You are viewing a free preview of this lesson.
Subscribe to unlock all 10 lessons in this course and every other course on LearningBro.
Why do people so often catch a cold in the run-up to exams, or after a bereavement, or during a stressful period at work? The answer lies in one of the most important discoveries in health psychology: that psychological stress can directly suppress the body's immune defences, leaving us more vulnerable to illness. This lesson follows the physiological story begun in the previous lesson — the SAM pathway, the HPA axis, and above all the hormone cortisol — through to its consequences for health. It examines the landmark research of Kiecolt-Glaser and colleagues on immunosuppression and wound healing, and extends the analysis to cardiovascular disorders, including the role of chronic anger studied by Williams (2000). The field that studies these mind–body–immune connections is called psychoneuroimmunology.
Key Definition: Immunosuppression is the reduction in the activity or effectiveness of the immune system. Psychoneuroimmunology is the study of how psychological factors (such as stress) influence the nervous and endocrine systems and, through them, the functioning of the immune system.
The central claim is straightforward but profound: stress is not "just in the mind." Through measurable hormonal pathways it changes the behaviour of white blood cells, slows the healing of wounds, and contributes to heart disease. Establishing this required psychologists to combine the methods of psychology with those of immunology and medicine, producing some of the most rigorous research in the discipline.
This lesson addresses the following points in AQA A-Level Psychology (7182), Paper 3, Section C (Stress):
Assessment objectives engaged: AO1 (knowledge of how stress affects the immune system, the mechanism of cortisol-induced immunosuppression, and the research of Kiecolt-Glaser et al. and Williams) and AO3 (evaluation of the stress–illness link — the strength of the evidence, the problem of inferring causation from correlational data, the acute–chronic distinction, and individual differences). This topic builds directly on the physiology of stress (the HPA axis and cortisol) studied in the previous lesson.
The immune system is the body's defence against pathogens such as bacteria, viruses, and tumour cells. Its key agents are white blood cells (leucocytes), including lymphocytes — among them the natural killer (NK) cells that destroy virus-infected and cancerous cells, and the T-cells and B-cells that coordinate the targeted (adaptive) immune response. Broadly, immunity has two arms: a fast, general non-specific (innate) response (including phagocytes that engulf pathogens and the inflammatory response) and a slower, targeted specific (adaptive) response in which B-cells produce antibodies and T-cells destroy infected cells and remember the pathogen for next time. Both arms can be measured in research — for example by counting lymphocytes, assaying NK-cell activity, or measuring antibody production — which is what allows psychologists to quantify the effect of stress on immune function.
The mechanism by which stress suppresses immunity runs through the physiology of the previous lesson. Under chronic stress, the HPA axis keeps cortisol persistently elevated. Cortisol has powerful immunosuppressive effects: it reduces the production of lymphocytes, decreases the activity of natural killer cells, and dampens the inflammatory and antibody responses. In evolutionary terms this made sense — during an acute emergency the body diverts resources away from "slow" maintenance functions such as immunity toward immediate survival. The problem is that when the stressor is chronic, this suppression is sustained, leaving the body persistently under-defended.
It is essential to distinguish acute from chronic stress here, because their effects on immunity differ:
| Stress type | Effect on the immune system |
|---|---|
| Acute (brief) | Short-term suppression, sometimes followed by a temporary enhancement of certain defences (an adaptive "ramping up" for a fight-or-flight emergency). |
| Chronic (prolonged) | Sustained immunosuppression — reduced lymphocyte production and NK-cell activity — increasing vulnerability to infection and slowing wound healing. |
This is why the most damaging effects on health are associated with chronic stress (caregiving, long-term illness, sustained work pressure), which corresponds to Selye's resistance and exhaustion stages and to prolonged HPA activation.
Key Definition: Natural killer (NK) cells are a type of lymphocyte that destroys virus-infected cells and tumour cells. NK-cell activity is a commonly used index of immune function in stress research because it can be measured from a blood sample.
The classic demonstration that naturally occurring stress suppresses immune function comes from Kiecolt-Glaser, Garner, Speicher, Penn, Holliday, and Glaser (1984), who studied medical students facing the predictable, real-world stressor of important examinations.
The strength of this study is that it used an objective physiological measure (NK-cell activity from blood) rather than relying on self-report of illness, and it captured a naturally occurring stressor of clear real-world relevance, giving it high ecological validity.
If chronic stress suppresses immunity, then it should also slow the body's ability to heal wounds, because healing depends on a coordinated immune and inflammatory response. Kiecolt-Glaser and colleagues tested this directly.
Kiecolt-Glaser et al. (1995) — caregivers.
Kiecolt-Glaser et al. (2005) — marital conflict. A later study using a controlled procedure created blister wounds on married couples and then had them engage in either a supportive discussion or a conflictual, hostile discussion. Wounds healed more slowly following the hostile interactions, and couples high in hostility healed more slowly overall, with associated changes in immune-relevant cytokines. This experimental manipulation of stress strengthens the causal inference that interpersonal stress directly impairs healing.
Kiecolt-Glaser and Glaser (1987) — caregivers. Complementing the wound-healing work, this study examined the immune function of people providing long-term care for relatives with Alzheimer's disease — one of the most studied models of chronic real-life stress. Compared with matched controls, the caregivers showed poorer immune functioning, including reduced activity on several immune indices, and reported more days of infectious illness. Because caregiving is an enduring, uncontrollable stressor lasting months or years, this study is an important demonstration that chronic stress, not just the acute spike of an examination, suppresses immunity.
Together with the 1984 examination study, these studies build a powerful, multi-method case that both acute (examinations, brief conflict) and chronic (long-term caregiving) stress suppress immune function in humans. A particular strength of this programme of research is that Kiecolt-Glaser and colleagues triangulated across very different designs — a natural experiment (exams), a quasi-experiment comparing caregivers with controls, and a true experiment manipulating marital conflict — and obtained convergent results. When findings replicate across methods with different strengths and weaknesses, confidence in the underlying effect is greatly increased, which is why the stress–immune link is one of the best-evidenced relationships in health psychology.
It is worth being precise about how cortisol produces immunosuppression, because the strongest exam answers explain the mechanism rather than merely asserting it. Cortisol binds to glucocorticoid receptors found inside many immune cells. Acting through these receptors, cortisol reduces the proliferation of lymphocytes, lowers the production of signalling molecules called cytokines that coordinate the immune response, and decreases the cytotoxic activity of natural killer cells. It also has a powerful anti-inflammatory effect — the very property that makes synthetic glucocorticoids (such as hydrocortisone and prednisolone) valuable drugs for treating inflammatory conditions. In the short term this anti-inflammatory action is adaptive, preventing an excessive immune reaction during an emergency. In the long term, however, sustained suppression of inflammation and lymphocyte activity leaves the body less able to mount an effective defence against pathogens and slows the inflammatory phase of wound healing — which is exactly what Kiecolt-Glaser's biopsy studies detected. This is the precise physiological chain that connects the abstract idea of "stress" to the concrete outcome of catching a cold or healing slowly.
The second major health consequence named by the specification is cardiovascular disorders — diseases of the heart and blood vessels, including coronary heart disease (CHD), hypertension (high blood pressure), and stroke. Stress contributes to these in two ways.
Direct physiological effects. Repeated or chronic activation of the SAM pathway and the HPA axis keeps heart rate and blood pressure elevated. Over time, the surges of adrenaline and the persistently raised blood pressure can damage the lining of the blood vessels, encouraging the build-up of fatty plaques (atherosclerosis) that narrow the arteries. Cortisol raises blood glucose and, with chronic exposure, contributes to higher cholesterol and blood pressure, all of which are risk factors for CHD and stroke.
Indirect behavioural effects. Stress also affects health indirectly by changing behaviour. People under chronic stress are more likely to smoke, drink alcohol, eat poorly, and exercise less — all of which independently raise cardiovascular risk. Disentangling the direct hormonal effects of stress from these behavioural pathways is one of the central difficulties in this field.
The two routes are summarised below.
| Pathway | How stress raises cardiovascular risk |
|---|---|
| Direct (physiological) | Repeated SAM/HPA activation keeps heart rate and blood pressure high; adrenaline surges and chronic cortisol damage blood-vessel linings, promote atherosclerosis, and raise blood glucose and cholesterol. |
| Indirect (behavioural) | Chronic stress encourages smoking, heavy drinking, poor diet, reduced exercise, and disturbed sleep — each an independent risk factor for heart disease. |
Both routes probably operate together in most people, which is one reason the contribution of stress to cardiovascular disease is real but hard to quantify precisely.
A particularly influential strand of research links a specific emotional component of stress — chronic anger and hostility — to heart disease.
This research connects directly to the Type A personality (characterised by competitiveness, time-urgency, and hostility) studied later in the option, where hostility has emerged as the most cardiotoxic component.
The link Williams identified is not arbitrary; it follows from the physiology of the previous lesson. Individuals who are chronically angry and hostile tend to react to everyday frustrations with repeated, exaggerated sympathetic arousal — frequent surges of adrenaline and noradrenaline, with the accompanying spikes in heart rate and blood pressure. Over many years, this repeated cardiovascular reactivity is thought to accelerate the damage to artery walls and the build-up of atherosclerotic plaque that leads to coronary heart disease. In other words, hostility functions as a kind of "stress amplifier": the hostile person turns minor, frequent annoyances into recurrent physiological stress responses, multiplying the cardiovascular wear-and-tear. This mechanistic account is important for exam answers because it links the psychological trait (anger) to the physiological pathway (SAM-driven cardiovascular reactivity) and the medical outcome (CHD), demonstrating exactly the kind of biopsychosocial integration that top-band evaluation rewards. It also explains why later refinements of the Type A research concluded that it is specifically the hostility component — rather than ambition or time-urgency on their own — that carries the cardiac risk.
Subscribe to continue reading
Get full access to this lesson and all 10 lessons in this course.