“Liking” and “Wanting” Linked to Reward Deficiency Syndrome (RDS): Hypothesizing Differential Responsivity in Brain Reward Circuitry

Department of Psychiatry and McKnight Brain Institute, University of Florida, Gainesville, FL 32610, USA.
Current pharmaceutical design (Impact Factor: 3.45). 01/2012; 18(1):113-8. DOI: 10.2174/138161212798919110
Source: PubMed

ABSTRACT In an attempt to resolve controversy regarding the causal contributions of mesolimbic dopamine (DA) systems to reward, we evaluate the three main competing explanatory categories: "liking,"learning," and "wanting" [1]. That is, DA may mediate (a) the hedonic impact of reward (liking), (b) learned predictions about rewarding effects (learning), or (c) the pursuit of rewards by attributing incentive salience to reward-related stimuli (wanting). We evaluate these hypotheses, especially as they relate to the Reward Deficiency Syndrome (RDS), and we find that the incentive salience or "wanting" hypothesis of DA function is supported by a majority of the evidence. Neuroimaging studies have shown that drugs of abuse, palatable foods, and anticipated behaviors such as sex and gaming affect brain regions involving reward circuitry, and may not be unidirectional. Drugs of abuse enhance DA signaling and sensitize mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Addictive drugs have in common that they are voluntarily selfadministered, they enhance (directly or indirectly) dopaminergic synaptic function in the nucleus accumbens (NAC), and they stimulate the functioning of brain reward circuitry (producing the "high" that drug users seek). Although originally believed simply to encode the set point of hedonic tone, these circuits now are believed to be functionally more complex, also encoding attention, reward expectancy, disconfirmation of reward expectancy, and incentive motivation. Elevated stress levels, together with polymorphisms of dopaminergic genes and other neurotransmitter genetic variants, may have a cumulative effect on vulnerability to addiction. The RDS model of etiology holds very well for a variety of chemical and behavioral addictions.

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    • "Alternatively, the increased propensity for DIO in offspring of obese mothers may be mediated via programmed dysregulation of the central mechanisms involved in palatable food intake: namely the mesocorticolimbic dopamine pathway from the ventral tegmental area (VTA) to the nucleus accumbens (NAcc). Dopaminergic signalling in the NAcc is thought to control incentive salience, or the motivated " wanting " of palatable foods, whilst opioidergic inputs onto the same pathway are thought to signal the pleasure associated with eating tasty foods and so influence food preferences or the " liking " of palatable foods (Blum et al., 2012; Egecioglu et al., 2011; Volkow et al., 2011). Connections between the reward system and the hypothalamus are critical for the regulation of reward-related feeding (Dietrich et al., 2012; Leinninger et al., 2011). "
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    ABSTRACT: Obesity in women of child-bearing age is a growing problem in developed and developing countries. Evidence from human studies indicates that maternal BMI correlates with offspring adiposity from an early age and predisposes to metabolic disease in later life. Thus the early life environment is an attractive target for intervention to improve public health. Animal models have been used to investigate the specific physiological outcomes and mechanisms of developmental programming that result from exposure to maternal obesity in utero. From this research, targeted intervention strategies can be designed. In this review we summarise recent progress in this field, with a focus on cardiometabolic disease and central control of appetite and behaviour. We highlight key factors that may mediate programming by maternal obesity, including leptin, insulin and ghrelin. Finally, we explore potential lifestyle and pharmacological interventions in humans and the current state of evidence from animal models. Copyright © 2015. Published by Elsevier Inc.
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    • "In this regard, the literature provides small, but convincing evidence for a link between biological brain abnormalities in patients addicted to substances and similar brain abnormalities in patients with IA. Blum et al. (2012) persuasively linked a reward-deficient aberrant behavior (RDAB) to abnormal dopaminergic function in the nucleus accumbens, and argued that RDABs can be observed both in conventional substance-use disorders, and also in excessive internet gaming and related activities that stimulate excessive dopamine release, such as gambling. "
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    • "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. These clusters seem to be convergent with the neurotransmitters involved in the brain reward circuitry like serotonin; endorphins; GABA; dopamine; cannabinoids; ACH and leptin, and specifically in the brain reward cascade (Yarnell et al., 2013) and RDS (Downs et al., 2013). "
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    ABSTRACT: Obesity and many well described eating disorders are accurately considered a global epidemic. The consequences of Reward Deficiency Syndrome, a genetic and epigenetic phenomena that involves the interactions of powerful neurotransmitters, are impairments of brain reward circuitry, hypodopaminergic function and abnormal craving behavior. Numerous sound neurochemical and genetic studies provide strong evidence that food addiction is similar to psychoactive drug addiction. Important facts which could translate to potential therapeutic targets espoused in this review include: 1) brain dopamine (DA) production and use is stimulated by consumption of alcohol in large quantities or carbohydrates bingeing; 2) in the mesolimbic system the enkephalinergic neurons are in close proximity, to glucose receptors; 3) highly concentrated glucose activates the calcium channel to stimulate dopamine release from P12 cells; 4) blood glucose and cerebrospinal fluid concentrations of homovanillic acid, the dopamine metabolite, are significantly correlated and 5) 2-deoxyglucose the glucose analogue, in pharmacological doses associates with enhanced dopamine turnover and causes acute glucoprivation. Evidence from animal studies and human fMRI support the hypothesis that multiple, but similar brain circuits are disrupted in obesity and drug dependence and DA-modulated reward circuits are involved in pathologic eating behaviors. Treatment for addiction to glucose and drugs alike, based on a consensus of neuroscience research, should incorporate dopamine agonist therapy, in contrast to current theories and practices that use dopamine antagonists. Until now, powerful dopamine-D2 agonists have failed clinically, due to chronic down regulation of D2 receptors instead, consideration of novel less powerful D2 agonists that up-regulate D2 receptors seems prudent. We encourage new strategies targeted at improving DA function in the treatment and prevention of obesity a subtype of reward deficiency.
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