Oxidized LDL and the Metabolic Syndrome
Arteriosclerosis, Thrombosis and Vascular Biology
men and women, age 70 to 79 years, were studied. In the Stockholm County cohort, only white men, age 62 to 64 years, were studied. The association between the metabolic syndrome and a higher prevalence of elevated levels of circulating oxidized LDL in the Health ABC cohort was independent of age, gender, and ethnicity. Although the Health ABC cohort was older, with a restricted age range, this suggests that the contrasting data are not likely to be attributable to differences in age, gender,
... in age, gender, and ethnicity. The Health ABC cohort appeared to be representative of the U.S. population. The prevalence of the metabolic syndrome as defined by ATP III (3 or more components) in the Health ABC cohort was 38% (1147 participants with metabolic syndrome) versus 42% in a similar-aged population in the Third National Health and Nutrition Examination Survey (NHANES III). In addition, the prevalence of diabetes, smoking, and hypertension, as well as the mean BMI and waist circumference, mean LDL and HDL cholesterol, and triglyceride levels were similar between the 2 study populations. Other than functional status, there were no other exclusion criteria. Individuals with the metabolic syndrome had twice the odds of having high oxidized LDL (Ͻ1.90 mg/dL, ie, Ͼ90 th percentile of distribution in individuals with no metabolic syndrome components) compared with those not having the metabolic syndrome, after adjusting for age, gender, ethnicity, smoking, and LDL cholesterol. The prevalence of the metabolic syndrome among 62-to 64-year-old men in the subset of the Stockholm County cohort was lower (8% or 22 participants) than what could be expected (Ϸ20%) from the NHANES data. One possible explanation for the lower than expected prevalence could be the exclusion of participants with manifest diabetes, treatment with antihypertensive agents, and BMI outside the range 19 kg/m 2 to 35 kg/m 2. The exclusion of obese and diabetics could have affected the relation between the metabolic syndrome and circulating oxidized LDL. Previously, we have shown that both obesity and diabetes contributed to the increase in oxidized LDL independent of LDL cholesterol levels.   Three other possible reasons for the observed differences, which cannot be excluded at this time are: (1) a small sample size, which limits statistical power and may have predisposed to type 2 error in the Sjogren article (nϭ22 for metabolic syndrome); (2) fundamental metabolic differences between the populations, possibly caused by differences in genetic architecture (we would consider this unlikely but still possible); and (3) a lack of adjustment for LDL levels in the Sjogren analyses, an adjustment we found to be critical because LDL and ox-LDL are highly correlated. Although we do not question the merits of this study, we wanted to put some of the data in a larger perspective.