Genetic Vulnerability and Addiction | AQA A-Level Psychology Revision

Revision Notes
Aug 7
31 min read

Updated: Aug 14

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 65 to 80 minutes

Genetic vulnerability and addiction A-Level Psychology revision examines how inherited biological differences may increase a person’s risk of developing addictive behaviour. Genes may influence the brain’s reward system, substance metabolism, personality and responses to stress, but they do not make addiction inevitable.

You will learn how family, twin, adoption and molecular-genetic research investigates inherited risk, why concordance below 100% points towards environmental influence, and why genetic vulnerability is best understood as one factor within a wider interactionist explanation. AQA requires genetic vulnerability as a risk factor in the development of addiction.

Learning Objectives 🎯

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

Define genetic vulnerability and genetic predisposition.
Explain how inherited differences may increase addiction risk.
Explain direct and indirect genetic pathways to addiction.
Apply genetic vulnerability to nicotine, substance and behavioural addictions.
Explain why possessing a vulnerability does not make addiction inevitable.
Interpret evidence from family, twin, adoption and molecular-genetic studies.
Evaluate genetic explanations using methodological issues, interactionism and psychological debates.

Revision Notes 📚

Genetic Vulnerability and Addiction A-Level Psychology Revision Focus

A risk factor is a biological, psychological or environmental characteristic that increases the likelihood of an outcome.

In addiction, risk factors may include:

Genetic vulnerability.
Personality characteristics.
Stress.
Family influence.
Peer influence.
Exposure to addictive substances or activities.

A risk factor changes probability.

It is not:

A guaranteed cause.
A diagnosis.
Proof that addiction will develop.
Evidence that the individual has no control.

The June 2025 AQA mark scheme defines risk factors as biological, personality or environmental factors that increase the chance of a person developing addictive behaviour.

What Is Genetic Vulnerability?

Genetic vulnerability is an inherited predisposition that increases the likelihood of developing an addiction.

The person may inherit genes that affect characteristics such as:

Sensitivity to reward.
Dopamine functioning.
The number or activity of particular receptors.
The metabolism of an addictive substance.
Impulsivity.
Sensation seeking.
Stress responsiveness.
The severity of withdrawal.
How rewarding an addictive behaviour feels.

A suitable definition is:

Genetic vulnerability is an inherited biological predisposition that increases a person’s risk of addiction without making addiction certain.

Vulnerability Is Not Inevitability

The word vulnerability is essential.

A person may inherit characteristics that make addiction more likely, but addiction will usually require further conditions.

For example, a genetic vulnerability to nicotine addiction cannot lead to nicotine dependence unless the person is exposed to nicotine.

The broad process may be:

Genetic predisposition + exposure + psychological and social influences → increased probability of addiction

A person with genetic vulnerability may never develop addiction because they:

Never encounter the substance or behaviour.
Reject opportunities to begin.
Have strong anti-addiction attitudes.
Receive effective family support.
Possess good coping skills.
Experience little environmental stress.
Stop experimenting before dependence develops.
Receive early treatment.

Genes and DNA

A gene is a section of DNA containing instructions that contribute to biological characteristics.

People inherit genetic material from their biological parents.

Different forms of a gene are called alleles.

Genetic differences may contribute to variation in:

Proteins.
Enzymes.
Receptors.
Neurotransmitter activity.
Brain development.
Behavioural tendencies.

Genes do not normally contain direct instructions such as:

“Become addicted to nicotine.”

Instead, they may influence biological or psychological characteristics that make addiction more or less likely.

Genotype and Phenotype

A person’s genotype is their genetic make-up.

Their phenotype is the observable outcome produced through interaction between genotype and environment.

In addiction:

The genotype may contain variants associated with greater vulnerability.
The phenotype may include craving, dependence or addictive behaviour.
The environment affects whether and how the vulnerability is expressed.

This can be represented as:

Genotype + environment → phenotype

Two people with similar genetic risk may therefore develop different outcomes because they experience different environments.

Addiction Is Likely to Be Polygenic

What Is Polygenic Inheritance?

A characteristic is polygenic when it is influenced by several genes rather than one gene.

Addiction is unlikely to result from a single universal “addiction gene”.

Instead, several genetic variants may each make a small contribution to:

Reward sensitivity.
Substance metabolism.
Impulse control.
Stress reactivity.
Learning from rewards.
Withdrawal experiences.

The overall vulnerability may result from the combined effect of many genes.

The Problem with the Phrase “Addiction Gene”

The phrase suggests that:

One gene causes addiction.
Everyone with the gene becomes addicted.
Everyone without the gene is protected.
The same gene explains every addiction.

These conclusions are too simplistic.

A more accurate statement is:

Several genes may contribute to a biological vulnerability, which interacts with environmental and psychological influences.

Different Genes May Influence Different Addictions

Genetic influences may not operate identically across:

Nicotine addiction.
Alcohol addiction.
Gambling addiction.
Other substance addictions.
Behavioural addictions.

Some genetic factors may affect a general reward or impulse-control system.

Others may influence processes specific to a particular substance, such as how quickly it is metabolised.

This means genetic vulnerability may be:

Partly general.
Partly addiction-specific.

Direct Genetic Effects

Genes may influence addiction risk directly by affecting biological processes involved in reward, dependence and metabolism.

AQA’s June 2022 mark scheme identifies genetic effects on dopamine-receptor numbers and the activity of enzymes involved in the metabolism of addictive substances as relevant genetic-vulnerability content.

Genes and Dopamine Receptors

Dopamine is a neurotransmitter involved in reward and motivation.

Genes may influence:

The number of dopamine receptors.
Receptor sensitivity.
Dopamine transmission.
How strongly a person experiences a reward.

One proposed possibility is that some people have less efficient reward-system functioning.

They may then need greater stimulation to experience a satisfying reward.

This could increase attraction to:

Nicotine.
Alcohol.
Gambling.
Other highly stimulating activities.

The process might be:

A person inherits a variant affecting dopamine functioning.
Ordinary rewards produce weaker stimulation.
An addictive substance or behaviour produces a stronger effect.
The person experiences the activity as highly rewarding.
Repetition becomes more likely.
Dependence may eventually develop.

This is a vulnerability rather than an unavoidable sequence.

The DRD2 Gene

DRD2 is associated with dopamine D2 receptors.

AQA mark-scheme material accepts DRD2 as a possible genetic determinant relevant to nicotine addiction and brain reward functioning.

A careful exam statement is:

Variations in genes such as DRD2 may influence dopamine-receptor functioning and therefore alter sensitivity to rewarding effects.

Avoid stating that:

DRD2 is the addiction gene.
Everyone with a particular variant becomes addicted.
DRD2 alone explains nicotine addiction.
The gene directly produces smoking behaviour.

The gene is one possible contributor within a complex pathway.

Genes and Substance Metabolism

Metabolism is the process through which the body breaks down and removes a substance.

Genes may influence the enzymes involved in metabolism.

This could affect:

How quickly a substance is processed.
How long its effects remain.
How strongly unpleasant effects are experienced.
How rapidly tolerance develops.
The amount consumed.

For example, inherited differences in alcohol-metabolising enzymes may influence how rewarding or unpleasant alcohol consumption feels.

The genetic factor changes the biological response to the substance.

It does not force the person to begin drinking.

Genes and Withdrawal

Genetic differences may affect the severity of:

Physical dependence.
Craving.
Withdrawal symptoms.
Emotional responses during abstinence.

A person experiencing severe withdrawal may find stopping more difficult.

The process could be:

Genetic difference → stronger withdrawal response → greater motivation to resume use → increased risk of maintained addiction

This link connects with physical dependence, tolerance and withdrawal syndrome [Lesson 1: Describing addiction].

Indirect Genetic Effects

Genes may also affect addiction indirectly.

AQA’s June 2022 mark scheme recognises genetic effects on mediating characteristics such as personality and other individual differences.

Genes and Personality

Inherited tendencies may contribute to characteristics such as:

Impulsivity.
Sensation seeking.
Novelty seeking.
Neuroticism.
Reward dependence.
Low self-control.

These characteristics may then increase addiction risk.

For example:

Genetic influence → greater sensation seeking → experimentation with stimulating substances or gambling → increased exposure → possible addiction

The gene does not directly cause the addiction.

It influences a personality characteristic that changes the person’s behaviour.

These characteristics are developed in individual and social risk factors for addiction [Lesson 3: Personality and social influences].

Genes and Stress Responsiveness

Genes may influence how strongly a person responds to stress.

One individual may experience:

Strong emotional reactions.
Prolonged physiological arousal.
Greater anxiety.
Greater difficulty returning to a calm state.

If an addictive substance or behaviour provides temporary relief, it may be repeated.

The possible chain is:

Genetic influence on stress response → strong distress → substance or behaviour provides relief → negative reinforcement → increased addiction risk

The genetic factor and stressful environment work together.

Genes and Sensitivity to Social Influence

Genetic differences may indirectly affect how a person responds to:

Peer approval.
Social reward.
Risk.
Novelty.
Group pressure.

For example, a highly reward-sensitive individual may find peer approval for gambling especially reinforcing.

This does not mean that conformity is genetically determined.

It means inherited characteristics may alter a person’s response to the social environment.

Genes May Influence Several Risk Factors

A genetic influence might contribute to:

Personality.
Stress responsiveness.
Reward sensitivity.
Substance metabolism.

These factors may then interact with:

Family behaviour.
Peer norms.
Availability.
Learning.
Life events.

AQA’s 2022 mark scheme notes that genetic influence may partly underlie other risk factors by affecting responses to stress and social influences.

Genetic Vulnerability and the Reward System

The Reward Pathway

Addictive substances and activities can stimulate brain systems involved in reward.

A genetically vulnerable person might experience differences in:

Baseline reward activity.
Dopamine release.
Dopamine-receptor response.
Motivation to seek rewards.
Adaptation following repeated stimulation.

The relationship with dopamine is studied more fully in brain reward systems and nicotine use [Lesson 4: Neurochemistry and nicotine addiction].

For this lesson, the key point is:

Genes may influence neurochemical systems that change how rewarding an addictive substance or activity feels.

Initiation and Maintenance

Genetic vulnerability may operate differently during different stages of addiction.

Initiation

Genetic factors may influence:

Curiosity.
Risk taking.
Reward seeking.
Initial response to a substance.
Whether first use feels pleasant or unpleasant.

Maintenance

Genetic factors may influence:

Tolerance.
Withdrawal.
Craving.
Reward sensitivity.
Difficulty stopping.
Relapse risk.

An explanation should be precise about which stage it addresses.

For example:

A gene influencing nicotine metabolism may help explain maintenance or amount smoked, but peer modelling may better explain why the first cigarette was tried.

Genetic Vulnerability and Nicotine Addiction

A genetically vulnerable person may inherit biological differences affecting:

Nicotine response.
Dopamine activity.
Nicotinic receptor functioning.
Nicotine metabolism.
Withdrawal severity.
Reward sensitivity.

A possible process is:

The person experiments with smoking.
Nicotine stimulates the reward system.
Their inherited biology makes the effect particularly reinforcing.
Repeated use produces dependence.
Withdrawal occurs during abstinence.
Smoking removes the discomfort.
Addiction becomes established.

The person must still encounter and use nicotine before the vulnerability can be expressed.

Applying Genetic Vulnerability to Smoking

Consider this scenario:

Several of Noah’s biological relatives have experienced nicotine addiction. Noah begins smoking with friends and finds nicotine highly rewarding. He later experiences intense cravings whenever he attempts to stop.

A developed application could state:

Addiction among biological relatives suggests possible inherited vulnerability.
Noah may share genes affecting nicotine response or dopamine functioning.
His intense reward response may encourage repeated smoking.
Severe cravings may increase maintenance and relapse risk.
Smoking with friends provides an environmental opportunity.
Family history alone does not prove that Noah inherited an addiction.
Genetic and social factors may have interacted.

Family Smoking Has Two Possible Meanings

When a question states that a person’s parents smoke, this could indicate:

Genetic influence

The person may have inherited biological vulnerability from biological parents.

Environmental influence

The person may have:

Observed smoking.
Imitated the behaviour.
Learned that smoking is acceptable.
Had easier access to cigarettes.

AQA’s specimen mark scheme accepts both genetic vulnerability and social-learning explanations when a family-smoking pattern is described.

A strong answer distinguishes the two interpretations.

Genetic Vulnerability and Gambling Addiction

Gambling addiction does not involve metabolising an ingested substance.

Genetic vulnerability may nevertheless contribute through inherited differences in:

Reward sensitivity.
Impulsivity.
Sensation seeking.
Risk taking.
Dopamine functioning.
Sensitivity to uncertain rewards.

For example:

A person with high inherited reward sensitivity may find the unpredictable excitement of gambling especially reinforcing.

However, genetic vulnerability cannot explain specific gambling beliefs such as:

“I am due to win.”
“My lucky number improves the odds.”
“A near miss means success is close.”

These are examined in cognitive bias and gambling behaviour [Lesson 7: Cognitive explanations of gambling addiction].

Applying Genetic Vulnerability to Gambling

Several members of Ruby’s biological family have experienced addictive behaviours. Ruby is highly impulsive and finds risky betting unusually exciting. Her partner dislikes gambling and she did not encounter it until adulthood.

A possible application is:

Family patterns may suggest inherited vulnerability.
Impulsivity could be an indirectly inherited risk factor.
Strong reward sensitivity may make gambling especially reinforcing.
The absence of gambling exposure earlier may explain why addiction did not develop in childhood.
Adult exposure provided the opportunity for vulnerability to be expressed.
The family pattern is not proof because relatives may share environments as well as genes.

Methods Used to Investigate Genetic Vulnerability

Researchers cannot ethically manipulate a person’s genes to see whether addiction develops.

They therefore use naturally occurring variation.

Common methods include:

Family studies.
Twin studies.
Adoption studies.
Linkage studies.
Candidate-gene research.
Genome-wide research.

The June 2022 AQA mark scheme recognises twin, adoption and linkage evidence as relevant to genetic vulnerability in addiction.

Family Studies

How Family Studies Work

Family studies examine whether addiction occurs more frequently among biological relatives of an addicted person than among the wider population.

The logic is:

If closer biological relatives show greater similarity, genetic influence may be involved.

Researchers might compare:

Parents and children.
Siblings.
Extended relatives.
People with and without an addicted biological relative.

Strength of Family Evidence

A family pattern is consistent with inherited vulnerability.

For example:

If addiction repeatedly appears among biological relatives, shared genetic material may contribute to the similarity.

Limitation of Family Evidence

Families share both genes and environments.

They may share:

Attitudes towards substances.
Access to addictive activities.
Stressful circumstances.
Modelling.
Socioeconomic conditions.
Cultural beliefs.

A family pattern cannot separate:

Genetic inheritance from social learning

This is one reason twin and adoption studies are valuable.

Twin Studies

Monozygotic and Dizygotic Twins

Monozygotic twins, or MZ twins, develop from the same fertilised egg and share virtually all their genes.

Dizygotic twins, or DZ twins, develop from separate fertilised eggs and share approximately half their segregating genes, like ordinary siblings.

Twin studies compare addiction similarity in MZ and DZ pairs.

Concordance Rate

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

For example:

MZ concordance: 55%
DZ concordance: 25%

The higher MZ rate would be consistent with genetic influence because MZ twins are genetically more similar.

Interpreting Twin Evidence

Pattern	Possible interpretation
MZ concordance greater than DZ concordance	Supports genetic influence
MZ and DZ concordance similar	Provides little evidence of additional genetic influence
MZ concordance below 100%	Shows genes are not sufficient
Both rates are high	Shared environmental influence may be important
Both rates are low	The characteristic may depend strongly on particular experiences

AQA’s June 2025 mark scheme identifies Kendler’s twin research as relevant evidence when evaluating genetic risk in addiction.

The supplied mark scheme does not provide the study’s detailed procedure or figures, so these should not be invented.

Why MZ Concordance Below 100% Matters

Suppose MZ concordance is 60%.

This means that in 40% of the identified pairs, one twin shows addiction while the other does not.

Because MZ twins share virtually all their genes, this difference points towards:

Different experiences.
Different peer groups.
Different stress.
Different exposure.
Individual choices.
Measurement error.
Other non-shared environmental influences.

Genetic vulnerability cannot therefore be a complete explanation.

The Equal Environments Assumption

Twin studies often assume that MZ and DZ twins experience equally similar environments.

This is called the equal environments assumption.

However, MZ twins may be:

Treated more similarly.
Dressed more similarly.
Encouraged to share activities.
More likely to have the same friends.
More emotionally close.

Higher MZ concordance could therefore result partly from more similar environments rather than greater genetic similarity.

Shared and Non-Shared Environment

The shared environment includes experiences both twins have, such as:

Family home.
Parenting.
Neighbourhood.
Some social attitudes.

The non-shared environment includes experiences that differ, such as:

Different friends.
Different teachers.
Different stressful events.
Different opportunities to use substances.
Different relationships.

Non-shared environments help explain why genetically identical twins may develop different addiction outcomes.

Adoption Studies

How Adoption Studies Work

Adoption studies compare an adopted person with:

Biological relatives who share genes.
Adoptive relatives who share the rearing environment.

The logic is:

Similarity with biological relatives supports genetic influence.
Similarity with adoptive relatives supports environmental influence.

Strength of Adoption Studies

Adoption studies attempt to separate genetic inheritance from family upbringing more clearly than ordinary family studies.

AQA’s June 2022 mark scheme identifies Kendler’s adoption research as relevant evidence when discussing addiction risk factors.

Again, the supplied source does not provide detailed figures, so the evidence should be used cautiously.

Limitation: Selective Placement

Adoptive families may not be completely different from biological families.

Agencies may place children in families with similar:

Cultural backgrounds.
Socioeconomic circumstances.
Educational values.
Community environments.

This is known as selective placement.

Similarity between adopted people and biological relatives may therefore not be entirely genetic.

Limitation: Prenatal Environment

An adopted child shares prenatal conditions with the biological mother.

Possible prenatal influences include:

Exposure to substances.
Maternal stress.
Nutrition.
Health complications.

These are environmental rather than genetic, but they may be wrongly attributed to heredity.

Limitation: Age at Adoption

If adoption takes place after the child has already spent time with biological relatives, some learning may have occurred before separation.

This makes it harder to distinguish genetic and early environmental influences.

Molecular-Genetic Research

Linkage Studies

Linkage studies examine whether particular genetic markers are associated with addiction within families or populations.

AQA accepts evidence from linkage studies showing genetic components in addictions such as alcohol and nicotine.

An association may suggest that a relevant gene is located near the identified marker.

It does not necessarily identify the exact causal mechanism.

Candidate-Gene Studies

A candidate gene is selected because researchers believe it may influence a biological process relevant to addiction.

Examples might involve genes connected with:

Dopamine receptors.
Neurotransmitter transmission.
Substance metabolism.
Stress responses.

Researchers compare the frequency of a genetic variant among:

People with an addiction.
People without that addiction.

Limitations of Candidate-Gene Research

Finding an association does not show that the gene directly causes addiction.

Problems include:

Small effects.
Multiple genes being involved.
Population differences.
Failure to replicate.
Environmental confounding.
Different definitions of addiction.
Multiple statistical comparisons.

A candidate gene should therefore be described as a possible contributor.

Genome-Wide Approaches

Genome-wide research examines large numbers of genetic variants without limiting the investigation to one candidate gene.

This approach is compatible with the idea that addiction is polygenic.

However, identified variants may each explain only a small proportion of individual differences.

Heritability

What Is Heritability?

Heritability estimates how much variation in a characteristic within a particular population is associated with genetic differences.

It does not mean:

The percentage of one person’s addiction caused by genes.
How fixed the characteristic is.
That environmental interventions cannot work.
That the estimate applies to every population.

Heritability depends on the population and environment being studied.

Heritability Is Not Destiny

A characteristic can be highly heritable and still be influenced by environmental change.

For example, genetic vulnerability may remain present while:

Access to the addictive substance is reduced.
Peer norms change.
Treatment is provided.
Coping strategies improve.
Stress decreases.

Genes contribute to vulnerability, but environmental conditions influence expression.

Why Genetic Vulnerability Does Not Necessarily Lead to Addiction

Exposure Is Required

A vulnerability cannot produce addiction to a substance or behaviour that the person never encounters.

For example:

A person cannot develop nicotine addiction without nicotine exposure.
A person cannot develop gambling addiction without gambling opportunities.

Exposure is a necessary environmental condition.

The First Experience May Differ

Even after exposure, people may respond differently.

One person may find the experience:

Rewarding.
Exciting.
Calming.

Another may find it:

Unpleasant.
Frightening.
Boring.
Physically uncomfortable.

Inherited biology may contribute to this difference, but learning and expectations also matter.

Social Influences Matter

Family and peers may:

Model addictive behaviour.
Provide access.
Approve or disapprove.
Reward participation.
Create social pressure.
Teach coping strategies.

A vulnerable person surrounded by strong anti-smoking attitudes may never begin smoking.

A person with lower biological vulnerability may still develop addiction within a highly reinforcing social environment.

Stress May Act as a Trigger

Stress may increase the likelihood that a vulnerability is expressed.

For example:

The person has inherited high stress sensitivity.
A major stressful period occurs.
Smoking or gambling provides temporary relief.
Relief negatively reinforces the behaviour.
Repetition increases addiction risk.

Without the stressful experience, the vulnerability may remain unexpressed.

Personality May Mediate the Effect

Genetic vulnerability may influence personality traits that alter exposure.

For example:

Inherited sensation seeking → greater willingness to experiment → increased exposure → greater addiction risk

A low sensation-seeking individual may avoid opportunities even if another biological vulnerability is present.

Protective Factors

A protective factor reduces risk.

Protective factors may include:

Supportive family relationships.
Strong coping strategies.
Accurate knowledge about addiction.
Prosocial peers.
Limited availability.
Good mental-health support.
High self-efficacy.
Early intervention.
Alternative sources of reward.

Risk and protection operate together.

Gene-Environment Interaction

A gene-environment interaction occurs when the effect of genetic vulnerability depends on environmental conditions.

A simple model is:

Genetic vulnerability	High-risk environment	Likely risk
Low	Low	Lower
High	Low	Increased but vulnerability may remain unexpressed
Low	High	Addiction may still develop through strong environmental influence
High	High	Greatest predicted risk

This is a probabilistic model rather than a fixed formula.

Diathesis-Stress Interpretation

Genetic vulnerability can be understood as a diathesis, meaning an underlying predisposition.

Environmental pressures or opportunities act as triggers.

The process is:

Genetic diathesis + environmental trigger → increased likelihood of addiction

Possible triggers include:

Substance availability.
Peer modelling.
Chronic stress.
Family conflict.
Gambling opportunities.
Social approval.
Major life changes.

The model explains why genetically similar people can develop different outcomes.

Applying an Interactionist Explanation

Consider this scenario:

Biological twins Ava and Mia were raised together. Several close relatives had alcohol problems. During adulthood, Ava experienced chronic stress and began drinking heavily with colleagues. Mia rarely drank and received strong support during stressful periods.

A strong explanation would state:

Both twins may share genetic vulnerability.
The family pattern is consistent with inherited risk.
Ava experienced environmental exposure through drinking colleagues.
Alcohol may have provided temporary stress relief.
Repeated use could have produced dependence.
Mia’s limited drinking reduced exposure.
Social support provided a protective factor.
Different outcomes show that vulnerability is not sufficient.

Evaluating Genetic Explanations

Strength: Twin Studies Support Genetic Influence

If MZ twins show higher concordance for addiction than DZ twins, this supports inherited vulnerability.

The reasoning is:

MZ twins share more genes.
Greater similarity accompanies greater genetic similarity.
Genetic differences may therefore contribute to addiction risk.

AQA identifies Kendler’s twin research as relevant evidence supporting genetic risk in addiction.

Limitation: Twin Evidence Cannot Fully Separate Nature and Nurture

MZ twins may share more similar environments than DZ twins.

They may receive:

More similar treatment.
More similar expectations.
More shared activities.
Greater mutual influence.

Higher concordance may therefore exaggerate genetic influence.

The June 2022 mark scheme identifies difficulty disentangling genetic and environmental influences as a central problem in interpreting twin evidence.

Strength: Adoption Studies Provide Further Evidence

Adoption research improves on ordinary family studies by separating biological relatedness from the rearing environment.

Similarity between adopted individuals and biological relatives is consistent with inherited vulnerability.

Using different methods can provide converging evidence.

For example:

Family patterns.
Twin concordance.
Adoption similarity.
Molecular associations.

If they point towards genetic influence, confidence increases.

Limitation: Adoption Studies Are Not Perfect Natural Experiments

Adoption studies may be affected by:

Selective placement.
Prenatal conditions.
Contact with biological relatives.
Age at adoption.
Unusual experiences associated with adoption.

They do not provide a complete separation of genes and environment.

Strength: Biological Mechanisms Can Be Proposed

Genetic explanations have greater value when they explain a mechanism.

For example:

Genetic variation → altered dopamine-receptor functioning → different reward sensitivity → increased repetition of addictive behaviour

This is more informative than merely saying:

Addiction runs in families.

AQA’s mark scheme recognises dopamine-receptor numbers and substance-metabolising enzymes as possible mechanisms.

Limitation: Mechanisms Are Complex

Addiction involves many systems, including:

Several neurotransmitters.
Multiple receptors.
Learning.
Cognition.
Stress.
Social reward.

A single gene-to-dopamine pathway may oversimplify this complexity.

The same genetic variant may also have different effects depending on:

Other genes.
Development.
Substance exposure.
Environment.

Limitation: Findings Are Mostly Correlational

Researchers do not experimentally assign human participants:

Genetic variants.
Addictions.
Family histories.

Studies therefore identify associations.

A relationship between a genetic variant and addiction could mean:

The gene increases addiction risk.
Another linked gene is responsible.
Population or environmental differences create the association.
The finding occurred by chance.
The relationship is indirect through personality or stress.

The June 2025 mark scheme identifies causality and third variables as key evaluation issues for addiction risk factors.

Limitation: Family History Is Not Purely Genetic

A person with addicted relatives may share:

Genes.
Substance availability.
Attitudes.
Stress.
Modelling.
Social norms.

Writing:

“Their parent smokes, so they inherited smoking”

is inaccurate.

The evidence supports possible inherited vulnerability, but environmental explanations must also be considered.

Limitation: Genes Cannot Explain Exposure

A genetic explanation may help explain:

Sensitivity to reward.
Dependence.
Withdrawal.
Difficulty quitting.

It cannot fully explain:

Why the first cigarette was available.
Why a peer group encouraged gambling.
Which gambling beliefs were learned.
Which environmental cues trigger craving.

Learning and social explanations may be more useful for these processes.

Limitation: Addiction Is Heterogeneous

Heterogeneous means varied.

People may reach similar addictive outcomes through different pathways.

For example:

One person begins because of peer pressure.
Another uses a substance to cope with stress.
Another is highly sensation seeking.
Another develops dependence after medical exposure.
Another becomes addicted through repeated gambling rewards.

A single genetic account may not explain every individual.

Limitation: Addiction May Be Polygenic and Multifactorial

The polygenic nature of addiction makes precise prediction difficult.

A person may have:

Several risk variants.
Several protective variants.
A low-risk environment.
Strong protective relationships.

Addiction is also multifactorial, meaning influenced by multiple biological, psychological and social factors.

This limits attempts to identify one simple biological cause.

Strength: Interactionism Explains Different Outcomes

An interactionist explanation accounts for:

MZ twins who are discordant for addiction.
Vulnerable individuals who never develop addiction.
People without family history who become addicted.
Different effects of stress and peer environments.

This provides a more complete account than pure genetic determinism.

AQA mark schemes encourage evaluation of single-factor explanations against approaches recognising several interrelated risk factors.

Limitation: Interactions Are Difficult to Measure

Although interactionism is realistic, it creates methodological challenges.

Researchers must measure:

Genetic variants.
Substance exposure.
Stress.
Personality.
Family influence.
Peer influence.
Availability.
Protective factors.

These factors may influence one another.

It is difficult to determine the relative contribution of each.

AQA’s June 2022 mark scheme states that addiction risk factors are often linked, making their separate effects difficult to assess.

Biological Reductionism

The genetic explanation may be criticised as biologically reductionist because it explains addiction using:

Genes.
Receptors.
Enzymes.
Neurotransmitters.

This focus has advantages.

It allows:

Objective biological measurement.
Testable predictions.
Possible personalised treatments.
Identification of biological mechanisms.

However, it may neglect:

Learning.
Beliefs.
Stressful experiences.
Family modelling.
Peer pressure.
Availability.
Cultural attitudes.

This connects with the strengths and limitations of biological reductionism [Lesson 5: Holism and reductionism].

Biological Determinism

A genetic explanation may appear biologically deterministic if it suggests that inherited characteristics control addiction.

This could lead to the belief:

“Addiction is in my genes, so I cannot change.”

This is problematic because:

Concordance is not 100%.
Treatment can be successful.
Environmental changes affect outcomes.
People can avoid exposure.
Coping skills can be learned.
Social support can reduce risk.

A more accurate interpretation is probabilistic:

Genes influence vulnerability, but behaviour is not biologically fixed.

This links with biological influence and personal control [Lesson 3: Free will and determinism].

Socially Sensitive Implications

Genetic research into addiction may have harmful consequences.

Possible risks include:

Labelling individuals as future addicts.
Discrimination by insurers or employers.
Stigma towards families.
Reduced expectations about recovery.
Pressure to undergo genetic testing.
Treating addiction as inevitable.
Ignoring environmental inequality.

A genetic association found at group level cannot identify with certainty whether one individual will develop addiction.

Blame and Responsibility

Genetic explanations can reduce moral blame by presenting addiction as partly influenced by biology.

This may be beneficial because it can:

Reduce the idea that addiction is simply weakness.
Encourage treatment.
Increase understanding.
Reduce shame.

However, an overly deterministic interpretation may:

Reduce personal agency.
Lower motivation to change.
Suggest treatment is pointless.
Ignore responsibility for managing risk.

A balanced position recognises both vulnerability and the possibility of change.

Practical Applications

Understanding genetic vulnerability may support:

Early education for people with family histories.
Monitoring of high-risk individuals.
Personalised prevention.
Treatment matched to biological differences.
Greater attention to environmental triggers.
Early support during stressful periods.

The June 2022 examiner report identifies implications for intervention and prevention as useful discussion of addiction risk factors.

Ethical Problems with Genetic Screening

Screening for addiction vulnerability would face several problems.

False positives

A person is identified as vulnerable but never develops addiction.

False negatives

A person is classified as low risk but develops addiction through environmental influence.

Limited predictive power

Many genes each contribute small effects.

Stigma

The person may be labelled before displaying any addictive behaviour.

Privacy

Genetic information could be used by other organisations.

Genetic information may be useful for prevention, but it should not be treated as a prediction of destiny.

Implications for Treatment

A biological vulnerability might suggest treatments addressing neurochemical processes, such as drug therapies designed to reduce addictive behaviour [Lesson 8: Drug therapy].

However, genetic vulnerability does not imply that only biological treatment will work.

Environmental and psychological interventions may include:

Reducing cues.
Changing peer groups.
Managing stress.
Developing coping skills.
Challenging addictive beliefs.
Increasing self-efficacy.

A multifactorial cause may require a combined treatment.

Comparing Genetic and Social Risk Factors

Genetic vulnerability	Social influence
Inherited biological predisposition	Environmental exposure and learning
May affect reward, metabolism or personality	May affect attitudes, access and modelling
Present before addictive behaviour begins	Develops through social experience
Investigated through twin, adoption and molecular studies	Investigated through family, peer and social-learning studies
Does not explain first exposure alone	Can explain how initiation occurs
May affect maintenance and withdrawal	May reinforce initiation and continued use
Probabilistic	Probabilistic
Interacts with the environment	Interacts with personal vulnerability

The strongest account may combine both.

Comparing Genetic Vulnerability and Neurochemistry

Genetic vulnerability and neurochemistry are connected but not identical.

Genetic vulnerability

Focuses on inherited DNA differences.

Neurochemical explanation

Focuses on neurotransmitter and receptor activity involved in addiction.

The relationship might be:

Gene variant → altered receptor functioning → different dopamine response → increased addiction vulnerability

The genetic explanation identifies an inherited source of variation.

The neurochemical explanation identifies the biological mechanism through which the variation may operate.

A Complete Interactionist Example

Ellis has biological relatives with nicotine addiction and may have inherited greater reward sensitivity. He does not smoke during school because his friendship group strongly rejects cigarettes. After beginning a stressful job, he joins colleagues who smoke during breaks. Nicotine provides pleasure and temporary stress relief, and repeated smoking leads to dependence.

A complete explanation includes:

Genetic vulnerability: Family history and possible reward sensitivity.
Exposure: Cigarettes become available through colleagues.
Social influence: Smoking is modelled and normalised.
Stress: Work pressure creates motivation for relief.
Learning: Nicotine reward reinforces smoking.
Dependence: Repeated use produces withdrawal and continued use.

The genetic factor contributes to the outcome but does not explain it alone.

Overall Evaluation

Genetic vulnerability provides a biologically plausible risk factor for addiction. Genes may influence dopamine receptors, substance-metabolising enzymes, withdrawal, stress responsiveness and personality characteristics such as impulsivity or sensation seeking.

Family, twin, adoption and molecular-genetic evidence supports an inherited contribution. In particular, greater concordance among more genetically similar relatives is consistent with genetic influence.

However, family and twin evidence cannot fully separate genes from shared environments, adoption studies contain confounding variables and molecular associations do not demonstrate causation. Addiction is polygenic and multifactorial, and no single gene explains every addiction.

Most importantly, vulnerability is not inevitability. Exposure, stress, family behaviour, peers, learning and protective factors influence whether the predisposition is expressed. The most defensible conclusion is therefore interactionist: inherited biology changes risk, while environmental and psychological experiences shape the final outcome.

Key Words 🔑

Key word	Student-friendly definition	How it may be used in an exam
Risk factor	A characteristic that increases the likelihood of an outcome	Define genetic vulnerability as one addiction risk
Genetic vulnerability	An inherited predisposition increasing addiction risk	Introduce the biological risk factor
Genetic predisposition	Another term for inherited vulnerability	Explain why risk is present before addiction develops
Gene	A section of DNA contributing to biological characteristics	Explain genetic transmission
Allele	A particular form of a gene	Explain genetic variation
Genotype	A person’s genetic make-up	Distinguish inherited risk from observable behaviour
Phenotype	The observable outcome produced by genes and environment	Explain why vulnerability may or may not be expressed
Polygenic	Influenced by several genes	Reject the idea of one addiction gene
Multifactorial	Influenced by several biological, psychological and environmental factors	Reach an interactionist conclusion
Candidate gene	A gene selected because it may influence a relevant biological process	Describe molecular-genetic research
DRD2	A gene associated with dopamine D2 receptor functioning	Give a cautious example of possible genetic influence
Dopamine	A neurotransmitter involved in reward and motivation	Explain a possible genetic pathway
Receptor	A structure that responds to a neurotransmitter or chemical signal	Explain inherited differences in reward sensitivity
Metabolism	Biological breakdown and processing of a substance	Explain genetic differences in substance response
Enzyme	A protein that helps a biological reaction occur	Explain inherited differences in metabolism
Reward sensitivity	The extent to which a person responds to rewarding outcomes	Link genes with repeated addictive behaviour
Indirect genetic effect	A genetic influence operating through another characteristic	Explain genes acting through personality or stress
Family study	Research examining whether characteristics occur among relatives	Introduce evidence for inherited risk
Monozygotic twins	Twins from one fertilised egg who share virtually all their genes	Explain twin-study comparisons
Dizygotic twins	Twins from separate fertilised eggs who share about half their segregating genes	Provide the comparison group in twin research
Concordance rate	The percentage of twin pairs sharing a characteristic	Interpret evidence for genetic influence
Equal environments assumption	The assumption that MZ and DZ twins experience equally similar environments	Evaluate twin evidence
Adoption study	Research comparing adopted people with biological and adoptive relatives	Explain attempts to separate genes and environment
Selective placement	Placing adopted children into families similar to their biological families	Evaluate adoption evidence
Linkage study	Research locating genetic markers associated with a characteristic	Explain molecular evidence
Heritability	The proportion of population variation associated with genetic differences	Avoid interpreting genetic influence as individual destiny
Protective factor	A characteristic that reduces the likelihood of addiction	Explain why vulnerability may remain unexpressed
Gene-environment interaction	A process in which genetic effects depend on environmental conditions	Explain different outcomes among similarly vulnerable people
Diathesis	An underlying predisposition or vulnerability	Explain interaction with environmental triggers
Biological reductionism	Explaining addiction mainly through genes and biological systems	Evaluate the explanation’s limited focus
Biological determinism	The view that inherited biology governs behaviour	Evaluate implications for control and recovery
Correlation	A relationship between measured variables	Evaluate genetic associations
Third variable	Another factor producing an apparent relationship	Evaluate family and molecular research

Hints from the Examiner Reports 💡

Define Risk as Increased Probability

Examiner hint: Risk factors make addiction more likely rather than certain.

A clear answer is:

Genetic vulnerability is an inherited biological predisposition that increases the chance of addiction.

Avoid:

A person with addiction genes will become addicted.

The June 2025 mark scheme explicitly defines risk factors through increased likelihood.

Explain a Psychological or Biological Mechanism

The June 2022 examiner report found that stronger answers explained risk factors through relevant psychological processes rather than racing through lists of factors and studies.

Do not write only:

Genes cause addiction.

Explain a pathway:

Genes may influence dopamine-receptor functioning, making an addictive substance or activity especially rewarding and increasing the likelihood of repetition.

Distinguish Family History from Genetic Proof

A family history may suggest:

Shared genes.
Shared modelling.
Shared access.
Shared stress.

A strong application acknowledges both possibilities.

Use Twin Evidence Carefully

A useful argument is:

Greater MZ than DZ concordance supports genetic influence because MZ twins share more genes. However, MZ concordance below 100% and possible environmental differences show that genes are not sufficient.

This gives both AO1 and AO3 value.

Do Not Invent Kendler’s Findings

AQA names:

Kendler’s twin research.
Kendler’s adoption research.

The supplied mark schemes do not provide detailed samples or numerical results.

Use them as examples of relevant evidence without inventing:

Participant numbers.
Exact concordance rates.
Exact risk percentages.
Details of particular addictions not provided by the source.

Explain the Interaction of Factors

The June 2025 examiner report states that successful evaluation often recognised that studying risk factors separately is unrealistic because the factors are interrelated.

A strong conclusion is:

Genetic vulnerability may affect reward sensitivity or stress responses, while peers, family and availability determine exposure and reinforcement.

Use Correlation Correctly

Do not say:

Twin studies prove genes cause addiction.

Write:

Twin studies demonstrate an association between genetic similarity and addiction similarity, but cannot completely control shared environmental influence.

Apply Family Information Precisely

When a stem states that several biological relatives are addicted:

Identify possible inherited vulnerability.
Explain what biological process may have been inherited.
State that the family also shares environmental influences.
Apply any additional triggers in the stem.
Conclude that risk has increased, not that addiction was inevitable.

Keep Genetic Vulnerability Separate from Neurochemistry

Genetic material is relevant where it explains inherited variation.

Neurochemistry is relevant where it explains how dopamine or other brain systems operate.

Connect them with a clear sequence:

Inherited genetic variation may influence receptor functioning, which changes the rewarding effect of nicotine.

Explain Why Vulnerability May Remain Unexpressed

Useful reasons include:

No exposure.
Strong protective factors.
Low stress.
Prosocial peers.
Effective coping.
Early intervention.

Do not merely state that “the environment matters”.

Develop Determinism and Reductionism

The 2022 examiner report warned against vague references to reductionism and determinism.

Develop each point:

The explanation is biologically reductionist because it focuses on genes and receptors while overlooking learned cues, social approval and cognitive beliefs.

It may appear deterministic because inherited risk is present from birth, but concordance below 100% and successful environmental intervention show that addiction is not fixed.

Include Practical Implications

Understanding vulnerability may support:

Early prevention.
Education.
Monitoring.
Treatment tailored to individual risk.
Protection during periods of stress.

How to improve:

Explain that genetic accounts may neglect cognition, learning, stress and social influence.

Mistake 15

Mistake: Inventing sample sizes or percentages for genetic studies.

Why this is risky:

Unsupported details weaken factual accuracy.

How to improve:

Use only evidence that can be described accurately and explain its relevance.

Exam-Style Questions ✍️

Question 1

What is meant by genetic vulnerability as a risk factor in addiction? [2 marks]

Question 2

Explain one way in which genes may influence the brain’s reward system. [3 marks]

Question 3

Explain one indirect pathway through which genes may increase addiction risk. [3 marks]

Question 4

Several of Ben’s biological relatives have experienced nicotine addiction. Ben begins smoking with colleagues during a stressful period and finds it difficult to stop.

Use your knowledge of genetic vulnerability to explain Ben’s addiction risk. [4 marks]

Question 5

Explain why genetic vulnerability does not necessarily lead to addiction. [4 marks]

Question 6

A hypothetical twin study produced the following results:

Twin type	Number of pairs studied	Number concordant for addiction
MZ twins	80	48
DZ twins	80	24

Calculate the concordance rate for each twin type. Explain what the pattern suggests and give one limitation of the conclusion. [6 marks]

Question 7

Explain one advantage of adoption studies over ordinary family studies when investigating genetic vulnerability to addiction. [3 marks]

Question 8

Explain one difference between genetic vulnerability and social influence as risk factors in addiction. [4 marks]

Question 9

Explain one strength and one limitation of genetic explanations of addiction. [6 marks]

Question 10

Discuss genetic vulnerability as a risk factor in the development of addiction. [16 marks]

Answers and Mark Scheme

Question 1

Award one mark for each of the following:

An inherited or biological predisposition.
The predisposition increases the likelihood of developing addiction but does not make it inevitable.

Maximum: 2 marks

Question 2

Award one mark for each linked point, up to three marks:

Genes may influence dopamine receptors or dopamine transmission.
This may change sensitivity to rewarding effects.
An addictive substance or behaviour may therefore feel particularly reinforcing.
Greater reward may increase repetition.
Repeated behaviour may contribute to dependence.

Question 3

Award one mark for each linked point, up to three marks.

Possible answers include:

Personality pathway

Genes may influence impulsivity or sensation seeking.
The person may be more likely to experiment with addictive substances or risky gambling.
Greater exposure increases the opportunity for addiction to develop.

Stress pathway

Genes may influence stress responsiveness.
The person may experience strong distress.
An addictive behaviour may be repeated because it provides temporary relief.

Withdrawal pathway

Genes may influence dependence or withdrawal severity.
Strong withdrawal makes abstinence more difficult.
Resuming the behaviour removes discomfort and maintains addiction.

Question 4

Award up to four marks for effective application:

Addiction among biological relatives suggests possible inherited vulnerability.
Ben may have inherited differences in reward sensitivity, nicotine response or metabolism.
The family pattern does not prove a genetic cause because relatives may also share environments.
Colleagues provided exposure and a social opportunity to smoke.
Stress may have acted as an environmental trigger.
Smoking may have provided reward or relief.
Difficulty stopping may reflect dependence or withdrawal.
Genetic, social and stress factors may have interacted.

Question 5

Award one mark for each relevant point, up to four marks:

Genetic vulnerability increases probability rather than guaranteeing addiction.
The person must normally be exposed to the substance or behaviour.
Social attitudes or peer groups may discourage initiation.
Stressful triggers may be absent.
Protective factors may reduce risk.
Effective coping or treatment may prevent addiction.
Several genes and environmental factors are involved.
MZ concordance below 100% shows that identical genetic vulnerability does not always produce the same outcome.

Question 6

Award one mark for each correct calculation:

MZ concordance=8048×100=60%DZ concordance=8024×100=30%

Award up to two marks for interpretation:

MZ concordance is twice the DZ concordance.
The higher MZ rate is consistent with genetic influence because MZ twins share more genes.
MZ concordance is below 100%, so genes cannot be sufficient.
Environmental differences must also contribute.

Award up to two marks for one limitation:

MZ twins may experience more similar environments than DZ twins.
Shared family exposure may contribute to both rates.
The research is correlational.
The sample may not represent the wider population.
The measure of addiction may lack validity.
The study does not identify a particular gene or biological mechanism.

Question 7

Award one mark for each linked point, up to three marks:

Adopted people share genes with biological relatives.
They share the rearing environment mainly with adoptive relatives.
Similarity with biological rather than adoptive relatives therefore provides stronger evidence of genetic influence than an ordinary family study.
This helps separate nature and nurture.

Credit limitations such as selective placement only where the advantage is still explained.

Question 8

Possible answer:

Genetic vulnerability is an inherited biological predisposition that may affect reward sensitivity, metabolism or personality. Social influence develops through environmental experiences such as observing family members, receiving peer approval or gaining access to addictive activities. Genetic vulnerability may alter how a person responds to an addictive substance, whereas social influence helps explain exposure, attitudes and learning. The two factors may interact.

For four marks, both risk factors should be accurate and the difference explicit.

Question 9

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

Possible strength:

Twin research has found greater similarity in addiction among MZ twins than DZ twins. Because MZ twins share more genetic material, this pattern is consistent with inherited vulnerability. Evidence from adoption and molecular studies provides additional support, increasing confidence that genes contribute to addiction risk.

Possible limitation:

MZ twins may be treated more similarly than DZ twins, so their higher concordance could partly reflect shared environmental experiences. Twin evidence is also correlational and cannot show that genes caused the addiction. Genetic influence may therefore be overestimated.

Other creditworthy points include:

Adoption evidence.
Biological mechanisms involving receptors or metabolism.
Polygenic complexity.
Gene-environment interaction.
Reductionism.
Determinism.
Practical applications.
Socially sensitive implications.

Question 10

A high-level response should include accurate knowledge and developed evaluation.

Indicative AO1 content

Definition of risk factor.
Definition of genetic vulnerability.
Predisposition rather than certainty.
Genes and inherited DNA.
Genotype and phenotype.
Polygenic inheritance.
Multifactorial addiction.
Genes affecting dopamine receptors.
Reward sensitivity.
Substance-metabolising enzymes.
Withdrawal and dependence.
Indirect genetic effects through personality.
Impulsivity and sensation seeking.
Genetic influence on stress responsiveness.
Family studies.
Twin studies.
MZ and DZ twins.
Concordance rates.
Adoption studies.
Linkage or candidate-gene research.
Possible example of DRD2.
Gene-environment interaction.
Protective and triggering factors.

Indicative AO3 content

Twin evidence supporting inherited vulnerability.
Kendler’s twin research as relevant evidence.
MZ concordance below 100%.
Equal environments assumption.
Adoption evidence.
Kendler’s adoption research.
Selective placement.
Prenatal environmental influences.
Converging evidence from different methods.
Problems with candidate-gene associations.
Polygenic complexity.
Correlation and causation.
Shared family environment.
Genes not explaining exposure.
Differences between initiation and maintenance.
Heterogeneity of addiction.
Gene-environment interaction.
Single-factor compared with multifactorial explanations.
Biological reductionism.
Biological determinism.
Socially sensitive implications.
Genetic privacy and labelling.
Practical applications for prevention and treatment.
Need to combine genetic, personality and social risk factors.

Thirteen to sixteen marks: Knowledge is accurate and generally detailed. Discussion is thorough, focused and effective. The answer consistently treats genes as a vulnerability rather than destiny and uses evidence, methodological issues and interactionism to reach a reasoned conclusion.

Nine to twelve marks: Knowledge is mostly accurate and discussion is generally effective. Genetic mechanisms and relevant research methods are explained, although some evaluative arguments may lack depth or balance.

Five to eight marks: Some relevant knowledge is present, but the response is mainly descriptive. The answer may state that addiction runs in families without explaining mechanisms, or evaluation may be generic.

One to four marks: Knowledge is very limited or confused. The response may claim that a single gene guarantees addiction, treat family history as proof or provide little relevant evaluation.