4.3.6 - Biological explanations for anorexia nervosa

Biological vulnerability and mechanisms

Biological accounts distinguish inherited vulnerability from neural processes that may influence the onset or maintenance of anorexia nervosa.

A careful biological answer should avoid two mistakes.

First, it should not say anorexia nervosa is "just genetic" or "just chemical". The disorder is complex, and biological factors interact with psychological and social contexts. Those contexts belong mainly in the next lesson, but interaction is important AO3 here.

Second, it should not treat biology as destiny. A person can inherit a vulnerability without developing anorexia nervosa. Equally, changes in the brain may be part of the cause, part of the maintenance of symptoms, or a consequence of starvation. A strong answer keeps these possibilities separate.

For AQA, organise the topic like this:

AO2 starting point: If an item describes someone with a family history of eating disorders, do not stop at "genes caused it". Family history is consistent with inherited vulnerability, but shared environment is another possible explanation. The timing of onset may reflect development, environmental influences and maintaining processes.

Genetic vulnerability

Genetic vulnerability changes the probability of an outcome; it does not specify an inevitable individual future.

Genetic explanations propose that some people inherit variants of genes that make anorexia nervosa more likely. This does not mean there is one "anorexia gene". The current evidence points to anorexia nervosa as polygenic: many genetic variants each contribute a small amount of risk.

Family studies

Family studies ask whether anorexia nervosa occurs more often among biological relatives of people diagnosed with the disorder than among relatives of people without the disorder. Strober et al. (2000) found that full-syndrome anorexia nervosa was much more common among female first-degree relatives of people with anorexia nervosa than among relatives of comparison participants. This supports familial aggregation.

The methodological problem is immediate: biological relatives usually share both genes and environment. Family studies can show that risk clusters in families, but they cannot by themselves prove that genes are the cause.

Twin studies

Twin studies compare monozygotic (MZ) twins, who share almost all their DNA, with dizygotic (DZ) twins, who share about half their segregating DNA on average. If a disorder is partly genetic, MZ twins should be more similar for that disorder than DZ twins, provided their disorder-relevant environments are comparably similar. If MZ pairs experience more similar pressures than DZ pairs, this equal-environments assumption is weakened.

Bulik et al. (2006) used the Swedish Twin Registry and reported a heritability estimate of about 0.56 for narrowly defined DSM-IV anorexia nervosa. In plain English, genetic differences accounted for a substantial part of the variation in liability to anorexia nervosa in that population. The estimate had a very wide 95% confidence interval, from 0.00 to 0.87, so this single study cannot establish a precise genetic contribution. Its estimate is heritability, not a 56% concordance rate. Other evidence is needed alongside it.

Genome-wide association studies

Modern genetic research looks across the whole genome rather than searching only for a few candidate genes. Watson et al. (2019) combined data from the Anorexia Nervosa Genetics Initiative and the Psychiatric Genomics Consortium. Their genome-wide association study included 16,992 cases and 55,525 controls and identified eight significant risk loci.

The most exam-useful conclusion is that anorexia nervosa showed genetic links with both psychiatric traits and metabolic traits. This supports the idea that anorexia nervosa is a metabo-psychiatric disorder: biological risk may involve systems related to mood, anxiety, reward, physical activity, body mass and metabolism.

AO3 precision: GWAS findings strengthen the biological explanation because they use very large samples and direct genetic data. However, finding risk loci is not the same as finding a simple cause. The identified variants have small effects, and genetic risk needs to be understood alongside environment and development.

Neural systems

Neural accounts link altered appetite, anxiety and reward processing to the development or maintenance of restriction.

The neural explanation for anorexia nervosa usually focuses on two neurotransmitter systems: serotonin and dopamine. These systems do not operate in isolation, but separating them helps with AO1.

Serotonin

Serotonin is involved in mood, anxiety, satiety and behavioural inhibition. These functions are relevant because many people with anorexia nervosa experience high anxiety, rigid control and intense preoccupation with food, weight or shape.

Research has linked anorexia nervosa with altered serotonin activity. Kaye et al. (1988) reported reduced cerebrospinal-fluid 5-HIAA, a serotonin metabolite, in underweight participants, with values normalising after weight gain. A metabolite is a product of chemical breakdown, so it is an indirect index rather than a direct measurement of thoughts or anxiety. PET studies have also reported differences in serotonin receptor binding in people who are ill or recovered.

AO1 chain: altered serotonin activity may increase anxiety and behavioural inhibition. Restricting intake may then feel subjectively calming or controlling, which can help maintain the disorder. This is a biological maintenance explanation, not a moral judgement about the person.

AO3 caution: starvation itself changes brain chemistry. If serotonin measures differ during acute illness, those differences may be a consequence of undernutrition rather than an original cause. Studies with recovered participants help reduce this problem, but they still cannot fully prove what came first.