Hypothesizing Darkness Induced Alcohol Intake Linked to Dopaminergic Regulation of Brain Function

Abstract

Understanding the role of neurotransmission in the prefrontal cortex and mesolimbic brain regions has become the subject of intensive neuroscience research worldwide. In the 1970s, our group provided evidence that rats exposed to darkness significantly augmented their alcohol intake. At that time, we proposed that melatonin was the culprit. At around the same time, our laboratory, amongst a few others, proposed that dopamine-adducts with acetaldehyde to induce alcohol intake both in rodents and in humans. While the work in these areas has declined considerably over the years, more recent scientifically sound studies continue to show the importance of these earlier controversial ideas involving alcohol abuse and alcoholism. A review of the literature has provided impetus to systematically access the newer genetic and molecular neurobiological findings relevant to the physiological and psychological motives for high alcohol consumption in animals and humans alike. Thus, we hypothesize that darkness-induced alcohol intake is linked not only to serotonergic-melatonin mechanisms, but also to dopaminergic regulation of brain mesolimbic pathways involving neuronal expression switching in response to long photoperiods affecting gene expression.

Molecular neuro-biological and systemic health benefits of achieving dopamine homeostasis in the face of a catastrophic pandemic (COVID- 19): A mechanistic exploration

“…This research provides insight into a novel mechanistic intervention that reveals a potential role for dopamine and melatonin in resolving retinal degeneration [47]. However, while regulating melatonin is important, health care professionals must be cognizant that increased levels of brain melatonin can lead to increased alcohol intake [48].…”

Invited Expert Opinion- Bio-informatic and Limitation Di-rectives to Help Adopt Ge-netic Addiction Risk Screening and Identify Preaddictive Reward Dysregulation: Re-quired Analytic Evidence to Induce Dopamine Homeo-statsis

“…Earlier work from Reiter's laboratory involving darkness induced excessive drinking framed the importance of circadian rhythm revealing the role of melatonin in alcoholism and the pineal gland [31][32][33]. Certainly, the field is rift with both animal and human studies related to at least seven neurotransmitter systems and receptology especially related to dopamine and NMDA, neurotrophic factors, and CLOCK genes in terms of genetically and neuroepigenetically induced reward deficiency and all addictive behaviors [34][35][36][37][38][39].…”

Researching Mitigation of Alcohol Binge Drinking in Polydrug Abuse: KCNK13 and RASGRF2 Gene(s) Risk Polymorphisms Coupled with Genetic Addiction Risk Severity (GARS) Guiding Precision Pro-Dopamine Regulation

“…The goal of such a strategy is to augment brain reward functional connectivity and to target reward deficiency along with the stress-like anti-reward symptomatology of addiction [ 84 , 85 ]. Binge drinkers’ phenotypes can be characterized using the Genetic Addiction Risk Score (GARS) that identifies reward gene risk polymorphisms across the brain reward cascade [ 86 , 87 , 88 , 89 , 90 ]. Dopamine homeostasis may thus be achieved via “Precision Addiction/Behavioral Management” (PAM/PBM), the customization of neuronutrient supplementation based on the GARS test result, along with behavioral intervention [ 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 ].…”