Abstract

Overweight and obesity are associated with functional and structural alterations in the brain, but how these associations change across critical developmental periods remains unknown. Here, we examined the relationship between age, body mass index (BMI) and cortical thickness (CT) in healthy adolescents (n = 70; 14–19 y) and adults (n = 75; 25–45 y). We also examined the relationship between adiposity, impulsivity, measured by delay discounting (DD), and CT of the inferior frontal gyrus (IFG), a region key to impulse control. A significant age-by-BMI interaction was observed in both adolescents and adults; however, the direction of this relationship differed between age groups. In adolescents, increased age-adjusted BMI Z-score attenuated age-related CT reductions globally and in frontal, temporal and occipital regions. In adults, increased BMI augmented age-related CT reductions, both globally and in bilateral parietal cortex. Although DD was unrelated to adiposity in both groups, increased DD and adiposity were both associated with reduced IFG thickness in adolescents and adults. Our findings suggest that the known age effects on CT in adolescence and adulthood are moderated by adiposity. The association between weight, cortical development and its functional implications would suggest that future studies of adolescent and adult brain development take adiposity into account.

Highlights

  • While obesity is defined as excess fat mass (body mass index (BMI) > 29.9 kg/m2), it is increasingly recognised as a neurobehavioural condi­ tion with metabolic consequences (O’Rahilly and Farooqi, 2008)

  • We examined the functional correlates of adiposity-related alterations by assessing whether adiposity and delay discounting, taken as a measure of impulsivity, related to cortical thickness (CT) of the inferior frontal gyrus (IFG), a brain region strongly linked to impulse control (Aron et al, 2014)

  • Because a priori hypotheses focused on the interaction of age and weight status an interaction term was added to the main effect model

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Summary

Introduction

While obesity is defined as excess fat mass (body mass index (BMI) > 29.9 kg/m2), it is increasingly recognised as a neurobehavioural condi­ tion with metabolic consequences (O’Rahilly and Farooqi, 2008). Adolescent overweight re­ lates to reduced cardiometabolic health (Reilly and Kelly, 2011) and to poorer psychological outcomes, including increased inci­ dence of depression and problematic alcohol use (Anderson et al, 2007; Fonseca et al, 2009). These findings may be explained, in part, by the effect of adiposity on cortical morphometric features, such as cortical thickness (CT) or grey matter volume (GMV), which undergo dynamic changes throughout adolescence

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