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.