Article

The drive to eat: Comparisons and distinctions between mechanisms of food reward and drug addiction

Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA.
Nature Neuroscience (Impact Factor: 16.1). 09/2012; 15(10):1330-1335. DOI: 10.1038/nn.3202

ABSTRACT

The growing rates of obesity have prompted comparisons between the uncontrolled intake of food and drugs; however, an evaluation of the equivalence of food- and drug-related behaviors requires a thorough understanding of the underlying neural circuits driving each behavior. Although it has been attractive to borrow neurobiological concepts from addiction to explore compulsive food seeking, a more integrated model is needed to understand how food and drugs differ in their ability to drive behavior. In this Review, we will examine the commonalities and differences in the systems-level and behavioral responses to food and to drugs of abuse, with the goal of identifying areas of research that would address gaps in our understanding and ultimately identify new treatments for obesity or drug addiction.

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    • "We and other have previously reported that sucrose overconsumption during adolescence decreased the motivation of rats (Vendruscolo et al., 2010a,b) and mice (Frazier et al., 2008) to obtain palatable foods in adulthood, using operant progressive ratio schedules. Interestingly, such effects have not been observed with drugs of abuse such as cocaine or alcohol (Vendruscolo et al., 2010a,b), indicating some differences in the neurobiological substrates underlying the intake of food and of drugs of abuse (DiLeone et al., 2012). Here, in accordance with the previous studies, we report that sucrose overconsumption during adolescence induced a protracted decrease in the consumption of both sucrose and saccharin using a two-bottle free choice test. "
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    ABSTRACT: Adolescence is a critical period characterized by major neurobiological changes. Chronic stimulation of the reward system might constitute an important factor in vulnerability to pathological development. In spite of the dramatic increase in the consumption of sweet palatable foods during adolescence in our modern societies, the long-term consequences of such exposure on brain reward processing remain poorly understood. Here, we investigated in rats the long-lasting effects of sugar overconsumption during their adolescence on their adult reactivity to the hedonic properties of sweet rewards. Adolescent rats with continuous access to 5% sucrose solution (from postnatal day 30-46) showed escalating intake. At adulthood (post-natal day 70), using two-bottle free choice tests, sucrose-exposed rats showed lower intake than non-exposed rats suggesting decreased sensitivity to the rewarding properties of sucrose. In Experiment 1, we tested their hedonic-related orofacial reactions to intraoral infusion of tasty solutions. We showed that sucrose-exposed rats presented less hedonic reactions in response to sweet tastes leaving the reactivity to water or quinine unaltered. Hence, in Experiment 2, we observed that this hedonic deficit is associated with lower c-Fos expression levels in the nucleus accumbens, a brain region known to play a central role in hedonic processing. These findings demonstrate that a history of high sucrose intake during the critical period of adolescence induces long-lasting deficits in hedonic treatment that may contribute to reward-related disorders.
    Full-text · Article · Jan 2016 · European Journal of Neuroscience
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    • "Binge eating (BE) in humans is defined as overconsumption of food, not necessarily driven by hunger, in a discrete time period, concomitantly with a sense of loss of control over eating during the binge (American Psychological Association 2013; Babbs, Wojnicki, & Corwin 2012). BE shares similar behavioral features with drug seeking, including incontrollable consummatory behavior , tolerance as represented by escalation of food or drug intake, and withdrawal-like symptoms—and even craving—when the food or drug is not available (DiLeone, Taylor, & Picciotto 2012; Wise 2013). BE and drug seeking in humans increase the risk for various negative consequences, including overweight and obesity for BE, and anxiety and mood disorders for drug seeking (Calero-Elvira et al. 2009; Field et al. 2012; Piran & Robinson 2011; Sonneville et al. 2013). "
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    ABSTRACT: Binge eating (BE) and drug seeking share similar behavioral features, including loss of control over consumption and compulsive seeking of the craved substance. Previous studies in animal models have demonstrated a complex interaction between 'state' BE, produced by intermittent access to a palatable diet, and 'trait' BE, a phenotypical proneness towards overeating. In the present study, we examined the relationship between state and trait BE and cocaine seeking. We used Otsuka Long Evans Tokushima Fatty rats, a genetic model for obesity that demonstrates BE-like behavior, and Long Evans Tokushima Otsuka controls. They received a schedule of limited access to a palatable diet (3 days/week or 5 days/week access to Ensure for a month). Next, they underwent cocaine self-administration training (1 mg/kg, 1 hour/day for 10 days) followed by extinction sessions (7 days). We found that the degree of BE-like behavior and the state and trait BE combination predicted cocaine craving patterns. Lower levels of dopamine D2 receptors in the prefrontal cortex were correlated with increased drug craving. Moreover, restricted access to an attractive diet was found to be a risk factor for heightened cocaine craving, particularly in trait binge eaters, as rats on the 3 days/week access schedule persistently failed to cease cocaine seeking throughout extinction. Hence, we postulate a joint role of state and trait BE as risk factors for heightened cocaine craving.
    Full-text · Article · Sep 2015 · Addiction Biology
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    • "These observations raise the question of the specific contribution of ARC versus extra-ARC neurons in the balance between reward-driven or energy-driven nutrient intake. This question becomes crucial when sugar-and fat-rich diets are readily available and may contribute to addictive-like feeding behavior (DiLeone et al., 2012). Mouse models with transient or chronic loss of AgRP neuron activity provide an ideal tool to dissect the role of homeostatic versus non-homeostatic regulation of energy intake. "
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    ABSTRACT: Feeding behavior is exquisitely regulated by homeostatic and hedonic neural substrates that integrate energy demand as well as the reinforcing and rewarding aspects of food. Understanding the net contribution of homeostatic and reward-driven feeding has become critical because of the ubiquitous source of energy-dense foods and the consequent obesity epidemic. Hypothalamic agouti-related peptide-secreting neurons (AgRP neurons) provide the primary orexigenic drive of homeostatic feeding. Using models of neuronal inhibition or ablation, we demonstrate that the feeding response to a fast ghrelin or serotonin receptor agonist relies on AgRP neurons. However, when palatable food is provided, AgRP neurons are dispensable for an appropriate feeding response. In addition, AgRP-ablated mice present exacerbated stress-induced anorexia and palatable food intake-a hallmark of comfort feeding. These results suggest that, when AgRP neuron activity is impaired, neural circuits sensitive to emotion and stress are engaged and modulated by food palatability and dopamine signaling. Copyright © 2015 Elsevier Inc. All rights reserved.
    Full-text · Article · Aug 2015 · Cell metabolism
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