It is the consensus among researchers today that there are both genetic and environmental contributions to schizophrenia. Studies with families and twin/adoption studies have favored the genetic disposition while labeling theory and developmental models corroborate environmental evidence. With due gratification to adoption studies, evidence for genetic factors in the etiology of schizophrenia has been found. However, how it is transmitted and the extent of genetic determination are still unknown. Since not all identical twins of schizophrenics are schizophrenic (only about 45-55%), nongenetic events must have some influence. The problem, however, is the ambiguity of what nongenetic environments and factors could contribute to the susceptibility and development of schizophrenia, e.g. pre- or postnatal environment, or psychosocial or physical environment (Matthysse & Kidd, 1978).
Indeed, attributing a cause to schizophrenia, be it genetic or environmental, seems to be something that a modern researcher would be very unlikely to do, at least professionally. According to Plomin & McClearn (1993),
The obvious familiality of schizophrenia does not lend itself to instant conclusions about the causes of the disorder; naive theorists of a psychodynamic persuasion would use the observations to implicate one or another dysfunctional aspects of shared experiences or environments; naive theorists of a sociological or biological-but-not-genetic orientation would use the far-from-perfect familiality to implicate cultural and unshared factors, including viruses; and naive genetically oriented theorists would use the same observations to confirm their belief that schizophrenia runs in families because genotypes run in families. (p. 233)Despite this observation, Plomin & McClearn point out that among 660 schizophrenic patients in a study done in Germany in 1932, 3.7% of the parents were also schizophrenic, as were 8.3% of the siblings, significantly higher than the 1% incidence in the general population. Further studies with parents and children yielded relatively close results to those aforementioned. Interestingly, Warner (2000) reports the same statistics for siblings (10%), but also points out that this rate remains the same even if children were raised by adoptive parents, suggesting a major genetic component. Due to anticipated advances in the application of molecular genetic techniques, these types of family studies were thought to have supposed to have been rendered obsolete. However, Murray, Jones, Susser, van Os & Cannon (2003) note that despite the movement toward molecular genetic techniques, these advances have not yet occurred, and consequently there has been a revival of interest in these classical family studies.
Though the simplest of environmental potential causes for schizophrenia taught to most students is something not unlike the diathesis-stress model, whereby a person has a biological predisposition to a disorder and decreased amounts of stress are needed to trigger its onset, there are several other non-genetic factors that have been offered as potential causes or catalysts to the development of schizophrenia.
Warner (2000) mentions both obstetric complications and viruses as potential causes. Data seem to show that nearly forty percent of schizophrenics had a history of obstetric complications, such as prolonged labor, and that children born of complications have twice the risk for developing schizophrenia as those who had no complications during birth. The risk of intrauterine brain damage is increased if a woman contracts a viral illness during pregnancy. Data show that more schizophrenics are born in late winter or spring as well, and that this trend increases sometimes after viral illnesses like influenza, measles or chickenpox occur.
Another major cluster of potential catalysts for the development and triggers for schizophrenia are the abuses: physical especially. Warner (2000) promptly notes, and devotes an entire section to it, that “bad parenting” does not cause schizophrenia. This is meant to clarify that neglect, confusing parenting styles and other such conditions that may not cause optimal developmental outcome do not cause or even greatly enhance the risk for schizophrenia. However, data has shown that severe physical abuses seem to lend themselves to greater risks for developing psychoses.
A study done by Belkin in 1994 looked at sexual abuse as a potential catalyst to the development of schizophrenia. The Minnesota Multiphasic Personality Inventory (MMPI) was administered to 105 sexually abused patients, and a matching sample of 105 control patients in order to compare their personality characteristics. The survivors of sexual abuse were found to have scored higher on the Psychopathic Deviate and Schizophrenia scales. The researchers feel that this indicates higher levels of interpersonal discord and social alienation among sexually abused subjects and control subjects with no history of sexual abuse. It was found that more psychopathology existed with histories of male-to-male abuse, and the age that was most impressionable to inducing social discomfort among victims is six to eleven years (subjects abused in this time scored higher on the measures than those of other age groups). Though this study seems to find a correlation between abuse as a child and a greater risk for psychopathologies in later life, it does not find a causal relationship in such things. In other words, sexual abuse as a child could not be proven to be a precursor to developing schizophrenia; merely, it demonstrated a greater chance that such abuse was conducive to developing such psychopathologies.
A study done by Wexler (1997) expanded on the earlier research of Belkin by including physical abuse in his research. His aim was to examine the relationship between childhood sexual and physical abuse and adult psychiatric illness in a sample of diagnostically diverse patients. For his study, he took a sample of 264 patients that had histories of abuse, and 689 who had no histories of this abuse. Through analyzing hospital records and conducting interviews, the primary finding was that there was a greater incidence (three for every one) of major depression and schizophrenia in subjects with histories of abuse than subjects with no such history. This study was only problematic in that it demonstrates only a correlation, and tells us nothing about the actual validity of the thought that abuse contributes to the development of depression and schizophrenic symptoms. However, paired with other research in the same subject matter, it seems to support the general findings that abuse certainly highly positively correlates to the development of psychopathological symptoms.
Based on all of these such findings, and other studies of the same and similar subjects, Read (2001) proposed a new model for the development of schizophrenia. It was intended to offer a more comprehensive look at the problem than the diathesis-stress model. The traumagenic neurodevelopmental model (TN model) was proposed in response to the high incidences of child abuse in subjects diagnosed with schizophrenia and schizophrenic symptoms. According to Read, a genetic deficit creates a predisposing vulnerability in the form of oversensitivity to stress. Highly stressful situations can trigger the onset of schizophrenic symptoms, and so children who have been sexually, emotionally and physically abused stand much higher risks of developing this disorder. Those with a genetic predisposition to the oversensitivity to stress have an even greater chance of this development. A very prominent aspect of this theory is the notion that those people who are severely enough abused as children can actually develop abnormalities in the brain that underlie the heightened sensitivity to stress so often found in schizophrenics. These people do not necessarily need to have a genetic predisposition. This model seems to be very comprehensive, but is still in testing stages. It is relatively new, and seems to have promise.
Holowka (2003) addresses dissociation. This study strengthens the TN model by finding strong correlations between emotional, physical and sexual abuse and dissociative symptoms and schizophrenia in adulthood. Twenty-six patients were administered the Dissociative Experiences Scale and the Childhood Trauma Questionnaire. What the study found was that emotional abuse had the greatest correlation between schizophrenic and dissociative symptoms, corroborating the theory that heightened levels of stress physiologically can trigger dissociative symptoms. Physical abuse has a lower correlation but is still high. The authors of this study maintain that emotional abuse may play an important role in the etiology of dissociation in schizophrenia. This is still controversial.