Unjali P. Gujral, PhD; Eric Vittinghoff, PhD; Morgana Mongraw-Chaffin, PhD; Dhananjay Vaidya, PhD; Namratha R. Kandula, MD, MPH; Matthew Allison, MD, MPH; Jeffrey Carr, MD; Kiang Liu, PhD; K.M. Venkat Narayan, MD; Alka M. Kanaya, MD
Acknowledgment: The authors thank the other investigators, the staff, and the MASALA and MESA participants for their valuable contributions. A full list of participating MESA investigators and institutions may be found at www.mesa-nhlbi.org.
Grant Support: The MASALA study was supported by NIH grants R01HL093009 and K24HL112827. Data collection at the University of California, San Francisco, was supported by NIH/NCRR grant UL1 RR024131. The MESA study was supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the NHLBI and by grants UL1-TR-000040 and UL1-TR-001079 from the NCRR.
Disclosures: Dr. Vittinghoff reports grants from the National Institute of Diabetes and Digestive and Kidney Diseases during the conduct of the study. Authors not named here have disclosed no conflicts of interest. Disclosures can also be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M16-1895.
Editors' Disclosures: Christine Laine, MD, MPH, Editor in Chief, reports that she has no financial relationships or interests to disclose. Darren B. Taichman, MD, PhD, Executive Deputy Editor, reports that he has no financial relationships or interests to disclose. Cynthia D. Mulrow, MD, MSc, Senior Deputy Editor, reports that she has no relationships or interests to disclose. Deborah Cotton, MD, MPH, Deputy Editor, reports that she has no financial relationships or interest to disclose. Jaya K. Rao, MD, MHS, Deputy Editor, reports that she has stock holdings/options in Eli Lilly and Pfizer. Sankey V. Williams, MD, Deputy Editor, reports that he has no financial relationships or interests to disclose. Catharine B. Stack, PhD, MS, Deputy Editor for Statistics, reports that she has stock holdings in Pfizer and Johnson & Johnson.
Reproducible Research Statement:Study protocol: MASALA protocol available from Dr. Kanaya (e-mail, email@example.com); MESA protocol available at www.mesa-nhlbi.org. Statistical code: Available from Dr. Gujral (e-mail, firstname.lastname@example.org). Data set: Available with steering committee approval from both MESA and MASALA.
Requests for Single Reprints: Unjali P. Gujral, PhD, Emory University, Hubert Department of Global Health, Rollins School of Public Health, 1518 Clifton Road, CNR 7040-K, Atlanta, GA 30322; e-mail, email@example.com.
Current Author Addresses: Dr. Gujral: Emory University, Hubert Department of Global Health, Rollins School of Public Health, 1518 Clifton Road, CNR 7040-K, Atlanta, GA 30322.
Dr. Vittinghoff: Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, 550 16th Street, 2nd Floor, San Francisco, CA 94158.
Dr. Mongraw-Chaffin: Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157.
Dr. Vaidya: Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8025, Baltimore, MD 21287.
Dr. Kandula: Center for Community Health, 420 East Superior, 6th Floor, Chicago, IL 60640.
Dr. Allison: Department of Family and Preventive Medicine, University of California, San Diego, 8950 Villa La Jolla Drive, Suite B122, Mailcode 0811, La Jolla, CA 92037.
Dr. Carr: Department of Radiology, Vanderbilt University, 1161 21st Avenue South, Nashville, TN 37232.
Dr. Liu: 680 North Lakeshore Drive, Suite 1200, Chicago, IL 60640.
Dr. Narayan: Rollins School of Public Health, Emory University, 1518 Clifton Road Northeast, Room 7047, Atlanta, GA 30322.
Dr. Kanaya: Division of General Internal Medicine, University of California, San Francisco, 1545 Divisadero Street, Suite 311, San Francisco, CA 94115.
Author Contributions: Conception and design: U.P. Gujral, M. Mongraw-Chaffin, K.M.V. Narayan, A.M. Kanaya.
Analysis and interpretation of the data: U.P. Gujral, E. Vittinghoff, M. Mongraw-Chaffin, D. Vaidya, N.R. Kandula, M. Allison, J. Carr, K.M.V. Narayan, A.M. Kanaya.
Drafting of the article: U.P. Gujral.
Critical revision for important intellectual content: U.P. Gujral, M. Mongraw-Chaffin, D. Vaidya, N.R. Kandula, M. Allison, J. Carr, K. Liu, K.M.V. Narayan, A.M. Kanaya.
Final approval of the article: U.P. Gujral, E. Vittinghoff, M. Mongraw-Chaffin, D. Vaidya, N.R. Kandula, M. Allison, J. Carr, K. Liu, K.M.V. Narayan, A.M. Kanaya.
Provision of study materials or patients: N.R. Kandula, A.M. Kanaya.
Statistical expertise: U.P. Gujral, E. Vittinghoff, M. Mongraw-Chaffin, D. Vaidya.
Obtaining of funding: N.R. Kandula, A.M. Kanaya.
Administrative, technical, or logistic support: J. Carr, A.M. Kanaya.
Collection and assembly of data: N.R. Kandula, J. Carr, A.M. Kanaya.
The relationship between body weight and cardiometabolic disease may vary substantially by race/ethnicity.
To determine the prevalence and correlates of the phenotype of metabolic abnormality but normal weight (MAN) for 5 racial/ethnic groups.
2 community-based cohorts.
2622 white, 803 Chinese American, 1893 African American, and 1496 Hispanic persons from MESA (Multi-Ethnic Study of Atherosclerosis) and 803 South Asian participants in the MASALA (Mediators of Atherosclerosis in South Asians Living in America) study.
Prevalence of 2 or more cardiometabolic abnormalities (high fasting glucose, low high-density lipoprotein cholesterol, and high triglyceride levels and hypertension) among normal-weight participants was estimated. Correlates of MAN were assessed by using log-binomial models.
Among participants of normal weight (n = 846 whites, 323 Chinese Americans, 334 African Americans, 252 Hispanics, and 195 South Asians), the prevalence of MAN was 21.0% (95% CI, 18.4% to 23.9%) in whites, 32.2% (CI, 27.3% to 37.4%) in Chinese Americans, 31.1% (CI, 26.3% to 36.3%) in African Americans, 38.5% (CI, 32.6% to 44.6%) in Hispanics, and 43.6% (CI, 36.8% to 50.6%) in South Asians. Adjustment for demographic, behavioral, and ectopic body fat measures did not explain racial/ethnic differences. After adjustment for age, sex, and race/ethnicity–body mass index (BMI) interaction, for the equivalent MAN prevalence at a BMI of 25.0 kg/m2 in whites, the corresponding BMI values were 22.9 kg/m2 (CI, 19.5% to 26.3%) in African Americans, 21.5 kg/m2 (CI, 18.5% to 24.5%) in Hispanics, 20.9 kg/m2 (CI, 19.7% to 22.1%) in Chinese Americans, and 19.6 kg/m2 (CI, 17.2% to 22.0%) in South Asians.
Cross-sectional study design and lack of harmonized dietary data between studies.
Compared with whites, all racial/ethnic minority groups had a statistically significantly higher prevalence of MAN, which was not explained by demographic, behavioral, or ectopic fat measures. Using a BMI criterion for overweight to screen for cardiometabolic risk may result in a large proportion of racial/ethnic minority groups being overlooked.
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Gujral UP, Vittinghoff E, Mongraw-Chaffin M, Vaidya D, Kandula NR, Allison M, et al. Cardiometabolic Abnormalities Among Normal-Weight Persons From Five Racial/Ethnic Groups in the United States: A Cross-sectional Analysis of Two Cohort Studies. Ann Intern Med. [Epub ahead of print 4 April 2017]:. doi: 10.7326/M16-1895
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Published: Ann Intern Med. 2017.
Cardiology, Coronary Risk Factors, Diabetes, Dyslipidemia, Endocrine and Metabolism.
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