Describe two theories which explain the occurrence of schizophrenia

This paper sets out to odour at the mental illness of schizophrenia and leave examine two theories on the travail of this disorder and how they relate to genetic science and the env put rightment. The two theories we testament discuss argon, The dopamine Theory and The Genetic Theory schizophrenia is a chronic and disabling question disorder which is characterized by gross aberrance of reality. The name schizophrenia derives from the Greek rowing skhizein meaning to split and Phrenos (phren) meaning idea (Taylor, 2011).The condition is categorised by either Positive or Negative Symptoms which argon unique to each unmarried. Individuals suffering from autocratic symptoms of the disorder experience on-going episodes of psychosis affecting their talent to distinguish, what is real or imagined. Positive symptoms so-and-so be defined as symptoms of deportment that argon present but should be absent they include behaviours such as delusions, hallucinations, fragmented t hinking and unusual patterns of deliverance or behaviour.Negative symptoms on the another(prenominal) hand are the absence of average behaviours which resultant quality in symptoms such as flattened emotional response, inability to prove pleasure, apathy, poverty of deliverance and social climb-down (Norman, 2004 365). dementia praecox is a very complicated disorder, and despite on-going debates, investigateers squander failed to identify atomic number 53 and only(a) single ca persona of the disorder, hitherto, it would appear that the consensus is that near(prenominal) biological and environmental doers could break away an main(prenominal) single-valued function in the snuff itrence of the illness. angiotensin converting enzyme of the most well debated theories on the cause of Schizophrenia is the dopamine possibility. The dopamine theory postulates that schizophrenia occurs as a result of hyperactivity of the neurotransmitter dopamine in the synapse. There ar e four main dopamine pathways which sop up been interested 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). look has given much attention specifically to the mesolimbic pathway which is a brain round dependent on dopamine. The mesolimbic pathway is ofttimes referred to as the reward pathway due to its key role in linking accepted 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 turn up to accompaniment the theory that mesolimbic dopamine work ons a role in Schizophrenia, follows logically from the discussion of the disorder with antipsychotic person drugs such as chlorpromazine and fluphenazine.These drugs wo rk by stoppage dopamine D2 postsynaptic sense organ sites, which inhibits the binding of dopamine, then reducing positive symptoms (Seeman, 2011). Furthermore, several studies fuck off hinted that the use of Psychostimulant drugs (such as amphetamines and cocaine), which work by enhancing dopamine neurotransmission, bemuse been shown to induce psychotic symptoms such as hallucinations, delusions and disorganised speech and thinking, all of which demonst say a label resemblance to the positive symptoms exhibited in patients with insane Schizophrenia (Laruelle, et al. , 1996 Breier, et al. , 1997 Abi-Dargham, et al. 1998).Although some research has implicated excess dopamine as a affirmable cause of schizophrenia, there is hush up 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 mental block of the dopamine D2 receptor sites will only pass 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 signaled by Stahl (2008), that the reason for this whitethorn be, that unlike the mesolimbic pathway which is hyperactive in dopamine, the mesocortical pathway whitethorn already be deficient in dopamine, therefore block off of the D2 receptors in the mesocortical pathway could further add negative symptoms. Swerdlow (2010 359) suggests that an argument against the dopamine surmise whitethorn be that some patients whitethorn 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 unpredictable anti-psychotic drug called clozapine, claimed to show a 40-60% benefit in sympt oms for patients of schizophrenia who did not reply to the traditional neuroleptics (Pincus & Tucker, 2003 119). Clozapine still dallys a role in blocking the D2 receptor site but with less eagerness 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 express that dopamine does not operate in isolation, and may form only damp of the etiology in the manifestation of Schizophrenia. What is swooning is that the dopamine theory is far from conclusive, which would suggest that much more research is infallible 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 disfunction in the dopamine neurotransmitters?Studies to date have identified that several of the genes which are about linked with Schizophrenia are immediately involved in dopaminergic pathways (Howes & Kapur, 2009) this therefore leads us to a further conclusion that genetic science and gene mutation may play a key role in the readyment of schizophrenia. Evidence suggests that there is a strong genetic predisposition to underdeveloped the disorder and the more closely someone is related to an individual with Schizophrenia, the higher(prenominal) the disaster of them develop the disorder themselves (Nolen-Hesksema, et al. , 2009).Family, Twin and espousal studies demonstrate that there are higher concordance rates between monozygotic (Identical) agrees than there is with dizygotic (non-identical) fit. Studies conducted by Gotteman (1991) found that dizygotic twins had a 17% fortune factor if their twin sibling had the disorder however, for monozygotic twins, the rate change magnitude to a more probatory 48%. Further studies have revealed that children of schi zophrenic parents showed similar concordance rates of 46%, however, children born to schizophrenic mothers but pick out 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 prominent strength to the genetic theory, new research in epigenetics has found that, whilst monozygotic twins share the same desoxyribonucleic acid, 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 two dopamine and genetics play an important r ole 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 house greatly influence the development and animation 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 plan of attack of schizophrenia (Psychiatry, 2011). Research suggests that prenatal environmental insults such as viral bring on anaemia in the first and act 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) use rat models to produce viral induce iron deficiency, and found that the biochemical and behavio ural 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 copy of de novo mutations in Schizophrenics (Krebs & Rouleau, 2011).De novo mutations do not occur as a result of transmitted factors, but instead, are alterations which take identify around the time of early inclination (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 go about b y mental health professionals. It is seeming(a) 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.