Abstract
Understanding weight-related differences in functional connectivity provides key insight into neurocognitive factors implicated in obesity. Here, we sampled three groups from human connectome project data: 1) 47 pairs of BMI-discordant twins (n = 94; average BMI-discordancy 6.7 ± 3.1 kg/m(2)), 2) 47 pairs of gender and BMI matched BMI-discordant, unrelated individuals, and 3) 47 pairs of BMI-similar twins, to test for body mass dependent differences in between network functional connectivity. Across BMI discordant samples, three networks appeared to be highly sensitive to weight status; specifically, a network comprised of gustatory processing regions, a visual processing network, and the default mode network (DMN). Further, in the BMI-discordant twin sample, twins with lower BMI had stronger connectivity between striatal/thalamic and prefrontal networks (pFWE = 0.04). We also observed that individuals with a higher BMI than their twin had stronger connectivity between cerebellar and insular networks (pFWE = 0.04). Connectivity patterns observed in the BMI-discordant twin sample were not seen in a BMI-similar sample, providing evidence that the results are specific to BMI discordance. Beyond the involvement of gustatory and visual networks and the DMN, little overlap in results were seen between the two BMI-discordant samples. In concordance with previous findings, we hypothesize that stronger cortical-striatal-thalamic connectivity associated with lower body mass in twins may facilitate increased regulation of hedonically motivated behaviors. In twins with higher body mass, increased cerebellar-insula connectivity may be associated with compromised satiation signaling, an interpretation dovetailing prior research. The lack of overlapping results between the two BMI discordant samples may be a function of higher study design sensitivity in the BMI-discordant twin sample, relative to the more generalizable results in the unrelated sample. These findings demonstrate that distinct connectivity patterns can represent weight variability, adding to mounting evidence that implicates atypical brain functioning with the accumulation and/or maintenance of elevated weight.