Explaining OCD Flashcards
Genetics
- Polygenic
- Genetic variations
- Polygenic
However, like many conditions, OCD seems to be polygenic. this means that OCD is not caused by one single gene but that several genes are involved. Taylor (2013) as analysed findings of previous studies and found evidence that up to 230 different genes may be involved in OCD. Genes that have been studied in relation to OCD include those associated with the action of dopamine as well as serotonin, both neurotransmitters believed to have a role in regulating mood.
2) Genetic variations
COMT: 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.
SERT: 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 6 out of 7 of the family members having OCD.
Strength - Genetics
One strength of the genetic explanation of OCD is the strong evidence base. There is evidence from a variety of sources which strongly suggests that some people are vulnerable to OCD as a result of their genetic make-up. One source of evidence is twin studies. In one study, Gerald Nestadt et al. (2010) reviewed twin studies and found that 68% of identical twins (monozygotic or MZ) shared OCD as opposed to 31% of non-identical twins (dizygotic or DZ). Another source of evidence for a genetic influence on OCD is family studies. Research has found that a person with a family member diagnosed with OCD is around four times as likely to develop it as someone without (Marini and Stebnicki 2012). These research studies suggest that there must be some genetic influence on the development of OCD.
Weakness - Genetics
One limitation of the genetic model of OCD is that there are also environmental risk factors. There is strong evidence for the idea that genetic variation can make a person more or less vulnerable to OCD. However, OCD does not appear to be entirely genetic in origin and it seems that environmental risk factors can also trigger or increase the risk of developing OCD. In one study for example, Kiara Cromer et al. (2007) found that over half the OCD clients in their sample had experienced a traumatic event in their past. OCD was also more severe in those with one or more traumas. This means that genetic vulnerability only provides a partial explanation for OCD.
Neural - brain structures
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.
1) The basal ganglia
The basal ganglia is a brain structure involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD-like symptoms, following their recovery. Furthermore, Max et al. (1994) found that when the basal ganglia is disconnected from the frontal cortex during surgery, OCD-like symptoms are reduced, providing further support for the role of the basal ganglia in OCD.
2) The orbitofrontal cortex
Another brain region associated with OCD is the orbitofrontal cortex, a region which converts sensory information into thoughts and actions. PET scans have found higher activity in the orbitofrontal cortex in patients with OCD. One suggestion is that the heightened activity in the orbitofrontal cortex increases the conversion of sensory information to actions (behaviours) which results in compulsions. The increased activity also prevents patients from stopping their behaviours.
Neural - neurotransmitters
The role of serotonin
- One explanation for OCD concerns the role of the neurotransmitter serotonin, which is believed to help regulate mood. Neurotransmitters are responsible for relaying information from one neuron to another. If a person has low levels of serotonin then normal transmission of mood-relevant information does not take place and mood - and sometimes other mental processes - are affected. At east some cases of OCD may be explained by a reduction in the functioning of the serotonin system in the brain.
- 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.
Strength - Neural
One strength of the neural model of OCD is the existence of some supporting evidence. Antidepressants that work purely on serotonin are effective in reducing OCD symptoms and this suggests that serotonin may be involved in OCD. Also, OCD symptoms form part of conditions that are known to be biological in origin, such as the degenerative brain disorder Parkinson’s disease, which causes muscle tremors and paralysis (Nestadt et al. 2010). If a biological disorder produces OCD symptoms, then we may assume the biological processes underlie OCD. This suggests that biological factors (e.g. serotonin and the processes underlying certain conditions) may also be responsible for OCD.
Weakness - Neural
One limitation of the neural model is that the serotonin-OCD link may not be unique to OCD. Many people with OCD also experience clinical depression. Having two disorders together is called co-morbidity. This depression probably involves (though is not necessarily caused by) disruption to the action of serotonin. This leaves us with a logical problem when it comes to serotonin as a possible basis for OCD. It could simply be that serotonin activity is disrupted in many people with OCD because they are depressed as well. This means that serotonin may not be relevant to OCD symptoms.
