About OEA
Endogenous fatty acid ethanolamide produced in the small intestine after oleic acid consumption (e.g., olive oil). Acts as a PPAR-alpha agonist, promoting fatty acid oxidation and energy expenditure. Also activates GPR119 (incretin release) and TRPV1 (vagal satiety signaling). Strong preclinical evidence for appetite suppression, fat metabolism, and anti-inflammatory effects in animal models. However, human clinical evidence is very limited — only a few small trials exist, with no large RCTs or meta-analyses. Not an endocannabinoid (does not bind CB1/CB2 receptors despite structural similarity to anandamide). Generally well tolerated. No established RDA or UL.
What OEA supports
- May reduce appetite via PPAR-alpha activation and vagal satiety signaling
- Promotes fatty acid oxidation in preclinical models
How much OEA to take
The RDA prevents deficiency. The effective range is what clinical trials used to actually move the outcome.
Effective
100–300
mg
100–300 mg/day in supplements. No human dose-finding trials. Doses extrapolated from animal studies and early clinical research.
Clinical evidence
Limited clinical evidence. Endogenous lipid with strong preclinical rationale (PPAR-alpha, appetite regulation) but very limited human RCT data
Examine.com