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11.7: Biological Explanations for Schizophrenia and Other Psychotic Disorders

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    221774

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    Learning Objectives
    • Explain genetic studies, twin and adoption research, and biological explanations for schizophrenia

    Causes of Schizophrenia

    There is considerable evidence suggesting that genetic inheritance has a strong influence on the development of schizophrenia. For example, the risk of developing schizophrenia is nearly six 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).

    Genes

    Two identical twin girls
    Figure \(\PageIndex{1}\): Twin and adoptions studies estimate that the heritability of schizophrenia may be up to 80%.

    When considering the role of genetics in schizophrenia, as in any disorder, conclusions based on family and twin studies have some inherent flaws 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).

    Individual twin studies and meta-analyses of twin studies have estimated the heritability of risk for schizophrenia to be approximately 80% (this refers to the proportion of variation between individuals in a population that is influenced by genetic factors, not the degree of genetic determination of individual risk), but the heritability estimate varies from 41 to 87%. Concordance rates (the percentage of twins whose co-twin has the same condition) between monozygotic twins vary in different studies, with an average estimate of approximately 50%; whereas dizygotic twins was 17%. Some twin studies have found rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins, however. Genetics do appear to play a strong role in the etiology of schizophrenia, but others factors are also clearly involved as predicted by the biopsychosocial model.

    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. 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. Since 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 biopsychosocial 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.

    The diathesis-stress model of schizophrenia explains how an environmental trigger, such as severe stress or drug use, can catalyze the onset of a disease in a genetically susceptible person. This model does not mean that without the specific environmental trigger the person would be safe from developing schizophrenia, but it does display the importance of the environment on genetic expression. For example, a young woman in her early to mid-twenties who has a genetic propensity to develop schizophrenia can go through a traumatic relationship, and that experience then catalyzes the initial onset of schizophrenic symptoms known as the prodromal phase.

    Neurotransmitters

    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 positive symptoms (Howes & Kapur, 2009). These findings were the oldest biologically focused hypothesis about the etiology of schizophrenia that began with research first conducted in the 1950s.

    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

    Image of the brain showing enlarged ventricles in a schizophrenic brain.
    Figure \(\PageIndex{2}\): Schizophrenia is associated with enlarged ventricles in the brain.

    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 areas. We do not yet understand the mechanisms or processes involved in the apparent atrophy of brain tissue in the brains of persons with schizophrenia or when this process takes place as a person grows and matures.

    Link to Learning

    This PBS News Hour clip highlights some research conducted by Steven McCarroll, an associate professor of genetics at Harvard University, that identified specific genetic markers connected to schizophrenia.

    Watch It

    Watch this video to learn more about the biological explanations of schizophrenia.

    You can view the transcript for “Biological basis of schizophrenia | Behavior | MCAT | Khan Academy” here (opens in new window).

    Try It

    Glossary

    dopamine-hypothesis: the oldest and most widely accepted biochemical model of schizophrenia that suggests overactivity of dopamine in the brain; newer studies are now exploring the role and interaction of other neurotransmitter systems

    ventricles: hollow spaces in the brain

    1. Siegmann A. E. (1976). A classification of sociomedical health indicators: perspectives for health administrators and health planners. International journal of health services : planning, administration, evaluation, 6(3), 521–538. https://doi.org/10.2190/MY7U-4BGM-9QFY-N0TN↵
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