Genetic explanations of OCD | AQA A-Level Psychology Revision
Updated: Sep 9
For 7182 specification, first teach in September 2025
AQA A-Level Psychology | Free Revision Notes
Estimated study time: 45 minutes
These Genetic explanations of OCD A-Level Psychology revision notes explain how inherited biological differences may create a vulnerability to obsessive-compulsive disorder. OCD is not thought to result from one single gene. Instead, many candidate genes may influence neurotransmitter systems and increase risk. You will learn about polygenic inheritance, aetiological heterogeneity, family and twin evidence, and why possessing a genetic vulnerability does not make OCD inevitable. You will also evaluate genetic explanations using environmental influences, methodological limitations and the diathesis-stress model.
The AQA specification requires genetic and neural explanations as part of the biological approach to explaining OCD.
Learning Objectives 🎯
By the end of this revision page, you should be able to:
Explain how genes may contribute to OCD.
Explain the role of candidate genes.
Explain why OCD is described as polygenic.
Explain aetiological heterogeneity.
Explain the idea of genetic vulnerability.
Interpret evidence from family and twin studies.
Apply genetic explanations to unfamiliar scenarios.
Evaluate the strengths and limitations of genetic explanations.
Revision Notes 📚
Genetic explanations of OCD A-Level Psychology revision overview
A genetic explanation proposes that inherited variations in a person’s genetic material contribute to their likelihood of developing obsessive-compulsive disorder, usually shortened to OCD.
The explanation does not mean that a person directly inherits a complete disorder.
Instead, they may inherit:
Particular gene variants.
Differences in biological functioning.
A greater sensitivity to environmental stress.
A predisposition towards particular OCD symptoms.
The central idea is:
Genes may create a vulnerability to OCD, but environmental and psychological experiences help determine whether the disorder develops.
The biological approach
Genetic explanations are part of the biological approach.
This approach explains behaviour using factors such as:
Genes.
Neurotransmitters.
Brain structures.
Nervous-system functioning.
The general principles of inheritance are covered in genotype, phenotype and inherited influences.
Genetic and neural explanations are connected
Genes contain instructions that influence the development and functioning of biological systems.
Gene variants may affect:
The production of proteins.
Neurotransmitter transport.
Receptor functioning.
Enzyme activity.
The development of brain circuits.
Genetic explanations therefore overlap with the role of neurotransmitters and brain structures.
However, the explanations should remain distinct in an examination:
A genetic explanation focuses on inherited variation.
A neural explanation focuses on neurotransmitters and brain circuits.
A strong genetic answer links neural functioning back to genes rather than describing neurotransmitters alone.
Genes and inherited information
What is a gene?
A gene is a section of deoxyribonucleic acid, usually shortened to DNA, that contains instructions contributing to biological development and functioning.
Genes influence the production of proteins involved in processes such as:
Neurotransmitter transport.
Receptor activity.
Enzyme production.
Brain development.
People inherit genetic material from both biological parents.
Gene variants
Genes can exist in different forms or variants.
A particular variant may slightly alter:
How much of a protein is produced.
How efficiently a protein functions.
The way a neurotransmitter is transported.
The sensitivity of a receptor.
The activity of an enzyme.
A gene variant does not normally act as an on-and-off switch for OCD.
Its influence is usually probabilistic.
Genotype and phenotype
A person’s genotype is their inherited genetic information.
Their phenotype is the observable outcome produced by an interaction between:
Genotype.
Environment.
For OCD, the phenotype may include the obsessions, compulsions and associated emotions.
Two people with a similar genetic vulnerability may display different outcomes because their environments and experiences differ.
Genetic vulnerability
What is genetic vulnerability?
A genetic vulnerability is an inherited predisposition that increases the probability of developing a condition.
It does not make the condition inevitable.
A person may inherit gene variants linked with OCD but never develop significant symptoms.
Another person may possess the vulnerability and develop OCD following:
Trauma.
Prolonged stress.
Illness.
Major life change.
Other environmental difficulties.
Vulnerability compared with genetic certainty
Genetic vulnerability | Genetic certainty |
Increases probability | Guarantees an outcome |
Interacts with the environment | Operates independently of experience |
May never produce the disorder | Inevitably produces the disorder |
Allows individual differences | Predicts the same outcome for everyone |
Fits a diathesis-stress account | Fits strict genetic determinism |
The evidence supports vulnerability more strongly than certainty.
A predisposition may remain inactive
A genetic vulnerability may remain inactive unless combined with other risk factors.
For example:
A person inherits gene variants associated with OCD.
The person displays no clinically significant symptoms.
A stressful event occurs.
Biological and psychological responses are activated.
Obsessions or compulsions begin to develop.
Avoidance and rituals may maintain the symptoms.
The genes increase susceptibility but do not fully determine the outcome.
Why relatives may differ
Two siblings may inherit different combinations of gene variants.
They may also experience different:
Stressors.
Relationships.
Coping strategies.
Life events.
Learning experiences.
One sibling may develop OCD while the other does not.
This does not necessarily disprove genetic influence.
It shows that inheritance is probabilistic and complex.
Candidate genes
What is a candidate gene?
A candidate gene is a gene believed to contribute to the development of a particular characteristic or disorder.
Researchers identify genes that may be involved because they influence biological systems connected with OCD.
Several candidate genes have been investigated.
These include genes involved in the regulation of:
Serotonin.
Dopamine.
Neurotransmitter receptors.
Neurotransmitter transport.
Official AQA marking guidance identifies the SERT, COMT and 5-HT1D beta genes as examples that may be credited within a genetic explanation.
Candidate genes do not act alone
The term candidate means that a gene is considered a possible contributor.
It does not mean that researchers have identified one gene that:
Is present in everybody with OCD.
Produces the disorder by itself.
Predicts exactly which symptoms will develop.
Each candidate gene may make only a small contribution to overall vulnerability.
The SERT gene
What is the SERT gene?
The SERT gene provides instructions relating to the serotonin transporter.
A transporter helps move serotonin from the synapse back into the transmitting neuron.
Variations in the SERT gene may influence:
Serotonin transport.
Serotonin availability.
Communication between neurons.
Why serotonin is relevant
Serotonin is a neurotransmitter involved in several processes, including:
Mood.
Anxiety.
Behavioural control.
Information processing.
Some variants of the SERT gene may contribute to altered serotonin functioning, increasing vulnerability to OCD.
Genetic and neural connection
The complete argument should be:
A variant of the SERT gene may alter the functioning of the serotonin transporter, affecting serotonergic communication and increasing vulnerability to OCD.
A weaker explanation states only:
“OCD is caused by low serotonin.”
This is a neural claim rather than a developed genetic explanation.
It also treats a complex relationship too simply.
The COMT gene
What is the COMT gene?
The COMT gene provides instructions for producing an enzyme involved in the breakdown of dopamine.
Different variants may influence:
The activity of the enzyme.
The regulation of dopamine.
Communication within brain systems associated with behaviour and decision-making.
Possible relationship with OCD
A variant affecting COMT activity could contribute to atypical dopamine regulation.
This may influence vulnerability to:
Repetitive behaviour.
Difficulty controlling actions.
Particular compulsive symptoms.
The gene does not directly instruct a person to perform a compulsion.
Its possible influence occurs through biological processes.
The 5-HT1D beta gene
The 5-HT1D beta gene is involved in the functioning of a serotonin receptor.
Gene variants could influence how neurons respond to serotonin.
This provides another possible link between:
Inherited genetic variation.
Neurotransmitter functioning.
OCD vulnerability.
The existence of several possible candidate genes supports the view that OCD is genetically complex.
Polygenic inheritance
What does polygenic mean?
A condition is polygenic when many genes contribute to its development.
OCD is not explained by one single gene.
Instead, vulnerability may result from the combined influence of many genetic variants.
Taylor identified evidence suggesting that as many as 230 genes may be involved in OCD, supporting the conclusion that the disorder is polygenic. This example is included in official AQA marking guidance.
Combined genetic effects
Each gene may have a relatively small effect.
The overall vulnerability may depend on the combination inherited.
For example:
Person | Simplified inherited pattern | Possible outcome |
A | Few risk-associated variants | Lower genetic vulnerability |
B | Several risk-associated variants | Moderate genetic vulnerability |
C | Many interacting risk-associated variants | Higher genetic vulnerability |
This is a simplified illustration.
Researchers cannot calculate an individual’s exact OCD risk merely by counting a few genes.
Polygenic does not mean that every gene has the same effect
Different genes may influence different processes.
One may affect:
Serotonin transport.
Another may affect:
Dopamine regulation.
Another may affect:
Receptor sensitivity.
Another may influence:
Brain development.
The combined biological effect may increase vulnerability.
Why polygenic inheritance makes research difficult
When many genes are involved:
The effect of each gene may be small.
Different combinations may produce similar symptoms.
One gene may interact with several others.
Environmental factors may change the outcome.
Findings concerning individual genes may be difficult to reproduce consistently.
This makes a simple genetic test for OCD unlikely.
Aetiological heterogeneity
What is aetiology?
Aetiology means the cause or origin of a disorder.
What is aetiological heterogeneity?
Aetiological heterogeneity means that the same disorder may have different causes in different people.
For OCD, different individuals may possess different combinations of risk-associated genes.
Official AQA marking guidance identifies aetiological heterogeneity as a central feature of the genetic explanation.
Different genetic pathways
Person A’s vulnerability might involve gene variants mainly affecting:
Serotonin transport.
Person B’s vulnerability might involve variants affecting:
Dopamine regulation.
Person C’s vulnerability might involve:
Several neurotransmitter and developmental genes.
All three people might receive an OCD diagnosis, despite having different biological vulnerabilities.
Different symptom patterns
Different gene combinations may also contribute to different forms of OCD.
One person may mainly experience:
Contamination obsessions and washing compulsions.
Another may experience:
Doubts and repeated checking.
Another may experience:
Symmetry concerns and ordering rituals.
The diagnosis is the same, but:
The symptoms differ.
The biological pathways may differ.
The environmental triggers may differ.
Polygenic and heterogeneous are not identical
Polygenic | Aetiologically heterogeneous |
Many genes contribute to vulnerability | Different people may have different causes |
Concerns the number of genes involved | Concerns variation between individuals |
One person may inherit several relevant variants | Different people may inherit different combinations |
Explains genetic complexity | Explains why one explanation may not fit every case |
OCD may be both polygenic and aetiologically heterogeneous.
Family studies
What is a family study?
A family study investigates whether a disorder occurs more frequently among biological relatives of an affected person than within the wider population.
If OCD appears more often among close biological relatives, this is consistent with genetic influence.
Degree of genetic relatedness
Close relatives share more genes than distant relatives.
For example:
Biological parents and children share approximately 50% of their variable genetic material.
Full siblings share approximately 50% on average.
More distant relatives share less.
A genetic explanation predicts that OCD risk should generally increase with genetic relatedness.
Interpreting family evidence
Suppose researchers find that close relatives of people with OCD have an increased rate of the disorder.
This may support genetic influence because:
Relatives share inherited material.
Greater relatedness may be associated with greater similarity.
However, family members also share:
Environments.
Experiences.
Parenting.
Stressors.
Learned behaviour.
Attitudes towards anxiety and rituals.
Family evidence therefore cannot separate genes and environment completely.
Twin studies
Why twin studies are useful
Twin studies compare:
Monozygotic twins.
Dizygotic twins.
Monozygotic twins, usually shortened to MZ twins, develop from one fertilised egg and share virtually all their genes.
Dizygotic twins, usually shortened to DZ twins, develop from two fertilised eggs and share approximately 50% of their variable genetic material on average.
If OCD has a genetic component, concordance should be higher among MZ twins than DZ twins.
Concordance rates
What is concordance?
A concordance rate is the percentage of twin pairs in which both twins display a characteristic when at least one twin displays it.
For example:
A 70% concordance rate does not mean that each person has a 70% chance of developing OCD.
It means that both twins were affected in 70% of the relevant twin pairs.
Interpreting concordance
Pattern | Possible interpretation |
MZ concordance is higher than DZ concordance | Supports a genetic contribution |
MZ concordance is 100% | Could suggest extremely strong genetic determination |
MZ concordance is below 100% | Indicates non-genetic influences are also involved |
MZ and DZ rates are very similar | Weakens a simple genetic explanation |
Nestadt and colleagues
Nestadt and colleagues reported OCD concordance rates of approximately:
68% for MZ twins
32% for DZ twins
The substantially higher MZ rate supports a genetic contribution because MZ twins share more genes.
However, the MZ concordance rate was not 100%.
This suggests that genes alone are insufficient to explain every case.
What the study supports
The difference between 68% and 32% is consistent with genetic influence.
The MZ concordance rate is:
68%−32%=3668\% - 32\% = 3668%−32%=36
percentage points higher than the DZ rate.
This substantial difference supports inherited vulnerability.
What the study does not prove
The evidence does not prove that:
OCD is entirely inherited.
The identified genes directly cause the disorder.
Environmental factors are irrelevant.
Every person with the vulnerability will develop OCD.
The study demonstrates an association between genetic similarity and OCD similarity.
The equal-environments assumption
What is the assumption?
Twin studies often assume that MZ and DZ twin pairs experience equally similar environments.
This is known as the equal-environments assumption.
Why it matters
MZ twins may be treated more similarly because they:
Look more alike.
Are more often dressed alike.
Are confused for one another.
Spend more time together.
Receive similar expectations from others.
If MZ twins share more similar environments than DZ twins, their greater concordance may partly result from environment rather than genes.
Example
Suppose both MZ twins repeatedly observe and copy a parent’s checking rituals.
Their shared symptoms could reflect:
Shared genes.
Social learning.
Shared stress.
A combination of these factors.
The twin study alone cannot determine the exact contribution of each.
Genetic vulnerability and environmental stress
The diathesis-stress model
The diathesis-stress model proposes that psychological disorders develop through an interaction between:
A vulnerability.
Environmental stress.
A genetic predisposition is one possible diathesis.
Stress may involve:
Trauma.
Loss.
Illness.
Responsibility for another person’s safety.
Major change.
Prolonged anxiety.
The model can be represented as:
Genetic vulnerability + environmental stress → increased likelihood of OCD
Neither factor may be sufficient alone
A person may possess:
Genetic vulnerability without experiencing sufficient stress.
They may never develop OCD.
Another person may experience:
Significant stress without substantial genetic vulnerability.
They may experience distress but not develop OCD.
The disorder may be most likely when vulnerability and stress interact.
Example
Two people experience a frightening incident involving contamination.
Person A has a stronger inherited vulnerability affecting anxiety and serotonin regulation.
Person B has a lower vulnerability.
Person A may be more likely to develop persistent contamination obsessions and washing compulsions.
This remains a probability, not a certainty.
Trauma and OCD onset
AQA’s June 2022 mark scheme accepts evidence that many cases of OCD follow traumatic experiences as a challenge to a purely genetic explanation.
This suggests that:
Environmental events can trigger symptoms.
Genes may create sensitivity rather than direct causation.
A combined explanation may be more convincing.
Trauma does not disprove genes
A traumatic trigger does not mean that genetic factors played no role.
A trauma may have different effects depending on:
Inherited vulnerability.
Previous experiences.
Coping resources.
Social support.
Biological stress responses.
The evidence is therefore consistent with gene-environment interaction.
Why MZ concordance is not 100%
MZ twins share virtually all their genes.
If genes completely determined OCD, the disorder should occur in both twins whenever it occurs in one.
The lower concordance rate demonstrates the likely importance of:
Different experiences.
Different stressors.
Different relationships.
Illness.
Learning.
Random developmental processes.
Differences in gene expression.
This supports genetic vulnerability rather than strict genetic determinism.
Gene-environment interaction
What is gene-environment interaction?
A gene-environment interaction occurs when the effect of a genetic vulnerability depends on environmental conditions.
The environment may:
Trigger the vulnerability.
Strengthen or weaken symptoms.
Influence which symptoms develop.
Affect when symptoms begin.
Genes may affect exposure to environments
Genes and environments may also become correlated.
For example, a genetically influenced anxious temperament might make a person:
More alert to possible danger.
More likely to seek reassurance.
More likely to avoid uncertainty.
These behaviours could influence the environments they experience.
A simple division between “genetic” and “environmental” causes may therefore be misleading.
Applying genetic explanations to examples
Scenario 1: family history
Several of Mia’s close biological relatives have OCD.
Mia develops checking compulsions after a period of intense stress.
A genetic explanation would suggest that:
Mia may have inherited a vulnerability.
Several candidate genes may be involved.
Stress may have triggered the vulnerability.
The family history supports genetic risk but does not prove genetic causation.
Scenario 2: unaffected identical twin
One MZ twin develops OCD while the other does not.
This does not show that genes have no role.
It suggests that:
The twins share a genetic vulnerability.
Their environmental experiences may differ.
One twin may have experienced a relevant trigger.
Genetic influence is probabilistic rather than deterministic.
Scenario 3: no family history
Oscar develops OCD despite having no known family history of the disorder.
Possible interpretations include:
Relatives may possess vulnerability without showing symptoms.
Different gene combinations may be involved.
New genetic variation may contribute.
Environmental factors may be particularly important.
The disorder may have a different aetiology for Oscar.
A lack of diagnosed family history challenges a simple inherited explanation but does not eliminate every genetic influence.
Scenario 4: different symptoms within a family
A parent experiences contamination obsessions, while their child develops repeated checking.
A genetic explanation could suggest that:
Both inherited a general vulnerability.
Different gene combinations or environments produced different symptoms.
OCD is aetiologically heterogeneous.
Genes do not prescribe one exact form of compulsion.
Scenario 5: inherited risk without OCD
A person has several close relatives with OCD but never develops the disorder.
This illustrates that:
Vulnerability is not certainty.
Protective environments may reduce risk.
Relevant triggers may not occur.
Other genes may reduce or alter the risk.
The disorder requires more than family history alone.
Explaining vulnerability in an examination
A strong answer might state:
Genetic explanations suggest that a person inherits a predisposition rather than OCD itself. Several candidate genes may influence neurotransmitter systems associated with the disorder. The vulnerability may remain inactive unless it interacts with environmental stress, so the presence of risk-associated genes does not make OCD inevitable.
A weak answer might state:
OCD is passed directly from parents to children.
This is too deterministic and does not explain:
Polygenic inheritance.
Vulnerability.
Environmental interaction.
Individual differences.
Strengths of genetic explanations
Strength: twin evidence supports inherited influence
Nestadt and colleagues found higher concordance for MZ twins than DZ twins.
Because MZ twins share more genetic material, this difference supports a genetic component.
The evidence is especially useful because:
It compares different degrees of genetic similarity.
It produces measurable concordance rates.
The predicted pattern was observed.
The support is not complete
The MZ rate was below 100%.
The evidence therefore supports genetic contribution rather than complete genetic determination.
A developed evaluation should use both sides of the finding:
Higher MZ concordance supports genetics, but incomplete concordance supports environmental influence.
Strength: family patterns are consistent with inheritance
OCD is more common among biological relatives of affected individuals than among the general population.
This is consistent with the prediction that inherited vulnerability runs in families.
However, families share environments as well as genes.
Strength: specific biological mechanisms can be proposed
Candidate genes provide possible mechanisms connecting inheritance with OCD.
For example:
SERT variants may affect serotonin transport.
COMT variants may affect dopamine regulation.
Receptor genes may affect serotonergic communication.
This gives the explanation greater detail than simply saying that OCD “runs in families”.
Strength: polygenic theory explains complexity
A polygenic account helps explain why:
No single OCD gene has been identified.
Symptoms differ between individuals.
Severity varies.
Family members do not all develop the disorder.
Several biological systems may be involved.
Strength: aetiological heterogeneity explains individual differences
Different people may reach the same diagnosis through different combinations of:
Genes.
Neurotransmitter differences.
Environmental triggers.
This may explain why:
Symptoms differ.
Treatment response differs.
Some cases have a strong family history.
Other cases follow trauma without obvious family history.
Limitations of genetic explanations
Limitation: twin studies cannot fully separate genes and environment
MZ twins may experience more similar environments than DZ twins.
Higher MZ concordance might therefore reflect:
Genetic similarity.
Environmental similarity.
Social learning.
A combination of factors.
This limits the internal validity of purely genetic conclusions.
Limitation: family members share environments
A child may develop checking behaviour after observing a parent who:
Repeatedly checks locks.
Expresses high anxiety about mistakes.
Seeks constant reassurance.
Avoids uncertainty.
The similarity may partly result from social learning.
A family study cannot automatically show whether the transmission was:
Genetic.
Environmental.
Both.
Limitation: concordance is not perfect
The MZ concordance rate of approximately 68% leaves a substantial proportion of pairs in which only one twin has OCD.
This means genes cannot provide a complete explanation.
Non-genetic factors are required to explain the difference.
Limitation: trauma can trigger symptoms
Some cases begin following traumatic or stressful experiences.
This challenges a purely inherited explanation.
The diathesis-stress model explains the evidence more effectively by combining:
Genetic vulnerability.
Environmental trigger.
Limitation: some people have no known family history
OCD can develop in individuals whose relatives have no diagnosed disorder.
This may indicate:
Environmental causes.
Undiagnosed family vulnerability.
A different genetic combination.
A complex interaction of factors.
It weakens the simple claim that OCD is directly inherited through families.
Limitation: candidate genes explain only small parts of risk
OCD is polygenic.
This means:
The effect of one gene is limited.
Many combinations are possible.
A single gene cannot accurately predict the disorder.
Individual candidate-gene findings provide an incomplete explanation.
Limitation: cause and effect remain difficult to establish
Finding a gene variant associated with OCD does not prove that the gene causes it.
The variant may:
Affect another biological factor.
Interact with environmental stress.
Be linked with another nearby gene.
Increase general anxiety rather than OCD specifically.
Association does not establish a direct causal pathway.
Limitation: biological reductionism
Genetic explanations may be described as biologically reductionist.
They reduce a complex disorder to genes and biological functioning.
This creates a clear and testable explanation.
However, it may neglect:
Learning.
Cognition.
Trauma.
Family relationships.
Culture.
Social circumstances.
The meaning of obsessive thoughts.
OCD includes private thoughts and emotional experiences that may not be fully explained by DNA.
Limitation: genetic determinism
A strongly deterministic account suggests that behaviour is controlled by inherited biology.
This may underestimate:
Environmental influence.
Personal coping.
Treatment.
Psychological change.
Individual agency.
The genetic-vulnerability model is less deterministic because it recognises that genes alter probability rather than guarantee an outcome.
Limitation: socially sensitive implications
Genetic explanations may produce socially sensitive consequences.
People identified as genetically vulnerable could experience:
Stigma.
Anxiety about their future.
Unfair assumptions by employers or insurers.
Concern about having children.
The belief that change is impossible.
A responsible explanation should emphasise that risk is probabilistic.
Limitation: diagnosis may affect research findings
Genetic studies depend on identifying who has OCD.
Diagnosis may be affected by:
Symptom overlap.
Different diagnostic thresholds.
Co-occurring disorders.
Participants concealing symptoms.
Changes in diagnostic systems.
If classification is unreliable, estimates of genetic similarity may also be unreliable.
Limitation: samples may not represent all OCD
Twin and family studies may include people who:
Have severe symptoms.
Seek clinical treatment.
Belong to particular populations.
Are willing to participate in genetic research.
The findings may not generalise equally to:
Mild OCD.
Undiagnosed individuals.
Different cultural groups.
Every symptom pattern.
Animal research
Animal research may investigate genetically influenced repetitive or ritualistic behaviour.
AQA’s June 2022 mark scheme recognises animal evidence as possible support for a genetic basis.
Possible strength
Animal studies allow researchers to:
Control breeding.
Examine biological mechanisms.
Control environmental conditions.
Investigate gene and brain interactions.
This may provide evidence difficult to obtain from humans.
Possible limitation
Repetitive behaviour in an animal is not identical to human OCD.
Animals cannot clearly report:
Intrusive thoughts.
Guilt.
Insight.
Cognitive coping strategies.
The meaning attached to rituals.
Animal research may model compulsive behaviour more successfully than the full disorder.
Practical applications
Identifying biological pathways
Genetic research may help identify:
Neurotransmitter systems involved in OCD.
Biological pathways for further investigation.
Individuals who may be more vulnerable.
Reasons that people respond differently to treatment.
Connection with drug therapy
If genes influence serotonin functioning, this may help explain why medication affecting serotonin transmission can reduce symptoms for some clients.
However, the success of a drug does not prove that:
A gene caused the disorder.
Low serotonin was the original problem.
Every person has the same biological abnormality.
The treatment fallacy
The treatment fallacy occurs when the effectiveness of a treatment is incorrectly treated as proof of the disorder’s cause.
For example:
Selective serotonin reuptake inhibitors reduce OCD symptoms, therefore a serotonin-related gene must have caused OCD.
This conclusion is not justified.
A treatment may reduce symptoms without reversing the original cause.
Painkillers reduce headaches, but a lack of painkillers did not cause the headache.
Future genetic interventions
Identifying risk-associated genes may eventually contribute to:
More personalised treatment.
Better prediction of treatment response.
Improved understanding of biological pathways.
Gene therapy is sometimes suggested as a future practical application.
However:
OCD involves many genes.
Gene effects are small.
Environmental influences remain important.
Altering genes would create major ethical and practical difficulties.
The immediate value of genetic research is therefore mainly explanatory rather than providing a simple cure.
Genetic and neural explanations compared
Genetic explanation | Neural explanation |
Focuses on inherited gene variants | Focuses on neurotransmitters and brain circuits |
Explains vulnerability across generations | Explains current biological functioning |
Uses family and twin studies | Uses brain imaging, medication response and biological measurement |
Includes candidate genes | Includes serotonin, dopamine and brain structures |
May explain why a biological difference develops | Describes how that difference may influence symptoms |
Does not prove the current neural mechanism | Does not necessarily explain why the neural difference developed |
The explanations can be combined:
Gene variants may influence neurotransmitter systems and brain development, which may then increase vulnerability to OCD.
Genetic explanations and drug therapy
Genetic explanations may suggest that biological treatments could be useful.
For example, gene variants affecting serotonin regulation may be consistent with the use of drugs that alter serotonergic transmission.
However, treatment must be evaluated separately.
The effectiveness of a drug may depend on:
The client’s symptoms.
Their biological pathway.
Dosage.
Side effects.
Other treatments.
Environmental stress.
Aetiological heterogeneity may help explain why one medication does not work equally well for everyone.
A balanced interactionist account
A complete explanation may include several stages:
The person inherits a polygenic vulnerability.
The genes affect biological development or neurotransmitter functioning.
Environmental stress activates the vulnerability.
Intrusive thoughts or anxiety develop.
Compulsions temporarily reduce distress.
Learning processes maintain the rituals.
Social and cognitive factors affect severity.
This account combines:
Genetic factors.
Neural factors.
Environmental triggers.
Psychological maintenance.
It is more comprehensive than a single-factor explanation.
Interpreting genetic evidence
Higher concordance does not equal complete causation
A higher MZ than DZ rate supports genetic influence.
It does not show that the percentage difference is entirely genetic.
Family history does not prove inheritance
Family members share:
Genes.
Environments.
Behavioural models.
Stressors.
No family history does not prove an absence of genetic risk
Relatives may:
Carry vulnerability without developing OCD.
Have mild or undiagnosed symptoms.
Possess different gene combinations.
One candidate gene does not explain the whole disorder
OCD is polygenic and heterogeneous.
A single gene can only provide part of the explanation.
Applying the explanation to research findings
Finding 1
MZ twins show greater concordance than DZ twins.
Interpretation: Genetic similarity is associated with OCD similarity, supporting inherited influence.
Finding 2
MZ concordance is below 100%.
Interpretation: Environmental or other non-genetic factors are required.
Finding 3
Some cases begin following trauma.
Interpretation: Environmental stress may activate an inherited vulnerability.
Finding 4
Different candidate genes are associated with different cases.
Interpretation: OCD is aetiologically heterogeneous.
Finding 5
Many genes are implicated.
Interpretation: OCD is polygenic rather than controlled by one gene.
Answering application questions
Step 1: identify evidence of inherited risk
Look for:
OCD among biological relatives.
Greater similarity between identical twins.
A strong family history.
Reference to candidate genes.
Step 2: use vulnerability language
Write:
“May have inherited a predisposition.”
“Has an increased probability.”
“Possesses a possible genetic vulnerability.”
Avoid:
“Inherited OCD directly.”
“Will definitely develop OCD.”
Step 3: identify environmental influence
Look for:
Trauma.
Stress.
Major change.
Illness.
Different experiences between relatives.
Step 4: explain interaction
State that environmental stress may activate the inherited vulnerability.
Step 5: distinguish genetic and neural material
If the scenario mentions serotonin, connect it back to a gene variant if the question asks about genetics.
Example application paragraph
Theo may have inherited a genetic vulnerability because several of his close biological relatives have OCD. The vulnerability is likely to be polygenic, involving several candidate genes rather than one OCD gene. His symptoms began after a highly stressful event, suggesting that the genetic predisposition interacted with an environmental trigger. The genes therefore increased his risk but did not make the disorder inevitable.
A balanced assessment
Genetic explanations are valuable because they:
Explain why OCD runs in some families.
Are supported by higher MZ than DZ concordance.
Identify possible biological mechanisms.
Recognise polygenic inheritance.
Explain individual differences through aetiological heterogeneity.
Produce testable predictions.
Contribute to research into biological treatments.
However:
Twin and family studies cannot completely separate genes and environment.
MZ concordance is below 100%.
Trauma and stress may trigger symptoms.
Some people have no diagnosed family history.
Candidate genes each explain only a small amount of risk.
Genetic explanations may be reductionist and deterministic.
Treatment success does not prove genetic causation.
The most justified conclusion is:
Genes appear to contribute to vulnerability to OCD, but they do not provide a complete or deterministic explanation. The evidence is most consistent with an interactionist account in which several genes affect biological susceptibility and environmental experiences influence whether and how the disorder develops.
Hints from the Examiner Reports 💡
Examiner hint: Do not confuse a genetic explanation with a general biological explanation. Neurotransmitter or brain-structure material must be linked explicitly to inherited genes.
Examiner hint: Learn the difference between polygenic inheritance and aetiological heterogeneity. Polygenic means many genes are involved. Aetiological heterogeneity means different people may have different combinations of causes.
Examiner hint: Use candidate genes accurately. SERT and COMT are examples, but naming them without explaining their possible biological role gains limited value.
Examiner hint: Describe genetic vulnerability rather than saying that somebody inherits OCD directly.
Examiner hint: Use the full twin-study argument. Higher MZ than DZ concordance supports genetics, but MZ concordance below 100% demonstrates the contribution of non-genetic factors.
Examiner hint: Evaluate the equal-environments assumption. MZ twins may share more similar treatment and experiences than DZ twins, which could partly explain higher concordance.
Examiner hint: Family studies do not separate genetic inheritance from social learning because relatives share both genes and environments.
Examiner hint: Link environmental triggers to the diathesis-stress model rather than treating trauma as evidence that genes have no role.
The June 2022 examiner report found that stronger responses used SERT and COMT, neurotransmitter links and aetiological heterogeneity. Better evaluation used twin and family studies, incomplete MZ concordance, the equal-environments assumption and the diathesis-stress model.
The report also noted that some students described brain structures or neurotransmitters without connecting them to inheritance. Such material did not provide a focused genetic explanation.
Common Mistakes ⚠️
Mistake: Saying people inherit OCD directly
Why this is inaccurate:
People inherit gene variants that may increase vulnerability.
How to improve:
Use terms such as predisposition, vulnerability and probability.
Mistake: Saying one gene causes OCD
Why this is incorrect:
OCD is polygenic.
How to improve:
Explain that many genes contribute small effects.
Mistake: Confusing polygenic with aetiologically heterogeneous
Why this is incorrect:
The terms describe different aspects of complexity.
How to improve:
Polygenic means many genes. Heterogeneous means different causal combinations between people.
Mistake: Naming SERT or COMT without explanation
Why this limits credit:
A gene name alone does not show understanding.
How to improve:
Link SERT with serotonin transport and COMT with dopamine regulation.
Mistake: Describing serotonin with no reference to genes
Why this does not answer a genetic question:
It becomes a neural explanation.
How to improve:
Explain how inherited variants may affect the neurotransmitter system.
Mistake: Saying low serotonin is the SERT gene
Why this is incorrect:
A gene is a section of DNA, while serotonin is a neurotransmitter.
How to improve:
Explain that the gene may influence the transporter affecting serotonergic communication.
Mistake: Saying MZ twins share 100% concordance
Why this is incorrect:
They share virtually all their genes, but their concordance for OCD is lower.
How to improve:
Distinguish genetic similarity from similarity in disorder outcome.
Mistake: Saying a 68% concordance rate means a person has a 68% risk
Why this is incorrect:
Concordance refers to similarity within twin pairs.
How to improve:
Define concordance before interpreting the figure.
Mistake: Using higher MZ concordance as proof of genetic causation
Why this is too strong:
MZ twins may also experience more similar environments.
How to improve:
Discuss the equal-environments assumption.
Mistake: Saying family studies prove inheritance
Why this is incorrect:
Families share learning experiences and environments.
How to improve:
Describe family evidence as consistent with, rather than proving, genetic influence.
Mistake: Ignoring the MZ concordance shortfall
Why this weakens evaluation:
A rate below 100% shows that genes are not sufficient.
How to improve:
Use the same study as both support and a limitation.
Mistake: Saying environmental triggers disprove genes
Why this is too simplistic:
Stress may activate a genetic vulnerability.
How to improve:
Use a diathesis-stress explanation.
Mistake: Saying everybody exposed to trauma develops OCD
Why this is incorrect:
Individual vulnerability and coping differ.
How to improve:
Explain why the same event produces different outcomes.
Mistake: Saying no family history means no genetic vulnerability
Why this is inaccurate:
Vulnerability may be undiagnosed or based on different gene combinations.
How to improve:
Treat family history as one source of evidence rather than a requirement.
Mistake: Treating all forms of OCD as genetically identical
Why this is incorrect:
The disorder is aetiologically heterogeneous.
How to improve:
Explain that different gene combinations may contribute to different symptoms.
Mistake: Claiming drug effectiveness proves the genetic explanation
Why this is the treatment fallacy:
Reducing symptoms does not identify the original cause.
How to improve:
Use drug response as indirect evidence only.
Mistake: Listing reductionism or determinism without development
Why this gains limited evaluation credit:
The relevance to OCD has not been explained.
How to improve:
State which psychological or environmental factors the genetic explanation overlooks.
Mistake: Saying genetic determinism means genes have no influence
Why this is incorrect:
Determinism means genes control the outcome too completely.
How to improve:
Contrast deterministic inheritance with probabilistic vulnerability.
Mistake: Giving only research names
Why this is incomplete:
The examiner needs the finding and its implication.
How to improve:
State the concordance rates and explain what they show.
Mistake: Describing neural explanations for most of the answer
Why this loses focus:
The question asks about genes.
How to improve:
Keep every biological mechanism linked to inherited variation.
Mistake: Concluding that genetic explanations are completely wrong
Why this is not supported:
Twin evidence indicates that genes contribute to risk.
How to improve:
Reach a balanced interactionist conclusion.
Exam-Style Questions ✍️
Question 1
Which one of the following best describes a polygenic explanation of OCD?
A. OCD is caused by one dominant gene
B. Many genes contribute to vulnerability to OCD
C. OCD is caused entirely by environmental stress
D. One gene produces every type of compulsion
[1 mark]
reveal mark scheme and indicative content
Answer: B. Many genes contribute to vulnerability to OCD
Question 2
Define genetic vulnerability in relation to OCD.
[2 marks]
reveal mark scheme and indicative content
Mark scheme
AO1 = 2
2 marks: Clear definition referring to an inherited predisposition that increases the likelihood of developing OCD without making the disorder inevitable.
1 mark: Limited or partial definition.
Indicative content
Certain inherited genes may increase susceptibility to OCD.
Genes create a vulnerability or predisposition, rather than directly determining that OCD will develop.
Environmental factors may interact with the vulnerability.
Example answer
Genetic vulnerability is an inherited predisposition that increases a person's likelihood of developing OCD, although having the vulnerability does not mean that OCD will definitely develop.
Question 3
Explain what is meant by aetiological heterogeneity.
[3 marks]
reveal mark scheme and indicative content
Mark scheme
AO1 = 3
Award 1 mark each for:
Aetiology refers to the cause or origin of a disorder.
Different combinations of genes may contribute to OCD in different people.
Different genetic combinations may also contribute to different forms or symptoms of OCD.
Indicative content
There may therefore be no single genetic cause of OCD that applies to every person with the disorder.
AQA explicitly defines aetiological heterogeneity in terms of different combinations of genes causing OCD in different people, with different combinations potentially accounting for different types of OCD.
Example answer
Aetiological heterogeneity means that OCD may have different genetic causes in different people. One person may develop OCD because of one combination of genes, while another person's vulnerability may involve a different combination. Different combinations may also be associated with different forms of OCD.
Question 4
Briefly explain the possible role of one candidate gene in OCD.
[3 marks]
reveal mark scheme and indicative content
Mark scheme
AO1 = 3
Award credit for identifying a relevant candidate gene and explaining its possible role.
Indicative content
For example, SERT:
SERT is a candidate gene associated with the serotonin transporter.
Variations in the gene may affect the transport or reuptake of serotonin.
Altered serotonin functioning may increase vulnerability to OCD.
Alternatively, credit an appropriate account involving COMT or another relevant candidate gene.
AQA specifically accepts reference to genes including SERT, COMT and 5HT1-D beta, provided their function is linked to OCD.
Example answer
One candidate gene is SERT, which is involved in the functioning of the serotonin transporter. Variations in this gene may affect serotonin transmission in the brain. Because abnormal serotonin functioning has been associated with OCD, certain SERT variants may contribute to genetic vulnerability to the disorder.
Question 5
Researchers found concordance rates of 68% for monozygotic twins and 32% for dizygotic twins.
Explain one conclusion and one limitation that can be drawn from these findings.
[4 marks]
reveal mark scheme and indicative content
Mark scheme
AO3 = 4
Award up to 2 marks for the conclusion and 2 marks for the limitation.
Indicative content
Conclusion
MZ twins share approximately 100% of their genes and have a concordance rate of 68%.
DZ twins share approximately 50% of their genes and have a much lower concordance rate of 32%.
This supports a genetic contribution to OCD.
Limitation
The MZ concordance rate is only 68%, not 100%, despite MZ twins sharing their genes.
This suggests that genes alone cannot explain OCD and environmental factors must also contribute.
Alternatively, credit the problem that MZ twins may experience more similar environments than DZ twins, so the difference cannot necessarily be attributed entirely to genes.
These figures are those cited by AQA for Nestadt et al. (2010) as evidence for a genetic basis of OCD.
Example answer
The higher concordance rate for MZ twins, 68% compared with 32% for DZ twins, supports a genetic contribution because MZ twins are genetically more similar. However, MZ concordance is not 100%, even though MZ twins share the same genes. This suggests that genetic factors alone cannot explain OCD and that environmental influences must also be involved.
Question 6
Several members of Nadiya’s biological family have OCD. Nadiya did not experience symptoms until after a highly stressful life event.
Use genetic vulnerability and the diathesis-stress model to explain Nadiya’s OCD.
[6 marks]
reveal mark scheme and indicative content
Mark scheme
AO2 = 6
Award credit for effective application of genetic vulnerability and the diathesis-stress model.
Indicative content
The occurrence of OCD among Nadiya's biological relatives suggests that she may have inherited a genetic vulnerability.
Multiple genes may contribute to this predisposition because OCD is polygenic.
A genetic vulnerability does not mean OCD will inevitably develop.
In the diathesis-stress model, the inherited vulnerability is the diathesis.
Nadiya's highly stressful life event acts as the environmental stressor.
The interaction between vulnerability and stress may explain why symptoms appeared only after the stressful event.
Example answer
Nadiya may have inherited a genetic vulnerability to OCD because several members of her biological family have the disorder. This vulnerability is a predisposition rather than a guarantee that she will develop OCD. According to the diathesis-stress model, her genetic vulnerability represents the diathesis. The highly stressful life event acts as an environmental trigger. The interaction between the inherited vulnerability and this stressor could therefore explain why Nadiya only began experiencing OCD symptoms after the stressful event.
AQA's June 2022 mark scheme explicitly accepts the diathesis-stress model as an alternative to a purely genetic explanation.
Question 7
Explain one reason why evidence from family studies cannot prove that OCD is inherited.
[4 marks]
reveal mark scheme and indicative content
Mark scheme
AO3 = 4
Award credit for one clearly developed methodological limitation.
Indicative content
Biological relatives share both genes and environments.
For example, children may share experiences, parenting and learned behaviours with family members who have OCD.
A higher rate of OCD among relatives could therefore result partly from environmental influences or social learning.
Family studies cannot separate genetic inheritance from these shared environmental influences and therefore cannot establish genetic causation.
AQA specifically credits shared environments and social learning as methodological problems with family and twin research.
Example answer
Family studies cannot prove that OCD is inherited because relatives share environments as well as genes. For example, children may observe and learn anxious or compulsive behaviour from family members. Therefore, higher rates of OCD within families could reflect environmental or learning influences rather than genetic inheritance alone.
Question 8
A student says:
“Identical twins have the same genes, so if one twin has OCD, the other twin must also have it.”
Use your knowledge of genetic explanations to explain why the student is incorrect.
[4 marks]
reveal mark scheme and indicative content
Mark scheme
AO1/AO2 = 4
Award 1 mark each for:
Identical or MZ twins share virtually all of their genes.
Genetic explanations propose a vulnerability, not absolute genetic determination.
Concordance for MZ twins is less than 100%, for example the cited figure of 68%.
Environmental factors or stress may interact with genetic vulnerability, so one twin can develop OCD while the other does not.
Example answer
The student is incorrect because genes provide a vulnerability to OCD rather than making the disorder inevitable. Although identical twins share virtually all of their genes, concordance is not 100%. For example, research has found an MZ concordance rate of 68%. This suggests that environmental factors, such as stressful experiences, can interact with genetic vulnerability, so one identical twin may develop OCD while the other does not.
Question 9
Explain one strength and one limitation of genetic explanations of OCD.
[6 marks]
reveal mark scheme and indicative content
Mark scheme
AO3 = 6
Award up to 3 marks for the strength and 3 marks for the limitation.
Indicative content
Strength
Twin research provides support for a genetic contribution.
Nestadt et al. (2010) found concordance of 68% for MZ twins compared with 32% for DZ twins.
As MZ twins share more genetic material, the higher concordance supports genetic vulnerability.
Limitation
Concordance among MZ twins is substantially below 100%.
Genetic factors are therefore insufficient by themselves to explain the disorder.
Environmental factors and stress are likely to interact with genetic vulnerability.
Alternatively, credit:
shared environment problems in twin/family studies
evidence that some OCD cases follow trauma
biological reductionism
genetic determinism
aetiological heterogeneity making it difficult to identify a single genetic explanation.
AQA's official marking guidance accepts each of these lines of discussion.
Example answer
One strength is support from twin research. Nestadt et al. found a concordance rate of 68% for MZ twins but only 32% for DZ twins. Because MZ twins share more genetic material, this difference suggests that genetic factors contribute to OCD.
However, MZ concordance is still well below 100%. If genes completely determined OCD, genetically identical twins should always be concordant. This suggests that environmental experiences also contribute, so a genetic explanation alone is incomplete.
Question 10
Discuss genetic explanations of obsessive-compulsive disorder.
[8 marks]
reveal mark scheme and indicative content
Mark scheme
AO1 = 3, AO3 = 5
7 to 8 marks: Knowledge of the genetic explanation for OCD is accurate with some detail. Discussion is thorough and effective. The answer is clear, coherent and focused, with effective use of specialist terminology.
5 to 6 marks: Knowledge is evident but there are occasional inaccuracies or omissions. Discussion is mostly effective.
3 to 4 marks: Limited knowledge is present. The answer focuses mainly on description and discussion is limited.
1 to 2 marks: Knowledge and discussion are very limited.
0 marks: No relevant content.
Indicative content
AO1
Genetic explanations propose that vulnerability or predisposition to OCD can be inherited across generations.
OCD appears to be polygenic, meaning that many genes contribute to vulnerability rather than one single gene.
Taylor (2013) identified up to 230 possible candidate genes.
Candidate genes include SERT, COMT and 5HT1-D beta.
Aetiological heterogeneity means different combinations of genes may cause OCD in different people.
Different combinations may also contribute to different forms of OCD.
Genes may exert their effects through underlying neurochemical mechanisms.
These points reflect the official June 2022 indicative content.
AO3
Twin evidence: Nestadt et al. (2010) found concordance rates of 68% for MZ twins and 32% for DZ twins. Greater concordance among genetically identical twins supports genetic influence.
Concordance is not 100%: even MZ twins are not always concordant, indicating that genes alone are insufficient.
Shared environment: twin and family studies cannot completely separate genetic inheritance from environmental similarity or social learning.
Trauma: AQA's mark scheme notes that around half of OCD cases may follow trauma, which undermines a purely genetic explanation.
Diathesis-stress: a more complete explanation is that genetic vulnerability interacts with environmental stressors.
Aetiological heterogeneity: identifying many genes and different combinations makes a simple genetic explanation difficult.
Biological reductionism: reducing OCD to genes may neglect cognitive, learning and environmental influences.
Genetic determinism: a purely genetic account may incorrectly imply that OCD is inevitable when the evidence indicates vulnerability rather than certainty.
Practical applications, such as implications for future genetically informed treatments, may also be credited.
Example answer
Genetic explanations suggest that some people inherit a vulnerability to OCD. The disorder appears to be polygenic, meaning that many genes rather than one gene contribute to this vulnerability. Candidate genes include SERT and COMT, which are associated with neurotransmitter functioning. There is also aetiological heterogeneity, meaning that different combinations of genes may contribute to OCD in different people and possibly to different forms of the disorder.
One strength is evidence from twin studies. Nestadt et al. found an OCD concordance rate of 68% for monozygotic twins compared with 32% for dizygotic twins. Because MZ twins share more genetic material, this supports a genetic contribution. However, concordance for MZ twins is not 100%, showing that genes cannot be the only cause. Twin and family studies are also difficult to interpret because relatives often share similar environments as well as genes. Environmental factors therefore provide an alternative explanation for similarities within families. A diathesis-stress explanation may be more complete because inherited vulnerability could interact with stressful life events to produce OCD. Overall, there is good evidence that genes contribute to vulnerability, but genetic factors alone cannot provide a complete explanation of OCD.
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