第15章心理的障害

There is considerable evidence suggesting that schizophrenia has a genetic basis. The risk of developing schizophrenia is nearly 6 times greater if one has a parent with schizophrenia than if one does not (Goldstein, Buka, Seidman, & Tsuang, 2010). Additionally, one’s risk of developing schizophrenia increases as genetic relatedness to family members diagnosed with schizophrenia increases (Gottesman, 2001).

When considering the role of genetics in schizophrenia, as in any disorder, conclusions based on family and twin studies are subject to criticism. This is because family members who are closely related (such as siblings) are more likely to share similar environments than are family members who are less closely related (such as cousins); further, identical twins may be more likely to be treated similarly by others than might fraternal twins. Thus, family and twin studies cannot completely rule out the possible effects of shared environments and experiences. Such problems can be corrected by using adoption studies, in which children are separated from their parents at an early age. One of the first adoption studies of schizophrenia conducted by Heston (1966) followed 97 adoptees, including 47 who were born to mothers with schizophrenia, over a 36-year period. Five of the 47 adoptees (11%) whose mothers had schizophrenia were later diagnosed with schizophrenia, compared to none of the 50 control adoptees. Other adoption studies have consistently reported that for adoptees who are later diagnosed with schizophrenia, their biological relatives have a higher risk of schizophrenia than do adoptive relatives (Shih, Belmonte, & Zandi, 2004).

Although adoption studies have supported the hypothesis that genetic factors contribute to schizophrenia, they have also demonstrated that the disorder most likely arises from a combination of genetic and environmental factors, rather than just genes themselves. For example, investigators in one study examined the rates of schizophrenia among 303 adoptees (Tienari et al., 2004). A total of 145 of the adoptees had biological mothers with schizophrenia; these adoptees constituted the high genetic risk group. The other 158 adoptees had mothers with no psychiatric history; these adoptees composed the low genetic risk group. The researchers managed to determine whether the adoptees’ families were either healthy or disturbed. For example, the adoptees were considered to be raised in a disturbed family environment if the family exhibited a lot of criticism, conflict, and a lack of problem-solving skills. The findings revealed that adoptees whose biological mothers had schizophrenia (high genetic risk) and who had been raised in a disturbed family environment were much more likely to develop schizophrenia or another psychotic disorder (36.8%) than were adoptees whose biological mothers had schizophrenia but who had been raised in a healthy environment (5.8%), or than adoptees with a low genetic risk who were raised in either a disturbed (5.3%) or healthy (4.8%) environment. Because the adoptees who were at high genetic risk were likely to develop schizophrenia only if they were raised in a disturbed home environment, this study supports a diathesis-stress interpretation of schizophrenia—both genetic vulnerability and environmental stress are necessary for schizophrenia to develop, genes alone do not show the complete picture.

If we accept that schizophrenia is at least partly genetic in origin, as it seems to be, it makes sense that the next step should be to identify biological abnormalities commonly found in people with the disorder. Perhaps not surprisingly, a number of neurobiological factors have indeed been found to be related to schizophrenia. One such factor that has received considerable attention for many years is the neurotransmitter dopamine. Interest in the role of dopamine in schizophrenia was stimulated by two sets of findings: drugs that increase dopamine levels can produce schizophrenia-like symptoms, and medications that block dopamine activity reduce the symptoms (Howes & Kapur, 2009). The dopamine hypothesis of schizophrenia proposed that an overabundance of dopamine or too many dopamine receptors are responsible for the onset and maintenance of schizophrenia (Snyder, 1976). More recent work in this area suggests that abnormalities in dopamine vary by brain region and thus contribute to symptoms in unique ways. In general, this research has suggested that an overabundance of dopamine in the limbic system may be responsible for some symptoms, such as hallucinations and delusions, whereas low levels of dopamine in the prefrontal cortex might be responsible primarily for the negative symptoms (avolition, alogia, asociality, and anhedonia) (Davis, Kahn, Ko, & Davidson, 1991). In recent years, serotonin has received attention, and newer antipsychotic medications used to treat the disorder work by blocking serotonin receptors (Baumeister & Hawkins, 2004).