biological explanations

• According to the genetic explanation of schizophrenia, if some family members have schizophrenia, then it is more likely you will develop schizophrenia. This is because you may inherit a specific gene allele associated with schizophrenia.
• The genetic explanation of schizophrenia suggests there are multiple gene alleles that increase the risk of developing schizophrenia. The more genetic risk alleles a person has, the more likely they are to develop schizophrenia.
• A gene is a specific section of a person’s DNA that controls the production of a particular protein.
• An allele are the multiple variations of DNA sections that lead to different biological outcomes.
• Inheritance is the process by which a genetic trait is passed on from a parent to a child.
• Supporting evidence for genetic explanation of schizophrenia. Gottesman and Shields 1966 conducted a twin study and found 74% concordance rate in MZ twins and 24% concordance rate in DZ twins. This is positive as it suggests schizophrenia is partially influenced by our genetics and supports the genetic explanation. However, concordance rate for MZ twins is not 100% so schizophrenia is not just caused by genetics and development is also influenced by the environment.
• Supporting evidence for genetic explanation of schizophrenia. Tienari et al conducted an adoption study and found adopted children with biological mothers who have schizophrenia are more likely to develop the disorder than children whose biological mothers don’t have schizophrenia. This is positive as it suggests genetics plays an important role in the development of schizophrenia. However, adoption studies assume any similarity between biological parent and adopted child is solely down to genetics.
• The neural correlates explanation of schizophrenia suggests that schizophrenia is caused by abnormal brain structure. Individuals with schizophrenia have a smaller frontal cortex and larger ventricles.
• Supporting evidence for neural correlates explanation. Torrey 2002 conducted MRI scans comparing the brains of participants with schizophrenia and those of a healthy control group and found people with schizophrenia had 15% larger ventricles than those in the control group. This is positive as it supports the idea that those with schizophrenia have an abnormal brain structure.
• Evidence supporting neural correlates explanation is from MRI studies. MRI studies provide correlational data, therefore, there is not sufficient evidence to conclude that brain abnormalities cause schizophrenia and the drugs patients take to treat schizophrenia may act as a confounding variable. This is problematic as supporting evidence lacks internal validity.
• Neural correlates explanation ignores individual differences. This hypothesis claims abnormal brain structure causes schizophrenia. Some studies have found no significant difference in the size of ventricles, between control groups and groups of people with schizophrenia. This is problematic as it contradicts the suggestion that large ventricles are a cause of schizophrenia.
• The dopamine hypothesis of schizophrenia suggests people with schizophrenia have higher levels of dopamine than healthy people and the neurons of people with schizophrenia generate more electrical activity than those of healthy people. Abnormal brain function causes schizophrenia
• The dopamine hypothesis suggests neurons are overactive in the mesolimbic system which causes delusions.
• The revised dopamine hypothesis suggests people with schizophrenia have high levels of dopamine in the mesolimbic pathway and overactivity in the mesolimbic system causes positive symptoms. People with schizophrenia have lower levels of dopamine in the frontal cortex than usual and underactivity causes negative symptoms.
• Supporting evidence for dopamine hypothesis. Drug studies show when normal people take amphetamines, they can experience hallucinations and delusions and drugs that reduce dopamine decrease the likelihood of people with schizophrenia having hallucinations and delusions. This is positive as it exemplifies the role dopamine has in schizophrenia.
• Evidence supporting dopamine hypothesis isn't always conclusive. Montcrieff 2009 reviewed studies investigating dopamine hypothesis and found amphetamines affect other neurotransmitters such as serotonin so we can't be sure positive symptoms are caused by dopamine and some post-mortem studies reported increased levels of dopamine in the mesolimbic pathway, but other studies reported no difference compared to the control brains. This is problematic as it contradicts the dopamine hypothesis.
• Antipsychotics are biological treatments for schizophrenia which decrease levels of dopamine activity in the brain.
• Antipsychotics reduce the overactivity of neurons in the mesolimbic pathway by preventing dopamine from binding to post-synaptic receptors. This reduces the activity of dopamine.
• A limitation of antipsychotics is side effects. Antipsychotic drugs can cause extra-pyramidal symptoms involving loss of control over movement as well as increased risk of heart problems, obesity and diabetes. This is problematic because it may not be the most efficient treatment for schizophrenia.
• A limitation of antipsychotics is that they do not treat the negative symptoms of schizophrenia. The dopamine hypothesis suggests that negative symptoms are caused by low levels of dopamine in the frontal cortex. Antipsychotics decrease dopamine levels in the brain. This is problematic because antipsychotics can cause an increase in negative symptoms and is not a completely effective treatment for schizophrenia.
• Atypical antipsychotics are able to treat negative symptoms when typical antipsychotics are not. Atypical antipsychotics have fewer side effects than typical antipsychotics.
• Typical antipsychotics bind to dopamine receptors for long periods of time whereas atypical antipsychotics bind to dopamine receptors for shorter periods of time, and are able to treat negative symptoms of schizophrenia.
• Supporting evidence for effectiveness of antipsychotics. Leucht 2001 conducted a meta-analysis of 65 studies regarding typical and atypical antipsychotics were significantly more effective at treating symptoms than placebo pills. This is positive as it demonstrates that antipsychotic drugs are helpful in treating schizophrenia.
• Crossley 2010 conducted a meta-analysis of 15 studies comparing effectiveness of typical and atypical antipsychotics and found no significant difference in overall effectiveness. However, it was found typical antipsychotics are associated with extra-pyramidal side effects and antipsychotics have fewer side effects as they bind to dopamine receptors for shorter periods of time.
• A limitation of antipsychotics is effectiveness. Patients who stop taking atypical or typical antipsychotics are likely to experience a schizophrenic relapse. Antipsychotics block the symptoms and do not treat the underlying causes of the disorder. This is problematic because it is not effective as a long-term treatment for schizophrenia.