Palmitoylethanolamide (PEA) is a naturally-occurring anti-inflammatory and analgesic fatty acid amide. PEA is formed locally at sites of tissue inflammation as a defense and repair reaction. It modulates mast cell activity (hyperactive in inflammatory conditions) and activated glia cells (non-neuronal brain cells).
An interesting paper on palmitoylethanolamide (PEA) was published recently in the Journal of Pain Research. The author, Jan Keppel of the University of Witten/Herdecke in Germany, summarizes the advances in the scientific understanding of PEA and related compounds that occurred over the last 60 years or so, and makes a number of interesting observations, though some of the conclusions reached may be challenged.
Check out the video abstract below for a quick rundown, or read the full text here.
The history of PEA is an interesting and convoluted one, and the timeline presented in the study above looks something like this:
While the history lesson is certainly illuminating, the central thesis (that a lack of understanding held PEA back from clinical acceptance) is less well-supported.
The author states that:
“The paper demonstrates that plausible explanations for the mechanism of action of drugs are required before a treatment concept can be explored in more detail in science and in the clinic, and before it can be accepted. Efficacy of a compound alone will not be enough to convince the scientific community.”
The corollary of the author’s position is that scientific understanding of a drug’s mechanism of action is a prerequisite of clinical acceptance, which is at odds with a critical view of pharmaceutical history. A number of drugs have been widely used, despite patchy or non-existent scientific understanding of how they exerted their effects.
Valproic acid, for example, the most popular anti-epileptic drug in the world, has a complex pharmacodynamic profile that is still ill-understood today.
Perhaps the most apposite example here would be the class of drugs known as the fibrates. They have been in clinical use as hypolipidemic agents since the 1930s, though it wasn’t until the 1990s that it was discovered that (like PEA) they are PPARα agonists.
Further, the mooted theory offers a somewhat reductive understanding of clinical acceptance, which is subject to many more pressures and influences than the author acknowledges.
– Painkillers are among the most popular drugs on the market, both over-the-counter and by prescription. Drug companies have had a legal monopoly over the market since the criminalization of traditional pain-killing plants (like hemp, coca, and opium poppies).
– COX-inhibiting NSAIDs have been the go-to anti-inflammatory and analgesic pharmaceuticals, and the focus of pharmaceutical thinking, since PEA was first discovered.
– The cost of bringing a new drug to market can easily exceed a billion dollars and take over a decade.
– The difficulty in patenting natural products offers a strong disincentive for drug companies to bring PEA-based products to market, irrespective of efficacy.
– In the US particularly (thanks to a combination of private healthcare and heavy advertising) many patients now expect to be treated with the drugs of their choice.
While the paper, through the timeline it establishes, demonstrates a clear ‘boom’ in the number of papers published about PEA subsequent to its identification as a PPARa agonist, it fails to demonstrate that identification as a causative factor for either prior lack of clinical acceptance or subsequent increase in availability (through release as a nutraceutical).
Though the sociological conclusions may be a bit shaky, the concluding remark seems well-justified: that the available body of evidence warrants much wider use of this compound. And that seems likely to happen, thanks to its release in Europe as “Normast” and “PeaPure”, and worldwide as a component of the sports-injury supplement “Achilles” by Antaeus Labs.
© Total Flex Blog 2013