Silje Steinsbekk

Sleep Disorders in Preschoolers: Prevalence and Comorbidity with Psychiatric Symptoms

Objectives: This study provides data on the prevalence of diagnosable sleep disorders in preschoolers and examined the relationship between specific sleep disorders and a range of DSM-4–defined psychiatric symptoms. Methods: All children born in 2003 or 2004 in Trondheim, Norway, who attended regular community health checkups for 4 year olds were asked to participate (97.2% attendance; 82.0% consent rate, N = 2475). A screen-stratified subsample of 1250 children was recruited to participate in an additional comprehensive study that included a structured diagnostic interview (the Preschool-Age Psychiatric Assessment). Nine hundred ninety-five parents (79.6%) completed the interview. Results: The estimated sleep disorder rate was 19.2%. Rates of specific disorders were as follows: primary insomnia (16.6%), primary hypersomnia (0.8%), nightmare disorder (2.2%), and sleepwalking disorder (0.7%). When adjusted for a range of common psychiatric symptoms, primary insomnia was specifically related to symptoms of depression, generalized anxiety disorder, separation anxiety, and specific phobia. When sleep problems were excluded as a symptom of depression, the association between depression and primary insomnia was no longer significant. Nightmare disorder was significantly related to generalized anxiety disorder. Conclusions: This first study of the prevalence and comorbidity of diagnosable sleep disorders in preschoolers indicates that primary insomnia is common in young children, whereas other sleep disorders are rare. Sleep disorders are related to psychiatric symptoms, particularly symptoms of anxiety disorders.

Food fussiness and food neophobia share a common etiology in early childhood

Background ‘Food fussiness’ (FF) is the tendency to be highly selective about which foods one is willing to eat, and emerges in early childhood; ‘food neophobia’ (FN) is a closely related characteristic but specifically refers to rejection of unfamiliar food. These behaviors are associated, but the extent to which their etiological architecture overlaps is unknown. The objective of this study was to quantify the relative contribution of genetic and environmental influences to variation in FF and FN in early childhood; and to establish the extent to which they share common genetic and environmental influences. Method Participants were 1,921 families with 16‐month‐old twins from the Gemini birth cohort. Parents completed the Child Eating Behaviour Questionnaire which included three FF items and four FN items. Bivariate quantitative genetic modeling was used to quantify: (a) genetic and environmental contributions to variation in FF and FN; and (b) the extent to which genetic or environmental influences on FF and FN are shared across the traits. Results Food fussiness and FN were strongly correlated (r = .72, p < .001). Proportions of variation in FF were equally explained by genetic (.46; 95% CI: 0.41–0.52) and shared environmental influences (.46; 95% CI: 0.41–0.51). Shared environmental effects accounted for a significantly lower proportion of variation in FN (.22; 95% CI: 0.14–0.30), but genetic influences were not significantly different from those on FF (.58, 95% CI: 0.50–0.67). FF and FN largely shared a common etiology, indicated by high genetic (.73; 95% CI: 0.67–0.78) and shared environmental correlations (.78; 95% CI: 0.69–0.86) across the two traits. Conclusions Food fussiness and FN both show considerable heritability at 16 months but shared environmental factors, for example the home environment, influenced more interindividual differences in the expression of FF than in FN. FF and FN largely share a common etiology.

Stability of sleep disorders from preschool to first grade and their bidirectional relationship with psychiatric symptoms.

Objectives: To examine the prevalence and stability of DSM-4–defined sleep disorders from preschool to first grade and to explore the bidirectional relationship between sleep disorders and symptoms of psychiatric disorders. Method: All children born in 2003 or 2004 in Trondheim, Norway, who attended regular community health checkups for 4-year-olds, were invited to participate (97.2% attendance; 82.0% consent rate, n = 2475) in this study. The authors recruited a screen-stratified subsample of 1250 children and interviewed 994 parents (79.6%) using a structured diagnostic interview (the Preschool Age Psychiatric Assessment). Two years later, 795 of the parents completed the interview. Results: There was stability in insomnia (adjusted odds ratio [OR] = 4.03, confidence interval [CI] = 2.83–5.75) and sleepwalking (adjusted OR = 19.28, CI = 4.53–82.10), whereas none of the children with hypersomnia or nightmare disorder at age 4 had the same disorder 2 years later. Insomnia increased the risk for developing symptoms of conduct disorder, major depressive disorder (MDD), and social phobia when the initial levels of insomnia were adjusted for. Symptoms of attention-deficit hyperactivity disorder, oppositional defiant disorder, and MDD at age 4 were statistically linked to insomnia at age 6. Sleepwalking predicted later separation anxiety disorder, whereas hypersomnia was unrelated to symptoms of psychiatric disorders. Conclusion: Insomnia is a prevalent and stable disorder in children and is bidirectionally related to psychiatric symptoms.

Polygenic risk, appetite traits, and weight gain in middle childhood:A longitudinal study

IMPORTANCE Genome-wide association studies have identified genetic risks for obesity. These genetic risks influence development of obesity partly by accelerating weight gain in childhood. Research is needed to identify mechanisms to inform intervention. Cross-sectional studies suggest appetite traits as a candidate mechanism. Longitudinal studies are needed to test whether appetite traits mediate genetic influences on childrens weight gain. OBJECTIVE To test whether genetic risk for obesity predicts accelerated weight gain in middle childhood (ages 4-8 years) and whether genetic association with accelerated weight gain is mediated by appetite traits. DESIGN, SETTING, AND PARTICIPANTS Longitudinal study of a representative birth cohort at the Trondheim Early Secure Study, Trondheim, Norway, enrolled at age 4 years during 2007 to 2008, with follow-ups at ages 6 and 8 years. Participants were sampled from all children born in 2003 or 2004 who attended regular community health checkups for 4-year-olds (97.2% attendance; 82.0% consent rate, n = 2475). Nine hundred ninety-five children participated at age 4 years, 795 at age 6 years, and 699 at age 8 years. Analyses included 652 children with genotype, adiposity, and appetite data. MAIN OUTCOMES AND MEASURES Outcomes were body mass index and body-fat phenotypes measured from anthropometry (ages 4, 6, and 8 years) and bioelectrical impedance (ages 6 and 8 years). Genetic risk for obesity was measured using a genetic risk score composed of 32 single-nucleotide polymorphisms previously discovered in genome-wide association studies of adult body mass index. Appetite traits were measured at age 6 years with the Childrens Eating Behavior Questionnaire. RESULTS Of the 652 genotyped child participants, 323 (49.5%) were female, 58 (8.9%) were overweight, and 1 (0.2%) was obese. Children at higher genetic risk for obesity had higher baseline body mass index and fat mass compared with lower genetic risk peers, and they gained weight and fat mass more rapidly during follow-up. Each SD increase in genetic risk score was associated with a 0.22-point increase in BMI at age-4 baseline (for the intercept, unstandardized path coefficient B = 0.22 [95% CI, 0.06-0.38]; P = .008. Children with higher genetic risk scores also gained BMI points more rapidly from ages 4 to 6 years (B = 0.11 [95% CI, 0.03-0.20]; P = .01 ; β = 0.12) and from 6 to 8 years (B = 0.09 [95% CI, 0.00-0.19]; P = .05; β = 0.10), compared with their lower genetic risk peers. Children at higher genetic risk had higher levels of alleged obesogenic appetite traits than peers with lower genetic risk at age 6 years, but appetite traits did not mediate genetic associations with weight gain. The sum of the 5 indirect effects was B = -0.001 (95% CI, -0.02 -0.01); P = .86; β = 0.00. CONCLUSIONS AND RELEVANCE Genetic risk for obesity is associated with accelerated childhood weight gain. Interventions targeting childhood weight gain may provide one path to mitigating genetic risk. However, middle childhood appetite traits may not be a promising target for such interventions. Studies of early-childhood samples are needed to test whether appetite traits explain how genetic risks accelerate growth earlier in development.

Predictors of Change in BMI From the Age of 4 to 8

OBJECTIVES To examine appetite traits, level of physical activity, and television (TV) time as predictors of change in Body Mass Index Standard Deviation Score (BMI SDS) from age 6 to 8 and to explore the effect of BMI SDS (from age 4) on appetite traits. METHODS In all, 995 Norwegian children participated at age 4; 760 and 687 of these children took part in the assessment at ages 6 and 8, respectively. Appetite traits were assessed using the Childrens Eating Behavior Questionnaire, activity was measured using accelerometers, and TV time was based on parental reports. RESULTS High food responsiveness predicted a steeper increase in BMI SDS. A reversed effect was also observed: High BMI SDS predicted increased food responsiveness and decreased satiety responsiveness. Physical activity and TV time were unrelated to BMI SDS. CONCLUSION Children whose eating is especially triggered by the sight and smell of food show prospective increased weight gain. Excess weight and weight gain also predict increased food-approaching behavior.

Change in body fat during a family-based treatment of obesity in children: the relative importance of energy intake and physical activity.

Objective: The aim of the current study was to examine to what extent changes in reported energy intake and physical activity predict changes in body fat during a family-based outpatient treatment of obesity in children. Methods: Total body fat (DXA), reported energy intake (4-day diet record), and physical activity (accelerometer) was measured in 99 children (age 7–12 years, mean BMI SDS = 2.99) at baseline as well as after 6 months 2 years of treatment. Repeated measures (GLM), growth modeling, and structural equation modeling (SEM) were applied in the data analyses. Results: There was significant decrease in body fat, reported energy intake, and physical activity at both follow-ups (p < 0.001) compared to baseline. Changes in reported energy intake from baseline to 6 months predicted a decrease in body fat from baseline to 6 months (β = 0.68, p < 0.001). In addition, changes in reported energy intake had a strong indirect effect on body fat at 2-year follow-up, mediated by changes in body fat from baseline to 6 months (indirect β = 0.50, p < 0.001). Changes in physical activity did not predict changes in body fat during treatment. Conclusions: Changes in reported energy intake significantly affected body fat at 6 months and indirectly predicted the amount of body fat at 2-year follow-up. The indirect effect was mediated by a decrease in body fat obtained during the first phase of treatment.

Health in overweight children: 2-year follow-up of Finnmark Activity School—a randomised trial

Objective To compare a comprehensive lifestyle intervention for overweight children performed in groups of families with a conventional single-family treatment. Two-year follow-up data on anthropometric and psychological outcome are presented. Design Overweight and obese children aged 6–12 years with body mass index (BMI) corresponding to ≥27.5 kg/m2 in adults were randomised to multiple-family (n=48) or single-family intervention (n=49) in a parallel design. Multiple-family intervention comprised an inpatient programme with other families and a multidisciplinary team, follow-up visits in their hometown, weekly physical activity and a family camp. Single-family intervention included counselling by paediatric nurse, paediatric consultant and nutritionist at the hospital and follow-up by a community public health nurse. Primary outcome measures were change in BMI kg/m2 and BMI SD score after 2 years. Results BMI increased by 1.29 kg/m2 in the multiple-family intervention compared with 2.02 kg/m2 in the single-family intervention (p=0.075). BMI SD score decreased by 0.20 units in the multiple-family group and 0.08 units in the single-family intervention group (p=0.046). A between-group difference of 2.4 cm in waist circumference (p=0.038) was detected. Pooled data from both treatment groups showed a significant decrease in BMI SD score of 0.14 units and a significant decrease in parent-reported and self-reported Strength and Difficulty Questionnaire total score of 1.9 units. Conclusions Two-year outcome showed no between-group difference in BMI. A small between-group effect in BMI SD score and waist circumference favouring multiple-family intervention was detected. Pooled data showed an overall improvement in psychological outcome measures and BMI SD score. Trial registration number NCT00872807, http://www.clinicaltrials.gov.

Physical Activity, Sedentary Behavior, and Symptoms of Major Depression in Middle Childhood

OBJECTIVE: The prospective relation between physical activity and Diagnostic and Statistical Manual of Mental Disorders-defined major depression in middle childhood is unknown, as is the stability of depression. We therefore aimed to (1) determine whether there are reciprocal relations between moderate-to-vigorous physical activity (MVPA) and sedentary behavior, on one hand, and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition defined symptoms of major depressive disorder, on the other and (2) assess the extent of stability in depressive symptoms from age 6 to 10 years. METHODS: A community sample of children living in Trondheim, Norway, comprising a total of 795 6-year-old children was followed up at 8 (n = 699) and 10 (n = 702) years of age. Physical activity was recorded by accelerometry and symptoms of major depression were measured through semistructured clinical interviews of parents and children. Bidirectional relationships between MVPA, sedentary activity, and symptoms of depression were analyzed through autoregressive cross-lagged models, and adjusted for symptoms of comorbid psychiatric disorders and BMI. RESULTS: At both age 6 and 8 years, higher MVPA predicted fewer symptoms of major depressive disorders 2 years later. Sedentary behavior did not predict depression, and depression predicted neither MVPA nor sedentary activity. The number of symptoms of major depression declined from ages 6 to 8 years and evidenced modest continuity. CONCLUSIONS: MVPA predicts fewer symptoms of major depression in middle childhood, and increasing MVPA may serve as a complementary method to prevent and treat childhood depression.

Predictors of eating behavior in middle childhood: A hybrid fixed effects model

Children’s eating behavior influences energy intake and thus weight through choices of type and amount of food. One type of eating behavior, food responsiveness, defined as eating in response to external cues such as the sight and smell of food, is particularly related to increased caloric intake and weight. Because little is known about the potential determinants of such behavior, we focus herein on child and parent predictors of food responsiveness in a large community sample of Norwegian 6-year-olds, followed up at ages 8 and 10. To measure children’s food responsiveness, parents completed the Children’s Eating Behavior Questionnaire. Potential predictors were children’s inhibition and symptoms of attention-deficit/hyperactivity disorder and depression, and parents’ instrumental and controlling feeding practices as well as parental restrained eating. After accounting for children’s initial levels of food responsiveness within a hybrid fixed effects method that takes into consideration all unmeasured time-invariant confounders, more child attention-deficit/hyperactivity disorder symptoms and greater restrained eating by parents predicted more food responsiveness at both ages 8 and 10. These results may provide important insights for efforts to prevent overeating.

Predictors of Physical Activity in Middle Childhood. A Fixed-Effects Regression Approach

Background: Moderate-to-vigorous physical activity (MVPA) has a range of health benefits across the life span. Although many putative determinants of childrens MVPA have been identified, their causal status is uncertain due to difficulties in adjusting for potential confounders. Objective: To inform promotion of childrens MVPA we therefore aimed to examine well-known child-, family- and contextual predictors of MVPA in middle childhood, by applying a fixed effects regression approach, which rules out the influence of all unmeasured time-invariant confounders. Methods: Two birth cohorts of children living in the city of Trondheim, Norway were invited to participate (82.0% consented). The participants were followed-up biennially from age 6 to 10 years (n = 800) between 2009 and 2014. MVPA in children was recorded by accelerometers and child-, family- and contextual factors were obtained through interviews and questionnaires. Predictors included (i) child-level factors: the childs time outdoors, organized sports participation, athletic self-concept, self-reported screen time and objectively measured sedentariness; (ii) family factors: self-reported parental MVPA and actively transporting the child to school; and (iii) contextual factors: parental socio-economic status (SES), access to playgrounds and ballparks, traffic safety, and having a garden. A three-wave prospective study was conducted with a hybrid fixed effects regressions analysis adjusting for all time-invariant confounders to examine predictors of MVPA. Results: Children evidenced increased MVPA when they spent more time outside, spent less time being sedentary and when the family had a garden and lived in a traffic-safe area. Conclusion: Adjusting for measured time-varying and all unmeasured time-invariant confounders renders many previously identified child and family factors without impact on MVPA in children. However, several contextual factors may promote MVPA in middle childhood, and efforts to facilitate children being outside in environments that promote physical activity (e.g., being outside, in gardens, or otherwise traffic safe areas) may prove important.