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Träfflista för sökning "L773:0021 9630 OR L773:1469 7610 ;pers:(Anckarsäter Henrik 1966)"

Search: L773:0021 9630 OR L773:1469 7610 > Anckarsäter Henrik 1966

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1.
  • Pettersson, Erik, et al. (author)
  • Birth weight as an independent predictor of ADHD symptoms : a within-twin pair analysis
  • 2015
  • In: Journal of Child Psychology and Psychiatry. - Hoboken, USA : Wiley-Blackwell. - 0021-9630 .- 1469-7610. ; 56:4, s. 453-459
  • Journal article (peer-reviewed)abstract
    • Background Studies have found an association between low birth weight and ADHD, but the nature of this relation is unclear. First, it is uncertain whether birth weight is associated with both of the ADHD dimensions, inattentiveness and hyperactivity-impulsivity. Second, it remains uncertain whether the association between birth weight and ADHD symptom severity is confounded by familial factors.Method: Parents of all Swedish 9- and 12-year-old twins born between 1992 and 2000 were interviewed for DSM-IV inattentive and hyperactive-impulsive ADHD symptoms by the Autism - Tics, AD/HD and other Comorbidities (A-TAC) inventory (N = 21,775 twins). Birth weight was collected prospectively through the Medical Birth Registry. We used a within-twin pair design to control for genetic and shared environmental factors.Results: Reduced birth weight was significantly associated with a mean increase in total ADHD (β = -.42; 95% CI: -.53, -.30), inattentive (β = -.26; 95% CI: -.33, -.19), and hyperactive-impulsive (β = -.16; 95% CI: -.22, -.10) symptom severity. These results imply that a change of one kilogram of birth weight corresponded to parents rating their child nearly one unit higher (going from "no" to "yes, to some extent" on a given symptom) on the total ADHD scale. These associations remained within pairs of MZ and DZ twins, and were also present when restricting the analyses to full term births.Conclusions: There is an independent association between low birth weight and all forms of ADHD symptoms, even after controlling for all environmental and genetic confounds shared within twin pairs. These results indicate that fetal growth restriction (as reflected in birth weight differences within twin pairs) and/or the environmental factors which influence it is in the casual pathway leading to ADHD.
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2.
  • Larsson, Henrik, 1975-, et al. (author)
  • Childhood attention-deficit hyperactivity disorder as an extreme of a continuous trait: a quantitative genetic study of 8,500 twin pairs.
  • 2012
  • In: Journal of child psychology and psychiatry, and allied disciplines. - : Wiley. - 1469-7610 .- 0021-9630. ; 53:1, s. 73-80
  • Journal article (peer-reviewed)abstract
    • Although the clinical utility of categorically defined attention-deficit hyperactivity disorder (ADHD) is well established, there is also strong evidence supporting the notion of ADHD as an extreme of a continuous trait. Nevertheless, the question of whether the etiology is the same for different levels of DSM-IV ADHD symptoms remains to be investigated. The aim of this study was to assess genetic links between the extreme and the subthreshold range of ADHD symptoms.
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3.
  • Lundström, Sebastian, et al. (author)
  • Trajectories leading to autism spectrum disorders are affected by paternal age: findings from two nationally representative twin studies.
  • 2010
  • In: Journal of Child Psychology and Psychiatry, and Allied Disciplines. - : Wiley. - 0021-9630 .- 1469-7610. ; 51:7, s. 850-856
  • Journal article (peer-reviewed)abstract
    • Background: Despite extensive efforts, the causes of autism remain unknown. Advancing paternal age has been associated with various neurodevelopmental disorders. We aim to investigate three unresolved questions: (a) What is the association between paternal age and autism spectrum disorders (ASD)?; (b) Does paternal age moderate the genetic and environmental etiological factors for ASD? (c) Does paternal age affect normal variation in autistic-like traits? Methods: Two nationally representative twin studies from Sweden (n = 11, 122, assessed at age 9 or 12) and the UK (n = 13, 524, assessed at age 9) were used. Categorical and continuous measures of ASD, autistic-like traits and autistic similarity were calculated and compared over paternal age categories. Results: Both cohorts showed a strong association between paternal age and the risk for ASD. A U-shaped risk association could be discerned since the offspring of both the youngest and oldest fathers showed an elevation in the risk for ASD. Autistic similarity increased with advancing paternal age in both monozygotic and dizygotic twins. Both cohorts showed significantly higher autistic-like traits in the offspring of the youngest and oldest fathers. Conclusions: Phenomena associated with paternal age are clearly involved in the trajectories leading to autistic-like traits and ASD. Mechanisms influencing the trajectories might differ between older and younger fathers. Molecular genetic studies are now needed in order to further understand the association between paternal age and ASD, as well as normal variation in social, language, and repetitive behaviors in the general population.
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4.
  • Lichtenstein, P., et al. (author)
  • Associations between conduct problems in childhood and adverse outcomes in emerging adulthood: a longitudinal Swedish nationwide twin cohort
  • 2020
  • In: Journal of Child Psychology and Psychiatry and Allied Disciplines. - : Wiley. - 0021-9630 .- 1469-7610. ; 61:7, s. 798-806
  • Journal article (peer-reviewed)abstract
    • Background We examined whether childhood conduct problems predicted a wide range of adverse outcomes in emerging adulthood and whether the association with internalizing problems remained after adjusting for general comorbidity and externalizing problems. Methods Participants were 18,649 twins from the Child and Adolescent Twin Study in Sweden. At age 9/12, parents rated their children on eight conduct problems. Adverse outcomes were retrieved from national registers in emerging adulthood (median follow‐up time = 9.2 years), including diagnoses of six psychiatric disorders, prescriptions of antidepressants, suicide attempts, criminality, high school ineligibility, and social welfare recipiency. We estimated risk for the separate outcomes and examined if conduct problems predicted an internalizing factor above and beyond a general comorbidity and an externalizing factor. We used twin analyses to estimate genetic and environmental contributions to these associations. Results On the average, each additional conduct symptom in childhood was associated with a 32% increased risk of the adverse outcomes in emerging adulthood (mean hazard ratio = 1.32; range = 1.16, 1.56). A latent childhood conduct problems factor predicted the internalizing factor in emerging adulthood (βboys = .24, standard error, SE = 0.03; βgirls = .17, SE = 0.03), above and beyond its association with the externalizing (βboys = 0.21, SE = 0.04; βgirls = 0.17, SE = 0.05) and general factors (βboys = 0.45, SE = 0.03; βgirls = 0.34, SE = 0.04). These associations were differentially influenced by genetic and environmental factors. Conclusions It is important to monitor boys and girls with conduct problems not only for future externalizing problems, but also for future internalizing problems. Prevention of specific outcomes, however, might require interventions at different levels.
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5.
  • Pettersson, Erik, et al. (author)
  • Different neurodevelopmental symptoms have a common genetic etiology.
  • 2013
  • In: Journal of child psychology and psychiatry, and allied disciplines. - : Wiley. - 1469-7610 .- 0021-9630. ; 43:6, s. 536-536
  • Journal article (peer-reviewed)abstract
    • BACKGROUND:Although neurodevelopmental disorders are demarcated as discrete entities in the Diagnostic Statistical Manual of mental disorders, empirical evidence indicates that there is a high degree of overlap among them. The first aim of this investigation was to explore if a single general factor could account for the large degree of observed overlap among neurodevelopmental problems, and explore whether this potential factor was primarily genetic or environmental in origin. The second aim was to explore whether there was systematic covariation, either genetic or environmental, over and above that contributed by the potential general factor, unique to each syndrome. METHOD: Parents of all Swedish 9- and 12-year-old twin pairs born between 1992 and 2002 were targeted for interview regarding problems typical of autism spectrum disorders, ADHD and other neurodevelopmental conditions (response rate: 80 percent). Structural equation modeling was conducted on 6,595 pairs to examine the genetic and environmental structure of 53 neurodevelopmental problems. RESULTS: One general genetic factor accounted for a large proportion of the phenotypic covariation among the 53 symptoms. Three specific genetic subfactors identified 'impulsivity,' 'learning problems,' and 'tics and autism,' respectively. Three unique environment factors identified 'autism,' 'hyperactivity and impulsivity,' and 'inattention and learning problems,' respectively. CONCLUSION: One general genetic factor was responsible for the wide-spread phenotypic overlap among all neurodevelopmental symptoms, highlighting the importance of addressing broad patient needs rather than specific diagnoses. The unique genetic factors may help guide diagnostic nomenclature, whereas the unique environmental factors may highlight that neurodevelopmental symptoms are responsive to change at the individual level and may provide clues into different mechanisms and treatments. Future research would benefit from assessing the general factor separately from specific factors to better understand observed overlap among neurodevelopmental problems.
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