Revise Explanations of obsessive-compulsive disorder for Cambridge 9990 (1.5.2)

Genetic explanations propose that an individual's inherited genes create a vulnerability to developing OCD. Evidence comes from family and twin studies. For instance, Nestadt et al. (2010) reviewed previous twin studies and found that 68% of identical (monozygotic) twins shared OCD as opposed to 31% of non-identical (dizygotic) twins, suggesting a strong genetic influence. Researchers have identified specific 'candidate genes' that may be involved, such as the SERT gene, which affects the transport of serotonin, and the COMT gene, which regulates dopamine. However, OCD is considered polygenic, meaning it is not caused by a single gene but a combination of genetic variations. This genetic predisposition is often viewed through the diathesis-stress model, where genes create a vulnerability that is then triggered by environmental stressors.

The leading biochemical explanation for OCD centres on the neurotransmitter serotonin. The 'serotonin hypothesis' suggests that low levels of serotonin are a causal factor. Serotonin is believed to help regulate mood and prevent the repetition of tasks. Low levels may disrupt the functioning of a key brain circuit, sometimes called the 'worry circuit', which involves the orbitofrontal cortex (OFC), the caudate nucleus, and the thalamus. The OFC sends 'worry' signals, which are normally suppressed by the caudate nucleus. If the caudate nucleus is damaged or affected by low serotonin, it may fail to suppress these signals, leading to the obsessional thoughts characteristic of OCD. Evidence for this explanation comes from the effectiveness of Selective Serotonin Reuptake Inhibitors (SSRIs), which increase serotonin levels and reduce OCD symptoms.

The cognitive approach argues that OCD stems from faulty and irrational thought processes. It suggests that everyone experiences intrusive, unwanted thoughts, but individuals with OCD interpret these thoughts in a catastrophic way. They may hold specific cognitive biases, such as an inflated sense of personal responsibility or 'thought-action fusion'—the belief that thinking a negative thought is equivalent to acting it out or makes it more likely to happen. These interpretations generate significant anxiety and a powerful urge to 'neutralise' the thought. This leads to the development of compulsions, which are performed in an attempt to suppress the thought or prevent a feared outcome, thus creating a vicious cycle of obsession and compulsion.

The behavioural component of the cognitive-behavioural explanation focuses on how compulsions are learned and maintained. It uses the principles of operant conditioning, specifically negative reinforcement. The obsessive thought (a cognitive element) produces intense anxiety (an unpleasant state). The individual discovers that performing a specific behaviour, the compulsion (e.g., washing hands, checking a lock), temporarily reduces this anxiety. The removal of the unpleasant feeling of anxiety acts as a negative reinforcer, making it more likely that the individual will perform the same compulsive behaviour again when the obsession and anxiety return. This creates a powerful, self-perpetuating cycle where the compulsions are maintained because they are effective at providing short-term relief, preventing the person from learning that their obsessive fears are unfounded.