The risk of developing schizophrenia can be thought of as a mix of genetic vulnerability and environmental factors; an individual’s genes set the stage for them to become prone to the assaults of the environment.[Dean & Murray, 2005] Some of the environmental risks are shown on the slide, and include pre- and post-natal factors, and cannabis use.[Sadock et al., 2009; Lakhan & Vieira, 2009]
Indeed, it is now accepted that most common diseases involve discrete genetic and environmental risk factors, and that these two elements interact to form complex genetic–environmental joint risk.[Hunter, 2005] If the genetic, or the environmental, risk factors of a condition are studied in isolation, this element of joint effect can be overlooked.[Hunter, 2005] A simple example of gene–environment interaction is the interplay between skin colour and sun exposure when considering the risk of skin cancer.[Hunter, 2005] Although unarguably more complex, schizophrenia can be conceptualised in this manner.[Hunter, 2005; Dean & Murray, 2005]
References:
Dean K, Murray RM. Environmental risk factors for psychosis. Dialogues Clin Neurosci 2005; 7 (1): 69–80.
Hunter DJ. Gene–environment interactions in human diseases. Nat Rev Genet 2005; 6 (4): 287–298.
Lakhan SE, Vieira KF. Schizophrenia pathophysiology: are we any closer to a complete model? Ann Gen Psychiatry 2009; 8: 12.
Sadock BJ, Sadock VA, Ruiz P (eds). Kaplan & Sadock’s Comprehensive Textbook of Psychiatry. 9th Edition. Vol 1. Lippincott Williams & Wilkins, 2009.