The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 12 No. 3 • June 2009

Emerging Medicine/Speculation:

The Niacin Flush: Could It Signal a Heart Protective Pathway?

One new research paper1 reports efforts to separate the mechanisms that control niacin flushing from the beneficial antilipolytic effects of niacin in order to get rid of that pesky flushing that some people find annoying or even intolerable. But, not so fast. It may be that the flushing is part of something important that niacin is doing and that you wouldn’t want to get rid of it.

Prostaglandin D2 has been identified as the molecule that naturally causes niacin flushing.1 “Nicotinic acid-mediated stimulation of GPR109A receptors expressed on Langerhans cells in the skin leads to activation of cytosolic phospholipase A2 (cPLA2) and subsequent production and secretion of prostaglandin D (PGD2), which through activation of its own 7TMR [7 transmembrane receptors], leads to cutaneous flushing.”1 The title of a new paper published subsequently2 caught our eye when it implied that prostaglandin D2 produced and released in the heart, where the enzyme responsible for its synthesis is reported to be highly expressed, could be responsible for major heart protective effects. The study reported that glucocorticoids protected rodent hearts from ischemia/reperfusion injury, the protection being a result of increased synthesis of PGD2. Moreover, the “the activation of L-PGDS-mediated production of PGD2 was crucial for the cardioprotection against ischemia/reperfusion conferred by glucorticoid-GR [glucorticoid receptor] signaling.” “Indeed, L-PGDS-knockout mice are prone to develop atherosclerosis when fed a high-fat diet.”2

As the authors2 explain, glucocorticoids are anti-inflammatory and generally repress prostaglandin biosynthesis in most cells. However, in rat heart cells glucocorticoids upregulated the enzyme that synthesizes PGD2 and, in fact, they report, “PGD2 was the most prominently induced prostaglandin in vivo in mouse hearts and in vitro in cultured rat cardiomyocytes after exposure to GR [glucocorticoid receptor]-selective agonists.” Glucocorticoids are released as a natural part of the body’s protective response to a heart attack.

Although the authors of this paper2 did not mention niacin or the fact that the niacin flush is caused as a result of the release in the skin of PGD2, it is hard not to speculate that there may be a connection between the niacin flush and the very substantial (and not entirely explained) cardiovascular benefits of niacin. If PGD2 in skin is released in response to the same signals as that in heart cells, then the skin flush could be a part of a much more important process than the mere sensation of hot and itching skin. Perhaps we shouldn’t get rid of the niacin flush.

Aspirin has been reported to be a possible way to mitigate or eliminate the niacin flush. (It is a known anti-prostaglandin compound.) However, we personally have not noticed any interference between taking a daily 81 mg low dose aspirin and the occurrence of niacin flushing.


  1. Walters et al. Beta-arrestin 1 mediates nicotinic acid-induced flushing, but not its anti-lipolytic effect, in mice. J Clin Invest 119(5):1312-21 (2009).
  2. Tokudome et al. Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase-derived PGD2 biosynthesis. J Clin Invest 119(6):1477-88 (2009).

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