Search

Intellectual disability (ID) aggregates in families, but factors affecting individual risk and heritability estimates remain unknown.A population-based family cohort study of 4,165,785 individuals born 1973-2013 in Sweden, including 37,787 ID individuals and their relatives. The relative risks (RR) of ID with 95% confidence intervals (95% CI) were obtained from stratified Cox proportional-hazards models. Relatives of ID individuals were compared to relatives of unaffected individuals. Structural equation modeling was used to estimate heritability.Relatives of ID individuals were at increased risk of ID compared to individuals with unaffected relatives. The RR of ID among relatives increased proportionally to the degree of genetic relatedness with ID probands; 256.70(95% CI 161.30-408.53) for monozygotic twins, 16.47(13.32-20.38) for parents, 14.88(12.19-18.16) for children, 7.04(4.67-10.61) for dizygotic twins, 8.38(7.97-8.83) for full siblings, 4.56(4.02-5.16) for maternal, 2.90(2.49-3.37) for paternal half-siblings, 3.03(2.61-3.50) for nephews/nieces, 2.84(2.45-3.29) for uncles/aunts, and 2.04(1.91-2.20) for cousins. Lower RRs were observed for siblings of probands with chromosomal abnormalities (RR 5.53, 4.74-6.46) and more severe ID (mild RR 9.15, 8.55-9.78, moderate RR 8.13, 7.28-9.08, severe RR 6.80, 5.74-8.07, and profound RR 5.88, 4.52-7.65). Male sex of relative and maternal line of relationship with proband was related to higher risk (RR 1.33, 1.25-1.41 for brothers vs. sisters and RR 1.49, 1.34-1.68 for maternal vs. paternal half-siblings). ID was substantially heritable with 0.95(95% CI 0.93-0.98) of the variance in liability attributed to genetic influences.The risk estimates will benefit researchers, clinicians, families in understanding the risk of ID in the family and the whole population. The higher risk of ID related to male sex and maternal linage will be of value for planning and interpreting etiological studies in ID.

BACKGROUND More knowledge about risks of clinical outcomes associated with nonsuicidal self-injury (NSSI) and suicide attempts (SAs) is needed to inform risk assessment and intervention. METHODS Longitudinal cohort study based on 1,855 youths was clinically assessed for NSSI and SA, and followed up (from December, 2011 to December 2013) for the outcomes; diagnosed self-injury, alcohol/substance use disorder, and psychiatric inpatient care data derived from Swedish registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) of the outcomes were estimated with Cox regressions, and additionally adjusted for the potential effect of sex and the number of clinical assessments. NSSI and SA were treated as time-varying covariates. RESULTS Youths with NSSI had elevated risks of all outcomes, compared with youths without NSSI or SA; the HR was 2.3, 95% confidence interval [1.6, 3.4] for self-injury, 1.4 [0.9, 2.1] for alcohol/substance use disorder, and 1.3 [1.0, 1.7] for psychiatric inpatient care. Youths with SA displayed higher risks for the outcomes than the NSSI group; the HR was 5.5 [2.4, 12.6] for self-injury, 2.0 [0.9, 4.4] for alcohol/substance use disorder, and 2.6 [1.5, 4.5] for psychiatric inpatient care. Youths with both NSSI and SA showed similar risks as youths with SA; HR 4.1 [2.0, 8.3] for self-injury, 2.0 [1.1, 4.1] for alcohol/substance use disorder, but a higher risk of psychiatric inpatient care; HR 5.0 [3.1, 7.9]. All results remained virtually unchanged in the adjusted analyses. CONCLUSIONS Youths with NSSI and/or SA had higher risks for subsequent adverse clinical outcomes. These excess risks were more pronounced among youths with SA and youths with both NSSI and SA, and the risk for psychiatric inpatient care was particularly high in youths with both NSSI and SA. Our findings suggest that early interventions for youths with NSSI or SA should not exclusively focus on suicide prevention, but also consider the risk of subsequent alcohol/substance use disorder.

Background\ud \ud Familial and genetic associations between autism spectrum disorder (ASD) and other neurodevelopmental and psychiatric disorders have been reported, sometimes with conflicting results. We estimated familial and genetic associations between ASD and nine disorder groups, and explored differences in these associations for ASD in the context of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations.\ud Methods\ud \ud Individuals born between 1985 and 2009 living in Sweden on their seventh birthday were linked to their biological parents in order to identify different types of relatives. We retrieved information on all the disorders considered from the National Patient Register. Logistic regression was used to estimate the familial association between ASD and other neurodevelopmental and psychiatric disorders in the different groups of relatives. Structural equation modeling was used to estimate phenotypic (rp) and genetic associations (rg), as well as the contribution of genetic influences to rp.\ud Results\ud \ud The study included 2,398,608 individuals. Among relatives of individuals diagnosed with ASD, there was an increased risk of the disorders considered, compared to relatives of individuals who were not diagnosed with ASD. Stronger associations were detected for ASD without any additional diagnosis of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations. The strongest genetic correlation was estimated between ASD and other neurodevelopmental disorders (rg = 0.73; 95% CI = 0.66–0.79). Moderate genetic correlations were estimated for anxiety disorders (rg = 0.47; 95% CI = 0.33–0.61), depression (rg = 0.52; 95% CI = 0.37–0.66), and intentional self-harm (rg = 0.54; 95% CI = 0.36–0.71).\ud Conclusions\ud \ud ASD shows familial and genetic association not only with other neurodevelopmental disorders, but also with other psychiatric disorders, such as anxiety, depression, and intentional self-harm. Family history of ASD comorbid with intellectual disability, epilepsy, congenital malformations, or chromosomal abnormalities is less related to other psychiatric disorders, potentially suggesting a different etiology for this subgroup of patients.

BACKGROUND The prevalence of diagnosed Autism Spectrum Disorder (ASD) has increased substantially across the world. Much - or even most - prevalence increase seems to reflect changes in diagnostic practice and ascertainment. A key part of ASD assessment is to document that the relevant symptoms are associated with clinical impairment. The aim of the present study is to capitalize on a nationwide longitudinal study spanning 15 consecutive birth year cohorts in order to investigate whether there has been a secular change in how parents perceive the impairment and suffering conferred by autism symptomatology in their children. METHODS Data came from the Child and Adolescent Twin Study in Sweden (27,240 individuals), where parents had reported on their child's ASD symptoms and impairment. Impairment due to ASD symptoms was regressed on an ASD symptom score across time. This was done for five 3-year birth cohorts (1995-1997, 1998-2000, 2001-2003, 2004-2006, and 2007-2009). RESULTS Reported impairment increased with consecutively later birth cohorts. This was evident across all levels of autism symptomatology. At clinically relevant levels of symptomatology, parents of those born 2007-2009 reported a 23% higher degree of impairment as compared with parents of those born in 1995-1997. The relative difference, however, was even greater at levels that previously would have been considered below the diagnostic threshold. DISCUSSION The results presented here contribute to the notion of a growing diffuseness in the conceptualization of the ASD diagnosis by adding the element of secular changes in the parental perception of the consequences of ASD symptom expression.

BACKGROUND Attention-deficit/hyperactivity disorder (ADHD) frequently co-occurs with other psychiatric disorders. Twin studies have established that these co-occurrences are in part due to shared genetic risks. However, the strength of these genetic overlaps and the potential heterogeneity accounted for by type of psychiatric symptoms, age, and methods of assessment remain unclear. We conducted a systematic review to fill this gap. METHODS We searched PubMed, PsycINFO, Embase, and Web of Science until March 07, 2019. Genetic correlations (rg ) were used as effect size measures. RESULTS A total of 31 independent studies fulfilled the inclusion criteria. The pooled estimates showed that the associations between ADHD and other psychiatric symptoms were partly explained by shared genetic factors, with a pooled genetic correlation of 0.50, 95% confidence interval: 0.46-0.60. The genetic correlations (rg ) between ADHD and externalizing (rg = .49 [0.37-0.61]), internalizing (rg = .50 [0.39-0.69]), and neurodevelopmental (rg = .56 [0.47-0.66]) symptoms were similar in magnitude. The genetic correlations in childhood and adulthood were rg = .53 (0.43-0.63) and rg = .51 (0.44-0.56), respectively. For methods of assessment, the genetic correlations were also similar in strength, self-reports rg = .52 (0.47-0.58), other informants rg = .55 (0.41-0.69), and combined raters rg = .50 (0.33-0.65). CONCLUSIONS These findings indicate that the co-occurrence of externalizing, internalizing, and neurodevelopmental disorder symptoms in individuals with ADHD symptoms in part is due to a shared genetic risk.

Background A better understanding of the trajectories and economic burden of psychiatric and somatic disorders (multimorbidity) in ADHD from childhood to adulthood is important for guiding more targeted areas for treatment of ADHD and prevention of multimorbidity, and for forecasting demands on the medical infrastructure. This study aimed to investigate patterns of healthcare utilization and costs of multimorbidity across young adulthood in individuals with a childhood ADHD diagnosis, and additionally in individuals who continue to have ADHD-related contact with health services (persisters) and those who do not (remitters). Methods We prospectively followed a cohort (N = 445,790) born 1987-1990 from the ages of 18 to 26 years. Data on healthcare utilization were obtained from the Swedish National Patient Register (inpatient and outpatient care) and the Prescribed Drug Register (medication prescriptions). Results Mean annual costs per capita from multimorbidity was €890 ($1,223) in individuals with a childhood ADHD diagnosis (persisters/remitters: €1,060[$1,456]/€609[$837]) and €304 ($418) in individuals without. Costs were largely driven by inpatient hospital admissions, mainly from drug abuse and injuries. Healthcare utilization and costs of psychiatric and somatic disorders at 18 years was significantly higher in individuals with childhood ADHD compared to those without. These group differences remained stable or increased across young adulthood for most outcomes and were generally larger in women than in men. ADHD remitters continued to show significantly greater healthcare utilization and costs compared to individuals without childhood ADHD, although their profiles were not as severe as ADHD persisters. Conclusions Childhood ADHD has long-term associations with both psychiatric and somatic disorders. Findings demonstrate the individual and societal burden of ADHD in adulthood and highlight the importance of continued support from childhood-adolescent to adult health services and early prevention of multimorbidity. Findings also point to specific targets for intervention that may be effective, such as drug abuse and injuries.