Difficulty: Intermediate | Prerequisites: Introductory psychology; basic biology (nervous system, endocrine system)
This topic sits at the heart of health psychology. Stress is the bridge between everyday experience and physical illness, which is the central question of the course: how do psychological processes affect the body? You need a basic grasp of the autonomic nervous system and the endocrine system (particularly the adrenal glands) before diving in. Everything here feeds forward into coping, social support, health service use, and chronic disease management later in the course.
Stress is a negative emotional experience that triggers measurable biochemical and physiological changes. The body responds through the sympathetic nervous system (catecholamines) and the HPA axis (cortisol), and chronic activation of these systems damages immune function, cardiovascular health, and cognitive performance. Whether a situation becomes stressful depends on how a person appraises it (primary and secondary appraisal) and how well their resources match environmental demands.
Stress
A negative emotional experience accompanied by predictable biochemical, physiological, cognitive, and behavioural changes directed toward altering or accommodating the stressful event. In simple terms, it is the body and mind shifting into a higher gear when demands feel like they outstrip resources.
Primary appraisal
The initial evaluation of an event: is it harmful, threatening, or challenging? Think of it as the brain's first-pass filter asking, "What just happened, and what does it mean for me?"
Harm appraisal
Assessment of damage that has already been done.
Threat appraisal
Assessment of possible future damage.
Challenge appraisal
Assessment that the event carries potential to overcome or benefit from the situation.
Secondary appraisal
Evaluation of whether personal resources are sufficient to meet the demands of the environment. In simple terms, this is the brain asking, "Can I handle this?"
Person-environment fit
The degree to which a person's needs and resources complement the demands and resources of the environment. Stress increases when the fit is poor.
Fight-or-flight response
Walter Cannon's (1932) model of the stress response: the body mobilises for aggression (fight) or withdrawal and distraction (flight). Think of it as the original survival toggle.
General adaptation syndrome (GAS)
Hans Selye's (1956) three-phase model of stress response: alarm, resistance, and exhaustion. The body mounts the same physiological pattern regardless of the stressor type.
Tend-and-befriend
Taylor et al. (2000) proposed that, alongside fight-or-flight, people (especially women) respond to stress with social affiliation and nurturant behaviour toward offspring.
Sympathetic activation
Arousal of the sympathetic branch of the autonomic nervous system, stimulating the adrenal medulla to release catecholamines (epinephrine and norepinephrine). This drives increases in blood pressure, heart rate, and sweating.
Catecholamines (epinephrine and norepinephrine)
Hormones secreted by the adrenal medulla during sympathetic arousal. They raise blood pressure, heart rate, and sweating, constrict peripheral blood vessels, and modulate immune function.
HPA axis (hypothalamic-pituitary-adrenal axis)
A neuroendocrine pathway that, when activated by stress, triggers cortisol release. Repeated activation can compromise the axis's normal functioning.
Cortisol
A corticosteroid released via the HPA axis. Normally high upon waking and declining through the day, chronic stress can flatten or distort this daily rhythm.
Reactivity
The degree of change in autonomic, neuroendocrine, or immune responses resulting from stress. Influenced by genetics, prenatal experiences, and early life experiences.
Allostatic load
The accumulating adverse effects of stress combined with pre-existing risks on the body's biological stress-regulatory systems. Think of it as the long-term wear and tear from running the stress response too often.
Stress is the consequence of appraisal processes. When an event occurs, the person runs two evaluations back to back.
Primary appraisal asks what the event is and what it means. Three possible outcomes:
Harm: damage already done
Threat: possible future damage
Challenge: potential to overcome or benefit
Secondary appraisal asks whether the person's resources (skills, support, energy, time) are sufficient to meet the environment's demands.
The overall level of stress is determined by person-environment fit: how well the person's needs and resources align with what the environment demands and provides. A poor fit produces stress; a good fit buffers against it.
The earliest formal model of the stress response. The body mobilises for one of two actions:
Fight: aggression, direct confrontation
Flight: social withdrawal, avoidance, or distracting activities
Selye proposed that any stressor, regardless of type, triggers the same general physiological pattern in three phases:
Alarm: the body detects the stressor and mobilises resources
Resistance: sustained physiological effort to cope with the stressor
Exhaustion: prolonged activation depletes resources and the body can no longer maintain resistance
Criticisms of GAS:
It gives limited weight to psychological factors. Different people respond differently to the same stressor depending on personality, emotions, and biological constitution.
The model emphasises exhaustion (phase 3) as the danger zone, but continued activation during the resistance phase (phase 2) may be more important for accumulating physiological damage.
A complementary model to fight-or-flight. People and animals also respond to stress through:
Social affiliation (seeking closeness with others)
Nurturant behaviour toward offspring
This response is especially pronounced in women and highlights that stress responses are not limited to aggression and withdrawal.
Stress does not cause illness through a single pathway. It operates through at least four mechanisms working in parallel:
Direct physiological effects: elevated blood pressure, decreased immune function (reduced ability to fight infection), and changes in lipid levels.
Poorer health behaviours: stressed people are more likely to smoke, eat poorly, sleep less, exercise less, and increase drug or alcohol use.
Erosion of psychosocial resources: supportive social contacts protect health, but stress pushes people to withdraw from those contacts or to behave in ways that damage relationships.
Reduced treatment adherence: people under stress are less likely to follow medical treatment regimens and more likely to delay seeking care for disorders that need attention, sometimes avoiding care altogether.
Sympathetic arousal stimulates the medulla of the adrenal glands, which secrete catecholamines: epinephrine (EP) and norepinephrine (NE).
Effects of catecholamine release:
Increased blood pressure and heart rate
Increased sweating
Constriction of peripheral blood vessels
Modulation of immune system function
The parasympathetic nervous system normally acts as a brake on the stress response. Under chronic stress, this braking function can become dysregulated. Because parasympathetic activity governs rest and sleep, changes in heart rate variability under stress may represent a pathway to disturbed sleep and, from there, to increased illness risk and mortality.
Repeated activation of the HPA axis can compromise its normal functioning.
Normal cortisol pattern: cortisol is high upon waking, decreases through the day (with a small peak after lunch), and flattens to low levels by the afternoon and evening.
Chronic stress disrupts this pattern in several ways:
Elevated cortisol persisting into the afternoon or evening
General flattening of the daily cortisol rhythm
Exaggerated cortisol response to a new challenge
Protracted cortisol response that does not return to baseline after a stressor ends
Or, paradoxically, no cortisol response at all
Prolonged discharge of epinephrine and norepinephrine leads to:
Suppression of immune function
Sustained increases in blood pressure and heart rate
Heart rhythm variations, including ventricular arrhythmias (a precursor to sudden death)
Neurochemical imbalances
Catecholamines also affect lipid levels and free fatty acids, contributing to the development of atherosclerosis.
Corticosteroids (released via the HPA axis) have their own long-term consequences:
Immunosuppressive effects
Destruction of neurons in the hippocampus, leading to problems with verbal functioning, memory, concentration, and potentially dementia
Pronounced HPA activation is common in depression; episodes of cortisol secretion are more frequent and longer among depressed individuals
Stress compromises immune functioning broadly. It predicts a lower antibody response to flu vaccine, for instance. Chronic inflammation is implicated in many diseases, including coronary artery disease, and the impaired ability to terminate inflammation may be a key pathway by which stress affects illness outcomes.
Reactivity refers to the degree of change in autonomic, neuroendocrine, or immune responses as a result of stress. It varies across individuals and can be shaped by:
Genetic makeup
Prenatal experiences
Early life experiences
Allostatic load is the cumulative wear and tear on biological stress-regulatory systems. It reflects the accumulating adverse effects of stress combined with whatever pre-existing risks the person carries. A person with high allostatic load is more vulnerable to the next stressor because the baseline systems are already compromised.
Students often think the GAS model says all stressors produce identical biological responses. It does not hold up that cleanly: individual differences in personality, emotion, and biology mean people respond differently to the same stressor.
Students often assume the exhaustion phase (phase 3) of GAS is where all the damage happens. The resistance phase (phase 2), with its sustained activation, may actually be more important for accumulating physiological damage.
Students sometimes treat fight-or-flight as the complete picture of the stress response. Tend-and-befriend (social affiliation, nurturant behaviour) is a distinct and well-supported additional response, particularly in women.
Students often conflate cortisol being "high" with being stressed right now. Cortisol follows a daily rhythm, and disrupted patterns (flattening, protracted responses) matter more than any single high reading.
Know the difference between primary and secondary appraisal, and be able to give an example of each.
Be able to name the three phases of GAS and the main criticisms of the model.
Understand the four pathways by which stress contributes to illness (direct physiological, health behaviours, psychosocial resource erosion, treatment non-adherence).
Know what catecholamines are, where they come from, and what they do.
Be able to describe what a normal cortisol pattern looks like and how chronic stress alters it.
Understand the concept of allostatic load and how it differs from a single acute stress response.
Taylor et al. (2000) and tend-and-befriend: know the researcher, the year, and how it complements fight-or-flight.
True or false: In Selye's GAS model, every stressor produces the exact same biological response in every person. (False: individual differences in personality, emotion, and biology shape responses.)
Fill in the blank: The two catecholamines released during sympathetic activation are ______ and ______. (Epinephrine and norepinephrine.)
True or false: Tend-and-befriend responses to stress are observed equally in men and women. (False: especially pronounced in women.)
Fill in the blank: The accumulating wear and tear on biological stress systems is called ______. (Allostatic load.)
True or false: Secondary appraisal is the evaluation of whether personal resources are sufficient to handle the situation. (True.)
Q: What are the three types of primary appraisal?
A: Harm (assessment of damage already done), threat (assessment of possible future damage), and challenge (potential to overcome or benefit from the event).
Q: Name the three phases of the General Adaptation Syndrome and one major criticism of the model.
A: Alarm, resistance, and exhaustion. A key criticism is that the model underestimates the role of psychological factors: different people respond differently to the same stressor depending on personality, emotions, and biological constitution.
Q: How does chronic stress alter normal cortisol patterns?
A: Chronic stress can cause elevated cortisol persisting into the afternoon or evening, flattening of the normal daily rhythm, exaggerated or protracted cortisol responses to challenges, or paradoxically no cortisol response at all.
Q: Describe the tend-and-befriend response and identify the researcher who proposed it.
A: Taylor et al. (2000) proposed that people, especially women, respond to stress through social affiliation and nurturant behaviour toward offspring, complementing the fight-or-flight model.
Q: What is allostatic load, and why does it matter for long-term health?
A: Allostatic load is the cumulative adverse effect of repeated stress on the body's biological stress-regulatory systems. It matters because a person with high allostatic load is more vulnerable to further stressors, as their baseline regulatory systems are already compromised.
This material connects directly to Coping, Resilience, and Social Support: the coping chapter picks up where appraisal leaves off, covering what people do after they appraise a situation as stressful. Understanding the physiological mechanisms here (catecholamines, cortisol, allostatic load) is essential for later topics on chronic illness, cardiovascular disease, and psychoneuroimmunology. The concept of person-environment fit also recurs in discussions of workplace stress and health behaviours.
Stress, stress appraisal, primary appraisal, secondary appraisal, harm appraisal, threat appraisal, challenge appraisal, person-environment fit, fight-or-flight, Walter Cannon, General Adaptation Syndrome, GAS, Hans Selye, alarm phase, resistance phase, exhaustion phase, tend-and-befriend, Shelley Taylor, sympathetic nervous system, sympathetic activation, catecholamines, epinephrine, norepinephrine, adrenaline, noradrenaline, HPA axis, hypothalamic-pituitary-adrenal axis, cortisol, cortisol rhythm, diurnal cortisol, corticosteroids, parasympathetic nervous system, heart rate variability, reactivity, stress reactivity, allostatic load, allostasis, immunosuppression, atherosclerosis, chronic stress, PSY320, health psychology, Michigan State University