WJEC A2 Psychology PY4 - Aetiologies of Unipolar

3 Aetiologies of Unipolar

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Biochemical Aetiology of Depression

1. Biochemical Aetiology of Depression

  • unipolar may be a result of changing levels of a number of neurotransmitters (serotonin, noradrenaline, dopamine = biological biogenic amines)
  • Ketty's Serotonin Theory suggests that serotonin controls the levels of other transmitters and that if low levels of serotonin occur, other transmitters (noradrenaline + dopamine) can fluctuate wildly, producing unipolar
  • serotonin = affect mood and sleeping habits, dopamine = affect psychosis/negative thoughts; noradrenalineaffect energy levels including movement and lethargy


(+) NcNeil + Cimbolic (1986)

  • found major serotonin-by product is not found in the cerebrospinal fluid of suicidally depressed patients, suggesting it is deficient in depressive's brains
  • supports aetiology: low levels of serotonin have an influence on mood and therefore relates to causing depression
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Biochemical Aetiology of Depression

(-) HOWEVER...

  • this research study does not establish a cause-effect relationship; difficult to know whether the levels of serotonin caused the depression or whether depression alters the level of neurotransmitters

(+) Antidepressants

  • increases the levels of noradrenaline and serotonin to alleviate the symptoms of depression, supports the influence of biochemicals on mood

(-) Treatment Aetiology Fallacy

  • mistaken idea that the success of a treatment reveals the cause of the disorder
  • if antidepressants work, doesn't mean unipolar is caused by a lack of serotonin

(-) Lag Time Effects

  • antidepressants increase levels of brain chemicals immediately but can take weeks before they alleviate depression
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Biochemical Aetiology of Depression

(-) Lag Time Effects continued... 

  • contradicts the aetiology as challenges the simple direct link between neurotransmitters and depression
  • antidepressants don't work for all patients with low serotonin; similarly those with low serotonin don't always become depressed

(+) Delgado et al (1994)

  • gave depressed patients who were on anti-depressants a special diet that lowered their level of tryptophan (which is suggested to be important in the formation of serotonin)
  • patients returned to former depressed state until change back to normal diet
  • suggests that diet might indirectly influence the production of serotonin and if there's not enough, there are low levels of serotonin, which links to depression = possible to say that environmental factors cause biological effect = unipolar
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Genetic Aetiology of Depression

2. Genetic Aetiology of Depression

  • suggests a link between genetic makeup and unipolar, and the possibility of the presence of unipolar from genetic vulnerability
  • it is assumed that the more closely related you are to someone with depression, the more likely you are to develop it


(+) McGuffin et al (1996)

  • a sample of 177 pairs of twins, at least one had unipolar and being treated
  • found that 46% of the other MZ twin and 20% of the DZ twin had also suffered depression
  • suggests a link between genetic makeup and unipolar as the MZ twins who have identical genetics had a 46% chance of suffering from depression
  • also supports the assumption that being more closely related increases the chance of developing unipolar (100% identical g = 46%, 50% identical g = 20%)
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Genetic Aetiology of Depression

(-) not 100% concordance rate

  • if unipolar was 100% genetic, there should be 100% concordance rate among MZ twins, however McGuffin et al showed it was more likely you wouldn't develop depression if your other MZ twin had it (54%)
  • suggests that although there is a link between genetic makeup and unipolar, there must be other factors (environmental) that contribute to its development

(-) sample sizes

  • McGuffin et al's study had a very small sample size because of the limitations of finding suitable twins and families related to unipolar; the generalisability and population validity is low and restricted

(-) Reductionist

  • the aetiology reduces the cause of a major mental illness to simply being genetics and ignores the idea of environmental factors influencing someone having unipolar
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Genetic Aetiology of Depression

(+) Diathesis-stress model of unipolar

  • the diathesis-stress model of unipolar suggests that depression is not solely linked to genetic factors but a combination of genes and environmental factors
  • the model demonstrates that genes do not determine who will develop depression but if there has been depression within a family, this may leave a genetic vulnerability to depression, which could be triggered by other environmental factors
  • supports aetiology as acknowledges genetics being a factor of unipolar but acting as a vulnerability which is exposed when an environmental factor (such as the death of a family member) occurs
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Seligman's Learned Helplessness Aetiology (1974)

3. Seligman's Learned Helplessness Aetiology (1974)

  • based on classical conditioning principles: learned helplessness occurs when an individual tries but fails to control unpleasant experiences eg. by trying to overcome an unpleasant experience but results in failure, the individual learns not to overcome other things because they believe the attempt is futile even if another situation can be avoided/overcome
  • eg. only so many times someone will try to 'get back on their feet' after a tragic event; if a number of tragic events occur one after the other, it is argued the person will learn that 'getting back on your feet' is pointless and not try; when they can overcome a situation, they don't because they've learnt from past experiences that any actions result in failure


(-) Reductionist

  • behavioural explanation oversimplified as focus is on environmental factors and reduces depression to your past experiences, ignoring the influence of biology
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Seligman's Learned Helplessness Aetiology (1974)

(+) Seligman + Maier (1967)

  • tested "Learned Helplessness" by exposing dogs in hammocks to electric shocks to their hind legs which were unavoidable
  • when exposed later to the same shocks in a cage but this time they had the opportunity to avoid the shocks by jumping over the barrier, the dogs didn't do this, most laid in the corner and whined, loss of appetite and lethargy followed
  • if animal learns its responses are ineffective = learns there is no point in responding again and behaves passively
  • supports theory - S + M generalised this to humans with unipolar = stressful situations may be unavoidable, and LH may occur, which leads to depression including symptoms of lethargy and loss of appetite

(-) HOWEVER...

  • results in further studies haven't replicated results found in S + M's
  • the LH theory and this study doesn't consider cognitive reasons for depression
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Seligman's Learned Helplessness Aetiology (1974)

(+) Maier + Seligman (1976)

  • study on humans, subjecting them to inescapable noise shock/insoluble problems
  • failed to escape from similar situations later where escape was possible
  • supports generalisation of 1967 study and supports the LH theory

(-) No cause-effect

  • causation cannot be inferred as associations haven't been identified: lack of reinforcement in social interactions or helplessness may be a consequence of being depressed rather than a cause

(+) Miller (1977)

  • found that learned helplessness in dogs seemed to occur, then changes in neurotransmitters followed (noradrenaline dropped)
  • suggests experiences cause chemical changes; LH is not solely responsible for depression and may act as a trigger to affect biological chemical changes
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