1.2 theories on depression Flashcards

1
Q

Hopelessness theory

main ideas

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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2
Q

Hopelessness theory

3 kinds of inferences

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

there are 3 kinds of inferences people make when confronted with these situations which contribute to hopelessness and, in turn, depression:

  1. 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
  2. inferred consequences → viewed as likely to lead to other negative consequences
  3. inferred characteristics → construed as implying that the person is unworthy or deficient
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3
Q

Hopelessness theory

causal chain

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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4
Q

Hopelessness theory

cognitive style

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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)

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5
Q

Beck’s theory

main ideas

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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6
Q

Beck’s theory

causal chain

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

neg event + neg cog schema / dysfunctional attitudes

cog distortions

neg cognitive triad (neg automatic thoughts)

symptoms of depression

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7
Q

Beck’s theory

the role of individual differences

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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8
Q

Beck’s theory vs hopelessness theory

similarities

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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9
Q

Beck’s theory vs hopelessness theory

differences

(Abramson 2002)

Cognitive vulnerability-stress models of depression in a self-regulatory and psychobiological context

A

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

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10
Q

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

A

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

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11
Q

the 6 assumptions of CIIT

assumption 1

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

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12
Q

the 6 assumptions of CIIT

assumption 2

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

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13
Q

the 6 assumptions of CIIT

assumption 3

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

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14
Q

the 6 assumptions of CIIT

assumption 4

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

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15
Q

the 6 assumptions of CIIT

assumption 5

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

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16
Q

the 6 assumptions of CIIT

assumption 6

(Hopwood et al, 2021)

Six assumptions of contemporary integrative interpersonal theory of personality & psychopathology

A

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

17
Q

the serotonin theory

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

18
Q

results

serotonin & 5-HIAA

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

19
Q

results

serotonin receptors

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

20
Q

results

serotonin transporter (SERT)

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

21
Q

results

tryptophan depletion studies

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

22
Q

results

SERT gene and gene-stress interactions

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

23
Q

conclusion

(Moncrieff et al, 2022)

The serotonin theory of depression: a systematic umbrella review of the evidence

A

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

24
Q

critiques of Moncrieff

non-novelty of main finding

(Jacobsen, 2023)

Serotonin and depression - an alternative interpretation of the data in Moncrieff et al

A

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

25
Q

critiques of Moncrieff

serotonin biology and pharmacology misunderstandings

(Jacobsen, 2023)

Serotonin and depression - an alternative interpretation of the data in Moncrieff et al

A

Moncrieff is unfamiliar with serotonin biology and pharmacology and makes factual errors, in addition to selective choosing quotes in cited literature

specifically, they make misinterpretations regarding serotonin reuptake inhibitor antidepressants, which could lead to misconceptions among general practitioners and the public

26
Q

critiques of Moncrieff

heterogeneity of depression

(Jacobsen, 2023)

Serotonin and depression - an alternative interpretation of the data in Moncrieff et al

A

this critique emphasises the complexity and heterogeneity of depression, suggesting that no single biological anomaly, including those related to serotonin, consistently aligns with depression

the effectiveness of a therapy does not necessarily depend on correcting a primary biological anomaly

Moncrieff did not take this fundamental fact into consideration

27
Q

critiques of Moncrieff

specific issues with Moncrieff et al’s review

(Jacobsen, 2023)

Serotonin and depression - an alternative interpretation of the data in Moncrieff et al

A

mischaracterization of 5-HT1A receptors

speculative interpretations

misunderstanding of antidepressant effects

28
Q

critiques of Moncrieff

a depleted account of tryptophan depletion

(Jauhar, 2023)

A leaky umbrella has little value: evidence clearly indicates the serotonin system is implicated in depression

A

Moncrieff omitted data from a study which showed effect of tryptophan in people with MDD

they claimed that studies on those with MDD showed slightly greater mood reduction following tryptophan, but that these were taking antidepressants and the sample was small
HOWEVER, in the study they refer the sample of individuals not taking antidepressant was large, and so was the effect size (of depression reduction after tryptophan)

he gives the impression that tryptophan has no effect

29
Q

critiques of Moncrieff

simplistic (mis)interpretation of molecular imaging evidence

(Jauhar, 2023)

A leaky umbrella has little value: evidence clearly indicates the serotonin system is implicated in depression

A

authors make the simplistic interpretation that reduced binding suggests increased synaptic 5-HT → it could result of several factors

authors mistakenly assumed that 5HT(1A) receptors are exclusively presynaptic autoreceptors → in reality, most are postsynaptic heteroreceptors

30
Q

critiques of Moncrieff

an uncertain approach to SERT binding

(Jauhar, 2023)

A leaky umbrella has little value: evidence clearly indicates the serotonin system is implicated in depression

A

Moncrieff oversimplifies by making the assumption that lower SERT binding is always associated with higher synaptic 5-HT

Moncrieff suggests that the reason for this reduced SERT is due to prior antidepressant treatment

it has been found that almost all effective antidepressants have an effect on the 5-HT system, and 5-HT agonist remains one of the main mechanisms for the antidepressant qualities of psychedelics - against Moncrieff’s conclusions