The biological approach to explaining and treating OCD: genetic and neural explanations; drug therapy.
Researchers are reasonably confident in the neurochemicals involved in OCD. Many people believe that OCD reflects a deficiency in the neurotransmitter serotonin; a hormone important in transmitting nerve impulses. The evidence for this is that OCD can be eased (but not cured) by antidepressants in some patients, which boost levels of serotonin in the brain (e.g. Fineberg and Gale, 2005).
Serotonin & Dopamine
Anxiety disorders tend to respond to drugs that affect either dopamine or serotonin systems. Serotonin is known to regulate other neurochemicals in the brain, such as dopamine and GABA, such that it can dampen down or enhance their activity, thus an imbalance in serotonin might lead to an imbalance in these others.
Dopamine is the main neurotransmitter involved in the brain reward pathway. It is an important neurotransmitter in the caudate nucleus and the basal ganglia in general. It seems as though there is a decreased number of dopamine receptors in the basal ganglia of OCD patients.
Supporting evidence for the involvement of dopamine in OCD comes from two main sources:
- Some patients with OCD who take atypical antipsychotics (a treatment given to patients with schizophrenia, to reduce their levels of dopamine) see a reduction in their OCD symptoms.
- Long-term heroin addicts can develop OCD symptoms (Papageorgiou et al., 2003). Heroin is known to disrupt the brain’s dopamine levels, which may, in turn, lead to OCD symptoms.
There are some limitations of neurochemical explanations though. Although research in this area is promising, as it allows the opportunity for further medications to be developed, there are some problems:
- Cause & effect cannot be established. Is OCD caused by changes in neurochemistry, or does it cause them itself?
- If we are unsure of the exact neural mechanisms involved, we are medicating blindly. More research needs to be conducted into how the brain works before effective treatments – or even cures – for OCD can be found.
It is believe that people inherit a predisposition to developing anxiety disorders, such as OCD. Genetics explanations for OCD are less established that neurochemical, but research in this area is currently underway. There are three main sources of information for whether something might be genetic: family studies, twin studies and gene research.
Since first degree relatives share around 50% of their genetic material, researchers look at concordance rates between relatives; that is, the chance of other family members developing a disorder if a proband (person with disorder) has been diagnosed. The incidence of OCD in proband families and those without a known history of the disorder are then compared.
There are very few family studies into OCD, but the first was conducted by Pauls et al. in 1995. They discovered that the risk of developing OCD was 5x higher if a first degree had been diagnosed with the disorder. A similar study by Nestadt et al. (2000) found a similar risk of 11.7 percent for families when a first degree relative had been diagnosed with OCD, compared to a general risk of 2.7% in the general population. Both studies therefore support a genetic role in OCD. Nestadt’s study was particularly well-controlled and showed that obsessions were more likely to be shared than compulsions. An earlier onset of the disorder within a family member also appeared to heighten the risk of family members also developing the disorder. This seems to indicate that there may be at least two distinct forms of OCD.
Evaluation of family studies
It is difficult to untangle the effects of nature and nurture in the development of OCD. This is due to the fact that most family members share the same environment, so observational learning cannot be discounted.
More robust evidence comes from twin studies, especially looking at concordance rates between monozygotic (identical) twins. Unfortunately, again, few studies have been conducted into OCD. Twin studies that have been conducted either look at twins over a longer period of time (which is useful in separating the roles of nature and nuture), or have very small samples.
A review of twin studies by Grootheest et al (2005) estimates the hereditability of OCD symptoms (rather than the diagnosis) as between 27 and 47%. It is important to remember that this comes from limited data, however.
Evaluation of Twin Studies
- Lack of data: There is a distinct lack of twin studies into OCD, possibly because it is difficult to find a large enough sample of participants. Instead, research has focused more on OCD symptoms, rather than a full diagnosis (subclinical features, where a person has begun to develop symptoms, but the disorder is not yet apparent). Again, it is very difficult to separate the roles of nature and nurture though.
- General predisposition to anxiety: It may be that genetic predisposition is simply for anxiety, rather than OCD in particular. This is more promising research in terms of developing appropriate treatments, but is complicated by the heterogeneous nature of OCD and other anxiety disorders.
Other gene research
Advances in technology have allowed researchers to investigate potential candidate genes for OCD. Unfortunately, it is still early days though in terms of this research. Here is a list of potential candidate genes research has identified on the online genetics database SNPedia.com. Most research in this area if focused on the roles of dopamine and serotonin systems. No studies with a large sample have yet been conducted, but many candidate genes have been suggested (Pauls, 2008).
Below are research studies focusing on specific genes:
- [PMID 18444253] Additional functional variation at the SLC6A4 gene.
- [PMID 18824000] How the serotonin story is being rewritten by new gene-based discoveries principally related to SLC6A4, the serotonin transporter gene, which functions to influence all cellular serotonin systems.
- [PMID 23510579] Worldwide population variation and haplotype analysis at the serotonin transporter gene SLC6A4 and implications for association studies.
- [PMID 23630162] Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette’s disorder.
Clearly, however, genes do not appear to be the only factor in the development of the disorder, as concordance rates between monozygotic twins are nowhere near 100%!
Source: Collins student support material for AQA A2 Psychology