Italian professors reviewed the impressive body of evidence that the natural compound palmitoylethanolamide (PEA) plays in our cells and tissues. They explain that PEA and related molecules have been known since mid last century as vital molecules.
Among all lipid endogenous molecules, palmitoylethanolamide (PEA) is richly concentrated in the central nervous system (CNS) and is produced by neurons and glial cells. Many experiments point out that PEA can kill pain and protects neurons against damage. They ask more awareness for the role of PEA in diseases as Parkinson’s and Alzheimers, and stated:
“Growing evidence suggest that PEA may be neuroprotective during CNS neurodegenerative diseases.”
Palmitoylethanolamide: quick biological actions and long term resetting
PEA works via many natural mechanisms of action, both via quick and early molecular control, (via the Ca(+2)-activated intermediate- and/or big-conductance K(+) channels) and via long term resetting of nuclear receptors (PPAR).
They pointed out that the gene transcription-mediated mechanism of PEA helps to understand the long-term anti-inflammatory effects of this compound.
In their article they also highlighted the emerging evidence for PEA’s therapeutic effects in neurodegenerative diseases.
Recommendations for the use of PEA formulations
Palmitoylethanolamide should best be administered either as the Italian PEA tablets, based on PEA-um or PEA-m, or by administrating the Dutch PEA capsules containing PEA-opt. Dutch capsules do not contain any chemical excipients and are 100% pure in vegetarian capsules.
Only for these quality ormulations long term safety and efficacy data gathered under the supervision of MDs are available. And only for these formulations (PEA-um, PEA-m and PEA-opt) there are currently data available proving that after intake PEA levels in the body significantly rise. Such data do not exist for me-too PEA formulations.
Mattace Raso G, Russo R, Calignano A, Meli R. Palmitoylethanolamide in CNS health and disease. Pharmacol Res. 2014 Aug;86:32-41. doi: 10.1016/j.phrs.2014.05.006. Epub 2014 May 17.