Section Learning Objectives

• Describe the biological causes of schizophrenia spectrum and other psychotic disorders.
• Describe the psychological causes of schizophrenia spectrum and other psychotic disorders.
• Describe the sociocultural causes of schizophrenia spectrum and other psychotic disorders.

8.3.1 Biological

8.3.1.1 Genetics

Twin and family studies consistently support the role of genetics in schizophrenia spectrum and psychotic disorders. Specifically, if one identical twin develops schizophrenia, there is roughly a 50% chance that the other twin will also develop the disorder within their lifetime (Coon & Mitter, 2007). This percentage drops to 17% in fraternal twins. However, it should be noted that most people diagnosed with schizophrenia hae no family history of psychosis (APA, 2022). The disorder is polygenetic with a spectrum of risk alleles, both common and rare, that are also associated with other mental disorders (e.g., bipolar disorder, depression, autism) (APA, 2022). Family studies have also found similarities in brain abnormalities among individuals with schizophrenia and their relatives; the more similarities, the higher the likelihood that the family member also developed schizophrenia (Scognamiglio & Houenou, 2014).

8.3.1.2 Neurobiological

There is consistent and reliable evidence of a neurobiological component in the transmission of schizophrenia. More specifically, neuroimaging studies have found a significant reduction in overall and specific brain regions volumes, as well as in tissue density of individuals with schizophrenia compared to healthy controls (Brugger, & Howes, 2017). Additionally, there has been evidence of ventricle enlargement as well as volume reductions in the medial temporal lobe. Structures such as the amygdala (involved in emotion regulation), the hippocampus (involved in memory), as well as the neocortical surface of the temporal lobes (processing of auditory information) are all structures within the medial temporal lobe (Kurtz, 2015). Additional studies also indicate a reduction in the volume of the orbitofrontal regions of the brain, a part of the frontal lobe that is responsible for response inhibition (Kurtz, 2015).

8.3.1.3 Prenatal Factors

Advanced paternal age and complications during birth and pregnancy are associated with a higher risk of schizophrenia later in life. These include hypoxia, stress, infection, and malnutrition during the prenatal period (APA, 2022).

8.3.1.4 Stress Cascade

The stress-vulnerability model suggests that individuals have a genetic or biological predisposition to develop psychotic disorders; however, symptoms will not present unless there is a stressful precipitating factor that elicits the onset of the disorder. Researchers have identified the HPA axis and its consequential neurological effects as the likely responsible neurobiological component responsible for this stress cascade.

The HPA axis is one of the main neurobiological structures that mediate stress. It involves the regulation of three chemical messengers (corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and glucocorticoids) as they respond to a stressful situation (Corcoran et al., 2003). Glucocorticoids (e.g., cortisol) are the final neurotransmitter released which is responsible for the physiological change that accompanies stress to prepare the body to “fight” or “flight.”

It is hypothesized that in combination with abnormal brain structures, persistently increased levels of glucocorticoids may be the key to the onset of psychosis in individuals in a prodromal phase (Corcoran et al., 2003). More specifically, stress exposure (and increased glucocorticoids) affects the neurotransmitter system and exacerbates psychotic symptoms due to changes in dopamine activity (Walker & Diforio, 1997). While research continues to explore the relationship between stress and the onset of schizophrenia spectrum and other psychotic disorders, evidence for the implication of stress and symptom relapse is strong. More specifically, individuals with schizophrenia experience more stressful life events leading up to a relapse of symptoms. Similarly, it is hypothesized that the worsening or exacerbation of symptoms is also a source of stress as symptoms interfere with daily functioning (Walker & Diforio, 1997). This stress alone may be enough to initiate a relapse.

8.3.2 Psychological

The cognitive model utilizes some of the aspects of the diathesis-stress model in that it proposes that premorbid neurocognitive impairment places individuals at risk for aversive work/academic/interpersonal experiences. These experiences in turn lead to dysfunctional beliefs and cognitive appraisals, ultimately leading to maladaptive behaviors such as delusions/hallucinations (Beck & Rector, 2005).

Beck proposed a diathesis-stress model for the development of schizophrenia. Based on his theory, an underlying neurocognitive impairment makes an individual more vulnerable to experiencing aversive life events such as homelessness, conflict within the family, etc. Individuals with schizophrenia are more likely to evaluate these aversive life events with a dysfunctional attitude and maladaptive cognitive distortions. The combination of the aversive events and their negative interpretations of them, produces a stress response in the individual, thus igniting hyperactivation of the HPA axis. According to Beck and Rector (2005), it is the culmination of these events that leads to the development of schizophrenia.

8.3.3. Sociocultural

8.3.3.1 Expressed Emotion

Research in support of a supportive family environment suggests that families high in expressed emotion, meaning families that have highly hostile, critical, and/or overinvolved family members, are predictors of relapse (Bebbington & Kuipers, 2011). In fact, individuals who return to families post-hospitalization with high expressed emotion are twice as likely to relapse compared to those who return to families with low expressed emotion (Corcoran et al., 2003). Several meta-analyses have concluded that family atmosphere is causally related to relapse in individuals with schizophrenia and that these outcomes can be improved when the family environment is improved (Bebbington & Kuipers, 2011). Therefore, one major treatment goal in families of people with schizophrenia is to reduce expressed emotion within family interactions.

8.3.3.2 Family Dysfunction

Even for families with low levels of expressed emotion, there is often an increase in family stress due to the secondary effects of schizophrenia. Having a family member who has been diagnosed with schizophrenia increases the likelihood of a disruptive family environment due to managing their symptoms and ensuring their safety while they are home (Friedrich & Wancata, 2015). Because of the severity of symptoms, families with a loved one diagnosed with schizophrenia often report more conflict in the home as well as more difficulty communicating with one another (Kurtz, 2015).

8.3.3.3 Environmental Factors

Schizophrenia is more prevalent in those who grew up in an urban environment, in refugees and some migrant groups, and in groups that are socially oppressed and face discrimination. Social adversity, childhood trauma and neglect, and socioeconomic factors also appear to be associated with these disorders. These associations may be driven by increases in stress caused by these environmental factors.