Reciprocal relations between dimensions of attention-deficit/hyperactivity and anxiety disorders from preschool age to adolescence: sex differences in a birth cohort sample.

BACKGROUND: Symptoms of anxiety and attention-deficit/hyperactivity disorder (ADHD) are prospectively related from childhood to adolescence. However, whether the two dimensions of ADHD-inattention and hyperactivity-impulsivity-are differentially related to anxiety and whether there are developmental and sex/gender differences in these relations are unknown. METHODS: Two birth cohorts of Norwegian children were assessed biennially from ages 4 to 16 (N = 1,077; 49% girls) with diagnostic parent interviews used to assess symptoms of anxiety and ADHD. Data were analyzed using a random intercept cross-lagged panel model, adjusting for all unobserved time-invariant confounding effects. RESULTS: In girls, increased inattention, but not hyperactivity-impulsivity, predicted increased anxiety 2 years later across all time-points and increased anxiety at ages 12 and 14 predicted increased inattention but not hyperactivity-impulsivity. In boys, increased hyperactivity-impulsivity at ages 6 and 8, but not increased inattention, predicted increased anxiety 2 years later, whereas increased anxiety did not predict increased inattention or hyperactivity-impulsivity. CONCLUSIONS: The two ADHD dimensions were differentially related to anxiety, and the relations were sex-specific. In girls, inattention may be involved in the development of anxiety throughout childhood and adolescence and anxiety may contribute to girls developing more inattention beginning in early adolescence. In boys, hyperactivity-impulsivity may be involved in the development of anxiety during the early school years. Effective treatment of inattention symptoms in girls may reduce anxiety risk at all time-points, while addressing anxiety may decrease inattention during adolescence. Similarly, treating hyperactivity-impulsivity may reduce anxiety risk in boys during late childhood (at ages 8-10).

Emotions or cognitions first? Longitudinal relations between executive functions and emotion regulation in childhood.

Executive functions and emotion regulation develop from early childhood to adolescence and are predictive of important psychosocial outcomes. However, despite the correlation between the two regulatory capacities, whether they are prospectively related in school-aged children remains unknown, and the direction of effects is uncertain. In this study, a sample drawn from two birth cohorts in Norway was biennially examined between the ages of 6 and 14 (n = 852, 50.1% girls, 93% Norwegian). Parents completed the Emotion Regulation Checklist, and teachers completed the Behavior Rating Inventory of Executive Function. A random intercept cross-lagged panel model revealed that improved emotion regulation predicted increased executive functioning to the same extent throughout development, whereas enhanced executive functioning was unrelated to future changes in emotion regulation.

Depression and Personality Traits Across Adolescence-Within-Person Analyses of a Birth Cohort.

Depressive symptoms and personality traits covary in adolescents, but our understanding of the nature of this relation is limited. Whereas a predisposition explanation posits that specific personality traits increase the vulnerability for developing depression, a scar explanation proposes that depression may alter premorbid personality. Attempts to test these explanatory models have relied on analyses that conflate within-person changes and between-person differences, which limits the implications that can be drawn. Moreover, research on the early adolescent years is lacking. The present study therefore examined within-person associations between depressive symptoms and Big Five personality traits across ages 10 to 16. Children (n = 817; 49.9% boys) and parents from two birth cohorts in Trondheim, Norway, were assessed biennially with clinical interviews capturing symptoms of major depressive disorder and dysthymia, and self-reported Big Five personality traits. Analyses were conducted using a random intercept cross-lagged panel model, which accounts for all unmeasured time-invariant confounding effects. Increased Neuroticism predicted an increased number of depressive symptoms-and increased depressive symptoms predicted increased Neuroticism-across ages 10 to 14. Moreover, increased depressive symptoms forecast reduced Extraversion across ages 10 to 16, and reduced Conscientiousness from ages 12 to 14. Increases in Neuroticism may contribute to the development of depressive symptoms-in line with the predisposition model. As regards the scar model, depression may have an even wider impact on personality traits: increasing Neuroticism and reducing Extraversion and Conscientiousness. These effects may already be present in the earliest adolescent years.

Development of symptoms of oppositional defiant disorder from preschool to adolescence: the role of bullying victimization and emotion regulation.

BACKGROUND: Childhood oppositional defiant disorder (ODD) is associated with adverse outcomes which can continue to impair life well into adulthood. Identifying modifiable etiological factors of ODD is therefore essential. Although bullying victimization and poor emotion regulation are assumed to be risk factors for the development of ODD symptoms, little research has been conducted to test this possibility. METHODS: A sample (n = 1,042) from two birth cohorts of children in the city of Trondheim, Norway, was assessed biennially from age 4 to 14 years. Parents and children (from age 8) were assessed with clinical interviews to determine symptoms of ODD, children reported on their victimization from bullying, and teachers reported on children's emotion regulation. RESULTS: Oppositional defiant disorder symptoms increased from age 4 to 6, from age 8 to 10, and then started to wane as children entered adolescence. A Random Intercept Cross-Lagged Panel Model revealed that increased emotion regulation predicted a reduced number of ODD symptoms across development (ß = -.15 to -.13, p < .001). This prediction was equally strong for the angry/irritable and argumentative/defiant dimensions of ODD. No longitudinal links were observed between bullying victimization and ODD symptoms. CONCLUSIONS: Improving emotion regulation skills may protect against ODD symptoms throughout childhood and adolescence.

Validation of the adult eating behavior questionnaire in a Norwegian sample of adolescents.

Eating behaviors are related to health and well-being. To examine stability and change in eating behaviors throughout life, developmentally appropriate measures capturing the same eating behavior dimensions are needed. The newly developed Adult Eating Behavior Questionnaire (AEBQ) builds on the well-established parent-reported Children's Eating Behavior Questionnaire (CEBQ), and together with the corresponding Baby Eating Behavior Questionnaire (BEBQ), these questionnaires cover all ages. However, validation studies on adolescents are relatively sparse and have yielded somewhat conflicting results. The present study adds to existing research by testing the psychometric properties of the AEBQ in a sample of 14-year-olds and examining its construct validity by means of the parent-reported CEBQ. The current study uses age 14 data (analysis sample: n = 636) from the ongoing Trondheim Early Secure Study, a longitudinal study of a representative birth cohort of Norwegian children (baseline: n = 1007). Confirmatory factor analysis (CFA) was conducted to test the factorial validity of AEBQ. Construct validity was examined by bivariate correlations between AEBQ subscales and CEBQ subscales. CFAs revealed that a 7-factor solution of the AEBQ, with the Hunger scale removed, was a better-fitting model than the original 8-factor structure. The 7-factor model was respecified based on theory and model fit indices, resulting in overall adequate model fit (χ2 = 896.86; CFI = 0.924; TLI = 0.912; RMSEA = 0.05 (90% CI: 0.043, 0.051); SRMR = 0.06). Furthermore, small-to-moderate correlations were found between corresponding AEBQ and CEBQ scales. This study supports a 7-factor solution of the AEBQ without the Hunger scale and provide evidence of its construct validity in adolescents. Several of the CEBQ subscales were significantly associated with weight status, whereas this was the case for only one of the AEBQ scales.

Reciprocal relations between interparental aggression and symptoms of oppositional defiant and conduct disorders: a seven-wave cohort study of within-family effects from preschool to adolescence.

BACKGROUND: Interparental aggression is believed to increase the risk of behavioral disorders in offspring, and offspring behavioral problems may forecast interparental aggression. However, these assumptions have yet to be put to a strong test. This study, therefore, examined whether increased interparental aggression predicted increased symptoms of oppositional defiant disorder (ODD) and conduct disorder (CD) from preschool to adolescence and vice versa. METHODS: A sample (n = 1,077; 49.6% girls) from two birth cohorts of children in Trondheim, Norway, was assessed biennially from age 4 to 16. Children's symptoms of ODD and CD were assessed using semi-structured clinical interviews of parents (from age 4) and children (from age 8). One of the parents reported on their own and their partner's verbal and physical aggression. A random intercept cross-lagged model was estimated to test the within-family relations between interparental aggression, CD, and ODD symptoms. RESULTS: Across development, increased interparental aggression predicted increased CD symptoms 2 years later, whereas an increased number of ODD symptoms forecasted increased interparental aggression. CONCLUSIONS: The argumentative/defiant, aggressive, and vindictive behaviors seen in ODD are often directed toward parents and may take a toll on their relationship and possibly foster interparental aggression, whereas aggression between parents may promote symptoms of CD in their offspring, which commonly extend beyond the home. Incorporating effective and non-aggressive means to solve interparental conflict into parental management programs may reduce the development of symptoms of CDs in children.

Social skills and symptoms of anxiety disorders from preschool to adolescence: a prospective cohort study.

BACKGROUND: Prior research, mostly cross-sectional or prospective studies with short follow-up periods, has indicated that childhood anxiety is associated with difficulties with social interaction. However, the etiological role of social skills in the development of anxiety in childhood remains unknown. Moreover, it is not known whether childhood anxiety impedes the development of age-appropriate social skills. METHODS: The relation between anxiety and social skills was, therefore, examined in two birth cohorts of children who were assessed biennially from the ages of 4 to 14 years (n = 1,043). Semistructured psychiatric diagnostic interviews of children (from age 8) and parents were used to measure symptoms of separation, generalized, and social anxiety disorders as well as specific phobias. Social skills were measured through the parent-reported Social Skills Rating System. A random intercept cross-lagged panel model was used to analyze the data, adjusting for observed time-variant covariates (emotion regulation, secure attachment, bullying victimization, and global self-esteem) and all unobserved time-invariant confounding effects. RESULTS: Reduced social skills predicted increased symptoms of anxiety at ages 8, 10, and 12 (ß = -.26, ß = -.17, and ß = -.15, respectively), whereas an increased number of anxiety symptoms did not forecast changes in social skills. CONCLUSIONS: The findings suggest that reduced social skills may be involved in the development of anxiety symptoms in middle childhood and should, therefore, be considered in efforts to prevent and treat childhood anxiety.

Parental personality disorder symptoms and children's social skills: a prospective community study.

Acquiring age-appropriate social skills, arguably a major prerequisite for favorable psychosocial development in children, is targeted in a range of interventions. Hence, identifying factors that limit this acquisition may inform preventative and treatment efforts. Personality disorders are characterized by pervasive and enduring dysfunctional interpersonal functioning, including parenting, and could thus entail risk for offspring in not developing adaptive interpersonal skills. However, no study has tested this possibility. A representative sample drawn from two birth cohorts of Norwegian 4-year-olds (n = 956) and their parents was followed up at ages 6, 8, and 10 years. Parents' personality disorder symptoms were measured dimensionally with the DSM-IV and ICD-10 Personality Questionnaire, and children's social skills were evaluated by the Social Skills Rating System. A difference-in-difference approach was applied to adjust for all unmeasured time-invariant confounders, and parental symptoms of depression and anxiety were entered as covariates. Increased Cluster B symptoms in parents of children aged 4 to 6 years predicted decreased social skill development in offspring (B = -0.97, 95% CI -1.58, -0.37, p = 0.002). On a more granular level, increased symptoms of borderline (B = -0.39, CI -0.65, -0.12, p = 0.004), histrionic (B = -0.55, CI -0.99, -0.11, p = 0.018), and avoidant (B = -0.46, CI-0.79, -0.13, p = 0.006) personality disorders in parents predicted decreased social skill development in offspring. Subclinical levels of borderline, histrionic and avoidant personality disorders in parents may impair the development of social skills in offspring. Successfully treating these personality problems or considering them when providing services to children may facilitate children's acquisition of social skills.

The prospective relation between eating behaviors and BMI from middle childhood to adolescence: A 5-wave community study.

Some eating behaviors are associated with increased risk of childhood obesity and are thus potential targets for obesity prevention. However, longitudinal research, especially on older children and adolescents, is needed to substantiate such a claim. Using data from a representative birth cohort of Norwegian children followed up biennially from age 6 to age 14 (analysis sample: n = 802), we tested if change in eating behaviors predicts increased body mass index (BMI) throughout childhood and adolescence, or if it is the other way around; higher BMI predicting more obesogenic eating. Eating behaviors were measured using the Children's Eating Behaviour Questionnaire (CEBQ) and BMI was measured objectively using digital scales. To separate within-person- and between-person effects and control for all time-invariant confounders (i.e., variables that do not change over the study period), we applied an autoregressive latent trajectory model with structured residuals (ALT-SR). Results showed that increases in obesogenic eating behaviors did not predict higher BMI at any age. It was the other way around: Increased BMI predicted increases in food responsiveness and emotional overeating at all time points, and enjoyment of food from 8 to 10 years and from 10 to 12 years. Furthermore, increased BMI predicted decreases in satiety responsiveness at all time points except from age 12 to age 14, as well as diminished emotional undereating from 12 to 14 years. One implication of our findings, if replicated, is that targeting obesogenic eating behaviors to change weight outcomes may be less effective in children older than age 6.

Relations between physical activity, sedentary time, and body fat from childhood to adolescence: Do they differ by sex?

BACKGROUND: Efforts to reveal the direction of influence between physical activity (PA), sedentary time (ST) and body fat in youth have produced inconsistent results, possibly due to a lack of adjustment for confounders and other factors. Sex-specific associations have rarely been studied. METHODS: A sample from two Norwegian birth cohorts (n = 809) were followed biennially over five waves from the age of 6-14 years. Physical activity and ST were recorded by accelerometers, and body fat was assessed by bioelectrical impedance measurements. RESULTS: By applying a dynamic panel model (DPM) that adjusts for all time-invariant confounding factors, it was found that among boys, increased fat mass index (FMI) at ages 8, 10 and 12 years predicted decreased PA two years later (8-10 years: B = -0.67, (95% CI: -1.1, -0.24); 10-12 years: B = -0.33, (95% CI: -0.61, -0.05); 12-14 years: B = -0.29, (95% CI: -0.52, -0.06)). Regarding the opposite direction of influence, more PA at age 12 forecasted reduced FMI at age 14 (B = -0.16, (95% CI: -0.24, -0.07)), whereas increased FMI predicted increased ST across all time points in boys only (6-8 years: B = 0.23, (95% CI:0.02.43); 8-10 years: B = 0.23, (95% CI:.08.39); 10-12 years: B = 0.13, (95% CI:.03.23); 12-14 years: B = 0.17, (95% CI:.07, 26)). The revealed relationships were significantly stronger in boys compared to the (absent) relations in girls. Sensitivity analyses examining moderate to vigorous PA (MVPA) rather than total PA were in accordance with the main findings. CONCLUSIONS: In boys, increased FMI predicted reduced PA and increased ST two years later from childhood to adolescence. The opposite direction of influence was evident from only ages 12-14. There were no prospective relationships between FMI and PA or ST among girls.

Longitudinal relations between impaired executive function and symptoms of psychiatric disorders in childhood.

BACKGROUND: Malfunctioning of executive functions correlates with psychopathology in children. However, the directionality, the extent to which the relation varies for various disorders, and whether prospective relations afford causal interpretations are not known. METHODS: A community sample of Norwegian children (n = 874) was studied biennially from the age of 6 to 14 years. Executive functions were assessed using the Behavior Rating Inventory of Executive Function Teacher-report and symptoms of psychopathology were assessed using the Preschool Age Psychiatric Assessment (age 6; parents) and Child and Adolescent Psychiatric Assessment (ages 8-14; children and parents). Prospective reciprocal relations were examined using a random intercept cross-lagged panel model that adjusts for all unobserved time-invariant confounders. RESULTS: Even when time-invariant confounders were accounted for, reduced executive functions predicted increased symptoms of depressive disorders, anxiety disorders, attention-deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) 2 years later, even when previous changes in these symptoms were adjusted for. The level of prediction (B = .83, 95% CI [.37, 1.3]) was not different for different disorders or ages. Conversely, reduced executive functions were predicted by increased symptoms of all disorders (B = .01, 95% CI [.01, .02]). CONCLUSIONS: Reduced executive functioning may be involved in the etiology of depression, anxiety, ADHD, and ODD/CD to an equal extent. Moreover, increased depression, anxiety, ADHD, and ODD/CD may negatively impact executive functioning.

Prevalence and course of anxiety disorders and symptoms from preschool to adolescence: a 6-wave community study.

BACKGROUND: The rate of various anxiety disorders in early childhood and whether they continue into middle childhood or adolescence is not known. We therefore report on the prevalence and stability of DSM-5-defined anxiety disorders and their symptoms, capturing the period from preschool to adolescence. METHODS: By means of interviewer-based clinical interviews, anxiety was measured in a sample of Norwegian children at six measurement points from age 4 to 14 (n = 1,041). To adjust for time-invariant factors, we applied random intercept cross-lagged panel models (RI-CLPMs) capturing within-person changes. RESULTS: Nearly 10% (95% CI = 7.29, 12.63) had an anxiety disorder at some timepoint. Specific phobia was the most prevalent disorder in early and middle childhood, whereas generalized anxiety disorder (GAD) increased in prevalence and became the most common anxiety disorder at age 14 (4.51%, 95% CI = 2.78, 6.23). When time-invariant confounding was adjusted for, homotypic continuity in anxiety symptoms typically first emerged in late middle childhood or adolescence. Even so, such within-person analyses revealed a heterotypic path from increased number of early childhood symptoms of specific phobia to increased number of GAD symptoms in middle childhood (B = .41, 95% CI = .06, .75). Increased separation anxiety in middle childhood predicted increased symptoms of GAD in adolescence (B = .38, 95% CI = .14, .62), and vice versa (B = .05, 95% CI = .00, .09). Only minor gender differences were revealed. CONCLUSIONS: Anxiety disorders are prevalent in childhood. In early childhood, anxiety symptoms generally do not predict later anxiety symptoms. In middle childhood, however, such symptoms are less likely to vanish, indicating this developmental period to be particularly important for preventive and treatment efforts.

Predictors of diagnostically defined insomnia in child and adolescent community samples: a literature review.

Diagnostically defined insomnia is prevalent, persistent, and associated with a range of negative outcomes in childhood and adolescence. To inform prevention and treatment, we need to identify relevant predictors that can be addressed in such intervention efforts. Therefore, a systematic search for longitudinal studies involving child and adolescent samples (ages 4 to 19) examining predictors of diagnostically defined insomnia adjusted for previous insomnia was conducted. The search identified 6419 studies, resulting in six included papers involving five samples (n = 9949) conducted in five different countries (the US, New Zealand, Norway, China, and Japan). Few longitudinal studies investigated the predictors of diagnostically defined insomnia in children and adolescents, and insomnia is rarely defined according to diagnostic manuals. The results suggested that poor mental health (most notably depression) and female sex may be involved in the etiology of diagnostically defined insomnia. Stress might be the most modifiable factor identified. However, the diversity of the predictors studied in previous reports combined with the lack of replication prevent any firm conclusions from being drawn. This review serves as a summary of the best available evidence.

Child and family predictors of insomnia from early childhood to adolescence.

BACKGROUND: Insomnia is prevalent among children and adolescents and is associated with a wide range of negative outcomes. Knowledge about its determinants is therefore important, but due to the lack of longitudinal studies, such knowledge is limited. The aim of the present inquiry is to identify child and family predictors of future pediatric insomnia within a psycho-bio-behavioral framework. METHODS: A representative community sample (n = 1,037) was followed biennially from 4 to 14 years of age (2007-2017). Insomnia was defined based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria and was diagnosed by a semistructured clinical interview of children (from age eight years of age) and parents (all ages). Predictors included parent ratings of child emotional reactivity, family functioning, and marital conflict; self-reports of personality; and teacher-rated emotion regulation skills. RESULTS: Random intercept cross-lagged analyses revealed that within-person increases (ie, relative to the child's typical levels across childhood) in emotional reactivity and decreases in emotion regulation skills predicted insomnia diagnosis two years later from ages 4 to 14 after adjusting for previous insomnia and all unmeasured time-invariant factors. Previous insomnia was the strongest predictor of later insomnia, whereas family functioning and marital conflict did not predict insomnia. CONCLUSIONS: Increases in emotional reactivity and decreases in emotion regulation skills predicted insomnia above and beyond all unmeasured time-invariant factors and could be targets for interventions. Previous insomnia predicted later insomnia, thereby underscoring the importance of detecting, preventing, and treating insomnia at an early age.

Rhinosinusitis without nasal polyps is associated with poorer health-related quality of life in COPD.

Rhinosinusitis without nasal polyps (RSsNP) is prevalent in COPD. Previous studies on its association with health-related quality of life (HRQoL) have limitations, and RSsNP is currently not recognized as a comorbidity. This study investigates HRQoL in COPD including a focus on RSsNP. Generic HRQoL was assessed with the Short Form-36 (SF-36v2) questionnaire and compared between 90 COPD and 93 control subjects and in subgroups with and without RSsNP. The association between RSsNP and COPD versus not and generic HRQoL was assessed by multivariable linear regression with adjustments for age, education, and body mass index (BMI). Disease-specific HRQoL was assessed by Sinonasal outcome test-22 (SNOT-22), St. Georges Respiratory Questionnaire (SGRQ), and COPD Assessment Test (CAT) and compared between COPD with and without RSsNP, and their association to RSsNP was assessed by multivariable linear regression with adjustments for age, BMI, and FEV1% predicted. RSsNP was associated with poorer disease-specific HRQoL, with higher SNOT-22 total score (14.67 points; 95% CI, 7.06-22.28; P < .001) and psychological subscale score (3.24 points; 95% CI, 0.37-6.11; P = .03), SGRQ symptom score (13.08 points; 95% CI, 2.73-23.4; P = .014), and CAT score (4.41 points; 95% CI, 1.15-7.66; P = .009). Generic HRQoL was poorer in COPD patients than in the control subjects. In addition to COPD, concomitant RSsNP was associated with poorer physical functioning, general health, vitality, and physical component summary. RSsNP in COPD is associated with poorer disease-specific HRQoL that is clinically relevant and, as it is amenable for treatment, should be recognized as a comorbidity of COPD.

Shared genetic architecture underlying sleep and weight in children.

Meta-analyses suggest shorter sleep as a risk factor for obesity in children. The prevailing hypothesis is that shorter sleep causes obesity by impacting homeostatic processes. Sleep duration and adiposity are both heritable, and the association may reflect shared genetic aetiology. We examined the association between a body mass index (BMI) genetic risk score (GRS) and objectively-measured total sleep time (TST) in a cohort of Norwegian children (enrolled at age four in 2007-2008) using cross-sectional data at age six. The analytical sample included 452 six-year old children with complete genotype and phenotype data. The outcome was actigraphic total sleep time (TST) measured at age six years. Genetic risk of obesity was inferred using a 32-single nucleotide polymorphism (SNP) weighted GRS of BMI. Covariates were BMI-Standard deviation scores (SDS) (which takes into account age and sex) and, in a sensitivity analysis socioeconomic status. Analyses consisted of Pearson's correlations and linear regressions. In our sample, 54% of participants were male; mean (SD) TST, age and BMI were 9.6 (0.8) hours, 6.0 (0.2) years and 15.3 (1.2) kg/m2, respectively. BMI and TST were not correlated, r = -0.003, p = 0.946. However, the BMI GRS was associated with TST after adjusting for BMI-SDS, standardised ß = -0.11; 95% confidence interval (CI) = -0.22, -0.01. To our knowledge, this is the first study to establish a relationship between genetic risk of obesity and objective sleep duration in children. Findings suggest some shared genetic aetiology underlying these traits. Future research could identify the common biological pathways through which common genes predispose to both shorter sleep and increased risk of obesity.

Persistent Short Sleep from Childhood to Adolescence: Child, Parent and Peer Predictors.

PURPOSE: Many children have periods when they sleep too little, with widely recognized detrimental effects. Less is known about persistent short sleep during childhood. Therefore, the present study aimed to investigate the prevalence of persistent short sleep in school-aged children and identify a set of child, parent, and peer predictors thereof. PARTICIPANTS AND METHODS: Objectively measured sleep duration (hip-held accelerometer) was biennially assessed in a community sample followed from 6 to 14 years (n=801). A latent profile analysis was applied to assess whether a subgroup of children slept consistently short across time and predictors of persistent short sleep were determined through regression analysis. RESULTS: A subgroup of children (n=160; 20.2%) was identified as having persistent short sleep across time. Temperamental negative affectivity (ß=0.08; 95% CI=0.01, 0.15; p=0.03) and low observer-assessed parental emotional availability (ß=-.09; 95% CI=-.18, -.01; p=0.04) predicted membership to that group. Teacher ratings of victimization from bullying were not associated with persistent short sleep (ß=0.01; 95% CI: -.10, 11; p=0.88). CONCLUSION: High child temperamental negative affectivity and low parental emotional availability may be involved in the development of persistent short sleep through childhood.

The association between childhood adiposity and appetite assessed using the Child Eating Behavior Questionnaire and Baby Eating Behavior Questionnaire: A systematic review and meta-analysis.

This systematic review and meta-analysis aimed to quantify associations between Child Eating Behavior Questionnaire (CEBQ) and Baby Eating Behavior Questionnaire (BEBQ) appetitive traits (food approach: Food Responsiveness [FR], Enjoyment of Food [EF], Emotional Overeating [EOE], and Desire to Drink [DD]; food avoidant: Satiety Responsiveness [SR], Slowness in Eating [SE], Emotional Undereating [EUE], Food Fussiness [FF]) and measures of child adiposity. Searches of six databases up to February 2019 identified 72 studies (CEBQ, n = 67; BEBQ, n = 5), and 27 met the meta-analysis criteria. For cross-sectional studies reporting unadjusted correlations with body mass index z-scores (BMIz) (n = 19), all traits were associated with BMIz in expected directions (positive: FR, EF, EOE, and DD; negative: SR, SE, EUE, and FF). Pooled estimates ranged from r = 0.22 (FR) to r = -0.21 (SR). For cross-sectional studies reporting regression coefficients (n = 10), three traits (FR, EF, and EOE) associated positively, and three traits (SR, SE, and EUE) negatively, with BMIz (ß = -0.31 [SR] to ß = 0.22 [FR]). Eleven studies reported prospective relationships from appetite to adiposity measures for six scales (positive: FR, EF, EOE, and DD; negative: SR and SE). Five studies reported relationships from adiposity measures to appetite for five traits (positive: FR, EF, and EOE; negative: SR). All BEBQ traits were consistently cross-sectionally associated with adiposity measures. Overall, CEBQ/BEBQ-assessed appetitive traits show consistent cross-sectional relationships with measures of child adiposity.

The co-occurrence between symptoms of internet gaming disorder and psychiatric disorders in childhood and adolescence: prospective relations or common causes?

BACKGROUND: Internet gaming disorder (IGD) is highlighted as a condition for further study in the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5). Some studies indicate that IGD appears comorbid with other psychiatric disorders. We examine concurrent and prospective links between symptoms of IGD and symptoms of common psychiatric disorders in childhood and adolescence to determine whether observed comorbidity is a result of (a) reciprocal relations or (b) common underlying causes. METHODS: A community sample (n = 702) of Norwegian children completed the Internet Gaming Disorder Interview (IGDI) to assess DSM-5 defined IGD symptoms at ages 10, 12 and 14 years. The Child and Adolescent Psychiatric Assessment (CAPA) assessed symptoms of depression, anxiety, attention-deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and conduct disorder (CD) at the same time points. RESULTS: A Random Intercept Cross-lagged Panel Model (RI-CLPM), which captures pure within-person changes and adjusts for all unmeasured time-invariant factors (e.g., genetics, parent education) revealed no associations between IGD symptoms and psychopathology, except that increased IGD symptoms at ages 10 and 12 predicted decreased symptoms of anxiety two years later. CONCLUSIONS: No support emerged for concurrent or prospective relations between IGD and psychiatric symptoms, except in one case: increased IGD symptoms forecasted reduction in anxiety symptoms. Observed co-occurrence between IGD symptoms and mental health problems can mainly be attributed to common underlying factors.

Prevalence and stability of insomnia from preschool to early adolescence: a prospective cohort study in Norway.

BACKGROUND: There is limited knowledge about the prevalence and stability of insomnia defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM). We therefore provide such estimates from preschool to early adolescence and explore potential sex differences. METHODS: We followed a representative community sample (n=1037) biennially from 4 to 14 years of age (2007-2017). Insomnia diagnoses and symptoms were captured by a semistructured clinical interview of parents and children (from age 8 years). RESULTS: At ages 4 and 6 years approximately 2.5% of children met the criteria for insomnia, whereas at ages 8, 10, 12 and 14 years the prevalence ranged from 7.5% to 12.3%. During the 10-year period examined nearly 1 in 5 children had insomnia at least once (18.7%). Sex differences were apparent with DSM-IV, but not DSM-5, criteria: boys (8.1%) had more insomnia than girls (4.5%) did at ages 4-10 years, whereas girls (11.4%) had more insomnia than boys (7.1%) did at ages 12 and 14 years. Insomnia proved stable, with 22.9%-40.1% of children retaining their diagnosis 2 years later. Having current insomnia produced medium to large ORs of between 5.1 (95% CI 2.6 to 9.8) and 15.3 (95% CI 4.4 to 52.9) for subsequent insomnia 2 years later compared with not having preceding insomnia. CONCLUSIONS: Insomnia was less prevalent than previous research indicates, with nearly 1 in 5 participants having insomnia at least once between the ages of 4 and 14 years. Female preponderance emerged in early adolescence. Having insomnia at one time point was a considerable risk for subsequent insomnia, indicating that insomnia is persistent and warrants clinical attention.