Metabolic Effects of Melatonin in Patients Treated With Second Generation Antipsychotics

Schizophrenia and bipolar disorder are frequently associated with an elevated risk for obesity, metabolic syndrome, diabetes mellitus, dyslipidemia and other metabolic disturbances. Second Generation Antipsychotics (SGA) have a demonstrated efficacy in acute and long term treatment of these disorders and are considered a first option on most treatment guidelines. Unfortunately the use of SGA is associated to drug induced weight gain, disturbed glucose and lipid regulation and an increase of cardiovascular risk and mortality as well as non- adherence to treatment. There are several hypotheses attempting to explain the complex pathways that lead to antipsychotic therapeutic effects and their accompanying adverse effects. Recently, in animals receiving SGA, melatonin prevented to a large extent the body weight increase, which indicates a possible role for biological rhythms in SGA induced body weight accumulation. Melatonin is a hormone secreted by the pineal gland that follows a circadian rhythm with an increased secretion in the middle of the night. This hormone acts importantly on the suprachiasmatic nucleus and other areas in the brain and periphery. Thus melatonin is involved in a series of biological functions such as sleep regulation, blood pressure, regulation of circadian rhythms, mood, behavior, and more recently in the regulation of metabolic processes including insulin, leptin, and lipid regulation.

Given previous results in experimental animals, the purpose of the present study is to test the potential effect of melatonin in reducing or preventing some of the metabolic disturbances associated with SGA