“Outline and Evaluate one biological explanation for OCD” (16 marks)
The genetic explanation for OCD suggests that some people have a vulnerable
predisposition to acquiring OCD. Mckean and Murray found that patients with OCD are more
likely to have close relatives that also suffer with this disorder, and Bellodi et al (2001) uses
evidence from twin studies and family studies to show that close relatives are more likely to
have the disorder rather than distant relatives. This supports the genetic explanation.
Another possible genetic explanation is candidate genes- these are genes that are thought
to play key factors in the development of OCD. An example of a candidate gene is the SERT
gene- this regulates serotonin and facilitates message transfer across synapses. A
malfunction or mutation of the SERT gene causes the person to have lower serotonin levels,
meaning that people may be more aware of their environment- this creates anxious feelings
leading to compulsions such as handwashing or counting or checking. A second example of
a candidate gene is the COMT gene, which regulates the production of dopamine.
Dopamine affects drive and motivation. OCD is reinforced by a reward of temporary anxiety
relief from performing compulsions, therefore OCD sufferers tend to have abnormally high
levels of dopamine present. Higher dopamine levels lead to wanting more rewards, so
compulsions are performed more often. While there is evidence from family studies to
support the role of genes in OCD development, it is recognised that not everyone in a given
family has the disorder so there must be additional factors.
The Diathesis Stress Model acknowledges the fact that people gain a vulnerability to OCD
through genetics, but also states that an environmental stressor is also required, for example
a traumatic or stressful event such as a bereavement. OCD is thought to be polygenic, which
means that there is little predictability available from genetics, so the diathesis stress model
provides an accompanying explanation by suggesting that through the genetic vulnerability,
OCD is triggered by an environmental stressor. This is supported by Cromer (2007) who
found that over half of OCD patients in her sample had a traumatic event in the past.
In evaluation, while there is substantial evidence from twin and family studies that some
people have a genetic predisposition to the development of OCD, the genetic explanation
does not account for possible environmental factors, for example close relatives of OCD
sufferers could have observed and imitated the behaviour. Each genetic variation only
increases the risk of developing OCD by a fraction, therefore the genetic explanation is
ineffective in explaining the acquisition of OCD.
The genetic explanation for OCD suggests that some people have a vulnerable
predisposition to acquiring OCD. Mckean and Murray found that patients with OCD are more
likely to have close relatives that also suffer with this disorder, and Bellodi et al (2001) uses
evidence from twin studies and family studies to show that close relatives are more likely to
have the disorder rather than distant relatives. This supports the genetic explanation.
Another possible genetic explanation is candidate genes- these are genes that are thought
to play key factors in the development of OCD. An example of a candidate gene is the SERT
gene- this regulates serotonin and facilitates message transfer across synapses. A
malfunction or mutation of the SERT gene causes the person to have lower serotonin levels,
meaning that people may be more aware of their environment- this creates anxious feelings
leading to compulsions such as handwashing or counting or checking. A second example of
a candidate gene is the COMT gene, which regulates the production of dopamine.
Dopamine affects drive and motivation. OCD is reinforced by a reward of temporary anxiety
relief from performing compulsions, therefore OCD sufferers tend to have abnormally high
levels of dopamine present. Higher dopamine levels lead to wanting more rewards, so
compulsions are performed more often. While there is evidence from family studies to
support the role of genes in OCD development, it is recognised that not everyone in a given
family has the disorder so there must be additional factors.
The Diathesis Stress Model acknowledges the fact that people gain a vulnerability to OCD
through genetics, but also states that an environmental stressor is also required, for example
a traumatic or stressful event such as a bereavement. OCD is thought to be polygenic, which
means that there is little predictability available from genetics, so the diathesis stress model
provides an accompanying explanation by suggesting that through the genetic vulnerability,
OCD is triggered by an environmental stressor. This is supported by Cromer (2007) who
found that over half of OCD patients in her sample had a traumatic event in the past.
In evaluation, while there is substantial evidence from twin and family studies that some
people have a genetic predisposition to the development of OCD, the genetic explanation
does not account for possible environmental factors, for example close relatives of OCD
sufferers could have observed and imitated the behaviour. Each genetic variation only
increases the risk of developing OCD by a fraction, therefore the genetic explanation is
ineffective in explaining the acquisition of OCD.
