The biological approach suggests that abnormal behaviour is caused by something physical happening in the body, which may be the result of genes.
Genetic explanations: Genes may create a vulnerability (risk of developing) to OCD. There is evidence that OCD runs in families. Lewis (1936) found that 37% of patients with OCD had parents with the disorder. The diathesis-stress model suggests that, along with this vulnerability, the environment may trigger OCD. There are many candidate genes involved in OCD (for example, those involved in the serotonin and dopamine systems), and it is polygenic: several genes are involved (perhaps up to 230). OCD is aetiologically heterogeneous, meaning different combinations of genes cause different types of OCD in different people.
- Supporting evidence from Nestadt et al (2010) showed that 68% of identical twins were both diagnosed with OCD, compared to 31% of non-identical twins, suggesting there is a genetic basis.
- There are too many candidate genes for OCD- potentially hundreds. This means that finding a definitive genetic cause is very unlikely, reducing the usefulness of this explanation.
- There is evidence from Cromer et al (2007) that the environment is very influential- OCD was more severe in patients who had experienced traumatic events in their lives, and even more severe where patients had experience more than one event. This suggests the environment is more important than biology in developing OCD.
Neural explanations: Low levels of serotonin (a neurotransmitter) leads to impaired transmission of mood-relevant information, leading to a lowered mood. Low levels of serotonin are also linked to obsessive thoughts. Abnormal frontal lobe functioning leads to impaired decision-making, leading to symptoms of OCD. Abnormal functioning of the left parahippocampal gyrus leads to more processing of unpleasant emotions, which is a feature of OCD.
- Supporting evidence from antidepressant studies shows that increasing serotonin levels reduces OCD symptoms, suggesting serotonin has a role in the development of OCD
- There is a lack of understanding what neural mechanisms are involved, making this an incomplete explanation.
- The cause-effect relationship not known- it could be that changed in the brain are a result of OCD, rather than causing it in the first place. This weakens the neural explanation.
Drug therapies for abnormal behaviours aim to affect levels of neurotransmitter activity in the brain, by affecting the activity at synapses (gaps between neurons where neurotransmitters are active). Neurotransmitters are released from the pre-synaptic cell into the synapse, then are absorbed by the post-synaptic cell. Excess neurotransmitter is then reabsorbed by the pre-synaptic cell. Drugs increase synaptic activity by causing more neurotransmitter to be released, or introducing a chemical that acts like the neurotransmitter, or preventing reuptake of neurotransmitter. Activity may be decreased by increasing the rate of neurotransmitter breakdown, or blocking off receptors at synapses.
Drug therapy: SSRIs (selective serotonin reuptake inhibitors) are the most commonly prescribed drugs for OCD. These work by blocking the transporter mechanism that re-absorbs serotonin into the presynaptic cell after it has fired. As a result, more serotonin is left in the synapse to be absorbed by the post synaptic cells. Dosages vary with the patient, and it takes 3-4 months for benefits to show. An example of an SSRI is Fluoxetine. Often SSRIs will be combined with CBT.
Other drugs include tricyclics, for example Clomipramine, which work in the same way as SSRIs but have more side effects. SNRIs work on noradrenaline as well as serotonin, and may also be used. These other drugs will be prescribed where a patient is not responding well to SSRIs.
- One strength of drug therapy for OCD was shown by Soomro _et al _(2009). In this study, it was found that SSRIs were significantly better than placebos (fake drugs) at reducing OCD symptoms, showing that the drugs are effective.
- Compared to psychological treatments, drug therapy is easy and non-disruptive, as the patient just needs to take a pill rather than undergoing lengthy therapy sessions. This is a strength because the treatment suits people no matter what their lifestyle, job, and so on.
- A weakness of drugs is that they can have side effects, for example indigestion, loss of sex drive, blurred vision, weight gain and aggression. This weakens the use of drugs because patients may be less willing to take them, therefore their OCD symptoms will return.
- 'Acting in a way that is different to how we expect.'- Which abnormality definition is this?
- Who created a set of criteria for ideal mental health?
- Which of these is not a behavioural characteristic of phobias- panic, avoidance, irrational beliefs, endurance?
- Your answer should include: Irrational / Beliefs
- Which aspects of OCD are obsessive?
- According to the two-process model, how are phobias acquired?
- Your answer should include: Classical / Conditioning
- In systematic desensitisation, what do the therapist and patient construct?
- Your answer should include: Anxiety / Hierarchy
- What is Ellis’s explanation of depression known as?
- Which neurotransmitter is associated with OCD symptoms?
- What does SSRI stand for?
- Your answer should include: Selective / Serotonin / Reuptake / Inhibitor
- Who found that SSRIs were superior to placebos in treating OCD?