How information processing mode could affect prostaglandin E1 metabolism and lung inactivation: relevance of hemispheric specialization, neurotransmitter asymmetry and brain reactivity.
Due to asymmetry of brain neurotransmitters and differential hemispheric information processing modes, it is suggested that the excessive use of one information processing mode could engender a state of brain reactivity whose neurochemical correlates would be either a rise in melatonin or beta-endorphin in systemic circulation. Since melatonin and beta-endorphin have opposite effects on lung-mediated regulation of prostaglandins, it is further suggested that the pulmonary inactivation of prostaglandin E1 would either be increased or inhibited. Low levels of PGE1 would engender high levels of PGE2 whose effects would explain the findings in schizophrenics of: 'reducing' pattern of visual evoked response, cerebral atrophy, and viral and autoimmune phenomena. The primacy of the disordered cognitive style in leading up to the immunological, biochemical and neuropathological processes is stressed. Implications of this model for understanding depression, anxiety and phobic disorders, autism, attention deficit disorder, obesity, alcoholism, smoking, drug addiction, sexual deviations, and certain psychosomatic and psychophysiological disorders are suggested.
D000527:Alprostadil; D001921:Brain / Q000502:physiology*; D003071:Cognition / Q000502:physiology*; D003863:Depression / Q000503:physiopathology; D004723:Endorphins / Q000502:physiology; D006801:Humans; D008168:Lung / Q000378:metabolism; D008550:Melatonin / Q000502:physiology; D008960:Models, Psychological; D018377:Neurotransmitter Agents / Q000502:physiology; D011458:Prostaglandins E / Q000378:metabolism*; D012559:Schizophrenia / Q000209:etiology / Q000503:physiopathology; D001615:beta-Endorphin
D004723:Endorphins; D018377:Neurotransmitter Agents; D011458:Prostaglandins E; D001615:beta-Endorphin; D000527:Alprostadil; D008550:Melatonin