Palmitoylethanolamide And Endocannabinoids| Therapeutic Effect

Palmitoylethanolamide And Endocannabinoids

Palmitoylethanolamide (PEA)
Palmitoylethanolamide (PEA) is a fatty substance found in living organisms and certain food items. It acts as a transmitter which enables the transfer of information between cells in the body.

Early Studies

The earliest reports of Palmitoylethanolamide (PEA) date back to 1943. Alvin F. Coburn and Lucile V. Moore discovered a negative relationship between the consumption of egg and the reduced occurrence of rheumatic fever among poverty-stricken children. In a later study, Coburn and Moore confirmed that enriching the diet of toddlers with egg yolk will reduce the toddler’s risk of developing rheumatic fever.

In 1957, scientists at Merck Sharp & Dohme were able to isolate a therapeutic compound, soon to be known as palmitoylethanolamide (PEA), from soybean lecithin, peanut meal, and egg yolk. The following years, the structure of PEA was established, and its anti-inflammatory properties were demonstrated.

The pharmaceutical industry Spofa introduced Impulsin® (tablets of PEA), in 1970, in Czechoslovakia which was used to prevent and treat acute respiratory infections in children and adults.

Further research into PEA was abandoned and it was not until the 1990’s that the Nobel prize winner, Rita Levi-Montalcini drew the attention of researchers back into PEA. The research conducted by Levi-Montalcini showed that PEA is an intraoral regulator of inflammation. In other words, PEA could reduce pain and inflammation through oral consumption.

At the same time, the role and individual elements of the endocannabinoid system was also being researched

Relation Between Endocannabinoid System And Palmitoylethanolamide (PEA)

In short, the endocannabinoid system is a collection of endocannabinoids and cell receptors (primarily CB1 and CB2). Endocannabinoids bind to the cell receptors to transfer a message in our central nervous system. PEA does not show a significant affinity towards cannabinoid receptors.

Instead, PEA controls inflammation and other immune functions through other receptors such as TRPV1 receptors. The best-documented mechanism of action of PEA is agonist activity against PPARα receptors. The role of these receptors is to be a key messenger in various inflammation and pain signaling pathways in the central nervous system and peripheral tissues. In addition, PPARα receptors play a role in the metabolism of fatty acids, synthesis of endocannabinoids and regulation of dopamine and acetylcholine in the brain.

RELATED: THC and CBD, What Else Interacts With CB1 Cannabinoid Receptors?

Relevance & What It Means?

An increasing number of preclinical data outlined the significant therapeutic potential of PEA. Particularly in pain, inflammation, neurodegenerative disorders, traumatic brain injury or ischemia, multiple sclerosis and amyotrophic lateral sclerosis.

This means that people may start consuming PEA products instead of CBD and THC products to treat symptoms of many illnesses and diseases.

Since the 1990s, a number of such experiments have been reported, ranging from small observational studies with a limited number of patients to randomized clinical trials to check the effectiveness of PEA in various chronic pain syndromes. Positive or at least promising results have been reported for peripheral neuropathic pain (diabetic pain, lower back pain, carpal tunnel syndrome) and pain in central neuropathies.


It’s difficult to judge whether PEA is a helpful substance in the treatment of pain. Clinical trials do not show consistent results and as a result, we cannot be 100% sure. In addition, the experiments do not check the safety of PEA in chronic therapy. We know that PEA is easily broken down by digestive enzymes and is often consumed orally. However, another form of the substance could be developed in the future to increase the probability of obtaining a greater therapeutic effect, potentially replacing THC and CBD products.


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