The involvement of zinc is essential for all physiological systems, including neural function, where it participates in a variety of cellular processes. Converging clinical, molecular, and genetic discoveries illuminate key roles for zinc homeostasis in the context of clinical depression and psychosis that are not yet well appreciated at the clinical interface.
Intracellular deficiency may result from low circulating zinc levels due to nutritional deficiencies or impaired absorption due to aging or medical illness, including alcoholism. A variety of medications commonly given to psychiatric patients, including anticonvulsants, oral anti-diabetic medications, hormones, antacids, anti-inflammatories, and others, also affect zinc absorption. In addition, inefficient genetic variants in zinc transporter molecules that transport the ion across cell membranes impede its action, even when circulating zinc concentrations are in the normal range.
Well-conducted clinical trials have shown beneficial effects of supplemental zinc in depression, and it is important to continue research with zinc as a potential therapeutic option in psychosis as well. Meta-analyses support the adjunctive use of zinc for major depression, and a single study now supports zinc for psychotic symptoms.
Front Pharmacol.: The Emerging Role for Zinc in Depression and Psychosis
Found at Alkohol adé (german)
