Eating Behaviour

Explanations for food preferences

Explanations for food preferences: the evolutionary explanation, including reference to
neophobia and taste aversion; the role of learning in food preference, including social and
cultural influences.

Evolutionary Explanation for Food Preferences

The evolutionary approach suggests that our modern food preferences and eating behaviours evolved due to environmental demands placed on our ancestors during hunter-gatherer times.

According to this theory, specific preferences and aversions were naturally selected because they increased an individual’s chances of survival and successful reproduction.

The genes responsible for these beneficial traits were therefore passed down to subsequent generations.

Preference for Sweet and Fatty Foods

Early humans required significant energy resources to survive, making calorie-dense foods highly valuable.

Sweetness: A preference for sweet foods was highly adaptive because sweetness in nature is associated with ripe fruit, which provides readily accessible, fast-acting sugar and calories. Evolutionary psychology suggests this drive is encoded in our DNA; for example, specific genes like T1r2 and T1r3 code for specialised sweet taste receptors.
Fat: Similarly, humans developed an evolutionary preference for fatty, animal-based foods due to their high caloric density and rich energy resources, which were critical for survival during times of food scarcity.

Neophobia

Neophobia is defined as a natural aversion to or fear of trying new foods.

Evolutionary function: Neophobia serves an adaptive, protective function. By avoiding unfamiliar foods, our ancestors reduced the risk of ingesting something toxic, poisonous, or spoiled.
Animal-based foods: It is suggested that neophobia generally applies more strongly to animal-based foods than plant-based ones, owing to the greater health risk posed by consuming rotting meat.

Taste Aversion

Taste aversion (sometimes referred to as the Garcia effect) occurs when an organism learns to avoid a specific food after it has caused illness or nausea.

Biological Preparedness: This ties into Seligman’s concept of “prepared learning” or biological preparedness. Animals are genetically predisposed to quickly associate specific tastes with internal illness (like nausea) to prevent future poisoning, and this association requires minimal learning.
Animal Studies: Garcia and Koelling (1966) conducted the landmark “bright-noisy-tasty water experiment”, demonstrating that rats easily developed a conditioned aversion to saccharin-flavoured water when it was paired with a nausea-inducing poison (lithium chloride). In another study, Garcia (1977) found that coyotes and wolves developed a learned taste aversion to sheep meat after the meat was laced with lithium chloride to induce sickness.
Human Studies: Bernstein and Webster (1980) demonstrated this in adult humans, finding that patients developed an aversion to ice cream after consuming it prior to nausea-inducing chemotherapy sessions.

Strengths:

Innate Support: Research heavily supports the idea that basic taste preferences are hardwired rather than learned. Steiner (1987) and Grill and Norgren (1978) observed the facial expressions of newborn babies, finding that they show innate signs of acceptance and pleasure (smiling, licking lips) to sweet tastes, and expressions of disgust to bitter tastes. This innate reaction towards bitterness highlights an evolutionary mechanism designed to keep us away from toxins. Humans even possess a larger number of receptors to distinguish bitter flavours than sweet ones, reflecting the survival necessity of fine discrimination to avoid danger.
Real-World Application: Understanding taste aversion has provided highly useful medical applications. Because radiation and chemotherapy can cause severe gastrointestinal illness, cancer patients often develop a taste aversion to their regular diet. Drawing on this theory, a technique was developed where patients are given a “novel” food before treatment. They develop an aversion to this new “scapegoat” food instead of their familiar meals, allowing them to maintain their appetite and nutrition during treatment.

Limitations:

Maladaptive in the Modern World: What was beneficial for our hunter-gatherer ancestors is often maladaptive today. The food industry exploits our evolutionary bias toward sugary and fatty foods, creating an “obesogenic” environment filled with refined carbohydrates and saturated fats. Consequently, an innate preference for high-cholesterol fats now leads to obesity and heart disease rather than aiding survival. Furthermore, extreme neophobia can be actively maladaptive today by restricting an individual’s diet to the point where they fail to receive sufficient nutrients.
Alternative Explanations: The evolutionary explanation is often criticised for ignoring the vast impact of social learning and cultural influences. For example, while humans have an innate aversion to bitterness and spice (as capsaisin mimics pain), people in many cultures gradually acquire a preference for chilli through early exposure and cultural norms, which evolutionary theory struggles to explain on its own.
Gut Microbe Theory: Alcock et al. (2014) propose an alternative evolutionary view, suggesting that food preferences actually evolved as an adaptive response to benefit our gut microbes rather than the human host itself. They suggest that the pain of colic causes babies to cry, prompting parents to feed them more and thus increasing the nutrient supply to the infant’s gut microbes.

Role of Learning in Food Preferences

The learning approach suggests that our food preferences are not solely innate or hardwired by evolution, but are significantly acquired through experience and association.

This explanation highlights how psychological conditioning, alongside social and cultural environments, shapes our attitudes towards different foods.

Mechanisms of Learning

Our basic learning mechanisms play a fundamental role in what we choose to eat:

Classical Conditioning: We often learn to prefer certain foods by associating them with positive experiences and happiness. For example, if a specific traditional meal is frequently eaten during enjoyable family gatherings or celebrations, a person will form a temporal association between that food and the feeling of joy, leading to a long-term preference.
Operant Conditioning: Parents frequently use direct reinforcement to manipulate food preferences. They might offer certain foods, like cake, as a positive reward or “treat” for good behaviour. Furthermore, parents often use one desirable food as a reward for eating a distasteful food (e.g., “you can have dessert if you eat your vegetables”). However, research suggests that this specific tactic can actually decrease a child’s preference for the distasteful food.

Social Influences on Food Preference

Social learning theory suggests that eating behaviours are largely acquired through the observation, imitation, and modelling of others.

Parents and Family: Parents are the primary role models for young children. Research by Brown and Ogden (2004) suggests that a child’s eating habits are directly determined and reinforced by observing their parents’ relationship with food.
Peers: As children grow older, the influence of their family may weaken while the influence of their peer group becomes more prominent. Hare-Braun (2011) demonstrated that as children develop, the dietary choices of their peers strongly guide their own personal decisions about food.
Media and Advertising: The media also serves as a powerful symbolic model for food preferences. Children observe and imitate characters they see on television or the internet. This mechanism is often exploited by the food industry through cartoon characters to promote healthy eating, or detrimentally, to market unhealthy, sugary diets directly to children. Hare-Braun (2011) also found that high television consumption in children correlated with unhealthy food preferences, though this link weakened over time.

Cultural Influences on Food Preference

Cultural norms act as a guiding framework that dictates what is considered acceptable or desirable to eat, leading to distinct cultural differences in food likes and dislikes.

The Exposure Hypothesis: Culture dictates what foods a child is exposed to early in life. While evolutionary theory argues humans have an innate aversion to bitter or spicy foods, the learning explanation successfully explains why people still enjoy them. In cultures where chilli is common, children are gradually exposed to it by their families, allowing them to overcome the innate aversion and develop a learned preference for spice.
Geographical Location and Availability: Historically, geography limited the types of food a culture could consume, shaping regional cuisine. For example, potatoes did not originally grow in the Orient, which is why they are rarely found in traditional Asian cuisines. Today, an increase in food availability outside the home in Western cultures has led to a cultural shift, with 46% of food spending going towards “eating out,” thereby altering modern preferences.
Religion: Religious beliefs exert a massive influence on dietary habits through practices like fasting (e.g., during Ramadan in Islam), prohibition (e.g., banning pork in Judaism and Islam, or beef in Hinduism), feasting at specific calendar events (e.g., Christmas), and the ritualisation of food (e.g., communion wafers in Christianity).
The Acculturation Effect: A study by Ball and Kenardy (2002) found that when women from various ethnic groups immigrated to Australia, their food preferences gradually shifted. The longer they spent in Australia, the more their eating behaviours and attitudes mirrored those of Australian-born women. However, this is not absolute; other researchers like Leshman have noted that traditional food preferences can sometimes strongly persist across generations even after moving to new, urbanized environments.
Cultural Ideals: What a culture views as the “ideal” body shape also influences diet. Historically, and in some cultures today, being overweight was seen as a sign of high status and wealth. In the modern Western world, this has been largely replaced by a “supermodel culture” that pressures individuals, particularly women, to be thin, profoundly influencing the types of foods they prefer and avoid.

Strengths:

Explanatory Power: The learning theory successfully accounts for the wide diversity of food preferences across different cultures and explains how these preferences can change over an individual’s lifetime or after migrating to a new culture.

Limitations:

Fails to Explain Innate Preferences: A major limitation is that learning theory cannot adequately account for universal, hardwired preferences—such as the innate preference for sweet, calorie-dense foods or the instinctual rejection of bitter tastes in newborns. This indicates that evolutionary biology must also play a role.
Classical Conditioning Limitations: While classical conditioning is excellent at explaining how we develop taste aversions (e.g., avoiding a food after it makes us sick), it is generally considered less effective at explaining how we develop food preferences.
Reductionism: Relying solely on learning theory to explain diet is incomplete. Psychologists suggest that food preferences are complex and multifactorial, requiring a holistic approach that considers both our evolutionary/biological predispositions and our learned socio-cultural environments.

Neural & Hormonal Mechanisms

Neural and hormonal mechanisms involved in the control of eating behaviour, including the
role of the hypothalamus, ghrelin and leptin.

Role of the Hypothalamus (Neural Mechanisms)

The neural control of eating behaviour and appetite regulation is primarily managed by the hypothalamus, a small gland located in the rough centre of the brain that maintains the body’s internal homeostasis.

Two specific parts of the hypothalamus are involved in managing eating behaviour:

The Lateral Hypothalamus (LH): The LH is responsible for triggering feelings of hunger and the motivation to seek out food. It contains receptors that monitor blood sugar levels. When blood sugar drops below a certain threshold, the LH detects this and stimulates feelings of hunger. Once we eat, blood sugar levels rise rapidly, which then sends signals to the VMH to make us feel full and stop eating. This process is supported by experimental research, such as the work of Wynn et al. (1990).
The Ventromedial Hypothalamus (VMH): The VMH triggers the process of satiety—the feeling of being full and content that prevents us from eating any more. The VMH initiates this response when it detects specific hormonal messenger compounds transported in the bloodstream. A malfunctioning VMH leaves appetite unregulated; if it is damaged, an individual may never feel full, causing them to overeat continuously and gradually gain weight. Bayless et al. (1996) provided experimental evidence for this VMH process, although it was an animal study.

Role of Ghrelin (Hormonal Mechanisms)

Ghrelin is a chemical hormone released by the stomach and the intestinal tract into the bloodstream in relation to food intake.

Appetite Stimulation: Ghrelin levels are at their lowest immediately after eating a meal. Over time, as the body stops releasing it during digestion, the levels gradually rise bit by bit.
When ghrelin levels cross a certain threshold, they increase feelings of hunger and stimulate eating behaviour, which then resets the cycle once food is consumed.
Cummings et al. (2004) conducted a landmark study that proved a direct link between ghrelin levels and overall hunger.

Role of Leptin (Hormonal Mechanisms)

Leptin is an adipocyte-derived hormone, meaning it is produced by adipose (fat) tissue and secreted into the bloodstream.

Appetite Suppression: Leptin is predominantly involved in the long-term regulation of body weight and energy balance by acting as a hunger-suppressant or satiety signal to the brain. When a certain percentage of the body’s weight is composed of fat tissue, leptin is released to tell the body to stop eating. Low levels of leptin have also been found to be associated with biological explanations of anorexia nervosa.
The Link to Obesity: A malfunctioning VMH is often affected by low levels of leptin. It is argued that some obese individuals lack the hormone leptin, meaning they do not have the physiological control to stop eating when full.
Supporting Research: Zhang et al. (1994) studied a strain of mice that were obese, insulin-resistant, and ate voraciously. They discovered these mice had two copies of a defective ob (obesity) gene, causing a defect in leptin production. Injecting these mice with leptin caused them to lose weight dramatically, indicating that leptin deficiency was the root cause of their obesity. This is further supported by human research by Licinio et al., who studied a Turkish family with a genetic deficiency that left them unable to produce leptin. When the family members were given leptin supplements, their weight and eating behaviours normalised.

Evaluation of Biological Mechanisms of Eating

One significant limitation of explaining eating behaviour through neural and hormonal mechanisms is the heavy reliance on non-human animal research, such as studies involving mice or rats (e.g., Zhang et al., Halass et al., and Bayless et al.).

Extrapolating findings from non-human animals to humans is problematic.

Animals have a much more limited behavioural range, and humans rely on incredibly complex biochemical and cognitive processes that differ vastly from animal instincts.

Additionally, studying the brain mechanisms of eating behaviour using animals raises severe ethical issues, as animals cannot give informed consent and may be harmed or distressed by the experimental procedures.

Biological Explanations for Anorexia Nervosa

Biological explanations for anorexia nervosa, including genetic and neural explanations.

Genetic Explanations

The genetic explanation for anorexia nervosa (AN) proposes that the disorder is heritable and transmitted through DNA across generations.

To investigate this, researchers frequently use twin studies to compare concordance rates between monozygotic (MZ) twins, who share 100% of their DNA, and dizygotic (DZ) twins, who share 50%.

Holland et al. conducted twin studies demonstrating that MZ twins have a 56% concordance rate for developing AN, compared to just 5% for DZ twins.

This dramatic increase in likelihood aligned with a higher degree of genetic similarity strongly indicates a genetic basis for the disorder.

Anorexia is understood to be a polygenic condition, meaning it involves a combination of multiple genes rather than a single ‘anorexia gene’.

Researchers have identified several specific candidate genes that may increase a person’s vulnerability, including OPRD1, HTR1D, and EPHX2. Zeeland et al. (2014) highlighted the significance of the Ephx2 gene, which codes for an enzyme involved in the metabolism of cholesterol.

This genetic link is particularly notable because individuals exhibiting severe symptoms of anorexia nervosa frequently have abnormally high levels of cholesterol.

Additionally, evolutionary genetics provides another biological perspective.

Guisinger proposed the “adapted to flee famine” hypothesis, which suggests that the genetic traits leading to anorexia may have had an adaptive evolutionary function in our ancestral past.

Other biological correlates that increase vulnerability to AN include premature birth, birth complications, poor maternal nutrition, and even being born in the spring.

Neural Explanations

Neural explanations focus on biochemical imbalances in the brain, particularly involving the neurotransmitters serotonin and dopamine.

Serotonin: Serotonin is a neurotransmitter implicated in behaviours such as obsessiveness. Biological research on anorexia often measures 5-HIAA, the main metabolite (breakdown product) of serotonin, in patients’ urine. Bailer and Kaye (2011) found abnormally low levels of 5-HIAA in individuals with anorexia, demonstrating that reduced serotonin activity is strongly associated with the disorder.
Dopamine: The exact role of dopamine is controversial, as levels in AN patients have been recorded as lower, higher, or the same as neurotypical controls. However, increased dopamine activity in AN has been demonstrated by higher levels of homovanillic acid (HVA), dopamine’s main metabolite.
Kaye et al. (1991) found that HVA levels were lower in individuals who had recovered from AN compared to control groups. Furthermore, Bailer (2012) discovered that while eating food normally increases dopamine, in anorexic individuals this dopamine release triggers severe anxiety. As a result, individuals with AN may restrict their food intake specifically to avoid the anxiety caused by eating.

Other neural factors include abnormal activity of neurotransmitters like noradrenaline and GABA, as well as low levels of leptin, a hormone responsible for controlling satiety.

Structurally, there is evidence pointing to abnormalities in the brain’s feeding control centres, particularly the hypothalamus, and dysfunctional neural circuitry in the insula region of the cortex.

Evaluation of Biological Explanations

Methodological issues with twin studies:

A key weakness of the genetic explanation is that twin studies rely on the “equal environments” assumption.

While MZ twins show higher concordance rates, they are also treated more similarly by their families and society than DZ twins are.

Therefore, the higher concordance rate for MZ twins may be a result of greater environmental similarity rather than genetic inheritance alone.

Cause and effect (The “Chicken and Egg” problem):

A significant issue with neural explanations is determining whether altered neurotransmitter functions and structural brain abnormalities are the cause of anorexia, or merely a consequence of it.

Severe starvation and weight loss inherently produce dramatic changes in brain function, making findings difficult to interpret.

However, Kaye et al. (1999) provided compelling evidence by measuring HVA levels in recovered anorexics.

By testing patients who were no longer actively starving, the study avoided the confounding variables of weight loss.

They found that low HVA levels persisted after recovery, which supports the idea that dopamine imbalances are an underlying cause of AN rather than just an effect.

Reductionism and Determinism:

The biological approach to anorexia is biologically reductionist.

It attempts to reduce a highly complex behavioral and psychological disorder down to basic cellular, genetic, and chemical levels, largely ignoring the complex interaction between different neurotransmitters and psychological or family influences.

Furthermore, the explanation is biologically deterministic, suggesting that an individual’s biology dictates their destiny.

This raises ethical implications, as it removes the element of free will and alters expectations for recovery and treatment.

Diathesis-Stress Model:

Because genetics and neurochemistry alone cannot account for why some people develop the disorder and others do not, psychologists suggest that the diathesis-stress model is a far more effective explanation.

This model argues that genes and neural structures only create a biological vulnerability (diathesis) to anorexia.

The disorder only manifests if this vulnerability is triggered by an activating environmental event or stressor, such as a childhood trauma or media pressures.

Psychological explanations for anorexia nervosa

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.

Family systems theory

Family systems theory proposes that anorexia nervosa (AN) develops as a result of dysfunctional family dynamics and interactions.

Rather than looking strictly at the individual’s biology or personal cognitions, this psychological approach argues that certain characteristics of the family environment create the root cause of the disorder.

Minuchin et al. (1978) explored this influence, suggesting that families of anorexia sufferers often share distinct, problematic characteristics, primarily revolving around enmeshment, a lack of autonomy, and overbearing control.

Enmeshment

In family systems theory, enmeshment describes a family environment where the distinctions and boundaries between individual family members are blurred.

In an enmeshed family, there are intensely strong emotional bonds, to the point where members become completely emotionally dependent on one another and fail to develop clear, separated social roles.

This over-involvement inhibits an individual’s sense of personal identity and individuality.

Control and Overprotection

Closely linked to enmeshment is the issue of control and overprotection.

Families of individuals with anorexia are often highly controlling and overprotective, constantly watching over the child and telling them what to do.

This strict control means the child is unable to feel independent, seeing themselves merely as an extension of the family unit without a distinct sense of self whatsoever.

The family may also exhibit rigidity, upholding extremely strict rules and strongly held beliefs that the child feels completely powerless to break or challenge.

Furthermore, to keep the peace under these strict rules, the family often engages in conflict avoidance.

Autonomy Autonomy

is the feeling of being free to decide how to behave and having control over one’s own life.

Because enmeshment, overprotection, and rigidity strip the child of their independence, they are left with a profound lack of autonomy.

Consequently, anorexia nervosa often develops as a quest or struggle for autonomy.

Controlling their food intake and weight becomes the only aspect of their life that the individual feels they have absolute control over.

By refusing to eat, the individual is effectively rebelling against the family’s control to establish their own independent identity.

Research by Brockmeyer et al. (2013) supports this, demonstrating a strong desire for autonomy in patients with anorexia nervosa.

Evaluation and Limitations of Family Systems Theory

While there is experimental evidence supporting the role of family dysfunction in anorexia, psychologists have identified several significant limitations and issues with this theory:

Blaming the Family: A major criticism is that the theory places the blame for the disorder squarely on the parents and the family unit. This can be highly socially sensitive and raises ethical issues regarding who is responsible for the condition. It can cause immense distress to families already struggling with a severely ill child.
Cause and Effect: There is a significant problem in determining causality. It is difficult to know whether the controlling, enmeshed family dynamics actually cause anorexia, or if the severe stress of having a child with a life-threatening eating disorder results in the family becoming overprotective and controlling.
Continuation Outside the Home: Anorexia frequently persists long after the individual has left the family home, such as when a young adult moves away to university. This suggests that the immediate family environment cannot provide a complete explanation for the disorder and that other biological, cognitive, or media influences must be involved.
Treatment Practicalities: This explanation naturally suggests family therapy as the most appropriate treatment. However, trying to change the deeply ingrained behaviors and communication styles of an entire family unit is often very difficult, time-consuming, and expensive. In some cases, attempting to restructure the family dynamic may even inadvertently cause further interpersonal problems and harmful effects within the family.

social learning theory

Social learning theory proposes that anorexia nervosa is not innate, but rather a learned behaviour acquired through observation, imitation, and the principles of classical and operant conditioning.

Rather than looking strictly at biological causes, this approach argues that individuals learn to restrict their food intake by observing the actions and the subsequent consequences of others around them.

Modelling and Identification

According to this theory, individuals learn eating behaviours by observing role models, which can be real people in their immediate environment, such as parents and peers, or symbolic models, such as actors, TV characters, and figures in digital media.

An individual is most likely to imitate a model if they identify with them and admire their characteristics.

For example, a young girl might observe her mother failing to finish her meals; if the girl identifies with her mother, she may emulate this restrictive eating behaviour.

Vicarious and Direct Reinforcement

Imitation is heavily driven by vicarious reinforcement, which occurs when an individual observes a role model receiving positive consequences for their behaviour.

For instance, if a child observes their mother restricting food intake and subsequently being praised by the father for being “beautiful”, the child perceives these positive consequences and is encouraged to imitate the restrictive eating to gain similar rewards.

Similarly, when young people look up to media figures and see the fame, money, influence, and social success associated with being thin, they feel validated in attempting to replicate this appearance and behaviour.

Once an individual actually begins to lose weight, their restrictive eating is often sustained through direct reinforcement.

Friends and family may accidentally reinforce the disordered eating by giving praise or making positive comments about how “thin” or “healthy” the individual looks.

Influence of Media

The media plays a profound role in the social learning of anorexia, as magazines, television, films, and digital media consistently present and reinforce an idealised “thin” female body shape.

Altered Standards: In the age of the internet, altered images and manipulation technology project distorted and often physically unattainable body images that young, impressionable people try to emulate.
Supporting Research: The impact of the media is supported by research findings demonstrating a correlation between the increasing cultural focus on idealised thin women and a rise in anorexia cases. Furthermore, the introduction of television to previously isolated communities was followed by a subsequent increase in cases of anorexia nervosa, and the general prevalence of the condition has risen significantly since mass media became a common aspect of daily life in the 1950s and 1960s.

Evaluation of the Social Learning Theory

Strength:

Explaining Cultural Differences:
A major strength of the social learning theory is its ability to explain cultural changes and variations linked to anorexia.
Because social learning relies on observing specific cultural environments and media representations, it effectively accounts for why anorexia is heavily prevalent in Western cultures, where the ideal female body shape is thin, compared to other countries where a larger body shape may be culturally idealised.

Limitation:

The Problem of Susceptibility:
A significant limitation of this explanation is the issue of susceptibility. In modern Western society, almost all young women are exposed to the exact same media influences, role models, and pressures to be thin, yet only a fraction of them actually go on to develop anorexia nervosa.
This strongly suggests that media and environmental modelling alone cannot provide a complete explanation for the disorder, and that other factors must be involved.

Alternative Explanation:
Because environmental and media exposure cannot fully explain who develops the disorder, psychologists argue that the diathesis-stress model provides a much more effective explanation. This model proposes that an individual must first have an underlying genetic or biological vulnerability (the diathesis) to anorexia.
The disorder only manifests if this biological vulnerability is triggered by an activating environmental event or stressor, such as a childhood trauma or the intense media pressures and social reinforcement described by the social learning theory.

cognitive theory

The cognitive approach suggests that anorexia nervosa (AN) is primarily caused and maintained by maladaptive thought processes.

Rather than focusing on biological genetics or family dynamics, this explanation argues that individuals with AN suffer from severe cognitive distortions and irrational beliefs regarding food, eating, and their own body shape.

Cognitive Distortions

Cognitive distortions are instances where an individual’s perception of themselves and the world is not consistent with reality.

In the context of anorexia nervosa, these distortions present in several ways:

Distorted Body Image: Individuals with AN typically suffer from a distorted perception of their own body shape, often drastically overestimating their actual body size. This perception causes an intense obsession with food and body shape, leading them to severely restrict their eating to “rectify” their perceived size.
Misidentifying Emotions: Sufferers frequently misidentify their emotional states or distress as simply feelings of being “fat”. This misinterpretation reinforces their belief that they need to lose weight and causes them to continue undereating.

Irrational Beliefs

Alongside visual and emotional distortions, the cognitive explanation highlights the role of deeply ingrained, irrational beliefs:

All-or-Nothing Thinking and Self-Worth: Individuals with AN often tie their entire self-worth to their ability to control their weight. They may hold the irrational belief that they are fundamentally worthless if they cannot maintain absolute control over their food intake.
Catastrophising: This involves blowing small events entirely out of proportion. For example, a person with AN might eat a single biscuit and catastrophise the event, irrationally believing that this signifies they have absolutely no willpower left.
Perfectionism: Sufferers frequently hold beliefs that they must meet exceptionally demanding standards in all areas of their life. Crucially, once they reach their target weight or goal, they raise their standards even higher, meaning they are forever chasing unattainable goals.
Cognitive Inflexibility: Individuals with AN often display cognitive inflexibility, meaning they find it incredibly difficult or impossible to switch to a more adaptive or healthy way of thinking about their body size and eating habits.

Evaluation of the Cognitive Explanation

Strength:

Practical Applications to Treatment: A major strength of the cognitive explanation is that it lends itself effectively to treatment, specifically Cognitive Behavioural Therapy (CBT). By aiming to correct the underlying cognitive distortions that prevent an individual from recovering, therapies have shown significant success.
For instance, Grave et al. (2014) used enhanced CBT on patients and found that it caused significant weight gain that was successfully maintained for a full year after hospital discharge. The success of this treatment helps validate the cognitive explanation, suggesting that irrational thoughts are indeed a key component of the disorder.

Limitation:

Cause and Effect: A significant weakness of the cognitive theory is determining whether cognitive distortions are the cause of anorexia nervosa, or merely a symptom of starvation.
Shott et al. (2012) found that while older patients with AN demonstrated cognitive inflexibility, young people with the disorder did not show significant cognitive inflexibility compared to healthy controls.
This suggests that cognitive inflexibility does not make people vulnerable to the disorder initially, but rather, these cognitive distortions develop as a result of the illness over time.

Contradictory Evidence: Some research directly contradicts the core assumptions of the cognitive explanation. For example, Cornelissen (2013) found no significant differences between the accuracy of body size estimates made by non-anorexics and sufferers of AN. This challenges the fundamental idea that anorexia is driven by a distorted perception of one’s own body shape.

Methodological Issues with Retrospective Data: While research by Halmi et al. (2012) found that childhood perfectionism was a significant predictor of later developing AN in women over the age of 16, this study relied heavily on retrospective data.
Participants had to recall instances of perfectionism from their childhoods, meaning their memories may have been distorted or inaccurate.
This methodological flaw could artificially inflate or incorrectly strengthen the perceived link between early perfectionism and the later development of anorexia nervosa.

Biological explanations for obesity

Biological explanations for obesity, including genetic and neural explanations.

Genetic Explanations

Obesity is understood to have a strong genetic basis, with research indicating that the condition runs in families and is governed by inherited DNA.

To establish this heritability, researchers frequently use family, twin, and adoption studies, comparing the Body Mass Index (BMI) between relatives, such as between monozygotic and dizygotic twins, or between adopted children and their biological versus adoptive parents.

Nan (2012) investigated concordance rates for BMI, providing strong supporting evidence for the genetic transmission of obesity.

Rather than being caused by a single gene, obesity is polygenic and linked to multiple candidate genes, including the DRD2 gene, the FTO gene, and the “thrifty gene”.

The thrifty gene hypothesis provides an evolutionary perspective on obesity; Rowe (2007) suggests that the biological tendency to store fat for energy when food was freely available conferred a significant survival advantage for our ancestors.

Because modern environments offer an abundance of high-calorie foods, this once-adaptive trait has become an “evolutionary hangover,” which helps to explain the dramatic increase in modern obesity rates.

In addition to polygenic vulnerabilities, specific genetic variations have been directly linked to severe obesity.

For example, Bardet-Biedl syndrome is caused by gene mutations that affect cell development, leading to abnormal weight gain that begins in early childhood and persists throughout life.

Another crucial genetic discovery is the ob (obesity) gene, which was first identified in a strain of mutant mice that were deficient in the gene, causing them to become insulin-resistant, eat voraciously, and develop severe obesity.

Neural Explanations

Neural explanations focus on biochemical imbalances and structural dysfunctions within the brain’s feeding control centres.

A primary neural explanation for obesity is the malfunctioning of the hypothalamus, specifically the ventromedial hypothalamus (VMH), which leaves a person’s appetite unregulated.

This VMH dysfunction is closely tied to abnormally low levels of leptin, an adipocyte-derived (fat-derived) hormone.

Leptin plays a vital role in the long-term regulation of body weight and energy balance by acting as a hunger-suppressant signal to the brain.

It is argued that many obese individuals lack leptin, meaning they are deprived of the physiological control required to stop eating when they are full.

Beyond hormones, neurotransmitter imbalances in the brain are also heavily implicated in obesity.

Research by Wang (2001) linked low levels of dopamine activity to obesity, while abnormally low levels of serotonin have been associated with disinhibited eating behaviours.

Ohia (2013) provided further support for this neural mechanism by demonstrating a link between serotonin levels and obesity in mice.

Evaluation of Biological Explanations

Supporting Evidence and Practical Applications:

There is compelling experimental and clinical evidence supporting biological explanations, particularly regarding the role of leptin.

Zhang et al. (1994) discovered that obese mice with two defective copies of the ob gene failed to produce leptin, but when these mice were injected with leptin supplements, they lost weight dramatically.

This indicates that leptin deficiency was the root cause of their obesity.

Human research mirrors these findings; Licinio et al. studied a Turkish family with a genetic deficiency that left them unable to produce leptin.

Following leptin supplement treatment, the family members’ eating behaviours and weight successfully normalised.

This highlights a major strength of the biological approach, as understanding these mechanisms can lead to effective medical interventions.

Reductionism and Determinism:

A significant weakness of explaining obesity solely through genetics and neurochemistry is that the approach is biologically reductionist.

It attempts to reduce a highly complex condition down to the isolated action of a single hormone or gene, largely ignoring the complex psychological and environmental relationship humans have with food.

For example, cognitive theories propose that psychological factors—such as restrained eating—can actively lead to disinhibition and subsequent overeating, which biological models fail to account for.

Furthermore, biological explanations are highly deterministic, suggesting that obesity is dictated by an individual’s biology, thereby removing the element of free will and personal responsibility.

Comorbidity Issues:

Another complication in assessing the biological causes of obesity is the issue of co-morbidity.

Obesity frequently occurs alongside other psychological conditions, such as depression.

Because neurotransmitters like serotonin and dopamine are implicated in both depression and obesity, it becomes methodologically difficult to isolate specific biological mechanisms that solely cause obesity without being confounded by overlapping disorders.

Psychological explanations for obesity

Psychological explanations for obesity, including restraint theory, disinhibition and the
boundary model. Explanations for the success and failure of dieting.

Restraint Theory

The restraint theory, developed by Herman and Polivy (1975), proposes that attempting to actively restrict food intake is fundamentally self-defeating and ironically acts as a precursor to obesity.

Dieters establish strict, self-imposed rules about what they can and cannot eat, utilizing a high-control strategy to manage their weight.

Because their eating is driven by a strict regimen rather than natural physiological hunger, they often become intensely preoccupied with food.

This rigid control makes individuals highly vulnerable to losing control, ultimately resulting in disinhibited eating behaviour that causes them to put on weight and become obese.

Disinhibition

Closely tied to restraint is disinhibition, which occurs when a period of restrained eating is suddenly interrupted by an episode of uncontrolled, unrestrained eating.

This loss of cognitive control over dieting is typically triggered by external, food-related cues or emotional states, such as anxiety or the need to seek comfort.

When a restrained eater breaks their strict dietary rules, they frequently experience what is known as the “what the hell” effect (Herman and Mack, 1975).

Because they believe they have already failed or broken their diet for the day, they adopt the irrational belief that they might as well continue to eat, leading to significant overeating.

Boundary Model

Herman and Polivy (1984) further integrated these concepts into the boundary model, a holistic approach that considers both the physiological and psychological/cognitive processes involved in eating.

Physiological Boundaries: The model begins with the biological principle that both extreme hunger and extreme fullness (satiety) are physically aversive. When our energy levels drop below a certain biological boundary, the discomfort of hunger motivates us to eat. Similarly, eating until we are overly full pushes us past the satiety boundary, creating discomfort that motivates us to stop.
The Zone of Biological Indifference: Between these two biological extremes lies the ‘zone of biological indifference’, a state where we feel neither hungry nor completely full. In this zone, our eating behaviour is entirely under the control of psychological and cognitive factors.
The Cognitive Boundary: According to the model, restrained eaters purposefully set a strict cognitive boundary for themselves that lies well below their biological satiety boundary; they aim to stop eating long before they are physically full. However, if they eat past this self-imposed cognitive boundary, the “what the hell” effect is triggered. Once disinhibition takes over, they abandon their restraint and continue eating until they reach their biological satiety boundary. Furthermore, the model suggests that restrained eaters actually possess a higher biological satiety boundary than unrestrained eaters, meaning they must consume more food to feel satisfied, which actively contributes to obesity.

Evaluation of Psychological Explanations for Obesity

Supporting Evidence:

Experimental research strongly supports the role of restraint and disinhibition in overeating.

Wardle and Beales (1988) allocated obese women to different conditions and found that the group practicing restrained eating (the dieters) actually consumed significantly more food than those in the non-dieting control conditions.

This validates the theory’s claim that restraint acts as a causal factor for overeating and weight gain.

Similarly, Herman and Mack (1975) demonstrated this effect by giving participants varying amounts of milkshake (a “preload”) and then observing how much ice cream they subsequently ate, revealing marked differences in how restrained and unrestrained eaters react to breaking their diet.

Practical Applications:

A major strength of the restraint theory and the boundary model is their practical application in explaining why traditional diets frequently fail.

The multi-billion-dollar dieting industry often promotes “quick fixes” and blames the patient’s lack of willpower when they fail to lose weight.

The boundary model, however, accurately predicts that restricting food intake directly leads to disinhibition and weight gain.

Understanding these psychological mechanisms allows healthcare professionals to design more effective, long-term weight loss strategies that do not rely on rigid food restriction.

Methodological Issues and Contradictory Evidence:

Despite its strengths, the experimental research underpinning these theories has methodological flaws.

Studies like Herman and Mack’s milkshake experiment take place in highly controlled laboratory settings.

These environments lack ecological validity, meaning the artificial eating behaviour observed in the lab may not accurately reflect how people diet and binge in the real world.

Furthermore, some research directly contradicts the central assumption that restrained eating inevitably leads to obesity.

A longitudinal study by Savage et al. (2009) found that restrained eating while dieting actually led to short-to-medium-term weight loss, completely contradicting the restraint theory’s prediction of weight gain.

Psychologists argue that this discrepancy can be explained by separating restraint into two distinct categories: rigid restraint and flexible restraint.

It is argued that only rigid restraint leads to the “what the hell” effect and subsequent obesity, which could explain why some dieters in Savage et al.’s study successfully lost weight using flexible restraint.