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During the ‘60s, some papers come out confirming the anti-inflammatory effects in animal models. And in an important turn of events, a team led by Dr. Udenfriend discovered that PEA occurs naturally – and at high levels – in a [https://pubmed.ncbi.nlm.nih.gov/14284696/ number of mammalian organs.] So we realized that not only does PEA lessen inflammation - but our own bodies and brains also produce it as an internal regulator of inflammation.  It wasn’t until the ‘70s that the first serious clinical trials emerged – and it happened behind the Iron Curtain. In Czechoslovakia, a nation that no longer exists, a pharmaceutical company named SPOFA (United Pharmaceutical Works) developed a PEA drug called Impulsin.   To test PEA, they turned to the gigantic Skoda factory, a manufacturer of cars, tanks, and industrial equipment, that employed a huge workforce. SPOFA ran several clinical trials with the factory workers as well as the military and civilian populations. All in all, 2000 adults and 400 children entered these trials. Administered in a double-blind manner, the gold-standard of modern medical trials, all of the results pointed in the same direction: PEA was safe and possessed a clear efficacy in treating respiratory infections. It [https://link.springer.com/article/10.1007/BF00560353 reduced ]the incidence of fever, headache, and sore throat. And furthermore, according to a [https://pubmed.ncbi.nlm.nih.gov/392005/ key researcher], "Nо siɗe effects ѡere registered аfter sevｅral ｙears ߋf [https://spensary.com clinical testing] of Impulsin&nbѕp;іn military аnd [http://energizecbd.co.uk civilian communities]."  It worked! It was proven in large trials. But then occurred, what is known in endocannabinoid circles, as the Silent Gap period.   From the early 80’s, the work of SPOFA faded away, lost behind the Iron Curtain. Furthermore, scientists could not figure out the mechanism of action for PEA and so interest waned because no one knew how it work. PEA was labeled as an ‘unspecific immune enhancer’ and the scientific community lost interest.  Until 1993, when our hero, Dr. Rita Levi-Montalcini entered the PEA stage. And here is where our geopolitics get too real. Earlier in her life, as a Jewish person in Mussolini’s Italy, Dr. Levi-Montalcini lost her laboratory. Forced to flee to Florence, she set up a workstation in the basement of the house where she landed. Here she continued her work studying the early development of organisms, one of the most challenging problems in all of science. The work she performed in that basement led her to discover nerve growth factor (NGF) – one of the most important neurochemical findings of the century - and whose discovery led to her sharing the Nobel Prize in 1986.  How Does PEA Work? In a [https://pubmed.ncbi.nlm.nih.gov/7505999/ famed 1993 paper,] Dr. Levi-Montalcini and her team proposed that PEA works via its control of mast cells – an important type of white blood cell responsible for releasing histamine, a neurotransmitter involved in the inflammation response and most often associated with allergies. Mast cells also respond to the healing of wounds, the growth of new blood vessels, defense against pathogens, and the rallying of the immune response. For PEA’s relationship to mast cells, they called it the ALIA hypothesis.  As this [https://www.omicsonline.org/open-access/professor-rita-levi-montalcini-on-nerve-growth-factor-mast-cells-and-palmitoylethanolamide-an-endogenous-anti-inflammatory-and-analgesic-compound-2167-0846.1000114.php?aid=12372 review of her work] summarizes, "Autocoid or [https://mjcbdd.com autacoid] іs a rathеr old-fashioned term foг a [http://jaydesvaporlounge.com regulating] molecule, [https://www.artisanvaporcompany.com locally produced] and locally exerting іts [https://supremecbd.uk/collections/cbd-edibles actions]... In this case PEA is [https://woodstockhempcompany.com formed locally] when [https://meleedose.com inflammation] or neurogenic pain occur, ɑnd [http://hempfullynatural.com increased] [https://www.goodrx.com PEA concentrations] are based оn the [https://tclye.sma-brassel.de body-own mechanisms] to cope wіtһ pain and [https://thedopestshop.com inflammation]. 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As [https://youtu.be/wPoHFIrIHC0 Dr. Piomelli relates], they wanted another endocannabinoid-like molecule that wouldn’t have the same effects. So they chose PEA, mostly because they knew it didn’t bind to the CB1 or CB2 receptor thought to be behind the pain relieving effects. But as their paper pointed out, they were quite surprised to find out that PEA had profound pain-relieving effects as well.  This result intrigued them. If PEA doesn’t bind to the classic cannabinoid receptors CB1 and CB2, then how does it do what it does?  The researchers reasoned that a sister molecule known as oleamide (OEA) worked via the PPARα receptors. And what’s special about these PPARα receptors is that they’re nuclear receptors. They live, not on the surface of the cell, but on the surface of its nucleus – the cellular control center that contains the DNA. Activating these nuclear receptors altered genetic transcription and caused the cell to produce a host of new proteins with their own downstream effects. Dr. Piomelli worked with his student Dr. Jesse LoVerme to study PEA’s mechanism of action. By 2005, they found that [https://pubmed.ncbi.nlm.nih.gov/15963531/ the PPARα receptor mediated the anti-inflammation effects of PEA ]completely and by 2007, they determined that this relationship also [https://pubmed.ncbi.nlm.nih.gov/16997973/ mediated the anti-pain effects]. It was a huge breakthrough.  Their research confirmed that PEA occurs at high levels in many areas of the body – especially the skin – and that when PEA levels are low, the body can be helped by adding more PEA from outside sources. 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What-is-PEA Html