biological explanation for schizoprenia

• family studies increased risk of sz due to genetic similarity. gottesman 1991 large scale family study 9% siblings 48% identical twin
• candidate genes many genes are involved polygenic. most likely genes is coding neurotransmitters inc DA. Ripke 2014 all past data from genome wide study. genetic make up 37000 sz 11300 cg 108 seperate combinations aettologically heterogenous
• role of mutation. mutation can occur in parental DNA caused by radiation or ural infection. evidence correlation between parental age and sperm mutation and increased risk of sz. 0.7% of sperm from 20-24 year olds have mutations compared to 2% from 50+
• + supporting evidence. Tienari 2004 bio children of parents sz increased risk developing sz when growing up in adoptive household. eventhough growing up in a different household therefore different environmental factors genes still have a strong influence. therefore genes have a strong basis in the influence of developing sz.
• -not purely genetic better explained via dsm. morgan 2017 birth complications linked to the development of sz. DiForti 2015 smoking TCH rich cannibis users have higher risk of schizophrenia. this supports that stressful situations such as birth complications can increase the risk of developing sz. further emphasising the role the dsm does in explaining sz, as purely bio not sufficient enough
• +emphasis on genetic treatment as bio approach can be linked to genetic counselling. if either one or both of the parents have sz child is at an increased risk. shows that different gene combinations can influence genetic vulnerability especially greater relatedness. also, if child is at heightened risk then stressful situations which can trigger sz can be avoided
• original DA hypothesis: increased dopamine hyperdopamingeria in the ventral striatum leads to increased risk of sz
• updated DA hypothesis: davis 1991 hypodopamingeria. suggesterd cortical low da leads to subcortical high da levels causing sz
• +supports the idea of hyperdopaminergia. curran 2004 amphetamine to in crease da levels worsen symptoms with or induce symptoms without. suggests that increased da levels symptoms is an efficient explanation for sz as can cause speech poverty or language deficit. supports original da hypothesis
• -da not the only substance responsible for sz. mcchurtesh 2000 consistently found high levels of glutamate in several brain regions in sz sufferers. also several candidate genes are involved in the production of glutamate suggests unusual levels of glutamate cause mood swings and poor concentration which are symptoms of sz. therefore more research needs to be done on the role of glutamate
• -supports original hypothesis using rats. tenn 2013 gave rats sz using amphetamines and relieved symptoms using da drugs. shows that drugs reducing da relieves sz. emphasis on original hypothesis
• + research support neurotransmitter imbalance. Cannon et al 2004 found that dopamine receptors were increased in the brains of people with positive symptoms of sz. Kahn et al 2008 found that serotonin transporter gene was associated with negative symptoms of sz. However, both studies used small samples sizes meaning that the findings may not apply to everyone with sz. They also only looked at specific aspects of the disorder rather than the whole picture. Therefore, external validity is limited.