Biological explanations of OCD
Specification: The biological approach to explaining OCD: genetic and neural explanations.
Genetic explanations
Genetic explanations have focused on identifying specific candidate genes which are implicated in OCD. It is believed that OCD is a polygenic condition, which means that several genes are involved. Taylor (2003) suggests that as many as 230 genes may be involved in the condition and perhaps different genetic variations contribute to the different types of OCD, e.g. hoarding or obsession with religion. Two examples of genes that have been linked to OCD are the COMT gene and SERT gene.
The COMT gene is associated with the production of catechol‐O‐methyltransferase (COMT for short), which regulates the neurotransmitter dopamine. Although all genes come in different forms, one variation of the COMT gene results in higher levels of dopamine and this variation is more common in patients with OCD, compared to people without OCD.
Secondly, the SERT gene (also known as the 5‐HTT gene) is linked to serotonin and affects the transport of this neurotransmitter (hence SERotonin Transporter). Transportation issues cause lower levels of serotonin to be active within the brain and are associated with OCD (and depression). Ozaki et al. (2003) published results from a study of two unrelated families who both had mutations of the SERT gene. It coincided with six out of seven of the family members having OCD.
Neural explanations - neurotransmitters
The neurotransmitter serotonin is believed to play a role in OCD. Serotonin regulates mood and lower levels of serotonin are associated with mood disorders, such as depression. Some cases of OCD are also associated with the reduced levels of serotonin, which may be caused by the SERT gene. Evidence for the role of serotonin in OCD comes from research examining antidepressants (SSRIs) such as that conducted by Piggott et al. (1990) who found that drugs which increase the level of serotonin in the synaptic gap are effective in treating patients with OCD.
In addition, the neurotransmitter dopamine has also been implicated in OCD. In contrast to serotonin, higher levels of dopamine have been associated with some of the symptoms of OCD, in particular, the compulsive behaviours.
Neural explanations – brain structure
It is believed that several regions in the frontal lobes of the brain have abnormal brain circuits in patients with OCD. Two brain regions implicated specifically in OCD are: the basal ganglia and orbitofrontal cortex.
The basal ganglia is a cluster of neurons at the base of the forebrain, which is involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD‐like symptoms.
The orbitofrontal cortex is a region which converts sensory information into thoughts and actions. PET scans have found higher activity in the orbitofrontal cortex in patients with OCD when, for example, a patient is asked to hold a dirty item with a potential germ hazard. One suggestion is that the heightened activity in the orbitofrontal cortex increases the conversion of sensory information to actions (behaviours) which results in compulsions.
Evaluation
A strength of the biological explanation of OCD comes from research support seen in family studies. Lewis (1936) examined patients with OCD and found that 37% of the patients with OCD had parents with the disorder and 21% had siblings who suffered. Nestadt et al. (2000) take this point further and proposes that individuals who have a first‐degree relative with OCD are up to five times more likely to develop the disorder over their lifetime compared to members of the general population without this genetic link. Research from family studies like this provides support for a genetic explanation for OCD, although it does not rule out other (environmental) factors playing a role.
Further support for the biological explanation of OCD comes from twin studies which have provided strong evidence for a genetic link. Billett et al. (1998) conducted a meta‐analysis of 14 twin studies investigating the genetic inheritance rate of OCD. It was concluded that monozygotic (MZ) twins had double the risk of developing OCD compared to dizygotic twins (DZ) if one of the pair had the disorder. Since concordance rates in twin studies are never 100%, it suggests that the diathesis‐stress model may be a better explanation whereby a genetic vulnerability is inherited and triggered by a stressor in the environment.
There is an issue with understanding neural mechanisms involved in OCD. While there is evidence which suggests that certain neural systems do not function normally in patients suffering from OCD, such as the basal ganglia and orbitofrontal cortex, research has also identified other areas of the brain that are occasionally involved as well. This means that there is no brain system which has consistently been found to play a role in OCD. So, although there is evidence that neurotransmitters and brain structures are implicated, it must not be concluded that there is a cause and effect relationship since it is difficult to ascertain whether the biological abnormalities seen are a cause of OCD or the result of the disorder.
There are credible alternative explanations for the development of OCD. For example, the two‐process model proposed by behaviourists suggests that learning could play a crucial role in the disorder. Initial learning of the feared stimulus could occur through classical conditioning’s associative process where, for example, dirt is paired with anxiety. This behaviour pattern would be maintained through operant conditioning and negative reinforcement whereby the stimulus is avoided so the anxiety is removed. This could result in an obsession forming which is linked to the development of a compulsion, e.g. washing of hands, which serves to reduce the anxiety felt. Support for this alternative explanation is found in the success of behavioural treatments for OCD where symptoms of patients are improved for 60‐90% of adults (Albucher et al., 1998).
Possible exam questions
Suggest one limitation of the genetic explanation for obsessive compulsive disorder (OCD). (2 marks)
Explain one criticism of the neural explanation for obsessive compulsive disorder (OCD). (3 marks)
Briefly outline the biological approach to explaining obsessive compulsive disorder (OCD). You may refer to genetic and/or neural explanations in your answer. (4 marks)
When investigating psychopathology, researchers often analyse the behaviour of twins. A recent study has revealed that the concordance rate for monozygotic twins (MZ) for obsessive compulsive disorder (OCD) ranges from 45% to 65%. With reference to these statistics, what do the findings seem to suggest about the origins of OCD? (4 marks)
Evaluate genetic and/or neural explanations of obsessive compulsive disorder (OCD). (6 marks)
Two friends were discussing their peer, Molly, who has recently been diagnosed by her doctor as suffering from obsessive compulsive disorder (OCD). Stuart says, “It isn’t a shock to me that Molly has been diagnosed OCD because her dad is always checking light switches are off and the doors are locked”. Andrew says, “Really? I didn’t know that! I always assumed that anyone suffering with OCD had something not working properly in their brains which made them behave differently”. Discuss neural and genetic explanations for obsessive compulsive disorder (OCD). Refer to the conversation between Stuart and Andrew in your answer. (12 marks)
Discuss one or more biological explanation for obsessive compulsive disorder (OCD). (16 marks)
