biological explanations

• genetic explanation


  sz passed on through generations - 1st degree relatives more likely to develop disorder - believed to be polygenic - evidence from twin, family and adoption studies - used to establish concordance rate - e.g. mz and dz twins one of each pair has sz compared to see how often other twin shows sz, if sz genetic argued mz twins should have higher concordance rate than dz twins
• GENETIC EVALUATION - family studies

  Varma found 16% 1st degree ratlines of schizophrenics developed sz compared to 7% controls - suggests more genetically related you are, more likely you are to develop sz - however, increased rate of sz amongst those with parents with sz could be down to environment
• GENETIC EVALUATION - twin research

  Joseph found concordance rate of 40% for mz twins compared to 7% for DZ twins - schizophrenia may be partly genetic - however, could be possible that higher concordance rate is due to MZ twins being treated more similar than dz twins
• GENETIC EVALUATION - adoption research

  Tienari compared adopted children whose biological mother had sz compared to control group of adoptees without genetic risk - found much higher rate of sz amongst those with biological mothers with sz - even with environmental influence of biological mother removed, genetic risk still evident - however, found healthy adoptive family could protect against those with high genetic risk developing sz
• neural correlates and dopamine hypothesis 


  experience of sz associated with abnormalities to the structure or function of the brain - e.g. early research on schizophrenics showed they had enlarged ventricles associated with damage to pre frontal cortex which have links to disorder - positive symptoms result of overactive transmission of neurotransmitter dopamine - schizophrenics thought to have high numbers of D2 receptors on receiving neutrons, more dopamine binding, more neurone firing - dopamine plays key role in guiding attention disturbances may relate to problems relating to attention
• revised dopamine hypothesis

  Davis and Kahn - positive symptoms of sz caused by excess of dopamine in subcortical areas of the brain (mesolimbic pathway) - negative symptoms caused by deficit of dopamine in pre frontal cortex (mesocortical pathway) - suggests dopamine has important but complex role in development of sz
• DOPAMINE EVALUATION - drug research

  amphetamine drugs, dopamine antagonists (stimulate neurone containing dopamine causing synapse to be flooded with neurotransmitter) - found that large doses of these drugs cause hallucinations and delusions similar to symptoms seen in sz
• DOPAMINE EVALUATION - practical applications

  typical antipsychotic drugs used to treat sz all dopamine antagonists - means they work by reducing stimulation of neurons containing dopamine by blocking D2 receptors and reduce positive symptoms like delusions - benefits real peoples lives and supports dopamine overactivity explains sz as reducing levels reduces symptoms
• NEURAL CORRELATES EVALUATION - cause and effect unclear

  brain abnormalities could be the effect rather than the cause of sz - e.g. could be the symptoms that cause changes in brain function - we don't fully understand the role of neural correlates in development of sz
• BIOLOGICAL EVALUATION - determinist 


  sz caused by factors outside sufferers conscious control - positive as it removes the blame from the patient for developing the disorder - negative because if the individual thinks they have no control over developing the disorder they may engage in risk behaviours (substance abuse) which could in turn trigger onset of sz
• BIOLOGICAL EVALUATION - reductionist

  focus wholly on internal factors and ignore environmental factors - psychological explanations of sz like family explanations that argue the way parents treat their child is the main influence on sz onset - biology alone may not explain all aspects of sz