To begin with, there are a number of scientists who have thought that genes might have an important role in developing schizophrenia. Their starting point for analyzing the details of the disease was to study the brains of patients with schizophrenia. The robust findings and various hypotheses suggest that “schizophrenia is a disease of disordered neural circuitry involving multiple anatomical brain regions such as cortex, thalamus, basal ganglia and medial temporal lobe” (Sobell, Mikesell & McMurray, 2002, p.1070). A few kinds of techniques have allowed scientists to investigate particular regional metabolic abnormalities in the brains of schizophrenic patients. Computed tomography and magnetic resonance show that there are not only increased volumes of lateral and third ventricles in schizophrenic patients, but also decrease in overall brain volumes and in the size of medial temporal lobe structures, such as amygdala and hippocampus (Sobell, Mikesell & McMurray, 2002). Most studies which are conducted by using these techniques also demonstrate that changes in activity of prefrontal cortex is observed during cognitive activation tasks and working memory. Furthermore, abnormal activation of thalamus, hippocampus and limbic has been discovered during active auditory hallucinations (Sobell, Mikesell & McMurray, 2002). Hence, in the light of this information, it can be said that there are some remarkable differences, which can be underlying factors leading to schizophrenia, in the brains of schizophrenic patients.
Another area of research in schizophrenia is in common with the possibility of brain structure abnormalities in people with schizophrenia. Some brain imaging techniques give a chance to observe changes in living patients’ brain. Researchers who used these techniques found that gliosis, which is usually linked with adult-onset brain injuries and neurodegenerative conditions, is not seen in the brains of schizophrenic patients. This situation demonstrates that absent of gliosis is a developmental origin for any abnormalities (Sobell, Mikesell & McMurray, 2002). Moreover, there is some additional evidence for neurobiological component of schizophrenia. According to this evidence, children of schizophrenic patients demonstrate neurobiological abnormalities associated to predisposition to schizophrenia. Egan et al. (2001) stated that schizophrenic patients have impairment in several regions of cognition which includes working memory/executive function, verbal memory, language, oculomotor scanning/psychomotor speed, and general intelligence. Impairments have also been detected in unaffected children, which propose that they can be inheritable.
Furthermore, some gene studies provide strong evidence for cause of schizophrenia. They focused on autosomal genes and found such interesting results. Not only schizophrenia but also schizodia, which has increased prevalence of the disorder in families with schizophrenia, is a result of defect in an autosomal gene. According to Heston (1970), defect in a single autosomal gene, which is found on one of the 22 autosomal chromosome pairs, is an explanation for the genetic contribution to schizophrenia. The idea of schizodia and schizophrenia being a single genetical disease is supported by their clinical similarities and each having the same amount of risk to occur in monozygotic twins of schizophrenia.
Systematic studies of the genetics of schizophrenia, which includes family aggregation, twin and adoption studies, have been conducted since 1916. These studies have produced strong evidence that genes play a significant role in schizophrenic conditions. Family aggregation studies have indicated some statistical data. According to these data, risks to schizophrenics’ siblings of about 8 % and to schizophrenics’ parents about 5%. Also, in offspring of one schizophrenic parent, the risk is about 12 %. However, risks to the offspring of two schizophrenic patients of about 40 %. As regards to the rate of risks to second-degree relatives, who share about 25 % of their genetical material with a schizophrenic patient, they are at risk about 2 %. According to the recent studies, the risk of relapse is lower (3.2-5.5% among first-degree relatives of schizophrenia patients).Narrower diagnostic criteria is the reason of this decrease (Holzman & Matthysse, 1990).
Twin studies, in which concordance rates in monozygotic and dizygotic twins are compared, show consistent results with genetic transmission. Since monozygotic twins share all same genetic material, they are concordant in term of schizophrenia about four times as often as dizygotic twins (Heston, 1970). However, despite the fact that there are several supportive evidence, some scientists maintain that if schizophrenia were entirely genetical, identical twins would have to show 100 percent of concordance. Thus, it is obviously seen that more emphasis should be placed on twin studies in order to determine the role of genetics in schizophrenia.
Adoption studies have been considered as essential to demonstrate that genetical factors have role in schizophrenia. Such studies indicate that schizophrenia runs in the biological families of schizophrenic patients, not in their adoptive families (Holzman & Matthysse, 1990). One study attracted attention was of Wender et al (n.d., cited in Heston, 1970). They have studied biological and adoptive parents of ten normal people. The biological parents of schizophrenia patients display significantly more psychopathology than group of adoptive parents. Therefore, it can be possible to say that the results of adoptive studies are strikingly consistent.
Genes were not the only explanation for causes of schizophrenia. Some researchers are of the view that environment plays a significant role in the development of schizophrenia. Studies have led scientists to propose that particular environments trigger the developing of the disease. One of the interesting explanations for environmental contributions to schizophrenia is that seasonality of birth affects the developing schizophrenia. According to one study conducted by Tarrey et al (1977, cited in Tsuang, 2000) except one, all 19 appropriately controlled Northern American studies indicate that 5-8 % excess births of schizophrenia patients during December through May with peaks in January and February. Winter-spring excess births were not intrinsic to schizophrenia alone; there were also rises in manic depression and major depression; however these rises cannot be seen in other psychiatric disorders. Lately, Mortensen et al (1999, cited in Tsuang, 2000) discovered slight excess (1.1 times) of births of schizophrenic people in the winter months with peaks in March (Tsuang, 2000).
The other environmental factor that contributes to the development of schizophrenia is urban births. Some research revealed that there is a linear correlation between urban birth and schizophrenia. Tsuang (2000) contended that the decrease in incidence rate of subsequent defined schizophrenia is two times more in people who born in areas of highest population density than people who born in the areas with a general population. Excessive noise, pollution, crime, divorce and other negative factors lead to stress of the urban environment which may cause schizophrenia in people who have a tendency to develop the disease.
Apart from those explanations, scientists who have tried to find out the causes of schizophrenia have suggested that the cause may lie in the prenatal and perinatal period. Some scientists are of the opinion that viral infections in the central nervous system during the pregnancy period may contribute to the increased risk of schizophrenia. Data which was attained from Finnish study indicated that children who had infections in their central nervous system had a five times greater risk to develop schizophrenia than children who had no infections in their central nervous system. Moreover Takei et al (1995, cited in Tsuang, 2000) detected that female fetuses, which is subjected to the influenza virus in the fourth month of the pregnancy, had an enhanced risk to develop schizophrenia disease in adulthood (Tsuang & Faraone, 1995, cited in Tsuang, 2000).
Complications and pregnancy and delivery complications are among most extensively studied of assumed early risk factors for developing schizophrenia. Some scientists contend that pregnancy and delivery complications are independent risk factors for developing disease, but these complications can be an explanation for the abnormal developmental process that ultimately results in the onset of the schizophrenia. Accordingly, Tsuang (2000) stated that children of schizophrenic mothers who had pregnancy and delivery complications had a great risk of developing schizophrenia than children of schizophrenic mothers who did not experience any birth complications. Similar to Tsuang, McGuffin et al (1994) (cited in Geddes et al, 1999) found that there is an association between schizophrenia and birth weight lower than 2.500 g. However, significant interaction between these complications and sex cannot be detected. Geddes et al (1999) concluded that pregnancy and delivery abnormalities can be linked with development of schizophrenia.
Recently, scientists have started to examine the role of cannabis use in contribution to schizophrenia. Although there have been a lot of perspectives, most scientists seem to agree on an idea that “cannabis is neither a necessary nor a sufficient cause; it must be a component cause” (Henquet, Murray, Linszen & Os, 2005, p.610). That is to say, cannabis is dependent
on some other factors in order to affect the risk of schizophrenia. There are many plausible explanations that show the association between cannabis and schizophrenia. Studies show that cannabis use at an early adolescence raises the risk for later schizophrenia. Henquet and his colleagues (2005) analyzed that the individuals who had never used cannabis but who have a tendency to psychosis would be more likely to start using cannabis use in their future life period. They found that psychosis liability predicted individual’s future cannabis use. However, size of
effect was not big enough and statistically inaccurate. Although there are many evidence that cannabis use affect the development of schizophrenia, some scientist claim that association between cannabis and psychosis is completely owing to confounding factors such as age, ethnic group, family history, urbanity and use of other drugs. Obviously, whether cannabis use affects the development of the disease in those who have a tendency to schizophrenia has still been controversial.
Lastly, psychosocial factors appear to be most significant in determining the causes of schizophrenia. Some researchers who investigate that whether psychosocial factors trigger the onset of schizophrenia put an emphasis on migration / minority status. This kind of research has consistently discovered an increased risk of schizophrenia. Lim, Chang and Keefe (2009) stated that a meta-analysis of 18 studies indicated that first and second generation migrations, who are defined as people who born in a foreign place and people whose one or both parents born in a foreign country respectively, are at risk of 2.9 of developing schizophrenia. Moreover, the study demonstrates that people who migrated from developing countries are at higher risk of developing schizophrenia than people who migrated from developed countries. Another interesting aspect of this study is that people who migrated from where majority of citizens were classified as black people also had higher risk of developing schizophrenia than people who migrated from where the majority were white.
The other psychosocial factors that affect the later development of disease is childhood abuse. Lim, Chang and Keefe (2009) reported that children who had traumatic experiences in their childhood before the age of 16 have increased risk for psychosis symptoms. Moreover, a perspective study of individuals found that victims of both males and females who have been sexually abused in childhood, had a greater risk rate of psychiatric treatment; however there was not any differences between these two cases in the rate for schizophrenia and related disease. For some scientists, there seems to be an association between childhood abuse and development of schizophrenia because of the fact that particular brain regions cannot function properly due to the result of stress from childhood social deprivation.
In the light of all studies and research mentioned above, it can be said that although there are a lot of theories and hypotheses about causations of schizophrenia, scientists have not arrived at a consensus yet. Despite the fact that there is some strong evidence for genetic contribution to the development of the disease, some findings support the hypothesis that schizophrenia is determined by social environment. Neurobiological, brain structure, gene and family studies have showed that schizophrenia is caused by genetical factors whereas some other studies which examine the effects of seasonality of birth, urban births, prenatal factors, cannabis use and psychosocial factors on schizophrenia suggest that the disease is determined by environmental contributions. Therefore, it is possible to say that schizophrenia is a complex disease; that is to say it is difficult to determine the precise causes of the disease. Although the idea that there is strong genetic contribution to schizophrenia is acceptable, having the genes associated with schizophrenia is just a starting point. If one has the genes, but does not experience the environmental factor that contributes to the development of the disease, then one will never develop schizophrenia.
Those who find the origin of schizophrenia only in the genetics may claim that the idea that mental illnesses are products of bad early childhood experiences is hardly ever fully proven. To them, there is little association between parenting styles and schizophrenia. Furthermore, they claim that the connection between the disease and poor communication could not be causal but indicative of the illness. However, serious doubts can be arised against this. In fact, it is more likely that schizophrenic behavior results from the mother’s behaviour toward the child in early childhood. Mothers who are cold, rejecting and detached parenting style cause psychological distress in the child. Fromm-Reichman found the term “schizophrenogenic mother”, which is a directly associated poor familial relation with the development of a particular mental disease. According to Fromm-Reichman theory, the basic cause of schizophrenia was “schizophrenogenic mother”. The mother was described as cold and tyrannizing person. She was also overprotective and she was not able to let the child develop his or her character. Thus, it brings about schizophrenia in the child (Simon, McNeil, Franklin & Cooperman, 1991).
Those who are against the opinion that schizophrenia is determined by environmental factors would assert that the fact that patients relapse after they discharged from the hospital is not necessarily the primary causal factor of the development of the disease. They maintain that the reason which delays the recovery cannot be the same with what triggers the disease. Yet, this idea cannot be more than just a claim. Patients whose relatives and families showed certain emotional attitudes during the follow-up period are more likely to relapse than patients whose families and relatives did not show such attitudes. In a further study, both patients and their relatives who were highly emotionally interaction with patients were more likely to suffer from a relapse of florid symptoms. One another suggestion is that short-term and long-term effects might have a cumulative influence; for instance, that an increased level of tension in the home made relapse more possible in the event of critical change in the social environment of patients ( Brown, Birley & Wing, 1972). As they point out, patients who have environment with law warmth, over-involved of parents and hostility are more likely to relapse.
Those who are against the opinion that schizophrenia is determined by environmental factors might maintain that schizophrenia appears in all social strata; thus, low socioeconomic class is not likely to be the major cause of schizophrenia. To them, schizophrenics find it too difficult to integrate into society and; therefore, they lose their any existing high social status. However, these views are not always the case. In fact, schizophrenia is more prevalent among the lower socioeconomic classes and more common in lower class regions of many cities of the industrial world (Faris et al., cited in Warner, 1995). Stress, racism, unemployment and bad house conditions are blame for the development of the disease. The individual who have lower socioeconomic status is more likely to have mental illness (Hudson, 2005). Moreover, a large German study that used a cross-sectional design indicated that both low socioeconomic status and single-parent families were linked with the psychological stress among children (Franz et al., cited in Hudson, 2005). Briefly, if one lives in an environment where stress, racism and other bad conditions are common, then the person is more likely to develop schizophrenia.
One last claim is that development of schizophrenia cannot be entirely genetic. Many famous twin and quadruplet studies highlight the idea that schizophrenia could have a genetic basis; since all children who are twins or quadruplets developed the disease. Also, it can be claimed that monozygotic twins are more likely to develop schizophrenia than dizygotic twins which shows that the shared DNA is to blame. However, they seem to be mistaken. Because twins or quadruplets had a similar family history and family environment. This means that although the cause for all developed schizophrenia seems to be genetic association, they were all exposed to similar conditions in early childhood. Therefore, trigger just has been an environmental one. Moreover, there are a lot of identical twin studies reared apart or together; however, none of these studies eliminate the possibility of social causes of schizophrenia, so they cannot be prove the idea that schizophrenia is caused by genetic factors.
All in all, it is obvious that a variety of researchers who have specialized in different sciences accept that there is no clear causation of schizophrenia. Actually, even if the genetic factors that contribute to the development of the disease are clear, previously tested hypotheses have failed to determine the specific factors that lead to schizophrenia in individuals. Whether schizophrenia is a result of nature or nurture should be examined in detail in order to prevent individuals from developing schizophrenia. Also, examining causations of schizophrenia is important to provide effective treatment for people who show a tendency to develop the disease.
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