Schizophrenia is a partially genetic disorder, inherited through hereditary means (through the genes passed on to individuals from their parents) and therefore runs in families.
Schizophrenia runs in families.Probability of schizophrenia = 48% between MZ twins, 46% if both parents had it and 10% between DZ twins. Strong evidence that schizophrenia is genetic
Schizophrenia is polygenic(involves a combination of genes) and is aetiologically heterogenous(a number of different combinations of genes can lead to the illness)
Compared the entire genetic makeup of 37,000 patients compare to 113,000 healthy controls and found 108 separate genetic variations associated with increased risk of the disorder.
Children adopted from 19,000 Finnish mothers at birth were compared with a control group (no genetic risk). It was found that harsh parenting was associated with schizophrenia in the children but ONLY for those who had a genetic vulnerability. Biological children of parents with Sz are at a greater risk even if they grow up in an adoptive family. Genetics make people more vulnerable!
80% of Schizophrenics have enlarged ventricles (fluid-filled spaces between brain areas) = a loss of brain tissue. Enlarged ventricles is associated with damage to central brain regions and pre-frontal cortex. Often associated with the negative symptoms of schizophrenia
Neurotransmitters are fast chemicalmessengers that travel between neurons (brain cells) by crossing the synapse. They bind themselves to receptors on the next neuron and pass on their message in the form of a small electric charge. Dopamine is an important neurotransmitter that regulate mood and attention.
Abnormally high levels of dopamine in the sub-cortex (inner parts of the brain) causing an over activation of neurons, resulting in positive symptoms of schizophrenia e.g. in Broca’s area (responsible for speech production) associated with auditory hallucinations and speech poverty
Abnormally low levels of dopamine in the pre-cortex (responsible for decision making) causing an under activation of neurons. Goldman-Rakic et al(2004) Hypodopaminergia in the pre-frontal cortex could explain negative symptoms in Sz
Mixed evidence - limitations of the dopamine hypothesis
Noll: Argues that 1/3 of patients do not respond to drugs which block dopamine so other neurotransmitters may be involved. Suggests that there is mixed evidence for the dopamine hypothesis as research has shifted to the role of other neurotransmitters showing they also have a role in Sz
Chicken and the egg - limitations of dopamine hypothesis
Now criticism of the dopamine hypothesis is there is a problem with the chicken and the egg. Are raised dopamine levels the cause of the schizophrenia of is it the raised dopamine level the result of Sz. It is unclear which comes first ∴ we need to be careful when establishing cause and effect relationships in schizophrenic patients
Environmental factors - limitation of biological explanation
Evidence to suggest an important role for environmental factors. The probability of developing Sz even if your an MZ twin is less than 50%. This challenges genetic explanations as if Sz was caused purely by genetic factors the probability should be 100%
Demand characteristics in twin, family and adoption studies - limitation of biological explanation
Twin, family and adoption studies must be considered cautiously because they are retrospective and diagnosis may be biased by knowledge that other family members who may have been diagnosed. This suggests the findings may lack validity due to the possibility of demand characteristic