Bio explanation
Download
Report
Transcript Bio explanation
What do we need to know?
In relation to
their chosen
disorder:
schizophrenia
Information to know;
Clinical characteristics of the chosen disorder
Issues surrounding the classification and diagnosis of their chosen
Biological explanations of their chosen disorder, for example, genetics,
biochemistry
Psychological explanations of their chosen disorder; behavioural, cognitive,
psychodynamic and socio-cultural
Biological therapies for their chosen disorder, including their evaluation
in terms of appropriateness and effectiveness
Psychological therapies for their chosen disorder, for example,
behavioural, psychodynamic and cognitive-behavioural, including their
evaluation in terms of appropriateness and effectiveness
LEARNING OBJECTIVES
describe the role of genetics in
schizophrenia
describe family, twin and adoption studies
as a way of studying the role of genetics in
schizophrenia
explain how family, twin and adoption
studies support the genetic explanation of
schizophrenia
True/False
3% of the population suffer from
schizophrenia
The word schizophrenia means ‘split mind’
The DVM is used to diagnose
schizophrenia
A delusion is a positive symptom
The symptoms must persist for one year
in order to be diagnosed as schizophrenic
The flattening of emotion is a positive
symptom
Biological V Psychological explanations
On a post it note
write down what
you understand
the nature
nurture debate to
be about
Nature V Nurture
Biological explanations
of Schizophrenia
Genetic factors
Neuro -chemicals:
Dopamine hypothesis
Diathesis -stress
Assumptions of biological
explanations
All mental disorders have a physical
cause. (micro-organisms, genetics,
biochemistry or neuro-anatomy)
Mental illnesses can be described in
terms of clusters of symptoms.
Symptoms can be identified, leading to
the diagnosis of an illness.
Diagnosis leads to appropriate physical
treatments.
Genetics
• Individuals may inherit a
predisposition to certain
illnesses. These are
carried on genes,
through DNA, which pass
from one generation to
the next
• PREDISPOSITION = Increased
vulnerability to a particular disease
based on genetic factors or the existence
of certain underlying conditions not yet
.
active or revealed
Genetics
• Every human has 46
chromosomes (DNA)
divided into 23 pairs.
• During reproduction,
23 chromosomes from
mum and 23
chromosomes from
dad are combined to
make an embryo (cells
before a baby)
Genetics
• This is how we get our
characteristics from
both of our parents.
• If a disorder is caused
genetically then we
would expect
individuals who are
closely related to be
more likely to have it
Genetics
• How do we measure
this?
• Concordance rate:
measures how often
two individuals who
are closely related
have the same
disorder.
Schizophrenia: genetics
factors
Prevalence of schizophrenia is the same all over
the world (about 1%)
Supports a biological view as prevalence
does not vary
Is with
this aenvironment
problem of
diagnosis
or broad
However,reliability
there arein
variations
within
is areas
it the (e.g.
influence
of2002 –
geographical
Torrey
environmental
found high
rates of Sz in factors
Ireland, ?4% of the
population, the incidence is also high in
Croatia and Scandinavian countries but low
in Spain and Italy and very low in some
parts of Africa)
How do we study the influence
of genetic factors?
If the concordance rate is
100% in MZ twins it means
that the characteristic is
genetically determined.
Twin
If it less than the 100% but
higher that DZ twins What
studies
does it mean?
However one
is usually born
bigger than
Monozygotic
the other
twins
Share the same
genes and the
same
environment
Concordance rate:
the proportion of
pairs where both
individuals share a
certain characteristic.
However they
might be
treated
Dizygotic differently
twins
Share as many
genes as
ordinary
siblings but
share the same
environment
SO -Dizygotic twins (nonidentical twins) share similar
characteristics, much like
siblings.
Monozygotic twins (identical
twins) are the result of an
embryo viably splitting early
on in development. They
share almost exactly the
same Chromosomal DNA.
Genetics
• Twin Studies look at all types of
twins:
• Twins can be identical
(monozygotic,MZ) or fraternal
(dizygotic, DZ).
• Best of all Psychologists like to study
MZ twins who have been reared apart
to see if they develop the same
disorder
• Why do you think that is?
Family
studies
Gottesman
(1991)
Children share 50%
of their genes with
each of their
parents.
If one of their
parent is
schizophrenic the
child has a greater
chance of being
schizophrenic.
If he/she is Sz, are
only genetic factors
responsible?
Tienari
(2000)
Adoption
studies
Adopted children have
a higher concordance
rate for Sz with their
biological parents than
with their adoptive
parents, which
supports the influence
of genetic factors
Twin studies
Gottesman and Shields
Reviewed the results of 5 twin studies looking for concordance
rates for schizophrenia.
These studies looked at 210 MZ twins and 319 DZ twins
It was found that in MZ twins there was a concordance rate of
35-58% compared with dizygotic (DZ) twin rates that ranged
from 9-26%.
They also found a concordance rate in MZ twins of 75-91%
when the sample was restricted to the most severe form
of schizophrenia.
The milder forms of schizophrenia had concordance rates of 1733% suggesting that there may be greater genetic loading
with severe forms of schizophrenia.
Joseph (2004) calculated that the pooled data for studies
prior to 2001 show a concordance rate for MZ twins at 40%
and Dz twins at 7%.
But the twin studies have all assumed that the shared
environmental effects for MZ and DZ twins are equal which
may be incorrect….and
Twins are not representative of the wider
population.
It is a very small sample. There are very few MZ
twins in the population and only 1% are Sz.
We need to question if these diagnoses are made
using the same criteria
Adoption studies
Prevalence
Prevalence among
amongst biological adoptive relatives
relatives
Kety et al (1968)
schizophrenia only
13%
2%
Tienari et al (1994)
all ‘severe’ psych.
diagnoses
30%
15%
Could the psychiatrist making the diagnosis in the
Were
Were
child
How
Did
they
these
be
they
old
adopted
influenced
diagnosis
were
see their
children
by if
members
made
biological
he/she
when
using
isofthey
parents
aware
the
the same
were
extended
that
regularly?
adopted?
criteria?
onefamily?
of
both of the parents are Sz??
The overall picture
Diathesis-Stress Model
This model explains Sz as a result of both genetic factors ("nature"), and life
experiences ("nurture").
This model thus assumes that a disposition towards a certain disorder may
result from a combination of one's genetics and life experiences.
The term "diathesis" is used to refer to a genetic predisposition toward an
abnormal or diseased condition.
This theory suggests a mental illness like schizophrenia is produced by the
interaction of a vulnerable hereditary predisposition along with precipitating
events in the environment – like death of a loved one, becoming homeless,
stress at work etc
Vulnerability
The greater the underlying vulnerability, the less
stress is needed to trigger the disorder.
Conversely, where there is a smaller genetic
contribution greater life stress is required to
produce the particular result.
Even so, someone with a diathesis towards a
disorder does not necessarily mean they will ever
develop the disorder. Both the diathesis and the
stress are required for this to happen.
So have we found a gene
responsible for Sz?
In 2006, an Edinburgh University team
found people carrying a variant of a gene
called neuregulin had a higher chance of
developing psychotic symptoms.
However since then research has shown
that Sz involves a huge number of genes
with each of them making only a small
contribution to the development of the
disorder according to Robin Murray a
leading schizophrenia researcher.
From twin, family and adoption
studies we can conclude that risk
rises with the degree of genetic
relatedness
Spouse – 1% (same as general
population)
Child – 13%
DZ twin – 17%
MZ twin – 48%
Evaluation
Twin studies may be flawed there may be reasons other than
genetic which explain the higher
concordance rates in MZs.
Can you think what they are?
Environmental Effects
MZ twins tend to be treated much
more similarly to each other than
DZs do. Therefore parenting issues
could be duplicated, or applied more
completely to both children in the
pair. Also, there may be more
identity issues - a problem
experienced by some schizophrenics
- because MZs are treated more like
one person.
Methodological Effects
In the past, diagnosis of the disease
in twin pairs was carried out by
psychiatrists who knew all about the
study, including whether or not they
were assessing MZs or DZs!
The solution is to carry out a b***d
diagnosis.
When this is done, concordance
rates drop for MZs
However, the difference is still
significant….
Overall there is substantial evidence for a
genetic contribution
However some evidence is disputed:
Shared environment issues
Diagnostic criteria in adoption studies
(Joseph 2004)
Methodological issues
The evidence also suggests environmental
triggers: Epigenetics could explain why the
concordance rate is less than 100% in MZ
twins. Heritability is similar to other major
disorders such as breast cancer, hypertension, etc
Now, please plan it
Discuss
means
describe and
evaluate
June 2013
Discuss biological explanations for
schizophrenia. (8 marks + 16 marks)
At the moment just plan what you would
include in the answer based on the
genetic explanation
From the examiner’s report
The commonest explanations for
schizophrenia were genetics, the dopamine
hypothesis and neuroanatomy. Other
appropriate explanations included the roles
of other neurochemicals, viral links and
evolutionary explanations. The evaluations
of the explanations were of mixed quality.
There was a general lack of focus on the
extent to which the explanations
described could explain the
development of schizophrenia.
Do you remember how neurones
work?
https://www.youtube.com/watch?v=c5cab4hgmoE
DOPAMINE
HYPOTHESIS
Schizophrenia: Biochemical
The dysfunction of several neurotransmitter
systems are thought to play a part in
schizophrenia
Dopamine
5-hydroxytryptamine (5-HT; Serotonin)
Glutamate
We will concentrate on the Dopamine
Hypothesis
Schizophrenia & dopamine
The dopamine hypothesis suggests
Schizophrenia is caused by excessive
Dopamine activity.
The
This causes
abnormal functioning of
abbreviation
dopamine-dependent brain systems,
resultingfor
in schizophrenic
symptoms
dopamine
Dopamine can is
increase
DA or decrease
brain activity depending on the
system you’re looking at
Lets remind ourselves how
neurotransmitters work
DOPAMINE HYPOTHESIS
The Dopamine hypothesis states that the
brains of schizophrenic patients produces
more dopamine than normal brains. Sz are
also thought to have high numbers of D2
receptors resulting in more dopamine binding
and therefore more neurones firing
Evidence comes from
studies with drugs
post mortems
pet scans
Normal Level of
Dopamine In The
Human Brain
Elevated Level of Dopamine
In The Brain of a
Schizophrenic Patient
(specifically the D2 receptor)
Neurons that use the transmitter ‘dopamine’ fire too often
Certain D2 receptors are known to play a key role in guiding
attention. – disturbances in this process may lead to problems
relating to attention, perception and thought processes
EVIDENCE: Lowering dopamine activity helps remove the
symptoms of schizophrenia
Evidence from Parkinson’s disease
Parkinson’s sufferers have low
levels of dopamine
L-dopa raises DA activity
People with Parkinson's develop
schizophrenic symptoms if they take
too much L-dopa
EVIDENCE:
Chlorphromazine (given to schizophrenics) reduces
the symptoms of Sz by blocking D2 receptors
ROLE OF DRUGS
Amphetamines (agonists) lead to increases in
dopamine levels
Large quantities lead to delusions and
hallucinations
If amphetamines are given to schizophrenic
patients their symptoms get worse
Randrup et al
Rats given
amphetamines
developed
schizophrenia
type symptoms
Antipsychotic drugs
Antipsychotic drugs block the
activity of dopamine in the brain.
By reducing stimulation of the
dopamine system these drugs
eliminate symptoms like
hallucinations and delusions.
POST MORTEM evidence
Falkai et al (1988)
Autopsies have found that people with
schizophrenia have a larger than usual number
of dopamine receptors.
Increased levels of dopamine have been found
in certain brain structures - left amygdala and
caudate nucleus putamen.
They concluded that dopamine production is
abnormal for schizophrenia
Evidence from PET SCANS
Lindstroem et al (1999)
Radioactively labelled the chemical LDopa
This was then administered to 10
patients with schizophrenia and 10
with no diagnosis
The L-Dopa was taken up quicker in
the brain of schizophrenic patients
This suggests they were producing
more dopamine than the control
group
Which Came First?
The Chicken or the Egg?
Schizophrenia or Faulty
Chemicals?
Faulty chemicals cause
schizophrenia but schizophrenia
may cause faulty chemicals
Drugs may also influence other systems that impact
on schizophrenia so we cannot be 100% sure about
their effects
EVALUATION
There is a lack of correspondence between taking the drugs and
signs of clinical effectiveness. It takes 4 weeks to see any sign that
the drugs are working even when they begin to block dopamine
receptors immediately.
At present there is still no accepted explanation for this time
difference.
Drugs such as CHLOPROMAZINE are only effective at relieving the
Positive (type 1) Symptoms of the Illness.
They are not effective for negative symptoms. This may suggest that
Type 2 Sz is related to a different kind of abnormality such as brain
structure.
PET scans have suggested that drugs do not reduce symptoms of
patients diagnosed with Sz for 10 yrs or more
Post Mortem studies –
contradictory evidence
As drugs block the dopamine
receptors - the brain compensates
by making more dopamine
Post mortem studies reveal that
patients who have taken
antipsychotic drugs before they die
have higher than normal levels of
dopamine in their brain.
Evidence from neuro-imaging
research
Neuro-imaging studies (like
using PET scans) have not
yet provided convincing
evidence of altered
dopamine activity in the
brains of people with SZ
(Copolov 2000)
Clearly there are other
possible causes of Sz
Brain structure
Brain damage
Viral infection
Birth complications
Brain Structure
People with
schizophrenia have
abnormally large
ventricles in the
brain. Ventricles are
fluid filled cavities.
This means that the
brains of
schizophrenics are
lighter than normal.
Brain structure
Swayze (1990) reviewed 50
studies of schizophrenics and
found that many had abnormally
large amounts of liquid in the
cavities of the brain.
This has been supported using
MRI scans on schizophrenic twins.
Brain Structure Evidence
Andreasen (1990)–
conducted a very well
controlled CAT scan
study and found
significant
enlargement of the
ventricles in
schizophrenics
compared to controls.
However this was
only the case for men
and not for women.
Enlarged ventricles due to
medications?
Beng-Choon Ho (2010) in
a longitudinal
correlational study of
211 schizophrenics
found that antipsychotic
drugs have measurable
influence on brain tissue
loss over time. This was
supported by Lewis
(2009) who administered
antipsychotic drugs to
primates and found a
brain volume loss of
10% .
However this was a
correlational study so it
does not show cause and
effect. Lewis’s study was
carried out on animals so
we cannot extrapolate to
humans without caution.
Furthermore
If the reduction in
brain volume is the
cause of the
schizophrenic
symptoms then it
cannot explain why
after 30 years of the
initial onset, 35% of
the schizophrenics are
classified as "much
improved“ because
the cortex does not
grow back, if the
structural differences
were the cause then
no improvement
would be possible.
Viral Infection
In recent years, there has
been a build up of evidence
supporting the role of viral
infections in the development
of schizophrenia, including the
poliovirus, the flu virus and a
virus called encephalitis
lethargica ('inflammation of
the brain that makes you
tired‘).
Birth Complications
Complications during pregnancy,
abnormal foetal growth and
complications during delivery are
significant risk factors in the
development of schizophrenia.
Gender bias
Reductionism
Ethnocentrism
Nature/Nurture
•is the theory based on research carried out on an
unrepresentative sample?
•does the theory/approach attempts to explain phenomena in
terms of basic elements?
•is the theory based on research carried out in one particular
type of culture (i.e. indivicualistis culture) ?
•Does the theory/approach explain phenomena in terms of
nature i.e. gentics neglecting other factors i.e. social
factors?
Approach
•Situate the theory in one approach (biological, behavioural,
cognitive, psychodynamic)
Determinism
•Does the theory/approach acknoledge a sense of individual
free-will or does it argue that our behaviour is determined
by a particular set of factors?
Ethics
•Does the theory/approach propose/research issues which
could be socially controversial ? (i.e. correlation between
race and IQ)
Scientific method
•Is the theory based on evidence which is objective/ valid/
reliable?
Evaluating Ideas in a
boarder context
‘GRENADES’
These are the issues
and debates we will
be using as the
course develops