There is a genetic link to OCD. Lewis observed that of his OCD patients 37% had parents with OCD and 21% had siblings with it.
Researchers have identified candidate genes that create a vulnerability for OCD.
COMT gene:
In OCD patients the COMT gene is mutated, making it have a low activity level.
This means it produces less COMT enzymes to clear the synapse of dopamine.
The excess dopamine causes an increase in dopamine levels in the brain, which causes compulsions in OCD.
SERT gene:
In OCD patients the SERT gene is mutated, making it have a higher activity level.
This means that the number of transporter proteinsincreases and more serotonin is removed from the synapse in re-uptake.
This means that serotonin levels decrease, and this affects the brain, creating a low mood and anxiety.
Tukel et al discovered that low activity levels in the COMT gene led to higher levels of dopamine.
Ozaki et al found that two unrelated families had the mutatedSERT gene and 7/8 members had OCD.
Based on animal studies, it is indicated that high levels of dopamine cause movements resembling compulsive behaviours (Szechtman et al).
Serotonin levels are also lower, meaning antidepressants can be used to help OCD patients (Pigott et al).
There are several areas in the brain thought to be involved in the OCD worry circuit:
Caudate nucleus (located in the Basal Ganglia)
OFC
Thalamus
The caudate nucleus usually suppresses worry signals from the OFC, to stop them from reaching the thalamus.
A damaged caudate nucleus allows the worry signals to reach the thalamus, where the signals are sent back to the OFC in a loop.
The worry circuit is supported by PET scans, showing heightened activity in the OFC.
Serotonin and Dopamine are linked to regions of the frontal lobe. Comer reports that serotonin plays a key role in the operation of the caudate nucleus and OFC.
What did Nestadt et al find about first-degree relatives of OCD patients?
Screening for specificgenes could mean certain genes can be turned ‘off’.
Limitations for the biological approach of OCD:
Alternative explanations - behaviourism
Tourette’s syndrome - Pauls and Leckman found that OCD is one form of the same gene that determines Tourette’s. Obsessive behaviours are also found in children with Autism, as well as Anorexia Nervosa. Shoes that it is not purely nature.
SSRIS re-absorption of serotonin is inhibited.
Tricyclics work in a similar way to SSRIs but inhibit the re-uptake of serotonin and noradrenaline.
Tricyclics are a last resort due to their side effects. They can increase heart rate, causing potential life threatening heart problems.
Benzodiazepines are used to reduce anxiety and usually only used over a two week period.
BZs slow down the activity of the CNS enhancing the activity of the neurotransmitterGABA - a neurotransmitter that has a quieting effect on neurones.
BZ attaches to the GABA receptor site, resulting kin the channel being opened up more frequently. This allows more chloride ions to flow through the channel, making you feel more relaxed.
Strengths of drug treatments:
Effectiveness - Soomro et al found that SSRIs were more effective with OCD than placebos. (but little long term data exists)
Preferred treatment - very little cognitive input needed from the patient, plus they are cheaper and require little monitoring.
Limitations of drug treatments:
Side effects - Nausea and headaches are common for SSRIs. Tricyclics can cause hallucinations and irregular heartbeat. Benzodiazepines include increased aggressions and long term impairment of memory as well as problems with addiction.
Not a lasting cure.
Koren et al found that although drug therapies were useful, psychotherapies should be used first to provide long term help.
Publication bias - there may be a bias in the studies that show antidepressants being effective as they are mostly conducted by the drug companies themselves.