Willuhn et al., observed that habitual cocaine use was correlated with reductions
in D2/D3 receptors linked to decreased cue activation in occipital cortex and cerebellum.
Dopamine agonist therapy maintains dopamine function and is a relapse prevention tactic
focused on psychoactive drug and behavioral addictions. Medication Assisted Treatment
(MAT) with emphasis on glutaminergic medications fails in the long-term treatment of
Reward Deficiency Syndrome Behaviors (RDS). While the careful use of “dopamine
antagonist-therapy” short-term is supported, the research-based concept of “dopamine
agonist therapy” in long-term is proposed. Neurogenetics and epigenetics are important in
understanding treatment response and clinical outcomes. The neuro–mechanisms involving
“dopamine homeostasis” are key to understanding recovery from drug and non–drug addictive
behaviors. For example, patients who carry the DRD2 A1 allele (30-40 less D2
receptors) should consider Neuronutriant–Amino-Acid therapy (KB220 variants) a
prevention modality. DRD2 A1 allele carriers show amplified striatal function of L-amino acid decarboxylase,
prior to dopamine biosynthesis. Another example is the effect of Acute Tyrosine Phenylalanine Depletion
(ATPD) on decision-making and reward found carriers with amino-acid deficiency (ATPD). They experienced
attenuated reward and reduced decision-making ability as quantified by Iowa Gambling Task (IGT). Future research
should be directed at asking the question; Would “dopamine agonist therapy” using KB220 variants reduce
methylation and increase acetyl groups to enhance DRD2 expression especially in DRD2 A1 allele carriers and
lead to increased dopamine function and a reduction of drug and non-drug seeking behaviors?
Keywords: Dopamine homeostasis, dopamine resistance, neuronutrient–amino-acid therapy, neurogenetics, epigenetics, enkephalinase
inhibition, KB220 variants.
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