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Aetiology of schizophrenia

Genetic factors

Schizophrenia has been at the centre of a scientific debate concerning the role of nature and nurture in the development of mental health problems. Perhaps the dominant model of the aetiology of schizophrenia has been biological, driven by genetic factors. Evidence relating to genetic factors has therefore been closely scrutinized and has not been without controversy. Early genetic studies indicated that the risk for schizophrenia among relatives of an identified ‘case’ correlated with the degree of shared genes.

More methodologically sound studies (e.g. Kringlen 1993) have reported concordance rates for schizophrenia in MZ twins of between 30 and 40 per cent and between DZ twins of 10 –15 per cent, suggesting a part-genetically mediated risk for schizophrenia. While this evidence shows that schizophrenia runs in families, it does not necessarily mean that it has a genetic causation. Those closest to the affected individual may share a similar environment, or be affected by their behaviour. Attempts to disentangle environmental from biological issues have led to a number of studies comparing the risk for schizophrenia among relatives or twins of adopted-away children. Close examination of these studies reveals a far from clear set of evidence. The Danish Adoption Studies (Kety et al. 1975), for example, traced the biological relatives of 34 adopted children who later developed schizophrenia and those of 34 control cases with ‘clean pedigrees’, comparing the prevalence of schizophrenia among them. Interestingly, they found only one person diagnosed as having chronic schizophrenia among the relatives of either cases or controls.

Only when they extended the diagnoses assigned to those within the schizophrenic spectrum, including borderline state, inadequate personality and uncertain schizophrenia, did differences between the groups arise. Using these diagnoses, they found nine affected relatives in the families of the cases and two among the controls. This, some critics (e.g. Roberts 2000) have argued, provided no evidence that schizophrenia per se is inherited. Roberts also noted that at least some of the diagnoses assigned were taken from hospital notes and not confi rmed by the research team, and that at least one person’s reported diagnosis changed from inadequate personality to borderline schizophrenia over the course of two reports by the same research team. Worse was to come: subsequent reading of this individual’s notes showed an initial diagnosis of bipolar disorder.

A more recent study of genetics reported by Tienari et al. (2000) compared rates of schizophrenia in the adopted-away offspring of both mothers diagnosed with schizophrenia and those without the diagnosis. Risk for schizophrenia was four times greater among the children of the women diagnosed as having schizophrenia than among the children of the comparison mothers: a total incidence of 8.1 per cent versus 2.3 per cent.

However, this was not entirely due to genetic factors. Using data from the same study, Wahlberg et al. (2000b) reported an interaction between genetic and environmental factors. Children of women diagnosed with schizophrenia who lived in households where there was good communication between the family members were not at increased risk of schizophrenia. By contrast, the children of women diagnosed as having schizophrenia who were placed in families with evidence of communication deviance were at greater risk of developing schizophrenia than children with ‘normal’ mothers who were placed in such households. That is, the development of schizophrenia seemed to depend on both genetic risk and communication deviance within the adoptive family. Importantly, any communication deviance seemed to predate the adoption, and was not a consequence of the child’s behaviour. Together, these and other data have generally been seen by biological theorists as supporting a model in which genetic factors infl uence risk for schizophrenia but do not form the single causal agent. They form a vulnerability factor rather than a causal factor.

The search for the location of genes that increase risk of schizophrenia has also proven somewhat difficult. Perhaps the frustration of researchers is summed up by the title of a paper examining this phenomenon (Sanders et al. 2008): ‘No significant association of 14 candidate genes with schizophrenia in a large European ancestry sample’. Nevertheless, some candidate genes involved in the development of schizophrenia are emerging, including the ERBB4 gene, responsible for dopamine regulation (Lu et al. 2010), and the 5-HTR2Agene (Tee et al. 2010) which is involved in serotonin regulation. When considering the role of genetics in schizophrenia, one fi nal cautionary note should be borne in mind: 81 per cent of people diagnosed with schizophrenia have no known relative with the disorder (Shean 2004). Other factors are clearly implicated in the development of the disorder.

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