This is a summary of 3.4 Affective Disorder. Some of the literature might differ as this is based on literature used during covid and online tutorials. I added tables to summarise the main points which really helped me for the exam, I hope it helps you too!
- (1) What is depression?
- Symptoms, diagnosis, risk factors
- How does it develop?
- How can it be distinguished from ‘normal’ sadness?
- -> Focus on conclusions – basic evidence
- (2) Cognitive models Beck & Abramson
- How do the models differ?
- How do they explain depression?
- What types of treatments do they recommend?
- (3) What is electroconvulsive therapy (ECT)?
- What are pros & cons + side effects?
- -> No need for specific names of anti-depressants -> focus on class/type of these
Don’t focus on specific stuffs between subtypes of anti-depressants
Look at limitations of article in general
Focus on effectiveness of interventions (most important – basic findings)
- (4) How does depression affect brain activity?
- Is it similar to chronic pain?
- What are the neural mechanisms of depression? How is the imbalance of hormones
related to depression?
- KW = dopamine, norepinephrine, serotonin
- -> Don’t focus on exact brain locations
Focus on functional neurons (≠ dif between white & grey) – general units
Keep intro points in mind for Kaiser (checklist)
- !! Subtypes + criteria of depression + prevalence (WHO doc)
Part 1:
Reading 1: World Health Organisation (2017) – Depression and common mental disorders
• DEFINITION:
o Depressive disorders = sadness, loss of interest/pleasure, feelings of guilt, low self-
worth, disturbed sleep/appetite, feelings of tiredness, poor concentration
Can be long-lasting OR recurrent
o 2 major sub-categories:
Major depressive disorder/depressive episodes -> mild to severe
Dysthymia -> chronic form of mild depression – less intense than depressive
episodes but similar
• 2 years + no stop for over 2 months
• GLOBAL & REGIONAL ESTIMATES OF PREVALENCE:
o Prevalence in world = 4.4% in 2015 (= 322 million people)
More common in females (5.1%) > males (3.6%)
Variation from 2.6% in Western Pacific to 5.9% in African regions
Peak in older adults (55-74 years) – 7.5% in F & 5.5% in M
• Lower in under 15 years
Increase of 18.4% between 2005 and 2015
1
,• GLOBAL & REGIONAL ESTIMATES OF HEALTH LOSS:
o Years Lived with Disability (YLD) + Years of Life Lost (YLL) + Disability-Adjusted Life
Years (DALYs) => Global Burden of Disease (GBD)
Depressive disorders = over 50 million YLD
• Often in low/middle-income countries
Ranked as largest contributor to non-fatal health loss
2
,Part 2:
Reading 2: Abramson (2002): Cognitive vulnerability-stress models of depression in self-regulatory
and psychological context
• INTRODUCTION:
o Neglect of depression until 1970s
o Beck = psychiatrist -> cognitive theory (≠ psychoanalytic)
Emphasis on negative automatic thoughts
o Seligman also made a new model/theory -> emphasis on maladaptive cognitions
o Cognitive approaches to depression
1. Info-processing – social cognition
2. Cog processed mediate emotional reactions (through thoughts)
3. Psychoanalytic seems untestable – less popular now
• ≠ The 2 new theories are testable
4. Questioning of purely behavioural stuff on psych phenomena
• TWO COGNITIVE THEORIES OF DEPRESSION:
• Overview:
o Vulnerability to depression to meaning/interpretation people give to their
experiences
Explains why cognitive therapy works so well
• Hopelessness Theory (Abramson, 1989):
o Cause = expectation of no desired outcomes and many aversive outcomes +
hopelessness (can’t do anything about it)
Hopelessness Depression (HD)
o Negative life event + 3 kinds of inferences = lead to HD
Causal attribution – inferred consequences – inferred characteristics of self
= + attribute stable & global causes / likely to lead to other negative
consequences / imply person is unworthy
E.g. fail test + assume it’s due to low IQ + will prevent her from getting into uni +
means she is worthless
o Individual differences cognitive vulnerability (negative cognitive styles) + stress
(negative life event)
Cognitive vulnerability-stress interaction
Social support can help
3
, • Material, emotional, informational support
• Can give adaptive inferential feedback
• Beck’s Theory (1983-1987):
o Cause = maladaptive self-schemata
Idea that one’s happiness/worth depends on being perfect OR other’s
approval
Not triggered when no negative event
o Only applies to some forms of depression (nonendgenous, unipolar)
o High sociotropy = value social relationships + intimacy + acceptance
With social rejection/interpersonal loss Neg cog triad = D
o ≠ High autonomy = value independence + freedom + achievement schemas -> alter info
When experience failure or threat to personal control into neg thoughts of
self
• Comparison of the two theories – similarities & differences:
o Similarities = cognition leads to & maintains D
Cognitive vulnerability hypothesis (neg cog patterns = high risk)
Mediator between neg event & depressive symptoms
Heterogeneity of depression – existence of subtype of depression
• H theory -> explicitly
• B theory -> implicitly
o Difference =
Cognitive processes Cognitive products
Operation of cog system – e.g. retrieval End result of the cog system – thoughts
experienced
B theory -> H theory + B theory
H theory -> depressive vs non-depressive cognition differ in content (≠ process)
B theory -> depressive vs non-depressive cognition differ in content + process
• D = schema-driven – influenced in making negative inferences -> distorted
• Non-D = data-driven
• EMPIRICAL EVALUATION OF THE THEORIES:
o 5 central predictions
1. Cog vulnerability will moderate effect of negative event on depression
2. Mediating link (hopelessness or neg cog triad) between life event & D
3. Causal chains leading to particular subtype of D (e.g. HD)
4
, 4. Match between cog vulnerability (e.g. achievement) & event = D
5. B theory -> depressive cog is distorted
• Research designs for testing these:
o 1) Remitted depression paradigm
= Examine cog patterns of depressed people + when they are cured
If H is correct, the cog pattern should be personal – so stay the same
Based on error assumption that cog vulnerability is immutable
o Behavioural high-risk design
= Study participants who don’t have the disorder but are hypothesized to be
at high or low risk of developing it
• Compare these two groups (prospective – future + retrospective)
• Prospective is more powerful -> cog vulnerability may be scar of prior
D episode in retrospective (≠ causal factor)
• (2) Etiological hypotheses featured in hopelessness theory:
o Strong link proven between cog vulnerability & D
But don’t know which cause which
o Studies with high-risk design -> found cog vulnerability leads to D
Need more research on hopelessness as a mediator
Higher risk with academic > interpersonal + low grade
• (3) Hopelessness depression subtype hypothesis:
o Proof cog vulnerability + stress = HD
o HD stands out statistically from other depressive symptoms
• (3) Etiological & nonendogenous subtype hypothesis – Beck’s theory:
o Cog vulnerability -> depression-specific neg thoughts -> stress
o Sociotropic -> some found D after neg interpersonal event (+ neg achievement)
Autonomous -> less strong support – D with neg achievement (≠ interper)
o Cog vulnerability-stress + mediating components => nonendogenous subtype
• The cognitive vulnerability to depression project:
o Cognitive Vulnerability to Depression (CVD) Project -> used retrospective +
prospective behavioural high-risk design
Tested cog vulnerability + B’s theories of D + other hypotheses in depressive
symptoms + clinically depressed
Followed uni students for 2.5 + 3 years
-> Support for cog vulnerability hyp (retro + pro)
• High Risk with prior D = more likely to redevelop it than LR
• HR = higher suicidality
=> Cog vulnerability risk of onset + recurrence of D
• Also support for specific subtype HD
o Cog vulnerability (= neg cog style – H theory + dysfunctional attitudes – B theory)
o Tritration model of cog vulnerability-stress
= Low levels of stress are enough to trigger depression in HR people
• Need high levels in non-vulnerable people
• Beck’s cognitive distortion hypothesis:
o B = thought non-D were less susceptible to illusion
o ≠ Depressive realism effect -> people with D are more accurate than non-D
Non-D = illusion of control
Accuracy ≠ normal cog functioning baseline
Suggestions to alter the theory -> emphasis on content dif > process
5
, • HOW WELL CAN THE COGNITIVE THEORIES EXPLAIN THE “BIG FACTS” OF DEPRESSION?
o There are undisputed facts about depression -> how well do the cog theories explain
them?
1. Depression is recurrent
• Some are more prone -> consistent with cog vulnerability hyp +
findings from CVD Project (neg cog styles = D)
• Underlying processes of 1st & recurrent D ≠ identical
o Some predictors are stronger for recurrence than 1st
2. Life events play a role in D development
• Cog vulnerability-stress component of cog theories
3. D can be lethal – increased risk of suicide
• Hopelessness = key factor
• CVD -> cog vulnerable people –> hopelessness –> suicidality
4. D is a common disorder
• So typical (≠ rare) factors cause D
o Neg life events are common
o D people don’t have rare cog processes -> they differ in cog
content from non-D
5. Rates of D increase from middle to late adolescence
• Rise in neg life event (= stressor of cog vulnerability-stress)
o Cog vulnerability developed/implemented in late childhood
o Contributes to hopelessness
6. Gender differences in D in adults
• 2x more W than M
• W also show higher scores in 2 features of hopelessness chain theory
o Neg life events (interpersonal) + neg cog styles
o => More vulnerable to cog vulnerability-stress
• M show greater dysfunctional attitudes (cog vul in B theory)
o May be more adaptive (e.g. perfectionism + high ability ->
balance out)
o Low self-efficacy + low ability = more maladaptive
7. D is heterogeneous + multiple causes
• D subtypes in cog theories
o Cog theories meet the explanatory requirement
6
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