The biological approach to explaining OCD: genetic and neural explanations. The biological approach to treating OCD: drug therapy.

What this dot point is asking

AQA wants you to explain OCD through genetic and neural explanations and describe drug therapy. The exam skill is to name candidate genes and the diathesis-stress logic, to link low serotonin and the worry circuit to SSRIs, and to evaluate drug therapy in a balanced way.

Genetic explanation

The genetic explanation argues that people inherit a vulnerability to OCD rather than the disorder itself. Two candidate genes are named in the specification material: the COMT gene, which regulates the neurotransmitter dopamine (a variation of it appears more common in OCD patients and may lead to higher dopamine levels), and the SERT gene (also called 5-HTT), which affects the transport of serotonin and, when faulty, may lower serotonin activity. Crucially, OCD is polygenic, meaning that no single gene is responsible; instead many genes each contribute a small amount to the overall risk, and the specific combination differs between individuals (the condition is aetiologically heterogeneous). The genetic account is best framed as diathesis-stress: genes create a vulnerability that may only develop into OCD when triggered by environmental stress, which is why even identical twins are not always concordant. Twin studies by Nestadt et al. found a far higher concordance rate for OCD in identical than non-identical twins, providing the main supporting evidence while also showing (through the less-than-perfect concordance) that genes are not the whole story.

Neural explanation and drug therapy

The neural explanation looks at neurotransmitters and brain structures. Low levels of serotonin, which helps regulate mood, are associated with OCD, and this is supported by the fact that drugs which raise serotonin reduce symptoms. At the structural level, the basal ganglia (involved in coordinating movement and habitual behaviour) and the orbitofrontal cortex (involved in decision-making) are implicated in a "worry circuit": the orbitofrontal cortex sends signals about potential worries to the thalamus, and in OCD this circuit appears overactive, so the worries (obsessions) and the urges to act on them (compulsions) are not properly filtered out. Drug therapy follows directly from the neural explanation. The main treatment is selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, which block the reabsorption (reuptake) of serotonin into the presynaptic neuron, so more serotonin stays in the synapse and continues to stimulate the postsynaptic neuron, correcting the deficiency. SSRIs are often combined with CBT, and alternatives include tricyclics and SNRIs.