Discuss the Biological Explanations of Schizophrenia
AO1 Dopamine Hypothesis:
- The original dopamine hypothesis stated that schizophrenia was caused by
excess dopamine in the subcortical areas of the brain. However, updated
versions have stated low DA in the prefrontal cortex leads to negative
symptoms such as avolition whereas excess dopamine in the brain leads to
positive symptoms such as hallucinations.
Genetics:
- Family studies have confirmed that the risk of schizophrenia increases in
line with the genetic similarity of the relative with the condition. This is
supported by Gottesman who found that someone with an aunt with
schizophrenia has a 2% chance of developing it, with a sibling increases the
chance to 9% and with a MZ twin, increases the chance to 48%
- From this research, psychologists found that schizophrenia is polygenetic
and that schizophrenic genes would code for differences in dopamine.
- Schizophrenia can also have genetic basis even if there is no family history
of it. This is because genes can mutate to become schizogenesis. Evidence
for mutation comes from the positive correlations between paternal age
and the risk of schizophrenia increasing. This is because the increase in
age, increases the risk of mutation.
AO3 1. Further research support for the genetic basis of schizophrenia is from
Tienari et al who conducted an adoption study which showed that
adopted children into stressful homes with biological mothers with
schizophrenia were more likely to develop schizophrenia than adopted
children into stressful homes without schizophrenic mothers. Showing
genetics plays a greater role in the development of schizophrenia than
environment.
2. Biologically reductionist- this approach only takes into consideration
the effects of biology and no other factors such as the environment.
Furthermore, by separating biological and environmental influences
which could be combined in the development of schizophrenia, this
decreases the validity of the explanation. Hence why an interactionist
approach may be better at explaining schizophrenia, as it takes into
account both influences.
3. Biologically deterministic- this approach implies that if someone has
the genes or low dopamine, they are destined to develop schizophrenia
and it cannot be cured. However, this is not the case as we know some
people may have the genes, but they may not be expressed so therefore
the person won’t develop schizophrenia. Furthermore, it could leave
people feeling hopeless about recovery and lead to difficulties in
treatment when we know that treatments can significantly improve the
quality of life of sufferers.
4. Implications into drug treatment- because we know that
schizophrenia is caused by excess dopamine, drugs such as
antipsychotics can be used to reduce dopamine levels and therefore
reduce schizophrenia symptoms such as hallucinations.
5. Twin studies have provided evidence for the genetic basis of
, schizophrenia as there is a higher concordance rate in MZ twins than DZ
twins. However, as concordance rates are not 100%, genetics alone
cannot explain schizophrenia, there must be other factors. Furthermore,
the increase in concordance rates in MZ twins could be due to
environmental factors such as the increased similarity in treatment
compared to DZ twins and not similarities in genetics.
6. A limitation with the dopamine hypothesis is the issue with causation. It
is difficult to determine whether it is the excess dopamine that causes
schizophrenia or if schizophrenia causes excess dopamine.
Discuss Biological Therapies for Schizophrenia
AO1 Typical Antipsychotics
- For example, chlorpromazine are dopamine antagonists which bind to
the dopamine receptors in the mesolimbic pathway, blocking them and
therefore reducing the action of dopamine. These work to reduce
positive symptoms of schizophrenia such as hallucinations. However,
as they act on many receptors in the brain, they cause extrapyramidal
side effects.
- They also have a sedation effect as they work on histamine receptors
so they can be used in highly anxious patients, the syrup form absorbs
faster for faster action.
Atypical Antipsychotics
- For example, clozapine binds to the dopamine receptors like
antipsychotics, however, they also bind to serotonin and glutamate
receptors so can reduce depression and improve mood. This means
that atypical antipsychotics can work on both positive and negative
symptoms and produces fewer side effects than typical
antipsychotics due to the lower affinity to dopamine receptors.
- However, they can cause potentially fatal side effects related to the
blood, so it is given at a lower dosage and patients have regular blood
tests.
- Risperidone is another atypical antipsychotic which binds to both
dopamine and serotonin receptors. However, it binds more strongly to
dopamine receptors than clozapine so is more effective in smaller doses
and therefore leads to fewer side effects.
AO3 1. Evidence for effectiveness from Thornley et al who reviewed
studies comparing the effects of chlorpromazine to control conditions
(placebo). He found that participants chlorpromazine was associated
with better overall functioning and reduced symptom severity as
compared to placebo. Showing that antipsychotics are an effective
treatment for schizophrenia.
2. A limitation of antipsychotics is the likelihood of side effects. Both
typical and atypical antipsychotics are associated with side effects
which can cause patients to stop taking the drug, making it
ineffective. Some antipsychotics have also been proven to have
severe long term side effects such as coma’s which can be fatal. This
means that antipsychotics can do more harm than good in the long
AO1 Dopamine Hypothesis:
- The original dopamine hypothesis stated that schizophrenia was caused by
excess dopamine in the subcortical areas of the brain. However, updated
versions have stated low DA in the prefrontal cortex leads to negative
symptoms such as avolition whereas excess dopamine in the brain leads to
positive symptoms such as hallucinations.
Genetics:
- Family studies have confirmed that the risk of schizophrenia increases in
line with the genetic similarity of the relative with the condition. This is
supported by Gottesman who found that someone with an aunt with
schizophrenia has a 2% chance of developing it, with a sibling increases the
chance to 9% and with a MZ twin, increases the chance to 48%
- From this research, psychologists found that schizophrenia is polygenetic
and that schizophrenic genes would code for differences in dopamine.
- Schizophrenia can also have genetic basis even if there is no family history
of it. This is because genes can mutate to become schizogenesis. Evidence
for mutation comes from the positive correlations between paternal age
and the risk of schizophrenia increasing. This is because the increase in
age, increases the risk of mutation.
AO3 1. Further research support for the genetic basis of schizophrenia is from
Tienari et al who conducted an adoption study which showed that
adopted children into stressful homes with biological mothers with
schizophrenia were more likely to develop schizophrenia than adopted
children into stressful homes without schizophrenic mothers. Showing
genetics plays a greater role in the development of schizophrenia than
environment.
2. Biologically reductionist- this approach only takes into consideration
the effects of biology and no other factors such as the environment.
Furthermore, by separating biological and environmental influences
which could be combined in the development of schizophrenia, this
decreases the validity of the explanation. Hence why an interactionist
approach may be better at explaining schizophrenia, as it takes into
account both influences.
3. Biologically deterministic- this approach implies that if someone has
the genes or low dopamine, they are destined to develop schizophrenia
and it cannot be cured. However, this is not the case as we know some
people may have the genes, but they may not be expressed so therefore
the person won’t develop schizophrenia. Furthermore, it could leave
people feeling hopeless about recovery and lead to difficulties in
treatment when we know that treatments can significantly improve the
quality of life of sufferers.
4. Implications into drug treatment- because we know that
schizophrenia is caused by excess dopamine, drugs such as
antipsychotics can be used to reduce dopamine levels and therefore
reduce schizophrenia symptoms such as hallucinations.
5. Twin studies have provided evidence for the genetic basis of
, schizophrenia as there is a higher concordance rate in MZ twins than DZ
twins. However, as concordance rates are not 100%, genetics alone
cannot explain schizophrenia, there must be other factors. Furthermore,
the increase in concordance rates in MZ twins could be due to
environmental factors such as the increased similarity in treatment
compared to DZ twins and not similarities in genetics.
6. A limitation with the dopamine hypothesis is the issue with causation. It
is difficult to determine whether it is the excess dopamine that causes
schizophrenia or if schizophrenia causes excess dopamine.
Discuss Biological Therapies for Schizophrenia
AO1 Typical Antipsychotics
- For example, chlorpromazine are dopamine antagonists which bind to
the dopamine receptors in the mesolimbic pathway, blocking them and
therefore reducing the action of dopamine. These work to reduce
positive symptoms of schizophrenia such as hallucinations. However,
as they act on many receptors in the brain, they cause extrapyramidal
side effects.
- They also have a sedation effect as they work on histamine receptors
so they can be used in highly anxious patients, the syrup form absorbs
faster for faster action.
Atypical Antipsychotics
- For example, clozapine binds to the dopamine receptors like
antipsychotics, however, they also bind to serotonin and glutamate
receptors so can reduce depression and improve mood. This means
that atypical antipsychotics can work on both positive and negative
symptoms and produces fewer side effects than typical
antipsychotics due to the lower affinity to dopamine receptors.
- However, they can cause potentially fatal side effects related to the
blood, so it is given at a lower dosage and patients have regular blood
tests.
- Risperidone is another atypical antipsychotic which binds to both
dopamine and serotonin receptors. However, it binds more strongly to
dopamine receptors than clozapine so is more effective in smaller doses
and therefore leads to fewer side effects.
AO3 1. Evidence for effectiveness from Thornley et al who reviewed
studies comparing the effects of chlorpromazine to control conditions
(placebo). He found that participants chlorpromazine was associated
with better overall functioning and reduced symptom severity as
compared to placebo. Showing that antipsychotics are an effective
treatment for schizophrenia.
2. A limitation of antipsychotics is the likelihood of side effects. Both
typical and atypical antipsychotics are associated with side effects
which can cause patients to stop taking the drug, making it
ineffective. Some antipsychotics have also been proven to have
severe long term side effects such as coma’s which can be fatal. This
means that antipsychotics can do more harm than good in the long
