Biological explanations for depression

  • Created by: Amy
  • Created on: 10-06-13 17:39
using the Maudsley Twin Register, what concordance rates did MacGuffin et al find in MZ twins?
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what concordance rates did they find in DZ twins?
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how do these rates compare to the lifetime risk of getting depression?
they are significantly higher than the risk of the general population
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what is a weakness of this study?
concordance rates are not 100% so suggests there are other factors at work
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why are adoption studies useful?
they are a way of disentangling genetic and environmental factors
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what have most adoption studies shown?
an increased risk in the biological relatives
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what did Wender et al find?
biological relatives were 8 times more likely to have depression
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what is the diathesis stress model?
it claims that having a genetic predisposition to depression will make depression more likely in response to environmental factors
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what are strengths of this?
not reductionist because it focuses on nature and nature, not one. doesn't simplify a complex behaviour
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what did Kendler et al find in their Virginia Twin Study?
women who were genetically predisposed to depression were far more likely to develop depressive symptoms with negative life events than women who had a lower risk of depression
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what are some weaknesses of this study?
gender bias, culture bias
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the low levels of which two neurotransmitters may result in depression?
serotonin and noradrenaline
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what parts of the brain are these neurotransmitters associated with?
parts of the brain involved with reward(pleasure) and punishment
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what part of the brain do these neurotransmitters help regulate?
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what does the hypothalamus control?
physiological arousal and key areas affected by depression: sleep, appetite, sexuality
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how do anti-depressant drugs prove to be a strength for this theory?
they are an effective treatment because they increase the action of serotonin and noradrenaline in the brain; and Reserpine reduces levels of noradrenaline(side effect)
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how are anti-depressant drugs a weakness of this theory?
because drugs exert an immediate effect on neurotransmitter in the brain but it takes several weeks for the person to start feeling better
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what does this suggest?
low levels of serotonin and noradrenaline are an effect rather than a cause of depression
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how is this supported by Seligman's study of dogs?
they're restrained in harness and given electric shocks and cannot escape. they showed symptoms of depression but only after these symptoms occur, neurotransmitter levels drop
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high levels of what hormone are found in depressed people?
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when noradrenaline levels are low, what part of the brain loses its ability to regulate cortisol levels?
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how does post natal depression act as a strength for this theory?
10-15% of women develop postnatal depression after childbirth - suggests ovarian hormones have an effect on depression
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what is a weakness of this point?
majority of women who suffer from postnatal depression already have had bouts of depression. and experience other problems such as being a mother
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people who have suffered strokes and brain damage to what part of the brain are likely to have depression/
frontal lobes
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what is this part of the brain associated with
emotion and motivation
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what did Starkstein and Robinson find in their research of stroke patients?
damage may disrupt noradrenaline and serotonin pathways that connect to the frontal lobes to other brain structures that regulate mood;
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what have brain scans of people who have not suffered from brain damage (but have depression) show?
they have frontal lobe abnormality
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what concordance rates did they find in DZ twins?



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how do these rates compare to the lifetime risk of getting depression?


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what is a weakness of this study?


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why are adoption studies useful?


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