Purpose of review
To show which aspects of the environment increase the risk for schizophrenia and how they interact with pre-existing liability for psychosis.
Not only does cannabis survive as a risk factor for psychosis, but the evidence is showing concrete synergistic effects between cannabis and pre-existing liability to psychosis. The urban environment is, in terms of attributable risk, the most important proxy environmental risk factor. There is evidence that it interacts with genetic risk and it has been hypothesized that the mechanism involves the cumulative effects of altered social interactions at the individual level and possibly also at the level of the wider social environment, such as the neighbourhood. Early trauma is another aspect of the environment that has recently been linked prospectively to psychosis, and meta-analytic work demonstrates conclusively that minority status is a risk factor, part of which may be mediated by chronic exposure to discrimination. Prenatal environmental effects may involve folate or vitamin D deficiency, viral infections or adverse effects associated with low or high birth weight. The mechanism by which the environment is likely to impact on risk is through cognitive and emotional pathways on the one hand, and biological pathways, possibly involving dopamine sensitization, on the other.
Several synergistic mechanisms involving proxy measures of genes and proxy measures of the environment, such as gene–cannabis, gene–urbanicity and gene–stress interactions, offer concrete avenues to pursue research that stands a good chance of elucidating at least some of the causes of schizophrenia.