4.7 Editorial Material

Should Reward Deficiency Syndrome (RDS) Be Considered an Umbrella Disorder for Mental Illness and Associated Genetic and Epigenetic Induced Dysregulation of Brain Reward Circuitry?

期刊

JOURNAL OF PERSONALIZED MEDICINE
卷 12, 期 10, 页码 -

出版社

MDPI
DOI: 10.3390/jpm12101719

关键词

Reward Deficiency Syndrome (RDS); hypodopaminergia; Genetic Addiction Risk Severity (GARS) test; pro-dopamine regulation (KB220Z); dopamine homeostasis; epigenetics; brain reward cascade; addiction

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Reward Deficiency Syndrome (RDS) is a syndrome characterized by a breakdown of reward neurotransmission, resulting in various addictive, compulsive, and impulsive behaviors. RDS is associated with a lack of integration between perception, cognition, and emotions, caused by significant dopaminergic surges and hypo-functionality of glutamatergic neurotransmission. There is a significant risk of dopaminergic gene polymorphic allele overlap between RDS, depression, and subsets of schizophrenia. Repairing the hypodopaminergia causing addictive behaviors may involve precision DNA-guided therapy using the Genetic Addiction Risk Severity (GARS) test and a specific nutraceutical formulation.
Reward Deficiency Syndrome (RDS) is defined as a breakdown of reward neurotransmission that results in a wide range of addictive, compulsive, and impulsive behaviors. RDS is caused by a combination of environmental (epigenetic) influences and DNA-based (genetic) neurotransmission deficits that interfere with the normal satisfaction of human physiological drives (i.e., food, water, and sex). An essential feature of RDS is the lack of integration between perception, cognition, and emotions that occurs because of (1) significant dopaminergic surges in motivation, reward, and learning centers causing neuroplasticity in the striato-thalamic-frontal cortical loop; (2) hypo-functionality of the excitatory glutamatergic afferents from the amygdala-hippocampus complex. A large volume of literature regarding the known neurogenetic and psychological underpinnings of RDS has revealed a significant risk of dopaminergic gene polymorphic allele overlap between cohorts of depression and subsets of schizophrenia. The suggestion is that instead of alcohol, opioids, gambling disorders, etc. being endophenotypes, the true phenotype is RDS. Additionally, reward deficiency can result from depleted or hereditary hypodopaminergia, which can manifest as a variety of personality traits and mental/medical disorders that have been linked to genetic studies with dopamine-depleting alleles. The carrying of known DNA antecedents, including epigenetic insults, results in a life-long vulnerability to RDS conditions and addictive behaviors. Epigenetic repair of hypodopaminergia, the causative basis of addictive behaviors, may involve precision DNA-guided therapy achieved by combining the Genetic Addiction Risk Severity (GARS) test with a researched neutraceutical having a number of variant names, including KB220Z. This nutraceutical formulation with pro-dopamine regulatory capabilities has been studied and published in peer-reviewed journals, mostly from our laboratory. Finally, it is our opinion that RDS should be given an ICD code and deserves to be included in the DSM-VI because while the DSM features symptomology, it is equally important to feature etiological roots as portrayed in the RDS model.

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