Abstract
We have asked whether the prevalence of combined hyperlipidemia (CHL) differs by race/ethnicity, obesity, and insulin resistance in a contemporary, multiethnic, US cohort. We determined the prevalence and adjusted odds of CHL in a cohort of 5923 men and women free of clinically recognized cardiovascular disease and diabetes according to race/ethnicity (white, Chinese, African American, and Hispanic), obesity, and insulin resistance. Untreated lipid values were imputed for those on lipid-lowering therapy. Combined hyperlipidemia was defined using age- and sex-specific greater than or equal to 75th percentile cut points for low-density lipoprotein cholesterol and triglycerides obtained from a predominantly white North American population study. Compared with whites, adjusted odds ratios for CHL were 0.48 in African Americans (95% confidence interval [CI], 0.30-0.75), 1.33 in Hispanics (95% CI, 0.93-1.91), and 1.06 in Asians (95% CI, 0.62-1.82). Within the entire population, the adjusted odds of CHL were over 2-fold higher in overweight and obese participants compared with normal-weight participants and more than 4-fold higher in quartiles 2 through 4 of insulin resistance compared with quartile 1. African Americans had lower odds for CHL than whites despite higher body mass index and abdominal adiposity. Hispanics had a nonsignificantly higher trend, and Asians had no significantly different odds than whites. Modest increases in weight and insulin resistance were associated with significantly higher odds of CHL in a multiethnic US population. Further research is needed to determine the most efficacious diet, exercise, and drug management to decrease the risk of CHL and coronary heart disease among racial/ethnic groups in the United States.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 212-219 |
| Number of pages | 8 |
| Journal | Metabolism: clinical and experimental |
| Volume | 58 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2009 |
Bibliographical note
Funding Information:This research was supported by contracts N01-HC-95159 through N01-HC-95166 and N01-HC-95167 from the National Heart, Lung, and Blood Institute. The authors thank the other investigators, the staff, and the participants of the MESA for their valuable contributions. The authors gratefully acknowledge Robyn McClelland, PhD, at the University of Washington for providing the imputed lipid values for the MESA participants. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org . Dr Paramsothy was supported by a Pfizer Preventive Cardiology Award and is funded by grant 1KL2RR025015-01 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) and NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/ .
