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Replication of a Gene-Diet Interaction in 3 Independent Populations

Dolores Corella, PhD; Gina Peloso, MSc; Donna K. Arnett, PhD, MSPH; Serkalem Demissie, PhD; L. Adrienne Cupples, PhD; Katherine Tucker, PhD; Chao-Qiang Lai, PhD; Laurence D. Parnell, PhD; Oscar Coltell, PhD; Yu-Chi Lee, MSc; Jose M. Ordovas, PhD

Arch Intern Med. 2009;169(20):1897-1906.

Background  Nutrigenetics studies the role of genetic variation on interactions between diet and health, aiming to provide more personalized dietary advice. However, replication has been low. Our aim was to study interaction among a functional APOA2 polymorphism, food intake, and body mass index (BMI) in independent populations to replicate findings and to increase their evidence level.

Methods  Cross-sectional, follow-up (20 years), and case-control analyses were undertaken in 3 independent populations. We analyzed gene-diet interactions between the APOA2 –265T>C polymorphism and saturated fat intake on BMI and obesity in 3462 individuals from 3 populations in the United States: the Framingham Offspring Study (1454 whites), the Genetics of Lipid Lowering Drugs and Diet Network Study (1078 whites), and Boston–Puerto Rican Centers on Population Health and Health Disparities Study (930 Hispanics of Caribbean origin).

Results  Prevalence of the CC genotype in study participants ranged from 10.5% to 16.2%. We identified statistically significant interactions between the APOA2 –265T>C and saturated fat regarding BMI in all 3 populations. Thus, the magnitude of the difference in BMI between the individuals with the CC and TT+TC genotypes differed by saturated fat. A mean increase in BMI of 6.2% (range, 4.3%-7.9%; P = .01) was observed between genotypes with high– (22 g/d) but not with low– saturated fat intake in all studies. Likewise, the CC genotype was significantly associated with higher obesity prevalence in all populations only in the high–saturated fat stratum. Meta-analysis estimations of obesity for individuals with the CC genotype compared with the TT+TC genotype were an odds ratio of 1.84 (95% confidence interval, 1.38-2.47; P < .001) in the high–saturated fat stratum, but no association was detected in the low–saturated fat stratum (odds ratio, 0.81; 95% confidence interval, 0.59-1.11; P = .18).

Conclusion  For the first time to our knowledge, a gene-diet interaction influencing BMI and obesity has been strongly and consistently replicated in 3 independent populations.

Author Affiliations: Nutrition and Genomics Laboratory (Drs Corella, Lai, Parnell, and Ordovas and Ms Lee) and Dietary Assessment and Epidemiology Research Program (Dr Tucker), Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, and Department of Biostatistics, Boston University (Ms Peloso and Drs Demissie and Cupples), Boston, Massachusetts; Genetic and Molecular Epidemiology Unit and Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III School of Medicine, University of Valencia, Valencia, Spain (Dr Corella); Department of Epidemiology, School of Public Health, and Clinical Nutrition Research Center, University of Alabama, Birmingham (Dr Arnett); Department of Computer Sciences, Jaume I University, Castellón, Spain (Dr Coltell); and Department of Cardiovascular Epidemiology and Population Genetics, National Center for Cardiovascular Investigation (CNIC), Madrid, Spain (Dr Ordovas).

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