Achieving dopamine homeostasis to combat brain-gut functional impairment: behavioral and neurogenetic correlates of reward deficiency syndrome

A variety of behavioral disorders are associated with addictions, impulsivity, obsessive-compulsive behaviors, and some personality disorders, which are collectively known as reward deficiency syndrome. These disorders are also associated with diverse digestive disorders. The enteric nervous system, a complex subdivision of the peripheral nervous system, and the central nervous system secrete diverse neurotransmitters including acetylcholine, dopamine, and serotonin. These neurotransmitters can have impaired functional competence due to digestive dysfunction. Hypothalamic-gut axis plays a vital role in nutrient selection. Therapeutic targets to prevent food addiction and neuroendocrine-mediated obesity stem from prodopamine regulation. Altered dopamine reward circuits are an antecedent to genetically induced survival panic, stress intolerance, pathologic food consumption, increased fat synthesis and storage, and digestive disorders. In contrast to current methods that utilize dopamine antagonistic or very powerful agonistic therapies and are based on the commonality of neural mechanisms between drug and glucose addiction, evidence from neuroimaging epigenetic studies strongly indicates that gentle dopamine agonist strategies targeting disrupted dopamine pathways make a significant contribution to achieving dopamine homeostasis and remitting digestive distress and dysbiosis. As a result, precision dopamine agonistic therapies for chronic addiction depend on scientifically sound and appropriate evidence-based early genetic risk determinations leading to precision personalized care of the patient. Multifaceted systems biology-based therapies have been shown to rebalance the sequela of genetically mediated neurotransmitter transactions; restore competent genetically regulated feedback; rebalance neurochemical crosstalk; and optimize health.