3,5-Diiodo-L-thyronine (T2)
3,5-Diiodo-L-thyronine (T2) is an endogenous iodothyronine metabolite marketed as a fat-loss supplement. It is claimed to raise metabolic rate through a rapid, largely non-genomic action on mitochondria without the strong TSH suppression of T3, though human evidence is thin.
01 Overview
T2 is a deiodination product of T3 that acts primarily on mitochondria to increase substrate oxidation and resting energy expenditure. Rodent studies show it can raise metabolic rate and reduce adiposity with less impact on the thyroid axis than T3, which drove its adoption in over-the-counter fat burners.
Human data are sparse and mostly limited to small or uncontrolled reports, so its real-world potency and safety margin are poorly defined. Some commercial T2 products have been found adulterated with T3, complicating the anecdotal picture.
02 Mechanism
Acts largely non-genomically on mitochondria, stimulating oxygen consumption and fatty-acid oxidation and uncoupling substrate use; genomic thyroid-receptor effects appear weaker than T3, sparing TSH somewhat.
03 Dosing
| Tier | Dose | Route | Notes |
|---|---|---|---|
| Supplement | 100–300 mcg/day | Oral | Label doses; potency and content vary widely |
04 Effects
| Effect | Magnitude | Evidence | |
|---|---|---|---|
| Increased metabolic rateMitochondrial stimulation increases energy expenditure in animal models. | Raised BMR in rodents | Preclinical | |
| Reduced adiposityRodent studies show fat-mass reduction without proportional TSH suppression. | Preclinical |
05 Side effects
| Effect | Severity | Frequency | Evidence | Countermeasures |
|---|---|---|---|---|
| Possible TSH suppressionSome suppression seen at higher doses despite the sparing claim. | Mild | Uncertain | Preclinical | |
| Cardiac stimulationPalpitations and raised heart rate reported anecdotally, sometimes from T3 adulteration. | Moderate | Uncertain | Anecdotal |