Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 4 • August 2012

No Statistically Significant Linear Relationship
Between Oxidative Stress and Abnormal Lipid Profile
in Human Subjects with Coronary Artery Disease

An interesting paper1 published the results of an examination of 42 known human cases of coronary artery disease (CAD) (outpatients who had just survived a heart attack) for markers of oxidative stress (assessed by measuring MDA, malondialdehyde, a lipid peroxidation product) and lipid profile parameters (standard risk factors that include HDL cholesterol, LDL cholesterol, and triglycerides). The CAD outpatients were compared to 33 age- and sex-matched healthy controls who were evaluated for the same parameters.

The major finding of this study was that although, as expected, there was increased oxidative stress as well as significantly abnormal measures of HDL, LDL, and triglycerides in the CAD patients who had just survived a heart attack as compared to the healthy controls, there was a highly statistically insignificant correlation between MDA level and each lipid profile parameter in the CAD cases. This suggests, the researchers say, that “increased oxidative stress and abnormal lipid profile are two independent risk factors in the pathomechanism of atherogenesis.”1

This finding is potentially of considerable interest and, if verified with a larger sample size, may help explain why antioxidants have not, in very large human clinical trials, been consistently effective in reducing the risk of developing heart disease. In these large trials, there generally haven’t been measurements to establish participants’ baseline and later levels of oxidative stress. If one is going to test the hypothesis that the reduction of oxidative stress by antioxidants could reduce the risk of (say) heart disease, then it hardly makes sense to run the study without measuring oxidative stress.

In the previously conducted large trials, it was difficult to interpret the results because it was unclear what part oxidative stress was playing in the disease process. (It still is, which is why measurements assessing changes in oxidative stress are so important.) Clearly, a great deal more is going on in CAD than just oxidative stress and antioxidants can often do a great deal more than just suppressing the generation of and/or chemical reactions of ROS, such as acting as signaling molecules in the expression of genes that might be relevant to CAD. Indeed, in the design of these costly studies, researchers need to take into account that the proper dosage level of antioxidants is unlikely to be the same for the diverse mechanisms by which antioxidants could affect the course of a disease.

The authors1 suggest that their findings should be verified by a study with a larger sample size. We hope this is done. It would also be useful to include more than just a single marker for the formation of lipid peroxide breakdown products (MDA) to assess oxidative stress.


  1. Rao and Kiran. Evaluation of correlation between oxidative stress and abnormal lipid profile in coronary artery disease. J Cardiovasc Dis Res 2(1):57-60 (2011) www.jcdronline.com DOI: 10.4103/0975-3583.78598.

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