Neuroscientists and psychiatrists working in the areas of “pain and addiction”
are asked in this perspective article to reconsider the current use of dopaminergic blockade
(like chronic opioid agonist therapy), and instead to consider induction of dopamine homeostasis
by putative pro-dopamine regulation. Pro-dopamine regulation could help pharmaceutical
opioid analgesic agents to mitigate hypodopaminergia-induced hyperalgesia by inducing
transmodulation of dopaminergic signaling. An optimistic view is that early predisposition
to diagnosis based on genetic testing, (pharmacogenetic/pharmacogenomic monitoring),
combined with appropriate urine drug screening, and treatment with pro-dopamine
regulators, could conceivably reduce stress, craving, relapse, enhance well-being and attenuate
unwanted hyperalgesia. These concepts require intensive investigation. However,
based on the rationale provided herein, there is a good chance that combining opioid analgesics
with genetically directed pro-dopamine-regulation using KB220 (supported by 43
clinical studies). This prodopamine regulator may become a front-line technology with the
potential to overcome, in part, the current heightened rates of chronic opioid-induced hyperalgesia
and concomitant Reward Deficiency Syndrome (RDS) behaviors. Current research
does support the hypothesis that low or hypodopaminergic function in the brain may
predispose individuals to low pain tolerance or hyperalgesia.
Paracetamol modulates biofilm formation in Staphylococcus aureus clonal complex 8 strains
