The biological approach to explaining OCD

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Genetic explanations - COMT gene

May contribute to OCD. Regulates production of dopamine - implicated in OCD. All genes come in diff forms (alleles) + 1 form of COMT gene found more common in OCD patients than people w/o disorder. Variation produces lower activity of COMT gene + higher levels dopamine - Tukel et al (2013).

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Genetic explanations - SERT gene

Also called 5-HTT. Affects transport of serotonin, creating lower levels of neurotransmitter. Higher levels also implicated in OCD. 

Ozaki et al (2003) - found mutation of gene in 2 unrelated families where 6 of 7 family members had OCD.

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Genetic explanations - Diathesis-stress

Idea of link b/ween 1 gene + disorder eg OCD unlikely. Genes eg SERT gene implicated in number of other disorders eg depression. Other factors affect what condition develops or whether mental illness develops. Therefore, some could possess COMT or SERT gene variations but suffer no ill effects - other factors eg environmental factors trigger it.

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NE - abnormal levels of neurotransmitters

Dopamine levels abnormally high in people w/ OCD. Based on animal studies eg Szechtman et al (1988) - high doses drugs enhance dopamine inc stereotyped movements resembling compulsive behaviours found in OCD patients.

Serotonin levels low - Pigott et al (1990) - antidepressant drugs increase serotonin activity been shown to reduce OCD symptoms, whereas antidepressants less effect on serotonin don't reduce OCD symptoms - Jenicke (1992).

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NE - abnormal brain circuits

Several areas in frontal lobes thought to be abmormal in people w/ OCD. Caudate nucleus (in basal ganglia) normally suppresses signals from orbitofrontal crtext (OFC), which sends signals to thalamus about things that are worrying eg potential germ hazard. When caudate damaged, fails to suppress minor 'worry' signals, thalamus alerted, sends signals back to OFC, acting as 'worry circuit'.

Supported by PET scanes of those w/ OCD while symptoms active - show heightened activity in OFC.

Serotonin + dopamine linked to these regions of frontal lobe. Comer (1998) - serotonin plays key role in operation of OFC caudate nuclei, would appear abnormal levels serotonin might cause areas to malfunction. Sukel (2007), dopamine main neurotransmitter of basal ganglia. High levels dopamine -> overactivity of this region.

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Evaluation- Strengths

Family + twin studies. Nestadt et al (2000) - 80 patients w/ OCD + 343 of their 1st degree relatives, compared them w/ 73 control patients w/o mental illnes + 300 of their relatives. Found those w/ 1st degree relative w/ OCD 5x greater risk of having illness themselves compared to general population.

Menzies et al (2007) - MRI, produced images of brain activity in OCD patients + immediate family members w/o OCD + group of unrelated healthy people. OCD patients + relatives reduced grey matter in key regions of brain inc OFC. Supports anatomical diffs inherited, may -> OCD.

Real world app - mapping of human genome -> hope that specific genes linked to particular disorders. Eg, might be that where one or other parent-to-be has COMT gene, mother's fetilised eggs could be screened, giving parents choice of whether to abord eggs w/ gene. Presumes simple relationship, when there isn't.

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Evaluation - Weaknesses

Pauls + Leckman (1986) - patients w/ Tourette's + families, found oCD 1 form of ecpression of same gene determines Tourette's. Supports view not one specific gene unique to OCD - predisposing factor towards obsessive-type behaviour.

Alternative explanations - two-process model (behavioural approach) can be applied to OCD. Initial learning occurs when NS eg dirt associated w/ anxiety. Association maintained b/c anxiety-provoking stimulus avoided. Obsession formed then link learned w/ compulsive behaviours eg hand washing, appeats to reduce anxiety.

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