The Biological Approach to Explaining OCD

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GENETIC EXPLANATIONS- the COMT gene

  • the COMT gene regulates the production of dopamine
  • all genes come in different forms (alleles) and one form of the COMT gene is more common in OCD patients than those without the disorder
  • this variation produces lower activity of the COMT gene and higher levels of dopamine
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GENETIC EXPLANATIONS- the SERT gene

  • affects the transport of serotonin- creating lower levels
  • lower levels are associated with OCD
  • Ozaki et al. (2003) found that a mutation of this gene in two unrelated families where 6 of the 7 family members had OCD
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GENETIC EXPLANATIONS- diathesis-stress

  • one gene cannot determine complex behaviours
  • the SERT gene is also implicated in a number of other mental disorders e.g. depression and PTSD
  • the diathesis-stress suggests a vulnerability of OCD (and other mental disorders). Other factors (stressors) affect what condition develops (if any)
  • some people may posses the variatons but suffer no ill effects
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NEURAL EXPLANATIONS- abnormal levels of neurotrans

HIGH DOPAMINE LEVELS

  • based on animal studies- high doses of drugs that enhance dopamine induce stereotyped movements resembling the compulsive behaviours found in OCD patients (Szechtman et al., 1998)

LOW SEROTONIN LEVELS

  • antidepressant drugs which increase serotonin levels have been shown to reduce OCD symptoms (Pigott et al., 1990)
  • antidepressants that have less effect on serotonin do not reduce OCD symptoms (Jenicke, 1992)
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NEURAL EXPLANATIONS- abnormal brain circuits

THE WORRY CIRCUIT

  • the caudate nucleus normally surpresses signals from the orbitofrontal cortex (OFC)
  • in turn, the OFC sends signals to the thalamus about things that are worrying
  • when the caudate nucleus is damaged, it fails to surpress the minor 'worry' signals and the thalamus is altered, which in turn, sends signals back to the OFC
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EVALUATION- family and twin studies

EVIDENCE FOR

  • Billet et al. (1998) meta analysis of twins found 68% concordance with identical twins (MonoZygotic- MZ) compared to 31% concordance in non-identical twins (DiZygotic-DZ)
  • Pauls et al. (2005) found 10% of people with an immediate relative with OCD also suffered the disorder in comparison to 2% of the general population

EVIDENCE AGAINST

  • no study has found a 100% concordance rate, so there must be other factors e.g. learning
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EVALUATION- neural explanations

EVIDENCE FOR

  • by using MRI/ other brain scanning techniques to produce images of the activity in the brain of OCD patients and their immediate family members without OCD- reduced grey matter in key regions of the brain (inc. OFC). Supports the view that anatomical differences are inherited and may lead to OCD in certain individuals.

EVIDENCE AGAINST

  • Aylward et al. (1996) did not find any significant difference in basal ganglia impairment between OCD patients and controls
  • Basal ganglia damage hasn't been found in 100% of people with OCD so cannot be the full story
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EVALUATION- alternative explanations

PSYCHOLOGICAL EXPLANATION

  • two process model can be applied to OCD (intiation and maintenance)
  • initial learning occurs when a neutral stimulus e.g. dirt is associated with anxiety
  • this association is maintained because the anxiety-provoking stimulus is avioded, then the link is learned with compulsive behaviours, e.g. hand washing
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