Abstract
Objective:Standard approaches have found that rapid growth during the first 2 years of life is a risk factor for overweight in later childhood. Our objective was to test whether growth velocity, independent of concurrent size, was associated with overweight using a nonlinear random-effects model that allows for enhanced specifications and estimations.Methods:Longitudinal data from a birth cohort in Mexico (n=586) were used to estimate growth trajectories over 0–24 months for body mass index (BMI), length and weight using the SuperImposition by Translation and Rotation (SITAR) models. The SITAR models use a nonlinear random-effects model to estimate an average growth curve for BMI, length and weight and each participant's deviation from this curve on three dimensions—size, velocity and timing of peak velocity. We used logistic regression to estimate the association between overweight status at 7–9 years and size, velocity and timing of BMI, length and weight trajectories during 0–24 months. We tested whether any association between velocity and overweight varied by relative size during 0–24 months or birth weight.Results:SITAR models explained the majority of the variance in BMI (73%), height (86%) and weight (85%) between 0–24 months. When analyzed individually, relative BMI/length/weight (size) and BMI/length/weight velocity during 0–24 months were each associated with increased odds of overweight in late childhood. Associations for timing of peak velocity varied by anthropometric measure. However, in the mutually adjusted models, only relative BMI/length/weight (size) remained statistically significant. We found no evidence that any association between velocity and overweight varied by size during 0–24 months or birth weight.Conclusions:After mutual adjustment, size during 0–24 months of life (as opposed to birth size), but not velocity or timing of peak velocity, was most consistently associated with overweight in later childhood.
Highlights
Body size and growth during infancy and childhood may have lasting effects on adult health.[1]
The estimated average growth trajectories from the randomized controlled trial in infancy was not included as a the SuperImposition by Translation and Rotation (SITAR) models for body mass index (BMI), length and weight are displayed in confounder as it was not associated with our exposure or outcome
In contrast to standard approaches, our approach allowed for the mutual adjustment of size, velocity and timing of peak velocity of the early life growth trajectory, in order to examine which aspects of growth trajectories were independently associated with overweight later in childhood
Summary
Body size and growth during infancy and childhood may have lasting effects on adult health.[1]. Programming or a predictive adaptive response, where cues from the environment cause permanent changes to physiological functioning during certain periods of developmental plasticity is one set of mechanisms through which either small size, small size combined with rapid growth velocity or rapid growth velocity itself is hypothesized to affect health later in life.[7,14,15,16] Small size at birth may be indicative of suboptimal intrauterine environments that may create a physiology that is predisposed to energy conservation.[15,16] This fetal or neonatal predictive adaptation is thought to work at the epigenetic level, and animal studies suggest multiple common alterations as a consequence of mismatched fetal and postnatal nutrition environments that result in a physiology that favors an insulin-resistant state and an increased propensity for accumulation of fat mass.[13] These alterations include changes to appetite control, taste preference, the hypothalamus, pancreas function and endothelial functioning.[13] The programming will be maladaptive if the environment later in life differs substantially from intrauterine environment and this mismatch in environments is the mechanism by which faster growth velocity in combination with smaller size at birth is hypothesized to be detrimental.[17]
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