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Open AccessJournal ArticleDOI

Weight Gain Is Associated with Reduced Striatal Response to Palatable Food

TLDR
Testing whether overeating leads to reduced striatal responsivity to palatable food intake in humans using repeated-measures functional magnetic resonance imaging indicated that women who gained weight over a 6 month period showed a reduction in striatal response toPalatable food consumption relative to weight-stable women.
Abstract
Consistent with the theory that individuals with hypofunctioning reward circuitry overeat to compensate for a reward deficit, obese versus lean humans have fewer striatal D2 receptors and show less striatal response to palatable food intake. Low striatal response to food intake predicts future weight gain in those at genetic risk for reduced signaling of dopamine-based reward circuitry. Yet animal studies indicate that intake of palatable food results in downregulation of D2 receptors, reduced D2 sensitivity, and decreased reward sensitivity, implying that overeating may contribute to reduced striatal responsivity. Thus, we tested whether overeating leads to reduced striatal responsivity to palatable food intake in humans using repeated-measures functional magnetic resonance imaging. Results indicated that women who gained weight over a 6 month period showed a reduction in striatal response to palatable food consumption relative to weight-stable women. Collectively, results suggest that low sensitivity of reward circuitry increases risk for overeating and that this overeating may further attenuate responsivity of reward circuitry in a feedforward process.

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Citations
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Journal ArticleDOI

Reward mechanisms in obesity: new insights and future directions.

TL;DR: Recent advances in the understanding of the brain circuitries that regulate hedonic aspects of feeding behavior will be reviewed and emerging evidence suggesting that obesity and drug addiction may share commonHedonic mechanisms will also be considered.
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The dopamine motive system: implications for drug and food addiction.

TL;DR: Dopamine contributes to addiction and obesity through its differentiated roles in reinforcement, motivation and self-regulation, referred to here as the 'dopamine motive system', which, if compromised, can result in increased, habitual and inflexible responding.
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Neural Correlates of Food Addiction

TL;DR: Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in responseto food intake.
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Obesity and the brain: how convincing is the addiction model?

TL;DR: The current evidence for the link between addiction and obesity is examined, identifying several fundamental shortcomings in the model, as well as weaknesses and inconsistencies in the empirical support for it from human neuroscientific research.
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Interoception, contemplative practice, and health.

TL;DR: It is concluded that maladaptive construal of bodily sensations may lie at the heart of many contemporary maladies, and that contemplative practices may attenuate these interpretative biases, restoring a person’s sense of presence and agency in the world.
References
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Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats

TL;DR: Overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating, demonstrating that common hedonic mechanisms may underlie obesity and drug addiction.
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TL;DR: The hypothesis that there are two separate motivational systems: one orchestrating approach and another avoidance behaviours is supported, suggesting that the reward value of food is represented here.
Journal ArticleDOI

Neural responses during anticipation of a primary taste reward.

TL;DR: The findings indicate that when rewards are predictable, brain regions recruited during expectation are, in part, dissociable from areas responding to reward receipt.
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