Describe and evaluate one or more biological explanations of schizophrenia
Research has shown that schizophrenia is heredity and can runs in families. This suggests that genes play a significant role. The closer the genetic relationship the more likely the people are to share the disorder. Evidence from family studies by Gottesman showed that when bothparent are schizophrenic then there is a 46% chance of the child getting it, however, if only one parent had it, it dropped to 17%. This suggests that a genetic factor is involved.
MZ twins share 100% of their genes; DZ twins share 50% of their genes. If genes are a factor we would expect more identical twins to share the disorder than non-identical. Gottesman also looked at twin
…show more content…
Recent research has suggested that genetic factors affect the hard wiring of the brain. The research focused on the brain biochemistry (neurotransmitters). Although there have been many neurotransmitters associated with schizophrenia, Dopamine seems to be the most important. The dopamine hypothesis says that schizophrenia is caused by an increased reaction to dopamine in the brain. This could be because there is too much of the hormone dopamine in the brain, or conversely because there is an abnormally high number of dopamine receptors in the brain. This model says the excess sensitivity to dopamine results in the brain, causes the symptoms of schizophrenia.
Evidence comes from the fact that amphetamines increase the amounts of dopamine large doses of amphetamines given to people with no history of the disorder produced behaviour which is very similar to paranoid schizophrenia. Small doses given to people already suffering from the disorder tend to worsen their symptoms. L-dopa is a drug used to treat Parkinson 's disease it acts by increasing dopamine levels; it can also produce symptoms of schizophrenia in previously unaffected individuals, although not all patients developed these side effects. Main antipsychotic drugs such as Phenothiazine’s block the dopamine receptor cells and reduce symptoms
However Phenothiazine’s do not work for everyone diagnosed with schizophrenia, this suggests something else must cause schizophrenia as well otherwise
Likewise we can not say for sure that a Schizoprenogenic mother isn’t the result of having a schizophrenic child and not the cause of schizophrenia in the child. Both the psychological and biological explanation of schizophrenia are criticised for being too simplistic an explanation of the causes of schizophrenia. However, both theories are not rigid in their views and most scientists believe that is a complex interaction between biological and environmental factors which determine the development of schizophrenia. Although most supporters of the genetic explanation believe that there is a genetic predisposition to schizophrenia and therefore accept other psychological and environmental factors.
Schizophrenia is classified as a mental disorder that shows profound disruption of cognition and emotion which affects a person’s language, perception, thought and sense of self. The dopamine hypothesis states that schizophrenic’s neurones transmitting dopamine release the neurotransmitter too easily, leading to the characteristic symptoms of schizophrenia. This hypothesis claims that schizophrenics have abnormally high amounts of D2 receptors; receptors that receive dopamine, therefore resulting in a higher amount of D2 receptors binding to the receptors causing more impulses. Dopamine neurotransmitters play a
In support of this Kendler et al found that first degree relatives of those with schizophrenia are at 18 times more risk than the general population. Research has also found that schizophrenia symptoms may have a genetic component. This was suggested by Malaspina, who found that patients who have schizophrenia in their family histories are more likely to develop negative symptoms than those families who are schizophrenia free. In evaluation of family studies it may be concluded that they are not very reliable as they are retrospective. The studies for family studies where taken place when diagnosis was under a more liberal use of the term schizophrenia. Twin studies have also shown a genetic pre-disposition. Gottesman found 48% risk of schizophrenia in MZ twins compared to only 17% in DZ twins. Similar to the Gottesman study two other studies showed higher concordance rates for MZ twins and lower in DZ twins however each had slightly different results. McGuffin et al argues this is because of the use of different diagnostic criteria, which may affect the validity of the results. On the other hand the researchers used blind techniques to obtain the results eliminating any researcher bias.
Research by Johnstone in 1994, explained the biological approach of interventions, explanation and treating of schizophrenia patients (Hansell & Damour, 2005). In studies of Fisher in 2001, discoveries that the brain had more dopamine receptors know as B_2 receptors in a person suffering from schizophrenia, than a non-suffer (Hansell & Damour, 2005). Biological findings of schizophrenia suggest that a genetic factor was hereditary, but not conclusive because the element of environment does make a difference (Hansell & Damour, 2005).
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
Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal
The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine
Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).
The initial indication of schizophrenia being a factor of dopamine was amphetamine consumers. Amphetamine causes several symptoms of schizophrenia including: delusions and hallucinations. In schizophrenics there is an unsteady, high amount of dopamine in the brain. Antipsychotic drugs work to lower the presence of dopamine on the brain by impeding dopamine receptors. There are two primary dopamine receptors, D1 and D2. In schizophrenic patients the latter is split into D2, D3 and D4 subtypes. Dopamine activators are found in the striatum, prefrontal cortex and limbic system of the brain. Clinical research has observed an increase of dopamine in the emotion controlling striatum through PET and SPECT brain scans. Unfortunately there is no one pinpointed cause of high dopamine levels. Many of these causes are: Agitation, anxiety, cognitive acuity, feeling of pleasure, hedonism, high energy, high libido, insomnia, paranoia and
Schizophrenia is a serious mental disorder that affects millions of people and it should not be underestimated or ignored.
The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine
However, the evidence is inconclusive since other studies have failed to reveal an excess of dopamine receptors. Further problems with the dopamine hypothesis include the finding that antipsychotic drugs which block dopamine receptors, do not appear to help a significant number of people with Sz. They appear much more effective in cases of Type 1 Sz than in Type 2. Second, these drugs block dopamine receptors quickly, yet even when they are effective, the symptoms can take weeks or even months to subside. Furthermore, the developments of new types of drugs such as clozapine which are known as antipsychotic drugs block fewer dopamine receptors than traditional anti-psychotics. However, they block many receptors for the neurotransmitter serotonin. They appear particularly effective in reducing the symptoms of Type 2 schizophrenics. Recent research suggests that Sz may result from the interaction of serotonin and dopamine rather than dopamine alone. As Davison and Neale (1998) suggest, ‘Sz is a disorder with widespread symptoms covering perception, cognition, motor activity and social behaviour. It is
This article provides information as to how the brain historically has used dopamine as an inhibitory neurotransmitter in regards to schizophrenia. The research discussed in this article focuses on a new discovery that indicates that glutamate, GABA, acetylcholine and serotonin alterations are also involved with schizophrenia’s pathology. With use of schizophrenic animal models, both dopamine receptors and the antipsychotic effects of the treatments that target them, and how they interact with other various neurochemical types of schizophrenia. The final topic the author discusses is how the human brain and mental abilities has evolved, causing many schizophrenic patients to be affected.
The first theory being, the Genetic Theory. This theory proposes that schizophrenia is inherited and passed through genes. As stated in the Epidemiology in Neurobiological Research by Tsung, Stone and Faraone, “greater risks are associated with higher levels of shared genes. For example, third-degree relatives share about 12.5% of their genes, and show a risk of 2% for developing schizophrenia. Second-degree relatives share about 25% of their genes and show a risk of 6%. Most first-degree relatives siblings, dizygotic (DZ) twins share about 50% of their genes and show a risk of about 9%. Monozygotic (MZ) twins share 100%
There are many causes to Schizophrenia. Many causes are genetics, brain chemistry and structure, and the environment of a human being. Genetically Schizophrenia can run through a family and can be passed on generations at a time. “Individuals with a first degree relative (parent or sibling) who has schizophrenia have a 10 percent chance of developing the disorder, as opposed to the 1 percent chance of the general population.” (Helpguide.org) Identical twins are a good example of this. “If an identical twin is diagnosed with Schizophrenia the other twin is 50 percent more likely to also be diagnosed with the mental disorder (psychcentral.com).” Brain chemistry and structure is another big factor in the cause of Schizophrenia. Neurotransmitters-