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
• BLittle 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 built mainly from self-report data from human dieters
• DIt places too much weight on hormones such as leptin and ghrelin

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.

Tom once ate prawns at a restaurant and was violently sick a few hours later. He now feels nauseous at the smell of prawns, even though he knows the illness was a stomach bug he caught from his nephew.

Which explanation of food preference best accounts for Tom's reaction?

• ANeophobia, an innate wariness of foods that are completely new
• BTaste aversion, a form of learning that can occur after one pairing✓
• CRepeated exposure, where familiarity with a food increases liking
• DSocial learning, where food choices are copied from a role model

Answer: One pairing of a taste with sickness, even hours later, produced a lasting aversion that persists although Tom knows the prawns were not the cause. This is taste aversion, which evolutionary psychologists see as an adaptation for avoiding toxic foods. Prawns were not new to him, so it is not neophobia; repeated exposure would increase liking rather than create disgust; and nobody modelled the reaction.

Which brain-scanning finding has been used to support a neural (reward) explanation of obesity?

• AWang et al. (2001) found increased dopamine D2 receptor availability in the striatum of obese people
• BWang et al. (2001) found that obese people had a larger ventromedial hypothalamus than lean controls
• CWang et al. (2001) found reduced dopamine D2 receptor availability in the striatum of obese people✓
• DWang et al. (2001) found that leptin levels in the brain's striatum were raised by overeating in rats

Answer: Using PET scans, Wang et al. found that the more obese the person, the fewer D2 receptors were available in the striatum. The reward-deficiency account suggests that people with a less responsive dopamine system may overeat to compensate. The finding was a reduction, not an increase; the study measured dopamine receptors in humans rather than hypothalamic size or leptin in rats. As the data are correlational, overeating might also reduce receptors.

Maya skipped breakfast and has eaten nothing since the evening before. It is now just before lunch and her stomach is empty.

Which hormonal state best explains her strong feeling of hunger?

• AGhrelin is high, as the empty stomach releases it to stimulate appetite✓
• BGhrelin is low, as the stomach stops releasing it once meals are missed
• CLeptin is high, as adipose tissue releases it to stimulate appetite now
• DInsulin is high, as the pancreas releases it when blood glucose is low

Answer: Ghrelin is secreted mainly by the stomach when it is empty; levels rise before meals and act on the hypothalamus to increase hunger, then fall after eating. Leptin from fat tissue signals satiety rather than hunger, and insulin is released when blood glucose is high after a meal, not when it is low.

Lena is on a strict diet. At a party she eats one slice of cake, decides 'I've blown my diet for today anyway', and then eats most of the remaining cake.

Which psychological explanation of obesity does this behaviour illustrate?

• ADisinhibition, as breaking a self-imposed limit releases the restraint✓
• BLeptin resistance, as her brain no longer responds to satiety signals
• CNeophobia, as she avoids unfamiliar foods and overeats familiar ones
• DTaste aversion, as one slice of cake was paired with feeling unwell

Answer: Once a restrained eater believes the diet limit has been broken, cognitive control is abandoned and they overeat (the 'what the hell' effect); this is disinhibition, which links restraint theory to the boundary model. Leptin resistance is a biological explanation, cake at a party is not unfamiliar, and taste aversion would reduce rather than increase eating.

Which of the following findings from Herman and Mack's (1975) preload study supports restraint theory?

• ARestrained eaters who first drank a milkshake ate less ice cream afterwards than restrained eaters given none
• BRestrained eaters who first drank a milkshake ate more ice cream afterwards than restrained eaters given none✓
• CUnrestrained eaters who first drank a milkshake ate more ice cream afterwards than unrestrained eaters given none
• DRestrained eaters ate the same amount of ice cream afterwards whether or not they had first drunk a milkshake

Answer: Unrestrained eaters compensated for the preload by eating less, as normal satiety would predict, whereas restrained eaters ate more after the milkshake: once their diet seemed broken, disinhibition led to overeating. This counter-regulation supports restraint theory. Eating less after the preload was the UNRESTRAINED pattern, and restrained eaters did not eat the same amount whatever the preload.

What does the genetic explanation of obesity propose?

• AObesity is caused mainly by learned eating habits within the family
• BBody weight is fixed at birth and cannot be altered by later diet
• 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.

Which finding provides the strongest support for a genetic explanation of obesity?

• AStunkard et al. (1986) found adoptees' body weight was closer to their adoptive parents' than to their biological parents'
• BStunkard et al. (1986) found that identical and non-identical twins had equal concordance rates for obesity
• CHetherington and Ranson (1940) found that obesity runs in families regardless of the food available to them
• DStunkard et al. (1986) found adoptees' body weight was closer to their biological parents' than to their adoptive parents'✓

Answer: Adoptees share genes but not upbringing with their biological parents and the reverse with their adoptive parents, so a closer weight match to the biological parents points to inherited influence. Resemblance to adoptive parents would point to environment instead, equal twin concordance would argue against a genetic role, and Hetherington and Ranson studied hypothalamic lesions in rats, not family patterns.

Which finding provides the strongest support for an evolutionary explanation of the human preference for sweet tastes?

• ASteiner found newborn babies made disgust expressions to sweet tastes but readily accepted bitter ones
• BGarcia found newborn babies developed a liking for sweet tastes after repeated pairings with milk
• CSteiner found sweet preferences appeared at around five years, once children had watched adults eat
• DSteiner found newborn babies made positive facial expressions to sweet tastes before their first feed✓

Answer: Newborns tested before any feeding responded to sweet tastes with relaxed, accepting expressions and to bitter tastes with rejection, so the preference appears without learning, consistent with sweetness having signalled safe, energy-rich food in our evolutionary past. The reversed finding is false, Garcia's work was on taste aversion in rats, and a preference appearing only after observing adults would support social learning instead.