Environmental And Genetic Affects And Schizophrenia Essay
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the relative importance of genetic and environmental factors in the
aetiology of schizophrenia.
Graeme Gordon
...poor Ophelia, divided from herself and her fair judgement without the which we arepictures or mere beasts...
Shakespeare, Hamlet
The term 'schizophrenia' (a splitting of psychic function, Strange, 1992) was first introduced in 1911 by Eugen Bleuler to denote the breakdown of integration between emotions, thought and actions. The symptoms of this disease are heterogeneous and there is still disagreement about diagnosis.
The annual incidence of schizophrenia is between 0.1 and 0.5 per 1000 depending on the diagnostic criteria used - representing a lifetime risk of 1 per cent (Strange, 1992). Onset of the disease is most commonly in late adolescence or early adulthood. In the U.S.A., schizophrenia fills more beds than almost any other illness and the financial cost of schizophrenia due to direct
medical costs, lost productivity and Social Security pensions is between $30 billion and $48 billion according to Federal figures (American Pychological Association (APA), 1996).
There are many theories about the aetiology of schizophrenia, but research has failed to pinpoint the origins. There is evidence that environmental pathogens (for example, viruses) are involved in the causation of schizophrenia. There is also evidence for a role of hereditary influences and obstetric complications on the incidence of schizophrenia. Furthermore, psychological influences have also been suggested as important in precipitating episodes of schizophrenia (for example, significant life events and interactions within the family). The symptoms and syndromes of schizophrenia are complex and very heterogeneous. Thus, the resulting theories reflect this complexity. This heterogeneity causes disagreement about diagnosis, illustrating the huge importance to explain the basis of schizophrenia and to establish the root causes - if they due indeed exist. The term schizophrenia may infact be an umbrella term covering a number of different diseases. Even if this was to be the case, the importance
still lies in establishing the root causes as this is the route to successful treatment.
In past years, psychiatric researchers theorised that schizophrenia arose from bad parenting. It was believed that a mother could cause the symptoms of schizophrenia through inadequate care. Such a mother was characterised by being "cold, distant and unfeeling" and due to this was called "schizophrenigenic" (APA, 1996). This has since been discredited as a theory. However, it wasn't until more sophisticated techniques for examining brain structure in vivo were
introduced in the late 1970s that schizophrenia was thought to be due to 'organic' brain changes. Previously it was a "general feeling that...it was considered a purely 'functional' disease" (Strange, 1992). The initial finding of the brain scans in the late 70s was that the brain changes in many, but not all, schizophrenics were manifested as ventricular enlargement. From such an observation, a number of theories arose about the causes of schizophrenia related to ventricular enlargement (for example, Crow, cited in Strange, 1992). However, more recent brainimaging has found there to be no correlation. Even so, it is an example of how observations in schizophrenics can aid the development of theories of aetiology.
Further observations that have led to the development of theories of the aetiology of schizophrenia include the observations that schizophrenics "have a lower head circumference at birth, show behavioural peculiarities as children, have an increased rate of minor physical abnormalities, delayedrodevelopmental milestones, low IQ and behavioural abnormalities in
childhood, and have an increased size of cerebral ventricles" (Weinberger, 1995). These observations have become warning signals that a child has a predisposition to schizophrenia, as well as leading to the neurodevelopmental hypothesis of schizophrenia. The point that a child may have a predisposition, suggesting a hereditary factor, will be discussed.
A similar study looked back at the childhood of schizophrenics and found there to be "two roads to schizophrenia" (Neumann et al., 1995). Six female and 23 male schizophrenics (average age of 35) were compared with a psychiatrically normal brother or sister. Their mothers were asked to recall the children's behaviour during the four four-year periods from birth to age sixteen. The
symptoms included in a checklist included social withdrawal, anxiety, depression, attention deficits, delinquency, and aggression. They reported that: "as a group, the pre-schizophrenic children had more behavioural problems than their siblings. In the first four years they showed attention deficits. At ages five to eight, they suffered from anxiety, depression, and thought disturbances. As they grew older there were signs of aggression and social withdrawal".
However, it was found that these problems were concentrated in a smaller group consisting of only 27 per cent of the pre-schizophrenic children. The other three-quarters of pre-schizophrenic children differed only slightly from their brothers and sisters up to the age of sixteen. Although the study does appear to have limitations - for example, the subjects were almost all male and their families were all of high socio-economic class - it does have implications on the aetiology of schizophrenia. For example, pointing toward a eurodevelopmental cause of the disorder.
Another example of such observations is from a study on eye tracking and visual attention (Archives of General Psychiatry, cited in Ward, 1997). "Doctors have known that there was something different about the eyes of many people with schizophrenia - and the eyes of their family members too" (Ward, 1997). The study Ward reports on investigates eye tracking (the ability to follow a moving target with the eyes) in first degree relatives of schizophrenics. They
found that in comparison to the eight per cent of the general population who are unable to do this task, 50 to 85 per cent of schizophrenics and 45 per cent of their parents or siblings are unable to perform this relatively simple task. The implication of this finding is that it points to a clear genetic factor in schizophrenia. Offering further support to the overwhelming evidence of
clear hereditary influences in schizophrenia.
Studies within families have shown that there is a ten per cent chance of developing schizophrenia in first degree relatives of schizophrenics (compared with one per cent in the general population). Sibling's have a nine percent chance of developing the disease. The lifetime risk of developing schizophrenia is correlated with genetic relatedness to a schizophrenic. First degree relatives do have a higher risk than second or third degree relatives.
This is illustrated in Figure 1. Such an illustration shows a clear hereditary influence on schizophrenia.
However, no hereditary gene has been identified as yet, although studies have identified a number of regions of chromosomes that may be involved.
Barondes et al. (cited in Freeman, 1997) identified regions of chromosomes that may be linkedto a genetic predisposition to schizophrenia. Those chromosomes are 3, 6, 8, 9, 20 and 22 (the23 pairs of human chromosomes, including the sex chromosomes, are numbered 1 through 23). Further studies have identified genetic markers for schizophrenia on chromosomes 6, 8, 9, 13 and 22 (Gottesman, cited in DeAngelis, 1997). These genetic markers refer to parts of a gene that are suspected to be linked to specific problems or features; they are less specific than locating the gene itself. DeAngelis (1997) reports that some of these findings have been replicated - in particular on chromosomes 6 and 22. As with the diagnosis of schizophrenia, there is disagreement about which chromosomes are involved in the transmission of schizophrenia. This is exemplified above - the fact that the Barondes study found there to be one more chromosome linked to schizophrenia than that cited by DeAngelis. Such a failure to find wholly consistent results is further exemplified in a study by Maziade et al. (1997). Their investigation into regions where 'schizophrenic genes' are likely to be found resulted in the identification of four specific areas - chromosomes 11q, 3q, 18q, 6p. Again, an inconsistency to that of the other findings cited in above. Even so, what such studies do show is that there is clear evidence for an hereditary influence in schizophrenia.
It is important to note that schizophrenia is not inherited in the same way as the colour of one's eyes or hair. Like many other genetically related illnesses, schizophrenia appears when the body is undergoing the hormonal and physical changes of adolescence. It has thus been suggested that schizophrenia lies "dormant" during childhood (APA, 1996). However, it is clear from the observations mentioned above that the effects are noticeable during childhood.
Furthermore, it is important to understand how the onset of such a "severe form of psychopathy" (Gottesman, cited in DeAngelis, 1997) comes about and whether it may lie "dormant" for longer periods and even indefinitely - missing out a generation.
It is from such questions that the idea that environmental stressors trigger the onset of the illness has arisen. From this idea theories have been developed and an example of such a theory, that is a culmination of findings from a number of studies, is that of the "phospholipid hypothesis" (Peet et al., 1995). This hypothesis predicts that schizophrenics have a genetic predisposition towards a disorder, modulated by environmental factors, that causes schizophrenia.
The "phospholipid hypothesis" was provided by studies showing that polyunsaturated fatty acids (PUFA) of the omega-3 and omega-6 series are depleted in cell membranes of neuroleptic treated schizophrenics (Peet et al., 1995). Peet compared the PUFA composition of red blood cell (RBC) membranes from schizophrenics and control subjects. The results are shown in Glen et al. (cited in Peet et al., 1995) found that the lowest RBC membrane levels of PUFA were
in the 'worst-state' schizophrenics. Furthermore, Peet and colleagues found "reduced levels of omega-6 PUFA correlated with plasma levels of thiobarbituric acid reactive substances (TBARS), suggesting that there was increased oxidative breakdown of these PUFA in our patients" (Peet et al., 1995). Peet et al. (1997) also found this to be the case in untreated schizophrenics from India and Malaysia. Thus, it appears that PUFA breakdown is increased in schizophrenics. Peet et al. (1995) cite further evidence of this. For example, a study using
magnetic resonance spectroscopy (Pettegrew et al.) found "decreased levels of
phosphomonoesters and increased levels of phosphodiesters in the frontal cortex of drug free schizophrenics, consistent with increased breakdown and/or decreased synthesis of membrane phospholipids". In another study cited, this index of increased phospholipid breakdown correlates with the severity of schizophrenic symptoms expressed. Furthermore, they also found there to be increased pentane levels in air expired from schizophrenics compared to that of
control subjects. This is consistent with increased oxidative breakdown of PUFA. Peet et al. (1995) suggest a mechanism that would promote the increased breakdown of membrane PUFA is that of increased phospholipase activity (this is the enzyme that reaks down fat). They based this hypothesis on the finding that significant elevations of phospholipase A2 (cPLA2) were reported in the platelets of schizophrenics (Gattaz, cited in Peet et al., 1995). Also, they cite two reports of abnormalities in the cPLA2 gene of schizophrenics. A more recent study by Peet (unpublished) has found a significant genetic abnormality that is over-represented in schizophrenics relative to ethnically matched controls. It is because of this that it is hypothesised that schizophrenics have a genetic predisposition to depleted membrane levels of PUFA. Peet et al. (1995) suggest that this could be modulated by dietary intake in infancy and later life which could underlie the reported neurodevelopmental abnormalities in schizophrenia. The efficacy of dietary intake on the modulation of PUFA levels has yet to be established.
The suggestion that environmental factors are involved with the incidence of schizophrenia in the "phospholipid hypothesis" is concurrent with the present direction of thought as to the aetiology of schizophrenia.
It is a current belief that schizophrenics do have a genetic predisposition to the disease and that certain factors of the environment act either as triggers or in some cases direct causal influences. Further examples of such theories that have evolved from this belief shall follow.
From observations of the biochemistry of schizophrenics it has become clear that they have an neurochemical imbalance. Thus, much research has been focused on neurotransmitters...
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