Oleoylethanolamide

Oleoylethanolamide (OEA) is a fatty acid derivative that is involved in regulating hunger. High doses of OEA in supplemental form can inhibit hunger, and OEA is one of the reasons that dietary fatty acids can be seen as 'satisfying'.

Oleoylethanolamide also has fat burning effects in the liver and is potentially a Nootropic by increasing dopamine and oxytocin levels in the brain and offering neuroprotection (protecting brain cells).

It is commonly used with Tetradecyl Thioacetic Acid as a fat burning combination.

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Effects are seen at doses at or higher than 10mg/kg bodyweight. Higher doses should be safe as it is an instrinsic compound, but this has not been directly studied.

Edit1. Sources and Pharmacology

Oleoylethanolamide (Henceforth OEA) is a derivative of anandamide, an endocannabinoid involved in food regulation. OEA retains the anorectic properties of anandamide^[1] while also being a stimulator of lipolysis via PPAR-alpha agonism.

Its main effects in the body can be seen as either acting vicariously through PPAR-alpha agonism or through Vanniloid TRPV1 antagonism.^[2]

Edit2. Mechanisms of Satiety

OEA can induce satiety by a variety of mechanisms deemed as either hepatic, neural, or peripheral.^[3]

It is synthesized in vivo from dietary fatty acids, as when fat is packaged into chylomicrons (during intestinal absorption) they induce secretion of OEA as they are being digested.^[4]

It has been shown to increase Oxytocin levels in the brain via PPAR-alpha mediated mechanisms^[5] and potentially increase extracellular dopamine levels.^[6] Its periphery effects include modulating Ghrelin and Peptide YY levels which, via the paraventicular nuclei (PVN), can also reduce food intake.^[1]

Edit3. Mechanisms of Fat loss

References

1. Serrano A, et al. Oleoylethanolamide: effects on hypothalamic transmitters and gut peptides regulating food intake. Neuropharmacology. (2011)
2. Galan-Rodriguez B, et al. Oleoylethanolamide exerts partial and dose-dependent neuroprotection of substantia nigra dopamine neurons. Neuropharmacology. (2009)
3. Food intake is inhibited by oral oleoylethanolamide
4. Thabuis C, et al. Biological functions and metabolism of oleoylethanolamide. Lipids. (2008)
5. Gaetani S, et al. The fat-induced satiety factor oleoylethanolamide suppresses feeding through central release of oxytocin. J Neurosci. (2010)
6. Murillo-Rodríguez E, et al. Administration of URB597, oleoylethanolamide or palmitoylethanolamide increases waking and dopamine in rats. PLoS One. (2011)
7. Rondanelli M, et al. Administration of a dietary supplement ( N-oleyl-phosphatidylethanolamine and epigallocatechin-3-gallate formula) enhances compliance with diet in healthy overweight subjects: a randomized controlled trial. Br J Nutr. (2009)

(Common misspellings for Oleoylethanolamide include oleoilethanolamide, oloylethanolamide, OAE, EOA oleicethanolamide)

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