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.

Summary 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 (β = −0.31 [SR] to β = 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.

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Background: 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. Methods: 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. Results: 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). Conclusions: 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.

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.MethodParticipants 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.ResultsFood 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.ConclusionsFood 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.

BackgroundPicky eating is prevalent in childhood. Because pickiness concerns parents and is associated with nutrient deficiency and psychological problems, the antecedents of pickiness need to be identified. We propose an etiological model of picky eating involving child temperament, sensory sensitivity and parent-child interaction.MethodsTwo cohorts of 4-year olds (born 2003 or 2004) in Trondheim, Norway were invited to participate (97.2% attendance; 82.0% consent rate, n = 2475) and a screen-stratified subsample of 1250 children was recruited. We interviewed 997 parents about their child’s pickiness and sensory sensitivity using the Preschool Age Psychiatric Assessment (PAPA). Two years later, 795 of the parents completed the interview. The Children’s Behavior Questionnaire (CBQ) was used to assess children’s temperament. Parent- child interactions were videotaped and parental sensitivity (i.e., parental awareness and appropriate responsiveness to children’s verbal and nonverbal cues) and structuring were rated using the Emotional Availability Scales (EAS).ResultsAt both measurement times, 26% of the children were categorized as picky eaters. Pickiness was moderately stable from preschool to school age (OR = 5.92, CI = 3.95, 8.86), and about half of those who displayed pickiness at age 4 were also picky eaters two years later. While accounting for pickiness at age 4, sensory sensitivity at age 4 predicted pickiness at age 6 (OR = 1.25, CI = 1.08, 2.23), whereas temperamental surgency (OR = 0.88, CI = 0.64, 1.22) and negative affectivity (OR = 1.17, CI = 0.75, 1.84) did not. Parental structuring was found to reduce the risk of children’s picky eating two years later (OR = 0.90, CI = 0.82, 0.99), whereas parental sensitivity increased the odds for pickiness (OR = 1.10, CI = 1.00, 1.21).ConclusionsAlthough pickiness is stable from preschool to school age, children who are more sensory sensitive are at higher risk for pickiness two years later, as are children whose parents display relatively higher levels of sensitivity and lower levels of structuring. Our findings suggest that interventions targeting children’s sensory sensitivity, as well as parental sensitivity and structuring, might reduce the risk of childhood pickiness. Health care providers should support parents of picky eaters in repeatedly offering unfamiliar and rejected foods to their children without pressure and acknowledging child autonomy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12966-017-0542-7) contains supplementary material, which is available to authorized users.

IntroductionAppetitive traits, including Food Responsiveness, Enjoyment of Food, Satiety Responsiveness, Emotional Over- and Under-Eating, Food Fussiness and Slowness in Eating, have been captured across childhood using the Children’s Eating Behavior Questionnaire (CEBQ). The Adult Eating Behavior Questionnaire (AEBQ) has explored these traits in adults, but not adolescents. This study aimed to test the factor structure and reliability of the AEBQ in a sample of UK adolescents, and explore demographic differences.Materials and MethodsConfirmatory factor analysis (CFA) tested an 8-factor and a 7-factor AEBQ, based on valid, completed AEBQ responses (n = 913) from adolescents aged 11–18 recruited from four London secondary schools. Test–retest reliability was analyzed in a subsample (n = 106) 2-weeks later, and 492 participants completed the Dutch Eating Behavior Questionnaire (DEBQ) to assess convergent validity. Demographic differences were explored using a multiple indicator multiple cause (MIMIC) model.ResultsThe CFA revealed an adequate model fit for a 7-factor structure without Hunger [RMSEA = 0.038 (90% CI:0.035,0.041); CFI = 0.926, TLI = 0.916; and χ2(df = 595) = 8502.69, p < 0.001]. These seven subscales showed acceptable internal consistency (Cronbach’s α > 0.70). The ICC for the test–retest was above 0.70. Comparisons with the DEBQ supported the convergent validity of the AEBQ. Older age was associated with greater Food Responsiveness and Enjoyment of Food (all p-values < 0.005). Females reported higher levels of Emotional Over-Eating, Satiety Responsiveness, and Slowness in Eating than males (all p-values ≤ 0.003).ConclusionThis study supports the use of the 7-factor AEBQ as a reliable measure of appetitive traits in adolescents.

Emotional overeating (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be protective. Interestingly, EOE and EUE tend to correlate positively, but it is unclear whether they reflect different aspects of the same underlying trait, or are distinct behaviours with different aetiologies. Data were from 2054 five-year-old children from the Gemini twin birth cohort, including parental ratings of child EOE and EUE using the Child Eating Behaviour Questionnaire. Genetic and environmental influences on variation and covariation in EUE and EOE were established using a bivariate Twin Model. Variation in both behaviours was largely explained by aspects of the environment completely shared by twin pairs (EOE: C = 90%, 95% CI: 89%-92%; EUE: C = 91%, 95% CI: 90%-92%). Genetic influence was low (EOE: A = 7%, 95% CI: 6%-9%; EUE: A = 7%, 95% CI: 6%-9%). EOE and EUE correlated positively (r = 0.43, p < 0.001), and this association was explained by common shared environmental influences (BivC = 45%, 95% CI: 40%-50%). Many of the shared environmental influences underlying EUE and EOE were the same (rC = 0.50, 95% CI: 0.44, 0.55). Childhood EOE and EUE are etiologically distinct. The tendency to eat more or less in response to emotion is learned rather than inherited.