Abstract
This article argues that a new mental health policy and programmes are needed to deal with the major mental disorders (schizophrenia, major depression and bipolar disorder). Evidence has now accumulated to show that many of the persons who are afflicted with these disorders continue to suffer throughout their adult lives, despite treatment. In addition to their own suffering, their mental disorders lead to unmeasurable suffering for their families which often include young children. Not only do these individuals present all of the symptoms and social impairments usually associated with the major disorders, they are also at increased risk for premature death, substance abuse/dependence, criminality, violence, homelessness, and infectious disease. This situation cannot be left to continue. New policy and programmes designed to prevent the major mental disorders are needed. Two consistent findings suggest that prevention may be possible: 1) many of the children at risk for the major mental disorders can be identified by their family history of mental disorder; and 2) non - genetic factors, biological and/or psychosocial, can limit the expression of the hereditary factors associated with each of these disorders. Given what we know about the fate of children within these high risk families, it may be unethical to not intervene.
This article reviews recent findings on the major mental disorders (schizophrenia, major depression, and bipolar disorder). The results demonstrate that these disorders, in most cases, are chronic, devastating, and debilitating, and that they are associated with increased risk of premature death, alcohol and/or drug abuse, criminality, violence, homelessness, and infectious disease. Since the implementation of deinstitutionalization policies along with widespread use of antipsychotic and antidepressant medications, the social problems associated with the major disorders have increased substantially. However, as other findings clearly demonstrate, there is no reason for the current situation to persist. The prevention of the major disorders is a realistic goal because: 1) a large part of the population at risk for these disorders can be identified with relative accuracy; and 2) twin studies have consistently demonstrated that some individuals who carry the genetic predisposition for one or other of these disorders, never develop the disorder; some non - genetic factor protects them. Identification of these protective factors and of the factors which exacerbate the genetic predisposition could lead to the development of prevention programmes. Given current knowledge in this field, Canada needs a new mental health policy which emphasizes prevention of the major mental disorders, and an allocation of resources which would allow for the implementation and evaluation of experimental prevention programmes.
A BRIEF REVIEW OF CURRENT FINDINGS ON THE MAJOR MENTAL DISORDERS
Prevalence
Onset of the major mental disorders occurs, in most cases, in late adolescence or early adulthood. Schizophrenia afflicts about 1.0% of men and women (Robins & Regier, 1991), and bipolar disorder about 1.6% of men and women (Kessler et al., 1994). The Epidemiologic Catchment Area project which evaluated a random, stratified sample of more than 15,000 U.S. citizens in the early 1980s, documented the prevalence of major depression to be 2.6% among men and 7.0% among women (Robins & Regier, 1991). A similar epidemiological investigation conducted in the early 1990s, documented rates of 12.7% among men and 21.3% among women (Kessler et al., 1994). Several investigations, conducted in a number of different Western industrialized countries, have documented increasing prevalence rates of major depression in cohorts born since the 1940s (Klerman & Weissman, 1992).
Validity and reliability of diagnoses
There is now good consensus, and more than adequate reliability and validity, for the diagnoses of schizophrenia and bipolar disorder that are obtained using structured, standardized, diagnostic instruments administered by experienced clinicians trained in their use (see for example, Spitzer, Williams, Gibbon, & First, 1992). In fact, in our research projects we have, more than once, obtained perfect agreement between independent diagnosticians on these two diagnoses for samples of up to 100 subjects. However, while the current diagnostic criteria for schizophrenia and bipolar disorder can be reliably applied and appear to identify relatively homogeneous groups of subjects, this is not the case for major depression. Many subjects who report an episode of major depression at time 1, fail to report the same episode again at time 2, 24 months later (Kendler, Neale, Kessler, Heath, & Eaves 1993a; Rice, Rochberg, Endicott, Lavori, & Miller, 1992). In addition, subjects who are diagnosed with major depression differ in important ways: about one - half experience recurrent episodes within two years of the index episode, and about one - quarter never relapse (Klerman and Weissman, 1992; Lewinsohn Zeiss, & Duncan, 1989); about one - half present important biological symptoms, while the other half do not (Gold, Goodwin, & Chrousos, 1988a & b). Consequently, research findings on major depression (diagnosed according to DSM III or DSM III - R) must be interpreted with great caution. Recent evidence suggests that the diagnosis is being applied to persons with very different types of disorders, and is not being applied to many persons who fail to report past episodes.
Levels of impairment
The suffering inflicted by the major mental disorders to both those who develop the disorders, and to their families, is unmeasureable. These disorders seriously limit all aspects of an individual's functioning. Persons suffering from schizophrenia are unable to develop social relationships, even though they report wanting such relationships (Leveillee, 1994). Consequently, they do not maintain intimate relationships and only infrequently have children. Few are able to obtain or to maintain employment. Among persons suffering from major affective disorders, 12% may never recover to a non - symptomatic state (Keller, Lavori, Endicott, Coryell, & Klerman, 1983; Keller et al., 1992; Winokur, Coryell, Keller, Endicott & Akiskal, 1993), and most relapse (Klerman & Weissman, 1992; Lewinsohn, Zeiss, & Duncan, 1989)(f.1). These individuals endure a special horror; in between acute episodes, they realise that the symptoms are likely to return and that there is little that can be done to prevent a relapse (see for example, Endler, 1990). In addition, persons suffering from the major affective disorders have difficulty maintaining stable relationships as is evidenced by high rates of divorce and separation (Weissman, Bruce, Leaf, Florio, & Holzer, 1991); however, they may have as many children as do non - disordered persons (Slater, Hare & Price, 1971). It is often assumed that the major affective disorders are cyclical or even non - recurrent, and that consequently they have little or no impact on psychosocial functioning during periods of remission. However, recent empirical data seriously challenge this assumption. Psychosocial impairment associated with the major affective disorders is often severe and chronic (see for example, Harrow, Goldberg, Grossman, & Meltzer, 1990; Stoll, Tohen, Baldessarini, et al., 1993; Tohen, Waternaux, & Tsuang, 1990; Klerman & Weissman, 1992). For example, researchers from the U.S. National Collaborative Project on Depression have concluded: "The psychosocial impairment associated with mania and major depression extends to essentially all areas of functioning and persists for years, even among individuals who experience sustained resolution of clinical symptoms." (Coryell, Scheftner, Keller, Endicott, Maser & Klerman, 1993, p. 720).
Premature death
We are currently examining a birth cohort, from a small Nordic country, composed of 324,401 persons (Hodgins, Mednick, Brennan, Schulsinger, & Engberg, in press). Among subjects who were never admitted to a psychiatric hospital, 2.9% of the men and 1.7% of the women died before the age of 45, as compared to 16.6% of the men and 9.2% of the women who had been admitted to a psychiatric hospital with a diagnosis of a major mental disorder. These figures are similar to those reported by others (see for example, Baldwin, 1979; Black, Winokur, & Nasrallah, 1987a & b; Goodwin & Jamison, 1990, ch. 6; Gottesman & Shields, 1982). The increased rates of premature death are due in part to increased rates of death from particular diseases (see for example, Baldwin, 1979), and in part to suicide. Among those suffering from schizophrenia, close to 13% take their own lives (Johns, Stanley, & Stanley, 1986). The numbers of persons suffering from the major affective disorders who commit suicide are difficult to establish. This is partly due to the fact that the majority of persons with these disorders are never treated. In the U.S., less that one - third of those with major affective disorders may receive treatement (Goodwin, & Jamison, 1990, p.3; Shapiro et al., 1984). A recent Finnish investigation examined all suicides during a 12 month period. In a random sample diagnosed using the suicide autopsy procedure, 26% of the males and 46% of the females met the criteria for major depression (Henriksson et al., 1993). Among the 53 adolescents (44 boys and nine girls) who committed suicide in this period, 45% of the boys and 44% of the girls were judged to have suffered from major depression (Marttunen, Aro, Henriksson, &Lonnqvist, 1991). In a study of consecutive admissions to a Belgian hospital, 29% of men and 44% of women who had seriously attempted to kill themselves met criteria for major depression (Linkowski, de Maertelaer, & Mendlewicz, 1985). These findings are similar to older U.S. figures which indicted that 46% of persons who committed suicide suffered from a recurrent major affective disorder (Robins, Murphy, Wilkinson, Gassner, & Kayes, 1959). There are no studies of suicide among persons suffering from bipolar disorder which overcome the problem of documenting suicide among non - treated cases. However, after an extensive review, Goodwin and Jamison (1990) concluded that the "...mortality rate for untreated manic - depressive patients is higher than it is for most types of heart disease and many types of cancer." (p.227) Bipolar disorder may also be associated with adolescent suicide. One study has reported that 22% of a sample of adolescents who killed themselves suffered from bipolar disorder (Brent et al., 1988).
Associated disorders
Personality disorders and other non - major disorders are more prevalent among individuals who suffer from one of the three major disorders, than among samples of the general population. For example, after diagnosing three different samples of persons suffering from schizophrenia, we have calculated that the prevalence of antisocial personality disorder is 13 times more prevalent among those with schizophrenia than in the general population (Hodgins, Toupin, & Cote, in press). While there are few published studies of personality disorders among persons with major depression, all available findings indicate that individuals suffering from major depression are more likely than the general population to manifest other disorders (see for example, Kessler et al., 1994). A study of a cohort of female twins, (a cohort which includes cases of major depression regardless of whether or not they have received treatment) indicated that major depression is associated with high rates of phobias and anxiety disorders. High rates of personality disorders have also been documented (Charney, Nelson, & Quinlan, 1981). Goodwin and Jamison (1990) found only four studies which examined personality disorders among persons suffering from bipolar disorder. All four reported elevated rates of borderline personality disorder and antisocial personality disorder. In children and adolescents suffering from depression, rates of co - morbidity are very high. In a review of the literature on this issue, Angold and Costello (1993) concluded that rates of co - morbid conduct disorder/oppositional defiant disorder ranged from 21% to 83%, co - morbidity with anxiety disorder ranged from 30% to 75%, and co - morbidity with attention deficit disorder ranged from 0% to 57.1%. A recent retrospective study of childhood mental health records showed that a third of a sample of bipolar patients had been seen as children, most for externalizing disorders (Manzano & Salvador, 1993). A prospective study has now shown similar results (Carlson & Weintraub, 1993).
Substance use disorders
Even experienced clinicians using structured diagnostic interview protocols fail to reliably diagnose alcohol and drug use disorders among individuals suffering from major mental disorders (Bryant, Rounsaville, Spitzer, & Williams, 1992). Despite this fact, it is clear that the prevalence of substance abuse and/or dependence has skyrocketed in recent years among persons suffering from major mental disorders. As discussed elsewhere, prevalence rates of co - morbid substance abuse estimated in different studies are not comparable (Cote, Hodgins, Toupin, & Proulx, in press). Consequently, only some examples are presented here. In a cohort composed of all 15,117 persons born in Stockholm in 1953, and followed to age 30, 32.9% of the men with major mental disorders, and 10.0% of the women with major disorders had additional diagnoses of alcohol and/or drug use disorders. (The prevalence is very high given that these were file diagnoses made during a period when little or no attention was paid to co - occurring disorders.)
Among persons suffering from schizophrenia, the prevalence of alcohol and drug use disorders varies from one study to another, but in all studies it is very high (for a review of this work see a special issue of Schizophrenia Bulletin, 16, 1990, especially Mueser et al., 1990; Drake et al., 1990; for a review of studies concerning schizophrenic subjects who abuse alcohol and/or drugs see Ridgely, Goldman, & Talbott, 1986). For example, in a U.S. study of 115 schizophrenic subjects discharged to the community, 45% were using alcohol, and 22% were abusing alcohol (Drake, Osher, & Wallach, 1989). In the ECA study, the prevalence of schizophrenia among those subjects who met the criteria for an alcohol use disorder was four times greater than that for the general population (Helzer & Przybeck, 1988). In three samples of schizophrenic subjects in Montreal, one recruited from the penitentiaries, a second from psychiatric and forensic hospitals, and a third from general hospitals, the prevalence of alcohol use disorders varied from 74% to 23%, the prevalence of drug use disorders varied from 68% to 23% (Cote & Hodgins, 1990; Dube, 1992; Hodgins et al., in press).
In the Epidemiological Catchment Area study, 27% of subjects who had experienced at least one episode of major depression met criteria for a lifetime diagnosis of either an alcohol use disorder, a drug use disorder, or both(f.2). The prevalence of other drug use disorders was 18.0% among subjects with a lifetime diagnosis of major depression and 6.1% among the general population (Regier et al., 1990).
Substance abuse is very common among persons suffering from bipolar disorder. In the ECA study, 56.1% of bipolar patients received an additional diagnosis for alcohol and/or drug use disorders: 43.6% received additional diagnoses of alcohol abuse and/or dependence, and 33.6% received diagnoses of drug abuse and/or dependence (Regier et al., 1990). Three other investigations (Estroff, Dackis, Gold, & Pottash, 1985; Freed, 1969; Morrison, 1974) have reported that 60% to 75% of bipolar patients abuse alcohol.
Crime and violence
Persons who suffer from major mental disorders are more likely than non - disordered persons to commit crimes, and particularly crimes of violence (for review see Hodgins, 1995a; 1994a; 1993). Three lines of research provide support for this conclusion. Studies of unselected birth cohorts followed into adulthood demonstrate that subjects who develop schizophrenia and major affective disorders are much more likely than non - disordered subjects to be convicted for violent and for non - violent crime (Hodgins, 1992; Hodgins et al., in press). In these investigations, subjects with major disorders were convicted, on average, for as many or more offenses than were persons who had never been admitted to a psychiatric ward or who had not been identified as mentally retarded. The offenders with major disorders committed all types of offenses, but the difference between the disordered and non - disordered was greatest for violent offenses.
In addition to these prospective investigations of unselected birth cohorts, crime among persons suffering from major disorders has been studied by following patients discharged from inpatient services. These investigations have consistently shown that patients with major mental disorders commit more crimes and more crimes of violence than do non - disordered adults living in the same community (for reviews see Hodgins, 1993; Link, Andrews, & Cullen, 1992; Steadman, et al., 1993).
The third line of evidence which has addressed the relation between major mental disorders and crime includes diagnostic studies of random samples of convicted offenders. All of the North American studies have reported higher prevalence rates of the major disorders among offenders than in the general population (Hodgins & Cote, 1990). In addition, recent studies of unbiased cohorts of homicide offenders have found that individuals with major mental disorders represent anywhere from 20% to 53% of these cohorts (Cote & Hodgins, 1992; Gabrielsen, Gottlieb, & Kramp, 1987; Lindqvist, 1986).
There may be a difference in rates of crime and violence depending on diagnosis. The birth cohort studies have not distinguished subjects by specific diagnosis. The follow - up studies of patients discharged from hospitals suggest that male schizophrenics are more at risk for criminality than other patients. Similarly, all but one of the North American studies of incarcerated offenders have documented rates of schizophrenia among inmates that far exceed rates in the general population. A recent investigation in Finland which examined all 1423 homicides committed over a 12 year period, found that male schizophrenics without a secondary diagnosis of alcoholism were six times more likely than non - disordered males to kill, while male schizophrenics with alcoholism were seventeen times more likely to kill (Eronen, Tiihonen, & Hakola, 1996). The comparable figures for female schizophrenics were five and eighty - five.
In most studies of criminality and violence among persons suffering from major disorders, more of the offenders than the non - offenders have secondary diagnoses of substance abuse. However, what must be emphasized is that in all of these investigations many of the mentally disordered offenders had no history of drug or alocohol abuse. In fact, alcohol and drugs may play less of a role in the violence of the mentally disordered than in the violence of the non - disordered (Beaudoin, Hodgins, & Lavoie, 1993; Hodgins, 1994b; Lindqvist, 1986).
While historical data are scarce, all available findings indicate that there has been an increase in criminality among persons suffering from major mental disorders. This increase begins to become evident from the late 1940s or early 1950s (Coid, Lewis, & Reveley, 1993; Hodgins & Lalonde, in press; Rabkin, 1979).
Homeless, and infectious disease
Rates of homeless and infectious diseases among persons suffering from major mental disorders, particuliarly hepatitus, tuberculosis, and AIDS, are difficult to document. Homeless persons don't readily accept to participate in diagnostic interviews for research purposes. However, all indicators suggest that many of the homeless suffer from a major disorder and that many develop infectious diseases (Belcher, 1989; Gelberg, Linn, & Leake, 1988; Tessler, & Dennis, 1989). The rates vary no doubt from region to region even within the same country.
CONCLUSION
The above findings, and many, many more too numerous to cite here, indicate that current policies and services available to persons suffering from major mental disorders are inadequate. In order to better serve those directly afflicted, their families, and the society at large, a reorientation of current policies and programmes is in order. Direct services must take account of recent findings on the major disorders, and must be funded and organized in such a way as to respond to the difficulties which these individuals present. In addition to these changes, the new policy and programmes must focus on prevention. Only in this way can we avoid perpetuating the current situation.
REORIENTING POLICY AND SERVICES TOWARDS PREVENTION
As long ago as 1978, the U.S. President's Commission on Mental Health, recommended that the only feasible strategy for dealing with the major disorders, was to begin prevention programmes. Since then, little has been done. In 1994, a committee mandated by the U.S. congress made the following recommendation. "...a critical mass of knowledge relevant to the prevention of mental disorders has accumulated and ... opportunities now exist to effectively use this knowledge to launch a research agenda... This agenda should facilitate development in three major areas: Building the infrastructure to coordinate research and service programs and to train and support new investigators; Expanding the knowledge base for preventive interventions; Conducting well - evaluated preventive interventions." (Mrazek & Haggerty, 1994, p. xii). Canada needs to do likewise.
The motivation for reorienting policy and programmes with regard to the major mental disorders comes not only from the data reviewed above, but also from studies of the cost of caring for persons with major disorders. For example, "...the financial burden of schizophrenia in the United States [is] approximately equal to that of all cancers combined." (Keith, Regier, & Rae, 1991, p. 34). The reason for the optimism concerning prevention comes from the fact that significant proportions of the populations at risk for the major mental disorders can be identified with relative accuracy. Identification of the population at risk is the first step in any prevention strategy (Price, Cowen, Lorion, & Ramos - McKay, 1988).
Family aggregation of the major mental disorders
The identification of populations at risk for the major mental disorders is possible because these disorders are not randomly distributed through the population, but rather they aggregate in a limited number of families. Table 1 presents examples of rates of disorders found among first degree relatives (parents, siblings, and offspring) of persons suffering from major mental disorders. In assessing the risks among the relatives of persons with schizophrenia it is important to remember that very few of them have children (Erlenmeyer - Kimling, Wunsch - Hitzig, & Deutsch, 1980). Consequently, comparisons with the first degree relatives of persons with affective disorders or persons with no disorders are inappropriate. Gottesman & Shields (1982) estimated the morbid risk of schizophrenia among the relatives of individuals with schizophrenia as follows: parents 5.6%, siblings when one parent is schizophrenic 16.7%, siblings when no parent is schizophrenic 9.6%, children 12.8%, children of two schizophrenic parents 46.3%. More recent investigations suggest that these morbid risks are slightly low (Kendler, McGuire, Gruenberg, O'Hare, Spellman, & Walsh, 1993b; Cannon, Mednick, Parnas, Schulsinger, Praestholm, & Vestergaard, in press). It is important to add that the first degree relatives of persons with schizophrenia are also at increased risk for other schizophrenia spectrum disorders (Kendler et al., 1993b). In fact, approximately 40% of them are diagnosed with one or other of the spectrum disorders (Kendler & Gruenberg, 1984).
Recent studies (Grove, Andreasen, Winokur, Clayton, Endicott, and Coryell, 1987; McGuffin, Katz, Aldrich, & Bebbington, 1988; Weissman, Kidd, & Prusoff, 1982; Weissman & Boyd, 1984) provide compelling evidence that the prevalence of the major affective disorders among the biological relatives of patients with major depression far exceed the prevalence in the general population. Table 1 presents for comparison, rates of disorders in the general population. However, the studies of the relatives of persons with major depression included comparison groups composed of relatives of subjects with no disorders. The difference between the rates in the two groups of relatives are much greater than what is observed in Table 1. For example, among the relatives of non - disordered persons, Weissman and colleagues (1982) documented rates of major depression of 3% in men and 9% in women. By contrast, major depression was identified among 11% of the male and 19% of the female relatives of their subjects with mild major depression, and among 9% of the male and 21% of the female relatives of subjects with severe major depression. Similarly, a British investigation (McGuffin, Katz, Aldrich, & Bebbington, 1988) estimated age morbid risk for depression among the relatives of their non - disordered subjects to be 8.9%, as compared to 22.4% among the relatives of subjects with depression.
As is indicated in Table 1, the first degree relatives of persons suffering from bipolar disorder are at increased risk for major affective disorders. All of the family studies to date have indicated that they are at higher risk for major depression than for bipolar disorder. For example, in one of the largest family studies conducted to date, among the relatives of persons with bipolar disorder the prevalence of major depression was higher (23.9%) than the prevalence of bipolar disorder (8.5%) (Andreasen, Rice, Endicott, Coryell, Grove, & Reich, 1987). Also, one - in - two of the offspring of persons suffering from major depression or bipolar disorder developed a major affective disorder by age 20 (Pauls, Morton, & Egeland, 1992; Weissman, Fendrich, Warner, & Wickramaratne, 1992).
It is essential to appreciate the magnitude of these family studies and to underline the rigour with which they were conducted. For example, Andreasen, Rice, Endicott, Coryell, Grove, & Reich (1987) used 942 index subjects diagnosed as having a major affective disorder. Two thousand, two hundred and twenty - six relatives of these patients were interviewed, and information was collected on another 1,197. Strengths of these family studies, other than the large sample sizes, include the use of standardized diagnostic instruments (SADS or SCID) administered by clinicians, documented rates of inter - diagnostician reliability, comparisons of results obtained with interviewed and non - interviewed relatives, and results calculated to take account of the age of relatives. The principal weakness of these family studies concerns the ascertainment of the index subjects. They were all patients. To what extent this biases the results is unknown. Another weakness is that calculations of prevalence rates do not take account of differential death rates among the relatives of persons with major affective disorder and those with no mental disorder.
CONCLUSION
These studies provide compelling evidence that each of the major mental disorders aggregate within a limited number of families. The closer the biological relationship to the index subject, the higher the risk of disorder in the relative. This aggregation allows for the identification of families and children at risk. In all three disorders, the aggregation is due, at least in part, to hereditary factors. Twin studies and adoption studies have confirmed the existence and the strength of these genetic factors (see for example, Goodwin & Jamison, 1990; Gottesman, 1991; Hammen, 1991). These same investigations have also demonstrated that some individuals carry the gene or genes for a disorder without ever developing the disorder. In other words, some genetically vulnerable individuals are being protected - somehow - from developing the disorder. The investigations of series of monozygotic twins who are discordant for one or other of the three major disorders elegantly demonstrate that non - genetic factors determine whether the disorder develops among individuals who are genetically vulnerable for one of these disorders (see for example, Torrey, Bowler, Taylor, & Gottesman, 1994). If these protective factors could be identified prevention would be possible. Similarly, if the negative factors which interact with the genetic vulnerability to determine the disorder, could be identified, prevention could include strategies to eliminate the factors or at least help the risk population to avoid them. Herein lies the importance of identifying the children - at - risk: 1) prospective longitudinal studies of these children and their families could be readily conducted in order to document factors associated with resiliency, and factors which exacerbate the genetic predisposition; and 2) in order to provide these children with mental health services, for the difficulties which they are experiencing and to promote resiliency.
Disorders among the children of parents with major mental disorders
The family studies demonstrated that the offspring of persons with major mental disorders are at increased risk for major mental disorders as adults. However, during childhood many of them experience difficulties to the point of meeting diagnostic criteria for a mental disorder.
In the early 1960s, when it was recognized that there was a hereditary factor contributing to the development of schizophrenia, the National Institutes of Mental Health in the U.S. began funding a number of prospective, longitudinal studies comparing the development of children of schizophrenic mothers to that of children of mothers with no mental disorder. These studies did not use diagnostic criteria to assess the children. However, most used developmental scales, IQ tests, academic performance, teacher ratings, and psychosocial functioning measures. The most consistent and important difficulties shown by a subgroup of the children of schizophrenic mothers from an early age were motor impairments and neuromotor integrative deficits. As they moved into adolescence, difficulties in interpersonal functioning became more and more apparent (Asarnow, 1988). Of all the original schizophrenia high risk studies only the subjects in the Copenhagin project have passed through the age of risk for schizophrenia. In this study, subjects who developed schizophrenia with predominately negative symptoms were described by their teachers in late childhood/early adolesence as passive, socially isolated and unresponsive to praise and were as well, unreponsive on galvanic skin conductance (GSR) measures. By contrast, those who developed schizophrenia with predominately positive symptoms had been described by their teachers as overactive, irritable, distractible and aggressive, and were over - reponsive on GSR measures (Cannon, Mednick, & Parnas, 1990). Almost nothing is known about the children who develop other schizophrenia spectrum disorders, but this same study is suggesting that they suffer some of the same brain damage observed in persons who suffer from schizophrenia (Cannon et al., 1994).
We have recently completed a literature review on the risk of disorders during childhood among offspring with one parent with a lifetime diagnosis of major depression (Lavoie & Hodgins, 1994). All studies indicate high rates of disorder among children of parents with major depression. A meta - analysis (Hunter & Schmidt, 1990; Hunter, Schmidt & Jackson, 1982; slightly modified to accomodate contingency tables, Haccoun, 1994) was conducted using data from the seven published studies which included a control group of children of parents with no mental disorder. A weighted average correlation of 0.27 was obtained between the presence of a lifetime major depressive disorder in the parent and the presence of any mental disorder in the child. The variation of the individual study correlations around the weighted average correlation was not significant (S'Symbol not transcribed'2 'Symbol not transcribed'T = 0; X'Symbol not transcribed'2 = 2.66; p > 0.70) and was attributed to sampling error. A weighted average correlation of 0.23 was obtained between the presence of a lifetime major depressive disorder in the parent and the presence of any affective disorder in the child. The variation around the weighted mean was not significant and was attributed to sampling error (S'Symbol not transcribed'2'Symbol not transcribed'T = 0.0143; X'Symbol not transcribed'2 = 3.70; p > 0.50). We concluded that the findings of the studies are consistent and indicate that children of parents with major depression are more likely than children of parents with no disorder to develop mental disorders.
Table 2 presents data cumulated from these studies. The numbers of subjects for each diagnostic category vary because the different authors do not report results for the same diagnostic categories. Further, and unfortuneately, these studies do not report results for age groups, for children pre - and post - puberty, or by gender. The children studied vary in age from 3to 20 years, with an average age of 11 to 12 years. As shown in Table 2, many of these children are experiencing considerable difficulty. For example, Weissman, Fendrich, Warner, and Wickramaratne (1992) examined 121 children with at least one parent with a lifetime diagnosis of major depression and 53 children of parents with no mental disorder. The offsprings' ages varied from under 12 to 23 years. Diagnoses were made with the Kiddie SADS or SCIDR and RDC. By age 20, over 50% of the offspring of parents with a lifetime diagnosis of major depression met criteria for major affective disorder as compared to 28% of the offspring of non - disordered parents. (The prevalence of major affective disorder in this latter group is surprisingly high.)(f.3) The rate of conduct disorder among the offspring of parents suffering from major depression was high, 40%, compared to that among the offspring of non - disordered parents, 20%. In another study (Hammen, Burge, Burney, & Adrian, 1990), the incidence of major depression up to age 19 was 67% for offspring of parents with major depression, 45% for offspring of medically ill parents, and 12% for offspring of non - disordered parents. Rates of conduct disorder were again elevated among the offspring of persons with major depression, 32%, compared to 8% among the offspring of non - disordered parents.
The rates of alcoholism and conduct disorder are increased by about three - fold among offspring under age 18 of parents with major depressive disorder and secondary alcoholism as compared with offspring of parents with only major depression (Merikangas, Leckman, Prusoff, Pauls, & Weissman, 1985). The prevalence of antisocial personality disorder is also greater among the adult offspring of parents with only major depression as compared to non - disordered parents and is even higher among the adult offspring of parents with major depression and secondary alcoholism (Merikangas et al., 1985; Weissman et al., 1992). The findings presented in Table 2 are not surprising when considered in the light of studies of infants and young children of mothers with depressive symptoms. Even at a very early age, these children are showing impairments in their interactions with their mothers which generalize to interactions with other adults (for a review, see Kratzer & Rubin, 1994).
We have also conducted a similar review of studies of children of parents with bipolar disorder (Lapalme, Hodgins, & LaRoche, 1994). In general, the 26 studies included in our review concur in demonstrating that children of parents with bipolar disorder are at increased risk for mental disorders, particularly affective disorders. The prevalence of disorders among these children was higher than that found among children of parents with no mental disorders, with no affective disorder, with no major mental disorder, or with a physical disorder. Again, a meta - analysis was conducted using data from nine studies which included a comparison group of children of parents with no mental disorder. The meta - analysis indicates that the relation between the prevalence of affective disorders among the children and the parents' diagnosis of bipolar disorder or no mental disorder is constant across these studies and that, on average, the strength of the relation is r = .35. Table 3 presents the cumulated results of these investigations. Again, the number of children assessed for each diagnostic category varies. Results were not reported by age group, for children pre - and post - puberty, or by gender. The average age of the children included in the analyses varied from 5 to 20 years. As can be observed in Table 3, children of parents suffering from bipolar disorder are at significantly increased risk for mental disorders as compared to the children of non - disordered parents. This table also shows that many of these children develop non - affective disorders. Carlson and Weintraub (1993), using data from a prospective longitudinal investigation, have shown that conduct disorder precedes the development of major affective disorders in many of these children. This finding concurs with the clinical observation that adolescents, especially boys, who are developing bipolar disorder are often initially diagnosed as presenting conduct disorder or antisocial personality disorder (Bowden & Sarabia, 1980).
Children of parents with major disorders are invisible
Presently, the children of parents with major depression and bipolar disorder are not being identified and are not receiving mental health services. A recent investigation conducted in Montreal illustrates the situation (Vanharen, LaRoche, Heyman, Massabki, & Colle, 1993). Of one hundred patients (50 inpatients and 50 outpatients) studied, 47 had a total of 138 children. Of the 47 patients who had children, 19 reported that at least one of their children had received some type of mental health service. "Only four of these 19 patients reported that the psychiatrist who treated them had inquired about the mental health of their children. In only one case did the psychiatrist refer the child for professional care." (Vanharen et al., 1993, p. 679) It is important to note that this study was conducted in a hospital in which the child psychiatry department has been particularly active, for a number of years, in describing the needs of this "invisible" population of children. In our experience, mental health professionals treating adults with major depression and bipolar disorder do not generally inquire about the children of their patients. In many cases, we have found, they do not even know if their patients have children.
Identifying the populations at risk for the major mental disorders
The first step to prevention is the identification of the population - at - risk (Price et al., 1988). This could be easily accomplished by identifying the children of adults who are treated for schizophrenia or a major affective disorder. A screening instrument used by adult patients to describe their children was developed and tested by Jellinek, Bishop, & Murphy (1991). It is well accepted and understood by patients and can be easily integrated into routine adult psychiatric services.
While this strategy would identify a large proportion of the children at risk for the major affective disorders, the identification of most of the children at risk for schizophrenia will be more difficult. The children of persons who suffer from schizophrenia constitute a risk population and can be identified by those treating the parent. However, such a procedure will identify only one - in - twenty persons who will eventually develop schizophrenia. Many of the others are to be found within the families in which the schizophrenic spectrum disorders occur at higher rates than in the general population. As many of the individuals with spectrum disorders are not seen in treatment, the best strategy now available is the identification of the first degree relatives of schizophrenic patients. These relatives will include a large number of children at risk for schizophrenia. It may be argued that identifying a population at risk for major mental disorders would stigmatize these children and/or lead to psychological problems as a result of a self - fulfilling prophecy. However, in this era when the news media report discoveries of the role of genetic factors in various disorders on a weekly bases, it is becoming common knowledge that hereditary factors are involved in the development of the major mental disorders. For example, many non - disordered parents with a first degree relative who suffers from schizophrenia worry that their child will develop this disorder. They often search for signs in their child's behaviour that he or she is disordered. They have nowhere to turn for help or support. Parents who suffer from a major mental disorder and their spouses feel guilty and worry that they will transmit the disorder to their children. Again, these couples often have no one with whom they can discuss these feelings and no one to provide skills training which may lessen the negative impact of their disorder on their children. In this context, and given the knowledge currently available, the advantages of early identification of these children at risk far out - weigh the possible disadvantages.
It is necessary to acknowledge that using family history of mental disorder as an index of risk will only identify some portion of the children who are at risk for the major mental disorders. Consider the analogy with breast cancer. In this disorder, most cases are sporadic, only a few hereditary. Yet no one denies the importance of early intervention with the daughters of women who have had breast cancer, even though all the other women - at - risk cannot yet be identified. Similarly, because we cannot yet identify all the children who will eventually develop major mental disorders is no reason not to begin working with those that we know are at risk.
There is presently no way of knowing which of the children in these families are at genetic risk for the major mental disorders. No biological markers exist either for the genes associated with the major disorders or for the disorders (for a review, see Lane & Palmour, 1994; Gottesman, 1991). This situation is likely to change in the coming years, as either biological markers for the genes and/or for the disorder are discovered. Such knowledge will permit accurate identification of the children at risk for the major disorders. Presently, by identifying children of parents with a major affective disorder or those within families with schizophrenia spectrum disorders, as a risk population, we are over - predicting the numbers who will develop major disorders in adulthood. Among children within families where schizophrenia spectrum disorders aggregate, investigations indicate that approximately 60% will not develop a disorder within the schizophrenia spectrum. Among children with parents who have a major affective disorder, the most recent evidence suggests that one - in - two will not develop a major affective disorder.
Over - prediction of the children at risk for major mental disorders should in no way be used as an excuse for continuing the present practice of not doing anything. Over - prediction is inconsequential for several reasons. One, the types of services to be offered to these children would be helpful to them all, regardless of whether or not they are genetically vulnerable for a major mental disorder. These children are being raised in families in which one parent suffers from a major mental disorder, or a severe personality disorder. That fact, in and of itself, is sufficient to signal their need for services. The kinds of services likely to be offered include helping families develop better management strategies, developing non - conflictual communication styles, parenting courses, setting up contingency plans for periods when the disordered parent is hospitalized or not functioning, self - esteem programmes, discussions of the parent's illness, of suicide attempts, etc. (see for example, Beardslee et al., 1993). These interventions would be useful and helpful to both the children who are genetically vulnerable and to those who are not genetically vulnerable. They would in no way harm those who are not genetically vulnerable.
Over - prediction of the children - at - risk for the major mental disorders in adulthood is inconsequential for a second reason. The children in these families, at one time or another, note the aggregation of disorders in their family as compared to the families of their friends. They wonder if they will succumb to the disorder. This seems to be particularly true of children of parents with a major affective disorder. Without professional support, it is often difficult for parents to discuss this issue with their children and to provide them with accurate information about the disorder. Prevention programmes aimed at the children of parents with major disorders could deal directly with this issue.
The third reason why over - prediction must not be used as an excuse to do nothing, is that mentally disordered parents have negative effects on their children. As noted above, these effects may begin to appear even in the early months of life and many of these children develop problems severe enough to meet diagnostic criteria for a mental disorder.
Prevention Programmes(f.4)
Once the policy decision has been made to identify the children - at - risk for major mental disorders and to provide them with services, the next step is to establish an infrastructure to co - ordinate research and service efforts designed to assess the needs of these children and to evaluate the efficacy of preventive interventions. (This is the recommendation noted previously, Mrazek & Haggerty, 1994).
The content of prevention programmmes will differ for the two populations: (1) children of parents who suffer from a major mental disorder; and (2) children with non - disordered parents who may have inherited a vulnerability for one of the major disorders. Consider first, children being raised in a family in which one parent has a major disorder. Most of these parents suffer from a major affective disorder and a few from schizophrenia. The first step in prevention of disorders in the children is adequate and appropriate treatment of the disordered parent. Adequate treatment involves not only medications to treat acute symptomalogy and to stabilize mood cycles, but also cognitive and behavioural interventions aimed at increasing self - esteem, and improving life and social skills (Corrigan, 1995; Hunter, 1995). The next step is to provide the couple with accurate information about the disorder, its treatment and course, and if necessary to provide them with programmes to facilitate communication, and conflict resolution. The third step is to ensure that these couples can provide good parenting to their children. This may necessitate parenting courses, helping these couples discuss the parental disorder openly with the children, helping the couple develop strategies for caring for the children during periods when the disordered parent requires hospitalization. Finally, assessments of these children - at - risk are necessary in order to determine if they require interventions to help them develop effective coping skills in stressful situations, problem solving skills, and good self esteem. This fourth step is where we need to begin with the children who have parents with no major disorder, but who may have inherited a vulnerability for a major disorder. Very little is known about them. Needs assessments of these children are essentiel and urgent to determine if problems can be identified and treated at a young age. Both of these groups of children would probably benefit from programmes that are effective in increasing competency and resilience in other populations (see for example Spivack, Platt, & Shure, 1976; the programmes described by Mrazek & Haggery, 1994; Piotrkowski, Collins, Knitzer, & Robinson, 1994; Zigler & Styfco, 1994).
Growth in knowledge about the factors, both protective and harmful, associated with each of the major disorders can be used to make prevention programmes more specific to each risk group. Interestingly, in the last few years, a common pattern has emerged in the research on the etiologies of the three major mental disorders. It appears as if the genetic vulnerabilities associated with each of the disorders significantly increases the fragility of the central nervous system. Other non - genetic factors, biological or psychosocial, damage the fragile CNS. Consequently, the same event will cause irreversible damage to the CNS of the genetically vulnerable foetus or child, but not to the non - genetically vulnerable child (for a detailed discussion, see Hodgins, 1995b; Post, Weiss, & Leverich, 1994). For example, recent investigations on the etiology of schizophrenia suggest that in addition to genetic vulnerability, prenatal factors, particularly events occuring during the second trimester of pregnancy, may be responsible for much of the CNS damage observed in adults suffering from schizophrenia. Evidence to date suggests that these are negative events (the mother learning that her husband had been killed, the mother being malnourished, the mother getting a flu virus) but not rare events. However, while these events adversely affect the foetuses who are genetically vulnerable to schizophrenia, they do not appear to damage the others. If this work is further substantiated, good prenatal care for women within the families - at - risk could prove to be an important component of an effective prevention strategy (see for example, Mednick, Cannon, Barr, & LaFosse, 1991; Schulsinger, & Parnas, 1990). As noted earlier, such a prevention programme would in no way be harmful to the babies who are not genetically vulnerable for schizophrenia. The other factors which have been repeatedly identified as being determinants of schizophrenia are removal of the child from the mother during the early months of life (Schulsinger, & Parnas, 1990) and family communication style (Tienari et al, 1987). As is the case with perinatal factors, the genetically vulnerable children appear to be damaged by these factors, whereas the non - genetically vulnerable children overcome them with no long - term sequelae. These two issues could be addressed within a prevention strategy, and again, the proposed interventions would be unlikely to harm the child who is not genetically vulnerable for schizophrenia.
Much less is known about etiology of the major affective disorders. Factors which have been identified to date include dysfunctional and/or dysynchronous neuroendocrine rhythms (Wehr, 1992a, & b), and excessive negative life events combined with the personality trait of neuroticism (Kendler et al., 1993c, & d). Accumulation of stress may cause changes in the CNSs of children who carry a genetic vulnerability to a major affective disorder but not to other children. In time, these abnormalities in the CNS lead to the symptoms of a major affective disorder (Post et al, 1994). Prevention strategies could consequently test the effectiveness of teaching individuals within the families - at - risk to structure daily activities (eating, sleeping) so as to reguliarize bodily rhythms (Frank, 1994), problem solving, strategies for coping with stress, and relaxation techniques. Again, none of these interventions would be detrimental to the children within these families who are not at genetic risk for a major affective disorder.
Conclusion
Much scientific evidence is available to permit us to begin developing prevention programmes for children who are at risk for the major mental disorders. Because we do not yet know exactly why and how these disorders develop is no reason to not begin testing the effectiveness of prevention interventions. We do know who the risk populations are, and we do know that they are at considerable risk as adults for major mental disorders, premature death, substance abuse, criminality, violence, homelessness, and infectious disease. The question may be posed whether it is morally acceptable not to provide help to these children given what we know.
This work was completed with funds from the Social Sciences and Humanities Research Council, the Conseil Quebecois de la Recherche Sociale, the FCAR, and the Strategic Fund for Children's Mental Health.
For reprints, write to Dr. S. Hodgins, Department of Psychology, Universite de Montreal, C.P. 6128, succ. Centre - ville, Montreal (Quebec) H3C 3J7.
References
Andreasen, N.C., Rice, J., Endicott, J., Coryell, W., Grove, W.M., & Reich, T. (1987). Familial rates of affective disorder. Archives of General Psychiatry, 44, 461 - 469.
Angold, A., & Costello, E. J. (1993). Depressive comorbidity in children and adolescents: Empirical, theoretical, and methodological issues. American Journal of Psychiatry, 150, 1779 - 1791.
Asarnow, J.R. (1988). Children at risk for schizophrenia: Converging lines of evidence. Schizophrenia Bulletin, 14, 613 - 631.
Asarnow, J.R., & Koegel (1994). Prevention of mental disorders in children. In P.J. Mrazek and R.J. Haggerty (Eds.), Reducing risks for mental disorders: Frontiers for preventive intervention research (pp. 3 - 22). Washington, D.C.: National Academy Press.
Baldwin, J.A. (1979). Schizophrenia and physical disease. Psychological Medicine, 9, 6]1 - 618.
Bauwens, F., Tracy, A., Pardoen, D., Vander Elst, M., & Mandlewicz, J. (1991). Social adjustment of remitted bipolar and unipolar out - patients. British Journal of Psychiatry, 159, 239 - 244.
Beardslee, W.R., Salt, P., Porterfiels, K., Rothberg, P.C., Van de Velde, P., Swatling, S., Hoke, L., Moilanen, D.L., & Wheelock, I. (1993). Comparison of preventive interventions for families with parental affective disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 32, 254 - 263.
Beaudoin, M.N., Hodgins, S., & Lavoie, F. (1993). Homicide, schizophrenia and substance abuse or dependency. Canadian Journal of Psychiatry, 38, 1 - 7.
Belcher, J.R. (1989). On becoming homeless: A study of chronically mentally ill persons. Journal of Community Psychology, 17, 173 - 185.
Black, D.W., Winokur, G., & Nasrallah, A. (1987a). Is death from natural causes still excessive in psychiatric patients? A follow - up of 1593 patients with major affective disorder. The Journal of Nervous and Mental Disease, 175, 674 - 680.
Black, D.W., Winokur, G., & Nasrallah, A. (1987b). Suicide in subtypes of major affective disorder: A comparison with general population suicide mortality. Archives of General Psychiatry, 44, 878 - 880.
Bowden, C.L., & Sarabia, F. (1980). Diagnosing manic - depressive illness in adolescents. Comprehensive Psychiatry, 21, 263 - 269.
Brent, D.A., Perper, J.A., Goldstein, C.E., Kolko, D.J., Allan, M.J., Allman, C.J., & Zelenak, J.P. (1988). Risk factors for adolescent suicide: A comparison of adolescent suicide victims with suicidal inpatients. Archives of General Psychiatry, 45, 581 - 588.
Bryant, K.J., Rounsaville, B., Spitzer, R.L., & Williams, J.B.W. (1992). Reliability of dual diagnosis: Substance dependence and psychiatric disorders. The Journal of Nervous and Mental Disease, 180, 251 - 257.
Cannon, T.D., Mednick, S., & Parnas, J. (1990). Antecedents of predominantly negative and predominantly positive symptom schizophrenia in a high risk population. Archives of General Psychiatry, 47, 622 - 632.
Cannon, T.D., Mednick, S., &., Parnas, J., Schulsinger, F., Praestholm, J., & Vestergaard, A. (1994). Developmental brain abnormalities in the offspring of schizophrenic mothers: II structural brain characteristics of schizophrenia and schizotypal personality disorder. Archives of General Psychiatry, 51, 955 - 962.
Carlson, G.A., & Weintraub, S. (1993). Childhood behavior problems and bipolar disorder - relationship or coincidence? Journal of Affective Disorders, 28, 143 - 153.
Charney, D.S., Nelson, J.C., & Quinlan, D.M. (1981). Personality traits and disorder in depression. American Journal of Psychiatry, 138, 1601 - 1604.
Coid, B., Lewis, S.W., & Reveley, A.M. (1993). A twin study of psychosis and criminality. British Journal of Psychiatry, 162, 87 - 92.
Corrigan, P.W. (1995). Wanted: Champions of psychiatric rehabilitation. American Psychologist, 50, 514 - 521.
Coryell, W., Scheftner, W., Keller, M., Endicott, J., Maser, J., & Klerman, G.L. (1993). The enduring psychosocial consequences of mania and depression. American Journal of Psychiatry, 150, 720 - 727.
Cote, G., & Hodgins, S. (1990). Co - occurring mental disorders among criminal offenders. Bulletin of the American Academy of Psychiatry and the Law, 18, 271 - 283.
Cote, G., & Hodgins, S. (1992). The prevalence of major mental disorders among homicide offenders. International Journal of Law and Psychiatry, 15, 89 - 99.
Cote, G., Hodgins, S., Toupin, J., & Proulx, J. (In press). Les problemes toxicomaniaques et la conduite antisociale chez les sujets en demande d'aide psychologique dans une salle d'urgence generale. Les actes du colloque de psychiatrie et neurologie de langue francaise. Paris: Masson.
Dinges, N.G. (1994). Mental health promotion. In P.J. Mrazek and R.J. Haggerty (Eds.), Reducing risks for mental disorders: Frontiers for preventive intervention research (pp. 23 - 37). Washington, D.C.: National Academy Press.
Drake, R.E., Osher, F.C., Noordsy, D.L., Hurlbut, S.C., Teague, G.B., & Beaudett, M.S. (1990). Diagnosis of alcohol use disorders in schizophrenia. Schizophrenia Bulletin, 16, 51 - 67.
Drake, R.E., Osher, T.C., & Wallach, M.A. (1989). Alcohol use and abuse in schizophrenia: A prospective community study. The Journal of Nervous and Mental Disease, 177, 408 - 414.
Dube, M. (1992). Une comparaison entre l'histoire des comportements d'agression des hommes et des femmes souffrant de schizophrenie et ceux et celles ne manifestant aucun trouble mental grave. Unpublished master's thesis, Universite de Montreal.
Elkin, I. (1994). The NIMH treatment of depression collaborative research program: Where we began and where we are. In A.E. Bergin & S.L. Garfield (Eds.). Handbook of Psychopathology and behavior change (pp. 114 - 139). New York: Wiley.
Endler, N.S. (1990). Holiday of darkness: A psychologist's personal journey out of his depression. Toroto: Wall & Thompson.
Erlenmeyer - Kimling, L., Wunsch - Hitzig, R.A., & Deutsch, S. (1980). Family formation by schizophrenics. In L.N. Robins, P.J. Clayton, & S.K. Wing (Eds.), The Social Consequences of Psychiatric Illness. New York: Brunner/Mazel.
Eronen, M., Tiihonen, J., & Hakola, P. (1996). Mental disorders and homicidal behavior. Schizophrenia Bulletin, 22.
Estroff, T.W., Dackis, C.A., Gold, M.S., & Pottash, A.L.C. (1985). Drug abuse and bipolar disorders. International Journal of Psychiatry and Medicine, 15, 37 - 40.
Frank, E. (1994, June). Development of new psychotherapies. Paper presented at the First International Conference on Bipolar Disorder, Pittsburgh.
Freed, E.X. (1969). Alcohol abuse by manic patients. Psychological Reports, 25, 280.
Gabrielsen, G., Gottlieb, P., & Kramp, P. (1987). The increase in homicide in Copenhagen 1959 - 1963 statistical analysis. Technical Report, Institute of Theoretical Statistics Copenhagen Business School, Denmark.
Gelberg, L., Linn, L.S., & Leake, B.D. (1988). Mental health, alcohol and drug use, and criminal history among homeless adults. American Journal of psychiatry, 145, 191 - 196.
Glynn, S., Mueser, K., & Herbert, J. (1.994). Treatment of adult psychiatric disorders: Implications for prevention efforts. In P.J. Mrazek and R.J. Haggerty (Eds.), Reducing risks for mental disorders: Frontiers for preventive intervention research (pp. 89 - 128). Washington, D.C.: National Academy Press.
Gold, P.W., Goodwin, F.K., & Chrousos, G.P. (1988a). Clinical and biochemical manifestations of depression. The New England Journal of Medicine, 319, 348 - 353.
Gold, P.W., Goodwin, F.K., & Chrousos, G.P. (1988b). Clinical and biochemical manifestations of depression. The New England Journal of Medicine, 319, 413 - 420.
Goodwin, F.D., & Jamison, K.R. (1990). Manic - depressive illness. New York: Oxford University Press.
Gordon, R.S. (1983). An operational classification of disease prevention. Public Health Reports, 98, 107 - 109.
Gottesman, I.I. (1991). Schizophrenia Genesis: The origins of madness. New York: W.H. Freeman and Company.
Gottesman, I.I., & Shields, J. (1982). The social biology of schizophrenia. The Epigenetic Puzzle (pp. 187 - 194). Cambridge: Cambridge University Press.
Grove, W.M., Andreasen, N.C., Winokur, G., Clayton, P.J., Endicott, J., & Coryell, W.H. (1987). Primary and secondary affective disorders: Unipolar patients compared on familial aggregation. Comprehensive Psychiatry, 28, 113 - 126.
Haccoun, R. (1994). Personal communication on the use of phi correlation coefficient for the meta - analysis.
Hammen, C. (1991). Depression runs in families: The social context of risk and resilience in children of depressed mothers. New York: Springer - Verlag.
Hammen, C., Burge, D., Burney, E., & Adrian, C. (1990). Longitudinal study of diagnoses in children of women with unipolar and bipolar affective disorder. Archives of General Psychiatry, 47, 1112 - 1120.
Harrow, M., Goldberg, J.F., Grossman, L., & Meltzer, H. (1990). Outcome in manic disorders. Archives of General Psychiatry, 47, 665 - 671.
Helzer, J.E., & Przybeck, T.R. (1988). The co - occurrence of alcoholism with other psychiatric disorders in the general population and its impact on treatment. Journal of Studies on Alcohol, 49, 219 - 224.
Henriksson, M.M., Aro, H.M., Marttunen, M.J., Heikkinln, M.E., Isometsa, E.T., Kuoppasalmi, K.I., & Lonnqvisv, J.K. (1993). Mental disorders and comorbidity in suicide. American Journal of Psychiatry, 150, 935 - 940.
Hodgins, S. (1995a). Major mental disorder and crime: An overview. Psychology, Crime and Law, 2, 5 - 17.
Hodgins, S. (1995b). Une recension des e'crits portant sur les facteurs de risque des trorbles mentaux graves. Report submitted to the CQRS.
Hodgins, S. (1994a). Schizophrenia and violence: Are new mental health policies needed? Journal of Forensic Psychiatry, 5, 473 - 477.
Hodgins, S. (1994b). Letter to the Editor. Archives General of Psychiatry, 51, 71 - 72.
Hodgins, S. (1993). The criminality of mentally disordered persons. In S. Hodgins (Ed.), Mental Disorder and Crime (pp. 1 - 21). Newbury Park, CA: Sage.
Hodgins, S. (1992). Mental disorder, intellectual deficiency and crime: Evidence from a birth cohort. Archives of General Psychiatry, 49, 476 - 483.
Hodgins, S., & Cote, C. (1990). The prevalence of mental disorders among penitentiary inmates. Canada's Mental Health, 38, 1 - 5.
Hodgins, S., & Lalonde, N. (in press). Major mental disorders and crime: Changes over time? In P. Cohen, L. Robins & C. Slomkowski (Eds.), Where and when: Geographical and historical aspects of psychopathology. Mahwah, NJ: Lawrence Erlbaum Associates.
Hodgins, S., Mednick, S.A., Brennan, P., Schulsinger, F., & Engberg, M. (in press). Mental disorder and crime: Evidence from a Danish birth cohort. Archives of General Psychiatry.
Hodgins, S., Toupin, J., & Cote, G. (in press). Schizophrenia and antisocial personality disorder: A criminal combination. In L.B. Schlesinger (Ed.), Explorations in Criminal Psychopathology: Clinical Syndromes with Forensic Implication. Spingfield, IL: Charles C. Thomas Publisher.
Hunter, R.H. (1995). Benefits of competency - based treatment programs. American Psychologist, 50, 509 - 513.
Hunter, J.E., & Schmidt, F.L. (1990). Methods of meta - analysis: correcting error and bias in research findings. Newberry Park, Sage.
Hunter, J.E., Schmidt, F.L., & Jackson, G.B. (1982). Meta - analysis: Cumulating research findings across studies. Beverley Hills, CA, Sage.
Jellinek, M.S., Bishop, S.J., & Murphy, J.M. (1991). Screening for dysfunction in the children of outpatients at a psychopharmacology clinic. American Journal of Psychiatry, 148, 1031 - 1036.
Johns, C.A., Stanley, M., & Stanley, B. (1986). Suicide in schizophrenia. Annals of the New York Academy of Science, 487, 294 - 299.
Keith, S.J., Regier, D.A., & Rae, D.S. (1991). Schizophrenic disorders. In L.N. Robins, & D.A. Regier (Eds). Psychiatric Disor - ders in America (pp. 33 - 52). New York: The Free Press.
Keller, M.B., Lavori, P.W., Endicott, J., Coryell, W., & Klerman, G. (1983). Double depression: Two - year follow - up. American Journal of Psychiatry, 140, 689 - 694.
Keller, M.B., Lavori, P.W., Mueller, T.I., Endicott, J., Coryell, W., Hirschfeld, R.M.A., & Shea, T. (1992). Time to recovery, chronicity, and levels of psychopathology in major depression. Archives of General Psychiatry, 49, 809 816.
Kendler, K.S., & Gruenberg, A.M. (1984). An independent analysis of the Danish Adoption Study of schizophrenia. Archives of General Psychiatry, 41, 555 - 564.
Kendler, K.S., McGuire, M., Gruenberg, A.M., O'Hare, A., Spellman, M., & Walsh, D. (1993b). The Roscommon Family Study. Archives of General Psychiatry, 50, 527 - 540.
Kendler, K.S., Neale, M.C., Kessler, R.C., Heath, A.C., & Eaves, L.J. (1993a). Major depression and phobias: the genetic and environmental sources of co - morbidity. Psychological Medicine, 23, 361 - 371.
Kendler, K.S., Neale, M.C., Kessler, R.C., Heath, A.C., & Eaves, L.J. (1993c). A Longitudinal Twin Study of Personality and Major Depression in Women. Archives of General Psychiatry, 50, 853 - 862.
Kendler, K.S., Kessler, R.C., Neale, M.C., Heath, A.C., & Eaves, L.J. (1993d). the Prediction of Major Depression in Women: Toward an Integrated Etiologic Model. American Journal of Psychiatry, 150, 1139 - 1148.
Kessler, R.C., McGonagle, KA., Zhao, S., Nelson, C.B., Hughes, M., Eshleman, S., Wittchen, H. - U., Kendler, K.S. (1994). Lifetime and 12 - month prevalence of DSM - III - R psychiatric disorders in the United States, Archives General of Psychiatry, 51, 8 - 19.
Klerman, G.L., & Weissman, M.M. (1992). The Course, Morbidity, and Costs of Depression. Archives of General Psychiatry, 49, 831 - 834.
Kratzer, L., & Rubin, N. (1994). A review of studies of mothers with depression and their young children. In S. Hodgins (Ed.). Children at risk for major affective disorders (pp. 196 - 237). Report commissioned by the Minister of Health, Canada.
Lane, C., & Palmour, R. (1994). Are there biological markers to indicate risk of affective disorders in children? In S. Hodgins (Ed.) Children at risk for major affective disorders (pp. 149 - 195). Report commissioned by the Minister of Health, Canada.
Lapalme, M., Hodgins, S., & LaRoche, C. (1994). Risk of mental disorders among children with a parent who suffers from bipolar disorder. In S. Hodgins (Ed.) Children at risk for major affective disorders (pp. 93 - 140). Report commisioned by the Minister of Health, Canada.
Lavoie, F., & Hodgins, S. (1994). Mental disorders among children with one parent with a lifetime diagnosis of major depression. In S. Hodgins (Ed.). Children at risk for major affective disorders (pp. 37 - 82). Report commissioned by the Minister of Health, Canada.
Leveillee, S. (1994). Evaluation multidimensionnelle du support social des sujets schizophrenes. Unpublished doctoral thesis, Universite de Montreal.
Lewinsohn, P.M., Zeiss, A.M., & Duncan, E.M. (1989). Probability of relapse after recovery from an episode of depression. Journal of Abnormal Psychology, 98, 107 - 116.
Lindqvist, P. (1986). Criminal homicide in Northern Sweden 1970 - In 1981: Alcohol intoxication, alcohol abuse and mental disease. International Journal of Law and Psychiatry, 8, 19 - 37.
Link, B.G., Andrews, H., & Cullen, F.T. (1992). The violent and illegal behaviour of mental patients reconsidered. American Sociological Review, 57, 275 - 292.
Linkowski, P., de Maertelaer, V., & Mendlewicz, J. (1985). Suicidal behaviour in major depressive illness. Acta Psychiatrica Scandinavica, 72, 233 - 238.
Manzano, J., & Salvador, A. (1993). Antecedents of severe affective (mood) disorders. Patients examined as children or adolescents and as adults. Acta Paedopsychiatrica, 56, 11 - 18.
Marttunen, M.J., Aro, H.M., Henriksson, M.M., & Lonnqvist, J.K. (1991). Mental disorders in adolescent suicide. DSM - III - R Axes I and 11 diagnoses in suicides among 13 - to 19 - year - olds in Finland. Archives of General Psychiatry, 48, 834 - 839.
McGuffin, P., Katz, R., Aldrich, J., & Bebbington, P. (1988). The camberwell collaborative depression study. II. Investigation of family members. British Journal of Psychiatry, 152, 766 - 774.
Mednick, S.A., Cannon, T.D., Barr, C.E., & LaFosse, J.M. (1991). Developmental neuropathology of schizophrenia. Series A: Life Sciences, vol. 17, New York: Plenum Press.
Merikangas, K.R., Leckman, J.F., Prusoff, B.A., Pauls, D.L., & Weissman, M.M. (1985). Familial transmission of depression and alcoholism. Archives of General Psychiatry, 42, 367 - 372.
Miklowitz, D.J., Goldstein, M.J., Nuechterlein, K.H., Snyder, K.S., & Mintz, J. (1988). Family factors and the course of bipolar affective disorder. Archives of General Psychiatry, 45, 225 - 231.
Morrison, J.R. (1974). Bipolar affective disorder and alcoholism. American Journal of Psychiatry, 131, 1130 - 1133.
Mrazek, P.J., & Haggerty, R.J. (1994). Reducing risks for mental disorders: Frontiers for preventive intervention research. Washington, D.C.: National Academy Press.
Mueser, K.T., Yarnold, P.R., Levinson, D.F., Singh, H., Bellack, A.S., Kee, K., Morrison, R.L., & Yadalam, K.G. (1990). Prevalence of substance abuse in schizophrenia. Schizophrenia Bulletin, 16, 31 - 56.
Pardoen, D., Bauwens, F., Tracy, A., Martin, F., Mendlewicz, J. (1993). Self - esteem in recovered bipolar and unipolar out - patients. British Journal of Psychiatry, 163, 755 - 762.
Pauls, D.L., Morton, L.A., & Egeland, J.A. (1992). Risks of affective illness among first - degree relatives of bipolar I old - order Amish probands. Archives of General Psychiatry, 49, 703 - 708.
Piotrkowski, C.S., Collins, R.C., Knitzer, J., & Robinson, R. (1994). Strengthening mental health services in head start: A challenge for the 1990s. American Psychologist, 49, 133 - 139.
Post, R.M. (1993). Issues in the long - term management of bipolar affective illness. Psychiatric Annal, 23, 86 - 93.
Post, R.M., Weiss, S.R.B., & Leverich, G.S. (1994). Recurrent affective disorder: Roots in developmental neurobiology and illness progression based on changes in gene expression. Development and Psychopathology, 6, 781 - 813.
Price, R.H., Cowen, E.L., Lorion, R.P., & Ramos - McKay, J. (1988). 14 Ounces of Prevention. Washington, D.C.: American Psychological Association.
Rabkin, J.G. (1979). Criminal behaviour of discharged mental patients. A critical appraisal of the research. Psychological Bulletin, 86, 1 - 29.
Regier, D.A., Farmer, M.E., Rae, D.S., Locke, B.Z., Keith, S.J., Judd, L.L., & Goodwin, F.K. (1990). Co - morbidity of mental disorders with alcohol and other drug abuse. Journal of the American Medical Association, 264, 2511 - 2518.
Rice, J.P., Rochberg, N., Endicott, J., Lavori, P.W., & Miller, C. (1992). Stability of psychiatric diagnoses: An application to the affective disorders. Archives of General Psychiatry, 49, 824 - 830.
Ridgely, M.S., Goldman, H.H., & Talbott, J.A. (1986). Chronic mentally ill young adults with substance abuse problems: A review of relevant literature and creation of a research agenda. Baltimore, MD: University of Maryland school of medicine. Mental Health Policy Studies.
Robins, E., Murphy, G.E., Wilkinson, R.H., Gassner, S., & Kayes, J. (1959). Some clinical considerations in the prevention of suicide based on a study of 134 successful suicides. American Journal of Public Health, 49, 888 - 899.
Robins, L.N., & Regier, D.A. (1991). Psychiatric disorders in America: The Epidemiologic catchment area study. New York: The Free Press.
Rutter, M. (1994). Genetic knowledge and prevention of mental disorders. In P.J. Mrazek and R.J. Haggerty (Eds.), Reducing risks for mental disorders: Frontiers for preventive intervention research (pp. 157 - 179). Washington, D.C.: National Academy Press.
Schulsinger, F., & Parnas, J. (1990). Risk factors in schizophrenia: Interaction between genetic liability and environmental factors. In A. Kales, C.N. Stefanis, & J. Talbott (Eds.). Recent advances in schizophrenia (pp. 117 - 129). New York: Springer Verlag.
Shapiro, S., Skinner, E.A., Kessler, L.G., Von Korff, M., German, P.S., Tischler, G.R., Leaf, P.J., Benham, L., Cottler, L., & Regier, D.A. (1984). Utilization of health and mental health services. Three epidemiologic catchment area sites. Archives of General Psychiatry, 41, 971 - 978.
Slater, E., Hare, E.H., & Price, J. (1971). Marriage and fertility of psychotic patients compared with national data. In I.I. Gottesman & L. Erlenmeyer - Kimling (Eds.), Fertility and reproduction in physically and mentally disordered individuals. Social Biology, 18, Supplement.
Spitzer, R.L., Williams, J.B.W., Gibbon, M., & First, M.B. (1992). The structured clinical interview for DSM - III - R (SCID). I. History, rationale, and description. Archives of General Psychiatry, 49, 624 - 629.
Spivack, G., Platt, J.J., & Shure, M.B. (1976). The problem - solving approach to adjustment. San Francisco, CA: Jossey - Bass.
Steadman, H.J., Monahan, J., Robbins, P.C., Appelbaum, P., Grisso, T., Klassen, D., Mulvey, E.P., & Roth, L. (1993). From dangerousness to risk assessment: Implications for appropriate research strategies. In S. Hodgins (Ed). Mental disorder and crime (pp. 39 - 22). Newbury Park, CA: Sage.
Stoll, A.L., Tohen, M., Baldessarini, R.J., Goodwin, D.C., Stein, S., Katz, S. Geenens, D., Swinson, R., Goethe, J.W., & Glashan, T. (1993). Shifts in diagnostic frequencies of schizophrenia and major affective disorders at six North American psychiatric hospitals. American Journal Psychiatry, 150, 1668 - 1673.
Suppes, T., Baldessarini, R.J., Faedda, G.I., & Tohen, M. (1991). Risk of recurrence following discontinuation of lithium treatment in bipolar disorder. Archives of General Psychiatry, 48, 1082 - 1088.
Tessler, R.C., & Dennis, D.L. (1989). A synthesis of NlMH - funded research concerning persons who are homeless and mentally ill. Research report.
Thase, M. (1994). What's become of this good prognosis illness? First International Conference on Bipolar Disorder.
Tienari, P., Sorri, A., Lahti, I., Naarala, M., Wahlberg, K., Moring, J., Pohjola, J., & Wynne, L. (1987). Genetic and psychosocial factors in schizophrenia: The Finnish adoptive family study. Schizophrenia Bulletin, 13, 477 - 484.
Tohen, M., Waternaux, C.M., & Tsuang, M.T. (1990). Outcome in mania: A 4 - year prospective follow - up of 75 patients utilizing survival analysis. Archives General of Psychiatry, 47, 1106 - 1111.
Torrey, E.F., Bowler, A.E., Taylor, E.H., & Gottesman, I.I. (1994). Schizophrenia and Manic Depressive Disorder, New York: Basic Books.
Vanharen, J., LaRoche, C., Heyman, M., Massabki, A., & Colle, L. (1993). Have the invisible children become
visible? Canadian Journal of Psychiatry, 38, 678 - 680. Wehr, T.A. (1992a). Seasonal vulnerability to depression: Implications for etiology and treatment. L'Encephale, 18, 479 - 483.
Wehr, T.A. (1992b). Improvement of depression and triggering of mania by sleep deprivation. Journal of the American Medical Association, 267, 548 - 551.
Weissman, M.M., & Boyd, J.H., (1984). The epidemiology of mental disorders. In: R.M. Post and J.C. Ballenger (Eds.), Neurobiology of Mood Disorders. (pp. 60 - 75). Baltimore: Williams & Wilkins.
Weissman, M.M., Bruce, M.L., Leaf, P.J., Florio, L.P., & Holzer, C.III. (1991). Affective Disorders. In L.N. Robins & D. Regier (Eds.), Psychiatric Disorder in America (pp. 53 - 80). New York: MacMillan/Free Press.
Weissman, M.M., Fendrich, M., Warner, V., & Wickramaratne, P. (1992). Incidence of psychiatric disorder in offspring at high and low risk for depression. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 640 - 648.
Weissman, M.M., Kidd, K.K., & Prusoff, B.A. (1982). Variability in rates of affective disorders in relatives of depressed and normal probands. Archives of General Psychiatry, 39, 1397 - 1403.
Winokur, G., Coryell, W., Keller, M., Endicott, J., & Akiskal, H. (1993). A prospective follow - up of patients with bipolar and primary unipolar affective disorder. Archives of General Psychiatry, 50, 457 - 465.
Zigler, E., & Styfco, S.J. (1994). Head start: Criticisms in a a constructive context. American Psychologist, 49, 127 - 132.
Footnotes:
(f.1) Only in recent years have methodologically sound follow - up studies been conducted of persons suffering from major affective disorders. The findings from these studies consistently indicate that in the large majority of cases, these are chronic, recurrent disorders. For example, in a recent article Robert Post and his group from the NIMH, echoing Jules Angst from Switzerland, stated that "...only a small portion of patients have spontaneous burnout of their affective disorder." (Post, Weiss, & Leverich, 1994, p. 808) The conclusion to the first 18 month follow - up in the NIMH Treatment of Depression Collaborative Research Programme was summarized by the project coordinator: "What is most striking in the follow - up findings is the relatively small percentage [24%] of patients [with major depression] who remain in treatment, fully recover, and remain completely well throughout the 18 month follow - up period." (Elkin, 1994, p. 131) In another follow - up within this same project, it was reported that at 5 years 11.5% of subjects with major depression had not recovered (Keller et al., 1992). Similar results were reported by Winokur, Coryell, Keller, Endicott and Akiskal (1993). As noted by Klerman and Weissman in 1992 "Major depression is an episodic condition with relapses, recurrences, and some chronicity." (1992, p. 833).
At the First International Conference on Bipolar Disorder held in June of 1994, M. Thase concluded: "... the results of both controlled clinical trials and naturalistic follow - up studies conducted over the past decade indicate that the prognosis of many patients with manic depression is surprisingly poor. Moreover, rates of sustained remission of finite periods of time, such as 3 or 5 year intervals seldom exceed 50% despite prophylactic treatment." (p. 229) This conclusion is supported by the few follow - up studies which have been published. For example, Tohen, Waternaux and Tsuang (1990) followed 75 bipolar patients for four years after discharge from an inpatient ward. Only 21 (28%) did not relapse during the follow - up period. Given that all the subjects in this investigation were in treatment, relapse rates are high. Another study reveals even a poorer outcome for bipolar patients. While 50% of patients were found to relapse within five months of terminating lithium treatment, 80 - 90% relapsed within two years (Suppes, Baldessarini, Faedda, & Tohen, 1991). These findings concur with those from other investigations in identifying high relapse rates even for treated cases, and poor psychosocial functioning in periods between acute episodes of mania or depression (Bauwens, Tracy, Pardoen, Vander Elst, & Mendlewicz, 1991; Harrow, Goldberg, Grossman, & Meltzer, 1990; Miklowitz, Goldstein, Nuechterlein, Snyder, & Mintz, 1988; Pardoen, Bauwens, Tracy, Martin, & Mendlewicz, 1993; Post, 1993).
(f.2) The prevalence of alcohol use disorders among subjects who had met the lifetime criteria for major depression was 16.5% as compared to 13.5% in the population. While it has often been thought in the past that the prevalence of alcohol use disorders was very elevated among subjects with major depression, this appears to be due to a difference in "true" prevalence rates and "treated" prevalence rates. Results from the ECA, have shown that among individuals with alcohol use disorders, those with depressive symptoms are more likely to seek treatment than those with no co - morbid disorders. Consequently, in clinical samples of patients with alcohol use disorders or with major depression the proportions of patients with both disorders is much greater than in the population (Helzer & Pryzbeck, 1988). Just as major depression is more prevalent among women than among men, major depression is almost four times more prevalent among women than among men with alcohol use disorders. Further, in 78% of the males with alcohol use disorders, the onset of the alcoholism precedes the onset of depression. However, the reverse was found to be true for women. Among the females who met lifetime criteria for alcohol use disorder and for depression, in 66% of the cases the depression preceded the alcoholism (Helzer & Pryzbeck, 1988).
(f.3) The rates of disorders among the children of comparison group parents are high. This may result, at least in part, from parents who observe problems in their children seeking out research projects in lieu of assessments and treatments which are not affordable.
(f.4) Here, the argument is in favour of what has been called "targeted interventions" which are "...designed for individuals within the larger population who are at high risk." (Asarnow & Koegel, 1994, p. 12) This is not meant to imply that universal interventions designed to promote mental health in the general populations, nor interventions aimed at children with problems are not warranted (Dinges, 1994; Glynn, Mueser, & Herbert, 1994, Gordon, 1983; Rutter, 1994).
TABLE 1
The Prevalence of Major Mental Disorders Among the First Degree Relatives of Subjects with Major Mental Disorders
Prevalence of major Prevalence of major
disorders among relatives disorders among
of persons with relatives of persons
schizophrenia'Symbol not with major
transcribed'1 depression'Symbol
not transcribed'2
Schizophrenia 6.5% 0.2%
Schizoaffective disorder 6.8% 0.75%
Other non affective 5.1%
psychoses
Major depression psychotic and 17.6%
non - psychotic illness
Bipolar disorder 3.2% 2.5%
Table continued...
Prevalence of major Prevalence of major
disorders among relatives disorders among
of persons with bipolar general population
disorder'Symbol not
transcribed'3
Schizophrenia 0.8% 0.85%'Symbol not
transcribed'4
Schizoaffective disorder 0.1% ?
Other non affective
psychoses
Major depression 23.9% 4.9%'Symbol not
transcribed'5 - 17.1%
'Symbol not transcribed'6
Bipolar disorder 8.5% 1.3%'Symbol not
transcribed'5 - 1.6%
'Symbol not transcribed'6
1 Kendler et al., 1993
2 Weissman, & Boyd, 1984, figures for "severe major depressive disorder" averaged for sites 1 and 2
3 Andreasen, Rice, Endicott, Coryell, Grove, & Reich, 1987
4 Gottesman, & Shields, 1982
5 Weissman, Bruce, Leaf, Florio, & Holzer, 1991
6 Kessler et al., 1994
TABLE 2
Prevalence of Mental Disorders Among children with One Parent with a Lifetime Diagnosis of Major Depression
Children-one Children - parents X'Symbol
parent with no mental not
major depression disorder transcribed
Any mental disorder 61.36% 24.05% 79.30*
(N = 589)
Any affective disorder 22.26% 6.75% 30.80*
(N = 648)
Major depression 22.16% 3.81% 34.17*
(N = 562)
Bipolar disorder 2.36% 0 2.82
(N = 245)
Dysthymia 11.01% 2.93% 14.38*
(N = 609)
Any anxiety disorder 27.12% 13.18% 18.27*
(N = 682)
p = .001
Source: Lavoie, & Hodgins, 1994
Biederman, Rosenbaum, Bolduc, Faraone, & Hirshfeld, 1991
Breslau, Davis, & Prabucki, 1987
Grigoroiu-Serbanescu, Christodorescu, Jipescu, Narinescu, & Ardelean, 1990
Hammen, Gordon, Burge, Adrian, Jaenicke, & Hiroto, 1987
Kashani, Burk, Horwitz, & Reid, 1985
Klein, Clark, Dansky, & Margolis, 1988
McClellan, Rupert, Reichler, & Sylvester, 1990
Orvaschel, Walsh-Allis, & Ye, 1988
Radkle-Yarrow, Nottelman, Martinez et al., 1992
Weissman, Gammon, John, Merikangas, Warner, Prusoff, & Sholomskas, 1987
TABLE 3
Prevalence of Mental Disorders Among Children with One Parent suffering from Bipolar Disorder
Children of Children of
parents with parents with X'Symbol
bipolar no mental not
disorder disorder transcribed
Any mental disorder (N = 973) 52.0% 29.0% 51.44**
Any affective disorder (N = 614) 26.5% 8.3% 30.58**
Bipolar disorder (N = 795) 5.4% 0 18.22*
Unipolar, major depression (N = 350) 8.5% 7.5% 0.12
Non-affective disorders (N= 505) 20.6% 20.4% .006
p = .000
p = .00001
Source: Lapalme, Hodgins & LaRoche, 1994
Decina & al., 1983
Gershon & al., 1985
Grigoroiu-Serbanescu & al., 1989
Hammen & al., 1987
Hammen & al., 1990
Nurnberger & al., 1988
Radke-Yarrow & al., 1992
Radke-Yarrow & al., 1992
Carlson & Weintraub 1993

No comments:
Post a Comment