Abstract
We hypothesize that individuals with genetic predisposition to Substance Use Disorder (SUD) may have greater likelihood of experiencing work related accidents. We further hypothesize that high risk populations will carry single or multiple polymorphisms associated with brain reward circuitry and/or brain reward cascade, including: Dopaminergic (i.e. DRD2 receptor genes); Serotonergic (i.e. 5-HTT2 receptor genes); Endorphinergic (i.e. pre-enkephalin genes); Gabergic (i.e. GABAA receptor genes); Neurotransmitter Metabolizing genes (i.e. MAO and COMT genes) among others (GARSRXTM). Analgesic addiction as well as “pseudoaddiction” must be treated to improve pain control and its management. We propose that non-pharmacological alternatives to pain relief, in high risk, addiction-prone individuals, are Electrotherapeutic Device(s) and Programs. We further propose patented KB220Z, a nutraceutical designed to release dopamine at the nucleus accumbens, will reduce craving behavior, in genetically programmed individuals. By utilizing both alternatives in DNA analyzed injured workers, a reduction in analgesic addiction (genuine or pseudo) leads to improved health and quicker return to work. We also hypothesize that this novel approach will impact costs related to injuries in the workforce. Effective management of chronic pain, especially in high addiction-prone workforce populations, is possible in spite of being particularly elusive. A series of factors encumber pain assessment and management, including analgesia addiction, pharmacogenomic response to pain medications, and genetically inherited factors involving gene polymorphisms. Additional research is required to test these stipulated hypotheses related to genetic proneness to addiction, but also proneness to accidents in the workplace and reduction of craving behavior. Our hypothesis that genotyping coupled with both KB220ZTM and the pharmaceutical-free Electrotherapy, will reduce iatrogenic induced analgesia addiction. This approach will achieve attainable effective pain management and quicker return to work. We propose outcomes such as the Reward Deficiency System SolutionTM may become an adjunct in the war against iatrogenic pain medication addiction.
Highlights
In this paper we have suggested that individuals presenting with work related accidents may have a number of reward gene polymorphisms that lead to a hypodopaminergic trait and as such enhance addictive behaviors
We theorize that the mechanisms involved in the effect of the Electrotherapy device include the following: 1) to elicit low tension, non-fatiguing and non-tetanizing muscle contractions for smooth lymphatic muscle as well as skeletal muscle fibers, closely mimicking natural and voluntary contraction of the muscle through low frequency (2 Hz); 2) to stimulate small fibers through waveform exponential decay and constant activity of the current generator; 3) to not activate motor nerves of sensory Delta and C pain fibers or white muscle fibers, thereby removing any pain caused by such stimulation; 4) to effect pain disorders anesthetically when utilized at higher frequency (60 HZ), intrinsically affecting the nerve through nerve fiber sodium pump deactivation inducing an enduring analgesic/anesthetic effect via an accumulative post-synaptic depression
Being cognizant that many more studies are required in terms of our proposal as well understanding many negative reports on certain gene associations regarding Reward Deficiency Syndrome” (RDS), we are still encouraged
Summary
In this paper we have suggested that individuals presenting with work related accidents may have a number of reward gene polymorphisms that lead to a hypodopaminergic trait and as such enhance addictive behaviors. We propose that coupling Genetic Addiction Risk Score (GARSRX) with dopaminergic agonistic modalities (such as KB220Z and an electrotherapeutic anti-pain device) will reduce unwanted accidents and reduce the chance of becoming addicted to opioids in the workplace
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