AO1: Social Causation Hypothesis
Psychologists such as Brian Cooper (2005) have been aware of the link between schizophrenia and environmental risk factors for many years. Supporters of the social causation hypothesis suggest that these factors may be ‘causally implicated’ or at least precipitate relapse in those who already have a diagnosis. Risk factors are many and varied and include family dysfunction and childhood trauma; however, some of the best supported risk factors are social adversity, urbanicity and immigration and/or minority group status. The question though is how do these factors cause schizophrenia?
All human beings have the same basic needs. These needs can be physical such as nutrition, warmth and shelter but they can also be intellectual, emotional and social. Some children grow up in environments which are less favourable than others due to socio-economic inequality and this can make them vulnerable to mental health disorders in the future. Families affected by unemployment, poverty and a poorer standard of living may be exposed to considerably more stress than other families. Furthermore, people from lower socio-economic groups, particularly the so-called social underclass may not be able to access treatment, leaving them even more vulnerable and further exacerbating their problems.
Many researchers have commented on the association between urban living and schizophrenia. William Eaton (1974) suggests that city life is more stressful than rural life and long term exposure to such stress may trigger a psychotic episode. There are many stressors linked to city life including air, noise and light pollution, criminality and substance abuse, the ‘24 hour’ society, faster pace, greater anonymity and lack of social cohesion and neighborliness. Collectively these factors may make a person more vulnerable to schizophrenia. Furthermore, increased population density makes life more competitive, whether it’s for a seat on the tube or a job and this arguably increases the experience of chronic social defeat, a stressor which may elicit schizophrenic symptoms (see stretch and challenge).
Immigration and minority status
Research in many countries has shown that first and second generation immigrants are at greater risk of schizophrenia than the general population, however, the risk decreases as the number of people from the same ethnic background increases, (Boydell et al. 2001). This indicates that it is minority or outgroup status that is the key, as opposed to belonging to any particular ethnic group. The implication is that marginalisation of outgroups may leave people vulnerable to schizophrenia.
Wim Veling and colleagues (2008) suggest that schizophrenia may be a reaction toward the chronic experience of prejudice and discrimination. Furthermore, some second generation immigrants may be at greater risk than first generation immigrants, due to weaker ethnic or cultural identity. Second generation immigrants may not fully identify with their parents due to primary socialisation having taken place in different countries, but they may feel that they fit in neatly alongside their indigenous peers, whose beliefs and expectations may be at odds with that of their parents and extended family members.
Stretch and challenge: The Social Defeat Hypothesis
In 2005, Jean-Paul Selten and Elizabeth Cantor-Graae (2005) proposed the Social Defeat Hypothesis to explain how social factors can alter dopaminergic activity. It is thought that long term feelings of isolation or marginalisation can lead to a sense of social defeat and exclusion and that people occupy ‘subordinate positions’ in society or have ‘outsider status’ are at increased risk of schizophrenia. The ‘intruder rat paradigm’ involves placing a male rat (the intruder) into another rat’s cage (the resident). The resident generally attacks the intruder, who shows signs of submission, in order to stop the attacker. Following the defeat, the intruder shows increased levels of dopaminergic activity in the mesolimbic system and this is believed to be the mechanism that links social defeat and schizophrenia (see p000). This interactionist theory appears to explain why people who are made to feel that they do not belong are more at risk of schizophrenia. They believe that social defeat can leave people more sensitive to dopamine in the future, making a future psychotic episode more likely.
Link to Developmental Psychology: Does city life sensitise the developing brain to social stress?
In a highly controlled experimental study Florian Lederbogen and colleagues (2011) used FMRI to reveal a link between growing up in an urban environment and later sensitivity to social stress. Participants had to solve challenging arithmetic problems whilst receiving negative feedback about their performance. The participants who grew up in cities showed greater activity in the amygdala and the anterior cingulate nucleus (ACC) compared with those who grew up in rural locations. These brain regions regulate emotion and stress responses and research has previously shown that people with schizophrenia have reduced ACC volume. From a developmental perspective, this study seems to have shown that where we are brought up can alter brain function in later life. These differences may make us more resilient or more vulnerable to mental health disorders, such as schizophrenia, in adulthood.
AO3: Evaluation of social causation hypothesis
Meta-analyses support the role of urban dwelling
One strength of the social causation hypothesis is that research has shown a significant correlation between urban dwelling and schizophrenia.
For example, Evangelos Vassos and colleagues (2012) performed a meta-analyses on data from four studies conducted in Sweden, the Netherlands and Denmark, including nearly 24,000 cases of schizophrenia. They found that the risk was 2.37 times higher for people living in the most urban environments compared with the most rural environments.
This is important as it shows that relative risk ofschizophrenia increases in line with population density.
Competing argument: One problem is that much of the supporting data is correlational, meaning it is not possible to say that schizophrenia is caused by urbanicity or adversity; the social drift hypothesis suggests people with schizophrenia find it hard to complete their education or hold down a job, leading them to ‘drift’ into a lower social class than their parents and siblings. This can lead to them migrating into deprived inner-city areas. Goldberg & Morrison (1988), for example, found that sons with schizophrenia were frequently in a lower social class than their fathers, suggesting that schizophrenia had caused them to become downwardly socially mobile. This said, many of the more recent studies, such as the one above, control for this issue by only looking at urban dwelling before symptoms were first observed, i.e. where people spent their childhood years.
Evidence from MZ/DZ twin studies
One weakness of social causation is that Gottesman and Shields (1966) clearly demonstrate that schizophrenia has a genetic component.
The concordance rate for schizophrenia in monozygotic twins was 42% compared with just 9% dizygotic twins. When the co-twin did not have schizophrenia the researchers checked to see whether they had any other psychiatric diagnosis or sub-clinical signs of abnormality of any sort, and in this case the concordance rate was 79% for MZ twins and 45% for DZs.
This shows that environmental factors may only trigger the onset of schizophrenia in people who are genetically predisposed to the condition. This is known as the diathesis-stress model of schizophrenia.
Strength or weakness (preferably a weakness to keep it balanced)
One strength of weak ethnic identity as predictive of schizophrenia is the support found in a complex analysis of self-reported questionnaire data performed by Wim Veling and colleagues (2010).
People classed as marginalised (weak national and ethnic identity) and assimilated (strong national identity but weak ethnic identity) were at greater risk of schizophrenia than people classed as integrated (strong national and ethnic identity) or separated (weak national bit strong ethnic identity).
This suggests that stronger than average ethnic identity, meaning people identify and embrace their ethnic ‘differentness’ appear less likely to develop schizophrenia.
One strength of the social causation hypothesis is that it draws attention to factors which affect mental health at the community level.
Housing projects which reduce overcrowding and provide more defensible and community projects which encourage neighborhood cohesion and celebrate cultural diversity should foster the courage, fortitude and resilience which will help communities arm themselves against mental breakdown.
This is a critical step in developing a sense of collective social responsibility, not only our own mental wellbeing, but also that of other people.
EXTRA: Issues and debates
One highly pertinent debate here is that of nature versus nurture.
In Pekka Tienari and colleagues’ adoption study (1985) none of the 43 Finnish offspring of biological mothers with schizophrenia who had been adopted into healthy or even in mildly disturbed adoptive families, were diagnosed with schizophrenia. Furthermore, 37% of offspring without biological mothers with schizophrenia but raised in severely disturbed families were classed as severely mentally disturbed themselves.
These findings demonstrate the importance of nurture in protecting offspring from mental disturbance, suggesting that community and government support for families is critical.
Overall, the evidence suggests that environmental factors relating to urbancity, including lack of social cohesion and being a victim of crime, in addition to one’s national and ethnic identity apparently play an important role to play in determining who will is likely to develop schizophrenia later in life. These factors may be critical in determining the way in which genetic potentiality is expressed throughout life. Although social causation is an important consideration, the role of biology cannot be cast aside; understanding the neuroscientific mechanisms which turn psychological subjective experiences into shattering psychotic symptomology is the next step for researchers.
- Describe one non-biological explanation of schizophrenia (5)
- Compare two explanations of schizophrenia (4)
- Evaluate one non-biological explanation of schizophrenia with reference t research evidence (8)
- You will have studied various explanations of schizophrenia on your course. Assess the usefulness of at least two of these explanations with reference to the their applications to society (20)