During the 1950’s & 60’s there were several British psychologists, notably Laing who rejected the medical model of mental disorder and were hostile to organic and genetic explanations of schizophrenia. According to his family interaction model (1961) he stated that “schizophrenia can only be understood as something that occurs between people, rather than something taking place inside a person as is maintained by the medical model” he went on to say “schizophrenia refers to an interpersonal ploy used by some people (ie parents, doctors and psychiatrists) in their interactions with suffers”.
Laing tried to get ‘inside the heads’ of schizophrenics. He proceeded from the assumption that what the schizophrenic says and does are intelligible if you listen carefully enough and can relate to ‘being in their world’. He found that there was a split in the patient’s relationship with the world and the self. The sufferer experiences an extreme form of ontological insecurity and everyday events may threaten a schizophrenic’s very existence.
According to Laing’s psychedelic model (1967) schizophrenia is in fact, an exceptionally eloquent critic of society and schizophrenia is “itself a natural way of healing our own appalling state of alienation called normality”
Many studies have investigated the possible role of brain neurotransmitters in the development of schizophrenia. Most of these studies have focused on the neurotransmitter called dopamine. The “dopamine theory of schizophrenia” is caused by an overactive dopamine system in the brain. There is strong evidence that supports the dopamine theory but there is also data that does not.
EVIDENCE FOR THE DOPAMINE THEORY OF SCHIZOPHRENIA.
- Drugs that block dopamine reduce schizophrenic symptoms.
- Drugs that block dopamine have side effects similar to Parkinson’s disease. (Parkinson’s disease is caused by a lack of dopamine in a part of the brain called the basal ganglia).
- The best drugs to treat schizophrenia resemble dopamine and completely block dopamine receptors.
- High doses of amphetamines cause schizophrenic like symptoms in a disorder called “amphetamine psychosis” Amphetamine psychosis is a model for schizophrenia because drugs that block amphetamine psychosis also reduce schizophrenic symptoms. Amphetamines also make schizophrenia worse.
- Children at risk of schizophrenia may have brain wave patterns similar to adult schizophrenics. These abnormal brain wave patterns in children can be reduced by drugs that block dopamine receptors.
EVIDENCE AGAINST THE DOPAMINE THEORY OF SCHIZOPHRENIA.
- Amphetamines do more than increase dopamine levels. They also alter other neurotransmitter levels.
- Drugs that block dopamine receptors act on receptors quickly, however these drugs may take days to change the behaviour of schizophrenics.
- The effects of dopamine blockers may be indirect. These drugs may influence other systems that have more impact on the schizophrenic symptoms.
- New drugs for schizophrenia, for example, clozapine, block receptors for both serotonin and dopamine.
Overall the evidence regarding the Dopamine theory is inconclusive (Lavender 2000). For example, there is no consistent difference in dopamine levels between drug free schizophrenics and people without the disease, Nor is there any evidence of higher levels of metabolites indicating greater dopamine activity. (Jackson 1986). Even if such evidence did exist, this could just as easily be a result of the schizophrenia as its cause, and if dopamine were found to be a causative factor, this may only be indirect. (For example, abnormal family circumstances give rise to high levels of dopamine, which in turn trigger the symptoms. (Lloyd et al 1984).
It is unlikely that any problems with dopamine production / receptivity will prove to be the basic biochemical abnormality underlying all forms of schizophrenia, although it may play a crucial role in some forms. (Jackson1990).
It is crucial to remember however that physical factors may be an affect as opposed to a cause and that medical models may be appropriate for physical illness, but are not so for mental illness where the symptoms are less objective and are often defined in terms of social difficulty. Biological modes purport to be value free, but are actually affected by cultural attitudes.
It is also worth bearing in mind that the biological approach to schizophrenia appears to blame illness rather than the patient. Also, some disorders do have a biological basis, but this may mean that other important factors may be overlooked.
The causes of schizophrenia cannot be identified as either solely biological or genetic. Studies of twins also demonstrate the environmental impact on the development of schizophrenia. Not all genetically identical twins, for example, develop schizophrenia if their twin sibling suffers from schizophrenia. Since their genetic makeup is completely identical, if schizophrenia was 100% genetic, both twins would develop the disease. Clearly the role of the environment plays a part. Problems in early mother- infant bonding, strong parental intrusiveness, chaos and mixed messages all appear to play a role in the development of schizophrenia in some individuals. Peer rejection and rejection of peers has also been explored in schizophrenia. While it is likely that the environment plays a part, the exact role of the environment in the development of schizophrenia remains a mystery.
Non-genetic factors that may influence the development of schizophrenia include family stress, poor social interactions, infections or viruses at an early age, or trauma at an early age. It is thought that somehow the genetic make up combines with environmental factors to cause schizophrenia.
At least 50 different investigations have been able to identify a relationship between schizophrenia and early “environmental factors”. Examples are: obstetric complications, early infections, (especially influenza) and maternal stress during pregnancy, birth and childhood in urban areas, birth during the winter etc. since the environmental factors cause more cases of schizophrenia that genetics (a recent Danish study supports this theory), the correlation between schizophrenia and environmental factors is especially important to the development of schizophrenia. In contrast to the knowledge regarding the genetic factors, knowledge exists on the effects of oxygen deficiency and early infections on the brain development. Scientists can also identify individuals who have been exposed to these environmental factors.
Possible environmental factors include obstetric complications such as exposure to influenza or nutritional deprivation during pregnancy. It has also been suggested that stress and trauma can cause the emergence of schizophrenia. Family factors causing stress may affect the course of the illness, however there is no convincing evidence to show that they have a causative role.
People diagnosed with Schizophrenia come from all kinds of social backgrounds, but most appear to come from socio economic groups and live in the poorest areas of cities. This leads us to believe that social factors may be of some importance.
The sociogenic hypothesis suggests that poor social conditions create stresses that trigger schizophrenia in some people. Dohrenwend et al (1955) studied 65 individuals with recent history of schizophrenic breakdown and concluded that the schizophrenic group were more likely than a control group to have:
- One or more major or minor life event in the immediate past.
- Small social network with few confiding relationships.
- A noisome occupation.
- Vulnerable personality profile
However, the social drift hypothesis suggests that people with schizophrenia are unable to function properly and that a downward slide in quality of life is a consequence of the failure of the individual to cope with the developing psychosis. It has been suggested that fathers of schizophrenics more frequently come from lower social classes and that schizophrenics generally have lower occupational status than their fathers.
Some psychologists suggest that dysfunctional family relations with abnormal communication may have a part to play in creating highly stressful environments, however this may be due to difficulties in coping with the family member who is mentally disturbed and NOT the reason for the illness itself.
Most researchers believe that there is a biological & genetic basis for schizophrenia; however, they agree that these factors should only be seen as a predisposition to the disorder. Ie, they make people more vulnerable to the disorder, but they do not actually result in schizophrenia.
Biological & environmental factors do not operate in a vacuum, they operate in an environment. This environment includes, culture, social relationships in general, and in particular family
relationships. Environmental factors can encourage or discourage the predisposition for schizophrenia into the disorder itself.
This argument forms the basis of the Diathesis Stress Model. Diatheses means predisposition and stress refers to the environmental stress, ie traumatic events such as the death of a close relative or disturbing social situations such as dysfunctional families.
The Diatheses Stress Model explains psychological disorders as an interaction between a predisposition to the disorder and environmental stress. Both of which are necessary for the disorder to develop.
Support for the Diatheses Stress Model comes from an important ongoing study in Finland (Teinari et al 1994). The researchers found 171 women diagnosed with schizophrenia and who had adopted a child under the age of 4. The adoptive parents were interviewed and given a series of tests. On this basis, they were judged to be either
- Healthy.
- Mildly disturbed.
- Severely disturbed.
None of the adopted children raised in ‘healthy’ families developed schizophrenia, however, 9% raised in ‘mildly disturbed’ families and 11% in severely disturbed families developed the disorder.
This suggests that a well-adjusted family environment protects children whom may be predisposed to schizophrenia, whereas a disturbed family environment may encourage this predisposition to express itself the form of the disorder.
However all these cases also showed signs of neuropsychological abnormalities at the time of the initial assessment. (13 years previously) which raises the question of whether these abnormalities had influenced the parent child interaction.
These studies are ongoing and many of the children have not yet passes through the critical period for the onset of schizophrenia. However the evidence so far strongly supports the diatheses stress model.
No single cause for schizophrenia has yet been identified. Biological & environmental research suggests a complex interplay between factors for example; a person may have an inherited tendency towards schizophrenia, which is triggered by environmental circumstances. Researchers have many differing opinions on the origin of schizophrenia. Almost all agree that both biological & environmental factors are important for the development of the disease. However, opinions differ on the relative importance of biological versus environmental. New knowledge on the plasticity of the brain and its continuous development during life will most likely turn many “obvious facts” upside down. Researchers will now have to reassess their findings along with their attitude towards different theories regarding factors in schizophrenia.