Lesson 2 Biological Explanations Of SZ Flashcards
Biological explanations of SZ
Biological explanations of schizophrenia are based on two factors: the genetic basis and neural correlates including the dopamine hypothesis.
Genetic basis
Genetic factors are normally tested through family, twin and adoption studies
Family studies
Family studies find individuals who have SZ and determine whether their biological relatives are similarly affected more often than non-biological relatives. Family studies have shown that the closer the genetic relatedness, the greater the risk. Gottesman (1991) found that if both parents were schizophrenic, then the likelihood of the offspring also having SZ was 46%, if one parent was schizophrenic, then the likelihood dropped to 13% and if a sibling (brother or sister) had SZ, the likelihood was 9% - this study shows that the more closer you are genetically related the more likely you are to get SZ.
Twin studies
Twin Studies are an opportunity for researchers to investigate the nature/nurture debate in terms of the contribution of heredity and environmental influences in having SZ. As Monozygotic twins (MZ) (identical twins) share 100% of their genes whereas as Dizygotic twins (DZ) (non-identical) twins share 50% of their genes, if SZ is genetic, then the concordance rates should be much higher for MZ rather than DZ twins! Gottesman (1991) found a 48% concordance rate for MZ twins and 17% concordance rate for DZ twins- this study shows that the more genetically similar you are then the more likely you are to get SZ.
Furthermore in a more recent study, Joseph (2004) did a review of twin studies that were carried out up to 2001, and found an overall concordance rate for MZ twins as 40% but DZ twins as 7.4%. As the concordance rate is still relatively high for the MZ twins, his study supports the idea of genes playing a big part in SZ
Adoption studies
Adoption Studies - because it is difficult to separate genetic from environmental influences in twin and family studies, adoption studies are often carried out to understand the influence of nature and nurture. For example, adoption studies are researched to see the nature/nurture influences when MZ twins may be reared apart or offspring of SZ parents are adopted. Tienari et al (2001) carried out a study in
Finland. 164 adoptees whose biological mothers had been diagnosed with SZ, 11 (6.7%) were also diagnosed with SZ compared to a control group of 197 adoptees where only 4 (2%) were diagnosed with SZ. This study shows that although the overall percentage of children (who have been adopted by non- schizophrenic parents) having SZ was very low,
as there was a small link between genes and SZ with children whose biological mothers were schizophrenic.
Candidate genes
There are specific candidate genes that seemed to be associated with SZ (such as the PCM1) although it is now agreed that SZ is polygenic – this means that there is a combination of different genes that have been implicated in SZ.
Gurling et al (2006) used evidence from family studies indicating that SZ was associated with chromosome 8p21-22 to identify a high-risk sample. Using gene mapping, the PCM1 gene was implicated in susceptibility to SZ, providing more evidence for genetics. Also, Benzel et al. (2007) used gene mapping to find evidence suggesting that NRG3 gene variants interact with both NRG1 and ERBB4 gene variants to create
susceptibility to developing SZ, suggesting an interaction of genetic factors.
Furthermore, Ripke et al (2014) compared the genetic makeup of 37000 SZ patients worldwide with 113000 controls. They found that 108 separate genetic variations were associated with an increased risk of SZ. The genes that were particularly vulnerable were the ones that had some connection to the functioning of certain neurotransmitters
such as dopamine.
Advantages of genetic basis of SZ
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
Disadvantages of genetic basis of SZ
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.
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.
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.
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 an 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.
Neural correlates of SZ
Neural correlates are patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.
Advantages of neural correlates
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.
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.
Disadvantages of neural correlates
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.
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?
Neural correlates: The Dopamine Hypothesis
One of the best known and researched example of neural correlates is the neurotransmitter dopamine – known as the Dopamine Hypothesis
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. DA 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 neurons that transmit dopamine fire too easily and often, leading to
hallucinations and delusions. Schizophrenics are thought to have particularly high levels of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing
What is dopamine
Dopamine is one of the brain’s neurotransmitters—a chemical that ferries information between neurons. Dopamine 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. Dopamine 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.
From paying attention to hallucinating, and experiencing sexual arousal, dopamine is a key
molecule in the puzzle of how humans navigate the world. Accordingly, scientists who study neurological and psychiatric disorders have long been interested in how it works and how relatively high or low levels in the brain relate to behavioural challenges and disability. The brain systems underlying conditions such as schizophrenia, ADHD, and substance abuse disorder are complex—the activity of the dopamine system depends on the state of one’s dopamine
receptors, for instance—and in people with these conditions, the chemical interacts with other
factors in ways that have yet to be completely explained.
Two consequences of the dopamine hypothesis
Hyperdopaminergia and hyposopaminergia
Hyperdopaminergia
Hyperdopaminergia in the subcortex – 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). For example, 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.
