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.
"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. "
"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. "
[Show abstract][Hide abstract] 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
"Brain reward processing and pleasurable experiences are ubiquitous in human behaviors such as tasting and eating food (Small et al., 2001), smelling odorants (Royet et al., 2000), listening to music (Menon and Levitin, 2005), reacting to sexual stimulation (Demos et al., 2012), winning games or money (Rademacher et al., 2010) and engaging in affiliative interactions (Krach et al., 2010). Moreover, abnormalities or alterations in reward processing are related to a range of disorders, including obesity (Stice et al., 2013) and psychiatric disorders (e.g., affective and eating disorders, schizophrenia) (Der-Avakian and Markou, 2012; Dichter et al., 2012; DiLeone et al., 2012). For example, anhedonia (i.e., the decreased response to pleasurable stimuli) and avolition (the lack of motivation) are considered primary features of major depression and schizophrenia (Der-Avakian and Markou, 2012). "
[Show abstract][Hide abstract] ABSTRACT: Brain reward systems mediate liking and wanting for food reward. Here, we explore the differential involvement of the following structures for these two components: the ventral and dorsal striatopallidal area, orbitofrontal cortex (OFC), anterior insula, and anterior cingulate. Twelve healthy female participants were asked to rate pleasantness (liking of food and non-food odors) and the desire to eat (wanting of odor-evoked food) during event-related functional magnetic resonance imaging (fMRI). The subjective ratings and fMRI were performed in hunger and satiety states. Activations of regions-of-interest were compared as a function of task (liking vs. wanting), odor category (food vs. non-food), and metabolic state (hunger vs. satiety). We found that the nucleus accumbens and ventral pallidum were differentially involved in liking or wanting during the hunger state, which suggests a reciprocal inhibitory influence between these structures. Neural activation of OFC subregions was correlated with either liking or wanting ratings, suggesting an OFC role in reward processing magnitude. Finally, during the hunger state, participants with a high body mass index exhibited less activation in neural structures underlying food reward processing. Our results suggest that food liking and wanting are two separable psychological constructs and may be functionally segregated within the cortico-striatopallidal circuit.
Social Cognitive and Affective Neuroscience 06/2014; 10(4). DOI:10.1093/scan/nsu086 · 7.37 Impact Factor
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