2025 CMI Session 11 - Understanding Sadness

Learning Objectives (Page 10)

    • Critically discuss and synthesize different approaches to understanding sadness and depression.

    • By next week:

    • Explain different approaches to treating depression and evaluate their

Historical Context of Sadness (Page 12)

  • Artwork: ‘Melancholy madness’ and ‘Raving madness’ statues at the Royal Bethlem Hospital, symbolizing historical views on mental illness.

DSM-5 Diagnostic Criteria for Depression (Page 13 - Page 14)

  • Diagnosis requires 5+ symptoms over a two-week period, including:

    • Depressed mood

    • Diminished interest or pleasure

    • Weight changes

    • Sleep disturbances

    • Psychomotor agitation or retardation

    • Fatigue

    • Feelings of worthlessness or excessive guilt

    • Trouble concentrating

    • Recurrent thoughts of death or suicide

  • Significant distress and impairment in functioning are required.

  • Additional specifiers: with mixed features and with anxious distress.

Normative Response to Loss (Page 15)

  • Various life events can lead to temporary sadness (e.g., relationship breakdown, bereavement).

  • Reactive/event-related depression defined when symptoms persist beyond the triggering event.

Duration of Depressive Episodes (Page 16)

  • Depressive episode durations:

    • 25% less than 1 month

    • 50% less than 3 months

    • 25-30% last up to 1 year

    • Nearly 25% last up to 2 years.

Prevalence of Depression (Page 17)

  • About 5% of the population is depressed at any given time.

  • 17% will experience depression in their lifetime.

  • Gender differences: 26% of women vs 12% of men report lifetime prevalence.

  • First onset typically between ages 24-29.

  • Often co-morbid with anxiety

Biological Basis of Depression (Page 18 - Page 21)

  • Depression's nature is episodic, like physical disorders.

  • Symptoms related to physical functions (e.g., sleep, eating).

  • Genetic components: heritability estimated at 40-50%.

  • Neurophysiological abnormalities contribute to mood regulation.

  • Neuroendocrine link: stress responses affect neurotransmitter function.

Depression and Heredity

  • Heritability of depression based on twin studies is estimated at 40%-50% (Levinson, 2006)

  • §One study found that biological relatives of adoptees with major depression were eight times more likely to have suffered major depression than controls (Wender et al., 1986)

    Genetic Evidence

  • §Replicability is extremely low – many inconsistent findings.

    §Kato (2007) – meta-analysis:

    →166 genes that had been linked with bipolar disorder and major depressive disorder

    →BUT only 6 have been replicated in more than 75% of relevant studies.→This highlights the challenges faced in genetic research related to mood disorders, indicating a need for more rigorous methodologies and larger sample sizes to enhance replicability.

    §Moderate genetic contribution to depression, and likely to be multiple alleles, not just one.

    §Maybe more likely that genetic factors contribute to a predisposition to depression – moderated by other factors.

    §Genes could be involved in stress responses, neurotransmitter function, and/or neurophysiology, so could underpin the other theories

Neurotransmitter Theories (Page 22 - Page 27)

  • Neurotransmitter dysregulation, particularly with monoamines (serotonin, norepinephrine, dopamine), as a significant factor.

  • Increased levels of neurotransmitters following antidepressant use, but symptom alleviation can take weeks.

  • Suggests complex interaction beyond neurotransmitter imbalances.

Antidepressants and Treatment (Page 28 - Page 29)

  • Antidepressants are commonly used yet may not be as effective as claimed.

  • There is significant discontinuation effects and doubts about the 'brain chemical imbalance' model.

  • Future discussions will focus on this treatment approach.

Psychological Factors in Sadness (Page 30 - Page 34)

  • Psychodynamic Models:

    →elegant explanations of sadness (especially in cases where there isn’t obvious trauma or material hardship), but emphasis on unconscious processes make them fundamentally untestable and unfalsifiable

    → typically long (and unpredictable) treatment length of psychodynamic therapies make them prohibitive for many individuals

  • Behaviourist Models:focus on conditioning
    → Learned helplessness (Seligman, 1975) – depression associated with internal, global, stable attributions

    → Low rate of positive social reinforcement leads to withdrawal, low mood, reduction of behaviour like to increase social contact.

  • Cognititve Models: Aaron Beck (1979)

    → Depression results from inaccurate cognitive responses to events that affect us – automatic negative thoughts.

    → Conscious thought influenced by depressogenic schema, established during childhood.

    →Beck’s cognitive triad – beliefs about self, events and the future.

    →These thoughts can create a cycle of negativity, reinforcing feelings of hopelessness and further contributing to depressive symptoms.

  • Emergence of talking cures influenced by historical societal changes.

  • Psychodynamic models highlight emotions tied to unconscious processes and significant losses.

  • Behavioral models emphasize learned helplessness and social withdrawal.

Cognitive Models of Sadness (Page 35 - Page 39)

  • Beck's cognitive theory links depression to negative automatic thoughts and cognitive triads.

  • Cognitive-behavioral models provide empirical frameworks but can risk increasing stigma and overlooking sociocultural factors.

Cognitive-behavioral models of sadness

→Pros:

  • §Offer a testable model of sadness

    §Many features applicable cross-culturally

    §Integrate biological aspects of sadness (e.g. reinforcement of fatigue through behavioural inactivity)

    Inform cognitive-behavioural therapies, which appear to have a strong

  • Provides structured approaches to identifying and challenging negative thoughts.

  • Encourages active participation from individuals in their own treatment.

  • Evidence-based strategies can lead to measurable improvements in mood and functioning.

→Cons:

  • §Focus on the individual’s thoughts and behaviours can risk increasing, rather than decreasing, stigma

    §Not entirely culturally sensitive (e.g. individual vs collectivist social orientation)

    §Insufficient attention to sociocultural  factors linked to sadness

Sociocultural Factors in Sadness (Page 42 - Page 48)

  • Gender impact on depression: societal roles, victimization, and economic disparities contribute to women's higher diagnosis rates.

  • Cultural variations : in prevalence and expression of depression; different groups experience distinct symptoms.

    →Annsseau et al. (2018) found that 12.8% of their sample (GP patients) with a degree met criteria for an anxiety or depression diagnosis, versus 22.1% of those without a degree (…Good news for you next year?!)…

    →But also found that 27.7% of those who were unemployed met criteria, versus 15.5% of those employed in management roles (…so better hurry up and get a job next year?!)

    →

Summary of Factors Influencing Sadness (Page 55)

  • Theories emphasize importance of biological, psychological, and sociocultural factors in depression's development.

  • Next discussions will explore treatment implications of these models.

Further Reading (Page 56)

  • Includes articles on biological, psychological, and social determinants of depression for deeper insights.

Case Study: Marie (Page 57 - Page 60)

  • Marie, a 39-year-old woman, exhibits symptoms of sadness potentially linked to familial and social stressors, including the death of her partner and challenges with her children.

  • Group tasks include exploring biological, psychological, and sociocultural factors in her case.

  • Preparation for next week involves reading specific chapter on sadness and depression.