Whole-grain intake, metabolic syndrome, and mortality in older adults.

the lipid part. We agree that the peroxidation of lipids present in LDL is not the only way to generate LDL oxidation. Direct oxidation of the protein moiety of the lipoprotein also occurs. The process of LDL oxidation leads to the modification of the protein moiety of LDL, either directly—via aldehydes released from endothelial cells, as Holvoet described, or via myeloperoxidase-derived hypochlorous acid (1)—or indirectly—via peroxidation of polyunsaturated fatty acids (2). In turn, direct and indirect pathways can be related. For example, the tyrosyl radical generated by myeloperoxidase is also a physiologic catalyst for the initiation of lipid peroxidation in lipoproteins (3). The advantage of the antibody against oxidized LDL developed by Holvoet and colleagues is that it is directed against the most harmful of the LDLs, a modified apolipoprotein B-100 lipoprotein that can be recognized by the scavenger receptor of the macrophages and, hence, promotes the development of atherosclerosis. It is currently thought that oxidized LDL is more damaging to the arterial wall than is native LDL (4). Holvoet et al (5) showed that, with the exception of blood pressure, all components of the metabolic syndrome were significantly associated with high concentrations of oxidized LDL in US men and women aged 70–79 y. Most importantly, high concentrations of oxidized LDL increased the risk of myocardial infarction in this population. The central role of abdominal obesity in the metabolic syndrome and the increased risk of high waist circumferences with high oxidized LDL concentrations (6) underscore the need for routine medical examination of waist circumferences.