Eating Behaviour

In the evolutionary explanation of food preference, what is neophobia?

• AA strong preference for foods that are high in refined sugar
• BA reluctance to eat foods that are unfamiliar to the individual✓
• CA learned dislike of a food which once caused nausea or an illness
• DAn inherited preference for the foods eaten by one's parents

Answer: Neophobia is the avoidance of unfamiliar foods. It is adaptive because an unknown plant or animal may be poisonous, so caution protects the individual until the food has been shown to be safe. A learned dislike following illness is taste aversion, which is a separate mechanism.

Garcia and Koelling's (1966) research on taste aversion in rats mattered because it showed that learning could:

• AOccur after only a single pairing and across a long delay in time✓
• BRequire a great many pairings presented closely together in real time
• CHappen only when an animal sees the true source of its illness
• DDepend entirely on the sheer strength of the unconditioned stimulus

Answer: The rats formed an aversion to a flavour after just one pairing with nausea, even when the illness followed hours later. That breaks the usual conditioning rules of repeated trials and close contiguity, and supports biological preparedness: animals are predisposed to link a taste with sickness specifically.

How does the evolutionary approach explain the human preference for sweet foods and dislike of bitter ones?

• ASweetness signalled scarce protein and bitterness signalled spoiled meat
• BSweet foods were rare in our ancestral past and bitter foods were common
• CSweet foods needed no cooking whereas bitter foods had to be prepared first
• DSweetness signalled ripe, energy-rich food and bitterness signalled toxins✓

Answer: A sweet taste reliably indicated ripe fruit dense in calories, while bitterness was a common marker of plant toxins, so preferring one and rejecting the other improved survival. The preferences persist even though sweet food is now abundant, which is part of why they contribute to obesity today.

Which finding best supports the role of social learning in the development of food preferences?

• AChildren reject a food that once made them feel unwell some hours later
• BNewborn infants show a clear preference for sweet solutions from birth
• CChildren eat more of a vegetable after seeing their own peers choose it✓
• DChildren begin to eat more once their blood glucose level has fallen

Answer: Watching a model eat and enjoy a food raises a child's willingness to eat it, which is vicarious reinforcement rather than any biological signal. The newborn sweet preference is innate, rejection after illness is taste aversion, and falling glucose is a physiological cue.

Which of these is the clearest example of a cultural influence on food preference?

• AAn infant grimacing in response to a bitter taste placed on the tongue
• BA rat avoiding a flavour that was followed by it feeling nauseous
• CFoods eaten quite routinely in one country being refused in another✓
• DAppetite rising as the stomach releases ghrelin shortly before a meal

Answer: Cultural norms determine which foods count as edible at all, which is why insects or offal are staples in some countries and refused in others. The bitter grimace is innate, the rat example is taste aversion, and ghrelin release is a hormonal mechanism.

In the dual-centre model of eating, what is the role of the lateral hypothalamus?

• AIt acts as a satiety centre, and damage to it causes overeating
• BIt releases leptin into the blood once the fat stores have risen
• CIt stores the long-term memory of the meals that were eaten
• DIt acts as a feeding centre, and damage to it causes aphagia✓

Answer: Stimulating the lateral hypothalamus makes an animal eat, and lesioning it produces aphagia — a refusal to eat that is fatal without intervention. The ventromedial hypothalamus plays the opposite, satiety role, and leptin is released by adipose tissue rather than by the brain.

A rat is given a lesion to its ventromedial hypothalamus. What is the most likely result?

• AAphagia, with the animal refusing food and losing weight
• BNo change at all, since the region has no role in appetite
• CA rise in leptin that fully suppresses the animal's appetite
• DHyperphagia, with the animal overeating and gaining weight✓

Answer: The ventromedial hypothalamus signals satiety, so removing it removes the stop signal and the animal eats its way to obesity. Aphagia follows a lateral hypothalamus lesion instead. One caution: such lesions often damage the neighbouring paraventricular nucleus as well, so the region's role is less clean than the model suggests.

What is the role of ghrelin in the control of eating?

• AIt is released by fat cells and decreases feelings of hunger
• BIt is released by the stomach and increases feelings of hunger✓
• CIt is released by the liver and converts stored glycogen to glucose
• DIt is released by the pancreas and lowers the blood glucose level

Answer: Ghrelin is secreted by the stomach lining, rises sharply before a meal and falls once food has been eaten, acting on the hypothalamus to stimulate appetite. Leptin from adipose tissue does the opposite, and insulin regulates glucose rather than appetite directly.

Leptin is secreted by adipose tissue. What does a rising leptin level normally signal?

• AThat fat stores are depleted, so appetite should now be increased
• BThat blood glucose has fallen well below its usual resting level
• CThat fat stores are adequate, so appetite should then be reduced✓
• DThat the stomach is empty and another meal should now be sought

Answer: The more adipose tissue the body carries, the more leptin it releases, so leptin works as a long-term signal of energy reserves and dampens appetite. Many people living with obesity have high leptin but a reduced sensitivity to it, which is described as leptin resistance.

Which is the strongest criticism of the dual-centre model of eating behaviour?

• AEating is controlled by a far wider network than just these two regions✓
• BThe hypothalamus plays no part whatsoever in the control of any eating
• CThe model was never tested using any research on non-human animals
• DHormonal signals have been shown to have no real effect at all on appetite

Answer: Feeding involves the arcuate nucleus, the paraventricular nucleus, neuropeptide Y and hormonal signals from the gut and fat stores, so reducing it to one hunger centre and one satiety centre is an oversimplification. The hypothalamus is still centrally involved, so the objection is to the model's scope rather than to its basic premise.

Twin studies of anorexia nervosa typically report which pattern of concordance?

• AHigher concordance for non-identical than for identical twins
• BHigher concordance for identical than for non-identical twins✓
• CAlmost identical concordance across both of the types of twin
• DConcordance close to zero for both identical and other twins

Answer: Monozygotic twins share all of their genes and consistently show higher concordance for anorexia than dizygotic twins, which supports a genetic contribution. Concordance falls well short of 100% even in identical twins, so genes raise vulnerability rather than determine the disorder on their own.

Which neural explanation has been proposed for anorexia nervosa?

• AA complete absence of dopamine throughout the whole of the brain
• BDamage to the ventromedial hypothalamus caused by prolonged fasting
• CDisturbed serotonin activity, linked to anxiety and rigid control✓
• DAn enlarged hippocampus that is present from birth in every case

Answer: Altered serotonin function is associated with the anxiety, perfectionism and rigidity often seen in anorexia, and disturbed dopamine activity in reward pathways has also been implicated. Claims that a neurotransmitter is wholly absent, or that a structural feature appears in every case, go well beyond what the evidence shows.

In family systems theory, what is meant by enmeshment?

• AFamily members are over-involved, so the individual boundaries blur✓
• BFamily members are distant, and rarely speak to one another at all
• CThe family openly confronts and resolves each conflict as it arises
• DThe family pushes each child towards independence unusually early

Answer: Minuchin described the psychosomatic family as enmeshed, overprotective, rigid and conflict-avoiding. Where the boundaries between members are blurred, an adolescent can struggle to establish autonomy, and controlling their own food intake may become one of the few areas of independent control still available to them.

How does social learning theory explain the development of anorexia nervosa?

• AVery thin models are imitated because they are seen to be rewarded✓
• BIrrational beliefs about weight distort how the body is then judged
• CAn inherited vulnerability is triggered by a stressful life event
• DDisturbed serotonin activity produces the rigid control over eating

Answer: Social learning points to modelling and vicarious reinforcement: seeing admired, very thin figures rewarded with attention and status makes the behaviour more likely to be copied. Becker's research in Fiji found that disordered eating attitudes rose among adolescent girls after television was introduced.

Which cognitive distortion is most characteristic of anorexia nervosa?

• ABelieving that other people are conspiring against the individual
• BOverestimating one's own body size despite being very underweight✓
• CRecalling only those events that occurred in the last few months
• DAssuming that a single failure guarantees later success instead

Answer: Body image distortion means the person perceives themselves as larger than they are, so losing weight never resolves the concern. Alongside it, dichotomous thinking treats eating as either total control or total failure, which makes any small lapse feel like a complete collapse.

What does the genetic explanation of obesity propose?

• AObesity is caused entirely by the amount of food that a person eats
• BBody weight is fixed at birth and cannot be altered at all later on
• COnly people carrying one specific gene are able to become obese
• DInherited factors influence appetite, metabolism and fat storage✓

Answer: Adoption and twin studies find that body weight resembles that of biological rather than adoptive relatives, which points to inherited influences on appetite regulation, metabolic rate and fat storage. Genes set a susceptibility that an environment full of cheap, energy-dense food then acts upon.

Why does a high leptin level often fail to suppress appetite in obesity?

• AThe body stops producing any leptin at all once fat stores grow
• BThe brain becomes less sensitive to the leptin signal it receives✓
• CLeptin is converted into ghrelin inside the adipose tissue itself
• DLeptin acts only on the stomach and never reaches the brain at all

Answer: Adipose tissue keeps releasing leptin, and levels are typically high rather than low, but the hypothalamus responds to it weakly. This leptin resistance means the satiety signal is present but not acted upon, which is why simply giving more leptin is rarely an effective treatment.

What is the central and somewhat paradoxical claim of restraint theory?

• ATrying to restrict food intake can actually lead to eating more✓
• BTrying to restrict food intake reliably produces steady weight loss
• CPeople who never diet consume far more than those who do diet
• DHunger is entirely under conscious control in almost everyone

Answer: Herman and Mack found that restrained eaters given a high-calorie preload went on to eat more than unrestrained eaters, not less. Once the self-imposed limit has been breached, restraint collapses, so the very act of dieting can raise overall consumption.

In the boundary model, what distinguishes a restrained eater from an unrestrained one?

• AA much narrower gap between the hunger and the satiety boundaries
• BA complete absence of any physiological hunger signal at all
• CA wider gap between hunger and satiety, plus a set diet limit✓
• DA satiety boundary that is reached far sooner after every meal

Answer: Restrained eaters have a larger range between the point where hunger starts and the point where satiety is felt, and they impose a cognitive diet boundary inside it. Crossing that self-set limit removes the restraint, and eating then continues all the way to the physiological satiety boundary instead.