correlation method to determine if behaviour is due to nature or nurture
use twin studies to determine a concordance between characteristics
if one twin develops SZ the chances of the other doing so is high
the higher the concordance the higher the chance of genetic relatedness of the disorder
genetic vulnerability 

proposed that there is a genetic component to SZ which predisposes some individuals to the illness~
explanation suggests that whether a person develops SZ is partly due to their genes, why patients often have other family members with SZ
family studies: find individuals who have SZ and determine whether their biological relatives are similarly affected more often than non-biological relatives using correlation
family studies:
Gottesman (1991): concluded that if both parents suffer from SZ, there is a 46% chance of also developing the disorder
shows that genes play an important role however if they were the only factor the percentages would be 100%
could be deterministic: just because we are 'predisposed' by our genes doesn't mean we necessarily get SZ
researchers now accept that SZ concordance rates in families may be more to do with common rearing patterns or other environmental factors that have nothing to do with heredity: interactionist approach
twin studies:
if MZ twins have a higher concordance than DZ twins, a genetic link?
researchers worked out if nature or nurture had a bigger influence
Gottesman and Shields (1972): found that the concordance rate for SZ in the MZ twins was 48% compared to 17% in DZ twins, suggests heredity
indicate a strong component, demonstrate a predisposition to developing SZ but not always, suggesting an environmental influence
concordance rate isn't 100% so SZ can't be account for by genetics alone
sample sizes are always small so difficult to generalise to wider pop
adoption studies
these studies allow researchers to overcome problem of disentangling genetic environmental influences
Heston (1966) compared 47 children whose biological mother had SZ with a control group of children with no history of SZ, none were diagnosed but 16% with biological influence were diagnosed
suggests a geneticbasis to the disorder
SZ could be a polygenetic disorder (more than one gene causing it)
nature vs nature debate, accepts an interactionist approach
the dopamine hypothesis:
dopamine: a neurotransmitter (NT) that serves as a chemical messenger in the brain, can function as both an excitatory and inhibitory NT, causing diverse effects on the brain, body and behaviour
function: associated with pleasure, reward, motivation and motor control, linked to feelings of gratification and is implicated in mood disorders, addiction and certain behaviour when levels are imbalanced
cognitive neuroscience studies are highly scientific: causal explanations
drugs that increase dopamine activity:
claims that an excess of the NT dopamine in certain regions of the brain is associated with the positive symptoms of SZ
SZ's are thought to have abnormally high numbers of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing
evidence: amphetamine is a dopamine agonist, stimulates nerve cells containing dopamine causing the synapse to be flooded with this NT
normal people exposed to large doses of dopamine releasing drugs can develop characteristic symptoms of a SZ episode, disappear when the drug stops
drugs that decrease dopamine activity:
antipsychotic drugs: block the activity of dopamine in the brain, these drugs were found to eliminate symptoms, like hallucinations/delusions
the fact that these drugs that block dopamine activity alleviated many of the symptoms of SZ strengthened the case for the role of dopamine
revised dopamine hypothesis:
Davis and Kahn (1991): positive symptoms of SZ are caused by an excess of dopamine in sub-cortical areas especially the mesolimbic pathway
the negative symptoms are thought to arise from a deficit in dopamine in the mesocortical pathway
dopamine hypothesis evidence:
PET scans show lower levels of dopamine in the dorsolateral prefrontal cortex compared to normal controls
the dorsolateral prefrontal cortex is where the mesocortical dopamine pathway is therefore support for low dopamine in this pathway leads to deficit of dopamine activity and negative symptoms of SZ
lots of success of drug treatment to change levels of dopamine activity
Leutch et al (2013) carried out a meta-analysis of 212 studies that analysed the effectiveness of different antipsychotics with a placebo, all drugs were more effective than the placebo
evaluation:
biological determinism: PET scans can establish a cause for SZ symptoms by measuring dopamine in normal and SZ patients but may be limited as other NT may be involved
explains how both positive and negative symptoms simultaneously as different parts of the brain are affected by dopamine differently led onto the development of more advanced drugs targeting specific sites so biological reductionism is good, more specific treatment
biological reductionism also led to a loss of a holistic understanding experience of SZ symptoms and led to the simplification of the disorder
neural correlates
measurements of the structure or function of the brain that occur in conjunction with an experience, SZ
evidence shows SZ is caused by structural abnormalities in the brain
brain scanning techniques have made it possible to investigate living brain images, cognitive neuroscience
prefrontal cortex: main area of the brain involved in executive function (planning, reasoning and judgement), its impaired in SZ patients
hypothesised that the cognitive systems of SZ results from deficits within the prefrontal cortex and its connections to other areas of the brain
prefrontal cortex:
several studies have reported anatomical changes in the hippocampus of SZ patients
deficits in the nerve connections between the hippocampus and the PFC have been found to correlate with the degree of working memory impairments
white matter: found in the brain and spinal cord and made up of nerve fibres covered in myelin, creates an insulating sheath around fibres speeding up information through the CNS
research found reduced myelination of white matter pathways in SZ patients compared to healthy controls
grey matter:
reduced volume of grey matter in SZ's brains especially in temporal and frontal lobes
found those displaying negative symptoms have enlarged ventricles, they are thought to be the result of nearby parts of the brain not developing properly
evaluation of neural correlates:
findings are inconsistent so inconclusive
MRI's made it possible to investigate living brain images
cause and effect cannot be established with brain abnormalities as its uncertain whether structural abnormalities/reduced functioning predispose to SZ
correlational data, there is a relationship between neural correlates in the brain and SZ
evaluation of biological explanations
inconsistent and there are contradictory findings
cause and effect is difficult to establish as many P's have suffered from SZ for a long time, enlarged ventricles may be the result of taking antipsychotics
biological explanations are reductionist in attempting to explain a complex multi-faced disorder at the levels of cells and genes
deterministic: assumption its inherited and unavoidable
diathesis-stress relationship may be at work, someone could be predisposed to SZ but its caused by environmental factors (interactionism)