Parental History Of Mental Disorder Research Articles

Association Between Intrauterine System Hormone Dosage and Depression Risk.

The authors compared the associated risk of incident depression between first-time users of low-, medium-, and high-dose levonorgestrel-releasing intrauterine systems (LNG-IUSs). This national cohort study was based on Danish register data on first-time users of LNG-IUSs, 15-44 years of age, between 2000 and 2022. Cox regression and a G-formula estimator were used to report 1-year average absolute risks, risk differences, and risk ratios of incident depression, defined as initiation of an antidepressant or receipt of a depression diagnosis, standardized for calendar year, age, education level, parental history of mental disorders, endometriosis, menorrhagia, polycystic ovary syndrome, dysmenorrhea, leiomyoma, and postpartum initiation. In total, 149,200 women started using an LNG-IUS, among whom 22,029 started a low-dose one (mean age, 22.9 years [SD=4.5]), 47,712 a medium-dose one (mean age, 25.2 years [SD=6.2]), and 79,459 a high-dose one (mean age, 30.2 years [SD=5.6]). The associated subsequent 1-year adjusted absolute risks of incident depression were 1.21% (95% CI=1.06-1.36), 1.46% (95% CI=1.33-1.59), and 1.84% (95% CI=1.72-1.96), respectively. For the users of high-dose LNG-IUSs, the risk ratios were 1.52 (95% CI=1.30-1.74) and 1.26 (95% CI=1.10-1.41) compared with users of the low- and medium-dose LNG-IUSs, respectively. For users of medium-dose LNG-IUSs, the risk ratio was 1.21 (95% CI=1.03-1.39) compared with users of low-dose LNG-IUSs. First-time use of an LNG-IUS was positively associated with incident depression in an LNG-dose-dependent manner across low-, medium-, and high-dose LNG-IUSs. Although the observational design of the study does not permit causal inference, the dose-response relationship contributes to the body of evidence suggesting a relationship between levonorgestrel exposure and risk of depression.

The Intergenerational Transfer of Mental Disorders: A Population-Based Multigenerational Linkage Study: Le transfert intergénérationnel des troubles mentaux : une étude sur les liens multigénérationnels basée sur la population.

The aetiology of mental disorders involves genetic and environmental factors, both reflected in family health history. We examined the intergenerational transmission of multiple mental disorders from parents and grandparents using population-based, objectively measured family histories. This population-based retrospective cohort study used administrative healthcare databases in Manitoba, Canada and included adults living in Manitoba from 1977 to 2020 with linkages to at least one parent and one grandparent. Index date was when individuals turned 18 or 1 April 1977, whichever occurred later. Mental disorder diagnoses (mood and anxiety, substance use and psychotic disorders) were identified in individuals, parents and grandparents from hospitalization and outpatient records. Cox proportional hazards regression models included sociodemographic characteristics, individual's comorbidity and mental disorder history in a grandparent, mother and father. Of 109,359 individuals with no mental disorder prior to index date, 47.1% were female, 36.3% had a mental disorder during follow-up, and 90.9% had a parent or grandparent with a history of a mental disorder prior to the index date. Both paternal and maternal history of a mental disorder increased the risk of the disorder in individuals. Psychotic disorders had the strongest association with parental history and were mostly influenced by paternal (hazards ratio [HR] 3.73, 95% confidence interval [CI] 2.99 to 4.64) compared to maternal history (HR 2.23, 95% CI, 1.89 to 2.64). Grandparent history was independently associated with the risk of all mental disorders but had the strongest influence on substance use disorders (HR 1.42, 95% CI, 1.34 to 1.50). Parental history of mental disorders was associated with an increased risk of all mental disorders. Grandparent history of mental disorders was associated with a small risk increase of the disorders above and beyond parental history influence. This three-generation study further highlights the need for family-based interventional programs in families affected by mental disorders. The Intergenerational Transfer of Mental Illnesses.

There is no association between combined oral hormonal contraceptives and depression: a Swedish register-based cohort study.

To investigate whether users of hormonal contraceptives (HCs) are at increased risk of depression compared with non-users. Register-based cohort study. Sweden. Women aged 15-25 years between 2010 and 2017 with no prior antidepressant treatment, psychiatric diagnose or contraindication for HCs (n = 739 585). Women with a prescription of HC were identified via the Swedish Prescribed Drug Register (SPDR). Relative risks (RRs) for first depression diagnosis in current HC-users compared with non-users were modelled by Poisson regression. Adjustments included age, medical indication for HC-use and parental history of mental disorders, among others. Depression, captured by a redeemed prescription of antidepressant treatment, or a first depression diagnosis in the SPDR and the National Patient Register. Compared with non-users, women on combined oral contraceptives (COCs) and oral progestogen-only products had lower or no increased risk of depression, relative risk (RR) 0.89 (95% CI 0.87-0.91) and 1.03 (95% CI 0.99-1.06) after adjustments, respectively. Age-stratified analyses demonstrated that COC use in adolescents conferred no increase in risk (RR 0.96, 95% CI 0.93-0.98), whereas use of progestogen-only pills (RR 1.13, 95% CI 1.07-1.19), contraceptive patch/vaginal ring (RR 1.43, 95% CI 1.30-1.58), implant (RR 1.38, 95% CI 1.30-1.45) or a levonorgestrel intrauterine device (RR 1.59, 95% CI 1.46-1.73) were associated with increased risks. This study did not find any association between use of COCs, which is the dominating HC in first time users, and depression. Non-oral products were associated with increased risks. Residual confounding must be addressed in the interpretation of the results. There is no association between combined hormonal contraceptives and depression.

Is there a social gradient in how youth with mental disorder perform academically? Findings from a Swedish longitudinal register-based study

BackgroundIt is well established that academic achievement and other school-related outcomes are associated with mental health status in children and youths. However, few studies have examined the influence of socioeconomic background on the relationship between poor childhood/adolescent mental health and school performance. From an equity perspective, it is important to explore how school-related outcomes are affected for young people with mental disorder and if these outcomes differ depending on gender and socioeconomic background. This study aimed to investigate social gradients in the prospective association between childhood/adolescent mental disorder and academic achievement.MethodsThis register based study used data from the Umeå SIMSAM Lab of linked Swedish registers on all children born between 1990 and 1994 and their parents (N = 642 558). The outcome was school grades achieved upon compulsory school graduation (age 15/16). Mental disorder was indicated by number of hospitalisations due to ICD classified mental disorders and prescription of psychoanaleptic drugs. Indicators of socioeconomic position were parental level of education and family income in four categories respectively. Parental history of mental disorder was controlled for. Linear regressions, including interaction analyses, were performed.ResultsMental disorder in childhood/adolescence was related to lower grades, particularly in boys. The drop in academic achievement among youth with mental disorder was more pronounced among girls in mid SEP categories than among their less and more advantaged peers. A less clear interaction pattern was identified in boys.ConclusionsBased on theory and existing research we expected a typical social gradient in the strength of the association between mental disorder and academic achievement. However, we identified a U-shaped social gradient among girls. Analyses of the links between mental health and academic outcomes need to take both gender and social position into account. More research is needed to investigate these patterns further.

Adolescent residential mobility, genetic liability and risk of schizophrenia, bipolar disorder and major depression.

Residential mobility during upbringing, and especially adolescence, is associated with multiple negative mental health outcomes. However, whether associations are confounded by unmeasured familial factors, including genetic liability, is unclear. We used a population-based case-cohort study to assess whether polygenic risk scores (PRSs) for schizophrenia, bipolar disorder and major depression were associated with mobility from ages 10-14 years, and whether PRS and parental history of mental disorder together explained associations between mobility and each disorder. Information on cases (n = 4207 schizophrenia, n = 1402 bipolar disorder, n = 18 215 major depression) and a random population sample (n = 17 582), born 1981-1997, was linked between Danish civil and psychiatric registries. Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of separate, large meta-analyses. PRSs for schizophrenia and major depression were weakly associated with moving once (odds ratio 1.07, 95% CI 1.00-1.16; and odds ratio 1.10, 95% CI 1.04-1.17, respectively), but not twice or three or more times. Mobility was positively associated with each disorder, with more moves associated with greater risk. Adjustment for PRS produced slight reductions in the magnitude of associations. Adjustment for PRS and parental history of mental disorder together reduced estimates by 5-11%. In fully adjusted models mobility was associated with all three disorders; hazard ratios ranged from 1.33 (95% CI 1.08-1.62; one move and bipolar disorder) to 3.05 (95% CI 1.92-4.86; three or more moves and bipolar disorder). Associations of mobility with schizophrenia, bipolar disorder and depression do not appear to be attributable to genetic liability as measured here. Potential familial confounding of mobility associations may be predominantly environmental in nature.

Association of Substance Use Disorders With Conversion From Schizotypal Disorder to Schizophrenia

Understanding the role of substance use disorders in conversion from schizotypal disorder to schizophrenia may provide physicians and psychiatrists with important tools for prevention or early detection of schizophrenia. To investigate whether substance use disorders, in particular cannabis use disorder, are associated with conversion to schizophrenia in individuals with schizotypal disorder. This prospective cohort study included a population-based sample of all individuals born in Denmark from January 1, 1981, through August 10, 2014, with an incident diagnosis of schizotypal disorder and without a previous diagnosis of schizophrenia. Follow-up was completed on August 10, 2014, and data were analyzed from March 10, 2017, through February 15, 2018. Information on substance use disorders combined from 5 different registers. Cox proportional hazards regression using time-varying information on substance use disorders and receipt of antipsychotics and adjusted for parental history of mental disorders, sex, birth year, and calendar year were used to estimate hazard ratios (HRs) and 95% CIs for conversion to schizophrenia. A total of 2539 participants with incident schizotypal disorder were identified (1448 men [57.0%] and 1091 women [43.0%]; mean [SD] age, 20.9 [4.4] years). After 2 years, 16.3% (95% CI, 14.8%-17.8%) experienced conversion to schizophrenia. After 20 years, the conversion rate was 33.1% (95% CI, 29.3%-37.3%) overall and 58.2% (95% CI, 44.8%-72.2%) among those with cannabis use disorders. In fully adjusted models, any substance use disorder was associated with conversion to schizophrenia (HR, 1.34; 95% CI, 1.11-1.63). When data were stratified by substance, cannabis use disorders (HR, 1.30; 95% CI, 1.01-1.68), amphetamine use disorders (HR, 1.90; 95% CI, 1.14-3.17), and opioid use disorders (HR, 2.74; 95% CI, 1.38-5.45) were associated with conversion to schizophrenia. These associations were not explained by concurrent use of antipsychotics, functional level before incident schizotypal disorder, or parental history of mental disorders. Substance use disorders, in particular cannabis, amphetamines, and opioids, may be associated with conversion from schizotypal disorder to schizophrenia. However, conversion rates are high even in those without substance use disorders, indicating a need for universal and substance-targeted prevention in individuals with schizotypal disorder.

O9.1. CANNABIS AND OTHER SUBSTANCE USE DISORDERS PREDICT CONVERSION FROM SCHIZOTYPAL DISORDER TO SCHIZOPHRENIA

BackgroundSchizotypal disorder has been linked to conversion to schizophrenia, with a quarter to half of patients converting over a course of two to five years. Substance use disorders are common in patients with schizotypal disorder, and cannabis has been shown to be a risk factor for developing schizotypal disorder. Cannabis has also been linked to an increased risk of schizophrenia. Other substance use disorders, in particular alcohol, may also increase risk of later schizophrenia. These previous results suggest that substance use, in particular cannabis, may predict conversion to schizophrenia in people with schizotypal disorder.MethodsWe used the nationwide, unselected Danish registers. The study population was all people born since 1981 in Denmark with incident diagnosis of schizotypal disorder, without previous diagnosis of schizophrenia. Information on substance use disorders was combined from five different registers. Cox regression using time-varying information on substance use disorders and antipsychotic medication, and adjusted for parental history of mental disorders, sex, birth year, and calendar year were used to estimate hazard ratios (HR) and 95% confidence intervals (CI).ResultsAfter two years, 16.3% (95% CI 14.8%-17.8%) of the people with schizotypal disorder had converted to schizophrenia. After 20 years, the conversion rate was 33.1% (95% CI 29.3–37.3) overall, and 58.2% (95% CI 44.8%-72.2%) in those with cannabis use disorders. In fully adjusted models, any substance use disorder predicted conversion to schizophrenia (HR=1.34, 95% CI 1.11–1.63). Dividing by substances, cannabis use disorders (HR=1.30, 95% CI 1.01–1.68), amphetamine use disorders (HR=1.90, 95% CI 1.14–3.17), and opioid use disorders (HR=2.74, 95% CI 1.38–5.45) predicted conversion to schizophrenia. These associations were not explained by concurrent use of antipsychotic medication, functional level before incident schizotypal disorder, or parental history of mental disorders.DiscussionSubstance use disorders, in particular cannabis, amphetamines, and opioids, are important predictors of conversion from schizotypal disorder to schizophrenia. However, conversion rates are high even in those without substance use disorders, indicating a need for both universal and substance-targeted prevention in people with schizotypal disorder.

F137. INFECTIONS OF THE CENTRAL NERVOUS SYSTEM AS A RISK FACTOR FOR MENTAL DISORDERS AND COGNITIVE IMPAIRMENT: A NATIONWIDE REGISTER-BASED STUDY

BackgroundInfections and inflammatory diseases have long been suggested as risk factors for cognitive decline and mental disorders, most notably schizophrenia and affective disorders. However, largescale studies have been lacking. This study aims to investigate the association between specific CNS-infections and the risk of developing mental disorders, and whether the causal agent of the CNS-infection has an effect on the association. Furthermore, this study will investigate the possible effect of CNS-infections on cognition in the largest study to date.MethodsWe will utilize the unique personal registration number to link nationwide Danish registers in order to identify all individuals born in Denmark between January 1, 1977, and December 31, 2010, with follow-up from birth. We will investigate the association between CNS-infections with the risk of 1) developing mental disorders and 2) affected cognition (defined as the highest completed level of education, completion of the 9th grade and grade average score at the end of the 9th grade). Further analyses will estimate the risk within every psychiatric diagnostic category based on the International Classification of Diseases, 10th edition (ICD-10), e.g. organic mental disorders (ICD-10: F00-09), substance abuse disorders (ICD-10: F10-19) and schizophrenia spectrum disorders (ICD-10: F20-29). The risk related to the different pathogens causing the CNS-infection will also be investigated. Data will be analysed using survival analysis to approximate relative risks estimated by Poisson regression, and will be adjusted for age, sex, calendar year, first-born status, parental history of mental disorders and educational level of the parents.ResultsAll analyses are expected to be completed no later than February 2018 and ready to be presented at the conference in April 2018.DiscussionThis population-based cohort study will be the largest to date investigating the association between CNS-infections and mental disorders, and whether there’s a difference in risk depending on the pathogen responsible for the CNS-infection. Additionally, it will be one of the largest studies investigating the effect of CNS-infections on cognition. It will add important knowledge to our understanding of the association between CNS-infections and mental disorders, and between CNS-infections and cognition.

The association between school exam grades and subsequent development of bipolar disorder.

Prior studies have indicated that both high and low school grades are associated with development of bipolar disorder (BD), but these studies have not adjusted for parental history of mental disorder, which is a likely confounder. Furthermore, the association between school grades and bipolar I disorder (BD-I) has not been studied. Therefore, we aimed to study the association between school exam grades and subsequent development of BD and BD-I while adjusting for parental history of mental disorder. We conducted a register-based nationwide cohort study following 505 688 individuals born in Denmark between 1987 and 1995. We investigated the association between school exam grades and development of BD or BD-I with a Cox model adjusting for family history of mental disorder and other potential confounders. During follow-up, 900 individuals were diagnosed with BD and 277 of these with BD-I. The risk for BD and BD-I was significantly increased for individuals not having completed the exams at term [adjusted hazard ratio (aHR) for BD (aHR=1.71, 95% CI: 1.43-2.04) and for BD-I (aHR=1.57, 95% CI: 1.13-2.19)]. Also, having low exam grades in mathematics was associated with increased risk of both BD (aHR=2.41, 95% CI: 1.27-4.59) and BD-I (aHR=2.71, 95% CI: 1.41-5.21). Females with very high exam grades in Danish (percentile group>97.7) had a significantly increased risk of BD-I (aHR=2.49, 95% CI: 1.19-5.23). The potential to develop BD seems to affect the school results of individuals negatively even before BD is diagnosed - with females having the potential to develop BD-I as a possible exception.

Parenting style and mental disorders in a nationally representative sample of US adolescents

We examined associations between parenting style and past-year mental disorders in a nationally representative cross-sectional survey of US adolescents and whether the associations differed by adolescent demographic characteristics. The sample included 6483 adolescents aged 13-18years who were interviewed for a full range of DSM-IV mental disorders. Parenting style was assessed by adolescent-reported maternal and paternal care and control using items from the Parental Bonding Instrument. We controlled for socio-demographics, parental history of mental disorders, stressful life events, sexual violence, inter-parental conflict, and household composition. We also tested for two-way interactions between parental care and control and adolescent age, sex, and race/ethnicity. In adjusted models, high maternal care was associated with lower odds of depressive, eating, and behavioral disorders, and high maternal control was associated with greater odds of depressive, anxiety, eating, and behavioral disorders. High paternal care was associated with lower odds of social phobia and alcohol abuse/dependence. High paternal control was associated with greater odds of agoraphobia and alcohol abuse/dependence but with lower odds of attention-deficit/hyperactivity disorder. Associations of maternal and paternal control with anxiety disorders and substance abuse/dependence differed by sex. High paternal care was associated with lower odds of anxiety disorders only among Hispanics and non-Hispanic blacks. Perceived parental care and control were associated with adolescent mental disorders after controlling for multiple potential confounders. Differential patterns of association were found according to adolescent sex and race/ethnicity. Findings have implications for prevention and intervention programs that incorporate familial contextual factors.

Parent-dependent stressors and the onset of anxiety disorders in children: links with parental psychopathology

Exposure to stressors is associated with an increased risk for child anxiety. Investigating the family origins of stressors may provide promising avenues for identifying and intervening with children at risk for the onset of anxiety disorders and their families. The aim of this study was to compare the frequency of parent-dependent negative life events and chronic adversities experienced by children with an anxiety disorder (n = 34) in the 12 months prior to the onset of the child’s most recent episode, compared to healthy controls (n = 34). Life events and chronic adversities were assessed using maternal report during an investigator-based interview, which provided independent panel ratings of the extent that reported experiences were related to parent behaviour. There were no group differences in the number of parent-dependent negative life events for anxious children compared to controls. However, significantly more parent-dependent chronic adversities were present for anxious children compared to controls. Findings suggest that parents contribute to an increased frequency of chronic adversities but not negative life events prior to their child’s most recent onset of anxiety. Furthermore, increased child exposure to parent-dependent chronic adversities was related to parental history of mental disorder.

The role of genetic liability in the association of urbanicity at birth and during upbringing with schizophrenia in Denmark.

Studies have indicated that the association of urbanicity at birth and during upbringing with schizophrenia may be driven by familial factors such as genetic liability. We used a population-based nested case-control study to assess whether polygenic risk score (PRS) for schizophrenia was associated with urbanicity at birth and at age 15, and to assess whether PRS and parental history of mental disorder together explained the association between urbanicity and schizophrenia. Data were drawn from Danish population registries. Cases born since 1981 and diagnosed with schizophrenia between 1994 and 2009 were matched to controls with the same sex and birthdate (1549 pairs). Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of a separate, large meta-analysis. Those with higher PRS were more likely reside in the capital compared with rural areas at age 15 [odds ratio (OR) 1.19, 95% confidence interval (CI) 1.01-1.40], but not at birth (OR 1.09, 95% CI 0.95-1.26). Adjustment for PRS produced almost no change in relative risks of schizophrenia associated with urbanicity at birth, but slightly attenuated those for urban residence at age 15. Additional adjustment for parental history led to slight attenuation of relative risks for urbanicity at birth [incidence rate ratio (IRR) for birth in capital = 1.54, 95% CI 1.18-2.02; overall p = 0.016] and further attenuation of relative risks for urbanicity at age 15 (IRR for residence in capital = 1.32, 95% CI 0.97-1.78; overall p = 0.148). While results regarding urbanicity during upbringing were somewhat equivocal, genetic liability as measured here does not appear to explain the association between urbanicity at birth and schizophrenia.

35. The Role of Genetic Liability in the Association Between Urbanicity and Schizophrenia

Abstract Background: The association of urbanicity at birth and during upbringing with schizophrenia remains unexplained. Some studies have indicated that it may be driven by familial selective factors such as genetic liability. However, no studies have used measures of genetic risk other than family history to test this hypothesis with respect to urbanicity at birth. We assessed whether genetic liability to schizophrenia, measured by polygenic risk score (PRS), was associated with being born and raised in urban areas, and whether adjustment for PRS and parental history of mental disorder together explained the effect of urbanicity. Methods: We conducted a nested case–control study using Danish population registry data. Cases in the Danish Psychiatric Central Register (n = 1692) who were born since 1981 and diagnosed with schizophrenia between 1994 and 2009 were matched to controls (n = 1724) with the same sex and birthdate. Genome-wide data were obtained from the Danish Neonatal Screening Biobank, and PRSs were calculated based on a Psychiatric Genomics Consortium meta-analysis that excluded Danish samples. PRSs were adjusted for ancestry using the first 10 principal components. Results: PRS generally increased with increasing level of urbanicity. Those with higher PRSs were significantly more likely to reside in the capital compared to rural areas at age 15 (odds ratio [OR] = 1.19, 95% confidence interval [CI] =1.00–1.42) but not at birth (OR = 1.09, 95%CI = 0.94–1.26). Adjustment for PRS produced almost no change in the excess risk of schizophrenia associated with urbanicity at birth (relative risk [RR] = 1.67, 95%CI = 1.29–2.17). However, the RR associated with urbanicity at age 15 decreased from 1.58 (95%CI = 1.20–2.09) to 1.47 (95%CI = 1.10–1.97) after adjustment for PRS. After adjustment for PRS and parental history together, the association between urbanicity at birth and schizophrenia remained (P = .016) but that for urbanicity at age 15 was fully attenuated (P = .148). Conclusion: We found evidence consistent with a role of selective migration in the association between urbanicity and schizophrenia, especially with respect to urbanicity during upbringing. However, our results failed to support the notion that genetic liability fully explains the excess risk of schizophrenia associated with urbanicity at birth. Additional research is needed to identify other familial mechanisms or constituent exposures that explain the robust association between urbanicity at birth and schizophrenia.

A population-based study of the risk of schizophrenia and bipolar disorder associated with parent-child separation during development.

There is growing interest in the role of childhood adversities, including parental death and separation, in the etiology of psychotic disorders. However, few studies have used prospectively collected data to specifically investigate parental separation across development, or assessed the importance of duration of separation, and family characteristics. We measured three types of separation not due to death: maternal, paternal, and from both parents, across the ages of 1-15 years among a cohort of 985 058 individuals born in Denmark 1971-1991 and followed to 2011. Associations with narrowly and broadly defined schizophrenia and bipolar disorder in the psychiatric register were assessed in terms of separation occurrence, age of separation, and number of years separated. Interactions with parental history of mental disorder were assessed. Each type of separation was associated with all three outcomes, adjusting for age, sex, birth period, calendar year, family history of mental disorder, urbanicity at birth and parental age. Number of years of paternal separation was positively associated with both schizophrenia and bipolar disorder. Associations between separation from both parents and schizophrenia were stronger when separation occurred at later ages, while those with bipolar disorder remained stable across development. The first occurrence of paternal separation appeared to increase risk more when it occurred earlier in childhood. Associations differed according to parental history of mental disorder, although in no situation was separation protective. Effects of parental separation may differ by type, developmental timing and family characteristics. These findings highlight the importance of considering such factors in studies of childhood adversity.

Criminal conviction among offspring with parental history of mental disorder

Offspring of parents with mental disorder are at risk of a range of adverse outcomes. We sought to establish whether such risks extend to offending by examining rates of criminal conviction, including conviction for violent and sexual offences, among offspring of parents with mental disorder compared to offspring without parental disorder. From a random sample of the Danish population, a cohort aged ≤15 years (n=412,117) was followed for the occurrence of conviction between January 1981 and December 2006. Incidence rate ratios (IRRs) and cumulative incidences for offspring conviction by parental mental disorder status were calculated using a Cox regression model. Analyses were repeated for conviction for a serious first offence. Offspring with history of parental mental disorder had higher rates of conviction than those without parental disorder; rates were highest for those with two affected parents [IRR 3.39, 95% confidence interval (CI) 3.08-3.73]. The association persisted when parental gender, offspring gender and the nature of parental disorder were considered. Absolute rates were lower but relative rates higher for female offspring (IRR 3.26 for males with two affected parents, 4.52 for females). Similar patterns were seen for conviction for serious offences. Associations were attenuated after adjustment was made for family socio-economic position (SEP) and parental criminality. Offspring of parents with mental disorder represent a group at elevated risk of criminality. This raises the possibility of shared familial vulnerability for mental disorder and criminal behaviour, and highlights the need to consider early identification and intervention in this group.

Full Spectrum of Psychiatric Outcomes Among Offspring With Parental History of Mental Disorder

While concordant parent/offspring risks for specific mental disorders are well established, knowledge of the broader range of psychiatric outcomes among offspring with parental history of mental disorder is lacking. To examine the full range of mental health outcomes among offspring of parents with serious and other mental disorders compared with those whose parents had no such history. Population-based cohort study. Offspring were followed up from their 14th birthday for the development of mental disorders based on both outpatient and inpatient hospital data. Danish population. All offspring born in Denmark between 1980 and 1994 (N = 865 078) with follow-up to December 2008. Incidence rates, incidence rate ratios, and cumulative incidences for offspring psychiatric outcomes. Parental serious mental disorder (SMD) (nonaffective or affective psychosis) was found to be positively associated with virtually all offspring psychiatric outcomes, including those not hitherto regarded as clinically related. Offspring of parents without SMD but with a history of "other mental disorder" were also found to be at increased risk of developing a range of mental disorders. The strongest associations were found where both parents had a history of mental disorder (eg, offspring of 2 parents with SMD were 13 times more likely to develop schizophrenia). Elevated risks were not confined to concordant parent/offspring disorders (eg, offspring of 2 parents with SMD were 8 times more likely to develop substance misuse disorders). The impact of parental history of mental disorder was not confined to elevated offspring risk of concordant disorders but rather offspring are at increased risk of a wide range of mental disorders, particularly those with 2 affected parents. Our results imply an important role for etiological factors giving rise to broad, as well as specific, familial vulnerabilities. These findings also have potential implications for diagnostic classification.

Social phobia and potential childhood risk factors in a community sample

This study examined the relationship between potential childhood risk factors and social phobia in an epidemiological sample. Identifying risk factors such as childhood adversities can often uncover important clues as to the aetiology of a disorder. This information also enables health care providers to predict which individuals are most likely to develop the disorder. Data came from the Mental Health Supplement to the Ontario Health Survey of a survey of 8116 Canadian respondents, aged 15-64. Social phobia was diagnosed using the Composite International Diagnostic Interview (CIDI). Childhood risk factors were assessed by a series of standardized questions. A positive relationship was observed between social phobia and lack of close relationship with an adult, not being first born (in males only), marital conflict in the family of origin, parental history of mental disorder, moving more than three times as a child, juvenile justice and child welfare involvement, running away from home, childhood physical and sexual abuse, failing a grade, requirement of special education before age 9 and dropping out of high school. Many of these variables remained significant after controlling for phobias, major depressive disorder and alcohol abuse. The data also suggest that some childhood risk factors may interact with gender to influence the development of social phobia. Although an association was detected between social phobia and childhood risk factors, naturalistic prospective studies are needed to clarify the aetiological importance of these and other potential risk factors for the disorder.