Explanations for Anorexia Nervosa

Anorexia nervosa is a serious eating disorder. For the AQA specification you need a clear clinical definition and then two families of explanation: biological and psychological.

Clinically, anorexia nervosa is characterised by three core features:

Core feature	What it means
Restriction of intake	A persistent restriction of energy intake leading to a low body weight
Intense fear	An intense fear of gaining weight, even when body weight is already low
Distorted perception	A distorted perception of one's own body shape or weight

That third feature — the disturbance in how body shape and weight are experienced — is central, and it reappears later in the cognitive explanation as a distorted body image.

Anorexia nervosa involves a restriction of energy intake leading to low body weight, an intense fear of weight gain, and a distorted perception of one's own body shape or weight.

The specification asks you to explain why the disorder develops. The rest of this lesson covers the biological account (genetic and neural) and the psychological account (family systems theory, social learning theory and cognitive theory), followed by an AO3 evaluation.

The genetic explanation proposes that a person can inherit a vulnerability to anorexia. The starting observation is that anorexia runs in families: a person is at higher risk if a close relative has the disorder.

Two lines of evidence support a heritable component:

• Twin studies. Concordance rates are consistently higher in monozygotic (MZ) twins, who share around 100% of their genes, than in dizygotic (DZ) twins, who share around 50%. A higher MZ concordance points to a genetic contribution.
• Family studies. First-degree relatives (parents, siblings, children) of someone with anorexia are at raised risk of developing it themselves, compared with the general population.

Researchers have looked for candidate genes that might carry this vulnerability, including genes affecting appetite regulation and the serotonin system, which links the genetic account directly to the neural one.

Higher MZ than DZ twin concordance, plus raised risk in first-degree relatives, suggests anorexia has a heritable component. It does not mean anorexia is a single-gene condition.

The genetic explanation does not claim anorexia is purely inherited. It claims a person can inherit a predisposition that makes them more susceptible when other factors are present.

The neural explanation focuses on the brain: specifically, dysregulation of neurotransmitters and abnormal activity in brain regions linked to reward and body image.

Two neurotransmitters are central to the AQA account:

Neurotransmitter	Proposed role in anorexia
Serotonin	Involved in appetite, mood and anxiety; abnormal serotonin activity is linked to the disorder
Dopamine	Central to the brain's reward circuitry; linked to the reinforcing quality of restriction

The dopamine account is worth unpacking. Dopamine underpins the experience of reward, and in anorexia it has been linked to the way restriction itself becomes rewarding or reinforcing — the behaviour that maintains the disorder is tied into the brain's reward system. Alongside this, brain-imaging research points to abnormal activity in areas involved in reward and in body-image processing.

The neural explanation proposes that dysregulation of serotonin and dopamine, together with abnormal activity in reward and body-image circuits, contributes to anorexia.

A key point to hold for the evaluation: much of the neural evidence is correlational. Finding altered neurotransmitter levels does not, on its own, establish that they caused the disorder.

Family systems theory shifts from biology to the family environment. It comes from Minuchin, who described the "psychosomatic family" — a pattern of family functioning that he argued could contribute to anorexia. Three interrelated features are named on the specification.

Feature	What it describes
Enmeshment	Family members are over-involved in each other's lives, with blurred personal boundaries
Autonomy	The young person struggles to develop independence and a separate sense of self
Control	With little control over their life, restricting food becomes a way to exert control

The logic runs like this. In an enmeshed family, the individual is not able to separate and develop autonomy. Feeling that they have little control over their own life, they turn to the one thing they can control — their eating. Restriction becomes a means of exerting control where the person feels they have none elsewhere.

Family systems theory attributes anorexia to enmeshment, a lack of autonomy, and issues of control within the "psychosomatic family". Restriction functions as an attempt to gain control.

This explanation is influential because it directly informs family-based treatment, a point returned to in the evaluation.

The two remaining psychological explanations focus on learning and on thinking.

Social learning theory argues anorexia is learned from the social environment through three mechanisms:

• Modelling — imitating thin role models, such as celebrities and peers, whose behaviour is observed and copied.
• Reinforcement — thinness or dieting is rewarded with praise and attention. This can be direct (praise received personally) or vicarious (seeing others praised for being thin).
• Media — repeated exposure to a thin ideal in advertising, television and online content normalises and promotes it.

Cognitive theory locates the problem in faulty information processing — in how the person thinks:

• Distortions — most importantly a distorted body image, in which the person overestimates their own body size, perceiving themselves as larger than they are.
• Irrational beliefs — rigid, perfectionist thinking that ties weight, food and self-worth together, so that weight becomes the measure of the self.

Social learning theory explains anorexia through modelling, reinforcement and media; cognitive theory explains it through distortions (distorted body image) and irrational, perfectionist beliefs.

These are distinct: social learning theory asks how the behaviour was acquired from others; cognitive theory asks what faulty thinking maintains it.

The specification rewards AO3 evaluation: weighing the strengths and limitations of each explanation.

Biological — twin and family support, but limits. Twin and family studies do support a genetic contribution. However, MZ concordance is well below 100%, so genes cannot be the whole story — the environment must also matter. Neurotransmitter findings are largely correlational: it is unclear whether abnormal serotonin or dopamine activity causes anorexia or is a consequence of the effects of starvation on the brain. This cause-and-effect ambiguity weakens the neural account.

Family systems theory — useful but hard to test. A clear strength is clinical usefulness: it informs family-based treatment, which has practical value. However, the supporting evidence is largely retrospective and correlational, gathered after the disorder has developed, so it cannot establish that family patterns came first. The theory also risks blaming families and parents, which is both ethically sensitive and may not be justified.

Social learning theory — media evidence. Support comes from Becker et al. (2002), who found that disordered eating attitudes rose among adolescent girls in Fiji after the introduction of Western television, supporting the influence of media on the thin ideal. A limitation is that not everyone exposed to thin ideals develops anorexia, so social factors alone are insufficient to explain who develops the disorder and who does not.

Cognitive theory — support, but origins unclear. Studies do show that people with anorexia tend to overestimate their body size, supporting the idea of distorted cognition. However, the theory describes the distorted thinking without fully explaining its origin, and cause-and-effect remains unclear: distorted cognition may be a cause of anorexia, a maintaining factor, or partly a result of it.

The most credible account is multi-factorial (interactionist): a biological vulnerability interacts with psychological and social triggers. No single explanation is sufficient on its own.

1. Treating one explanation as the sole cause

The evidence points to a multi-factorial account. Presenting genetics, family dynamics, learning or cognition as the single cause misrepresents the research and misses the interactionist conclusion that AO3 answers reward.

2. Confusing enmeshment with autonomy and control

These are three distinct features of the psychosomatic family. Enmeshment is over-involvement with blurred boundaries; autonomy is the struggle to become independent; control is restriction used to exert control. Blurring them together loses precision marks.

3. Assuming media exposure guarantees anorexia

Media and modelling are contributory influences, not guarantees. Most people exposed to a thin ideal do not develop anorexia, so social factors alone cannot explain who develops the disorder. State the influence, then acknowledge this limitation.

4. Presenting correlational neural findings as proven cause

Altered serotonin or dopamine activity is often correlated with anorexia, but the direction of causation is unclear — it may be a consequence of starvation rather than a cause. Writing that abnormal neurotransmitters "cause" anorexia overstates what the evidence shows.

5. Describing symptoms instead of explaining causes

The question asks for explanations for anorexia. Listing clinical features earns little credit unless you use them to build an argument about why the disorder develops (genetic, neural, family, learning or cognitive).