The impact of anorexia nervosa and BMI polygenic risk on childhood growth: A 20-year longitudinal population-based study.

Growth deviating from the norm during childhood has been associated with anorexia nervosa (AN) and obesity later in life. In this study, we examined whether polygenic scores (PGSs) for AN and BMI are associated with growth trajectories spanning the first two decades of life. AN PGSs and BMI PGSs were calculated for participants of the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 8,654). Using generalized (mixed) linear models, we associated PGSs with trajectories of weight, height, body mass index (BMI), fat mass index (FMI), lean mass index (LMI), and bone mineral density (BMD). Female participants with AN PGSs one standard deviation (SD) higher had, on average, 0.004% slower growth in BMI between the ages 6.5 and 24 years and a 0.4% slower gain in BMD between the ages 10 and 24 years. Higher BMI PGSs were associated with faster growth for BMI, FMI, LMI, BMD, and weight trajectories in both sexes throughout childhood. Female participants with both a high AN PGS and a low BMI PGS showed slower growth compared to those with both a low AN PGS and a low BMI PGS. We conclude that AN PGSs and BMI PGSs have detectable sex-specific effects on growth trajectories. Female participants with a high AN PGS and low BMI PGS likely constitute a high-risk group for AN, as their growth was slower compared to their peers with high PGSs on both traits. Further research is needed to better understand how the AN PGS and the BMI PGS co-influence growth during childhood and whether a high BMI PGS can mitigate the effects of a high AN PGS.

Associations between parent and child latent eating profiles and the role of parental feeding practices.

Previous research employing the person-centred approach of Latent Profile Analysis (LPA) with parent-reported data of their child's eating behaviour identified four distinct eating profiles in 3-6-year-old children: typical, avid, happy, and avoidant eating (Pickard et al., 2023). In this follow-up study, the same parents were asked to self-report their own eating behaviour (N = 785) and LPA was conducted to determine the latent eating profiles of the parents/caregivers. The LPA showed that a four-profile solution best represented the sample of parents, termed: typical eating (n = 325, 41.4%), avid eating (n = 293, 37.3%), emotional eating (n = 123, 15.7%) and avoidant eating (n = 44, 5.6%). Multiple mediation analysis was then conducted to examine both the direct associations between parents' eating profiles and the child's probability of eating profile membership, as well as the indirect associations through the mediatory role of specific parental feeding practices. The results suggested direct links between parent and child eating profiles, with the 'avid eating' and 'avoidant eating' profiles in parents predicting similar profiles in their children. Feeding practices, such as using food for emotional regulation, providing balanced and varied food, and promoting a healthy home food environment, mediated associations between parent and child eating profiles. This research provides novel evidence to reinforce the need for interventions to be specifically tailored to both the parent's and child's eating profiles. The work also provides an interesting avenue for future longitudinal examination of whether the parents' provision of a healthy home food environment could protect against intergenerational transmission of less favourable eating behaviours.

Examining parents' experiences and challenges of feeding preschool children with avid eating behaviour.

Avid eating behaviours, including greater responsiveness to food cues and emotional over-eating, have been linked to child overweight and obesity. Parental feeding practices are modifiable components of a child's food environment and may be key levers for behaviour change in tailored interventions to support parents of children with avid eating behaviour. However, there is a lack of research examining parents' experiences in this context. This study aimed to explore parents' experiences of feeding children with avid eating behaviour and to understand any challenges experienced in this context. Semi-structured interviews with parents (N = 15) of a preschool child (3-5 years) identified as having an avid eating behaviour profile explored how children's avid eating manifests, the parental feeding practices used to manage avid eating, and the perceived effectiveness of these strategies. Data were analysed using reflexive thematic analysis. Four core themes were generated. Theme one, 'Have they got worms? Children's insatiable hunger', captures parents' interpretation of the complex ways in which avid eating behaviour manifests. Theme two, 'Parenthood as a duty', illustrates how parents' perceived responsibilities shape their feeding practices. Theme three, 'Lifelong habits', captures parents' use of responsive feeding practices to support children's healthy relationship with food. Theme four, 'Picking battles', captures the structure- and coercive-based feeding strategies commonly used to manage children's avid eating. This novel study provides an in-depth understanding of the complex ways that children's avid eating behaviour manifests, and the strategic and creative parental feeding practices used to manage these behaviours. Such findings are valuable for informing the development of future support resources for parents/caregivers to help their children with avid eating behaviours to develop a healthy relationship with food.

The network structure of mania symptoms differs between people with and without binge eating.

OBJECTIVES: People with bipolar disorder who also report binge eating have increased psychopathology and greater impairment than those without binge eating. Whether this co-occurrence is related to binge eating as a symptom or presents differently across full-syndrome eating disorders with binge eating is unclear. METHODS: We first compared networks of 13 lifetime mania symptoms in 34,226 participants from the United Kingdom's National Institute for Health and Care Research BioResource with (n = 12,104) and without (n = 22,122) lifetime binge eating. Second, in the subsample with binge eating, we compared networks of mania symptoms in participants with lifetime anorexia nervosa binge-eating/purging (n = 825), bulimia nervosa (n = 3737), and binge-eating disorder (n = 3648). RESULTS: People with binge eating endorsed every mania symptom significantly more often than those without binge eating. Within the subsample, people with bulimia nervosa most often had the highest endorsement rate of each mania symptom. We found significant differences in network parameter statistics, including network structure (M = 0.25, p = 0.001) and global strength (S = 1.84, p = 0.002) when comparing the binge eating with no binge-eating participants. However, network structure differences were sensitive to reductions in sample size and the greater density of the latter network was explained by the large proportion of participants (34%) without mania symptoms. The structure of the anorexia nervosa binge-eating/purging network differed from the bulimia nervosa network (M = 0.66, p = 0.001), but the result was unstable. CONCLUSIONS: Our results suggest that the presence and structure of mania symptoms may be more associated with binge eating as a symptom rather than any specific binge-type eating disorder. Further research with larger sample sizes is required to confirm our findings.

Reciprocal associations between parental feeding practices and child eating behaviours from toddlerhood to early childhood: bivariate latent change analysis in the Gemini cohort.

BACKGROUND: Parental feeding practices (PFPs) are a key component of a child's food environment. Parent-child feeding relationships are hypothesised to be bidirectional; however, to date, few large prospective studies have examined this, instead focussing on unidirectional relationships. As such, the direction of relationships between PFPs and children's eating behaviours remains unclear. METHODS: Data were from Gemini, a population-based sample of children born in England and Wales in 2007. Children's eating behaviours and PFPs were measured at 15/16 months and 5 years using validated psychometric measures (n = 1,858 children). Bivariate Latent Change Score Modelling was used to examine the nature of relationships between PFPs and children's eating behaviours at 15/16 months and 5 years. Models were adjusted to account for clustering of twins within families and for sex of the child, socioeconomic status, gestational age and age of the child at measurement time points. RESULTS: A reciprocal relationship was observed between instrumental feeding and emotional overeating, with greater instrumental feeding predicting greater increases in emotional overeating (ß = .09; 0.03-0.15; p = .004) and vice versa (ß = .09; 0.03-0.15; p = .005). Reciprocity was also observed between encouragement to eat nutritious foods and children's enjoyment of food, with greater encouragement predicting greater increases in enjoyment of food (ß = .08; 0.02-0.13; p = .006) and vice versa (ß = .07; 0.02-0.11; p = .003). Parent-child associations and child-parent associations were also observed. CONCLUSION: These findings are consistent with the hypothesis that certain feeding practices are used as a 'natural' response to a child expressing a greater interest in and enthusiasm for food, but at the same time, such practices impact the development of eating behaviours by nurturing and encouraging the expression of higher emotional overeating and greater enjoyment of food in preschool years. The findings provide important insights into the PFPs and eating behaviour traits that could be targeted as part of a tailored feeding intervention to support parents of children during the preschool formative years.

Parental feeding practices as a response to child appetitive traits in toddlerhood and early childhood: a discordant twin analysis of the Gemini cohort.

BACKGROUND: Parental feeding practices (PFPs) have been implicated in the development of children's eating behaviours. However, evidence suggests that feeding practices may also develop in response to their child's weight or emerging appetitive traits. We used the twin design to test the hypothesis that parents develop their feeding practices partly in response to their child's appetite. METHODS: Data were from Gemini, a population-based cohort of 2402 British families with twins born in 2007. Psychometric measures of PFPs and appetite were completed by parents when their twins were 16-months and 5-years. Within-family analyses including all twins with available data in the sample (n = 1010-1858 pairs), examined if within-pair differences in PFPs were associated with differences in appetitive traits, controlling for differences in birth weight-SDS, early feeding method and child sex. In a subsample of twin pairs who were considerably discordant for appetitive traits by ≥ 1SD (n = 122-544 pairs), the direction and magnitude of within-pair differences in feeding practices was explored. RESULTS: Within-family variation in parental feeding practices in toddlerhood and early childhood was low (discordance ranged from 0.1 to 6% of the sample), except for pressure to eat (toddlerhood: 19%; early childhood: 32%). Within-pair differences in all appetitive traits were associated with differential use of 'pressure to eat' at both 16-months and 5-years. In the subsample of twins most discordant for appetitive traits, parents used more pressure with the twin expressing lower food responsiveness, lower emotional overeating, lower food enjoyment, higher satiety responsiveness, slower speed of eating, higher emotional undereating and greater fussiness in toddlerhood and early childhood (p-values < 0.001). Effect sizes were small to large at 16-months (η2=0.02-0.09) and 5-years (η2=0.05-0.21). CONCLUSION: Parents rarely varied their feeding practices between twins in toddlerhood and early childhood, except for pressure. Parents exerted greater pressure on their twin who expressed a poorer appetite compared to their co-twin, suggesting that parents develop a pressuring feeding style when their child expresses a poorer appetite or lower interest in, and enthusiasm for, eating. These findings could be used to guide interventions seeking to support parents in feeding their children in a way that nurtures the development of healthy eating behaviours.

Gone too soon: Studying mortality in eating disorders.

Eating disorders (anorexia nervosa, bulimia nervosa, binge eating disorder, and other specified feeding and eating disorder) are not only common mental health disorders but they also affect an individual's physical, psychological, and social well-being, with high impact and burden. Importantly, previous research has found that eating disorders have high mortality, higher than many other psychiatric disorders. Here, we discuss findings from Castellini and colleagues in the context of previous studies.

Could interventions on physical activity mitigate genomic liability for obesity? Applying the health disparity framework in genetically informed studies.

Polygenic scores (PGS) are now commonly available in longitudinal cohort studies, leading to their integration into epidemiological research. In this work, our aim is to explore how polygenic scores can be used as exposures in causal inference-based methods, specifically mediation analyses. We propose to estimate the extent to which the association of a polygenic score indexing genetic liability to an outcome could be mitigated by a potential intervention on a mediator. To do this this, we use the interventional disparity measure approach, which allows us to compare the adjusted total effect of an exposure on an outcome, with the association that would remain had we intervened on a potentially modifiable mediator. As an example, we analyse data from two UK cohorts, the Millennium Cohort Study (MCS, N = 2575) and the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 3347). In both, the exposure is genetic liability for obesity (indicated by a PGS for BMI), the outcome is late childhood/early adolescent BMI, and the mediator and potential intervention target is physical activity, measured between exposure and outcome. Our results suggest that a potential intervention on child physical activity can mitigate some of the genetic liability for childhood obesity. We propose that including PGSs in a health disparity measure approach, and causal inference-based methods more broadly, is a valuable addition to the study of gene-environment interplay in complex health outcomes.

Risk and protective factors for new-onset binge eating, low weight, and self-harm symptoms in >35,000 individuals in the UK during the COVID-19 pandemic.

OBJECTIVE: The disruption caused by the COVID-19 pandemic has been associated with poor mental health, including increases in eating disorders and self-harm symptoms. We investigated risk and protective factors for the new onset of these symptoms during the pandemic. METHOD: Data were from the COVID-19 Psychiatry and Neurological Genetics study and the Repeated Assessment of Mental health in Pandemics Study (n = 36,715). Exposures were socio-demographic characteristics, lifetime psychiatric disorder, and COVID-related variables, including SARS-CoV-2 infection/illness with COVID-19. We identified four subsamples of participants without pre-pandemic experience of our outcomes: binge eating (n = 24,211), low weight (n = 24,364), suicidal and/or self-harm ideation (n = 18,040), and self-harm (n = 29,948). Participants reported on our outcomes at frequent intervals (fortnightly to monthly). We fitted multiple logistic regression models to identify factors associated with the new onset of our outcomes. RESULTS: Within each subsample, new onset was reported by: 21% for binge eating, 10.8% for low weight, 23.5% for suicidal and/or self-harm ideation, and 3.5% for self-harm. Shared risk factors included having a lifetime psychiatric disorder, not being in paid employment, higher pandemic worry scores, and being racially minoritized. Conversely, infection with SARS-CoV-2/illness with COVID-19 was linked to lower odds of binge eating, low weight, and suicidal and/or self-harm ideation. DISCUSSION: Overall, we detected shared risk factors that may drive the comorbidity between eating disorders and self-harm. Subgroups of individuals with these risk factors may require more frequent monitoring during future pandemics. PUBLIC SIGNIFICANCE: In a sample of 35,000 UK residents, people who had a psychiatric disorder, identified as being part of a racially minoritized group, were not in paid employment, or were more worried about the pandemic were more likely to experience binge eating, low weight, suicidal and/or self-harm ideation, and self-harm for the first time during the pandemic. People with these risk factors may need particular attention during future pandemics to enable early identification of new psychiatric symptoms.

Prospective associations between parental feeding practices used in toddlerhood and preschool children's appetite vary according to appetite avidity in toddlerhood.

Parental feeding practices are a key modifiable component of children's food environments. Evidence suggests that certain feeding practices may differentially influence children's eating behaviour or weight, depending on the child's temperament (e.g. emotionality). Building on this work, we tested the hypothesis that feeding practices during toddlerhood influence children's developing eating behaviours differently, depending on their appetite avidity (which is characterised by a larger appetite and greater interest in food). Data were from Gemini, a population-based cohort of British twin children born in 2007. Parental feeding practices were assessed at 15/16-months, and child appetite at 15/16-months and 5-years, using validated psychometric measures (n = 1858 children). Complex samples general linear models examined prospective associations between PFPs at 15/16-months and child appetitive traits at 5-years, adjusting for clustering of twins within families and for the corresponding child appetitive trait at 15/16-months, difference in age between timepoints, child sex, gestational age, and socioeconomic status. Moderation analyses revealed that pressuring a child to eat led to greater increases in emotional overeating from 15/16-months to 5-years, only for children with high (1 SD above the mean: B = 0.13; SE± = 0.03,p < 0.001) or moderate emotional overeating (mean: B = 0.07 ± 0.03,p < 0.001) in toddlerhood. Greater covert restriction predicted greater reductions in emotional overeating and food responsiveness from 15/16-months to 5-years, only for children with high emotional overeating (1 SD above the mean: B = -0.06 ± 0.03,p = 0.03) and low food responsiveness (1 SD below the mean: B = -0.06 ± 0.03,p = 0.04) in toddlerhood. These findings are consistent with the hypothesis that children with a more avid appetite in toddlerhood are differentially affected by parental feeding practices; caregivers of toddlers may therefore benefit from feeding advice that is tailored to their child's unique appetite.

Identifying an avid eating profile in childhood: Associations with temperament, feeding practices and food insecurity.

This study aimed to identify distinct eating behaviour profiles in young children and examine how other key predictors of children's eating behaviour, including child temperament, the experience of food insecurity, or parental feeding practices, may vary by identified profiles. An online survey was conducted with 995 parents/carers living in England and Wales (N = 995, Mage = 35.4 years, 80% female, 88% White). Participants reported on their child's eating behaviour using the Child Eating Behaviour Questionnaire and completed measures of child temperament, household food security and parental feeding practices. Latent Profile Analysis (LPA) was carried out to identify distinct eating profiles amongst the children (36-72 months, Mage = 48.8 months, 52% female). Four eating profiles emerged from the sample of children: (a) avid eating, (b) avoidant eating, (c) happy eating, and (d) typical eating. Avid eating (21.9% of children) was characterised by higher levels of food responsiveness, enjoyment of food, and emotional over-eating in combination with lower satiety responsiveness, slowness in eating and food fussiness. Children with an avid eating profile were reported to be more surgent and experienced greater food insecurity than all other eating profiles. Parents of children belonging to the avid eating profile showed significantly greater use of food for emotional regulation, varied and balanced food provision, restriction of food for health, and restriction of food for weight feeding practices than the three other eating profiles.

Attachment and mentalization as predictors of outcome in family therapy for adolescent anorexia nervosa.

Anorexia nervosa-focussed family therapy (FT-AN) is the first-line treatment for adolescent anorexia nervosa (AN), but the predictors of poor treatment response are not well understood. The main aim of this study was to investigate the role of attachment and mentalization in predicting treatment outcome. The secondary aims of the study were to investigate therapeutic alliance at 1 month as a predictor of outcome, and to test the associations between alliance and baseline attachment and mentalization. 192 adolescents with AN and their parents were recruited as they began family therapy in out-patient specialist eating disorder services. Self-report measures of attachment, mentalization, and emotion regulation were completed at the start of treatment by adolescent patients and one of their parents. Self-reported alliance scores were collected at one month. Higher scores on the Certainty Scale of the Reflective Functioning Questionnaire, completed by parents, which indicate over-certainty about mental states, were the strongest predictor of poor outcome (Odds Ratio: 0.42, CI: 0.20-0.87). Similarly, for adolescents, higher Lack of Clarity scores on the Difficulties in Emotion Regulation Scale, representing being unclear about one's feelings, were predictive of positive treatment outcome (OR: 1.10, CI: 1.00-1.21). Higher alliance scores at 1 month predicted positive outcome, and were associated with attachment security and mentalization. These novel findings suggest that, particularly in parents, a tendency towards excessive certainty about mental states in others may predict poor outcome in FT-AN. Further research is warranted to replicate the finding and characterise families at risk of poor outcome.

Parental feeding and childhood genetic risk for obesity: exploring hypothetical interventions with causal inference methods.

BACKGROUND: Parental-feeding behaviors are common intervention targets for childhood obesity, but often only deliver small changes. Childhood BMI is partly driven by genetic effects, and the extent to which parental-feeding interventions can mediate child genetic liability is not known. Here we aim to examine how potential interventions on parental-feeding behaviors can mitigate some of the association between child genetic liability and BMI in early adolescence, using causal inference methods. METHODS: Data from the Avon Longitudinal Study of Parents and Children were used to estimate an interventional disparity measure for a child polygenic score for BMI (PGS-BMI) on BMI at 12 years. The approach compares counterfactual outcomes for different hypothetical interventions on parental-feeding styles applied when children are 10-11 years (n = 4248). Results are presented as adjusted total association (Adj-Ta) between genetic liability (PGS-BMI) and BMI at 12 years, versus the interventional disparity measure-direct effect (IDM-DE), which represents the association that would remain, had we intervened on parental-feeding under different scenarios. RESULTS: For children in the top quintile of genetic liability, an intervention shifting parental feeding to the levels of children with lowest genetic risk, resulted in a difference of 0.81 kg/m2 in BMI at 12 years (Adj-Ta = 3.27, 95% CI: 3.04, 3.49; versus IDM-DE = 2.46, 95% CI: 2.24, 2.67). CONCLUSIONS: Findings suggest that parental-feeding interventions have the potential to buffer some of the genetic liability for childhood obesity. Further, we highlight a novel way to analyze potential interventions for health conditions only using secondary data analyses, by combining methodology from statistical genetics and social epidemiology.

The longitudinal association of eating behaviour and ADHD symptoms in school age children: a follow-up study in the RHEA cohort.

Previous evidence suggests a link between attention deficit hyperactivity disorder (ADHD) symptoms and disordered eating behaviours; however, the direction of the causal association remains unclear. Building on our previous research, we aimed to examine the longitudinal association between eating behaviours at 4 years, ADHD symptoms at 6 years of age, and the role of body mass index (BMI). We included children from the RHEA mother-child cohort in Greece, followed up at 4 and 6 years (n = 926). Parents completed the Children's Eating Behaviour Questionnaire (CEBQ) to assess children's eating behaviour at 4 years and the ADHD Test (ADHDT) and Child Behaviour Checklist for ages 6-18 (CBCL/6-18) to evaluate ADHD symptoms at 4 and 6 years, respectively, as well as measures of BMI. Longitudinal structural equation modeling (SEM) was carried out to evaluate the associations of all variables between 4 and 6 years. Food responsiveness at 4 years was positively associated with hyperactivity at age 6, whereas emotional overeating was negatively associated with hyperactivity. There was no evidence of an association between eating behaviours of preschoolers and BMI at 6 years, or BMI at 4 years and later ADHD symptoms and vice versa. Findings suggest that food responsiveness is an early marker of ADHD symptoms at 6 years of age. In contrast to our hypothesis there was no significant association between ADHD at age 4 and BMI at age 6.

Associations between childhood autistic traits and adolescent eating disorder behaviours are partially mediated by fussy eating.

OBJECTIVE: Previous literature shows an increased risk for eating disorders in autistic individuals. This study tested whether fussy eating contributes to the association between childhood autistic traits and adolescent eating disorder behaviours. METHOD: Using data from the Avon Longitudinal Study of Parents and Children, we estimated the intercept and slope of parent-rated autistic traits and fussy eating between 7 and 14 years (N = 8982) and their association with self-reported eating disorder behaviours at age 14 years, including the indirect path from autistic traits to eating disorder behaviours via fussy eating. Analyses were adjusted for child sex, maternal age at delivery, maternal body mass index and maternal education. RESULTS: Analyses found a small indirect pathway from autistic traits intercept to eating disorder behaviours via fussy eating slope (b = 0.017, 95% CI = 0.002-0.032, p = 0.026), with higher levels of autistic traits at age 7 years being associated with a shallower decline in fussy eating, which in turn was associated with greater eating disorder behaviours. CONCLUSION: Findings point towards fussy eating as a potential link between childhood autistic traits and later disordered eating. Addressing fussy eating patterns before they become entrenched may decrease risk for eating disorders later in development.

Eating disorder symptoms and their associations with anthropometric and psychiatric polygenic scores.

BACKGROUND: Eating disorder (ED) symptoms are prevalent in the general population, but their shared genetic underpinnings with psychiatric, metabolic, and anthropometric traits are not known. Here, we examined if polygenic scores (PGSs) of traits associated with anorexia nervosa are also associated with adolescent ED symptoms in the Avon Longitudinal Study of Parents and Children (ALSPAC). METHODS: A total of 8654 participants with genotype data and at least one phenotypic measure were included from the ALSPAC study. We associated PGS from 25 traits (16 psychiatric, 4 metabolic, and 5 anthropometric) with eight ED symptoms, including behaviours such as fasting for weight loss and cognitions such as body dissatisfaction. RESULTS: Higher attention deficit hyperactivity disorder PGS and lower educational attainment PGS were associated with fasting for weight loss. Higher insomnia PGS was associated with increased body dissatisfaction. We found no evidence of an association between metabolic trait PGS and any ED symptom. Fat-free mass, fat mass, and body fat percentage PGSs, were positively associated with binge eating, excessive exercise, fasting for weight loss, body dissatisfaction, and weight and shape concern. CONCLUSIONS: ED symptoms are genetically associated with psychiatric and anthropometric, but not with metabolic traits. Our findings provide insights for future genetic research investigating on why some individuals with ED symptoms progress to develop threshold EDs while others do not.

One size does not fit all. Genomics differentiates among anorexia nervosa, bulimia nervosa, and binge-eating disorder.

OBJECTIVE: Genome-wide association studies have identified multiple genomic regions associated with anorexia nervosa. No genome-wide studies of other eating disorders, such as bulimia nervosa and binge-eating disorder, have been performed, despite their substantial heritability. Exploratively, we aimed to identify traits that are genetically associated with binge-type eating disorders. METHOD: We calculated genome-wide polygenic scores for 269 trait and disease outcomes using PRSice v2.2 and their association with anorexia nervosa, bulimia nervosa, and binge-eating disorder in up to 640 cases and 17,050 controls from the UK Biobank. Significant associations were tested for replication in the Avon Longitudinal Study of Parents and Children (up to 217 cases and 3,018 controls). RESULTS: Individuals with binge-type eating disorders had higher polygenic scores than controls for other psychiatric disorders, including depression, schizophrenia, and attention deficit hyperactivity disorder, and higher polygenic scores for body mass index. DISCUSSION: Our findings replicate some of the known comorbidities of eating disorders on a genomic level and motivate a deeper investigation of shared and unique genomic factors across the three primary eating disorders.

Common etiological architecture underlying reward responsiveness, externally driven eating behaviors, and BMI in childhood: findings from the Gemini twin cohort.

BACKGROUND: Studies have reported that impulsivity predicts childhood BMI and that the association is mediated by eating behaviors. One aspect of impulsivity-potentially crucial in the obesity context-is reward responsiveness, which may predispose to responsiveness to palatable food cues. The behavioral susceptibility theory hypothesizes that genetic susceptibility to obesity operates partly via genetically determined differences in appetite regulation. Reward responsiveness may therefore be one of the neuro-endophenotypes that mediates genetic susceptibility to obesity. OBJECTIVE: To test whether reward responsiveness, eating behaviors, and child BMI share common genetic architecture. METHODS: We examined reward responsiveness, eating behaviors, and BMI in 5-year-old children from Gemini, a UK birth cohort of 2402 twin pairs born in 2007. All measures were collected by parent report. Reward responsiveness was derived from the Behavioral Approach System. Compulsion to eat and eating for pleasure was measured with the "food responsiveness" scale of the Child Eating Behavior Questionnaire. Wanting to eat in response to environmental food cues was measured with the "external eating" scale of the Dutch Eating Behavior Questionnaire. Maximum-likelihood structural equation modeling was used to establish underlying common genetic and environmental influences. RESULTS: There were significant positive phenotypic correlations between all traits except for reward responsiveness and BMI. Genetic factors explained the majority of the association between food responsiveness and external eating (74%, 95% CI: 61, 87), whereas common shared environmental factors explained the majority of the associations between reward responsiveness with both food responsiveness (55%, 95% CI: 20, 90) and external eating (70%, 95% CI: 39, 100). CONCLUSIONS: Our study demonstrates the importance of common environmental factors in the shared etiology between reward responsiveness and childhood eating behaviors. However, the common etiology underlying both reward responsiveness and BMI is unclear, as there was no phenotypic correlation between reward responsiveness and BMI at this age. Further longitudinal research needs to detangle this complex relationship throughout development.

Eating behavior trajectories in the first 10 years of life and their relationship with BMI.

BACKGROUND: Child eating behaviors are highly heterogeneous and their longitudinal impact on childhood weight is unclear. The objective of this study was to characterize eating behaviors during the first 10 years of life and evaluate associations with BMI at age 11 years. METHOD: Data were parental reports of eating behaviors from 15 months to age 10 years (n = 12,048) and standardized body mass index (zBMI) at age 11 years (n = 4884) from the Avon Longitudinal Study of Parents and Children. Latent class growth analysis was used to derive latent classes of over-, under-, and fussy-eating. Linear regression models for zBMI at 11 years on each set of classes were fitted to assess associations with eating behavior trajectories. RESULTS: We identified four classes of overeating; "low stable" (70%), "low transient" (15%), "late increasing" (11%), and "early increasing" (6%). The "early increasing" class was associated with higher zBMI (boys: ß = 0.83, 95% CI: 0.65, 1.02; girls: ß = 1.1; 0.92, 1.28) compared with "low stable." Six classes were found for undereating; "low stable" (25%), "low transient" (37%), "low decreasing" (21%), "high transient" (11%), "high decreasing" (4%), and "high stable" (2%). The latter was associated with lower zBMI (boys: ß = -0.79; -1.15, -0.42; girls: ß = -0.76; -1.06, -0.45). Six classes were found for fussy eating; "low stable" (23%), "low transient" (15%), "low increasing" (28%), "high decreasing" (14%), "low increasing" (13%), and "high stable" (8%). The "high stable" class was associated with lower zBMI (boys: ß = -0.49; -0.68-0.30; girls: ß = -0.35; -0.52, -0.18). CONCLUSIONS: Early increasing overeating during childhood is associated with higher zBMI at age 11. High persistent levels of undereating and fussy eating are associated with lower zBMI. Longitudinal trajectories of eating behaviors may help identify children potentially at risk of adverse weight outcomes.

A longitudinal study of eating behaviours in childhood and later eating disorder behaviours and diagnoses.

BACKGROUND: Eating behaviours in childhood are considered as risk factors for eating disorder behaviours and diagnoses in adolescence. However, few longitudinal studies have examined this association. AIMS: We investigated associations between childhood eating behaviours during the first ten years of life and eating disorder behaviours (binge eating, purging, fasting and excessive exercise) and diagnoses (anorexia nervosa, binge eating disorder, purging disorder and bulimia nervosa) at 16 years. METHOD: Data on 4760 participants from the Avon Longitudinal Study of Parents and Children were included. Longitudinal trajectories of parent-rated childhood eating behaviours (8 time points, 1.3-9 years) were derived by latent class growth analyses. Eating disorder diagnoses were derived from self-reported, parent-reported and objectively measured anthropometric data at age 16 years. We estimated associations between childhood eating behaviours and eating disorder behaviours and diagnoses, using multivariable logistic regression models. RESULTS: Childhood overeating was associated with increased risk of adolescent binge eating (risk difference, 7%; 95% CI 2 to 12) and binge eating disorder (risk difference, 1%; 95% CI 0.2 to 3). Persistent undereating was associated with higher anorexia nervosa risk in adolescent girls only (risk difference, 6%; 95% CI, 0 to 12). Persistent fussy eating was associated with greater anorexia nervosa risk (risk difference, 2%; 95% CI 0 to 4). CONCLUSIONS: Our results suggest continuities of eating behaviours into eating disorders from early life to adolescence. It remains to be determined whether childhood eating behaviours are an early manifestation of a specific phenotype or whether the mechanisms underlying this continuity are more complex. Findings have the potential to inform preventative strategies for eating disorders.