ocd - eval

• support

  • there is research support for the genetic explanation
  • research has confirmed there are up to 230 genes involved with ocd (taylor, 2013)
  • nestadt (2010) reviewed twin studies and found a concordance rate of 68% for mz twins compared to 31% in dz
  • this strongly supports the genetic explanation of ocd
• counter

  • studies have been unsuccessful at identifying all the genes involved and there seem to be several involved. each genetic variation only increases the risk of ocd by a fraction
  • the consequence is that a genetic explanation is very unlikely to ever be very useful because it provides little predictive value
• alternative

  • two-process model works here
  • initial learning occurs when a neutral stimulus is associated with anxiety. this association is maintained because the anxiety-provoking stimulus is avoided. thus an obsession is formed and then a link is learned with compulsive behaviours which appear to reduce the anxiety
• application 1

  • if biology is responsible for ocd then drugs can address the disorder. if genes influence neurotransmission levels, drugs can adjust them to more appropriate levels
  • soomro et al reviews 17 studies comparing ssri’s to placebos in the treatment of ocd. all 17 showed significantly better results for ssris than for the placebo conditions
• application 2

  • the mapping of the human genome has led to the hope that specific genes could be linked to particular disorders. in future, we could screen fertilised eggs to give parents choices about continuing with a pregnancy
  • alternatively, gene therapy may produce a means of turning genes ‘off’ so that a disorder is not expressed
• i&d

  • the diathesis-stress model suggests that genes do contribute to the development of ocd, but are not the sole cause
  • cromer 2007 found that over half of the ocd patients in the study sample had experienced a traumatic event in their past. ocd was more severe in those having faced trauma