasma in 1952 (Gross & Pitt-Rivers, Lancet 1952).
Liothyronine sodium has the formula C₁₅H₁₁I₃NNaO₄ and a molecular weight of 672.95 g/mol; the free acid weighs 650.97 g/mol (PubChem). Its effects come from binding thyroid hormone receptors in the cell nucleus, which switch gene transcription on and off (Cytomel label). Thyroid hormones raise oxygen use and basal metabolic rate and speed the turnover of carbohydrate, fat and protein (liothyronine injection label).
The library has a separate page for T4 (thyroxine). The main differences, as described in the labels:
| Feature | T3 (liothyronine) | T4 (levothyroxine) |
|---|---|---|
| Role | Active hormone | Prohormone, converted to T3 |
| Nuclear receptor affinity | Roughly 10 times higher than T4 | Lower |
| Binding to blood proteins | Loose, so it enters tissues faster | Tight, giving higher blood levels and a longer half-life |
| Onset after a dose | Within a few hours; peak response in 2–3 days | Slower |
| Approximate dose equivalence | 25 mcg | 100 mcg |
Pharmacokinetics
The Cytomel label states that T3 is almost completely absorbed, about 95% within 4 hours. It is broken down mainly in the liver by stepwise removal of iodine, and is also conjugated and excreted in bile. The label gives a biological half-life of about 2.5 days (Cytomel label).
Studies that measured T3 in blood directly report shorter values:
| Study | Population | Key findings |
|---|---|---|
| Nicoloff et al., JCI 1972 (radio-labeled T3) | 31 people across thyroid states | Half-life 1.0 day if euthyroid, 0.63 days if hyperthyroid, 1.38 days if hypothyroid; normal T3 production ≈27.6 mcg/day |
| Jonklaas et al., Ther Drug Monit 2015 | 12 healthy adults, single 50 mcg dose | Peak at 2.5 h; mean peak 346 ng/dL from a baseline of 120 ng/dL; half-life 22 h |
| Van Tassell et al., Thyroid 2019 | 14 thyroid cancer patients without their own thyroid hormone | Peak at 1.8 h; fast distribution phase (half-life 2.3 h), then elimination half-life 22.9 h |
Two points follow from these data:
- Levels spike quickly. A single 50 mcg dose nearly tripled blood T3 within a few hours in healthy adults. The 2019 authors modeled twice-daily low doses as a way to avoid peaks above the reference range when T3 is added to T4.
- Half-life depends on thyroid state and on how it is measured. T3 clears faster when someone is already hyperthyroid. In the 2015 study, the calculated half-life ranged from 22 h to 71 h depending on which time points were used.
The normal daily T3 production of roughly 28 mcg is in the same range as the labeled starting dose of 25 mcg, which is why replacement doses are measured in micrograms.
Approved medical use
Oral liothyronine is approved for the following uses (Cytomel label):
| Indication | Labeled dosing |
|---|---|
| Hypothyroidism (primary, pituitary or hypothalamic; congenital or acquired) | Adults: 25 mcg once daily, raised by 25 mcg every 1–2 weeks if needed; usual maintenance 25–75 mcg/day. Elderly or heart disease: start at 5 mcg/day |
| TSH suppression in well-differentiated thyroid cancer, alongside surgery and radioiodine | Dose set to reach the target TSH; may require higher doses |
| Thyroid suppression test (to tell mild hyperthyroidism or an autonomous gland from normal) | 75–100 mcg daily for 7 days; a 50% or greater fall in radioiodine uptake indicates a normal thyroid-pituitary axis |
The label states that it is not indicated for benign thyroid nodules or nontoxic goiter in iodine-sufficient patients, and not for hypothyroidism during recovery from subacute thyroiditis.
Intravenous liothyronine is indicated for myxedema coma and precoma. Its label recommends initial doses of 25–50 mcg (10–20 mcg with known or suspected heart disease), given with glucocorticoids. Case-report data showed lower mortality with at least 65 mcg/day in the first days, and there is limited experience above 100 mcg/day. No controlled clinical studies of the injection exist (liothyronine injection label).
What the research shows
T3 instead of T4 for hypothyroidism
Levothyroxine (T4) is the standard treatment for hypothyroidism. The 2014 American Thyroid Association (ATA) guideline concluded that levothyroxine should remain the standard of care, and found no consistently strong evidence that alternatives, including T4/T3 combinations or thyroid extracts, improve health outcomes (Jonklaas et al., Thyroid 2014).
One small trial compared T3 alone with T4 alone. Fourteen hypothyroid patients took each drug three times daily in a randomized, double-blind crossover design, with doses adjusted to the same TSH target of 0.5–1.5 mU/L (Celi et al., JCEM 2011):
| Outcome on T3 vs T4 | Result |
|---|---|
| Body weight | 68.5 vs 70.6 kg (p = 0.009) |
| Total cholesterol | −10.9% |
| LDL cholesterol | −13.3% |
| Apolipoprotein B | −18.3% |
| Heart rate, blood pressure, exercise tolerance, insulin sensitivity | No significant difference |
These were patients without a working thyroid, treated to a normal TSH. The result does not show that adding T3 to a normal thyroid causes fat loss.
T4 plus T3 combination therapy
A 2021 meta-analysis of 18 studies found no difference between T4/T3 combination therapy and T4 alone on quality of life, psychological distress, depressive symptoms or fatigue (low-to-moderate certainty evidence). When asked, 43% of patients preferred the combination, 23% preferred T4 alone and 30% had no preference (Millan-Alanis et al., Thyroid 2021).
A joint ATA, British and European thyroid association consensus noted that 14 clinical trials had not shown a consistent benefit of combination therapy. It recommended new trials using twice-daily T3 or a slow-release preparation in patients who remain dissatisfied on T4 (Jonklaas et al., Thyroid 2021).
Weight loss in people without hypothyroidism
A systematic review of controlled studies of T3 or T4 given to obese people during calorie restriction found that T3 suppressed TSH and T4 levels, but consistent effects on weight loss, protein breakdown, metabolic rate and heart rate could not be established. The authors concluded that the data were inconclusive for effectiveness, while they did show that such therapy induces subclinical hyperthyroidism (Kaptein et al., JCEM 2009).
Where extra weight loss did occur, it was not necessarily fat:
- Obese dieters. Patients losing weight slowly on 2 MJ/day (≈480 kcal) were given T3 20 mcg three times daily for about two weeks. Weight loss sped up, but urinary nitrogen excretion rose, and the authors concluded the extra loss came from lean body mass rather than fat (Wolman et al., Int J Obes 1985).
- Healthy young adults. Eighteen healthy people (mean age 26) took T3 100 mcg/day for 2 weeks. Lean body mass fell, whole-body protein breakdown rose, type IIA muscle fiber area fell 15%, muscle oxidative enzyme activity fell 21–37%, and maximal oxygen uptake dropped from 3.08 to 2.94 L/min (Martin et al., JCI 1991).
About “T3 burns fat, not muscle.” This is a common claim in bodybuilding circles. The controlled human data point the other way: excess T3 increased protein breakdown and reduced lean mass in both obese dieters and healthy young adults. The FDA label states that doses in the normal replacement range are ineffective for weight reduction in people with normal thyroid function.
T3 combined with testosterone
Direct evidence is minimal. In one bed-rest study, 10 healthy men received T3 50 mcg/day for 28 days as a model of catabolic stress. The 6 men randomized to testosterone enanthate 200 mg/week kept nitrogen balance and lean body mass, but knee-extensor strength fell about as much as in the 4 men on placebo (Zachwieja et al., JCEM 1999). The study was not designed to test fat loss and was too small to say anything about safety.
Side effects and risks
Boxed warning: not for weight loss
Both the tablet and injection labels carry the same boxed warning. In people with normal thyroid function, replacement-range doses do not cause weight loss, and larger doses “may produce serious or even life-threatening manifestations of toxicity,” especially when combined with sympathomimetic amines such as appetite-suppressing stimulants (Cytomel label). The label also notes a narrow therapeutic index, meaning the gap between an effective and a harmful dose is small.
Adverse reactions are those of hyperthyroidism from too much hormone. The label lists:
- Heart: palpitations, fast heart rate, arrhythmias, raised blood pressure, heart failure, angina, myocardial infarction and cardiac arrest;
- Nervous system: headache, nervousness, anxiety, irritability, insomnia, tremor;
- Muscle: weakness and cramps;
- General: heat intolerance, sweating, fever, increased appetite, weight loss, diarrhea;
- Other: hair loss, menstrual irregularities, impaired fertility and reduced bone mineral density.
Overdose can add confusion and disorientation; cerebral embolism, seizure, shock, coma and death have been reported. Symptoms may not appear until several days after ingestion.
Heart
Even a single replacement-size dose has measurable cardiac effects. After 50 mcg in healthy adults, mean heart rate rose by up to 18 beats/min within 12 hours, peaking about 10 hours after the dose (Jonklaas et al., Ther Drug Monit 2015).
Long-term over-replacement carries larger risks. In a population cohort of 17,684 people on long-term T4 therapy in Scotland, those whose TSH was fully suppressed (≤0.03 mU/L) had higher rates of the following compared with people with a normal TSH (Flynn et al., JCEM 2010):
| Outcome | Adjusted hazard ratio (95% CI) |
|---|---|
| Cardiovascular disease | 1.37 (1.17–1.60) |
| Dysrhythmias | 1.6 (1.10–2.33) |
| Fractures | 2.02 (1.55–2.62) |
People with a low but not fully suppressed TSH (0.04–0.4 mU/L) did not have a raised risk. These data come from T4 users; no comparable cohort exists for T3. The label notes that atrial fibrillation is the most common arrhythmia with thyroid hormone overtreatment in the elderly.
Bone
The label warns that over-replacement increases bone resorption and decreases bone mineral density, particularly in postmenopausal women. The fracture data above point the same way.
Muscle loss and thyrotoxic periodic paralysis
Excess T3 increases protein breakdown and reduced lean mass in the trials described above. Case reports in bodybuilders describe a more acute problem, thyrotoxic hypokalemic periodic paralysis: sudden attacks of muscle weakness or paralysis with very low blood potassium. A 29-year-old bodybuilder had recurrent attacks of myalgia and weakness that resolved after potassium replacement and stopping liothyronine (van Bokhorst et al., Eur J Case Rep Intern Med 2021).
Another report describes a 25-year-old bodybuilder first treated for presumed sepsis because of persistent tachycardia. Tests later showed a markedly raised T3 with undetectable TSH and free T4, and he disclosed taking testosterone and T3 (Warner et al., BMJ Case Rep 2020). The authors note that clinicians may not recognize this kind of hormone use unless a thorough drug history is taken.
Suppression of the body’s own thyroid
Taking thyroid hormone lowers TSH, the pituitary signal that drives the thyroid. After one 50 mcg dose of T3, TSH reached its low point at 12 hours and stayed below baseline for 2–3 days (Jonklaas et al., Ther Drug Monit 2015).
Recovery after long-term use is not immediate. In seven euthyroid women taken off prolonged thyroid-suppression therapy, the pituitary’s TSH reserve stayed reduced for 2–5 weeks, and serum T4 took at least 4 weeks to return to normal (Vagenakis et al., NEJM 1975). During that window, thyroid hormone levels can be below normal.
Interactions
Key interactions from the Cytomel label:
| Drug or class | Effect |
|---|---|
| Sympathomimetics (stimulants, decongestants, appetite suppressants) | Effects of both can increase; higher risk of coronary insufficiency in people with coronary disease |
| Tricyclic and tetracyclic antidepressants | Effects and toxicity of both may increase, including arrhythmias |
| Ketamine | Marked high blood pressure and fast heart rate |
| Warfarin and other oral anticoagulants | Stronger anticoagulant effect; dose may need lowering |
| Insulin and other diabetes drugs | Blood sugar control may worsen |
| Digitalis glycosides | Reduced digitalis effect |
| Bile acid sequestrants, sevelamer | Reduced T3 absorption; label advises dosing liothyronine at least 4 hours before these drugs |
| Androgens / anabolic steroids, glucocorticoids | Lower thyroxine-binding globulin, which changes total hormone measurements |
Who should not use it
The tablet label contraindicates liothyronine in uncorrected adrenal insufficiency, because thyroid hormone speeds the clearance of cortisol and can trigger an adrenal crisis. It also advises starting at lower doses in the elderly and in people with heart disease, and warns that oral thyroid hormone should not be used to treat myxedema coma (Cytomel label).
Legal status and use outside medicine
In the US, liothyronine is a prescription drug. It is not among the anabolic steroids named in Schedule III (21 CFR 1308.13). Thyroid hormones are not named on the WADA 2026 Prohibited List.
An American Association of Clinical Endocrinology position statement describes rising off-label use and misuse of thyroid hormone for fatigue, obesity, depression and athletic performance in people without a thyroid diagnosis, and calls the balance of risks and benefits unfavorable (Irwig et al., Endocr Pract 2020). Case reports describe bodybuilders taking T3 together with testosterone and other drugs, often without telling their doctors. Combining thyroid hormone with sympathomimetic stimulants, a class that includes beta-agonists such as clenbuterol, is the scenario the boxed warning singles out.
Key takeaways
- The active thyroid hormone. Liothyronine is synthetic T3, about four times as potent per microgram as T4, with a fast onset and a blood half-life of about one day.
- Approved for thyroid disease only. Indications are hypothyroidism, TSH suppression in thyroid cancer, a diagnostic suppression test and (IV) myxedema coma. Labeled oral maintenance is 25–75 mcg/day.
- Boxed warning against weight-loss use. Replacement doses do not cause weight loss in people with normal thyroid function, and larger doses can be life-threatening, especially with stimulants.
- Extra weight loss can be muscle. In controlled studies, excess T3 raised protein breakdown and reduced lean mass in both dieters and healthy young adults.
- Heart and bone are the main long-term risks. Fully suppressed TSH on thyroid hormone was linked to more cardiovascular disease, arrhythmias and fractures.
- It switches off the body’s own thyroid. TSH falls within hours of a single dose, and recovery after long-term use took weeks in a small study.
Sources
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- XGen Pharmaceuticals DJB. Liothyronine sodium injection (T3) prescribing information. DailyMed, 2023. DailyMed.
- National Center for Biotechnology Information. Liothyronine sodium, CID 23666110. PubChem.
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- World Anti-Doping Agency. The 2026 Prohibited List. WADA.