Biological explanations

• Biological explanations


  - Genetic explanations

  - Neural corelates
• Genetic explanations


  Schizophrenia is transmitted through hereditary means, no single 'schizophrenic gene' several involved which increases an individuals overall vulnerability to developing schizophrenia
• Gottesman and Shields (1976)

  Reviewed 5 twin studies and reported a concordance rate between 75% and 91% for MZ twins with severe forms of schizophrenia suggesting that genetics play a larger role with chronic forms of the disorder.
• Torrey et al (1994)

  Supported the findings but Gotterman and Shields

  - if one MZ twin developed schizophrenia there is a 28% chance the second twin will do so too.
• Overlook nurture


  Whilst twin studies suggest a genetic factor in the onset of schizophrenia they overlook the influence of environments on the onset of schizophrenia

  - MZ twins treated more similarly than DZ twins

  - makes it difficult to separate the effects of nature and nurture in the onset of schizophrenia.
• Sample size


  Similarly the samples from which such results are derived are very small, therefore the findings should not be generalised to the whole population - only MZ twins with 1 being schizophrenic.
• Lack of 100% CR

  If genes alone caused schizophrenia concordance rates for MZ twins would be 100%, which they aren't

  - this suggests that other factors must contribute to the onset of schizophrenia

  - the diathesis model suggests that a person may have a genetic vulnerability but a stressor, (poverty, environment) causes the vulnerability to manifest into schizophrenia.

  - this proposes further explanations for the onset of schizophrenia with a more interactionalist viewpoint.
• Kety and Ingraham (1992)

  Found prevalence rates of schizophrenia were 10 times higher among genetic relatives rather than adoptive relatives of schizophrenia.

  - genetics play a larger role than environmental factors
• Parmas et al (1993)

  Conducted a longitudinal family study of schizophrenia, finding that 16% of children whose mothers had schizophrenia developed the disorder, compared to 2% of children whose mother did not.

  - Suggesting a genetic link
• Sorry et al (2004)

  Performed a longitudinal study over 21 years on Finnish adoptees with biological mothers with schizophrenia comparing them with adoptees whose biological mother didn't have schizophrenia.

  - also considered family rearing styles withing the adoptive families.

  - those adoptees who developed schizophrenia were more sensitive to non-healthy rearing patterns, suggesting environmental factors are also important.
• Interactionist Approach


  Acknowledges that a range of factors, including biological and psychological factors, are involved in the development of schizophrenia
• Diathesis - Stress model

  Consists of a vulnerability to schizophrenia and a stressor/trigger causes the onset of schizophrenia

  - Meehl's model + original d-s vulnerability was completely genetic (schizogene). without schizogene no amount of stress could lead to the development of schizophrenia

  - in carriers of the gene, chronic stress, in particular the presence of a schizophrenogenic mother, could result in the development of schizophrenia
• Modern understanding of diathesis

  Clear many genes appear to increase genetic vulnerability

  - also range in factors other than genetic eg. trauma

  - read et al (2001) neurodevelopmental model where early trauma alters developing brain
• Modern understanding of stress

  Modern definition of stress is anything that risks triggering schizophrenia (Houston et al 2008)

  - most research concerns cannabis use

  - stressor as it increases risk up to 7 times according to dose - interferes with dopamine system - most people unaffected
• Treatment


  Combine drug therapies and CBT

  - Turkington et al (2006) impossible to believe in biological causes and practise CBT to relieve psychological symptoms
• Tienari et al (2004)
• Overly simplified
• Turkington et al (2006)
• Gene-Mapping


  Gene-mapping studies recently used that look for genetic material commonly found between sufferers

  - identified a number of genes that seem to exert an influence
• Benzel et al (2007)

  Used gene mapping to find evidence suggesting that NRG3 gene variants interact with both NGRI and ERBB gene variants to create susceptibility to developing schizophrenia

  - supports idea that there isn't 1 singular gene responsible for schizophrenia but rather an interaction of a number of genes
• Avramopoulos et al (2013)

  Sequenced genes associated with the neuregulin signalling pathway, which relays signals within the nervous system

  - they found that some families with high levels of schizophrenia had multiple neuregulin signalling-related variants whilst others had none

  - those that did, experienced more hallucinations but less impairment than those that didn't

  - suggests that individually harmless genetic variation my unite to increase vulnerability to schizophrenia
• Test development - AO3

  Gene-mapping offers the possibility of developing tests to identify high-risk individuals, though this raises concerns on what we do with this information
• Criticisms - AO3


  - Biological determinist as the approach says that what happens is because of biological factors that are out of our control

  - can be considered biologically reductionist as it overlooks the influence of any factors other than the biological ones.
• Neural Correlates


  The idea of neural correlates is that abnormalities with specific brain areas may be associated with the development of schizophrenia

  - originally evidence was limited to post-mortems conducted upon the brains of dead schizophrenics

  - now research uses non-invasive scanning techniques such as fMRI
• Cause or result

  Must consider whether brain abnormalities found in schizophrenic patients are caused by genetic factors or are the result of the disorder

  - this can be investigated by comparing the brain of sufferers with non-schizophrenic family members if similar brain abnormalities are found in both it suggests a genetic link
• Boss et al (2012)

  Performed MRI scans of 155 schizophrenic patients, 186 of schizophrenic non-schizophrenic siblings and 122 non-related schizophrenics to find that schizophrenics have decreased grey matter + cortical thinning compared with other participants

  - suggests brain tissue differences in schizophrenics are an effect of having schizophrenia rather tan being due to a genetic factor
• Tilo et al (2001)

  Gave fMRI scans to 6 schizophrenics and 6 non-schizophrenics whilst they looked at and spoke about Rorschach ink blots

  - in schizophrenics it was found that the severity of thought disorder was negatively correlated with the production of coherent speech

  - supports the idea of abnormal functioning in specific areas being related to schizophrenia
• Enlarged ventricles


  Early research was focussed on schizophrenics having enlarged ventricles

  - enlarged ventricles are especially associated with damage to the central brain areas and the pre-frontal cortex, which more recent scanning studies have also linked to the disorder, such damage has often been associated with negative symptoms
• Johnstone et al (1976)

  Found that schizophrenics had enlarged ventricles whilst non-schizophrenics didn't

  - supports early research looking into the idea that schizophrenics have enlarged ventricles however this could be an affect of the disorder

  - in this vein, it appears that those schizophrenics that are medication resistant are also those who have enlarged ventricles, could mean its an effect of suffering from schizophrenia over an extended period rather than a cause of schizophrenia
• Weyandt (2006)


  Reported that enlarged ventricles are associated with negative symptoms only, implying that it can't explain all symptoms and incidences of schizophrenia

  - as not all schizophrenics have enlarged ventricles and not all people with enlarged ventricles have schizophrenia it refutes the idea that schizophrenia is due to a loss of brain tissue

  - lacks aetiological validity as a theory as there isn't 1 cause of schizophrenia
• Other factors - AO3

  When assessing the role that brain abnormalities play in the development of schizophrenia, consideration must be given to environmental factors, such as substance abuse and stress levels, which may also be having a damaging influence on brain tissue.
• Longitudinal studies - AO3

  Structural brain damage is often evident at first onset of schizophrenia, but only by performing longitudinal studies would it be possible to assess whether damage progressively worsens as the disorder continues

  - sufferers from people dropping out (attrition rate) and reducing validity
• Dopamine Hypothesis


  Dopamine is important in the functioning of several brain areas that may be implicated in the symptoms of schizophrenia
• Original Dopamine hypothesis


  Focused on the possible role of high levels of dopamine (hyperdopaminergic) in the subcortex

  - eg. an excess of dopamine receptors in Broca's area may be associated with poverty of speech and/or the experience of auditory hallucinations
• More recent Dopamine Hypothesis

  Focussed on abnormal dopamine systems in the brain's cortex

  - Goldman-Rakic et al (2004) identified a role of low levels of dopamine (hypodopaminergic) in negative symptoms
• Combination


  May be that both hyper- and hypodopaminergia are both correct explanations and that both high and low levels of dopamine in different areas of the brain are responsible for schizophrenia
• Curran et al (2004) - AO3

  Found that dopamine agonists such as amphetamines that increase levels of dopamine make symptoms of schizophrenia worse and produce schizophrenic-like symptoms in non-sufferers

  On the other hand antipsychotics work by reducing levels of dopamine, both drugs suggest that dopamine does play a role in schizophrenia
• Lindstroem et al (1999)

  Used radioactive labelling to identify that the chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics than non-schizophrenics
• Randrup and Munkvad (1966)

  Created schizophrenic-like behaviour in rats by giving them amphetamines and raising Dopamine levels.

  Support for Dopamine Hypothesis
• Alternative


  Evidence to suggest that dopamine may not be the sole cause of schizophrenia.

  - Moghaddam and Javitt (2012) conducted research which implicated another neurotransmitter known as glutamate