Unfortunately, most of the high-risk or cohort studies have not included measures of the kinds of social-cognitive processes which, I have argued, play a crucial role in depression, mania and paranoia. In fact, so far as I am aware, only the Israeli High-Risk Study has included a measure of this sort.79 In that study, the adolescent children of schizophrenia patients were administered a questionnaire measure of locus of control, a construct that is similar to but predates the concept of attributional style. Individuals are said to have an external locus of control if they believe that important facets of their life, including their own behaviour, are controlled by external influences, whereas they are said to have an internal locus of control if they believe that they control their own destinies. In the Israeli study, high-risk adolescents who later became psychotic were found to have a more external locus of control than those who did not later become psychotic. If verified by future studies, this finding suggests that the attributional abnormalities observed in some psychotic patients may be present, to some degree, well before the onset of their delusional ideas.
The role of early brain damage
Many investigators have assumed that the neurodevelopmental abnormalities found in pre-psychotic children must be genetically determined. However, others have argued that other kinds of influences on the developing nervous system may affect a person’s vulnerability to psychosis. In the Copenhagen study it was found that high-risk children who were later to become ill were more likely to have experienced difficult births than children who stayed well.80 As complications during birth can cause the brain to be temporarily starved of oxygen, this observation is consistent with early versions of the biological time-bomb hypothesis. Although some studies have replicated this finding,81 others have not,82 or have found that the association between birth complication and psychosis exists only for males.83 For these reasons, the contribution of birth complications to psychosis remains uncertain.
A more recent hypothesis suggests that foetal exposure to a virus contracted by the expectant mother might be the cause of early neurodevelopmental abnormalities responsible for psychosis. This suggestion was originally made to explain the much repeated observation of a very slightly increased risk of psychosis in people born in the late winter or early spring (and who were therefore second trimester foetuses during the winter, when viral infections are most common).84* A bizarre version of this theory, proposed by American psychiatrists E. F. Torrey and Robert Yolken, holds that the ‘schizovirus’ can be caught by expectant mothers from domestic house cats, which tend to spend more time indoors during the winter. (Fuller and Yolken claim that schizophrenia is especially common in countries where people keep cats as pets.)85 However, most researchers have focused on the influenza virus. Although some retrospective studies have reported evidence that mothers of psychotic patients suffered from influenza during pregnancy more often than mothers of non-psychotic people,86 many others have failed to find this association.87
Even if the influenza virus is not the culprit, one piece of evidence suggests that the role of maternal infections in conferring vulnerability to psychosis should not be dismissed entirely. Several studies have found that the season-of-birth effect is especially evident in patients born in urban areas characterized by high population density and crowded housing but is absent or almost absent in patients born in rural areas.88 Of course, the importance of this observation can be debated. In one study the combined effect of season of birth and urban birth was only evident in females.89 However, in another, more recent, study, it was calculated that the population risk (number of cases) attributable to place and season of birth exceeded the risk associated with having a first-degree relative suffering from psychosis.90Of course, the urban environment probably contains a number of psychological hazards to the developing child, as we will see in the next chapter. Nonetheless, one explanation for the greater evidence of the season-of-birth effect in urban environments is infections; in crowded conditions viruses and other infectious agents are easily passed from one person to another.
Viral infections are not the only conceivable cause of the season-of-birth effect. As there is no seasonal bias in the births of brothers and sisters of psychotic patients, the hypothesis that the effect is caused by the seasonal reproductive enthusiasms of parents can probably be ruled out.91 However, the possibility that poor maternal nutrition in the winter months plays a role is raised by a study that found that a higher than expected number of future schizophrenia patients were born during the Dutch ‘hunger winter’ of 1944 to 1945, when a Nazi blockade precipitated a severe famine in western Holland.92
Unfortunately the interactions between these kinds of factors and others that appear to contribute to psychosis are not understood. Attempts to determine whether birth complications play a greater role in patients with or without a family history of mental illness have yielded almost entirely inconsistent results,93 so it is not clear whether early brain damage and genetic vulnerability represent separate or interacting contributions to later psychosis. Attempts to demonstrate an association between birth complications and the kinds of structural brain abnormalities sometimes observed in brain scans of adult patients have also been inconclusive.94 Nor can interactions with psychological and social factors be excluded. The authors of a recent study, which found an association between schizophrenia and maternal bleeding during pregnancy,95 speculate that some aspects of maternal lifestyle (for example, smoking during pregnancy, failure to comply with routines of antenatal care) may partially explain their observations. As some of these lifestyle characteristics are especially evident in mothers who suffer from psychiatric problems, this hypothesis suggests a non-genetic mechanism that might explain why psychosis sometimes runs in families.
What can we Conclude from Neurodevelopmental Studies?
Overall, the findings from developmental studies consistently show that unusual characteristics are present in at least some future psychotic patients many years before they become obviously ill. The findings on birth complications and prenatal exposure to viruses or malnutrition lend further support to the theory that early brain damage can make individuals more vulnerable to becoming psychotic in later life. However, it is important not to leap from these observations to simple conclusions. Other types of challenges to the developing brain, for example prenatal exposure to high levels of alcohol,96 have been proposed as potential causes of vulnerability to psychosis. Perhaps any kind of early brain damage can have this effect.
Nor are these effects specific to people who later receive a particular diagnosis. Although most of the relevant studies have been conducted by investigators who have been searching for the origins of schizophrenia, whenever comparable data have been collected, similar observations have been made for children who later develop psychotic mood disorders.97 For example, in one study it was found that the average IQ scores of future schizophrenia and future bipolar patients were both slightly lower than normal during middle childhood.98 In the NSHD, there was evidence that those who later developed severe depression, on average, showed poor performance on IQ measures, together with speech irregularities.99 Retrospective reports by parents suggest that future bipolar patients, like future schizophrenia patients, show impaired social functioning in adolescence.100 The season-of-birth effect has also been found for bipolar patients101 who, like future schizophrenia patients, may have experienced higher than expected rates of obstetric birth complications.102 Unexpectedly high rates of depression and bipolar disorder, as well as schizophrenia, have been found in children born in the Dutch ‘hunger winter’.103 It is pretty clear from this evidence that non-specific kinds of early brain damage cause a non-specific vulnerability to psychotic symptoms later in life (a conclusion that could obviously be interpreted as consistent with a unitary psychosis model).
The magnitude of this effect is drawn into question by the low prevalence of psychotic illness. As we have seen, studies of birth complications and prenatal influenza reveal, at best, a
very modest increase in exposure to these phenomena in future patients in comparison to ordinary people. In this context it is important to remember that, for every person who receives a diagnosis of schizophrenia or bipolar disorder, there are about 100 people who do not. Simple arithmetic reveals that, even if exposure to these challenges to the nervous system were three times more common in future patients than in others(which would certainly be more than a modest increase), the number of people who suffer these insults without becoming psychotic would still be more than thirty times greater than the number who do so and later become ill.*
A final, and very important, qualification about the evidence we have examined concerns the logic of the neurodevelopmental time-bomb hypothesis. Whether theories of this kind implicate processes early or late in development, their main strength is that they explain the age of onset data discussed at the beginning of this chapter. Herein also lies their fundamental weakness. Whereas adolescents and young adults are more vulnerable to developing psychotic symptoms than any other age group, symptoms can appear as early as the age of 10 or as late as the age of 70 or afterwards. In fact, despite the over-representation of adolescents among people experiencing their first episode of psychosis, it seems likely that the number of non-adolescents experiencing psychotic symptoms for the first time exceeds the number of adolescents.†
Because biological researchers have attempted to explain the typical age of onset exclusively in terms of some kind of endogenous process – the biological time-bomb that ‘explodes’ during a critical period of development – they struggle to explain the very wide range of ages at which psychotic symptoms first appear. In order to explain this range, it will be necessary to take into account factors external to the individual, in particular the life-experiences of those who become psychotic.
18
The Trials of Life
There is but one truly serious philosophical problem and that is
suicide. Judging whether life is or is not worth living amounts to
answering the fundamental problem of philosophy. Albert Camus1
Life’s a bitch, and then you die… Common saying
My mother telephoned me on a Sunday evening to tell me that my brother had killed himself. It was a brief conversation, muted by shock. Afterwards, the fact of Andrew’s death seemed so big and difficult to absorb that I sat silently on my living-room couch, searching my brain for appropriate thoughts but finding none. The coldness of my home – the small house I had retreated to after the break-up of my marriage – suddenly became more evident. As minutes passed into hours, guilt began to lay siege to my defences. I had visited my mother earlier in the day. She had telephoned me only an hour after my return. Andrew had also planned to visit her but for some reason, probably because he and I did not get on very well, she had asked him not to come until the following weekend. He had killed himself that morning by leaping from the fourteenth floor of the tower block in which he lived.
Visiting a police station early the next day, my sister and I were relieved to discover that our brother’s body had already been identified by one of his friends. However, other grim tasks fell to us later in the week – clearing out the shabby flat in which he had lived in his final years; sitting in an empty courtroom to hear the coroner open and then adjourn the inquest; organizing the funeral, which was attended by a surprising number of his friends, most of whom were previously unknown to us. In the middle of the week, a local priest called on my mother and, knowing my profession, remarked that Andrew’s suicide must have been especially difficult for me to cope with.
Tragedy always unleashes an immediate search for explanations. We launch into attributional overdrive. However, as the priest who had visited my mother had shrewdly observed, it was unlikely that the concepts I had absorbed during my training would adequately satisfy my need to understand my brother’s final and most decisive act. Of course, Andrew had always been different. At school, he had constantly been at loggerheads with his teachers and his peers. He had dropped out from formal education without achieving qualifications, and had drifted in to a life of drug-taking and unemployment. From the comfortable perspective of a professional clinical psychologist, some of his behaviour could be described as schizotypal. He complained of flashback hallucinatory experiences that he attributed to his experiments with LSD. He sometimes professed strange and magical beliefs, at one time telling my mother’s elderly neighbour of his ambition to absorb all the knowledge in the universe. And yet, this kind of diagnostic labelling does not seem to do justice to the story of my brother’s life. He might have been ‘schizotypal’, for want of any better word, but he was not schizotypal in a vacuum. The more he became disengaged from his roots, and the middle-class values of his family, the more his relationships with us came under stress. We became angry and distant from him and ultimately, for my own part, quite rejecting. At his funeral, the friend who had identified his body told me that all Andrew had wanted from us was to be treated as ‘an acceptable failure’.
Yet Another Interminable Debate
They fuck you up, your mum and dad.
They may not mean to, but they do.
They fill you with the faults they had
And add some extra, just for you.
But they were fucked up in their turn
By fools in old-style hats and coats,
Who half the time were soppy-stern
And half at one another’s throats.
Man hands on misery to man,
It deepens like a coastal shelf.
Get out as early as you can,
And don’t have any kids yourself.
Philip Larkin2
The idea that environmental factors, and especially family relationships, contribute to madness is so difficult for many patients and their relatives that many professionals treat it as taboo.3 Most of those who have worked on the concept of expressed emotion, in particular, have been at pains to argue that, although families may influence the course of illness, ‘We consider that families do not exert a causal influence.’4 In making this kind of assertion, psychologists and psychiatrists have attempted to distance themselves from the equally extreme viewpoint of an earlier era, in which the causes of madness were exclusively laid at the door of ‘schizogenic’ parents. In the late 1950s, for example, the American anthropologist Geoffrey Bateson argued that the parents of future schizophrenia patients drove their children mad by giving them simultaneous but logically contradictory messages (known as ‘double-binds’).5 A few years later, the British anti-psychiatrists R. D. Laing and Aaron Esterson suggested that young schizophrenia patients were victimized and scapegoated by family members who wished to avoid dwelling on their own inadequacies.6 One consequence of characterizing the parents of psychiatric patients as evil in this way was described by the philosopher Peter Sedgwick, who witnessed a meeting between trainee social workers and a group of parents in the late 1970s, in which the former greeted the latter with undisguised hostility.7
The taboo against considering the role of environmental influences on psychosis has bolstered exclusively biological accounts of madness, particularly genetic accounts that portray the close relatives of patients as passive victims of a preordained tragedy. However, prejudicial assumptions of any sort are a poor basis for a scientific analysis. As we have seen in previous chapters, debates about the origins of madness have tended to focus exclusively on single causes that are either biological or environmental, as if the two were mutually exclusive. Advocates of both positions have often naively assumed that a focus on family relationships amounts to holding parents morally culpable for the troubles of their children.
In the last chapter we saw some evidence that environmental factors play a role in the development of psychosis. For example, in the adoption study reported by Tienari and his colleagues, an interaction was observed between genetic and environmental influences on thought disorder. In the Copenhagen high-risk study, patients with positive symptoms were especially
likely to have suffered separation from their parents at an early age. Of course, many different kinds of environmental factors might, in theory, help to determine whether or not an individual eventually becomes mad. In this chapter I will consider what these factors might be, focusing on three broad types of influences: family relationships, the general social environment, and traumatic experiences. Wherever possible, I will try to indicate how specific environmental influences contribute to specific complaints.
Family Influences
We begin with the difficult question of whether family relationships play a role in the aetiology of psychosis. One impediment to thinking clearly about this issue has been some over-simplistic ideas about how family relationships can go awry. The early family causation theories of schizophrenia created an image of the ‘schizogenic’ parent as a kind of monster. However, we do not need to assume that the parents of future psychotic patients are wilfully neglectful, deranged or cruel in order to accept that they have some influence on their children’s mental health.
Madness Explained Page 53
