Palmitoylethanolamide, or PEA, is a compound which has analgesic, anti-inflammatory and neuroprotective effects. PEA is found in a number of common foods, including cow’s milk, breast milk, beans, peas, tomatoes, alfalfa, corn, soy lecithin and peanuts.
Neuropathic pain, caused by the compression of nerves leading to nerve inflammation, is ordinarily difficult to treat. Such pain is often shooting, radiating, tingling stabbing or burning. In many instances, people experience ongoing pain even after the source has been removed. However, PEA is particularly effective in treating trapped nerve pain, such as sciatica and carpal tunnel syndrome.
In addition, PEA’s anti-inflammatory action may be useful in treating a range of other conditions, such as osteoarthritis, shingles, peripheral neuropathy, lower back pain, fibromyalgia, depression, autism and colds and flus.
PEA vs CBD oil
The use of cannabinoids (CBD) faces legality issues in many parts of the world and this has opened up the space for alternative anti-inflammatory pain management solutions such as palmitoylethanolamide (PEA) to come to the fore. The THC component of cannabinoids are the most effective for pain management but many users do not tolerate the ‘high’ or ‘stone’ that comes with the THC containing oils.
PEA is produced in the body as a biological response and as a repair mechanism for inflammation. It is a simple fatty acid amide that is structurally related to the endogenous cannabinoid transmitter, anandamide (AEA). AEA is associated with regulating pain and the more AEA in the bloodstream, the less discomfort a person may feel. PEA has numerous clinical studies demonstrating its potential as an effective and safe anti-inflammatory, analgesic and tissue-protective nutrient.PEA is essentially an endogenously produced cannabimimetic compound.
However, this does not mean that PEA is just an alternative. In places where cannabinoids face no regulatory issues, PEA can be used in combination with CBD to boost health benefits.
Cannabinoid type 2 (CB2) receptors are almost solely expressed in the microglia of the central nervous system. When you stimulate these receptors you promote neuroprotection, the release of anti-inflammatory cytokines and pain relief. PEA does not directly bind to these cannabinoid receptors it works by enhancing CB2 receptor expression.
PEA further information
Around 50% of people with diabetes have some peripheral neuropathy, which can affect sleep and daily activities. Studies indicate that PEA can significantly improve this.
PEA accumulates in brain tissue following injury, leading researchers to hypothesise that it may have neuroprotective properties. Several preclinical studies support this, indicating that it may assist with Alzheimer’s disease, and may be able to reduce some Parkinson’s disease related motor deficits, as well as and behavioural, biochemical and functional changes triggered by traumatic brain injury.
In clinical trials, the daily dosage of PEA has ranged from 300-1200mg for chronic pain, and up to 1800mg for acute colds and flu.
It is suggested that an initial dose of 600-1200mg for 3-4 weeks, followed by a maintenance dose of 300-600mg may be appropriate for chronic pain. Smaller doses of PEA can be used with liposomal forms due to the increased absorption and better penetration into the cells. Liposomal PEA dosages of 300-600mg for 3-4 weeks, followed by a maintenance dose of 150-300mg may be appropriate for chronic pain.
As PEA is a fat soluble compound, consuming it with a fat-containing meal may enhance its absorption.
PEA does not have any known contra-indications and has been found to be highly tolerable.