The biological approach focuses on the genetic and neural explanations.
The genetic explanation suggest OCD is inherited and that individuals inherit specific genes
that cause OCD. The genetic explanation focuses on identifying specific genes which can
leave people more likely to suffer from OCD, known as candidate genes. The Sert gene
(5HT1-D beta), is linked to the neurotransmitter serotine which affects the transport of
serotine across synapses, decreased levels of this neurotransmitter is associated with OCD
and depression. The Compt gene is associated with the production of dopamine, which is
also implicated in OCD. Moreover, OCD is not caused by 1 single gene but several genes (it
polygenic). There is evidence that different types of OCD may be the result of certain genetic
variations.
The neural explanation of OCD focuses on neurotransmitters and the brain structure. A
neurotransmitter is responsible for relaying info from one neuron to another, abnormal
levels of neurotransmitter is believed to cause OCD. The neurotransmitter serotine is
believed to play a role in OCD as reduction in the levels of serotine in the brain, lowers
mood and it is used to explain some cases of OCD and high levels of dopamine may lead to
OCD. Other cases of OCD, (hoarding disorder) are associated with impaired decision making,
this is when the lateral frontal lobes are functioning abnormally, (part of the brain
responsible for logical thinking and making decision). There is evidence to suggest an area in
the brain called the Parahippocampal gyrus, which is associated with processing unpleasant
emotion, functions abnormally in OCD.
A strength of the genetic explanation for OCD is there is good supporting evidence for it. For
example, Nestadt et al reviewed twin studies and found that 68% of identical twins (MZ)
shared OCD as opposed to 31% of non-identical twins (DZ). This evidence suggests that
some individuals are more vulnerable to OCD because of their genetic makeup in particular
MZ twins. Thus, this is a strength to the genetic explanation as it strongly supports the
genetic influence on OCD.
A limitation of the genetic explanation is that environmental factor can also increase the risk
of developing OCD. For example, Cromer et al found that over half of OCD patients in their
sample had a traumatic event in their past, and OCD was more severe in those with one or
more traumas. This evidence suggests that OCD is not entirely genetic in origin and that
environmental risk factors can also trigger them. Thus, this is a limitation to genetic
explanation of OCD as it supports the diathesis stress model in explaining OCD as it factors
the effects of both genetics and the environment.
A strength of the neural explanation is there is supporting evidence for the role of some
neural mechanism in OCD. For example, antidepressants that work purely on the serotonin
system increasing the levels of this neurotransmitters are effective in reducing OCD
symptoms and this suggests that the serotonin system may be involved in OCD. Also, OCD
symptoms form part of biological conditions such as Parkinson’s disease. Thus, this suggests
that the biological processes that cause the symptoms in those conditions may also be
responsible for OCD.