Highlights BMI was associated with widespread structural differences in cortical thickness, surface area, subcortical gray matter volumes and in white matter estimates of fractional anisotropy and mean diffusivity. BMI was also associated with altered resting-state functional connectivity and working memory during an EN-back task but, contrary to some extant findings, was not related to reward or inhibitory control (as assessed by the Monetary Incentive Delay task and Stop Signal Task). Excessive weight gain (i.e., more than 20 pounds in a year) was associated at baseline with thicker cortices, and differences in surface area and white matter in regions associated with attention and appetite control (e.g., insula, parahippocampal gyrus), but no functional associations were observed. All analyses quantified generalizability to an unseen test set. These findings suggest that brain structure, resting state and working memory are associated with current weight and that brain structure may have potential as an MRI biomarker to identify children at risk for pathological weight gain.
Effect sizes are commonly interpreted using heuristics established by Cohen (e.g., small: r = .1, medium r = .3, large r = .5), despite mounting evidence that these guidelines are mis-calibrated to the effects typically found in psychological research. This study’s aims were to 1) describe the distribution of effect sizes across multiple instruments, 2) consider factors qualifying the effect size distribution, and 3) identify examples as benchmarks for various effect sizes. For aim one, effect size distributions were illustrated from a large, diverse sample of 9/10-year-old children. This was done by conducting Pearson’s correlations among 161 variables representing constructs from all questionnaires and tasks from the Adolescent Brain and Cognitive Development Study® baseline data. To achieve aim two, factors qualifying this distribution were tested by comparing the distributions of effect size among various modifications of the aim one analyses. These modified analytic strategies included comparisons of effect size distributions for different types of variables, for analyses using statistical thresholds, and for analyses using several covariate strategies. In aim one analyses, the median in-sample effect size was .03, and values at the first and third quartiles were .01 and .07. In aim two analyses, effects were smaller for associations across instruments, content domains, and reporters, as well as when covarying for sociodemographic factors. Effect sizes were larger when thresholding for statistical significance. In analyses intended to mimic conditions used in “real-world” analysis of ABCD data, the median in-sample effect size was .05, and values at the first and third quartiles were .03 and .09. To achieve aim three, examples for varying effect sizes are reported from the ABCD dataset as benchmarks for future work in the dataset. In summary, this report finds that empirically determined effect sizes from a notably large dataset are smaller than would be expected based on existing heuristics.
ImportanceAlthough most research has linked video gaming to subsequent increases in aggressive behavior in children after accounting for prior aggression, findings have been divided with respect to video gaming’s association with cognitive skills.ObjectiveTo examine the association between video gaming and cognition in children using data from the Adolescent Brain Cognitive Development (ABCD) study.Design, Setting, and ParticipantsIn this case-control study, cognitive performance and blood oxygen level–dependent (BOLD) signal were compared in video gamers (VGs) and non–video gamers (NVGs) during response inhibition and working memory using task-based functional magnetic resonance imaging (fMRI) in a large data set of 9- and 10-year-old children from the ABCD study, with good control of demographic, behavioral, and psychiatric confounding effects. A sample from the baseline assessment of the ABCD 2.0.1 release in 2019 was largely recruited across 21 sites in the US through public, private, and charter elementary schools using a population neuroscience approach to recruitment, aiming to mirror demographic variation in the US population. Children with valid neuroimaging and behavioral data were included. Some exclusions included common MRI contraindications, history of major neurologic disorders, and history of traumatic brain injury.ExposuresParticipants completed a self-reported screen time survey including an item asking children to report the time specifically spent on video gaming. All fMRI tasks were performed by all participants.Main Outcomes and MeasuresVideo gaming time, cognitive performance, and BOLD signal assessed with n-back and stop signal tasks on fMRI. Collected data were analyzed between October 2019 and October 2020.ResultsA total of 2217 children (mean [SD] age, 9.91 [0.62] years; 1399 [63.1%] female) participated in this study. The final sample used in the stop signal task analyses consisted of 1128 NVGs (0 gaming hours per week) and 679 VGs who played at least 21 hours per week. The final sample used in the n-back analyses consisted of 1278 NVGs who had never played video games (0 hours per week of gaming) and 800 VGs who played at least 21 hours per week. The VGs performed better on both fMRI tasks compared with the NVGs. Nonparametric analyses of fMRI data demonstrated a greater BOLD signal in VGs in the precuneus during inhibitory control. During working memory, a smaller BOLD signal was observed in VGs in parts of the occipital cortex and calcarine sulcus and a larger BOLD signal in the cingulate, middle, and frontal gyri and the precuneus.Conclusions and RelevanceIn this study, compared with NVGs, VGs were found to exhibit better cognitive performance involving response inhibition and working memory as well as altered BOLD signal in key regions of the cortex responsible for visual, attention, and memory processing. The findings are consistent with videogaming improving cognitive abilities that involve response inhibition and working memory and altering their underlying cortical pathways.
Effect sizes are commonly interpreted using heuristics established by Cohen (e.g., small: r = .1, medium r = .3, large r = .5), despite mounting evidence that these guidelines are mis-calibrated to the effects typically found in psychological research. Here we summarize Pearson’s correlations among all questionnaire and task data from the ABCD Study® to illustrate effect size distributions in a large, diverse sample of 9/10-year-old children. The median in-sample effect size was .03, and values at the first and third quartiles were .01 and .07. Effects were smaller for associations across instruments, content domains, and reporters, as well as when covarying for sociodemographic factors. To help modify researcher expectations, we provide benchmark examples for varying effect sizes. In summary, this report finds that empirically determined effect sizes from a notably large dataset are smaller than would be expected based on existing heuristics.
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