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August 28, 2004
Can the Social Environment Cause Schizophrenia?
Krabbendam and van Os (2004) have recently raised the question of socio-cultural etiology in the schizophrenic disorders (“Can the social environment cause schizophrenia? in “Schizophrenia: Challenging the Orthodox” edited in 2004 by Colm McDonald, Katja Schulze, Robin Murray & Padraig Wright for Taylor & Francis). They begin their affirmative argument with population variation, an approach demonstrating between-population variation. Incidence rates of schizophrenia vary widely, within the same country, between urban and rural populations, as well as between majority and minority populations. They hypothesized that the mean level of symptoms would increase with the rate of disorder across increasingly urbanized areas. In a random sample of 7076 women and men (the Dutch NEMESIS Study), it was demonstrated that the level of urbanicity was not only associated with DSM psychotic disorder, but also, independently, with any symptom of delusions and/or hallucinations, and any rating of a psychosis-like symptom. These investigators concluded: “These findings suggest that the increased prevalence of psychotic disorder should be interpreted in light of increased levels of ‘psychosis proneness’ in urban populations” (p. 50).
Ethnic minority status is another robust source of variance between populations at risk for developing schizophrenia. (Anecdotally, I remember a much higher proportion of ethnic patients at the state hospital in which I worked, as well as harsher precautions taken against them, e.g., use of seclusion room, loss of therapeutic passes, etc, should they engage in what was perceived as ‘threatening’ behavior, e.g., raised voices, cursing, insulting staff, etc). A well-known population in which ethnic minority status has been associated with higher rates of schizophrenia in first and second generation individuals is the African-Caribbean people living in the UK. These populations are not or are much less risk in situations where they become majority populations, indicating that genetic factors alone could not be explanatory. A recent study by Boydell et al reported in 2001 in the British Medical Journal, demonstrated that as the proportion of non-white ethnic minorities in a given neighborhood decreases, the rate of incidence of schizophrenia increases (for non-whites). Investigators have raised the issue of racial discrimination as a powerful factor in these results. Additionally, I would raise the issue of separation anxiety and/or ‘anxiety of the strange’ when one is in a minority population, surrounded by persons who do not look like you, have different cultural features and who, in addition, may fail to resonate and respond to the minority person, verbally and non-verbally, or even may evidence signs of anxiety and fear or indifference in response to minority persons.
The effect of discrimination on the development of psychotic symptoms in the Dutch NEMESIS cohort was investigated prospectively (Krabbendam & van Os 2004). In brief, psychotic symptoms, e.g., delusions, were associated with reported discrimination. No association was found between baseline discrimination and onset of hallucinatory experiences. The researchers concluded that perceived discrimination may induce delusional ideation and thus contribute to the high observed rates of psychotic disorder in exposed minority populations.
Data from the NEMESIS Study were analyzed to investigate the role of childhood trauma and early childhood adversities. The results suggested that reported childhood abuse predicts psychotic disorder and psychosis-like symptoms (perhaps demonstrating that there is a continuous and normal distribution of psychotic traits in the general population - a similar hypothesis has recently been proposed and demonstrated by Daniel Freeman and Philippa Garety in their excellent volume “Paranoia: The Psychology of Persecutory Delusions” published in 2004 by Psychology Press). Krabbendam and van Os (2004), based on the above research concluded: “Early adverse experiences such as social marginalization, childhood loss or severe childhood trauma, may create an enduring cognitive vulnerability, characterized by negative schematic models of the self and the world (e.g. beliefs about the self as vulnerable to threat, or about others as dangerous) that facilitate external attributions. This tendency to externally attribute events may lie beneath paranoid ideation” (p.52).
Krabbendam and van Os (2004) also noted the effects of prenatal stress and inconvenience of pregnancy as associated with increased risk for pregnancy. Myhrman et al (1996) in “Unwantedness of a pregnancy and schizophrenia in the child” (British Journal of Psychiatry; 169: 637-640) demonstrated that experiential factors in relation to the ‘receiving’ environment to the child can play a significant role in increasing risk for the later development of schizophrenia (see the clinical and theoretical work of Finnish psychiatrist-psychoanalyst Martti Siirala, in particular, his excellent volume, years ahead of its time, “From Transfer to Transference, on the transgenerational transmission of trauma and its relation to psychosis). The Early Developmental Stages of Psychopathology (Lieb et al., Archives of General Psychiatry 2000; 57: 859-866) study (EDSP), a longitudinal study of 963 adolescents aged 15-20 years and their parents, demonstrated that stress during pregnancy (as I have shown in many previous ISPS postings and papers using research studies from various countries, prenatal stress is a behavioral teratogen, affecting the developing fetal neuroaxis) and inconvenience of pregnancy were associated with an increased risk of expression of psychosis in the adolescents and similar, but more enhanced, results were obtained with narrowly defined psychotic experiences. These effects remained after controlling for gender, socioeconomic status, as well as psychiatric diagnosis and current level of depression and mania in the parents. From an attachment perspective, these risk variables (prenatal stress, unwantedness of pregnancy) would be seen as disrupting the developing child’s psychobiological homeostasis (affective misattunement leading to affective dysregulation in the child) and the needed connection, for survival purposes, with the primary caregivers (e.g., failures to establish a secure base). See the research of Myron Hofer (a researcher at Columbia University-NYS Psychiatric Institute) for research evidence of the massive psychobiological effects of separation (what he calls “hidden regulators” of the attachment bond).
Krabbendam and van Os concluded: “The significance of these findings lies in the fact that prenatal risk factors may influence expression of psychosis outside the clinical phenotype. This suggests that the pathway from risk factors in early life to adult schizophrenia may involve an intermediary vulnerability state characterized by subtle but non-clinical psychotic experiences that may subsequently make the transition to clinical psychotic disorder, under the influence of other, more distal risk factors” (p. 53).
The data presented demonstrate that established proxy etiological factors for schizophrenia such as urbanicity, racial discrimination, childhood trauma and abuse, prenatal stress and unwantedness of pregnancy, affect both the occurrence of non-clinical psychosis-like experiences in addition to occurrence of narrowly defined schizophrenic disorders.
Krabbendam and van Os (2004) noted that the: “environmental factors associated with these [above] variables cause whole populations to have higher levels of non-clinical psychotic experiences, rather than causing a few individuals to develop a rare disorder. In other words, the psychosis phenotype appears to be a continuous function that varies with different levels of social environmental stresses. What is called schizophrenia may just be the extreme manifestation of this continuum. In conclusion, therefore, not only common sense but also research findings suggest that the mental states associated with schizophrenia are not the exception to the rule that psychological and environmental experiences go hand in hand” (p. 53).
Brian Koehler PhD
New York University Postdoctoral Program
80 East 11th street #339
New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net
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