Kulisch Leonard Konstantin, Arumäe Kadri, Briley Daniel A, Vainik Uku
Institute of Psychology, University of Tartu, Tartu, Estonia.
Wilhem Wundt Institute for Pschology, Leipzig University, Leipzig, Germany.
Dev Sci. 2023 Nov;26(6):e13392. doi: 10.1111/desc.13392. Epub 2023 Mar 23.
Childhood obesity is a serious health concern that is not yet fully understood. Previous research has linked obesity with neurobehavioral factors such as behavior, cognition, and brain morphology. The causal directions of these relationships remain mostly untested. We filled this gap by using the Adolescent Brain Cognitive Development study cohort comprising 11,875 children aged 9-10. First, correlations between the age- and sex-specific 95th BMI percentile (%BMIp95) and neurobehavioral measures were cross-sectionally analyzed. Effects were then aggregated by neurobehavioral domain for causal analyses. Behavioral genetic Direction of Causation modeling was used to test the direction of each relationship. Findings were validated by longitudinal cross-lagged panel modeling. %BMIp95 correlated with impulsivity, motivation, psychopathology, eating behavior, and cognitive tests (executive functioning, language, memory, perception, working memory). Greater %BMIp95 was also associated with reduced cortical thickness in frontal and temporal brain areas but with increased thickness in parietal and occipital areas. Similar although weaker patterns emerged for cortical surface area and volume. Behavioral genetic modeling suggested causal effects of %BMIp95 on eating behavior (β = 0.26), cognition (β = 0.05), cortical thickness (β = 0.15), and cortical surface area (β = 0.07). Personality/psychopathology (β = 0.09) and eating behavior (β = 0.16) appeared to influence %BMIp95. Longitudinal evidence broadly supported these findings. Results regarding cortical volume were inconsistent. Results supported causal effects of obesity on brain functioning and morphology. The present study highlights the importance of physical health for brain development and may inform interventions aimed at preventing or reducing pediatric obesity. RESEARCH HIGHLIGHTS: A continuous measure related to obesity, %BMIp95, has correlations with various measures of brain functioning and structure Behavioral genetic and longitudinal modeling suggest causal links from personality, psychopathology, and eating behavior to %BMIp95 Results also indicate directional links from %BMIp95 to eating behavior, cognition, cortical thickness, and cortical surface area Obesity may play a role for healthy brain development during childhood.
儿童肥胖是一个尚未被完全理解的严重健康问题。先前的研究已将肥胖与神经行为因素联系起来，如行为、认知和脑形态。这些关系的因果方向大多仍未得到检验。我们通过使用包含11875名9至10岁儿童的青少年大脑认知发展研究队列填补了这一空白。首先，对按年龄和性别划分的第95百分位体重指数（%BMIp95）与神经行为指标之间的相关性进行横断面分析。然后按神经行为领域汇总效应以进行因果分析。使用行为遗传因果方向模型来检验每种关系的方向。研究结果通过纵向交叉滞后面板模型进行验证。%BMIp95与冲动性、动机、精神病理学、饮食行为和认知测试（执行功能、语言、记忆、感知、工作记忆）相关。较高的%BMIp95还与额叶和颞叶脑区的皮质厚度减少有关，但与顶叶和枕叶脑区的厚度增加有关。皮质表面积和体积也出现了类似但较弱的模式。行为遗传模型表明%BMIp95对饮食行为（β = 0.26）、认知（β = 0.05）、皮质厚度（β = 0.15）和皮质表面积（β = 0.07）有因果效应。人格/精神病理学（β = 0.09）和饮食行为（β = 0.16）似乎会影响%BMIp95。纵向证据广泛支持了这些发现。关于皮质体积的结果不一致。结果支持肥胖对脑功能和形态的因果效应。本研究强调了身体健康对脑发育的重要性，并可能为旨在预防或减少儿童肥胖的干预措施提供参考。研究亮点：与肥胖相关的连续指标%BMIp95与各种脑功能和结构指标相关 行为遗传和纵向模型表明从人格、精神病理学和饮食行为到%BMIp95的因果联系 结果还表明从%BMIp95到饮食行为、认知、皮质厚度和皮质表面积的方向性联系 肥胖可能在儿童期健康脑发育中起作用
