OCD

• OCD suggests obsessions (irrational thinking causing anxiety) leads to compulsions(repetitive behaviours that they carry out to temporarily relieve the anxiety caused by obsessions)
• behavioural characteristics are compulsive behaviours - repetitive behaviours that gives temporary relief from anxiety caused by obsessions

  avoidance - avoiding situations which may trigger anxiety, inducing obsessions
• cognitive characteristics are obsession - reoccurring thoughts which are unpleasant and produce anxiety typically irrational and catastrophic

  selective attention - hyper focussed on the source of obsessions

  awareness - aware their obsessions are irrational which differs it from psychosis.
• emotional characteristics are anxiety - feelings of distress caused by obsessions and temporarily relieved by compulsions

  depression - low mood and lack of enjoyment in activities

  guilt and disgust - irrational guilt over minor issues and disgust towards themselves or something external(dirt)
• biological explanation of OCD is that its genetic as Lewis 1936 identified 37% of patients with OCD had parents with it however concordance rates aren't 100% so it isn't completely genetic and can be due to the environment. Diathesis stress model says someone may have predisposition to OCD but an environmental stressor is needed to trigger the condition.
• 2 genes have been linked to OCD. COMT gene regulates dopamine high levels of dopamine are more common with OCD patients. SERT gene transportation of serotonin. Transportation issues causes lower levels of serotonin which is associated with OCD.
• What is one strength of the biological explanation of OCD?

  There is supporting research indicating a genetic component.
• What did Lewis find in his research on OCD?

  37% of people with OCD had a parent with OCD, and 21% had a sibling with OCD.
• What does the finding that 37% of individuals with OCD had a parent with OCD suggest?

  It suggests that OCD has a genetic component.
• Why is the research by Lewis considered valid?


  Because it supports the predictions made by the biological explanation of OCD.
• What is a limitation of the research conducted by Lewis?

  The research is correlational, which means cause and effect cannot be established.
• What does the correlational nature of the research imply about the relationship between family history and OCD?

  It implies that confounding variables may be causing the observed relationship.
• How does the correlational research affect the internal validity of the biological explanation of OCD?

  It lowers the internal validity due to the inability to establish cause and effect.
• one limitation of the biological explanation is that there's alternative explanations for example the diathesis stress model suggests environmental stressors can cause OCD to present itself in someone if they already have the genes relating to OCD. This may be more appropriate because it accounts for both genetic and environmental factors for OCD and account for the fact concordance rates aren't 100%-weakens the validity
• Another biological explanation for OCD is neural systems
• serotonin regulates mood so low serotonin means the relevant info isn't transmitted can lead to low mood and anxiety which could explain the anxiety they feel when experiencing obsessions.
• Brain structures - basal ganglia (dopamine is it's main neurotransmitter)

  orbitofrontal cortex (converts sensory info into thoughts and actions. Hyperactivity increases the conversion of sensory info to actions)
• evaluation of the neural explanation - one strength is that there's supporting evidence. Soomro et al 2009 found SSRIs a type of anti depressants that increase serotonin reduce symptoms of OCD in 70%. Suggesting low levels of serotonin are elated to OCD symptoms as raising the levels relieves the symptoms. Valid as supporting evidence supports the predictions it makes.
• one limitation of the neural explanation is that its based on correlational research for example whilst a relationship has been found between damage to the basal ganglia and OCD it doesn't suggest causation. This is because we can't determine if abnormal brain functions cause OCD or if OCD causes abnormal brain functions. Lacks internal validity as cause and effect relationship between neural structure and OCD cant be established.
• OCD treatments - Drug treatments (SSRIs) selective serotonin reuptake inhibitors. They work by blocking the reuptake of serotonin and ensuring the serotonin continues to stimulate the post synaptic neuron
• Alternative drugs are Tricyclics which are an older type of anti depressant increases serotonin and are associated more with side effects only used if they don't respond to SSRIs
• Alternative drugs are SNRIs serotonin norepinephrine reuptake inhibitors. New type of anit depressants increases serotonin and norepinephrine
• Evaluation of treatments - strength is that there's supporting research into its effectiveness. Soomro et al found 70% of people taking SSRIs had a reduction in their symptoms and SSRIs were more effective in reducing OCD than placebos. Meaning they have real life effects on OCD symptoms and can help treat them. Improved quality of life and economic implications as they can maintain employment. However an interactionist approach wold be more effective because it takes into account genetics and the environment which could have a cumulative effect on improving their quality of life.