Depression Part 1 Flashcards
1
Q
What are the key symptoms of depressive disorders as defined by WHO (2017)?
A
- Loss of interest
- Feeling low
- Insomnia or hypersomnia
- Increased or decreased appetite
- Lack of focus
- Feelings of worthlessness and guilt
- Lack of energy
2
Q
What are the two main categories of depressive disorders?
A
- Major Depressive Disorder/Depressive Episode
- Symptoms: diminished interest, low mood, reduced energy levels.
- Classified as mild, moderate, or severe.
- Dysthymia
- Chronic, persistent mild depression.
- Symptoms are longer-lasting but less intense than a depressive episode.
3
Q
What impact does depression have on an individual’s life?
A
- Functional impairment in school, work, or daily life.
- Can be long-lasting or repetitive.
- May lead to suicide.
4
Q
How significant is depression globally according to WHO (2017)?
A
- Main contributor to global disability.
- Significant role in the prevalence of suicide-related deaths.
- Affects more than 300 million people (4.4% of the world’s population).
- Numbers are increasing, especially in low-income countries.
5
Q
What are the two main common mental disorders?
A
- Depressive disorders
- Anxiety disorders
Characteristics: Varying duration and severity, influence on emotional states, and common occurrence.
6
Q
What factors can increase the risk of depression?
A
- Stressful life events (e.g., illnesses, unemployment, poverty, substance use, deaths of loved ones).
7
Q
What is the global prevalence of depression?
A
- More prevalent in women.
- Less common in older age, even lower in adolescents and children under 15.
- More frequent in low- and middle-income countries.
8
Q
What is the relationship between suicide and depression?
A
- Suicide accounts for 1.5% of deaths globally.
- Common in ages 15–29.
- Suicide frequency varies by sex, region, and income level.
9
Q
How does ICD-11 define depression?
A
Depression is a condition with clinically identifiable symptoms and observed behaviors related to distress and disturbance of personal functions.
10
Q
What are the diagnostic criteria for depression according to ICD-11?
A
- At least 5 symptoms from a list of 10.
- Symptoms must be present most of the day, nearly every day, for at least 2 weeks.
- Symptoms must negatively affect personal functioning.
Exclusions:
* Not due to another medical condition.
* Not caused by medication or substances.
* Not better explained by grief or mourning.
11
Q
What is the unique symptom in ICD-11 not present in DSM?
A
“Hopelessness about the future,” a strong indicator distinguishing people with and without depression.
12
Q
What are subthreshold depressions, and why are they significant?
A
- Cases with fewer than 5 symptoms but similar outcomes as diagnosed depression.
- Outcomes include psychiatric comorbidity, future depressive episodes, and personal functioning issues.
- Highlights the need for alternative diagnostic approaches.
13
Q
What are two alternative solutions for addressing subthreshold depression?
A
- At least 1 main symptom (loss of pleasure or depressed mood) for at least 2 weeks.
- Any 2 depressive symptoms for at least 2 weeks, with evidence of social impairment.
14
Q
What is the Patient Health Questionnaire (PHQ-9)?
A
- A self-reported questionnaire based on the DSM.
- Assesses 9 symptoms of depression.
- Scored on a 4-point Likert scale to evaluate severity.
15
Q
What distinguishes complicated depression from uncomplicated depression?
A
Complicated Depression includes at least 1 of the following symptoms:
* Suicidal ideation
* Feelings of guilt or worthlessness
* Psychotic symptoms
* Functional impairment –> moet volgens mij psychomotorische retardatie zijn.
Het hebben van een functionele beperking is een DSM-V voorwaarde om de diagnose MDD te krijgen.
16
Q
How do descriptors aid in diagnosing depression in ICD and DSM?
A
Descriptors like psychotic features, melancholia, and atypical features refine diagnosis rather than serving as separate categories.
17
Q
What are some characteristics and research biases in depression?
A
- More common in women.
- Most research comes from high-income, English-speaking countries, leading to cultural biases.
- Common comorbidities: substance use, anxiety, chronic physical disorders (e.g., diabetes, cardiovascular disease).
- Majority of suicide victims had depression
18
Q
What areas of functioning are impacted by depression?
A
- Early study discontinuation.
- Decreased personal income.
- Increased likelihood of intimate partner violence (males).
- Adverse effects on children of depressed parents (e.g., anxiety, health complications).
- Isolation for caregivers of depressed individuals.
19
Q
What are protective factors against depression?
A
- Social support
- Personality characteristics
- Personal interests
Risk factors include forced migration and pessimistic attitudes toward depression.
20
Q
What is depression literacy, and why is it important?
A
- Understanding strategies to achieve and maintain positive mental health and depression treatments.
- Improves help-seeking behavior, adherence to treatment, and reduces stigma.
21
Q
What challenges do countries face in managing depression?
A
- Insufficient resources.
- Lack of skilled providers.
- Underfunded mental health care systems.
22
Q
What are the core diagnostic criteria for depression in ICD-11 and DSM-5?
A
At least 5 symptoms present for most of the day, nearly every day, for at least 2 weeks.
One symptom must be low mood or decreased interest/pleasure.
Symptoms include:
* Low mood
* Decreased interest/pleasure
* Lack of focus/indecisiveness
* Feelings of guilt/worthlessness
* Suicidal ideation
* Changes in appetite/weight
* Insomnia/hypersomnia
* Energy loss/tiredness
* Functional impairment
23
Q
What are the three classes of depressive symptoms in ICD-11?
A
- Cognitive-behavioral
- Neurophysiological
- Affective
Note: These divisions are for clinical convenience and lack empirical support.
24
Q
What are the two traditional clinical subtypes of depression?
A
- Melancholic Depression (autonomous): Thought to stem from biological disruption.
- Lack of pleasure and movement-related activity.
- Non-Melancholic Depression (situational): Arises from situational factors.
25
What are the DSM-5 criteria for depression with melancholic features?
Lack of reaction to positive stimuli.
Loss of pleasure in almost all activities.
Plus at least 3 of the following:
* Depression worse in the morning.
* Early morning awakening.
* Excessive guilt.
* Significant weight loss/anorexia.
* Decreased movement-related activity.
26
What defines psychotic depression?
* Presence of hallucinations or delusions during depressive episodes.
* Psychotic symptoms are absent outside depressive episodes.
* Associated with increased suicide risk and higher likelihood of death from biological causes.
27
What defines mixed depression?
At least 3 manic symptoms present (e.g., elevated mood, racing thoughts, increased energy, grandiosity).
Not included in ICD-11.
Associated with:
* Increased anxiety and suicide risk.
* Substance use and impaired functioning.
* Poor response to treatment.
28
What defines anxious depression?
At least 2 of the following symptoms:
* Feeling strained.
* Excessive anxiety.
* Fear of something bad happening.
* Difficulty focusing due to worry.
* Feeling out of control.
Associated with chronicity, suicidal ideation, poor performance, and reduced quality of life.
29
What is seasonal depression, and what are its common symptoms?
Linked to seasonal patterns (spring/summer or autumn/winter).
Common symptoms:
* Excessive eating.
* Carbohydrate cravings.
* Hypersomnia.
30
How do DSM-5 and ICD-11 classify depression severity?
DSM-5:
* Mild: Manageable symptoms, slight impact on functioning.
* Moderate: Between mild and severe.
* Severe: Unmanageable symptoms, significant functional impairment.
ICD-11:
* Mild: Intense symptoms absent, some challenges in functioning.
* Moderate: More intense symptoms, greater impairment.
* Severe: Most symptoms present, significant impairment in all areas.
Note: Suicidality is not a determinant of severity in either manual.
31
What is the Five Factor Model (FFM) of personality, and how does it relate to depression?
The FFM includes:
* Extraversion/introversion
* Openness to experience/unconventionality
* Agreeableness/antagonism
* Neuroticism: Linked to increased risk of depression due to sensitivity to stress and negative emotional responses.
* Conscientiousness/disinhibition
32
What is the cognitive triad in depression?
People with depression often have a negative view of:
1. The world.
2. Themselves.
3. The future.
33
What are common health comorbidities and risks associated with depression?
* Metabolic conditions: Hypertension, obesity, insulin resistance.
* Chronic diseases: Cardiovascular issues, anxiety.
* Depression is a risk factor for cardiovascular disease and is associated with reduced immunity.
34
What are the two cognitive theories of depression discussed in Abramson et al. (2002)?
1. Hopelessness Theory
2. Beck’s Theory
35
What is the central idea of the Hopelessness Theory?
Depression arises from a belief of having no control over situations where favorable outcomes are unlikely or unfavorable outcomes are expected. This leads to hopeless depression (HD) symptoms.
36
What are the symptoms of hopeless depression (HD)?
* Sadness
* Sleep disturbance
* Lack of concentration
* Lack of energy
* Negative cognitions
* Suicidality
* Reduced cognitive and motor functioning
37
What are the key inferences in the Hopelessness Theory that lead to hopelessness?
1. Stable and global attributions: Negative events are persistent and affect many life areas.
2. Belief in further negative outcomes.
3. Negative view of self: Unworthiness or inadequacy.
38
What is an example of hopelessness leading to depression?
A student fails a test and believes:
* “I have low intelligence” (stable and global attribution).
* “I won’t get accepted to a university” (extreme negative consequence).
* “I’m insignificant” (negative self-view).
39
What is the cognitive vulnerability-stress component of Hopelessness Theory?
* Cognitive vulnerability: Negative inferential style (depressogenic thinking).
* Stress: Negative life events.
* Interaction between the two leads to hopelessness and depression.
40
What is the central idea of Beck’s Theory?
Depression results from dysfunctional self-schemas activated by negative life events, leading to the negative cognitive triad:
1. Negative views of self.
2. Negative views of the world.
3. Negative views of the future.
41
How do sociotropy and autonomy relate to Beck’s Theory of depression?
Sociotropy: Vulnerability to depression from interpersonal losses and social rejection.
Autonomy: Vulnerability to depression from threats to independence and personal control.
42
What are the similarities between Hopelessness Theory and Beck’s Theory?
Both emphasize the role of cognition in depression.
Both highlight cognitive vulnerability and stress as triggers.
Both suggest that negative inferences mediate depression.
Both propose depression can be cognitively mediated.
43
What are the differences between Hopelessness Theory and Beck’s Theory?
Focus on cognitive processes vs. products:
* Hopelessness Theory focuses on cognitive products (content of thoughts).
* Beck’s Theory focuses on both cognitive processes and products.
Schema-driven vs. data-driven inference:
* Beck’s Theory suggests depressed individuals use schema-driven processing.
* Hopelessness Theory does not distinguish processes.
44
What are the five main predictions of both cognitive theories?
1. Interaction between cognitive vulnerability and stress leads to depression.
2. A mediating link (hopelessness or negative cognitive triad) between stress and depression.
3. Both theories propose specific depression subtypes (e.g., hopeless depression).
4. A match between cognitive vulnerability content and stressor content increases depression likelihood.
5. Beck’s theory emphasizes distorted cognition, while Hopelessness Theory does not.
45
How does the Hopelessness Theory describe the role of cognitive vulnerability in the absence of negative life events?
People with negative cognitive styles (depressogenic inferential style) DO experience more depression when negative life events do not occur.
46
What is an example of a negative cognitive schema in Beck’s Theory?
“I am nothing if a person I love doesn’t love me!”
This dysfunctional schema leads to automatic negative thoughts during negative life events.
47
How does Beck’s Theory define cognitive vulnerability in depression?
Cognitive vulnerability arises from dysfunctional self-schemas that generate negative automatic thoughts in response to stress.
48
What role does stress play in both cognitive theories of depression?
* Stress activates cognitive vulnerabilities.
* Interaction with stress leads to depressive symptoms.
* Importance of the stressor is based on individual values (e.g., sociotropy vs. autonomy).
49
What is the Contemporary Integrative Interpersonal Theory (CIIT)?
CIIT is a model of personality and mental disorders emphasizing how individuals interact with others. It highlights recurring interpersonal patterns as the core of personality and psychopathology, rather than stable individual traits.
50
What is the first assumption of CIIT?
Personality and mental health issues are shown through interpersonal interactions.
* These include face-to-face interactions and internal mental interactions.
Example: Feeling depressed after not receiving a promotion can involve interpersonal conflict (e.g., disappointment with others) and unmet self-expectations.
51
What dimensions does CIIT use to organize interpersonal functioning? (second assumption)
1. Agency: Assertiveness vs. passivity.
2. Communion: Emotional closeness vs. social reserve.
These dimensions form the interpersonal circumplex (agency on the vertical axis, communion on the horizontal axis) to differentiate disorders and interpersonal behaviors.
52
What does the interpersonal circumplex illustrate? (third assumption)
It organizes interpersonal functioning across levels:
* Motives
* Stable traits
* Specific behaviors
The circumplex helps measure problems, values, strengths, and sensitivities, offering insights across different experiences.
53
What motivates interpersonal behavior according to CIIT? (fourth assumption)
Interpersonal behavior is driven by the need to satisfy agentic and communal motives.
* These motives vary between individuals and situations.
* Satisfying or failing to satisfy these motives affects psychopathology.
54
How does the CIIT model explain interpersonal conflicts in psychopathology?
Example: Passive-aggressive personality disorder
* Perceives manipulative dominance.
* Conflict arises between agency (control) and communion (connection).
* Resolves by showing non-compliant behavior, provoking negative responses that reinforce the pattern.
55
What is the interpersonal transaction cycle in CIIT? (fifth assumption)
* Dominant behavior typically triggers submissive behavior.
* Warm behavior tends to elicit warm behavior in return.
This cycle helps predict interpersonal behavior patterns based on perception, motivation, affect, and behavior.
56
What do deviations from the interpersonal transaction cycle indicate? (sixth assumption)
Deviations suggest psychopathology, revealing:
* How a patient differs from others (between-person comparisons).
* Contexts that trigger symptoms (within-person comparisons).
57
How can interpersonal styles vary within the same diagnosis?
Variations in interpersonal styles among individuals with the same disorder can identify symptom triggers, internal experiences, and tailored therapy approaches.
58
What is an example of how CIIT guides therapy for depression?
Failure-focused depression: Struggles with dominance-submission. Therapy should enhance agency and provide opportunities for success.
Rejection-focused depression: Struggles with warmth-coldness. Therapy should focus on communion and provide a supportive, warm environment.
59
What makes CIIT useful for understanding personality and psychopathology?
* Focuses on dynamic interpersonal patterns rather than stable traits.
* Integrates motives, traits, and behaviors to explain mental health and personality.
* Allows predictions about behavior and psychopathology using the interpersonal circumplex.
60
What is the serotonin theory of depression? (Moncrieff et al. (2022))
The serotonin theory posits that abnormalities in serotonin levels or function contribute to depression, supporting the use of antidepressants to correct these imbalances.
61
What are alternative explanations for antidepressant effects? (Moncrieff et al. (2022))
1. Placebo effect: Antidepressants may work due to increased patient expectations.
2. Blunting emotions: Antidepressants might limit emotional responses rather than directly addressing depression.
62
What are the six areas of evidence reviewed for the serotonin hypothesis? (Moncrieff et al. (2022))
1. Serotonin and serotonin metabolite (5-HIAA) levels in body fluids.
2. Serotonin receptor levels in people with depression.
3. Serotonin transporter (SERT) levels in depression.
4. Effects of tryptophan depletion on mood.
5. SERT levels measured through imaging or post-mortem studies.
6. SERT gene-environment interactions (e.g., gene-stress interactions).
63
What evidence exists about serotonin and 5-HIAA levels in depression? (Moncrieff et al. (2022))
No link found between 5-HIAA concentrations and depression.
Antidepressants were associated with lower serotonin levels, regardless of depression status.
64
What is the role of the 5-HT1A receptor in depression? (Moncrieff et al. (2022))
5-HT1A receptors reduce presynaptic serotonin release.
Evidence shows no consistent difference in receptor levels between people with and without depression.
A lower receptor level might suggest higher serotonin concentration in depression.
65
What role does the serotonin transporter (SERT) play in depression? (Moncrieff et al. (2022))
SERT reduces serotonin availability by removing it from the synapse.
Antidepressants (SSRIs) are thought to work by inhibiting SERT.
Evidence shows mixed results; some studies suggest higher SERT activity in depression, not lower.
66
What is the effect of tryptophan depletion on mood? (Moncrieff et al. (2022))
Decreased tryptophan, which reduces serotonin, lowered mood in people with depression.
No significant effect was observed in individuals without depression.
Results from depletion studies were largely mixed.
67
What does the research say about the SERT gene and gene-stress interaction? (Moncrieff et al. (2022))
Early studies suggested a link between the short version of the SERT gene, stress, and depression.
Recent high-quality studies found no consistent evidence of this interaction.
68
What are the overall results of the serotonin theory review? (Moncrieff et al. (2022))
No clear evidence links serotonin abnormalities to depression.
Antidepressants may lower serotonin rather than increase it.
Mixed results across studies investigating serotonin activity, receptors, and genetic factors.
High serotonin activity may be linked with depression.
69
How does this review challenge the serotonin theory of depression? (Moncrieff et al. (2022))
Evidence does not strongly support serotonin abnormalities as the cause of depression.
Antidepressant efficacy may be better explained by placebo effects or emotion-blunting mechanisms.
70
What was the central claim of Moncrieff et al. (2022)?
Moncrieff et al. concluded that “there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity.”
71
What are the main criticisms Jacobsen (2023) raises against Moncrieff et al.?
1. Factual errors: Misunderstanding serotonin biology and pharmacology.
2. Selective citations: Ignoring studies opposing their conclusions.
3. Misinterpretation of data:
* Claiming SSRIs decrease serotonin, which is uncertain.
* Equating reduced plasma serotonin after SSRI use with lower brain serotonin, which is incorrect.
72
How does Jacobsen (2023) critique Moncrieff et al.’s interpretation of 5-HT1A receptor changes?
Moncrieff et al. claimed fewer 5-HT1A receptors in depression might reflect higher extracellular serotonin, but this is uncertain.
Their suggestion that antidepressants reduce 5-HT1A receptors as a response to lower serotonin lacks evidence.
73
What does Jacobsen (2023) state about tryptophan depletion and serotonin levels?
Tryptophan depletion causes depression in SSRI-treated individuals, suggesting high serotonin is crucial for antidepressant efficacy.
Moncrieff et al. ignored results showing tryptophan depletion’s impact on mood.
74
What is Jacobsen’s (2023) conclusion about Moncrieff et al.?
Moncrieff et al.’s review:
* Adds little innovation.
* Selective and questionable conclusions may not benefit scientific discussion or patients.
75
What methodological weaknesses does Jauhar (2023) highlight in Moncrieff et al.’s review?
1. Combined meta-analyses and umbrella reviews instead of separating them.
2. Selective exclusion of studies, leading to unreliable interpretations.
3. Inconsistent quality standards for included studies.
76
How did Moncrieff et al. misinterpret tryptophan depletion studies, according to Jauhar?
They downplayed evidence that tryptophan depletion impacts mood in people prone to depression.
Moncrieff et al. selectively cited studies on healthy individuals to claim tryptophan depletion had no effect.
77
What does Jauhar (2023) say about molecular imaging evidence in Moncrieff et al.’s review?
Moncrieff et al. claimed inconsistencies in SERT binding findings across brain regions.
In reality, these findings were consistent across studies and demonstrated disturbances in the serotonin system.
78
What are Jauhar’s (2023) conclusions about Moncrieff et al.’s review?
1. The review lacked consistency for an umbrella review.
2. Selective criteria and biased interpretations undermined conclusions.
3. Neuroscience complexities were oversimplified, leading to invalid conclusions.
79
According to Jauhar (2023), what should Moncrieff et al. have concluded?
1. Tryptophan depletion indicates serotonin involvement in vulnerable individuals.
2. Molecular imaging evidence points to disturbances in the serotonin system in depression.
80
What was the purpose of Zhou et al. (2020)’s study?
To analyze evidence on the efficacy and acceptability of antidepressants, psychotherapies, and their combinations for treating depressive disorders in children and adolescents.
81
Why is treating depression during childhood and adolescence critical?
Depression during these periods increases the risk of:
* Impaired educational and social functioning.
* Substance abuse and smoking.
* Obesity.
* Suicide.
82
What antidepressants and control conditions were used in the study?
Antidepressants:
* Tricyclic Antidepressants (TCAs)
* Selective Serotonin Reuptake Inhibitors (SSRIs)
* Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
* Other drugs
Control Conditions:
* Pill placebo for pharmacological treatments.
* Waiting list or psychological placebo for psychological treatments.
83
What were the key findings about the efficacy of treatments?
Fluoxetine + CBT and fluoxetine alone were more effective than placebo or psychological controls.
Fluoxetine + CBT was better than CBT alone.
Interpersonal therapy (IPT) outperformed all psychological controls.
84
What were the key findings about the acceptability of treatments?
* Fluoxetine and psychological treatments had similar dropout rates.
* TCAs (e.g., imipramine) had higher dropout rates than other treatments.
* SNRIs (e.g., venlafaxine) increased the risk of suicide in young people.
85
How do these results differ from adult depression treatment findings?
For adults, most antidepressants and psychotherapies outperform placebo.
In children and adolescents, fluoxetine (alone or with CBT) showed the best results, and many treatments did not significantly outperform placebo.
86
What are possible explanations for the differences between youth and adult depression treatments?
1. Hormonal sensitivity to emotional stimuli in adolescents.
2. Fewer studies and smaller sample sizes for youth.
3. Higher placebo response rates in youth trials.
4. Psychotherapies developed for adults may not suit adolescents’ cognitive, emotional, and behavioral traits.
87
What is the conclusion of Zhou et al. (2020)?
Fluoxetine (alone or with CBT) appears to be the most effective acute treatment for youth depression.
Limitations include:
* Scarcity of high-quality evidence.
* Potential publication bias in efficacy outcomes.
88
Why is treating adolescent depression uniquely challenging?
* Adolescent depression differs due to biological, psychological, and social factors.
* Treatments designed for adults may not address these differences effectively.
* The prevalence of depression and suicide among adolescents is rising.
89
How does Harmer (2020) summarize Zhou et al.’s (2020) results?
* Efficacy: Fluoxetine + CBT was most effective.
* Acceptability: Fluoxetine and psychological treatments had similar dropout rates.
* Suicidality: SNRIs (e.g., venlafaxine) increased suicide risk, but other treatments did not differ from placebo.
90
What additional points does Harmer (2020) highlight from Zhou et al.’s findings?
* Treatment responses in youth differ from adults.
* More research is needed on long-term antidepressant effects in adolescents.
* There’s a need for personalized treatment options for youth.
91
What are the findings of the #ActivelngredientsMH project?
* SSRIs can be effective but don’t work for everyone.
* Antidepressants affect brain regions responsible for emotional regulation, potentially improving mood.
* Long-term effects of SSRIs in adolescents remain unknown.
* Risks and benefits must be carefully weighed, allowing for informed treatment decisions.
92
What are Harmer’s (2020) recommendations for treating adolescent depression?
* Develop therapies tailored to adolescents’ needs.
* Study which patients benefit most from antidepressants.
* Provide young people with informed choices regarding treatment options.
