Individual-level longitudinal data on biological, behavioural, and social dimensions are becoming increasingly available. Typically, these data are analysed using mixed effects models, with the result summarised in terms of an average trajectory plus measures of the individual variations around this average. However, public health investigations would benefit from finer modelling of these individual variations which identify not just one average trajectory, but several typical trajectories. If evidence of heterogeneity in the development of these variables is found, the role played by temporally preceding (explanatory) variables as well as the potential impact of differential trajectories may have on later outcomes is often of interest. A wide choice of methods for uncovering typical trajectories and relating them to precursors and later outcomes exists. However, despite their increasing use, no practical overview of these methods targeted at epidemiological applications exists. Hence we provide: (a) a review of the three most commonly used methods for the identification of latent trajectories (growth mixture models, latent class growth analysis, and longitudinal latent class analysis); and (b) recommendations for the identification and interpretation of these trajectories and of their relationship with other variables. For illustration, we use longitudinal data on childhood body mass index and parental reports of fussy eating, collected in the Avon Longitudinal Study of Parents and Children.

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.

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

Background: Food preferences vary substantially among adults and children. Twin studies have established that genes and aspects of the shared family

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.

The COVID-19 pandemic has led to the implementation of stay-at-home and lockdown measures. It is currently unknown if the experience of lockdown leads to long term changes in individual's eating behaviors. The objectives of this study were: i) to derive longitudinal trajectories of change in eating during UK lockdown, and ii) to identify risk factors associated with eating behavior trajectories. Data from 22,374 UK adults from the UCL COVID-19 Social study (a panel study collecting weekly data during the pandemic) were analyzed from 28th March to 29th May 2020. Latent Class Growth Analysis was used to derive trajectories of change in eating. These were then associated with prior socio-economic, health-related and psychological factors using multinomial regression models. Analyses suggested five trajectories, with the majority (64%) showing no change in eating. In contrast, one trajectory was marked by persistently eating more, whereas another by persistently eating less. Overall, participants with greater depressive symptoms were more likely to report any change in eating. Loneliness was linked to persistently eating more (OR = 1.07), whereas being single or divorced, as well as stressful life events, were associated with consistently eating less (OR = 1.69). Overall, higher education status was linked to lower odds of changing eating behavior (OR = 0.54–0.77). Secondary exploratory analyses suggest that participants self-reported to have overweight were more commonly categorised into the group consistently eating more, whereas participants with underweigh persistently ate less. In this study, we found that one third of the sample report changes in quantities eaten throughout the first UK lockdown period. Findings highlight the importance of adjusting public health programs to support eating behaviors in future lockdowns both in this and potential future pandemics. This is particularly important as part of on-going preventive efforts to prevent nutrition-related chronic diseases.