Genome–Environment Interactions and Psychiatric Disorders

Environmental factors are known to interact with the genome by altering epigenetic mechanisms regulating gene expression and contributing to the pathogenesis of psychiatric disorders. This article is a narrative review of how the major environmental factors contribute to the pathogenesis of common psychiatric disorders such as schizophrenia, bipolar disorder, major depressive disorder, and anxiety disorder this way. The cited articles were published between 1 January 2000 and 31 December 2022 and were obtained from PubMed and Google Scholar. The search terms used were as follows: gene or genetic; genome; environment; mental or psychiatric disorder; epigenetic; and interaction. The following environmental factors were found to act epigenetically on the genome to influence the pathogenesis of psychiatric disorders: social determinants of mental health, maternal prenatal psychological stress, poverty, migration, urban dwelling, pregnancy and birth complications, alcohol and substance abuse, microbiota, and prenatal and postnatal infections. The article also discusses the ways by which factors such as drugs, psychotherapy, electroconvulsive therapy, and physical exercise act epigenetically to alleviate the symptoms of psychiatric disorders in affected patients. These data will be useful information for clinical psychiatrists and those researching the pathogenesis and treatment of psychiatric disorders

Inhibition of Contractility of Isolated Caprine Detrusor by the Calcium Channel Blocker Cilnidipine and Reversal by Calcium Channel Openers

ABSTRACT: Background: Cilnidipine is a fourth-generation calcium channel blocker that is clinically used to treat hypertension. It is a dihydropyridine that blocks L- and N-type calcium channels. The inhibitory effect of cilnidipine on isolated detrusor muscle contractility has not been studied. This study investigated the inhibitory effect of cilnidipine on isolated caprine (goat) detrusor muscle contractility and the reversal of the inhibition by calcium channel openers. Methods: Fourteen caprine detrusor strips were made to contract using 80 mM potassium chloride before and after addition of three concentrations (20, 40, and 60 µM) of cilnidipine. Two reversal agents, the L-type calcium channel opener FPL64716, and the N-type calcium channel opener GV-58, were investigated for their ability to reverse the inhibitory effect of 40 µΜ cilnidipine on potassium chloride-induced detrusor contractility. Results: Cilnidipine caused a dose-dependent and statistically significant inhibition of detrusor contractility at all concentrations of cilnidipine used (20, 40, and 60 µΜ). The inhibitory effect of 40 µM cilnidipine on detrusor contractility was significantly reversed by the addition of FPL64716 and GV-58. Conclusions: Cilnidipine inhibits the contractility of the isolated detrusor by blocking L- and N-type calcium channels. Cilnidipine could be evaluated for treating clinical conditions requiring relaxation of the detrusor such as overactive bladder

An epigenetic basis for an omnigenic model of psychiatric disorders

An Epigenetic Basis for an Omnigenic Model of Psychiatric Disorder