Blood pressure and the capacity-load model in 8-year-old children from Nepal: Testing the contributions of kidney size and intergenerational effects.

Jonathan C.K Wells,Anthony Costello,David Osrin,Dharma S Manandhar,Delan Devakumar,Carlos S Grijalva‐Eternod

doi:10.1002/ajhb.22829

Jonathan C.K Wells, Anthony Costello + Show 4 more

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https://doi.org/10.1002/ajhb.22829

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Abstract

ObjectivesGrowth patterns in early life are increasingly linked with subsequent cardio-metabolic risk, but the underlying mechanisms require elucidation. We have developed a theoretical model of blood pressure, treating it as a function of homeostatic metabolic capacity, and antagonistic metabolic load. We sought to differentiate prenatal and postnatal components of metabolic capacity, and to identify intergenerational contributions to offspring capacity and load.MethodsWe followed up at 8 years a cohort of children originally recruited into a randomized trial of maternal micronutrient supplementation in pregnancy. Maternal anthropometry was measured at recruitment. Offspring anthropometry was measured at birth, 2 years and 8 years. Offspring blood pressure, kidney size, and body composition were measured at 8 years. Regression analysis was used to investigate potential associations of maternal phenotype, birth phenotype, and current body composition with kidney size and blood pressure.ResultsBlood pressure was positively associated with body fat, but negatively associated with birth weight and relative leg length. Kidney size was positively associated with birth weight but not with relative leg length. Adjusting for adiposity, blood pressure was independently negatively associated with birth weight, relative leg length, and kidney length. Maternal height and BMI predicted offspring size at birth and at 8 years, but not blood pressure.ConclusionsOur data provide support for the capacity-load model of blood pressure in Nepalese children. Fetal and postnatal growth and kidney dimensions all contribute to metabolic capacity. Maternal phenotype contributed to offspring capacity and load, but these associations did not propagate to blood pressure.

Highlights

There is compelling evidence that growth patterns in early life are associated with subsequent metabolic phenotype (Barker et al, 1989; Bhargava et al, 2004; Eriksson et al, 2006; Hales et al, 1991; Lakshmy et al, 2011; Leon et al, 1996; Lithell et al, 1996)
They hypothesized that nutritional insufficiency in utero induced the fetus to sacrifice growth of some organs in order to spare the brain (Hales and Barker, 1992; Latini et al, 2004). Such reallocation of energy between organs and tissues would favor short-term survival, but at the cost of reduced tolerance of “affluent lifestyle” in later life. While this approach emphasized the detrimental effects of low birth weight, it did not explain why inverse associations between birth weight and later disease risk are apparent across the entire range of birth weight (e.g., Rich-Edwards et al, 1997), and apply to those with adequate fetal growth
We introduced relative leg length and kidney dimensions into the model as potential independent components of metabolic capacity, or as mediating factors

Summary

Introduction

There is compelling evidence that growth patterns in early life are associated with subsequent metabolic phenotype (Barker et al, 1989; Bhargava et al, 2004; Eriksson et al, 2006; Hales et al, 1991; Lakshmy et al, 2011; Leon et al, 1996; Lithell et al, 1996). To shed more light on these associations between early growth and later risk, we have built on the thrifty phenotype hypothesis of Hales and Barker (1992) They hypothesized that nutritional insufficiency in utero induced the fetus to sacrifice growth of some organs (e.g., pancreatic beta-cell mass, muscle mass, liver, and kidney mass) in order to spare the brain (Hales and Barker, 1992; Latini et al, 2004). Such reallocation of energy between organs and tissues would favor short-term survival, but at the cost of reduced tolerance of “affluent lifestyle” in later life. Others have clarified that postnatal weight gain at any age is positively associated with later blood pressure, mediated by increases in tissue masses (Adair et al, 2009; Leunissen et al, 2012)

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