Abnormal - analyse etiologies of depression Flashcards
1
Q
etiology
A
- scientific study of causes/origins of disorders or abnormal behaviour
- important because of the idea that treatment should be related to the cause of the disorder (i.e. if the disorder is caused by biological factors, a biomedical approach to treatment should be used)
2
Q
biological etiologies
A
- evolutionary theory (Hagen et al., 2004)
- genetic predisposition (Kendler et al., 2006)
- serotonin hypothesis (Coppen, 1967)
- cortisol hypothesis
3
Q
biological etiologies: evolutionary theory
A
Hagen et al. (2004):
- depression signals need/attention
- to elicit help from members of the group
- however, like all evolutionary theories this is impossible to test experimentally
4
Q
biological etiologies: genetic predisposition
A
Kendler et al. (2006):
- massive twin study on 42000 participants
- found that concordance rates among monozygotic twins of 44% for female and 31% for male, while dizygotic twins exhibited 16% for female and 11% for male
- if the disorder were purely genetic, we might expect the monozygotic concordance rates to be much higher
- but the difference between monozygotic and dizygotic concordance rates is enough to indicate a strong genetic component
5
Q
biological etiologies: evaluation of genetic predisposition
A
- some evidence for genetic predisposition (Kendler et al., 2006)
- but depression is a complex disorder
- environmental factors (e.g. stress) also play an important role
6
Q
biological etiologies: serotonin hypothesis
A
Main idea: depression is caused by low serotonin levels (Coppen, 1967)
- supported by the effectiveness of the drug Prozac, which improves mood by inhibiting serotonin reuptake
7
Q
biological etiologies: against serotonin hypothesis
A
- short alleles of the 5-HTT gene also inhibits serotonin reuptake like Prozac, but its carriers are more likely to suffer depression
NOTE: Levinson (2005) argues that the 5-HTT gene simply makes individuals more sensitive to stressful life events, and doesn’t necessarily cause depression
Sarek (2006): tianeptine, a drug used in Europe and South America to treat depression, enhances serotonin reuptake…
Lacasse and Leo (2005):
- lack of evidence that low serotonin causes depression
- the effectiveness of a treatment doesn’t imply a causal effect (e.g. aspirin alleviates headaches, but headaches are not caused by a lack of aspirin)
8
Q
biological etiologies: evaluation of serotonin hypothesis
A
- some evidence that serotonin may be involved in depression (effect of Prozac)
- but research doesn’t show a clear link between serotonin and depression
- see how short allele of 5-HTT gene and Prozac generally has same biological effect but opposite physiological effect
- there may be a confounding variable we are unaware of
9
Q
biological etiologies: cortisol hypothesis
A
- the stress hormone cortisol may play a role in the development of depression
- particularly high cortisol levels appears to have damaging effects on a developing brain
- Burke et al (2005): cortisol activity differs between depressed and non-depressed – non-depressed’s cortisol levels rise and fall rapidly during and after stressful situations, but depressed’s cortisol levels remain high for longer after stressful situations
- Cutuli et al. (2010): significant correlation between high levels of cortisol and a history of negative life events
10
Q
evaluation of biological etiologies
A
- lots of evidence of physiological correlations to mental state
- but we don’t have a clear understanding of how depression might develop biologically
- still need to research more about interactions between stressful life events, genes, hormones, and neurotransmitters
11
Q
cognitive triad
A
Beck (1976):
- depression is caused by a cluster of negative thoughts in 3 categories: the self, the world, and the future
- these thoughts form a vicious cycle of negative automatic thoughts
- the triad is perpetuated by cognitive biases like over-generalization (about negative aspects, e.g. “I never do well in tests”), polar reasoning (i.e. does not take any ambiguities), and selective abstraction (i.e. only focusing on the negatives)
- contradicts traditional depression theories: negative thinking is typically considered to be a symptom of depression, not the cause
cognitive triad in action: self (“I’m not good at anything”) → world (“Everyone hates me because I’m worthless”) → future (“I’ll never be good at anything because everyone hates me”) → repeat
12
Q
evaluation of cognitive triad
A
Strengths:
- descriptively very powerful
- Robins and Block (1989): depressed people have negative thinking styles
- Lewinshohn et al. (2001): negative thinking and high stress levels often preceded the onset of depression
- Boury et al. (2001): there is a significant correlation between amount of negative automatic thoughts and the severity of depression (BUT they also note that correlation =! causation)
- treatment: Beck’s cognitive triad resulted in the creation of CBT (cognitive-behavioural therapy)
Weaknesses:
- Boury et al. (2001): correlation =! causation
- no explanations: unclear whether this model reflects cause of depression or simply disordered thinking
- Taylor and Brown (1988): depressed people interpret events more realistically
13
Q
sociocultural etiologies
A
- unemployment/poverty (Brown and Harris, 1978)
- social inequality
- individualist vs collectivist
14
Q
sociocultural etiologies: unemployment/poverty
A
Brown and Harris (1978):
- interviewed 450 London women
- unemployed single mothers who lacked social support were most likely to undergo depression
- thus Brown and Harris identified 3 vulnerability factors: unemployment/poverty, lack of social support, and social responsibilities (e.g. children to take care of)
15
Q
sociocultural etiologies: evaluation of unemployment/poverty
A
- received much support on vulnerability factors
- but it can be argued that the factors are unlikely to be responsible for creating feelings of sadness, only propagating it
