the biological approach to explaining OCD

the genetic explanation

Genetic explanations focus on whether individuals inherit a genetic pre-disposition to developing OCD.

This would mean that individuals inherited specific genes from their parents that are related to the onset of OCD. OCD is likely to involve many genes so it is a polygenic disorder. Taylor (2013) found evidence that up to 230 different genes may be involved in OCD.

different types of OCD

One group of genes may cause OCD on one person but a different set of genes may cause the disorder in another person:- known as aetiologically heterogenous (more than one cause).

family and twin studies

Family studies have shown that relatives of OCD are more vulnerable to developing OCD. e.g. Nestadt et al (2000) → first-degree relatives (i.e. parents, siblings) of OCD sufferers had an 11.7% chance of developing the disorder compared to a 2.7% risk in first-degree relatives of control patients without OCD.

Twin studies have also been used to investigate the role genetics play in developing OCD. They involve a comparison between MZ and DZ twins. MZ twins share 100% of their genes and DZ share only 50% of their genes so if genes do play a role in developing OCD we would expect to find a higher concordance rate for MZ than DZ. e.g. Carey and Gottesman (1981) found MZ twins had a concordance rate of 87% for obsessive symptoms and features compared to 47% in DZ twins.

candidate genes

Genes that give a person a vulnerability to OCD.

COMT and SERT genes

candidate genes - the COMT gene

regulates the production of the neurotransmitter dopamine that has been implicated in OCD. All genes come in different forms and one form of the COMT gene has been found to be more common in OCD patients than with people without the disorder.

Tukel et al (2013) → this form of the COMT gene produces higher levels of dopamine. This in turn can lead to over activity in the basal ganglia (the worry circuit in the brain).

candidate genes - the SERT gene

Also called the 5-HTT, the SERT gene is thought to affect the transport of serotonin creating lower levels of the neurotransmitter. These changed levels of serotonin are also implicated in OCD.

candidate genes - the diathesis-stress model

Genotype & phenotype: Although evidence suggests that OCD can have a genetic biological cause, it can also be seen that biology, specifically genetics, aren’t the sole reason why an individual can develop OCD. an individual may have a genetic vulnerability to develop OCD (i.e. they have the SERT or the COMPT gene) but, this gene alone does not cause the OCD, the interaction with our environmental triggers (e.g. stress, our upbringing) and the gene combined causes the OCD.

Diathesis-stress model: genetic mutations in the COMT or SERT genes may lead to a vulnerability to OCD, other factors (stressors) need to be present for the condition to manifest itself. Diathesis - biological predisposition or tendency towards. Stress- environmental trigger e.g. childhood experiences.

neural explanations

The neural explanations for OCD include biochemical causes (e.g. the role of neurotransmitters) and neurophysiological causes (certain areas of the brain e.g. the orbitofrontal cortex)

biochemical causes

neurotransmitters, in particular serotonin and dopamine, have been found to play a role in OCD.

Serotonin: If a person has low levels of serotonin then normal transmission of mood-relevant info doesn’t take place which means mood, and sometimes other mental processes, are affected. e.g. when low serotonin levels are experienced by someone with OCD, it can make them edgier and more hyperaware of their environments than usual, resulting in increased OCD-related behaviours such as obsessive hand-washing, counting or organising. Piggott et al (1990) → drugs which increase the level of serotonin in the synaptic gap are effective in treating patients with OCD, suggesting that serotonin is a contributory factor.

Dopamine: High levels of dopamine have been linked to OCD. This may be cuz dopamine is thought to influence concentration which could explain why OCD individuals experience an inability to stop focussing on obsessive thoughts and repetitive behaviours.

neurophysiological causes

Research has found sufferers of OCD have elevated levels of activity in the orbitofrontal cortex and the caudate nucleus (located in the basal ganglia).

PET scans of patients with OCD have shown higher levels of activity in the OFC. The orbitofrontal cortex is part of a brain circuit; one of the functions of this circuit appears to be turning sensory info into thoughts and actions. Primitive impulses, e.g. to check and clean, arise from the orbitofrontal cortex in response to sensory inputs.

how does the circuit relate to OCD?

The orbital frontal cortex sends a message of panic to the caudate nucleus. A normal brain would decide whether or not this issue is important and if it is, it would get passed on to the thalamus to take action. If the message isn't important or has already been dealt with it will filter out ending the circuit. but, in a brain of an OCD sufferer, the caudate nucleus doesn’t work correctly and sends the potentially faulty message of panic to the thalamus which then sends strong signals back to the OFC which carries out the action e.g. washing hands. This will keep repeating on a loop which is why someone with OCD performs compulsions which are repetitive rituals.

e.g. a non-suffer of OCD may have an impulse to wash dirt from their hands; once this is done the impulse to perform the activity stops and so does the behaviour. It may be that the brains of those with OCD have difficulty switching off these impulses so that they turn into obsessions, resulting in compulsive behaviour.

AO3 - strength of genetic explanation

evidence from twin studies. Nestadt et al. (2010) reviewed twin studies and found that 68% of MZ shared OCD as opposed to 31% of DZ twins.

evidence from 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).

AO3 - limitation of genetic explanation

there are environmental risk factors.

There’s strong evidence for the idea that genetic variation can make a person more or less vulnerable to OCD. but, OCD doesn’t appear to be entirely genetic in origin and it seems that environmental risk factors can also trigger or increase the risk of developing OCD.

Cromer et al. (2007) → 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.

AO3 - strength of neural explanation

Antidepressants that work purely on serotonin are effective in reducing OCD symptoms 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.

AO3 - limitation of neural explanation

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 (though isn’t necessarily caused by) 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’re depressed as well.

This means that serotonin may not be relevant to OCD symptoms.