How do OCs operate within the etiology of Schizophrenia?

An array of models has been proposed to explain how OCs contribute to the causes of schizophrenia. We cover the most prominent models in schizophrenia research and discuss which model is best supported by empirical research.

Some theorists have proposed that there may be a subgroup of patients with schizophrenia who acquire the disorder from entirely nongenetic origins. According to this model, an obstetric insult could cause schizophrenia independently of genetic contributions. If this model were correct, then exposure to OCs (with a given degree of severity and during a sensitive period of gestation) would lead to expression of schizophrenia with a fair degree of reliably. The prevailing evidence suggests that this model is unlikely, because the rate of OCs in the general population is far higher than the rate of schizophrenia (approximately 1% of the population). Even if OCs during particularly critical periods of gestation only were considered, there would likely still be a much higher rate of schizophrenia in the population if OCs were the sole cause of the disease onset. Therefore, there currently is little support for the idea that OCs alone can produce schizophrenia.

Another model, the gene - environment covariation model, posits that OCs are associated with the genes for the disorder, but OCs do not exert any etiological role in the disease. This model predicts an increase in the number of OCs in individuals who carry genes associated with schizophrenia, regardless of whether they develop the disorder. The main support for the gene - environment covariation model comes from studies that found increased birth complications in offspring of mothers with schizophrenia (who carry the disease-producing genes given that they express the disorder phenotypically), but it is inconsistent with the finding that unaffected siblings of patients with schizophrenia do not differ from the general population in the incidence of OCs. Siblings of patients with schizophrenia would be expected to share some of the disease-promoting genes, therefore leading to increased risk of OCs, if the gene - environment covariation model were correct.

In addition, interpretation of increases in OCs among mothers with schizophrenia is complicated by the elevated occurrence of health-risk behaviors during pregnancy among this cohort. Specifically, women with schizophrenia are less likely to receive prenatal care, more likely to be polydrug users, more likely to drink alcohol, more likely to be on psychiatric medications, and more likely to smoke cigarettes than women without schizophrenia, all of which have been associated with increases in OCs. Moreover, discontinuation of antipsychotic medication has been associated with a worsening of symptoms, often leading to psychotic episodes in relatively asymptomatic women. The onset of a psychotic episode likely has many consequences for prenatal health, including increased stress, poor nutrition, poor self-care, suicide attempts, attempts at premature delivery, and other risky behaviors that could lead to deleterious pregnancy and birth outcomes.