Biological Explanations of Schizophrenia

Published: 2021-06-28 02:55:04
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Describe and evaluate biological explanations of schizophrenia (24 marks) Schizophrenia is a psychotic disorder characterized by distorted thinking, impaired emotional responses, poor interpersonal skills and a distortion of reality. It is the most common of psychotic disorders that, in most countries around the world, affects around 1 per cent of the population.
In terms of explanations for the disorder, two central types of explanations arise – psychological explanations and biological explanations. Whereas psychological explanations tend to focus on cognitive, emotional and environmental factors that may cause the disorder, biological explanations tend to focus on genetic, biochemical and neuro-anatomical factors as the cause of the disorder. One biological explanation of schizophrenia is ‘the genetic hypothesis’.
Schizophrenia appears to run in families, and Gottesman (1991) has shown through a series of controlled genetic correlational studies that the likelihood of an individual developing schizophrenia is proportional to the amount of genes they share with somebody affected by schizophrenia. For example, children with two schizophrenic parents have a concordance rate of 46 per cent, monozygotic (MZ) twins have a concordance rate of 48 per cent, and dizygotic (DZ) twins have a concordance rate of 17 per cent.
However, from these studies it has also been made clear that genetic factors cannot be the only explanation for schizophrenia. Although genetic studies support the argument for a genetic basis for the disorder, they have also shown that even when the relative is genetically identical – like monozygotic twins – the chance of developing schizophrenia is below 50 per cent. This implies therefore, that heredity factors are not the primary cause of schizophrenia, other factors are clearly involved.
In addition to this, many researchers have suggested that the reason that schizophrenia appears to run in families could be due to common rearing patterns and that genetic factors are comparatively uninvolved. Research on expressed emotion shows that negative emotional climates that are high in expressed emotion could lead to stress beyond an individual’s coping mechanisms, and could thus trigger a schizophrenic episode (Linzen et al, 1997), further exemplifying the importance of environmental factors in the onset of schizophrenia.
In an attempt to disentangle controversy surrounding genetic and environmental factors, twin studies and adoption studies have been carried out. With twin studies the underlying assumption has been that monozygotic twins will show a greater concordance rate than dizygotic twins as they are genetically identical, and many studies have supported this assumption. Although many twin studies do consistently reveal a greater concordance rate in monozygotic twins than dizygotic twins, the extent to which this is the case varies greatly.
For example, Cardno et al (2002) showed a concordance rate of 26. 5 per cent for monozygotic twins and 0 per cent for dizygotic twins based on the ‘Maudsley Twin Register’, compared to Joseph (2004) who, when using pooled data for all schizophrenia twin studies carried out prior to 2001, found a concordance rate of 40. 4 per cent in monozygotic twins and 7. 4 per cent for dizygotic twins. There are several issues with this kind of research, however. As only 1 per cent of the population is schizophrenic and around 0.3 per cent of the population are monozygotic twins, statistically only 0. 003 per cent of the entire population is a schizophrenic monozygotic twin.
This means that sample sizes in these studies are usually very small and so researchers have difficulty generalizing results to the entire population. In addition, twin studies do not all use the same diagnostic criteria and so comparisons cannot always be made (McGuffin et al, 1984), and concordance rates can be calculated in different ways and vary depending on the method used – meaning that twin studies can lack reliability.
Also a crucial assumption underlying twin studies is that, in general, the environments for monozygotic and dizygotic twins are equivalent and therefore the greater concordance rate in monozygotic twins is due to genetic factors. As Joseph (2004) pointed out, however, this is not always the case. Monozygotic twins are more likely to be treated in a similar way, encounter more similar environments, and be to be thought of as ‘the twins’ rather than two separate individuals. This, in turn, can lead to ‘identity confusion’ and so potentially a higher concordance rate amongst monozygotic twins.
Therefore Joseph argues that the greater concordance rate seen in monozygotic twins than in dizygotic twins is a result of the differing attitudes and environments experienced by the two types of twins. Adoption studies have also been used to determine whether home environment or genetic disposition are more influential in the causation of schizophrenia, as usually in twin studies twins are both genetically related and experience the same environment. Kety (1994) found high rates of schizophrenia in individuals whose biological parents were schizophrenic but were adopted by psychologically healthy parents.
The most methodologically sound of adoption studies, though, was carried out by Tienari et al (2000) in Finland. In the study 164 adoptees whose biological mothers were schizophrenic were compared to 197 adoptees whose mothers were psychologically healthy. It was found that 6. 7 per cent of the experimental group (those with schizophrenic mothers) developed schizophrenia compared to just 2 per cent of individuals in the control group, suggesting that genetic factors are indeed involved. Despite this, there are still potential problems with adoption studies.
It is assumed that adoptees are not ‘selectively placed’ and are randomly allocated to families. In countries like the US, for example, potential adoptive parents would be aware of the child’s biological family and so be aware of any family history of schizophrenia. This could lead to differences in the type of adoptive parents and thus could account for some of the differences seen in the development of schizophrenia between adoptees whose biological mother was schizophrenic and adoptees whose biological mother was psychologically healthy.
Another biological explanation of schizophrenia is to do with biochemical factors, including the ‘dopamine hypothesis’. The dopamine hypothesis states that the positive symptoms of schizophrenia are produced by overactivity of synapses that use dopamine as a transmitter substance. A variety of drugs used in the treatment of schizophrenia could support the dopamine hypothesis. Phenothiazines, for example, that work by blocking dopamine at the synapse, have been effective in alleviating major symptoms of schizophrenia.
L-dopa, used for the treatment of Parkinson’s disease, could also support the dopamine hypothesis. The drug works by increasing dopamine levels, but this has also been known to simultaneously provoke the development of schizophrenic-type symptoms (Grilly,2002). Amphetamines, used as stimulant drugs that act by increasing the availability of dopamine and noradrenaline in the brain, can also induce severe symptoms of paranoid schizophrenia in those who were previously unaffected by the disorder.
Evidence from PET scans can also support the dopamine hypothesis. For example, Wong et al (1986) found a two-fold increase in the density of dopamine receptor sites in schizophrenic patients that had never been treated with drugs compared to schizophrenic patients who had been treated with drugs. Issues with the dopamine hypothesis are in abundance in spite of supporting evidence. Drugs used to treat schizophrenia, like phenothiazines, do not work for everybody and, even when they do, only alleviate the positive symptoms of schizophrenia.
Also, post-mortem examinations used as evidence to support the dopamine hypothesis are usually carried out on patients that have been taking neuroleptic drugs for years, meaning that it is difficult to tell whether alterations in dopamine receptor sites were caused by schizophrenia or the drugs themselves. It has, in fact, been found that the drugs used to treat schizophrenia by blocking dopamine activity can, paradoxically, increase it as neurons struggle to compensate for the sudden deficiency.
Haracz (1982), in a review of post-mortem studies of schizophrenics, found that many of those who displayed elevated dopamine levels were receiving antipsychotic drugs shortly before death. Although it is likely that dopamine is implicated in producing several symptoms of schizophrenia, it is an oversimplified explanation on its own. A third explanation for schizophrenia, are neuro-anatomical factors which are present in the structures of the brain. This explanation, supported by studies, states that schizophrenia maybe caused by abnormal sizes of neuro-anatomical structures in the brain.
Buchsbaum (1990), for example, used PET scans to reveal reduced cerebral blood flow to the frontal lobes (specifically the frontal hippocampus and the amygdale) in the brains of schizophrenic patients. Frontal lobes, which are imperative in higher-intellectual thinking, have also been shown to be smaller in schizophrenic patients than in those who are psychologically healthy. Research into ventricles, which are cavities that store cerebro-spinal fluid in the brain, have also revealed that these are larger in people with schizophrenia than in those without (Brown et al, 1986).
Interestingly, this was only the case for men and not for women. Despite the fact that abnormalities have been found in neuro-anatomical structures in the brains of schizophrenic patients, findings have been controversial and it has been occasionally difficult to pinpoint exactly how these abnormalities could be causing schizophrenic symptoms. Furthermore, a reoccurring mediating factor in research into neuro-anatomical structures is that patients that are studied have usually been schizophrenic for years, and therefore have been taking antipsychotic drugs for this length of time.
This means that it is sometimes difficult to distinguish between the effects that schizophrenia has had on the brain of schizophrenic patients and the effects of the antipsychotic drugs. Another issue has been that abnormalities in neuro-anatomical structures have not been found in the brains of all schizophrenic patients, leading researchers, such as Crow (1985), to believe that there is more than one type of schizophrenia.
These are: “Type 1” schizophrenia: a genetically inherited condition that is characterized by positive symptoms such as hallucinations and responds well to antipsychotic medication and “Type 2” schizophrenia: a neuro-developmental disorder that arises from prenatal insults (factors that might have an effect on the baby whilst it is in the womb) and perinatal insults (problems that could occur around the time of birth). This type of schizophrenia does not respond well to antipsychotic medication.
By distinguishing between two types of schizophrenia it has been possible for other researchers to settle some of the controversy surrounding research data. Having said this, the two types of schizophrenia cannot explain research whereby schizophrenic patients have shown both positive and negative symptoms, and so this ‘two-syndrome hypothesis’ could be deemed as over-simplistic. To conclude, while there is evidence to suggest that biological factors are clearly involved in the development of schizophrenia, there is also evidence to suggest that biological factors are not the only factors involved.
For example, although monozygotic twins consistently show a higher concordance rate than dizygotic twins, monozygotic twins never show a conclusive 100 per cent concordance rate. This suggests that possibly environmental and cognitive factors may also be strongly involved. Taking biological factors as the only explanation would be too reductionist because of the multi-factorial nature of the complex disorder itself. Since it is unlikely that a single cause to the disorder can be identified, most researchers now accept an integrative approach that works on the principles of the diathesis-stress model (Zubin & Spring, 1977).
The diathesis-stress model draws together biological, environmental and psychological explanations for the onset and maintenance of schizophrenia. The model attempts to explain schizophrenia as a genetic predispositional vulnerability and the extent to which it develops in severity may lie within the individual’s experience of stress from life experiences, combined with issues within the individual’s uniqueness in terms of his/her personality factors (Barlow & Durand, 2009).
Because arange of individual differences exist between sufferers in their vulnerability to the development of this serious disorder, arguably, this model could be the most plausible account for the onset and maintenance of such a complex and universal disorder as schizophrenia is. To summarise, it is therefore a useful model for the purposes of understanding the complex interplay of ‘nature and nurture’ in the susceptibility to psychological disorders like schizophrenia, being experienced acutely and or chronically (as a lifespan prognosis).

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