| 31. |
- Rodriguez, Alina, et al.
(author)
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Fetal origins of non-right-handedness and child mental health
- 2008
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In: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 49:9, s. 967-976
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Journal article (peer-reviewed)abstract
- Background: Environmental risk during fetal development for non-right-handedness, an index of brain asymmetry, and its relevance for child mental health is not fully understood. Methods: A Swedish population-based prospective pregnancy-offspring cohort was followed-up when children were five years old (N = 1714). Prenatal environmental risk exposures were the number of ultrasound examinations and maternal distress during pregnancy. Child mental health, including symptoms of attention deficit hyperactivity disorder (ADHD), language difficulties, and care-seeking for child behavior problems, was assessed via maternal and/or kindergarten teacher's ratings. Results: Prenatal exposure to maternal depressive symptoms and critical life events were associated with increased risk of child non-right-handedness and mixed handedness, after adjustment for parity, maternal age, birth outcomes, infant sex, and parental handedness. No association was found between handedness and number of ultrasound examinations. Non-right and mixed-handedness, rather than left-handedness, were associated with increased risk of language difficulties and particularly with ADHD symptoms, after adjustment for current parental ADHD symptoms, current maternal depressive symptoms, birth outcomes, smoking during pregnancy, depressive symptoms and critical life events. Problems were significant enough to prompt mothers to seek care for children's behavioral problems, and parents were more likely to have received advice from the children's kindergarten teachers to seek care. Conclusions: This study suggests that mixed-handedness, i.e., reflecting atypical brain laterality, can be a marker of both severity of prenatal exposure to maternal distress and of increased risk of ADHD symptoms in childhood. Our results support the idea that the fetal environment plays a role in subsequent child mental health.
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| 32. |
- Rodriguez, Alina, et al.
(author)
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Is prenatal alcohol exposure related to inattention and hyperactivity symptoms in children? : Disentangling the effects of social adversity
- 2009
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In: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 50:9, s. 1073-1083
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Journal article (peer-reviewed)abstract
- Background: Studies concerning whether exposure to low levels of maternal alcohol consumption during fetal development is related to child inattention and hyperactivity symptoms have shown conflicting results. We examine the contribution of covariates related to social adversity to resolve some inconsistencies in the extant research by conducting parallel analyses of three cohorts with varying alcohol consumption and attitudes towards alcohol use.Methods: We compare three population-based pregnancy2013offspring cohorts within the Nordic Network on ADHD from Denmark and Finland. Prenatal data were gathered via self-report during pregnancy and birth outcomes were abstracted from medical charts. A total of 21,678 reports concerning inattention and hyperactivity symptoms in children were available from the Strengths and Difficulties Questionnaire or the Rutter Scale completed by parents and/or teachers.Results: Drinking patterns differed cross-nationally. Women who had at least some social adversity (young, low education, or being single) were more likely to drink than those better off in the Finnish cohort, but the opposite was true for the Danish cohorts. Prenatal alcohol exposure was not related to risk for a high inattention-hyperactivity symptom score in children across cohorts after adjustment for covariates. In contrast, maternal smoking and social adversity during pregnancy were independently and consistently associated with an increase in risk of child symptoms.Conclusions: Low doses of alcohol consumption during pregnancy were not related to child inattention/hyperactivity symptoms once social adversity and smoking were taken into account.
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| 33. |
- Rodriguez, Alina
(author)
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Maternal pre-pregnancy obesity and risk for inattention and negative emotionality in children
- 2010
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In: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 51:2, s. 134-143
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Journal article (peer-reviewed)abstract
- Objective:This study aimed to replicate and extend previous work showing an association between maternal pre-pregnancy adiposity and risk for attention deficit hyperactivity disorder (ADHD) symptoms in children.Methods:A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714). Mothers and kindergarten teachers rated children's ADHD symptoms, presence and duration of problems, and emotionality. Dichotomized outcomes examined difficulties of clinical relevance (top 15% of the distribution). Analyses adjusted for pregnancy (maternal smoking, depressive symptoms, life events, education, age, family structure), birth outcomes (birth weight, gestational age, infant sex) and concurrent variables (family structure, maternal depressive symptoms, parental ADHD symptoms, and child overweight) in an attempt to rule out confounding.Results:Maternal pre-pregnancy overweight and obesity predicted high inattention symptom scores and obesity was associated with a two-fold increase in risk of difficulties with emotion intensity and emotion regulation according to teacher reports. Means of maternal ratings were unrelated to pre-pregnancy body mass index (BMI). Presence and duration of problems were associated with both maternal over and underweight according to teachers.Conclusions:Despite discrepancies between maternal and teacher reports, these results provide further evidence that maternal pre-pregnancy overweight and obesity are associated with child inattention symptoms and extend previous work by establishing a link between obesity and emotional difficulties. Maternal adiposity at the time of conception may be instrumental in programming child mental health, as prenatal brain development depends on maternal energy supply. Possible mechanisms include disturbed maternal metabolic function. If maternal pre-pregnancy obesity is a causal risk factor, the potential for prevention is great.
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| 34. |
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| 35. |
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| 36. |
- Sjöberg, Rickard L.
(author)
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Child testimonies during an outbreak of witch hysteria : Sweden 1670-1671
- 1995
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In: Journal of Child Psychology and Psychiatry. - : Blackwell Publishing. - 0021-9630 .- 1469-7610. ; 36:6, s. 1039-1051
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Journal article (peer-reviewed)abstract
- Eight hundred and nine testimonies given by children between the ages of 1 and 16 to the priests of the parish of Rättvik, and to the Royal commission of inquiry, during an outbreak of witch hysteria in 1670-71 are examined. The result implies that the capacity to separate reality from fantasy as well as the tendency to give stereotyped testimonies are related to age, social influence from other children and sex. The results also suggest that the testimonies were influenced by the person investigating the child.
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| 37. |
- Thorell, Lisa B.
(author)
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Do delay aversion and executive function deficits make distinct contributions to the functional impact of ADHD symptoms? : A study of early academic skill deficits
- 2007
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In: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 48:11, s. 1061-1070
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Journal article (peer-reviewed)abstract
- Background: The present study examined the distinct properties of executive functioning in relation to ADHD symptoms, as well as functional outcomes associated with ADHD. In line with the dual-pathway model of ADHD, executive functioning and delay aversion were expected to show independent effects on ADHD symptoms. Furthermore, relations to early academic skills were examined, and it was hypothesized that the two processes of the dual-pathway model can be differentiated in terms of their effect on academic skill deficits, such that EF deficits, but not delay aversion, mediate the link between ADHD and academic functioning. Results: As hypothesized, both EF deficits and delay aversion were independently related to ADHD symptoms. However, when conducting separate analyses for the two ADHD symptom domains, only the effect of EF deficits was independently related to symptoms of inattention, whereas only the effect of delay aversion was independently related to symptoms of hyperactivity/ impulsivity. The mediation analysis showed that EF deficits, but not delay aversion, act as a mediator in the relation between symptoms of inattention and both mathematics and language skills. In addition, there was also a significant direct effect of inattention on early academic skills. Conclusions: The findings of the present study are of importance for current models of heterogeneity in ADHD as they 1) provide further support for the notion that EF deficits and delay aversion are two possible pathways to ADHD, 2) add new interesting knowledge by showing that EF deficits and delay aversion can be differentiated in terms of their relations to the two ADHD symptom domains, and 3) indicate that the two processes of the dual-pathway model can also be differentiated in terms of their effect on functional impairments associated with ADHD.
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| 38. |
- Tuvblad, Catherine, 1968-, et al.
(author)
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Heritability for adolescent antisocial behavior differs with socioeconomic status : gene–environment interaction
- 2006
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In: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 47:7, s. 734-743
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Journal article (peer-reviewed)abstract
- Background: Socioeconomic status is often assumed to be of importance for the development of antisocial behavior, yet it explains only a fraction of the variance. One explanation for this paradox could be that socioeconomic status moderates the influence of genetic and environmental effects on antisocial behavior.Method: TCHAD is a Swedis h longitudinal population-based twin study that contains 1,480 twin pairs born 1985-1986. The present study included 1,133 twin pairs, aged 16-17 years. Antisocial behavior was measured through self-report. Family socioeconomic status was assessed by parentalreported education and occupational status. Neighborhood socioeconomic conditions were assessed using five aggregated level variables: ethnic diversity, basic educational level, unemployment level, buying power, and crime-rate. We used structural equation modeling to test whether socioeconomic status interacted with latent genetic and environmental effects for antisocial behavior.Results: Gen etic influences on antisocial behavior were more important in adolescents in socioeconomically more advantaged environments, whereas the shared environment was higher in adolescents in socioeconomically less advantaged environments. Heritability for antisocial behavior was higher in girls than in boys, irrespective of socioeconomic background.Conclusions: Our results suggest that differe nt intervention policies should be considered in different socioeconomic areas. In socioeconomically advantaged areas, it might be more fruitful to focus on individually based preventions and treatments. In socioeconomically disadvantaged areas, intervention and prevention policies might be more effective on a community level, to account for shared environmental risk factors.
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| 39. |
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| 40. |
- Ahlberg, Richard, et al.
(author)
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Shared familial risk factors between autism spectrum disorder and obesity : a register‐based familial coaggregation cohort study
- 2022
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In: Journal of Child Psychology and Psychiatry. - : John Wiley & Sons. - 0021-9630 .- 1469-7610. ; 63:8, s. 890-899
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Journal article (peer-reviewed)abstract
- Background: Meta-analyses suggest an association between autism spectrum disorder (ASD) and obesity, but the factors underlying this association remain unclear. This study investigated the association between ASD and obesity stratified on intellectual disability (ID). In addition, in order to gain insight into possible shared etiological factors, the potential role of shared familial liability was examined.Method: We studied a cohort of 3,141,696 individuals by linking several Swedish nationwide registers. We identified 35,461 individuals with ASD and 61,784 individuals with obesity. Logistic regression models were used to estimate the association between ASD and obesity separately by ID and sex and by adjusting for parental education, psychiatric comorbidity, and psychotropic medication. Potential shared familial etiologic factors were examined by comparing the risk of obesity in full siblings, maternal and paternal half-siblings, and full- and half-cousins of individuals with ASD to the risk of obesity in relatives of individuals without ASD.Results: Individuals with ASD + ID (OR = 3.76 [95% CI, 3.38-4.19]) and ASD-ID (OR = 3.40 [95% CI, 3.23-3.58]) had an increased risk for obesity compared with individuals without ASD. The associations remained statistically significant when adjusting for parental education, psychiatric comorbidity, and medication. Sex-stratified analyses indicated a higher relative risk for males compared with females, with statistically significant interaction effects for ASD-ID, but not for ASD+ID in the fully adjusted model. First-degree relatives of individuals with ASD+ID and ASD-ID had an increased risk of obesity compared with first-degree relatives of individuals without ASD. The obesity risk was similar in second-degree relatives of individuals with ASD+ID but was lower for and ASD-ID. Full cousins of individuals with ASD+ID had a higher risk compared with half-cousins of individuals with ASD+ID). A similar difference in the obesity risk between full cousins and half-cousins was observed for ASD-ID.Conclusions: Individuals with ASD and their relatives are at increased risk for obesity. The risk might be somewhat higher for males than females. This warrants further studies examining potential common pleiotropic genetic factors and shared family-wide environmental factors for ASD and obesity. Such research might aid in identifying specific risks and underlying mechanisms in common between ASD and obesity.
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