Linear enamel hypoplasia and growth in an Australian Aboriginal community: not so small, but not so healthy either

While much is strongly suspected about synergisms linking courses of growth and development with nutrient intakes, immune function, disease exposures, and energy expenditures, debates remain regarding the probability of permanent impairments to growth and function under various circumstances.This study tests a series of related hypotheses in an attempt to reconcile evidence of increasing physiological stress among Warlpiri and Pintubi infants and young children following settlement in the 1940s with their frequently rapid and undelayed longitudinal growth in stature during adolescence.The study used archived cross-sectional and longitudinal records of stature, weight, and dental casts collected by the Dental School at the University of Adelaide beginning in 1951 at the then recently settled community of Yuendumu. Longitudinal modelling of height data and all statistical tests were accomplished using SYSTAT 10. Height, weight, and BMI (kg m-2) for age z-scores were calculated using NCHS reference data. Dental casts were scored for linear enamel hypoplasia (LEH) with each defect assigned to an enamel developmental unit. The extent of height catch-up was estimated using conditional height gain.Cross-sectional analyses indicate significant associations between birth year and women's heights (n = 105, p = 0.02) or height for age z-scores (p = 0.003), but no similar associations among men. Final height for age z-score was significantly associated with sex (p0.0005), onset (p = 0.031), and an onset by number of enamel defects interaction (p = 0.033). Late adolescent height z-scores were only significantly negatively associated with increasing numbers of defects among individuals with enamel defects appearing prior to about 18 months of age (n = 60, p = 0.019). With longitudinally estimated age at peak height velocity (APHV) statistically controlled, peak height velocity (PHV) was similarly significantly positively associated with conditional height gain in males (n = 50, p = 0.01) and females (n = 31, p = 0.05). Exploratory analyses suggest that with timing and intensity of PHV controlled, childhood body mass was only significantly positively associated with catch-up in height among those who experienced defect onset relatively early (n = 80, p = 0.005).Results help explain previously documented, and apparently contradictory, outcomes of settlement processes. Rapid and relatively undelayed late childhood and adolescent growth associated with catch-up in height occurred through a confluence of increasing early childhood systemic stress followed by increases in net energy consumption that probably increased as children aged.