The biological approach to explaining OCD Flashcards
Correlation and causality
There is clear evidence to strongly suggest that some neural systems (such as the neurotransmitter serotonin) do not work normally in people with OCD. According to the biological model of mental disorder the most obvious way to explain this brain–OCD link is to say that the brain dysfunction comes first and causes the OCD. In other words this becomes a causal explanation.
However, the relationship between neural abnormality and OCD is just a correlation, and such correlations do not necessarily indicate a causal relationship. It is quite possible that the OCD (or its accompanying depression) causes the abnormal brain function. Alternatively, both OCD and neural abnormality may be influenced by a third factor – for example trauma. Traumatic events can both affect the brain and have a range of psychological effects. Trauma could thus be the cause of both the neural abnormality and the OCD/depression.
In conclusion, correlations are not enough to say categorically that there is a neural basis to OCD.
Animal studies
On one hand evidence from twin studies suggests there is a possible genetic basis to OCD. However it has proved hard to find candidate genes, i.e. genetic variations, that are consistently associated with OCD. There is evidence though from animal studies that show that particular genetic variations are associated with repetitive behaviours (similar to e.g. repetitive hand-washing) in other mammal species, for example mice (Ahmari 2016).
On the other hand, although mice and humans share most of their genes (i.e. you can find the same genes in both species), the human mind and brain are much more complex than those of other mammal species. For example the human brain is capable of complex thinking and problem-solving. This means we should always be very cautious about generalising from animal to human brains. Also, it may not be possible to generalise from the tendency for repetitive behaviour in mice to human OCD behaviours or even the wider aspects of what is characteristic of OCD.
This means that animal studies probably only provide weak support for the idea of candidate genes for OCD in humans.
Research supports
One strength of the genetic explanation for OCD is the strong evidence base.
There is evidence from a variety of scurces 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 (MZ) shared OCD as opposed to 31% of non-identical (DZ) twins. 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.
Environmental risk factors
One limitation of the genetic model of OCD is that there are also environmental risk factors.
There in strong avidone 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.
Research support
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 (see next spread for evidence) 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 disorders) may also be responsible for OCD
No unique neural system
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 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.
