Schizophrenia is caused by environmental not genetic factors
PSYCHOLOGY - The medical condition Schizophrenia (not to be confused with multiple personality disorder) is a debilitating psychological condition, and although there are treatments available it is unclear as to what causes schizophrenia in the first place. Some theories suggest the condition may originate from poor parenting or difficult conditions in adolescence, whilst other research has shown genes, dopamine and serotonin levels may be to blame. So is it deficient care or abnormal makeup that causes psychologically stable individuals to develop such a condition?
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Schizophrenogenic mother theory (Fromm-Reichman 1948)
It was proposed that scizophrenic behaviour stems from the mother's behaviour toward the child in early childhood. Mothers with cold, rejecting or detached styles of parenting create psychological distresss in the child. Later in childhood these mothers create 'double blind' situations - scenarios in which whatever the child does is not right. Evidence has shown that in families where there is Schizophrenia communication is much less clear.
The somewhat Freudian approach that all mental disorders are products of bad early childhood experiences is hardly ever fully evidenced. There is little evidence to link parenting styles to Schizophrenia and even the link between the illness and poor communication could be symptomatic not causal. Studies [Liem 1974]] showed that even parents of 'normal' children were confused when talking to schizophrenic children and thus it is less a fault with the parents than an effect of dealing with Schizophrenic patients.
Expressed Emotion Theory (Brown 1959)
In the 'Camberwell Family study' Brown measured relapse rates of Schizophrenia when patients returned home, and when patients returned to hostels after treatment. He found that they differed but there was a third factor present which helped determine the success of their recovery which he termed 'expressed emotion'(EE). High EE was characterised by a family environment with low warnth, parental over-involvement and hostility. Of the three test groups in the study the group that spent the longest time in the high EE environment ws the group that was most likely to relapse.
This study demonstrates why a patient might relapse but this is not necessarily the initial causal factor of the development of the illness. What delays recovery may not be the same as what triggers illness.
Schizophrenia is statistically more prevalent in lower socio-economic classes. Perhaps factors such as stresss, racism, unemployment and bad housing are to blame for the development of the illness?
The socioeconomic pattern disappears when the patients are categorized by their fathers' occupations [Goldberg and Morrison 1963]]. When this is done the illness appears in all social strata, thus we can only conclude that it is more 'social drift' than 'sociogenesis' - the schizophrenics find it hard to integrate into society and thus they lose any existing high social status.
The famous case of the Genain quadrupets highlights the idea that schizophrenia could have a genetic basis. All four of these quadruplets developed schizophrenia. Also, monozigotic twins are more likely to develope the illness (44.3%) than dizigotic (12.1) indicating that the shared DNA is to blame.
In the case of the Genain quadruplets they had a family history of physical and sexual abuse and their family environment was categorised as having high 'Expressed Emotion' (see earlier point). This means that although it appears to be a genetic link that all four developed the illness, they were all subject to similar circumstances in childhood and therefore the 'trigger' could just as easily have been an environmental one.
Patients diagnosed with schizophrenia were initially treated with antipsychotics. Doctors knew through clinical trials that these worked, but were not aware of why. The drugs sometimes produced Parkinsonian side-effects (usually caused by low dopamine levels) it was thus deduced that the antipsychotics were reducing excess Dopamine, which was the cause of the illness. The drugs work by blocking post-synaptic dopamine receptors.
Patients with Schizophrenia do not have increased levels of homovillic acid (the main metabolite of Dopamine) so thier Dopamine levels cannot be higher than average.
Also, to be theraputic anti-psychotics have to reduce dopamine levels to below normal (which produces the parkinsonian side effects). If 'excess' Dopamine was to blame why would it not be effective to reduce it to normal levels?
Increased dopamine receptors
Perhaps it is not the dopamine itself that is elevated (as this would result in increased homovillic acid) but the dopamine receptors. PEt scans and post mortems have shown this to be the case [Goldsmith et al 1997]].
Anti psychotics block dopamine receptors rapidly yet symptoms only reduce gradually. If excess receptors were to blame why is there such a delay?
Schizophrenia cannot be merely environmental because evidence from post mortems and MRI and CT scans indicates that there are physical abnormalities present in the brains of schizophrenics which are not demonstrated in the 'healthy' brain. The most consistent finding is that schizophrenic brains demonstrate enlarged ventricles (which indicates loss of brain cells)[Nopoulous et. al 1997]]. Structural abnormalities have also been found in the temporal-limbic areas and the prefontal temporal cortex [Dwork 1997]]. There is also a reduction in cortical grey matter [Gur et al 2000]] and reduced volume in the basal ganglia and limbic structures [Velahoulis et al 1999]].
These findings are at best contradictory and the many studies have been incolclusive. There have also been no longitudinal studies to see whether these brain structure abnormalities are congenital (indicating a genetic factor) or whether they could develop as a result of external developmental factors in childhood.
What do you think?