Explain the stress response (the SAM system, the HPA axis and fight-or-flight), models of stress and how chronic stress harms health directly and through behaviours such as eating and smoking, and evaluate the research.
Each is in the Psychology glossary, with every other term in the subject.
The process by which a person evaluates whether a situation is relevant and threatening (primary appraisal) and whether they have the resources to cope with it (secondary appraisal).
The cognitive and behavioural efforts a person makes to manage a stressful situation and the emotions it causes, either by changing the problem (problem-focused) or by regulating the emotions (emotion-focused).
The rapid set of physiological changes, such as increased heart rate, blood pressure, breathing and blood glucose, that prepares an organism to confront or escape an immediate threat.
Selye’s model of the body’s non-specific response to any prolonged stressor, in three stages: alarm, resistance and exhaustion, in which illness becomes more likely.
The slower stress pathway in which the hypothalamus releases CRH, the pituitary gland releases ACTH and the adrenal cortex releases cortisol, which keeps energy available during continuing stress.
A form of chronic work stress in which high demands are combined with low control over how and when the work is done, linked to a higher risk of coronary heart disease.
The study of the interactions between psychological processes, the nervous and endocrine systems and the immune system, including how stress can suppress immune function.
Describe stress, stressors and the difference between acute and chronic stress.
Explain the physiological stress response, including the SAM system, the HPA axis and the fight-or-flight response.
Describe and evaluate the general adaptation syndrome and the transactional model of stress.
Explain how stress affects health directly, through the immune and cardiovascular systems, and indirectly, through behaviours such as eating and smoking.
Explain the role of stress in one or more health problems, especially obesity and tobacco addiction.
Discuss how biological, cognitive and sociocultural factors interact in the relationship between stress and health.
Evaluate research on stress and health with reference to causality, measurement, bias and responsibility.
Stress is the response that occurs when a person judges that the demands of a situation are greater than their ability to cope. Short bursts of stress help people meet challenges, but long-lasting stress is linked to infections, slower healing, heart disease, weight gain and addiction, which makes it one of the main psychological factors in physical health.
Stress shows clearly how the approaches work together in the health and well-being context. The body’s stress response is biological, whether a situation is stressful depends on cognitive appraisal, and many of the most powerful stressors, such as poverty, discrimination and job strain, are sociocultural. Research in this area raises questions of causality, because most evidence links stress and illness without manipulating stress, and of measurement, because stress can be measured as an event, a feeling or a hormone level.
With a free account, Augment remembers where you stopped and what you have practiced.
The fast stress pathway in which the hypothalamus activates the sympathetic nervous system, which stimulates the adrenal medulla to release adrenaline and noradrenaline into the bloodstream.
A physiological and psychological response that occurs when a person perceives that the demands of a situation exceed their resources to cope with it.
Eating in response to stress or negative emotions rather than hunger, typically with a preference for energy-dense, sweet or fatty comfort foods.
Any event, situation or demand, physical or psychological, that can trigger a stress response, such as a deadline, a bereavement or long-term caring for a sick relative.
Lazarus and Folkman’s model in which stress results from an interaction between person and environment, depending on the person’s appraisal of the demands of a situation and of their resources for coping.
Scope: An area of study in health problems in the health and well-being context: the role of stress in one or more health problems. The physiology of the stress response (the SAM system, the HPA axis, fight-or-flight) and models of stress are taught here; obesity and tobacco addiction are the main health problems used. The hormones cortisol and adrenaline are taught as chemical messengers and only recapped.
Psychologists separate the cause of stress from the response to it. A stressor is any event or situation that can trigger stress, such as a deadline, an illness in the family or a noisy neighbourhood. Stress is the physical and psychological state that results when the stressor is judged to be more than the person can handle.
Stressors can be classified in several ways. Acute stressors are short-lived, such as giving a speech or sitting an important test. Chronic stressors last for months or years, such as caring for a relative with dementia, long-term unemployment or living in poverty. Major life events, such as bereavement or divorce, are rare but demanding, while daily hassles, such as traffic, arguments and lost keys, are minor but frequent and can add up.
The way stress is defined decides how it is measured, and each definition is linked to a different research tradition.
Approach | Stress is… | Typical measure | Associated researchers |
|---|---|---|---|
Stimulus-based | a demand in the environment (the stressor) | life-event checklists such as the Social Readjustment Rating Scale | Holmes and Rahe (1967) |
Response-based | the body’s reaction to any demand | cortisol in saliva or blood, heart rate, blood pressure | Selye (1936, 1956) |
Transactional | a relationship between the person and the situation, decided by appraisal | perceived stress questionnaires, appraisal ratings | Lazarus and Folkman (1984) |
Holmes and Rahe (1967) developed the Social Readjustment Rating Scale, which lists 43 life events, each with a score in “life change units” that reflects how much readjustment it demands. The death of a spouse scores 100, divorce 73 and a change in residence 20. People add up the scores of events in the past year, and higher totals have been linked to a greater chance of later illness. The scale treats stress as a stimulus: it assumes that the same event is equally stressful for everyone, an assumption the transactional model rejects.
When a situation is perceived as a threat, the hypothalamus in the brain activates two systems. The first acts within seconds through nerves; the second acts over minutes to hours through hormones carried in the blood. Both release energy and prepare the body for physical action.
In the SAM system (sympathetic–adrenal–medullary system), the hypothalamus activates the sympathetic branch of the autonomic nervous system. Sympathetic nerves stimulate the adrenal medulla, the inner part of the adrenal glands, to release adrenaline and noradrenaline into the blood. These hormones raise heart rate and blood pressure, widen the airways, release glucose from the liver, send blood to the muscles and slow digestion.
Together these changes make up the fight-or-flight response, first described by the physiologist Walter Cannon in the early 20th century. In an emergency, such as an attack by an animal, it prepares the body to fight or to run. Once the threat has passed, the parasympathetic nervous system returns the body to its resting state.
The HPA axis (hypothalamic–pituitary–adrenal axis) is slower and maintains the response when stress continues. The hypothalamus releases corticotropin-releasing hormone (CRH), which travels to the pituitary gland. The pituitary releases adrenocorticotropic hormone (ACTH) into the blood, and ACTH stimulates the adrenal cortex, the outer layer of the adrenal glands, to release cortisol.
Cortisol raises blood glucose, so that energy stays available, and damps down functions that are not needed in an emergency, including digestion, growth, reproduction and parts of the immune response. Cortisol also acts on the hypothalamus and pituitary to reduce the release of CRH and ACTH. This negative feedback normally switches the response off once the stressor has gone.
Feature | SAM system | HPA axis |
|---|---|---|
Speed | seconds | minutes to hours |
Route | nerves, then hormones | hormones only |
Gland | adrenal medulla | pituitary, then adrenal cortex |
Main hormones | adrenaline, noradrenaline | CRH, ACTH, cortisol |
Main effects | heart rate, blood pressure, alertness | glucose release, immune and digestive suppression |
Risk when chronic | high blood pressure, damage to blood vessels | immune suppression, abdominal fat, impaired memory |
YouTubeThe stress response evolved to deal with short physical emergencies. Many modern stressors are psychological and long-lasting, such as debt, insecure work or caring for a sick relative, and fighting or running solves none of them. When the response is activated again and again, or stays switched on, the same changes that help in an emergency begin to cause harm: blood pressure stays high, cortisol keeps suppressing the immune system, and glucose and fat are released into the blood without being used.
With long exposure, negative feedback can become less effective, so cortisol levels remain high. This idea, that the costs of a protective system build up when it is overused, links the biology of stress to long-term illness.
YouTubeThe first general model of the stress response came from the endocrinologist Hans Selye. In experiments with rats in the 1930s, he found that very different harmful agents, such as cold, injury, toxic substances and forced exercise, all produced the same pattern of physical changes: enlarged adrenal glands, a shrunken thymus (an organ of the immune system) and stomach ulcers. Selye (1936) concluded that the body responds to any demand with the same non-specific response, which he called the general adaptation syndrome (GAS).
Alarm. The body recognises the stressor and the SAM system and HPA axis are activated. After a brief drop in resistance (shock), arousal rises and the body prepares for action.
Resistance. If the stressor continues, the body adapts to it. Stress hormones remain high and the person appears to cope, but bodily resources are being used up.
Exhaustion. If the stressor continues for a long time, the body can no longer maintain its response. Selye thought resources became depleted, leading to “diseases of adaptation” such as ulcers, high blood pressure and lowered immunity.
The GAS was the first model to link stress to illness through physiology, and its central idea, that prolonged stress responses damage the body, has been supported by later research on cortisol and immunity. It also explains why illness tends to follow long periods of stress rather than short ones.
The model has important limitations. It was based on rats exposed to physical stressors, which raises questions of extrapolation to humans, whose most common stressors are psychological. Later research showed that the response is less uniform than Selye claimed: Mason (1971) argued that the emotional reaction to a physical stressor, rather than the stressor itself, is what triggers the hormonal response. Exhaustion is also not usually a depletion of stress hormones, which often remain high; harm comes from their long-term effects. Most importantly, the GAS ignores cognition: it cannot explain why the same event is highly stressful for one person and hardly stressful for another.
Lazarus and Folkman (1984) argued that stress is neither a property of the event nor simply a bodily reaction. In their transactional model of stress, stress arises from a transaction between a person and their environment, and the key link is cognitive appraisal: the person’s judgement of what the situation means and whether they can deal with it.
Primary appraisal asks whether the event matters and how: it may be judged irrelevant, benign, or stressful. A stressful event can be appraised as a harm (damage already done), a threat (possible future harm) or a challenge (an opportunity for gain or growth).
Secondary appraisal asks whether the person has the resources to cope: skills, time, money, information and support from others.
Stress occurs when the demands are judged to exceed the resources. The person then copes, and the outcome feeds back into a reappraisal of the situation.
Speisman et al. (1964) showed participants a silent film of a painful initiation ritual in which adolescent boys underwent genital cutting. Participants heard one of several soundtracks: one emphasised the pain and danger (trauma), one denied that the rite was painful (denial), one described it in a detached, anthropological way (intellectualisation), and a control group saw the film without sound. Physiological arousal, measured mainly by skin conductance, was highest with the trauma soundtrack and lower with the denial and intellectualisation soundtracks, although the film was identical.
Changing the appraisal changed the physiological response, which is strong evidence that appraisal sits between the event and the body’s reaction. The study also raises ethical questions, both about deliberately distressing participants and about using film of a sacred ritual of an Aboriginal Australian community as a laboratory stressor.
Later research on the challenge–threat distinction supports the same idea. People who appraise a demanding task as a challenge show a different cardiovascular pattern, with the heart pumping efficiently and blood vessels widening, from people who appraise it as a threat, whose blood vessels constrict. Appraisal therefore shapes the physiology, which links the cognitive and biological approaches.
Coping is what people think and do to manage a stressful situation. Lazarus and Folkman distinguished problem-focused coping, which tries to change the situation (making a revision plan, asking for an extension, looking for a new job), from emotion-focused coping, which tries to manage the feelings the situation causes (seeking comfort, distraction, relaxation, reappraising the situation more positively). Some emotion-focused strategies, such as eating, drinking alcohol or smoking to feel better, reduce distress in the short term but damage health in the long term.
Problem-focused coping tends to work best when the stressor can be controlled, and emotion-focused coping when it cannot, as in bereavement or a chronic illness. The model predicts that health suffers most when stressors are uncontrollable and coping relies on harmful behaviours.
Social support is one of the most important coping resources, but cultures differ in how it is sought. Kim, Sherman and Taylor (2008) reviewed research showing that people in Asian cultures and Asian Americans are more reluctant than European Americans to ask others explicitly for help with their problems, because they are more concerned about burdening others and harming relationships. They benefit more from implicit support, such as spending time with close others without discussing the problem. A stress intervention that encourages people to “talk it through” may therefore suit individualist cultures better than collectivist ones.
Culture also shapes appraisal. Dressler et al. (2005) studied cultural consonance in a city in Brazil: how closely people’s lives matched the shared local model of a good life, such as owning certain household goods and having a supportive network. People with lower cultural consonance had higher blood pressure, a pattern the researchers had found before in the same community. Falling short of one’s culture’s expectations appears to act as a chronic stressor, which shows how a sociocultural factor can reach the cardiovascular system.
The transactional model explains individual differences that the GAS cannot, and it is supported by experiments in which changing appraisal changes physiology. It has also led to effective interventions that train people to reappraise stressors and to cope more effectively. However, appraisals are measured mainly by self-report, which is open to social desirability and to people’s limited insight into their own thinking. The model is also hard to falsify, since almost any reaction can be explained after the event by assuming a particular appraisal. Finally, by focusing on individual perception, it can underplay stressors such as poverty and discrimination that are harmful whatever the person thinks of them.
Stress affects health through two kinds of pathway. Direct pathways are physiological: stress hormones change the immune and cardiovascular systems. Indirect pathways are behavioural: stressed people often sleep less, exercise less, eat more energy-dense food, smoke and drink more. The two kinds interact, since poor sleep and diet also change hormone levels and immunity.
Psychoneuroimmunology (PNI) is the study of how psychological processes, the nervous system and the immune system influence each other. Cortisol suppresses several parts of the immune response, including the activity of natural killer (NK) cells, which destroy virus-infected cells, and the production of cytokines needed for inflammation and healing. Chronic stress should therefore make people more vulnerable to infection and slower to heal.
Kiecolt-Glaser et al. (1984) took blood samples from 75 first-year medical students one month before their final examinations and again on the first day of the examinations. NK cell activity fell significantly between the two samples, and students who scored higher on stressful life events and loneliness had lower NK activity. Because each student was compared with themselves, individual differences in immunity were controlled, but the study could not rule out other changes at the time, such as less sleep.
Cohen, Tyrrell and Smith (1991) provided stronger evidence on illness itself. 394 healthy volunteers completed stress questionnaires and were then given nasal drops containing one of five common cold viruses, while 26 received harmless saline drops. Participants were quarantined and monitored. Rates of infection and of clinical colds rose with psychological stress in a dose–response pattern: clinical colds ranged from about 27% at the lowest stress levels to about 47% at the highest. The effect remained after controlling for age, sex, allergies, weight, season and health behaviours such as smoking, alcohol, exercise, diet and sleep.
Segerstrom and Miller (2004) combined more than 300 studies in a meta-analysis. Brief stressors lasting minutes produced a potentially adaptive increase in some parts of the immune response, short naturalistic stressors such as examinations suppressed some functions, and chronic stressors, such as caregiving or unemployment, suppressed a broad range of immune functions. The pattern supports the idea that the duration of stress matters more than its intensity.
Repeated activation of the SAM system raises heart rate and blood pressure, and over years this can damage blood vessels and contribute to coronary heart disease (CHD). Much of the evidence comes from research on work. In the Whitehall II study of British civil servants, Marmot et al. (1997) followed 7,372 men and women for about five years. Employees in the lowest grades were more likely to develop CHD than those in the highest, and low control over one’s work made the largest contribution to this social gradient, more than smoking, blood pressure or other standard risk factors.
Kivimäki et al. (2012) pooled individual data from 197,473 workers in 13 European cohort studies in which no one had heart disease at the start. Over an average of 7.5 years, workers who reported job strain (high demands with low control) had about 23% higher risk of CHD than other workers, after adjusting for age and sex.
The effect remained when heart attacks in the first few years were excluded, which reduces the chance that early illness caused the strain rather than the other way round. The effect was larger in published than in unpublished studies, a sign of publication bias, and job strain explained only about 3% of all cases of CHD.
Stress is linked to obesity through both kinds of pathway. Behaviourally, many people eat more, and choose more energy-dense food, when they are stressed. Physiologically, cortisol increases appetite, especially for sweet and fatty food, and promotes the storage of fat around the abdomen. Stress-related eating connects the two.
Epel et al. (2001) tested whether the size of a person’s cortisol response predicts eating after stress. Fifty-nine healthy pre-menopausal women took part in a stress session, with a series of demanding tasks, and a control session on different days, and their eating was measured afterwards. Women who released more cortisol in response to stress (high reactors) ate more calories after the stress session than low reactors but similar amounts after the control session, and high reactors ate more sweet food. Increases in negative mood also predicted greater eating.
The study shows that individual differences in the biological stress response affect eating behaviour, although it was a short laboratory study of one group of women, and eating a snack in a laboratory is a narrow measure of everyday diet.
Dallman et al. (2003) proposed a biological explanation from research with rats. Chronically high cortisol increases the reward value of pleasurable foods such as sugar and fat, which encourages eating “comfort food”, and promotes fat storage in the abdomen. Abdominal fat in turn sends signals that damp down the chronic stress-response network, so comfort eating may temporarily reduce stress. The model explains why stress-related eating is rewarding and therefore hard to stop. Much of it rests on animal research, however, and the authors noted that chronically stressed rats usually lose weight, whereas stressed humans may either gain or lose it.
Stress-related eating also depends on the person. People who are restrained eaters, who try hard to control their weight, often eat more under stress, as do people who use eating as an emotion-focused coping strategy. A cognitive explanation is that stress uses up the attention needed to keep to dietary goals, so eating falls under the control of fast, habitual System 1 processes and food cues. Sociocultural factors decide what comfort food is available and cheap: in an obesogenic environment, the easiest comfort is energy-dense food.
Stress is also one of the strongest factors in addiction, including tobacco addiction. Stress makes people more likely to start using drugs, to continue using them and to relapse after quitting. Many smokers say they smoke to cope with stress, which makes smoking a form of emotion-focused coping.
Parrott (1999) argued that this belief reverses the real relationship. Adult smokers report slightly higher stress than non-smokers, adolescents report rising stress as they become regular smokers, and stress falls after people successfully stop smoking. Between cigarettes, nicotine levels drop and dependent smokers become tense and irritable; the next cigarette relieves this withdrawal and feels relaxing. On this view, smoking does not reduce stress but creates a cycle in which the drug relieves the stress that dependence itself causes.
Biological, cognitive and sociocultural factors also interact in addiction. Stress hormones and nicotine both act on the brain’s reward system, which may make stressed people more sensitive to the rewarding effects of drugs. The belief that smoking relieves stress is a cognitive expectation that keeps the behaviour going. Chronic stressors such as poverty and discrimination are concentrated in the same groups that have the highest smoking rates, which helps explain the social gradient in the prevalence of tobacco use.
The same stressor harms some people much more than others. Biological differences, such as how strongly a person’s HPA axis reacts, cognitive differences in appraisal and coping, and social differences in support and resources all play a part. The diathesis-stress model offers a general framework: illness develops when a vulnerability meets enough stress.
Taylor et al. (2000) also argued that the classic fight-or-flight model describes male responses better than female ones, and that women’s behavioural response to stress more often takes the form of tend-and-befriend: protecting offspring and seeking social contact, possibly supported by oxytocin. The proposal has been influential but is based on limited human evidence and risks overstating sex differences.
Kiecolt-Glaser and her colleagues aimed to find out whether chronic psychological stress slows the healing of a physical wound, and whether this is linked to changes in the immune response.
The study was a quasi-experiment with an independent samples design, carried out at Ohio State University in the United States. The stressed group was 13 women caring for a relative with Alzheimer’s disease or another form of dementia, a well-established chronic stressor; their mean age was about 62. The control group was 13 women who were not caregivers, matched for age and family income. Caregiving was not assigned by the researchers, so the independent variable was naturally occurring.
All 26 participants received a standard 3.5 mm punch-biopsy wound, in which a small circle of skin is removed. Healing, the dependent variable, was measured in two independent ways: photographs of the wound taken regularly, and a test in which hydrogen peroxide was applied to the wound, with healing defined as the point at which the wound no longer foamed. The researchers also took blood samples and measured how much interleukin-1β (IL-1β), a cytokine needed in the early stages of wound repair, the participants’ white blood cells produced when stimulated.
Wounds took significantly longer to heal in caregivers than in controls: a mean of 48.7 days compared with 39.3 days, a difference of about nine days, or roughly 24% longer (p < 0.05). Caregivers’ white blood cells produced significantly less IL-1β messenger RNA than those of controls.
Sources: Kiecolt-Glaser, J. K., Marucha, P. T., Malarkey, W. B., Mercado, A. M., & Glaser, R. (1995). Slowing of wound healing by psychological stress. _The Lancet, 346(8984), 1194–1196._
Chronic stress was associated with substantially slower wound healing, and the lower production of IL-1β suggests a biological mechanism: stress, probably through cortisol, suppresses the immune processes needed to repair tissue. The authors pointed out that stress-related delays in healing could matter for recovery from surgery.
Because caregiving could not be assigned at random, this is a quasi-experiment, and the groups may have differed in ways other than stress, such as sleep, diet, exercise or health. Matching for age and income controls some of these, but not all. Later research strengthened the causal case. Marucha, Kiecolt-Glaser and Favagehi (1998) gave 11 dental students two small wounds on the roof of the mouth, one during the summer vacation and one three days before major examinations. Each student acted as their own control, and wounds took on average three days, or 40%, longer to heal during examinations, while IL-1β production fell by 68%.
Healing was measured objectively, with two independent methods (photographs and the peroxide test), and a biological mechanism was measured in the blood, which avoids the problems of self-reported health. The wound itself was standardised in size and position. Stress, however, was inferred from group membership: caregivers were assumed to be more stressed than controls, so the study shows an effect of a stressful life situation rather than of a measured level of stress.
The sample was very small and consisted of older American women, so the results may not generalise to men, younger people or other cultures. Older adults already heal more slowly and may have weaker immune responses, which could make stress effects easier to detect. The replication with young dental students, a different age group and type of stressor, increases confidence that the effect is not limited to one group.
Deliberately wounding participants raises clear ethical issues. The wounds were small and standardised, healing was monitored closely, and the knowledge gained has practical value for surgery and care, so a cost–benefit analysis can justify the procedure if participants give fully informed consent. Even so, researchers had a special responsibility towards caregivers, an already burdened group, which includes making participation easy to refuse and not adding to their stress.
Research on stress and health uses a wide range of methods, from animal experiments to large cohort studies. Its strengths and weaknesses can be organised through the concepts.
Most human evidence is correlational or quasi-experimental, because stress cannot ethically be imposed for months to see whether people fall ill. Third variables are a constant problem: stressed people may sleep less, smoke more and eat worse, so an apparent effect of stress may run through behaviour, or may be caused by something else entirely, such as low income. Reverse causation is also possible, since early, undiagnosed illness can make people feel more stressed.
Several designs strengthen the causal case. Prospective designs, such as Cohen et al. (1991) and Kivimäki et al. (2012), measure stress before illness appears. Repeated-measures designs, such as Marucha et al. (1998), compare the same people under high and low stress. Experiments manipulate stress in the short term, as in Epel et al. (2001), and animal research, as in Selye’s and Dallman’s work, can manipulate stress over longer periods, though with problems of extrapolation. Together, these designs make a consistent case that chronic stress contributes to illness, while showing that it is one cause among many.
Stress can be measured as an event (life-event scales such as the Social Readjustment Rating Scale), as a perception (questionnaires such as the Perceived Stress Scale) or as a physiological response (cortisol, heart rate, blood pressure). Each measure captures something different, and they often correlate only weakly.
Life-event scales ignore appraisal and depend on accurate memory; self-report is open to social desirability bias; cortisol varies across the day, peaking soon after waking, so samples must be taken at standard times. Segerstrom and Miller (2004) found that self-reported stress was generally less closely related to immune change than objective stressors, a reminder that the measure chosen can decide the result. Triangulation across several measures gives the most credible picture.
Much of the classic research used narrow samples: Selye’s rats, American medical students, older American women caring for relatives. Early stress research also focused mainly on men, which led Taylor et al. (2000) to argue that the fight-or-flight model had been generalised from male responses without testing women. Cultural bias is another concern: what counts as stressful, how it is appraised and which coping strategies help depend on culture, as the research on social support by Kim et al. (2008) and on cultural consonance by Dressler et al. (2005) shows.
A purely biological account of stress, in terms of hormones and immune cells, explains how stress damages the body but not why one person is stressed by an event and another is not. A purely cognitive account explains individual appraisal but can underplay the effect of poverty, discrimination and job strain, which harm health partly through conditions people cannot change by thinking differently. The most complete explanations are biopsychosocial: sociocultural conditions create stressors, cognitive appraisal decides how stressful they are, and the SAM system and HPA axis turn that stress into physical change.
Studies that expose people to viruses, wounds or stressful tasks require careful cost–benefit judgements, full informed consent and medical monitoring. Applications of stress research also raise questions of responsibility. Findings on job strain place some responsibility for health on employers and governments, not only on individuals, while advice to “manage stress better” can unfairly put the burden on people whose stressors, such as poverty, are not under their control.
Concept | Strength of the research | Limitation of the research |
|---|---|---|
Causality | prospective, repeated-measures and experimental designs converge on a causal role for chronic stress | most human evidence is correlational or quasi-experimental; third variables and reverse causation |
Measurement | objective outcomes (healing time, infection, CHD events) and biological measures | stress itself is measured in different ways that agree only weakly |
Bias | large, multi-country cohorts in recent research | early research on rats, men and WEIRD samples |
Perspective | links biological, cognitive and sociocultural levels | single-level explanations are reductionist |
Stress occurs when the demands of a situation are judged to exceed a person’s resources; a stressor is the event that triggers it.
The SAM system acts in seconds: the sympathetic nervous system stimulates the adrenal medulla to release adrenaline, producing the fight-or-flight response.
The HPA axis acts over minutes: CRH from the hypothalamus, ACTH from the pituitary and cortisol from the adrenal cortex, with negative feedback.
Selye’s general adaptation syndrome (alarm, resistance, exhaustion) explains why chronic stress leads to illness but ignores appraisal.
The transactional model explains individual differences through primary and secondary appraisal and coping; Speisman et al. (1964) showed that appraisal changes physiology.
Stress affects health directly, through immune suppression and cardiovascular strain, and indirectly through behaviour; key evidence includes Kiecolt-Glaser et al. (1995), Cohen et al. (1991) and Kivimäki et al. (2012).
Stress contributes to obesity through cortisol and stress-related eating, as Epel et al. (2001) showed, and to tobacco addiction, where Parrott (1999) argued that dependence itself creates stress.
Research is evaluated through causality (few true experiments), measurement (event, perception or hormone), bias (narrow samples) and perspective (a biopsychosocial explanation is needed).
I can describe stress and stressors and distinguish acute from chronic stress.
I can explain the SAM system, the HPA axis and the fight-or-flight response, and draw both pathways from memory.
I can describe and evaluate the general adaptation syndrome and the transactional model.
I can explain the direct and indirect pathways from stress to illness, with evidence.
I can explain the role of stress in obesity and in tobacco addiction.
I can describe and evaluate Kiecolt-Glaser et al. (1995).
I can discuss how biological, cognitive and sociocultural factors interact in stress and health.
I can evaluate stress research with reference to causality, measurement, bias and responsibility.