4.3.7 - The role of stress in illness

How stress can become illness

Stress does not cause every illness, and it is not a simple "one stressor equals one disease" relationship. For AQA, the key idea is more precise: stress can increase vulnerability to illness through two main routes. One route is immunosuppression, where stress reduces the effectiveness of the immune system. The other is increased risk of cardiovascular disorders, where stress affects the heart and blood vessels.

The second route concerns the heart and blood vessels.

AO1: the direct route. When the hypothalamic-pituitary-adrenal (HPA) axis is activated, the adrenal cortex releases cortisol. In the short term, cortisol helps the body mobilise energy. If cortisol remains high over time, it can reduce lymphocyte production and activity. Lymphocytes are white blood cells involved in recognising pathogens, producing antibodies and destroying infected cells. Effects depend on the duration and pattern of stress. Natural killer cells contribute to innate defence, whereas T and B lymphocytes contribute to acquired immunity; chronic stress can dysregulate these responses rather than simply switching the immune system off.

AO1: the indirect route. Stress also affects illness through behaviour. A chronically stressed person may sleep poorly, smoke more, drink more alcohol, eat less well or exercise less. These behaviours can weaken immune functioning and increase cardiovascular risk, so stress may be part of a chain rather than the only cause.

AO2: applying the idea. If Aisha has been caring for a relative for several months, sleeping badly and catching repeated infections, a strong answer should link her chronic stress to HPA activation and cortisol, then add the indirect route through sleep and lifestyle. The examiner is not looking for "stress made her ill" as a slogan. They are looking for the mechanism.

Evidence for immunosuppression

Research measures immune functioning during naturally occurring stressors and compares it with lower-stress periods.

One influential line of research comes from Janice Kiecolt-Glaser and colleagues. Their work is useful because it studied real-life stressors rather than only artificial laboratory stress.

Kiecolt-Glaser et al. (1984) studied exam stress in 75 first-year medical students. The students gave blood samples twice: about one month before final examinations, when stress was lower, and on the first day of final examinations, when stress was higher. The researchers measured aspects of immune functioning, especially natural killer (NK) cell activity. NK cell activity declined from the first to the second sample, and students with higher life stress and loneliness showed lower NK cell activity. The finding supports an association between an examination period and reduced NK activity. Because the researchers did not randomly allocate exam stress, it does not isolate stress from changes in sleep, diet or other exam-period experiences.

Kiecolt-Glaser et al. (1991) extended this to a more chronic stressor. They compared 69 spousal caregivers of people with dementia with 69 sociodemographically matched controls. The caregivers had already been caring for an average of about five years, so this was a long-term stressor. Across a follow-up of about 13 months, caregivers showed poorer cellular immune measures than controls, reported more days of infectious illness and had higher levels of depressive disorder. At follow-up, 32% of caregivers met criteria for depressive disorder, compared with 6% of controls. This supports a relationship between a chronic caregiving context, immune measures and health. Matching reduces some group differences, but it cannot eliminate every difference in sleep, resources or prior health.

The contrasting category is chronic stress.

AO3: the acute/chronic distinction matters. Dhabhar's review of stress and immune function argues that acute stress can sometimes be immunoenhancing: immune cells are redistributed around the body so the organism is prepared for possible injury or infection. Chronic stress, by contrast, is more likely to suppress or dysregulate immune function. This is a strong evaluation point because it prevents a simplistic answer. Stress is not always harmful in the same way; duration, intensity and context matter.

What the immune result actually shows

NK activity means how effectively the cells perform their measured function; it is not the same as counting how many NK cells are present. The 1984 result therefore supports reduced activity, not the claim that all white blood cells disappeared or that every student developed an infection.

Comparing each student with their own earlier sample reduces differences due to stable characteristics such as genetic background. However, an exam period changes several things together. A student might sleep less and feel more threatened at the same time. The design establishes a change associated with that period, while leaving the separate contributions of stress appraisal and sleep unresolved.