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Cel pracyDokonanie porównań w zakresie funkcji rodzin nastolatków (13-16 lat) z rozpoznaniem ADHD lub ADHD i opozycyjno-buntowniczych zaburzeń zachowania (ODD).MetodaOcena przy użyciu Kwestionariusza do Oceny Rodziny w trzech grupach nastolatków, wychowujących się w rodzinach biologicznych: (1) grupie ADHD/ODD (n=40), (2) grupie ADHD (n=40) oraz (3) grupie K (kontrolnej) nastolatków (n=40), którzy nie korzystali obecnie lub w przeszłości z opieki psychologicznej lub psychiatrycznej.WynikiMatki, ojcowie i nastolatkowie z grupy ADHD/ODD istotnie gorzej ocenili wszystkie istotne aspekty funkcjonowania rodziny w porównaniu z grupą kontrolną. W grupie ADHD stwierdzono mniej korzystnie w odniesieniu do grupy kontrolnej oceny matek i ojców dla wszystkich obszarów funkcjonowania rodziny oraz oceny nastolatków w wymiarze Pełnienia ról, Emocjonalności, Afektywnego nawiązywania relacji oraz Kontroli. Badani z grupy ADHD/ODD i ich rodzice gorzej ocenili funkcjonowanie rodziny w odniesieniu do grupy ADHD: matki-we wszystkich opisywanych obszarach, nastolatkowie-w większości z opisywanych obszarów poza wymiarem Kontroli, a ojcowie w większości z opisywanych obszarów poza wymiarem Emocjonalności.WnioskiFunkcjonowanie rodzin pacjentów z ADHD i opozycyjno- buntowniczymi zaburzeniami zachowania oraz rodzin pacjentów z ADHD istotnie negatywnie różni się we wszystkich lub większości badanych wymiarów w odniesieniu do rodzin osób bez diagnozy, przy czym funkcjonowanie rodzin pacjentów z ADHD i opozycyjno- buntowniczymi zaburzeniami zachowania można opisać jako bardziej nieprawidłowe niż rodzin pacjentów z ADHD.

To examine the association of childhood-onset type 1 diabetes (T1D) and attention-deficit/hyperactivity disorder (ADHD) with educational outcomes from compulsory school to university.Using multiple Swedish nationwide registers, we followed up on 1,474,941 individuals born in Sweden from 1981-1995 to December 31, 2013. Associations of T1D and ADHD with achieving educational milestones (from compulsory school to university) and school performances were estimated using logistic and linear regression models and sibling comparison models.Compared to their peers, children with both T1D and ADHD were less likely to achieve any of the educational attainments, including completing compulsory school (adjusted OR [aOR] [95% CI]: 0.43 [0.26, 0.72]), be eligible to and finishing upper secondary school (0.26 [0.19, 0.36], 0.24 [0.17, 0.35], respectively), and starting university (0.38 [0.17, 0.90]). The odds of achieving these educational milestones were substantially lower in children with ADHD alone (aORs: 0.14-0.44), but were slightly worse or no differences in children with T1D alone (aORs: 0.86-1.08). All associations above remained similar in the sibling comparison models.Children and adolescents with both T1D and ADHD had long-term educational underachievement, with ADHD being the major contributor. Our findings suggest the importance of assessing ADHD in children with T1D and targeted support for minimising the education gap between the affected children and their peers.

Cel pracyOcena wzorców przywiązania wśród nastolatków (13-16 lat) z rozpoznaniem ADHD lub ADHD i opozycyjno- buntowniczymi zaburzeniami zachowania (ODD).MetodaOcena przy użyciu Inwentarza Przywiązania do Rodziców i Rówieśników (IPPA) oraz Kwestionariusza Przywiązania do Rodziców (PBI) w trzech grupach nastolatków, wychowujących się w rodzinach biologicznych: (1) grupie ADHD/ODD (n=40), (2) grupie ADHD (n=40) oraz (3) grupie K (kontrolnej) nastolatków (n=40), którzy nie korzystali obecnie lub w przeszłości z opieki psychologicznej lub psychiatrycznej.WynikiWzorce przywiązania do rodziców w obszarze Zaufania, Komunikacji i Alienacji (IPPA) oraz Troski i Kontroli (PBI) w grupie ADHD/ODD różnią się istotnie w porównaniu z grupą kontrolną. Nastolatki z grupy ADHD/ODD opisują istotnie mniej doświadczanego Zaufania i Komunikacji (IPPA) oraz Troski (PBI) w relacjach z rodzicami a więcej Alienacji (IPPA) i Kontroli (PBI), niż nastolatki z grupy ADHD. Wzorce przywiązania do rówieśników w obu grupach klinicznych i kontrolnej różnią się istotnie. W grupie ADHD/ODD dominuje lękowo – unikający styl przywiązania do matki oraz ojca, w grupie ADHD styl bezpieczny w relacji z matką oraz lękowo-unikający w relacji z ojcem. W relacjach z rówieśnikami w grupie ADHD/ODD oraz grupie ADHD dominuje styl lękowo-unikający.WnioskiObraz przywiązania istotnie różni się u nastolatków z rozpoznaniem ADHD i opozycyjno – buntowniczych zaburzeń zachowania i nastolatków z rozpoznaniem ADHD. W grupie ADHD/ODD oraz grupie ADHD w odróżnieniu od grupy nastolatków bez diagnozy psychiatrycznej, dominują pozabezpieczne wzorce przywiązania do rodziców i rówieśników (głównie styl lękowo- unikający).

Background Intellectual disability (ID) is associated with violent and sexual offending and victimization, but the importance of neuropsychiatric comorbidity and severity of disability remains unclear. Methods In a register-based cohort study of people born in Sweden 1980–1991 (n = 1 232 564), we investigated associations of mild and moderate/severe ID with any, violent and sexual crimes, and with assault victimization, stratified by comorbid autism and attention deficit hyperactivity disorder (ADHD). We defined ID by attendance at a special school or registered diagnosis and obtained data on criminal convictions and injuries or deaths due to assaults from nationwide registers until end of 2013. Results Compared to people without ID, autism or ADHD, men and women with mild or moderate/severe ID and comorbid ADHD had elevated risks of violent crimes [range of hazard ratios (HRs) 4.4–10.4] and assault victimization (HRs 2.0–7.7). Women with mild ID without comorbidities or with comorbid autism also had elevated risks of violent crimes and victimization (HRs 1.8–4.6) compared to women without ID, autism or ADHD. The relative risks of sexual offending and victimization were elevated in men and women with ID without comorbidities (HRs 2.6–12.7). The highest risks for sexual offending in men (HRs 9.4–11.0) and for sexual assault victimization in women (HRs 11.0–17.1) related to ID and comorbid ADHD. Conclusions The elevated risk of violent offending and assault victimization in people with ID is largely explained by comorbid ADHD, whereas ID is independently associated with sexual crimes and victimization, even though absolute risks are low.

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is associated with an increased risk of poor mental health. However, the understanding of ADHD-related burden and impairments in women during the postpartum period is limited. The aim with the present study was to examine the risk of depression and anxiety disorders during the postpartum period among women with and without an ADHD diagnosis.METHODS: We used register-based data to identify women who gave birth to their first and/or second child between 2005 and 2013 in Sweden (n = 773,047), of which 0.5 % (n = 3515) had a diagnosis of ADHD prior to pregnancy. Diagnoses of depression and anxiety disorders up to one year after delivery were collected from the national patient register.RESULTS: A total of 16.76 % of the women with an ADHD diagnosis were also diagnosed with depression disorders in the postpartum period, prevalence ratio (PR) 5.09 (95 % confidence interval (CI), 4.68-5.54). A total of 24.92 % of the women with an ADHD diagnosis were also diagnosed with anxiety disorders in the postpartum period, PR 5.41 (5.06-5.78). Stratified results revealed that having a diagnosis of ADHD increased the risk for both depression and anxiety disorders postpartum, beyond other well-known risk factors.LIMITATIONS: There is a potential risk of surveillance bias as women diagnosed with ADHD are more likely to have repeated visits to psychiatric care and might have an enhanced likelihood of also being diagnosed with depression and anxiety disorders postpartum, compared to women without ADHD.CONCLUSIONS: ADHD is an important risk factor for both depression and anxiety disorders postpartum. Therefore, ADHD needs to be considered in the maternal care, regardless of sociodemographic factors and the presence of other psychiatric disorders.

Background Turner syndrome is the result of the partial or complete absence of an X chromosome in phenotypic girls. This can cause an array of medical and developmental difficulties. The intelligence quotient in females with Turner syndrome has previously been described as uneven, but considered within normal range. Although their social, intellectual, and psychiatric profile is described, it is unclear to what extent these females meet the clinical criteria for neurodevelopmental or psychiatric diagnoses. The aim of this study was to examine the prevalence of neurodevelopmental and psychiatric disorders in females with Turner syndrome. Methods A retrospective cohort study was performed with a total of 1392 females with Turner syndrome identified through the Swedish National Patient Register and compared with 1:100 age- and sex-matched controls from the general population. The associations between Turner syndrome and diagnoses of neurodevelopmental and/or psychiatric disorders were calculated using conditional logistic regression and is presented as estimated risk (odds ratio, OR, 95% confidence interval, CI) in females with Turner syndrome compared with matched controls. Results Females with Turner syndrome had a higher risk of neurodevelopmental or psychiatric disorder (OR 1.37, 95% CI 1.20–1.57), an eightfold increased risk of intellectual disability (OR 8.59, 95% CI 6.58–11.20), and a fourfold increased risk of autism spectrum disorder (OR 4.26, 95% CI 2.94‑6.18) compared with the controls. In addition, females with Turner syndrome had twice the risk of a diagnosis of schizophrenia and related disorders (OR 1.98, 95% CI 1.36–2.88), eating disorders (OR 2.03, 95% CI 1.42–2.91), and behavioral and emotional disorders with onset in childhood (OR 2.01, 95% CI 1.35–2.99). Conclusions Females with Turner syndrome have an increased risk of receiving a diagnosis of neurodevelopmental or psychiatric disorder. This warrants extensive assessment of intellectual and cognitive functions from early age, and increased psychiatric vigilance should be a part of lifelong healthcare for females with Turner syndrome.

Psychiatric disorders are common among autistic children and adults. Little is known about sex differences in psychiatric disorders and hospitalization in early adulthood.To examine sex differences in psychiatric diagnoses and hospitalizations in autistic compared with nonautistic young adults.This population-based cohort study assessed all individuals born in Sweden between 1985 and 1997. A total of 1 335 753 individuals, including 20 841 autistic individuals (7129 [34.2%] female individuals), were followed up from age 16 through 24 years between 2001 and 2013. Analysis took place between June 2021 and August 2022.Autism was defined as having received at least 1 clinical diagnosis of autism based on the International Classification of Diseases.The cumulative incidence of 11 psychiatric diagnoses up until age 25 years was estimated, and birth year-standardized risk difference was used to compare autistic female and male individuals directly. Sex-specific birth year-adjusted hazard ratios (HRs) with 95% CIs were calculated using Cox regression. Analyses were repeated for inpatient diagnoses to assess psychiatric hospitalization.Of 1 335 753 individuals included in this study, 650 314 (48.7%) were assigned female at birth. Autism was clinically diagnosed in 20 841 individuals (1.6%; 7129 [34.2%] female) with a mean (SD) age of 16.1 (5.1) years (17.0 [4.8] years in female individuals and 15.7 [5.2] years in male individuals) for the first recorded autism diagnosis. For most disorders, autistic female individuals were at higher risk for psychiatric diagnoses and hospitalizations. By age 25 years, 77 of 100 autistic female individuals and 62 of 100 autistic male individuals received at least 1 psychiatric diagnosis. Statistically significant standardized risk differences were observed between autistic female and male individuals for any psychiatric disorder (-0.18; 95% CI, -0.26 to -0.10) and specifically for anxiety, depressive, and sleep disorders. Risk differences were larger among autistic than nonautistic individuals. Compared with nonautistic same-sex individuals, autistic female individuals (HR range [95% CI], 3.17 [2.50-4.04.]-20.78 [18.48-23.37]) and male individuals (HR range [95% CI], 2.98 [2.75-3.23]-18.52 [17.07-20.08]) were both at increased risk for all psychiatric diagnoses. Any psychiatric hospitalization was statistically significantly more common in autistic female individuals (32 of 100) compared with autistic male individuals (19 of 100). However, both autistic female and male individuals had a higher relative risk for psychiatric hospitalization compared with nonautistic female and male individuals for all disorders (female individuals: HR range [95% CI], 5.55 [4.63-6.66]-26.30 [21.50-32.16]; male individuals: HR range [95% CI], 3.79 [3.22-4.45]-29.36 [24.04-35.87]).These findings highlight the need for profound mental health services among autistic young adults. Autistic female individuals, who experience more psychiatric difficulties at different levels of care, require increased clinical surveillance and support.

Objective To assess the association and familial co-aggregation between early-onset type 2 diabetes (diagnosed before age 45) and mood, anxiety, and stress-related disorders, and estimate the contribution of genetic and environmental factors to their co-occurrence. Research Design and Methods This population-based cohort study included individuals born in Sweden 1968-1998, from whom pairs of full-siblings, half-siblings, and cousins were identified. Diagnoses of early-onset type 2 diabetes and mood (including unipolar depression and bipolar disorder), anxiety, and stress-related disorders were obtained from the National Patient Register. Logistic and Cox regression models were used to assess the phenotypic association and familial co-aggregation between type 2 diabetes and psychiatric disorders. Quantitative genetic modeling was conducted in full- and maternal half-sibling pairs to estimate the relative contributions of genetic and environmental factors to the association. Results Among a total of 3,061,192 individuals, 7,896(0.3%) were diagnosed with early-onset type 2 diabetes. These individuals showed higher risks of any diagnosis (Odds Ratio [OR][95%CI]: 3.62[3.44,3.80]) and specific diagnosis of unipolar depression (3.97[3.75,4.22]), bipolar disorder (4.17[3.68,4.73]), anxiety (3.76[3.54,3.99]) and stress-related disorders (3.35[3.11,3.61]). Relatives of individuals with early-onset type 2 diabetes also had higher overall risks of the examined psychiatric disorders (ORs:1.03-1.57). These associations are largely explained by genetic factors (51%-78%), with the rest explained by non-shared environmental factors. Conclusion Our findings highlight the burden of mood, anxiety, and stress-related disorders in early-onset type 2 diabetes and demonstrate that shared familial liability may contribute to their co-occurrence, suggesting that future research should aim to identify shared risk factors and ultimately refine preventive and intervention strategies.

Objective To estimate the association and familial co-aggregation of childhood-onset type 1 diabetes with depression, anxiety, and stress-related disorders. Research design and methods Population-based cohort study using data from Swedish nationwide registers. A total of ~3.5 million individuals born in Sweden 1973-2007 were linked to their biological parents, full- and half-siblings, and cousins. Cox models were used to estimate the association and familial co-aggregation of type 1 diabetes with depression, anxiety, and stress-related disorders. Results Individuals diagnosed with childhood-onset type 1 diabetes (n=20,005) were found to be at greater risks of all outcomes: any psychiatric diagnosis (adjusted Hazard Ratio [aHR] [95% Confidence Intervals]: 1.66 [1.59-1.72]) or specific diagnoses of depression (1.85 [1.76-1.94]), anxiety (1.41[1.33-1.50]), stress-related disorders (1.75 [1.62-1.89]), as well as using antidepressants or anxiolytics (1.30 [1.26-1.34]), compared to individuals without type 1 diabetes. Overall, relatives of individuals with type 1 diabetes were at elevated risks of developing these outcomes, with the highest risks seen in parents (aHRs: 1.18-1.25), followed by full-siblings (aHRs: 1.05-1.20), and the magnitudes of risk estimates appear proportional to familial relatedness. Conclusion These results support existing evidence that children and adolescents with type 1 diabetes are at greater risks of developing depression, anxiety, and stress-related disorders and indicate that shared familial factors might contribute to these elevated risks. Our findings highlight the need for psychological consulting for children and their families in diabetes care. Quantitative and molecular genetic studies are warranted to further understand the etiology of these psychiatric disorders in type 1 diabetes.

Context Neurodevelopmental disorders are more prevalent in childhood-onset type 1 diabetes than in the general population, and the symptoms may limit the individual’s ability for diabetes management. Objective This study investigated whether comorbid neurodevelopmental disorders are associated with long-term glycemic control and risk of diabetic complications. Methods This population-based cohort study used longitudinally collected data from Swedish registers. We identified 11 326 individuals born during 1973-2013, diagnosed with type 1 diabetes during 1990-2013 (median onset age: 9.6 years). Among them, 764 had a comorbid neurodevelopmental disorder, including attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, and intellectual disability. We used multinomial logistic regression to calculate odds ratios (ORs) of having poor glycemic control (assessed by glycated hemoglobin [HbA1c]) and Cox regression to estimate hazard ratios (HRs) of nephropathy and retinopathy. Results The median follow-up was 7.5 years (interquartile range [IQR] 3.9, 11.2). Having any neurodevelopmental disorder (ORadjusted 1.51 [95% CI 1.13, 2.03]), or ADHD (ORadjusted 2.31 [95% CI 1.54, 3.45]) was associated with poor glycemic control (mean HbA1c > 8.5%). Increased risk of diabetic complications was observed in patients with comorbid neurodevelopmental disorders (HRadjusted 1.72 [95% CI 1.21, 2.44] for nephropathy, HRadjusted 1.18 [95% CI 1.00, 1.40] for retinopathy) and patients with ADHD (HRadjusted 1.90 [95% CI 1.20, 3.00] for nephropathy, HRadjusted 1.33 [95% CI 1.07, 1.66] for retinopathy). Patients with intellectual disability have a particularly higher risk of nephropathy (HRadjusted 2.64 [95% CI 1.30, 5.37]). Conclusion Comorbid neurodevelopmental disorders, primarily ADHD and intellectual disability, were associated with poor glycemic control and a higher risk of diabetic complications in childhood-onset type 1 diabetes.

Aims/hypothesis The aim of this study was to investigate the effect of childhood-onset type 1 diabetes on the risk of subsequent neurodevelopmental disorders, and the role of glycaemic control in this association. We hypothesised that individuals with poor glycaemic control may be at a higher risk of neurodevelopmental disorders compared with the general population, as well as compared with individuals with type 1 diabetes with adequate glycaemic control. Methods This Swedish population-based cohort study was conducted using data from health registers from 1973 to 2013. We identified 8430 patients with childhood-onset type 1 diabetes (diagnosed before age 18 years) with a median age of diabetes onset of 9.6 (IQR 5.9–12.9) and 84,300 reference individuals from the general population, matched for sex, birth year and birth county. Cox models were used to estimate the effect of HbA1c on the risk of subsequent neurodevelopmental disorders, including attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD) and intellectual disability. Results During a median follow-up period of 5.6 years, 398 (4.7%) individuals with type 1 diabetes received a diagnosis of any neurodevelopmental disorder compared with 3066 (3.6%) in the general population, corresponding to an adjusted HR (HRadjusted) of 1.31 (95% CI 1.18, 1.46) after additionally adjusting for other psychiatric morbidity prior to inclusion, parental psychiatric morbidity and parental highest education level. The risk of any neurodevelopmental disorder increased with HbA1c levels and the highest risk was observed in patients with mean HbA1c >8.6% (>70 mmol/mol) (HRadjusted 1.90 [95% CI 1.51, 2.37]) compared with reference individuals without type 1 diabetes. In addition, when compared with patients with diabetes with HbA1c 1c >8.6% (>70 mmol/mol) had the highest risk of any neurodevelopmental disorder (HRadjusted 3.71 [95% CI 2.75, 5.02]) and of specific neurodevelopmental disorders including ADHD (HRadjusted 4.16 [95% CI 2.92, 5.94]), ASD (HRadjusted 2.84 [95% CI 1.52, 5.28]) and intellectual disability (HRadjusted 3.93 [95% CI 1.38, 11.22]). Conclusions/interpretation Childhood-onset type 1 diabetes is associated with an increased risk of neurodevelopmental disorders, with the highest risk seen in individuals with poor glycaemic control. Routine neurodevelopmental follow-up visits should be considered in type 1 diabetes, especially in patients with poor glycaemic control. Graphical abstract

OBJECTIVE To ascertain the association and coaggregation of eating disorders and childhood-onset type 1 diabetes in families. RESEARCH DESIGN AND METHODS Using population samples from national registers in Sweden (n = 2,517,277) and Demark (n = 1,825,920), we investigated the within-individual association between type 1 diabetes and eating disorders and their familial coaggregation among full siblings, half siblings, full cousins, and half cousins. On the basis of clinical diagnoses, we classified eating disorders into any eating disorder (AED), anorexia nervosa (AN) and atypical AN, and other eating disorder (OED). Associations were determined with hazard ratios (HRs) with 95% CIs from Cox regressions. RESULTS Swedish and Danish individuals with a type 1 diabetes diagnosis had a greater risk of receiving an eating disorder diagnosis (HR [95% CI] Sweden: AED 2.02 [1.80–2.27], AN 1.63 [1.36–1.96], OED 2.34 [2.07–2.63]; Denmark: AED 2.19 [1.84–2.61], AN 1.78 [1.36–2.33], OED 2.65 [2.20–3.21]). We also meta-analyzed the results: AED 2.07 (1.88–2.28), AN 1.68 (1.44–1.95), OED 2.44 (2.17–2.72). There was an increased risk of receiving an eating disorder diagnosis in full siblings in the Swedish cohort (AED 1.25 [1.07–1.46], AN 1.28 [1.04–1.57], OED 1.28 [1.07–1.52]); these results were nonsignificant in the Danish cohort. CONCLUSIONS Patients with type 1 diabetes are at a higher risk of subsequent eating disorders; however, there is conflicting support for the relationship between having a sibling with type 1 diabetes and an eating disorder diagnosis. Diabetes health care teams should be vigilant about disordered eating behaviors in children and adolescents with type 1 diabetes.

BACKGROUND: Attention deficit/hyperactivity disorder (ADHD) medications are used by increasing numbers of reproductive-aged women. Findings from studies exploring the safety of these medications during pregnancy are mixed, and it is unclear whether associations reflect causal effects or could be partially or fully explained by other factors that differ between exposed and unexposed offspring. OBJECTIVES: The aim of this systematic review was to evaluate the adverse pregnancy-related and offspring outcomes associated with exposure to prescribed ADHD medication during pregnancy, with a focus on how studies to date have handled the influence of confounding. METHODS: We searched PubMed, Embase, PsycINFO, and Web of Science up to July 1(st), 2019, without any restrictions on language or date of publication. We included all observational studies (e.g. cohort studies, case control studies, case-crossover studies, cross-sectional studies, and registry-based studies) with pregnant women of any age or from any setting who were prescribed ADHD medications and evaluated any outcome, including both short- and long-term maternal and offspring outcomes. Two independent authors then used the Newcastle-Ottawa Scale (NOS) to rate the quality of the included studies. RESULTS: Eight cohort studies that estimated adverse pregnancy-related and offspring outcomes associated with exposure to ADHD medication during pregnancy were included in the qualitative review. There were substantial methodological differences across the included studies regarding data sources, type of medications examined, definitions of studied pregnancy-related and offspring outcomes, types of control groups, and confounding adjustment. There was no convincing evidence for teratogenic effects according to the relative risk of pregnancy-related and offspring outcomes, and the observed differences in absolute risks were overall small in magnitude. Inadequate adjustment for confounding existed in most studies, and none of the included studies adjusted for ADHD severity in the mothers. CONCLUSION: The available data are too limited to make an unequivocal recommendation regarding the use of ADHD medication during pregnancy. Therefore, physicians should weigh whether the advantages of using ADHD medication outweigh the potential risks for the developing fetus according to the different situation of each particular woman. Future research should attempt to triangulate research findings based on a combination of different designs that differ in their underlying strengths and limitations and should investigate specific confounding factors, the potential impact of timing of exposure, and potential long-term outcomes in the offspring.

ImportanceResearch shows that children and adolescents with type 1 diabetes (T1D), compared with their peers without diabetes, have a greater risk of psychiatric disorders. However, no study has comprehensively examined whether having psychiatric disorders is associated with educational outcomes in children and adolescents with T1D.ObjectiveTo investigate educational outcomes in children and adolescents with T1D with and without psychiatric disorders.Design, Setting, and ParticipantsThis cohort study used data from multiple Swedish registers. The main study cohort included individuals born in Sweden between January 1, 1973, and December 31, 1997, who were followed up from birth through December 31, 2013. Data analyses were conducted from March 1 to June 30, 2022.ExposuresType 1 diabetes and psychiatric disorders (including neurodevelopmental disorders, depression, anxiety disorders, eating disorders, bipolar disorder, psychotic disorder, and substance misuse) diagnosed before 16 years of age.Main Outcomes and MeasuresAchieving educational milestones (completing compulsory school [primary and lower secondary education], being eligible to and finishing upper secondary school, and starting and finishing university) and compulsory school performances.ResultsOf 2 454 862 individuals (51.3% male), 13 294 (0.5%; 53.9% male) were diagnosed with T1D (median [IQR] age at diagnosis, 9.5 [6.0-12.5] years), among whom 1012 (7.6%) also had at least 1 psychiatric disorder. Compared with healthy individuals (without T1D and psychiatric disorders), individuals with T1D alone had slightly lower odds of achieving the examined educational milestones. However, those with both T1D and any psychiatric disorder had much lower odds of achieving milestones, including completing compulsory school (odds ratio [OR], 0.17; 95% CI, 0.13-0.21), being eligible for (OR, 0.25; 95% CI, 0.21-0.30) and finishing (OR, 0.19; 95% CI, 0.14-0.26) upper secondary school, and starting (OR, 0.36; 95% CI, 0.29-0.46) and finishing (OR, 0.30; 95% CI, 0.20-0.47) university. They also showed lower grade point averages for compulsory school subjects. These findings remained similar in sibling comparison analyses, suggesting independence from familial confounding.Conclusions and RelevanceIn this cohort study of Swedish-born children and adolescents, those with T1D alone had minor difficulties with their educational outcomes, whereas those with both T1D and psychiatric disorders had universal long-term educational underachievement. These findings highlight the importance of identifying psychiatric disorders in pediatric patients with T1D and the need for targeted educational intervention and support to minimize the education gap between the affected children and their peers.

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.

Monogenic diabetes caused by mutation in the glucokinase gene (GCK-MD) is a rare disorder manifesting in childhood as mild, prevalent hyperglycemia. By consensus, it is managed by dietary supervision and infrequent consultations. However, its impact on the mental health of the affected children is largely unknown.To estimate the prevalence of psychiatric comorbidities in children with monogenic glucokinase-related diabetes (GCK-MD) and evaluate their association with quality of life (QoL).The study invited children with GCK-MD aged 5-18 years identified in the Central National Registry and treated in 3 pediatric diabetes centers in Poland. The control group comprised children with type 1 diabetes (T1D, the most common diabetes type in youth) matched for age and family history of diabetes. Participants underwent a semistructured clinical interview diagnostic for psychiatric comorbidities, questionnaires assessing behavioral problems, depressive symptoms, parental stress, and measuring general and diabetes-related QoL (PedsQl).We included 35 patients with GCK-MDMD and 199 with T1D. Eight (22.9%) GCK-MD patients were diagnosed with psychiatric disorder in their lifetime, compared with 16 (8.1%) in the T1D group (odds ratio 3.4 [95% confidence interval: 1.3-8.7]). Patients with GCK-MD showed better parent-reported general QoL (87.1 ± 11.9 vs 82.0 ± 14.0, P = 0.0060) and higher diabetes-related QoL in both parental (84.5 ± 13.8 vs 74.1 ± 15.2, P0.0001) and child's perspective (87.6 ± 10.9 vs 77.3 ± 13.9, P0.0001). Psychiatric disorders (+P) were associated with worse child-reported diabetes QoL (T1D+P 66.6 ± 16.7, T1D-P 78.2 ± 13.3, GCK-MD+P 79.6 ± 16.3, GCK-MD-P 90.1 ± 7.5, P = 0.0002).High prevalence of psychiatric disorders in children with GCK-MD and lower QoL emphasizes the need for psychologic surveillance in those otherwise mildly-treated patients.

Several gastrointestinal and allergic diseases have been linked to psychiatric disease, but there are limited data on psychiatric disease in eosinophilic esophagitis (EoE). Our aim was to study the association between EoE and later psychiatric disorders.This was a population-based nationwide cohort study. Individuals with EoE diagnosed during 1989-2017 in Sweden (n = 1,458) were identified through the ESPRESSO histopathology cohort that represents all gastrointestinal biopsy reports in Sweden's 28 pathology departments. Individuals with EoE were matched with up to 5 reference individuals on sex, age, county, and calendar year (n = 6,436). Cox proportional hazard modeling estimated adjusted hazard ratios (HRs). In a secondary analysis, we compared individuals with EoE with their siblings to adjust for intrafamilial confounding.The median age at EoE diagnosis was 39 years, and 76% of the enrolled individuals with EoE were male. During a median follow-up of 4 years, 106 individuals with EoE (15.96/1,000 person-years) developed a psychiatric disorder compared with 331 reference individuals (10.93/1,000 person-years), corresponding to an HR of 1.50 (95% confidence interval = 1.20-1.87). The increased risk was seen in the first 5 years of follow-up, but not thereafter. The highest relative risks were seen in individuals diagnosed with EoE in childhood. Compared with siblings, individuals with EoE were at an increased risk of psychiatric disease (HR = 1.62; 95% confidence interval = 1.14-2.31). EoE was linked to mood disorders, anxiety disorder, and attention-deficit hyperactivity disorder.Individuals with EoE may be at greater risk of psychiatric disease than their siblings and the general population. This risk needs to be considered in clinical care to detect, prevent, and treat comorbidity.

Although highly heritable, environment also contributes to the etiology of autism spectrum disorder (ASD), with several specific environmental factors previously suggested. A registry-linked population-based twin cohort of 15,701 pairs (586 individuals with an ASD diagnosis), was established within the Child and Adolescent Twin Study in Sweden. Participants were evaluated for autistic symptoms at age 9 using the Autism-Tics, ADHD and other Comorbidities parental interview. A series of binary cut-offs indicated whether participants scored over various ASD symptom percentiles. Three early medical factors previously associated with ASD, beyond familial confounding (low birth weight, congenital malformations and perinatal hypoxia), were summed up creating an individual cumulative exposure load. A series of unconditional logistic regressions between all individuals and conditional regressions within twin pairs were performed for each outcome and exposure level. Between all individuals increasing cumulative early exposure loads were associated with increasing risk of ASD diagnosis (OR 3.33 (95%CI 1.79–6.20) for three exposures) and autistic symptoms (ranging from OR 2.12 (1.57–2.86) for three exposures at the 55th symptom percentile cut-off to OR 3.39 (2.2–5.24) at the 95th). Within twin pairs, the association between three exposures and an ASD diagnosis remained similar, but not statistically significant (OR 2.39 (0.62–9.24)). Having a higher load of early cumulative exposure was consistently associated with autistic symptoms after adjusting for familial confounding and sex (OR 3.45 (1.66–7.15) to OR 7.36 (1.99–27.18)). This study gives support to the cumulative stress hypothesis of ASD, and the dimensional model regarding environmental exposures, after adjustment for familial confounding.

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.

Knowledge of the health challenges and mortality in people with intellectual disability (ID) should guide health policies and practices in contemporary society.To examine premature mortality in individuals with ID.This population-based longitudinal cohort study obtained data from several national health care, education, and population registers in Sweden. Two registers were used to identify individuals with ID: the National Patient Register and the Halmstad University Register on Pupils With Intellectual Disability. Two cohorts were created: cohort 1 comprised young adults (born between 1980 and 1991) with mild ID, and cohort 2 comprised individuals (born between 1932 and 2013) with mild ID or moderate to profound ID; each cohort had matched reference cohorts. Data analyses were conducted between June 1, 2020, and March 31, 2021.Mild or moderate to profound ID.The primary outcome was overall (all-cause) mortality, and the secondary outcomes were cause-specific mortality and potentially avoidable mortality.Cohort 1 included 13 541 young adults with mild ID (mean [SD] age at death, 24.53 [3.66] years; 7826 men [57.8%]), and its matched reference cohort consisted of 135 410 individuals. Cohort 2 included 24 059 individuals with mild ID (mean [SD] age at death, 52.01 [16.88] years; 13 649 male individuals [56.7%]) and 26 602 individuals with moderate to profound ID (mean [SD] age at death, 42.16 [21.68] years; 15 338 male individuals [57.7%]); its matched reference cohorts consisted of 240 590 individuals with mild ID and 266 020 with moderate to profound ID. Young adults with mild ID had increased overall mortality risk compared with the matched reference cohort (odds ratio [OR], 2.86; 95% CI, 2.33-3.50), specifically excess mortality in neoplasms (OR, 3.58; 95% CI, 2.02-6.35), diseases of the nervous system (OR, 40.00; 95% CI, 18.43-86.80) and circulatory system (OR, 9.24; 95% CI, 4.76-17.95). Among deaths that were amenable to health care (OR, 7.75; 95% CI, 4.85-12.39), 55% were attributed to epilepsy. In cohort 2, increased risk of overall mortality was observed among both individuals with mild ID (OR, 6.21; 95% CI, 5.79-6.66) and moderate to profound ID (OR, 13.15; 95% CI, 12.52-13.81) compared with the matched reference cohorts. Those with moderate to profound ID had a higher risk in several cause-of-death categories compared with those with mild ID or the matched reference cohort. Adjustment for epilepsy and congenital malformations attenuated the associations. The relative risk of premature death was higher in women (OR, 6.23; 95% CI, 4.42-8.79) than in men (OR, 1.99; 95% CI, 1.53-2.60), but the absolute risk of mortality was similar (0.9% for women vs 0.9% for men).This study found excess premature mortality and high risk of deaths with causes that were potentially amenable to health care intervention among people with ID. This finding suggests that this patient population faces persistent health challenges and inequality in health care encounters.

Background and Aims Inflammatory bowel disease [IBD] is linked to psychiatric morbidity, but few studies have assessed general population comparators. We aimed to investigate the risk of psychiatric morbidity and suicide in adult-onset IBD patients. Methods We used a nationwide population-based cohort study in Sweden [1973–2013]. We studied the risk of psychiatric disorders and suicide in 69,865 adult-onset IBD patients [ulcerative colitis, UC: n = 43,557; Crohn’s disease, CD: n = 21,245; and IBD-unclassified: n = 5063] compared to 3,472,913 general population references and 66 292 siblings. Results During a median follow-up of 11 years, we found 7465 [10.7%] first psychiatric disorders in IBD [incidence rate, IR/1000 person-years 8.4] and 306 911 [9.9%] in the general population [IR 6.6], resulting in 1.8 extra psychiatric morbidity per 100 patients followed-up for 10 years and a hazard ratio [HR] of 1.3 [95% confidence interval, 95%CI = 1.2–1.3]. The highest risk of overall psychiatric morbidity was seen in the first year after IBD diagnosis [HR = 1.4, 95%CI = 1.2–1.6] and in patients with extraintestinal manifestations [HR = 1.6, 95%CI = 1.5–1.7]. Psychiatric morbidity was more common in all IBD subtypes [HR 1.3–1.5]. An increased risk of suicide attempts was observed among all IBD types [HR = 1.2–1.4], whereas completed suicide was explicitly associated with CD [HR = 1.5] and elderly-onset [diagnosed at the age of > 60 years] IBD [HR = 1.7]. Conclusion Adult-onset IBD was associated with an increased risk of psychiatric disorders and suicide attempts. Psychological follow-up should be provided to patients with IBD, especially those with extraintestinal manifestations and elderly-onset IBD. This follow-up should be within the first year after IBD diagnosis.

Summary Background Emerging evidence suggests increased risk of several physical health conditions in people with ADHD. Only a few physical conditions have been thoroughly studied in relation to ADHD, and there is little knowledge on associations in older adults in particular. We aimed to investigate the phenotypic and aetiological associations between ADHD and a wide range of physical health conditions across adulthood. Methods We did a register study in Sweden and identified full-sibling and maternal half-sibling pairs born between Jan 1, 1932, and Dec 31, 1995, through the Population and Multi-Generation Registers. We excluded individuals who died or emigrated before Jan 1, 2005, and included full-siblings who were not twins and did not have half-siblings. ICD diagnoses were obtained from the National Patient Register. We extracted ICD diagnoses for physical conditions, when participants were aged 18 years or older, from inpatient (recorded 1973–2013) and outpatient (recorded 2001–13) services. Diagnoses were regarded as lifetime presence or absence. Logistic regression models were used to estimate the associations between ADHD (exposure) and 35 physical conditions (outcomes) in individuals and across sibling pairs. Quantitative genetic modelling was used to estimate the extent to which genetic and environmental factors accounted for the associations with ADHD. Findings 4 789 799 individuals were identified (2 449 146 [51%] men and 2 340 653 [49%] women), who formed 4 288 451 unique sibling pairs (3 819 207 full-sibling pairs and 469 244 maternal half-sibling pairs) and 1 841 303 family clusters (siblings, parents, cousins, spouses). The mean age at end of follow-up was 47 years (range 18–81; mean birth year 1966); ethnicity data were not available. Adults with ADHD had increased risk for most physical conditions (34 [97%] of 35) compared with adults without ADHD; the strongest associations were with nervous system disorders (eg, sleep disorders, epilepsy, dementia; odds ratios [ORs] 1·50–4·62) and respiratory diseases (eg, asthma, chronic obstructive pulmonary disease; ORs 2·42–3·24). Sex-stratified analyses showed similar patterns of results in men and women. Stronger cross-disorder associations were found between full-siblings than between half-siblings for nervous system, respiratory, musculoskeletal, and metabolic diseases (p

Background Attention-deficit/hyperactivity disorder (ADHD) has been associated with several autoimmune diseases (AD), both within individuals and across relatives, implying common underlying genetic or environmental factors in line with studies indicating that immunological mechanisms are key to brain development. To further elucidate the relationship between ADHD and autoimmunity we performed a population-wide familial co-aggregation study. Methods We linked Swedish national registries, defined a birth cohort with their biological relatives and identified individuals diagnosed with ADHD and/or 13 ADs. The cohort included 5 178 225 individuals born between 1960 and 2010, of whom 118 927 (2.30%) had been diagnosed with ADHD. We then investigated the associations between ADHD and ADs within individuals and across relatives, with logistic regression and structural equation modelling. Results Within individuals, ADHD was associated with a diagnosis of any of the 13 investigated ADs (adjusted odds ratio (OR) =1.34, 95% confidence interval (CI) = 1.30-1.38) as well as several specific ADs. Familial co-aggregation was observed. For example, ADHD was associated with any of the 13 ADs in mothers (OR = 1.29, 95% CI = 1.26–1.32), fathers (OR = 1.14, 95% CI = 1.11–1.18), full siblings (OR = 1.19, 95% CI = 1.15–1.22), aunts (OR = 1.12, 95% CI = 1.10–1.15), uncles (OR = 1.07, 95% CI = 1.05–1.10) and cousins (OR = 1.04, 95% CI = 1.03–1.06). Still, the absolute risks of AD among those with ADHD were low. The genetic correlation between ADHD and a diagnosis of any of the investigated ADs was 0.13 (95% CI = 0.09–0.17) and the environmental correlation was 0.02 (95% CI = -0.03–0.06). Conclusions We found that ADHD and ADs co-aggregate among biological relatives, indicating that the relationship between ADHD and autoimmune diseases may in part be explained by shared genetic risk factors. The patterns of familial co-aggregation of ADHD and ADs do not readily support a role of maternal immune activation in the aetiology of ADHD. The findings have implications for aetiological models of ADHD. However, screening for autoimmunity among individuals with ADHD is not warranted.

Objective: Evidence regarding comedication among individuals with ADHD is lacking, especially in adults. This study investigated comedication and polypharmacy with ADHD medications in adults. Method: We identified adults dispensed with ADHD medications during 2013 in Sweden and matched them to controls. Logistic regression was used to calculate odds ratios (ORs) of receiving other medications. Results: Individuals receiving ADHD medications had higher risk of receiving any major classes of somatic medications (ORs ranged from 4.1, 95% confidence interval [CI] = [4.0, 4.3], to 7.4, 95% CI = [6.5, 8.5] across age groups). They were more likely to receive respiratory system, alimentary tract and metabolic system, and cardiovascular system medications. In addition, they had higher risk of receiving any other psychotropic medications. The proportion of polypharmacy with five or more medication classes increased from 10.1% to 60.4% from 18 to 64 years. Conclusion: Comedication was more common in adults receiving ADHD medications. Potential benefits and harms of comedication and polypharmacy require further research. (J. of Att. Dis. XXXX; XX[ X] XX-XX)

Background Type 1 diabetes mellitus (T1DM) is a chronic condition with major effect on health-related quality of life (HRQoL) and mental health. In 1990s, high rates of psychiatric disorders were reported among children with T1DM. Little is known, however, about current prevalence of psychiatric disorders in children with T1DM and the relation between psychiatric diagnosis and HRQoL. Objective The aim of the study was to determine the prevalence of Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision) psychiatric disorders and the association between psychiatric comorbidity and HRQoL in the pediatric population with T1DM. Methods We conducted a cross-sectional study of 207 children, aged 8−18 years, diagnosed with T1DM. The presence of psychiatric disorders has been assessed by the standard diagnostic interview according to Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision) criteria. HRQoL was measured by the general and diabetes mellitus−specific modules of the Paediatric Quality of Life Inventory. Results Of the evaluated patients, 26.6% ( N = 55) met the criteria for psychiatric disorders at the time of evaluation. The most common diagnoses were anxiety ( N = 32; 15.5%) and mood disorders ( N = 8; 3.9%). One-third of the patients ( N = 66, 31.9%) met the criteria for at least 1 psychiatric diagnosis in their lifetime. The presence of psychiatric disorders was related to an elevated hemoglobin A1c level (8.6% vs 7.6%) and a lowered HRQoL level in the general pediatric quality of life inventory. In the diabetes mellitus−specific pediatric quality of life inventory, children with psychiatric disorders revealed more symptoms of diabetes mellitus, treatment barriers, and lower adherence than children without psychiatric disorders. Conclusions T1DM in children is associated with a very high prevalence of psychiatric comorbidity, which is related to elevated hemoglobin A1c and lower HRQoL levels.

Objective Knowledge concerning mental health outcomes is important to optimize the health of individuals with disorders or differences of sex development (DSD). Thus, the aim of this study was to estimate if the prevalence of psychiatric morbidity in adult women diagnosed with complete androgen insensitivity syndrome (CAIS) or complete gonadal dysgenesis (46,XY GD and 46,XX GD) differs from that in women with premature ovarian insufficiency (POI) or age-matched population controls. Methods This cross-sectional study was conducted at the Karolinska University Hospital, Stockholm, Sweden, and included 33 women with different DSDs: 20 CAIS, 6 46,XY GD, 7 46,XX GD, 21 women with POI and 61 population-derived controls. Psychiatric morbidity was assessed using the Mini International Neuropsychiatric Interview plus (MINI +). To complement the MINI +, three self-report questions were used to evaluate current and previous psychiatric history. Results are presented as p values and estimated risks (odds ratio [OR], 95% confidence intervals [CI]) of psychiatric conditions among women with CAIS or GD in comparison with women with POI and age-matched population-derived controls. Results Twenty-eight of the 33 women (85%) with CAIS or GD met the criteria for at least one psychiatric disorder according to the MINI +, with depression and anxiety disorders being most common. This was significantly higher compared with population controls (52%) (OR 5.1, 95% CI 1.7–14.9), but not compared to women with POI, who had a high frequency of psychiatric diagnoses (76%). Conclusion The increased psychiatric morbidity in women with CAIS and GD highlights the need for clinical awareness of the psychiatric vulnerability in these patients.

Congenital adrenal hyperplasia (CAH) is a chronic condition and individuals are exposed to elevated androgen levels in utero as a result of the endogenous cortisol deficiency. Prenatal androgen exposure has been suggested to influence mental health, but population based studies on psychiatric morbidity among girls and women with CAH are lacking. Therefore, we performed a cohort study based on Swedish nationwide registers linked with the national CAH register. Girls and women with CAH due to 21-hydroxylase deficiency (n = 335) born between January 1915 and January 2010 were compared with aged-matched female (n = 33500) and male controls (n = 33500). Analyses were stratified by phenotype [salt wasting (SW), simple virilizing (SV), and non-classical type (NC)] and by CYP21A2 genotype subgroups (null, I2splice, I172N, and P30L). Results are presented as estimated risks (OR, 95%CI) of psychiatric disorders among girls and women with CAH compared with age-matched controls. Any psychiatric diagnoses were more common in CAH females compared with female and male population controls [1.9 (1.4–2.5), and 2.2 (1.7–2.9)]. In particular, the risk of alcohol misuse was increased compared with female and male population controls [2.8 (1.7–4.7) and 2.1 (1.2–3.5)], and appeared most common among the girls and women with the most severe null genotype [6.7 (2.6–17.8)]. The risk of stress and adjustment disorders was doubled compared with female population controls [2.1 (1.3–3.6)]. Girls and women with CAH have an increased risk of psychiatric disorders in general and substance use disorders in particular compared with unexposed females, with the highest risk among those with the most severe genotype. Prenatal androgen exposure and deficient endogenous cortisol and/or adrenaline production may provide explanations for these findings, but other factors related to CAH cannot be excluded.

OBJECTIVE To assess the risk of psychiatric disorders and suicide attempts in children with type 1 diabetes and their healthy siblings. RESEARCH DESIGN AND METHODS We performed a population-based case-cohort study of individuals born in Sweden between 1973 and 2009. Children with type 1 diabetes (n = 17,122) and their healthy siblings (n = 18,847) were identified and followed until their 18th birthday. Their risk of psychiatric disorders was compared with that of matched control subjects. RESULTS The risk of psychiatric morbidity in children with type 1 diabetes compared with the general population was tripled within 6 months after the onset of diabetes (hazard ratio [HR] 3.0 [95% CI 2.7–3.4]) and doubled within the total observation period (HR 2.1 [95% CI 2.0–2.2]). An increased risk was noted in suicide attempts (HR 1.7 [95% CI 1.4–2.0]) and in most categories of psychiatric disorders. The risk of psychiatric disorders in probands declined from HR 2.7 (95% CI 2.2–3.3) for those in the cohort born 1973–1986 to 1.9 (95% CI 1.8–2.0) in those born 1997–2009. The risk for any psychiatric disorders among siblings of patients with type 1 diabetes was estimated to be HR 1.1 (95% CI 1.0–1.1), and there was no increased risk in any of the specific category of disorders. CONCLUSIONS Children with type 1 diabetes are at high risk of psychiatric disorders, which seems to be a consequence of the disease rather than due to a common familial etiology. The results support recommendations on comprehensive mental health surveillance in children with type 1 diabetes, especially in recently diagnosed children.

Cel pracyPodjęto próbę oceny mineralizacji kości i częstości złamań u kobiet, które w okresie dorastania były leczone z powodu jadłowstrętu psychicznego ( j.p.).Metoda47 kobiet (wiek 20-36,8lat) zbadano ponownie po 6,33-21,2latach od pojawienia się objawów j.p. U 46 kobiet zbadano gęstość mineralną kości (BMD) całego szkieletu, kręgosłupa lędźwiowego, szyjki kości udowej, bliższego końca kości udowej oraz dokonano densytometrycznej oceny złamań kręgosłupa (VFA). Oznaczenia BAP, P1NP, CTX, estradiolu, testosteronu, kortyzolu, IGF-1, leptyny, DHEA-S wykonano u 45 kobiet uczestniczących w obecnym badaniu. Aktualne wyniki BMD porównano z dostępnymi wynikami z okresu hospitalizacji.WynikiObecnie obniżone BMD (Z-scoreWnioskiPomimo wczesnego rozpoczęcia i dobrych wyników leczenia j.p. w okresie dorastania obniżone BMD występowało obecnie u 60,9% kobiet. Podczas obserwacji w większości przypadków obserwowano znaczącą poprawę lub normalizację wcześniej obniżonych wyników BMD całego szkieletu i kręgosłupa lędźwiowego.

Background Hypospadias (aberrant opening of the urethra on the underside of the penis) occurs in 1 per 300 newborn boys. It has been previously unknown whether this common malformation is associated with increased psychiatric morbidity later in life. Studies of individuals with hypospadias also provide an opportunity to examine whether difference in androgen signaling is related to neurodevelopmental disorders. To elucidate the mechanisms behind a possible association, we also studied psychiatric outcomes among brothers of the hypospadias patients. Methods Registry study within a national cohort of all 9,262 males with hypospadias and their 4,936 healthy brothers born in Sweden between 1973 and 2009. Patients with hypospadias and their brothers were matched with controls by year of birth and county. The following outcomes were evaluated (1) any psychiatric (2) psychotic, (3) mood, (4) anxiety, (5) eating, and (6) personality disorders, (7) substance misuse, (8) attention-deficit hyperactivity disorder (ADHD), (9) autism spectrum disorders (ASD), (10) intellectual disability, and (11) other behavioral/emotional disorders with onset in childhood. Results Patients with hypospadias were more likely to be diagnosed with intellectual disability (OR 3.2; 95% CI 2.8–3.8), ASD (1.4; 1.2–1.7), ADHD (1.5; 1.3–1.9), and behavioral/emotional disorders (1.4; 1.2–1.6) compared with the controls. Brothers of patients with hypospadias had an increased risk of ASD (1.6; 1.3–2.1) and other behavioral/emotional disorders with onset in childhood (1.2; 0.9–1.5) in comparison to siblings of healthy individuals. A slightly higher, although not statistically significant, risk was found for intellectual disability (1.3; 1.0–1.9). No relation between other psychiatric diagnosis and hypospadias was found. Conclusions This is the first study to identify an increased risk for neurodevelopmental disorders in patients with hypospadias, as well as an increased risk for ASD in their brothers, suggesting a common familial (genetic and/or environmental) liability.

We read with interest the recently published work in Gut by Imhann et al .1 Although this paper suggests that genetics plays an important role in IBD,1 environmental factors clearly contribute to its aetiology.2 When Ng et al 2 reviewed environmental risk factors for IBD in this journal they noted that urbanisation may be linked to both Crohn’s disease (CD) and ulcerative colitis (UC). We used Cox regression to estimate the effect of urbanisation and deprivation during childhood on future IBD. From the Swedish Total Population Register,3 the government agency Statistics Sweden selected all individuals born in Sweden between 1973 and 2013 (n=4 161 280). Among these there …

IMPORTANCE: Inflammatory bowel disease (IBD) has been associated with psychiatric morbidity in adults, although previous studies have not accounted for familial confounding. In children, IBD has an even more severe course, but the association between childhood-onset IBD and psychiatric morbidity remains unclear. OBJECTIVE: To examine the risk of psychiatric morbidity in individuals with childhood-onset IBD, controlling for potential confounding shared between siblings. DESIGN, SETTING, AND PARTICIPANTS: A population-based cohort study was conducted using data from the Swedish national health care and population registers of all children younger than 18 years born from 1973 to 2013. The study included 6464 individuals with a diagnosis of childhood-onset IBD (3228 with ulcerative colitis, 2536 with Crohn disease, and 700 with IBD unclassified) who were compared with 323 200 matched reference individuals from the general population and 6999 siblings of patients with IBD. Cox proportional hazards regression was used to estimate hazard ratios (HRs) with 95% CIs. Statistical analysis was performed from January 1, 1973, to December 1, 2013. MAIN OUTCOMES AND MEASURES: The primary outcome was any psychiatric disorder and suicide attempt. Secondary outcomes were the following specific psychiatric disorders: psychotic, mood, anxiety, eating, personality, and behavioral disorders; substance misuse; attention-deficit/hyperactivity disorder; autism spectrum disorders; and intellectual disability. RESULTS: The study included 6464 individuals with a diagnosis of childhood-onset IBD (2831 girls and 3633 boys; mean [SD] age at diagnosis of IBD, 13 [4] years). During a median follow-up time of 9 years, 1117 individuals with IBD (17.3%) received a diagnosis of any psychiatric disorder (incidence rate, 17.1 per 1000 person-years), compared with 38 044 of 323 200 individuals (11.8%) in the general population (incidence rate, 11.2 per 1000 person-years), corresponding to an HR of 1.6 (95% CI, 1.5-1.7), equaling 1 extra case of any psychiatric disorder per 170 person-years. Inflammatory bowel disease was significantly associated with suicide attempt (HR, 1.4; 95% CI, 1.2-1.7) as well as mood disorders (HR, 1.6; 95% CI, 1.4-1.7), anxiety disorders (HR, 1.9; 95% CI, 1.7-2.0) eating disorders (HR, 1.6; 95% CI, 1.3-2.0), personality disorders (HR, 1.4; 95% CI, 1.1-1.8), attention-deficit/hyperactivity disorder (HR, 1.2; 95% CI, 1.1-1.4), and autism spectrum disorders (HR, 1.4; 95% CI, 1.1-1.7) Results were similar for boys and girls. Hazard ratios for any psychiatric disorder were highest in the first year of follow-up but remained statistically significant after more than 5 years. Psychiatric disorders were particularly common for patients with very early-onset IBD (