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The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.

ABSTRACT: What we eat, when and how much, all are influenced by brain reward mechanisms that generate "liking" and "wanting" for foods. As a corollary, dysfunction in reward circuits might contribute to the recent rise of obesity and eating disorders. Here we assess brain mechanisms known to generate "liking" and "wanting" for foods and evaluate their interaction with regulatory mechanisms of hunger and satiety, relevant to clinical issues. "Liking" mechanisms include hedonic circuits that connect together cubic-millimeter hotspots in forebrain limbic structures such as nucleus accumbens and ventral pallidum (where opioid/endocannabinoid/orexin signals can amplify sensory pleasure). "Wanting" mechanisms include larger opioid networks in nucleus accumbens, striatum, and amygdala that extend beyond the hedonic hotspots, as well as mesolimbic dopamine systems, and corticolimbic glutamate signals that interact with those systems. We focus on ways in which these brain reward circuits might participate in obesity or in eating disorders.

SUBMITTER: Berridge KC

PROVIDER: S-EPMC2913163 | biostudies-other | 2010 Sep

REPOSITORIES: biostudies-other

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The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.

Berridge Kent C KC Ho Chao-Yi CY Richard Jocelyn M JM DiFeliceantonio Alexandra G AG

Brain research 20100411

What we eat, when and how much, all are influenced by brain reward mechanisms that generate "liking" and "wanting" for foods. As a corollary, dysfunction in reward circuits might contribute to the recent rise of obesity and eating disorders. Here we assess brain mechanisms known to generate "liking" and "wanting" for foods and evaluate their interaction with regulatory mechanisms of hunger and satiety, relevant to clinical issues. "Liking" mechanisms include hedonic circuits that connect togethe ...[more]

PMID: 20388498

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Project description:According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with psychotherapy. Genetic and other biological factors (toxic, infectious, or traumatic) may increase sensitivity to the induction of relevant neuroplastic changes. Reversal or compensation of these neuroplastic adjustments may explain the effects of biological therapies in treating depression.

Project description:The aims of this review were to map and summarize data currently available about 1) key dimensions of eating pleasure; 2) associations of eating pleasure, and its key dimensions, with dietary and health outcomes and 3) the most promising intervention strategies using eating pleasure to promote healthy eating. Using the scoping review methodology, a comprehensive search of the peer-reviewed literature (Medline, PsycInfo, Embase, ERIC, Web of Science, CINAHL, ABI/Inform global and Sociology Abstract) and of the grey literature (ProQuest Dissertations & Theses and Google) was carried out by two independent reviewers. We included 119 of the 28,908 studies found. In total, 89 sub-dimensions of eating pleasure were grouped into 22 key dimensions. The most frequently found related to sensory experiences (in 50.9% of the documents), social experiences (42.7%), food characteristics besides sensory attributes (27.3%), food preparation process (19.1%), novelty (16.4%), variety (14.5%), mindful eating (13.6%), visceral eating (12.7%), place where food is consumed (11.8%) and memories associated with eating (10.9%). Forty-five studies, mostly cross-sectional (62.2%), have documented links between eating pleasure and dietary and/or health outcomes. Most studies (57.1%) reported favorable associations between eating pleasure and dietary outcomes. For health outcomes, results were less consistent. The links between eating pleasure and both dietary and health outcomes varied according to the dimensions of eating pleasure studied. Finally, results from 11 independent interventions suggested that strategies focusing on sensory experiences, cooking and/or sharing activities, mindful eating, and positive memories related to healthy food may be most promising. Thus, eating pleasure may be an ally in the promotion of healthy eating. However, systematically developed, evidence-based interventions are needed to better understand how eating pleasure may be a lever for healthy eating.

Dataset Information

The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.

Publications

The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.

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