AQA Syllabus focus:
'Biological explanations for anorexia nervosa, including genetic and neural explanations.'
Anorexia nervosa can be explained biologically by inherited vulnerability and brain-based differences. These notes focus on how genes and neural systems may increase risk, shape symptoms, and help maintain severe food restriction.
Genetic explanations
A genetic explanation argues that anorexia nervosa is partly influenced by inherited factors. The disorder does not appear to be caused by one single gene. Instead, biological vulnerability is likely to reflect the combined effect of many genes, each making a small contribution. What may be inherited are tendencies linked to the disorder, such as anxiety, perfectionism, obsessional thinking, and unusual sensitivity to reward or punishment.
Family and twin evidence
Support for genetic influence often comes from family studies and twin studies. If anorexia nervosa is more common among biological relatives than in the general population, this suggests inherited vulnerability. Twin research strengthens this logic by comparing monozygotic twins, who share almost all their genes, with dizygotic twins, who share about half on average.
Researchers often compare concordance rates across these groups.
Concordance rate: The extent to which both individuals in a pair, such as twins, show the same disorder.
Twin studies usually find higher concordance for monozygotic twins than for dizygotic twins. This pattern suggests that heredity matters. However, concordance is not 100%, so genes cannot be the full explanation. Even when one identical twin has anorexia nervosa, the other may not develop it. This means environmental influences, life events, and the effects of dieting or starvation must also play a role.
Family evidence is useful because it shows that risk clusters in biologically related people. A limitation is that relatives often share environments as well as genes, so family similarity does not prove genetic causation by itself.
Candidate genes and polygenic risk
Molecular genetics has tried to identify specific genes linked to anorexia nervosa. Early research focused on candidate genes, especially genes involved in serotonin and dopamine functioning, because these systems affect mood, anxiety, reward, and motivation. Some research has also examined genes linked to brain-derived neurotrophic factor, which is involved in brain development and neural communication.
Current thinking is more complex than a single-gene account:
anorexia nervosa is probably polygenic
different genes may influence different vulnerability traits
genetic risk may help explain why the disorder often co-occurs with anxious or obsessive characteristics
A strength of the genetic explanation is that it matches evidence that biological vulnerability exists before the illness becomes severe. A weakness is that many early candidate-gene studies used small samples and produced inconsistent findings. This means genes are better understood as creating a predisposition, not a direct and unavoidable cause.
Neural explanations
A neural explanation focuses on brain systems and neurotransmitters that may create or maintain anorexic behavior. In this context, the most important accounts focus on serotonin and dopamine, because these chemicals are closely linked to anxiety, mood, reward, and motivation.
Serotonin and anxiety
Serotonin is associated with mood regulation and anxiety. One neural explanation suggests that some people with anorexia nervosa have disturbed serotonin activity, which may contribute to high anxiety, rigid thinking, and an exaggerated need for control. These traits fit the clinical picture of many individuals with the disorder.
Food intake affects serotonin-related processes because eating changes levels of tryptophan, a chemical involved in serotonin production.
This diagram maps the metabolic route from L-tryptophan to serotonin (via 5-hydroxytryptophan), showing the key enzymatic steps. It helps explain why changes in dietary intake can alter availability of serotonin precursors, linking food restriction to mood/anxiety-related neurochemistry. Source
Restricting food may therefore reduce uncomfortable internal states in some people. This helps explain why starvation may feel temporarily calming, even though it is physically harmful. In this way, abnormal serotonin functioning may help both to trigger the disorder and to maintain restriction once it has begun.
Dopamine and reward processing
Dopamine plays a major role in reward, motivation, and the learning of habits.
This figure illustrates the core dopaminergic reward circuitry, highlighting projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and the prefrontal cortex (PFC). It provides an anatomical “map” for discussing how altered reward processing could make food less rewarding while reinforcing weight-loss or control-related behaviors. Source
Neural explanations suggest that people with anorexia nervosa may process reward differently from healthy controls. Food may produce less pleasure or more anxiety, while weight loss, self-control, or excessive exercise may become unusually rewarding.
This altered reward response could help explain:
persistent food restriction
compulsive exercise
why losing weight may be experienced as achievement rather than danger
Brain-imaging studies sometimes report unusual activity in areas involved in reward and emotional processing, such as the insula and anterior cingulate cortex. These neural differences may contribute to disturbed responses to hunger signals, food cues, and body-related experiences.
Issues in evaluating biological explanations
Biological explanations have clear strengths. They are supported by evidence from twin research, genetics, and neuroscience. They also help explain why anorexia nervosa can be severe, persistent, and difficult to change through advice alone.
However, there are important limitations:
causality is hard to establish because starvation itself changes brain chemistry and brain structure
shared environments can inflate estimates of genetic influence in families
biological accounts can become reductionist if they ignore the person’s wider experience
This is especially important for neural explanations. If someone has been malnourished for a long time, altered serotonin or dopamine activity may be a consequence of the illness rather than its original cause. For that reason, the strongest biological account is not that genes or neurotransmitters act alone, but that they create vulnerability that can be triggered and maintained over time.
Practice Questions
Outline one finding from twin research into anorexia nervosa. (2 marks)
1 mark for stating that monozygotic twins show a higher concordance rate than dizygotic twins.
1 mark for linking this finding to a genetic influence or inherited vulnerability.
Discuss genetic and neural explanations for anorexia nervosa. (6 marks)
AO1: Up to 3 marks for accurate knowledge of genetic and neural explanations.
1 mark for describing inherited vulnerability or polygenic risk.
1 mark for describing evidence from family or twin studies.
1 mark for describing a neural explanation such as disturbed serotonin or dopamine functioning.
AO3: Up to 3 marks for discussion or evaluation.
1 mark for using supporting evidence, such as higher monozygotic than dizygotic concordance or brain-imaging findings.
1 mark for explaining that concordance below 100% means genes are not deterministic.
1 mark for noting that starvation may cause neural changes, so causality is unclear, or that biological explanations can be reductionist.
FAQ
An endophenotype is a measurable trait that sits between genes and the full disorder. In anorexia research, possible examples include cognitive rigidity, high harm avoidance, or unusual reward sensitivity.
Researchers value endophenotypes because they may be easier to measure consistently than the disorder itself. They can also appear in unaffected relatives, which makes them useful for tracing inherited vulnerability.
Candidate-gene studies test a small number of genes chosen in advance because researchers think they are biologically relevant. In anorexia nervosa, these often focused on serotonin or dopamine-related genes.
Genome-wide association studies scan the whole genome without assuming where the effect will be found. They usually need much larger samples, but they can give a broader and often more reliable picture of genetic risk.
Epigenetics refers to changes in gene activity that do not alter the DNA sequence itself. Chemical markers can make genes more or less active.
This matters because stress, malnutrition, and hormonal changes may affect gene expression over time. Epigenetics may help explain how inherited vulnerability and experience work together, rather than acting as separate influences.
If a trait appears in someone with anorexia nervosa and also in their healthy biological relatives, that trait may reflect vulnerability rather than being only a result of starvation.
This approach helps researchers identify possible inherited markers, such as rigid thinking styles or atypical reward responses. It is a useful way to separate pre-existing risk from illness effects.
Most diagnosed cases in research samples are female, so many genetic and neural studies mainly include girls and women. This means the evidence base is often narrower than it looks.
The result is a generalizability problem. Some biological risk factors may apply across sexes, but male-specific patterns could be missed if the sample is too small to detect them.
