The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 4 • August 2015

Author’s Summary of “Why the Niacin Flush May Be
Surprisingly Beneficial to Your Health

i.e. It May Reduce the Risk of Alzheimer’s Disease,
Atherosclerosis, Type II Diabetes, and other
Inflammatory Diseases

“The devil is in the details,
but so are the angels.”

— Sandy Shaw

by Sandy Shaw and Durk Pearson

Here I provide a sketch of what my heavily documented paper on this subject (available at the website) discusses in detail. You can get a pretty good idea of the main dots that are connected by all the technical detail by reading this summary. Durk contributed to this summary on the basis of discussions with Sandy on her paper, not having had the time to read her lengthy paper before the publication of this issue of the Durk Pearson & Sandy Shaw Life Extension Newsletter.

1. Niacin is called “immediate-release” for plain powdered or crystalline niacin that causes the most intense flush; “extended-release” or “prolonged release” niacin is released gradually over time (the flush is attenuated).

2. The niacin flush is caused by an acute release of prostaglandin D2. Prostaglandin D2 is made in the body from arachidonic acid, which is produced by a long chain of biochemical reactions from polyunsaturated fatty acids of the omega-6 class, such as linoleic acid, but not from the omega-3 (fish oils) class of polyunsaturated fatty acids (such as eicosapentaenoic acid, EPA, and docosahexaenoic acid, DHA).

3. Prostaglandin D2 can be released acutely (in a pulse) or chronically (at an elevated level over an extended period of time). The effects of prostaglandin D2 depend critically on whether it is released acutely or chronically. An acutely released pulse of prostaglandin D2 is generally ANTIINFLAMMATORY whereas chronically high release of prostaglandin D2 is generally PROINFLAMMATORY. Other important factors determining whether it is proinflammatory or antiinflammatory include the inflammatory state of the tissue where it is released and the amount that is released.

4. A chronically high level of prostaglandin D2 signaling has been reported in published papers on Alzheimer’s disease as well as in male pattern baldness, the inflammation resulting from gout, and other chronic inflammatory diseases (atherosclerosis, type 2 diabetes, data on these will be discussed in our next newsletter).

5. Whereas a chronically high level of prostaglandin D2 in Alzheimer’s disease is known to be proinflammatory, causing the death of brain cells, we (and possibly others) hypothesize that the pulsatile release of large quantities of prostaglandin D2 (which has a short biological half life) as occurs during the niacin flush might be protective against the adverse effects of chronically high levels of prostaglandin D2 as reported in Alzheimer’s disease and other inflammatory diseases by acting as a signal that attenuates the chronically high level signaling, perhaps by down-regulating its receptors and/or by reducing its chronic production and release.

6. If the pulsatile release of prostaglandin D2 of fast acting (immediate release) niacin is replaced by the longer, more chronic release of prostaglandin D2 by extended release (or prolonged release) niacin, it is more likely to cause inflammatory liver damage, even in patients whose liver can tolerate immediate release niacin in equally high doses.

7. Immediate release niacin combined with a prostaglandin D2 antagonist such as lanoprost that inhibits the niacin flush will not produce the full antiinflammatory benefits of fast acting high dose niacin.

8. The effects of a drug may be related to its time course as well as its dose. Many signaling molecules are released in a pulsatile or cyclic manner, and produce adverse effects when dosed as a prolonged constant level. Examples include insulin, growth hormone, luteinizing hormone, follicle stimulating hormone, thyroid hormone, testosterone, and many others.

9. A signalling molecule released in a pulse into an environment with a high background level of that signalling molecule is likely to be impaired in its ability to transmit the signal carried by the pulse to the tissue where that molecule is part of background “noise.”

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