L3 - Depression Flashcards

(47 cards)

1
Q

Learning objectives for this lecture

A
  1. Define depression and differentiate it from normal sadness
  2. Identify key symptoms of depression
  3. Understand the burden of depression in terms of prevalence, disability adjusted life years, and economic costs
  4. Identify key risk factors (e.g., stress, trauma, chronic illness) that contribute to the epidemiology of depression,
  5. Recognise the interaction between biological, psychological, and social factors in depression (biopsychosocial model)
  6. Summarise current evidence-based treatments for depression, including pharmacological (e.g., SSRIs) and psychotherapeutic approaches (e.g., CBT, IPT)
  7. Describe the effectiveness and limitations of different treatment options
  8. Discuss emerging research in novel treatments (e.g., digital interventions).
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2
Q

What are the symptoms of depression?

A

They are grouped into 3 clusters - complex disorder that affects multiple aspects of the human experience

Emotional symptoms:

  • Depressed mood
  • Anhedonia (loss of interest)
    ↪ one of these is required for diagnosis, alongside 5 or more of the following
  • Irritability
  • Sadness

Physical symptoms:

  • Sleep disturbances
  • Appetite disturbances
  • Psychomotor retardation/ agitation
  • Catatonia
  • Fatigue

Cognitive symptoms:

  • Poor attention / concentration
  • Indecisiveness
  • Sense of worthless/ guilty
  • Hopelessness
  • Suicidal thoughts
  • Delusions/ hallucinations
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3
Q

What are the different types of depressive disorders?

A
  1. Major Depressive Disorder
  2. Subthreshold/ minor depression
  3. Depression with melancholic features
  4. Depression with psychotic features
  5. Perinatal depression
  6. Depression with catatonic features
  7. Seasonal affective disorder
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4
Q

Article - Beyond classifications

What points are raised in the article about oversimplification of depression?

A
  • Psychopathological oversimplification
  • The subjective experience of depression might not be fully covered by current diagnoses
  • In reality, patients are more complex, there is great comorbidity - have we oversimpified it? Should we make it dimensional?
  • Depression is very cultural thing - different symptoms and some don’t even have the word depression; might have a completely different word
    ↪ Are the symptoms and criteria applicable across different populations? - picture 5
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5
Q

What does the article argue about the dimensional approach to depression?

A
  • Depression co-exists with bodily distress and anxiety
  • Depressive, anxiety and somatic symptoms might be different representations of a common latent phenomenon and might require common therapeutic approaches
  • Some propose a higher order category of common mental disorders
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6
Q

What are the facts about depression?

prevalence, comorbidity, recurrance risk…

A
  • ~ 280 million people
  • 6 months average episode duration
  • 20 - 33% of depressive episodes are linked to a history of bipolar spectrum disorder
  • Prevalence varies across continents and gender (women: 5.8% in Africa and Americas & 2.8% in Western Pacific; men: 4.8% in Africa, 2.8% in Western Pacific)
  • Recurrence risk – 71-85% in clinical samples over 5 years
  • Early onset: 24y in LMICs; 26y in HICs
  • Underdiagnosis in certain age groups: adolescence, older people
  • Gender differences – peak at age 16 years - Females higher risk of depression (gender stereotype? Men don’t want to talk about it?)
  • High Comorbidity with anxiety and SUD
  • Comorbidities with physical diseases (e.g., cancer, diabetes, cardiovascular disease)
    ↪ increases prevalence of these diseases (depression = predictor of onset of those + behaviours connected with depression increases chances of development: smoking -> heart disease)
    ↪ worse course of the disease because of depression
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7
Q

How is depression a major contributor to the disease burden?

A
  • Increases all-cause mortality: 2.2 million excess deaths globally
  • Excess rates of suicides
  • Burden increases during early aduldhood (20s and 30s)
  • Occupy lot of GP’s care (even though they need a help from psychologist/psychiatrist)
  • Sub-threshold syndromes of depressive symptoms prevalence of 17% - prevention would help a lot with developing into major depression
  • Disability - Poor functioning:
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8
Q

What are the areas of a person’s life that are affected by depression and hence the person’s poor functioning in those adds to the disease burden

A
  • education (premature termination)
  • unemployment
  • work disability (calling in sick)
  • economic consequences (personal earnings and household income lower in depressed individuals)
  • Intimate relationships (low probability of marriage, predicts divorce - marital discord and dissatisfaction)
  • Intimate partner violence
  • Poor parental functioning and offspring outcomes (especially maternal depression on the baby - low birth weight, poor school performance, anxiety, substance abuse…)
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9
Q

How does the reduction in the global burden of depression evolved over the years compared to ischemic heart disease?

A

Ischemic heart disease has a clear decline in disease burden over 30 years but depression doesn’t - surprising since treatment, research… = need to do something else/more

Picture 6

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10
Q

What can be done to reduce the disease burden?

A
  1. Decreasing stigma and improving depression literacy
  2. Prevention
  3. Treatment
  4. Maintanance

Picture 1

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11
Q

How do different interventions help reduce stigma around depression?

A
  • Mass media campaigns - short-term improvements un knowledge and attitudes but limited long-term effects on help-seeking behaviour and stigma
  • Social contact-based approaches (interaction with experts by experience) - more long-term effects in reducing stigma and improving empathy
  • Biomedical models - framing depression through biological explanations (e.g., chemical imbalances) increases stigma by reinforcing stereotypes of unpredictability and dangerousness
    ↪ combined bio-psycho-social approach more effective
  • higher depression literacy of health workers = higher rates of depression recognition and better quality of care
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12
Q

What should be considered when deciding on interventions for a person with depressive symptoms

A

What stage of life they are in

  • adressing risk factors uniqur to each life period can be very helfpul for delivering targetted and effective intervention
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13
Q

What are the different life stages that require different approach of interventions?

A
  1. Perinatal and early childhood intervention
  2. Childhood and adolescence (school-based programs on emotional regulation and anti-bullying)
  3. Adulhood and workplace interventions
  4. Older adults (adressing loneliness and isolation - use of technology to promote social support and sense of belonging)
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14
Q

What are prevention interventions mostly focused on in perintal stage and early childhood?

A
  • Maternal depression increases risk for childhood-onset depression - intervention with mothers with history of depression or socio-economic and demographic factors
    ↪ exercise during pregnancy
  • Psychological interventions (e.g., Thinking Healthy Programme) effectively reduce postpartum depression
  • Parental support programs in the perinatal period and ealry childhood promote healthy parenting, family bonding; improve attachment, emotional regulation, and mental health outcomes in children
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15
Q

How can interventions in adulhood, especially workplace interventions, protect against depression?

A
  • Employment is protective against depression due to its role in financial stability, social engagement, increase in autonomy and improved socioeconomic status
  • Workplace programs that increase employee control and promote physical activity improve mental health
  • CBT-based workplace interventions show smal but cost-saving effects on reducing depressive symptoms
  • Preventive interventions targetting smoking and physical actvity - improved anxiety and depression
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16
Q

What is the staged model of depression care?

A
  • It organizes interventions according to severity and risk
  • Helpful due to heterogeneity of depression
  • Identifies where an individual lies along a continuum of risk for the illness progression
  • Stages don’t have to progress from one to another or in linear way (you can go from stage 4 to 3)
  • Staging provides a model for responding to the needs of the individual and reducing the risks of progression to a more advanced stage
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17
Q

What are the stages in the stage model?

A

Stage 0: Universal and selective preventive interventions
Stage 1: Indicated prevention of depression
Stage 2: Interventions early in the course of a depressive disorder, first episode
Stage 3: adressing recurrent depression
Stage 4: Present with persistent depression

Picture 4

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18
Q

What three types of prevention are there and what are their strategies?

A
  1. Universal preventive interventions - targeted at entire communities regardless of risk
    ↪ psychoeducation, stress management, social-emotional learning programs
  2. Selective preventive interventions - targeted at high-risk groups within a community, chosen by demographic characteristics rather than individual risk profiles
  3. Indicated preventive interventions - targeted at individuals with early signs or symptoms but who do not meet criteria for MDE
    ↪ mild symptoms but don’t meet criteria (sub-threshold depression)
    ↪ self-help, internet-based CBT, psychoeducation
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19
Q

How do we define treatment?

A

Treatment refers to interventions occurring after the onset of the disorder, to bring a quick end to the clinical episode

20
Q

What are the four aims of treatment?

A
  1. Reduce symptoms
  2. Improve quality of life, reduce impairment
  3. Shorten episode
  4. Prevent recurrence
21
Q

Which two maintanance interventions can be done?

A
  1. Long-term treatment
  2. After-care: to prevent another episodes
22
Q

What is an important thing to remember so that treatment is effective?

A

To treat we need to understand how it develops and how it’s maintained

  • No single factor explains depression = complex disorder
23
Q

Etiology

What were the two competing views on epidemiology of depression that dominated psychology for decades?

A
  1. The Biomedical Model
    ↪ Depression is caused by chemical imbalances, brain structure changes, or genetics
    ↪ Treatment: Medication, brain stimulation (e.g., transcranial magnetic stimulation)
  2. The Psychosocial Model
    ↪ Depression is caused by negative life experiences, stress, or maladaptive thoughts
    ↪ Treatment: Psychotherapy, social support, lifestyle changes
24
Q

However, over time it became clear that these two as a stand-alone models don’t explain depression. What new model is now dominant?

A

The biopsychosocial model

  • no single factor explains depression
  • depression is not just a chemical imbalance, a negative mindset, or a social problem → it’s an interaction of all three
25
What are the biological factors of depression proposed by the biopsychosocial model?
1. **Genetics** – Depression often runs in families along with SUD, BD, and anxiety disorders (40% risk for offsprings of parents with depression) ↪ In most cases is preceded by childhood onset disorders (e.g., ADHD) 2. **Brain Damage Before Birth** – Low birth weight, infections during pregnancy, or birth complications increase the risk 3. **Medical & Drug-Related Causes** – Some illnesses, medications, and substances (e.g., alcohol, drugs) trigger depression 4. **Brain Imaging Studies** – Depressed individuals often have reduced brain volume in areas controlling emotion
26
What are the psychological factors of depression proposed by the biopsychosocial model?
1. **Early Psychological Stress** – Childhood trauma makes people more vulnerable to depression later in life 2. **Personality Traits** – People high in neuroticism are at greater risk 3. **Cognitive Biases** – Depressed individuals focus more on negative thoughts and struggle to shift attention away from them
27
What are the social factors of depression proposed by the biopsychosocial model?
1. **Life Stressors** – Events like job loss, divorce, or death of a loved one often trigger depressive episodes 2. **Social Support Matters** – Having strong relationships can protect against depression, while loneliness increases risk
28
The biopsychosocial model explains depression in three phases, what are those?
1. **Predisposing Factors**: Genetics, childhood trauma, personality traits create a foundation for risk ↪ prevention works well 2. **Precipitating Factors**: A major stressor, like losing a job or a breakup ↪ indicated prevention 3. **Sustaining Factors**: Negative thoughts, social withdrawal, and low energy reinforce the depressive state, making it harder to recover ↪ treatment, maintenance
29
What are the implications for treatment from this model?
- **Biological Approaches** : e.g., Antidepressants (restore neurotransmitter balance), brain stimulation (e.g., TMS) (reactivate underactive brain areas) - **Psychological Approaches**: e.g., Cognitive Behavioural Therapy (CBT) (helps change negative thought patterns) - **Social Approaches**: e.g., Building social support (connecting with friends & family), improving life circumstances (work, finances, relationships) Usually the combination of these is the thing that does the trick = Multimodal approach and focus on the individual rather than treating people generally
30
What are the different types of antidepressants and what are the disadvantages?
1. SSRIs (selective serotonin reuptake inhibitor) 2. SNRIs (serotonin and norepinephrine reuptake inhibitor) 3. TCAs (Tricyclic Antidepressants) - Strong placebo effect (38% respond after placebo, 52% after medication) - Not advised in children and adolescents (maybe an increased suicide risk) - Some side effects: Suicidality, agitation, irritability, sleep problems, weight gain, gastrointestinal, sexual problems
31
What different psychological treatments are there for depression? What are the effects?
Many different types, the most important ‘families’: 1. Cognitive behavioral therapy 2. Interpersonal therapy 3. Behavioral activation 4. Problem solving therapy - Effects are moderate to large - But considerably overestimated because of problems of randomized trials examining the effects - no possibility of placebo so not as clear cut as with medication - Effects are measured in ‘Standardized mean differences’ (smd) indicating the difference between treatment and untreated control group in terms of standard deviations: 0.2 is small, 0.5 is moderate, .8 is large
32
# Theories on depression What is the core idea and the cognitive triad in Beck's Cognitive Model (1967)?
Core Idea: Depression results from maladaptive thought patterns shaped by negative schemas **The Cognitive Triad** (negative beliefs reinforcing each other): - Negative view of self - Negative view of the world - Negative view of the future
33
What are some cognitive distortions that people with depression experience?
1. **Overgeneralization** – Making broad conclusions from a single event, e.g., “I failed this test, so I’ll fail everything in life” 2. **Catastrophizing** – Expecting the worst possible outcome, e.g., “If I make a mistake, my entire career is over” 3. **All-or-Nothing Thinking** – Viewing situations in extreme, black-and-white terms, e.g., “If I’m not perfect, I’m a total failure” 4. **Unrealistic Standards** – Setting impossibly high expectations and feeling inadequate when they aren’t met, e.g., “I should always be the best at everything” 5. **Discounting Any Positives** – Ignoring achievements and focusing only on failures, e.g., “I got good feedback, but that doesn’t count because I made a small mistake” 6. **Magnifying Negative Events** – Focusing only on the worst parts of a situation while ignoring the positives, e.g., “I did well on the project, but I stumbled during my presentation, so I embarrassed myself” 7. **Making Negative Predictions About the Future** – Assuming things will turn out badly without real evidence, e.g., “I’ll never be happy again” 8. **Taking Things Personally** – Assuming that other people’s actions or words are directed at you, e.g., “They didn’t say hi, so they must not like me” 9. **Mind-Reading** – Believing you know what others are thinking, usually in a negative way, e.g., “They think I’m boring”
34
What is the maintainance cycle?
Picture 2 Thoughts cause the feeling, behaviour, physical symptoms and so on - vicious cycle and cbt tries to alter this thinking by breaking this pattern
35
# Theories on depression What is Bower's Associative Network Theory (1981)? What is its core idea and how does depression become chronic according to this theory?
Core Idea: Thoughts, emotions, and memories are stored in interconnected networks. - **Mood-Congruent Memory Bias**: Depressed mood → Activates negative memories → Reinforces depression ↪ Explains why negative thoughts persist even after a depressive episode ends **How Depression Becomes Chronic**: - Negative emotions strengthen connections to negative memories - Depressed individuals are more likely to recall negative experiences than positive ones
36
What cognitive deficits can be observed in depressed individuals?
1. **Executive Functioning**: ↪ *Problem-Solving Difficulties*: Challenges in developing effective solutions, leading to feelings of helplessness ↪ *Inhibition Challenges*: Reduced ability to suppress inappropriate responses, resulting in impulsivity. 2. **Working Memory Impairments**: ↪ *Retention Issues*: Difficulty holding onto positive information, perpetuating negative thought patterns ↪ *Task Management*: Struggles in maintaining and manipulating information, hindering planning and organization 3. **Slowed Processing Speed**: ↪ *Delayed Reaction Times*: Noticeable slowing in cognitive processing, leading to delayed responses ↪ *Information Processing*: Taking longer to understand and respond, affecting decision-making and daily tasks
37
What cognitive biases can be observed in depressed individuals?
1. **Self-Referential Processing Bias**: Depressed individuals are more likely to recall negative information about themselves, reinforcing a negative self-image 2. **Attentional Biases**: Difficulty disengaging from negative stimuli, leading to prolonged focus on negative aspects 3. **Interpretation Biases**: Tendency to interpret ambiguous situations negatively, contributing to feelings of hopelessness 4. **Memory Biases**: Preferential recall of negative over positive information, perpetuating a negative worldview
38
Which cognitive emotion regulation strategies do individuals with depression engage in?
1. **Rumination**: Repeatedly thinking about negative emotions and their causes 2. **Distraction**: Avoiding negative thoughts (considered an adaptive strategy but not a long-term solution) 3. **Reappraisal**: Changing how one interprets a negative situation (healtiest one, but less used by depressed individuals)
39
Diagram explaining how cognitive control, cognitive bias, cognitive emotional regulation relate and interact which leads to depression
Picture 3 If we can intervene in any of those domains we might be able to treat depression
40
How does understanding depression help in therapy?
Understanding cognition and depression has led to better treatments: 1. **Cognitive Behavioral Therapy** (CBT) - based on changing negative thought patterns ↪ If we teach people how to challenge their negative thoughts, we can break the cycle of depression 2. **Cognitive Training & Attention Exercises** ↪ New research is exploring ways to train the brain to overcome negative biases using: - *Computer-based tasks* that help people focus on positive information - *Eye-tracking technology* to study how depressed people focus on sadness These new interventions could complement therapy in the future!
41
What is the difference in effectiveness between psychotherapy and antidepressants?
Psychotherapy more lasting effects; right after treatment with medication and psychotherapy have the same effects - the best approach in terms of effects sizes is their combination
42
What do researchers think is the reason why almost all psychotherapies have almost the same effect sizes?
Since each of the psychotherapies is targetting a different aspect of depression and they still have the same effect sizes, it must be that the thing they have in common is the reason for the effectiveness of them, e.g. empathy of the therapist, therapeutic relationship... This however, she said that the more important thing is to approach everyone individually so even increase the effectiveness of treatment because everyone is different and has different needs. So each treatment should be tailored on each individual, which right now is not happening as the treatment is based on averages
43
What is a way to deliver individualised treatment to people?
**Internet-based interventions** - can be guided or unguided - can even be blended with face-to-face treatment - they use interactive prediction tool to show who needs therapeutic guidance and who doesn’t based on hundreds of randomised trials done on individuals with depression ↪ Shows whether there is a difference between guided and unguided intervention ↪ Might be able to give individualised advice which treatment will be more suitable and beneficial for that specific individual ↪ Assist clinicians in their judgment - used in combination with clinical judgment
44
What is the conclusion from her study where they used the internet-based interventions with the interactive prediction tools?
Focusing on giving individualised treatment might help to overcome the disease burden - Decreases the wasting of treatment and clinicians’ resources - These tools meant to be used with clinical judgment and patient preferences to optimise the outcomes of treatment for each individual
45
# Article What is the difference between first-line and second/third- line treatment?
Distonguished based on their application in the course of the disorder and their complexity **First-line treatment**: initial interventions delivered early in the course of a depressive disorder, specifically from its first episode ↪ consist of evidence-based treatments for acute episodes of clinical-threshold depression (e.g. CBT, interpersonal therapy, antidepressants for moderate or severe depression) **Second-line treatment**: more complex interventions provided for people who do not respond to first-line interventions or who present with recurrent or persistent depression ↪ Consists of switching to or augmenting medication or combining treatments (psychotherapy plus medication) **Third-line treatment**: Considered when depression is treatment-resistant, refractory, difficult to treat or persistent, meaning that the individual has not responded to at least two courses of antidepressants ↪ More intensive interventions such as neuromodulation therapies (e.g. ECT or rTMS), drugs that target specific systems in the brain, novel psychological treatments (e.g. mindfulness-based CBT, acceptance and commitment therapy)
46
# Article How can relapse and recurrence be prevented?
1. Pharmacotherapy Continuation: continuing antidepressant medication after symptom remission reduces relapse risk by 50% 2. Psychotherapy for Maintenance: increases the likelihood of maintanance by 12-16% compared to starting with medication alone ↪ E.g. Mindfulness-Based Cognitive Therapy (MBCT), preventive CBT, and interpersonal psychotherapy effectively prevent relapse
47
What are the principles of care?
- Care should be timely, accessible, and of the same quality as for physical illnesses - **Collaborative care**: Integrating mental health professionals, primary care providers, and social workers improves outcomes ↪ Involving caregivers in treatment decisions enhances recovery and promotes sustained wellness - Accurate assessment and formulation are crucial for personalised treatment recommendations - Personalised care: involves placing the person at the centre of clinical decisions and identifying individual characteristics associated with treatment outcomes