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- Sujan, Ayesha C., et al.
(författare)
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A Genetically Informed Study of the Associations Between Maternal Age at Childbearing and Adverse Perinatal Outcomes
- 2016
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Ingår i: Behavior Genetics. - New York, USA : Springer. - 0001-8244 .- 1573-3297. ; 46:3, s. 431-456
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Tidskriftsartikel (refereegranskat)abstract
- We examined associations of maternal age at childbearing (MAC) with gestational age and fetal growth (i.e., birth weight adjusting for gestational age), using two genetically informed designs (cousin and sibling comparisons) and data from two cohorts, a population-based Swedish sample and a nationally representative United States sample. We also conducted sensitivity analyses to test limitations of the designs. The findings were consistent across samples and suggested that, associations observed in the population between younger MAC and shorter gestational age were confounded by shared familial factors; however, associations of advanced MAC with shorter gestational age remained robust after accounting for shared familial factors. In contrast to the gestational age findings, neither early nor advanced MAC was associated with lower fetal growth after accounting for shared familial factors. Given certain assumptions, these findings provide support for a causal association between advanced MAC and shorter gestational age. The results also suggest that there are not causal associations between early MAC and shorter gestational age, between early MAC and lower fetal growth, and between advanced MAC and lower fetal growth.
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| 2. |
- Wiggs, Kelsey K., et al.
(författare)
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A Family-Based Study of the Association Between Labor Induction and Offspring Attention-Deficit Hyperactivity Disorder and Low Academic Achievement
- 2017
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Ingår i: Behavior Genetics. - Stockholm : Springer. - 0001-8244 .- 1573-3297. ; 47:4, s. 383-393
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Tidskriftsartikel (refereegranskat)abstract
- The current study examined associations between labor induction and both (1) offspring attention-deficit hyperactivity disorder (ADHD) diagnosis in a Swedish birth cohort born 1992-2005 (n = 1,085,008) and (2) indices of offspring low academic achievement in a sub-cohort born 1992-1997 (n = 489,196). Associations were examined in the entire sample (i.e., related and unrelated individuals) with adjustment for measured covariates and, in order to account for unmeasured confounders shared within families, within differentially exposed cousins and siblings. We observed an association between labor induction and offspring ADHD diagnosis and low academic achievement in the population. However, these associations were fully attenuated after adjusting for measured covariates and unmeasured factors that cousins and siblings share. The results suggest that observed associations between labor induction and ADHD and low academic achievement may be due to genetic and/or shared environmental factors that influence both mothers' risk of labor induction and offspring neurodevelopment.
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| 3. |
- Andersson, Anneli, 1992-, et al.
(författare)
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Genetic overlap between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms : a systematic review and meta-analysis
- 2018
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 48:6, s. 455-456
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder (Wilens, Biederman & Spencer 2002) and affects approximately 5% of children (Polanczyk, de Lima, Horta, Biederman & Rohde 2007). About half of those diagnosed in childhood continue to have the diagnosis and symptoms in adulthood (Kessler et al. 2006). The co-occurrence of ADHD with other psychiatric disorder symptoms (Burt et al. 2001; Cole et al. 2009; Polderman et al. 2014) has been suggested to be partly explained by a shared genetic vulnerability (Polderman et al. 2014). However, the strength of the genetic overlap is currently unclear. Also, no study has examined whether the genetic correlations differs between age groups (childhood versus adulthood), by rater (self-report, other informant, combined (parent-teacher, parent-twin, teacher-twin)), or by type of psychiatric disorder symptoms (externalizing, internalizing, neu-rodevelopmental). To address this gap, we conducted a systematic literature search to identify relevant twin studies, in PubMed, PsycINFO, and EMBASE. A total of 31 articles were identified and included in the present study. The pooled estimates showed that the comorbidity between ADHD and diverse psychiatric disorder symptoms were explained by shared genetic effectsrg= 0.50 (0.43–0.56). A similar shared genetic overlap between ADHD and psychiatric disorder symptoms was observed in both childhood rg= 0.51(0.42–0.61) and adulthood rg= 0.47 (0.40–0.53). Similar results werealso found for self-reports rg= 0.49 (0.42–0.55), other informants rg= 0.50 (0.40–0.60), and combined raters rg= 0.51 (0.30–0.69). Further, the strength of the genetic correlations of ADHD with the externalizing rg= 0.49 (0.39–0.59), internalizing rg= 0.55 (0.40–0.68) and neurodevelopmental rg= 0.47 (0.40–0.53) spectrums were similar in magnitude. These findings emphasize the presence of a shared genetic liability between ADHD and externalizing, internalizing and neurodevelopmental disorder symptoms, independent of age and rater.ReferencesBurt, S. A., Krueger, R. F., McGue, M., Iacono, W. G. (2001).Sources of covariation among attention-deficit/hyperactivity disorder,oppositional defiant disorder, and conduct disorder: the importance ofshared environment.Journal of Abnormal Psychology, 4, 516–525.Cole, J., Ball, H. A., Martin, N. C., Scourfield, J., McGuffin, P.(2009). Genetic overlap between measures of hyperactivity/inatten-tion and mood in children and adolescents.J Am Acad Child AdolescPsychiatry48, 1094–1101.Kessler, R. C., Adler, L., Barkley, R., Biederman, J., Conners, C.K., Demler, O., Faraone, S. V., Greenhill, L. L., Howes, M. J., Secnik,K., Spencer, T., Ustun, T. B., Walters, E. E., Zaslavsky, A. M. (2006).The prevalence and correlates of adult ADHD in the United States:results from the National Comorbidity Survey Replication.Am JPsychiatry, 163, 716–723.Polanczyk, G., de Lima, M. S., Horta, B. L., Biederman, J., Rohde,L. A. (2007). The worldwide prevalence of ADHD: a systematicreview and metaregression analysis.Am J Psychiatry, 164, 942-8.Polderman, T. J., Hoekstra, R. A., Posthuma, D., Larsson, H.(2014). The co-occurrence of autistic and ADHD dimensions inadults: an etiological study in 17,770 twins.Transl Psychiatry2014;4: e435.Wilens, T. E., Biederman, J., Spencer, T. J. (2002). Attentiondeficit/hyperactivity disorder across the lifespan.Annual Review Med53:113–131.
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| 7. |
- Baker, Laura, et al.
(författare)
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The genetic and environmental etiology of internalizing and externalizing behavior in adolescent twins
- 2011
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Ingår i: Behavior Genetics. - : Springer Science and Business Media LLC. - 0001-8244 .- 1573-3297. ; 41:6, s. 927-927
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Comorbidity between internalizing (anxious, depressive) and externalizing (aggressive, delinquent) behavior is a well-established and common clinical reality throughout the lifespan, but perhaps becomes more significance in adolescence, when individuals are awarded more freedom. However, the genetic and environmental etiology of this comorbidity has rarely been examined in a behavioral genetic setting, especially during the period of adolescence. Additionally, research suggests that while caregivers may be more reliable reporters of externalizing behavior in youth, youth themselves are more reliable reporters of internalizing symptoms, raising the question of how different raters affect data patterns. Using the parent report Child Behavior Checklist (CBCL) as well as the youth report version (Youth Self Report—YSR), this research uses a twin study design to examine the etiology of coexisting internalizing and externalizing symptoms in mid adolescence (age 14–16 years) using a common pathway model that examined all data concurrently. Female comorbidity was accounted for by genetic and shared environmental influences, and male comorbidity by shared environmental influences, exclusively. Genetic influences emerged for all but self-report male externalizing behavior. Every scale showed unique influences as well, some of which were correlated between same-rater scales (e.g. parent report internalizing and externalizing), suggesting that some of the influences on covariation are rater-specific. These results contribute to our understanding of the nature of comorbid psychological disorders during adolescence, and suggest the importance of shared environment to the development of both internalizing and externalizing behavior
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| 8. |
- Baker, Laura, et al.
(författare)
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The Relationship between IQ and PM2.5 : Findings from the University of Southern California Twin Study
- 2016
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 46:6, s. 772-773
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Tidskriftsartikel (refereegranskat)abstract
- We examined the longitudinal relationship between IQ and fine particulate matter (\2.5lm aerodynamic diameters; PM2.5) exposure in urban-dwelling children, using prospective longitudinal data from the USC Twin Study of Risk Factors for Antisocial Behavior (RFAB; Baker et al. 2013). Residential addresses were collected via selfreports. Verbal and Performance IQ during childhood (age 9–10) and young adulthood (age 19–20) were evaluated by the Wechsler Abbreviated Intelligence Scale (Wechsler, 1999) using four subtests: VIQ=Vocabulary Similarities; PIQ=Block Design Matrices. Based on residential addresses and spatiotemporal generalized additive model of local monitoring data for PM2.5, we estimated 1-year average exposure before each assessment. A three-level mixed effects model regressing IQ scores at each assessment on time-varying air pollution exposures, accounting for both within-family (random intercepts) and within-individual (random slopes) was used. PM2.5 exposure had significant adverse effects on PIQ (95 % CI of b:-7.29 to-1.01, p\.05) but not VIQ (95 % CI of b:-4.50 to-1.96). Adverse effects of PM2.5 exposure remained significant after adjusting for age, family SES, sex, race/ethnicity, parental cognitive abilities, neighborhood SES, neighborhood quality and neighborhood greenness; the association was still significant after further adjusting for traffic distance (300 m), temperature, humidity and annual NOx. PM2.5 exposure confers stronger adverse effects on PIQ in low SES families, males, and during pre-adolescence. Our findings reveal social disparities and sexual dimorphism in the adverse PM2.5 exposure effects on PIQ. Baker, L., Tuvblad, C., Wang, P., Gomez, K., Bezdjian, S., Niv, S., & Raine, A. (2013). The Southern California Twin Register at the University of Southern California: III. Twin Research and Human Genetics, 16(1), 336–343; Wechsler, D. (1999). Wechsler Abbreviated Scale of Intelligence (WASI). San Antonio, Texas: Harcourt Assessment.
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| 9. |
- Baldwin, Jessie R., et al.
(författare)
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Adverse Childhood Experiences and Mental Health : A Genetically Informed Study
- 2021
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 51:6, s. 691-692
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Children exposed to adverse childhood experiences (ACEs) have an elevated risk of mental health problems, but it is unclear whether these associations reflect genetic confounding. We tested (1) whether children with genetic liability to psychopathology are more likely to experience ACEs, and (2) the extent to which the associations between ACEs and mental health are genetically confounded. Par-ticipants were 6411 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). ACEs (including maltreatment, domestic violence, and parental psychopathology, substance abuse, criminality, and separation) were prospectively measured through parent reports at multiple assessments between birth and age 9. Internalizing and externalizing problems at age 9 were assessed through parent reports on the Development and Wellbeing Assessment. We derived polygenic scores for a range of psychiatric disorders. Children with greater genetic liability to psychopathology had a small elevation in risk of ACEs (pooled odds ratio = 1.05, 95% CI 1.01–1.09). Measured polygenic scores accounted for a very small proportion of the associations between ACEs with internalizing problems (pooled average across ACEs = 3.6%) and externalizing problems (pooled average = 4.8%). However, latent polygenic scores capturing SNP heritability in mental health outcomes explained a larger proportion of the associations between ACEs with internalizing problems (pooled average = 63%) and externalizing problems (pooled average = 17%). Risk of mental health problems in children exposed to ACEs is partly, but not completely driven by pre-existing genetic liability to psychopathology. Assuming the absence of nongenetic confounding, these findings are consistent with a partly causal effect of ACEs on mental health.
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