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

Abstract

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.

Keywords: Addiction transfer; Bariatric surgery; Cross tolerance; Dopamine; Reward Deficiency Syndrome; Reward genes.

Conflict of interest statement

Conflict of Interest

Kenneth Blum, PhD owns patents related to KB220Z and has provided LifeGen, Inc, San Diego, California with worldwide exclusive rights. Kenneth Blum owns stock in LifeGen, Inc. John Giordano is a Lifegen, Inc partner. No other author claims any conflict of interest.

Figures

Figure 1. Illustrates a positive response to KB220Z compared to placebo in triple blind randomized placebo controlled study in psychostimulant abusers undergoing protracted abstinence (modified from Blum et al. [94]

This is the first report to demonstrate involvement of the prefrontal cortex in the qEEG response to a natural putative D2 agonist, especially evident in dopamine D2 A1 allele subjects in agreement with NIDA scientists as well as others in terms of the use of D2 agonist therapy to treat additive behaviors [95,96]. These authors concluded that DA/5-HT releasers and D2 agonists might be useful therapeutic adjuncts for the treatment of cocaine and alcohol addiction, obesity, and even attention deficit disorder and depression [95]. Of particular interest germane to bariatric surgery Brandacher et al. [97] reported that Tryptophan depletion in morbidly obese patients due to chronic immune activation persists in spite of significant weight reduction following bariatric surgery. They suggest that this finding might be responsible for diminished serotonin functions, leading to unchanged satiety dysregulation and play a role in reward-deficiency-syndrome.