Neuro-Genetics of Reward Deficiency Syndrome (RDS) as the Root Cause of "Addiction Transfer": A New Phenomenon Common after Bariatric Surgery

Department of Psychiatry, Mcknight Brain Institute, University of Florida, College of Medicine, Gainesville, Florida, USA
Journal of genetic syndrome & gene therapy 12/2011; 2012(1). DOI: 10.4172/2157-7412.S2-001
Source: PubMed


Now after many years of successful bariatric (weight-loss) surgeries directed at the obesity epidemic clinicians are reporting that some patients are replacing compulsive overeating with newly acquired compulsive disorders such as alcoholism, gambling, drugs, and other addictions like compulsive shopping and exercise. This review article explores evidence from psychiatric genetic animal and human studies that link compulsive overeating and other compulsive disorders to explain the phenomenon of addiction transfer. Possibly due to neurochemical similarities, overeating and obesity may act as protective factors reducing drug reward and addictive behaviors. In animal models of addiction withdrawal from sugar induces imbalances in the neurotransmitters, acetylcholine and dopamine, similar to opiate withdrawal. Many human neuroimaging studies have supported the concept of linking food craving to drug craving behavior. Previously our laboratory coined the term Reward Deficiency Syndrome (RDS) for common genetic determinants in predicting addictive disorders and reported that the predictive value for future RDS behaviors in subjects carrying the DRD2 Taq A1 allele was 74%. While poly genes play a role in RDS, we have also inferred that disruptions in dopamine function may predispose certain individuals to addictive behaviors and obesity. It is now known that family history of alcoholism is a significant obesity risk factor. Therefore, we hypothesize here that RDS is the root cause of substituting food addiction for other dependencies and potentially explains this recently described Phenomenon (addiction transfer) common after bariatric surgery.

Download full-text


Available from: Marlene Oscar-Berman, Oct 06, 2015
90 Reads
  • Source
    • "The finding of decreased D2/D3 availability may explain in part the increased risk of drug seeking behavior reported following bariatric surgery. Our hypothesis that the real culprit in obesity may be RDS is supported by this finding (Blum et al., 2011a,b). Increased alcohol intake following bypass surgery was reported by Hajnal et al. (2012) and a reduced reward-related (e.g., striatal) neural activation has been observed following bariatric surgery. "
    [Show abstract] [Hide abstract]
    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.
    Frontiers in Psychology 09/2014; 5:919. DOI:10.3389/fpsyg.2014.00919 · 2.80 Impact Factor
  • Source
    • "This phenomenon has been thought to be connected with the Reward Deficiency Syndrome (RDS), which is related to dopamine receptor defects, and has been described as a genetic disease [85]. It has been thought that, in those subjects where “Transfer of Addiction” takes place after bariatric surgery, obesity and thus compulsive eating behavior could be a sort of defense mechanism towards other addictions [86]. It is known that insulin can affect dopamine receptors and vice versa [87], the activity of the dopamine transporter can in fact be increased by high insulin levels {{96}}. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Consensus exists that several bariatric surgery procedures produce a rapid improvement of glucose homeostasis in obese diabetic patients, improvement apparently uncorrelated with the degree of eventual weight loss after surgery. Several hypotheses have been suggested to account for these results: among these, the anti-incretin, the ghrelin and the lower-intestinal dumping hypotheses have been discussed in the literature. Since no clear-cut experimental results are so far available to confirm or disprove any of these hypotheses, in the present work a mathematical model of the glucose-insulin-incretin system has been built, capable of expressing these three postulated mechanisms. The model has been populated with critically evaluated parameter values from the literature, and simulations under the three scenarios have been compared. The modeling results seem to indicate that the suppression of ghrelin release is unlikely to determine major changes in short-term glucose control. The possible existence of an anti-incretin hormone would be supported if an experimental increase of GIP concentrations were evident post-surgery. Given that, on the contrary, collected evidence suggests that GIP concentrations decrease post-surgery, the lower-intestinal dumping hypothesis would seem to describe the mechanism most likely to produce the observed normalization of Type 2 Diabetes Mellitus (T2DM) after bariatric surgery. The proposed model can help discriminate among competing hypotheses in a context where definitive data are not available and mechanisms are still not clear.
    Theoretical Biology and Medical Modelling 05/2012; 9(1):16. DOI:10.1186/1742-4682-9-16 · 0.95 Impact Factor
  • [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
Show more