Biological Explanations for Schizophrenia [AQA ALevel]

Summary

This video explores the biological explanation of schizophrenia, focusing on genetics, neural structures, and neurotransmitters. It highlights how schizophrenia is polygenic, with multiple genes increasing risk, and reviews studies showing genetic links through family, twin, and adoption studies. The video also discusses neural correlates like the dopamine hypothesis and enlarged brain ventricles. Lastly, it evaluates the deterministic and reductionist views, contrasting biological explanations with the diathesis-stress model, which integrates genetic and environmental factors in the development of schizophrenia.

Takeaways

• 🧬 Schizophrenia has a biological basis, involving physical processes such as genetics and neurotransmitter activity, especially dopamine.
• 🔬 Schizophrenia is polygenic, meaning multiple genes increase the risk, with over 108 gene loci identified in studies like Ripke's.
• 👨‍👩‍👧‍👦 Family and twin studies, including Gottesman's research, suggest a genetic link, with higher concordance rates in identical twins (48%) compared to non-identical twins (17%).
• 📊 Aetiological heterogeneity means that different gene combinations cause schizophrenia in different individuals.
• 👶 Adoption studies show that biological risk for schizophrenia can be influenced by the environment, as seen in Tienari's research.
• 🧠 Neural correlates, such as hyperdopaminergia and hypodopaminergia, are linked to symptoms of schizophrenia like hallucinations and avolition.
• 💊 The dopamine hypothesis is supported by the effectiveness of antipsychotic drugs, which reduce dopamine and alleviate symptoms.
• 🔎 Enlarged ventricles in the brain have been observed in people with schizophrenia, but it's unclear if this is a cause, effect, or side effect of medication.
• ⚖️ Determinism vs. free will: The biological explanation of schizophrenia suggests it is inevitable, but cognitive perspectives allow for potential control over thought processes.
• 🌍 A more holistic approach, the diathesis-stress model, combines genetic predisposition with environmental triggers like family dysfunction to explain schizophrenia.

Q & A

What does it mean to say schizophrenia has a biological cause?

Saying schizophrenia has a biological cause implies that the disorder arises from physical processes in the body, particularly involving genetic factors, neural structures, and neurotransmitter activity.

Is there a single gene responsible for schizophrenia?

No, there is no single gene responsible for schizophrenia. It is polygenic, meaning that multiple genes contribute to the risk of developing the disorder.

What did Ripke's research on schizophrenia genetics discover?

Ripke's research, which studied over 36,000 individuals with schizophrenia, identified 108 gene loci associated with the condition. Many of these genes are linked to the nervous and immune systems.

What is meant by schizophrenia being 'aetiologically heterogeneous'?

'Aetiologically heterogeneous' means that schizophrenia can arise from different combinations of genes, causing variations in how the disorder develops in different individuals.

How do family and twin studies support the genetic basis of schizophrenia?

Family and twin studies show that schizophrenia is more common in close relatives of those with the disorder. For example, research by Gottesman found a 48% concordance rate in identical twins and a 17% rate in non-identical twins, suggesting a genetic component.

Why doesn't the concordance rate for identical twins reach 100% in schizophrenia studies?

Although identical twins share the same DNA, the concordance rate for schizophrenia is only 48%, which suggests that environmental factors also play a significant role in the development of the disorder.

How do adoption studies provide insight into the genetic basis of schizophrenia?

Adoption studies, such as those by Tienari, show that children of schizophrenic mothers raised in healthy environments had a lower chance of developing schizophrenia (5.8%) compared to those raised in dysfunctional families (36.8%). This suggests both genetic and environmental factors influence the disorder.

What is the dopamine hypothesis of schizophrenia?

The dopamine hypothesis suggests that an imbalance or excess of dopamine in certain areas of the brain, such as Broca's area, contributes to positive symptoms like hallucinations, while low dopamine levels in areas like the frontal cortex may lead to negative symptoms.

What role do other neurotransmitters like glutamate and serotonin play in schizophrenia?

In addition to dopamine, lower levels of glutamate, which regulates learning and memory, and the involvement of serotonin, particularly through treatments like clozapine, are also implicated in the development of schizophrenia.

What does research about enlarged ventricles in the brains of people with schizophrenia suggest?

Research by Johnstone in the 1970s showed that people with schizophrenia tend to have larger brain ventricles, but this finding is correlational, and it is unclear if enlarged ventricles cause schizophrenia, result from it, or are a side effect of medication.

What is the difference between determinism and reductionism in the context of schizophrenia's biological explanation?

Determinism suggests that schizophrenia is inevitable if one has the genetic predisposition, while reductionism focuses on simplifying the disorder to basic biological processes, ignoring psychological factors. Holism, in contrast, acknowledges both genetic and environmental causes.

Outlines

00:00

🧠 Introduction to the Biological Explanation of Schizophrenia

This paragraph introduces the biological explanation of schizophrenia, emphasizing the role of genetics, neural structures, and neurotransmitters, particularly dopamine. It outlines the scope of the video, focusing on genetic and neural aspects, as well as evaluating the strength of biological explanations.

05:04

🧬 The Genetic Explanation of Schizophrenia

Here, the genetic basis of schizophrenia is discussed, explaining that there isn't a single gene responsible but rather a polygenic model, where multiple genes contribute to the risk. Research by Ripke identifies 108 gene loci associated with schizophrenia, with some genes related to the nervous and immune systems. The idea of etiological heterogeneity—different gene combinations causing schizophrenia in different people—is introduced.

👨‍👩‍👧‍👦 Family and Twin Studies Supporting Genetic Links

The paragraph discusses family and twin studies as a method to support the genetic explanation. It introduces the concept of concordance rates, which measure the occurrence of schizophrenia among relatives, particularly focusing on higher rates in monozygotic twins (48%) compared to dizygotic twins (17%). The studies suggest a genetic component, though the environment also plays a role, as identical twins don't show a 100% concordance rate.

👶 Adoption Studies and Gene-Environment Interaction

Adoption studies, particularly Tienari’s research, highlight the genetic risk of schizophrenia and its interaction with the environment. Children of schizophrenic mothers raised in healthy environments had a 5.8% risk, compared to 36.8% when raised in dysfunctional environments. This supports the idea that while genetics play a role, environmental factors significantly influence the development of schizophrenia.

🔬 Neural Correlates and the Dopamine Hypothesis

This section introduces the concept of neural correlates and focuses on the dopamine hypothesis, which suggests that too much or imbalanced dopamine contributes to schizophrenia symptoms. Hyperdopaminergia in speech centers may cause auditory hallucinations, while hypodopaminergia in the frontal cortex could explain negative symptoms like avolition. Drugs affecting dopamine levels provide evidence supporting this hypothesis.

📊 Further Evidence Supporting Dopamine and Other Neurotransmitters

The role of other neurotransmitters, such as glutamate and serotonin, is mentioned. Lower glutamate levels in schizophrenic individuals impact learning and memory, while serotonin is implicated due to the effectiveness of clozapine, which targets serotonin systems. A meta-analysis by Leucht of 212 studies confirms the dopamine hypothesis by showing that antipsychotic drugs, which reduce dopamine, effectively treat symptoms.

🧠 Enlarged Ventricles and Neural Structures in Schizophrenia

This paragraph discusses research on enlarged ventricles in schizophrenic individuals, as identified by Johnstone's 1970s study. The finding of larger cerebrospinal fluid-filled voids in the brain is correlational, meaning it's unclear whether they cause schizophrenia or are a result of the condition or medication.

🧐 Determinism and Reductionism in Biological Explanations

The concluding section addresses the concepts of determinism and reductionism. Biological determinism implies that schizophrenia is inevitable if you have the right genes, which can be disempowering. Reductionism simplifies schizophrenia to a cellular process, aiding research but ignoring psychological causes. The alternative is holism, as seen in the diathesis-stress model, which incorporates both genetic predispositions and environmental triggers.

Keywords

💡Genetics

Genetics refers to the hereditary transmission of traits through DNA. In the context of schizophrenia, the video explains that while there is no single gene responsible, the disorder is polygenic, meaning multiple genes contribute to an individual's risk of developing it. Research has identified 108 gene loci involved, linking genetics to both the nervous and immune systems.

💡Concordance rate

The concordance rate measures how often both individuals in a pair, such as twins, share a condition like schizophrenia. It provides evidence for genetic involvement. For example, identical twins have a concordance rate of 48%, compared to 17% for non-identical twins, suggesting a genetic component but also indicating environmental influences.

💡Dopamine hypothesis

The dopamine hypothesis suggests that an imbalance in the neurotransmitter dopamine is linked to schizophrenia. Excess dopamine (hyperdopaminergia) in areas like Broca’s area may cause auditory hallucinations, while low levels (hypodopaminergia) in the frontal cortex might contribute to negative symptoms like avolition. This theory is supported by the effectiveness of antipsychotic drugs that target dopamine.

💡Polygenic

Polygenic refers to a condition or trait that is influenced by multiple genes. Schizophrenia is described as polygenic because no single gene causes it; instead, various combinations of genes increase the likelihood of developing the disorder. This complexity makes it etiologically heterogeneous, meaning different genetic combinations may lead to schizophrenia in different people.

💡Neural correlates

Neural correlates refer to the brain structures or processes associated with a particular mental disorder. In schizophrenia, these include the activity of neurotransmitters like dopamine and physical brain abnormalities, such as enlarged ventricles. These neural correlates provide a biological basis for understanding symptoms and the disorder's progression.

💡Adoption studies

Adoption studies examine individuals adopted at birth and compare the rates of schizophrenia in those with biological parents who have schizophrenia versus those without. These studies provide evidence for genetic influence while controlling for the environment. For example, children with schizophrenic mothers had a higher likelihood of developing schizophrenia, especially in dysfunctional family environments.

💡Determinism

Determinism, in this context, refers to the idea that schizophrenia is predetermined by biological factors, such as genetics, leaving little room for change or control over the condition. This can be disempowering, as it suggests that individuals with certain genes are fated to develop schizophrenia, contrasting with cognitive explanations that allow for personal agency.

💡Reductionism

Reductionism involves explaining complex phenomena, such as schizophrenia, in terms of simpler biological processes. While this approach provides clear, evidence-based explanations (e.g., focusing on genetics and neurotransmitters), it may overlook other contributing factors, like psychological or environmental influences, which a more holistic approach would consider.

💡Diathesis-stress model

The diathesis-stress model is a holistic explanation for schizophrenia, suggesting that a genetic predisposition (diathesis) interacts with environmental stressors, such as family dysfunction, to trigger the disorder. This approach bridges biological and psychological explanations, recognizing that while genetics may create vulnerability, environmental factors are critical in determining if the disorder manifests.

💡Enlarged ventricles

Enlarged ventricles are large fluid-filled spaces in the brain that have been found in people with schizophrenia. This physical abnormality, discovered through CT scans, serves as a neural correlate. However, the relationship is correlational, meaning it's unclear if enlarged ventricles cause schizophrenia, are a result of it, or are influenced by medication use.

Highlights

Schizophrenia has a biological cause involving genetics, neural structures, and neurotransmitters.

There is no single 'schizophrenia gene'; it is polygenic with many genes increasing the risk.

Research identified 108 gene loci associated with schizophrenia, some linked to the nervous and immune systems.

Schizophrenia is aetiologically heterogeneous, with different gene combinations causing it in different individuals.

Family studies show higher concordance rates of schizophrenia in close relatives, especially in siblings.

Twin studies reveal a 48% concordance rate in identical twins, suggesting a genetic aspect.

Adoption studies show biological children of schizophrenic mothers have a higher risk even in healthy environments.

Neural correlates of schizophrenia include the dopamine hypothesis, suggesting imbalances cause symptoms.

Dopamine imbalances might cause auditory hallucinations and negative symptoms like avolition.

Antipsychotic drugs that influence the dopamine system support the dopamine hypothesis.

Other neurotransmitters like glutamate and serotonin may also play a role in schizophrenia.

Ventricles are larger in individuals with schizophrenia, but the causality is unclear.

Determinism suggests schizophrenia is inevitable if one has the genes.

Reductionism simplifies schizophrenia to cellular and chemical processes, ignoring psychological causes.

Holism, specifically the diathesis-stress model, combines genetic predisposition with environmental stressors.

Gottesman and Tienari's studies provide evidence for genetic and environmental influences on schizophrenia.

Transcripts

Hello and welcome to psych  boost. In this video we will  

be covering what it means to say that  schizophrenia has a biological cause.

As part of that discussion we will  touch on genetics, neural structures  

and the activity of neurotransmitters,  in particular the role of dopamine.

And of course we will consider the strength  of the biological explanation argument  

with evaluations. So let's begin CONTENT The Genetic Explanation

To say that schizophrenia is  biological we are suggesting  

it comes about through physical processes.

One of the main drivers of physical processes in  the body is how genetic information is expressed.

Now let me make clear right away  that while there is evidence for  

schizophrenia to have a genetic basis  there is not one schizophrenia gene.

Instead it seems that schizophrenia is polygenic,  this means there are a large number of individual  

genes that increase the risk of developing  schizophrenia. Infact research looking directly at  

the genetic code of over 36 thousand schizophrenia  sufferers by Ripke has identified 108 gene loci  

that are implicated, a number of these genes  are also associated with the nervous system, and  

interestingly the immune system. But the genetic  cause is complex, with different combinations of  

genes causing schizophrenia in different people,  we can call that aetiologically heterogeneous.

Now there is another way to  investigate if schizophrenia  

is genetic. And that is family studies.  If schizophrenia has a genetic basis  

we would expect to see schizophrenia in  close relatives of schizophrenia sufferers.

Now we can measure this statistical relationship  with a concordance rate. When we use concordance  

rate in schizophrenia research we mean how  often we see schizophrenia in both people.

So for example we would expect the  concordance rate to be higher in siblings  

than in cousins, because siblings share more DNA.

Of particular interest are twins, identical  twins have identical DNA, so we would expect  

to in twin studies see a higher concordance  rate in monozygotic twins than dizygotic twins.

So let's consider some evidence, research  by gottesman. This was a review of a large  

number of cases, looking for schizophrenia  in family members. What was found was a  

concordance rate of 48% in identical twins  dropping to 17% in non identical twins.  

Now considering the concordance rate  in the general population is only 1%  

this does seem to be strong evidence that  there is a genetic aspect to schizophrenia.  

The higher the genetic similarly the more  likely someone is to share the condition.

But you may have spotted some issues with this  data, characteristics that are fully genetic  

should have a 100% concordance rate in  identical twins. Think of blue eyes for  

example, that's not what we see with the  48% rate in genetically identical twins.

But we do expect both types of  twins to share a family environment,  

often sharing the same educational experiences,  family events and even diets, so the difference  

between the types of twins is likely due  to genetics. This data suggests a genetic  

aspect to schizophrenia, but also a complex  relationship between genes and the environment.

Adoption studies also provide evidence  for a genetic basis to schizophrenia.  

Tienari showed that when adopted and raised  in a psychologically healthy environment  

5.8% children of schizophrenic  mothers developed schizophrenia,  

compared to 2% of children who did not  have biologically schizophrenic mother's.  

This suggests that there is a biological risk,  however as 36.8% of those children whose mothers  

had schizophrenia went on to develop schizophrenia  if raised in a dysfunctional family, again this  

suggests that while important any biological  causes are influenced by psychological factors.

Neural Correlates

Genes code for biological processes within  the body, biological processes that are  

in the nervous system and are correlated with  schizophrenia we would call neural correlates.

The main neural correlate we will talk about here  is the dopamine hypothesis, this suggests that too  

much or an imbalance of the neurotransmitter  dopamine is responsible for symptoms.

Now the exact mechanism isn't known, but too  much dopamine, known as hyperdopaminergia in  

the brain's speech centers like Broca's area  may be responsible for auditory hallucinations.

And negative symptoms like  avolition and speech poverty  

could be due to low dopamine levels known  as hypodopaminergia in the frontal cortex.

This theory first came about from observations  that dopamine releasing drugs such as  

L-dopa would produce schizophrenia  like symptoms in healthy people.  

And that antipsychotics that work by reducing  levels of dopamine decrease symptoms.

Now while dopamine is the main neurotransmitter  

implicated in schizophrenia, there  are others that may play a role.  

Glutamate is in lower levels in people with  schizophrenia and it regulates learning,  

attention and memory. Serotonin, as clozapine  is an effective treatment for schizophrenia,  

and acts on a range of neurotransmitter  systems including the serotonin system.

When looking for evidence  for the dopamine hypothesis  

we can look at the success of antipsychotic drugs  

that work influence the dopamine system  as evidence for the dopamine hypothesis.

For example leueht's meta-analysis of 212  studies, as these drugs work in the dopamine  

system and were more effective than a placebo at  treating symptoms, then this supports the argument  

that dopamine is responsible for symptoms,  otherwise the drugs wouldn’t be effective.

But quick point, if you are asked a question about  the biological explanation for schizophrenia,  

don't allow yourself to start writing an essay  about drug treatments, all we are doing here is  

using the effectiveness of the drugs to support  the dopamine hypothesis, keep your essay focused.

Moving on to another neural correlate we can  mention ventricles, these are large voids in the  

brain, these voids are filled with cerebrospinal  fluid. Research by Johnstone in the 1970's  

showed using CT scans that these structures are  larger on average in people with schizophrenia.

enlarged ventricles is an interesting  observation, but a problem with this  

research is it's correlational. We don't know  if larger ventricles cause schizophrenia or  

the other other way around. Or maybe enlarged  ventricles are a side effect of medication.

I'm going to finish this exploration of  the biological basis of schizophrenia  

by considering both determinism  and reductionism as evaluations.

Now I would advise not to use both of  these evaluations together in an essay,  

mostly because many students get  them confused with each other,  

and there are always other  evaluations available to us.

But I'm going to use them both now so I can show  you clearly the difference between the concepts.  

And you may want to pick  one to use in your essay.  

So starting with determinism

Using a biological explanation for schizophrenia,  such as the genetic explanation assumes that  

schizophrenia is inevitable, you have the genes  or you don't. Schizophrenia is biologically  

determined for you. As you can imagine that can be  disempowering and could make you feel like you are  

unable to change your situation. The alternate  cognitive explanation is a soft determinist  

perspective, there may be causal reasons for the  origin of schizophrenia, however the individual  

can alter their own thought processes via  free will and ultimately control the disorder.

Looking now at reductionism

Being able to explain the origin of schizophrenia  as a basic cellular and chemical process is  

biologically reductionist, this has benefits, for  example the biological explanation has parsimony,  

it explains the disorder simply using the  available evidence, allowing future research  

on schizophrenia’s origins and treatments  to be focused. However this reductionist  

approach ignores a range of valid evidence  for psychological causes of schizophrenia.

We can add on to this reduction  argument its opposite, holism.

A better explanation for schizophrenia may be a  holistic approach, the diathesis-stress approach  

accepts the cause of schizophrenia is genetic  in origin acting as a weakness or diathesis.  

But includes psychological environmental  stressors like family dysfunction as a trigger.

Have a look again at the gottesman and  Tenari research studies in this video  

and see if you can make a little  more sense of the results now.