AJCN 19th International Congress of Nutrition
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American Journal of Clinical Nutrition, Vol. 83, No. 6, 1438-1439, June 2006
© 2006 American Society for Nutrition

LETTER TO THE EDITOR

Reply to P Holvoet

Helmut Schröder and Maria-Isabel Covas

Institut Municipal d'Investigació Mèdica
Unitat de Lipids i Epidemiologia Cardiovascular
Carrer Doctor Aiguader, 80
08003 Barcelona
Spain
E-mail: hschroeder{at}imim.es

Dear Sir:

We are grateful for the interest shown by Holvoet concerning our article. In his letter he noted that the antibody used in our study is directed against the modified protein part of the LDL lipoprotein, not 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.

ACKNOWLEDGMENTS

None of the authors had a conflict of interest related to the letter.

REFERENCES

  1. Hazen SL, Crowley JR, Mueller DM, Heinecke JM. Mass spectrometric quantification of 3-chlorotyrosine in human tissues with attomole sensitivity: a sensitive and specific marker for myeloperoxidase-catalyzed chlorination at sites of inflammation. Free Radic Biol Med 1997;23:909–16.[Medline]
  2. Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol: modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med 1989;320:915–24.[Medline]
  3. Savenkva MI, Mueller DM, Heinecke JW. Tyrosil radical generated by myeloperoxidase is a physiological catalyst for initiation of lipid peroxidation in low density lipoprotein. J Biol Chem 1994;269:20394–400.[Abstract/Free Full Text]
  4. Navab M, Berliner JA, Watson AD, et al. The Ying and Tang of oxidation in the development of the fatty streak. Arterioscler Thromb Vasc Biol 1996;16:831–42.[Abstract/Free Full Text]
  5. Holvoet P, Kritchevsky SB, Tracy RP, et al. The metabolic syndrome, circulating oxidized LDL, and risk of myocardial infarction in well-functioning elderly people in the Health, Aging, and Body Composition cohort. Diabetes 2004;53:1068–73.[Abstract/Free Full Text]
  6. Weinbrenner T, Schroder H, Escurriol V, et al. Circulating oxidized LDL is associated with increased waist circumference independent of body mass index in men and women. Am J Clin Nutr 2006;83:30–5.[Abstract/Free Full Text]




This Article
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