OCD

• Obsessive-Compulsive Disorder (OCD)


  • Behavioural characteristics: compulsions and avoidance behaviour
  • Emotional characteristics: guilt, disgust, depression, and anxiety
  • Cognitive characteristics: acknowledgement that anxiety is excessive and irrational, development of cognitive strategies to deal with obsessions, and obsessive thoughts
• Genetic explanation for OCD

  • Some have a genetic vulnerability towards developing OCD because of inherited familial influence/genetic factors
  • based this theory on the concordance rates within family and twin studies
• Supporting evidence for genetic basis of OCD- credibility

  • Nestadt et al. reviewed previous twin studies
  • 68% of identical twins, compared to 31% of non-identical twins, share OCD
  • genetics must play a role as the more genetic material, the higher the concordance rate
• Methodological issues with twin studies- reduces validity and credibility. Makes the incorrect assumption that MZ are only more concordant bc of genetics, fails to consider that MZ twins are more likely to share the same environment than DZ twins. Environment could affect the concordance rate, not genetics.
• Genetic explanation is biologically reductionist- suggests that OCD can be explained by using a low level, narrow construct: genes. Doesn't consider the broader experience e.g. environment. Cromer et al found that over half of his clients with OCD had experienced a traumatic event in the past
• Tricyclics and selective noradrenaline-reuptake inhibitors (SNRIs)


  Have a similar effect, but are reserved for those who do not respond well to SSRIs
• Drug therapy for OCD has serious side effects that can have implications on everyday life
• Effective treatments for OCD


  Can reduce time off work through sick days, increasing workforce productivity and tax revenue
• Drug treatments for OCD

  Are cost-effective and non-disruptive compared to psychological treatments
• obsessions

  Recurrent, persistent thoughts, impulses or images. They are excessive, unreasonable and interfere with daily life. Obsessions are an example of internal symptoms.
• compulsions

  these are repetitive behaviours that the person feels driven to perform, they interfere with daily life. Compulsions are an example of external symptoms.
• 3 genetic explanations

  • candidate genes
  • polygenic
  • aetiology heterogenous
• candidate genes

  create a vulnerability for OCD. Some of these genes are involved in regulating the development of the serotonin system.

  E.g. The COMT gene may contribute to OCD. This gene regulates the production of dopamine. Individuals with OCD are thought to have a mutation in their COMT gene which results in higher levels of dopamine in their brain
• polygenic

  research suggests that OCD is not caused by one single gene. Several genes are implicated in the development of OCD.

  Taylor (2013) found evidence of up to 230 different genes may be involved in OCD.
• Aetiology Heterogenous

  research suggests that one group of genes may cause OCD in one person, but a different group may cause the disorder in another person. Perhaps the different combinations of genes may account for the different types of OCD.
• Research suggests that neurochemicals such as serotonin and dopamine are associated with the onset of OCD- the abnormal transmission of these neurotransmitters may lead to obsessive thoughts.
• serotonin

  • Serotonin is a neurotransmitter, which helps to regulate mood
  • Low levels of serotonin in the brain is associated with the symptoms of OCD
  • The brains of individuals with OCD seem to remove serotonin too quickly - before it has had time to transmit its signal to the postsynaptic neuron. This causes low amounts of serotonin transmission
  • Low levels of serotonin is associated with mood disorders such as OCD
• dopamine

  • High levels of dopamine is associated with OCD and has been linked with compulsive/stereotypical movements seen in OCD
  • Research on animals has found that drugs, which increase levels of dopamine lead to stereotyped movements that resemble the compulsive behaviours seen in OCD patients
• +ve for biochemical explanations- RWA

  Soomro et al reviewed 17 studies into drug treatments for OCD which combined, studied over 3000 participants. They compared drugs which increased serotonin in the brain with placebo drugs. They found drugs which altered levels of serotonin in the brain were more effective at reducing symptoms of OCD than placebos. The effectiveness of the therapy suggests that low levels of serotonin may contribute to the onset of symptoms of OCD. The success of the therapy also highlights the value of the biological explanation in helping to develop treatments for OCD.
• -ve for biochemical explanations

  research has found that SSRI's (drugs, which increase levels of serotonin) only reduce symptoms in 50% of people with OCD.

  Furthermore, there is a time delay as the drug do not reduce symptoms immediately; this can take a few weeks. This suggests that the biological, biochemical explanation that low levels of serotonin causes OCD are incomplete.
• -ve of biochemical explanations

  biologically deterministic- assumes that biochemical imbalances cause OCD, assumes we have no control over our own behaviour and therefore does not account of the role of free will. Deterministic theories such as the biological explanation are useful because they can help us to predict the onset of OCD and treat OCD however, they have social implications. Patients with OCD may feel that they cannot control their own behaviour and therefore may not engage with any psychological therapies to treat their OCD
• how SSRIs work

  • SSRI's increase the level of serotonin available in the synapse by binding to the presynaptic neuron and preventing the reabsorption of the serotonin
  • This in turn increases the level of serotonin in the synapse, which in turn improves the amount of serotonin the postsynaptic receptor receives
  • Serotonin therefore continues to stimulate the postsynaptic neuron leading to increased levels of serotonin in the brain, which helps to regulate mood
• normal path of serotonin

  when serotonin is released from the pre-synaptic cell into the synapse, it travels to the receptor sites on the postsynaptic neuron. Serotonin, which is not absorbed into the postsynaptic neuron, is reabsorbed into the pre-synaptic cell