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WIREs Cogn Sci
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How we decide what to eat: Toward an interdisciplinary model of gut–brain interactions

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Abstract Everyday dietary decisions have important short‐term and long‐term consequences for health and well‐being. How do we decide what to eat, and what physiological and neurobiological systems are involved in those decisions? Here, we integrate findings from thus‐far separate literatures: (a) the cognitive neuroscience of dietary decision‐making, and (b) growing evidence of gut–brain interactions and especially influences of the gut microbiome on diet and health outcomes. We review findings that suggest that dietary decisions and food consumption influence nutrient sensing, homeostatic signaling in the gut, and the composition of the gut microbiome. In turn, the microbiome can influence host health and behavior. Through reward signaling pathways, the microbiome could potentially affect food and drink decisions. Such bidirectional links between gut microbiome and the brain systems underlying dietary decision‐making may lead to self‐reinforcing feedback loops that determine long‐term dietary patterns, body mass, and health outcomes. This article is categorized under: Economics > Individual Decision‐Making Psychology > Brain Function and Dysfunction Psychology > Reasoning and Decision Making
The homeostatic regulation of eating behavior. (a) Energy intake and expenditure need to be balanced in order to maintain a healthy body weight. Energy (food) intake is regulated by hunger and satiety signals. Becoming overweight is the consequence of a dysregulation of these systems and a resulting excessive energy intake. (b) The energy‐rich macronutrients and their metabolism in the gastrointestinal tract control energy intake by causing feelings of hunger and satiety in the CNS either directly or via metabolic and hormonal signals. Orexigenic signals (e.g., ghrelin) promote eating and feelings of hunger, while anorexigenic (e.g., insulin, leptin, CCK, GLP‐1, and PYY) signals decrease eating and promote feelings of satiety. Additionally, the gut microbiota interacts with the gut metabolism and thereby also influences the regulation of hunger and satiety. CCK, cholecystokinin; GLP‐1, glucagon‐like peptide 1; PYY, peptide YY
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A reinforcing feedback loop of dieting behavior, gut microbiome, and food reward processing. Gut microbial diversity strongly depends on the nutrient composition in the gut. Thus, gut microbial composition varies with dietary patterns. In turn, gut microbial signaling via bacterial metabolites, gut peptides, neurotransmitters, and immune pathways affects dietary decision‐making in the CNS. Several behaviors that are relevant for dietary decisions (e.g., impulsivity, reward seeking) are sensitive to gut microbial changes. 5‐HT, serotonin; CCK, cholecystokinin; CNS, central nervous system; DA, dopamine; GLP‐1, glucagon‐like peptide 1; Phe, phenylalanine; SCFA, short‐chain fatty acids; Trp, tryptophan
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Schematic representation of the several brain circuits, including the homeostatic system (green), valuation system (red), and cognitive control system (yellow) that interactively regulate eating behavior. Metabolic signals are forwarded to the brain by circulating hormones and the vagus nerve and are processed in the hypothalamus. The metabolic signals that arrive in the hypothalamus are integrated with reward signals that are generated in the valuation system and are modulated by the cognitive control system. ACC, anterior cingulate cortex; dlPFC, dorsolateral prefrontal cortex; GLP‐1, glucagon‐like peptide 1; Hyp, hypothalamus; LH, lateral hypothalamus; PVN, paraventricular nucleus; VMH, ventromedial hypothalamus; vmPFC, ventromedial prefrontal cortex; vStr, ventral striatum
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Psychology > Reasoning and Decision Making
Psychology > Brain Function and Dysfunction
Economics > Individual Decision-Making

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