Schizophrenia

• Genetic hypothesis states: the closer you are in relation to the family member w/ SZ, the greater their chance of developing the disorder.

  • concordance rates show, as genetic similarity increases so does the probability of sharing SZ (Gottesman 1991)
  • risk of developing SZ is nearly 3x as high in MZ twins compared to DZ twins (MZ= 48% and DZ=17%)
• Genes consist of DNA strands that contain ‘instructions’ for general physical features and specific physical features. Therefore, genetic variation may be responsible for some neurochemical irregularities.
• Heritability of SZ is 79% (Hilker et al. 2018). This suggests a large role of genetic factors in determining the disorder. One way of understanding the genetic underwire of SZ is to identify responsible genes:

  • Wright (2014) indicated that up to 700 genes are present and by now this figure is likely to be 1000.
• The DNA code in one or more genes may spontaneously mutate to develop SZ: mutations can result from an environmental factor or an error in cell division (deletion or duplication).
• For ex. DiGeorge Syndrome is caused by the deletion of 30-40 neighbouring genes located in a specific region and 25% of people w/ DiGeorge Syndrome = develop SZ
• • The COMT gene: provides instructions for the creation of an enzyme that breaks down NTs such as dopamine in the frontal cortex: hence the link between SZ and the DiGeorge Syndrome may be because of the deletion of the COMT gene (deletion of the COMT gene will mean that dopamine levels are poorly regulated resulting in SZ symptoms)
• The DISC1 gene: people with an abnormality in the gene are 1.4x more likely to develop SZ than people w/o this abnormality (Kim et al. 2012).

  • this gene codes for the creation of GABA, which regulates other neurotransmitters ie glutamate and dopamine in the limbic system
• A person may possess SZ genes (diathesis) but the condition is only triggered by other biological or environmental effects

  Original diathesis-stress model = stated that stress was psychological

  • Houston et al 2008 suggests that nowadays the definition of stress is more broader and includes anything that might trigger SZ
• Recent research into factors triggering an episode of SZ shows that cannabis use inc risk up to 7x (as the cannabis interferes with the dopamine system)
• Credibility for bio cause of SZ:

  • Gotessman (1991): analysed concordance rates for people of different genetic similarity - showed clear relationship between genetic similarity and an increase in two related individuals both having SZ
  • Gotessman and Shields (1966): identified a concordance rate of 42% for MZ twins and 9% for DZ twins = greater rate for MZ shows that while SZ is not entirely a genetic disorder, biology does play a significant role
• Objections for bio cause of SZ:

  • be more cautious in interpreting the findings of twin studies: MZs not only share more DNA than DZs, they are also treated more similarly (always the same sex and same appearance).
  • Similarity in genetic relatives may also be due to shared environment = reduces validity of the conclusion that the greater shared DNA is responsible for the similar pathology
• Differences for bio cause of SZ (1):

  • concordance rates in twin studies are far from 100% suggesting a significant role for the environment. Pedersen and Mortensen (2006) show the risk of developing SZ increases with greater exposure to city life and higher population density. Hence, rural dwelling may help protect a person from developing a disorder to which they are genetically predisposed.
• Differences for bio cause of SZ (2):

  • Dahoun et al (2017) concluded that DISC1 is associated with presynaptic dopamine dysregulation, and Egan et al (2001) found a link between decreased dopamine activity in the PFC and one form of the COMT gene = this shows how genetic variations support neurochemical differences which can predispose a person towards SZ
• Applications for bio cause of SZ:

  • When a family member receives a diagnosis of SZ, the family may want more info about heritability: ‘recurrence risk’ can be calculated and the counsellor will then help the family to interpret it. This provides support, helps put to rest fears about developing SZ and inform choices about family planning.
• There are many environmental risk factors but some of the best supported risk factors are social adversity, urbanicity, social isolation and immigration/minority status (Tiwari et al 2010).
• Growing up in an environment that is less favourable than others, makes children vulnerable to mental health disorders in the future

  • people from lower socioeconomic groups may not be able to access treatment for SZ = leaving them more vulnerable
  • AO3 (Hjem et al. 2004) showed that ‘social adversity’ in childhood relates to the development of SZ in later life
• Urbanicity may play a role: city life is more stressful than rural life - noise, light, pollution, pace and greater anonymity:

  • high pop density makes life more competitive, which may increase the experiences of chronic social defeat (stressor that may be due to hostile confrontations)
  • Inner-city areas with poor housing + overcrowding, and high levels of crime and drug use
• Faris (1934) has suggested that people with SZ withdraw because they feel that contact with others is stressful. Such self-imposed isolation cuts the individual off from feedback about what behaviours and thoughts are inappropriate and in the absence of corrective feedback they begin behaving strangely.
• Research in many countries has shown that 1st and 2nd gen immigrants are at a higher risk of SZ, however this risk decreases as the number of people from the same background increases; it is a minority status that is the key, as opposed to belonging to any particular ethnic group; marginalisation of outgroups may leave people vulnerable to SZ.
• Veling 2008 suggests SZ may be a reaction against chronic experience of prejudice. 2nd gen immigrants are at greater risk because:

  • weaker cultural identity
  • learned to fit in with the norms
  • their beliefs and expectations may be at odds with those around them
• Credibility for non-bio expl of SZ:

  • Vassos et al (2012) analysed data from 4 studies to correlate location; risk was 2.37x higher for those living in more urban environments (nearly 24,000 cases of SZ). They correlated location (urban to rural) with SZ risk and found a link = risk of SZ was 2.37x higher for people living in the most urban environments compared with the most rural environments. Hence risk of SZ links with population density.
• Objections for non-bio expl of SZ:

  • the data is correlational thus we cannot say SZ is caused by urbanicity or adversity. Social drift hypothesis suggests those with SZ find it hard to hold down a job, so they drift into a lower social class
• Differences for non-bio expl of SZ:

  • (STRENGTH) Veling studied people classed as marginalised and assimilated: they were at greater risk of SZ than people classed as integrated or separated = strong ethnic identity may be a protective factor against SZ
• Applications for non-bio expl of SZ:

  • drawing attention to factors affecting mental health: housing projects reduce overcrowding, celebrate cultural diversity and help foster resilience against mental breakdowns = critical step in developing a sense of collective social responsibility
• Hyperdopaminergia (NTs)

  Antipsychotic drugs (ie chlorpromazine) help symptoms of SZ - but also induce side effects of tremors and muscle rigidity; these are symptoms of Parkinson’s, hence SZ was linked to high dopamine.
• Dopamine deficiency (NTs)

  Davis et al (1991) suggested that the +ve symptoms of SZ may result from excess of dopaminergic activity in the mesolimbic pathway
• What is hypodopaminergia?(NTs)

  lack of dopaminergic activity in mesocortical pathway
• Role of serotonin (NTs)


  Later research focused on the roles of other NT’s: clozapine binds to D1 and D4 receptors but only weakly to D2.

  • clozapine binds to S receptors and reduces +ve and -ve symptoms of SZ = -ve symptoms may be caused by irregular serotonergic activity
• Dopamine dysregulation (NTs):

  Howes and Kapurs (2009) version of the hypothesis:

  • D impairment is the common pathway to psychosis
  • attention should be on high presynaptic D levels as opposed to irregularities of D2 receptors
  • D hypothesis should be viewed as an explanation for ‘psychosis proneness’ and not for specifically SZ
• Credibility for NT expl SZ:

  • study in 2003 found that rats given 9 amphetamine injections over 3wks showed SZ-like symptoms: D antagonists successfully reversed these effects = inc D levels may be a cause of SZ
• Objections for NT expl SZ:

  • Dépatie and Lal (2001) showed that a dopamine agonist which stimulates D2 receptors does not induce/worsen psychotic symptoms
  • neurochemical theories can't explain why some groups are more prone to SZ: Veling showed that Moroccan immigrants were diagnosed than Turkish immigrants = environmental factors may interact with internal neurochemistry
• Applications for NT expl SZ:

  • D antagonists binding to D2 receptors and atypical drugs which block S receptors = successfully reduce symptoms
• Antipsychotic drugs (ie chlorpromazine) help symptoms of SZ - but also induce side effects of tremors and muscle rigidity; these are symptoms of Parkinson’s, hence SZ was linked to high dopamine.
• Antipsychotic drugs (ie chlorpromazine) help symptoms of SZ - but also induce side effects of tremors and muscle rigidity; these are symptoms of Parkinson’s, hence SZ was linked to high dopamine.
• Dopamine deficiency (NT's)

  Davis et al (1991) suggested that the +ve symptoms of SZ may result from excess of dopaminergic activity in the mesolimbic pathway

  • -ve symptoms may result from hypodopaminergia (lack of dopaminergic activity in the mesocortical pathway
• Role of Serotonin (NT's)

  Later research focused on the roles of other NT’s: clozapine binds to D1 and D4 receptors but only weakly to D2.

  • clozapine binds to S receptors and reduces +ve and -ve symptoms of SZ = -ve symptoms may be caused by irregular serotonergic activity
• Dopamine dysregulation (NT's)

  Howes and Kapurs (2009) version of the hypothesis:

  • D impairment is the common pathway to psychosis
  • attention should be on high presynaptic D levels as opposed to irregularities of D2 receptors
  • D hypothesis should be viewed as an explanation for ‘psychosis proneness’ and not for specifically SZ
• Credibility for NTs (bio expl):

  • study in 2003 found that rats given 9 amphetamine injections over 3wks showed SZ-like symptoms: D antagonists successfully reversed these effects = inc D levels may be a cause of SZ
• Objections for NTs (bio expl):

  • Dépatie and Lal (2001) showed that a dopamine agonist which stimulates D2 receptors does not induce/worsen psychotic symptoms
  • neurochemical theories cannot explain why certain groups are more prone to SZ: Veling showed that Moroccan immigrants were diagnosed than Turkish immigrants = environmental factors may interact with internal neurochemistry
• Differences for NTs (bio expl):

  • 1985 study showed that chlorpromazine is an antagonist at many D receptors = suggests that excess activity at specific D receptors is implicated in development of symptoms