Was the Historic Contribution of Spain to the Mexican Gene Pool Partially Responsible for the Higher Prevalence of Type 2 Diabetes in Mexican-Origin Populations?

Was the Historic Contribution of Spain to the Mexican Gene Pool Partially Responsible for the Higher Prevalence of Type 2 Diabetes in Mexican-Origin Populations? The Spanish Insulin Resistance Study Group, the San Antonio Heart Study, and the Mexico City Diabetes Study Carlos Lorenzo , MD 1 , Manel...

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Published inDiabetes care Vol. 24; no. 12; pp. 2059 - 2064
Main Authors Carlos Lorenzo, Manel Serrano-Rios, Maria T. Martinez-Larrad, Rafael Gabriel, Ken Williams, Clicerio Gonzalez-Villalpando, Michel P. Stern, Helen P. Hazuda, Steven M. Haffner
Format Journal Article
LanguageEnglish
Published American Diabetes Association 01.12.2001
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Summary:Was the Historic Contribution of Spain to the Mexican Gene Pool Partially Responsible for the Higher Prevalence of Type 2 Diabetes in Mexican-Origin Populations? The Spanish Insulin Resistance Study Group, the San Antonio Heart Study, and the Mexico City Diabetes Study Carlos Lorenzo , MD 1 , Manel Serrano-Rios , MD 2 , Maria T. Martinez-Larrad , MD 2 , Rafael Gabriel , MD 3 , Ken Williams , MS 1 , Clicerio Gonzalez-Villalpando , MD 4 , Michel P. Stern , MD 1 , Helen P. Hazuda , PHD 1 and Steven M. Haffner , MD 1 1 Department of Medicine, Division of Clinical Epidemiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 2 Department of Internal Medicine, Hospital Universitario de San Carlos, Madrid, Spain 3 Department of Internal Medicine, Hospital de La Princesa, Madrid, Spain 4 Center of Studies in Diabetes, American British Cowdray Hospital, Mexico City, Mexico Abstract OBJECTIVE —Mexican-American populations in San Antonio, Texas (SA-MA) and Mexico have a higher prevalence of type 2 diabetes than non-Hispanic whites in San Antonio (SA-NHW). However, the higher prevalence of type 2 diabetes in Mexican-origin populations might be related, in part, not to Native American genetic admixture but to Spanish genetic admixture. RESEARCH DESIGN AND METHODS —Four population-based epidemiological surveys conducted with Mexican-origin and European-origin samples provided data relevant to this question. In all four surveys, type 2 diabetes was defined as fasting plasma glucose ≥7.0 mmol/l or 2-h glucose ≥11.1 mmol/l or use of antidiabetic agents. RESULTS —A comparison of the two Mexican-origin populations showed that the age- and sex-adjusted prevalence of type 2 diabetes was lower in Mexico than in SA-MA (15.1 vs. 17.9%, P = 0.032). Between the two European-origin populations, the prevalence of type 2 diabetes was lower in SA-NHW than in Spain (6.2 vs. 9.1%, P < 0.0001), but differences were attenuated by adjustment for BMI or after stratification by education. In logistic regression analyses, type 2 diabetes was associated with Mexican ethnic origin after adjusting for age, education, BMI, and waist-to-hip ratio. CONCLUSIONS —The prevalence of type 2 diabetes in Spain was intermediate between that in Mexican-origin populations and SA-NHW. Although the higher degree of Native American admixture is a major contributor to the higher rates of type 2 diabetes, we cannot completely rule out a partial contribution of Spanish admixture to diabetes susceptibility among Mexican- origin populations. MCDS, Mexico City Diabetes Study OR, odds ratio SAHS, San Antonio Heart Study SA-NHW, non-Hispanic whites in San Antonio SA-MA, Mexican-Americans in San Antonio SIRS, Spanish Insulin Resistance Study WHR, waist-to-hip ratio Footnotes Address correspondence and reprint requests to Carlos Lorenzo, MD, Department of Medicine, Division of Clinical Epidemiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284-7873. E-mail: lorenzo{at}uthscsa.edu . Received for publication 4 May 2001 and accepted in revised form 4 September 2001. A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
ISSN:0149-5992
1935-5548
DOI:10.2337/diacare.24.12.2059