Abstract
Obesity as a result of overeating as well as a number of well described eating disorders has been accurately considered to be a world-wide epidemic. Recently a number of theories backed by a plethora of scientifically sound neurochemical and genetic studies provide strong evidence that food addiction is similar to psychoactive drug addiction. Our laboratory has published on the concept known as Reward Deficiency Syndrome (RDS) which is a genetic and epigenetic phenomena leading to impairment of the brain reward circuitry resulting in a hypo-dopaminergic function. RDS involves the interactions of powerful neurotransmitters and results in abnormal craving behavior. A number of important facts which could help translate to potential therapeutic targets espoused in this focused review include: (1) consumption of alcohol in large quantities or carbohydrates binging stimulates the brain’s production of and utilization of dopamine; (2) in the meso-limbic 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) a significant correlation between blood glucose and cerebrospinal fluid concentrations of homovanillic acid the dopamine metabolite; (5) 2-deoxyglucose (2DG), the glucose analog, in pharmacological doses is associated with enhanced dopamine turnover and causes acute glucoprivation. Evidence from animal studies and fMRI in humans support the hypothesis that multiple, but similar brain circuits are disrupted in obesity and drug dependence and for the most part, implicate the involvement of DA-modulated reward circuits in pathologic eating behaviors. Based on a consensus of neuroscience research treatment of both glucose and drug like cocaine, opiates should incorporate dopamine agonist therapy in contrast to current theories and practices that utilizes dopamine antagonistic therapy. Considering that up until now clinical utilization of powerful dopamine D2 agonists have failed due to chronic down regulation of D2 receptors newer targets based on 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.
Highlights
Reward Deficiency Syndrome (RDS; Blum et al, 1996) caused by a Brain Reward Cascade dysfunction is linked to polymorphisms in the Dopaminergic system that cause hypo-dopaminergic function and result in abnormal craving behavior (Zhu and Shih, 1997)
For example, high levels of enkephalins are associated with pain suppression and low serotonin levels with depression, an individual with the Taq1 A1 allele of the Dopamine Receptor Gene (DRD2), lacks enough dopamine receptor sites to release the normal amount of dopamine into the Reward Center of the brain and dopamine function is reduced (Noble et al, 1991; Delis et al, 2013)
Humans possessing the A1 variant crave and seek substances and behaviors known to cause dopamine release preferentially at the nucleus accumbens (NAc) in the meso-limbic system (Stice and Dagher, 2010). They may become serious cocaine abusers or have unhealthy appetites, which lead to, eating disorders like obesity, overeating or at the other extreme, anorexia nervosa (AN), they suffer from high levels of stress over an extended period of time
Summary
Reward Deficiency Syndrome (RDS; Blum et al, 1996) caused by a Brain Reward Cascade dysfunction is linked to polymorphisms in the Dopaminergic system that cause hypo-dopaminergic function and result in abnormal craving behavior (Zhu and Shih, 1997).
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