Auxological perspectives on ‘growth’ in DOHaD M. Lampl 1,2 *, A. Mummert 1,2 and M. Schoen 1 1 Center for the Study of Human Health, Emory University, Atlanta, GA, USA 2 Department of Anthropology, Emory University, Atlanta, GA USA David Barker established growth as a seminal link between early development and later health attainment and disease risk. This was nothing less than a paradigm shift in health and medicine, turning the focus of disease causality away from contemporary environmental influences to earliest growth as a time when functional anatomy and physiology sets in place critical structures and function for a lifetime. Barker’s prodigious work investigated time- and place-specific interactions between maternal condition and exogenous environmental influences, focusing on how growth unfolds across development to function as a mechanistic link to ensuing health. Subsequent applications do not always attend to the specificity and sensitivity issues included in his original work, and commonly overlook the long-standing methods and knowledge base of auxology. Methodological areas in need of refinement include enhanced precision in how growth is represented and assessed. For example, multiple variables have been used as a referent for ‘growth,’ which is problematic because different body dimensions grow by different biological clocks with unique functional physiologies. In addition, categorical clinical variables obscure the spectrum of variability in growth experienced at the individual level. Finally, size alone is a limited measure as it does not capture how individuals change across age, or actually grow. The ground-breaking notion that prenatal influences are important for future health gave rise to robust interest in studying the fetus. Identifying the many pathways by which size is realized permits targeted interventions addressing meaningful mechanistic links between growth and disease risk to promote health across the lifespan. Received 27 June 2015; Revised 15 July 2015; Accepted 16 July 2015 Key words: auxology, developmental origins, fetal growth, fetology, lifespan health The field of auxological epidemiology has long acknowledged growth during childhood as a sensitive indicator of the environ- ment, in recognition of the small size among children and adults alike living in poor circumstances. 1 Appreciation of maternal health and well-being as an environmental exposure, and the identi fica- tion of these effects on prenatal growth, has been more nuanced. Maternally derived influences on fetal development ranging from genetics to growth-regulating substances 2 were postulated in early investigations. Animal studies documented the importance of maternal environment over genetics in classic cross-breeding experiments (e.g., horses 3 ), identifying restrictive effects on offspring size from maternal size and litter size (e.g., rabbits 2,4 ) and limitations in intrauterine blood supply (e.g., mice 5 ). Observations among humans recognized that smaller infants are born to smaller mothers with influences from interactions between maternal age, infant birth order and placental size on fetal growth rate, 6–10 as well as parental economic circumstances, which exert effects on both birth size and the likelihood of death during infancy. 11,12 The specific relationships between infant size and placental size and function 10,13 contributed to the formalization of the maternal constraint concept 14,15 and supported an emerging clinical focus on fetal growth retardation 16 as the field of neonatology emerged in the 1960s. 17 An appreciation for poor growth as a predictor of adult morbidity and mortality has been more recent. Observations of high mortality from cardiovascular disease in later life among people born into regions characterized by high infant mortality rates led to speculations that poor infant, 18,19 childhood and adolescent environments 20 might be causal. One interpretation of this association is that a cumulative biological effect of poor circumstances across the lifespan leads to higher mortality 21 through allostatic load. 22 Another viewpoint on these correlations is that high infant mortality results from reduced fetal growth and lower birthweight neonates who have increased susceptibilities as a product of generations of poorly nourished mothers. 23 In this scenario, it is not neonatal smallness itself that underlies the link, but how the infant became small that generates both early survival challenge and later health risk. Small infants may be constitutionally different, in ways that increase their susceptibility to cardiac stress across the lifespan. In lieu of general allostatic load stress, the mortality correlations were postulated to reflect specific patterns of altered prenatal organ growth, subsequently tried by the rapid postnatal growth in length and weight following small birth size 24–27 and exacerbated in the face of potentially abundant resources thereafter. 20,28–30 Gennser et al. 31 postulated a specific mechanistic link to explain increased diastolic blood pressure among young adults who had been born small for gestational age (SGA). They suggested that increased fetal circulatory pressure to sustain placental *Address for correspondence: M. Lampl, Center for the Study of Human Health, Emory University, 107 Candler Library, 550 Asbury Circle, Atlanta, GA 30322, USA. (Email mlampl@emory.edu) Journal of Developmental Origins of Health and Disease (2015), 6(5), 390–398. © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2015 ORIGINAL ARTICLE doi:10.1017/S2040174415001403 Themed Issue: David Barker commemorative meeting, September 2014; the future of the science he inspired