Another line of research, explored over the same time period as the schizophrenogenic mother and the double bind, concerned theories that distortions in the marital relationship of a mother and father might impact adversely on a child and cause schizophrenia. Theodore Lidz was one of the leading researchers in this field. Lidz hypothesised that there are two different kinds of distortion in parental marital relationships which alternatively selected boys and girls as candidates for schizophrenia.
The first kind of distortion Lidz called ‘marital skew’.[80] This occurs when one parent yields to the idiosyncrasies and over-bearing dominance of the other. This situation was thought to be particularly relevant to the cause of schizophrenia in male children.[81] In families with marital skew the dominant parent was usually the mother, and in contrast to her the father was perceived as being a weak passive type of person who provided a poor role model for his son. In these families the mother was believed to turn away from her husband as a source of emotional comfort and to fixate on her son in a search for solace. The combination of a poor paternal role model and a fixated, dominant and often eccentric mother was thought to be a frequent cause of schizophrenia in male children.[82]
The cause of schizophrenia in female children was thought to be usually caused by a variation on this theme and due to a condition called ‘marital schism’. Marital schism occurred when there was conflict between the mother and father but neither party yielded to the other.[83] In this situation each partner was constantly striving to satisfy their own needs while ignoring the other partner’s needs. This perpetual battle for ascendancy between parents inevitably involved the children as the parents competed for their affections and enrolled them as supporters. The schismatic family was thought to be far more selective in causing schizophrenia in females than in males.[84]
In both the skewed and schismatic types of family, Lidz hypothesised that children are reared in an abnormal environment because there is an absence of parental cooperation and the normal delineations between generations are not observed. He believed these conditions could lead to anxieties in children involving the induction of incestuous feelings. Lidz’s basic approach to schizophrenia was similar to Bateson’s in that he believed it is the manifestation of inappropriate behaviour that has been learned in the family environment.[85]
Although a considerable amount of research has been conducted over the years to test Lidz’s theories, most of the results have not supported them. A particularly thorough study was undertaken by Sharan in the middle 1960s.[86] Sharan’s study involved twelve families with a schizophrenic son, and twelve with a schizophrenic daughter. Each of these groups of families were symmetrically balanced by dividing them into six families with a healthy sibling of the same sex as the schizophrenic, and six families with a healthy sibling of the opposite sex to the schizophrenic.
The core of the study required each family to complete a questionnaire. This was done under tape-recorded supervision with the family members assembled in groups of three, firstly comprising the two parents and the schizophrenic child, and secondly comprising the two parents and the healthy child. Different questionnaires were used each time, and answering the questionnaires required discussion amongst each separate group. The objective was to score the individual parents for indications of dominance by assessing how often one parent’s answers became the group’s decision. Support between individuals was also scored by recording how often supportive and non-supportive remarks were directed at individual family members.
Sharan could find no clear pattern confirming Lidz’s theories about either the relationship of parental marital skew to schizophrenia in male children or the relationship of marital schism to female schizophrenia. Nor could he uncover any clear pattern of parental support or non-support for schizophrenic children as compared to their healthy siblings.[87]
Another line of research assuming an environmental cause involved studying the families of schizophrenics as whole units to see if the cause of schizophrenia could be found in group deviance, rather than in the deviations of individual members.[88] One influential hypothesis postulated that when there are mutual expectations amongst family members of reciprocal fulfilment, which have no basis in reality, the false atmosphere in the family is often accompanied by disjointed forms of communication and irrational shifts in the focus of family attention. This situation was thought to give rise to conditions where all family communications were polarised between superficiality at one pole and fragmented, disjointed thinking at the other. These conditions in turn influenced the cognitive development of children who were subjected to them. Schizophrenia was thought to be one of the outcomes.
More recently deviance in the language of schizophrenic patients has been compared to similar deviations in the language of their parents in the hope that some light may be shed on the cause by understanding how the language deviations of schizophrenia are learned.[89] Research is now also turning to focus on positively identifying a link between genetic vulnerability and environmental stresses in family life that might trigger schizophrenia. One recent study compared adopted children of schizophrenic mothers, who were thought to have an enhanced genetic risk, with a control group of adoptees with normal genetic risk profiles, to see whether there were any consistent patterns of thought deviation in the two groups of children that might be associated with environmental triggers. However, no clear pattern has emerged from this research yet.[90]
Stress in the family environment has been extensively researched as both an originating cause of schizophrenia and as a factor in relapse. Two types of stresses have largely been the focus of attention: the ambient stresses of everyday life and abnormal stresses brought on by important life events such as a death in the family.[91] Ambient stresses are often measured in the form of ‘expressed emotion’ (EE). Schizophrenics are thought to come from families with higher than normal levels of EE and some researchers claim that when there is a high level of EE between a mother and child, for instance, this deepens the emotional bond, but it also puts the child at higher risk of developing schizophrenia.[92] Comparisons have been drawn between the key components of EE research—that is, critical comments and the over-involvement of family members in the schizophrenic’s life—with the rejection and over-protection that was formerly attributed to the schizophrenogenic mother.[93] This suggests that EE researchers might be merely extending the schizophrenogenic concept from the mother to the whole family.
One type of important event that has attracted research attention is the death of a grandparent within two years of the birth of a schizophrenic person. Researchers found that a grandparent of 41 per cent of a large sample of schizophrenics had died within this period. This rate was significantly higher than the rate in a control group of normal people, and it was hypothesised that the additional stresses introduced into family life by two major events—a birth followed by death, or vice versa—might confuse the parenting and mourning roles. In this situation a bereaved parent might be emotionally unavailable to an infant and a spouse or, alternatively, a child might be used as a distraction from mourning and as a result could inadvertently absorb the painful feelings of the bereaved parent.[94]
Next: Social Stress
[80] Theodore Lidz et al., Schizophrenia and the Family, pp. 142–5.
[81] Ibid., p. 249.
[82] Julian Leff, ‘Social and Psychological Causes of the Acute Attack’, p. 143.
[83] Lidz et al., op.cit., pp. 136–142, 264.
[84] Leff, op.cit., p. 143.
[85] Theodore Lidz, ‘Patients whose children became schizophrenic’, pp. 408–11.
[86] Leff, op.cit., p. 144.
[87] Ibid., p. 145.
[88] Deborah J. Lieber, ‘Parental focus of attention in a videotape feedback task as a function of hypothesised risk for offspring schizophrenia’, pp. 467–75.
[89] N. M. Docherty, ‘Communication deviance, attention, and schizotypy in parents of schizophrenic patients’, pp. 750–56.
[90] K. E. Wahlberg et al., ‘Gene-environment interaction in vulnerability to schizophrenia: findings from the Finnish Adoptive Family Study of Schizophrenia’, pp. 355–62.
[91] Ian R. Falloon, ‘Family stress and schizophrenia: Theory and practice’, pp. 165–82.
[92] William L. Cook et al., ‘Expressed emotion and reciprocal affective relationships in families of disturbed adolescents’, pp. 337–48.
[93] Parker, op.cit., pp. 452–62.
[94] Froma W. Walsh, ‘Concurrent grandparent death and birth of schizophrenic offspring: An intriguing finding’, pp. 457–63.