Depression - biological explanations

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  • Created by: Roisin
  • Created on: 11-03-16 20:23

AO1 - GENES

  • depression can be passed on via genes
  • twin studies - MZ twins share genes and the environment so if MZ concordance rates are high, this suggests a genetic cause
  • Allen: MZ 40%, DZ 11%
  • adoption studies - separate environmental factors as indivudals experience different environments to people they share genes with
  • Wender et al: adopted children are 8x more likely to be depressed if biological parents are
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AO2 - GENES

  • McGuffin et al: MZ 46%, DZ 20%
  • MZ not 100% so environment does have an impact but genes have a larger influence
  • people inherit a gene that covers a range of disorders, e.g. anxiety and depression
  • Kendler et al: concordance rates were higher for depression AND anxiety
  • Tully et al: adopted children were more likely to be depressed if their adoptive parents are depressed - suggests environmental impact as adoptive parents haven't passed on genes so must be enviornment (nature vs nurture)
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AO1 - BIOCHEMICALS

  • imbalances of neurotransmitters in brain cause depression
  • catecholamine hypothesis: low levels of noradrenaline cause depression
    • e.g. reserpine (drug that lowers blood pressure) lowered noradrenaline levels and caused a side effect of acute depression in patients, confirms the link
  • serotonin hypothesis: low levels of serotonin causes low mood
    • e.g. MDMA increases serotonin levels and causes euphoria (opposite to depression)
  • Kety et al's permissive amine theory: serotonin controls the fluctuations of noradrenaline, so if serotonin levels decreases the fluctuations of noradrenaline are not controlled so noradrenaline levels can increase (and cause mania) or decrease (and cause depression)
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AO2 - BIOCHEMICALS

  • success of treatments:
    • e.g. SSRIs (such as prozac) treat depression by inhibiting the reuptake of serotonin at the presynaptic neuron and so increase the levels of serotonin in the brain, confirms the link
    • Versiani compared NRIs to placebos and found NRIs to be more effective
  • drugs don't work straight away:
    • MAOIs increase neurotransmitter levels in minutes but have no effect on mood for weeks
    • shows that the interaction of neutrotransmitters in the brain is more complex, and drugs don't work by simply increasing neurotransmitter levels
    • Kennett et al: the time delay is because the drugs work by changing the brain structure to make the neurons more sensitive to the neurotransmiiters
  • after recovery neurotransmitter levels are still low:
    • depression may cause the low levels of biochemicals, not the other way around
    • questions the very basis o the biochemical explanation of depression
    • treating individuals with drugs to change the neurotransmitters therefore does not address the underlying problem
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IDA - REDUCTIONIST

  • Bentall:a purely biological explanation is reductionist
  • depression is a complex disorder and can't be reduced to just genes / neurotransmitters
  • the environment is important too
  • it is deterministic to assume those with the gene will definitely develop depression - significant life stressors will also have an effect
  • nature vs nurture - some psycholgists favour the nurture argument (faulty thinking,early experiences) over the nature argument (genes)
  • a solely biologcaly explanation of depression is inadequate
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IDA - DIATHESIS STRESS MODEL

  • diathesis stress model: individuals may inherit a vulnerability for depression but only develop it if they experience significant life stressors
  • explains the lack of 100% concordance in MZ twins - both may have the gene but only one develops depression due to different life events / stressors
  • Claridge and Davis: gave non-depression participants drugs to lower neurotransmitter levels and participants didn't show depresive symptoms
  • shows that the biochemical explanation isn't complete so cannot solely explain depression
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