From monosaturated dietary fatty acid, oleic acid, the body can synthesize fatty acids ethanolamides such as PEA (Palmitoylethanolamide) and OEA(oleoylethanolamide).
These fatty acid amides have demonstrated, mostly in animal research for OEA and broadly in human research for PEA, being effective as dietary supplement additions in battling obesity and its untoward sequelae.
OEA exposure has been shown to stimulate fatty acid uptake, lipolysis, and β-oxidation, and also promote food intake control, as well as for its positive and protective actions on the pancreatic beta cells, decreasing inflammation and body weight.
Palmitoylethanolamide, PEA, is produced in the body naturally to combat pain and inflammation. Many animals and plants also produce PEA. It also supports our endocannabinoid system helps support our anti-hunger hormone leptin and has significant immune-enhancing properties.
Considering that obesity is an endocrinopathy, PEA’s influence on a number of the metabolic pathways of WAT makes this natural ingredient to be available in higher amounts as a supplement than what the body can create or what the diet can offer.
OEA has ideal compatibility and physiological synergy with its cannabinoid enhancing cousin “PEA” as well as its ease in designing expanded applications with its similar physical properties that make them both excellent for great application versatility from encapsulation to use in functional foods and beverages.
The right kind of fats and fatty acids are essential nutritional components for healthy brain aging–actually at any age. The human brain is nearly 60 percent fat. We’ve learned in recent years that fatty acids are among the most crucial molecules that determine your brain’s integrity and ability to perform.
High carbohydrate diets that sacrifice fats are ironically the antithesis for brain health.
This is an additional reason to include OEA and PEA as part of a smart overall lipid strategy for brain and neurological health.
RECOMMENDED REFERENCES
Ottaviani E, Malagoli D, Franceschi C. The evolution of the adipose tissue: a neglected enigma. Gen Comp Endocrinol. 2011;174:1–4. [PubMed] [Google Scholar]
Bernlohr DA, Jenkins AE, Bennaars AA. Adipose tissue and lipid metabolism. In: Vence JE, Vence D, editors. Biochemistry of lipids, lipoproteins and membranes. 4th ed. Elsevier Science: Amsterdam; 2002. pp. 263–89. [Google Scholar]
Ahima RS, Flier JS. Adipose tissue as an endocrine organ. Trends Endocrinol Metab. 2000;11:327–32. [PubMed] [Google Scholar]
Bès‐Houtmann S, Roche R, Hoareau L et al. Presence of functional TLR2 and TLR4 on human adipocytes. Histochem Cell Biol 2007; 127: 131– 137.
Hoareau L, Ravanan P, Gonthier MP et al. Effect of PEA on LPS inflammatory action in human adipocytes. Cytokine 2006; 34: 291– 296.
Coenen KR, Gruen ML, Chait A, Hasty AH. Diet‐induced increases in adiposity, but not plasma
Xu H, Barnes GT, Yang Q et al. Chronic inflammation in fat plays a crucial role in the development of obesity‐related insulin resistance. J Clin Invest 2003; 112: 1821– 1830.
Weisberg SP, McCann D, Desai M et al. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 2003; 112: 1796– 1808.
Gonthier MP, Hoareau L, Festy F et al. Identification of endocannabinoids and related compounds in human fat cells. Obesity (Silver Spring) 2007; 15: 837– 845.
