L2 - Biological Explanations Of SZ

Question 1

What are the two main factors in biological explanations of schizophrenia?

Answer 1

Genetic basis and neural correlates including the dopamine hypothesis

Question 2

How are genetic factors tested in schizophrenia research?

Answer 2

Through family, twin, and adoption studies

Question 3

Family studies

Answer 3

• find ppl with SZ & see if biological relatives are similarly affected more then non-biological relatives
• Gottesman (1991) found if that the chances of getting SZ:
• 46% if both parents are schizophrenic
• 13% if one parent is schizophrenic
• 9% if a sibling has schizophrenia
• This shows a clear trend that closer genetic relatedness increases the risk of developing schizophrenia.

Question 4

Twin studies

Answer 4

• They investigate the nature/nurture debate regarding heredity and environmental influences
• Monozygotic twins share 100% of their genes, while dizygotic twins share 50%
• Gottesman (1991) found the concordance rates are:
• 48% for monozygotic twins
• 17% for dizygotic twins
• Higher concordance in monozygotic twins supports the genetic basis of schizophrenia, as more genetically similar, more likely to get SZ

Question 5

More twin study support

Answer 5

• Joseph (2004) did a review of twin studies carried up to 2001 & found concordance rates to be
• 40% for monozygotic twins
• 7.4% for dizygotic twins
• still relatively high for MZ twins
• reinforces the idea that genetics play a significant role in schizophrenia

Question 6

What is the purpose of adoption studies in schizophrenia research?

Answer 6

• To understand the influence of nature and nurture by observing adopted individuals with biological parents diagnosed with schizophrenia
• Tienari et al. (2001) carried out a study in Finland using 164 ppt whose bio mothers had SZ
• 6.7% of adoptees with biological mothers diagnosed with SZ were also diagnosed
• 2% in a control group of adoptees of 197 ppt (parents don’t have SZ)
• although percentage is low, there is a small link between SZ genes with children whose bio mothers were schizophrenic
• although not as good as gottesman studies

Question 7

What does it mean that schizophrenia is considered polygenic?

Answer 7

• It means that multiple genes contribute to the risk of developing schizophrenia
• combination of different genes that have been implicated in SZ
• there are specific candidate genes that are associated with SZ e.g. PCM1

Question 8

chromosome study

Answer 8

• Gurling et al (2006) used family study evidence indicating that SZ was associated with Chromosome 8p21-22 to identify a high risk sample
• gene mapping also used to implicate PCM1 gene in susceptibility to SZ
• also benzel et al. (2007)

Question 9

Benzel et al. (2007)

Answer 9

• used gene mapping to find evidence suggesting that NRG3 gene variants interact with NRG1 and ERBB4 gene variants to create susceptibility to develop SZ suggesting interaction of genetic factors

Question 10

What did Ripke et al (2014) find in their comparison of genetic makeup of schizophrenia patients and controls?

Answer 10

108 separate genetic variations associated with increased risk of schizophrenia
Genes that were particularly vulnerable were the ones that had so,e connection to the functioning of certain neurotransmitters such as dopamine

This study involved a large sample size of 37,000 SZ patients and 113,000 controls.

Question 11

Evaluation of the genetic basis of SZ

Answer 11

strengths
- research support
weaknesses
- separating nature vs nurture
- absence of family history
- biologically reductionist
- diathesis stress model

Question 12

Research support (genes)

Answer 12

There is a wealth of research evidence to support the genetic basis for SZ as can be seen from the findings of Gottesman, Joseph’s and Tienari’s study, thus there is a link between genes and SZ. This is a strength because it shows that if a child grows up in a family where both their biological parents has SZ, then the chances of them getting it is heightened compared to if only one parent or none of the parents have it suggesting that genetics is an important factor

Question 13

Separating nature from nurture

Answer 13

However, the problem with twin and family studies is separating nature (genes) from nurture (the environment). For example, MZ twins are normally reared together and sent to the same school, where the same clothes (in childhood), this then makes it difficult to separate upbringing from genes. Even if we look at adoption studies that attempt to separate genes from the environment, children tend to be adopted by relatives who may still rear the child similarly to its biological parents – thus adoption studies may not always be a good comparison for the effects of nature and nurture.

Question 14

Absence of family history

Answer 14

More importantly, SZ can take place in the absence of a family history. One explanation is that there may be a mutation in parental DNA, for example in paternal sperm cells. This can be caused by radiation, poison or infection. Evidence for role of mutation comes from Brown et al’s. (2002) study which showed a positive correlation between paternal age and increased risk of SZ increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. This suggests that although no direct genes are involved, a person can still get SZ if their father was older at the time of fertilisation. This suggests that the role of nature and nurture may both play a part rather than just genes

Question 15

Biologically reductionist

Answer 15

The Genetic explanation of SZ is also biologically reductionist as it is stating that one cause of SZ is simply your genes. In other words it is insinuating that if you possess the PCM1 gene then you will have SZ. This means that this explanation is ignoring other factors such as psychological factors and family upbringing which could be more important in explaining SZ – for example it has been found that certain parenting styles (e.g. the schizophrenogenic mother) in an individuals childhood could trigger symptoms of SZ in adulthood

Question 16

Diathesis stress model

Answer 16

Similarly, the diathesis stress model states that there is a genetic vulnerability in schizophrenia but this vulnerability is only likely to be triggered if there is a stress trigger in the individual’s life. In other words, you may be born with a gene which makes you particularly vulnerable to SZ but if your life is relatively stress free, then you may not end up having the disorder at all. Thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ. Therefore taking a more holistic
perspective in understanding the causes of SZ may lead to more effective treatments rather than just focusing on genes alone.

Question 17

Neural correlates

Answer 17

• they are patterns or structure or activity in the brain that occur in conjunction with an experience & may be implicated in the origins of that experience
• both positive and negative symptoms have neural correlates

Question 18

Neural correlates - different brain regions (extra)

Answer 18

• Using brain-imaging techniques, researchers have discovered that many schizophrenics have enlarged ventricles, cavities in the brain that supply nutrients and remove waste – the ventricles of a person with SZ are on average about 15% bigger than normal (Torrey, 2002)
• People with SZ who have enlarged ventricles tend to display more negative than positive symptoms.
• These people also tend to respond poorly to typical antipsychotic drugs.
• The enlarged ventricles may be the result of poor brain development or tissue damage, and these problems may lead to the development of SZ.

Question 19

Prefrontal cortex (PFC)

Answer 19

The prefrontal cortex (PFC) is the main area of the brain involved in executive control (i.e. planning, reasoning and judgement) and research has shown that this is impaired in schizophrenic patients (Weinberger and Gallhofer, 1997).

Question 20

Hippocampus

Answer 20

Also, the hippocampus is an area of the brain in the temporal lobe and several studies have reported anatomical changes in the hippocampus in schizophrenic patients (Conrad et al., 1991). Deficits in the nerve connections between the hippocampus and prefrontal cortex have found to correlate with the degree of memory impairments in schizophrenics.

Question 21

Evaluation of neural correlates - different brain regions

Answer 21

strengths
- research evidence
- brain scanning
weaknesses
- individual differences
- exact region/cause and effect

Question 22

Research evidence (neural correlates)

Answer 22

There is research evidence to support the structural changes in the brain between SZ and non SZ such as Torrey’s study with reference to enlarged brain ventricles and Conrad’s study with regards to the hippocampus.

Question 23

Brain scanning

Answer 23

Furthermore, this research evidence can be validated through brain scanning which is an objective method suggesting that there is face validity to the neural correlates explanation because one can actually observe the structural brain changes that occur with schizophrenic patients – this can then help to tailor make treatments that will reduce the symptoms of SZ.

Question 24

Individual differences

Answer 24

The problem with looking at different brain regions is the fact that there are individual differences in sufferers of schizophrenia and not all patients have deficits in the functioning of different brain regions.

Question 25

Exact region/cause & effect

Answer 25

• Also as there are different brain regions involved in SZ, it may be difficult to pinpoint
  which brain region is causing the symptoms.
• Furthermore, it may be difficult to establish cause and effect in terms of neuroanatomy as evidence is correlational in other words, did the sufferer have abnormalities in a particular brain region and then contract schizophrenia or did the individual contract schizophrenia and then show brain abnormalities

Question 26

What is dopamine?

Answer 26

• Dopamine is a neurotransmitters it helps regulate movement, attention, learning, and emotional responses.
• It also enables us not only to see rewards, but to take action to move toward them. Since dopamine contributes to feelings of pleasures and satisfaction as part of the reward system, the neurotransmitter also plays a part in addiction.
• Dopamine is heavily involved in the motor system. When the brain fails to produce enough dopamine, it can result in Parkinson’s disease.
• A primary treatment for Parkinson’s disease, therefore, is a drug called L-dopa, which spurs the production of dopamine.
• it has also been implicated in schizophrenia and ADHD, but its role is not fully understood. People with low dopamine activity may also be more prone to addiction.
• The presence of a certain kind of dopamine receptor is associated with sensation-seeking, more commonly known as risk taking.

Question 27

Neural correlates - the dopamine hypothesis

Answer 27

• one of the best known examples of neural correlates
• Neurotransmitters are the brains chemical messengers. These appear to work differently in the brains of schizophrenics.
• In particular, dopamine (DA) seems to have an important role since DA is necessary in the functioning of several brain systems, it has also been implicated in SZ.
• Thus the dopamine hypothesis claims that an excess of the neurotransmitter dopamine
  in certain regions of the brain is associated with the positive symptoms of SZ. Thus messages from neurones that transmit dopamine fire too easily and often, leading to hallucinations and delusions.
• Schizophrenics are thought to have particularly high levels of DA receptors on receiving
  neurons resulting in more dopamine binding and therefore more neurons firing

Question 28

2 consequences of the dopamine hypothesis

Answer 28

• Hyperdopaminergia in the sub cortex
• Hypodopaminergia in the cortex

Question 29

Hyperdopaminergia in the sub cortex

Answer 29

• this is based on the original version of the dopamine hypothesis in explaining SZ – this states that there are high levels of activity of dopamine in an area of the brain known as the subcortex (i.e. the central areas of the brain).
  E.g. an excess of dopamine receptors in the Broca’s area (which is responsible for speech production) may be associated with problems in speech and/or the experience of auditory hallucinations.

Question 30

Hypodopaminergia in the cortex

Answer 30

• recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex. - This too can explain symptoms of SZ e.g low levels of dopamine in the prefontal cortex (responsible for thinking)
• could explain the cognitive problems in the negative symptoms of SZ for example speech poverty where low levels of dopamine can lead to an inability to construct grammatical Sentences
• has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia so both high and low levels of dopamine in different brain regions are part of an updated version of explaining the symptoms of SZ

Question 31

Evaluation of neural correlates - dopamine hypothesis

Answer 31

strengths
Research support
Antipsychotic drugs
Speed of chemicals
weaknesses
Biologically determinists
Cause & effect

Question 32

Research support (dopamine hypothesis)

Answer 32

With regards to the dopamine hypothesis, this neural correlates explanation is supported through drug research since dopamine agonists like amphetamines tend to increase dopamine levels and make the schizophrenic symptoms worse in sufferers andcan produce schizophrenic-like symptoms in non-sufferers thus supporting this idea of Hyperdopaminergia

Question 33

Anti-psychotic drugs

Answer 33

Also, antipsychotic drugs act like antagonists – which act to reduce the levels of dopamine in schizophrenic patients (which thus help control the symptoms of SZ) supporting the idea that dopamine levels are high in SZ and can be reduced through drugs (e.g. Tauscher et al, 2014).

Question 34

Speed of chemicals

Answer 34

Furthermore, Lindstroem et al. (1999) have found that that chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics compared to controls again suggesting that schizophrenics produce more dopamine. Thus the abundance of evidence suggests that the dopamine hypothesis is definitely relevant in understanding schizophrenia

Question 35

Biologically determinist

Answer 35

the dopamine hypothesis could be criticised to being biological determinist which means an individual has no control over this whatsoever. However, the dopamine hypothesis alone cannot be seen as the sole cause of SZ since there are other biological and psychological factors that contribute such as upbringing in terms of family dysfunction or cognitive explanations which focus on impaired thinking which could definitely explain the hallucinations and delusions. Also much more recent research has also focused on the attention of glutamate – another neurotransmitter that has been implicated in SZ (Moghadamm and Javitt, 2012) suggesting that dopamine might not be the only neurotransmitter responsible for SZ and other neurotransmitters may also be involved

Question 36

Cause and effect

Answer 36

-there are a number of neural correlates of SZ such as brain structure and neurotransmitters and although studies support neural correlates, there are some important questions that are left unanswered with such evidence. Most importantly, does high or low levels of dopamine cause SZ
- There could be other explanations for the correlation.
e.g. there is a correlation between high levels of dopamine and experiencing symptoms of SZ.
- However, did the individual start having excess levels of dopamine in that brain region and start experiencing symptoms of SZ or did the individual first experience symptoms of SZ and consequently have high levels of dopamine? This point poses a serious problem to the neural correlates explanation as it does not really explain the cause and effect