Biological approach OCD

Genetic Explanations: (A01)

The genes we inherit from our parents can predispose us to OCD.  For example, Lewis (1936) found that 37% of his OCD patients had parents with the disorder, suggesting that specific genes are related to the onset of OCD.  Researchers have been able to identify two of these genes.

1.    The COMT Gene

COMT is an enzyme that regulates dopamine however in people with OCD, this gene mutates, preventing the COMT enzyme from regulating dopamine levels.  This in turn, causes the high levels of dopamine seen in many patients with OCD.

2.    The SERT gene.

The SERT gene is involved in the transportation of serotonin, an inhibitory neurotransmitter. When levels of serotonin are low, a person is more likely to get OCD.  In people with OCD, the SERT gene mutates, causing lower levels of serotonin.

OCD is Polygenic

It appears that OCD is polygenic.  This means that OCD is not caused by one single gene but that several genes are involved.  For example, Taylor, 2013, found that up to 230 different genes may be involved in OCD, including the SERT and the COMT genes.

There is also evidence to suggest that different types of OCD may be due to different gene combinations.

Neural Explanations: (A01)

The genes associated with OCD affect the level of certain neurotransmitters as well as particular structures within the brain.

Abnormal Neurotransmitter levels

Serotonin helps to regulate mood.  Low levels of serotonin have been linked to depression and anxiety disorders, such as OCD.  Support for this comes from the fact that drugs which increase serotonin levels are effective in treating OCD.

Additionally, the neurotransmitter dopamine has also been implicated in OCD, with high levels of dopamine being associated with compulsive behaviours, such as hand washing.

Abnormal Brain Structures - Worry circuit

The orbital prefrontal cortex (OFC) is a region in the brain which converts sensory information into thoughts and actions.  The OFC sends signals about potential hazards (e.g. concerns about harmful germs after using a dirty toilet) to the thalamus.  However, if these ‘worry signals’ are not serious, they will be suppressed by the caudate nucleus, preventing them from reaching the thalamus.

When the caudate nucleus is damaged, it fails to suppress minor or unimportant ‘worry’ signals. Thus, unnecessary thoughts and impulses are allowed to alert the thalamus. These signals are then sent back to the OFC, reinforcing the belief that these unnecessary thoughts and impulses are a major concern that need an immediate and powerful response.

Evaluation – Biological explanations of OCD (A03)

P: The biological explanation for OCD has a great deal of supporting evidence.

E: E.g., Nestadt et al (2010) carried out a meta-analysis of twin studies and found that MZ (identical) twins had an overall concordance rate of 68% compared to only 31%in DZ  (non-identical) twins. Additional supporting evidence comes from family studies.  E.g., Nestadt et al (2000) found that people with a first-degree relative with OCD (e.g. parents, sibling) were five times more likely to develop the illness themselves, compared to the general population. This evidence further increases the validity of the biological explanation of OCD.

L: This supports the link between genetics and OCD.

However, it should be noted that concordances rates for twin studies are never 100%, which means that environmental factors must also play a part.

P: Support for the biological explanation of OCD comes from the use of anti-depressants.

E: Anti-depressants typically work by increasing the levels of the neurotransmitter serotonin. Thus, the effectiveness of these drugs at reducing the symptoms of OCD provides support for the neural explanation of OCD.

E: For example, Soomro et al (2009) found that SSRIs were significantly more effective than placebos in treating OCD.

L: This supports the view that abnormal neurotransmitter levels must be contributing to the cause of OCD.

P: Research evidence supports the role of the OFC in OCD.

E: Menzies (2007) conducted MRI scans on OCD patients and their immediate family members without OCD, and also a healthy control group.

E: He found that OCD patients and their immediate close family members had reduced grey matter in the OFC.

L: This is a strength as it supports the view that differences in this brain region are inherited and may be contributing to the disorder.

However, researchers have been unable to successfully identify which genes are causing this reduction in grey matter. The consequence is that a genetic explanation is unlikely to ever be very useful because it provides little predictive value.  For example, it is unable to predict which relatives with the reduction in grey matter will develop OCD.  

P: The diathesis-stress model may be better at explaining the cause of OCD than the biological explanation.

E: This is because it acknowledges that both genes and the environmental play a role in OCD. It suggests that individual genes could cause a vulnerability for OCD but whether the illness develops depends on environmental factors.

E: For example, Cromer et al (2007) found that over half of their OCD patients had experienced a traumatic life event and that OCD was more severe in patients who had experienced more than one traumatic event.

L: This supports the diathesis-stress model and the view that genes alone cannot predictive who is likely to develop OCD.

Antidepressants: SSRIs (A01)

The standard medical treatment used to tackle the symptoms of OCD involves a type of antidepressant called a selective serotonin reuptake inhibitor (SSRI for short).fd900/

Low levels of the neurotransmitter serotonin are associated with depression as well as OCD, so drugs that increase levels of serotonin are used with both mental disorders. This summarizes how SSRI’s work:

·      Serotonin is released into the synapse by the pre-synaptic neuron.

·      Normally, after serotonin has crossed the synapse from the presynaptic neuron, it is reabsorbed by the presynaptic neuron (reuptake mechanism) ready to be re-used.

·      SSRIs work by preventing (or ‘inhibiting’) this reabsorption. This results in more serotonin staying in the synapse for longer.  This allows the serotonin to stimulate the postsynaptic neuron for longer, compensating for the deficiency in the serotonin system.  SSRI’s help to reduce the anxiety associated with OCD and ‘normalise’ the worry circuit.

A typical daily dose of an SSRI, such as fluoxetine (Prozac) is 20mg.  It takes three to four months of daily use for SSRIs to have much impact on symptoms.

Anti-anxiety drugs (A01)

Benzodiazepines (e.g., Valium) are commonly used to reduce anxiety.  Benzodiazepines work by increasing the activity of the neurotransmitter GABA.  GABA has a quietening effect on neurons in the brain and therefore, helps to slow down brain activity.

How GABA works:

·      GABA is released into the synapse by the presynaptic neuron.

·      It locks onto receptors on the postsynaptic neuron

·      This opens a channel that increases the flow of chloride ions into the neuron.

·      Chloride ions make it harder for the neuron to be stimulated by other neurotransmitters, thus slowing down its activity, reduces the anxiety experienced due to obsessions and makes the person with OCD feel more relaxed.

(Optional A01)

Other drugs used:

-       SNRIs (Serotonin Noradrenaline Reuptake Inhibitors).

These drugs work by preventing the reuptake mechanism of both serotonin and noradrenaline, thus increasing the levels of both of these neurotransmitters and reducing anxiety.

-       Tricyclics

These are an older drug which work in the same manner as SNRIs but have more severe side effects.

Evaluation (A03)

P: There is clear evidence for the effectiveness of drug therapy in reducing the symptoms of OCD.

E: For example, Soomro et al (2009) reviewed studies comparing SSRIs to placebos in the treatment of OCD.  They found that SSRIs were significantly more effective than placebos in treating OCD.

E: Additionally, Kahn et al (1986) compared placebos and Benzodiazepine (BZs) in 250 patients. They found that BZs were significantly superior to placebos in treating anxiety.

L: This is a strength because drug therapy enables people with OCD to cope with their symptoms, such as anxiety, thereby improving the quality of their lives.

P: A further strength of drug therapy as a treatment for OCD is that they are cost-effective compared to psychological treatments.

E: For example, they do not require a trained therapist and are less disruptive to the patients’ lives.

E: Drugs allow patients to reduce their symptoms without having to engage with much of the hard work needed by psychological therapies such as CBT.

L: For these reasons, drug therapies are the preferred method of treatment for many doctors and patients.  They enable people to control their symptoms with minimal effort, saving time and money.

Additionally, drug therapy combines well with CBT by reducing a patient’s anxiety, thereby enabling them to engage more successful with the techniques.

P: Although drug therapies are more commonly used to treat OCD, in a comprehensive review of treatments for the disorder, Koran (2007) argued that psychotherapies such as CBT should be tried first.

E: This is because drugs only treat the symptoms of OCD rather than the root cause. Whilst drug therapy is effective in the short-term by placing a ‘chemical mask’ on symptoms, they are not a lasting cure.

E: For example, patients normally relapse within a few weeks after medication is stopped.

L: This is an issue as alternative therapies such as CBT or a combined approach of drugs and CBT, may be seen as more appropriate in the long-term.

P: A major weakness of drug therapy are the side effects that most patients experience.

E: Common side effects of SSRIs include blurred vision, indigestion and loss of sex drive. These may not seem that terrible but often are enough to make a patient prefer not to take the drug.  Some patients also experience more serious side effects like hallucinations, erection problems and raised blood pressure.

E: BZs are renowned for being highly addictive and can also cause increased aggression and long-term memory impairments. As a result, BZs are usually only prescribed for short-term treatment.

L: Consequently, these side effect diminish the effectiveness of drug treatments, as patients will often stop taking medication if they experience these side effects.