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
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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Available from: Liza Bekker
- "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.
Addiction Biology 09/2015; DOI:10.1111/adb.12315 · 5.36 Impact Factor
Available from: Marie Schaeffer
- "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.
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Cell metabolism 08/2015; 22(4). DOI:10.1016/j.cmet.2015.07.011 · 17.57 Impact Factor
Available from: Minati Singh
- "On the other hand, several imaging studies from obese population shows that greater BMI and overeating are associated with neurobiological pathways similar to those observed in drug addicts (Stice and Dagher, 2010; Stice et al., 2010; Volkow et al., 2012, 2013). In humans, feeding behaviors are more complex but pattern of food addiction appears to parallel substance dependence (Gearhardt et al., 2011; Dileone et al., 2012). Some argue that food addiction should be included in the DSM manual (Volkow and O'brien, 2007; Taylor et al., 2010) even though food addiction is not a categorized diagnosis within DSM-5. "
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ABSTRACT: Food is a potent natural reward and food intake is a complex process. Reward and gratification associated with food consumption leads to dopamine (DA) production, which in turn activates reward and pleasure centers in the brain. An individual will repeatedly eat a particular food to experience this positive feeling of gratification. This type of repetitive behavior of food intake leads to the activation of brain reward pathways that eventually overrides other signals of satiety and hunger. Thus, a gratification habit through a favorable food leads to overeating and morbid obesity. Overeating and obesity stems from many biological factors engaging both central and peripheral systems in a bi-directional manner involving mood and emotions. Emotional eating and altered mood can also lead to altered food choice and intake leading to overeating and obesity. Research findings from human and animal studies support a two-way link between three concepts, mood, food, and obesity. The focus of this article is to provide an overview of complex nature of food intake where various biological factors link mood, food intake, and brain signaling that engages both peripheral and central nervous system signaling pathways in a bi-directional manner in obesity.
Frontiers in Psychology 09/2014; 5:925. DOI:10.3389/fpsyg.2014.00925 · 2.80 Impact Factor
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