PSYC 2161: Chapter 9: Stress

🌸 Case Example: Ms. A

• Who she is: 46-year-old lawyer, married, has irritable bowel syndrome (IBS) since age 20.

• Stressors: Pressured job + stressful marriage.

• Symptoms: IBS flares right after arguments or deadlines → crampy pain, diarrhea, constipation, bloating.

• Mental health: Developed major depression (low mood, fatigue, poor sleep, crying, impaired concentration).

• Medication journey:

  • Amitriptyline → helped depression, but worsened constipation ❌

  • Fluoxetine → worsened diarrhea ❌

  • Trazodone → too sedating ❌

  • Nortriptyline → worked ✅ (depression lifted + IBS improved).

• Big reveal: Her husband was also depressed → after he got treatment, marital conflict decreased, and her IBS stabilized.

✨ Takeaway: Stress + relationships + physical health are interconnected. Treating one person’s issues sometimes means looking at the social system around them too (biopsychosocial model).

🌱 What this shows us

1. Stress has many forms → it can impact both mind + body.

2. Mind-body link → physical illness worsens emotional well-being, and vice versa.

3. Life stressors = catalysts → marital conflict made her IBS flare.

4. Social context matters → husband’s depression was a hidden factor.

5. Fits biopsychosocial model → biology (IBS), psychology (depression, stress), social (marital discord).

🏠 Roy Romanow’s “Tips for Health” (2003)

These are big-picture public health ideas about reducing stress and improving health in Canada:

1. Don’t be poor → socioeconomic status is the #1 predictor of health.

2. Get a good start in life → prenatal & early childhood matter long-term.

3. Graduate from school → more education = better health outcomes.

4. Get a job → unemployment worsens stress + health.

5. Choose your community → where you live and your sense of belonging impacts health.

6. Live in quality housing → environment affects disease risk.

7. Look after yourself → eat well, exercise, avoid substances.

8. Men and women differ → women live longer but report poorer health.

✨ Takeaway: These are social determinants of health. Poverty, education, housing, community, and lifestyle shape physical + psychological well-being.

📖 Stress-Related Disorders in DSM-5

DSM-5 created a new category: Trauma- and Stressor-Related Disorders. These include:

• PTSD → long-lasting maladaptive reaction to trauma.

• Reactive Attachment Disorder (RAD) → emotionally withdrawn child, due to neglect.

• Disinhibited Social Engagement Disorder (DSED) → child is overly friendly with strangers (neglect/chaotic caregiving).

• Acute Stress Disorder → trauma symptoms 3 days–1 month after trauma (often in first responders).

• Adjustment Disorders → emotional/behavioural symptoms after major stressor (but not enough for depression/anxiety diagnosis).

💊 Psychophysiological Disorders

• Definition: Real physical illnesses that are caused/worsened by emotional stress.

• Examples: Asthma, hypertension, headaches, gastritis.

• Used to be called psychosomatic disorders.

• Important: Not imaginary — stress can cause actual organ damage and even death (e.g., uncontrolled high BP).

🧠 Fields of Study

• Behavioural medicine & health psychology → study how psychology influences health/illness, and how to prevent/treat stress-related illness.

• Examples: biofeedback for headaches, studying health care delivery.

• Prevention focus: cardiovascular disease (CVD) is the leading cause of death in Canada, often linked to lifestyle factors (smoking, diet, alcohol). Health psychologists try to reduce risk.

🌟 Big Takeaways from Part 1

• Stress deeply impacts both mental and physical health.

• Social determinants (poverty, education, housing, community, lifestyle) are central to health outcomes.

• DSM-5 recognizes stress-related disorders as a distinct category.

• Psychophysiological disorders are real medical conditions tied to stress.

• Health psychology = prevention, treatment, and understanding the mind-body link.

🌸 Defining Stress

• Originally, stress = environmental condition that can trigger psychopathology.

• We also learned about self-generated stress (basically when your own behaviours/thought patterns create stress for you).

• Here → the text digs deeper into what stress is and the struggles in pinning down its definition.

👨‍🔬 Hans Selye: The Father of Stress

• Who he was:

  • Endocrinologist, originally from Europe, became Canadian 🇨🇦.

  • Worked at McGill University in Montreal.

  • Authored 30 books + hundreds of research papers on stress.

  • Companion of the Order of Canada (1968) + even on a postage stamp!

• His big contribution:

  • Coined the term “stress” (though later wished he’d said “strain” because “stress” already had a physics meaning).

  • Defined stress as the non-specific response of the body to any demand for change.

🩺 General Adaptation Syndrome (GAS) – Selye’s Model (1936)

This is a biological stress response that happens when you’re under ongoing pressure:

1. Alarm Reaction 🚨

   • Autonomic nervous system is activated (fight-or-flight).

   • If too intense → physical consequences (GI ulcers, enlarged adrenal glands, thymus atrophy).

2. Resistance 🛡

   • The body tries to adapt/calm things down using coping mechanisms.

   • How long this stage lasts = depends on your adaptability + intensity of the stressor.

3. Exhaustion 🥀

   • If stressor continues, body’s resources run out.

   • Can lead to irreversible damage or death.

✨ Key idea: Stress is linked to all diseases (directly or indirectly).

🌈 Types of Stress

• Distress → negative, damaging, unpleasant stress (e.g., anxiety, marital fights).

• Eustress → positive, motivating stress (e.g., excitement before a big presentation).

  • Both increase physiological arousal, but only distress is harmful.

🧠 Stress & Illness (Selye’s own story)

• Selye himself developed a rare, usually fatal cancer.

• He believed his survival came from his strong desire to keep doing research.

• This shows how psychological factors (like meaning, motivation, faith) may influence physical outcomes (e.g., cancer).

🌀 Problems with Defining Stress

• If you define stress only as a response, you run into issues:

  • Emotional upset, poor performance, sweating, or high cortisol levels can all happen for non-stressful reasons (like being hyped for a concert 🎶).

• So researchers realized → stress = more complex than just “body reactions.”

🌟 Big Takeaways from this Part

1. Hans Selye gave us the language and biological framework for stress.

2. Stress = nonspecific body response to demands for change.

3. GAS model (alarm → resistance → exhaustion) explains how prolonged stress harms health.

4. Stress can be bad (distress) or good (eustress).

5. Defining stress is tricky — body changes alone aren’t enough to label something as stress

⚡ The Autonomic Nervous System (ANS) & Stress

• Two big systems in the nervous system:

  • Somatic NS = voluntary, conscious movements (like moving your arm).

  • Autonomic NS = automatic/involuntary (like heart rate, digestion, glands).

• The ANS controls:

  • Endocrine glands 🧪

  • Heart ❤

  • Smooth muscles in blood vessels, stomach, intestines, kidneys, etc.

✨ Even though it’s “automatic,” biofeedback research shows we can influence it more than we used to think (e.g., lowering heart rate with relaxation training).

🔄 Sympathetic vs. Parasympathetic

• Sympathetic NS = “fight or flight” 🚨

  • ↑ Heartbeat

  • Dilates pupils

  • ↓ Digestion

  • ↑ Sweating/electrodermal activity

  • Gets body ready for action

• Parasympathetic NS = “rest and digest” 🛌

  • Calms the body back down

  • Restores lower activation

💡 Problem: If you’re chronically stressed → sympathetic system stays ON → prolonged stress hormones → health problems like immune suppression, hypertension, and organ damage.

🌪 Stress as a Stimulus = Stressors

• Stressors = external things/events that cause stress.

• Can be:

  • Major → death of a loved one

  • Minor → traffic jam

  • Acute → failing an exam

  • Chronic → hostile workplace

• Types of stressors:

  • Psychogenic = psychological (e.g., anticipating bad news)

  • Neurogenic = physical (e.g., surgery, injury)

✨ Other dimensions of stressors (Anisman & Merali, 1999):

• Controllable vs. uncontrollable

• Predictable vs. unpredictable

• Short-term vs. chronic

• Intermittent vs. recurring

⚖ Allostatic Load

• If stressors are chronic, unpredictable, or intense, body’s systems struggle to adapt.

• This wear-and-tear is called allostatic load.

• Leads to pathological outcomes (illnesses, immune breakdown, etc.).

🧩 Problems with Defining Stressors

• Not just negative events — even positive life events (marriage, new job) are stressors because they demand adaptation.

• People differ widely in their responses → depends on:

  • Financial resources 💰

  • Social support 🤝

  • Personality/cognitive appraisal 🧠

Example: After the 2016 Fort McMurray fire, families with money + friends recovered better than those without support.

🧠 Stress as Cognitive Appraisal (Lazarus, 1966)

• Stress = not just the event itself, but how you perceive it.

• If you think demands > resources, you feel stressed.

• Example: Same exam might feel like a challenge to one student but overwhelming to another.

• Ottawa study: women’s stress in breast cancer screening was linked to how they interpreted the experience.

💪 Coping Styles

According to Lazarus & Folkman (1984):

1. Problem-focused coping 📝

   • Tackling the stressor directly (e.g., making a study schedule, finding solutions).

2. Emotion-focused coping 💆‍♀

   • Managing feelings (e.g., distraction, relaxation, seeking comfort).

🔀 Transactional Model of Stress (Lazarus, Neufeld)

• Stress = interaction between situation + person.

• Stressors and coping evolve over time → it’s a dynamic process.

🎯 Goodness-of-Fit Hypothesis

• Effectiveness of coping depends on whether it matches the situation:

  • Distraction → good before surgery (calms nerves).

  • Distraction → bad if you find a breast lump (you need problem-solving).

• Continuing to fight an unsolvable problem = frustration and harm (Terry & Hynes, 1998).

🌟 Big Takeaways

• ANS = stress highway → Sympathetic (on) vs. Parasympathetic (off).

• Chronic sympathetic activation = big health problems (hypertension, immune suppression).

• Stressors can be psychological, physical, controllable/uncontrollable, etc.

• Stress = not just what happens, but how you appraise it.

• Coping = problem-focused vs. emotion-focused → best if matched to the situation.

• Stress is a transactional process (situation + person + time).

🔑 Coping & Controllability

• Whether stress-coping is effective depends on controllability of the situation:

  • Controllable situation → best to use problem-focused coping (e.g., study schedule for exams, asking for help).

  • Uncontrollable situation → problem-solving won’t help, better to use emotion-focused coping (venting, expressing feelings, relaxation).

• Denial & avoidance:

  • Common response to shocking/stressful events.

  • But escape/avoidance coping (“I wish this would just go away”) = least effective long-term.

  • Works short-term for overwhelming shocks, but harmful over time.

📏 Measuring Stress

Stress is hard to define → also hard to measure. Two main approaches are highlighted:

1. 🗂 The Social Readjustment Rating Scale (SRRS)

• Developed by Holmes & Rahe (1967).

• Method: people rated life events by how stressful & how much adjustment they required.

• Marriage was the reference point (set at 500 originally, then rescaled to 50).

• Example (Miller & Rahe, 1997 rescale):

  • Death of a child → 123

  • Death of a spouse → 119

  • Death of a sibling → 102

  • Death of a parent → 100

  • Divorce → 96

• 💡 Findings: Higher Life Change Unit (LCU) scores linked with illnesses (heart attacks, leukemia, colds/fevers).

• BUT caution: illness itself can increase life-change scores (e.g., job loss from being sick). → stress-illness link is correlational, not always causal.

• 🔁 Best studies are longitudinal (track stress + health changes over time).

2. 📓 Assessment of Daily Experience (ADE)

• Developed by Stone & Neale (1982).

• Focus = daily prospective records (instead of long-term memory, which is biased).

• Why? Daily recall is more accurate + avoids retrospective bias.

• Results:

  • Desirable events ↓ 3–4 days before respiratory illness.

  • Undesirable events ↑ 4–5 days before illness.

  • Suggests life events may play a causal role in illness vulnerability.

🧩 Daily Hassles

• Minor hassles often predict health outcomes better than major events.

• Original Hassles Scale (Kanner et al., 1981) had issues:

  1. Contamination → included symptoms of distress (like fatigue) instead of hassles.

  2. Relevance → designed for middle-aged adults, not all groups.

• Revised versions:

  • Anita DeLongis (UBC 💙) refined the Hassles Scale (1988).

  • Tailored versions for students and teens:

    • Brief College Hassles Scale (BCHS) → 3 main themes:

      1. Academic hassles 🎓 (deadlines, bureaucracy)

      2. Interpersonal hassles 💔 (dating, parents)

      3. Financial hassles 💸 (debt, expenses)

    • Also included time management, chores, noise, job prospects, etc.

🌟 Big Takeaways

1. Coping effectiveness depends on controllability.

   • Problem-focused = good if solvable.

   • Emotion-focused = better if unsolvable.

   • Avoidance = worst long-term.

2. SRRS: measures big life events → shows correlation between stress & illness, but not perfect (illness can inflate scores).

3. ADE: measures daily events prospectively → stronger evidence for stress → illness link.

4. Daily hassles may matter more than big life events in predicting health outcomes

🌸 Daily Hassles & Health

• BCHS (Brief College Hassles Scale) findings:

  • Higher scores → more psychological distress (Blankstein, 1991).

  • Linked to more headaches (Bottos & Dewey, 2004).

  • Students with lower emotional intelligence & stress management → more hassles + more symptoms (Day et al., 2005).

• Illness-specific hassles (Fillion et al., 2001):

  • For cancer patients → hassles like future worries (“what happens to my family if I die”), disability, body image.

  • Associated with ↑ anger, fatigue, depression.

  • Important: these measures are precise but population-specific (don’t generalize beyond the group studied).

🎓 Student Perspectives 9.1: Health Status of Students

• Myth busted: Students don’t rate their health better than older adults.

• Negative health ratings linked with:

  • Poor child–parent relationships

  • Lower school achievement/interest

  • Low self-esteem

  • Smoking 🚬

  • Being female (replicated internationally).

• European study: worst predictor of self-rated health = psychosomatic symptoms.

• ACHA National College Health Assessment (2008, USA):

  • 66% → excellent/very good health

  • 27% → good

  • 7% → fair/poor

• Ontario campuses (2009):

  • 10.8% rated health as fair/poor.

  • 21.2% reported a traumatic health problem in past year.

  • Stress levels high → 43.2% “more than average stress,” 11.4% “tremendous stress.”

💡 Mortality link: Students rating their health as poor had double the risk of death compared to those who rated excellent (DeSalvo, 2005).

Top student health problems (USA survey):

1. Allergies (47.9%)

2. Back pain (46.1%)

3. Sinus infection (30.7%)

4. Depression (17%)

5. Strep throat (13.8%)

• ~10% asthma.

Top academic disruptors:

• Stress (33.9%)

• Cold/flu/sore throat (28.8%)

• Sleep difficulties (25.6%)

• Concern for friend/family (18.8%)

• Internet/gaming (16.9%)

✨ Takeaway: Student health is fragile → stress, inactivity, and poor coping are major risks.

💼 Stress in Work Contexts

• Job stress:

  • Comes from personal traits or high-stress occupations (nurses, doctors, accountants at tax season).

  • Consistently linked to depression and negative health outcomes.

• Nurses study (Shields & Wilkins, 2005):

  • Survey of 18,676 nurses across Canada.

  • ~1/3 had high job stress/strain.

  • Predicted poorer physical & mental health + more sick leave.

• Job spillover: stress from work spreads into family life.

🔥 Job Burnout

Concept developed by Christina Maslach & colleagues.
Three components:

1. Emotional exhaustion 😩

2. Depersonalization (becoming detached/insensitive to others)

3. Reduced personal accomplishment (feeling ineffective, unproductive).

• Burnout linked with:

  • CVD (Melamed, 2006)

  • Depression

• Sometimes reflects work addiction/workaholism (Burke, 2006).

• Vital exhaustion = extreme burnout → severe depletion, linked to heart disease.

🧠 Coping Research

• How measured: questionnaires (e.g., COPE inventory) → ask which strategies people use.

• Best research = longitudinal → shows coping style → predicts later outcomes.

Example: Breast Cancer Coping Studies

• Carver et al., 1993:

  • Women with acceptance + humor → less distress.

  • Avoidant coping (denial, disengagement) → more distress.

• Heim et al., 1997 → replicated negative effects of denial.

• Epping-Jordan et al., 1994:

  • Avoidant coping predicted greater cancer progression after 1 year.

• 💡 Key idea: It’s not just the stress, but how you cope that drives outcomes.

🍁 Canadian Contributions 9.2: Norman Endler

• Big name in coping, stress, and anxiety research.

• Later partnered with James Parker (Trent University) → focused on coping with health/illness.

• Parker = Canada Research Chair in emotion & health.

• Examined predictors of outcomes like emotional intelligence and alexithymia (difficulty identifying/expressing emotions).

🌟 Big Takeaways

1. Daily hassles strongly linked with distress, headaches, and illness-specific struggles (esp. in vulnerable populations like cancer patients).

2. Students face high stress and health problems, with stress being the #1 academic disruptor.

3. Job stress & burnout → major risk factors for depression and cardiovascular disease.

4. Coping matters: avoidance is the worst, while acceptance and humor are protective.

5. Canadian researchers (DeLongis, Endler, Parker) are leaders in advancing stress and coping research.

🇨🇦 Norman Endler: Interaction Model of Anxiety, Stress, and Coping

• Who he was:

  • Famous Canadian psychologist (York University).

  • Awarded the Donald O. Hebb Award (1997) + Innis-Gerin medal by the Royal Society of Canada.

  • Died in 2003.

• Early work:

  • Developed the interaction model of anxiety with David Magnusson (1976).

  • Idea: trait anxiety + situation = state anxiety.

    • People anxious about physical danger → most anxious in dangerous settings.

    • People anxious about social evaluation → most anxious in public situations.

🧠 Expanding to Stress & Coping

• Later, Endler (with James Parker, Trent University) added stress and coping into the model.

• Key idea: Coping is a personality trait.

• They developed the Coping Inventory for Stressful Situations (CISS) → measures 3 coping styles:

  1. Task-oriented coping (problem-solving).

  2. Emotion-oriented coping (rumination, self-blame).

  3. Avoidance-oriented coping (distraction, social diversion).

🩺 Coping with Health Injuries and Problems (CHIP)

• Created to measure coping with illness.

• 4 scales:

  1. Emotional preoccupation (ruminative worry).

  2. Distraction (keeping busy).

  3. Instrumental coping (task/problem solving).

  4. Palliative coping (self-soothing, e.g., rest, comfort).

• Findings:

  • Chronic illness → ↑ emotional preoccupation, ↓ instrumental coping.

  • Cancer patients: emotional preoccupation stable across phases; palliative coping predicted emotional distress (Jadoulle, 2006).

  • Fibromyalgia patients not adhering to meds → low instrumental coping.

  • HIV/AIDS patients → well-being ↑ if high instrumental coping.

  • Mindfulness training → ↑ palliative coping.

🔄 Rumination & Perseverative Cognition

• Rumination = replaying negative thoughts → prolongs stress response (perseverative cognition hypothesis).

• Effects:

  • Prolonged cortisol elevation.

  • Linked with hypertension & cardiovascular activation (Key et al., 2008; Johnson et al., 2012).

  • Stronger in people with high hostility, self-directed anger, depression, anxiety.

• Interpersonal rumination (e.g., thinking about an argument):

  • ↑ cortisol and blood pressure (McCullough, 2007; Ottaviani, 2011).

• Fix: Cognitive distraction works short-term → but long-term requires cognitive control & thought-stopping techniques.

👭 Social Support as a Moderator

• Stress effects vary depending on coping + social support.

Types of Social Support

• Structural support: size of social network (friends, marital status).

• Functional support: perceived quality (having someone to call on).

• Forms:

  • Emotional support 💞 (feeling cared for).

  • Instrumental support 🛠 (practical help like meals, money).

Research Findings

• Adult survivors of abuse → more emotional than instrumental support (Muller, 2000).

• Structural support = predictor of mortality → fewer friends = higher death rates.

• Functional support linked with:

  • ↓ atherosclerosis (Seeman & Syme, 1989).

  • Better adjustment to chronic rheumatoid arthritis (Goodenow, 1990).

  • Loneliness = ↑ morbidity + mortality (Cacioppo, 2015).

Lab Studies

• Women under stress + close friend support → lower blood pressure (Kamarck, 1995).

• Support must come from a friend (not a stranger) to reduce physiological stress (Christenfeld, 1997).

• Oxytocin hypothesis: social bonding releases oxytocin → calms sympathetic nervous system (Uvnas-Moberg, 1997).

🌟 Big Takeaways

1. Endler’s model: Stress response = interaction of trait, situation, and coping style.

2. CISS/CHIP tools show how coping strategies predict health outcomes.

   • Instrumental coping = protective.

   • Emotional preoccupation/rumination = maladaptive.

3. Rumination prolongs stress → worsens physical health (cortisol, hypertension).

4. Social support (structural + functional) = key buffer for stress effects.

5. Not all support helps → must be trusted, meaningful support.

❓ Big Questions

Researchers ask:

1. Why does stress make some people sick but not others?

2. Why does stress cause illness in some but psychological disorder in others?

3. Why does stress cause different types of illness (e.g., asthma vs. hypertension) in different people?

➡ Most explanations use a diathesis–stress model (predisposition + stressor = illness). The “diathesis” can be biological 🧬 or psychological 🧠.

🚨 Problems with Self-Report Data

• A lot of early research = correlations between stress and self-reported illness.

• BUT: self-reports may not equal actual physical illness.

  • Watson & Pennebaker (1989): negative emotions linked to illness reporting, not necessarily illness itself.

  • Neuroticism → more complaints, but not “hard endpoints” like verified heart disease (Stone & Costa, 1990).
    ➡ This chapter focuses more on objective measures beyond self-report.

🧬 Biological Theories of Stress–Illness

1. Somatic-Weakness Theory

• Idea: Certain organs are genetically or biologically weaker → stress targets them.

• Example: Weak respiratory system → more likely to develop asthma when stressed.

2. Specific-Reaction Theory

• People have idiosyncratic autonomic response patterns to stress.

• Example:

  • One person → stress ↑ heart rate.

  • Another person → stress ↑ respiration.

  • Someone prone to BP spikes → more vulnerable to hypertension.

3. Prolonged Exposure to Stress Hormones (McEwen’s Theory of Allostatic Load)

• Short-term → stress responses are adaptive (mobilize energy, fight/flight).

• Long-term → cost to body from repeated HPA axis + sympathetic activation.

Mechanism:

1. Stress → sympathetic nervous system + HPA axis activated.

   • Epinephrine (adrenal medulla) + ACTH (pituitary) → cortisol (adrenal cortex).

2. Prolonged cortisol exposure →

   • Alters immune system → ↑ susceptibility to illness.

   • Kills hippocampal cells (hippocampus regulates cortisol itself).

   • → makes person even more vulnerable to stress.

Individual differences:

• Most people adapt (e.g., repeated public speaking → cortisol decreases).

• About 10% don’t adapt → cortisol keeps rising → these people are at higher disease risk (Kirschbaum, 1995).

Meta-analysis (Miller, Chen & Zhou, 2007, UBC):

• Stress → sometimes ↑, sometimes ↓ HPA activity. Why?

  • Timing: cortisol rises after stress, but normalizes over months.

  • Nature of stressor: traumatic, survival-related, or threats to self (like divorce) → prolonged activation.

  • Controllability: uncontrollable stressors → persistent HPA activation.

🌟 Big Takeaways

1. Stress → illness depends on individual vulnerabilities (weak organ systems, unique stress response patterns).

2. Somatic-weakness explains “why this organ,” specific-reaction explains “why different people react differently.”

3. Chronic cortisol exposure (allostatic load) explains long-term damage: immune suppression, brain changes, vulnerability.

4. Uncontrollable, traumatic, socially threatening stressors are the worst for long-term illness.

🦠 Stress & the Immune System

• Stress affects autonomic nervous system, hormones, and brain.

• Immune system = key in infectious disease, cancer, allergies, autoimmune disease.

🌡 Stress & Autoimmunity

• Stress can trigger autoimmune diseases (e.g., rheumatoid arthritis).

• Stressors shown to alter immune function: exams, bereavement, divorce, job loss, caregiving, disasters.

🧬 Psychoneuroimmunology

• Stress dysregulates immunity → vaccine responses delayed, weakened, shorter.

• Stress linked to tumour cytokine secretion (Antoni, 2006) → role in cancer progression.

• ⚖ Caveat:

  • Short-term stress → can be beneficial (immune boost).

  • Chronic stress → undermines immunity.

🛡 Secretory Immunity & sIgA

• sIgA antibodies in saliva, tears, nasal/gut secretions = first line of defense.

• Study: Dental students → saliva tested 3x/week.

  • Negative mood → ↓ sIgA antibodies.

  • Positive mood → ↑ sIgA antibodies.

• Mechanism: ↑ undesirable events + ↓ desirable events → negative mood → ↓ sIgA → ↑ infection risk.

🥶 Stress & Respiratory Infection Studies

• Volunteers exposed to cold virus nasal drops.

• Results: More stress → more likely to get sick.

• Stressors = interpersonal + work-related.

• Social support buffered risk (Cohen, 1997).

• Positive emotional style (happy, calm, energetic) predicted protection better than absence of negativity (Cohen, 2006).

📊 Meta-Analysis (Segerstrom & Miller, 2004)

• 300+ studies reviewed.

• Findings:

  • Short-term stress → can up-regulate immunity (“fight-or-flight” prep).

  • Even short-term stressors (like exams) → can suppress cellular immunity.

  • Chronic stress → suppresses both cellular + humoral immunity.

  • Low self-efficacy → diminished immune function.

🧠 Psychological Theories

1. Cognitive & Behavioural Factors

• Humans create stress beyond physical threats → regrets, worries, “what ifs.”

• These cognitive-emotional loops prolong stress hormone activation → “storms” body can’t withstand.

• Appraisal matters: perceiving life events as “too much” → chronic stress risk.

• Coping style matters: e.g., coping with anger linked to hypertension.

• Personality traits: high negative affect → higher risk of cardiovascular disease.

2. Psychoanalytic Theories

• Franz Alexander → father of psychoanalytic explanations for psychophysiological disorders.

• Idea: specific unconscious conflicts → disorder-specific emotional states.

• Example: Anger-in theory (essential hypertension)

  • Hostile impulses repressed → bottled-up anger → chronic stress state → hypertension.

  • Quote: repression = “damming up hostile impulses,” leading to defensive measures, occupational failure, envy, hostility.

🌟 Big Takeaways

1. Stress directly weakens immune defenses, esp. with chronic exposure.

2. sIgA studies show mood + daily hassles → immediate effects on infection vulnerability.

3. Experimental virus studies prove stress → illness risk, moderated by support + positive emotion.

4. Psychological theories emphasize appraisal, coping, and personality traits.

5. Psychoanalytic theories highlight unconscious conflicts (e.g., unexpressed anger → hypertension).

💔 Cardiovascular Disorders (CVDs) Overview

• CVDs = diseases of heart + circulation system.

• Focus here: Hypertension + Coronary Heart Disease (CHD).

• CHD = leading cause of death in CVD.

🇨🇦 Canadian Stats

• 1997 → CVD cost = $17 billion/year.

• 2000 → ↑ to $22.2 billion (direct + indirect).

• Still the second-leading cause of death in Canada → 1 in 5 deaths.

• Risk varies by region + ethnicity:

  • Higher in Eastern Canada.

  • South Asian Canadians = especially high risk.

📊 Canadian Heart Health Survey (1986–1992)

• Sample: >5,000 Canadians (55–74 yrs).

• Findings:

  • 52% hypertensive (!!)

  • 26% = isolated systolic hypertension.

  • 30% = cholesterol high enough for intervention.

  • 52% of hypertensives were untreated.

  • Nearly 50% had 3+ risk factors → and risk factors are synergistic (together they multiply risk, not just add it).

🧠 Public Knowledge (Kirkland et al., 1999)

• Asked: “What causes heart disease?”

  • Stress (44%), worry (44%), smoking (41%) = top answers.

  • BUT: cholesterol (23%), hypertension (16%) barely mentioned.

• Many didn’t know their own risk status:

  • ⅔ with high cholesterol didn’t know.

  • ⅓ women + 43% men didn’t know they were hypertensive.

💡 Canadian Hypertension Education Program

• Led by Dr. Norm Campbell.

• Aim = increase awareness, treatment, and control.

• Results:

  • Mortality + hospitalization ↓ 30% (1994–2004).

  80% premature CVD deaths are preventable (Capewell & O’Flaherty, 2009).

  • Canada + US: big improvements, but still high prevalence.

🔴 Essential Hypertension (High BP with no clear physical cause)

• Why important? → predisposes to atherosclerosis, heart attack, stroke, kidney failure.

• Called the “silent killer” because often symptomless until severe.

📏 Blood Pressure Basics

• Systolic (top) → heart contracting (normal ~120).

• Diastolic (bottom) → heart resting (normal ~80).

• CVD risk now considered to start at 115/75 mmHg → doubles with each 20/10 mmHg increase.

• AMA emphasizes systolic > diastolic as the key risk after age 50.

🌍 Prevalence

• Wolf-Maier et al. (2003):

  • 28% Canadians/Americans hypertensive.

  • 44% Europeans hypertensive.

• Worldwide: >1 billion people, ~7.5 million deaths/yr → leading global risk factor for death.

• Canada (2007–2009 survey):

  • 19% hypertensive.

  • Another 20% pre-hypertensive.

  • ~1 in 5 Canadians still hypertensive (2011).

📈 Progress in Canada

• 1992 vs. 2009:

  • Awareness: ↑ from 56.9% → 82.5%

  • Treatment: ↑ from 34.6% → 79%

  • Control: ↑ from 13.2% → 64.6%

• Now only ~1 in 5 Canadians with HTN not receiving treatment.

⚙ Causes & Risk Factors

• Essential hypertension = heterogeneous (many causes).

• Biological/physiological contributors:

  • Genes 🧬

  • Sympathetic nervous system activation

  • Hormones

  • Salt metabolism

  • CNS mechanisms

  • Cardiac output & vascular resistance

• Lifestyle contributors:

  • Obesity

  • High alcohol use

  • Salt-heavy diet (e.g., Inuit diet change study → hypertension doubled with Western diet, Picard 2009).

• Psychological contributors: stress + coping style.

🔟 Top 10 Risk Factors for Hypertension (Canadian Expert Working Group)

1. Excess body weight

2. High salt intake

3. Low potassium intake

4. Physical inactivity

5. Heavy alcohol use

6. Stress

7. Socioeconomic status (low SES = ↑ risk)

8. Family history/genetics

9. Age

10. Poor coping styles

🌟 Big Takeaways (Hypertension)

• Huge health + economic burden in Canada.

• Awareness and treatment improving thanks to national programs, but prevalence remains high.

• It’s multifactorial → genes, biology, lifestyle, psychology, SES.

• “Silent killer” because many don’t know they have it.

• Stress + coping = major psychological links.

🔼 Psychological Stress & Blood Pressure

• Short-term BP spikes = seen in stressful situations:

  • Natural disasters (earthquakes), stressful interviews, job stress.

  • Lab stressors: anger, fear, sadness, mental arithmetic, mirror drawing, cold pressor test (ice water!), public speaking → all ↑ BP (Cacioppo, 1993; Obrist, 1978).

  • Classic study: reaction-time task with threat of electric shock → ↑ HR + systolic BP.

• Ambulatory BP monitoring (real life):

  • Both positive and negative emotions raise BP (Jacob, 1999; Kamarck, 1998).

  • Paramedic studies: high-stress ambulance calls → ↑ BP, especially for those high in anger/defensiveness (Shapiro, 1993).

  • General effect = modest, but subset of people show very large increases (e.g., 20-point systolic jump).

  • Suggests: only those with diathesis/predisposition develop long-term hypertension.

🧬 Predisposing Factors for Hypertension

• Genetics:

  • Highly heritable, but only recently identified → meta-analyses (159,000 people!) found 13 new gene regions linked to BP (Levy, 2009; Newton-Cheh, 2009).

  • Each has small effect, but opens new directions.

• Cardiovascular Reactivity (CVR):

  • Individual differences in how strongly BP/HR respond to stress.

  • Longitudinal evidence:

    • 3,000 young adults → BP reactivity to a video game predicted coronary calcification 13 yrs later (Matthews, 2006).

  • Neurobiology:

    • High stress-evoked BP → ↑ amygdala activation, ↓ amygdala grey matter, and stronger connectivity with ACC + brainstem pons (Gianaros, 2008).

    • High CVR linked to heightened resting corticolimbic activity (Gianaros, 2009).

  • Takeaway → CVR = biological diathesis for hypertension/CHD.

❤ Coronary Heart Disease (CHD)

• Two main forms:

  1. Angina Pectoris → chest pain from ischemia (lack of oxygen to heart). Pain radiates to back/arm, relieved by rest or meds. Usually no permanent damage.

  2. Myocardial Infarction (MI, heart attack) → full artery blockage → oxygen cut off → permanent heart muscle damage.

• Risk factors (biological/lifestyle):

  • Age, sex (men > risk), smoking 🚬, high BP, high cholesterol, enlarged left ventricle, obesity, inactivity, alcohol overuse, diabetes.

  • Risk = cumulative (the more factors, the higher).

⚡ Stress & Heart Attacks

• Acute triggers:

  • Physical exertion, episodes of anger (Mittleman, 1997).

  • Acute stress (e.g., Tel Aviv missile attack → MI spike).

• Chronic stressors:

  • Marital conflict, financial problems.

  • Theory: chronic stress → immune activation → inflammation → CHD (Miller & Blackwell, 2006).

• Job stress (biggest studied factor):

  • High strain jobs = ↑ MI risk.

  • British civil servants study → low job control = more CHD (Marmot, 1997).

  • Finland → demanding jobs = ↑ atherosclerosis + CVD mortality (Lynch, 1997).

🧠 Psychological Diatheses for CHD

• Type A Behavior Pattern (Friedman & Rosenman, 1958):

  • Intense competitiveness, urgency, hostility/aggressiveness.

  • Western Collaborative Group Study (8.5 yrs, 3,154 men):

    • Type A men = 2x more likely to develop CHD than Type B.

    • Effect held even after controlling for cholesterol etc.

• Key insight: Hostility/aggression within Type A is the most toxic component for CHD risk.

🌟 Big Takeaways

• Stress → short-term BP spikes for everyone, but only predisposed individuals → sustained hypertension.

• Predispositions include genes, CVR, and neurobiological differences.

• CHD develops from both traditional biological risks + psychological/behavioral factors (Type A, job strain, anger).

🔥 Beyond Type A: The Real Culprit = Hostility + Negative Emotions

• Type A pattern (urgency, competitiveness, hostility) originally linked with CHD.

• BUT → follow-up studies showed hostility is the most toxic element.

  • Meta-analysis (25 studies): anger & hostility → higher risk for CHD outcomes in healthy + cardiac populations (Chida & Steptoe, 2009).

• Anxiety & CHD:

  • Linked to increased CHD risk (Kawachi, 1994).

  • Animal research: inducing anxiety → triggered heart attacks in atherosclerotic animals (Carpeggiani, 1991).

• Depression & CHD:

  • ~20% of CHD patients meet full criteria for depression, many more show symptoms.

  • Quebec study → depressed cardiac patients = 3x more likely to die within 5 years (Lésperance, 2002).

  • Baseline depression & anxiety predict future adverse cardiac events (Frasure-Smith & Lésperance, 2008).

  • Biological mechanisms: ↑ inflammation, clotting, oxidative stress, HPA overactivation (Nemeroff & Goldschmidt-Clermont, 2012).

Type D Personality (Distressed Type)

• Defined as: Negative affectivity (anxiety, anger, depression) + Social inhibition (suppressing emotions).

• Outcomes:

  • ↑ CVD morbidity & mortality (independent of other risks).

  • Poorer quality of life + less treatment benefit (Pedersen & Denollet, 2003).

  • Linked to avoidance coping, low problem-solving, and emotional preoccupation with illness (Montreal CHIP study).

• Prevalence:

  • UK/Ireland → ~38.5%.

  • Other Europe → 21–33%.

  • Canada (Toronto rehab patients) → ~33%.

• Key: Type D = risky blend of chronic distress + repression → maladaptive coping → worsens heart outcomes.

🧬 Biological Diatheses

• Cardiovascular Reactivity (CVR):

  • Magnitude of HR/BP increases in response to stress.

  • Excessive CVR → arterial damage → ↑ MI risk (Bongard, 2012).

  • Type D + chronic heart failure patients = inadequate stress response in psychosocial challenges (public speaking) (Kupper, 2013).

• Shows how psych + bio factors interact in CVD vulnerability.

💊 Treating Hypertension & Reducing CHD Risk

Non-Pharmacological Interventions

• Lifestyle changes:

  • Weight loss, lower salt intake, quit smoking, aerobic exercise, moderate alcohol.

  • Statins (e.g., lovastatin) → lower LDL & prevent atherosclerosis.

• Key Study (TONE, Whelton 1998):

  • Older obese hypertensive adults → lost just ~8 lbs + reduced salt by 25%.

  • ~50% stopped meds and maintained normal BP!

  • Benefits lasted 3+ years.

• Exercise:

  • Lifestyle activities (stairs, walking) = as effective as structured programs (Dunn, 1999).

  • Moderately intense 30 min/day = ↓ BP by ~10 points + reduced mortality (Wannamethee, 1998).

  • Can sometimes replace or reduce meds.

Psychological Approaches

• Relaxation therapy:

  • Small BP reductions, but evidence = weak (Dickinson, 2008).

• Biofeedback:

  • Initially promising (Harvard studies: could change HR & BP).

  • But meta-analyses show only modest or no long-term benefit (Linden, 2006; Greenhalgh, 2009).

  • Recommendation: use only as supplement to other treatments.

🏥 Cardiac Rehabilitation

• IHDLSM (Montreal):

  • Stress-monitoring + psychosocial support = ↓ mortality/MI at first (Frasure-Smith, 1989).

  • Later studies: mixed. Helped anxious men most, but sometimes worsened outcomes for women/repressors (Frasure-Smith, 2002).

• Meta-analyses:

  • Comprehensive rehab = effective (Sandercock, 2013; Zwisler, in press).

  • BUT only ~⅓ of eligible Canadians access programs (Grace, 2014).

  • Barriers: lack of referral, travel, distance. National push for systematic referrals now underway.

🌟 Big Takeaways

• Hostility, anxiety, and depression → strong psychological risk factors for CHD.

• Type D personality = chronic distress + repression → major cardiac vulnerability.

• Biological diatheses (CVR, HR reactivity) interact with psychological styles to increase risk.

• Best protection: lifestyle interventions (weight, salt, exercise), combined with medical treatment + cardiac rehab.

• Challenge: Many patients don’t access rehab despite strong evidence of benefits.

🌪 9.4 Post-Traumatic Stress Disorder (PTSD)

📖 Description & Symptoms

• Definition: An extreme response to a severe stressor, with hallmark symptoms of:

  • Heightened anxiety

  • Avoidance of trauma reminders

  • Emotional numbing

  • Intrusive re-experiencing (flashbacks, nightmares)

• DSM-5:

  • Now recognizes broader trauma types (not just “outside the range of human experience”).

  • Requires symptoms lasting > 1 month.

  • 4 symptom clusters (20 total symptoms):

    1. Intrusions (distressing memories, dreams, flashbacks)

    2. Avoidance (of thoughts, feelings, reminders)

    3. Negative alterations in cognition/mood (added in DSM-5)

    4. Altered arousal/reactivity (hypervigilance, exaggerated startle, irritability, sleep/concentration difficulties).

🧍 Case Examples

• Sergeant Bob Bilodeau (RCMP):

  • Served in Bosnia (Srebrenica, 1993).

  • Flashbacks, nightmares, low self-esteem, concentration issues.

  • Used alcohol as “self-medication.”

  • Ongoing intrusive memories triggered by reminders (e.g., dusk drive → danger flashback).

• Nicholas John Arnold (2001 accident, BC):

  • Witnessed a fatal crash → panic attacks, PTSD, bipolar depression.

  • Symptoms: anxiety driving, flashbacks, sleep disturbance.

  • Precedent: awarded $11,000 compensation for trauma after witnessing strangers’ deaths.

  • Raises legal/ethical questions: how much should witnessing trauma be compensated?

🧠 Theoretical Issues & Controversies

• Conceptual bracket creep: Debate over what counts as trauma.

  • PTSD initially required events “outside the range of human experience.”

  • DSM-5 tightened rules: witnessing must be in person (not just on TV/news).

• Critiques:

  • Excludes some major losses (e.g., parent losing child to cancer, soldier losing a respected leader).

  • Some argue broadened criteria may pathologize normal distress.

📊 Prevalence & Impact

• Canada:

  • Lifetime prevalence ≈ 10%

  • One-month prevalence ≈ 4% (Van Ameringen et al., 2008).

• Risk varies by trauma severity:

  • ~3% → civilians exposed to physical attack.

  • ~20% → Vietnam veterans (wounded).

  • ~50% → rape victims, POWs (WWII, Korea).

  • ~46% → volunteers in Swissair disaster cleanup.

• Dose-response: More severe/closer trauma → higher PTSD risk.

  • Example: 9/11 direct exposure = 6x more PTSD vs. indirect exposure (Henriksen et al., 2010).

🧩 Intrusion: Core Symptom

• Repeated nightmares, flashbacks, symbolic triggers.

• Holocaust survivors study (Toronto):

  • Nightmares in 87–90% of survivors (Kuch & Cox, 1992).

• Theories:

  • PTSD = failure to integrate trauma into existing schemas, leading to intrusive re-experiencing (Foa, Horowitz).

🔄 Acute Stress Disorder (ASD) vs. PTSD

• Acute Stress Disorder:

  • Distress lasting 3 days–1 month post-trauma.

  • Often a precursor to PTSD.

  • Prevalence depends on trauma type:

    • 90% after rape

    • 13% after car accidents

• PTSD:

  • Symptoms persist > 1 month.

  • Can last decades (Vietnam veterans: 271,000 still meet criteria 40 years later).

💡 Key Takeaways

• PTSD = chronic dysregulation of stress systems after trauma.

• Symptoms cluster around intrusion, avoidance, negative cognition/mood, and hyperarousal.

• Severity and proximity of trauma matter → dose-response.

• Controversy remains about definition and scope.

• Prevalence is high in Canada and especially among first responders, veterans, and survivors of severe interpersonal trauma.

🇨🇦 PTSD in Canadian Veterans, Peacekeepers & Civilians

📜 Historical Context

• WWI (Farrar, 1917):

  • 10% of invalided Canadian soldiers were “nervous and mental cases.”

  • 58% = neurotic reactions (some “shell shock”), 14% = mental diseases/defects (e.g., “dementia praecox,” “psychopathic inferiority”).

• Shows PTSD-like symptoms were recognized long before the modern diagnosis.

🎖 Canadian Military Veterans

• Vietnam War (Stretch, 1990, 1991):

  20,000 Canadians volunteered with US forces.

  • Sample of 164 veterans: 65.4% reported PTSD symptoms.

  • PTSD linked to poor health, depression, anxiety, anger, shame.

  • Worse adjustment vs. US veterans → more isolation, less recognition/support.

• Dieppe Raid (Beal, 1995, 50-year follow-up):

  • 276 veterans studied, 68% casualty rate.

  • 43.4% of POWs and 29.9% of non-POWs had PTSD 50 years later.

  • POWs with PTSD: reported more maltreatment (beatings, death threats, torture).

  • Symptoms persisted decades later → higher depression, anxiety, suicidal ideation.

  • Only 5.4% received disability pensions (despite 37% PTSD prevalence).

🕊 Peacekeepers & Modern Recognition

• 2000 → Canadian gov’t officially recognized PTSD for disability pensions (Thorne, 2000).

• Roméo Dallaire (Rwanda, 1994 genocide):

  • Witnessed mass atrocities, Belgian soldiers’ murder.

  • Public struggles with PTSD, alcohol, suicide attempts.

  • Opened national discussion on PTSD in peacekeepers.

• Studies:

  • PTSD symptoms linked to poor health in both deployed & non-deployed personnel (Asmundson et al., 2002).

  • PTSD strongly comorbid with depression; 87% of French-Canadian male veterans reported significant pain, with depression mediating PTSD–pain link (Poundja et al., 2006).

  • PTSD & depression severity predicted poorer quality of life (Richardson et al., 2008).

⚕ Treatment-Seeking & Access Barriers

• Fikretoglu et al. (2007, CCHS-Canadian Forces Supplement):

  • 5.3% 12-month PTSD; 11.1% lifetime PTSD.

  • 1/3 never sought treatment; comorbid depression ↑ treatment-seeking (x3.75).

• Barriers:

  • Shortage of providers (needed ↑ 22% staff, Daigle, 2012).

  • Auditor General (2014): 20% waited up to 8 months for approval.

  • Dallaire (2015): publicly criticized Veterans Affairs for being “cheap.”

⚠ Afghanistan War & Suicide Crisis

• 2007–2015: PTSD diagnoses among Canadian veterans tripled (>14,000 cases).

• Suicides: At least 54 soldiers/veterans died by suicide post-deployment (D’Alesio, 2016).

• Canadian Forces Mental Health Survey (2013):

  • 1 in 6 reported depression, anxiety, PTSD, or substance abuse.

  • PTSD: 5.3% (12-month), 11.1% (lifetime).

  • PTSD ~2x higher in Afghanistan veterans.

🌍 PTSD Beyond the Military

• Natural Disasters:

  • China earthquake (2008): 45.5% PTSD prevalence (Peng et al., 2009).

  • Hurricane Katrina (2005): PTSD prevalence increased from 14.9% → 20.9% one year later (Kessler et al., 2008).

• Canadian Floods (Alberta, 2012):

  • $50 million allocated for post-trauma mental health supports.

• Air Transat Flight 236 (2001):

  • Engine failure, emergency landing.

  • ~50% developed PTSD.

  • Research: PTSD survivors recalled more non-traumatic details; trauma linked with amygdala activation (McKinnon et al., 2015; Palombo et al., 2016).

  • Researcher Margaret McKinnon was herself a passenger.

🎓 PTSD in Students

• York University (Muller et al., 2012):

  • 30% scored above trauma cut-off.

• US Universities (Read et al., 2011):

  • 66% exposed to trauma, 9% had PTSD.

  • Follow-up (Read et al., 2016): most recovered, but 11% remained symptomatic after 1 year.

• Virginia Tech shooting (2007): 15% PTSD prevalence (Hughes et al., 2011).

• Dawson College shooting (2006, Montreal):

  • 30% developed at least one disorder; 18% = first onset.

  • Closer exposure → greater PTSD risk.

  • Majority did not seek help (Miquelon et al., 2014).

💡 Key Takeaways

• Canadian veterans/peacekeepers show long-lasting PTSD (Dieppe → 50 years later; Afghanistan vets).

• PTSD strongly linked to depression, pain, poor quality of life, suicide risk.

• Systemic issues: inadequate government support, long wait times, stigma, and shortages of mental health providers.

• Civilians & students are also vulnerable → disasters, accidents, shootings show dose-response relationships.

• Universal theme: not everyone exposed develops PTSD → vulnerability factors (biological, psychological, social) are critical.

🧠 Etiology of PTSD

🔹 Risk Factors

• Gender & Exposure

  • Men experience more trauma overall (except sexual assault/child sexual abuse).

  • Women more likely to develop PTSD after trauma (Breslau, 2002; Tolin & Foa, 2006).

• Psychosocial & Developmental Factors

  • Perceived life threat.

  • Early parental separation.

  • Family history of mental disorder.

  • Pre-existing anxiety/depression.

  • Previous trauma (strongest predictor of future trauma exposure).

• Symptom-Specific Predictors (Cougle et al., 2009)

  • Re-experiencing → predicted later exposure to interpersonal violence (non-intimate perpetrators).

  • Hyperarousal → predicted other traumatic stressors.

• Protective Factor: High IQ (≥115) linked to better coping (Breslau et al., 2006).

• Dissociation (amnesia, out-of-body experience during trauma):

  • ↑ PTSD risk and maintains symptoms by preventing memory integration.

  • Rape survivor study → high dissociation scores predicted PTSD symptoms; paradoxical pattern = high subjective stress but low physiological arousal.

• Cognitive/Personality Vulnerabilities:

  • Taking personal responsibility for failures; emotion-focused coping (Mikulincer & Solomon, 1988).

  • Insecure attachment style (negative self-view) predicts PTSD (Muller et al., 2000, 2004).

  • Symptom reductions after therapy were accompanied by ↑ secure attachment (Muller & Rosenkrantz, 2009).

🔹 Psychological Theories

• Learning Theories

  • Classical conditioning of fear (CS = trauma cues; UCS = trauma).

  • Avoidance negatively reinforces fear reduction (Mowrer’s two-factor theory).

  • Supported by evidence (Foy et al., 1990).

• Cognitive Theories

  • PTSD = memory disorder (McNally, 2006).

  • Features:

    • Involuntary recollections/intrusions.

    • Impaired memory of neutral stimuli (esp. verbal).

    • Working memory deficits (Shaw et al., 2009).

    • Linked to vmPFC functioning (Dickie et al., 2008).

  • Cognitive protection: above-average ability.

  • Biological vulnerability: smaller hippocampal volume (Bremner, 2006).

• Psychodynamic Theory (Horowitz, 1990):

  • Constant painful memories → repression or suppression.

  • Internal struggle to integrate trauma into worldview.

🔹 Biological Theories

• Genetic & Twin Studies

  • Some trauma exposures (e.g., violent crimes) influenced by genetics + environment.

  • PTSD symptoms moderately heritable in community samples, incl. women (Stein et al., 2002).

  • Trait neuroticism may be a heritable diathesis.

• Neurocognitive Function (Gilbertson et al., 2006):

  • Combat-unexposed twins of PTSD veterans showed same cognitive deficits as brothers → some deficits are premorbid risk factors.

• Noradrenergic System (Krystal et al., 1989):

  • Trauma ↑ norepinephrine → heightened startle & emotional reactivity.

  • PTSD patients = ↑ norepinephrine than schizophrenia/mood disorder patients (Kosten et al., 1987).

  • Stimulating system → panic in 70%, flashbacks in 40% (Southwick et al., 1993).

  • ↑ sensitivity of noradrenergic receptors tied to specific PTSD symptom clusters (O’Donnell et al., 2004).

🛠 Tailoring Treatment for PTSD

🔹 Early Intervention

• Psychological First Aid (Vernberg et al., 2008):

  • Frontline support after disasters/terrorism.

• Crisis Intervention (Foa & Meadows, 1997):

  • Recreate & discuss trauma details.

  • Normalize anxiety reactions.

  • Encourage open processing (Mitchell & Bray, 1990).

🔹 Cognitive-Behavioural Approaches

• CBT for Assault Survivors (Foa et al., 1995):

  • Combination of exposure, relaxation, and cognitive restructuring (esp. reducing self-blame).

• Prolonged Exposure Therapy (Foa & McLean, 2016):

  • Based on emotion processing theory (PTSD = failure to process trauma due to avoidance).

  • Step-by-step imaginal + in-vivo exposure, plus cognitive restructuring and breathing control.

  • 8–15 sessions (90 minutes each).

  • Supported by meta-analysis (Powers et al., 2010).

• Limitations:

  • ⅓–½ of patients show little improvement.

  • Up to ⅔ of military PTSD patients still meet diagnostic criteria after treatment.

  • ~25% drop out (Steenkamp et al., 2015).

🔹 Mechanisms of Exposure

• Extinction of fear responses.

• Corrects maladaptive beliefs:

  • (a) Trauma reminders ≠ danger.

  • (b) Remembering ≠ reliving.

  • (c) Anxiety decreases without avoidance.

  • (d) Anxiety/PTSD symptoms ≠ loss of control.

✅ Summary: PTSD arises from an interplay of risk factors (trauma exposure, gender, attachment, dissociation, neuroticism), psychological processes (conditioning, memory disruption, avoidance), and biological vulnerabilities (hippocampal volume, noradrenergic sensitivity). Treatments, especially prolonged exposure CBT, are effective but not universally — hi🛠 Treatments for PTSD

🔹 1. Virtual Reality Exposure Therapy (VRET)

• Developer: Albert “Skip” Rizzo — Virtual Iraq program.

• Features:

  • Immersive 3D scenarios with visual, audio, vibration, and even smell cues.

  • Two settings:

    1. Humvee convoy ambushed in desert.

    2. Middle Eastern town with unpredictable attacks.

• Procedure: Typically introduced after rapport (e.g., by 4th session).

• Advantages: Less stigmatizing for military personnel than “seeing a shrink.”

• Evidence:

  • Effective for enlisted soldiers (McLay et al., 2012; Rizzo et al., 2010).

  • Used preventively in resilience training pre-deployment (Rizzo et al., 2013).

• Case Example (Gerardi et al., 2008):

  • 29-year-old Iraq veteran with intrusive memories, hypervigilance, concentration problems.

  • Humvee scenario → initial symptom flare, but gradual exposure reduced symptoms.

  • Emotional shift: horror, guilt → pride, acceptance.

  • Outcome expectancy (belief in treatment effectiveness) predicted success.

🔹 2. Cognitive-Behavioural Therapy (CBT)

• Key Mechanism: Change in dysfunctional trauma appraisals precedes symptom reduction (Kleim et al., 2013).

• Prolonged Exposure Therapy (PET):

  • Gold standard; 8–15 × 90-min sessions (Foa & McLean, 2016).

  • Involves imaginal + in-vivo exposure, breathing regulation, and cognitive restructuring.

  • Meta-analysis confirms efficacy (Powers et al., 2010).

• Limitations:

  • 1/3–1/2 show little improvement.

  • Up to 2/3 of military PTSD clients still meet criteria post-treatment.

  • ~25% dropout (Steenkamp et al., 2015).

🔹 3. Eye Movement Desensitization and Reprocessing (EMDR)

• Method (Shapiro, 1989): Trauma recall + eye tracking of therapist’s finger, then restructuring negative → positive cognitions.

• Claims: Rapid (1–2 sessions), highly effective.

• Controversy:

  • Some studies: eye movements add nothing beyond exposure (Cahill et al., 1999).

  • Exposure > EMDR in direct comparison (Taylor et al., 2003).

  • Early studies had methodological flaws (Rosen, 1999).

• Support:

  • Canadian study: alternating bilateral stimulation ↓ subjective distress (Servan-Schreiber et al., 2006).

  • Meta-analysis (Lee & Cuijpers, 2013): EMDR has moderate significant effect.

• Consensus: Exposure to trauma memories = core active ingredient.

🔹 4. Psychodynamic Approach (Horowitz, 1990)

• Focus: Integration of trauma into self-schema.

• Methods:

  • Discuss trauma in depth.

  • Explore defenses & transference.

• Evidence: Limited, small controlled studies show some benefit (Foa & Meadows, 1997).

🔹 5. Psychotherapy Meta-Analyses

• Bradley et al. (2005): 26 studies, 44 treatments.

  • ⅔ no longer met PTSD criteria after therapy.

  • Residual symptoms common; combat trauma = lowest effect sizes.

• Benish, Imel, & Wampold (2008):

  • All bona fide psychotherapies equally effective (no superiority).

🔹 6. Pharmacological Treatments

• SSRIs (e.g., sertraline): Some success, especially with comorbid depression (Yehuda et al., 1998).

• Client Preferences (Feeny et al., 2009):

  • Most trauma victims prefer exposure over medication.

  • Those with comorbid major depression more likely to choose SSRIs.

• MDMA (Ecstasy):

  • Mithoefer et al. (2011): RCT, 83% improved with MDMA-assisted therapy vs. 25% in placebo.

  • Approved Canadian trial (2012).

  • Still controversial due to legal and safety concerns.

🔹 7. Social Support

• Critical protective factor: Family, community, religious groups, peer listening (Hobfoll et al., 1991).

• Example: Westray mining disaster — community support vital in recovery.

• Helping others can also help the helper.

✅ Summary

• Best-supported approaches:

  • Prolonged exposure CBT (gold standard).

  • Virtual Reality exposure = promising, esp. for military (engagement + stigma reduction).

  • EMDR works, but likely because of exposure rather than eye movements.

• Mixed approaches:

  • Psychodynamic useful but less evidence-based.

  • Pharmacological options (SSRIs, MDMA trials) can help, esp. with comorbid conditions or when CBT is not accessible.

• Universal principle: Social support dramatically impacts prognosis.ghlighting need for tailored and early interventions.