PEA

Supports comfort and inflammation balance.
Micronized palmitoylethanolamide, or PEA, is a naturally occurring fatty acid compound. It's found in the body and some foods. When converted to a micronized form, its smaller particles may boost absorption. It’s often used in supplements aimed at supporting comfort, healthy inflammatory responses, and nervous system balance.

About PEA

Understanding Micronized PEA

Palmitoylethanolamide, commonly known as PEA, has piqued interest among researchers and supplement users alike. It interacts with pathways that help manage discomfort and soothe irritated nerves. Your body produces PEA in small amounts, especially when tissues are stressed or inflamed. In its micronized form, absorption is enhanced, akin to how fine sand passes more easily through a sieve compared to larger rocks.

Mechanism of Action

PEA acts by supporting natural cellular responses through proteins known as peroxisome proliferator-activated receptors (PPAR-alpha). These proteins moderate inflammation signals and maintain cellular balance, affecting nerves and immune cells. This function makes micronized PEA a popular choice in formulations for nerve health and overall comfort.

Supplement Uses

You’ll often find PEA in supplements addressing joint comfort, neurological wellness, or recovery routines. It’s sometimes paired with ingredients like curcumin or resveratrol for potential complementary effects. Since your body already produces PEA, it’s a familiar compound for your cells.

Common Applications

Micronized PEA appears in blends for calming overactive nerves, supporting joint and muscle comfort after physical activity, bolstering healthy immune responses, and encouraging balance during periods of stress or discomfort. It also plays a role in gut and brain health.

Practical Considerations

Micronized PEA is typically available as capsules or powders. The micronization process doesn’t alter the substance itself, but it does enhance digestibility. It’s often combined with other bioactive compounds for neurological, gut, or musculoskeletal wellness. Checking if a product uses a micronized form can impact its absorption efficiency.

Related Products

Formulated With

Learn about other ingredients that PEA is used alongside throughout the LVLUP range.

Detailed Information

Scientific Insights into PEA

Palmitoylethanolamide (PEA) is an endogenous N-acylethanolamine involved in the modulation of inflammation and nociplastic processes through activation of nuclear receptors including peroxisome proliferator-activated receptor alpha (PPAR-alpha), as well as indirect modulation of endocannabinoid signaling by FAAH inhibition. Micronization reduces the crystallinity and particle size of raw PEA from several hundred microns to the low-micron range (typically less than 10ÎĽm), substantially increasing its surface area-to-volume ratio for improved gastrointestinal dissolution kinetics and subsequent bioavailability.

Homeostatic Function

PEA acts as an autacoids localis; under conditions of oxidative or inflammatory stress – such as mast cell degranulation or neural irritation – its tissue concentrations rise transiently to facilitate restoration of homeostasis via inhibition of pro-inflammatory cytokine release (including TNF-α and IL-1β) from non-neuronal cells such as microglia and mast cells. Exogenous supplementation with micronized PEA appears to mimic endogenous mechanisms by augmenting local tissue concentrations beyond physiological baseline without disrupting systemic endocannabinoid tone.

Supplement Design Considerations

In supplement design, micronized PEA is favored both for its improved pharmacokinetic profile and its ability to act at multiple tissue sites – including central nervous system glial populations – where unmicronized forms may exhibit limited permeability. Its favorable safety profile supports its inclusion alongside polyphenolic compounds for multifaceted support of neuroimmune interactions implicated in pain modulation, mitochondrial function, cellular recovery post-injury, and homeostatic restoration following acute stressors.