The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 11 No. 2 • March 2008

Prevention of HDL Oxidation that Is
Associated with Loss of HDL Atheroprotection

Much has been published of late on the fact that HDL levels alone do not tell you how much protection HDL is affording your cardiovascular system. Under inflammatory conditions and under oxidative stress, the main HDL protein, apolipoprotein A-I, can be modified by reactive oxygen species, and HDL becomes proatherogenic rather than atheroprotective.1

That’s why we were so excited by a recent paper showing that albumin-bound quercetin repairs vitamin E oxidized by apolipoprotein radicals in native HDL3 and LDL2. As the authors explained, the oxidation of tryptophan and tyrosine by hydroxyl radicals may be involved in the myeloperoxidase-induced loss of apoAI structure and activity.2 Vitamin E can repair, but incompletely, the apoAI damage by reduction of tyrosine radicals but not tryptophan radicals. The researchers then found that quercetin bound to albumin, its physiological carrier, “can indeed repair the portion of [tryptophan] and [tyrosine] radicals generated in apoAI, apoAII, and apoB not repairable by [vitamin E].” In fact, it also effectively repairs the tocopheryl radicals formed when the vitamin E scavenges radicals, thereby replenishing the supplies of vitamin E in LDL and HDL3. These were test tube studies that used human HDL3 and LDL.

We include quercetin (130 mg in the recommended 12 capsules daily) in our Personal Radical Shield™.

This effect could be very important; we hope to see more published on it.


  1. Navab et al. Mechanisms of disease: proatherogenic HDL—an evolving field. Nature Clin Pract Endocrinol Metab 2(9):504-11 (2006).
  2. Filipe et al. Albumin-bound quercetin repairs vitamin E oxidized by apolipoprotein radicals in native HDL3 and LDL. Biochemistry 46:14305-15 (2007).

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