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.

Objectives The aim of this study was to estimate the incidence of lost to follow up from anti-retroviral therapy (ART) care and identify the associated factors among human immunodeficiency virus (HIV) infected patients after first-line ART initiation at University of Gondar comprehensive specialized hospital, Northwest Ethiopia between January 2012 and January 2018. Results The overall incidence rate of lost to follow up was 12.26 per 100 person years (95% CI (10.61–14.18)). Being underweight (< 18.5 kg/m 2 ) (AHR, 1.52, 95% CI 1.01–2.28), jobless (AHR, 2.22, 95% CI 1.2–4.11), substance abuser (AHR, 1.84 95% CI 1.19–2.86), having sub-optimal adherence (fair/poor) (AHR 6.33, 95% CI (3.90–10.26)), not receiving isoniazid prophylaxis (AHR 2.47, 95% CI (1.36–4.48)), ambulatory functional status (AHR 1.94, 95% CI (1.23–3.06)), having opportunistic infections (AHR, 1.74 95% CI 1.11–2.72), having CD4 count 201–349 cells/µL (AHR 0.58, 95% CI (0.38–0.88)) were found to be significant predictors of lost to follow up from ART service.

BackgroundEating behaviours in childhood are considered as risk factors for eating disorder behaviours and diagnoses in adolescence. However, few longitudinal studies have examined this association.AimsWe 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.MethodData 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.ResultsChildhood 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).ConclusionsOur 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: Tourette syndrome (TS) has a well-established genetic background, but its genetic architecture remains largely unknown. The authors investigated the role of polygenic risk scores (PRS) derived from a TS genome-wide association study (GWAS) in relation to the occurrence of tics and associated traits in a general population cohort.