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 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).

Brain Anatomy

Brain imaging studies reveal that people with schizophrenia have enlarged ventricles, the cavities within the brain that contain cerebral spinal fluid (Green, 2001). This finding is important because larger than normal ventricles suggests that various brain regions are reduced in size, thus implying that schizophrenia is associated with a loss of brain tissue. In addition, many people with schizophrenia display a reduction in gray matter (cell bodies of neurons) in the frontal lobes (Lawrie & Abukmeil, 1998), and many show less frontal lobe activity when performing cognitive tasks (Buchsbaum et al., 1990). The frontal lobes are important in a variety of complex cognitive functions, such as planning and executing behavior, attention, speech, movement, and problem solving. Hence, abnormalities in this region provide merit in explaining why people with schizophrenia experience deficits in these of areas.

Events During Pregnancy

Why do people with schizophrenia have these brain abnormalities? A number of environmental factors that could impact normal brain development might be at fault. High rates of obstetric complications in the births of children who later developed schizophrenia have been reported (Cannon, Jones, & Murray, 2002). In addition, people are at an increased risk for developing schizophrenia if their mother was exposed to influenza during the first trimester of pregnancy (Brown et al., 2004). Research has also suggested that a mother’s emotional stress during pregnancy may increase the risk of schizophrenia in offspring. One study reported that the risk of schizophrenia is elevated substantially in offspring whose mothers experienced the death of a relative during the first trimester of pregnancy (Khashan et al., 2008).


Another variable that is linked to schizophrenia is marijuana use. Although a number of reports have shown that individuals with schizophrenia are more likely to use marijuana than are individuals without schizophrenia (Thornicroft, 1990), such investigations cannot determine if marijuana use leads to schizophrenia, or vice versa. However, a number of longitudinal studies have suggested that marijuana use is, in fact, a risk factor for schizophrenia. A classic investigation of over 45,000 Swedish conscripts who were followed up after 15 years found that those individuals who had reported using marijuana at least once by the time of conscription were more than 2 times as likely to develop schizophrenia during the ensuing 15 years than were those who reported never using marijuana; those who had indicated using marijuana 50 or more times were 6 times as likely to develop schizophrenia (Andréasson, Allbeck, Engström, & Rydberg, 1987). More recently, a review of 35 longitudinal studies found a substantially increased risk of schizophrenia and other psychotic disorders in people who had used marijuana, with the greatest risk in the most frequent users (Moore et al., 2007). Other work has found that marijuana use is associated with an onset of psychotic disorders at an earlier age (Large, Sharma, Compton, Slade, & Nielssen, 2011). Overall, the available evidence seems to indicate that marijuana use plays a causal role in the development of schizophrenia, although it is important to point out that marijuana use is not an essential or sufficient risk factor as not all people with schizophrenia have used marijuana and the majority of marijuana users do not develop schizophrenia (Casadio, Fernandes, Murray, & Di Forti, 2011). One plausible interpretation of the data is that early marijuana use may disrupt normal brain development during important early maturation periods in adolescence (Trezza, Cuomo, & Vanderschuren, 2008). Thus, early marijuana use may set the stage for the development of schizophrenia and other psychotic disorders, especially among individuals with an established vulnerability (Casadio et al., 2011).