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, including genetic and neural explanations.
Anorexia nervosa clusters in families, and the biological claim is that what is inherited is a vulnerability rather than the illness itself. Twin studies carry the weight: Holland reported concordance of about 56% in identical twins against roughly 5% in non-identical pairs, and Strober found first-degree relatives of sufferers some eleven times more likely to develop it. Candidate genes cluster on the serotonin system, notably the serotonin transporter gene. Neurally, Kaye found raised serotonin metabolites in the cerebrospinal fluid of recovered patients, implying a chronically over-aroused, anxious state that starving temporarily quiets, while imaging shows altered dopamine activity in the striatum, which may turn eating from something rewarding into something aversive.
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 accounts, each naming a different culprit. Minuchin's family systems view puts the illness in the family rather than the person: boundaries blur into enmeshment, a parent answers for the child, conflict is never resolved, and refusing food becomes the one act of autonomy and control left - Bruch called it a bid for effectiveness by someone who feels she has none. Social learning theory looks outward to modelled thin ideals and praise for weight loss; Becker's Fiji study is the evidence, disordered-eating scores rising from roughly 13% to 29% of adolescent girls in the three years after television arrived. Cognitive theory looks inward, to perceptual distortion of body size and irrational beliefs such as 'one biscuit means I have failed completely'.
Biological explanations for obesity, including genetic and neural explanations.
Obesity clusters in families, and adoption studies separate out why. Stunkard's Danish study found adoptees' body weight tracked their biological parents and not the adoptive parents who actually fed them, and twins reared apart stay strikingly alike, putting heritability estimates near 70%. The best-known gene is FTO: carrying two risk copies is associated with being roughly three kilograms heavier and with clearly raised odds of obesity. The thrifty gene idea says why such alleles persisted - storing fat efficiently paid when food ran out. Neurally, leptin resistance leaves the satiety signal loud but unheard, and Wang found lower striatal dopamine receptor availability in obese participants, falling further as body mass rose, so more food is needed for the same reward.
Psychological explanations for obesity, including restraint theory, disinhibition and the boundary model. Explanations for the success and failure of dieting.
The counter-intuitive finding is that trying not to eat makes eating more likely. Herman and Mack gave restrained and unrestrained eaters a milkshake preload and then unlimited ice cream; the dieters given two milkshakes ate more than dieters given none, which is counterregulation, or disinhibition. The boundary model explains it: hunger and satiety are physiological limits with a wide indifferent zone between them that cognition governs, and a dieter imposes a diet boundary well before hunger ends. Crossing it triggers 'what the hell' eating that runs on to a satiety boundary set higher than average. Mann's review of long-term trials found most dieters regain what they lost, and a sizeable minority end up heavier.
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 26 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 Holland's twin concordance and Strober's family risk figures as evidence of an inherited vulnerability.
- Explain the serotonin and dopamine account of anorexia, including Kaye's raised metabolites in recovered patients.
- Explain why starvation itself makes it hard to tell whether neural differences cause anorexia or follow it.
- Evaluate the biological account against the female preponderance, rising incidence and cultural patterning it cannot explain.
- Describe Minuchin's enmeshment, overprotectiveness, rigidity and conflict avoidance and how the symptom stabilises the family.
- Explain how autonomy and control make food refusal a bid for effectiveness in Bruch's account.
- Explain body-size distortion and dichotomous thinking as the irrational beliefs cognitive therapy targets.
- Apply social learning theory to Becker's Fiji figures on disordered eating after television arrived.
- Evaluate family systems theory as a socially sensitive account built on uncontrolled clinical observation.
- Describe Stunkard's Danish adoption findings and the heritability estimate near 70% for body weight.
- Explain the neural account of obesity through leptin resistance and Wang's reduced striatal dopamine receptors.
- Apply gene-environment interaction to explain the rise in obesity since the 1980s without any change in the gene pool.
- Evaluate the dopamine evidence, since chronic overeating may downregulate receptors rather than low density driving it.
- Describe Herman and Mack's preload study and state what counterregulation looked like in restrained eaters.
- Explain the boundary model's hunger, satiety and diet boundaries and the indifferent zone between them.
- Apply the boundary model to explain the burst of overeating that follows a dieter crossing the diet boundary.
- Explain what makes dieting fail and what makes it succeed, naming flexible restraint and self-monitoring.
- Evaluate restraint theory using anorexia, where restriction succeeds and weight keeps falling.
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.
- AO1: state the diathesis - genes confer a vulnerability that environmental stressors trigger, rather than causing anorexia directly.
- AO1: quote twin concordance (Holland: about 56% identical against 5% non-identical) and raised first-degree family risk (Strober).
- AO1: name a candidate gene or system, most usefully the serotonin transporter gene.
- AO1: give the neural account - serotonin dysregulation with raised metabolites in recovered patients (Kaye), plus altered striatal dopamine and reduced grey matter.
- AO3: concordance far below total shows genes cannot be sufficient, so a purely genetic account is incomplete.
- AO3: identical twins share a more similar environment as well as their genes, so twin data overstate heritability.
- AO3: direction of causality is the strongest point - starvation itself alters neurotransmitter levels and shrinks brain tissue, so neural differences may be an effect of the illness rather than its cause.
- AO3: biology cannot explain the heavy female preponderance, the rise in incidence or the cultural patterning, all of which favour psychological and social explanations.
- AO1: family systems - name enmeshment, overprotectiveness, rigidity and conflict avoidance, and explain how the symptom stabilises the family (Minuchin).
- AO1: link autonomy and control to Bruch's sufferer who feels ineffective and controls the one domain she can.
- AO1: social learning - modelling of thin models, peers and family, vicarious and direct reinforcement through compliments, and the media as source; evidence from Becker in Fiji.
- AO1: cognitive - perceptual distortion of body size, dichotomous thinking, and over-evaluation of shape and weight as irrational core beliefs.
- AO3: Minuchin's evidence is clinical observation of families already in treatment with no controls and is retrospective, so dysfunction may be a consequence of living with a seriously ill child.
- AO3: family systems theory is socially sensitive and has been criticised for blaming parents, with real harm to families in treatment.
- AO3: social learning cannot explain why the overwhelming majority of media-exposed girls never develop anorexia, so an individual vulnerability factor is still needed.
- AO3: cognitive distortions may be symptoms rather than causes, although the success of cognitive-behavioural therapy targeting over-evaluation of weight supports a causal role.
- AO1: separate the genetic claim (inherited differences in metabolism, appetite and fat storage) from the neural claim (how hunger and reward circuits behave).
- AO1: cite adoption and twin evidence - Stunkard's Danish adoptees resembling biological parents, twins reared apart, heritability estimates near 70%.
- AO1: name a candidate gene such as FTO or a leptin-pathway mutation and state its measured effect on weight.
- AO1: give the neural mechanisms - hypothalamic dysfunction, leptin resistance, and reduced striatal dopamine receptor availability (Wang).
- AO3: genes cannot explain how fast obesity rose from the nineteen-eighties onwards, because the gene pool did not change; genotype interacting with an obesogenic environment is required.
- AO3: identified genes account for only a small fraction of the variance in body weight, so the explanation is partial.
- AO3: causality is uncertain in the dopamine evidence - chronic overeating may downregulate receptors rather than low receptor density driving overeating.
- AO3: implications cut both ways - a biological account reduces blame and stigma, but its determinism can discourage the behavioural change that treatment needs.
- AO1: define restraint theory - deliberately restricting intake paradoxically raises the likelihood of overeating.
- AO1: describe Herman and Mack's preload study and the counterregulation result, distinguishing restrained from unrestrained eaters.
- AO1: define disinhibition and give its triggers - preload, alcohol, anxiety and low mood.
- AO1: set out the boundary model's hunger, satiety and self-imposed diet boundaries and the zone of biological indifference between them.
- AO1: explain failure through the heightened salience of forbidden food, the all-or-nothing diet boundary and metabolic adaptation, and success through flexible rather than rigid restraint, realistic goals, self-monitoring and social support.
- AO3: restraint theory cannot explain anorexia nervosa, where restraint succeeds and weight keeps falling, so restriction alone is not the whole account.
- AO3: preload studies are laboratory tasks with student samples and transparent aims, so ecological validity and demand characteristics are problems.
- AO3: the practical value is real - flexible restraint and relapse-prevention techniques derive directly from the boundary model.
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.
- 💡Concordance evidence only gains full credit when the two twin types are compared explicitly - the contrast is the argument, not the figure.
- 💡Keep the descriptive section to three or four evidenced points; the marks live in the evaluation.
- 💡If the stem mentions a relative who also has the illness, use it: say why that fits genetics and why it equally fits shared family environment and modelling.
- 💡The specification names nine technical terms here and questions quote them, so be able to define enmeshment, autonomy, control, modelling, reinforcement, media influence, distortions and irrational beliefs.
- 💡When evaluating psychological explanations, use the biological account as the counterweight and argue for an interactionist position rather than declaring a winner.
- 💡In scenario questions, quote the stem: if a mother answers questions put to her daughter, name that as enmeshment before you explain it.
- 💡The strongest single evaluation point is gene-environment interaction; keep the timeline of rising obesity ready as the evidence for it.
- 💡Name adoption studies as a design, not just a finding, because they answer the shared-environment criticism of twin studies rather than repeating it.
- 💡For 'discuss biological explanations', write genetic and neural as two clearly separated paragraphs so the examiner can credit both.
- 💡The statement has two halves; a dieting question expects the boundary model as the framework, not a list of practical diet tips.
- 💡Scenario stems often describe someone breaking a rule then eating the whole packet - name disinhibition and the 'what the hell' effect explicitly to earn the application marks.
- 💡When evaluating, set the psychological account against the biological one and argue for interaction rather than choosing between them.
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.
- Writing that there is 'a gene for anorexia'. No single gene has been identified and the explanation is polygenic and probabilistic.
- Quoting concordance rates without explaining what a concordance rate is or why the identical against non-identical comparison is the argument.
- Missing the cause-or-consequence problem, which is the most creditworthy evaluation available on this content.
- Sliding from biological explanation into biological treatment and describing antidepressant drugs instead.
- Defining enmeshment loosely as 'a close family' rather than as blurred boundaries where members speak and feel for one another.
- Asserting that the media causes anorexia with no study attached, which earns no knowledge credit.
- Blurring the three explanations into one undifferentiated psychological account instead of separating family, learning and cognitive claims.
- Confusing perceptual distortion of body size with the irrational beliefs about eating; the specification names both and they are different things.
- Claiming a gene 'causes' obesity rather than raising risk by a measurable amount within a particular environment.
- Using twin similarity as proof of genetics while ignoring that twins usually share a kitchen as well as a genome.
- Stating that obese people lack leptin; in most cases leptin is high and the receptors are insensitive to it.
- Drifting into dieting and willpower, which belong to the psychological explanations and gain nothing here.
- Explaining dieting failure as a lack of willpower, which contradicts the very theory being examined.
- Muddling the self-imposed diet boundary with the physiological satiety boundary.
- Reporting Herman and Mack backwards: it is the restrained eaters, not the unrestrained, who eat more after the preload.
- Answering only on why diets fail when the specification asks for success and failure.