1. 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

2. 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

3. 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

4. Biological V Psychological explanations
On a post it note write down what you understand the nature nurture debate to be about
Nature V Nurture

5. Biological explanations of Schizophrenia
Genetic factors
Neuro -chemicals: Dopamine hypothesis
Diathesis -stress

6. 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.

7. 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.

8. 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)

9. 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

10. Genetics How do we measure this?
Concordance rate: measures how often two individuals who are closely related have the same disorder.

11. Schizophrenia: genetics factors
Prevalence of schizophrenia is the same all over the world (about 1%)
Supports a biological view as prevalence does not vary with environment
However, there are variations within broad geographical areas (e.g. Torrey 2002 – found high rates of Sz in 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)
Is this a problem of reliability in diagnosis or is it the influence of environmental factors ?

12. How do we study the influence of genetic factors?
Concordance rate: the proportion of pairs where both individuals share a certain characteristic.
If the concordance rate is 100% in MZ twins it means that the characteristic is genetically determined.
If it less than the 100% but higher that DZ twins What does it mean?
Twin studies
However they might be treated differently
However one is usually born bigger than the other
Dizygotic twins
Monozygotic twins
Share as many genes as ordinary siblings but share the same environment
Share the same genes and the same environment

13. SO -Dizygotic twins (non- identical 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.

14. 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?

15. Children share 50% of their genes with each of their parents.
Family studies
Gottesman (1991)
Adoption studies
Tienari (2000)
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
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?

16. 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 % 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 % suggesting that there may be greater genetic loading with severe forms of schizophrenia.

17. Twins are not representative of the wider population.
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

18. Adoption studies
Prevalence amongst biological relatives
Prevalence among adoptive 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 child be influenced if he/she is aware that one of both of the parents are Sz??
Were they adopted by members of the extended family?
Were these diagnosis made using the same criteria?
Did they see their biological parents regularly?
How old were children when they were adopted?

19. The overall picture

20. 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

21. 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.

22. 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.

23. 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%

24. 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?

25. 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.

26. 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….

27. 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

28. Discuss means describe and evaluate
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

29. 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.

30. Do you remember how neurones work?

31. DOPAMINE HYPOTHESIS

32. 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

33. Schizophrenia & dopamine
The abbreviation for dopamine is DA
The dopamine hypothesis suggests
Schizophrenia is caused by excessive Dopamine activity.
This causes abnormal functioning of dopamine-dependent brain systems, resulting in schizophrenic symptoms
Dopamine can increase or decrease brain activity depending on the system you’re looking at

34. Lets remind ourselves how neurotransmitters work

35. 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

36. Neurons that use the transmitter ‘dopamine’ fire too often
Elevated Level of Dopamine In The Brain of a Schizophrenic Patient
(specifically the D2 receptor)
Normal Level of Dopamine In The Human Brain
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

37. 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

38. 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

39. Rats given amphetamines developed schizophrenia type symptoms
Randrup et al
Rats given amphetamines developed schizophrenia type symptoms

40. 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.

41. 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

42. Evidence from PET SCANS
Lindstroem et al (1999)
Radioactively labelled the chemical L- Dopa
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

43. Schizophrenia or Faulty Chemicals?
Which Came First?
The Chicken or the Egg?
Schizophrenia or Faulty Chemicals?
Faulty chemicals cause schizophrenia but schizophrenia may cause faulty chemicals
Movie clip: house (ao2 points …… ethics & side effects of biological model approach)
Drugs may also influence other systems that impact on schizophrenia so we cannot be 100% sure about their effects 

44. 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

45. 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.

46. 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)

47. Clearly there are other possible causes of Sz
Brain structure
Brain damage
Viral infection
Birth complications

49. 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.

50. 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.

51. 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.

52. 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.

53. 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.

54. 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‘).

55. Birth Complications
Complications during pregnancy, abnormal foetal growth and complications during delivery are significant risk factors in the development of schizophrenia.

56. Evaluating Ideas in a boarder context
is the theory based on research carried out on an unrepresentative sample?
Gender bias
does the theory/approach attempts to explain phenomena in terms of basic elements?
Reductionism
is the theory based on research carried out in one particular type of culture (i.e. indivicualistis culture) ?
Ethnocentrism
Does the theory/approach explain phenomena in terms of nature i.e. gentics neglecting other factors i.e. social factors?
Nature/Nurture
Situate the theory in one approach (biological, behavioural, cognitive, psychodynamic)
Approach
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?
Determinism
Does the theory/approach propose/research issues which could be socially controversial ? (i.e. correlation between race and IQ)
Ethics
Is the theory based on evidence which is objective/ valid/ reliable?
Scientific method
Evaluating Ideas in a boarder context
‘GRENADES’
These are the issues and debates we will be using as the course develops 