Stress and illness | AQA A-Level Psychology Revision

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 65 minutes

These stress and illness A-Level Psychology revision notes explain how prolonged physiological activation may affect the immune and cardiovascular systems. You will examine how sustained cortisol production can cause immunosuppression and how repeated cardiovascular arousal may be associated with high blood pressure and heart problems. The lesson applies knowledge of cortisol during prolonged stress [The HPA system] and rapid cardiovascular arousal [The sympathomedullary pathway], before evaluating evidence linking stress with physical illness.

Learning Objectives 🎯

By the end of this revision page, you should be able to:

• Define immunosuppression and cardiovascular disorders.

• Explain how prolonged cortisol production may reduce immune functioning.

• Explain how stress may increase vulnerability to infection.

• Explain the relationship between stress and cardiovascular disorders.

• Apply physiological explanations to unfamiliar examples of stress-related illness.

• Analyse research evidence linking stress with immune and cardiovascular outcomes.

• Evaluate the strength of the evidence that stress causes illness.

Revision Notes 📚

What does the AQA specification require?

Within the Stress option, AQA requires students to study:

• The physiology of stress, including general adaptation syndrome, the hypothalamic-pituitary-adrenal system, the sympathomedullary pathway and cortisol.

• The role of stress in illness, including immunosuppression and cardiovascular disorders.

The specification therefore requires more than a general statement that stress is unhealthy. You must explain the biological processes that may connect stress with illness and evaluate the evidence supporting those connections.

For this lesson, you need to understand:

1. How stress activates physiological pathways.

2. How sustained cortisol may suppress immune activity.

3. Why immunosuppression may increase vulnerability to infection.

4. How repeated increases in heart rate and blood pressure may affect cardiovascular health.

5. What research has found about stress and illness.

6. Why associations between stress and illness do not necessarily prove causation.

How can stress affect physical health?

Stress is a response to demands or threats that require adaptation.

In the short term, physiological stress responses may be useful. They prepare the body to act, maintain alertness and make energy available.

Problems may arise when:

• Stress is severe.

• Stress continues for a long period.

• Stressors occur repeatedly.

• The body has insufficient opportunity to recover.

• The person has other sources of vulnerability.

The overall relationship can be represented as:

Continuing or repeated stress → prolonged physiological activation → disruption to normal bodily functioning → increased vulnerability to illness

Two important routes are required by the specification:

• Effects on the immune system.

• Effects on the cardiovascular system.

Acute and chronic stress

It is important to distinguish short-term from long-term stress.

Acute stress is a brief response to an immediate stressor.

Chronic stress continues over a prolonged period or repeatedly returns.

Acute stress	Chronic stress
Short-lived	Long-lasting or frequently repeated
May help the person respond to an immediate demand	Requires continued physiological adaptation
Often involves rapid fight-or-flight arousal	Often involves sustained HPA activity and cortisol
Recovery can occur when the stressor ends	The body may have little opportunity to return to its resting state
May be adaptive	May increase vulnerability to illness

The distinction matters because evidence linking stress and illness usually concerns prolonged or repeated stress, not every brief experience of pressure.

The physiological pathways linking stress and illness

Stress can activate two linked physiological systems.

The sympathomedullary pathway

The sympathomedullary pathway produces rapid arousal.

The sequence is:

1. A stressor activates the hypothalamus.

2. The hypothalamus activates the sympathetic nervous system.

3. The sympathetic nervous system stimulates the adrenal medulla.

4. The adrenal medulla releases adrenaline and noradrenaline.

5. Heart rate, breathing rate and blood pressure increase.

These changes prepare the body for fight or flight.

This is normally adaptive in a short-lived emergency. However, frequent or prolonged cardiovascular arousal may place repeated demands on the heart and blood vessels.

The complete immediate response is covered in adrenaline and fight or flight [The sympathomedullary pathway].

The HPA system

The hypothalamic-pituitary-adrenal system, usually called the HPA system, produces a more sustained response.

The sequence is:

1. The hypothalamus releases corticotrophin-releasing hormone, or CRH.

2. CRH stimulates the pituitary gland.

3. The pituitary gland releases adrenocorticotrophin hormone, or ACTH.

4. ACTH stimulates the adrenal cortex.

5. The adrenal cortex releases cortisol.

Cortisol helps maintain energy availability while the stressor continues.

If cortisol production remains sustained, it may interfere with immune functioning.

This process builds directly on the prolonged stress pathway [The HPA system].

Stress does not automatically cause illness

Stress should be described as a risk factor, not an automatic cause of illness.

A person experiencing stress will not necessarily become ill because outcomes may be affected by:

• The duration and severity of the stress.

• Individual differences.

• Personality.

• Hardiness.

• Social support.

• Existing health.

• Other environmental or behavioural influences.

A careful examination sentence would be:

Prolonged stress may increase vulnerability to illness by suppressing immune functioning or maintaining cardiovascular arousal.

Avoid stating:

Stress always causes illness.

That claim is too deterministic and is not supported by the evidence.

Immunosuppression

What is immunosuppression?

Immunosuppression occurs when the immune system becomes compromised and cannot protect the individual against disease as effectively.

The immune system normally helps defend the body against:

• Viruses.

• Bacteria.

• Infected cells.

• Other potential threats to health.

If immune activity is reduced, the person may become more vulnerable to infection or may take longer to recover.

AQA has previously defined immunosuppression as the immune system becoming compromised so that it cannot protect the individual against disease.

The role of white blood cells

White blood cells, also called leucocytes, are involved in the immune response.

Their activity helps the body identify and respond to infection.

Sustained cortisol production may interfere with the activity of these cells. The immune system may therefore become less effective at defending the body.

AQA’s June 2024 mark scheme identifies the following pathway:

• Sustained cortisol reduces immune functioning.

• Cortisol interferes with white blood-cell activity.

• The body’s ability to fight infection is reduced.

Natural killer cells

Natural killer cells, often abbreviated to NK cells, form part of the body’s immune defence.

Research into stress and immune functioning may measure natural killer-cell activity. Lower activity suggests that one aspect of the immune response has been weakened.

Do not write that lower natural killer-cell activity proves that a person will become ill. It indicates reduced immune functioning and potentially increased vulnerability.

How cortisol may produce immunosuppression

Cortisol is adaptive when it helps the body maintain energy during a continuing stressor.

However, sustained cortisol production can suppress processes that are not immediately required for dealing with the demand.

The proposed process is:

1. A stressor continues.

2. The HPA system remains active.

3. The adrenal cortex continues releasing cortisol.

4. Cortisol interferes with white blood-cell activity.

5. Immune functioning becomes less effective.

6. The person becomes more vulnerable to infection or slower recovery.

A useful exam chain is:

Chronic stress → sustained cortisol → reduced leucocyte activity → immunosuppression → increased vulnerability to illness

Why would the stress response suppress immunity?

During an immediate threat, the body prioritises processes needed for rapid action.

Energy is directed towards:

• Maintaining alertness.

• Supporting muscles.

• Making glucose available.

• Continuing physiological activity.

Immune defence is important, but it may not be the body’s immediate priority during an emergency.

Temporarily reducing immune activity may therefore be manageable. The problem occurs when the stress response remains active and immune activity is suppressed for too long.

Immunosuppression and infection

If the immune system is compromised, a person may be more likely to:

• Develop a cold or viral infection.

• Experience repeated minor infections.

• Show slower recovery.

• Take longer to heal after an injury.

The correct link is:

Stress does not create a virus, but it may reduce the body’s ability to defend itself against one.

For example, a student exposed to a cold virus during a prolonged examination period may be more likely to develop symptoms if their immune functioning has been suppressed.

Immunosuppression and wound healing

An effective immune response contributes to healing.

Research cited in AQA assessment material has found increased wound-healing times in stressed populations. This is consistent with the claim that stress can interfere with processes involved in repair.

The conclusion should remain cautious:

Slower healing in a stressed group supports a relationship between stress and immune functioning, but other differences between the groups may also contribute.

Chronic caring stress

Long-term carers are frequently used in research because caring responsibilities can provide a naturally occurring source of continuing stress.

A carer may experience:

• Extended responsibility.

• Limited opportunities for recovery.

• Sleep disruption.

• Emotional demands.

• Repeated daily stressors.

If carers show poorer immune functioning than an appropriate comparison group, this is consistent with the prediction that chronic stress may produce immunosuppression.

However, caregiving cannot ethically or practically be assigned experimentally. Carers may differ from non-carers in other ways, creating problems when drawing causal conclusions.

Applying immunosuppression to a scenario

Consider this example:

Amira has cared for an unwell relative for more than a year while continuing to work. She sleeps poorly and has recently developed several infections.

A developed application would explain:

• Amira’s caring responsibilities are a chronic stressor.

• Her HPA system may remain active over a prolonged period.

• The adrenal cortex may continue releasing cortisol.

• Sustained cortisol may interfere with white blood-cell activity.

• This could produce immunosuppression.

• Reduced immune functioning may help explain her increased vulnerability to infection.

A weak answer would state only:

Amira is stressed, so she gets infections.

This does not explain the physiological mechanism.

Immunosuppression is not complete immune failure

The prefix immuno- relates to the immune system, while suppression means reduction.

Immunosuppression therefore means that immune functioning is reduced or compromised. It does not necessarily mean that the immune system has stopped working completely.

Use careful language:

• “Reduced immune activity.”

• “Compromised immune functioning.”

• “Increased vulnerability.”

• “Lower ability to fight infection.”

Avoid:

• “The immune system disappears.”

• “Cortisol destroys every white blood cell.”

• “Stress guarantees disease.”

Evidence for Stress and Immunosuppression

Kiecolt-Glaser and examination stress

Research identified in AQA mark schemes compared immune functioning during periods of lower and higher stress.

Kiecolt-Glaser and colleagues found that:

• Natural killer-cell activity was significantly lower during the high-stress examination period than during a lower-stress period.

• The reduction was greater among students who reported greater social isolation.

This supports the prediction that stress is associated with reduced immune activity.

Why the research supports the explanation

The evidence is consistent with immunosuppression because:

1. Examination periods provide an identifiable source of stress.

2. Immune activity was measured.

3. Immune functioning was lower during the higher-stress period.

4. The result matches the prediction that stress compromises immunity.

Limitation of the evidence

The research does not prove that stress alone caused the reduction.

Other differences during examination periods might include:

• Reduced sleep.

• Changes in diet.

• Changes in routine.

• Differences in social contact.

These variables may also influence immune functioning.

Kiecolt-Glaser and caregiving

Another study identified by AQA compared people caring for relatives with Alzheimer’s disease with a control group over a 13-month period.

The carers showed:

• Increased antibodies to the Epstein-Barr virus.

• More infectious illness than controls.

This finding is consistent with poorer immune control during chronic stress.

A strength is that caregiving represents genuine, prolonged stress, so the research has real-world relevance.

A limitation is that carers and controls may differ in several ways besides stress.

Cohen and the common cold

Cohen’s research found that the likelihood of developing a cold was positively associated with scores on a questionnaire measuring stressful life events.

A positive association means that higher stress scores were linked with a greater likelihood of illness.

This supports the claim that stress may increase susceptibility to infection.

However, the relationship does not by itself prove that stress caused the cold. People with high stress scores may also differ in health behaviour, personality or other relevant factors.

Evidence of immunoenhancement

Not all evidence suggests that every form of stress suppresses immune activity.

AQA assessment material recognises research reporting immunoenhancing effects of stress.

This may indicate that:

• Short-term stress can temporarily increase some aspects of immune activity.

• The effect of stress depends on its duration.

• Acute and chronic stress should not be treated as identical.

• Different parts of the immune system may respond differently.

This does not disprove the relationship between chronic stress and immunosuppression. It suggests that the relationship is more complex than “all stress weakens immunity”.

Stress and Cardiovascular Disorders

What is the cardiovascular system?

The cardiovascular system consists of the heart and blood vessels.

Its functions include:

• Pumping blood around the body.

• Delivering oxygen and nutrients.

• Removing waste products.

• Maintaining circulation.

A cardiovascular disorder is a health problem affecting the heart or blood vessels.

Within the stress topic, relevant examples include:

• High blood pressure.

• Heart problems.

• Coronary heart disease.

• Heart attack.

How acute stress affects the cardiovascular system

During the fight-or-flight response:

1. The hypothalamus activates the sympathetic nervous system.

2. The adrenal medulla releases adrenaline and noradrenaline.

3. Heart rate increases.

4. Blood pressure increases.

5. Blood is circulated more quickly.

6. Oxygen and glucose are delivered to the muscles.

These changes are useful during an immediate emergency.

For example, a faster heart rate may help someone move rapidly away from danger.

Why repeated cardiovascular arousal may be harmful

The cardiovascular response is designed to help meet an immediate demand.

If the response occurs frequently or remains activated:

• Heart rate may be repeatedly elevated.

• Blood pressure may remain raised.

• The heart and blood vessels experience continued physiological demand.

• Vulnerability to cardiovascular illness may increase.

The proposed relationship is:

Repeated or chronic stress → continued cardiovascular arousal → raised blood pressure and strain on cardiovascular functioning → increased risk of cardiovascular disorder

This does not mean that one brief increase in heart rate produces heart disease.

The concern is repeated or sustained physiological activation over time.

High blood pressure

Blood pressure is the force exerted by circulating blood against the walls of blood vessels.

Stress-related sympathetic activation can temporarily increase blood pressure.

If high blood pressure becomes prolonged or repeatedly occurs, it may be associated with poorer cardiovascular health.

In an exam scenario, a doctor taking a stressed person’s blood pressure may be checking their cardiovascular functioning. This was an explicit application point in AQA’s June 2024 mark scheme.

Stress and heart rate

A pounding or rapidly beating heart may indicate sympathetic arousal.

This does not mean the person has a cardiovascular disorder. It is a normal part of the immediate stress response.

The distinction is:

• Temporary increased heart rate is a physiological stress response.

• Long-term or repeated cardiovascular activation may contribute to health risk.

• A cardiovascular disorder is an illness affecting the heart or blood vessels.

Stress and coronary heart disease

Coronary heart disease, often abbreviated to CHD, is a cardiovascular disorder.

AQA materials connect chronic stress, low workplace control and particular personality characteristics with increased CHD risk.

Stress may be one contributing factor among several rather than the only cause.

This topic links with:

• workload and occupational control [Workplace stress]

• behavioural patterns linked to stress [Personality types and stress]

• commitment, challenge and control [Hardiness]

Stress and heart attacks

AQA’s June 2024 mark scheme identifies Yusuf’s research as evidence of a link between chronic stress and heart attacks.

This evidence supports the broader claim that prolonged psychological stress is associated with serious cardiovascular outcomes.

However, such evidence is generally correlational. It is difficult to conclude that stress alone caused the heart attacks because other variables may contribute.

Direct and indirect relationships

Stress may be related to cardiovascular illness through a direct physiological route:

• Sympathetic activation.

• Increased heart rate.

• Raised blood pressure.

• Prolonged cardiovascular arousal.

The evidence may also be affected by indirect or mediating influences.

For example, people under stress may differ in:

• Diet.

• Personality.

• Existing health.

• Other behaviours or circumstances affecting health.

AQA examiner commentary specifically identifies diet and personality as mediating variables that students could use when assessing the stress-illness relationship.

Applying cardiovascular effects to a scenario

Consider this example:

Tariq has experienced intense pressure at work for several months. He often feels his heart pounding and his doctor records persistently raised blood pressure.

A developed application would explain:

• Tariq’s workload is a continuing stressor.

• Stress may repeatedly activate the sympathomedullary pathway.

• Adrenaline and noradrenaline increase heart rate and blood pressure.

• Continuing activation may prevent cardiovascular functioning from returning fully to its resting level.

• Persistently raised blood pressure may indicate increased cardiovascular risk.

A cautious answer should not diagnose Tariq with a specific disorder unless the scenario provides that information.

Comparing immune and cardiovascular effects

Immune route	Cardiovascular route
Primarily linked with sustained cortisol	Primarily linked with repeated sympathetic arousal
Involves reduced white blood-cell activity	Involves increased heart rate and blood pressure
May increase vulnerability to infection	May increase vulnerability to heart and blood-vessel disorders
Immunosuppression is the key concept	Cardiovascular arousal is the key process
Strongly linked with prolonged HPA activation	Strongly linked with repeated sympathomedullary activation

The pathways can operate together. A person experiencing chronic stress may show both sustained cortisol and repeated cardiovascular arousal.

Evaluating Evidence Linking Stress and Illness

Strength: evidence uses objective physiological measures

Research into stress and illness may measure:

• Natural killer-cell activity.

• White blood-cell functioning.

• Antibodies.

• Wound-healing time.

• Blood pressure.

• Heart rate.

• Diagnosed illness.

These measures are less dependent on a participant’s subjective opinion than simply asking whether they feel unhealthy.

This can increase the scientific credibility of the evidence.

However, an objective measure does not automatically establish causation. Lower immune activity and high stress may still be produced by another variable.

Strength: evidence comes from several populations

Evidence has been found among:

• Students during examinations.

• Long-term carers.

• People reporting stressful life events.

• People exposed to workplace stress.

• Populations experiencing chronic stress.

Finding similar associations in different settings increases confidence that the relationship is not limited to one unusual group.

It also suggests that stress may affect health across several kinds of real-life demand.

Strength: real-world stress improves validity

Studies of examinations, caregiving and work investigate naturally occurring stress.

This gives the research ecological validity because participants are experiencing genuine demands rather than an artificial laboratory task.

For example, caring for a relative over many months resembles the kind of chronic stress the theory is intended to explain.

The limitation is that real-world research gives the investigator less control over extraneous variables.

Limitation: much of the evidence is correlational

A large amount of research identifies a relationship between:

• Stress scores and illness.

• Stressful circumstances and immune activity.

• Workplace stress and cardiovascular illness.

A correlation shows that variables are associated. It does not establish that one caused the other.

Possible interpretations include:

1. Stress causes poorer health.

2. Poor health increases stress.

3. Another variable causes both stress and illness.

4. Stress and illness influence each other over time.

AQA’s June 2024 mark scheme explicitly identifies cause and effect as a central evaluation issue because being ill may itself cause or intensify stress.

Reverse causality

Reverse causality occurs when the presumed effect may actually influence the proposed cause.

For example:

A person may report high stress because they are already experiencing pain, fatigue, treatment demands or concerns about their health.

This means that an association between stress and illness cannot always establish which occurred first.

Longitudinal research can help by measuring stress before later illness develops, although it still cannot control every possible influence.

Limitation: mediating variables

A mediating variable affects the relationship between two other variables.

The effect of stress on illness may depend on:

• Personality.

• Hardiness.

• Social isolation.

• Social support.

• Diet.

• The duration of the stress.

• The person’s existing vulnerability.

For example, the reduction in natural killer-cell activity in examination research was greater among students reporting social isolation.

This suggests that stress may not act in exactly the same way for everyone.

Understanding these differences prepares you for personality and stress-related behaviour [Personality types and stress] and hardy responses to demanding events [Hardiness].

Limitation: self-report measures of stress

Some studies measure stress using questionnaires about:

• Life events.

• Perceived stress.

• Social isolation.

• Daily experiences.

Self-report data may be affected by:

• Inaccurate recall.

• Different interpretations of questions.

• Social desirability.

• Differences in how people label and report stress.

If the measure of stress is inaccurate, the estimated relationship with illness may also be inaccurate.

This limitation connects with questionnaire-based stress assessment [Measuring stress through self-report].

Limitation: participants cannot be randomly assigned to severe chronic stress

It would be unethical to deliberately expose participants to severe, prolonged stress in order to see whether they become seriously ill.

Researchers therefore often rely on:

• Naturally occurring stress.

• Correlational designs.

• Quasi-experimental comparisons.

• Shorter and less harmful laboratory stressors.

This protects participants but limits experimental control.

The strongest causal experiment would often be ethically unacceptable, creating a tension between scientific control and participant welfare.

Limitation: evidence can be muddled if studies are not learned precisely

Different studies may examine:

• Natural killer cells.

• Antibodies.

• Cold symptoms.

• Wound healing.

• Cardiovascular outcomes.

These are related but are not interchangeable.

For example:

• Lower natural killer-cell activity is a measure of immune functioning.

• Developing a cold is an illness outcome.

• Wound-healing time is a recovery outcome.

• Blood pressure is a cardiovascular measure.

A strong answer identifies exactly what each study measured and found.

Not all stress is harmful

Moderate or short-term stress may sometimes be beneficial.

It may:

• Increase alertness.

• Mobilise energy.

• Prepare the immune system for an immediate challenge.

• Help a person respond effectively.

This challenges a simplistic view that every experience of stress damages health.

The health risk appears more closely linked with:

• Severe stress.

• Chronic stress.

• Repeated activation.

• Insufficient recovery.

Stress may be one factor within an interaction

An interactionist explanation proposes that illness may result from several factors working together.

These might include:

• Physiological predisposition.

• Personality or temperament.

• Exposure to external stressors.

• Social support.

• Coping resources.

• Existing health.

AQA’s mark scheme recognises the value of explanations involving the combined effects of physiological predisposition, personality and external stressors.

This is more balanced than claiming either:

• Stress alone causes illness.

• Stress has no meaningful effect on illness.

Practical applications

Evidence linking stress and illness has practical value.

It suggests that reducing chronic stress may help protect health.

Possible implications include:

• Addressing the source of workplace stress.

• Increasing control over demanding situations.

• Developing effective coping strategies.

• Providing appropriate social support.

• Monitoring cardiovascular and immune health in highly stressed groups.

AQA’s mark scheme emphasises that it may be important to address the source of stress rather than merely mask its symptoms.

Later lessons examine ways of developing psychological coping skills [Stress inoculation therapy] and using physiological feedback to reduce arousal [Biofeedback].

Biological reductionism

The explanation may be criticised as biologically reductionist if illness is explained only through:

• Cortisol.

• White blood cells.

• Heart rate.

• Blood pressure.

Focusing on biological processes has advantages:

• The mechanisms can be measured.

• Predictions can be tested.

• The explanation identifies possible health pathways.

However, it may neglect:

• The meaning of the stressor.

• Perceived control.

• Social circumstances.

• Personality.

• Coping.

• Social support.

A fuller account should connect physiological activity with the person’s psychological and social context.

Biological determinism

A strongly deterministic account could suggest that stress automatically produces physiological damage.

This would underestimate:

• Differences in coping.

• The possibility of recovery.

• Individual resilience.

• The protective role of social support.

• The fact that associations are probabilistic.

A better conclusion is that stress increases risk under some conditions rather than fixing an inevitable outcome.

Overall evaluation

There is convincing evidence that stress is associated with changes in immune activity and cardiovascular health. Research involving students, carers and people experiencing chronic stress supports the proposed relationship.

However, much of the evidence is correlational and vulnerable to confounding variables. Illness may also increase stress, while personality, diet, social isolation and other factors may affect both variables. The most defensible conclusion is that prolonged stress is one important risk factor within a wider interactionist explanation of illness.

Planning an extended response

For a question asking you to discuss the role of stress in illness, organise your answer around the assessment objectives.

Knowledge and understanding

Explain:

• The difference between acute and chronic stress.

• HPA activity and sustained cortisol.

• The effect of cortisol on white blood cells.

• Immunosuppression and vulnerability to infection.

• Sympathomedullary activation.

• Increased heart rate and blood pressure.

• The possible link with cardiovascular disorders.

Application

For every scenario detail:

1. Identify the source or duration of stress.

2. Select the relevant physiological pathway.

3. Explain the biological mechanism.

4. Link it to the health symptom or measurement.

For example:

Repeated sore throats may indicate infection. Long-term stress may sustain cortisol production, suppressing white blood-cell activity and increasing vulnerability to infection.

Evaluation

Develop points such as:

• Supporting immune and cardiovascular evidence.

• Objective physiological measures.

• Real-world validity.

• Correlational evidence.

• Reverse causality.

• Mediating variables.

• Individual differences.

• Acute stress possibly enhancing some immune responses.

• Practical applications.

• Interactionist explanations.

A 16-mark answer should not consist entirely of research studies. You must first explain the biological links between stress and illness.

Key Words 🔑

Key word	Student-friendly definition	How it may be used in an exam
Stress	A physiological and psychological response to demands requiring adaptation	Identify the response linked with changes in health
Acute stress	A short-term response to an immediate stressor	Contrast immediate arousal with chronic health effects
Chronic stress	Stress that continues or repeatedly occurs over a prolonged period	Link it with sustained cortisol and cardiovascular activation
Immune system	The body’s defence system against infection and disease	Explain which system is affected by immunosuppression
Immunosuppression	Compromised immune functioning that reduces protection against disease	Use it to explain increased vulnerability to infection
White blood cells	Cells involved in the body’s defence against infection	Explain how sustained cortisol may interfere with immunity
Leucocytes	Another name for white blood cells	Recognise and use the specialist term accurately
Natural killer cells	Immune cells whose activity may be measured in stress research	Use when describing evidence from examination-stress research
Cortisol	A hormone released by the adrenal cortex during HPA activation	Link sustained production with reduced immune functioning
HPA system	The prolonged stress pathway involving the hypothalamus, pituitary gland and adrenal cortex	Explain the physiological route to cortisol release
Sympathomedullary pathway	The rapid pathway involving sympathetic activation and the adrenal medulla	Explain increases in heart rate and blood pressure
Cardiovascular system	The heart and blood vessels	Identify the bodily system affected by cardiovascular disorders
Cardiovascular disorder	A health problem affecting the heart or blood vessels	Use when discussing high blood pressure, CHD or heart attacks
Blood pressure	The force exerted by circulating blood against blood-vessel walls	Apply it as a cardiovascular measure in a scenario
Coronary heart disease	A cardiovascular disorder affecting the heart’s blood supply	Use as an example of illness associated with chronic stress
Correlation	A measured association between two variables	Explain why stress and illness may be related without proving causality
Reverse causality	The possibility that the proposed outcome affects the supposed cause	Explain how illness might increase reported stress
Mediating variable	A factor that affects the relationship between stress and illness	Apply personality, diet or social isolation in evaluation
Interactionist explanation	An explanation involving several factors working together	Conclude that stress combines with biological and psychological vulnerability

Hints from the Examiner Reports 💡

Examiner hint: Explain the biological mechanism before presenting supporting studies. The June 2024 examiner report found that many students described evidence instead of explaining how stress affects the immune and cardiovascular systems.

Examiner hint: Keep research studies separate and accurate. The same report noted that some students combined details from several different studies, producing muddled evidence.

Examiner hint: Distinguish what each study measured. Natural killer-cell activity, antibodies, cold incidence, wound healing and blood pressure are different outcomes.

Examiner hint: Use the whole scenario. A long-term caring role may indicate chronic stress, a sore throat may suggest infection, heart pounding may indicate sympathetic arousal and a blood-pressure check concerns cardiovascular functioning.

Examiner hint: Application requires psychological knowledge. Do not simply state that the person is ill because they are stressed. Name cortisol, immunosuppression or cardiovascular arousal and explain the connection.

Examiner hint: Develop mediating variables. The 2024 report found that stronger evaluations recognised factors such as diet and personality when considering the relationship between stress and illness.

Examiner hint: A 16-mark response requires knowledge, application and discussion. Strong answers explain the mechanism, apply it to several details and then evaluate the strength of the evidence.

Examiner hint: Use cautious causal language. Most evidence demonstrates an association, so phrases such as “may increase vulnerability” are more accurate than “definitely causes”.

Common Mistakes ⚠️

Mistake: Saying stress directly creates infections.

Why this is incorrect:Stress does not create a virus or bacterium. It may reduce the immune system’s ability to defend the body.

How to improve:Explain that immunosuppression increases vulnerability after exposure to a pathogen.

Mistake: Defining immunosuppression as complete immune failure.

Why this is incorrect:Immunosuppression means that immune functioning is reduced or compromised, not necessarily absent.

How to improve:Use terms such as reduced activity, compromised defence and increased vulnerability.

Mistake: Saying adrenaline causes immunosuppression through the HPA system.

Why this is incorrect:The HPA system releases cortisol from the adrenal cortex. Adrenaline belongs to the sympathomedullary pathway.

How to improve:Separate the immune route from the cardiovascular route.

Mistake: Saying cortisol is released by the pituitary gland.

Why this is incorrect:The pituitary releases ACTH. The adrenal cortex releases cortisol.

How to improve:Recall the full HPA sequence before explaining immunosuppression.

Mistake: Stating that cortisol is always harmful.

Why this is incorrect:Cortisol helps maintain energy during a continuing demand. Problems are associated particularly with sustained production.

How to improve:Distinguish its adaptive short-term role from the possible effects of chronic activation.

Mistake: Saying that a pounding heart means the person has heart disease.

Why this is incorrect:An increased heart rate is a normal part of sympathetic arousal. It is not itself a diagnosis.

How to improve:Explain that repeated or sustained cardiovascular activation may increase long-term risk.

Mistake: Confusing cardiovascular disorders with immunosuppression.

Why this is incorrect:Cardiovascular disorders affect the heart and blood vessels. Immunosuppression affects immune defence.

How to improve:Learn the two biological routes separately before connecting them.

Mistake: Describing several research studies without explaining stress and illness.

Why this is incorrect:Evidence does not replace knowledge of the physiological mechanism.

How to improve:Begin with cortisol, leucocytes, heart rate and blood pressure, then use studies to support or challenge those processes.

Mistake: Combining findings from different studies.

Why this is incorrect:A study of examination stress and natural killer cells is not the same as research into cold incidence or wound healing.

How to improve:Learn each study using four headings: participants, stressor, health measure and finding.

Mistake: Claiming that correlation proves causation.

Why this is incorrect:Illness might increase stress, or another factor might influence both variables.

How to improve:Use the phrase “is associated with” and discuss reverse causality.

Mistake: Naming a confounding variable without explaining it.

Why this is incorrect:The examiner needs to understand how the factor affects the conclusion.

How to improve:For example, explain that changes in diet during examinations could influence immune functioning independently of stress.

Mistake: Treating acute and chronic stress as identical.

Why this is incorrect:Short-term stress may be adaptive and may not produce the same effects as sustained stress.

How to improve:State the duration of the stressor and explain why prolonged activation creates greater health risk.

Mistake: Diagnosing illness from limited scenario information.

Why this is incorrect:Heart pounding or a sore throat may have several explanations.

How to improve:Use cautious language such as “may indicate” or “is consistent with”.

Exam-Style Questions ✍️

Question 1

Which of the following best defines immunosuppression?

A. A rapid increase in heart rate during stressB. A complete absence of white blood cellsC. Compromised immune functioning that reduces protection against diseaseD. Increased immune functioning during all forms of stress

[1 mark]

Question 2

Outline what is meant by a cardiovascular disorder.

[2 marks]

Question 3

Explain how prolonged stress may lead to immunosuppression.

[4 marks]

Question 4

Explain how repeated activation of the sympathomedullary pathway may be associated with cardiovascular disorders.

[4 marks]

Question 5

A researcher measures natural killer-cell activity in the same group of students twice.

Measurement period	Mean relative natural killer-cell activity
Four weeks before examinations	82
During final examinations	61

Explain what the results suggest about stress and immune functioning. Identify one conclusion that cannot be drawn from the results.

[4 marks]

Question 6

Rosa has cared for her father for eighteen months while working full time. She sleeps poorly and has recently experienced repeated colds. During a medical appointment, her doctor takes a blood sample.

Use your knowledge of stress and illness to explain Rosa’s experiences.

[6 marks]

Question 7

Explain one methodological limitation of evidence linking stress with illness.

[4 marks]

Question 8

Evaluate evidence linking stress with immunosuppression.

[8 marks]

Question 9

Dominic has experienced heavy workload and family difficulties for several months. He frequently feels his heart pounding and has persistently raised blood pressure. He has also developed several minor infections. Dominic says, “The stress must be the only reason I am unwell.”

Discuss the role of stress in illness. Refer to Dominic in your answer.

[16 marks]

Answers and Mark Scheme

Question 1

Answer: C

Immunosuppression means that immune functioning is compromised, reducing the body’s ability to protect itself against disease.

[1 mark]

Question 2

Award up to two marks:

• A cardiovascular disorder is an illness or health problem affecting the cardiovascular system.

• This means that it affects the heart or blood vessels, for example high blood pressure, coronary heart disease or heart attack.

[2 marks]

Question 3

Award one mark for each relevant point, up to four marks:

• Prolonged stress causes continuing activation of the HPA system.

• The adrenal cortex continues releasing cortisol.

• Sustained cortisol interferes with white blood-cell or leucocyte activity.

• Immune functioning is suppressed, increasing vulnerability to infection or slowing recovery.

[4 marks]

Question 4

Award up to four marks:

• Stress activates the sympathetic nervous system.

• The adrenal medulla releases adrenaline and noradrenaline.

• These hormones increase heart rate and blood pressure.

• If cardiovascular activation is frequent or prolonged, it may place continued demand on the heart and blood vessels and increase vulnerability to cardiovascular illness.

Answers must connect the immediate response with possible long-term risk.

[4 marks]

Question 5

Award up to four marks:

• Natural killer-cell activity is lower during examinations than before examinations.

• Examinations are likely to produce a period of increased stress.

• The result is consistent with stress being associated with reduced immune activity or immunosuppression.

• The researcher cannot conclude that examination stress caused the reduction because other variables, such as sleep, diet or changes in routine, were not controlled.

Credit other accurate interpretations and limitations.

[4 marks]

Question 6

Award one mark for each clear application, up to six marks:

• Caring for eighteen months represents chronic or prolonged stress.

• Rosa’s HPA system may remain activated.

• The adrenal cortex may continue releasing cortisol.

• Sustained cortisol may interfere with white blood-cell activity.

• Immunosuppression could increase Rosa’s vulnerability to repeated colds.

• The blood sample could be used to investigate markers of immune activity, infection or physiological stress.

Credit other accurate applications linked to the scenario.

[6 marks]

Question 7

Award marks as follows:

• One mark for identifying a relevant methodological limitation.

• Up to three further marks for developing its effect on the conclusion.

Possible answer:

Much evidence is correlational because researchers cannot ethically assign people to severe chronic stress. A correlation between stress and illness cannot establish which variable caused the other. Illness may increase reported stress, or another variable such as personality or diet may influence both, so a causal conclusion is not justified.

Other relevant limitations include:

• Self-report measures may be inaccurate.

• Naturally stressed groups may differ in several uncontrolled ways.

• Findings from one population may not generalise.

• Different studies measure different aspects of immune functioning.

[4 marks]

Question 8

Indicative content may include:

Knowledge and evidence

• Immunosuppression involves compromised immune functioning.

• Sustained cortisol can interfere with white blood-cell activity.

• Kiecolt-Glaser found lower natural killer-cell activity during examinations.

• Greater reductions were associated with social isolation.

• Caregiving research found poorer immune outcomes among long-term carers.

• Cohen found an association between stressful life events and cold incidence.

• Stressed populations have shown slower wound healing.

Evaluation

• Objective physiological measures increase scientific credibility.

• Real-life stressors improve ecological validity.

• Findings across different populations provide converging support.

• Naturally occurring stress is difficult to control.

• Correlational findings cannot establish causation.

• Illness may itself increase stress.

• Diet, personality, sleep or social isolation may mediate the relationship.

• Self-reported stress may be inaccurate.

• Some short-term stress may enhance rather than suppress immune functioning.

• Stress is likely to be one factor within an interactionist account.

For the highest marks, evidence should be described accurately and its implications developed.

[8 marks]

Question 9

Indicative content may include:

Knowledge and understanding

• Chronic stress involves prolonged or repeated physiological activation.

• The HPA system results in cortisol release from the adrenal cortex.

• Sustained cortisol may interfere with leucocyte activity.

• This may produce immunosuppression and increased vulnerability to infection.

• Sympathetic activation releases adrenaline and noradrenaline.

• These hormones increase heart rate and blood pressure.

• Repeated cardiovascular arousal may increase vulnerability to cardiovascular disorders.

• Stress is a risk factor rather than an inevitable cause of illness.

Application to Dominic

• Workload and family difficulties lasting several months indicate chronic stress.

• Dominic’s pounding heart suggests sympathetic arousal.

• Persistently raised blood pressure concerns cardiovascular functioning.

• Repeated activation may increase cardiovascular risk.

• Minor infections may be consistent with reduced immune functioning.

• Sustained cortisol may have interfered with white blood-cell activity.

• Dominic’s claim that stress is the only cause is too definite because other factors may contribute.

Evaluation

• Research involving students, carers and people reporting stressful events supports a relationship with immune functioning.

• Cardiovascular research supports an association between chronic stress and heart problems.

• Objective measures such as blood pressure and immune-cell activity are a strength.

• Many studies use genuine stressors, improving ecological validity.

• Much of the evidence is correlational.

• Illness may increase stress, creating reverse causality.

• Personality, diet, existing health and social support may mediate the relationship.

• Acute stress may have different effects from chronic stress.

• An interactionist explanation involving stress and vulnerability is more convincing than a single-cause account.

• Evidence has practical implications for reducing long-term stress and monitoring health.

A high-level answer will explain both immunosuppression and cardiovascular disorders, apply several details from Dominic’s situation and develop its evaluation rather than listing studies or generic limitations.

[16 marks]