Biological approach explaining and treating OCD

Question 1

OCD

Answer 1

Obsessive-compulsive disorder (OCD) can be defined as ‘a mental health condition where a person has obsessive thoughts and compulsive activity’.

We all find ourselves double checking things from time to time.
For example, you might double check to make sure you locked
your front door or that you turned off your straighteners. But
people with OCD feel the need to check things repeatedly, or
have certain thoughts or perform routines and rituals over and over. The thoughts and rituals associated with OCD cause distress and get in the way of daily life because they cannot be controlled.

Question 2

The Biological Approach to Explaining OCD

Answer 2

The biological approach assumes that abnormal behaviour such as OCD is caused by problems within the body or brain and that mental illness has a physical cause. Factors that cause mental illness are genes, neuroanatomy (brain structure) and neurotransmitters (brain chemicals).

Question 3

Genetic explanations of OCD

Answer 3

The genetic explanation is that OCD can be passed from parent to child through genetic inheritance. Geneticists have been trying hard to isolate a candidate gene for OCD, they have identified 2 genes that might be implicated in a vulnerability for OCD

1. COMT gene
   It has been suggested that the COMT gene may contribute to OCD. This gene is involved in the production of an enzyme (COMT)
   that regulates the production of dopamine. One form of the COMT gene leads to lower activity of the enzyme and therefore higher levels of dopamine. It is this form of the COMT gene that is commonly found in individuals with OCD.
2. SERT gene
   The SERT gene has also been linked to OCD. This gene is involved in the production of a protein that removes serotonin from the synapse between neurons. A mutation of this gene leads to higher activity of this protein and therefore lower levels of serotonin. A mutation of the SERT gene has been found in families where many members have OCD.

Question 4

Evaluation of genetic arguments, research support

Answer 4

There is research to support the genetic argument for OCD. For example, Nestadt (2010) reviewed twin studies and found 68% of identical twins showed concordance for OCD compared to 31% in non-identical twins. This strongly suggests a genetic element in OCD

Question 5

Evaluation of genetic arguments, weakness

Answer 5

However, it is difficult to draw firm conclusions about the influence of genes from twin studies alone. Twins are generally exposed to the same environmental factors and the higher MZ concordance rates could be explained away by identical twins being treated in a more similar way and so sharing the same behaviors. Furthermore, there are no studies that show 100% concordance in MZ twins, suggesting that other factors must be involved. This is consistent with the diathesis- stress model which brings nature and nurture together, suggesting that genetic factors predispose an individual to developing OCD, but environmental factors (e.g. life events/learning) are needed to trigger the disorder.

Another limitation is that too many candidate genes have been identified. Like many disorders, OCD seems to be polygenic. This means that it is caused by several genes, maybe up to 230, rather than a single gene. This means that the genetic explanation may not be very useful in predicting OCD.

Question 6

Neural explanations of OCD

Answer 6

(Neural means ‘the brain’, so these explanations will place the cause of OCD at brain structure or brain chemistry)

The genes that are associated with OCD are likely to affect the levels of neurotransmitters as well as the structures of the brain. Therefore, neural explanations say that OCD can be caused by abnormal levels of neurotransmitters such as serotonin and certain structures within the brain (neuroanatomy) such as the areas that make up the ‘worry circuit’.

Question 7

Neural arguement 1: serotonin

Answer 7

OCD may be caused by a disruption of serotonin levels which has a knock-on effect on regulating the levels of other neurotransmitters, such as GABA, and dopamine. This idea is based on drug therapy evidence which indicates a reduction in symptoms of OCD seen in
individuals who take anti-depressant drugs that increase serotonin activity (in other words if someone takes a pill to increase serotonin and gets better, surely the low serotonin was the problem?). It is argued that low levels of serotonin are responsible for the symptoms of OCD and may explain why OCD is comorbid with depression.

Question 8

Evaluation of Neural Argument 1: Serotonin

Answer 8

There is research to support the role of serotonin in OCD. Evidence based on drug therapy seems to support the notion that serotonin plays a role in OCD. Zohar et al (1996) found that drugs which increase serotonin have been beneficial for up to 60% of patients with OCD. This supports the idea that low levels of serotonin may be associated with OCD.(and why it might be comorbid with depression!)

However, a weakness is that it is not known if the problems with neurotransmitters are a cause or a consequence of OCD. This is known as the treatment-aetiology fallacy - just because serotonin reduces symptoms of OCD doesn’t necessarily mean the symptoms were caused by lack of serotonin. In the same way aspirin may cure a headache, but this doesn’t mean the headache was caused by lack of aspirin.

Question 9

Neural Argument 2: Neuroanatomy: The ‘worry circuit’

Answer 9

A further neural argument is that the symptoms of OCD arise from structural damage to the brain. It is argued that there are impairments in an area of the brain termed the basal ganglia, specifically within this region, an area termed the caudate nucleus.

There are three areas in the brain that form a ‘worry circuit’: the orbitofrontal cortex (OFC), the caudate nucleus (part of the basal ganglia) and the thalamus. The OFC is responsible for sending ‘worry’ signals to the thalamus when we are concerned or anxious about something (e.g. a potential germ hazard). These signals are usually suppressed by the caudate nucleus. However, if damaged, the caudate nucleus fails to block the signal and the thalamus is alerted. The thalamus then sends signals back to the OFC, creating a circuit. In typical brains the OFC regulates the transmission of information regarding worrying events between the thalamus and the OFC; but in OCD the Orbito-Frontal Cortex is impaired and therefore incorrectly regulates the worrying information. This makes it difficult for the individual with OCD to pay attention to anything other than the worrying event and to plan behaviours other than their compulsions.
Therefore, OCD could be caused by a damaged caudate nucleus.

Question 10

Evaluation of Neural Argument 2: Neuroanatomy

Answer 10

There are inconsistent findings from research studies. For example, Neuroimaging studies have not identified basal ganglia impairments in all OCD sufferers and some people with impairments in the basal ganglia show no sign of OCD. Equally, Twin and family studies have not all found the same concordance rates. Therefore it is difficult to draw firm conclusions about the role of biology in OCD.

Question 11

General Evaluation of the Biological Approach to Explaining OCD, strength

Answer 11

Such ways of thinking about OCD have been very useful in providing practical applications to treat OCD. Drug therapies attempt to correct faults in the brain by rebalancing the chemical that are thought to be causing OCD (e.g. dopamine and serotonin). This is a strength because it requires little commitment and motivation from the client and can therefore support the economy and reduce the burden on the NHS.

Question 12

General Evaluation of the Biological Approach to Explaining OCD, weakness

Answer 12

It is very difficult to determine cause and effect between an individual’s biology and mental illness. It is not clear whether neural abnormalities in people with OCD are a cause of the condition or develop as a result of the condition. This is a weakness because the explanation does not fully explain what it set out to.

A weakness of the biological approach is that it is heavily focused on the nature side of the nature nurture debate (thus reductionist). The explanations look just at physical causes for OCD and ignore the impact that our experiences have. Twin studies have shown that both members of a pair of identical twins do not always develop OCD when one does. This is a weakness because it is more likely that individuals inherit a biological vulnerability that puts them at risk of developing OCD but only if they are exposed to particular life conditions and experiences.

Question 13

The biological approach to treating OCD, 2 ways of drug therapy

Answer 13

anti-depressants and anti-anxiety drugs

Question 14

drug therapy

Answer 14

Drugs are an easy and accessible treatment for people with OCD which deal with their obsessions and compulsions by rebalancing the neurotransmitters in the brain. There are a number of different types of drug that can be prescribed as a treatment for OCD.

Question 15

Anti-depressants: Selective Serotonin Reuptake Inhibitors (SSRI’s e.g. Prozac)

Answer 15

Selective serotonin reuptake inhibitors (SSRIs) work by increasing the amount of serotonin that passes around the brain. Raising serotonin levels helps to reduce symptoms of OCD in those suffering with the disorder.

These drugs act by preventing the serotonin that flows from one neurone to the next from being reabsorbed or removed from the system, leaving greater amounts of serotonin in the synapse, continuing to stimulate the post synaptic neuron.

Question 16

Other anti-depressant have also been used such as Tricyclics

Answer 16

(an older type of anti- depressant) block the transporter mechanism that reabsorbs both serotonin and noradrenaline into the presynaptic cell after it has fired. Clomipramine was the first antidepressant used for OCD and today is primarily used for OCD rather than depression. However, tricyclics generally have more side effects than SSRI’s.

Question 17

Anti-anxiety drugs: BZs (e.g. Valium)

Answer 17

Benzodiazepines (BZs) help to control feelings of extreme anxiety by reducing the level of brain activity and bringing about feelings of being calm.

Benzodiazepines act on chemicals within the brain and slow down activity within the central nervous system. By doing this, they reduce anxiety and make an individual feel calmer.

Benzodiazepines work by enhancing the action of a neurotransmitter called GABA.
GABA is the body’s natural form of anxiety relief. When released, GABA has a calming effect on many of the neurons in the brain – it is an inhibitory neurotransmitter.
During synaptic transmission, GABA binds with GABA-A receptors on the post-synaptic neuron. This opens a channel
that increases the flow of chloride ions into the post-synaptic neuron, making it more difficult for the post-synaptic neuron to be stimulated by other neurotransmitters. This means that signals are less likely to be passed from one neuron to the next.
Benzodiazepines enhance this natural process by binding with GABA receptors. This allows more chloride ions to enter the post-synaptic neuron. The neuron is then even less responsive to other excitatory neurotransmitters, further reducing neuron activity in the brain.

Question 18

Evaluation of drug therapy, effectiveness

Answer 18

One strength is that there is evidence for the effectiveness of drugs to treat OCD. Soomro (2009) conducted a meta-analysis of 17 studies of OCD patients being treated with SSRIs found in all 17 studies, SSRI’s were more effective at reducing symptoms of OCD than a placebo (a fake drug).

Research has also shown that BZs are more effective at reducing anxiety than a placebo. Taking the fake drug makes people feel a little calmer simply because they believe they have had a treatment – a psychological process known as the placebo effect. BZs make people feel even better than when they just think they have had a treatment so showing that there is an actual therapeutic process taking place in altering brain chemistry. This means that BZs are an effective treatment for anxiety conditions such as OCD.

However, not all evidence supports the effectiveness of drug therapies. For example Zohar found that only 60% of clients improved with drugs that increase serotonin. This suggests that there are individual differences in how people respond to drug therapy and might also cast doubt upon the biological explanation of OCD

Question 19

Evaluation of drug therapy, appropriateness

Answer 19

A strength of this type of therapy is that drugs are relatively fast acting and require little effort on the part of the individual. For example, CBT requires a lot of motivation and insight from the individual whereas drug therapies require virtually no input in terms of time or motivation. This is a strength because the therapy may be appropriate for people with OCD who lack insight into their thought processes and emotions or who cannot commit the time that other therapies require.

A weakness of drug therapies is that they do not cure OCD. They reduce the symptoms of the illness but once the person stops taking the drugs the symptoms of OCD return. This means that the underlying problem (the real cause of their obsessions and compulsions) has not been dealt with. Psychological therapies aim to cure mental illness by addressing the root cause of the conditions. This is a weakness because a better form of treatment for OCD might be to combine drug treatment and psychological therapy to maximise the benefit to the patient. Drug therapy alone is not effective enough.

Another weakness of this therapy is that there are negative side effects to taking drugs. For example, nausea, headaches and insomnia are often reported by people taking SSRIs and possible side effects of BZs include increase aggression and long-term memory impairment. BZs are also associated with dependency and so can only be taken for a few weeks. This is a weakness because, although they are an effective treatment, some people with OCD prefer not to take such medication and therefore it is not an appropriate treatment for all. Indeed, it has been suggested that 30-50% of clients with OCD derive no benefit from them, so they are not effective for a large minority. Furthermore, relapse rates are thought to be as high as 90%. Therefore drugs do not provide a permanent ‘cure’ for the disorder as soon after treatment stops, symptoms return.