Dual Roles of Dopamine in Food and Drug Seeking: The Drive-Reward Paradox

Abstract

The question of whether (or to what degree) obesity reflects addiction to high energy foods often narrows to the question of whether the overeating of these foods causes the same long-term neuroadaptations as are identified with the late stages of addiction. Of equal or perhaps greater interest is the question of whether common brain mechanisms mediate the acquisition and development of eating and drug-taking habits. The earliest evidence on this question is rooted in early studies of brain stimulation reward. Lateral hypothalamic electrical stimulation can be reinforcing in some conditions and can motivate feeding in others. That stimulation of the same brain region should be both reinforcing and drive-inducing is paradoxical; why should an animal work to induce a drive-like state such as hunger? This is known as the “drive-reward paradox.” Insights into the substrates of the drive-reward paradox suggest an answer to the controversial question of whether the dopamine system—a system “downstream” from the stimulated fibers of the lateral hypothalamus—is more critically involved in “wanting” or in “liking” of various rewards including food and addictive drugs. That the same brain circuitry is implicated in the motivation for and the reinforcement by both food and addictive drugs extends the argument for a common mechanism underlying compulsive overeating and compulsive drug-taking.

Dopamine and glucose, obesity, and reward deficiency syndrome

“…Behaviors reported by self-identified food addicts conform to the seven DSM-5 criteria for substance use disorders (Campbell et al, 2013). This notion of commonality has been confirmed by studies that show that food craving, in both normal weight and obese patients, activates similar areas of the brain to those indicated in drug seeking (Wise, 2013). Avena (2010) adequately defined binging, withdrawal, and craving by presenting evidence from animal models of binge eating of sucrose or glucose, in a review that summarized evidence for “food addiction.” In a PANTHER analysis of gene array expression performed on 152 unique genes, resulting in a total of 193 multiple-factor (MF) assignments, sorted into 20 categories (Avena et al, 2010; Blum et al, 2012a,b) found gene clusters expressed significantly differently, in the ad libitum sucrose group compared to the sucrose binge eating group.…”

A comparison of neural responses to appetitive and aversive stimuli in humans and other mammals

“…Our focus on animal studies which use the passive presentation of both aversive and appetitive stimuli has precluded many of the seminal studies in this area, but it is important to acknowledge the work of some of the main contributors not otherwise noted here. For instance, Fibiger and Phillips sketched an early brain map of dopamine's impact on positive reinforcement (Phillips et al, 1992;Phillips and Fibiger, 1973), Shultz and colleagues were instrumental in uncovering the role of dopaminergic responses in prediction errors (Lak et al, 2014;Mirenowicz and Schultz, 1996), Carelli, Deadwyler and colleagues were integral in separating dopaminergic responses to drug vs. 'natural' rewards (Carelli et al, 2000;Deadwyler, 2010), and the work of both Wise and Salamone continue to greatly influence our conceptual understanding of this neurotransmitter in response to both appetitive and aversive stimuli (for interesting recent reviews see Salamone and Correa, 2013;Wise, 2013).…”

Neuroendocrine abnormalities in Parkinson's disease

“…Dopaminergic dysfunction : owing to the role of dopamine in the regulation of the hedonic mechanisms of feeding behaviour,93 dopamine dysfunction producing anorexigenic signals in the hypothalamus has been proposed to contribute to weight loss in PD.…”