Biological Approach to Explaining OCD (AQA AS Psychology)

A genetic explanation of OCD assumes that mental illnesses are heritable (i.e. they are generationally transmitted)

The risk of developing OCD is higher for first-degree relatives (siblings or children) and the risk of inheriting OCD is higher in some families than in others (though research so far cannot explain why this is so)

Researchers have identified candidate genes as genes that code for vulnerability to OCD 

• OCD is polygenic, it is not caused by one single gene but by a combination of genetic variations that together cause significantly increased vulnerability

A specific gene variation or group of genes may result in OCD in one person, but not for everyone with that genetic profile

OCD-relevant genes include those involved in serotonergic and dopaminergic pathways

• Both dopamine and serotonin are neurotransmitters linked to mood, emotion and motivation

Research suggests a variation of the COMT gene is linked to OCD

• COMT plays an important role in de-activating dopamine

  • Irregular dopamine levels are implicated in OCD

  • COMT gene helps to balance dopamine levels

  • Hence, COMT gene variation may contribute to OCD as it may help to control compulsive behaviours

The SERT gene has also been linked with OCD, affecting the transport of serotonin

• Lower levels of serotonin activity are implicated in OCD

• Serotonin plays a role in balancing mood which in turn may help to regulate obsessive thoughts

There is some strong research support for a genetic explanation of OCD

• Nestadt et al. (2010) found that 68% of monozygotic (MZ; identical) twins both had OCD compared to 31% of dizyogotic (DZ; non-identical) twins

  • This increases the validity of the theory, suggesting that OCD can be partly explained by genetics

Twin studies are a useful way to investigate the heritability of OCD

• Each twin acts as the control for the other twin which means that individual differences are accounted for to some extent

• Twin studies tend to use large samples which results in robust quantitative data i.e. the research has good reliability

Ignoring the role that the environment plays in the development of a mental illness means that a genetic explanation is prone to biological reductionism

• Twins are reared in the same environment which means that they are likely to respond to upbringing, family life etc. similarly

• If the environment also contributes to OCD then a genetic explanation lacks fully explanatory power

Pato et al. (2001) noted that although there does seem to be a genetic explanation for OCD, there is insufficient understanding of the actual genetic mechanisms surrounding OCD

• The above observation means that a genetic explanation alone may lack validity

A neural explanation of OCD assumes that neurotransmitters play a role in the development of the disorder

The two key neurotransmitters here are serotonin and dopamine (see the section above for the relevance of gene variations linked to these two neurotransmitters)

Serotonin is known to play a role in regulating mood

• Low or disrupted levels of serotonin have been implicated in mood disorders such as depression

• Low mood may also be accompanied by cognitive disturbances such as faulty information processing

• Faulty information processing can be located to the frontal cortex of the brain

  • The frontal cortex has been linked to executive functioning

  • If serotonin levels are irregular/low in the frontal cortex then it is likely that someone will experience difficulty in applying logic, reason and rationality to their thoughts and behaviours

  • Obsessive thoughts are thus more likely if serotonin levels in the frontal cortex are irregular/low

Dopamine is also implicated as a neural explanation of OCD

• Dopamine activity in the dorsomedial striatum (DSM) has been linked to the development of compulsive behaviours

• Neural circuits connecting the cerebral cortex to the DSM are thought to control movement and reward-seeking behaviours

• There is good evidence to suggest that dopamine plays a key role in movement and reward

• High levels of dopamine in the DSM increase compulsive reward-seeking

  • This reward-seeking may explain OCD as compulsive behaviours are performed to decrease obsessive thoughts by reducing anxiety

  • Thus, dopamine reinforces the compulsive behaviours which are necessary to reduce obsessive thoughts

Antidepressants such as SSRIs, which are used to regulate serotonin levels, have been effective in reducing OCD symptoms

• This finding supports the idea that irregular levels of serotonin are linked to the development of OCD, which increases the validity of the theory

Research into a neural explanation of OCD tends to use objective, clinical methods such as fMRI scanning which is high in reliability

Not all OCD sufferers respond positively to SSRIs which reduces the external validity of the theory

• If SSRIs cannot treat all individuals with OCD, then the cause may not be solely neural

Although sophisticated apparatus (such as fMRIs) are used to measure brain activity this in itself is not 100% evidence of neurotransmission

• The brain activity measured in an fMRI may be the result of other factors e.g. excitement/nervousness at being in the scanning machine

• It is not yet possible to track and measure 'live' neurotransmission

• Thus, it is only possible to claim that OCD have neurological correlates, there is no absolute 'proof' that irregular serotonin and dopamine levels cause OCD