Describe two theories which explain the occurrence of schizophrenia

This paper sets out to look at the mental illness of Schizophrenia and will examine two theories on the cause of this disorder and how they relate to genetics and the environment. The two theories we will discuss are, ‘The Dopamine Theory’ and ‘The Genetic Theory’ Schizophrenia is a chronic and disabling brain disorder which is characterized by gross distortion of reality. The name ‘Schizophrenia’ derives from the Greek words skhizein meaning “to split” and Phrenos (phren) meaning “mind” (Taylor, 2011).
The condition is categorised by either Positive or Negative Symptoms which are unique to each individual. Individuals suffering from positive symptoms of the disorder experience on-going episodes of psychosis affecting their ability to distinguish, what is real or imagined. Positive symptoms can be defined as symptoms of behaviour that are present but should be absent; they include behaviours such as delusions, hallucinations, fragmented thinking and unusual patterns of speech or behaviour.
Negative symptoms on the other hand are the absence of normal behaviours which result in symptoms such as flattened emotional response, inability to express pleasure, apathy, poverty of speech and social withdrawal (Norman, 2004: 365). Schizophrenia is a very complex disorder, and despite on-going debates, researchers have failed to identify one single cause of the disorder, however, it would appear that the consensus is that both biological and environmental factors could play an important role in the occurrence of the illness.

One of the most well debated theories on the cause of Schizophrenia is the dopamine theory. The dopamine theory postulates that schizophrenia occurs as a result of hyperactivity of the neurotransmitter dopamine in the synapse. There are four main dopamine pathways which have been implicated in the disorder of Schizophrenia and they are; the Nigrostriatal pathway which is involved in motor control, Tuberoinfundibular pathway associated with sensory processes and the Mesolimbic and Mesocortical pathways which are connected to memory, motivation and emotional responses (Stahl, 2002: 10).
Research has given much attention specifically to the mesolimbic pathway which is a brain circuit dependent on dopamine. The mesolimbic pathway is often referred to as the ‘reward pathway’ due to its key role in linking certain behaviours to the sensation of pleasure, such as those associated with the use of psychostimulant drugs like amphetamine, MDMA (Ecstasy) and cocaine (Stahl, 2008: 272). The evidence to support the theory that mesolimbic dopamine plays a role in Schizophrenia, follows logically from the treatment of the disorder with antipsychotic drugs such as chlorpromazine and fluphenazine.
These drugs work by blocking dopamine D2 postsynaptic receptor sites, which inhibits the binding of dopamine, thus reducing positive symptoms (Seeman, 2011). Furthermore, several studies have suggested that the use of Psychostimulant drugs (such as amphetamines and cocaine), which work by enhancing dopamine neurotransmission, have been shown to induce psychotic symptoms such as hallucinations, delusions and disorganised speech and thinking, all of which demonstrate a marked resemblance to the positive symptoms exhibited in patients with Paranoid Schizophrenia (Laruelle, et al. , 1996; Breier, et al. , 1997; Abi-Dargham, et al. 1998).
Although some research has implicated excess dopamine as a possible cause of schizophrenia, there is still much controversy surrounding this theory. It could be argued that the theory is reliable because research demonstrates that alterations in levels of dopamine either exacerbate or reduce symptoms, however, there are limitations with this theory, as blocking of the dopamine D2 receptor sites will only have an impact on the positive symptoms of schizophrenia, and not the negative symptoms such as apathy, speech and working memory, which are associated with the mesocortical pathway (Wayandt, 2006: 130).
It has been suggested by Stahl (2008), that the reason for this may be, that unlike the mesolimbic pathway which is hyperactive in dopamine, the mesocortical pathway may already be deficient in dopamine, therefore blocking of the D2 receptors in the mesocortical pathway could further increase negative symptoms. Swerdlow (2010: 359) suggests that an argument against the dopamine hypothesis may be that some patients may be unresponsive to the more traditional neuroleptic drugs such as chlorpromazine which acts upon the D2 receptor sites.
However, studies conducted by Brier and Buchanan (1996) on the use of a new atypical anti-psychotic drug called clozapine, claimed to show a 40-60% improvement in symptoms for patients of schizophrenia who did not respond to the traditional neuroleptics (Pincus & Tucker, 2003: 119). Clozapine still plays a role in blocking the D2 receptor site but with less intensity than traditional antipsychotics. However, it is also responsible for blocking a variety of other receptor sites including dopamine D4, 5-HT (serotonin), norepinephrine, acetylcholine, and histamine (Moses, 2012).
With this in mind, it could be said that dopamine does not operate in isolation, and may form only part of the etiology in the manifestation of Schizophrenia. What is clear is that the dopamine theory is far from conclusive, which would suggest that much more research is needed to examine the role that other neurotransmitters may play in the disorder. Furthermore, if dopamine does play a primary role in schizophrenia then this leads us to the question, what causes this dysfunction in the dopamine neurotransmitters?
Studies to date have identified that several of the genes which are closely linked with Schizophrenia are directly involved in dopaminergic pathways (Howes & Kapur, 2009); this therefore leads us to a further conclusion that genetics and gene mutation may play a key role in the development of schizophrenia. Evidence suggests that there is a strong genetic predisposition to developing the disorder and the more closely someone is related to an individual with Schizophrenia, the higher the chance of them developing the disorder themselves (Nolen-Hesksema, et al. , 2009).
Family, Twin and adoption studies demonstrate that there are higher concordance rates between monozygotic (Identical) twins than there is with dizygotic (non-identical) twins. Studies conducted by Gotteman (1991) found that dizygotic twins had a 17% risk factor if their twin sibling had the disorder; however, for monozygotic twins, the rate increased to a more significant 48%. Further studies have revealed that children of schizophrenic parents showed similar concordance rates of 46%, however, children born to schizophrenic mothers but adopted by non-schizophrenic mothers only showed a risk factor of 17% (Kalat, 2009: 451).
These findings suggest that Schizophrenia is not entirely genetic, and that environmental factors may also play a role in the development of the disorder. However, in giving strength to the genetic theory, new research in epigenetics has found that, whilst monozygotic twins share the same DNA, there are variations in the levels of methylation detected in a gene called ST6GALNAC1, which has been found in individual schizophrenic twins (Times, 2011).
Whilst these changes in segments of DNA offer some explanations for the discordance in monozygotic twin studies in Schizophrenia, it is suggested that these mutations develop as a result of environmental influences (Coghlan, 2011: 16). Moving on, it has become apparent, that both dopamine and genetics play an important role in the predisposition towards schizophrenia. However, evidence appears to suggest that, whilst an individual may have a predisposition, this is not a guarantee that they will develop the disorder.
Theorists believe that for those individuals who do have a predisposition towards schizophrenia, environmental factors can greatly influence the development and life course of the condition. One environmental factor which may be linked to the dopamine theory is the associated risk between prenatal exposure to viral infections and adult onset of schizophrenia (Psychiatry, 2011). Research suggests that prenatal environmental insults such as viral induced anaemia in the first and second trimesters, may lead to deficiency in myelination of neurons and dysfunction in the dopaminergic pathways (Brown, 2011).
In support of this claim, a study by (Aguilar-Valles, et al. , 2010) used rat models to produce viral induced iron deficiency, and found that the biochemical and behavioural changes which occurred in the rats were characteristic of those found in adult schizophrenia. Moreover, Brown (2011) also suggests that iron deficiency significantly contributes to de novo mutations in DNA, and this may be due to a possible disruption of oxidation in the cells. Consequently, researchers have also identified significant representation of de novo mutations in Schizophrenics (Krebs & Rouleau, 2011).
De novo mutations do not occur as a result of hereditary factors, but instead, are alterations which take place around the time of early conception (Reference, 2012). These findings may support the theory that prenatal environmental insults could be responsible for the increased risk in someone developing the disorder. Furthermore, this may also offer some explanation for the manifestation of schizophrenia in individuals who have no family history of the disorder.
In conclusion, schizophrenia still remains one of the most perplexing and misunderstood disorders faced by mental health professionals. It is evident that dopamine, genetics and the environment all play a role in schizophrenia, however not one of these factors appears to work in isolation. In short, it would appear that the environment interacts with both biochemical and genetic factors and determines whether or not an individual is likely to develop the disorder.