| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Fat Oxidation In animal models, OEA promotes fatty acid oxidation through PPARα activation, the same nuclear receptor targeted by fibrate drugs. Rodent studies show increased lipid metabolism markers following OEA administration (PMID:25832022). No human supplementation data available. | Improves (the measure goes up) | Small effect | 2 studies | |||
Supplement
Oleoylethanolamide (OEA) is a fat-derived molecule your gut makes after a meal, where it activates a receptor called PPARα to help signal fullness and guide how the body handles fat. People mostly look at it for appetite, and the evidence is limited: animal studies consistently found less food intake, while in people, higher OEA after gastric bypass surgery was linked to metabolic improvements. No human trials have tested OEA supplements for appetite, so those findings are mostly from animals and observation rather than supplementation.
Sources: PMID 25413674; PMID 25832022
- Updated
- How we grade
- 12 studies cited
- Best evidence
- Grade C
- Conditions studied
- 4
- Outcomes
- 8
- Graded outcomes
- 0017
Evidence by condition
- Strong
- Moderate
- Limited
- Very limited
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Appetite Reduction Consistently reduces food intake across multiple animal species via vagal afferent signaling and PPARα activation. Human observational studies link post-bariatric surgery OEA increases to metabolic improvements (PMID:30702457, PMID:25413674), but direct oral supplementation has not been validated in human trials. | Improves (the measure goes down) | Moderate effect | 4 studies | |||
Studies that measured appetite reduction
| ||||||
General
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Pain Sensitivity Circulating OEA levels are associated with individual differences in human pain sensitivity in a quantitative sensory testing study (PMID:41324391). Animal studies show OEA activates TRPV1 receptors (PMID:18261748) and PPARα blockade exacerbates inflammatory pain (PMID:34072060). Human evidence is correlational, not interventional. | Improves (the measure goes down) | Small effect | 4 studies | 100 people | ||
Studies that measured pain sensitivity
| ||||||
| Neuroprotection Preclinical studies demonstrate anti-inflammatory and neuroprotective effects via PPARα activation in brain tissue, studied in rodent models of Parkinson's disease, stroke, and neuroinflammation. FAAH inhibition (which raises endogenous OEA) attenuates TLR-induced neuroinflammatory gene expression in animal models (PMID:28237711, PMID:34265624). | Improves (the measure goes up) | Small effect | 3 studies | |||
Studies that measured neuroprotection
| ||||||
| Adipose Tissue Inflammation A clinical observational study found gastric bypass in morbidly obese patients was associated with reduced adipose tissue inflammation via OEA-mediated pathways (PMID:25413674). Plasma OEA levels inversely correlate with markers of metabolic dysfunction (PMID:29935920). No direct OEA supplementation trials in humans. | Improves (the measure goes down) | Small effect | 3 studies | 50 people | ||
Studies that measured adipose tissue inflammation
| ||||||
| Intestinal Inflammation Preclinical evidence suggests OEA reduces intestinal inflammation via PPARα-dependent mechanisms. OEA is produced endogenously in the gut after fat consumption and may modulate local immune responses. Evidence is limited to animal and in vitro models. | Improves (the measure goes down) | Small effect | 2 studies | |||
Body Composition
- Fat Oxidation: improves
Cardiovascular Health
- Intimal Hyperplasia: changes; see studies
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Intimal Hyperplasia A single animal study demonstrated that OEA suppresses intimal hyperplasia after balloon injury in rats through the AMPK/PPARα signaling pathway (PMID:29305859). No human data available for this cardiovascular outcome. | Changes; see studies | Small effect | 1 study | |||
Studies that measured intimal hyperplasia | ||||||
Barth Syndrome
- Mitochondrial Function (Barth Syndrome): improves
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Mitochondrial Function (Barth Syndrome) An in vitro study found OEA treatment of Tafazzin-deficient lymphoblasts (a model of Barth syndrome) improved cell growth, mitochondrial morphology, and mitochondrial dynamics (PMID:35676289). No in vivo or clinical data available. | Improves (the measure goes up) | Small effect | 1 study | |||
Studies that measured mitochondrial function (barth syndrome) | ||||||
Key findings
- Appetite ReductionImproves (the measure goes down)
- Pain SensitivityImproves (the measure goes down)
- NeuroprotectionImproves (the measure goes up)
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- Grade C
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Studies cited
12 studies from PubMed
- The contribution of baseline circulating endocannabinoids to individual differences in human pain sensitivity: a quantitative sensory testing study.
- N-oleoylethanolamide treatment of lymphoblasts deficient in Tafazzin improves cell growth and mitochondrial morphology and dynamics.
- Pharmacological Blockade of PPARα Exacerbates Inflammatory Pain-Related Impairment of Spatial Memory in Rats.
- N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARα.
- Oea Signaling Pathways and the Metabolic Benefits of Vertical Sleeve Gastrectomy.
- N-oleoylethanolamide suppresses intimal hyperplasia after balloon injury in rats through AMPK/PPARα pathway.
- Profiling plasma N-Acylethanolamine levels and their ratios as a biomarker of obesity and dysmetabolism.
- Pharmacological inhibition of FAAH modulates TLR-induced neuroinflammation, but not sickness behaviour: An effect partially mediated by central TRPV1.
- Gastric bypass in morbid obese patients is associated with reduction in adipose tissue inflammation via N-oleoylethanolamide (OEA)-mediated pathways.
- Synthesis and evaluation of fatty acid amides on the N-oleoylethanolamide-like activation of peroxisome proliferator activated receptor α.
- Actions of 3-methyl-N-oleoyldopamine, 4-methyl-N-oleoyldopamine and N-oleoylethanolamide on the rat TRPV1 receptor in vitro and in vivo.
- 'Entourage' effects of N-palmitoylethanolamide and N-oleoylethanolamide on vasorelaxation to anandamide occur through TRPV1 receptors.