Schizophrenia is a devestating psychiatric disorder that affects approximately one percent of the world's adult population. Despite substantial investigative efforts over the last decades, the exact mechanisms and pathogenesis of this condition are not yet fully understood. Published data support certain infectious agents as potential risk factors for schizophrenia. Since its discovery, Helicobacter pylori has been implicated in a variety of extradigestive diseases, but its potential role in the pathogenesis of psychiatric disorders has thus far been neglected. It is hypothesized here that infection with H. pylori occurring in early childhood may induce persisting systemic biochemical aberrations, including dopaminergic dysfunction, decreased levels of essential polyunsaturated fatty acids, subtle inflammation, and homocysteine alterations, that may play a crucial role in the development of schizophrenia in genetically predisposed individuals. Evidence in favor of this hypothesis is provided and possible therapeutic implications are discussed.