Association between childhood trauma and risk for obesity: a putative neurocognitive developmental pathway.
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Luo Qiang, Zhang Lingli, Huang Chu-Chung, Zheng Yan, Kanen Jonathan W, Zhao Qi, Yao Ye, Quinlan Erin B, Jia Tianye, Banaschewski Tobias, Bokde Arun L W, Bromberg Uli, Büchel Christian, Flor Herta, Frouin Vincent, Garavan Hugh, Gowland Penny, Heinz Andreas, Ittermann Bernd, Martinot Jean-Luc, Martinot Marie-Laure Paillère, Nees Frauke, Orfanos Dimitri Papadopoulos, Poustka Luise, Hohmann Sarah, Fröhner Juliane H, Smolka Michael N, Walter Henrik, Whelan Robert, Sahakian Barbara J, Schumann Gunter, Li Fei, Feng Jianfeng, Desrivières Sylvane, Robbins Trevor W, IMAGEN consortium
Аннотация
METHODS: 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.
RESULTS: 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%).
CONCLUSIONS: 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.