Association between childhood trauma and risk for obesity: a putative neurocognitive developmental pathway.
Qiang Luo,Qiang Luo,Lingli Zhang,Chu Chung Huang,Yan Zheng,Jonathan W. Kanen,Qi Zhao,Ye Yao,Erin Burke Quinlan,Tianye Jia,Tianye Jia,Tobias Banaschewski,Arun L.W. Bokde,Uli Bromberg,Christian Büchel,Herta Flor,Herta Flor,Vincent Frouin,Hugh Garavan,Penny A. Gowland,Andreas Heinz,Bernd Ittermann,Jean-Luc Martinot,Marie-Laure Paillère Martinot,Frauke Nees,Dimitri Papadopoulos Orfanos,Luise Poustka,Luise Poustka,Sarah Hohmann,Juliane H. Fröhner,Michael N. Smolka,Henrik Walter,Robert Whelan,Barbara J. Sahakian,Barbara J. Sahakian,Barbara J. Sahakian,Gunter Schumann,Gunter Schumann,Fei Li,Jianfeng Feng,Jianfeng Feng,Sylvane Desrivières,Trevor W. Robbins,Trevor W. Robbins +43 more
TL;DR: The findings highlight that a malfunctioning, top-down cognitive or behavioral control system, independent of genetic predisposition, putatively contributes to excessive weight gain in a particularly vulnerable population, and may inform treatment approaches.
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Abstract: Childhood trauma increases the risk for adult obesity through multiple complex pathways, and the neural substrates are yet to be determined. Participants from three population-based neuroimaging cohorts, including the IMAGEN cohort, the UK Biobank (UKB), and the Human Connectome Project (HCP), were recruited. Voxel-based morphometry analysis of both childhood trauma and body mass index (BMI) was performed in the longitudinal IMAGEN cohort; validation of the findings was performed in the UKB. White-matter connectivity analysis was conducted to study the structural connectivity between the identified brain region and subdivisions of the hypothalamus in the HCP. In IMAGEN, a smaller frontopolar cortex (FPC) was associated with both childhood abuse (CA) (β = − .568, 95%CI − .942 to − .194; p = .003) and higher BMI (β = − .086, 95%CI − .128 to − .043; p < .001) in male participants, and these findings were validated in UKB. Across seven data collection sites, a stronger negative CA-FPC association was correlated with a higher positive CA-BMI association (β = − 1.033, 95%CI − 1.762 to − .305; p = .015). Using 7-T diffusion tensor imaging data (n = 156), we found that FPC was the third most connected cortical area with the hypothalamus, especially the lateral hypothalamus. A smaller FPC at age 14 contributed to higher BMI at age 19 in those male participants with a history of CA, and the CA-FPC interaction enabled a model at age 14 to account for some future weight gain during a 5-year follow-up (variance explained 5.8%). The findings highlight that a malfunctioning, top-down cognitive or behavioral control system, independent of genetic predisposition, putatively contributes to excessive weight gain in a particularly vulnerable population, and may inform treatment approaches.
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