Addiction by Any Other Name is Still Addiction: Embracing Molecular Neurogenetic/Epigenetic Basis of Reward Deficiency

Drew Edwards, A. Kenison Roy III, Brent Boyett, Rajendra D. Badgaiyan, Panayotis K. Thanos, David Baron, Mary Hauser, Sampada Badgaiyan, Raymond Brewer, David B. Siwicki, William Downs, David E. Smith and Kenneth Blum

 

Abstract

The Human Genome Project and the database it created established a plausible observatory, so to speak, for scientists to identify the etiology of genetic variants and their expression. It is well-known that “Single Nucleotide Polymorphisms” (SNPs) which involve the cumulative presence of nucleic acids in sufficient volume and proximity along the DNA strands to create novel variants in the transcription and encoding of replicate genes–thus creating phenotypical risk for pathological expression [1]. One of these created phenotypes involves the molecular rearrangement of known base pairs sitting in chromosomes leading to an uncontrollable desire to self-administrate various drugs and even risky behaviours to overcome a known neurochemical deficiency or hypodopaminergia resulting in drug or non-drug seeking behaviours [2].

Published on: January 21, 2020
doi: 10.17756/jas.2020-043
Citation: Edwards D, Roy III AK, Boyett B, Badgaiyan RD, Thanos PK, et al. 2020. Addiction by Any Other Name is Still Addiction: Embracing Molecular Neurogenetic/Epigenetic Basis of Reward Deficiency. J Addict Sci 6(1): 1-4.
 
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