Estimates of lifetime risk of suicide in mental disorders were based on selected samples with incomplete follow-up.
To estimate, in a national cohort, the absolute risk of suicide within 36 years after the first psychiatric contact.
Prospective study of incident cases followed up for as long as 36 years. Median follow-up was 18 years.
Individual data drawn from Danish longitudinal registers.
A total of 176,347 persons born from January 1, 1955, through December 31, 1991, were followed up from their first contact with secondary mental health services after 15 years of age until death, emigration, disappearance, or the end of 2006. For each participant, 5 matched control individuals were included.
Absolute risk of suicide in percentage of individuals up to 36 years after the first contact.
Among men, the absolute risk of suicide (95% confidence interval [CI]) was highest for bipolar disorder, (7.77%; 6.01%-10.05%), followed by unipolar affective disorder (6.67%; 5.72%-7.78%) and schizophrenia (6.55%; 5.85%-7.34%). Among women, the highest risk was found among women with schizophrenia (4.91%; 95% CI, 4.03%-5.98%), followed by bipolar disorder (4.78%; 3.48%-6.56%). In the nonpsychiatric population, the risk was 0.72% (95% CI, 0.61%-0.86%) for men and 0.26% (0.20%-0.35%) for women. Comorbid substance abuse and comorbid unipolar affective disorder significantly increased the risk. The co-occurrence of deliberate self-harm increased the risk approximately 2-fold. Men with bipolar disorder and deliberate self-harm had the highest risk (17.08%; 95% CI, 11.19%-26.07%).
This is the first analysis of the absolute risk of suicide in a total national cohort of individuals followed up from the first psychiatric contact, and it represents, to our knowledge, the hitherto largest sample with the longest and most complete follow-up. Our estimates are lower than those most often cited, but they are still substantial and indicate the continuous need for prevention of suicide among people with mental disorders.
There is a high prevalence of smoking and physical inactivity among individuals with severe mental illness (SMI). The current study assessed the acceptability of introducing physical activity, including perceived advantages and disadvantages, as an adjunct to a smoking cessation service within this population.
109 participants with SMI who were receiving smoking cessation treatment completed a survey assessing perceived interest in physical activity and a 24-item decisional balance questionnaire reflecting potential advantages and disadvantages of becoming more physically active.
The majority of the participants reported being interested in assistance in becoming more active [63% (69/109)]. The highest rated advantages reported were 'It would improve my health or reduce my risk of disease' and 'It would improve how I feel about myself'. Cost, and being active by oneself were the most frequently reported barriers.
This study suggests that many individuals with SMI seeking treatment for smoking cessation may also be receptive to assistance in becoming more physically active. Such individuals endorse both advantages and disadvantages more frequently than those not interested.
This study provides preliminary support for the acceptability of adding physical activity as a smoking cessation strategy with SMI individuals. Addressing salient barriers will be critical to integrating physical activity within this smoking cessation service.
The phenomenon of acculturation stress is described with particular reference to the subsequent development of the transitional role conflict. The adolescent and young adult male Eskimo is especially susceptible to the anxiety generated by the process of acculturation and it is the interaction of this external stress with the bio-psychosocial characteristics of the individual within his ecological group, that may lead to an increased incidence of mental disorder. The clinical picture that develops will depend on the complex interaction of this psychosocial stressor and the level of ego development and its accompanying defence and coping strategies. We see how the development of manifest psychopathology in two young Inuit males was intimately associated with the stresses of acculturation acting upon personalities characterized by a low self-esteem and negative self-image, feelings of emasculation and a state of anomie. Coping and defensive strategies exhibited both similarities (drugs, alcohol, withdrawal, actin out) and differences (psychosis versus dissociation). The value of modified supportive therapy with continuity of care aimed at increasing self-esteem through sublimation, identification, reduction of dependency and encouragement of growth and autonomy is described, as are measures aimed at primary prevention.
From: Fortuine, Robert et al. 1993. The Health of the Inuit of North America: A Bibliography from the Earliest Times through 1990. University of Alaska Anchorage. Citation number 2319.
Acute intermittent porphyria (AIP) has been associated with schizophrenia in some studies, but prior research is limited by the absence of comparison populations. Here, we linked Swedish registers to examine the risk of schizophrenia and bipolar disorder in 717 individuals diagnosed with AIP and their first-degree relatives, compared with matched individuals without AIP and their first-degree relatives. Individuals with AIP had a fourfold increased risk of schizophrenia or bipolar disorder. Similarly, relatives of individuals with AIP had double the risk of schizophrenia or bipolar disorder, suggesting that these associations may be as a result of common genetic influences.
The objective was to assess the presence of different subgroups, via age-at-onset (AAO) analysis, in a schizophrenia population consecutively recruited through an Early Psychosis Service in London, Canada.
Admixture analysis was applied in order to identify a model of separate normal distribution of AAO characterized by different means, variances and population proportions to allow for evaluation of different subgroups in a sample of 187 unrelated patients with a Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, diagnosis of schizophrenia.
The best-fitting model suggested three subgroups with means and standard deviations of 16.8 ± 1.9, 22.3 ± 2.1 and 32.7 ± 5.9 years comprising 41%, 30% and 29% of the schizophrenia sample, respectively. These three subgroups were categorized as early, intermediate and late onset with cutoffs determined by admixture analysis to be 19 and 26 years of age, respectively. In our investigation, the definition of early-onset schizophrenia is the main outcome. We considered the clinical variables mainly related to the heritability and neurobiology of schizophrenia. Single status was strongly associated with early onset (P
In the context of a Finnish birth cohort, we tested the hypothesis that viral infection during the latter two thirds of fetal development would increase the risk of adult schizophrenic outcome. Psychiatric hospital diagnoses were recorded for all individuals in greater Helsinki who were fetuses during the 1957 type A2 influenza epidemic. Those exposed to the viral epidemic during their second trimester of fetal development were at elevated risk of being admitted to a psychiatric hospital with a diagnosis of schizophrenia. This was true for both males and females and independently in several psychiatric hospitals. The second-trimester effect was seen in the elevated proportion of schizophrenics among those admitted to a psychiatric hospital and also in higher rates of schizophrenia per 1000 live births in the city of Helsinki. The study has several limitations: (1) We have no direct evidence that the subjects actually suffered a viral infection. (2) The psychiatric data were obtained only for subjects up to the age of 26 years, 56 days. (3) The findings are based on hospital diagnoses. (4) The determination of stage of gestation at time of exposure to the epidemic is based on date of birth. The viral infection might have occurred outside the official epidemic window; the infant may have had a preterm or postterm delivery. These sources of error, however, should not serve to enhance the findings. The observed viral effect is interpreted as being one of many potential perturbations of gestation. We suggest that it is less the type than the timing of the disturbance during fetal neural development that is critical in determining risk for schizophrenia.
Advanced paternal age (APA) is a risk factor for nonaffective psychosis (NAP) in the offspring, although the mechanism(s) of this association are not clear. The aim of this study was to examine whether later childbearing can be explained by parental schizophrenia, and in doing so, further evaluate the "de novo mutation" hypothesis for the association between APA and NAP.
Using binary logistic regression, the association between APA and parental history of schizophrenia in the offspring, considering maternal and paternal history separately, was examined in 1) all persons with NAP born in Finland between 1950 and 1969 (Finnish NAP Cohort, n = 13,712), and 2) members of the Northern Finland 1966 Birth Cohort (NFBC 1966, n = 10,224), a general population birth cohort.
In the Finnish NAP Cohort, having a mother with schizophrenia was associated with APA (Odds Ratio [OR] for linear trend = 1.20, 95% confidence interval 1.12-1.29, p
Advanced paternal age has been linked with an increased risk of schizophrenia in the offspring. If age-related de novo mutations in the male germ line underlie this association, grandpaternal and paternal age would both be expected to influence the risk of schizophrenia. The aim of the current study was to explore the links between both paternal and grandpaternal age with respect to the risk of schizophrenia in a large, national register-based cohort.
We linked the Swedish Multi-Generation and Hospital Discharge Registers and compared parents' ages at offspring birth for 20,582 schizophrenia-affected and 100,176 non-affected individuals. Grandparents' ages at the birth of the parent were compared between 2511 affected and 15,619 non-affected individuals. The risk of schizophrenia was examined with logistic regression when the predictor variable (parent or grandparent age) varied across age strata.
After adjusting for maternal age, birth year and proband sex, we confirmed that offspring of older fathers had an increased risk of schizophrenia. Compared to those with paternal age 20-24years, those with fathers >55years had a two-fold increased risk of schizophrenia. With respect to grandparent age, older maternal (but not paternal) grandfather age was associated with an increased risk of schizophrenia. Compared to maternal grandfather age 20-24years, those with maternal grandfathers >55years had a significantly increased risk of schizophrenia (adjusted odds ratio and 95% confidence intervals; 2.79, 1.71-4.56). The pattern of results was essentially unchanged when we examined male and female probands separately.
This is the first study to report an association between grandpaternal age and risk of schizophrenia. The selective effect of advanced maternal grandfather age suggests that the biological mechanisms involving the X-chromosome may differentially contribute to the association between paternal age and offspring risk of schizophrenia.
Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly because of increased de novo mutations during spermatogenesis with older paternal age. Because severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending. Interlinked Swedish national registers provided information on fathers' age at childbirth and violent criminal convictions in all offspring born from 1958 to 1979 (N = 2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences. In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-family analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.
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