Source: Abnormal Psychology, University of Florida
Difficulty: Intermediate | Prerequisites: Part 1 of these notes (eating disorder types and DSM-5 criteria). Familiarity with basic neurotransmitter functions (serotonin, dopamine, norepinephrine) is helpful.
Tags: eating disorders, aetiology, biological factors, heritability, hypothalamus, serotonin, dopamine, thin ideal, body dissatisfaction, cognitive factors, emotion regulation, family dynamics, athletes and eating disorders, sociocultural factors, abnormal psychology
Understanding why eating disorders develop requires pulling together biological, psychological, and sociocultural threads. No single factor is sufficient on its own. Genetic predisposition sets a baseline of vulnerability, neurochemical systems (particularly serotonin and the hypothalamus) regulate hunger and satiety, and societal pressures around thinness create the context in which those vulnerabilities express themselves. This section covers what the research says about each contributing factor, and where the evidence is still uncertain.
Eating disorders arise from a combination of genetic vulnerability (56% heritability for anorexia, 41% for binge-eating), disrupted neurochemical systems in the brain, societal idealisation of thinness, cognitive distortions about body image, difficulties regulating emotions, and family environments that emphasise control and perfectionism. No single cause is enough; the factors interact.
Heritability (of eating disorders)
The proportion of variance in a trait attributable to genetic differences. Twin studies estimate 56% heritability for anorexia nervosa and 41% for binge-eating. Genes appear to carry a general risk for eating disorders rather than risk for one specific type.
In simple terms, your genes load the gun, but environment pulls the trigger.
Hypothalamus
A brain structure that regulates eating by receiving messages about recent food consumption and nutrient levels, then signalling the body to stop eating once nutritional needs are met. Dysfunction here can disrupt hunger and satiety signals.
Think of it as the brain's thermostat for appetite.
Set point theory (implied)
The idea that the body has a natural weight range it tries to maintain through metabolic and appetite regulation. Disruption of hypothalamic signalling may interfere with this regulation.
Thin ideal
The culturally promoted standard that equates attractiveness and worth with extreme thinness. Internalisation of this ideal is a significant risk factor for eating disorders, particularly in Western and Westernised cultures.
Body dissatisfaction
A negative evaluation of one's own body, particularly weight and shape. It is one of the strongest psychological predictors of eating disorder development. In one study, 24% of high-school girls with the greatest body dissatisfaction developed a diagnosable eating disorder, compared to 6% with lower dissatisfaction.
Dichotomous thinking
An all-or-nothing cognitive style in which things are judged as entirely good or entirely bad, with no middle ground. Common in individuals with eating disorders, this style is applied to food ("forbidden" vs "allowed"), body weight, and self-evaluation.
In simple terms, one biscuit eaten means the entire diet is ruined.
Diet subtype (of binge-eating)
A disordered eating pattern in which the individual is greatly concerned about body shape and size, maintains strict low-calorie dieting, and uses vomiting or exercise to compensate after binges.
Depressive subtype (of binge-eating)
A disordered eating pattern in which concern about weight coexists with significant depression and low self-esteem, and the individual eats to soothe negative feelings. This subtype carries greater social and psychological consequences and is less responsive to treatment. Roughly 80% develop clinical depression.
Genetics:
Twin studies: 56% heritability for anorexia, 41% for binge-eating
Genes confer a general vulnerability to eating disorders, not a specific risk for one diagnosis
Genetic risk interacts with the biological changes of puberty to contribute to eating disorder onset in girls (but not in boys)
Changes in female hormones at puberty may activate a latent genetic predisposition
The hypothalamus and neurochemical regulation:
The hypothalamus receives information about recent food intake and nutrient levels via neurotransmitters (norepinephrine, serotonin, dopamine) and hormones (cortisol, insulin)
It sends signals to cease eating when the body's nutritional needs are met
Dysregulation of any of these neurochemicals, or structural or functional problems in the hypothalamus, can produce disordered eating behaviour
This can manifest as difficulty detecting hunger accurately or difficulty stopping eating when full
Anorexia and brain function:
Individuals with anorexia show lowered functioning of the hypothalamus and abnormalities in serotonin and dopamine
Unresolved question: these abnormalities could be a cause of the disorder or a consequence of prolonged starvation
It remains unclear whether these neurochemical changes persist after weight is restored
Bulimia and serotonin:
Serotonin deficiency may lead the body to crave carbohydrates
This is consistent with the clinical observation that binge episodes frequently centre on carbohydrate-rich and high-fat foods
The ideal female body shape in developed nations has become progressively thinner since the mid-20th century
Most fashion models have a figure that is physically unattainable for most women
Women who internalise the thin ideal are at significantly higher risk for eating disorders
Both anorexia and bulimia are more common in women, consistent with the greater cultural pressure on women to be thin
Research evidence:
24% of high-school girls with the highest body dissatisfaction went on to develop a diagnosable eating disorder (versus 6% of those with lower dissatisfaction)
Exposure to media promoting thinness increases body dissatisfaction: women who watched "The Swan" (a makeover show) reported greater perceived pressure to be thin than those who watched a home-improvement programme
Peer influence matters: in one study, women exposed to a thin peer who complained about her weight and described her extreme diet became significantly more dissatisfied with their own bodies; those exposed to the same peer discussing neutral topics (classes, weekend plans) did not
Fiji study: girls with access to media and the internet were at much higher risk of eating-disorder symptoms; having friends who watch the most television amplified the risk further
Sports that emphasise aesthetics or weight class carry elevated risk: gymnastics, ice skating, dancing, horse racing, wrestling, bodybuilding, diving, figure skating, judo, karate
Female athletes report that the physical changes of puberty undermine their competitive edge, leading to severe dieting to maintain a prepubescent figure
Bodybuilders show eating-and-exercise patterns as obsessive as those seen in clinical eating disorders, but directed toward gaining muscle rather than losing fat
46% report bingeing after most competitions
85% report gaining significant weight in the off-season (average of 15 lbs), then dieting to lose roughly 14 lbs before competition
Among female bodybuilders: 42% report having been anorexic, 67% report being terrified of becoming fat, 58% report being obsessed with food
Ephedrine abuse is documented (used to reduce body fat)
Important caveat: in sports where thinness is not emphasised, athletes show lower rates of eating problems than non-athletes
Women who feel they need a perfect body, are dissatisfied with their current body, and have low self-esteem are more likely to adopt maladaptive weight-control strategies
These individuals tend to be heavily influenced by others' opinions and more conforming to social expectations, making them especially susceptible to thin-ideal pressures
Dichotomous (all-or-nothing) thinking is characteristic: food, behaviour, and self-worth are categorised as entirely good or entirely bad
Obsessive planning of eating routines and daily schedules, down to the smallest detail
Concern about body size operates at an unconscious level as well
Bulimic women are more likely to classify women in photographs by body size rather than facial expression
Individuals experiencing depression or persistent negative affect are at elevated risk for eating disorders
Among women with both elevated depressive symptoms and body dissatisfaction, 43% developed an eating disorder
Two subtypes of disordered eating patterns involving binge-eating:
Diet subtype: primary concern is body shape and size; individuals maintain a strict low-calorie diet and use vomiting or exercise to purge after binges
Depressive subtype: concern about weight is present, but depression and low self-esteem dominate; eating serves as emotional regulation
Greater social and psychological consequences over time
More distressed relationships with family and friends
More likely to develop additional psychiatric disorders
Less likely to respond to treatment
80% develop clinical depression
Anorexia nervosa commonly occurs in girls described as "good girls," high achievers who are dutiful, compliant, and eager to please
These families tend to feature:
Overinvestment in the daughter's compliance and achievement
Overcontrolling parenting
Suppression of emotional expression, particularly negative emotions
As a result, daughters do not learn to identify and accept their own feelings; instead, they learn to monitor and satisfy others' needs
Girls from overcontrolling families deeply fear separation because they have not developed the capacity for independent thought or action
They distrust their own judgement and do not understand their own feelings
Controlling food intake becomes a way to:
Gain a sense of control over one's own life
Elicit concern and attention from parents
Avoid peer relationships
Research findings:
Families of girls with eating disorders show high levels of conflict, discourage the expression of negative emotions, and emphasise control and perfectionism
Mothers in these families are more likely to believe their daughters should lose weight, to criticise their daughters' bodies, and to have exhibited disordered eating patterns themselves
Students sometimes assume eating disorders are purely sociocultural. Heritability figures (56% for anorexia) make clear that biology plays a substantial role.
It is easy to assume that serotonin and dopamine abnormalities in anorexia are a cause. They may well be a consequence of starvation. The research has not settled the direction of causality.
The thin ideal is often treated as the sole cause of eating disorders. Many people internalise the thin ideal without developing a disorder. Additional psychological factors (dichotomous thinking, low self-esteem, emotion-regulation difficulties) are needed to push the vulnerability into a clinical presentation.
Athletes are sometimes seen as uniformly at risk. In sports that do not emphasise thinness or weight class, athletes show lower rates of eating problems than non-athletes.
⚠️ Know the heritability estimates: 56% for anorexia, 41% for binge-eating. Be prepared to explain that genes confer a general eating-disorder risk, not a disorder-specific one.
⚠️ Understand the role of the hypothalamus and the key neurotransmitters/hormones involved (serotonin, dopamine, norepinephrine, cortisol, insulin).
⚠️ The cause-versus-consequence problem for neurochemical abnormalities in anorexia is a favourite exam question.
⚠️ Be able to describe at least two pieces of research evidence for the role of the thin ideal (e.g. the peer study, the Fiji study, the body-dissatisfaction prospective data).
⚠️ Know the two subtypes of binge-eating (diet subtype vs depressive subtype) and which carries worse outcomes.
⚠️ Family dynamics: be able to describe the overcontrolling family pattern and explain how controlling food intake functions as a bid for autonomy.
Fill in the blank: Twin studies estimate ________% heritability for anorexia nervosa.
True or false: Serotonin abnormalities in anorexia are definitively established as a cause rather than a consequence of the disorder.
Fill in the blank: In the binge-eating depressive subtype, roughly ________% develop clinical depression.
True or false: Athletes in sports that do not emphasise thinness have higher rates of eating disorders than non-athletes.
True or false: Genes appear to carry a general risk for eating disorders rather than risk for one specific type.
Answers: 1. 56. 2. False (the direction of causality is unresolved). 3. 80. 4. False (they show lower rates). 5. True.
Q: What is the heritability of anorexia nervosa, and what does this figure tell us about genetic versus environmental contributions?
A: Heritability is approximately 56%, meaning that just over half of the variance in anorexia risk is attributable to genetic factors. The remaining variance is environmental. Genes confer a general vulnerability to eating disorders rather than risk for one specific diagnosis.
Q: Explain the "cause or consequence" problem with neurochemical abnormalities in anorexia.
A: Individuals with anorexia show lowered hypothalamic functioning and abnormalities in serotonin and dopamine. However, prolonged starvation itself disrupts these same systems. Researchers cannot yet determine whether the neurochemical abnormalities preceded the disorder or resulted from it, and it is unclear whether they persist after weight is restored.
Q: Describe two pieces of evidence supporting the role of the thin ideal in eating disorder development.
A: (1) A prospective study found that 24% of high-school girls with the greatest body dissatisfaction developed a diagnosable eating disorder, compared to only 6% of those with less dissatisfaction. (2) In the Fiji study, girls with access to media and the internet showed a much higher risk of eating disorder symptoms, and having friends who watched the most television amplified that risk.
Q: Compare the diet subtype and depressive subtype of binge-eating. Which has a worse prognosis?
A: The diet subtype is primarily concerned with body shape and size and uses vomiting or exercise to compensate after binges. The depressive subtype is driven more by low mood and low self-esteem, with eating serving to soothe negative feelings. The depressive subtype carries worse outcomes: greater social and psychological consequences, more strained relationships, higher rates of co-occurring psychiatric disorders, lower treatment responsiveness, and an 80% rate of developing clinical depression.
Q: How do family dynamics contribute to the development of anorexia nervosa?
A: Anorexia tends to develop in girls from overcontrolling families that suppress emotional expression and emphasise achievement and perfectionism. Daughters in these families do not learn to identify their own feelings or act independently. Controlling food intake becomes a means of asserting autonomy, gaining a sense of control, and eliciting parental concern. Research confirms that these families show high conflict, discourage negative emotion, and include mothers who are more likely to criticise their daughters' weight and to exhibit disordered eating themselves.
The biological material here connects to the neuroscience foundations covered earlier in the course (neurotransmitter systems, brain structures). The sociocultural discussion of the thin ideal ties into cultural psychology and the broader debate about how Western diagnostic categories apply cross-culturally (revisit Criterion B of anorexia from Part 1). Family dynamics link to the developmental psychopathology material and to attachment theory. Emotion-regulation difficulties connect to mood disorders and the broader transdiagnostic literature on how poor affect regulation underlies multiple forms of psychopathology.
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