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.
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.
Previous studies of bipolar disorders indicate that childhood abuse and substance abuse are associated with the disorder. Whether both influence the clinical picture, or if one is mediating the association of the other, has not previously been investigated.
A total of 587 patients with bipolar disorders were recruited from Norway and France. A history of childhood abuse was obtained using the Childhood Trauma Questionnaire. Diagnosis and clinical variables, including substance abuse, were based on structured clinical interviews (Structured Clinical Interview for DSM-IV Axis I disorders or French version of the Diagnostic Interview for Genetic Studies).
Cannabis abuse was significantly associated with childhood abuse, specifically emotional and sexual abuse (? 2 = 8.63, p = 0.003 and ? 2 = 7.55, p = 0.006, respectively). Cannabis abuse was significantly associated with earlier onset of the illness (z = -4.17, p
We have previously reported an increase in schizophrenia diagnoses in a population exposed during the second trimester to the 1957 influenza epidemic. These basic findings together with a fair number of replications have been interpreted as supporting a neurodevelopmental contribution to the origins of schizophrenia. Recent neuroimaging findings suggest that affective illness may also have a neurodevelopmental origin. We examined the hypothesis that exposure to an influenza epidemic during the second trimester would increase the risk for adult major affective disorder.
The subjects had been exposed as fetuses to the type A2/Singapore influenza epidemic in greater Helsinki, Finland. Control subjects were born in the 6 years before the epidemic.
We found a significant (P .05) were similar. The second-trimester effect remained when we estimated population-based rates (2.1 vs 0.6 per 1000) (P .05) elevation was observed for the bipolar forms of major affective disorder.
These data are consistent with the hypothesis concerning the possible neurodevelopmental contribution to the origins of some forms of major affective disorder, especially unipolar depressive disorder. These encouraging findings, if replicated, may suggest that some mental disorders may stem, in part, from a disturbance in the development of the fetal brain during the second trimester.
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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OBJECTIVE: The aim of this study was to determine the treatment incidence, diagnostic stability and clinical and social outcome of affective disorders in the Greenlandic population. METHODS: A cohort of Greenlanders first hospitalized in 1980-1983 and diagnosed with an affective disorder at least once during the period 7 to 12 years after first admission formed the study population. The manic-depressive patients who were still alive at follow-up were invited for a Present State Examination, and information about clinical and social condition was obtained for the total cohort. RESULTS: The rates of manic-depressive psychoses diagnosed at first admission or later were 6.6 for men and 20.4 for women per 100,000 individuals of over 15 years of age. The unipolar:bipolar ratio was very low, namely 1:3 for men and 1:2 for women. Outcome was relatively poor. CONCLUSION: Manic-depression is a recognizable diagnostic category in Greenland. Extremely low rates of unipolar disorders in both sexes and high rates of bipolar disorders among women were the most marked findings.
The high co-occurrence between borderline personality disorder and affective disorders has led many to believe that borderline personality disorder should be considered as part of an affective spectrum. The aim of the present study was to examine whether the prevalence of affective disorders are higher for patients with borderline personality disorder than for patients with other personality disorders.
In a national cross-sectional study of patients receiving mental health treatment in Norway (N?=?36 773), we determined whether psychiatric outpatients with borderline personality disorder (N?=?1 043) had a higher prevalence of affective disorder in general, and whether they had an increased prevalence of depression, bipolar disorder or dysthymia specifically. They were compared to patients with paranoid, schizoid, dissocial, histrionic, obsessive-compulsive, avoidant, dependent, or unspecified personality disorder, as well as an aggregated group of patients with personality disorders other than the borderline type (N?=?2 636). Odds ratios were computed for the borderline personality disorder group comparing it to the mixed sample of other personality disorders. Diagnostic assessments were conducted in routine clinical practice.
More subjects with borderline personality disorder suffered from unipolar than bipolar disorders. Nevertheless, borderline personality disorder had a lower rate of depression and dysthymia than several other personality disorder groups, whereas the rate of bipolar disorder tended to be higher. Odds ratios showed 34% lower risk for unipolar depression, 70% lower risk for dysthymia and 66% higher risk for bipolar disorder in patients with borderline personality disorder compared to the aggregated group of other personality disorders.
The results suggest that borderline personality disorder has a stronger association with affective disorders in the bipolar spectrum than disorders in the unipolar spectrum. This association may reflect an etiological relationship or diagnostic overlapping criteria.
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Cites: Arch Gen Psychiatry. 2001 Jun;58(6):590-611386989
Many studies have shown associations between a history of childhood trauma and more severe or complex clinical features of bipolar disorders (BD), including suicide attempts and earlier illness onset. However, the psychopathological mechanisms underlying these associations are still unknown. Here, we investigated whether affective lability mediates the relationship between childhood trauma and the severe clinical features of BD.
A total of 342 participants with BD were recruited from France and Norway. Diagnosis and clinical characteristics were assessed using the Diagnostic Interview for Genetic Studies (DIGS) or the Structured Clinical Interview for DSM-IV Axis I disorders (SCID-I). Affective lability was measured using the short form of the Affective Lability Scale (ALS-SF). A history of childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ). Mediation analyses were performed using the SPSS process macro.
Using the mediation model and covariation for the lifetime number of major mood episodes, affective lability was found to statistically mediate the relationship between childhood trauma experiences and several clinical variables, including suicide attempts, mixed episodes and anxiety disorders. No significant mediation effects were found for rapid cycling or age at onset.
Our data suggest that affective lability may represent a psychological dimension that mediates the association between childhood traumatic experiences and the risk of a more severe or complex clinical expression of BD.
Advancing paternal age has been linked to psychiatric disorders. These associations might be caused by the increased number of de novo mutations transmitted to offspring of older men. It has also been suggested that the associations are confounded by a genetic liability for psychiatric disorders in parents. The aim of this study was to indirectly test the confounding hypotheses by examining if there is a genetic component to advancing paternal age and if men with a genetic liability for psychiatric disorders have children at older ages.
We examined the genetic component to advancing paternal age by utilizing the twin model in a cohort of male twins (N = 14 679). We also studied ages at childbirth in men with or without schizophrenia, bipolar disorder and/or autism spectrum disorder. Ages were examined in: (1) healthy men, (2) affected men, (3) healthy men with an affected sibling, (4) men with healthy spouses, (5) men with affected spouses, and (6) men with healthy spouses with an affected sibling.
The twin analyses showed that late fatherhood is under genetic influence (heritability = 0.33). However, affected men or men with affected spouses did not have children at older ages. The same was found for healthy individuals with affected siblings. Instead, these men were generally having children at younger ages.
Although there is a genetic component influencing late fatherhood, our data suggest that the associations are not explained by psychiatric disorders or a genetic liability for psychiatric disorders in the parent.
This study aimed to investigate the relationship between age at onset and time to first pharmacological treatment in patients with either bipolar I or II disorder. A total of 146 consecutive in-patients acutely admitted from the same catchment area were included. Patients were divided into four age groups: 0-12 years (23%); 13-18 years (32%); 19-29 years (26%); and > or =30 years (18%). Mean age at first affective episode was 20.2 years (s.d.=11.8). This represents a similar pattern to the age at onset seen in out-patients in the USA. Early age at onset predicted a longer time to first pharmacological treatment (rho =-0.695, P