Author
MERINO, JORDI - Massachusetts General Hospital | |
LANE, JACQUELINE - Massachusetts General Hospital | |
BARTZ, TRACI - University Of Washington | |
MCKEOWN, NICOLA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University | |
SMITH, CAREN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University | |
TANAKA, TOSHIKO - National Institute On Aging (NIA, NIH) | |
LEMAITRE, ROZENN - University Of Washington | |
RUTTER, MARTIN - University Of Manchester | |
SAXENA, RICHA - Massachusetts General Hospital |
Submitted to: Meeting Abstract
Publication Type: Abstract Only Publication Acceptance Date: 1/17/2018 Publication Date: 6/9/2018 Citation: Merino, J., Lane, J.M., Bartz, T.M., McKeown, N.M., Smith, C.E., Tanaka, T., Lemaitre, R.N., Rutter, M.K., Saxena, R. 2018. Biological insights from genetics of breakfast intake [abstract]. American Society of Nutrition. Abstract No. 436282. Interpretive Summary: Technical Abstract: Objectives: Breakfast consumption is a heritable dietary behavior associated with lower body weight and cardiometabolic disease risk, yet, variation exists in whether breakfast is consumed. Discovery of genetic variants influencing diet beyond composition is hindered by the lack of data on meal preference captured by traditional dietary assessment methods. The objectives of this study were to identify genetic factors that influence breakfast intake and unravel shared biological links with other traits. Methods: We leveraged the power of the UK Biobank (n=500,000) to identify genetic variants related to breakfast cereal intake as a proxy for breakfast. Breakfast cereal frequency was estimated using data from up to five web-based 24-hr diet recalls, and responses were categorized as "never," "sometimes," and "always" (n=193,860). We performed genome-wide association study (GWAS) using linear mixed models adjusting for age, sex, 10 PCs, and genotyping array in related participants of European ancestry. We then verified observed links in the Cardiovascular Health Study (CHS) that captured breakfast intake frequency as assessed by "How often do you eat breakfast?" ("never" vs. "always") by performing GWAS using age- and sex-adjusted logistic regression (n=3,044). Results: From the UK Biobank, we identified 6 independent genome-wide significant loci. Associations included genes implicated for caffeine intake/metabolism (CYP1A1), carbohydrate intake (FGF21), and schizophrenia (ZNF804A). Genome-wide genetic correlations indicated shared biological links between infrequent breakfast and insomnia, depression, obesity, coronary artery disease, and smoking (P<2.14x10-4). We also observed that a genetic-risk score for higher coffee intake was associated with lower breakfast intake (P<0.05), suggesting shared genetics among foods. In the CHS, we confirmed links with insomnia and schizophrenia by using genetic-risk scores for those traits (P<0.05). Replication analyses to confirm UK Biobank top signals are underway upon inclusion of other CHARGE consortium cohorts. Conclusions: The present findings provide novel understanding of the genetic architecture of breakfast behavior including shared genetic links. |