Abstract

Abstract Introduction Previous studies indicate that lack of sleep might increase risk for unhealthy eating and obesity. This is particularly important during adolescence, when most youth sleep less than the recommended 8-10 hours/night and dietary habits are developed that extend into adulthood. This study investigated the relationship between multi-night sleep restriction and the appeal of food, including neuroimaging to examine the impact on brain responses to food-related stimuli. Methods Healthy 14-17 year-old adolescents (n=39) completed an experimental sleep manipulation across consecutive five-night periods to compare nightly sleep of approximately 9 hours (healthy sleep duration) vs. about 6.3 hours (mild sleep restriction). At the end of each week, participants underwent functional MRI while performing a visual food appeal task. The task included 42 photos in each of four food categories (sweets, snacks, fast-food, meat/fruit/vegetable) and one non-food category. Photos were presented every 3 seconds in blocks of 7 within each category; 6 interleaved blocks per category. Teens rated the appeal of each block of photos. General linear modeling explained regional brain response according to categorical presentation time-courses. Results The pattern of brain responses to the different food types was similar across the two sleep conditions. However, the sleep manipulation led to significant regional effects when contrasting the totality of food vs non-food images. Specifically, when compared to non-food, food images overall resulted in greater activation in the ventral tegmental area (VTA) and substantia nigra (SN) during sleep restriction. Both regions have been previously shown to be involved in processing reward-related information. Conclusion Our findings suggest neuronal responses in reward circuitry for teens viewing food images are influenced by sleep duration. Sleep restriction may affect reward processing of food in teens by increasing brain activation in VTA/SN network components that underlie dopamine-mediated motivational drive. Support Supported by NIH R01HL120879

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