Cognitive Connie
The Psychology of Stress
Stress is the body's response to demands that exceed its resources — a cascade of neural, hormonal, and immunological changes that evolved to handle short-term physical threats but are repeatedly activated by the chronic psychological pressures of modern life. Understanding stress means understanding three interlocking questions: what happens in the body when we encounter a stressor, what kinds of stressors are most damaging and how they are measured, and why some people remain healthy under high stress while others do not.
Defining features
01. Overview
Selye's General Adaptation Syndrome.
Selye (1936) proposed that any sufficiently intense or prolonged stressor — physical or psychological — produces the same three-stage physiological response. The insight that diverse stressors produce identical biological patterns was groundbreaking.
Alarm Reaction
Initial fight-or-flight activation: SAM axis fires, adrenaline floods the system, and there is an initial drop in physiological resistance as resources mobilise. The organism is primed for immediate action.
Resistance / Adaptation
The organism adapts to the stressor. HPA axis sustains cortisol elevation; physiological resistance to the specific stressor rises above normal. But resources are being consumed, and resistance to other stressors may fall — the body is running on reserves.
Exhaustion
If the stressor persists, physiological resources are exhausted. Adrenal glands hypertrophy then fail; immune function collapses; peptic ulcers develop; disease vulnerability soars. In extreme cases, death can result. Selye called these the "diseases of adaptation."
Key figures
Walter Cannon
1871–1945American physiologist who described the fight-or-flight response (1915) and coined the term "homeostasis." Identified the sympathetic nervous system as the driver of the acute stress response — the foundation for the SAM pathway concept.
Hans Selye
1907–1982Hungarian-Canadian endocrinologist who discovered the General Adaptation Syndrome and coined the term "stress" in its modern biological sense. His work established that diverse physical and psychological stressors produce the same nonspecific physiological response — founding the scientific study of stress.
Richard Lazarus
1922–2002American psychologist who developed the transactional (cognitive appraisal) model of stress with Susan Folkman. Proposed that stress is not in the stimulus or the response, but in the person-environment transaction — mediated by primary appraisal (is this threatening?) and secondary appraisal (can I cope?). Co-developer of the Hassles and Uplifts Scale.
Donald Meichenbaum
1940–presentCanadian clinical psychologist and founder of cognitive-behaviour modification. Developed Stress Inoculation Training (1977) — a structured, three-phase protocol for building coping capacity that remains one of the most widely used evidence-based stress management interventions.
Suzanne Kobasa
1949–presentSocial psychologist who identified the hardiness construct — the three-C personality buffer against stress — in a landmark study of executives during the AT&T divestiture. Her work established personality as a moderator of the stress-illness relationship and influenced both clinical practice and organisational health psychology.
Janice Kiecolt-Glaser
1951–presentClinical psychologist and pioneer of psychoneuroimmunology at Ohio State University. Her research programme (with immunologist Ronald Glaser) produced landmark findings on stress and immune suppression, wound healing, vaccine response, and the biological costs of relationship conflict and caregiving.
Key concepts
General Adaptation Syndrome (GAS)
Selye's (1936, 1950) three-stage model of the body's nonspecific response to prolonged stress: alarm (SAM activation, initial resistance drop) → resistance (HPA-sustained adaptation, depleting reserves) → exhaustion (resource depletion, immune collapse, disease). The key insight: diverse stressors produce the same biological pattern.
Sympathomedullary (SAM) pathway
The fast stress-response axis: threat → amygdala/hypothalamus → sympathetic nervous system → adrenal medulla → adrenaline and noradrenaline into bloodstream. Activates within seconds. Produces the fight-or-flight response (increased heart rate, bronchodilation, glucose mobilisation). Repeated SAM activation contributes to cardiovascular disease through endothelial damage and hypertension.
HPA axis
The slower stress-response axis: stressor → hypothalamus (CRH) → anterior pituitary (ACTH) → adrenal cortex → cortisol. Peaks at 15–30 minutes. Cortisol mobilises energy, suppresses immune and inflammatory responses, and enhances memory consolidation of emotional events. Negative feedback: rising cortisol suppresses CRH and ACTH. Chronic stress impairs this feedback, producing sustained cortisol elevation.
Social Readjustment Rating Scale (SRRS)
Holmes and Rahe's (1967) self-report measure listing 43 life events each weighted in life change units (LCUs). Total LCU score over 12 months predicts illness probability. Key weakness: assigns fixed LCU values ignoring individual appraisal; conflates positive and negative events; retrospective; modest correlations with health outcomes (r ≈ 0.12–0.30).
Hassles & Uplifts Scale
Kanner et al.'s (1981) alternative to life-event measurement: 117 everyday hassles (losing keys, traffic, arguments) rated for frequency and intensity, plus 135 uplifts (pleasant daily events). DeLongis et al. (1982) found hassles predicted somatic and psychological health outcomes better than major life events, supporting Lazarus's argument that chronic micro-activation is more pathogenic than infrequent major events.
Demand–control model
Karasek's (1979) model of occupational stress: health risk is greatest in "high-strain" jobs combining high psychological demands with low decision latitude (control). Active jobs (high demand/high control) are challenging but not pathogenic. Extended by Siegrist's (1996) effort–reward imbalance (ERI) model: high effort combined with low reward (pay, esteem, security) violates the social contract of work and drives stress.
Immunosuppression
The suppression of immune function by chronic stress. Cortisol binds glucocorticoid receptors on immune cells, reducing T-cell proliferation, NK cell activity, cytokine production, and antibody secretion. Key studies: Kiecolt-Glaser et al. (1984) — lower NK cell activity in medical students during exams; Cohen et al. (1991) — higher stress scores predicted clinical cold development after deliberate rhinovirus exposure (dose-dependent).
Type A behaviour pattern
Friedman and Rosenman's (1959) personality cluster: time urgency, competitive drive, and free-floating hostility. The WCGS (Rosenman et al., 1975) found Type A men had ~2× CHD rate over 8.5 years. Refinement: Miller et al. (1996) meta-analysis showed cynical hostility — not global Type A — is the "toxic ingredient" that independently predicts CHD.
Hardiness (Kobasa)
Kobasa's (1979) personality buffer against stress: three Cs — Commitment (engagement with life vs alienation), Control (belief that actions affect outcomes vs helplessness), Challenge (appraising change as opportunity vs threat). Identified in 837 Illinois Bell executives during AT&T divestiture. Critique (Funk, 1992): hardiness scales overlap substantially with low neuroticism; discriminant validity is contested.
Stress-buffering hypothesis
Cohen and Wills's (1985) model in which functional social support specifically protects against health effects of high-stress events by redefining the stressor as less threatening (appraisal stage) and/or providing coping resources (response stage). Distinct from the main-effects model (social integration is beneficial regardless of stress level). Strongest evidence for buffering when support is measured functionally and stress is high.
Stress Inoculation Training (SIT)
Meichenbaum's (1977) CBT-based stress management protocol. Three phases: (1) Conceptualisation — client learns about stress and appraisal; (2) Skills acquisition — relaxation, cognitive restructuring, coping self-statements, problem-solving; (3) Application — graduated exposure to stressors to practise skills under pressure. Effective for PTSD, medical procedure anxiety, anger management, and occupational stress.
Biofeedback
A technique providing real-time information about a physiological signal (skin conductance/GSR, muscle tension/EMG, heart rate variability, peripheral temperature) to enable operant conditioning of normally involuntary autonomic responses. Used in stress management to teach sympathetic downregulation. Strongest evidence: EMG biofeedback for tension headaches, HRV biofeedback for anxiety and hypertension, thermal biofeedback for Raynaud's syndrome.
Test your knowledge
Frequently asked questions
What is the difference between the SAM pathway and the HPA axis?+
Both are stress response systems but they differ in speed, hormones, and function. The SAM (sympathomedullary) pathway activates within seconds: the sympathetic nervous system triggers the adrenal medulla to release adrenaline and noradrenaline into the bloodstream, producing the immediate fight-or-flight response (increased heart rate, dilated airways, elevated blood glucose). The HPA axis activates over 15–30 minutes: the hypothalamus releases CRH → the anterior pituitary releases ACTH → the adrenal cortex releases cortisol. Cortisol sustains the stress response by mobilising energy reserves, suppressing immune function, and enhancing memory for threatening events. The SAM response is fast and short; the HPA response is slower and more sustained. Both activate simultaneously — SAM handles the immediate threat, HPA sustains and modulates the response. Repeated activation of both systems — without adequate recovery — contributes to cardiovascular disease and immunosuppression.
Why do daily hassles predict health outcomes better than major life events?+
Major life events (measured by the SRRS) are infrequent and allow the organism time to adapt between episodes. Daily hassles — the recurring frustrations of everyday life — activate the stress response repeatedly, with little opportunity for full recovery. Lazarus argued that chronic micro-activation of the HPA axis (repeated cortisol spikes from traffic, arguments, minor frustrations) produces more cumulative biological damage than occasional major events. DeLongis et al. (1982) found that hassle frequency and intensity predicted somatic symptoms and health status better than SRRS scores, even after controlling for major life events. The hassles measure also captures the subjective meaning of daily experience more accurately than the SRRS, which assigns fixed severity values regardless of individual appraisal.
How does social support protect against the health effects of stress?+
Cohen and Wills (1985) identified two mechanisms. The main-effect model holds that social integration — simply belonging to and participating in social networks — provides direct health benefits through positive affect, sense of belonging, and access to information and resources, regardless of stress level. The buffering model holds that functional social support specifically moderates the stress-illness relationship: when matched to the demands of a stressor (emotional support for interpersonal crises, informational support for practical problems), support reduces the threat appraisal of the stressor and/or provides resources to manage it, reducing physiological activation. Biologically, social support is associated with attenuated cortisol responses to stressors, lower inflammatory markers, and improved immune function. Conversely, social isolation is as damaging as smoking ~15 cigarettes daily in terms of mortality risk (Holt-Lunstad et al., 2015).
Sources
Last reviewed July 2025- 1.
Selye, H. (1956). The stress of life. McGraw-Hill.
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Introduced the General Adaptation Syndrome (GAS) and the concept of non-specific biological stress.
- 2.
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal, and coping. Springer.
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Established the transactional model of stress, centring primary and secondary appraisal as mediators of the stress response.
- 3.
Cohen, S., Kamarck, T., & Mermelstein, R. (1983). A global measure of perceived stress. Journal of Health and Social Behavior, 24(4), 385–396.
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Introduced the Perceived Stress Scale (PSS), one of the most widely used instruments in stress research.
- 4.
Holt-Lunstad, J., Smith, T. B., Baker, M., Harris, T., & Stephenson, D. (2015). Loneliness and social isolation as risk factors for mortality. Perspectives on Psychological Science, 10(2), 227–237.
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Meta-analysis showing social isolation increases mortality risk comparably to established risk factors such as smoking.