Twin studies have shown that the lifetime risk in monozygotic twins is less than 100%. Therefore, this indicates the importance of non- genetic, environmental factors. However, the most compelling evidence for genetic effects is the adoption studies. These studies have shown that the risk of schizophrenia for those offspring that were ‘adopted away’, was comparable with those that remained with family members that were affected. These various studies not only have provided clear evidence for a genetic based aetiology, but have also highlighted the importance an environmental influence to schizophrenia.
​
Furthermore, numerous susceptible genes have been identified which relates to schizophrenia. Emphasis has been placed on the fact that these genes do not directly cause schizophrenia, however, polymorphisms of each gene can be a contributing causative factor and is associated with a slight increased risk of the condition.



Environmental factors​

​
Obstetric complications
It has been identified that a range of complications that occur before and during birth, have been associated with an increased risk of schizophrenia. Specific complications that are relevant include:

 

• Birth before 37 weeks
• Premature rupture of membranes
• Use of a incubator or resuscitator
• Low birth weight.

It has been postulated that the possible explanation for the obstetric complications associated with schizophrenia may be due to hypoxic events. Hypoxia can lead to structural and neurochemical modification; which in turn can cause schizophrenia. Moreover, obstetric complications may be more significant for those individuals that have a genetic predisposition to schizophrenia.



Maternal influenza & Winter birth

Evidence from numerous studies have indicated that schizophrenia is relatively common in those individuals born in late winter or early spring, which suggests a relation to maternal respiratory viral infections. It has therefore been proposed that there is a relationship between exposure to influenza during early pregnancy and an increased risk of subsequently developing schizophrenia in the offspring.
​
Urban population
An urban environment appears to be a risk factor for schizophrenia and other psychoses. The risk of psychotic symptoms has been also seen to increase with population size.

Migration
Rates of schizophrenia are greater with migration. Moreover, the incidence of schizophrenia is larger when the proportion of the ethnic minorities in the population is smaller.



Substance use

Evidence has shown that the use of certain drugs can lead to an elevated risk of schizophrenia. The evidence for cannabis has been the most robust. A study carried out in 1987 found that those individuals who used cannabis, the relative risk of developing schizophrenia was 2.5 times greater. Furthermore, there was a six- fold increase in the risk of schizophrenia for those subjects who were heavy users. In addition, the risk is further increased for those individuals who are predisposed to psychosis for reasons such as genetic factors.

Family environment
Family environment has not been known to be a direct causative factor of schizophrenia. However, evidence has shown that an environment with emotions such as aggression, conflict or over-involvement, may have a substantial effect on the rate of relapse.

Social factors
Studies have supported factors such as alienation from society, low socio-economic class, an unsatisfactory standard of living and discrimination governing to some degree the risk of schizophrenia.

​

Stress- vulnerability model
A well established concept to the aetiology of schizophrenia is the ‘stress vulnerability’ model. The theory proposes that the degree to which an individual is vulnerable to schizophrenia is determined by a combination of biological, social and psychological factors. Furthermore, schizophrenia can be triggered by traumatic or stressful events.

The individuals that have a high vulnerability only require relatively low levels of stress to trigger schizophrenia. Conversely, for those individuals that have a low vulnerability, may require a significant level of stress before schizophrenia is triggered.