biological explanations of ocd Flashcards
genetic explanations
- focused on identifying specific candidate genes implicated in ocd, ocd is believed to be polygenic
- taylor (2003) said as many as 230 genes may be involved, and perhaps diff genetic variations contribute to diff types of ocd
- the COMT gene and SERT gene have both been linked to ocd
the COMT gene
- associated with the production of catechol-O-methyltransferase (COMT) which regulates dopamine
- one variation of the COMT gene results in higher dopamine levels which is common in patients with ocd
the SERT gene (5-HTT)
- linked to serotonin, affecting its transport
- transportation issues cause lower levels of serotonin active in the brain and are associated with ocd
- a study of 2 unrelated families with mutations of the SERT gene found 6 of the 7 family members had ocd
neural explanations: neurotransmitters
- serotonin regulates mood (lower levels are linked to mood disorders) and some ocd cases are linked to reduced serotonin levels (may be caused by the SERT gene
- research into SSRIs found drugs that increase levels of serotonin in the synaptic gap are effective in treating OCD
- high dopamine levels are linked to some ocd symptoms, specifically compulsions
neural explanations: brain structure
- believed several regions in the frontal lobes have abnormal brain circuits in those with ocd
- 2 regions implicated in ocd are the basal ganglia and the orbitofrontal cortex
the basal ganglia
- a cluster of neurons at the base of the forebrain
- involved in multiple processes like the coordination of movement
- people who suffer injuries here often develop ocd like symptoms
the orbitofrontal cortex
- converts sensory info into thoughts and actions
- pet scans have found higher activity here in those with ocd when for example they are asked to hold a dirty item with a potential germ hazard
- its suggested the heightened activity in this area increases the conversion of sensory info to actions, resulting in compulsions
give a strength of biological explanations
1/2
supported by family studies. lewis (1936) found 37% of the patients examined with ocd had parents with it, and 21% had siblings with it. nestadt et al (2000) proposed that those with a 1st degree relative with ocd are 5x more likely to develop it during their life. these studies support a genetic explanation of ocd, but don’t rule out other (environmental) factors playing a role
give a strength of biological explanations
2/2
supported by twin studies. billett et al (1998) did a meta-analysis of 14 twin studies and found mz twins had double the risk of developing ocd than dz twins if one twin had it. since concordance rates in twin studies are never 100%, the diathesis-stress model may be a better explanation
give a limitation of biological explanations
1/2
there’s an issue in understanding neural mechanisms involved in ocd. evidence suggests certain neural systems don’t function normally in those with ocd, but research has also identified other areas sometimes involved. this means there is no brain system consistently found to play a role. so although there is evidence that neurotransmitters and brain structures are implicated we can’t establish a cause and effect relationship as we can’t determine if the biological abnormalities are the case of result of ocd
give a limitation of biological explanations
2/2
there are credible alt explanations. the 2 process model suggests initial learning of the feared stimulus could occur via cc, and the fear is maintained via oc and neg reinforcement. this could lead to obsessions which is linked to developing compulsions. this is supported by the success of behavioural treatments where symptoms are improved for 60-90% of adults