Eating Behaviour
Explanations for Food Preferences
Evolutionary Explanation
Food preferences are thought to be adaptive because they increase survival. Humans have evolved to prefer certain tastes that indicate nutritional value.
A preference for sweetness is adaptive because sweet foods are high in energy. Steiner (1977) found that babies show a natural preference for sweet tastes such as fructose.
Preference for salt develops at around four months and helps maintain fluid balance and physiological functioning. Harris et al. (1990) found that babies preferred salted cereal, even though breast milk contains little salt.
Preference for fat is adaptive because fat provides a high number of calories, which would have been valuable in environments where food was scarce. Fat also enhances taste.
Neophobia refers to the innate tendency to avoid unfamiliar foods. This is adaptive because new foods could be poisonous. It is strongest between ages 2 and 6, when children begin exploring different foods.
Taste aversion is a learned response where individuals avoid foods that have previously caused illness. This occurs through biological preparedness, meaning humans are evolved to quickly associate certain tastes, particularly bitterness, with danger.
Evaluation of the Evolutionary Explanation
There is support for evolutionary explanations from research on stress. Torres et al. (2008) found that people consume more high-fat foods under stress, suggesting that these preferences are linked to the body’s energy needs.
However, neophobia may no longer be adaptive in modern environments, as food safety regulations reduce the risk of poisoning. It may instead limit children’s willingness to try beneficial foods.
There are also individual differences in taste sensitivity. Some individuals can detect bitter chemicals such as PROP more easily than others, which suggests that food preferences are not entirely universal.
The Role of Learning
Food preferences can also be explained through learning processes.
Classical conditioning explains food preferences through flavour–flavour learning. A new food paired with a liked flavour becomes preferred over time.
Operant conditioning explains preferences through reinforcement. Children may be rewarded for eating certain foods and punished for refusing them, increasing the likelihood of desired eating behaviour.
Social learning theory explains food preferences through observation. Children imitate role models such as parents, peers, or media figures, particularly when these behaviours are rewarded through vicarious reinforcement.
Cultural influences also shape food preferences. Cultural norms determine what is considered appropriate to eat, such as traditional meals or dietary practices. Food may also be associated with emotional experiences through conditioning.
Evaluation of the Role of Learning
Research suggests that learning may explain aversion better than preference. Baeyens et al. (1996) found that children developed strong aversions to flavours paired with unpleasant tastes, but not strong preferences for flavours paired with sweetness.
There is support for social learning theory. Birch and Fisher (2000) found a correlation between mothers’ and daughters’ restrained eating, suggesting modelling. Tenney (2001) found that children preferred foods modelled by others.
However, cultural explanations are not always supported. Mumford et al. (1988) found higher rates of eating disorders in Asian girls than white girls, suggesting that ethnicity does not always predict attitudes toward food.
Neural and Hormonal Mechanisms
The Role of the Hypothalamus
The hypothalamus regulates food intake by monitoring glucose levels.
The lateral hypothalamus (LH) is responsible for hunger. When glucose levels fall, the LH is activated and releases neuropeptide Y, which stimulates eating.
The ventromedial hypothalamus (VMH) is the satiety centre. When glucose levels rise, it inhibits the LH and produces feelings of fullness.
Ghrelin and Leptin
Ghrelin is released by the stomach and increases hunger. Levels rise when the body has not eaten for a period of time, stimulating the LH.
Leptin is released by fat cells and suppresses appetite. It signals the VMH when sufficient energy stores are present, reducing food intake.
Evaluation of Neural and Hormonal Mechanisms
The explanation is reductionist because many other factors influence eating behaviour. Neurotransmitters such as serotonin and dopamine also play a role, as well as hormones like cholecystokinin.
There is strong support from animal studies. Hetherington and Ranson (1942) found that damage to the VMH caused overeating, while Anand and Brobeck (1951) found that damage to the LH led to a lack of eating.
However, social factors may be more important in everyday eating behaviour. Woods (2004) argued that eating is often triggered by environmental cues rather than biological need.
Biological Explanations for Anorexia Nervosa
Genetic Explanations
Twin studies provide evidence for a genetic basis. Holland et al. (1988) found higher concordance rates in monozygotic twins compared to dizygotic twins.
Anorexia nervosa is likely polygenic, involving multiple genes. One gene identified is epoxide hydrolase 2, which is linked to cholesterol metabolism.
Genome-wide studies have identified many genetic variations associated with anorexia, although no single gene has been confirmed as the cause.
Neural Explanations
Low levels of serotonin metabolites have been found in individuals with anorexia, which may affect mood and appetite regulation.
Low levels of dopamine metabolites have also been observed, which may influence reward processing. Increasing dopamine levels can increase anxiety in those with anorexia.
Evaluation of Biological Explanations for Anorexia Nervosa
The lack of a single gene supports the view that anorexia is polygenic and may involve interactions with environmental factors.
Neural explanations may be oversimplified. Instead of one neurotransmitter, multiple systems may be involved.
There are real-world applications. SSRIs have been used to reduce relapse rates, although no drug has been consistently effective, suggesting biological explanations are incomplete.
Psychological Explanations for Anorexia Nervosa
Family Systems Theory
Family systems theory suggests that dysfunctional family dynamics contribute to anorexia.
Enmeshment refers to blurred boundaries, where family members are overly involved in each other’s lives.
Overprotectiveness involves parents being overly controlling and making decisions for the child.
Rigidity refers to resistance to change within the family.
Conflict avoidance means families avoid addressing problems.
Anorexia may allow individuals to gain autonomy and control by refusing to eat.
Evaluation of Family Systems
There is limited scientific support. Aragona et al. (2011) found no evidence for key features such as enmeshment.
The concepts are difficult to measure objectively, reducing validity.
However, the theory has applications in therapy. Behavioural family systems therapy has been shown to improve outcomes for some patients.
Family factors alone cannot explain anorexia. Davis et al. (2004) found that family influences interact with factors such as anxiety.
Social Learning Theory
Social learning theory explains anorexia nervosa as being learned through observation and imitation of role models. A child is more likely to imitate someone they identify with, particularly if that individual is perceived as attractive, successful, or similar to themselves.
Vicarious reinforcement plays an important role. If an individual observes a role model being rewarded for losing weight, such as receiving praise, attention, or social approval, they are more likely to imitate this behaviour. Media figures are especially influential because they are often associated with success, attractiveness, and status.
Dittmar et al. (2006) demonstrated the influence of media role models by showing that young girls who were exposed to images of Barbie dolls reported lower body satisfaction compared to those exposed to more realistic dolls. This suggests that unrealistic body standards can act as powerful role models in the development of anorexic behaviours.
Evaluation of Social Learning Theory
There is support for the role of media. Becker et al. (2002) found that after the introduction of television in Fiji, rates of disordered eating increased, suggesting media can transmit body ideals.
Social learning theory explains cultural differences, as rates of anorexia increase in cultures adopting Western ideals.
However, the theory has limited application to treatment, as changing role models alone has not been particularly effective in reducing anorexia symptoms.
Cognitive Theory
Cognitive theory suggests anorexia nervosa is caused by distorted thinking about body image, food, and weight.
Disturbed perceptions involve overestimating body size and being highly critical of appearance. Williamson et al. (1993) found individuals with anorexia were less accurate than controls when estimating body size.
Irrational beliefs include all-or-nothing thinking, such as “if I am not thin, I am fat,” and perfectionism, where individuals set increasingly unrealistic standards.
Cognitive inflexibility refers to difficulty adapting behaviour, meaning individuals continue harmful eating patterns even when they recognise the negative consequences.
Evaluation of Cognitive Theory
There is support for cognitive distortions. Sachdev et al. (2008) found altered brain activity when individuals with anorexia viewed their own bodies.
Perfectionism has also been linked to anorexia, with Halmi et al. (2012) showing it can be a risk factor.
However, Cornelissen et al. (2013) found no difference between anorexic individuals and controls in body size estimation, suggesting distorted body image may not always be present.
Biological Explanations for Obesity
Genetic Explanations
Family and twin studies show higher concordance rates among relatives. Chaput et al. (2014) and Nan et al. (2012) found strong evidence for genetic influence.
Obesity is polygenic, meaning it is influenced by many genes. Locke et al. (2015) identified numerous genes linked to body mass index.
Neural Explanations
Low serotonin levels may reduce satiety signals, leading to overeating.
Lower dopamine receptor levels may reduce reward from eating, causing individuals to eat more to feel satisfied.
Evaluation of Biological Explanations for Obesity
The diathesis-stress model explains that genetic vulnerability requires environmental triggers such as stress.
Ohia et al. (2013) found mice without serotonin receptors developed obesity, supporting a neural role.
However, drug treatments have side effects and are not always effective long term.
Psychological Explanations for Obesity
Restraint Theory
Restrained eating involves cognitive control over food intake, which can increase preoccupation with food.
This may lead to disinhibition, where individuals overeat after breaking dietary restraint.
Boundary Model
The boundary model proposes that eating occurs between hunger and satiety boundaries, with a zone of biological indifference in between.
Restrained eaters have a wider zone, making them more influenced by external cues and more likely to overeat when boundaries are exceeded.
Evaluation of Psychological Explanations for Obesity
Boyce and Kuijer (2014) found that rigid restraint leads to overeating, while flexible restraint does not.
Savage et al. (2009) found restrained eating may lead to weight loss, challenging the theory.
Wardle and Beales (1988) found restrained eaters consumed more calories due to disinhibition.
Bergh et al. (2009) suggested focusing on eating behaviour rather than dieting may be more effective.