PEA er et naturlig fettstoff som kroppen produserer selv. Det finnes i mange matvarer, særlig i kjøtt, egg, soyabønner og andre peanøtter.

Kroppen produserer PEA spesielt ved betennelsestilstander, og man ser det øker i konsentrasjon lokalt der betennelsen er. PEA har en beskyttende rolle i en betennelsestilstand. Men om betennelsestilstandende vedvarer kan kroppens naturlige PEA brukes opp. Da får man mindre beskyttelse og det blir lettere å få andre plager eller vedvarende plager. Siden det er kosttilskudd må man regne med å bruke minst 2-3 måneder for å se om det hjelper.

PEA gjør at kroniske betennelsesreaksjoner lettere kan brytes slik at regenerering kan inntre igjen. PEA er spesielt interessant fordi det virker på nervetråder. Nevropati (ødelagte nervetråder) er en svært vanskelig tilstand å behandle, men PEA har potensiale til å være både et effektivt og bivirkningsfri tilskudd for å starte regenereringen av nervetråder. PEA er et endokannabinoid-lignende stoff. Man får alle de medisinske og smertedempende effektene lik kannabinoider, men uten noen form for rus.

Her er en lang rekke med studier som har blitt gjort på nevropati og PEA:

Micronized palmitoylethanolamide reduces the symptoms of neuropathic pain in diabetic patients. (Free in PMC)

These results suggest that PEA-m could be considered as a promising and well-tolerated new treatment for symptomatology experienced by diabetic patients suffering from peripheral neuropathy.

Chronic idiopathic axonal neuropathy and pain, treated with the endogenous lipid mediator palmitoylethanolamide: a case collection. (Free in PMC)

In all these patients, PEA reduced pain significantly, without side effects. PEA can be administered in addition to other analgesics, without negative drug-drug interactions, or can be used as a stand-alone analgesic. Due to a favorable ratio between efficacy and safety, PEA should be considered more often as a treatment for neuropathic pain.

Palmitoylethanolamide is a disease-modifying agent in peripheral neuropathy: pain relief and neuroprotection share a PPAR-alpha-mediated mechanism. (Free in PMC)

These results strongly suggest that PEA, via a PPAR- α -mediated mechanism, can directly intervene in the nervous tissue alterations responsible for pain, starting to prevent macrophage infiltration.

Therapeutic utility of palmitoylethanolamide in the treatment of neuropathic pain associated with various pathological conditions: a case series. (Free in PMC)

Probably due to the fact that PEA is an endogenous modulator as well as a compound in food, such as eggs and milk, no serious side effects have been reported, nor have drug-drug interactions.

Palmitoylethanolamide restores myelinated-fibre function in patients with chemotherapy-induced painful neuropathy.

In a severe condition such as painful neuropathy associated with multiple myeloma and chemotherapy, a safe substance such as PEA provides significant restoration of nerve function.

Use of palmitoylethanolamide in the entrapment neuropathy of the median in the wrist.

The data support the hypothesis of protection against inflammatory and neuropathic pain by PEA.

Palmitoylethanolamide in CNS health and disease.

Overall, the integration of these different modes of action allows PEA to exert an immediate and prolonged efficacious control in neuron signaling either on inflammatory process or neuronal excitability, maintaining cellular homeostasis.

Palmitoylethanolamide, a naturally occurring disease-modifying agent in neuropathic pain.

Collectively, the findings presented here propose that palmitoylethanolamide merits further consideration as a disease-modifying agent for controlling inflammatory responses and related chronic and neuropathic pain.

Mast cells, glia and neuroinflammation: partners in crime?

N-Palmitoylethanolamine has proven efficacious in mast-cell-mediated experimental models of acute and neurogenic inflammation.

Her er en rekke studier som har blitt gjort på betennelser og PEA:

Gastric bypass in morbid obese patients is associated with reduction in adipose tissue inflammationvia N-oleoylethanolamide (OEA)-mediated pathways.

Palmitoylethanolamide regulates development of intestinal radiation injury in a mast cell-dependent manner.

Palmitoylethanolamide normalizes intestinal motility in a model of post-inflammatory accelerated transit: involvement of CB₁ receptors and TRPV1 channels.

Palmitoylethanolamide inhibits rMCP-5 expression by regulating MITF activation in rat chronic granulomatous inflammation.

Palmitoylethanolamide and luteolin ameliorate development of arthritis caused by injection of collagen type II in mice.

An apPEAling new therapeutic for ulcerative colitis?

Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-α activation.

A new co-ultramicronized composite including palmitoylethanolamide and luteolin to prevent neuroinflammation in spinal cord injury.

Glia and mast cells as targets for palmitoylethanolamide, an anti-inflammatory and neuroprotective lipid mediator.

New insights in mast cell modulation by palmitoylethanolamide.