Stress.

HookThe rats that were all stressed the same way

MechanismThe physiology of stress — two pathways and one syndrome

Selye's General Adaptation Syndrome (GAS) describes three stages. In alarm, a stressor is perceived and the body mobilises. In resistance, the body copes and appears to function normally, but resources are draining. In exhaustion, prolonged demand overwhelms the system, defences collapse, and stress-related illness appears. GAS is the umbrella; underneath it sit two distinct physiological routes.

The sympathomedullary pathway (SAM) handles acute, moment-to-moment stress. A stressor activates the sympathetic branch of the autonomic nervous system, which stimulates the adrenal medulla to release adrenaline and noradrenaline. Within seconds the heart pounds, breathing quickens, pupils dilate and blood is shunted to the muscles — the fight-or-flight response. When the threat passes, the parasympathetic branch restores calm. The hypothalamic-pituitary-adrenal (HPA) system handles chronic stress and works more slowly. The hypothalamus releases CRH, which tells the pituitary to secrete ACTH, which tells the adrenal cortex to release cortisol. Cortisol keeps blood glucose high for sustained energy and dampens inflammation — useful in the short term, corrosive over months, because persistently high cortisol suppresses the immune system and damages blood vessels. A negative feedback loop is meant to switch cortisol off once levels are high; chronic stress blunts that feedback, and the tap stays running. Two pathways, two timescales — get the SAM/HPA distinction sharp and half the physiology marks are secured.

MechanismStress and illness — the immune system and the heart

The bridge from stress to disease runs mainly through cortisol's suppression of the immune system. The landmark evidence is Kiecolt-Glaser's work. In one study, medical students' natural killer cell activity was measured before and during exams; immune function dropped during the high-stress exam period, and dropped further in students who were also lonely. In a second, celebrated study she inflicted small standardised wounds on carers of relatives with dementia and on matched controls: the chronically stressed carers' wounds healed significantly more slowly — around nine days longer on average — direct evidence that stress impairs the body's repair machinery. Cohen's common-cold research added a dose-response element: people scoring higher on a stress index were more likely to develop a cold after controlled exposure to the virus.

Stress also damages the cardiovascular system. Repeated SAM activation raises blood pressure and heart rate; chronically raised cortisol promotes the build-up of fatty plaques (atherosclerosis) and the release of glucose and lipids into the blood. Personality feeds in here too — Williams' large-scale study found that people scoring high on anger and hostility had substantially more coronary events over follow-up. The evaluation to carry is that most of this evidence is correlational: stress reliably associates with illness, but third variables (poor diet, smoking, lost sleep in stressed people) muddy the causal claim, and individual differences mean stress harms some people far more than others.

ModelSources of stress — life changes, daily hassles and the workplace

Life changes are major, relatively rare events that force readjustment — bereavement, divorce, moving house, even positive changes like marriage. Holmes and Rahe argued that any change, good or bad, is stressful because it demands adaptation, a claim built into their Social Readjustment Rating Scale (next block). Rahe's study of naval personnel found a positive correlation between the total life-change score in the months before a voyage and illness during it, though the correlation was weak (around +0.12).

Daily hassles are the small, frequent irritations of ordinary life — traffic, misplaced keys, a difficult colleague. Kanner argued these accumulate, and DeLongis found that hassles were actually a better predictor of ill health than major life changes, perhaps because their sheer frequency gives the stress response no time to recover. Workplace stress turns on two factors above all: workload and, crucially, control. Johansson's study of Swedish sawmill workers found that 'finishers', whose work was repetitive, machine-paced and isolating, showed higher stress hormones and more illness than workers with more control. Marmot's Whitehall study of civil servants found the counter-intuitive result that lower-grade staff — not the overloaded executives — had more cardiovascular disease, and that low job control was the key predictor. The lesson examiners want is that it is not simply how much work you have, but how much say you have over it.

DataMeasuring stress — self-report and physiology

Because stress is invisible, psychologists measure it two ways, each with a trade-off. Self-report scales ask people to report their experience. The Social Readjustment Rating Scale (SRRS) (Holmes and Rahe) lists 43 life events, each assigned a weighting in Life Change Units (LCUs) — death of a spouse tops the list at 100, marriage sits at 50, a minor law violation near the bottom. You tick the events you experienced over a period, sum the LCUs, and higher totals predict greater illness risk. The rival Hassles and Uplifts Scale (Kanner) instead samples the small daily stressors (hassles) and the small daily boosts (uplifts) that the SRRS ignores entirely.

Physiological measures bypass the reporting problem by recording the body directly: cortisol levels in blood or saliva, heart rate and blood pressure, and skin conductance (the galvanic skin response, which rises as sweat glands activate under sympathetic arousal). The evaluation writes itself as a comparison. Self-report is cheap and captures the subjective, cognitive appraisal that makes stress personal — but it is vulnerable to social desirability, memory error, and the fact that the SRRS lumps positive and negative change together and ignores how much an event actually mattered to that individual. Physiological measures are objective and quantitative — but arousal is not stress-specific (exercise or excitement raise cortisol too), and they miss the psychological meaning of the event entirely. Neither is complete; the strongest research triangulates both.

ModelIndividual differences — personality and hardiness

The same stressor floors one person and barely touches another, and personality is a large part of why. Friedman and Rosenman defined Type A personality as competitive, time-urgent, impatient and hostile, against the relaxed, easy-going Type B. Their Western Collaborative Group Study followed around 3,000 men for eight and a half years and found Type A men were roughly twice as likely to develop coronary heart disease — later re-analysis suggested the toxic ingredient was specifically the hostility, not the ambition. Type C personality, added later, describes people who suppress emotions (especially anger), are conscientious and self-sacrificing, and may be more prone to cancer — a weaker and more contested link.

Kobasa's concept of hardiness flips the question from what makes people vulnerable to what makes them resilient. Hardy individuals share the three Cs: commitment (deep involvement in life and work), challenge (seeing change as an opportunity, not a threat), and control (a belief that they influence events). Hardiness buffers the impact of stressors — the same objective pressure produces less illness in a hardy person. The evaluation to reach for: personality research is largely correlational (Type A does not prove causation, and hostility may reflect an underlying physiological reactivity), the A/B typology is criticised as too crude a dichotomy, and there is overlap between low control in hardiness and the workplace-control finding — a neat chance to link this block back to sources of stress.

MechanismManaging and coping with stress

Management strategies divide into treating the body and retraining the mind. Drug therapy targets physiology directly: benzodiazepines (BZs) enhance the inhibitory neurotransmitter GABA, slowing the nervous system and reducing anxiety, while beta-blockers block adrenaline's effects on the heart, lowering heart rate and blood pressure. Drugs are fast and effective but treat symptoms not causes, can produce dependence and side effects, and stop working when you stop taking them. Stress inoculation therapy (SIT), Meichenbaum's cognitive approach, 'inoculates' people against future stress in three phases: conceptualisation (understanding the sources and appraisal of one's stress), skills acquisition and rehearsal (learning coping techniques such as relaxation and positive self-talk), and application (practising them in graded real situations). Biofeedback gives the person real-time readouts of a bodily function (heart rate, muscle tension) so they can learn, through operant conditioning and relaxation, to bring it under voluntary control.

Coping is also shaped by whom you have and who you are. Social support comes in types — instrumental (practical help), emotional (comfort and reassurance) and esteem (encouragement that builds confidence) — and buffers the effect of stressors. And there are gender differences: where the classic fight-or-flight model was built largely on male samples, Taylor argued women are more likely to tend-and-befriend — to protect offspring and seek social contact under stress, possibly mediated by oxytocin. The evaluative payoff is that cognitive methods like SIT tackle causes and build durable, transferable skills but are effortful and time-consuming, whereas drugs are effortless but shallow — so the 'best' approach depends on whether the goal is immediate relief or lasting change.

VocabularyKey terms the mark scheme pays for

TrapsMisconceptions that cost marks

ExamWhat examiners want