"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: 3.29). 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.


Available from: Marlene Oscar-Berman, Jun 02, 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is pandemic worldwide, and hyperphagia remains extremely difficult for physicians to treat. Currently, appetite suppression continues to be the focus of antiobesity drugs, and these drugs are clearly unsuccessful in the long term. Although the food addiction concept remains controversial, this hypothesis provides a matrix in which to examine disordered eating behaviors and their similarities to addiction. This article looks at food addiction as the high end of an eating disorder continuum, with anorexia nervosa as the low end. Similarities with drug addiction provide an avenue leading to new and potentially more successful treatments.
    06/2014; 1(2):83-88. DOI:10.1007/s40429-014-0010-2
  • Source
    Internet Addiction. Neuroscientific Approaches and Therapeutical Interventions, 1^ edited by Christian Montag, Martin Reuter, 02/2015: chapter 10: pages 151-165; Springer International Publishing., ISBN: 978-3-319-07241-8
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Alcohol-dependent patients have been shown to faster approach than avoid alcohol stimuli on the Approach Avoidance Task (AAT). This so-called alcohol approach bias has been associated with increased brain activation in the medial prefrontal cortex and nucleus accumbens. Cognitive bias modification (CBM) has been used to retrain the approach bias with the clinically relevant effect of decreasing relapse rates one year later. The effects of CBM on neural signatures of approach/avoidance tendencies remain hitherto unknown. In a double-blind placebo-controlled design, 26 alcohol-dependent in-patients were assigned to a CBM or a placebo training group. Both groups performed the AAT for three weeks: in CBM training, patients pushed away 90 percent of alcohol cues; this rate was 50 percent in placebo training. Before and after training, patients performed the AAT offline, and in a 3 T magnetic resonance imaging scanner. The relevant neuroimaging contrast for the alcohol approach bias was the difference between approaching versus avoiding alcohol cues relative to soft drink cues: [(alcohol pull > alcohol push) > (soft drink pull > soft drink push)]. Before training, both groups showed significant alcohol approach bias-related activation in the medial prefrontal cortex. After training, patients in the CBM group showed stronger reductions in medial prefrontal cortex activation compared with the placebo group. Moreover, these reductions correlated with reductions in approach bias scores in the CBM group only. This suggests that CBM affects neural mechanisms involved in the automatic alcohol approach bias, which may be important for the clinical effectiveness of CBM.
    Addiction Biology 02/2015; DOI:10.1111/adb.12221 · 5.93 Impact Factor