What is PEA？

Palmitoylethanolamide (PEA) is a naturally occurring fatty acid compound that exists endogenously in animal and plant cells. In the human body, PEA is part of the expanded endocannabinoid family and acts as a protective and repair molecule, supporting the body's ability to repair itself and having anti-inflammatory and analgesic effects.

What Does PEA Do?

PEA in its microparticulate form, exhibits a complex mechanism of action that operates through multiple cellular pathways. Let me detail its mechanism comprehensively.

PEA functions primarily as an endogenous lipid mediator, with its microparticulate form offering enhanced bioavailability and cellular penetration. The compound’s primary mechanism involves activation of peroxisome proliferator-activated receptor alpha (PPAR-α), which triggers a cascade of anti-inflammatory and pain-modulating effects. This interaction with PPAR-α leads to the downregulation of pro-inflammatory genes and the reduction of inflammatory mediator production.

At the molecular level, PEA demonstrates what’s known as the “entourage effect” through its interaction with endocannabinoid systems. While it doesn’t directly bind to cannabinoid receptors, it enhances the process of endocannabinoids by inhibiting the enzyme FAAH, which normally breaks down endocannabinoids. This indirect modulation of the endocannabinoid system contributes to its anti-inflammatory and analgesic properties.

The microparticulate form specifically enhances these mechanisms through improved absorption and distribution. The smaller particle size supports and enhances the surface area for biological interactions, leading to better bioavailability and more efficient cellular uptake. This formulation effectively engages cellular targets more effectively, particularly in neuroinflammatory conditions.

Additionally, PEA demonstrates mast cell stabilization properties, reducing the production and presence of pro-inflammatory mediators from these cells. This mechanism is particularly important in neurogenic inflammation and pain conditions. The compound also influences microglial cell function, modulating their activation state and reducing neuroinflammatory responses through direct and indirect pathways.

Recommended Dosage and Usage

• For Pain Relief: Typical dosages range from 300 to 1,200 mg daily, often divided into multiple doses.
• For Neurological Health: Dosages may vary based on clinical guidance and formulation.

Specifications: