AQA A-Level Psychology: Stress & Eating Behaviour — Complete Revision Guide (7182)
AQA A-Level Psychology: Stress & Eating Behaviour — Complete Revision Guide
Paper 3 of AQA A-Level Psychology (7182/3) is titled Issues and Options in Psychology, and it is where the specification finally lets you specialise. The paper is a two-hour exam worth 96 marks (33.3% of the A-Level), split into four sections. Section A — Issues and Debates — is compulsory and sat by everyone. Sections B, C and D each present a menu of option topics, and your school chooses one topic per section for you to study in depth. Each section is worth 24 marks and typically blends short-answer questions with one extended 16-mark essay.
This guide focuses on Section C, which offers a choice of three clinically and biologically rich options: Schizophrenia, Eating Behaviour, or Stress. Most centres teach just one of these, but Stress and Eating Behaviour are the two most popular non-clinical-diagnosis choices, and they reward students who can move fluently between the biological, cognitive and social levels of explanation. If you would like a structured route through the whole course, the AQA A-Level Psychology learning path sequences every topic with exam-style practice, and the AQA A-Level Psychology Exam Guide explains how each question type is marked.
Below we work topic by topic through both options. Every study named is a genuine, examinable piece of research — there are no invented findings, statistics or dates.
Section C at a Glance
| Section C option | Core themes you must know |
|---|---|
| Stress | Physiology of stress; stress and illness; sources of stress; measuring stress; individual differences; managing stress; social support |
| Eating Behaviour | Food preference; neural and hormonal control of eating; explanations of anorexia nervosa; explanations of obesity |
| Schizophrenia | (Also examinable here, but covered in our separate Schizophrenia guide) |
Whichever option you sit, the skill set is the same: precise AO1 description of theories and studies, accurate AO3 evaluation, and the ability to apply ideas to novel scenarios for the AO2 application marks in the shorter questions.
Stress
Stress is one of the most coherent topics on the A-Level: it builds logically from biology, through the evidence linking stress to illness, out to the social and individual factors that shape how we cope. You can explore it through the AQA A-Level Psychology: Stress course, which has interactive questions for every sub-topic.
The Physiology of Stress
Stress begins as a bodily response to a perceived threat or stressor. Two systems carry that response, and a third framework — Selye's model — describes how the body behaves over time.
The General Adaptation Syndrome (GAS). Hans Selye proposed that the body responds to any prolonged stressor through the same three stages, regardless of its source. In the alarm reaction, the threat is detected and physiological arousal increases. In the resistance stage, the body adapts and appears to cope, but resources are being depleted. In the exhaustion stage, prolonged demand overwhelms the body's reserves, arousal systems can no longer function effectively, and stress-related illness becomes more likely. Selye's great contribution was the idea that chronic stress is physiologically costly; his model is criticised for being based largely on animal research and for underplaying the role of psychological appraisal.
The sympathomedullary (SAM) pathway and fight-or-flight. Acute, short-term stressors are handled by the SAM pathway. The hypothalamus activates the sympathetic branch of the autonomic nervous system, which signals the adrenal medulla to release adrenaline (and noradrenaline). This produces the classic fight-or-flight response: increased heart rate, raised blood pressure, dilated pupils and the diversion of blood to the muscles, all preparing the body for rapid action. Once the threat passes, the parasympathetic branch returns the body to its resting state.
The hypothalamic-pituitary-adrenal (HPA) axis. Chronic, ongoing stressors are managed by a slower hormonal system. The hypothalamus releases CRH, which stimulates the pituitary gland to release ACTH, which in turn stimulates the adrenal cortex to release cortisol. Cortisol mobilises energy by raising blood glucose and helps maintain steady arousal, but persistently high cortisol suppresses immune function and is associated with the long-term health costs of stress. The system is self-regulating: high cortisol feeds back to the hypothalamus and pituitary to dampen further release.
A useful exam table:
| System | Speed | Key structures | Key chemical(s) | Best for |
|---|---|---|---|---|
| SAM pathway | Fast | Sympathetic ANS, adrenal medulla | Adrenaline, noradrenaline | Acute stressors |
| HPA axis | Slower | Hypothalamus, pituitary, adrenal cortex | CRH, ACTH, cortisol | Chronic stressors |
The Role of Stress in Illness
The biology matters because stress is implicated in physical illness, mainly through two routes.
The immune system. Chronic stress suppresses immune function, partly through the action of cortisol. The landmark research is by Kiecolt-Glaser. In one well-known study, medical students gave blood samples during a low-stress period and again during their exam period; natural killer cell activity was significantly lower during the high-stress exam window, indicating reduced immune function. A later study found that wounds healed more slowly in people experiencing chronic stress (such as carers), demonstrating a real clinical consequence. These studies are valued for using objective biological measures, though the populations are specific and the effects are correlational.
The cardiovascular system. Repeated activation of the stress response strains the heart and blood vessels. Raised blood pressure and heart rate, the effect of stress hormones on blood vessel walls, and stress-linked behaviours such as poor diet or smoking together contribute to a higher risk of cardiovascular problems over time — one reason the workplace and personality research below matters.
Sources of Stress
Life changes. Major life events — even positive ones like marriage — require adjustment, and that adjustment is stressful. Holmes and Rahe developed the Social Readjustment Rating Scale (SRRS), which assigns each major life event a score in "life change units" based on how much readjustment it demands. By summing the events someone has experienced in a given period, researchers can correlate total scores with subsequent illness. The SRRS pioneered the systematic measurement of life stress; critics note that it does not distinguish desirable from undesirable events and ignores how the individual interprets each one.
Daily hassles. Kanner argued that the minor, everyday irritations of life — traffic, deadlines, misplaced keys — may predict health outcomes better than rare major events, precisely because they accumulate. The Hassles and Uplifts Scale measures both the daily annoyances that drain us and the small positives that buffer us. Research suggests daily hassles are at least as strong a predictor of stress symptoms as life changes.
Workplace stress. Two strands of evidence dominate here. The Whitehall studies of British civil servants found that those in lower-grade, lower-control jobs had higher rates of stress-related illness, including cardiovascular disease, than those in higher grades — highlighting job control (and lack of it) as a key workplace stressor. Johansson studied Swedish sawmill workers and found that those in a high-stress group, whose work was repetitive, machine-paced and socially isolated, showed higher stress-hormone levels and more stress-related illness and absenteeism than a low-stress comparison group. Together these point to control, workload and the social conditions of work as critical factors.
Measuring Stress
| Method | Examples | Strengths | Limitations |
|---|---|---|---|
| Self-report scales | SRRS, Hassles and Uplifts Scale | Quick, large samples, captures subjective experience | Social desirability, recall bias, interpretation varies |
| Physiological measures | Heart rate, blood pressure, cortisol assays, skin conductance | Objective, not easily faked | Affected by other factors (caffeine, exercise); may feel intrusive |
A strong answer recognises that the two approaches are complementary: self-reports capture how stressed a person feels, physiological measures capture how the body is responding, and the two do not always agree.
Individual Differences in Stress
Personality types. Friedman and Rosenman identified the Type A behaviour pattern — competitiveness, time-urgency and hostility — and linked it, in their long-running study of men, to a higher incidence of coronary heart disease compared with the more relaxed, easy-going Type B pattern. Later work suggested hostility may be the most damaging component. A third pattern, the Type C ("cancer-prone") personality, describes individuals who suppress emotions, particularly negative ones, and tend to be passive and people-pleasing; this pattern has been tentatively associated with poorer outcomes in some illnesses, though the evidence is weaker and more contested.
Hardiness. Kobasa proposed that some people resist the harmful effects of stress because they are psychologically hardy, a quality made of three Cs: control (a belief that one can influence events), commitment (deep involvement in life and its activities) and challenge (viewing change as an opportunity rather than a threat). Hardiness offers a more optimistic, trainable counterpart to the Type A research — it suggests resilience can be developed, not just inherited.
Managing and Coping with Stress
Drug therapy. Two drug families feature on the specification. Benzodiazepines (BZs) enhance the action of the neurotransmitter GABA, the body's natural anxiety-dampener, slowing central nervous system activity and reducing the psychological experience of anxiety. Beta-blockers (BBs) act more peripherally, reducing the physical symptoms of stress — they lower heart rate and blood pressure by blocking the action of stress hormones on the heart. Drugs are fast-acting and effective for many people, but they treat symptoms rather than causes, can produce side effects and dependence (particularly BZs), and do nothing to change the stressor itself.
Stress Inoculation Therapy (SIT). Meichenbaum's cognitive-behavioural approach treats coping as a skill that can be learned in advance, much as a vaccine prepares the immune system. It has three phases: conceptualisation (the therapist and client analyse the sources and nature of the stress), skills acquisition (the client learns coping techniques such as positive self-talk and relaxation), and application (the client practises these skills in increasingly demanding real and imagined situations). SIT is praised for tackling causes and building lasting resilience, but it is time-consuming and demands considerable effort and commitment from the client.
Biofeedback. This technique gives the individual real-time information about a normally involuntary physiological process — such as heart rate or muscle tension — usually via a monitor, and trains them to bring it under voluntary control using relaxation. Because it produces a genuine, learnable change in the body's stress response and has no drug side effects, it appeals to many; however, it requires equipment and training, and some argue that the relaxation itself, rather than the feedback, does most of the work.
Social Support and Gender Differences in Coping
Social support — emotional, instrumental (practical) and esteem-based — buffers the impact of stress, and people with strong support networks tend to show better health outcomes. There also appear to be gender differences in coping. Taylor proposed the tend-and-befriend model: where the classic fight-or-flight account was based largely on male physiology, females under stress may be more likely to protect and nurture offspring (tend) and to form protective social alliances (befriend). This response is linked to the hormone oxytocin and offers an evolutionary explanation for why support-seeking is a particularly common female coping strategy. The model is a valuable corrective to the beta bias of early stress research, which assumed male findings applied universally.
Eating Behaviour
Eating Behaviour sits squarely on the nature-nurture fault line: what, when and how much we eat is shaped by evolved biology, hormones, learning and culture all at once. You can revise it sub-topic by sub-topic in the AQA A-Level Psychology: Eating Behaviour course.
A note on register before we begin. This guide discusses anorexia nervosa and obesity clinically and objectively, as the specification requires. These are serious matters that affect real people and deserve to be treated with care and dignity. You will not find specific weights, BMI or calorie figures, dieting methods, or any framing that glamorises disordered eating here, and your own exam answers should keep the same clinical, respectful tone.
Explanations for Food Preference
Evolutionary explanations. Our preferences are partly inherited adaptations. A preference for sweet and fatty tastes made sense for ancestors needing scarce, energy-dense calories, while a wariness of bitter tastes helped avoid toxins. Neophobia — a reluctance to eat unfamiliar foods — is adaptive because novel foods carried a risk of poisoning; this caution is especially pronounced in young children. Taste aversion is a powerful, fast-forming learned avoidance: Garcia demonstrated that animals which became ill after consuming a novel flavour developed a strong aversion to it after a single pairing, even when the illness occurred hours later. This biological preparedness to associate taste with sickness is highly adaptive, as it helps an organism avoid foods that have made it ill.
Learning, social and cultural influences. Beyond biology, preferences are learned. Classical conditioning can attach positive associations to foods eaten in pleasant contexts, and operant conditioning operates when food is used as a reward. Social learning matters too: children imitate the eating of parents, peers and media figures, so observing others enjoy a food increases the likelihood of trying it. Cultural influences are powerful — what counts as a desirable, normal or taboo food varies enormously between cultures, and food forms part of cultural and religious identity. Together these factors explain why food preference cannot be reduced to evolution alone.
Neural and Hormonal Mechanisms in the Control of Eating
The control of eating is, at its core, a homeostatic system that keeps energy balance roughly stable, and the hypothalamus is central to it.
- The lateral hypothalamus (LH) has traditionally been described as a "hunger centre": stimulating it promotes eating, while damage to it is associated with reduced food intake.
- The ventromedial hypothalamus (VMH) has been described as a "satiety centre": stimulating it inhibits eating, while damage to it is associated with overeating.
This dual-centre model is a useful framework, though modern neuroscience treats it as an oversimplification, since many brain regions and circuits contribute to appetite. Two hormones provide the key signals:
| Hormone | Source | Effect on appetite |
|---|---|---|
| Ghrelin | Stomach (rises when empty) | Stimulates hunger — the "hunger hormone" |
| Leptin | Fat (adipose) tissue | Signals satiety and energy stores to the brain |
Ghrelin is secreted by the stomach and rises before meals when the stomach is empty, signalling hunger to the hypothalamus. Leptin is released by the body's fat stores and signals to the brain how much energy is held in reserve; higher leptin should reduce appetite. Disruption to these signalling systems — for example, the brain becoming less responsive to leptin — is one route by which appetite regulation can be impaired, which links this topic to the explanations of obesity below.
Anorexia Nervosa: Biological and Psychological Explanations
Anorexia nervosa is a serious psychological disorder characterised by an intense fear of weight gain, a distorted body image, and a sustained restriction of food intake. The specification asks you to consider both biological and psychological explanations; the most balanced position is that several factors interact.
Biological explanations.
- Genetic. Anorexia runs in families, and twin studies show higher concordance for the disorder in monozygotic (identical) twins than in dizygotic (non-identical) twins, indicating a heritable component. No single "anorexia gene" exists; vulnerability is polygenic and is best understood as a predisposition rather than a cause.
- Neural. Research implicates neurotransmitters, particularly serotonin and dopamine, in the regulation of appetite, mood and reward, and abnormalities in these systems may contribute to the disorder. Such evidence is largely correlational, so it is difficult to establish whether neural differences are a cause or a consequence of the illness.
Psychological explanations.
- Family systems theory (Minuchin). Minuchin proposed that anorexia can emerge within a particular family environment characterised by features such as enmeshment (over-involvement and blurred boundaries between family members), over-protectiveness, rigidity and an avoidance of open conflict. In this view, the disorder serves a function within the family's dynamics. The account is influential but difficult to test scientifically and risks unfairly attributing blame to families.
- Social learning theory. Anorexia may be partly learned through modelling and reinforcement. The internalisation of a culturally promoted "thin ideal" — observed in family members, peers and media — and the reinforcement that thinness can attract may shape disordered eating. This explanation accounts for cultural patterns but struggles to explain why most people exposed to the same ideals do not develop the disorder.
- Cognitive theory. This approach emphasises distorted thinking — most notably a distorted body image and irrational beliefs about food, weight and control. Cognitive biases such as all-or-nothing thinking maintain the disorder, which is one reason cognitive-based therapies are used in treatment. The cognitive account is supported by the success of those therapies, though it describes the faulty thinking better than it explains its ultimate origin.
Obesity: Biological and Psychological Explanations
Obesity is the medical condition of carrying excess body fat to a degree that may affect health. As with anorexia, the specification expects both biological and psychological explanations, treated objectively and without judgement of the people affected.
Biological explanations.
- Genetic. A predisposition towards obesity is heritable, and twin and adoption studies support a genetic contribution. Genes can influence factors such as metabolic rate, fat storage and appetite regulation, meaning some individuals are biologically more vulnerable in an environment of abundant food.
- Neural. Disruption to the appetite-control mechanisms described earlier can contribute to overeating — for instance, reduced sensitivity to leptin's satiety signal (so the "I have enough energy stored" message is weakened), or dysregulation of the hypothalamic circuits involved in hunger and satiety.
Psychological explanations.
- Restraint theory. Herman and Polivy observed the paradox that deliberately trying to restrict eating can, in some circumstances, lead to increased eating. People who consciously restrain their intake (restrained eaters) may, once that restraint is broken, eat more than they otherwise would — the so-called disinhibition effect — which can be counter-productive.
- The boundary model (Herman and Polivy). This refines restraint theory. It proposes that eating is governed by two physiological boundaries — a lower hunger boundary and an upper satiety boundary — with a cognitively set zone between them. Restrained eaters impose a self-imposed "diet boundary" below their natural satiety point; once that cognitive boundary is crossed (for example, by a perceived dietary "lapse"), eating may continue up to the higher satiety boundary, producing overeating. The model is valuable because it integrates physiological limits with cognitive control and helps explain why rigid restriction is often ineffective.
Exam Technique: Mastering the 16-Mark Essay
Whichever Section C option you sit, the 16-mark essay is where the marks are won or lost. These extended questions are marked across two assessment objectives: roughly 6 marks for AO1 (accurate, detailed description of the relevant theory, study or explanation) and 10 marks for AO3 (evaluation, analysis and discussion). That weighting is the single most important thing to internalise: more than half the marks reward evaluation, not description. Students who simply write everything they know about, say, the HPA axis or the dual-centre model rarely climb out of the middle band.
Aim for a clear structure. Open with concise, precise AO1 — define terms accurately, name the right researchers, and resist the temptation to over-describe. Then spend the majority of the essay on developed AO3 points. A strong evaluation point does not just state a criticism; it explains why it matters and what it implies. A useful discipline is the point, evidence, explain, link approach: make the evaluative point, support it with evidence or a counter-argument, explain its significance, and link it back to the question. Effective AO3 content includes the strength and quality of supporting research, methodological issues (such as the correlational nature of much stress-illness and neural research), competing explanations, real-world applications such as therapies derived from a theory, and relevant debates such as nature-nurture, reductionism or the biological versus psychological tension that runs through both options.
A few habits pay off across the whole paper:
- Prepare at least two strengths and two limitations for every named theory, study and therapy.
- Use specialist terminology precisely — "adrenal cortex," "ghrelin," "disinhibition effect" — because marks are awarded for accurate psychological language.
- In Eating Behaviour especially, keep the clinical, respectful register described above; objectivity is part of writing like a psychologist.
- Reach a reasoned conclusion that weighs the arguments rather than just restating them, and where appropriate favour an interactionist view, since both Stress and Eating Behaviour are best explained by biological, cognitive and social factors working together.
Prepare with LearningBro
Stress and Eating Behaviour both reward students who can hold the biological, cognitive and social levels in mind at once and then evaluate sharply under timed conditions. The most effective revision is active retrieval — testing yourself on the explanations and studies — rather than passively re-reading notes.
To revise each topic with exam-style questions, work through our courses:
- AQA A-Level Psychology: Stress — the physiology of stress, stress and illness, sources, measurement, individual differences and stress management.
- AQA A-Level Psychology: Eating Behaviour — food preference, the neural and hormonal control of eating, and explanations of anorexia nervosa and obesity.
- AQA A-Level Psychology learning path — the full guided route through every topic on the 7182 specification.
Use these alongside the AQA A-Level Psychology Exam Guide to build both the knowledge and the exam technique you need to excel in Paper 3, Section C.