Oren Contreras-Rodríguez1, Cristina Martín-Pérez2, Raquel Vilar-López3, Antonio Verdejo-Garcia4. 1. Red de Trastornos Adictivos, Universidad de Granada, Granada; Psychiatry Department, Bellvitge University Hospital, Bellvitge Biomedical Research Institute-IDIBELL, and Centro de Investigación Biomédica en Red de Salud Mental, Barcelona. 2. Red de Trastornos Adictivos, Universidad de Granada, Granada; Institute of Neuroscience F. Oloriz, Universidad de Granada, Granada, Spain. 3. Red de Trastornos Adictivos, Universidad de Granada, Granada; Mind, Brain and Behavior Research Center, Universidad de Granada, Granada, Spain. 4. Red de Trastornos Adictivos, Universidad de Granada, Granada; Institute of Neuroscience F. Oloriz, Universidad de Granada, Granada, Spain; School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne, Australia. Electronic address: Antonio.Verdejo@monash.edu.
Abstract
BACKGROUND: The food addiction model proposes that obesity overlaps with addiction in terms of neurobiological alterations in the striatum and related clinical manifestations (i.e., craving and persistence of unhealthy habits). Therefore, we aimed to examine the functional connectivity of the striatum in excess-weight versus normal-weight subjects and to determine the extent of the association between striatum connectivity and individual differences in food craving and changes in body mass index (BMI). METHODS: Forty-two excess-weight participants (BMI > 25) and 39 normal-weight participants enrolled in the study. Functional connectivity in the ventral and dorsal striatum was indicated by seed-based analyses on resting-state data. Food craving was indicated with subjective ratings of visual cues of high-calorie food. Changes in BMI between baseline and 12 weeks follow-up were assessed in 28 excess-weight participants. Measures of connectivity in the ventral striatum and dorsal striatum were compared between groups and correlated with craving and BMI change. RESULTS: Participants with excess weight displayed increased functional connectivity between the ventral striatum and the medial prefrontal and parietal cortices and between the dorsal striatum and the somatosensory cortex. Dorsal striatum connectivity correlated with food craving and predicted BMI gains. CONCLUSIONS: Obesity is linked to alterations in the functional connectivity of dorsal striatal networks relevant to food craving and weight gain. These neural alterations are associated with habit learning and thus compatible with the food addiction model of obesity.
BACKGROUND: The food addiction model proposes that obesity overlaps with addiction in terms of neurobiological alterations in the striatum and related clinical manifestations (i.e., craving and persistence of unhealthy habits). Therefore, we aimed to examine the functional connectivity of the striatum in excess-weight versus normal-weight subjects and to determine the extent of the association between striatum connectivity and individual differences in food craving and changes in body mass index (BMI). METHODS: Forty-two excess-weight participants (BMI > 25) and 39 normal-weight participants enrolled in the study. Functional connectivity in the ventral and dorsal striatum was indicated by seed-based analyses on resting-state data. Food craving was indicated with subjective ratings of visual cues of high-calorie food. Changes in BMI between baseline and 12 weeks follow-up were assessed in 28 excess-weight participants. Measures of connectivity in the ventral striatum and dorsal striatum were compared between groups and correlated with craving and BMI change. RESULTS:Participants with excess weight displayed increased functional connectivity between the ventral striatum and the medial prefrontal and parietal cortices and between the dorsal striatum and the somatosensory cortex. Dorsal striatum connectivity correlated with food craving and predicted BMI gains. CONCLUSIONS:Obesity is linked to alterations in the functional connectivity of dorsal striatal networks relevant to food craving and weight gain. These neural alterations are associated with habit learning and thus compatible with the food addiction model of obesity.
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