Hypothesizing that Putative Dopaminergic, Melatonin, Benzodiazepine Reward Circuitry Receptor(s) Activator Provides Sleep Induction Benefits

Abstract

The issue of insomnia is a global phenomenon which requires additional in-depth research. Insomnia especially in alcohol-dependent patients, for example, may lead to suicide. It is noteworthy that childhood sleep problems predict the onset of drinking in boys. We now know that while there are multi-faceted reasons for sleep problems and disturbances (e.g. sleep drive homeostasis, circadian rhythm physiology, and genetic influences), the scientific community has not been able to deliver an appropriate solution. Some benefit has been noted with cognitive behavioral therapy, but it has minimal effects in patients relapsing from drugs especially alcohol, cocaine and opiates. While there are a number of pharmaceutical drugs developed to treat insomnia, most have associated side effects and even addiction liability. We do know that benzodiazepines hijack the midbrain dopamine system leading to addiction. Finally, it has been proposed that dopamine D2 receptors are involved in rapid eye movement sleep, suggesting as proposed herein that dopaminergic activation is a worthwhile mechanism to explore in the future. The concepts presented herein on potential nutrigenomic therapy warrants further in-depth analysis. In this regard we hypothesize based on both literature review and empirical data that a putative dopaminergic, melatonin, benzodiazepine reward circuitry receptor(s) activator provides sleep induction benefits