Biological approach to explaining + treating OCD

• Explanations for OCD (Neural) -

  • Neurotransmitters are chemical messengers that send signals around the brain + body. Relay info from 1 neuron to another. Serotonin regulates mood & lower levels of serotonin are associated with mood disorders. High levels of dopamine are associated with symptoms of OCD e.g. compulsive behaviour. The chemical imbalance of low levels of serotonin & high levels of dopamine is associated with OCD.
• Explanations for OCD (Neural) - Brain Structures:

  • Basal Ganglia: involved in multiple processes e.g. coordination of movement. After a lesion in this area many develop OCD-like symptoms following recovery.
  • Orbitofrontal Cortex: converts sensory info to thoughts & actions. PET scans found higher activity here in patients with OCD. Heightened activity increases sensory info into actions may lead to compulsions, increased activity also prevents patients from stopping their compulsive behaviours.
• Explanations for OCD (Genetic) -

  • Genes are predisposed. With an environmental trigger it may lead to the expression of OCD. Taylor proposed OCD is polygenic and up to 230 different genes are associated to it.
  • Candidate Genes -
  • COMT Gene: associated with dopamine (pleasure + reward). 1 variation results in high levels of dopamine & this variation is more common in patients with OCD (Tukel et al, 2013).
  • SERT Gene: associated with serotonin, affects transportation of serotonin, lower levels are linked to OCD. Ozaki et al (2003) found a mutation of this gene in 2 families with OCD.
• AO3: Biological explanation for OCD -

  • Biological reductionism, no twin study has a concordance rate of 100% suggests other factors must also impact OCD e.g. environmental. Too simplistic.
  • Anti-depressants work by increasing serotonin levels e.g. SSRI's. RLA, improves patients quality of life supports neural & SERT gene.
  • Can't establish cause + effect, reduces scientific credibility, abnormalities could be due to OCD rather than causing OCD.
• AO3: Biological explanation for OCD -

  • OCD is polygenic, too simplistic.
  • Twin studies provide evidence for a strong genetic link e.g. 68% MZ twins, 31% DZ twins which suggests nature does have an impact on OCD.
• • Biological Treatment for OCD: Drug Therapy (SSRI's) -
  • most common, assumes there is a chemical imbalance in the brain.
• • Without SSRI's: serotonin is released by pre-synaptic neuron & travels across the synapse to receptor sites on the post-synaptic neuron but doesn't bind to the receptors.
  • With SSRI's: serotonin is released from the pre-synaptic neuron into the synapse, travels to the receptor site on the post-synaptic neuron. SSRI's block reabsorption of serotonin from pre-synaptic neuron. This increases serotonin levels in the synapse allowing more serotonin to be received in the post-synaptic neuron.
• Combining SSRI's with other treatments -

  • Drugs are often used alongside CBT. Drugs reduce emotional symptoms e.g. anxiety but patients may also improve if they engage with CBT if their OCD was expressed through an environmental trigger.
• AO3 Treating OCD (Biological: SSRI's) -

  • Soomro reviewed 17 studies comparing SSRI's to placebo's. All 17 showed significantly better results for SSRI's.
  • ~May have publication bias as drug companies often provide unreliable evidence as many drug companies are sponsored & need to sell their drugs.
  • Dependency
  • Side effects: 1 in 10 experience weight gain, loss of sex drive, affects patients quality of life, may lead to drop-outs.
  • Cost-effective, less strain on the NHS.
• AO3 Treating OCD (Biological: SSRI's) -

  • Less disruptive to the patients lives as you just take the drugs until your symptoms reduce unlike psychological therapies.
  • Drugs treat symptoms not causes. In some cases biological factors may not lead to the expression of OCD. Rather it could be psychological factors affecting the expression of OCD e.g. trauma in which case drugs may not be as useful.
• • the role of neurochemicals such as serotonin and dopamine – levels associated with abnormal transmission of mood-related information/obsessive thoughts
  • structural deficits – abnormal functioning in the parahippocampal gyrus which processes unpleasant emotions; hyperactivity in the basal ganglia linked to repetitive actions (compulsions); the orbito-frontal cortex ‘the worry circuit’ – the caudate nucleus-thalamus loop, inability to filter small worries in OCD so worry circuit is overactive
• Treating depression -

  • use of drug therapy to ‘correct’ imbalance of neurochemicals, e.g. serotonin, to reduce symptoms associated with OCD
  • SSRIs – prevent the reabsorption and breakdown of serotonin in the brain, continue to stimulate the postsynaptic neuron
  • timescale – 3–4 months of daily use for SSRIs to impact upon symptoms
• Genetic Explanation for OCD -

  • suggests that OCD is an inherited condition, vulnerability/predisposition is passed on across generations
  • a number of candidate genes have been implicated as a possible cause for OCD, e.g. Taylor (2013) identified up to 230 suggesting OCD is polygenic
  • different combinations may also account for different types of OCD
  • credit reference to specific genes and their function, e.g. SERT, COMT
• AO3 Genetic Explanation -

  • use of evidence to support genetic basis, e.g. Nestadt et al (2010) – twin study (68% MZs, 32% DZs)
  • methodological problems with twin and family studies such as shared environments, social learning
  • cannot account for OCD in families where there is no previous history
  • broader issues of biological reductionism, determinism, causation
  • discussion of alternatives, e.g. diathesis-stress model use of an interactionist approach