The long-term association between sleep duration and mental health in children is currently unknown.
To investigate the prospective associations between sleep duration and symptoms of emotional and behavioral disorders at ages 6, 8, 10, and 12 years.
This population-based cohort study obtained data from the Trondheim Early Secure Study in Trondheim, Norway. A representative, stratified random sample of children born between January 1, 2003, and December 31, 2004, were invited to participate. Participants were followed up biennially from age 4 years (2007-2008) to 12 years (2013-2014). Data analysis was conducted from January 2, 2019, to May 28, 2019.
Sleep duration was assessed with 1 week of continuous use of a triaxial accelerometer. Symptoms of emotional (anxiety and depression) and behavioral (oppositional defiant, conduct, and attention-deficit/hyperactivity) disorders were measured by semistructured clinical interviews (using the Preschool Age Psychiatric Assessment and the Child and Adolescent Psychiatric Assessment) with parents (at all ages) and children (from age 8 years).
The analytical sample comprised 799 children (mean [SD] age at time point 2, 6.0 [0.2] years; 405 [50.7%] boys; and 771 [96.5%] Norwegian). Shorter sleep duration at age 6 years (ß [unstandardized regression coefficient]?=?-0.44; 95% CI, -0.80 to -0.08; P?=?.02) and 8 years (ß?=?-0.47; 95% CI, -0.83 to -0.11; P?=?.01) forecasted symptoms of emotional disorders 2 years later. Comparatively short sleep duration at age 8 years (ß?=?-0.65; 95% CI,?-1.22 to -0.08; P?=?.03) and 10 years (ß?=?-0.58; 95% CI,?-1.07 to -0.08; P?=?.02) was associated with symptoms of behavioral disorders 2 years later among boys but not among girls at age 8 years (ß =?-0.14; 95% CI,-?0.52 to 0.24; P?=?.48) or 10 years (ß?=?-0.05; 95% CI,?=?-0.49 to 0.40; P?=?.84). These associations were statistically significant among boys compared with girls at age 8 years (??21?=?13.26; P?
Research suggests a role for both fat mass and muscle mass in appetite regulation, but the longitudinal relationships between them have not yet been examined in children. The present study therefore aimed to explore the prospective relationships between fat mass, muscle mass and the appetitive traits food responsiveness and satiety responsiveness in middle childhood.
Food responsiveness and satiety responsiveness were measured using the parent-reported Children's Eating Behavior Questionnaire in a representative sample of Norwegian 6?year olds, followed up at 8 and 10?years of age (n?=?807). Body composition was measured by bioelectrical impedance.
Applying a structural equation modeling framework we found that higher fat mass predicted greater increases in food responsiveness over time, whereas greater muscle mass predicted decreases in satiety responsiveness. This pattern was consistent both from ages 6 to 8 and from ages 8 to 10?years.
Our study is the first to reveal that fat mass and muscle mass predict distinct changes in different appetitive traits over time. Replication of findings in non-European populations are needed, as are studies of children in other age groups. Future studies should also aim to reveal the underlying mechanisms.
Cites: Appetite. 2007 Jan;48(1):104-1316962207
Cites: BMC Pediatr. 2015 Oct 12;15:15326459321
Cites: Dis Model Mech. 2012 Sep;5(5):608-1322915022
Cites: Neuroimage. 2013 Jan 1;64:712-2122974975
Cites: Br J Nutr. 2012 Feb;107(3):445-921733267
Cites: Child Obes. 2015 Oct;11(5):650-526332367
Cites: Science. 2005 Mar 25;307(5717):1909-1415790843
Cites: Int J Behav Nutr Phys Act. 2012 Oct 30;9:13023110748
Eating more or eating less in response to negative emotions, called emotional over- and undereating, is common in children, but research on the etiology of these behaviors is in its infancy. Drawing on a large, representative community sample of Norwegian children followed up on a biennial basis from 6 to 10 years of age (analysis sample: n = 802), child and contextual predictors (i.e., child temperament, depression symptoms, serious life events, family functioning, parental sensitivity and structuring) of change in emotional over- and undereating were examined. Results revealed that low (temperamental) soothability and less parental structuring at age 6 predicted increased emotional overeating at age 10 and that lower family functioning at age 6 predicted more emotional undereating during the same period.
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.
Overweight and obese children aged 6-12 years with body mass index (BMI) corresponding to =27.5 kg/m(2) 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/m(2) and BMI SD score after 2 years.
BMI increased by 1.29 kg/m(2) in the multiple-family intervention compared with 2.02 kg/m(2) 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.
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.
Childhood psychiatric disorders and their symptoms evince both within-disorder (homotypic) and between-disorder (heterotypic) continuities. These continuities may be due to earlier symptoms causing later symptoms or, alternatively, that the same (unknown) causes (e.g., genetics) are operating across time. Applying a novel data analytic approach, we disentangle these two explanations.
Participants in a Norwegian community study were assessed biennially from 4 to 10 years of age with clinical interviews (n = 1,042). Prospective reciprocal relations between symptoms of disorders were analyzed with a dynamic panel model within a structural equation framework, adjusting for all unmeasured time-invariant confounders and time-varying negative life-events.
Homotypic continuities in symptoms characterized all disorders; strongest for attention-deficit/hyperactivity disorder (ADHD) (r = .32-.62), moderate for behavioral disorders (r = .31-.48) and for anxiety and depression (r = .15-.40), and stronger between 8 and 10 than between 4 and 6 years. Heterotypic continuity also characterized all disorders. A dynamic panel model showed that most continuities were due to unmeasured time-invariant factors rather than effects of earlier symptoms on later symptoms, although symptoms of behavioral disorders, which evinced two-year homotypic continuity (B = .14, 95% CI: .04, .25), did influence later symptoms of ADHD (B = .13, CI: .03, .23), and earlier ADHD symptoms influenced later anxiety disorder symptoms (B = .07, CI: .01, .12).
Homotypic and heterotypic continuities of symptoms of childhood psychiatric disorders are mostly due to unobserved time-invariant factors. Nonetheless, symptoms of earlier behavioral disorders may affect later symptoms of such disorders and of ADHD, and ADHD may increase the risk of later anxiety. Thus, even if interventions do not alter basic etiological factors, symptom reduction may itself cause later symptom reduction.
Parental feeding practices and children's eating behavior are consistently related to childhood obesity. However, it is not known whether parents' feeding practices predict obesogenic eating behavior or vice versa. In a Norwegian cohort (n = 797), it was found that greater parental use of food as a reward (instrumental feeding) when children were 6 predicted increased emotional overeating and food responsiveness, whereas greater parental encouragement to eat forecasted increased enjoyment of food 2 years later. No evidence of child effects emerged. Although children's eating behavior is relatively stable and established at an early age, findings suggest that parental feeding practices can serve as targets of intervention to prevent the development of obesogenic eating behavior.
According to prominent models of child development, parental factors may contribute to individual differences in children's executive functioning (EF). Here, we examine the relative importance of parents' socio-economic status, mental health, and parenting as predictors of EF development, drawing on a large (n = 1,070) community sample of Norwegian children who received biennial EF assessments from 6 to 10 years of age. We measure EF by means of the Behavior Rating Inventory of Executive Function. We assess parenting through observer ratings of parent-child interactions and parental mental health via the Beck Anxiety Inventory, Beck Depression Inventory, and Hopkins Symptom Checklist. When we adjust for all time-invariant unmeasured confounders, higher parental education predicts superior EF development, whereas harsh parenting forecasts poorer EF development. However, parenting does not mediate the effect of parental education. These results indicate that harsh parenting should be targeted in interventions aimed at improving EF. Statement of contribution What is already known on this subject? Parental factors seem to affect child development of executive functions (EF). Specifically, parental socio-economic status, mental health, and their parenting seem to influence the developmental course of child EF. What does this study add? To what degree the parental influence on EF development is likely to be driven by time-invariant factors, for example, genetics. The relative influence of positive and negative parenting on EF development.
Personality disorder (PD) symptomatology is characterized by interpersonal problems and emotional dysregulation, which may affect offspring of parents with PD symptoms. Notably though, studies are needed to discern (i) whether parental PDs forecast symptoms of psychiatric disorders in offspring during their childhood years and (ii) whether such prospective relations obtain after accounting for common causes (e.g., genetics, common methods). To address these issues, we followed up a community sample of Norwegian children biennially from ages 4 to 8 (n?=?594), using a semi-structured psychiatric interview (PAPA/CAPA) to capture DSM-IV defined symptoms of emotional disorders. Parental symptoms of personality disorders were captured by the DSM-IV and ICD-10 Personality Questionnaire (DIP-Q), whereas depression and anxiety in caregivers were measured using the Beck Depression Inventory -II and Beck Anxiety Inventory, respectively. Upon applying a hybrid fixed and random effects method that takes into account all unmeasured time-invariant confounders, we found that: (i) Parental symptoms of DSM-IV defined Cluster A and C were related to symptoms of anxiety disorders in offspring two years later, even after accounting for children's initial levels of anxiety and parental anxiety, whereas (ii) Parental DSM-IV Cluster B predicted symptoms of depressive disorders in children, adjusted for children's initial levels of depression and parental depression. Clinical implications of the results are discussed.