Chapter 8: Mood Disorders and Suicide

🧠 SECTION 8.1 – Part 1: General Characteristics of Mood Disorders

🌧 What Are Mood Disorders?

Mood disorders are psychological disorders that cause disturbances in emotion, ranging from:

• 🥀 Deep sadness and hopelessness (depression)

• 💥 To extreme elation or irritability (mania)

They're often disabling and can co-occur with:

• Panic attacks

• Substance use

• Sexual dysfunction

• Personality disorders

📉 Comorbidity = poorer prognosis and more severe symptoms.

🔵 DEPRESSION: SIGNS & SYMPTOMS

🫠 What is depression?
A persistent emotional state marked by:

• Great sadness

• Feelings of worthlessness

• Guilt

• Withdrawal from others

• Loss of interest in things once enjoyed (including sex)

• Changes in sleep/appetite (↑ or ↓)

• Low energy, low motivation, and cognitive fog

🧠 Cognitive symptoms:

• Trouble focusing or remembering

• Conversations feel exhausting

• Speech is slow, quiet, and monotonous

• May neglect hygiene or appearance

• Repetitive self-blame and hopeless thoughts

🧍‍♀ Behavioural symptoms:

• Sitting silently for long periods

• Some are agitated (pacing, sighing, wringing hands)

🧒👵 Depression Across Age Groups

• Children: more likely to show physical symptoms (e.g. tummy aches, headaches)

• Older adults: more distracted, forgetful

🌍 Cultural Differences

• Depression is less prevalent in China than in North America (likely due to cultural stigma about emotional expression)

• Non-Western cultures are often said to emphasize somatic (physical) symptoms more than emotional ones

• But even in Canada, most depressed patients in medical settings emphasize somatic symptoms rather than emotions

  • Only 15% are psychologizers (those who emphasize emotional/psychological symptoms)

🔁 Recurrent but Treatable

• Most episodes resolve on their own with time

• But chronic depression means the person may never fully “bounce back” to their old self between episodes

🟡 MANIA: SIGNS & SYMPTOMS

🔥 What is mania?
A mood state marked by:

• Intense elation or irritability

• Hyperactivity

• Talkativeness with fast speech (flight of ideas)

• Grandiose plans

• Distractibility

• Can include risky or impractical behaviours (e.g., spending sprees, impulsive sexual acts)

💡 Mania often occurs with depression (bipolar), but mania without depression is rare.

🧪 MR. W’s Case of Mania

A 32-year-old postal worker suddenly:

• Quit his job

• Spent all the family’s savings on tropical fish gear

• Believed he’d become a millionaire

• Wanted to ride a child’s bicycle across the country

• Was sexually inappropriate with his therapist

😮 His speech was:

• Fast, loud, pun-filled

• Hard to interrupt

• Jumped from topic to topic (flight of ideas)

📅 Duration: Mania can last days to months
😡 Attempts to stop or redirect manic individuals can cause anger/rage

🌪 DSM-5 Mood Disorders Overview

DSM-5 organizes mood disorders into two major categories:

1. Depressive Disorders

   • e.g., Major Depressive Disorder (MDD), Persistent Depressive Disorder, Disruptive Mood Dysregulation Disorder, Premenstrual Dysphoric Disorder

2. Bipolar and Related Disorders

   • e.g., Bipolar I, Bipolar II, Cyclothymic Disorder

📍 Fun fact: Bipolar disorders are placed between schizophrenia and depressive disorders in DSM-5 to reflect how it shares features of both (e.g., mood disturbances + possible psychosis).

🌧 Diagnosis of Major Depressive Disorder (MDD)

To be diagnosed with MDD, a person must have at least 5 of the following symptoms, present nearly every day for at least 2 weeks. One of the symptoms must be either:

• 1⃣ Depressed mood

• 2⃣ Loss of interest/pleasure (anhedonia)

🧠 Other Symptoms (Need 4+ more from this list):

• Changes in sleep (insomnia or hypersomnia)

• Psychomotor agitation or retardation (restlessness or slowed movement)

• Change in appetite (up or down)

• Fatigue or energy loss

• Feelings of worthlessness or inappropriate guilt

• Difficulty concentrating or indecisiveness

• Recurrent thoughts of death or suicide

➡ MDD is still diagnosed categorically, but DSM-5 encourages rating severity, duration, and frequency for a more dimensional approach.

💬 Is It Really All-or-Nothing?

Researchers have debated whether depression is categorical (you have it or don’t) or dimensional (a spectrum of severity).

• 🧪 Twin studies show even people with 3 symptoms for <2 weeks can still have significant future risk or genetic links.

• 💭 So the line between "depressed" and "not depressed" might be blurrier than we think!

📊 Prevalence of MDD

• Lifetime prevalence: Varies between 5.2% – 17.1% in U.S. studies.

• Canadian data (CCHS 2012): Lifetime prevalence = 11.3%

• Epidemiologist Scott Patten suggests it may be even higher — possibly up to 50% over a lifetime!

• About 3.9% of Canadians met criteria for MDD in the past year

• Two-thirds of people with recent MDD sought treatment

• One-third were taking antidepressants

🚺 Gender Differences in Depression

• MDD is ~2x more common in women than in men

• This gender difference is universal — found in most countries and ethnic groups

• Often starts appearing in adolescence

🧠 Why Might Women Be More Prone to Depression?

1. Ruminative Coping

• Women are more likely to brood over emotions (e.g., “Why do I feel this way?”)

• Men tend to distract themselves with activities (e.g., sports)

2. Co-Rumination

• Especially in girls — friends brood together over problems

• 🔀 Linked to more depression but also stronger friendships

3. Silencing the Self (Dana Jack)

• Women may "suffer in silence" to preserve relationships — more internalized distress

4. Objectification Theory

• Constantly being judged based on appearance can harm girls’ self-esteem and increase shame → depression risk

5. Trauma Exposure

• 52% of women in a Toronto psych ward for depression had experienced sexual abuse

6. Stress Generation

• Women may unknowingly create or magnify interpersonal stress (e.g., conflict)

7. Hormones

• Estrogen and progesterone have some links to mood, but the evidence is mixed

➡ Most likely: a mix of social, psychological, and biological factors = biopsychosocial model

⏳ Persistent Depressive Disorder (PDD)

• Formerly known as dysthymia

• Chronic depression lasting 2+ years

• Lifetime prevalence = 4.6%

• Predictors include:

  • Female gender

  • Being unmarried

  • Comorbid conditions

  • Limited physical functioning

  • Reduced family/social support

📉 PDD patients:

• Often need longer treatment

• May respond to therapy, but have lower remission rates

• Identifying them early can help tailor treatment plans

🧨 Impact on Functioning

• WHO ranked depression as a leading cause of disability

• By 2030, it may be #1 in disease burden in high-income countries

• Lost workdays:

  • MDD = ~27 days/year

  • Bipolar disorder = ~65.5 days/year

💡 KEY TERMS FROM THIS SECTION:

🌧 Diagnosis of Bipolar Disorder

🔹 Bipolar I Disorder (aka classic bipolar)

• Definition: At least one full manic episode is required for diagnosis (depression usually also occurs, but it’s not required).

• DSM-5 Criteria for a manic episode:
  You need:

  • Elevated or irritable mood AND

  • Increased goal-directed activity or energy

  • Plus 3 more symptoms (or 4 if the mood is only irritable):

    ✅ Increased goal-directed activity
    ✅ More talkative / pressured speech
    ✅ Flight of ideas / racing thoughts
    ✅ Less need for sleep
    ✅ Inflated self-esteem or grandiosity
    ✅ Easily distracted
    ✅ Risky behaviours (shopping sprees, sex, gambling)

• New in DSM-5: Increased goal-directed activity is now a required symptom.

⚖ Prevalence and Course

• Lifetime prevalence for Bipolar I + II = ~4.4%

• Age of onset = typically early 20s

• Men = Women, but:

  • Women = more depression

  • Men = more mania

• 50% relapse within 1 year 🌀

• Many remain functionally impaired even after treatment or hospitalization 😢

😵‍♀ Heterogeneity in Mood Disorders

🔸 Types:

🧠 Psychotic or Melancholic Features in Depression

• Psychotic depression = Depression + hallucinations/delusions
  🧪 Needs antipsychotics + antidepressants

• Melancholic features:

  • No pleasure in anything (anhedonia)

  • Worse in the morning

  • Early morning awakening

  • Weight/appetite loss

  • Extreme agitation or lethargy

👶 Peripartum Depression (aka Postpartum Depression)

• Affects up to 12% of Canadian mothers

• Can start during pregnancy (peripartum), not just after birth

• Risk factors:

  • Past depression

  • Low income

  • Low social support

  • Interpersonal violence

  • Stressful life events

• One study found that peer support backfired because struggling moms compared themselves to thriving peer coaches and felt worse 😢
  ✅ Interventions work better when done by trained nurses.

• Fathers also experience postpartum mental health issues (~10%) but rarely seek help

❄ Seasonal Affective Disorder (SAD)

• Depression that follows a seasonal pattern, usually winter

• Caused by reduced sunlight → decreased serotonin activity in hypothalamus

• Prevalence:

  • General Canadian pop: ~2.9%

  • Inuit community: 18% (!!)

  • Icelanders: very low (1.2%) — possibly due to diet (fish?) or genetic adaptation

💫 Cyclothymic Disorder

• Low-grade bipolar: chronic ups and downs

• Symptoms:

  • Periods of hypomania and mild depression

  • No full-blown manic or depressive episodes

  • Lasts at least 2 years (1 year in kids)

• Not common (<1% prevalence), but can be a precursor to bipolar disorder

🌟 Wrap-Up: Mood Disorders Overview

🧠 Key Terms Review

• Mania: Elation, hyperactivity, poor judgment

• Hypomania: Mild mania, doesn’t impair functioning

• Anhedonia: Loss of pleasure

• Mixed episode: Mania + depression symptoms at same time

• Melancholic features: Severe depressive symptoms with specific pattern

• Psychotic features: Delusions/hallucinations with depression

• SAD: Seasonal depressive pattern (often winter)

• Cyclothymic disorder: Chronic mood instability, less severe than bipolar

• Peripartum depression: Depression during or after pregnancy

🧠 8.2 Psychological Theories of Mood Disorders (Part 1)

This section answers the question:

To answer that, we explore:

• Psychoanalytic theory (Freud)

• Cognitive theory (Beck)

• Personality factors (e.g., self-criticism)

• Diathesis-stress model

Let’s go through each!

💭 1. Psychoanalytic Theory of Depression (Freud)

🎭 Core Idea:

Depression comes from unconscious conflict related to loss and grief, especially if you’re overly dependent on others.

🍼 How it starts (in childhood):

• If a child’s needs are over- or under-fulfilled during the oral stage (first stage of psychosexual development), they can become fixated.

• This fixation leads to dependency on others for self-esteem.

🧠 How it turns into depression (as adults):

• When someone they love is lost (e.g., through death, separation, or rejection), they introject (mentally "absorb") that person.

• Any anger or negative feelings toward that person (even if unconscious) now get turned inward.

• This becomes self-blame, guilt, and self-criticism = ✨depression✨.

🌀 Why it gets worse:

• Normally, grieving ends with “mourning work” (separating from the lost person emotionally).

• Depressed people don’t finish this mourning work — they stay stuck in guilt and blame.

🍁 2. Canadian Research: Personality Factors & Depression

Let’s now look at research that supports or builds on Freud’s ideas (even if indirectly).

💡 Sociotropy & Autonomy (Aaron Beck, 1983 – cognitive theory)

🧪 Canadian Research:

• David Clark (UNB) and others developed the SAS-R Scale to measure these styles.

• Found: Both styles predict depression risk and number of past episodes.

• Autonomy in particular = risk of recurrence.

🧠 Introjective vs. Anaclitic Personality Styles (Sidney Blatt)

🧪 Canadian research (Zuroff, Mongrain, etc.):

• Used the DEQ to measure:

  • Maladaptive dependency (neediness)

  • Adaptive dependency (healthy connectedness)

• Found: Self-criticism = strongest predictor of depression, but dependency still matters.

💡 Perfectionism and Depression

🧪 Canadian researchers (Hewitt & Flett) found:

• People with MDD or bipolar often have high perfectionism.

• Self-criticism + perfectionism = 🔥 high risk for chronic depression.

🔁 Congruency Hypothesis (Diathesis–Stress)

This theory says:

Example:

🧪 Results: Mixed support. Sometimes congruent stressors matter. Sometimes stress in general is enough.

💊 Personality & Treatment Outcomes (Rector et al., 2000)

• Self-criticism = bad response to cognitive therapy (CT)

• But NOT to meds 💊

• The best CT outcome = when self-critical clients reduce self-criticism over time.

🧠 This shows that personality traits affect which treatments work!

🔬 SCPS: Self-Critical Perfectionism Scale

• Combines:

  • Self-criticism

  • Autonomy

  • Perfectionism

• Captures ✨shared patterns✨ across theories.

• Best predictor of depressive symptoms (esp. in MDD & social anxiety).

Traits of someone with high SCPS:

• Unrealistic goals

• Fear of criticism

• Self-critical evaluation

• Prefers solitude

• Concerned about rejection

💡 Targeting self-critical perfectionism may be key to improving therapy for depression.

✅ Summary of Key Concepts So Far:

💡 Core Concept: Beck’s Theory of Depression

Beck believed that depression is caused and maintained by distorted, negative thought patterns.

🧠 1. Negative Schemas

• Schemas = mental structures or patterns that help us interpret information.

• Depressed individuals develop negative schemas early in life (e.g., from trauma, loss, rejection, criticism).

• These schemas lie dormant until triggered by stress or reminders of past events.

🔄 2. The Negative Cognitive Triad

These schemas feed into a “triad” of pessimistic thoughts:

1. Negative view of self ("I’m worthless")

2. Negative view of world ("Life is unfair")

3. Negative view of future ("Things will never get better")

⚠ 3. Cognitive Distortions (Biases)

These are irrational ways of thinking that keep the depression going:

📏 4. Dysfunctional Attitudes

• Beliefs that make people vulnerable to depression.

• Examples:

  • “If I’m not perfect, I’m worthless”

  • “I must be liked by everyone”

🧪 Measured by: Dysfunctional Attitude Scale (DAS)

• High DAS scores = more vulnerability to recurrent depression

• Themes: need for approval and need for perfection

🧪 5. Canadian Research Highlights

• Self-Referent Encoding Task: Depressed people are more likely to:

  • Endorse negative adjectives (e.g., “stupid”) as self-descriptive

  • Recall negative words more easily (cognitive bias!)

• Stroop Task: Depressed individuals take longer to name the colour of depression-related words = those themes are more cognitively accessible

• Attention Tasks: Non-depressed ppl avoid negative info (protective bias); depressed ppl focus on it

• Schema Organization: Depressed people have:

  • Highly interconnected negative self-schema

  • Poorly organized positive schema

🧠 6. Beck’s Expanded Model

• Negative schemas become part of a “depressive mode”:

  • A system of thoughts, emotions, behaviours, and physical reactions

  • Once activated, this mode dominates thinking and fuels rumination

• Depression is on a continuum with normal functioning—everyone has some vulnerability

🧩 7. Cause or Effect?

• Do negative thoughts cause depression or does depression cause negative thoughts?

• Beck says: it’s bidirectional

  • Depression worsens negative thinking

  • Negative thinking can trigger and maintain depression

Clinical Importance

• Beck’s model is highly testable and influential in therapy

• Forms the basis of Cognitive Behavioural Therapy (CBT)!

• CBT changes thought patterns to improve emotional state

💥 8.2 Psychological Theories of Mood Disorders – Part 2: Helplessness & Hopelessness

🐶 1. Learned Helplessness Theory (Seligman, 1975)

Key idea:
After repeated exposure to uncontrollable stress (like trauma or failure), people learn to be passive and believe they can’t change things, even when they later can.

Based on animal studies:

• 🐶 Dogs were shocked and couldn’t escape.

• Later, even when escape was possible, they gave up and didn’t even try.

• Symptoms: passivity, appetite/weight loss, low norepinephrine (just like human depression).

In humans:
This models depression where people feel powerless, don’t attempt solutions, and feel like they’ve lost the will to act.

🧠 2. Attributional Reformulation (Abramson, Seligman & Teasdale, 1978)

This version adds cognition to the mix—how people explain failure affects whether they become depressed.

🧩 Three dimensions of attributions:

🧠 Depressive Attributional Style =
Internal + Stable + Global = 🚨 DEPRESSION RISK

This creates the "depressive paradox":
You feel helpless but also blame yourself, which deepens the depression.

😞 3. Hopelessness Theory (Abramson, Metalsky & Alloy, 1989)

This expanded on the attribution model to say:

Definition of hopelessness:
Believing bad things:

• Will happen

• Cannot be stopped or changed

• Will have severe consequences

🎯 3 diatheses (vulnerabilities) in this model:

1. Depressive attributional style (internal, stable, global)

2. Low self-esteem

3. Tendency to assume extreme negative consequences

🧪 Research support:
People with these styles:

• Had more frequent and severe depressive episodes

• Had more chronic depression

• Developed depression only if hopelessness was present

🧠 Anxiety → Hopelessness → Depression:

• At first, helplessness leads to anxiety.

• If bad events are seen as certain, hopelessness forms.

• Then you get depression with anxiety mixed in.

This explains comorbidity of anxiety and depression!

🔑 Key Terms to Remember:

• Learned helplessness = Passive behavior after uncontrollable stress

• Depressive paradox = Feeling helpless but still blaming yourself

• Depressive attributional style = Internal, stable, global attributions for bad outcomes

• Hopelessness = Belief that bad outcomes will definitely happen and can’t be changed

• Depressive predictive certainty = Believing bad events are inevitable

🌟 PART 1: Interpersonal Theory of Depression 💔🧍‍♀🧍‍♂

This theory focuses on how depressed people interact with others and how this can actually worsen or even cause depression.

💬 Main Points:

1. Sparse, unsupportive social networks:
   Depressed people often have few social supports and feel like those they do have aren’t helpful → this makes them more vulnerable to stressful life events.

2. Negative reactions from others:
   People around them may reject them due to:

   • Low enjoyment of their company

   • High levels of negativity

   • Repetitive self-focused convo (conversational self-focus)

   EX: Roommates of depressed students reported more aggression toward them & less enjoyment.

3. Reassurance seeking 🥺👉👈
   Depressed people constantly ask “Do you still love me?” or “Are you mad at me?” but:

   • They don’t believe the reassurance

   • It irritates others

   • Eventually → rejection

4. Interpersonal problems = cause and consequence of depression
   EX: If someone has low social skills or poor eye contact, they may struggle to make friends → feel isolated → become more depressed → spiral worsens.

🌪 PART 2: Stress Generation Theory ⚡

🧠 Who made it?

• Constance Hammen (1991)

🔑 Key idea:

People who are depressed (especially girls & women) sometimes create their own stress, especially interpersonal stress, like fights or breakups.

This stress is:

• Dependent (they played a role in it)

• Not just bad luck or random (not independent)

😔 How?

• Picking toxic partners

• Acting clingy or conflict-triggering

• Constant reassurance seeking

• Being high in interpersonal sensitivity

🧬 Stress Generation + Childhood Maltreatment + Genes = 💥

• Girls who had childhood maltreatment + a genetic risk factor (s-allele of serotonin transporter gene) → more self-caused stress → higher depression

⚡ PART 3: Psychological Theories of Bipolar Disorder Bipolar has been less studied psych-wise, but now we have ideas like:

1. Stress triggers bipolar episodes

• Life stress → both depression AND mania episodes

2. Cognitive problems like:

• Negative self-esteem even when not symptomatic

• Dysfunctional thinking (like Beck’s stuff)

• Memory issues, trouble with problem-solving

3. Mania as a defence mechanism:

• Some say manic episodes protect against horrible internal feelings, like:

  • Low self-esteem

  • Hopelessness

• So mania = psychological escape from deeper pain

4. BAS Dysregulation Theory 🔥 (Behavioural Activation System)

• Proposed by Alloy & Abramson (2010)

• BAS = reward system in brain

• Depressed = low BAS → no motivation

• Manic = HYPER BAS → too sensitive to rewards
  → Chases goals too hard
  → Overreacts to success
  → Leads to risky behaviour, impulsivity, mania

🌟 OVERVIEW:

This section explains how genetics, brain chemistry, and biology contribute to depression and bipolar disorder. TLDR: there’s no one magic cause, but biological vulnerability plays a huge role.

🧬 GENETIC VULNERABILITY

🧠 GENE–ENVIRONMENT INTERACTIONS (GxE)

✨ These findings emphasize that depression isn’t all genes or all environment—it’s how they mix together.

🧪 NEUROCHEMISTRY & ANTIDEPRESSANTS

Let’s talk brain chemicals 🧠✨

💡 Even though these meds work, it doesn’t mean depression is only caused by low serotonin. There’s more to the story (receptors, transporters, brain circuits, etc.), but this is a foundational clue.

🔑 KEY TAKEAWAYS SO FAR:

• 🧬 Bipolar has strong genetic roots; MDD is also heritable but less so.

• 🔁 Gene–environment interactions (like trauma + certain genes) shape depression risk.

• 💊 Antidepressants target serotonin, norepinephrine, and dopamine—but neurotransmitter levels alone don’t explain everything.

🧪 1. Neurotransmitters: Why the Old Theories Weren’t Enough

• Old belief: Depression = low serotonin/norepinephrine/dopamine. Mania = high levels.

• Problem:

  • Tricyclics and MAOIs raise neurotransmitter levels immediately… but clinical effects take 7–14 days.

  • By the time mood improves, neurotransmitter levels have returned to baseline → ❌ inconsistent.

  • Measuring metabolites (breakdown products of neurotransmitters) doesn't always reflect actual brain activity → not reliable.

🧠 2. Newer Theory: Postsynaptic Receptor Sensitivity

• Instead of focusing only on neurotransmitter levels, scientists started to study how sensitive the brain receptors are.

• Overly sensitive dopamine receptors may trigger manic episodes (like with dopamine-increasing drugs).

• Serotonin receptor sensitivity and dysfunction are also implicated, especially in people with family histories of depression.

• 🧪 Tryptophan Depletion Studies:

  • Lowering tryptophan (a precursor to serotonin) causes return of depression in those in remission — but not in people with no depression history.

  • Shows serotonin hypersensitivity may be tied to genetic vulnerability.

🧬 3. Structural and Functional Neuroimaging Findings

🧠 Brain Areas Involved:

📌 Beck (2008): Combo of overactive amygdala + underactive prefrontal cortex → depression and cognitive bias (tendency to interpret things negatively).

🧪 4. MAO-A and New Neurochemical Evidence

• Jeffrey Meyer’s breakthrough: People with untreated MDD have ↑ 35% MAO-A enzyme levels → breaks down serotonin, dopamine, norepinephrine = contributes to lower monoamine levels.

• Same effect found in postpartum depression.

• MAO-A may be the main reason monoamine levels are low in depression.

• 🧪 = stronger evidence than just "low serotonin" theory.

💡 5. Challenges in Bipolar Imaging Studies

• Inconsistent findings due to:

  • Small sample sizes

  • Equipment differences

  • Patient differences (age of onset, suicide attempt history)

• Solution proposed: Focus on specific symptoms (e.g., emotional reactivity) instead of whole bipolar diagnosis.

🧪 6. HPA Axis (Neuroendocrine System)

• HPA axis = stress hormone system: hypothalamus → pituitary → adrenal → cortisol

• Found to be overactive in people with depression:

  • ↑ cortisol levels

  • ↑ adrenal gland size

  • Dexamethasone suppression test: depressed people don’t suppress cortisol properly

• Interpretation: body’s stress system is hyperactive and doesn’t shut down even when it should.

• Tied to vegetative symptoms like sleep and appetite disturbances.

• 🧬 Genetic tie-in: 5-HTTLPR short allele carriers have higher cortisol response + cognitive bias + amygdala hyperactivation (Gotlib et al., 2008)

🧠 7. Brain Hemispheres

• Right hemisphere dysfunction = flat affect, indifference

• Left hemisphere dysfunction = sadness, agitation

• Depression involves dysfunction in both hemispheres, but symptoms vary depending on which is more affected.

🔁 8. Biological vs Psychological: NOT Opposites

• Even if depression has biological roots (like cortisol and serotonin), psychological factors like negative thinking still matter.

• Beck (2008) proposed a combined model → see below!

🧠 9. Beck’s "Deconstructing Depression" Model

🔁 This creates a cycle that maintains and worsens depression.

🧪 Summary Table: Biological Hypotheses

🧠 KEY TAKEAWAYS

• Neurotransmitter levels alone don’t explain depression.

• Postsynaptic sensitivity, MAO-A activity, and the HPA axis are better biological indicators.

• Brain imaging shows consistent amygdala hyperactivity and prefrontal underactivity in MDD.

• Structural changes like reduced hippocampus size may result from chronic depression.

• Beck’s integrative model links biology and cognition, not one or the other.

✨

🧠 BIG PICTURE:

Mood disorders like MDD and bipolar disorder can be treated with psychological therapies or biological therapies (or both). Even though depression can go away on its own, treatment is important because:

• It's debilitating

• It often recurs

• Suicide is a risk

Many people in BC (and elsewhere) don’t get proactive care — usually only their GP sees them (not a psychiatrist). So we need a flexible, stepped-care approach

🌪 Psychodynamic Therapies

📉 Evidence:

• Mixed results.

• Older studies say: not much evidence for long-term psychodynamic therapy.

• Some newer ones say: short-term psychodynamic therapy is just as good as antidepressants for mild/moderate MDD.

• One version, Interpersonal Therapy (IPT) = focuses on current relationships and communication 💬. Very good at preventing relapse!

🧠 Cognitive-Behavioural Therapy (CBT)

✅ Evidence:

• CT can work better than meds in some people (especially mild/moderate MDD).

• Works best when the person:

  • Doesn’t have super chronic or early-onset depression

  • Doesn’t have comorbid personality disorders

• Long-term CBT helps prevent relapse (yay!).

🧠 Problem-Solving Therapy (PST) = a form of CBT that focuses on:

• Identifying problems

• Finding practical solutions

• It works well too!

🧘 Mindfulness-Based Cognitive Therapy (MBCT)

✅ Evidence:

• Cuts relapse in half for people with ≥3 depressive episodes.

• Helps reduce rumination 🌀 and improves autobiographical memory specificity (less vague, more precise memories).

• Also helps current depression, anxiety, and chronic suicidal thoughts.

🔁 Similar idea:

• Preventive Cognitive Therapy = booster-style CBT given after someone improves. Helps prevent future depression too.

TL;DR Summary Table:

Here’s how we’ll break it down for clarity:

💭 1. Depression in University Students

• Being in university ≠ protection from depression.

  • Key stressors: identity confusion, being away from home, constant evaluations, and social comparison 😣

• Prevalence:

  • ~12% of college students report depression in a year (Blanco et al., 2008)

  • 13.8% undergrads vs. 11.3% grad students (Eisenberg et al.)

  • A review found self-reported depressive symptoms in 30.6% of students (not necessarily diagnosed depression)

• Prevention Programs:

  • Most effective when:

    • Delivered by trained professionals

    • Target negative thinking + teach problem-solving

  • 🧠 CBT & relaxation training help reduce symptoms

  • Workshops encouraging optimistic thinking lowered symptoms (Seligman et al.)

  • Perfectionism-focused online CBT helped high-risk students (reduced both perfectionistic thoughts and depressive symptoms)

⚠ Many programs underused. Male students underrepresented in prevention programs!

🧠 2. Psychological Treatment of Bipolar Disorder

• Bipolar patients often struggle with interpersonal and cognitive issues (especially after manic episodes).

• CBT can help:

  • Focuses on thoughts + behaviours during mood swings (Basco & Rush, 1996)

  • Educating patients improves medication adherence and reduces relapses 💊

• Family dynamics matter: Returning to a home with high “expressed emotion” (hostility, overinvolvement) → more relapses

  • Family education + stress reduction = fewer relapses

• Mixed evidence:

  • Scott et al. (2006): CT worked best for those with <12 past episodes

  • Lam (2006): Emphasized structure, early warning signs, routine, and mood tracking as key strategies

  • Beynon et al. (2008): CBT + psychoeducation may prevent relapse

  • Miziou et al. (2015): Only psychoeducation had consistent evidence

Bottom line: Psychotherapy can help alongside meds, but results vary. About ⅓ of people with bipolar seek psychotherapy.

⚡ 3. Biological Therapies – ECT

• Electroconvulsive Therapy (ECT) = dramatic treatment for severe depression

• Introduced by Cerletti & Bini in the 1930s

• 💡 Inspired by seizures in animals at a slaughterhouse (wild origin story 😵)

• Used for severe, unresponsive depression after other treatments fail

How it works:

• Induces a seizure via electrical current (70–130 volts)

• Unilateral ECT (right side) now preferred over bilateral to reduce memory loss

• Patients receive anesthesia + muscle relaxants → wake up with no memory of procedure

📉 How effective?

• Fast results, but unknown mechanism

• Risks: confusion + memory loss

• 50% remission rate; high relapse rate (~51% in a year, even with continuation meds)

💥 Controversial:

• Some feel it saved their lives

• Others report long-term harm (e.g., Wendy Funk's memoir)

• Media spotlight: Ontario use ↑350% in 7 years (2010–11) 😬

⚠ Needs:

• Informed consent

• Strict guidelines and standards

🧠 Quick Recap Table

🌟 PART 1: New Biological Treatments for Depression

🧠 1. Deep Brain Stimulation (DBS)

• What it is: Surgically implanted electrodes deliver electrical impulses to the brain.

• Target area: Subgenual cingulate region (Brodmann area 25) — overactive in treatment-resistant depression.

• Why it’s used: For people who didn’t respond to meds, ECT, or psychotherapy.

• Evidence: Showed promise in unipolar and bipolar depression, and even other conditions like OCD, addiction, Alzheimer’s, and anorexia.

• Downside: Extremely expensive (~$250,000 per person ).

🧲 2. Repetitive Transcranial Magnetic Stimulation (rTMS)

• What it is: Non-invasive brain stimulation using magnetic pulses.

• How it works: Pulses pass through the skull → stimulate brain tissue → elevate mood.

• Uses: Depression, chronic pain.

• Evidence: Better than placebo; increases glutamate levels (linked to improvement).

💊 PART 2: Drug Therapies for Depression

Three Main Categories:

❗ Key Points:

• Antidepressant use has skyrocketed in Canada.

• SSRIs are most commonly prescribed, especially for younger patients.

• Effectiveness varies a lot — some don’t respond, and we can’t predict who will.

• Best outcomes = combo of meds + CBT (esp. when social or cognitive issues are involved).

💫 PART 3: STAR*D Study

(Sequence Treatment Alternatives to Relieve Depression)

• Main idea: Flexible, multi-step treatment.

• Started with: citalopram (SSRI)

• If no improvement after 8–12 weeks → other drugs or CBT

• Takeaways:

  • Only ~70% achieved remission after 4 steps.

  • No clear predictors of who’ll respond to what.

  • People with anxiety had poorer outcomes.

  • Minority groups (esp. Black participants) had higher drop-out rates and worse outcomes → need for earlier and culturally safe interventions!

💎 PART 4: Drug Therapy for Bipolar Disorder

💡 Lithium Carbonate (1st Mood Stabilizer)

• Works in 80% of patients! 👑

• Effective for: both manic and depressive episodes.

• Slow onset → often started with antipsychotic (e.g., Haldol) for quick relief.

• Side effects: tremors, dizziness, thyroid/parathyroid issues (→ monitor calcium!).

• Discontinuation = relapse risk 🚨

• Use has declined due to side effects & newer “mood stabilizers.”

☀ PART 5: Seasonal Affective Disorder (SAD)

• Treatment: Phototherapy (bright white light therapy).

• CBT + Light therapy = better long-term outcomes!

  • CBT helps challenge negative winter thoughts.

  • Behavioural activation encourages daily pleasure activities.

• 🧠 This is based on Lewinsohn’s theory — depression = lack of positive reinforcement.

🛡 PART 6: Preventing Depression

• Prevention is possible — but not many studies focus on reducing actual diagnoses.

• CBT and IPT-based prevention programs can reduce incidence by ~22%.

• Most effective = multi-component, targeted programs (e.g., cognitive + interpersonal + parent involvement).

💀 Suicide & Mood Disorders (8.5 Part 1)

📊 Suicide Stats in Canada (2012 data):

• Suicide = 9th leading cause of death in Canada overall.

• Top 2 cause of death for youth (15–24) (after accidents).

• 3,926 total suicides in Canada that year (10.4 per 100,000).

• Males = 2,972 suicides (75% of total suicides).

• Gender paradox:

  • Women attempt more often, but

  • Men die more often (use more violent methods).

• Suicide rates are increasing in places like the U.S. too.

🔄 Important Definitions:

🔍 Who’s most at risk?

• Having a plan → increases chance of attempt (31.9% with plan vs. 9.6% without).

• Unplanned attempts = still very common (43% of attempts).

• Biggest predictor of future attempt = past attempt 😔

🧠 Suicide Attempt vs. Gesture (from Nock & Kessler, 2006):

Suicide attempters:

• More likely to be male

• Lower education

• Psychiatric diagnoses (depression, impulsivity, aggression)

• Comorbid mental illnesses

• History of physical/sexual abuse

💔 Predictors of Completed Suicide (Brown et al., 2000):

• Strong suicidal ideation

• Hopelessness

• Depression

• Unemployment

• Diagnosis of bipolar depression

🧍‍♀ Impact on Survivors:

• Emotional aftermath: shock, guilt, shame, anger, etc.

• Higher mortality among survivors in the year after a loved one’s suicide.

• Double stigma: suicide + mental illness.

🧠 Suicide & Psychological Disorders:

MDD:

• ~15% of MDD patients die by suicide.

• Warning signs: weight loss, insomnia, guilt, suicidal thoughts.

• Insomnia is a strong immediate risk sign.

Bipolar Disorder:

• Risk increases in depressive phases (hopelessness), mixed phases (severity, younger age).

• Childhood neglect increases suicide risk in females.

Borderline Personality Disorder:

• Especially high suicide risk in those with mood instability (emotional swings).

Alcohol Use Disorder:

• Very high suicide risk, especially if co-occurring with depression.

Schizophrenia:

• Suicide risk similar to MDD. Risk signs: depression, psychosis, family history, low negative symptoms.

👶 Early Warning Signs (Sourander et al., 2009):

• Male suicides often had mental health issues by age 8, especially anxiety + conduct issues.

• Females: no strong predictors found at that age.

⚠ Clinical Insight:

• Suicidal behaviour often missed in diagnosis.

• Researchers recommended adding a separate diagnosis for suicidality in DSM, but DSM-5 removed Axis system, so it didn’t happen.

🌍 1. Sociological Perspective – Durkheim’s Theory

Émile Durkheim (1951) viewed suicide as a social phenomenon, not just an individual issue.

He proposed 3 types of suicide:

🧠 2. Psychological Theories

Many motives have been proposed:

• Freud: Aggression turned inward.

• Others: Retaliation, escaping pain, joining loved ones, guilt, or the desire to end unbearable emotional suffering.

💡 Key point: Most people are ambivalent.

• People often communicate their intent (e.g., giving away items, making final plans).

• Suicide often happens in a narrowed state of awareness, where options feel limited.

🔁 3. Risk Factor Model (Government of Canada, 2006)

Breaks suicide risk into 4 categories:

🚪 4. Baumeister’s Escape Theory

• Suicide = escape from aversive self-awareness 😖

• People feel inadequate, ashamed, and blame themselves.

• Rooted in:

  • Unrealistic self-expectations

  • Emotional suffering from self-perceived failure

• Perfectionists = especially vulnerable

🎯 5. Perfectionism Social Disconnection Model (PSDM)

• Interpersonal perfectionism = need to appear flawless → creates isolation & hopelessness.

• Bullying + need to seem perfect = toxic combo for suicidal ideation.

🧍‍♂ 6. Joiner’s Interpersonal Theory of Suicide

🔑 Two main factors that lead to suicidal desire:

1. Thwarted belongingness (“I am alone”)

2. Perceived burdensomeness (“I am a burden”)

If a person feels both ➕ has the capability to die by suicide, the risk is high.

➕ Capability to act = separate from desire

• Can be acquired through:

  • Nonsuicidal self-injury (e.g., cutting)

  • High distress tolerance

  • Sensation-seeking

💡 Prevention Insight:

• Enhance social belonging in schools or communities.

• Target perceived burdensomeness in therapy.

• Teach coping for emotional pain tolerance.

💬 Quick Summary Recap:

🧠 Section 8.5 Part 2: Psychological & Biological Theories of Suicide

🔹 Shneidman’s Approach: Suicide = a Solution to Psychache

• Edwin Shneidman saw suicide not as an illness but as a conscious effort to escape intense psychological pain (“psychache”).

• Psychache = unbearable emotional suffering → the main proximal cause of suicide.

• Psychiatric disorders like depression are only relevant in how much they contribute to psychache.

📝 Example:

• Research shows psychache:

  • Mediates the link between perfectionism and suicidality.

  • Predicts suicide risk better than depression or hopelessness (especially in homeless men and high-risk students).

🔹 Additional Psychological Factors

• 💭 Cognitive rigidity & problem-solving deficits: Suicidal people may feel “trapped” with only one perceived option — death.

• 💥 Impulsivity & neuroticism: Increase risk.

• 🌀 Hopelessness: Often a stronger predictor than depression.

• 🔮 Cognitive distortions like fortune-telling (e.g., "things will never get better") are common in suicidal individuals.

  • These distortions often lose significance when hopelessness is accounted for — showing how central hopelessness is.

🍁 Canadian Perspectives: Suicide Among Aboriginal People

Suicide rates in some Indigenous communities are astonishingly high:

• Ex: Innu of Labrador → 13× national rate.

• Ex: Pikangikum (Ojibwa reserve) → 213 per 100,000.

• Cluster suicides, poverty, trauma, solvent abuse, and sexual abuse are common factors.

• Inuit children → up to 30× more likely to die by suicide than other Canadian children.

📊 Protective factors:

• Church attendance

• Doing well in school

💔 Risk factors:

• Male gender

• Peer suicide

• Physical/sexual abuse

• Family alcohol/drug issues

🔐 Cultural Identity = KEY

• Suicide rates are lower in communities that preserve their cultural identity and self-determination (Chandler & Lalonde, 1998).

🧭 SPAG Report (2003):

• Multi-level prevention:

  1. Support cultural continuity

  2. Build youth identity

  3. Improve integrated health services

  4. Focus on community-led approaches

🛑 Crisis continues:

• 2016: 11 suicide attempts in one night in Attawapiskat → State of emergency declared.

💡 Linehan's Reasons for Living Inventory:

• Assesses reasons people don’t want to die (e.g., family, morality, fear of suicide)

• Helpful for therapeutic interventions 💖

🧬 Biological & Physical Factors in Suicide

⚠ Chronic Traumatic Encephalopathy (CTE)

• Found in athletes (e.g., NFL players) with repeated head trauma.

• Symptoms: impulsivity, irritability, decision-making issues.

• Diagnosed post-mortem via brain autopsy.

🧬 Genetics and Brain Chemistry

• Monozygotic twins → higher suicide concordance than dizygotic twins = genetic risk.

• Traits like impulsive-aggression may be intermediate traits passed in families.

🧪 Serotonin and Suicide

• Low serotonin (measured via 5-HIAA levels) → linked to impulsive/violent suicides.

• Brains of suicide victims show increased serotonin receptor binding, likely compensating for low serotonin.

• SPECT studies: Suicide attempters show impaired ability to regulate serotonin & dopamine under stress.

✨ KEY TERMS TO REMEMBER

• Psychache: unbearable emotional pain driving suicide (Shneidman).

• Hopelessness: strongest predictor of suicide, more than depression.

• Cognitive rigidity: inability to see alternatives to suicide.

• CTE: brain damage from repeated head injury.

• 5-HIAA: serotonin metabolite, low levels linked to suicide.

• Reasons for Living Inventory: tool to identify life-protective beliefs.

• Cluster suicide: multiple suicides in one community in a short time.

🌍 Global + National Suicide Prevention Strategies

• WHO’s SUPRE-MISS (1999):

  • “SUPRE” = Suicide prevention

  • “MISS” = Multi-site intervention study

  • Focuses on evaluating suicide treatment strategies + community surveys

• U.S. National Strategy (2012):

  • 4 key themes:

    1. Health-empowered people (individuals, families, schools)

    2. Preventive services (community + clinical)

    3. Treatment/support services

    4. Surveillance, research, evaluation

  • Goals: e.g., promoting responsible media reporting and countering myths (e.g., that suicide can’t be prevented)

• Canada:

  • No national suicide prevention strategy yet 😔

  • But groups like CASP (Canadian Association for Suicide Prevention) and MHCC (Mental Health Commission of Canada) are pushing hard

  • Working together to form a National Collaborative on Suicide Prevention

🧠 Treating the Underlying Mental Disorder

• Suicide is often linked to treatable mental disorders (e.g., depression, borderline personality disorder)

• Example: A Canadian study found almost all young men who died by suicide had an Axis I disorder, and over half had a personality disorder

• CBT and dialectical behaviour therapy (DBT) can reduce suicide risk by treating the underlying condition

Treating Suicidality Directly

• Some approaches focus directly on the suicidal state, not just mental illness

• Edwin Shneidman’s 3-part strategy:

  1. Reduce psychological pain

  2. Expand the person’s view of their options

  3. Pull them back from the brink of suicide (even temporarily)

📌 Example: Helping a suicidal pregnant student consider all options—even if none are ideal—gave her enough space to pause and reevaluate her situation.

☎ Suicide Prevention Centres (Crisis Lines)

• Modelled after the 1958 Los Angeles Suicide Prevention Center

• Staffed mostly by trained non-professionals under mental health supervision

• Main goals:

  • Provide 24/7 consultation to people in crisis

  • Use risk checklists to assess lethality

  • Build empathy and personal connection (phenomenological stance, “tuning in”)

• ✨Warning signs like suicidal threats or detailed plans are cries for help that centres try to respond to

📞 Canada-specific examples:

• First Canadian crisis line: Sudbury, 1965

• Major centres: Toronto (800,000+ calls/year), Montreal (French), Kamatsiaqtut Crisis Line in Iqaluit (culturally adapted to Inuit values despite being individual-focused)

💔 Survivors & Peer Support

• Survivors of suicide (including friends, family, even therapists present at the time) often face:

  • Guilt, grief, self-blame

  • Grieving can last longer than other types of loss

• Peer support groups can offer:

  • Social support, shared understanding, referrals, and venting space

⚖ Clinical and Ethical Issues

• Therapists are ethically responsible for preventing suicide, even if that means breaking confidentiality

• Malpractice suits can occur if a therapist fails to meet the standard of care

• There's a dilemma: How far should clinicians go?
  e.g., hospitalization, forced sedation, or physical restraint

💊 Physician-Assisted Suicide in Canada

• Brought into public eye by:

  • Jack Kevorkian in U.S. (helped 100+ people, jailed in 1999)

  • Canadian cases: Austin Bastable, Gloria Taylor, etc.

• Key legal milestone:

  • Carter v. Canada (2015): Supreme Court ruled assisted suicide bans were unconstitutional

  • Led to Bill C-14 in 2016: allows assisted dying for mentally competent adults with serious, terminal illness

📌 Debate continues:

• Some say it's too restrictive, others say not restrictive enough

• In 1999, 60% of Canadian doctors surveyed were in favour of legalization

🧪 Evidence-Based Treatments

• CBT and IPT (interpersonal therapy) = best psychological approaches

• Antidepressants may help, esp. newer ones (controversial but possibly effective)

• Lithium = reduces suicidality in bipolar and possibly unipolar depression

• Clozapine = helps reduce suicidality in schizophrenia

• ⚠ Often, clinicians must use interventions without strong evidence, because suicidal clients are in crisis

🚨 Challenges in Help-Seeking

• Only 29.5% of people with suicide ideation/attempts seek help

• More research is needed on how to increase help-seeking behaviour