| 341. |
- Rydell, Mina, et al.
(författare)
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Has the attention deficit hyperactivity disorder phenotype become more common in children between 2004 and 2014? : Trends over 10 years from a Swedish general population sample
- 2018
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Ingår i: Journal of Child Psychology and Psychiatry. - Stockholm : Blackwell Publishing. - 0021-9630 .- 1469-7610. ; 59:8, s. 863-871
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Studies have reported increases in clinically diagnosed and treated attention deficit hyperactivity disorder (ADHD) during the last decade, but it is unclear if this reflects an increase in the underlying ADHD phenotype. We aimed to clarify if there has been an increase in the prevalence of ADHD-like traits in the general population from 2004 to 2014.METHOD: Data were collected from 9-year-old twins (19,271), participating in the population-based Child and Adolescent Twin Study in Sweden between 2004 and 2014. We assessed lifetime ADHD symptoms using the Autism-Tics, ADHD and other Comorbidities inventory. Research proxies for diagnostic-level ADHD and subthreshold ADHD were derived from this scale. We modeled the lifetime prevalence of diagnostic-level and subthreshold ADHD with logistic regression, and assessed mean ADHD scores each year with linear regression. Lifetime prevalence of clinically diagnosed ADHD was retrieved from the National Patient Register and modeled with logistic regression.RESULTS: The prevalence of diagnostic-level ADHD based on parent ratings did not differ significantly over time from 2004 to 2014 (OR 1.37; 95% CI: 0.77-2.45; p-value .233). Both subthreshold ADHD and mean ADHD scores increased significantly over time (both p-values <.001). Clinically diagnosed ADHD increased more than fivefold from 2004 to 2014 (OR 5.27, 95% CI: 1.85-14.96).CONCLUSIONS: We found no evidence of an increase in ADHD-like traits at the extreme end of the distribution from 2004 to 2014, but small increases in normal and subthreshold variations of ADHD-like traits were observed. This suggests that the increased rates of clinically diagnosed ADHD might reflect changes in diagnostic and treatment practices of ADHD, administrative changes in reporting diagnoses, greater awareness of ADHD, better access to healthcare, or current overdiagnosis, rather than an increase in the ADHD phenotype.
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| 342. |
- Råstam, Maria, 1948, et al.
(författare)
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Eating Problems and Overlap with ADHD and Autism Spectrum Disorders in a Nationwide Twin Study of 9- and 12-Year-Old Children.
- 2013
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Ingår i: Scientific World Journal. - : Hindawi Limited. - 1537-744X .- 2356-6140.
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Tidskriftsartikel (refereegranskat)abstract
- Aim. To establish the prevalence of restrictive eating problems, the overlap and association with attention-deficit/hyperactivity disorder (ADHD), and autism spectrum disorders (ASD) and to estimate the heritability of eating problems in a general population sample of twins aged 9 and 12. Methods. Parents of all Swedish 9- and 12-year-old twin pairs born between 1993 and 1998 (n = 12,366) were interviewed regarding symptoms of ADHD, ASD, and eating problems (EAT-P). Intraclass correlations and structural equation modelling were used for evaluating the influence of genetic and environmental factors. Cross-twin, cross-trait correlations were used to indicate a possible overlap between conditions. Results. The prevalence of eating problems was 0.6% in the study population and was significantly higher in children with ADHD and/or ASD. Among children with eating problems, 40% were screened positive for ADHD and/or ASD. Social interaction problems were strongly associated with EAT-P in girls, and impulsivity and activity problems with EAT-P in boys. The cross-twin, cross-trait correlations suggested low correlations between EAT-P and ADHD or EAT-P and ASD. Genetic effects accounted for 44% of the variation in liability for eating problems. Conclusions. In the group with eating problems, there was a clear overrepresentation of individuals with ADHD and/or ASD symptoms.
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| 343. |
- Sahlin, Hanna, et al.
(författare)
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Association Between Deliberate Self-harm and Violent Criminality
- 2017
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Ingår i: JAMA psychiatry. - : AMER MEDICAL ASSOC. - 2168-6238 .- 2168-622X. ; 74:6, s. 615-621
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Tidskriftsartikel (refereegranskat)abstract
- IMPORTANCE Individuals who self-harm may have an increased risk of aggression toward others, but this association has been insufficiently investigated. More conclusive evidence may affect assessment, treatment interventions, and clinical guidelines. OBJECTIVE To investigate the association between nonfatal self-harm and violent crime. DESIGN, SETTING, AND PARTICIPANTS This population-based longitudinal cohort study, conducted from January 1, 1997, through December 31, 2013, studied all Swedish citizens born between 1982 and 1998 who were 15 years and older (N = 1 850 252). Individuals who emigrated from Sweden before the age of 15 years (n = 104 051) or immigrated to Sweden after the age of 13 years (ie, <2 years before the beginning of the follow-up; n = 22 009) were excluded. Data analysis was performed from April 21, 2016, to June 4, 2016. EXPOSURES Receipt of self-harm-associated clinical care. MAIN OUTCOMES AND MEASURES Conviction of a violent crime according to the Swedish penal code. RESULTS The study cohort consisted of 1 850 525 individuals (950 382 males and 900 143 females), and the mean (SD) follow-up time was 8.1 (4.7) years (range, 0-17.0 years; minimum age, 15 years; maximum age, 32 years). During a mean follow-up period of 8.1 years, 55 185 individuals (3.0%) received clinical care for self-harm. The crude hazard ratio was 4.9 (95% CI, 4.8-5.0) for violent crime conviction in exposed individuals compared with the unexposed group. Women who self-harm were at particularly high risk for expressing violent behaviors. After adjustment for relevant psychiatric comorbidities and socioeconomic status, an almost doubled hazard of violent offense remained (hazard ratio, 1.8; 95% CI, 1.8-1.9). CONCLUSIONS AND RELEVANCE Self-harm is associated with an increased risk of conviction for a violent offense in both sexes. The risk of violence, as well as the risk of suicide and self-harm, should be assessed among offending and self-harming individuals.
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| 344. |
- Salvatore, Jessica E., et al.
(författare)
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Alcohol use disorder and divorce : evidence for a genetic correlation in a population-based Swedish sample
- 2017
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Ingår i: Addiction. - : Wiley. - 0965-2140 .- 1360-0443. ; 112:4, s. 586-593
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Tidskriftsartikel (refereegranskat)abstract
- Aims: We tested the association between alcohol use disorder (AUD) and divorce; estimated the genetic and environmental influences on divorce; estimated how much genetic and environmental influences accounted for covariance between AUD and divorce; and estimated latent genetic and environmental correlations between AUD and divorce. We tested sex differences in these effects. Design: We identified twin and sibling pairs with AUD and divorce information in Swedish national registers. We described the association between AUD and divorce using tetrachorics and used twin and sibling models to estimate genetic and environmental influences on divorce, on the covariance between AUD and divorce and the latent genetic and environmental correlations between AUD and divorce. Setting: Sweden. Participants: A total of 670 836 individuals (53% male) born 1940–1965. Measurements: Life-time measures of AUD and divorce. Findings: AUD and divorce were related strongly (males: rtet = +0.44, 95% CI = 0.43, 0.45; females rtet = +0.37, 95% CI = 0.36, 0.38). Genetic factors accounted for a modest proportion of the variance in divorce (males: 21.3%, 95% CI = 7.6, 28.5; females: 31.0%, 95% CI = 18.8, 37.1). Genetic factors accounted for most of the covariance between AUD and divorce (males: 52.0%, 95% CI = 48.8, 67.9; females: 53.74%, 95% CI = 17.6, 54.5), followed by non-shared environmental factors (males: 45.0%, 95% CI = 37.5, 54.9; females: 41.6%, 95% CI = 40.3, 60.2). Shared environmental factors accounted for a negligible proportion of the covariance (males: 3.0%, 95% CI = −3.0, 13.5; females: 4.75%, 95% CI = 0.0, 6.6). The AUD–divorce genetic correlations were high (males: rA = +0.76, 95% CI = 0.53, 0.90; females +0.52, 95% CI = 0.24, 0.67). The non-shared environmental correlations were modest (males: rE = +0.32, 95% CI = 0.31, 0.40; females: +0.27, 95% CI = 0.27, 0.36). Conclusions: Divorce and alcohol use disorder are correlated strongly in the Swedish population, and the heritability of divorce is consistent with previous studies. Covariation between AUD and divorce results from overlapping genetic and non-shared environmental factors. Latent genetic and non-shared environmental correlations for alcohol use disorder and divorce are high and moderate.
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| 345. |
- Samuelsson, Åsa, et al.
(författare)
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Disability Pension Among Swedish Twins - Prevalence Over 16 Years and Associations With Sociodemographic Factors in 1992
- 2012
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Ingår i: Journal of Occupational and Environmental Medicine. - : Wolters Kluwer. - 1076-2752 .- 1536-5948. ; 54:1, s. 10-16
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To investigate annual prevalence of disability pension (DP) from 1992 to 2007 and associations with sociodemographic factors in 1992.Methods: All twins born between 1928 and 1958 were identified from the Swedish Twin Registry and linked to national records on DP. Descriptive statistics and logistic regressions were applied.Results: The annual prevalence of DP was 10.7% (9.6% to 11.3%). High age (odds ratio [OR] 9.17; 95% confidence interval [CI] 8.43 to 9.98), low education (OR 4.84; 95% CI 4.31 to 5.42), and being unmarried (OR 2.36; 95% CI 2.22 to 2.50) were associated with DP. The associations remained after adjusting for familial factors.Conclusions: The fact that the associations remained after control for familial factors indicates that factors not shared by family members, such as choices in adulthood, are of relevance for the associations found.
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| 346. |
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| 347. |
- Sandin, Sven, et al.
(författare)
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The familial risk of autism
- 2014
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Ingår i: Journal of the American Medical Association (JAMA). - Chicago, USA : American Medical Association. - 0098-7484 .- 1538-3598. ; 311:17, s. 1770-1777
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Tidskriftsartikel (refereegranskat)abstract
- Importance: Autism spectrum disorder (ASD) aggregates in families, but the individual risk and to what extent this is caused by genetic factors or shared or nonshared environmental factors remains unresolved.Objective: To provide estimates of familial aggregation and heritability of ASD.Design, setting and participants: A population-based cohort including 2,049,973 Swedish children born 1982 through 2006. We identified 37,570 twin pairs, 2,642,064 full sibling pairs, 432,281 maternal and 445,531 paternal half sibling pairs, and 5,799,875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.Main outcomes and measures: The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.Results: In the sample, 14,516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100,000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).Conclusions and relevance: Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
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| 348. |
- Sandin, Sven, et al.
(författare)
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The Heritability of Autism Spectrum Disorder
- 2017
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Ingår i: Journal of the American Medical Association (JAMA). - : American Medical Association. - 0098-7484 .- 1538-3598. ; 318:12, s. 1182-1184
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Tidskriftsartikel (refereegranskat)
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| 349. |
- Sariaslan, Amir, et al.
(författare)
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Childhood family income, adolescent violent criminality and substance misuse : quasi-experimental total population study
- 2014
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Ingår i: British Journal of Psychiatry. - London, United Kingdom : Royal College of Psychiatrists. - 0007-1250 .- 1472-1465 .- 0300-5771. ; 205:4, s. 286-290
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Tidskriftsartikel (refereegranskat)abstract
- Background: Low socioeconomic status in childhood is a well-known predictor of subsequent criminal and substance misuse behaviours but the causal mechanisms are questioned. Aims To investigate whether childhood family income predicts subsequent violent criminality and substance misuse and whether the associations are in turn explained by unobserved familial risk factors.Method: Nationwide Swedish quasi-experimental, family-based study following cohorts born 1989-1993 (n(total) = 526 167, n(cousins) = 262 267, n(siblings) = 216 424) between the ages of 15 and 21 years.Results: Children of parents in the lowest income quintile experienced a seven-fold increased hazard rate (HR) of being convicted of violent criminality compared with peers in the highest quintile (HR = 6.78, 95% CI 6.23-7.38). This association was entirely accounted for by unobserved familial risk factors (HR = 0.95, 95% CI 0.44-2.03). Similar pattern of effects was found for substance misuse.Conclusions: There were no associations between childhood family income and subsequent violent criminality and substance misuse once we had adjusted for unobserved familial risk factors.
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| 350. |
- Sariaslan, Amir, et al.
(författare)
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Does population density and neighborhood deprivation predict schizophrenia? A nationwide Swedish family-based study of 2.4 million individuals
- 2015
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Ingår i: Schizophrenia Bulletin. - Oxford, United Kingdom : Oxford University Press. - 0586-7614 .- 1745-1701. ; 41:2, s. 494-502
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Tidskriftsartikel (refereegranskat)abstract
- People living in densely populated and socially disorganized areas have higher rates of psychiatric morbidity, but the potential causal status of such factors is uncertain. We used nationwide Swedish longitudinal registry data to identify all children born 1967-1989 (n = 2361585), including separate datasets for all cousins (n = 1715059) and siblings (n = 1667894). The nature of the associations between population density and neighborhood deprivation and individual risk for a schizophrenia diagnosis was investigated while adjusting for unobserved familial risk factors (through cousin and sibling comparisons) and then compared with similar associations for depression. We generated familial pedigree structures using the Multi-Generation Registry and identified study participants with schizophrenia and depression using the National Patient Registry. Fixed-effects logistic regression models were used to study within-family estimates. Population density, measured as ln(population size/km(2)), at age 15 predicted subsequent schizophrenia in the population (OR = 1.10; 95% CI: 1.09; 1.11). Unobserved familial risk factors shared by cousins within extended families attenuated the association (1.06; 1.03; 1.10), and the link disappeared entirely within nuclear families (1.02; 0.97; 1.08). Similar results were found for neighborhood deprivation as predictor and for depression as outcome. Sensitivity tests demonstrated that timing and accumulation effects of the exposures (mean scores across birth, ages 1-5, 6-10, and 11-15 years) did not alter the findings. Excess risks of psychiatric morbidity, particularly schizophrenia, in densely populated and socioeconomically deprived Swedish neighborhoods appear, therefore, to result primarily from unobserved familial selection factors. Previous studies may have overemphasized the etiological importance of these environmental factors.
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