AQA · A-Level · Psychology

    Course version: 7182-2025 · Exams from 2027

    Biological explanations for anorexia nervosa: genetic and neural.

    Full specification wording

    Eating behaviour: Biological explanations for anorexia nervosa: genetic and neural.

    Biological explanations for anorexia nervosa (AN) focus on genetic vulnerability and neural mechanisms.

    Checked against the AQA 7182-2025 specification (opens in a new tab) on .

    • Point 3 of 6
    • 3 key terms

    Study notes

    From the checked teaching notes for this specification point.

    The idea

    Biological explanations for anorexia nervosa (AN) focus on genetic vulnerability and neural mechanisms. Genetic explanations suggest AN is heritable, supported by twin studies showing higher concordance rates for monozygotic twins compared to dizygotic twins. Candidate gene studies investigate specific genes, such as the EPHX2 gene, which is involved in cholesterol metabolism, as altered cholesterol processing is often seen in AN. Neural explanations highlight neurotransmitter imbalances, particularly serotonin and dopamine. Overactivity in dopamine receptors in the basal ganglia may alter reward perception, making eating anxiety-inducing rather than pleasurable. Additionally, altered serotonin pathways can explain comorbid symptoms like perfectionism and obsessive traits often seen in AN.

    What earns the marks

    • Genetic explanations rely on twin and family studies demonstrating higher concordance rates for AN in monozygotic twins than dizygotic twins.
    • Candidate genes, such as EPHX2 (involved in cholesterol metabolism) and those linked to serotonin receptors, are implicated in genetic vulnerability to AN.
    • Neural explanations focus on the role of serotonin, where altered levels are linked to appetite dysregulation, anxiety, and perfectionism.
    • Dopamine imbalances, particularly overactivity in the basal ganglia, are proposed to disrupt the brain's reward system, making food restriction rewarding and eating aversive.
    • Evaluation can include the diathesis-stress model, arguing that biological vulnerabilities require environmental triggers to manifest as AN.

    Common mistakes and how to put them right

    • Stating that a single gene causes anorexia nervosa.

      Put it right: Explain that AN is polygenic, meaning multiple genes contribute to a vulnerability rather than a single gene determining the disorder.

    • Error: Confusing the roles of dopamine and serotonin in AN. Correction: Clearly distinguish that serotonin is typically linked to mood, anxiety, and perfectionism, while dopamine is linked to the reward system and altered responses to food.

    • Ignoring the issue of cause and effect in neural explanations.

      Put it right: Point out that neurotransmitter imbalances might be a consequence of starvation rather than the root cause of the disorder.

    Exam tips

    • Always use the terms monozygotic (MZ) and dizygotic (DZ) instead of identical and non-identical when discussing twin studies.
    • Highlight the difficulty in separating genetic and environmental factors, as families share both DNA and living environments.
    • Use the diathesis-stress model as a sophisticated evaluation point to show how biological and psychological explanations can be integrated.

    Try the lesson

    The start of the Eating behaviour: Biological explanations for anorexia nervosa: genetic and neural. lesson, made from checked teaching notes for this specification point.

    Have a go first

    Which of the following findings from twin studies provides the strongest evidence for a genetic explanation of anorexia nervosa?

    Listen

    Biological explanations for anorexia nervosa (AN) focus on genetic vulnerability and neural mechanisms. Genetic explanations suggest AN is heritable, supported by twin studies showing higher concordance rates for monozygotic twins compared to dizygotic twins. Candidate gene studies investigate specific genes, such as the EPHX2 gene, which is involved in cholesterol metabolism, as altered cholesterol processing is often seen in AN. Neural explanations highlight neurotransmitter imbalances, particularly serotonin and dopamine. Overactivity in dopamine receptors in the basal ganglia may alter reward perception, making eating anxiety-inducing rather than pleasurable. Additionally, altered serotonin pathways can explain comorbid symptoms like perfectionism and obsessive traits often seen in AN. A strong answer earns marks for these points. Genetic explanations rely on twin and family studies demonstrating higher concordance rates for AN in monozygotic twins than dizygotic twins. Candidate genes, such as EPHX2 (involved in cholesterol metabolism) and those linked to serotonin receptors, are implicated in genetic vulnerability to AN. Neural explanations focus on the role of serotonin, where altered levels are linked to appetite dysregulation, anxiety, and perfectionism. Dopamine imbalances, particularly overactivity in the basal ganglia, are proposed to disrupt the brain's reward system, making food restriction rewarding and eating aversive. A common slip: Stating that a single gene causes anorexia nervosa. Instead, Explain that AN is polygenic, meaning multiple genes contribute to a vulnerability rather than a single gene determining the disorder. Exam tip: Always use the terms monozygotic (MZ) and dizygotic (DZ) instead of identical and non-identical when discussing twin studies.

    See it

    A top-down flowchart. The top node, 'Biological explanations for AN', branches into two nodes: 'Genetic explanations' and 'Neural explanations'. The genetic node branches into two further nodes: 'Twin studies: higher concordance in MZ than DZ' and 'Candidate genes, e.g. EPHX2 (cholesterol metabolism)'. The neural node branches into two further nodes: 'Serotonin: altered levels linked to appetite dysregulation, anxiety, perfectionism' and 'Dopamine: overactivity in basal ganglia alters reward perception'. The dopamine node leads to one final node: 'Eating aversive, food restriction rewarding'.
    It shows how biological explanations of anorexia nervosa divide into genetic explanations (twin studies and candidate genes) and neural explanations (serotonin and dopamine).

    Key words

    Say what each word means before you turn the card.

    Genetic inheritance

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    Neurochemistry

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    Biological reductionism

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    See every definition
    Genetic inheritance
    Suggests anorexia nervosa is heritable, supported by twin studies showing higher concordance rates for monozygotic twins compared to dizygotic twins.
    Neurochemistry
    Highlights neurotransmitter imbalances, particularly serotonin and dopamine, where altered serotonin pathways can explain comorbid symptoms like perfectionism and obsessive traits.
    Biological reductionism
    An issue used to evaluate biological explanations of anorexia nervosa, alongside cause-and-effect.

    Label the diagram

    Some boxes have lost their names. Pick the right name for each number.

    The diagram again, with 3 boxes numbered instead of named. A top-down flowchart. The top node, 'Biological explanations for AN', branches into two nodes: 'Genetic explanations' and 'Neural explanations'. The genetic node branches into two further nodes: 'Twin studies: higher concordance in MZ than DZ' and 'Candidate genes, e.g. EPHX2 (cholesterol metabolism)'. The neural node branches into two further nodes: 'Serotonin: altered levels linked to appetite dysregulation, anxiety, perfectionism' and 'Dopamine: overactivity in basal ganglia alters reward perception'. The dopamine node leads to one final node: 'Eating aversive, food restriction rewarding'.
    • 1Box 1

    • 2Box 2

    • 3Box 3

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