Abstract
The Karlberg model of human growth describes the infancy, childhood, and puberty (ICP) stages as continuous and overlapping, and defined by transitions driven by sequential additional effects of several endocrine factors that shape the growth trajectory and resultant adult size. Previous research has suggested that a delayed transition from the infancy to the childhood growth stage contributes to sub-optimal growth outcomes. A new method developed to analyze the structure of centile crossing in early life has emerged as a potential tool for identifying the infancy-childhood transition (ICT), through quantifying patterns of adjacent monthly weight-for-age z-score (WAZ) deviation correlations. Using this method, the infancy-childhood transition was identified as taking place at around 12 months of age in two cohorts of UK infants. Here, we apply this method to data collected as part of a longitudinal growth study in rural Gambia [the Hormonal and Epigenetic Regulators of Growth, or HERO-G study, N = 212 (F = 99, M = 113)], in order to identify the ICT and assess whether timing of this transition differs across groups based on sex or birth seasonality. We calculated Pearson correlation coefficients for adjacent monthly WAZ score deviations. Based on the patterns of change in the correlation structure over time, our results suggest that the infancy-childhood transition occurs at around 9 months of age in rural Gambian infants. This points to an accelerated ICT compared to UK infants, rather than a delayed ICT. A comparatively later transition, seen in UK infants, allows maximal extension of the high rates of growth during the infancy stage; an earlier transition as seen in Gambian infants cuts short this period of rapid growth, potentially impacting on growth outcomes in childhood while diverting energy into other processes critical to responses to acute infectious challenges. Growth in later developmental stages in this population offers an extended window for catch-up.
Highlights
The human growth trajectory is complex compared to other large-bodied mammals; passing through infancy, childhood, juvenility, and adolescence before reaching adulthood [1] it is relatively prolonged via the extension of the pre-pubertal period [2], and is best described as sinuous and containing periods of both relatively slow growth and accelerated growth
Cole et al [28] identified two ‘phases’ of deviation correlations within the first year of infant life: [1] positive feedback during the first few months, and [2] negative feedback from 6 to 10/11 months. These feedback phases were proposed as the mechanism by which an individual finds and tracks their growth canal
Cole et al [28], and [2] the ICT in Gambian infants born in the wet season would be delayed (DICT) relative to the ICT in infants born in the dry season
Summary
The human growth trajectory is complex compared to other large-bodied mammals; passing through infancy, childhood, juvenility, and adolescence before reaching adulthood [1] it is relatively prolonged via the extension of the pre-pubertal period [2], and is best described as sinuous and containing periods of both relatively slow growth and accelerated growth. Earlier perspectives held that certain stages of growth are uniquely derived in humans (e.g., childhood), and the insertion of these stages into an ancestral primate growth trajectory are responsible for the prolongation of growth overall in humans—itself hypothesized to permit a longer period of brain development [3], to build metabolic and cognitive capital to use in later life [4], or to increase chances of success in relationship to extrinsic mortality risk both in adulthood and during immaturity [5, 6]. More recent analyses have suggested that while the human growth trajectory is extended relative to that of our closest living relatives, those stages previously considered novel are present in other non-human primate species, and relatively accelerated, and/or compressed in their time course of expression [7,8,9,10,11,12]. Growth in early life has been linked to developmental and health outcomes across the life course such as childhood obesity [18]; childhood adiposity; and age at menarche [19]
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