Biological explanations of anorexia nervosa | AQA A-Level Psychology Revision

Revision Notes
Aug 6
33 min read

Updated: Aug 14

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 60 minutes

Biological explanations propose that vulnerability to anorexia nervosa may arise from inherited genetic factors and differences in brain chemistry or neural functioning. These Biological explanations of anorexia nervosa A-Level Psychology revision notes examine polygenic inheritance, candidate genes, serotonin, dopamine, leptin and the insula. Biological findings must be interpreted carefully because restrictive eating and substantial weight loss can themselves alter the brain and hormone levels. The current AQA specification requires both genetic and neural explanations of anorexia nervosa.

Learning Objectives 🎯

By the end of this revision page, you should be able to:

Explain genetic transmission and heritability in anorexia nervosa.
Explain evidence from family, twin and genome research.
Explain why anorexia nervosa is considered polygenic.
Describe candidate genes associated with biological vulnerability.
Explain neural accounts involving serotonin, dopamine, leptin and the insula.
Distinguish biological causes from biological consequences of restricted eating.
Apply biological explanations to unfamiliar scenarios.
Evaluate biological explanations using evidence, methodological issues and psychological alternatives.

Revision Notes 📚

Biological explanations of anorexia nervosa overview

Biological explanations locate vulnerability to anorexia nervosa within processes involving:

Genes and DNA.
Neurotransmitters.
Hormones.
Brain circuits.
Prenatal and developmental factors.

The main accounts required for this lesson are:

Genetic explanations
Neural explanations

AQA mark schemes accept biological content including:

Genetic transmission.
Family and twin research.
Polygenic inheritance.
Candidate genes.
Reduced serotonin activity.
Dopamine abnormalities.
Low leptin.
Dysfunctional neural circuitry involving the insula.

The central biological claim

The biological approach proposes that some people possess an underlying vulnerability that makes anorexia nervosa more likely.

A simplified pathway is:

inherited or developmental vulnerability → altered neural functioning → increased susceptibility to restrictive eating and related difficulties

This is a probabilistic explanation.

It does not mean that:

One gene inevitably produces anorexia nervosa.
Every biological relative will develop the condition.
Psychological and social experiences are irrelevant.
Brain differences remove all possibility of recovery.
A biological abnormality identified after diagnosis must have caused the condition.

Genetic explanations

What is a genetic explanation?

A genetic explanation proposes that vulnerability is partly transmitted through inherited DNA.

Genes contain biological instructions that influence:

Development.
Brain structure.
Neurotransmitter systems.
Hormonal functioning.
Responses to the environment.

A person may inherit genetic variants that increase susceptibility without directly inheriting anorexia nervosa itself.

The distinction is:

inherited vulnerability, not inherited certainty

Genotype and phenotype

A person’s genotype is their genetic makeup.

Their phenotype consists of observable characteristics arising through interaction between:

Genotype.
Development.
Environment.

Within a genetic explanation:

Risk alleles form part of the genotype.
Restrictive eating or other features form part of the phenotype.
Environmental and psychological experiences influence whether vulnerability is expressed.

This means two people with similar genetic risk may have very different outcomes.

Genetic transmission

What is genetic transmission?

Genetic transmission is the passing of genetic material from biological parents to their children.

Anorexia nervosa tends to occur more often among some biological relatives than would be expected by chance.

This pattern suggests a familial biological component.

The June 2023 mark scheme explicitly accepted a mother’s history of eating difficulties as evidence that could be applied to a genetic or familial explanation.

Family history as evidence of vulnerability

Suppose a person has several biological relatives who have experienced anorexia nervosa.

A genetic explanation would propose that:

The relatives share some DNA.
Some shared genetic variants may increase vulnerability.
The person may inherit a higher genetic loading.
This raises risk but does not guarantee the condition.

A family history is therefore evidence of possible predisposition rather than proof of a future diagnosis.

Family studies

What is a family study?

A family study examines whether a characteristic occurs more frequently among biological relatives of people with a condition.

Researchers may compare rates among:

Parents.
Children.
Siblings.
More distant biological relatives.
People without an affected relative.

Predicted finding

A genetic explanation predicts that:

risk should generally increase as biological relatedness increases

For example, close biological relatives should show greater similarity than unrelated individuals.

What family studies can show

Family studies can support the conclusion that:

Anorexia nervosa clusters within some families.
Biological inheritance may contribute to vulnerability.
Familial risk is greater than population risk.

What family studies cannot show

Relatives share more than genes.

They may also share:

Diets.
Family relationships.
Attitudes towards food.
Socio-economic circumstances.
Cultural expectations.
Modelling and reinforcement.

A family pattern could therefore result from:

shared genes + shared environment

Family studies alone cannot separate these influences confidently.

Twin studies

Monozygotic and dizygotic twins

Twin studies compare:

Monozygotic twins, usually abbreviated to MZ twins.
Dizygotic twins, usually abbreviated to DZ twins.

MZ twins share almost all their genetic material.

DZ twins share, on average, about half of the genes that vary between people.

Concordance

A concordance rate is the percentage of twin pairs in which both twins show the characteristic when one twin has it.

The genetic prediction is:

MZ concordance should be higher than DZ concordance

This is because MZ twins are more genetically similar.

Interpreting twin findings

Suppose an investigation finds:

Twin type	Concordance for anorexia nervosa
MZ twins	50%
DZ twins	15%

This pattern would support a genetic contribution because concordance is higher among the more genetically similar MZ twins.

However, MZ concordance is not 100%.

This suggests that genes are not sufficient by themselves.

Environmental and psychological factors must also contribute.

Similar environments

MZ twins may be:

Treated more similarly.
Dressed alike.
Encouraged to share activities.
More likely to identify closely with one another.

Their greater concordance could therefore partly reflect more similar environments rather than only genetic similarity.

This is known as the equal-environments problem.

Heritability

What is heritability?

Heritability is an estimate of the proportion of variation in a characteristic within a population that is associated with genetic variation.

It does not describe:

The percentage of one individual’s anorexia nervosa caused by genes.
The certainty that an individual will develop the condition.
Whether a characteristic can be changed.

A characteristic can be highly heritable while still being influenced by experience.

Population dependence

Heritability estimates apply to:

A particular population.
In a particular environment.
At a particular time.

If environments change, the relative contribution of genetic variation may also change.

Anorexia nervosa is polygenic

What does polygenic mean?

Polygenic means that vulnerability is influenced by many genes rather than one single gene.

AQA mark schemes identify anorexia nervosa as polygenic and recognise genome research and candidate genes as relevant biological material.

The genetic account is therefore:

many small genetic influences combine to produce different levels of susceptibility

Genetic loading

A person may inherit:

Few risk variants.
Several risk variants.
A combination carrying greater vulnerability.

The more relevant risk variants a person possesses, the greater their genetic loading may be.

However, a higher loading still does not make anorexia nervosa inevitable.

Different genetic pathways

Two people with anorexia nervosa may possess different combinations of risk alleles.

This means the condition may be:

Polygenic.
Genetically heterogeneous.
Influenced by several biological pathways.

There is no requirement that every person share one identical genetic profile.

Candidate genes

What is a candidate gene?

A candidate gene is a gene investigated because researchers believe its variation may be associated with a particular condition or relevant biological process.

AQA mark schemes accept candidate genes including:

OPRD1
HTR1D
EPHX2

Students do not need to claim that any one of these genes causes anorexia nervosa directly.

The safer conclusion is:

Variants of candidate genes may contribute to a broader polygenic vulnerability.

Candidate-gene pathway

A simplified explanation is:

A gene exists in different forms.
One variant is more common among people with anorexia nervosa.
The variant may influence a relevant biological system.
This creates a small increase in vulnerability.
Other genes and environmental factors are also required.

Association is not causation

Finding that a genetic variant is more common in one group does not show that it caused the condition.

The variant may:

Be linked with another causal gene.
Affect only a small subgroup.
Produce risk only in a particular environment.
Be associated by chance in a small sample.
Influence a related characteristic rather than anorexia nervosa directly.

Candidate-gene findings therefore need replication.

Genome research

What is genome research?

Genome research investigates genetic variation across many parts of the genome.

Rather than selecting only one candidate gene, researchers may search for patterns involving large numbers of variants.

Advantages

Genome research can:

Examine polygenic influences.
Use large samples.
Identify several risk variants.
Avoid relying entirely on one preselected gene.
estimate patterns of genetic vulnerability.

Limitations

Individual variants may each have:

A very small effect.
Different effects across populations.
Effects dependent on environmental circumstances.

A statistically significant association does not automatically create an accurate prediction for one person.

Genes do not code directly for complex behaviour

It is too simplistic to write:

“A gene causes somebody to stop eating.”

Genes influence biological systems.

These systems may affect:

Brain development.
Neurotransmitter activity.
Sensitivity to internal bodily signals.
Vulnerability to anxiety or rigid patterns of behaviour.
Responsiveness to environmental stress.

The relationship is therefore indirect:

genes → biological functioning → psychological vulnerability → increased risk

This is one reason anorexia nervosa is described as complex and polygenic.

Gene-environment interaction

A genetic vulnerability may be expressed only under particular environmental conditions.

Possible environmental influences include:

Family interaction.
Social modelling.
Media exposure.
Stress.
Cultural attitudes.
Cognitive beliefs.

The interaction can be represented as:

genetic susceptibility + environmental or psychological risk → increased likelihood of anorexia nervosa

The later lessons examine these influences through:

enmeshment, autonomy and control [Family systems theory and anorexia nervosa]
modelling, reinforcement and media [Social learning theory and anorexia nervosa]
distortions and irrational beliefs [Cognitive explanations of anorexia nervosa]

Applying genetic explanations

Scenario 1: affected biological relative

Naomi’s mother previously experienced anorexia nervosa. Naomi later develops serious restrictive eating.

A genetic explanation would suggest:

Naomi and her mother share genetic material.
The family history indicates possible inherited vulnerability.
Naomi may have inherited risk variants.
The relationship does not prove genetic causation because Naomi may also have learned attitudes or behaviour from her mother.

Scenario 2: MZ twins with different outcomes

One identical twin develops anorexia nervosa while the other does not.

This suggests:

The twins may share substantial genetic vulnerability.
Genes are not sufficient by themselves.
Different experiences may influence whether vulnerability is expressed.
The genetic explanation should be interactionist rather than fully deterministic.

Scenario 3: no known family history

A person develops anorexia nervosa despite having no known affected relatives.

This does not disprove a genetic account because:

Relatives may carry risk variants without developing the condition.
Several small genetic variants may be inherited.
Family history may be incomplete.
Non-genetic biological and psychological factors may contribute.

Neural explanations

What is a neural explanation?

A neural explanation focuses on differences involving:

Neurotransmitters.
Receptor activity.
Brain structures.
Neural circuits.
Hormonal signals received by the brain.

AQA mark schemes recognise neural explanations involving:

Serotonin.
Dopamine.
Noradrenaline.
GABA.
Leptin.
The insula.

Neural abnormality does not automatically mean cause

A person experiencing sustained food restriction undergoes major biological changes.

Therefore, an observed neural difference could be:

A pre-existing cause.
A vulnerability.
A consequence of restricted eating or low body weight.
A factor maintaining the condition.
A combination of these.

This direction-of-causality problem is central to evaluation.

Neurotransmitters

What is a neurotransmitter?

A neurotransmitter is a chemical messenger released by neurons.

It crosses a synapse and influences another neuron by binding with receptor sites.

Neural explanations propose that unusual levels or activity in neurotransmitter systems may contribute to anorexia nervosa.

The principal neurotransmitters accepted in AQA mark schemes are:

Serotonin.
Dopamine.
Noradrenaline.
GABA.

Serotonin

The serotonin explanation

AQA mark schemes accept reduced serotonin activity as one biological explanation of anorexia nervosa.

The account proposes that atypical serotonergic functioning may contribute to vulnerability.

This may involve differences in:

Serotonin production.
Release.
Receptor sensitivity.
Reuptake.
Metabolism.

The precise abnormality may vary between individuals and studies.

5-HIAA

5-HIAA is a breakdown product, or metabolite, of serotonin.

Researchers may measure 5-HIAA in urine or other biological samples as an indirect indicator of serotonin activity.

AQA mark schemes recognise:

lower levels of 5-HIAA in urine as evidence of reduced serotonin activity.

Proposed pathway

A simplified neural pathway is:

altered serotonin functioning → disrupted regulation of eating and related psychological processes → increased vulnerability to restrictive eating

The account should be presented cautiously because low serotonin activity measured during severe restriction may be an effect of inadequate nutrition.

Low 5-HIAA does not directly measure the brain

A urine measurement is indirect.

Its strength is that it produces:

Quantitative data.
An objective biological measure.
A testable comparison between groups.

Its limitation is that urinary levels may not perfectly represent:

Activity in a particular brain region.
Receptor sensitivity.
Synaptic serotonin at the time behaviour occurs.

Dopamine

The dopamine explanation

Dopamine has also been associated with anorexia nervosa.

However, AQA’s mark schemes explicitly describe its role as controversial.

Research findings have reported dopamine activity that is:

Lower than controls.
Higher than controls.
Similar to controls.

Students should therefore avoid a single absolute statement such as:

“Anorexia nervosa is caused by low dopamine.”

Homovanillic acid

Homovanillic acid, often abbreviated to HVA, is a breakdown product of dopamine.

Higher HVA levels have been used as evidence of increased dopamine activity in some people with anorexia nervosa.

D2 receptor activity

AQA mark schemes also recognise evidence of increased D2 receptor activity among people recovering from anorexia nervosa.

The importance of recovered participants is that some biological differences may continue after immediate nutritional recovery.

This could suggest a pre-existing or continuing vulnerability.

However, recovery does not guarantee that every consequence of the condition has disappeared.

Why dopamine evidence is difficult to interpret

Different results may arise because studies examine people who are:

At different stages of the condition.
Underweight or weight restored.
Taking different medication.
Experiencing different symptoms.
Measured using different biological methods.

The inconsistency weakens any simple dopamine explanation.

Other neurotransmitters

AQA mark schemes also accept:

Noradrenaline
GABA

as neurotransmitters potentially involved in anorexia nervosa.

These reinforce the idea that a single-neurotransmitter account may be too narrow.

A more cautious neural explanation proposes:

several interacting neurotransmitter systems may contribute to vulnerability and maintenance

Students are not required to present an unsupported claim that one particular level of noradrenaline or GABA causes all cases.

Leptin

What is leptin?

Leptin is produced by fat cells and provides the brain with information about stored energy.

Its normal role is explored in ghrelin, leptin and hypothalamic signalling [Hormonal control of eating].

AQA mark schemes accept low leptin as a biological correlate of anorexia nervosa.

Why leptin levels may be low

When body-fat stores are reduced:

Fat tissue produces less leptin.
The brain receives less stored-energy information.
Ordinary appetite-regulation processes may be disrupted.

Cause or consequence?

Low leptin may be:

A biological vulnerability.
A consequence of reduced body fat.
A mechanism maintaining altered eating.
Part of a feedback cycle.

For example:

severe restriction → loss of body fat → lower leptin → altered appetite and hormonal functioning

Finding low leptin after substantial weight loss does not show that low leptin initiated the restriction.

Important comparison

Leptin normally contributes to satiety.

It may therefore seem surprising that a person with low leptin continues to restrict food.

This illustrates that eating behaviour is not controlled by one hormone alone.

Cognitive, social and emotional influences may override or reinterpret biological hunger signals.

The insula

What is the insula?

The insula is a brain region involved in processing internal bodily and sensory information.

AQA mark schemes accept dysfunctional neural circuitry in the insula as a biological correlate of anorexia nervosa.

Possible relevance to eating

The insula contributes to processing information related to:

Taste.
Internal bodily states.
Hunger and fullness.
Emotional significance.

Dysfunctional insula circuitry may therefore affect how a person experiences or interprets:

Hunger.
Satiety.
Taste.
Bodily sensations.

Possible neural pathway

atypical insula functioning → distorted processing of internal food-related signals → increased difficulty responding normally to hunger or satiety

This is one possible explanation rather than a complete account.

Neural circuitry

The term neural circuitry is important.

Complex behaviour is rarely controlled by one isolated brain area.

The insula communicates with wider systems involved in:

Reward.
Emotion.
Decision-making.
Bodily regulation.

A circuit-based account is therefore more sophisticated than describing the insula as an on-off “anorexia centre”.

Neural control of hunger and anorexia nervosa

Normal eating involves interaction among:

The hypothalamus.
Hunger and satiety signals.
Hormones.
Wider neural circuits.

This is examined in the hypothalamus and homeostatic eating [Neural control of eating].

A neural explanation of anorexia nervosa may propose disruption in how these systems:

Detect energy need.
Process internal signals.
Attribute value to food.
Translate hunger into eating.

However, a person may still recognise hunger while deliberately restricting intake.

Neural control therefore cannot be treated as the only level of explanation.

Additional biological correlates

AQA mark schemes accept several additional biological associations:

Birth complications.
Premature birth.
Poor maternal nutrition.
Season of birth.
Dysfunctional insula circuitry.

Prenatal and birth-related influences

Birth complications, premature birth and poor maternal nutrition may affect:

Early neural development.
Later biological vulnerability.
Regulation of bodily systems.

These are developmental biological factors rather than inherited genes.

Season of birth

A statistical association with season of birth may reflect environmental influences acting during development.

However, season of birth is only a correlate.

It does not identify one precise causal mechanism.

Caution with biological correlates

A correlate is a factor associated with a condition.

It is not automatically:

A cause.
Present in every person.
Unique to anorexia nervosa.
Sufficient to produce the condition.

Genetic and neural explanations can be connected

Genes may influence neural systems.

A possible pathway is:

genetic variants → altered neurotransmitter or neural-circuit functioning → increased biological vulnerability → environmental and psychological factors influence whether anorexia nervosa develops

This provides a more integrated biological explanation.

For example:

A serotonin-related gene could affect serotonergic signalling.
Several genes could influence neural development.
Genetic differences could alter sensitivity to internal bodily signals.

The candidate genes should not be described as directly creating restrictive behaviour.

Biological vulnerability and symptom maintenance

Biological factors may contribute at different stages.

Predisposing factors

Present before the condition begins:

Genetic vulnerability.
Developmental neural differences.
Prenatal biological risks.

Precipitating factors

Contribute to onset:

Environmental pressure.
Stress.
Dieting.
Social or cognitive influences.

Maintaining factors

Help the pattern continue:

Changes in neurotransmitters.
Reduced body fat.
Low leptin.
Altered reward or internal bodily processing.
Effects of prolonged undernutrition.

This distinction helps solve the false choice between:

“The biological difference caused anorexia nervosa.”

and:

“The biological difference was only a consequence.”

It may have different roles at different stages.

A biological feedback cycle

A possible cycle is:

The person has a biological vulnerability.
Psychological or environmental factors encourage restriction.
Restricted intake alters hormones and neurotransmitter functioning.
Neural changes affect mood, cognition or eating regulation.
Restriction becomes harder to stop.
Further biological disruption occurs.

This is more interactionist than a one-way biological explanation.

Applying neural explanations

Scenario 1: low serotonin marker

Researchers find lower urinary 5-HIAA among a group of people currently experiencing anorexia nervosa.

A neural explanation would state:

5-HIAA is a serotonin metabolite.
Lower levels may indicate reduced serotonin activity.
This supports serotonergic involvement.
It does not establish cause because current food restriction may have altered serotonin metabolism.

Scenario 2: inconsistent dopamine evidence

One study reports increased dopamine activity, while another finds no difference from controls.

The correct conclusion is:

Dopamine may be involved.
The evidence is inconsistent.
A single direction of dopamine abnormality cannot be assumed.
Differences in participants, measurement or stage of recovery may explain the results.

Scenario 3: medication appears helpful

Elliot’s doctor prescribes medication, and his difficulties appear to improve.

AQA’s June 2023 mark scheme accepts this as application suggesting that the condition may have a neurochemical or biological component.

However:

Improvement supports biological involvement.
It does not prove the original cause.
A treatment may alter a maintaining process without removing every cause.

Scenario 4: disrupted hunger signals

Following substantial weight loss, a person has very low leptin but continues to restrict food.

A biological explanation might propose:

Reduced body fat has lowered leptin.
The hormone change indicates disrupted energy regulation.
Continuing restriction despite this hunger-related pressure shows that cognitive and social factors may override biological signals.
Low leptin may be a consequence rather than an initial cause.

Scenario 5: insula functioning

A brain-imaging study finds unusual activity in the insula when participants process food-related stimuli.

A neural explanation would suggest:

The insula contributes to processing taste and internal bodily information.
Dysfunctional activity may affect the experience of hunger, satiety or food.
The finding is correlational unless neural activity was measured before the condition developed.

Evaluating biological explanations

Strength: familial patterns support genetic vulnerability

Anorexia nervosa occurs more frequently among some biological relatives.

Twin and family studies provide evidence consistent with inherited risk.

This supports the genetic explanation because:

Biological relatives share genes.
MZ twins are more genetically similar than DZ twins.
Greater similarity among MZ twins is predicted by inheritance.

AQA identifies twin and family research as central evidence for biological explanations.

Limitation: shared environment

Family and twin similarities may arise from shared experiences.

Relatives may be exposed to similar:

Attitudes towards weight.
Meal patterns.
Parental modelling.
Family control.
Cultural expectations.

Familial clustering therefore does not separate nature from nurture automatically.

Strength: incomplete concordance supports an interactionist account

MZ concordance below 100% shows that genetic similarity does not produce identical outcomes.

This suggests:

genes create vulnerability, while environmental and psychological factors influence expression

The finding weakens hard genetic determinism while preserving a genetic contribution.

Limitation: candidate-gene effects are small

A complex condition is unlikely to be explained by one candidate gene.

Associations involving OPRD1, HTR1D or EPHX2 may:

Contribute only a small amount of risk.
Apply to some participants but not others.
Depend on other genes.
Depend on environmental conditions.

A polygenic model is therefore more appropriate than a single-gene account.

Strength: biological measurements can be objective

Researchers can measure:

Genetic variants.
Urinary 5-HIAA.
HVA.
Receptor activity.
Hormone concentrations.
Brain activity.

These produce quantitative data and may improve:

Objectivity.
Reliability.
Replication.
Scientific credibility.

The June 2023 mark scheme notes that biological explanations often use more traditionally objective methods than some family-based accounts.

Counterpoint

Objective measurement does not guarantee valid interpretation.

A highly reliable measurement of low leptin may still fail to show whether low leptin:

Caused restriction.
Resulted from weight loss.
Maintains the condition.
Reflects another factor.

Major limitation: cause and effect

This is one of the most important evaluation points.

People with anorexia nervosa may experience:

Restricted nutrition.
Substantial loss of body fat.
Physiological stress.
Hormonal changes.
Changes in brain chemistry.

Therefore:

observed biology may be a consequence rather than a cause

AQA’s 2020 and 2023 mark schemes explicitly recognise that altered neurotransmitter levels might be an effect of the condition.

Example: serotonin

Low serotonin activity could:

Contribute to vulnerability.
Result from inadequate dietary intake.
Be strengthened by continuing restriction.

Example: leptin

Low leptin may follow from low body-fat stores.

Example: neural circuitry

Altered brain activity may reflect:

A pre-existing difference.
The effects of undernutrition.
Medication.
A continuing adaptation.

Using recovered participants

Researchers may examine people after weight restoration or recovery.

Possible strength

If a biological difference remains, it is less easily explained as an immediate effect of current starvation.

Limitation

Recovery does not recreate the person’s brain and body exactly as they were before the condition.

A persistent difference could be:

A pre-existing vulnerability.
A lasting effect.
A scar of the condition.
A treatment effect.

Prospective longitudinal evidence is stronger for identifying vulnerability before onset.

Strength: treatment implications

Biological explanations suggest biological interventions, including medication targeting relevant neurochemical systems.

If medication produces improvement, this supports the idea that neural processes are involved.

In the June 2023 Elliot scenario, improvement following medication was accepted as application of a biological explanation.

Treatment does not prove cause

A treatment can alter a symptom without identifying its original cause.

For example:

Pain relief reduces a headache without explaining why it began.
Medication may alter neurotransmission without showing that neurotransmitter dysfunction initiated the condition.

Treatment evidence supports involvement more strongly than original causation.

Limitation: inconsistent dopamine evidence

AQA’s mark schemes explicitly state that dopamine findings are controversial.

Studies have reported:

Higher activity.
Lower activity.
No difference.

This inconsistency challenges a simple neural account.

It may indicate:

Different biological subtypes.
Measurement differences.
Changes across illness and recovery.
Medication effects.
Small or unrepresentative samples.

The correct conclusion is not that dopamine is irrelevant, but that its role is not straightforward.

Limitation: biological reductionism

Biological explanations may reduce anorexia nervosa to:

Genes.
Receptors.
Neurotransmitters.
Hormones.
Brain circuits.

This is valuable because individual mechanisms can be measured scientifically.

However, anorexia nervosa occurs within a social and psychological context involving:

Family relationships.
Media.
Cultural ideals.
Modelling.
Beliefs.
Perceptual distortions.
The need for control.

The June 2024 mark scheme directly accepted reductionism as a limitation of neural explanations because cells and chemicals cannot fully represent the wider social context of eating behaviour.

This connects with levels of explanation and biological reductionism [Holism and reductionism].

Limitation: biological determinism

A strongly biological explanation can imply:

Genes and brain chemistry determine restrictive eating.

This may lead people to believe that:

Change is impossible.
Treatment will be ineffective.
They have no role in recovery.
Psychological support is pointless.

AQA’s June 2024 mark scheme identifies this fatalistic implication as a limitation of neural explanations.

A more balanced position is soft determinism:

Biology influences vulnerability, but environment, cognition and treatment can affect outcomes.

This connects with biological determinism and behavioural change [Free will and determinism].

Strength: biological explanations may reduce personal blame

A biological explanation can show that anorexia nervosa is not simply:

A choice.
Attention-seeking.
Vanity.
A failure of willpower.

Recognising biological vulnerability may:

Reduce moral judgement.
Increase compassion.
Encourage scientific treatment.
Reduce blame directed at the individual or family.

Possible ethical cost

Genetic explanations can also create:

Fatalism.
Genetic stigma.
Fear among relatives.
Assumptions that a person is permanently biologically abnormal.

Biological evidence must be communicated probabilistically.

Limitation: temporal changes are difficult to explain biologically

AQA’s 2024 mark scheme accepts difficulty explaining rising rates of anorexia nervosa as a limitation of neural explanations.

Human genes and basic brain structures do not change rapidly across a few generations.

Changes over time may be better explained by:

Media exposure.
Cultural ideals.
Social learning.
Changes in family or social environments.

Counterargument

A stable biological vulnerability can interact with a changing environment.

For example:

genetic vulnerability remains relatively stable while environmental pressure increases

Biological and social explanations can therefore be complementary.

Limitation: gender and cultural patterns

An exclusively biological account may struggle to explain why diagnosis or incidence varies between:

Gender groups.
Cultures.
Historical periods.

AQA’s 2020 and 2023 mark schemes identify the ability to explain gender, cultural and temporal patterns as a useful basis for comparing explanations.

Social learning and cognitive explanations may account more directly for:

Exposure to particular body ideals.
Differential reinforcement.
Culturally specific beliefs.

Biological vulnerability may still affect who is most susceptible within those environments.

Comparison with family systems theory

Biological explanations and family interaction, enmeshment and autonomy [Family systems theory and anorexia nervosa] differ in several important ways.

Biological explanations	Family systems theory
Emphasise genes and neural functioning	Emphasises family interaction
Family contributes passively through inherited DNA	Family contributes actively through behaviour
Focus on neurotransmitters and neural circuits	Focus on control, enmeshment and autonomy
Suggest biological treatment implications	Suggest family-therapy implications
Mainly nature-based	Mainly nurture-based
Biologically deterministic if presented strongly	Environmentally deterministic if presented strongly
Often use quantitative biological measures	May use interviews, observations or case material

AQA’s November 2020 question directly required students to compare biological explanations with family systems theory and allocated ten of the sixteen marks to comparison and discussion.

Family blame versus biological blame

Family systems theory may risk blaming relatives.

Biological explanations may reduce this form of blame but create:

Genetic stigma.
Biological fatalism.
Concern that relatives carry “faulty” genes.

Neither account is ethically neutral.

Comparison with social learning theory

Biological explanations propose inherited and neural vulnerability.

Modelling, reinforcement and media influences [Social learning theory and anorexia nervosa] propose that behaviour and attitudes are learned from the environment.

Biological	Social learning
Genes and neural mechanisms	Observation and reinforcement
Nature	Nurture
Vulnerability may precede experience	Preferences and behaviour acquired through experience
Biological treatment implications	Modelling and media-related interventions
Explains familial similarity through DNA	Explains familial similarity through observation

Family similarity could support either explanation unless researchers separate genetic and environmental influences.

Comparison with cognitive explanations

Biological explanations focus on mechanisms such as serotonin and insula circuitry.

Cognitive distortions and irrational beliefs [Cognitive explanations of anorexia nervosa] focus on:

Distorted body perception.
Weight-related schemas.
Faulty beliefs.
Biased information processing.

The explanations may interact.

For example:

biological vulnerability affects neural processing → cognitive distortions become more likely → restrictive behaviour follows → starvation produces further biological changes

This feedback model is more complete than treating cognition and biology as mutually exclusive.

Multifactorial explanation

AQA mark schemes repeatedly recognise the multifactorial nature of anorexia nervosa as an important discussion point.

A multifactorial account may include:

Polygenic vulnerability.
Neural functioning.
Family systems.
Social modelling.
Media.
Cognitive distortions.
Cultural context.

The person’s pathway may therefore be:

biological predisposition + psychological vulnerability + environmental pressure → development and maintenance of anorexia nervosa

Research methods in genetic explanations

Twin studies

Strengths:

Compare people with different levels of genetic similarity.
Produce concordance data.
Allow naturally occurring genetic relationships to be studied.

Limitations:

No random allocation.
MZ and DZ environments may differ.
Small samples may be necessary.
Diagnosis may not be identical across studies.

Family studies

Strengths:

Identify familial clustering.
Can include several degrees of relatedness.
May use large medical records.

Limitations:

Shared environment.
Retrospective reporting.
Selective knowledge of family history.
Diagnosis may have changed over time.

Genome studies

Strengths:

Examine many genetic variants.
Fit a polygenic account.
Can use large samples.

Limitations:

Individual effects may be extremely small.
Population differences can affect results.
Statistical association does not reveal the psychological mechanism.

Research methods in neural explanations

Biochemical measures

Researchers may examine:

5-HIAA.
HVA.
Leptin.
Other neurotransmitter or hormonal markers.

Strengths:

Quantitative.
Objective.
Replicable.

Limitations:

May be indirect measures.
Values are affected by food intake and body weight.
One sample may not represent long-term activity.

Brain imaging

Researchers may examine activity or circuitry involving the insula.

Strengths:

Provides information about functioning in the living brain.
Allows comparison during food-related tasks.
Can identify regional patterns.

Limitations:

Usually correlational.
Neural differences may be effects of undernutrition.
Tasks in a scanner may not represent ordinary eating.
Small samples may limit generalisation.

Longitudinal research

A longitudinal study follows people over time.

Ideally, researchers would measure biological vulnerability before anorexia nervosa develops.

Strength:

Helps establish temporal order.

Limitation:

Very large samples may be required because relatively few participants develop the condition.
Repeated biological assessment is expensive.
Participants may withdraw.

Applying biological explanations to Elliot

The June 2023 AQA paper described Elliot as very underweight, experiencing distorted beliefs about his size, repeatedly arranging food, having a mother with previous eating difficulties and showing improvement with medication.

A biological application could state:

Elliot’s mother’s history indicates familial linkage and possible inherited genetic vulnerability.
Anorexia nervosa is likely to be polygenic rather than controlled by one gene.
Improvement following medication is consistent with neurochemical involvement.
Biological application should not ignore that his mother is also a model and part of his environment.
His distorted body perception is more directly explained by cognitive theory.
His mother’s control could be explained through family systems theory.

A high-level answer would therefore recognise that several details support several explanations.

Structuring an application paragraph

Use:

scenario evidence → biological mechanism → cautious conclusion → alternative possibility

Example:

“Mia’s biological sister previously experienced anorexia nervosa, suggesting familial genetic vulnerability. As close biological relatives share DNA, Mia may have inherited some of the polygenic risk associated with the condition. However, the similarity could also reflect shared family attitudes and modelling, so the family link does not prove genetic causation.”

Structuring a two-mark limitation

The June 2024 paper asked:

Outline one limitation of neural explanations for anorexia nervosa.

A full two-mark response needs:

A clear limitation.
An explanation linked specifically to neural accounts.

Model response

“Neural explanations are biologically reductionist because they explain anorexia nervosa through cells, neurotransmitters and brain circuits. This overlooks social and cognitive influences such as media ideals and distorted body beliefs, so neural activity cannot provide a complete explanation.”

Alternative full responses could use:

Biological determinism and fatalism.
Inability to explain rapid historical change.
Contradictory neural evidence.

Structuring an eight-mark evaluation

Paragraph 1: genetic evidence

Family or twin studies.
Higher concordance among closer relatives.
Shared-environment limitation.

Paragraph 2: neural evidence

Reduced serotonin or 5-HIAA.
Dopamine findings.
Objective measurements.
Inconsistency or causality.

Paragraph 3: consequence of starvation

Low leptin and neural changes.
Cause-and-effect problem.
Recovered or longitudinal participants.

Paragraph 4: broader explanation

Reductionism.
Psychological and cultural influences.
Multifactorial conclusion.

Structuring a 16-mark essay

Paragraph 1: biological overview

Genetic and neural explanations.
Vulnerability rather than inevitability.

Paragraph 2: genetic transmission

Familial link.
Twin and family studies.
Concordance.

Paragraph 3: polygenic inheritance

Many genes.
Candidate genes.
OPRD1, HTR1D and EPHX2.

Paragraph 4: serotonin

Reduced activity.
Low urinary 5-HIAA.
Possible contribution.

Paragraph 5: dopamine and other neural factors

Conflicting dopamine evidence.
HVA.
D2 activity.
Noradrenaline and GABA.

Paragraph 6: leptin and insula

Low leptin.
Stored body fat.
Insula circuitry.
Cause versus consequence.

Paragraph 7: evidence evaluation

Twin and family evidence.
Objective measures.
Shared environments.
Correlation.

Paragraph 8: broader discussion

Reductionism.
Determinism.
Gender, culture and temporal change.
Psychological alternatives.
Multifactorial conclusion.

Overall conclusion

Biological explanations propose that anorexia nervosa involves inherited and neural vulnerability.

Genetic explanations are supported by:

Familial clustering.
Twin and family studies.
Polygenic inheritance.
Candidate genes such as OPRD1, HTR1D and EPHX2.

Neural explanations involve:

Reduced serotonin activity and low 5-HIAA.
Controversial findings involving dopamine.
Possible roles for noradrenaline and GABA.
Low leptin.
Dysfunctional insula circuitry.
Other developmental biological correlates.

These explanations have scientific value because genes, hormones and neural activity can be measured objectively. They may also reduce the inaccurate idea that anorexia nervosa is simply a voluntary choice.

However, biological findings are difficult to interpret because restriction and weight loss themselves alter the body and brain. Genetic concordance is incomplete, dopamine findings conflict and biology alone struggles to explain cultural and historical variation.

The strongest conclusion is:

Biological factors create or maintain vulnerability, but anorexia nervosa is most convincingly understood through interaction among genetic, neural, cognitive, family and wider social influences.

Key Words 🔑

Key word	Student-friendly definition	How it may be used in an exam
Biological explanation	Account explaining behaviour through genes, brain activity or bodily processes	Introduce the approach
Genetic explanation	Account proposing that inherited DNA contributes to vulnerability	Explain family patterns
Genetic transmission	Passing genetic material from biological parents to children	Explain familial linkage
Genotype	Person’s genetic makeup	Distinguish genes from observed behaviour
Phenotype	Observable outcome produced by genes and environment	Explain interaction
Heredity	Biological transmission of characteristics	Link anorexia nervosa with family risk
Heritability	Population estimate of variation associated with genetic differences	Evaluate genetic influence
Predisposition	Increased vulnerability rather than certainty	Avoid deterministic claims
Genetic loading	Amount of inherited genetic risk	Explain individual differences
Family study	Investigation comparing rates among biological relatives	Evaluate genetic evidence
Twin study	Investigation comparing similarity among MZ and DZ twins	Explain genetic research
Monozygotic twins	Identical twins sharing almost all their genetic material	Apply concordance evidence
MZ twins	Abbreviation for monozygotic twins	Use specialist terminology
Dizygotic twins	Non-identical twins sharing about half their variable genes	Compare with MZ twins
DZ twins	Abbreviation for dizygotic twins	Use specialist terminology
Concordance rate	Percentage of twin pairs in which both show a characteristic	Interpret twin evidence
Equal-environments problem	MZ twins may share more similar experiences than DZ twins	Evaluate twin studies
Polygenic	Influenced by many genes	Explain complex inheritance
Candidate gene	Gene investigated as a possible contributor to vulnerability	Explain OPRD1, HTR1D or EPHX2
Risk allele	Gene variant associated with increased susceptibility	Explain probabilistic risk
Genome research	Research examining genetic variation across the genome	Explain polygenic evidence
Gene-environment interaction	Genetic effects depending partly on environmental experience	Reach an interactionist conclusion
Neural explanation	Account based on neurotransmitters, brain regions or circuits	Introduce brain-based explanations
Neuron	Cell transmitting electrical and chemical information	Explain neural processing
Neurotransmitter	Chemical messenger released between neurons	Explain serotonin or dopamine
Serotonin	Neurotransmitter whose altered activity has been linked with anorexia nervosa	Explain neural vulnerability
5-HIAA	Breakdown product used as an indirect indicator of serotonin activity	Interpret biochemical evidence
Dopamine	Neurotransmitter with a controversial association with anorexia nervosa	Explain conflicting evidence
Homovanillic acid	Dopamine breakdown product used as an indirect biological measure	Explain HVA findings
HVA	Abbreviation for homovanillic acid	Use specialist terminology
D2 receptor	Type of dopamine receptor investigated in neural research	Explain recovered-participant findings
Noradrenaline	Neurotransmitter accepted as another possible biological factor	Demonstrate breadth
GABA	Neurotransmitter accepted as another possible neural factor	Demonstrate breadth
Leptin	Hormone from fat cells providing information about stored energy	Explain hormonal correlates
Adipose tissue	Body-fat tissue producing leptin	Explain source of leptin
Insula	Brain region involved in processing internal bodily and sensory information	Explain neural circuitry
Neural circuitry	Connected network of brain regions	Avoid one-centre explanations
Biological correlate	Biological feature associated with a condition	Distinguish correlation from cause
Cause and effect	Whether one factor directly produces another	Evaluate neural evidence
Reverse causality	Possibility that the condition produces the biological difference	Evaluate starvation effects
Longitudinal study	Research following participants over time	Explain how temporal order may be tested
Objective measure	Measurement involving limited personal judgement	Evaluate biological methods
Biological reductionism	Explaining a complex condition through biological components	Evaluate neural accounts
Biological determinism	View that biology controls behaviour	Discuss fatalism
Familial linkage	Condition occurring more frequently among relatives	Apply family history
Multifactorial explanation	Account involving several biological and psychological influences	Reach a balanced conclusion
Interactionism	View that biological and environmental factors work together	Evaluate the overall approach

Hints from the Examiner Reports 💡

Examiner hint: Learn both required biological categories.

The specification requires:

Genetic explanations.
Neural explanations.

An answer describing only family history will not cover the full biological approach.

Examiner hint: Do not write that there is one anorexia gene.

AQA accepts:

Polygenic inheritance.
Genome research.
Candidate genes such as OPRD1, HTR1D and EPHX2.

Examiner hint: Explain family history cautiously.

Use:

“This suggests inherited vulnerability.”

Do not use:

“The mother passed anorexia nervosa directly to the child.”

Examiner hint: Serotonin and dopamine must not be treated as interchangeable.

AQA accepts reduced serotonin activity, including low 5-HIAA, but describes dopamine evidence as controversial and inconsistent.

Examiner hint: Avoid inventing one definitive dopamine direction.

The mark scheme permits evidence involving:

Increased dopamine.
Decreased dopamine.
No difference.

A strong answer uses this inconsistency as evaluation.

Examiner hint: Cause and effect is essential.

Altered neurotransmitters, leptin or brain activity may result from:

Food restriction.
Low body weight.
Treatment.

Do not assume that every measured biological difference existed before the condition.

Examiner hint: AQA directly assessed reductionism in June 2024.

A complete limitation should explain that neural accounts focus on cells and chemicals while overlooking social and cognitive influences.

Examiner hint: Name the consequence of determinism.

Do not stop at:

“The explanation is deterministic.”

Explain that a person may feel change is impossible, reducing hope or expectations of successful treatment.

Examiner hint: Apply each scenario clue to the most suitable explanation.

In the 2023 Elliot question:

His mother’s history supported familial or genetic vulnerability.
Medication appearing to help supported neurochemical involvement.
His distorted body perception supported a cognitive explanation.
His mother’s controlling behaviour supported family systems theory.

Examiner hint: Treatment effectiveness is not proof of original causation.

Why this is incomplete:

Genes can influence neural functioning.

How to improve:

Explain a genetic-to-neural vulnerability pathway.

Exam-Style Questions ✍️

Questions

1. What is meant by a genetic predisposition?[2 marks]

2. Explain what psychologists mean when they describe anorexia nervosa as polygenic.[3 marks]

3. Explain how twin studies may be used to investigate genetic explanations of anorexia nervosa.[4 marks]

4. Name two candidate genes that have been associated with anorexia nervosa.[2 marks]

5. Explain one limitation of family studies investigating anorexia nervosa.[3 marks]

6. Explain one neural explanation of anorexia nervosa involving serotonin.[4 marks]

7. Explain why dopamine evidence does not provide a simple explanation of anorexia nervosa.[4 marks]

8. Explain how leptin may be associated with anorexia nervosa.[4 marks]

9. Explain one way in which the insula may be involved in anorexia nervosa.[4 marks]

10. Outline one limitation of neural explanations for anorexia nervosa.[2 marks]

11. Hana’s identical twin has anorexia nervosa, but Hana does not.

Explain what this suggests about genetic explanations.[4 marks]

12. Researchers find that people currently experiencing anorexia nervosa have lower mean urinary 5-HIAA than a control group.

Explain one conclusion and one limitation of this finding.[4 marks]

13. Researchers obtain the following hypothetical concordance rates:

Twin type	Concordance
MZ twins	48%
DZ twins	18%

a) Calculate the difference in concordance rates.[1 mark]

b) Calculate how many times greater MZ concordance is than DZ concordance. Give your answer to two decimal places.[2 marks]

c) Explain one conclusion and one limitation of the results.[4 marks]

14. Elliot is very underweight. His mother previously experienced eating difficulties, and medication appears to improve some of Elliot’s difficulties.

Explain Elliot’s situation using biological explanations.[6 marks]

15. Explain one strength and one limitation of genetic explanations of anorexia nervosa.[6 marks]

16. Evaluate neural explanations of anorexia nervosa.[8 marks]

17. Compare biological explanations with family systems theory as explanations of anorexia nervosa.[16 marks]

18. Discuss biological explanations of anorexia nervosa. Refer to the following scenario in your answer.

Freya’s biological mother and aunt have both experienced anorexia nervosa. Freya severely restricts her food intake and has very low body-fat stores. Tests show low leptin and reduced urinary 5-HIAA. A brain scan also shows unusual activity in the insula.

[16 marks]

Answers and Mark Scheme

Question 1

Award up to two marks:

A genetic predisposition is an inherited vulnerability or susceptibility.
It increases the likelihood of anorexia nervosa but does not guarantee that the condition will develop.

Question 2

Award up to three marks:

Polygenic means influenced by many genes.
Each genetic variant may make a relatively small contribution.
Different combinations produce different levels of vulnerability.
Environmental and psychological influences affect whether the vulnerability is expressed.

Question 3

Award up to four marks:

Researchers compare concordance among MZ and DZ twins.
MZ twins share more genetic material than DZ twins.
A genetic explanation predicts higher MZ concordance.
Higher MZ concordance would support inherited vulnerability.
Concordance below 100% would show that non-genetic factors also matter.

Question 4

Award one mark for each valid candidate gene, up to two marks:

OPRD1.
HTR1D.
EPHX2.

Question 5

Award up to three marks:

Biological relatives share environments as well as genes.
They may share food practices, modelling, family interaction or cultural attitudes.
Familial similarity therefore cannot be attributed confidently to genetic transmission alone.

Question 6

Award up to four marks:

Serotonin is a neurotransmitter.
Reduced serotonin activity has been associated with anorexia nervosa.
Lower urinary levels of the serotonin metabolite 5-HIAA provide supporting evidence.
Atypical serotonergic activity may contribute to vulnerability or maintaining processes.
The evidence does not establish whether reduced activity is a cause or an effect of restriction.

Question 7

Award up to four marks:

Dopamine has been associated with anorexia nervosa.
Some studies report higher activity.
Others report lower activity or no difference from controls.
Evidence includes HVA and D2-receptor findings.
Inconsistent results prevent a simple claim that one particular dopamine level causes anorexia nervosa.

Question 8

Award up to four marks:

Leptin is produced by fat cells.
It provides the brain with information about stored energy.
People with anorexia nervosa may have low leptin because body-fat stores are low.
This may disrupt normal appetite regulation.
Low leptin may be a consequence of weight loss rather than the original cause.

Question 9

Award up to four marks:

The insula is involved in processing internal bodily and sensory information.
This includes food-related, taste, hunger or satiety signals.
Dysfunctional insula circuitry may alter how such information is experienced or interpreted.
This may contribute to abnormal eating behaviour.
The finding is correlational unless the difference existed before onset.

Question 10

Award up to two marks for one clear and developed limitation.

Possible answer:

Neural explanations are biologically reductionist because they explain anorexia nervosa through cells, chemicals and brain circuits.
This overlooks cognitive, family, social and cultural influences, so the neural account is incomplete.

Alternative limitations include:

Biological determinism and fatalism.
Contradictory neural evidence.
Difficulty explaining historical increases.
Cause-and-effect problems.

This reflects the June 2024 mark scheme.

Question 11

Award up to four marks:

Identical twins share almost all their genetic material.
Hana may therefore share considerable genetic vulnerability with her twin.
Different outcomes show that genes are not sufficient.
Different environmental, developmental or cognitive experiences may affect expression.
The finding supports an interactionist rather than fully deterministic genetic account.

Question 12

Award up to four marks.

Possible conclusion:

Lower 5-HIAA is consistent with reduced serotonin activity.
This supports serotonin involvement in anorexia nervosa.

Possible limitation:

The participants are currently experiencing the condition.
Restricted eating or undernutrition may have reduced serotonin metabolism.
The study therefore cannot show that low serotonin caused the condition.
Urinary 5-HIAA is also an indirect measure of brain activity.

Question 13a

48−18=30

The difference is 30 percentage points.

Question 13b

1848=2.666…

MZ concordance is 2.67 times the DZ concordance rate.

Question 13c

Award up to four marks.

Possible conclusion:

MZ twins have substantially higher concordance.
This supports a genetic contribution because MZ twins share more genetic material.

Possible limitation:

MZ twins may share more similar environments.
The figures provide no sample size or inferential test.
Concordance is below 100%, so genes do not provide a complete explanation.
Diagnosis or sampling procedures are not described.

Question 14

Award up to six marks:

Elliot’s mother’s eating history indicates familial linkage.
Elliot may have inherited some genetic vulnerability.
The vulnerability is likely to be polygenic rather than caused by one gene.
Shared environment and modelling could also explain similarity with his mother.
Medication improvement suggests that neurochemical processes may be involved.
Medication effectiveness supports biological involvement but does not prove that neural abnormality originally caused the condition.

This application is consistent with AQA’s June 2023 mark scheme.

Question 15

Award up to three marks for a developed strength and three marks for a developed limitation.

Possible strength:

Twin and family studies show that anorexia nervosa clusters among biological relatives. Higher concordance among more genetically similar twins is consistent with inherited vulnerability.

Possible limitation:

Relatives share environmental experiences as well as genes. Similar food attitudes, modelling and family relationships may produce familial similarity, so genetic causation cannot be isolated confidently.

Alternative creditworthy points include:

Polygenic genome research.
Objective genetic measures.
Incomplete concordance.
Small candidate-gene effects.
Genetic determinism.
Gene-environment interaction.

Question 16

A strong answer should include:

Evidence of reduced serotonin activity.
Low urinary 5-HIAA.
Objective biological measurement.
Problems using peripheral measures to represent brain activity.
Dopamine evidence involving HVA or D2 receptors.
Inconsistent dopamine findings.
Possible roles of noradrenaline and GABA.
Low leptin.
Low leptin as a likely consequence of low body fat.
Dysfunctional insula circuitry.
Neuroimaging evidence being correlational.
Neural abnormalities potentially being consequences of undernutrition.
Biological reductionism.
Biological determinism and fatalism.
Difficulty explaining cultural or historical change.
Treatment implications.
Psychological and social alternatives.
A multifactorial conclusion.

Question 17

A strong response should include:

Biological explanations

Genetic transmission.
Family and twin studies.
Concordance rates.
Polygenic inheritance.
Candidate genes.
Serotonin and 5-HIAA.
Dopamine and conflicting findings.
Leptin.
Insula circuitry.

Family systems theory

Enmeshment.
Overprotectiveness.
Rigidity.
Conflict avoidance.
Lack of autonomy.
Restriction as a means of exerting control.

Direct comparisons

Biological explanations implicate family passively through inherited DNA, whereas family systems theory gives family behaviour an active role.
Biological explanations emphasise nature, whereas family systems theory emphasises nurture.
Biological accounts are biologically deterministic, whereas family systems theory may be environmentally deterministic.
Biological explanations suggest medication, whereas family systems theory suggests family intervention.
Family systems theory may explain social and gender patterns more directly.
Biological explanations may use objective measures, whereas family accounts may rely more on observation or case material.
Neither establishes causality confidently.
Neural differences may follow starvation, while family dysfunction may develop in response to the condition.
Family systems theory risks parental blame.
Genetic accounts may create fatalism or genetic stigma.
Both are reductionist when presented alone.
A multifactorial interactionist account is more complete.

The November 2020 question allocated six marks to knowledge and ten marks to comparison and discussion.

Question 18

A strong response should include:

Knowledge and understanding

Biological explanations.
Genetic transmission.
Family studies.
Polygenic inheritance.
Candidate genes.
Neural explanations.
Serotonin.
5-HIAA.
Leptin.
Insula circuitry.
Cause-and-effect concerns.

Application

Freya’s biological mother and aunt provide evidence of familial linkage.
She may have inherited polygenic vulnerability.
Family history does not prove causation because relatives may share environments.
Her very low body-fat stores are associated with reduced leptin.
Low leptin may disrupt energy regulation.
It may also be a consequence of restricted intake and reduced fat stores.
Reduced 5-HIAA is consistent with reduced serotonin activity.
Current restriction may itself have affected serotonin metabolism.
Unusual insula activity may affect processing of taste or internal bodily signals.
The scan does not show whether the activity difference preceded the condition.

Evaluation

Familial patterns support inherited vulnerability.
Incomplete concordance indicates environmental influence.
Polygenic theory is more realistic than a single-gene account.
Candidate-gene effects may be small.
Biological measurements are objective and replicable.
Objective association does not establish cause.
Low leptin is particularly vulnerable to reverse-causality criticism.
Brain differences may result from undernutrition.
Recovered and longitudinal evidence would strengthen causal conclusions.
Neural findings may support biological treatment.
Treatment effectiveness would not prove original causation.
Biological accounts may reduce personal and family blame.
They may create fatalism or genetic stigma.
The explanation is biologically reductionist.
Cognitive, family and social-learning accounts explain influences biology omits.
A gene-environment and multifactorial explanation is most complete.

Higher-level responses will distinguish inherited vulnerability from certainty, explain neural mechanisms accurately and maintain the cause-versus-consequence issue throughout the discussion.