AQA A-level Psychology (7182): Paper 3 — Eating behaviour — Study Guide

This guide covers Eating behaviour, section 4.3.6 of the AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025. Eating behaviour is one of the three topics in Option 2 of the A-level, alongside Schizophrenia and Stress. It is assessed in Paper 3: Issues and Options in Psychology, a 2-hour written exam worth 96 marks and 33.3% of the A-level. Section C of that paper is “one topic from option 2”, with multiple choice, short answer and extended writing questions worth 24 marks.

Use it with the Eating behaviour revision notes and Eating behaviour practice questions. The AQA A-level Psychology hub lists every unit, and the 7182 checklist lets you tick off each point.

How Paper 3 is set out

The specification prints the Paper 3 rules like this. Compulsory content is Issues and debates in Psychology (Section A, 24 marks). You then answer on one topic from Option 1 (Relationships, Gender, Cognition and development) in Section B, one topic from Option 2 (Schizophrenia, Eating behaviour, Stress) in Section C, and one topic from Option 3 (Aggression, Forensic Psychology, Addiction) in Section D. Each section is worth 24 marks. The specification also says research methods, practical research skills and maths skills will be assessed in Paper 3, and that sections B, C and D contain extended response questions. Which option your school teaches is a school decision; your teacher will confirm it.

Coverage table

Syllabus reference	What you must know or be able to do (from the specification)	Where assessed
4.3.6 Food preferences	The evolutionary explanation, including neophobia and taste aversion; the role of learning, including social and cultural influences	Paper 3, Section C
4.3.6 Control of eating	Neural and hormonal mechanisms, including the role of the hypothalamus, ghrelin and leptin	Paper 3, Section C
4.3.6 Anorexia nervosa (biological)	Genetic and neural explanations	Paper 3, Section C
4.3.6 Anorexia nervosa (psychological)	Family systems theory (enmeshment, autonomy, control); social learning theory (modelling, reinforcement, media); cognitive theory (distortions, irrational beliefs)	Paper 3, Section C
4.3.6 Obesity (biological)	Genetic and neural explanations	Paper 3, Section C
4.3.6 Obesity (psychological)	Restraint theory, disinhibition and the boundary model	Paper 3, Section C
4.3 skills	Apply knowledge to contexts; analyse, interpret and evaluate theories, studies and research methods	Paper 3, all sections

Explanations for food preferences: evolution

Key idea. Our ancestors lived in an environment where food was scarce and some foods were poisonous. Preferences that helped them survive were passed on.

• Innate taste preferences. Sweet signals energy-rich food (ripe fruit). Salty signals sodium, needed for nerve and muscle function. Fat is energy-dense. Bitter and sour can signal toxins or spoiled food. Steiner (1979) reported that newborns show positive facial expressions to sweet tastes and rejection expressions to bitter ones, before any learning.
• Neophobia. A reluctance to try new foods. It protected young children, who could now walk away from their carers, from eating something harmful.
• Taste aversion. A learned avoidance of a food after it has been followed by illness. One pairing can be enough, even with a delay of hours. It is “prepared” learning: animals are biologically ready to link taste with sickness.

Evidence. Garcia and Koelling (1966) found rats easily learned to link a taste with illness, but not a light or sound with illness. This supports a biological readiness to link taste and sickness. Bernstein (1978) offered children receiving chemotherapy an unusual ice cream before drug treatment. Children whose treatment caused stomach and gut side effects were later less likely to choose that ice cream again than control children.

Evaluation.

• Strength: the innate face responses in newborns are hard to explain through learning.
• Strength: taste aversion has practical value. It explains why people having chemotherapy may go off foods eaten before treatment.
• Limitation: many adults prefer bitter foods such as coffee or dark chocolate. Learning can override innate preferences.
• Limitation: evolutionary accounts are hard to test directly, because we cannot observe the ancestral environment.

Worked paragraph. “Neophobia is a reluctance to eat unfamiliar food (AO1). It would explain why a toddler pushes away a new vegetable even though she is hungry (AO2). In the ancestral environment, a child who avoided unknown plants was less likely to be poisoned, so the trait was passed on (AO3 analysis). However, neophobia usually fades with repeated exposure, which shows that learning shapes how long it lasts (AO3 evaluation).”

Explanations for food preferences: learning

Classical conditioning. A flavour paired with something pleasant (calories, sweetness, a happy setting) becomes liked. A flavour paired with illness becomes disliked.

Operant conditioning. Food can be rewarded or used as a reward. Using a sweet as a prize for eating vegetables may increase liking for the sweet, not the vegetables.

Social influences. Children model parents and peers. Birch (1980) found preschool children changed their vegetable choices after eating with peers who preferred a different vegetable. Brown and Ogden (2004) found that parents’ and children’s snack intake, eating motivations and body dissatisfaction were consistently correlated.

Cultural influences. Culture decides what counts as food, how it is prepared and when it is eaten. A food that is a delicacy in one culture can cause disgust in another. Media and advertising spread cultural norms.

Mere exposure. Birch and Marlin (1982) found that the more often two-year-olds were exposed to new cheeses or fruits, the more they preferred them.

Evaluation.

• Strength: exposure research has practical use for parents and nurseries.
• Strength: cultural variation in diet is hard to explain through genes alone.
• Limitation: parent-child correlations cannot separate modelling from shared genes.
• Limitation: social learning is weaker for innate preferences such as sweet, which suggests an interaction between learning and evolution.

Worked paragraph. “Children model the food choices of people around them (AO1). A boy who refuses fish may start eating it after lunches beside classmates who enjoy it (AO2). Birch (1980) supports this with preschool children (AO3). However, family correlations cannot separate modelling from shared genes (AO3).”

Neural and hormonal control of eating

The hypothalamus. The dual-centre model says the lateral hypothalamus (LH) starts eating and the ventromedial hypothalamus (VMH) stops it. Anand and Brobeck (1951) found rats with LH damage stopped eating. Hetherington and Ranson (1940) found rats with VMH damage overate and became obese. The arcuate nucleus in the hypothalamus receives hormone signals and passes them on.

Ghrelin. A hormone released mainly by the stomach when it is empty. It acts on the hypothalamus to increase hunger. Cummings et al. (2001) found ghrelin rises before meals and falls after eating. Wren et al. (2001) found that giving people ghrelin increased their food intake.

Leptin. A hormone released by fat (adipose) tissue. It signals to the hypothalamus that energy stores are adequate and reduces appetite. Montague et al. (1997) described two severely obese children from the same family who had a gene mutation that left them with very low leptin (congenital leptin deficiency). Farooqi et al. (1999) reported large weight loss when a child with congenital leptin deficiency was given leptin treatment.

Evaluation.

• Strength: human cases of leptin deficiency give clear causal evidence.
• Limitation: the dual-centre model is too simple. LH damage also hit nerve fibres passing through it, and many brain areas control eating.
• Limitation: most people with obesity have high leptin levels, not low. This “leptin resistance” means leptin alone cannot explain obesity.
• Limitation: biological reductionism. People eat when not hungry, for comfort or company. Much early evidence is from rats.

Worked paragraph. “Ghrelin from an empty stomach signals the hypothalamus to start eating (AO1). This explains why someone who skips breakfast feels very hungry before lunch (AO2). Cummings et al. (2001) found ghrelin rises before meals (AO3). However, people also eat at set times when not hungry, so hormones are only part of the story (AO3).”

Biological explanations for anorexia nervosa

Genetic. Anorexia nervosa (AN) runs in families. Holland et al. (1988) found much higher concordance for AN in identical (MZ) twins than in non-identical (DZ) twins. Watson et al. (2019), a genome-wide association study, identified several gene locations linked to AN. It found genetic overlap with psychiatric traits and with metabolic traits, which suggests AN has both psychiatric and metabolic roots.

Neural. Kaye et al. (2009) reviewed evidence that serotonin and dopamine systems work differently in people with AN, including after recovery. Raised serotonin activity is linked to anxiety and perfectionism; restricting food may lower it and reduce anxiety for a time. Differences in dopamine reward pathways may mean food is less rewarding.

Evaluation.

• Strength: twin evidence supports a genetic role.
• Limitation: MZ concordance is well below 100%, so the environment must matter. A diathesis-stress view fits better.
• Limitation: cause and effect is unclear. Starvation itself changes brain chemistry. Studies of recovered patients help but cannot rule this out.
• Limitation: evidence that serotonin-based drugs help people with AN is mixed, which weakens the serotonin account.

Worked paragraph. “Twin studies suggest AN has a genetic basis, as MZ twins are more often concordant than DZ twins (AO1, AO3). But MZ concordance is far from 100%, so genes may create a vulnerability that a stressor, such as weight-focused comments, then triggers (AO3 analysis).”

Psychological explanations for anorexia nervosa

Family systems theory. Minuchin et al. (1978) described families in which AN developed as enmeshed: members are over-involved, with weak boundaries, over-protection and avoidance of conflict. Bruch (1978) argued that a young person in such a family struggles to develop autonomy. Restricting food becomes one area they can control.

Evaluation: family-based therapy has good support for adolescents, which suggests family processes matter. But the evidence is mostly from clinical observation and correlation; enmeshment could be a reaction to a child’s illness rather than a cause. The theory has been criticised for blaming parents.

Social learning theory. People model the eating and dieting of parents, peers and media figures. Weight loss may be reinforced by praise (direct) or seen to be rewarded in others (vicarious). The media presents a thin ideal. Becker et al. (2002) studied adolescent girls in a region of Fiji where television arrived in 1995. The proportion scoring above the risk threshold on an eating attitudes test rose from about 13% within a month of television arriving to about 29% three years later.

Evaluation: the Fiji study is a strong natural experiment. But nearly everyone sees thin-ideal media and few develop AN, so SLT cannot explain individual vulnerability. The Fiji study measured attitudes, not diagnosed AN.

Cognitive theory. People with AN show distortions, such as seeing their body as larger than it is. They hold irrational beliefs, such as “If I gain any weight I am a failure” or all-or-nothing thinking. Garner and Bemis (1982) described AN in terms of such beliefs and reasoning errors.

Evaluation: cognitive behavioural therapy targets these beliefs and has some support. But it is unclear whether distortions cause AN or are effects of starvation. The theory describes what the person thinks more than why it started.

Worked paragraph. “SLT says thin ideals are modelled and weight loss is reinforced (AO1). A dancer praised by a coach for looking ‘lighter’ receives direct reinforcement (AO2). Becker et al. (2002) support a media effect (AO3), but most people exposed to such media never develop AN (AO3).”

Biological explanations for obesity

Genetic. Stunkard et al. (1986) found that adopted adults’ weight was related to their biological parents’ weight, not their adoptive parents’. Frayling et al. (2007) found adults with two copies of a higher-risk variant of the FTO gene were on average about 3 kg heavier than people with no copies. Obesity is polygenic: many genes each add a small risk.

Neural. Leptin resistance and other hypothalamic changes reduce satiety signals. Wang et al. (2001) found people with obesity had lower dopamine D2 receptor availability in the striatum. One interpretation is a reward deficiency: some people eat more to get the same reward.

Evaluation.

• Strength: adoption and twin studies separate genes and environment better than family studies.
• Limitation: obesity rates have risen fast in recent decades. Genes do not change that quickly, so the food environment must matter. A diathesis-stress view fits.
• Limitation: the dopamine finding is correlational. Overeating could change receptors, rather than the other way round.

Psychological explanations for obesity

Restraint theory. Herman and Mack (1975) suggested that trying to limit eating can backfire. Restrained eaters who drank a milkshake “preload” then ate more ice cream than restrained eaters who had none; unrestrained eaters ate less after the preload. Wardle and Beales (1988) randomly assigned women with obesity to a diet group, an exercise group or no treatment; in laboratory tests the diet group ate more.

Disinhibition. Restraint can break down. Triggers include stress, low mood, alcohol and breaking a diet rule (“I’ve ruined it now”). Stunkard and Messick (1985) built disinhibition into their Three-Factor Eating Questionnaire.

Boundary model. Herman and Polivy (1984) proposed a hunger boundary below which hunger is aversive and a satiety boundary above which fullness is aversive. Between them is a zone where cognitive and social factors decide intake. Dieters have a wider zone and set a lower diet boundary. Once they cross it, they keep eating until the satiety boundary.

Evaluation.

• Strength: the theories explain why dieting often fails, which has practical use.
• Limitation: some people restrain successfully and keep weight off, so restraint does not always lead to overeating.
• Limitation: laboratory taste tests may not reflect everyday eating, so ecological validity is limited.

Worked paragraph. “The boundary model says that dieters set a diet boundary lower than their satiety boundary (AO1). A dieter who eats one biscuit at work may think the day is ruined and eat the whole packet (AO2). This shows disinhibition: crossing the self-set boundary removes cognitive control, so intake is governed only by satiety (AO3 analysis). Herman and Mack (1975) support this, but their laboratory taste test may lack ecological validity (AO3 evaluation).”

Common errors

• Saying ghrelin is made by fat cells. Ghrelin comes mainly from the stomach; leptin comes from fat tissue.
• Mixing up LH (“on”) and VMH (“off”).
• Treating taste aversion as innate. The readiness is innate; the aversion is learned.
• Describing AN or obesity as caused by one factor. Exams reward interactionist, diathesis-stress points.
• Using Becker et al. (2002) as evidence about diagnosed AN. It measured eating attitudes.
• Confusing restraint (the attempt to limit eating) with disinhibition (the breakdown of restraint).
• Using stigmatising language. Write “a person with anorexia nervosa” and “people with obesity”.

Where to go next

For the biological, social learning and cognitive approaches that underpin this topic, see the Approaches in Psychology study guide and the Approaches revision notes. Use the Issues and debates guide for evaluation themes. Then test yourself with the Eating behaviour practice questions.

Official syllabus

This guide follows section 4.3.6 Eating behaviour and the Paper 3 structure of the AQA AS and A-level Psychology (7181, 7182) specification, Version 1.4 (1 September 2025), for teaching from September 2025.