Stress and Health: Cognitive Appraisal, GAS, and Health Outcomes

Lazarus' Cognitive Appraisal Model

  • Focus on psychology of stress: perception shapes the stress response, not the event itself.
  • Core idea: stress is produced by a mismatch between demands of a stressor and the resources available to cope with it.
  • Appraisal determines the intensity and meaning of the stress experience.
  • Two levels of appraisal:
    • Primary appraisal: am I facing potential threat or harm?
    • Secondary appraisal: do I have the resources to cope?
  • Primary appraisal categories (four ways to interpret a stressor):
    • Irrelevant: the stressor has no bearing on me.
    • Benign/Positive: the stressor is interpreted as harmless or beneficial.
    • Harmful and Threat: it is seen as dangerous and threatening.
    • Harmful and Challenge: it is seen as a challenge from which I can learn or grow.
  • Examples used in class:
    • Friend says they’re mad and want to talk.
    • Irrelevant: you don’t care about this person’s issue.
    • Benign/Positive: conversation is an opportunity to resolve something and feels okay.
    • Harmful/Threat: feels scary and threatening to self.
    • Harmful/Challenge: scary but manageable; learning opportunity.
    • Exams or class material: may be irrelevant, benign/positive (a well-prepared situation), or harmful/threatening (fear of failing).
  • Stress is shaped by perception: interpretation changes physiological and emotional responses.
  • Secondary appraisal asks: can I handle it? what coping options do I have?
    • Coping strategies discussed: talking to the person, ignoring, seeking therapy, taking a nap, etc.
  • Cognitive reappraisal (a key CBT technique): changing how you frame a stressor to reduce emotional impact.
    • Example: failing a test could be reappraised as a challenge or growth opportunity rather than a catastrophe.
    • Reappraisal strategies discussed:
    • Look for past evidence of coping with similar stressors.
    • Frame as a learning opportunity: “I can study smarter for the next one.”
    • Consider the proportion of the grade the event represents: “this is only a small part of my overall grade.”
    • Emphasize growth: “I can only go up from here.”
  • Perceived resources influence stress: higher perceived resources can lower stress; lack of resources can increase stress.
  • Model takeaway: Stress experience results from the interaction of primary appraisal (threat level) and secondary appraisal (resources/coping), i.e., the sequence: primary appraisal → secondary appraisal → stress response.

Common Stressors (examples used in class)

  • School/schoolwork
  • Financial stress
  • Traffic and getting around on time
  • Personal relationships (conflicts, dating, friendships)
  • Other life demands

Practical implications of appraisal

  • Perception can alter physiological responses and mood even if the objective event is the same.
  • Cognitive-behavioral therapy uses cognitive reappraisal to mitigate stress by changing thought patterns.
  • The same event can be experienced as a threat or a challenge based on appraisal.
  • In everyday life, awareness of appraisal processes can guide coping strategies and reduce negative emotional impact.

Stress and Health: General Adaptation and Biopsychosocial Frameworks

Hans Selye and the General Adaptation Syndrome (GAS)
  • Hans Selye (1930s) introduced the GAS model based on experiments with rats and a non-specific stress response.
  • Core idea: the body’s stress response to a nonspecific demand is similar across stressors.
  • Three stages of GAS:
    • Alarm stage: fight-or-flight response; physiological mobilization for immediate threat. Involves rapid activation of stress systems.
    • Resistance (adaptation) stage: the body tries to adapt to a higher level of arousal; health resources are used to cope for a prolonged period; symptoms may include concentration difficulties and irritability.
    • Exhaustion stage: prolonged exposure depletes resources; risk of stress-related illness increases (digestive issues, headaches, sleep problems, depressive/anxiety symptoms).
  • If the stressor ends, the system can return to homeostasis; if it persists, exhaustion and illness can follow.
  • Connection to Lazarus: perception of stressors (appraisal) influences whether the GAS is activated and how intensely it is sustained.
Two main stress response systems: SAM and HPA
  • SAM system (Sympathetic-Adrenomedullary)
    • Triggered by sympathetic nervous system activation in response to threat (amygdala detects threat).
    • Adrenal medulla releases catecholamines: primarily epinephrine (adrenaline) and norepinephrine.
    • Immediate physiological effects: pupil dilation, increased heart rate and blood pressure, increased respiration, mobilization of glucose from liver, increased muscle readiness, reduced digestion.
    • Chronic activation can contribute to heart disease, type 2 diabetes risk, and other health issues due to sustained cardiovascular load and metabolic changes.
  • HPA axis (Hypothalamic-Pituitary-Adrenal axis)
    • Hypothalamus triggers pituitary to release ACTH (adrenocorticotropic hormone).
    • ACTH stimulates adrenal cortex to release cortisol.
    • Cortisol effects: increases blood glucose, modulates immune response, reduces inflammation; supports energy mobilization and tissue repair in acute stress.
    • Chronic HPA activation with elevated cortisol can suppress immune function, alter inflammatory processes, and contribute to chronic diseases (cardiovascular disease, diabetes, etc.).
  • Integrated view: amygdala detects threat → SAM and HPA axis activate → physiological changes prepare for action; chronic activation disrupts health.
  • Important note: the same stressor can trigger similar physiological responses whether the threat is physical or social/interpersonal; the perception of threat determines the intensity and duration of these responses.
Acute vs. Chronic Stress and Health Outcomes
  • Acute stress: short-term, can be adaptive; returns to baseline after threat passes.
  • Chronic stress: long-lasting; maintains elevated SAM/HPA activity; linked with diverse health problems (cardiovascular disease, immune suppression, sleep disturbances, mood disorders, digestive issues, etc.).
  • Broader examples mentioned in class: chronic stress associated with high blood pressure, heart disease, ulcers, diabetes risk, sleep problems, digestive issues, and immune suppression.
  • Japan example: kuroshi – death from overwork, illustrating severe consequences of chronic work-related stress.
Stress, Immunity, and the Brain
  • Psychoneuroimmunology: study of how psychological processes influence the immune system via nervous and endocrine pathways.
  • Stress and immune function: cortisol can suppress immune responses; chronic stress lowers resistance to infections, and may influence inflammatory processes.
  • Cortisol and immune suppression can increase susceptibility to illnesses and infections.
  • Brain effects: chronic stress can affect brain cells and neural networks; in animal studies, chronic stress altered hippocampal neurons (memory-related region).
  • Telomeres and aging: stress may accelerate telomere shortening, which is associated with aging and cellular aging; stress-related hormonal activity can influence cellular aging processes.
  • Oxytocin as a protective factor: “cuddle hormone” reduces stress responses and can promote vascular relaxation and potential heart repair; social contact and support can buffer against stress.
Diathesis-Stress Framework (Diathesis-Stress Model) and Precipitating vs. Predisposing Factors
  • Precipitating factors: environmental stressors that trigger illness or symptoms (e.g., chronic social stress, job insecurity, relationship conflicts).
  • Predisposing factors: inherent susceptibility (genetic risks) or early life experiences that increase vulnerability to illness.
  • Interaction: individuals with predisposing factors exposed to precipitating stressors are at higher risk for stress-related illnesses (e.g., PTSD, cardiovascular conditions, depression).
  • The diathesis-stress framework helps explain why stress does not cause illness in everyone but can precipitate disease in susceptible individuals.
Key Research Illustrations Discussed
  • Cohen et al. (1998) – Common Cold Study (psychoneuroimmunology in action)
    • Design: participants exposed to rhinovirus; tracked who developed a cold after exposure.
    • Key finding: chronic stress length is associated with higher likelihood of illness after exposure.
    • Data presentation: Relative risk (RR) for developing a cold increases with longer stress duration; approximate interpretation: for those with chronic stress lasting >2 years, RR ≈ 3.7 compared with those reporting no major stressors.
    • Expressed as: RR=3.7RR = 3.7 for stress duration > 2 years vs no major stressors.
    • Takeaway: chronic stress dampens immune defenses, increasing disease susceptibility after viral exposure.
  • Sapolsky and primate research (stress and brain/cognition)
    • Studies of baboons in social dominance hierarchies show differential brain health depending on social status.
    • Dominant, well-supported individuals showed healthier hippocampal neurons; subordinate, stressed individuals showed damaged hippocampal neurons.
    • Conceptual link: chronic social stress can affect brain structure and function, with implications for memory and cognition.
    • Uses diathesis-stress thinking: chronic stress acts as a precipitating factor that interacts with individual predispositions to influence health outcomes.
  • Telomeres and aging (illustrated in stress-and-health discussions)
    • Chronic stress may accelerate telomere shortening, contributing to cellular aging and aging-related disease risk.
  • Oxytocin and social buffering
    • Oxytocin can dampen stress responses; social support and positive social interactions act as moderators that reduce the negative health impact of stress.
    • Practical implication: social connection and supportive relationships can help safeguard health under stress.
Intersections with the Biopsychosocial Model
  • Stress and health are understood through a biopsychosocial lens: biology (HPA/SAM, cortisol, adrenaline), psychology (perception, appraisal, coping), and social context (support, relationships, cultural factors) all interplay to produce health outcomes.
  • The medical system’s tendency to segment psychology and biology can obscure the wide-reaching effects of stress on health; recognizing stress as a health determinant supports integrated care approaches.
Practical Takeaways for Exam Prep
  • Be able to describe the Lazarus cognitive appraisal model, including primary vs secondary appraisal and the four primary appraisal categories.
  • Understand cognitive reappraisal as a CBT technique to reduce stress by reframing the stressor.
  • Explain Hans Selye’s General Adaptation Syndrome (alarm, resistance, exhaustion) and how it relates to chronic stress.
  • Distinguish SAM and HPA axis activation, including key hormones and their effects: epinephrine (adrenaline), norepinephrine, and cortisol.
  • Tie stress physiology to health outcomes: immune suppression, cardiovascular risk, metabolic changes, brain effects, aging (telomeres), and the buffering role of oxytocin and social support.
  • Be able to explain the diathesis-stress model with precipitating vs predisposing factors.
  • Recall a key empirical finding: Cohen et al. 1998 common cold study showing higher illness risk with longer stress duration (RR ≈ 3.7 for stress > 2 years).
  • Recognize real-world examples and moderators (e.g., social support, coping strategies) as important for mitigating stress effects.

Reflection Paper Options and Logistics

  • Option 1: Intersectionality mapping (connection to health behavior and stress)
    • Create a circle diagram representing you: a large circle with smaller inner circles for different identities.
    • You may make circles overlapping or separate; size and arrangement reflect relative emphasis and interconnections.
    • After mapping, answer reflection questions connecting identities to health and health behavior.
    • Map submission is private if you choose; answers to reflection questions must be submitted. This option links to the biopsychosocial perspective and intersectionality.
  • Option 2: Sapolsky podcast analysis
    • Choose a podcast episode from Dr. Sapolsky’s stress and illness series.
    • Listen and respond to the set of questions provided in the assignment.
    • This option emphasizes stress-health mechanisms and specific health conditions.
  • Practical details
    • Reflections are due Friday, the 26th (date as given in class).
    • Each reflection has multiple options; minimum one paragraph per question; four questions total.
  • Course logistics discussed in class
    • First reading quiz: Thursday (five-minute quiz with three multiple-choice questions).
    • Bring a 3x5 index card with notes on one side and a discussion question on the other side.
    • Class guidelines and discussion norms were summarized and posted on Canvas; emphasis on active listening, respectful dialogue, avoiding assumptions, openness to different viewpoints, encouraging everyone to share, staying on topic, and confidentiality.

Quick Review: Key Terms and Concepts

  • Appraisal: perception and interpretation of a stressor.
  • Primary appraisal: threat assessment (Irrelevant, Benign/Positive, Harmful-Threat, Harmful-Challenge).
  • Secondary appraisal: assessment of coping resources and options.
  • Cognitive reappraisal: reframing a stressor to reduce negative emotion.
  • Coping strategies: direct talk, avoidance, therapy, rest, etc.
  • General Adaptation Syndrome (GAS): Alarm, Resistance, Exhaustion.
  • SAM system: sympathetic activation; adrenaline/epinephrine and noradrenaline/norepinephrine; rapid physiological changes.
  • HPA axis: hypothalamus–pituitary–adrenal axis; cortisol; metabolic and immune effects.
  • Psychoneuroimmunology: study of psychology–nervous system–immune system interactions.
  • Diathesis-stress model: predispositions plus environmental stressors increase illness risk.
  • Precipitating factors vs predisposing factors: environmental triggers vs inherent susceptibility.
  • Telomeres and aging: stress may accelerate telomere shortening.
  • Oxytocin: social-buffering hormone that can reduce stress responses.
  • Intersectionality: multiple identities shaping experiences of health, stress, and discrimination.
  • Biopsychosocial model: integration of biological, psychological, and social factors in health.

References to Data and Studies Mentioned

  • Cohen et al. (1998): Common Cold and Stress duration – higher illness risk with longer stress exposure; reported as RR=3.7RR = 3.7 for stressors lasting >2 years vs no major stressors.
  • Sapolsky’s primate research: social dominance hierarchies and hippocampal neuronal health differences between dominant vs. subordinate monkeys; illustrates chronic social stress effects on the brain.
  • General concepts of cortisol, epinephrine, norepinephrine, ACTH, and brain regions (amygdala, hippocampus) in stress responses.

Note: The above notes cover the major and minor points from the transcript, including concepts, examples, mechanisms, and study references discussed in the class session. The organization is designed to function as a comprehensive study resource that can stand in for the original source for exam preparation.