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There are many different factors that appear to contribute to the cause of schizophrenia in most people. In the previous article, we explored some of heredity and biological causative factors. This articles looks at additional possible causes of schizophrenia.
There is also considerable evidence indicating that stress may trigger episodes of schizophrenia psychosis. For example, emotionally turbulent families14 and stressful life events have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. In common with other forms of mental illness, abuse as a child and early traumatic experience have also been suggested to be a risk factor for developing schizophrenia later in life, although the "bad parenting" theory of causation is now largely held in disrepute on the grounds that it overlooks the likelihood that the parental incompetences may have been a result of schizophrenia in the parents, and the disorder itself in the offspring was actually transmitted genetically from the parents.
Factors such as poverty and discrimination may also be involved in increasing the risk of having a schizophrenic episode due to the high levels of stress that these lifestyles harbor. This may explain why minority communities have much higher rates of schizophrenia than when members of the same ethnic groups are resident in their home country. On the other hand, the "social drift hypothesis" suggests that people affected by schizophrenia may be less able to hold steady or demanding, higher-paying jobs, consigning them to lower incomes thereby increasing stress levels and leaving them susceptible to lapsing into a schizophrenic episode.
One particularly stable and replicable finding has been the association between living in an urban environment and risk of developing schizophrenia, even after factors such as drug use, ethnic group and size of social group have been controlled for19. A recent study of 4.4 million men and women in Sweden found a 68%-77% increased risk of psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be accounted for by schizophrenia.
One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.
It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia22. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939-1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy23, suggesting that even psychological trauma in the mother may have an effect.
Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered sensitive to features of dysfunctional social settings, such as trauma, violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. It is thought that the effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. This is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years.
Data from a recent PET study suggests the less the frontal lobes activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.
In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia, largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.
However, this theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments.
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in the development of schizophrenia. This theory has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia27 and the discovery that the glumatate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems of associated with the condition. The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can effect dopamine function, all of which have been implicated in schizophrenia, have suggested the glutamate hypothesis of schizophrenia as an increasingly popular explanation.