1.2 theories on depression Flashcards
Hopelessness theory
main ideas
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
the expectation that highly desired outcomes will not occur or that highly aversive outcomes will occur and that one cannot change this situation
- hopelessness is a proximal sufficient cause of depressive symptoms
depression occurs based on the way people interpret and make inferences about negative life events
Hopelessness theory
3 kinds of inferences
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
there are 3 kinds of inferences people make when confronted with these situations which contribute to hopelessness and, in turn, depression:
-
causal attributions → neg events are attributed to stable and global causes and viewed as important
- when the causal attribution is internal, stable, and global, hopelessness will be accompanied by lowered self-esteem and dependency - inferred consequences → viewed as likely to lead to other negative consequences
- inferred characteristics → construed as implying that the person is unworthy or deficient
Hopelessness theory
causal chain
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
neg event + neg cognitive style
↓
event specific inferences
(stable-global causes, neg consequences, neg self-characteristics)
↓
hopelessness
↓
symptoms of hopelessness depression
e.g. a student fails a test
- will become depressed if she believes the failure was: due to her low intelligence, will prevent her from getting into med school and/or means that she is worthless
- but will not become depressed if she believes the failure was: due to not studying hard enough, will motivate her to do especially well on the next test and/or has no implications for her self-worth
Hopelessness theory
cognitive style
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
informational cues in the situation + individual differences in cog style, influence people’s inferences about cause, consequence, and self when neg life events occur
cognitive vulnerability-stress component of the theory:
- negative cognitive styles - are the cognitive vulnerability
- negative life events - are the stress
- A cognitive vulnerability in a particular content domain (e.g., for interpersonal events) provides ‘specific vulnerability’ when a person is confronted with negative events in that same domain (e.g., social rejection)
Beck’s theory
main ideas
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
maladaptive self-schemata containing dysfunctional attitudes involving themes of loss, inadequacy, failure, and worthlessness constitute the cognitive vulnerability for depression
these attitudes often involve the theme that one’s happiness and worth depend on being perfect or on other people’s approval
when dysfunctional self-schemata are activated by neg life events (the stress), they generate specific neg cognitions (automatic thoughts)
- take the form of overly pessimistic views of oneself, the world, and the future = negative cognitive triad
Beck hypothesized that his cognitive vulnerability-stress model applies to only some forms of depression, particularly nonendogenous, unipolar depressions
Beck’s theory
causal chain
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
neg event + neg cog schema / dysfunctional attitudes
↓
cog distortions
↓
neg cognitive triad (neg automatic thoughts)
↓
symptoms of depression
Beck’s theory
the role of individual differences
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
differences in the value people place on different kinds of experiences influence whether or not particular neg events will activate the cognitive vulnerability (depressogenic self-schemata) for depression
those high in ‘sociotropy’
- people who value social relationships, intimacy, and acceptance from others
- likely to become depressed when they experience social rejection or interpersonal losses
those high in ‘autonomy’
- people who value independence, freedom, and achievement
- will become depressed when they experience failures related to their personal control
Beck’s theory vs hopelessness theory
similarities
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
both theories emphasize the role of cognition in the origins and maintenance of depression
both include a cognitive vulnerability hypothesis - neg cognitive patterns increase vulnerability to depression when experiencing neg incongruent or highly valued content domains
both propose a mediating sequence of negative inferences that influence whether negative events will lead to depressive symptoms
both recognize the heterogeneity of depression and either explicitly (hopelessness) or implicitly (Beck’s) propose the existence of a cognitively mediated subtype of depression
Beck’s theory vs hopelessness theory
differences
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
hopelessness theory:
- depressive and nondepressive cognition differ in content but not process
- e.g. stable, global vs unstable, specific causal attributions for neg events
Beck’s theory:
- depressive and nondepressive cognition differ not only in content but also in process
- the inference process is ‘schema-driven’ among depressed and ‘data-driven’ among nondepressed
So, Beck’s theory emphasized that depressive cognition is distorted whereas hopelessness theory is silent on the distortion issue
empirical evaluation of hopelessness & beck’s theory
research design for testing the etiological hypotheses of the theories
(Abramson 2002)
Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context
remitted depression paradigm: the cognitive patterns of depressed individuals are examined during the depressed state as well as when it has remitted
- any cognitive pattern not exhibited by previously depressed individuals cannot qualify as a vulnerability for depression
- argued that its not valid
high risk design: involves studying participants who do not currently have the disorder but who are hypothesized to be at high or low risk for developing it
the 6 assumptions of CIIT
assumption 1
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
important functional expressions of personality and psychopathology occur in interpersonal situations
the CIIT conceptualizes psychological functions as a dynamic interaction between self and other
SO, rather than focusing on stable features within individuals, they consider recurrent patterns within interpersonal situations as the basic units of personality and pathology
= encompasses direct in-person interactions and also internal mental representations of interactions
the 6 assumptions of CIIT
assumption 2
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
interpersonal functioning can be organized using the dimensions of agency and communion = interpersonal circumplex
- agency (vertical axis): tendencies to get ahead and be in control vs. tendencies to be passive and seek guidance from others
- communion (horizontal axis): tendencies to get along and be close to others vs. tendencies to be distant and socially aloof
the circumplex helps identify how different patterns of interpersonal behaviour relate to each other
the 6 assumptions of CIIT
assumption 3
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
the same structure (interpersonal circumplex) organises functioning across levels of experience
the circumplex can be used to organise functioning across several levels such as motives, stable traits, specific behaviors, values, sensitivities, etc
accordingly, the circumplex can be used to organise functioning and dysfunction with the same set of variables across levels of human experience
the 6 assumptions of CIIT
assumption 4
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
satisfying agentic and communal motives drives interpersonal behavior:
interpersonal behaviour aims to satisfy agentic and communal motives + individuals differ in their level of motives, giving rise to interpersonal traits
BUT, it is not this variation in levels or nature of motives that characterizes psychopathology, but the degree to which the motives are satisfied and by which methods
other dimentions that are important (other than agency & communion): interpersonal behavior, motives, emotions & perceptions of self and others
the 6 assumptions of CIIT
assumption 5
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
the interpersonal transaction cycle provides expectations for patterns of behaviour and falsifiable predictions about behavioral sequences
the CIIT predicts that dominant behaviour tends to elicit or invite submissive behavior, whereas warm behavior tends to elicit warm behavior
the 6 assumptions of CIIT
assumption 6
(Hopwood et al, 2021)
Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology
sustained deviations from these expected patterns (likely) reflect psychopathology
typical patterns of functioning provide a preliminary basis of comparison for identifying maladaptive functioning
both between and within-person comparisons are important
- between-person tell us about individual differences
- within person tell us about differences due to context
the serotonin theory
The serotonin theory of depression: a systematic umbrella review of the evidence
suggests that lower levels of serotonin (5-HT) within the CNS cause depressive symptoms
in other words, depression is caused by a chemical imbalance in serotonin
5-HT serotonin receptors: dysfunction of serotonin receptors (by reabsorbing serotonin) → results in lower levels of active serotonin → leads to depression
- serotonin is reabsorbed into presynaptic cleft meaning less serotonin in the cleft
serotonin transporter (SERT): higher levels of SERT lowers synaptic levels of serotonin → causes depression
- if there’s a lot of SERT action, serotonin taken away quickly = less serotonin
this is why SSRIs work: blocking the reuptake and transportation of serotonin back into the presynaptic neuron → leads to more serotonin available → leaving serotonin for as much/long as possible in cleft
results
serotonin & 5-HIAA
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
5-HIAA = a substance formed by the breakdown of serotonin
a study found lower levels of plasma serotonin in women with depression BUT it did not reach statistical significance after adjusting
analyses revealed that antidepressants were strongly associated with lower serotonin levels independently of depression
two meta-analyses of 5-HIAA in CSF found no evidence of an association between 5-HIAA concentrations and depression
results
serotonin receptors
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
5-HT1a receptors = auto-receptors which inhibit the release of serotonin presynaptically
- THUS, if depression is the result of reduced serotonin activity caused by abnormalities in the 5-HT1a receptor, people with depression would be expected to show increased activity of these receptors compared to those without
majority of results showed:
- no difference in these receptors between controls and depressed individuals
- a lower level of these inhibitory receptors → this would imply higher concentrations/activity of serotonin in depressed individuals
results
serotonin transporter (SERT)
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
if depression is caused by low serotonin activity or availability, and if SERT is the origin of this, then the amount of SERT would be expected to be higher in people with depression
research is mixed, mostly based on animal studies
results
tryptophan depletion studies
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
tryptophan depletion is thought to reduce serotonin levels
studies involving people diagnosed with depression showed slightly greater mood reduction following tryptophan depletion
more recent studies conducted on healthy volunteers showed no effects of tryptophan depletion on mood
no convincing effects of depletion → mixed results
results
SERT gene and gene-stress interactions
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
there could be a link between depression and 5-HTTLPR (polymorphism in the promoter region of the SERT gene)
the short version of this may only give rise to depression in the presence of stressful life events
results are mixed → some studies have found a significant association, while two recent large, high quality studies did not find an association
conclusion
(Moncrieff et al, 2022)
The serotonin theory of depression: a systematic umbrella review of the evidence
there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity
most studies found no evidence of reduced serotonin activity in people with depression
critiques of Moncrieff
non-novelty of main finding
(Jacobsen, 2023)
Serotonin and depression - an alternative interpretation of the data in Moncrieff et al
Moncrieff’s conclusion that depression is not generally linked with serotonin deficiency is not new information to neuropharmacologists
this has been a topic of discussion in the field since at least 1986
