Yosuke Inoue1,2, Mariaelisa Graff1,3, Annie Green Howard1,4, Heather M Highland3, Kristin L Young1,3, Kathleen Mullan Harris1,5, Kari E North1,3, Yun Li4,6, Qing Duan4,6, Penny Gordon-Larsen1,7. 1. Carolina Population Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 2. Department of Epidemiology and Prevention, National Center for Global Health and Medicine, Tokyo, Japan. 3. Department of Epidemiology, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 4. Department of Biostatistics, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 5. Department of Sociology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 6. Department of Genetics, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 7. Department of Nutrition, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Abstract
BACKGROUND: Few studies have focused on the role of adverse childhood experiences (ACEs) in relation to genetic susceptibility to obesity. OBJECTIVE: We aimed to examine the interaction between the presence of ACEs (i.e., physical, psychological and sexual abuse) before the age of 18 and BMI polygenic score. METHODS: Data came from the National Longitudinal Study of Adolescent to Adult Health (Add Health) Wave IV (2007/2008) where saliva samples were collected for DNA genotyping and information on BMI and ACEs were obtained from 5854 European American (EA), 2073 African American (AA) and 1448 Hispanic American (HA) participants aged 24 to 32 years old. Polygenic scores were calculated as the sum of the number of risk alleles of BMI-related SNPs which were weighted by effect size. A race/ethnicity-stratified mixed-effects linear regression model was used to test for differential association between BMI polygenic score and BMI by the presence of ACEs. RESULTS: We did not find any evidence of significant interaction between ACEs and polygenic score in relation to BMI among EA (p = 0.289), AA (p = 0.618) or HA (p = 0.870). In main effects models, polygenic score was positively associated with BMI in all race/ethnic groups, yet the presence of ACEs was associated with increased BMI only among EA. CONCLUSION: We did not find any evidence that ACEs exacerbate genetic predisposition to increased BMI in early adulthood.
BACKGROUND: Few studies have focused on the role of adverse childhood experiences (ACEs) in relation to genetic susceptibility to obesity. OBJECTIVE: We aimed to examine the interaction between the presence of ACEs (i.e., physical, psychological and sexual abuse) before the age of 18 and BMI polygenic score. METHODS: Data came from the National Longitudinal Study of Adolescent to Adult Health (Add Health) Wave IV (2007/2008) where saliva samples were collected for DNA genotyping and information on BMI and ACEs were obtained from 5854 European American (EA), 2073 African American (AA) and 1448 Hispanic American (HA) participants aged 24 to 32 years old. Polygenic scores were calculated as the sum of the number of risk alleles of BMI-related SNPs which were weighted by effect size. A race/ethnicity-stratified mixed-effects linear regression model was used to test for differential association between BMI polygenic score and BMI by the presence of ACEs. RESULTS: We did not find any evidence of significant interaction between ACEs and polygenic score in relation to BMI among EA (p = 0.289), AA (p = 0.618) or HA (p = 0.870). In main effects models, polygenic score was positively associated with BMI in all race/ethnic groups, yet the presence of ACEs was associated with increased BMI only among EA. CONCLUSION: We did not find any evidence that ACEs exacerbate genetic predisposition to increased BMI in early adulthood.
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