The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 5 • September 2015

by Sandy Shaw

A paper (Shimada, 2014) Durk found in a search provides an excellent summing up of how inflammatory prostaglandins, products of the omega-6 fatty acids through their conversion to arachidonic acid, are critically involved in epilepsy and what takes place during a seizure, whether it is tonic-clonic or temporal lobe epilepsy (the latter may have no convulsive features at all, resulting in sometimes subtle changes in mental state, to a sort of disassociated state, akin to the infamous “split personality” of schizophrenia, which may make it difficult to diagnose).

The paper describes the process as follows: “In addition to inflammatory cytokines, prostaglandins (PGs) are major factors that stimulate inflammation processes. PGs are known to markedly increase following seizures and they contribute to epileptogenesis and reduction in seizure threshold.” “The enzyme cyclooxygenase (COX) converts arachidonic acid to PGH2 and the specific PG synthase converts PGH2 to various PGs such as thromboxane A2, PGF2alpha, PGE2, PGI2, or PGD2.”

“Because PGs play an important role in inflammatory responses, the function of PGs in epileptogenesis have been studied for a considerable amount of time” One thing the researchers pointed out is the discrepancy in effects of COX inhibitors in the treatment of epilepsy, with some having positive effects, while others can even increase damage and mortality. The reason for this discrepancy is, I believe, due to failing to recognize that the release of prostaglandins in pulses can be antiinflammatory (with PGD2 being an excellent example, discussed at length in my niacin paper) while their release over an extended period of time is likely to be proinflammatory. So the time course of the release of prostaglandins resulting from the inhibition of COX is not being considered, so far as I have seen in the literature on prostaglandins. As prostaglandins are crucially involved in inflammatory diseases, which include just about every important disease afflicting man, this time course of the release of prostaglandins by COX inhibitors is itself critical to the outcome of treatment.

This information fits nicely into the paper I wrote on the niacin flush (which is caused by a pulsatile release of a particular prostaglandin, prostaglandin D2 (PGD2) and which has powerful antiinflammatory effects) and I have added it as part II of my niacin flush/inflammatory diseases paper at the Life Enhancement website (See “Why the Niacin Flush May Be Surprisingly Beneficial to Your Health” in the August 2015 issue.)

The researchers go on in their analysis of epilepsy: “...PGD2 and PGF2alpha can exhibit anticonvulsive functions. PGD2 synthase H-PGDS knockout (KO) mice [they cannot make PGD2] or PGD2 receptor DP1R-KO mice showed more severe seizures after pentylenetetrazol (PTZ) treatment than wild type mice whereas deficiencies of the other synthase L-PGDS or receptor DP2R did not alter seizure severity.” “By contrast, PGE2 mainly functions as a promotor of epileptogenesis and ictogenesis.” “...COX2 coupled PGE2 production can promote seizures through mechanisms that drive epileptogenesis.”

It is very interesting to note that PGD2 can act as a counter-regulatory factor to PGE2 but only when it is released in pulses, as occurs during the niacin flush. See my niacin flush paper PART I near the start of the text, just after the discussion of “What Is the Niacin Flush.”

Prostaglandin D2 release as an antiinflammatory pulse can be effected by a number of dietary supplements, including curcumin (and other constituents of turmeric root), niacin (in the immediate release form that causes flushing), selenium (shunts arachidonic acid production to antiinflammatory prostaglandins such as PGD2), EGCG (inhibits PGE2 production, possibly by releasing PGD2 in a pulse), ginger, sulforaphane (as found in cruciferous vegetables; stable metabolites with potent antiinflammatory activity also contained in the herb Moringa oleifera). These are just a few examples.

  • Shimada, Takemiya, et al. Role of inflammatory mediators in the pathogenesis of epilepsy. Mediators Inflamm. 2014;2014:901902. doi: 10.1155/2014/901902. Epub 2014 (Aug 13, 2014).
  • Shaw. Why the Niacin Flush May Be Surprisingly Beneficial to Your Health. Part I, (Aug. 2015), free access at and Part III (Sept. 2015), the discussion of epilepsy.

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