The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 8 • December 2015

Prostaglandins as Major Factors in Inflammation, Both as Pro-inflammatory and Anti-Inflammatory

Sandy Studies the Niacin Flush and Learns a Lot About the Regulation of Inflammation by Prostaglandins

When Sandy wrote her paper on the niacin flush (see the July, August, and September issues of the Durk & Sandy newsletter at the Life Enhancement website (, her purpose was to find out whether it was a good idea to eliminate the niacin flush in order to make niacin supplementation more pleasant for those who didn’t like the flush. It was not self-evident whether the flush played a part in the protective effects of niacin (the immediate release form that causes flushing) or whether it could be suppressed without reducing the very powerful beneficial effects of niacin in protecting against non-fatal heart attacks (the most common kind) and reducing the risk of a variety of diseases associated with dyslipidemia and inflammation, such as diabetes, cardiovascular disease, non-alcoholic fatty liver disease, and many others.

In the course of writing the paper, she learned a lot about how the niacin flush works (a major effect is the pulsatile release of prostaglandin D2, which suppresses the inflammatory prostaglandin E2, which appears to be a factor in every inflammatory disease. She also learned that finding out what was known at any particular time was very difficult, requiring many extensive literature searches, due to the disseminated understanding of a particular aspect of science, the “balkanization” of science (where many areas of science are not very well connected to other areas), and the level of understanding differing from one scientist to another. Sometimes it seemed that a particular fact that had been discovered years ago had to be rediscovered due to a sort of failure of the earlier knowledge to be kept alive in ongoing discussions. This is why the disclaimer “we are the first to discover what we report in this paper, to the best of our knowledge” has become ubiquitous, because you can never be entirely sure.

A good example of the last point, that you can find work that predates new research and anticipates its findings is the following: Sandy just found a 1998 paper (Prasad, 1998), a review that proposed that “PG [prostaglandin] induced elevation of Abeta [amyloid beta] may lead to an increased binding of Abeta...” and they report their prior work in which they show that “prostaglandins (PG), which are [] released during inflammatory reactions, cause rapid degenerative changes in differentiated murine neuroblastoma (NB) cells in culture.”

Sandy became very interested in prostaglandins D2 and E2 and their apparent ubiquitous appearance in inflammatory diseases. It seemed that the papers she read did not distinguish between the PULSATILE release of PGD2, which appeared to be an important anti-inflammatory signal, as compared to CHRONIC release of PGD2, which was pro-inflammatory, as she learned was the case in Alzheimer’s disease. Even now, this distinction does not seem to be mentioned in papers.

A recent paper (Das, 2011) describes inflammation and its resolution as follows: “During the early phase of inflammation, COX-2 derived PGs [prostaglandins] and TXs [thromboxanes] and lipoxygenase-derived LTs [leukotrienes] initiate exudate formation and inflammatory cell influx. TNF-alpha causes an immediate influx of neutrophils concomitant with PGE2 [prostaglandin E2] and LTB4 [leukotriene B4] production, whereas during the phase of resolution of inflammation, an increase in LXA4 [lipoxin A4, a pro-resolution molecule derived from arachidonic acid], PGD2 [prostaglandin D2] and its product 15deoxydelta12-14PGJ2 formation occurs that induces resolution of inflammation with a simultaneous decrease in PGE2 synthesis that stops neutrophil influx and enhances phagocytosis of debris.”


  • Das. A defect in the activities of delta6 and delta5 desaturases and pro-resolution bioactive lipids in the pathobiology of non-alcoholic fatty liver disease. World J Diabetes. 2(11):176-88 (2011).
  • Prasad, Hovland, La Rosa, et al. Prostaglandins as putative neurotoxins in Alzheimer’s disease. Proc Soc Exp Biol Med. 219:120-5 (1998).

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