Hormonal and Genetic Mechanisms in Aggression | AQA A-Level Psychology Revision
- Revision Notes
- Aug 7
- 21 min read
Updated: Aug 14
For 7182 specification, first teach in September 2025
AQA A-Level Psychology | Free Revision Notes
Estimated study time: 60 to 75 minutes
Hormonal and genetic mechanisms A-Level Psychology revision examines how testosterone and inherited biological factors may influence aggressive behaviour. You will learn how testosterone may affect the neural regulation of aggression and how variants of the monoamine oxidase A gene can create a genetic vulnerability. This lesson builds directly on brain structures and serotonin in aggression [Lesson 1: Neural mechanisms] and prepares you to compare biological explanations with environmental accounts later in the Aggression option.
The AQA specification requires students to study testosterone as a hormonal mechanism and genetic factors in aggression, including the monoamine oxidase A gene.
Learning Objectives 🎯
By the end of this revision page, you should be able to:
Define testosterone, genetic factors and the monoamine oxidase A gene.
Explain how testosterone may influence aggressive behaviour.
Explain how the MAOA gene may create a vulnerability to aggression.
Apply hormonal and genetic explanations to unfamiliar situations and data.
Compare hormonal and genetic mechanisms.
Evaluate these explanations using evidence, methodological issues and psychological debates.
Revision Notes 📚
Hormonal and Genetic Mechanisms A-Level Psychology Revision Focus
Hormonal and genetic explanations are biological explanations of aggression. They propose that aggressive behaviour is partly influenced by internal biological processes.
A hormonal explanation focuses on chemical messengers released into the bloodstream.
A genetic explanation focuses on inherited information carried in deoxyribonucleic acid, usually shortened to DNA.
Both explanations may affect the functioning of neural systems involved in emotional responses and behavioural control.
This reflects the assumptions of the biological explanation of behaviour [Lesson 7: The biological approach]. It is also important to understand that biological influence does not necessarily make aggressive behaviour inevitable.
What Is Testosterone?
Testosterone is an androgen, meaning that it is a hormone associated with male sexual development and functioning. It is secreted mainly by the testes, although testosterone is present in people of different sexes.
Hormones are chemical messengers released by glands and transported through the bloodstream. This process connects with your earlier study of hormonal communication in the body [Lesson 4: The endocrine system].
Testosterone has been linked with aggression. The proposed explanation is that relatively high testosterone activity may increase a person’s readiness to respond aggressively, particularly in situations involving threat, competition or provocation.
Testosterone and Aggressive Behaviour
Testosterone does not simply switch aggression on. Its effects may occur through the way it influences brain systems involved in emotion and behavioural control.
Testosterone may:
Influence the activity of the amygdala, which is involved in emotional responses to threat.
Affect the orbitofrontal cortex, which contributes to impulse control and evaluating consequences.
Make emotional responses more difficult to regulate in provocative situations.
Increase the likelihood that a strong emotional response is expressed as aggression.
The proposed process can be summarised as follows:
A person encounters a threat or provocation.
Limbic structures such as the amygdala respond to its emotional significance.
Frontal areas normally regulate the response and inhibit inappropriate behaviour.
Testosterone may affect the balance between limbic activity and frontal control.
An aggressive response may become more likely.
An AQA mark scheme has recognised that testosterone may mediate activity in the amygdala and orbitofrontal cortex. This means that hormonal and neural mechanisms should not always be treated as completely separate explanations.
Testosterone Increases Risk, Not Certainty
A hormonal explanation does not mean that a person with relatively high testosterone will always behave aggressively.
Aggression may also depend on:
The nature of the situation.
Whether a person interprets something as threatening.
Their previous learning experiences.
Social rules and expected behaviour.
The strength of their behavioural control.
Whether aggression has previously been rewarded.
Testosterone is therefore better described as one factor that may alter the probability of aggression.
A careful exam statement would be:
Relatively high testosterone activity may increase a person’s vulnerability to aggression, particularly when the person encounters a provocative or competitive situation.
An inaccurate statement would be:
High testosterone always causes aggression.
Evidence for the Role of Testosterone
Research has found associations between testosterone and aggressive behaviour. Evidence also comes from animal research in which hormonal activity can be studied or altered under controlled conditions.
This evidence is useful because it suggests that aggression has a biological component. However, different research methods permit different conclusions.
Type of evidence | Possible contribution | Main limitation |
Correlations between testosterone and aggression | Show whether the two variables are related | Cannot establish that testosterone caused aggression |
Animal experiments | Allow greater control and manipulation of hormonal activity | Animal aggression may not represent complex human aggression |
Studies of naturally occurring hormonal differences | Allow investigation of hormones without experimentally changing them | Other biological and environmental differences may affect behaviour |
Research examining testosterone and brain activity | Connects hormonal and neural mechanisms | Brain and hormone measures may still be correlational |
The Direction of Effect Problem
An association between testosterone and aggression does not reveal which variable came first.
Several explanations are possible:
Higher testosterone activity increases aggressive behaviour.
Participating in aggressive or competitive behaviour changes testosterone activity.
Another factor affects both testosterone and aggression.
This is known as a direction of effect problem.
Researchers must therefore avoid concluding that testosterone causes aggression merely because the two variables are correlated.
What Are Genetic Factors?
Genetic factors are inherited influences on behaviour. Genes are sections of DNA that contribute to biological characteristics and processes.
Genetic explanations of aggression propose that inherited differences may affect:
Neurotransmitter functioning.
Hormonal activity.
Brain development.
Impulse control.
Emotional responses to threat or provocation.
Aggression is not usually explained as the product of one simple “aggression gene”. Genetic influences are better understood as creating a predisposition or vulnerability.
The MAOA Gene
The monoamine oxidase A gene, abbreviated to MAOA, is located on the X chromosome. It provides instructions for producing the enzyme monoamine oxidase A.
This enzyme helps break down monoamine neurotransmitters, including:
Serotonin.
Dopamine.
Noradrenaline.
This creates a direct connection between genetic and neural explanations. Genes may influence aggression by affecting the neurochemistry involved in impulse control and emotional regulation.
Your understanding of neurotransmitter activity and inhibition [Lesson 3: Synaptic transmission] will help you follow this mechanism.
The Low-Activity MAOA Variant
A low-activity form of the gene is often called MAOA-L.
MAOA-L produces relatively low activity of the monoamine oxidase A enzyme. Consequently, monoamine neurotransmitters are not broken down as efficiently.
The proposed chain is:
A person inherits a low-activity MAOA variant.
Less active monoamine oxidase A enzyme is produced.
The regulation of serotonin, dopamine and noradrenaline is affected.
Neural systems involved in emotion and impulse control may function differently.
The person may become more vulnerable to impulsive or aggressive behaviour.
AQA mark schemes recognise MAOA-L, reduced enzyme activity, altered monoamine levels and impulsivity as relevant parts of a genetic explanation of aggression.
Avoiding an Oversimplified Serotonin Explanation
Students sometimes notice an apparent contradiction:
Neural explanations link low serotonin activity with reduced inhibition.
The MAOA account suggests that reduced enzyme activity can produce excessive monoamine availability.
Do not reduce either explanation to a rule such as “more serotonin causes aggression” or “less serotonin causes aggression”.
The MAOA explanation concerns the regulation of several neurotransmitters by an enzyme. The neural explanation focuses on serotonin functioning within particular brain systems involved in inhibition. In both cases, the important point is disrupted neurochemical regulation, rather than a simple total amount of serotonin throughout the brain.
Evidence from Selective Breeding
Selective breeding involves choosing animals with a particular characteristic and breeding them together.
If animals selected for aggression produce offspring that are also more aggressive, this suggests that inherited factors contribute to the behaviour.
A possible procedure would be:
Researchers assess aggression in a population of animals.
Animals showing relatively high aggression are bred together.
Aggression is measured in later generations.
Researchers examine whether aggressive traits become more frequent.
A strength of selective breeding is that the process can demonstrate how behavioural characteristics change across generations.
However, selective breeding does not identify a single gene responsible for the behaviour. It may select several inherited characteristics at the same time.
Evidence from Gene-Disabling Studies
Animal research has also examined the effects of disabling the MAOA gene.
When normal MAOA functioning is disrupted, animals may show increased aggression. This supports the view that the gene contributes to the neurochemical regulation of aggressive behaviour.
Such research may provide stronger evidence of cause and effect because researchers alter the gene and observe the resulting behaviour.
However, there are important limitations:
Human aggression involves language, beliefs, social rules and conscious decision-making.
Animal aggression may not be equivalent to human aggression.
Procedures involving gene disabling would be unacceptable in human research.
A gene may have different effects in different species.
Evidence from Twin Studies
Twin studies compare monozygotic twins, who share all their genes, with dizygotic twins, who share approximately half of the genes that vary between people.
Researchers may calculate concordance rates, which show the extent to which both members of a twin pair display the same characteristic.
The reasoning is:
If aggression is partly inherited, monozygotic twins should be more similar in aggression than dizygotic twins.
Higher concordance among monozygotic twins therefore supports a genetic contribution.
AQA mark schemes identify higher concordance for some forms of aggression in monozygotic twins than in dizygotic twins as relevant supporting evidence.
However, monozygotic twins may also experience more similar environments than dizygotic twins. This makes it difficult to separate genetic and environmental influences completely.
Evidence from Adoption Studies
Adoption studies compare an adopted person with:
Their biological relatives, with whom they share genes.
Their adoptive relatives, with whom they share an environment.
Greater similarity to biological relatives would support a genetic contribution. Greater similarity to adoptive relatives would support environmental influence.
Adoption evidence has indicated a significant genetic element in aggressive behaviour. Nevertheless, adoption does not create a perfectly clean separation of nature and nurture.
For example:
Adopted children experienced a prenatal environment before adoption.
Adoption agencies may place children in families similar to their biological families.
Contact with biological relatives may continue.
Adoption itself may affect development.
Gene-Environment Interaction
One of the most important evaluations is that a genetic vulnerability may only lead to aggression under particular environmental conditions.
This is a gene-environment interaction.
A person may inherit MAOA-L but not develop unusually aggressive behaviour. The effect of the gene may depend on experiences such as childhood trauma or stressful situations.
The interaction can be expressed as:
Genetic vulnerability + environmental trigger → increased likelihood of aggression
This does not mean that every person exposed to adversity becomes aggressive, or that every person with MAOA-L behaves aggressively. Both vulnerability and environment affect the outcome.
This explanation connects directly to interactionism in the nature-nurture debate [Lesson 4: The nature-nurture debate].
A Diathesis-Stress Interpretation
The gene-environment interaction can be expressed using the diathesis-stress model:
Diathesis means an underlying vulnerability, such as MAOA-L.
Stress means an environmental experience that activates or strengthens that vulnerability.
Aggression is most likely when the vulnerability and environmental trigger occur together.
This is more complete than a purely genetic account because it explains why people with the same genetic variant may behave differently.
How Testosterone and MAOA Differ
Feature | Testosterone explanation | MAOA explanation |
Type of biological factor | Hormonal | Genetic |
Main biological component | An androgen hormone | A gene coding for an enzyme |
Proposed mechanism | May influence emotional brain activity and behavioural control | Affects the breakdown and regulation of monoamine neurotransmitters |
Evidence | Hormone-behaviour correlations and animal research | Twin, adoption, selective breeding and gene-disabling research |
Main causal problem | Aggression may alter hormone activity | Genetic similarity may be confused with environmental similarity |
Environmental role | Situations may affect whether hormonal vulnerability is expressed | Environmental triggers may interact with genetic vulnerability |
Appropriate conclusion | Testosterone may increase the likelihood of aggression | MAOA variants may create a predisposition to aggression |
Applying Testosterone to an Unfamiliar Scenario
Consider this scenario:
Researchers find that Leon has a relatively high testosterone level. During a competitive match, an opponent deliberately pushes him. Leon immediately responds by pushing the opponent to the ground.
A weak application would be:
Leon is aggressive because he has testosterone.
This is vague and deterministic.
A stronger application would be:
Leon’s relatively high testosterone level may have increased his sensitivity to the competitive and provocative situation. Testosterone may influence activity in the amygdala and orbitofrontal cortex, making the emotional response more difficult to regulate. This could have increased the likelihood of Leon’s immediate aggressive reaction.
The stronger answer:
Uses details from the scenario.
Explains a mechanism.
Links the hormone to neural regulation.
Uses cautious language.
Does not claim that testosterone made aggression inevitable.
Applying the MAOA Gene to an Unfamiliar Scenario
Consider this scenario:
Genetic testing identifies a low-activity MAOA variant in Arun. Arun experienced serious adversity during childhood and now frequently responds impulsively during confrontations.
A strong application might state:
Arun may have a genetic vulnerability because the low-activity MAOA variant produces reduced activity of the monoamine oxidase A enzyme. This can disrupt the regulation of serotonin, dopamine and noradrenaline, affecting emotional and impulse control. Arun’s childhood adversity may have acted as an environmental trigger, illustrating a gene-environment interaction rather than genetic determinism.
Strength: Supporting Biological Evidence
Hormonal and genetic explanations are supported by several types of scientific evidence.
For testosterone, research has identified associations between hormone activity and aggression. For genetic explanations:
Twin studies have found greater similarity among monozygotic twins.
Adoption studies suggest a genetic contribution.
Selective breeding demonstrates inherited differences in animals.
Gene-disabling research links altered MAOA functioning with aggression.
MAOA-L has been associated with aggressive and impulsive behaviour.
The use of several methods produces converging evidence. When different research designs point towards biological influence, confidence in the broad explanation increases.
However, the methods do not all establish the same conclusion. Correlations show an association, while controlled animal studies provide stronger causal evidence but weaker generalisability.
Strength: Explanations Link Different Biological Levels
Hormonal and genetic mechanisms can be connected rather than treated as isolated causes.
For example:
Genes may affect the production of enzymes.
Enzymes influence neurotransmitter activity.
Neurotransmitters affect communication between brain structures.
Hormones may influence activity in emotional and regulatory brain systems.
These neural processes may affect aggressive behaviour.
This gives a more integrated biological explanation than simply stating that aggression is “in the genes”.
Limitation: Cause and Effect Is Difficult to Establish
Much human evidence is correlational.
Researchers cannot normally:
Assign participants to different genetic variants.
Experimentally alter a person’s genes.
Manipulate testosterone freely without ethical concerns.
Control every environmental influence across a person’s life.
As a result, an association between a biological factor and aggression may not demonstrate causation.
For testosterone:
Aggression may alter testosterone.
A competitive situation may increase both testosterone and aggression.
Personality may affect both variables.
For genetic factors:
Relatives share environments as well as genes.
Genetic variants may be associated with other inherited characteristics.
Environmental experiences may determine whether a vulnerability is expressed.
Limitation: Problems with Animal Research
Some of the strongest causal evidence comes from animals.
Animal studies allow researchers to:
Control breeding.
Manipulate hormonal activity.
Disable particular genes.
Standardise environmental conditions.
This increases control and helps researchers identify biological mechanisms.
However, extrapolation to humans is difficult because human aggression may involve:
Beliefs and intentions.
Moral judgement.
Social expectations.
Planned retaliation.
Language and communication.
Awareness of consequences.
Animal evidence supports a biological contribution, but it cannot explain the full complexity of human aggression.
Limitation: Problems with Twin Studies
Higher concordance among monozygotic twins may be taken as evidence of genetic influence, but monozygotic twins often share more similar environments than dizygotic twins.
They may:
Be treated more similarly by parents.
Spend more time together.
Be encouraged to share activities.
Experience similar expectations from others.
The greater similarity in aggression could therefore reflect both genes and environment.
Twin research supports a genetic contribution, but it cannot provide an exact measure of how much aggression is caused by genes.
Strength: Interactionism Explains Individual Differences
A gene-environment interaction provides a stronger explanation than genetic determinism.
It explains why:
Not everyone with MAOA-L becomes aggressive.
People exposed to similar adversity respond differently.
Aggression may appear only in particular situations.
Environmental support may reduce the expression of vulnerability.
This acknowledges both heredity and experience and therefore avoids presenting genes as an unavoidable behavioural destiny.
Limitation: Biological Reductionism
Hormonal and genetic explanations may be criticised for biological reductionism because they reduce aggression to hormones, genes, enzymes and neurotransmitters.
This may overlook:
Learning from aggressive role models.
Reinforcement of aggressive behaviour.
Group anonymity.
Frustration.
Cultural expectations.
Prison conditions.
Media influences.
For example, learning aggression through observation and reinforcement [Lesson 6: Social learning theory] explains why a person may copy behaviours that appear successful or rewarded.
A biological explanation may identify a vulnerability but may not explain why aggression occurs towards a particular person, at a particular time or in a particular social setting.
This criticism links to levels of explanation in psychology [Lesson 5: Holism and reductionism].
Limitation: Biological Determinism
Hormonal and genetic explanations can appear biologically deterministic because they suggest that aggressive behaviour is governed by internal biological forces.
This has important implications:
It may reduce the perceived responsibility of an aggressive person.
It raises questions about blame and punishment.
It may suggest that behaviour cannot be changed.
People identified as biologically vulnerable could be labelled or stigmatised.
Biological differences might be misused to make predictions about individuals.
However, the evidence does not show that aggression is inevitable. An interactionist account allows biological influences while recognising that people respond differently across environments.
This issue connects with biological determinism and personal responsibility [Lesson 3: Free will and determinism].
Limitation: Socially Sensitive Implications
Research into genes, hormones and aggression may be socially sensitive because findings could affect how individuals or groups are treated.
Possible risks include:
Labelling someone as dangerous because of a genetic variant.
Treating biological risk as proof of future behaviour.
Discrimination by employers, insurers or criminal justice agencies.
Ignoring social causes of aggression.
Assuming that intervention or rehabilitation is pointless.
Researchers must communicate that biological factors indicate probabilities, not certainties.
Comparison with Evolutionary Explanations
Genetic explanations can also be connected with the adaptive value of aggression [Lesson 4: Evolutionary explanations].
An evolutionary explanation proposes that inherited tendencies towards aggression may have remained in the population because they supported survival or reproductive success.
However, the two explanations have different emphases:
The MAOA explanation focuses on a specific genetic and neurochemical mechanism.
The evolutionary explanation focuses on why an inherited tendency might have been adaptive.
Do not replace an MAOA answer with a general account of natural selection unless the question allows more than one explanation.
Overall Evaluation
Testosterone and the MAOA gene provide scientifically testable explanations for biological differences in aggression. Evidence from hormonal research, twin studies, adoption research, selective breeding and gene-disabling studies supports the conclusion that aggression has a biological component.
However, the strongest human evidence is often correlational, while the strongest causal evidence often comes from animals. Neither testosterone nor MAOA-L makes aggression inevitable.
The most defensible conclusion is that hormones and genes create vulnerabilities whose effects depend on neural functioning, environmental experiences and the situation in which behaviour occurs.
Key Words 🔑
Key word | Student-friendly definition | How it may be used in an exam |
Hormone | A chemical messenger released by a gland and transported in the bloodstream | Introduce testosterone as a biological influence on aggression |
Testosterone | An androgen hormone linked with aggressive behaviour | Explain how hormonal activity may affect emotional and impulse-control systems |
Androgen | A class of hormones associated with male sexual development and functioning | Identify the type of hormone testosterone is |
Amygdala | A limbic structure involved in processing emotional significance and threat | Explain how testosterone may influence emotional responses |
Orbitofrontal cortex | A frontal brain area involved in evaluating consequences and controlling impulses | Explain how testosterone may affect behavioural regulation |
Genetic factor | An inherited biological influence carried in DNA | Introduce inherited explanations of aggression |
Gene | A section of DNA that contributes to a biological characteristic or process | Explain how inherited information can affect behaviour |
Predisposition | An increased vulnerability to develop a behaviour, rather than a certainty | Avoid claiming that genes determine aggression completely |
MAOA gene | A gene that provides instructions for producing monoamine oxidase A | Explain a specific genetic factor required by AQA |
Monoamine oxidase A | An enzyme involved in breaking down monoamine neurotransmitters | Explain how the MAOA gene affects neurochemistry |
MAOA-L | A low-activity variant of the MAOA gene | Link reduced enzyme activity with vulnerability to impulsive aggression |
Monoamine | A category of neurotransmitter that includes serotonin, dopamine and noradrenaline | Explain which neurotransmitters are affected by MAOA |
Selective breeding | Breeding animals with a chosen characteristic to examine inheritance | Use as evidence that aggression has a genetic component |
Concordance rate | The extent to which both members of a pair share a characteristic | Interpret evidence from twin studies |
Monozygotic twins | Twins who share all their genes | Explain why their aggression is compared with dizygotic twins |
Dizygotic twins | Twins who share approximately half of the genes that vary between people | Use as a comparison group in genetic research |
Gene-disabling study | Research in which the normal functioning of a gene is prevented | Evaluate causal evidence involving MAOA in animals |
Gene-environment interaction | The combined influence of inherited vulnerability and environmental experience | Evaluate a purely genetic explanation |
Diathesis-stress model | The idea that an underlying vulnerability may be activated by environmental stress | Explain why MAOA-L does not inevitably produce aggression |
Biological reductionism | Explaining complex behaviour through smaller biological components | Evaluate hormonal and genetic explanations |
Biological determinism | The view that behaviour is governed by biological forces outside conscious control | Discuss responsibility and the possibility of change |
Hints from the Examiner Reports 💡
Examiner hint: Focus on the precise explanation named in the question.
In the June 2022 examination, some students treated a question about genetic factors as a general question about biological explanations. Weaker answers concentrated almost entirely on neural mechanisms and barely discussed genes. Stronger responses gave accurate genetic explanations and supporting evidence.
For a question on genetic factors, prioritise:
Inheritance.
MAOA.
MAOA-L.
Monoamine oxidase A enzyme activity.
Neurotransmitter regulation.
Twin, adoption or selective-breeding evidence.
Gene-environment interaction.
Shape Related Material to the Question
Examiner hint: Neural material only becomes useful in a genetic answer when you establish the genetic link.
For example:
Serotonin is linked with aggression.
This is neural rather than genetic.
A better genetic link would be:
The MAOA gene controls the production of an enzyme involved in breaking down serotonin, dopamine and noradrenaline. A low-activity variant can therefore affect neural regulation and increase vulnerability to impulsive aggression.
The November 2020 examiner report similarly noted that material about genes in a neural-mechanisms question required an explicit connection to brain structure, functioning or neurochemistry.
Keep Testosterone Relevant
Examiner hint: Evidence about testosterone must be shaped to the behaviour named in the question.
Do not write a general paragraph explaining that testosterone is involved in biological sex. In an aggression answer, explain how testosterone may affect amygdala activity, orbitofrontal regulation or responsiveness to provocation.
Use Evidence as Part of an Argument
Examiner hint: Do not merely name a study and assume it counts as evaluation.
Use the pattern:
State the evidence.
Explain what it shows.
Link it to the hormonal or genetic explanation.
Identify a limitation where relevant.
Reach a reasoned conclusion.
For example:
Higher concordance for aggression in monozygotic than dizygotic twins supports a genetic contribution because monozygotic twins share more genes. However, monozygotic twins may also share more similar environments, so the difference cannot be attributed entirely to heredity.
Develop Evaluation Points
Examiner hint: Words such as “reductionist” and “deterministic” do not earn substantial credit unless they are explained.
A developed reductionism point should identify:
What the behaviour is reduced to.
What influences are omitted.
Why this limits the explanation.
Whether an interactionist account would be more complete.
The June 2022 report noted widespread misuse of the terms reductionism and determinism in extended responses.
Balance Description and Evaluation
For a 16-mark question asking you to discuss genetic factors, the 2022 mark scheme allocated:
AO1: 6 marks.
AO3: 10 marks.
This means a high-level answer needs substantial evaluation, not several pages of description followed by one brief limitation.
A useful structure is:
Explain inherited vulnerability and MAOA.
Explain relevant genetic evidence.
Evaluate animal evidence.
Evaluate twin or adoption evidence.
Develop gene-environment interaction.
Discuss reductionism, determinism or implications.
Reach a balanced conclusion.
Common Mistakes ⚠️
Mistake 1
Mistake: Describing testosterone as a neurotransmitter.
Why this is incorrect:
Testosterone is a hormone carried in the bloodstream. Serotonin is a neurotransmitter used in communication between neurons.
How to improve:
Learn the distinction:
Testosterone is an androgen hormone. Serotonin is a neurotransmitter.
Mistake 2
Mistake: Claiming that testosterone always produces aggression.
Why this is incorrect:
Testosterone may increase vulnerability or affect responsiveness to provocation, but behaviour also depends on neural control, learning and the situation.
How to improve:
Use phrases such as:
“May increase the likelihood.”
“Is associated with.”
“May influence.”
“Creates a vulnerability.”
Mistake 3
Mistake: Writing that the MAOA gene is itself a neurotransmitter.
Why this is incorrect:
MAOA is a gene. It provides instructions for producing the monoamine oxidase A enzyme, which affects the breakdown of neurotransmitters.
How to improve:
Use the chain:
MAOA gene → monoamine oxidase A enzyme → regulation of monoamine neurotransmitters → possible influence on aggression
Mistake 4
Mistake: Calling MAOA-L an “aggression gene”.
Why this is incorrect:
MAOA-L creates a possible vulnerability. It does not program a person to become aggressive.
How to improve:
Refer to a low-activity genetic variant associated with increased vulnerability to impulsive aggression.
Mistake 5
Mistake: Saying that MAOA only affects serotonin.
Why this is incorrect:
The enzyme is involved in breaking down several monoamine neurotransmitters, including serotonin, dopamine and noradrenaline.
How to improve:
Name all three when explaining the mechanism.
Mistake 6
Mistake: Assuming that higher monoamine levels always have one simple effect.
Why this is incorrect:
The MAOA account concerns disrupted regulation of several neurotransmitters. Behaviour cannot be predicted from a simple “more” or “less” rule.
How to improve:
Focus on altered neurotransmitter regulation, emotional control and impulsivity.
Mistake 7
Mistake: Using neural evidence without linking it to genetics.
Why this is incorrect:
A question about genetic factors requires inherited mechanisms. A paragraph about serotonin or the amygdala alone does not answer that question.
How to improve:
Explain how the MAOA gene influences the enzyme that regulates neurotransmitters.
Mistake 8
Mistake: Treating twin concordance as proof of genetic causation.
Why this is incorrect:
Monozygotic twins share environments as well as genes. Greater concordance may reflect both influences.
How to improve:
State that twin evidence supports a genetic contribution but cannot completely separate nature and nurture.
Mistake 9
Mistake: Evaluating animal research by saying only that “animals are different”.
Why this is incorrect:
This does not explain how the difference affects the conclusion.
How to improve:
Explain that human aggression involves social meanings, intentions and moral decisions, so genetically altered aggression in an animal may not generalise fully to human behaviour.
Mistake 10
Mistake: Using “reductionist” and “deterministic” as unexplained labels.
Why this is incorrect:
Evaluation requires a developed argument.
How to improve:
Explain precisely what is omitted by the explanation and why that weakens its account of aggression.
Exam-Style Questions ✍️
Question 1
What type of hormone is testosterone? [1 mark]
Question 2
Outline the role of the monoamine oxidase A gene in aggression. [2 marks]
Question 3
Explain how testosterone may influence aggressive behaviour. [4 marks]
Question 4
Explain how the low-activity variant of the MAOA gene may increase vulnerability to aggression. [4 marks]
Question 5
Researchers measure Vicky’s testosterone level before a competitive activity. Vicky has a relatively high testosterone level. During the activity, another participant deliberately prevents her from completing a task. Vicky immediately shouts at the participant and pushes their equipment onto the floor.
Using your knowledge of hormonal mechanisms, explain Vicky’s behaviour. [4 marks]
Question 6
Researchers compare concordance for high aggression in two types of twin pair.
Twin pair | Concordance for high aggression |
Monozygotic twins | $56%$ |
Dizygotic twins | $30%$ |
Calculate the difference in concordance between monozygotic and dizygotic twins. Show your working. Explain what the result suggests and identify one reason why it does not prove that aggression is genetically determined. [5 marks]
Question 7
Safiya has inherited the low-activity MAOA variant. She experienced a stable and supportive childhood and does not normally behave aggressively. Her cousin Idris has the same variant but experienced serious childhood adversity and frequently responds aggressively during confrontations.
Use your knowledge of genetic factors to explain the difference between Safiya and Idris. [4 marks]
Question 8
Explain one strength and one limitation of hormonal or genetic explanations of aggression. [6 marks]
Question 9
Discuss hormonal and genetic mechanisms in human aggression. [16 marks]
Answers and Mark Scheme
Question 1
Answer: An androgen. [1 mark]
Question 2
Award one mark for each of the following:
The MAOA gene provides instructions for producing the monoamine oxidase A enzyme.
This enzyme helps regulate or break down monoamine neurotransmitters.
A low-activity variant has been associated with increased impulsivity or aggression.
The gene therefore creates a possible vulnerability to aggression.
Maximum: 2 marks
Question 3
Award one mark for each relevant point, up to four marks:
Testosterone is an androgen hormone.
It has been associated with increased aggression.
Testosterone may influence activity in the amygdala.
The amygdala is involved in emotional responses to threat or provocation.
Testosterone may affect the orbitofrontal cortex.
The orbitofrontal cortex contributes to impulse control and evaluating consequences.
Hormonal influence may make an aggressive response more likely.
Testosterone does not make aggression inevitable.
A full-mark answer should explain a process rather than merely state that testosterone is linked with aggression.
Question 4
Possible content:
MAOA-L is a low-activity variant of the MAOA gene.
The gene controls production of the monoamine oxidase A enzyme.
The enzyme is involved in breaking down serotonin, dopamine and noradrenaline.
The low-activity variant produces reduced enzyme activity.
Monoamine neurotransmitter regulation is therefore altered.
This may affect emotional control, impulsivity or neural inhibition.
Aggressive behaviour may become more likely.
The variant is a vulnerability rather than a direct cause.
Award up to four marks for a clear and logically connected explanation.
Question 5
Award up to two marks for relevant knowledge and up to two marks for effective application.
Possible content:
Vicky’s relatively high testosterone may have increased her responsiveness to the competitive situation.
Being deliberately prevented from completing the task provides a clear provocation.
Testosterone may influence amygdala activity, strengthening the emotional response.
It may also affect regulation by the orbitofrontal cortex.
Reduced control could explain why Vicky responded immediately.
Shouting and pushing the equipment are aggressive responses.
Testosterone may have increased the likelihood of the behaviour, but it did not make it inevitable.
Question 6
Calculation:
56%−30%=26 percentage points
Award one mark for the correct answer with working.
Possible interpretation:
Concordance is 26 percentage points higher among monozygotic twins.
Monozygotic twins share more genes than dizygotic twins.
This pattern supports a genetic contribution to aggression.
Possible limitation:
Monozygotic twins may be treated more similarly.
They may experience more similar environments.
The study therefore cannot completely separate genes from environmental influences.
Concordance is not $100%$, showing that genes do not fully determine aggression.
Award:
One mark for the calculation.
Up to two marks for interpretation.
Up to two marks for the limitation.
Question 7
Possible content:
Safiya and Idris both have a genetic vulnerability associated with MAOA-L.
The variant alone does not inevitably produce aggression.
Safiya’s stable and supportive childhood may mean that the vulnerability was not activated or strengthened.
Idris’s childhood adversity may have acted as an environmental trigger.
The difference illustrates a gene-environment interaction.
It can also be explained using a diathesis-stress model.
Idris’s aggression results from the combination of genetic vulnerability and environmental stress.
Safiya’s behaviour demonstrates that genetic predisposition is not genetic destiny.
Award up to four marks for clear application to both people.
Question 8
Award up to three marks for one developed strength and up to three marks for one developed limitation.
Possible strength:
Genetic explanations are supported by twin evidence showing higher concordance for aggression among monozygotic twins than dizygotic twins. Because monozygotic twins share more genes, this pattern supports an inherited contribution. Similar conclusions from adoption, selective-breeding and MAOA research provide converging evidence.
Possible limitation:
Twin evidence cannot completely separate heredity from environmental influence. Monozygotic twins may be treated more similarly and have more similar experiences than dizygotic twins. Higher concordance may therefore be partly environmental, meaning genetic causation cannot be established.
Other creditworthy points include:
Supporting hormonal or gene-disabling evidence.
Problems generalising from animals.
Correlational evidence and direction of effect.
Biological reductionism.
Biological determinism.
Gene-environment interaction.
Socially sensitive implications.
Question 9
A high-level response should contain accurate explanation and substantial evaluation.
Indicative AO1 content:
Testosterone as an androgen hormone.
Association between testosterone and aggression.
Possible influence on amygdala and orbitofrontal activity.
Genetic inheritance and predisposition.
MAOA gene and monoamine oxidase A enzyme.
MAOA-L and reduced enzyme activity.
Effects on serotonin, dopamine and noradrenaline regulation.
Impulsivity and increased vulnerability to aggression.
Twin, adoption, selective-breeding or gene-disabling evidence.
Gene-environment interaction.
Indicative AO3 content:
Research supporting a hormonal contribution.
Correlation and direction of effect problems.
Support from twin and adoption research.
Shared-environment problems in twin studies.
Causal evidence from animal studies.
Difficulties extrapolating from animals to humans.
Converging evidence from different methods.
Gene-environment interaction.
Biological reductionism.
Biological determinism.
Moral, legal and socially sensitive implications.
Comparison with social psychological explanations.
Hormonal and genetic vulnerability rather than inevitability.
Thirteen to sixteen marks: Knowledge is accurate and generally detailed. Discussion is thorough, focused and well developed. Evidence is used to construct arguments, and specialist terminology is effective.
Nine to twelve marks: Knowledge is mostly accurate and discussion is mostly effective. Some points may lack development or the answer may lose focus occasionally.
Five to eight marks: Limited knowledge is present, but the response is mainly descriptive. Evaluation lacks development or relevance.
One to four marks: Knowledge is very limited or confused. Evaluation is absent, generic or poorly focused.
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