Eating behaviour — AQA A-Level Psychology
Test yourself on Eating behaviour with AQA A-Level practice questions.
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Eating behaviour explained
Food preference is not free choice but an inherited solution to an old problem.
Read the full explanation
Sweetness signalled ripe calories and bitterness signalled plant toxins, so those biases were selected for in ancestral foragers. Neophobia, the flat refusal of unfamiliar food that peaks between the ages of two and six, kept mobile toddlers from sampling poison. Taste aversion is the strongest evidence: Garcia and Koelling found rats avoided sweetened water after a single pairing with radiation-induced nausea, even with hours between taste and sickness, which breaks the contiguity rule of ordinary classical conditioning and shows biological preparedness. Learning matters too. Birch shifted preschoolers' vegetable choices simply by seating them beside peers who preferred the other vegetable, and culture decides what reaches the plate at all.
Neural and hormonal mechanisms involved in the control of eating behaviour, including the role of the hypothalamus, ghrelin and leptin.
Eating is homeostatic: the body defends a fairly stable store of energy, and the hypothalamus is where the signals are read. The classic dual-centre model makes the lateral hypothalamus the on switch and the ventromedial hypothalamus the off switch - lesion the ventromedial area in a rat and it overeats into obesity, lesion the lateral area and it starves. Hormones carry the news. Ghrelin is released by the empty stomach lining, acts on neuropeptide Y cells in the arcuate nucleus, and rises sharply in the minutes before a meal then falls once food arrives, as Cummings showed with repeated blood sampling. Leptin is secreted by fat cells in proportion to fat stored and tells the hypothalamus there is enough; mice bred without it eat until grossly obese.
Biological explanations for anorexia nervosa: genetic and neural.
Biological explanations for anorexia nervosa (AN) focus on genetic vulnerability and neural mechanisms. Genetic explanations suggest AN is heritable, supported by twin studies showing higher concordance rates for monozygotic twins compared to dizygotic twins. Candidate gene studies investigate specific genes, such as the EPHX2 gene, which is involved in cholesterol metabolism, as altered cholesterol processing is often seen in AN. Neural explanations highlight neurotransmitter imbalances, particularly serotonin and dopamine. Overactivity in dopamine receptors in the basal ganglia may alter reward perception, making eating anxiety-inducing rather than pleasurable. Additionally, altered serotonin pathways can explain comorbid symptoms like perfectionism and obsessive traits often seen in AN.
Psychological explanations for anorexia nervosa: family systems theory, including enmeshment, autonomy and control; social learning theory, including modelling, reinforcement and media; cognitive theory, including distortions and irrational beliefs.
Three psychological explanations for anorexia nervosa exist. Minuchin's family systems theory locates the illness in family dynamics: boundaries blur into enmeshment (e.g. a parent answering for a child), and refusing food becomes a bid for autonomy and control by someone feeling ineffective. Social learning theory focuses on the media, modelling of thin ideals, and direct or vicarious reinforcement (e.g. praise for weight loss). Becker's Fiji study provides evidence, showing disordered eating increased after television was introduced. Cognitive theory looks inward, distinguishing between perceptual distortions (overestimating body size) and irrational beliefs (e.g. 'one biscuit means I have failed completely').
Biological explanations for obesity, including genetic and neural.
Biological explanations for obesity focus on genetic inheritance and neural mechanisms. Genetic theories propose that obesity is polygenic, with research highlighting the FTO gene, which increases the likelihood of overeating by altering energy homeostasis. Evolutionary concepts like the 'thrifty gene' suggest ancestors who stored fat survived famines, making these genes maladaptive today. Neural explanations emphasise the hypothalamus and neurotransmitters. A deficiency in dopamine D₂ receptors means individuals experience less reward from eating, leading to overeating to compensate. Additionally, dysfunction in serotonin pathways, which normally signal satiety, can prevent the feeling of fullness, contributing to weight gain.
Psychological explanations for obesity, including restraint theory, disinhibition and the boundary model.
Psychological explanations for obesity focus on cognitive and behavioural factors. Restraint theory suggests that strict dieting and cognitive restriction of food intake paradoxically lead to overeating, as individuals become preoccupied with food. Disinhibition occurs when these restrained eaters encounter triggers, such as stress or high-calorie foods, causing them to lose control and binge eat. Herman and Polivy’s boundary model integrates these concepts, proposing a biological range between hunger and satiety. Restrained eaters impose a cognitive diet boundary below their biological satiety level. When this cognitive boundary is breached, known as the 'what the hell' effect, they continue eating until reaching maximum biological capacity.
Your focus
- Explain the evolutionary logic behind preferring sweet and fatty tastes and rejecting bitter ones.
- Describe taste aversion learning and why one-trial, long-delay conditioning in Garcia and Koelling shows preparedness.
- Apply neophobia to explain a three-year-old's refusal of an unfamiliar food and the advantage that gave ancestors.
Show all 21 objectives
- Evaluate the evolutionary account using its post-hoc reasoning and the deliberate liking of coffee and chilli.
- Describe the dual-centre model, naming which hypothalamic area starts feeding and which stops it.
- Explain how ghrelin and leptin differ in source, timescale and what each signals to the hypothalamus.
- Apply leptin resistance to explain why leptin replacement cures congenital deficiency but fails in common obesity.
- Evaluate the dual-centre model given that ventromedial lesions also damage the paraventricular nucleus and fibres of passage.
- Describe genetic explanations for anorexia nervosa including twin studies and candidate genes.
- Explain how neural mechanisms, specifically serotonin and dopamine, contribute to anorexia nervosa.
- Evaluate biological explanations of anorexia nervosa using issues such as reductionism and cause-and-effect.
- Describe Minuchin's concept of enmeshment and explain how food refusal acts as a bid for autonomy and control.
- Apply social learning theory to explain how the media, modelling, and reinforcement contribute to anorexia nervosa.
- Distinguish between perceptual distortions of body size and irrational beliefs in the cognitive explanation of anorexia nervosa.
- Evaluate family systems theory as a socially sensitive account built on uncontrolled clinical observation.
- Describe genetic explanations for obesity including the FTO gene.
- Explain neural mechanisms of obesity focusing on dopamine D₂ receptors and serotonin.
- Evaluate biological explanations using relevant research evidence and alternative approaches.
- Define restraint theory and explain how it leads to paradoxical overeating.
- Describe the process of disinhibition and identify common triggers for binge eating.
- Explain the boundary model and apply it to the eating behaviour of restrained eaters.
Eating behaviour exam tips
Marking Points
- AO1: state the evolutionary logic - preferences that raised survival in ancestral environments were selected, so energy-dense sweet and fatty tastes are preferred and bitterness is rejected as a toxin cue.
- AO1: define neophobia as the avoidance of unfamiliar foods, note that it peaks in early childhood, and give the adaptive advantage of not sampling unknown plants.
- AO1: describe taste aversion learning and credit Garcia and Koelling for one-trial, long-delay conditioning in rats.
- AO1: explain learning through association, social reinforcement, parental and peer modelling, and cultural availability and prohibition, using Birch's peer-modelling study.
- AO3: the evidence base is largely non-human, so extrapolation to human food choice is questionable.
- AO3: evolutionary accounts are post-hoc and hard to falsify, and cannot explain rapid modern dietary change or the deliberate liking of bitter foods such as coffee and chilli.
- AO3: the explanations combine better than they compete - preparedness sets what is easy to learn, culture sets what is actually learned.
- AO1: establish homeostasis and the hypothalamus as the control centre before naming any structure.
- AO1: the lateral hypothalamus initiates feeding and the ventromedial hypothalamus inhibits it, evidenced by aphagia and hyperphagia after lesioning in rats.
- AO1: ghrelin is a short-term hunger hormone from the stomach lining acting via the arcuate nucleus, rising before meals and falling afterwards.
- AO1: leptin is a long-term satiety hormone from adipose tissue signalling the size of fat stores to the hypothalamus.
- AO3: the dual-centre model is oversimplified - ventromedial lesions also damage the paraventricular nucleus and fibres of passage, so the overeating may not be caused by that nucleus at all.
- AO3: biologically reductionist - it cannot explain eating for pleasure, boredom or social occasion, when people eat although satiety signals say stop.
- AO3: application - leptin replacement cures congenital leptin deficiency but fails in common obesity, where leptin is already high and receptors are insensitive, which supports leptin resistance.
- Genetic explanations rely on twin and family studies demonstrating higher concordance rates for AN in monozygotic twins than dizygotic twins.
- Candidate genes, such as EPHX2 (involved in cholesterol metabolism) and those linked to serotonin receptors, are implicated in genetic vulnerability to AN.
- Neural explanations focus on the role of serotonin, where altered levels are linked to appetite dysregulation, anxiety, and perfectionism.
- Dopamine imbalances, particularly overactivity in the basal ganglia, are proposed to disrupt the brain's reward system, making food restriction rewarding and eating aversive.
- Evaluation can include the diathesis-stress model, arguing that biological vulnerabilities require environmental triggers to manifest as AN.
- Explain family systems theory by detailing enmeshment (blurred boundaries) and how food refusal is an attempt to gain autonomy and control.
- Apply social learning theory by explaining the modelling of thin ideals from the media, and reinforcement (e.g. vicarious reinforcement from seeing models praised).
- Outline cognitive theory by distinguishing perceptual distortions (misperceiving body size) from irrational beliefs (e.g. dichotomous thinking about food).
- Evaluate family systems theory by discussing its socially sensitive nature, as it potentially blames parents and relies on retrospective clinical observations.
- Evaluate social learning theory by noting it struggles to explain why most media-exposed individuals do not develop anorexia, suggesting a biological vulnerability is also required.
- Evaluate cognitive theory by questioning whether cognitive distortions and irrational beliefs are symptoms rather than underlying causes, though CBT's success supports their role in maintenance.
- Identify the role of the FTO gene in predisposing individuals to obesity through impaired energy balance.
- Explain the evolutionary 'thrifty gene' hypothesis as a genetic explanation for fat storage.
- Describe how a reduction in dopamine D₂ receptors leads to compensatory overeating to achieve reward.
- Explain the role of serotonin in signalling satiety and how deficits lead to a lack of fullness and subsequent weight gain.
- Evaluate biological explanations using twin and adoption studies to establish concordance rates for body mass index.
- Define restraint theory as the cognitive restriction of food intake which paradoxically increases the risk of overeating.
- Explain disinhibition as the loss of control over eating behaviour in response to specific internal or external cues.
- Describe the boundary model's biological zones of hunger and satiety, and the placement of the cognitive diet boundary.
- Explain the 'what the hell' effect within the boundary model, where breaching the cognitive boundary leads to eating up to maximum capacity.
- Evaluate psychological explanations by discussing their inability to explain why some restrained eaters successfully lose weight.
Examiner Tips
- 💡If the question names neophobia or taste aversion, both must appear; an answer on general evolution alone caps the knowledge marks.
- 💡For a scenario about a child refusing new food, name neophobia explicitly and then say what the parent should do - repeated neutral exposure and modelling - to earn the application marks.
- 💡In an extended essay covering both evolutionary and learning explanations, ensure both are credited as description (AO1) if requested, and evaluate them by contrasting their approaches, such as biological preparedness versus cultural transmission.
- 💡A frequent stem describes someone who has lost weight and cannot stop feeling hungry; apply falling leptin and rising ghrelin rather than discussing motivation.
- 💡Name each hormone's source, target and direction of effect in one sentence apiece - that structure banks the knowledge marks quickly and leaves room for evaluation.
- 💡'Neural and hormonal' means both; an answer that is all hypothalamus and no hormones is only half a response.
- 💡Always use the terms monozygotic (MZ) and dizygotic (DZ) instead of identical and non-identical when discussing twin studies.
- 💡Highlight the difficulty in separating genetic and environmental factors, as families share both DNA and living environments.
- 💡Use the diathesis-stress model as a sophisticated evaluation point to show how biological and psychological explanations can be integrated.
- 💡The specification names eight specific terms across the three theories (enmeshment, autonomy, control, modelling, reinforcement, media, distortions, irrational beliefs), so be prepared to define and apply each one.
- 💡When evaluating psychological explanations, use the biological account as a counterweight and argue for an interactionist position rather than declaring a single winner.
- 💡In scenario questions, quote the stem: if a mother answers questions put to her daughter, explicitly name that as enmeshment before explaining it.
- 💡Use twin studies, such as those by Stunkard, to provide supporting evidence for the genetic basis of obesity.
- 💡When evaluating, introduce the diathesis-stress model to explain how genetic vulnerability requires an environmental trigger.
- 💡Clearly distinguish between neural mechanisms, such as neurotransmitters, and genetic inheritance to ensure focused answers.
- 💡Describe the boundary model diagram in your answer to clearly illustrate the zones of biological hunger, satiety, and the cognitive boundary.
- 💡Use the 'what the hell' effect as a concrete example of disinhibition when evaluating the boundary model.
- 💡Contrast psychological explanations with biological ones to build a strong, synoptic evaluation paragraph.
Common Mistakes
- Describing taste aversion as ordinary classical conditioning without saying what makes it special: the single trial and the delay of hours between taste and sickness.
- Treating neophobia as fussiness or a disorder rather than an adaptive, age-related mechanism.
- Writing that a preference 'helped us survive' with no mechanism named, which credits nothing because any evolutionary answer could say it.
- Confusing taste aversion with food allergy, or with disgust acquired by watching other people react.
- Swapping the two hypothalamic centres, or writing that the lateral hypothalamus stops eating.
- Saying ghrelin and leptin 'cause hunger and fullness' without naming where each is made and where it acts.
- Reporting rat lesion findings as though they were human evidence, with no comment on extrapolation.
- Describing leptin as a meal-to-meal signal; it tracks stored fat over long periods, which is why it is the long-term signal.
- Error: Stating that a single gene causes anorexia nervosa. Correction: Explain that AN is polygenic, meaning multiple genes contribute to a vulnerability rather than a single gene determining the disorder.
- Error: Confusing the roles of dopamine and serotonin in AN. Correction: Clearly distinguish that serotonin is typically linked to mood, anxiety, and perfectionism, while dopamine is linked to the reward system and altered responses to food.
- Error: Ignoring the issue of cause and effect in neural explanations. Correction: Point out that neurotransmitter imbalances might be a consequence of starvation rather than the root cause of the disorder.
- Defining enmeshment loosely as 'a close family' rather than as blurred boundaries where members speak and feel for one another.
- Assuming that describing media effects without a named study earns no credit; explaining the mechanism of media influence (modelling and reinforcement) is valid knowledge even without citing Becker.
- Blurring the three explanations into one undifferentiated psychological account instead of separating family, learning and cognitive claims.
- Confusing perceptual distortion of body size with irrational beliefs about eating; the specification names both and they are distinct concepts.
- Error: Stating that a single gene causes obesity. Correction: Explain that obesity is polygenic, meaning multiple genes interact with environmental factors to influence weight.
- Error: Confusing the roles of dopamine and serotonin. Correction: Specify that dopamine is linked to the reward pathway and pleasure from eating, whereas serotonin is linked to satiety and feeling full.
- Error: Writing the dopamine receptor index on the baseline. Correction: Write the dopamine receptor subtype using a subscript, such as D₂ receptors, to denote the receptor subtype correctly.
- Error: Treating restraint theory and the boundary model as completely separate, unrelated theories. Correction: Explain that the boundary model was developed to integrate and explain the mechanisms behind restraint theory and disinhibition.
- Error: Stating that the cognitive diet boundary is placed above the biological satiety boundary. Correction: Specify that restrained eaters place their cognitive diet boundary below the biological satiety boundary to restrict intake.
- Error: Confusing biological hunger with cognitive boundaries. Correction: Clearly distinguish between the innate biological drive to eat and the self-imposed psychological limit.