SCHIZOPHRENIA ASSESSMENT
CONTENTS
CLASSIFICATION OF SCHIZOPHRENIA:
Positive symptoms of schizophrenia include hallucinations and delusions. Negative symptoms of schizophrenia include speech poverty and avolition.RELIABILITY AND VALIDITY IN DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA:
Including references to comorbidity, culture and gender bias, and symptom overlap.BIOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA:
Genetics and neural correlates, including the dopamine hypothesis.PSYCHOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA:
Family dysfunction and cognitive explanations, including dysfunctional thought processing.DRUG THERAPY":
Typical and atypical antipsychotics.COGNITIVE BEHAVIOUR THERAPY AND FAMILY THERAPY:
As used in the treatment of schizophrenia. Token economies are used in the management of schizophrenia.THE IMPORTANCE OF AN INTERACTIONIST APPROACH:
In explaining and treating schizophrenia: the diathesis stress model.
SUPPORT PSYCHSTORY
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SUPPORT PSYCHSTORY 〰️
DEAR STUDENTS
AQA requires you to formally know very little about the classification of schizophrenia, e.g., what schizophrenia actually is.
The specification says you must know:
Positive symptoms of schizophrenia, including hallucinations and delusions.
Negative symptoms of schizophrenia, including speech poverty and avolition.
And that’s it, which is surprising given the complexity of schizophrenia. It is one of the more difficult illnesses to understand. The truth is, AQA are never really going to ask you what schizophrenia is in the examination.
At most, they occasionally ask a five-mark question, such as
“Outline the classification of schizophrenia”
And when they do, the answer below is what the examiner is looking for :
ANSWER:
“Schizophrenia (SZ) is a complicated disorder to classify, as each individual can have different characteristics of the illness. It is a condition characterised by disordered, disorganised thought processes, manifesting in the patient’s language and behaviour. There is also a loss of contact with reality and a disturbance of form and thought content. Schizophrenia affects the mood of the person and their sense of self about the external world. The behaviour of schizophrenics may be purposeless, and they can distort reality and withdraw from society. Some types of schizophrenia develop slowly and insidiously, and the absence of emotion, language and self-initiation may dominate the early clinical picture. Yet other kinds of schizophrenia are dominated by auditory hallucinations, paranoid delusions, and excessive behaviours. As a result, schizophrenia is now classified as a spectrum disorder. “
You may also see multiple-choice or short-answer questions on the difference between positive and negative symptoms. But that is it. HONESTLY!
Yet students are often tempted to tell the examiner what schizophrenia is when asked, for example,
“Outline and evaluate biological explanations for schizophrenia”.
They produce a half-paragraph (or more) describing the disorder before finally getting to the biological explanation. In those cases, everything they wrote that “describes” what schizophrenia is earns no credit at all. This is because the question did not ask you what schizophrenia is. It asked you to “describe” two biological explanations (theories ) of schizophrenia. Therefore, the essay should have started like this:
“One biological explanation/theory of schizophrenia is the dopamine hypothesis/genetic theory …”
This naturally raises the question of why we bother studying the disorder in such depth. The short answer is that without a proper grasp of schizophrenia, the explanations make no sense. You cannot meaningfully understand the dopamine hypothesis if you have no firm idea of the symptoms dopamine is supposed to be influencing. The same applies to validity and reliability. How can anyone evaluate whether schizophrenia is a “valid” or “reliable” construct — whether it is, in effect, a social construction — if they are unclear on what the symptoms look like, how they present, or how effectively they respond to treatment?
That is why this section is so substantial, despite the specification itself appearing to ask for very little. If you do not understand the disorder, you cannot understand the explanations. If you do not understand the explanations, you cannot evaluate them. And if you cannot assess them, you cannot secure high marks. In other words, the foundation is non-negotiable.
CLASSIFICATION OF SCHIZOPHRENIA
Positive symptoms of schizophrenia include hallucinations and delusions.
Negative symptoms of schizophrenia include speech poverty and avolition.
POSITIVE / NEGATIVE SYMPTOM CLASSIFICATION ASSESSMENT
SHORT QUESTIONS
Which of the following are not negative symptoms: ( 1 mark for each correct answer)
Hallucinations
Avolition
Delusions
Anhedonia
Poverty of speech
Thought control
Give two examples of how language can be disordered in Schizophrenia. (4 marks)
What is a delusion? (3 marks)
What is a hallucination? (3 marks)
Outline two positive symptoms (4 marks)
Define positive symptoms (4 marks)
Define negative symptoms (4 marks)
Outline four negative symptoms. (8 marks)
What is meant by affect? (2 marks)
Name four different types of affect (4 marks)
Name and briefly outline one negative symptom of schizophrenia. (2 marks)
Using your knowledge of schizophrenia, explain why Louise is now showing symptoms of schizophrenia. (4 marks)
Read the item and then answer the question above:
Louise comes from a family with a history of schizophrenia, as both her grandfather and an aunt have been diagnosed with the disorder. Louise’s father has recently died from cancer, and she has just moved out of the family home to start a university course. Although she has always been healthy in the past, she has just begun to experience symptoms of schizophrenia, such as delusions and hallucinations.What is the difference between chronic and acute onset Schizophrenia? (4 marks)
What is Type One Schizophrenia? (4 marks)
Why is using the Type One Schizophrenia and Type Two Schizophrenia categorisations of schizophrenia fallible? (4 marks)
How long do symptoms have to be present before a diagnosis of Schizophrenia can be made for ICD-11 and DSM-5? (1 mark)
Name ICD subtypes (7 marks)
Name the DSM IV subtypes (5 marks)
Name two differences between the current ICD-11 and DSM-5 in Schizophrenia classification? 4 marks)
Outline the classification of Schizophrenia (5 marks)
Circle the relevant words or phrases in the examples below and identify the pathology shown.
State clearly whether the presentation indicates:
POSITIVE SYMPTOMS
If so, specify which: loose associations, knight’s move thinking, clang associations, neologisms, word salad, thought disorder, hallucinations, delusions (give exact examples from the text).NEGATIVE SYMPTOMS
If so, specify which: disturbances of motivation (avolition, apathy, anhedonia, social withdrawal) or disturbances of affect (flat affect, blunted affect, inappropriate/incongruent affect). Give exact examples
EXAMPLE ONE
I am a nun. If that’s not enough, you are still his. That is a brave cavalier; take him as your boon-swagger, Caroline; you know well you are my lord because I am bored, and you like a sword in the Fjord. If you are the habbicontin, Mrs K is still best by fear. Handle the gravy carefully. Where is my paintbrush? Where are you, Monet?
EXAMPLE TWO
“I am writing on paper. The pen which I am using is from a factory called ‘Perry & Co’. This factory is in England. I assume this. Behind the name of Perry Co., the city of London is inscribed, but not the city. The city of London is in England. I know this from my school days. Then, I always liked geography. My last teacher in that subject was Professor August A. He was a man with black eyes. I also like black eyes. There are also blue and grey eyes and other sorts, too. I have heard it said that snakes have green eyes. All people have eyes. There are some, too, who are blind. A boy leads about these blind people. It must be very terrible not to be able to see. There are people who can’t see and, in addition, can’t hear. I know some who hear too much. One can hear too much. There are many sick people in Burgholzi; they are called patients. One of them I like a great deal. His name is E. Sch. He taught me that in Burgholzi, there are many kinds of patients, inmates, and attendants. Then there are some who are not here at all. They are all peculiar people….”
EXAMPLE THREE
Carl was twenty-seven years old when he was first admitted to a psychiatric facility. Gangling and intensely shy, he was so incommunicative at the outset that his family had to supply initial information about him. They, it seemed, had been unhappy and uncomfortable with him for quite some time. His father dated the trouble to “sometime in high school.” He reported, “Carl turned inward, spent a lot of time alone, had no friends and did no schoolwork.” His mother was especially troubled about his untidiness. “He was really an embarrassment to us then, and things haven’t improved since. You could never take him anywhere without an argument about washing up. And once he was there, he wouldn’t say anything to anyone.” His twin sisters, six years younger than Carl, said very little during the family interview, instead passively agreeing with their parents.
One would hardly have guessed from their report that Carl graduated from high school in the upper quarter of his class and went on to college, where he studied engineering for 3 years. Though he had always been shy, he had had one close friend, John Winters, throughout high school and college. John had been killed in a car accident a year earlier. (Asked about Winters, his father said, “Oh, him. We don’t consider him much of anything at all. He didn’t go to church either. And he didn’t do any schoolwork.”)
Carl and John were unusually close. They went through high school together, served in the army at the same time, and, upon discharge, began college together and roomed in the same house. Both left college before graduating, much to the chagrin of Carl’s parents, took jobs as machinists in the same firm, and moved into a nearby apartment.
They lived together for three years until John was killed. Two months later, the company for which they worked went out of business. John’s death left Carl enormously distraught. When the company closed, he found himself without the energy and motivation to look for a job. He moved back home. Disagreements between Carl and his family became more frequent and intense. He became more reclusive, sloppy, and bizarre; they became more irritable and isolating. Finally, they could bear his behaviour no longer and took him to the hospital. He went without any resistance.
After ten days in the hospital, Carl told the psychologist who was working with him, “I am an unreal person. I am made of stone, or else I am made of glass. I am not wrong, precisely. But you will not find my key. I have tried to lose it. You can look at me closely if you wish, but you see more from far away.”
Shortly thereafter, the psychologist noted that Carl “…smiles when he is uncomfortable, and smiles more when in pain. He cries during television comedies. He seems angry when justice is done, frightened when someone compliments him, and roars with laughter on reading that a young child was burned in a tragic fire. He grimaces often. He eats very little but always carries food away.”
After two weeks, the psychologist said to him, “You hide a lot. As you say, you are wired precisely wrong. But why won’t you let me see the diagram?”
Carl answered: “Never, ever will you find the lever, the eternal lever that will sever me forever with my real, seal, deal, heel. It is not on my shoe, not even on my sole. It walks away.
EXAMPLE FOUR: MARY
Mary is 21 and was first presented to psychiatric services as an outpatient at the age of 19. She gave a two-month history of social withdrawal associated with paranoid delusions. A diagnosis of probable paranoid schizophrenia was made, and she was treated. However, her condition continued to deteriorate. Over the next two months, she became retarded and mute and was admitted to the hospital. At this time, she began having episodes of freezing and started walking backwards. During her freezing episodes, she would stand rigid for hours and ignore any instructions from nurses to move.
EXAMPLE FIVE TOMMY
According to his family, he has always been withdrawn, and his behaviour is sometimes inappropriate. His sister-in-law gave the example of him waking her up in the middle of the night to cook him breakfast. Over the last year, Tommy has frequently talked at length and struggled to understand. He often goes days without speaking to people.
EXAMPLE FIVE DAVE
Over the last three months, he has had visions of aliens walking around him at work. His speech has become rambling, and often his friends cannot tell what he is saying. A few weeks ago, Dave was told his old college friend had died, and in response, he laughed. He has stopped showering regularly and believes his water system has been poisoned. He has lost a lot of weight as he no longer bothers to cook. His neighbour was worried about Dave when she saw him sitting on the floor in the corner shop, grimacing.
EXAMPLE SIX: MIKE
Mike says he knows someone has removed his brain and replaced it with someone else's. He believes that this brain is controlling him and that he is not responsible for his actions. He works daily and has been in his current job for 15 years. He says he has many friends, but sometimes he thinks one of them did this to him. He is convinced he must protect his brain by wearing a hat (even to bed). He can speak fine and goes to work every day. He doesn’t think his thoughts are unusual.
EXAMPLE SEVEN” SUSAN
Susan is 20 years old. She suffered from depression when she was 15. She has now been discharged from her psychiatrist and has been free of depression for the last three years. She is taking her final university exams, has had trouble sleeping, and has had bad dreams over the past few weeks. She is feeling stressed out and overwhelmed
NEURAL CORRELATES AND DOPAMINE HYPOTHESES ASSESSMENT
THEORIES OF ABNORMALITY
Chemical theories explain psychological disorders in terms of neurotransmitter imbalance (for example, hyper or hypo levels).
Examples you already know from Year 1:
Depression → low serotonin
OCD → high dopamine and low serotonin
Schizophrenia fits the same model. It is explained partly by abnormal dopamine levels, which affect how the brain processes information. This forms the chemical explanation of schizophrenia.
NEURAL CORRELATES AND SCHIZOPHRENIA
A neural correlate is a feature of the brain that is linked to a particular behaviour or mental state.
It can be a difference in:
Brain structure (size or shape of an area)
Brain activity (more or less activity in a pathway)
Brain chemistry (for example, levels of a neurotransmitter such as dopamine)
These differences may be caused by genes, illness, or experiences in the environment.
Example: people who lose the ability to produce speech often have damage to Broca’s area in the left frontal lobe. This repeated pattern suggests that Broca’s area is closely linked to speech production.
In clinical psychology, neural correlates are used to link features in the brain with mental disorders. For example, if a group of patients with similar symptoms also share a similar brain abnormality, that abnormality is described as a neural correlate of the disorder.
Important: the word correlate means there is a relationship but not automatic proof of cause and effect. However, when brain damage is followed by a clear change in behaviour, and this is repeatedly found in different patients, it is reasonable to suggest a causal link.
NEURAL CORRELATES IN SCHIZOPHRENIA
A neural correlate of schizophrenia is any consistent physical or functional difference in the brains of people with schizophrenia compared with people without the disorder.
Examples include:
Differences in brain chemistry (especially dopamine systems)
Differences in brain structure (for example, enlarged ventricles)
Because this is a very large area, the AQA specification uses the dopamine hypothesis as its key example of a neural correlate.
DOPAMINE HYPOTHESIS AS A NEURAL CORRELATE
Dopamine is a neurotransmitter that has several different circuits in the brain, each doing slightly different jobs, for example controlling voluntary movement, creating feelings of reward and assigning importance to stimuli, supporting higher-level thinking and planning, and regulating hormone release from the pituitary gland.
Nigrostriatal → voluntary movement
Mesolimbic → reward, motivation, salience (what feels important)
Mesocortical → higher thinking and planning
Tuberoinfundibular → hormone regulation (prolactin control)
The original dopamine hypothesis was discovered after accidentally finding that antipsychotics reduced hallucinations and delusions in the early 1950s. It did not identify any of the dopamine circuits above and simply stated that schizophrenia was linked with excess dopamine and that this caused hallucinations and delusions.
However, the original dopamine hypothesis eventually fell out of favour for several reasons. Most importantly, it did not account for negative symptoms. It had been assumed that negative symptoms were a by-product of positive symptoms, but over time it became clear that antipsychotics were not effective for these symptoms and that negative symptoms such as flat affect, anhedonia, and poverty of speech were a category in their own right.
The dopamine hypothesis was reformulated and stated that two of the main dopamine circuits were involved in schizophrenia. These circuits are:
MESOLIMBIC PATHWAY
Dopamine is too high in this pathway, and this over-activates the brain’s salience system.
Salience means deciding what is important.
When dopamine is excessive, the brain cannot filter irrelevant information, so ordinary events feel meaningful or threatening.
This produces positive symptoms, for example hallucinations and delusions.
MESOCORTICAL PATHWAY
Dopamine is too low in this pathway, which connects to the prefrontal cortex, the area responsible for planning, thinking, and motivation.
When dopamine is reduced, these functions become under-stimulated.
This produces negative symptoms such as avolition, flat affect, and poverty of speech, as well as cognitive symptoms like poor decision-making
DOPAMINE RECEPTORS (WHY THERE ARE FIVE)
Students usually learn “dopamine” as if it were one
In reality, dopamine has several different “docking sites” in the brain, called receptors.
These receptors are slightly different shapes, so dopamine produces different effects depending on which one it binds to.
There are five dopamine receptors — D1, D2, D3, D4, D5. They are named in the order they were discovered:
They are not five different kind of dopamine. they are five ways different parts of the brain can read the same dopamine signal.
DOPAMINE RECEPTORS ARE DIVIDED INTO TWO PROMINENT FAMILIES
Scientists then group them based on how they behave:
D1-LIKE RECEPTORS (D1, D5): Generally stimulate neuron activity (excitatory effects).
D2-LIKE RECEPTORS (D2, D3, D4): Generally inhibit neuron activity (inhibitory effects).
These effects vary depending on brain region and neural pathway.
For schizophrenia, only two of these receptors matter: D1 and d2
MESOLIMBIC PATHWAY
(↑ D2 → positive symptoms (lack of salience → hallucination and delusions ).MESOCORTICAL PATHWAY
(↓ D1 → negative symptoms (cognitive deficits → poverty of speech, thought and lack of motivation).
Students are actually confused because hallucinations are caused by too much D2 activity even though D2 is described as inhibitory, and the opposite seems true for D1. The key is that “inhibitory” and “excitatory” describe what happens inside a single neuron, not what happens to the whole pathway.
D2 is inhibitory at the cell level, but when there is too much dopamine stimulating D2 receptors in the mesolimbic pathway, the entire circuit becomes overactive, not calmer. This overactivity disrupts salience (the ability to know what is important), which produces hallucinations and delusions.
D1 is excitatory at the cell level, but when there is too little dopamine acting on D1 receptors in the mesocortical pathway, the circuit becomes underactive. This underactivity leads to cognitive problems and negative symptoms such as poverty of speech, reduced thought, and lack of motivation.
So:
D2 = inhibitory, but overstimulation in the mesolimbic pathway → positive symptoms
D1 = excitatory, but understimulation in the mesocortical pathway → negative symptoms
SUPPORTING EVIDENCE
• Supporting evidence comes from the effects of amphetamines, which increase dopamine levels. When large doses are administered to individuals without any prior psychological issues, they can induce behaviour closely resembling paranoid schizophrenia. In people already diagnosed with schizophrenia, smaller doses of amphetamines typically make their symptoms worse.
• A later refinement of the hypothesis shifted focus from excessive dopamine itself to an increased number of dopamine receptors. A higher density of receptors leads to greater neuronal firing and an excess of messages. Post-mortem studies have revealed a generally higher number of dopamine receptors in the brains of people with schizophrenia (Owen et al., 1987). Other research has identified elevated dopamine concentrations in specific brain areas, including the left amygdala (Falkai et al., 1988) and the caudate nucleus and putamen (Owen et al., 1978).
EVALUATION A03
One major criticism of the dopamine hypothesis concerns the issue of causality—often described as a “chicken-and-egg” problem. It remains unclear whether abnormally high dopamine levels cause schizophrenia or whether they are a consequence of the disorder itself. This ambiguity means researchers must be cautious about assuming a direct cause-and-effect relationship in schizophrenia.
A significant challenge to the hypothesis emerged from Farde et al. (1990), who found no differences in dopamine levels (or D2 receptor densities) between individuals with schizophrenia and healthy controls.
Furthermore, Noll (2009) pointed out that approximately one-third of patients with schizophrenia do not improve when treated with dopamine-blocking antipsychotic drugs, indicating that other neurotransmitters are likely involved in the disorder.
A final limitation is that the dopamine hypothesis can be viewed as biologically deterministic. Even if someone has elevated dopamine activity, it does not inevitably mean they will develop schizophrenia. This approach overlooks the role of personal agency and free will, implying that biology alone dictates the onset of the condition.
Early support for the original dopamine hypothesis came from two observations. Which pair matches the text?
a. Antipsychotics reduced psychosis and amphetamines induced psychosis
b. Agonists reduced psychosis and Antagonists induced psychosis
c. L Dopa reduced psychosis and chlorpromazine induced psychosis
d. Lithium reduced psychosis and Thorazine induced psychosis
2. According to the text, why were amphetamine-induced psychotic states used as evidence for dopamine involvement?
a. They produced symptoms indistinguishable from acute paranoid schizophrenia
b. They produced only negative symptoms
c. They caused long term structural brain damage
d. They suppressed dopamine release
3. Which limitation of early post-mortem research is stated in the text?
a. Dopamine receptors cannot be seen under a microscope.
b. Dopamine activity cannot be measured in real time
c. Schizophrenia brains cannot be preserved after death
d. Post mortems always exaggerate dopamine levels
4. Which statement matches the text’s criticism of rat models?
a. Rats have no dopamine receptors
c. Rats do not respond to dopamine-altering substances
d. Rat brains lack limbic pathways
c. Researchers cannot assess hallucinations or disorganised thoughts in rats
5 MARKS
5. The text argues that excess dopamine in the striatum is not unique to schizophrenia. Which option lists three states that also show this pattern?
a. Psychotic bipolar mania, drug-induced psychosis, schizoaffective disorder
b. Dementia, phobias, autism
c. Obsessive compulsive disorder, anorexia, PTSD without psychosis
d. Alzheimer’s disease, depersonalisation, seasonal affective disorder
6 MARKS
6. Which option best contrasts the original and reformulated dopamine hypotheses as described?
a. Original: one pathway, excess dopamine only. Reformulated: different pathways, excess in mesolimbic and reduced in mesocortical.
b. Original: serotonin only. Reformulated: glutamate only.
c. Original: dopamine causes negative symptoms only. Reformulated: dopamine causes positive symptoms only.
d. Original: dopamine never changes across pathways. Reformulated: dopamine is unrelated to brain regions.
Using information from the text, outline two criticisms of the original dopamine hypothesis and explain why each criticism weakens the claim that “excess dopamine causes schizophrenia.”
What is a neural correlate? (1 marks)
What part of the brain is associated with Positive symptoms? (1 MARK).
What part of the brain is associated with Negative symptoms (1 MARK
What dopamine receptor is associated with positive symptoms of schizophrenia? (1 MARK
What dopamine receptor is associated with positive symptoms of schizophrenia? (1 MARK
3. Give two disadvantages of the neural correlates theory. (4 marks)
4. What do people typically experience when they produce too much dopamine? (4 marks)
5. What is the Dopamine 1 hypothesis? (4 marks)
7. What do people typically experience when they produce too little dopamine? (4 marks)
8. What is the Dopamine 2 hypothesis? (4 marks)
5 MARKS
The text argues that dopamine hyperactivity is not specific to schizophrenia. Describe three examples from the text where the same dopamine pattern appears in conditions or states other than schizophrenia and explain why this challenges the original hypothesis.
6 MARKS
Compare the original and reformulated dopamine hypotheses using only points from the text. Your answer should cover:
• how each model explains positive symptoms
• how the reformulated model accounts for negative and cognitive symptoms
• the different pathways each model focuses on
• how modern imaging and atypical antipsychotic findings support the reformulated model.
6. Name four disadvantages of the Dopamine 1 hypothesis. (8 marks)
9. Name four disadvantages of the Dopamine 2 hypothesis. (8 marks)
10. Give four disadvantages that pertain to both Dopamine hypotheses 1 and 2. (8 marks)
GENETIC EXPLANATIONS OF SCHIZOPHRENIA ASSESSMENT
Biological Explanations for Schizophrenia
Genetics
Family studies investigate people diagnosed with schizophrenia and examine whether their blood relatives are more likely to develop the condition compared to non-blood relatives.
Twins come in two forms: identical (monozygotic) and non-identical (fraternal or dizygotic). Identical twins develop when a single fertilised egg divides and forms two individuals who share identical genetic material.
AO1
• Gottesman (1991) reported a 48% concordance rate for schizophrenia in identical (MZ) twins, compared to a 17% rate in fraternal (DZ) twins. This indicates that greater genetic similarity is linked to a higher chance of developing the disorder.
• Benzel et al. (2007) identified three genes—COMT, DRD4, and AKT1—that are connected to elevated dopamine levels at certain D2 receptors, which can trigger acute episodes and positive symptoms such as delusions, hallucinations, and unusual beliefs.
• Miyakawa et al. (2003) analysed DNA from families impacted by schizophrenia and discovered that affected individuals were more likely to carry a faulty form of the PPP3CC gene, which plays a role in producing calcineurin, a protein involved in regulating the immune system. Additionally, Sherrington et al. (1988) identified a gene on chromosome 5 that appeared linked to the disorder in a limited number of large families.
• Supporting evidence shows that the risk of schizophrenia increases with closer biological ties. Kendler (1985) demonstrated that first-degree relatives of people with schizophrenia face an 18 times greater risk than the general population. Gottesman (1991) also showed that the condition occurs more frequently among the biological family members of those affected, with risk rising in line with the level of genetic closeness.
AO3
It is crucial to recognise that genetic factors account for only part of the risk; if genes were the sole cause, identical twins would show 100% concordance rates.
One limitation of the genetic explanation is the presence of methodological issues. Research involving families, twins, and adoptions needs careful interpretation because it is often retrospective, and diagnoses can be influenced by awareness that other relatives have already been identified as having the disorder. This raises concerns about potential bias or demand characteristics.
Another drawback relates to the nature-versus-nurture debate. Separating genetic influences from environmental ones is extremely challenging. Since concordance rates fall short of 100%, schizophrenia cannot be fully attributed to genetics alone; instead, individuals may inherit a vulnerability that increases their susceptibility when combined with certain environmental triggers. This means the biological approach does not provide a complete account of the condition.
A further weakness is that the genetic explanation can be seen as biologically reductionist. Advances from the Human Genome Project have highlighted the intricate nature of genes. With fewer genes identified than originally expected, it is now understood that individual genes can serve multiple purposes and that behaviour is influenced by numerous genes interacting in complex ways.
Schizophrenia is regarded as a polygenic and multifactorial condition, arising from the combined effects of several genes and environmental influences. This complexity indicates that efforts to pinpoint specific genes oversimplify the disorder, as it is not caused by any single genetic factor.
GENETIC EXPLANATION
SHORT QUESTIONS
What is a concordance rate? (2 marks)
What is meant by the term heritability in relation to schizophrenia? (2)
What percentage of genes do monozygotic (MZ) twins share? (1)
What is the general population risk of developing schizophrenia? (1)
Give three other significant concordance rates for relatives of schizophrenics. (3 marks)
What does it mean for genetic explanation of schizophrenia to be polygenic? (2)
Outline how twin studies are used to investigate the genetic basis of schizophrenia. (3)
Describe one adoption study that provides evidence for the genetic explanation of schizophrenia. (3)
what were the findings of the adoption study? (2 marks)
Give four criticisms of family studies. (8 marks)
Give two criticisms of twin studies. (4 marks)
Give two criticisms of separated twin studies. (4 marks)
Give two criticisms of adoption studies. (4 marks)
Give two other criticisms of genetic explanations of schizophrenia. (4 marks)
Explain the role of the C4 gene in schizophrenia. (4)
Describe how genome-wide association studies (GWAS) have contributed to genetic research on schizophrenia. (4)
Explain how molecular genetics has advanced the understanding of schizophrenia. (6)
Why are these concordance rates important for the genetic argument? (5 marks)
APPLICATION AND ANALYSIS QUESTIONS (A02)
A researcher finds that schizophrenia occurs more frequently in families where a close relative has already been diagnosed. Explain why this does not necessarily prove that schizophrenia is genetic. (3)
A clinician observes that two identical twins raised apart have both developed schizophrenia, while another set of identical twins raised together has only one twin with schizophrenia. What could this suggest about the causes of schizophrenia? (4)
A hospital records that patients with schizophrenia often have a biological parent with the disorder, but some do not. Using the diathesis-stress model, explain how this finding could be interpreted. (4)
Researchers find that children born to parents with schizophrenia but adopted into non-schizophrenic families still show an increased risk of developing the disorder. Explain what this suggests about the nature-nurture debate in schizophrenia. (4)
Explain why the diathesis-stress model provides a more comprehensive explanation of schizophrenia than purely genetic models. (6)
EVALUATION AND DISCUSSION QUESTIONS (A03)
Explain two weaknesses of using twin studies to investigate schizophrenia. (4)
Why might the difference in concordance rates between MZ and DZ twins not be purely genetic? (4)
Why is the lack of a single schizophrenia gene a challenge for the genetic explanation? (4)
Outline and evaluate family studies as evidence for the genetic explanation of schizophrenia. (6)
Evaluate adoption studies as evidence for the role of genetics in schizophrenia. (6)
Explain one strength and one limitation of genome-wide association studies (GWAS) in schizophrenia research. (6)
Explain why the discovery of overlapping genetic risk factors for schizophrenia and bipolar disorder weakens the genetic explanation of schizophrenia. (6)
Discuss the strengths and weaknesses of molecular genetic research into schizophrenia. (8)
Compare and contrast the genetic explanation and the diathesis-stress model of schizophrenia. (8)
Evaluate the strengths and limitations of twin studies as evidence for the genetic explanation of schizophrenia. (8)
EXTENDED RESPONSE QUESTIONS (A01/A02/A03)
Evaluate family, twin, and adoption studies as evidence for the genetic explanation of schizophrenia. (10)
Discuss the role of molecular genetics and genome-wide association studies in understanding schizophrenia. (10)
Explain how the C4 gene’s role in synaptic pruning may provide a biological explanation for schizophrenia. (10)
To what extent does research support the genetic explanation of schizophrenia? (12)
Discuss the strengths and limitations of genetic explanations for schizophrenia, using research evidence. (16)
Discuss one or more biological explanations for schizophrenia. (16 marks)
Discuss biological explanations for schizophrenia. (16 marks)
Describe and evaluate biological explanations for schizophrenia. Refer to the evidence in your answer. (16 marks)
There is considerable evidence that biological factors cause schizophrenia. These can be genetic, neuroanatomical, biochemical, viral, or a combination of such factors.” Discuss biological explanations of schizophrenia. (16 marks).
TASK: TURNING AO3 CRITIQUES INTO PEEL POINTS (SCHIZOPHRENIA – NATURE VS NURTURE)
INSTRUCTIONS FOR STUDENTS
You are given developed AO3 critiques. Your task is to restructure each critique into a PEEL paragraph. Follow the prompts carefully. Do not add new material. Do not generalise beyond what is stated.
CRITIQUE 1: DIFFICULTY ESTABLISHING CAUSE AND EFFECT
STEP 1 – POINT
Identify the core methodological problem being raised.
Sentence starter:
One limitation of family and twin studies is that…
STEP 2 – EVIDENCE
Select the specific evidence that supports this limitation. Use only what is given.
Prompt questions:
• Which types of twins are compared?
• What environmental factors do they share?
Sentence starter:
This is evident because MZ and DZ twins…
STEP 3 – EXPLAIN
Explain why this evidence weakens conclusions about genetics.
Prompt questions:
• Why do shared environments matter?
• How might genetic vulnerability and environmental stress interact?
Sentence starter:
This makes it difficult to isolate genetic influences because…
STEP 4 – LINK
Link back to the wider debate about schizophrenia.
Sentence starter:
Therefore, these studies cannot conclusively show that…
CRITIQUE 2: CHILDREN OF SCHIZOPHRENIC PARENTS
STEP 1 – POINT
Identify the assumption being challenged.
Sentence starter:
A limitation of interpreting concordance rates in children of schizophrenic parents is that…
STEP 2 – EVIDENCE
Use the named findings only.
Prompt questions:
• What concordance rates are cited?
• What does adoption research suggest?
Sentence starter:
For example, Gottesman reported…, however Tienari found that…
STEP 3 – EXPLAIN
Explain how the family environment could independently increase risk.
Prompt questions:
• What aspects of schizophrenia affect parenting?
• Why might this environment be stressful for a child?
Sentence starter:
Living with a schizophrenic parent may increase risk because…
STEP 4 – LINK
Link explicitly to the nature–nurture problem.
Sentence starter:
As a result, genetic and environmental influences…
CRITIQUE 3: DZ TWINS VERSUS SIBLINGS
STEP 1 – POINT
State the comparative issue clearly.
Sentence starter:
Evidence from DZ twins and siblings suggests that…
STEP 2 – EVIDENCE
Use numerical data accurately.
Prompt questions:
• How genetically similar are DZ twins and siblings?
• What are the respective concordance rates?
Sentence starter:
DZ twins share…, yet show a concordance rate of…, compared to…
STEP 3 – EXPLAIN
Explain why age and shared developmental context matter.
Prompt questions:
• How might siblings of different ages experience the same event differently?
• Why does timing matter?
Sentence starter:
This difference may be explained by shared developmental experiences because…
STEP 4 – LINK
Link back to causation.
Sentence starter:
This challenges purely genetic explanations by suggesting that…
EXTENSION (FOR STRONGER STUDENTS)
• Underline where cause and effect is assumed rather than demonstrated
• Identify one extraneous variable in each PEEL paragraph
• Rewrite the POINT sentence so it could apply across multiple studies
ANSWERS
DIFFICULTY ESTABLISHING CAUSE AND EFFECT
Point: Family and twin studies struggle to establish a clear cause and effect relationship between genetics and schizophrenia.
Evidence: Although higher concordance rates in MZ twins than DZ twins are often taken as evidence for genetic influence, both types of twins share significant environmental factors, including the same household, socioeconomic conditions, and family culture.
Explain: These shared environments may account for similarities in concordance rates, making it difficult to isolate genetic effects. In addition, individuals with a genetic vulnerability to schizophrenia may also be more likely to experience environmental stressors such as family conflict or trauma, further blurring the distinction between nature and nurture.
Link: As a result, twin and family studies cannot conclusively demonstrate that genetics are the primary cause of schizophrenia, as environmental influences cannot be adequately controlled.
CHILDREN OF SCHIZOPHRENIC PARENTS
Point: Concordance rates in children of schizophrenic parents cannot be assumed to reflect purely genetic transmission.
Evidence: Gottesman reported concordance rates of 27 to 39 percent for children with two schizophrenic parents, often interpreted as genetic. However, research by Tienari shows that many of these children are adopted away due to the severe impact of parental schizophrenia on child development.
Explain: Living with a schizophrenic parent is likely to be highly stressful and unpredictable, as the disorder can involve impaired cognition, language, and emotional regulation, as well as frightening delusions or hallucinations. This environment may disrupt emotional security and cognitive development, independently increasing the child’s risk of mental health problems.
Link: Therefore, genetic vulnerability and environmental stress are so closely intertwined that it is not possible to separate their individual contributions to the development of schizophrenia.
DZ TWINS VERSUS SIBLINGS
Point: Differences in concordance rates between DZ twins and non twin siblings suggest environmental influences play a causal role.
Evidence: Dizygotic twins share approximately 50 percent of their DNA, the same as ordinary siblings, yet DZ twins show higher concordance rates for schizophrenia (around 17 percent) than siblings (around 9 percent).
Explain: If schizophrenia were entirely genetic, these rates should be identical. The higher concordance in DZ twins may instead reflect shared environmental and psychological factors, such as being exposed to family events at the same developmental stage and interpreting family conflict in similar ways. Siblings of different ages experience family dynamics differently due to changing roles, stresses, and circumstances over time.
Link: This pattern supports the view that environmental and developmental factors contribute to schizophrenia risk, challenging purely genetic explanations.
PEELEd POINTS ADOPTION STUDIES
ADOPTION STUDIES – SUPPORT FOR A GENETIC EXPLANATION
Point: Adoption studies provide strong evidence for a genetic contribution to schizophrenia by separating biological inheritance from the rearing environment.
Evidence: Adoption research shows that children adopted from schizophrenic mothers have a 7 percent risk of developing schizophrenia, compared with 1.5 percent for adoptees from non schizophrenic mothers, despite being raised in different families. Tienari’s study was a prospective longitudinal natural experiment, avoiding many problems associated with retrospective family and twin studies. Similar findings were reported by Kety and Heston, increasing the reliability of the results.
Explain: Because the children were raised away from their biological parents, environmental explanations linked to direct parental influence are reduced, strengthening the argument that genetic factors increase vulnerability to schizophrenia. The prospective design also avoids recall bias and allows clearer observation of outcomes over time.
Link: This suggests that genetics play a significant role in schizophrenia risk, although this does not imply genetic determinism.
ISSUES WITH INTERNAL VALIDITY IN ADOPTION STUDIES
Point: Despite their strengths, adoption studies suffer from internal validity issues that weaken genetic conclusions.
Evidence: Although Tienari claimed to match experimental and control groups, schizophrenic adoptees were removed from their mothers before age four and adopted between ages five and seven, with no clear account of where they lived during the intervening period. It is also unknown whether these children experienced deprivation, privation, or abuse, whereas control adoptees did not experience similar late adoption or early disruption.
Explain: Early trauma, neglect, or institutional care are known to have long term effects on emotional regulation, language development, and relationships, as demonstrated by research on early deprivation. These uncontrolled early environmental factors may independently increase vulnerability to schizophrenia, making it impossible to attribute outcomes solely to genetics.
Link: Therefore, adoption studies cannot conclusively demonstrate that increased schizophrenia risk is purely genetic, as critical extraneous variables were not adequately controlled.
INTERACTION BETWEEN GENETIC VULNERABILITY AND ENVIRONMENT
Point: Adoption studies themselves support an interactionist explanation of schizophrenia rather than a purely genetic one.
Evidence: Tienari found that adoptees were more likely to develop schizophrenia if they were raised in disturbed adoptive families.
Explain: This indicates that genetic vulnerability alone is insufficient and that environmental stressors play a key role in triggering the disorder. A supportive environment may reduce risk, whereas a disturbed family context may activate underlying vulnerability.
Link: This supports the diathesis stress model, which proposes that schizophrenia results from an interaction between biological predisposition and environmental stress.
ETHICAL ISSUES IN TIENARI’S STUDY
Point: Tienari’s adoption research raises significant ethical concerns.
Evidence: Many of the children studied were likely taken from their biological mothers without informed consent. If the mothers were schizophrenic, they may have lacked the capacity to consent during active phases of illness.
Explain: Studying children who may have been removed under ethically questionable circumstances raises concerns about benefitting from decisions made without valid consent, particularly when mental incapacity is involved.
Link: These ethical issues complicate the interpretation of the findings and highlight the moral limitations of using adoption studies to investigate schizophrenia.
LIMITATIONS OF DIAGNOSTIC VALIDITY IN GENETIC RESEARCH
Point: Family, twin, and adoption studies investigating the genetics of schizophrenia are limited by problems with diagnostic validity.
Evidence: Many early studies relied on broad and inconsistent diagnostic criteria that predate the introduction of DSM III in 1980 and later refinements in DSM 5. These earlier classifications included subtypes and milder psychotic disorders that are no longer recognised within modern diagnostic frameworks.
Explain: As a result, individuals who would not meet current diagnostic thresholds for schizophrenia may have been included in research samples. This weakens construct validity and makes it difficult to determine whether findings genuinely relate to schizophrenia as currently defined.
Link: Therefore, conclusions drawn from early genetic studies must be treated with caution, as they may not accurately reflect the disorder recognised today.
IMPACT ON CONCORDANCE AND HERITABILITY ESTIMATES
Point: Outdated diagnostic criteria may have inflated concordance rates reported in genetic studies of schizophrenia.
Evidence: Studies analysed by Gottesman, as well as adoption research such as Tienari’s and Kety’s Danish American study, were conducted during periods when diagnostic standards varied considerably. Diagnoses often included conditions such as paranoid schizophrenia or other psychotic disorders that are no longer classified separately or at all.
Explain: Including a wider range of disorders increases the likelihood that twins or biological relatives will appear concordant, artificially raising estimates of heritability in both twin and adoption studies.
Link: This suggests that reported genetic influence in early research may be overstated due to inconsistent diagnostic boundaries.
IMPLICATIONS FOR MODERN RESEARCH
Point: Early genetic findings must be reinterpreted in light of modern diagnostic standards.
Evidence: While meta analyses, twin studies, and adoption studies consistently suggest a genetic component to schizophrenia, many were based on classifications that lack consistency with current DSM criteria.
Explain: Without applying contemporary diagnostic definitions, it is not possible to accurately quantify the genetic contribution to schizophrenia. Modern research requires stricter classification to distinguish schizophrenia from related but distinct psychotic conditions.
Link: Consequently, although early research supports a genetic role, its findings should be contextualised rather than taken as precise estimates of heritability.
C4 GENE PEELED
STRENGTHS OF THE C4 EVIDENCE BASE
Point: A major strength of the C4 explanation is the breadth and convergence of supporting evidence.
Evidence: Support for the C4 gene comes from genome wide association studies, post mortem brain analysis, animal experiments, cell culture research, biomarker studies, and brain imaging.
Explain: This triangulation across multiple methods increases confidence that the findings are robust and not artefacts of a single research approach. Unlike earlier genetic studies, the C4 explanation also provides a clear biological mechanism by showing how gene expression can influence synaptic pruning during brain development.
Link: As a result, the C4 explanation represents a more sophisticated and biologically grounded account of schizophrenia risk than earlier genetic associations without mechanisms.
EXPLANATORY POWER OF THE C4 THEORY
Point: The C4 explanation has high explanatory power for key features of schizophrenia.
Evidence: Excessive synaptic pruning linked to C4A expression explains reduced grey matter and synaptic density, the absence of neuron loss, and the typical onset of schizophrenia in late adolescence when pruning peaks.
Explain: This developmental account goes beyond adult neurotransmitter imbalance by explaining how structural brain changes emerge over time rather than appearing suddenly in adulthood.
Link: This makes the C4 explanation stronger than accounts that focus solely on dopamine dysfunction without addressing developmental changes.
LIMITATIONS OF THE C4 EXPLANATION
Point: Despite strong evidence, the C4 explanation is not deterministic and has limited predictive value.
Evidence: Many individuals with high C4A expression do not develop schizophrenia, indicating that the gene increases vulnerability rather than directly causing the disorder.
Explain: This means genetic risk alone is insufficient and must interact with other factors for schizophrenia to develop.
Link: Therefore, C4 cannot be treated as a single causal explanation for schizophrenia.
METHODOLOGICAL AND REDUCTIONIST LIMITATIONS
Point: The evidence base for C4 relies heavily on non human models and risks biological reductionism.
Evidence: Much of the mechanistic research uses animal models and laboratory systems such as mice and cell cultures.
Explain: While these methods allow experimental control, they may not fully represent the complexity of the human brain or the higher cognitive and social processes involved in schizophrenia. Focusing on synaptic pruning alone may also underplay established environmental risk factors such as childhood trauma, prenatal stress, social adversity, and cannabis use.
Link: This limits the extent to which the C4 explanation can account for schizophrenia in isolation.
RELATIONSHIP TO OTHER EXPLANATIONS
Point: The C4 explanation complements rather than replaces existing biological theories.
Evidence: Excessive pruning may disrupt cortical regulation of subcortical dopamine systems, helping to explain dopamine dysregulation observed in schizophrenia.
Explain: This supports an interactionist framework in which developmental brain changes and neurotransmitter abnormalities are linked rather than competing explanations.
Link: The C4 explanation therefore fits well alongside the dopamine hypothesis rather than contradicting it.
DIATHESIS STRESS MODEL
Point: The C4 explanation aligns closely with the diathesis stress model of schizophrenia.
Evidence: C4A expression represents a genetic vulnerability that only leads to schizophrenia when combined with environmental stressors.
Explain: This explains why not all individuals with genetic risk develop the disorder and highlights the role of environmental triggers.
Link: This strengthens the view that schizophrenia results from interacting biological and environmental factors.
PRACTICAL AND ETHICAL CONSIDERATIONS
Point: At present, C4 research has limited direct clinical application.
Evidence: There is no safe or ethical method for altering synaptic pruning during development.
Explain: Intervening in early brain development carries significant ethical risks, limiting immediate treatment implications. However, the findings may aid early identification of risk and encourage preventative approaches.
Link: This suggests the value of C4 research lies more in early intervention and prevention than direct treatment.
OVERALL CONCLUSION
Point: Overall, C4 research represents a major advance in biological explanations of schizophrenia.
Evidence: It provides a coherent developmental account supported by converging evidence across multiple research methods.
Explain: However, it explains increased risk rather than certainty and cannot account for schizophrenia without reference to environmental and psychological factors.
Link: Therefore, the C4 explanation is best understood as part of an interactionist framework rather than a standalone cause.
ESSAY EXEMPLARS
3-MARK A01 RESPONSE
Schizophrenia is believed to have a genetic basis, as studies show the risk increases with genetic similarity. Twin studies show that monozygotic (MZ) twins have a 48% concordance rate, while dizygotic (DZ) twins have only a 17% concordance rate, suggesting a strong genetic component. Adoption studies, such as Tienari’s Finnish Adoption Study, further support this, as children of schizophrenic biological parents were more likely to develop schizophrenia, even when raised in non-schizophrenic adoptive families.
Recent genetic research has identified specific genes, such as the C4 gene, linked to excessive synaptic pruning in the adolescent brain. This may contribute to the development of schizophrenia by affecting neural pathways involved in cognition and perception. However, schizophrenia is now understood to be polygenic, meaning multiple genes contribute to its growth rather than a single identifiable cause.
6-MARK A01 RESPONSE
The genetic explanation of schizophrenia suggests that the disorder is inherited, with research providing strong evidence for a genetic component. Twin studies have demonstrated that schizophrenia is more likely to occur in individuals with a higher degree of genetic relatedness. Gottesman and Shields (1991) found that monozygotic (MZ) twins have a 48% concordance rate, meaning if one twin has schizophrenia, there is a 48% chance the other will develop it. In contrast, dizygotic (DZ) twins have a significantly lower concordance rate of 17% despite sharing the same environment. This suggests that genetics plays a key role in the disorder. Family studies also show that schizophrenia runs in families: the risk for first-degree relatives (parents, siblings, children) is 9-13%, while for second-degree relatives (e.g., half-siblings, uncles, aunts) it is 2-6%, and for third-degree relatives (e.g., cousins) it is around 2%. The general population risk remains at 1%, supporting a genetic influence.
Adoption studies further support the genetic explanation by showing that schizophrenia risk remains even when individuals are raised in different environments. Tienari’s Finnish Adoption Study found that 7% of adoptees with schizophrenic biological mothers developed schizophrenia, compared to 1.5% in the control group, suggesting that biological inheritance plays a role. However, as not all genetically at-risk individuals develop schizophrenia, researchers have turned to specific genetic factors to understand its causes.
Recent genetic research has identified specific genes linked to schizophrenia. One of the most significant discoveries is the C4 gene, which regulates synaptic pruning—a process that removes excess neural connections during adolescence. Sekar et al. (2016) found that overactive C4 function leads to excessive synaptic loss, particularly in the prefrontal cortex, an area responsible for cognition, memory, and decision-making. This may explain why individuals with schizophrenia experience disorganised thinking and cognitive deficits.
Schizophrenia is now understood to be polygenic, meaning multiple genes contribute to its development rather than a single gene being responsible. Other genes, such as DISC1, CACNA1C, and GRIN2A, have been linked to schizophrenia, further supporting the idea that genetic and neurobiological factors interact in the development of the disorder.
10-MARK A03 EVALUATION RESPONSE (APPROX. 600 WORDS, PEC STRUCTURE)
POINT 1: FAMILY STUDIES PROVIDE EVIDENCE FOR A GENETIC LINK, BUT ENVIRONMENTAL FACTORS CANNOT BE RULED OUT
EXPLAIN: Family studies show that schizophrenia runs in families, suggesting a genetic basis. Gottesman and Shields (1991) found that first-degree relatives (parents, siblings, children) have a 9-13% risk, compared to 2-6% for second-degree relatives and 1% in the general population. This pattern of risk supports the idea that schizophrenia has a heritable component.
CRITIQUE: However, family studies fail to separate genetic influence from shared environmental factors. Families not only pass on genes but also provide shared experiences that may contribute to schizophrenia. Expressed emotion (EE), a pattern of high criticism, hostility, and emotional over-involvement, has been linked to schizophrenia relapse, showing that environment plays a role.
CONSEQUENCE: This suggests that family studies alone are not sufficient evidence for a purely genetic explanation, as they cannot disentangle whether schizophrenia is inherited biologically or learned through dysfunctional family dynamics.
POINT 2: TWIN STUDIES PROVIDE STRONGER GENETIC EVIDENCE, BUT ENVIRONMENT STILL MATTERS
EXPLAIN: Twin studies strengthen the genetic argument by comparing monozygotic (MZ) twins, who share 100% of their DNA, with dizygotic (DZ) twins, who share 50%. Gottesman and Shields (1991) found that MZ twins have a 48% concordance rate, whereas DZ twins have a 17% concordance rate, suggesting a strong genetic component.
CRITIQUE: However, if schizophrenia were purely genetic, the MZ concordance rate should be 100%, yet over half of genetically identical twins remain unaffected. This suggests that environmental factors must also contribute. Additionally, MZ twins often experience more similar environments (e.g., being treated alike by parents, sharing the same social experiences), which could inflate genetic estimates.
CONSEQUENCE: While twin studies support a genetic predisposition to schizophrenia, they also show that genes alone are not enough to trigger the disorder, supporting the diathesis-stress model, where genetic vulnerability interacts with environmental stressors.
POINT 3: ADOPTION STUDIES PROVIDE STRONGER EVIDENCE FOR GENETICS BUT HAVE METHODOLOGICAL ISSUES
EXPLAIN: Adoption studies help to separate genetic and environmental influences. Tienari’s Finnish Adoption Study found that 7% of adoptees with schizophrenic biological mothers developed schizophrenia, compared to 1.5% in control adoptees with no family history. This suggests that schizophrenia risk remains even when children are raised in non-schizophrenic households, supporting the genetic hypothesis.
CRITIQUE: However, adoption studies are not perfect. Many adoptees do not experience completely different environments, as adoption agencies often place children in homes that match their biological background (selective placement bias). Additionally, adopted children may have experienced trauma or neglect before adoption, which could independently increase their risk of schizophrenia.
CONSEQUENCE: Although adoption studies provide more substantial support for genetic factors than family studies, they cannot fully control for early environmental influences, meaning schizophrenia cannot be explained purely in terms of genetics.
POINT 4: MOLECULAR GENETICS HAS IDENTIFIED RISK GENES, BUT NO SINGLE "SCHIZOPHRENIA GENE" EXISTS
EXPLAIN: Recent genome-wide association studies (GWAS) have identified specific genes associated with schizophrenia. The C4 gene, which regulates synaptic pruning, has been associated with excessive neural loss in the prefrontal cortex, potentially explaining cognitive and thought disturbances in schizophrenia (Sekar et al., 2016). Other genes, such as DISC1, CACNA1C, and GRIN2A, have also been linked to dopamine regulation and brain development, supporting the idea that schizophrenia has a biological basis.
CRITIQUE: However, schizophrenia is now recognised as polygenic, meaning multiple genes contribute, and no single gene determines whether someone will develop the disorder. Additionally, many genes linked to schizophrenia, such as CACNA1C, are also associated with bipolar disorder and depression, raising questions about whether schizophrenia is a distinct genetic disorder or part of a broader psychiatric spectrum.
CONSEQUENCE: While molecular genetics has provided biological insights, genetic findings lack predictive power—having schizophrenia-related genes does not mean someone will develop the disorder. This suggests that environmental factors must interact with genetic risk, further supporting the diathesis-stress model.
POINT 5: THE DIATHESIS-STRESS MODEL PROVIDES A MORE BALANCED EXPLANATION
EXPLAIN: The diathesis-stress model suggests that schizophrenia develops due to a combination of genetic vulnerability (diathesis) and environmental stressors (stress). Evidence shows that schizophrenia risk increases with exposure to stressors such as childhood trauma, cannabis use, urban living, and social isolation.
CRITIQUE: This model explains why some individuals with genetic risk never develop schizophrenia, as they may not encounter the necessary environmental triggers. It also accounts for why identical twins do not always both develop schizophrenia, despite sharing the same genes.
CONSEQUENCE: The diathesis-stress model is more comprehensive than purely genetic explanations, as it integrates biological and environmental factors, making it a superior explanation of schizophrenia
16-MARK A01 RESPONSE
Jay has schizophrenia. His speech is rapid and confusing, constantly shifting from one idea to another. Jay’s father was treated for mental health problems when he was younger. Jay’s mother worries excessively about Jay. She often criticises his behaviour and tells him what to do. Jay’s doctor prescribes medication, which seems to reduce his symptoms.
Discuss one or more explanations for schizophrenia. Refer to Jay in your answer. (16 marks)
AO1 (6 marks)
One explanation for schizophrenia is the dopamine hypothesis. The original dopamine hypothesis proposes that positive symptoms—such as hallucinations, delusions, and disorganised thinking—arise from excess dopamine in the mesolimbic pathway, where overstimulation of D2 receptors distorts the brain’s salience system. This makes irrelevant stimuli feel meaningful.
However, the reformulated dopamine hypothesis argues that schizophrenia involves two opposite dopamine abnormalities:
• Hyperdopaminergia in the mesolimbic pathway → positive symptoms
• Hypodopaminergia in the mesocortical pathway → negative and cognitive symptoms due to reduced D1 receptor activity in the prefrontal cortex
A second biological explanation is genetic vulnerability. Schizophrenia is highly heritable, and having a first-degree relative with the disorder increases risk. Genes may influence dopamine regulation or early neurodevelopment.
AO2 (4 marks) – APPLYING TO JAY
Jay’s rapid, confusing speech and constant derailment reflect mesolimbic dopamine hyperactivity, which disrupts coherent thinking. His improvement after medication supports the dopamine hypothesis because antipsychotics reduce dopamine transmission.
Jay’s father, having been treated for mental health problems, suggests a genetic predisposition, fitting the genetic explanation. Jay’s mother’s excessive worry and criticism reflect high expressed emotion, an environmental stressor known to trigger relapse in genetically vulnerable individuals. This shows how biological vulnerability and stress interact to produce Jay’s symptoms.
AO3 (6 marks)
A significant strength of the dopamine hypothesis is drug evidence: antipsychotics that block D2 receptors reduce positive symptoms, while dopamine agonists (e.g., L-DOPA) can induce psychosis. Brain-imaging research (e.g., Howes et al.) also shows elevated dopamine synthesis in high-risk groups.
However, dopamine findings are correlational, meaning dopamine abnormalities may be a result of schizophrenia, not a cause. Around one-third of patients show little dopamine abnormality yet remain symptomatic, limiting the explanatory power of dopamine alone. The hypothesis also struggles to fully explain negative symptoms.
Genetic theories are supported by family, twin, and adoption studies showing higher concordance in genetically related individuals. Yet identical twins show only ~48% concordance, proving that genetics alone is insufficient. Environmental factors—such as the family stress Jay experiences—must interact with biological vulnerability, supporting a diathesis–stress model rather than a single cause.
CONCLUSION
Jay’s symptoms are well accounted for by biological explanations: mesolimbic dopamine hyperactivity explains his disorganised thoughts, and genetic vulnerability explains his family history. However, the role of High Expressed emotion in his home shows that schizophrenia is best explained by an interaction between biological risk and environmental stress, not biology alone.
PSYCHOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA QUESTIONS
COGNITIVE EXPLANATIONS ASSESSMENT
What is a dysfunctional thought process? (4 marks)
What is a cognitive explanation of schizophrenia? (6 marks)
Give two disadvantages of the cognitive explanation for schizophrenia. (4 marks)
Give two advantages of the cognitive explanation for schizophrenia. (4 marks)
DOUBLE-BIND THEORY (BATESON) ASSESSMENT
What terms are used by family systems theorists to describe A and B below? (2 marks)
Being free to decide how to behave and feel in control of one’s life.
When a family is overprotective, distinctions between family members are blurred.
Briefly outline family dysfunction as an explanation for schizophrenia. (2 marks).
What is a double bind? (3 marks).
How do researchers measure double binds? (4 marks).
Name and outline two studies that support the double bind theory. (4 marks).
Outline one psychological explanation of schizophrenia. (4 marks),
Briefly discuss two limitations of the family dysfunction explanation for schizophrenia. (4 marks)
What is a family's dysfunctional explanation of schizophrenia? (6 marks)
According to Bateson, schizophrenia is caused by double binds; explain how. (6 marks).
Evaluate one psychological explanation for schizophrenia. (6 marks).
Explain how family dysfunction might be involved in schizophrenia. Refer to one or more types of family dysfunction in your answer. (6 marks).
Why do psychological explanations of schizophrenia, such as the double bind theory, struggle to obtain scientifically valid and reliable studies to support their theories? (8 marks).
Jack has been diagnosed with schizophrenia. He describes his family background to his therapist:
"I could never talk to Mum. She fussed over me all the time. I tried to do what she said, but could never please her. One minute, she seemed all affectionate, and the next minute, she would make nasty comments. My dad hated all the arguments and stayed out of it."
Describe the family dysfunction explanation for schizophrenia, and explain how Jack’s experiences can be linked to the family dysfunction explanation. (8 marks)Evaluate psychological explanations of schizophrenia. (16 marks)
Outline and evaluate one or more psychological explanations for schizophrenia. (16 marks)
EXPLANATIONS FOR SCHIZOPHRENIA: EXPRESSED EMOTION (EE) ASSESSMENT
What is expressed emotion (EE), e.g., what is high expressed emotion (HEE)? (4 marks)
What is low-expressed emotion (LEE)? (4 marks)
How do researchers measure EE? (4 marks)
Name and outline two studies that support the expressed emotion theory. (6 marks)
Expressed emotion theory does not explain the cause of schizophrenia, only the course of the illness. Explain what that means, e.g., what is the difference between course and cause explanations of schizophrenia? (8 marks)
Why is it easier to research psychological explanations, such as EE theory, that investigate the course of the illness? (6 marks)
How does EE affect the course of schizophrenia? (4 marks)
What other evaluative points about EE theory should be considered? (4 marks)
INTERACTIONIST MODEL ASSESSMENT
What is the interactionist theory of schizophrenia? (4 marks)
What is the diathesis-stress model of schizophrenia? (4 marks)
What support does the interactionist model have that shows schizophrenia is caused by both nature and nurture? (6 marks)
DRUG TREATMENT FOR SCHIZOPHRENIA ASSESSMENT
Outline the function of dopamine, e.g., what does it do? (4 marks)
Describe problems people may experience with imbalances in dopamine production, e.g., excess and deficiency. (4 marks)
What is an agonist? (2 marks)
What is an antagonist? (2 marks)
What is an antipsychotic? (2 marks)
What is a typical or conventional antipsychotic? (2 marks)
How did antipsychotics originate? (2 marks)
Name two typical antipsychotics. (2 marks)
How do typical antipsychotics work? (2 marks)
What are the four adverse symptoms of taking typical antipsychotics? (2 marks)
Name two other issues that devalue the efficacy of typical antipsychotics. (2 marks)
What is an Atypical antipsychotic? (2 marks)
Name two Atypical antipsychotics. (2 marks)
Give two advantages of taking Atypical antipsychotics versus taking typical antipsychotics. (4 marks)
Name two disadvantages of taking Atypical antipsychotics. (4 marks)
What are the findings regarding the length of time on typical and Atypical antipsychotics? (4 marks)
PSYCHOLOGICAL TREATMENTS FOR SCHIZOPHRENIA ASSESSMENT
TOKEN ECONOMIC TREATMENTS FOR SCHIZOPHRENIA QUESTIONS
What is a token economy? (3 marks)
How is it theorised that a token economy helps schizophrenia patients? (3 marks)
What form of behaviourism is the token economy derived from? Give an example. (3 marks)
Give three disadvantages of using a token economy. (6 marks)
COGNITIVE BEHAVIOURAL THERAPY TREATMENTS FOR SCHIZOPHRENIA ASSESSMENT
What is cognitive behavioural therapy (CBT), and how is it used to treat schizophrenia? (4 marks)
Name two key techniques used in CBT for schizophrenia. (4 marks)
Explain one advantage and one disadvantage of using CBT to treat schizophrenia. (4 marks)
Why might CBT not be effective for all schizophrenia patients? (4 marks)
RELIABILITY AND VALIDITY OF SCHIZOPHRENIA ASSESSMENT
What does reliability mean in the context of diagnosing schizophrenia? (3 marks)
What does validity mean in the context of diagnosing schizophrenia? (3 marks)
Explain how co-morbidity affects the validity of the schizophrenia diagnosis. (4 marks)
Explain how symptom overlap affects the reliability of schizophrenia diagnosis. (4 marks)
Discuss how cultural bias can impact the diagnosis of schizophrenia. (6 marks)
Discuss how gender bias can impact the diagnosis of schizophrenia. (6 marks)
Describe one study that investigates the reliability of schizophrenia diagnosis. (4 marks)
Describe one study that investigates the validity of schizophrenia diagnosis. (4 marks)
Discuss issues associated with reliability and validity in diagnosing and classifying schizophrenia. (16 marks)
AQA SCHIZOPHRENIA EXAM QUESTIONS
FAMILY SYSTEMS AND PSYCHOLOGICAL EXPLANATIONS
NEURAL CORRELATES AND SCHIZOPHRENIA
Which of the following best describes neural correlates as an explanation for schizophrenia? Shade one box only. (1 mark)
A: There is a correlation between brain plasticity and symptoms of schizophrenia.
B: There is a correlation between brain structure and function and symptoms of schizophrenia.
C: There is a correlation between dysfunctional thinking and symptoms of schizophrenia.
INTERACTIONIST APPROACH
Discuss the use of an interactionist approach in explaining and treating schizophrenia. (16 marks)
Outline one or more biological explanations for schizophrenia. Compare biological explanation(s) for schizophrenia with the family dysfunction explanation for schizophrenia. (16 marks)
ANTIPSYCHOTIC DRUGS
Outline and evaluate the use of antipsychotic drugs to treat schizophrenia. (8 marks)
Apart from effectiveness, briefly explain one limitation of drug therapy for schizophrenia. (2 marks)
Read the item and then answer the questions that follow:
Two years ago, Jenny was diagnosed with schizophrenia. She has been taking an atypical antipsychotic drug, and there have been improvements in her positive symptoms. However, she still suffers negative symptoms and side effects. Her psychiatrist wants to change her medication from typical antipsychotics to one of the atypical antipsychotics and has also suggested cognitive behavioural therapy.
A. Outline one negative symptom of schizophrenia. (2 marks)
B. Concerning the item above, explain why Jenny’s psychiatrist wants to move her on to one of the atypical antipsychotics. (4 marks)
C. Briefly explain one advantage of cognitive behavioural therapy in treating schizophrenia. (2 marks)
TOKEN ECONOMIES
Below are four evaluative statements about token economies used in the treatment of schizophrenia. Which statement is TRUE? Shade one box only. (1 mark)
A: Token economies can be used effectively in any environment.
B: Token economies have a positive effect on thinking.
C: Token economies help to promote acceptable behaviours.
D: Token economies address the cause of the problem.
Discuss token economies as a method for managing schizophrenia. (8 marks)
COGNITIVE BEHAVIOURAL THERAPY (CBT)
Briefly outline how cognitive behavioural therapy (CBT) is used to treat schizophrenia and explain one limitation of using CBT to treat schizophrenia. (4 marks)
Jay and Mary are clinical psychologists. They each work with patients who have schizophrenia. Both Jay and Mary treat their patients without the use of drugs. Jay explains that he involves close relatives in treatment to reduce tension. Mary describes how she helps patients understand their thoughts and develop effective strategies to help themselves.
Describe and evaluate family therapy and cognitive behavioural therapy as treatments for schizophrenia. Refer to Jay and Mary in your answer. (16 marks)Martine has schizophrenia. She is afraid because she believes that her care workers are trying to hurt her. She hears voices telling her to lock the doors and windows so the care workers cannot enter her house. She thinks about nothing else. Explain how a cognitive behaviour therapist might treat Martine’s symptoms. (4 marks)
"Therapies can be time-consuming and, in some cases, uncomfortable for the client. Therefore, it is essential to offer the most appropriate and effective treatment."
Outline and evaluate two or more therapies used in the treatment of schizophrenia. (16 marks)Outline and compare two treatments for schizophrenia. (16 marks)
RELIABILITY AND VALIDITY IN SCHIZOPHRENIA DIAGNOSIS
What terms are used by psychologists to describe A and B below? (2 marks)
A When a person has two or more disorders at the same time.
B When two different disorders have a symptom in common.
Briefly outline and evaluate one study on the validity of the diagnosis of schizophrenia. (4 marks)
Discuss issues associated with reliability and validity in the diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias, and symptom overlap. (16 marks)
