Our results have implications for theory, research, and clinical practice. With respect to theory, our results are consistent with the hypothesis that genetic risk for obesity is quantitatively distributed and can be operationalized in a GRS 48. With respect to research methods, our findings illustrate one approach to operationalize quantitative genetic risk. A systematic and replicable approach to selecting SNPs from association studies to follow-up in etiological and treatment research will be especially important with the advent of next-generation sequencing approaches. Next generation sequencing is likely to uncover many new disease-associated loci for obesity and for other phenotypes of interest to clinicians and researchers. These variants, though rarer in the population, may have higher penetrance and thus greater clinical relevance. Future research can also make use of the GRS derived in this study as a measure of inherited obesity risk. With respect to clinical practice, results indicate that, for persons in middle age, GWAS SNP-based approaches to obesity risk assessment offer little in the absence of more detailed information about lifestyle and environment. Although genetic information reliably predicted risk for
