Abstract
In accord with the new definition of addiction published by American Society of Addiction Medicine (ASAM) it is well-known that individuals who present to a treatment center involved in chemical dependency or other documented reward dependence behaviors have impaired brain reward circuitry. They have hypodopaminergic function due to genetic and/or environmental negative pressures upon the reward neuro-circuitry. This impairment leads to aberrant craving behavior and other behaviors such as Substance Use Disorder (SUD). Neurogenetic research in both animal and humans revealed that there is a well-defined cascade in the reward site of the brain that leads to normal dopamine release. This cascade has been termed the "Brain Reward Cascade" (BRC). Any impairment due to either genetics or environmental influences on this cascade will result in a reduced amount of dopamine release in the brain reward site. Manipulation of the BRC has been successfully achieved with neuro-nutrient therapy utilizing nutrigenomic principles. After over four decades of development, neuro-nutrient therapy has provided important clinical benefits when appropriately utilized. This is a review, with some illustrative case histories from a number of addiction professionals, of certain molecular neurobiological mechanisms which if ignored may lead to clinical complications.
Highlights
Feelings of well being are experienced in the mesolimbic site of the brain
Basic research has revealed that there is a well-defined cascade in the reward site of the brain that leads to normal DA release
Empirical and clinical research has revealed that there is a well-defined cascade in the reward site of the brain that leads to normal DA release
Summary
Feelings of well being are experienced in the mesolimbic site of the brain. In this part of the brain termed the “reward center”, chemical messengers, including serotonin, enkephalin, and GABA work in concert to provide a net release of dopamine (DA) at the nucleus accumbens (NAc), a region in the mesolimbic system. At about the same time, but published a decade later, Blum and associates working on rodent models discovered that the substance D-phenylalanine (DPA) reduced the alcohol craving in genetically craving high alcohol preferring mice [52] The mechanism for such a finding resides in the important innate property of D-amino acids to block the enzyme enkephalinase (responsible for the catabolism–breakdown-of opioid peptides, including enkephalins) and as such significantly raise brain enkephalin levels [52]. No significant association of cue-elicited cravings was found with the nine-repeat allelic variants in DA transporter gene (DAT) SLC6A3 or with the dinucleotide repeat polymorphism (DRP) 148 bp allele in D5 dopamine receptor gene (DRD5) These results suggest that DA pathways in the human brain are involved in cueinduced heroin craving through this known mechanism and, as noted in many studies, the use of the NAAT can reduce craving behavior as well as stress [49,61,62]. Not providing any method to offset the impaired reward circuitry of discharged patients, by activation of brain dopaminergic pathways to prevent relapse, for them is like “Jumping out of a plane without a parachute” [67]
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