Abstract
Pregnancy and birth cohorts have been utilised extensively to investigate the developmental origins of health and disease, particularly in relation to understanding the aetiology of obesity and related cardiometabolic disorders. Birth and pregnancy cohorts have been utilised extensively to investigate this area of research. The aim of the present review was twofold: first to outline the necessity of measuring cardiometabolic risk in children; and second to outline how it can be assessed. The major outcomes thought to have an important developmental component are CVD, insulin resistance and related metabolic outcomes. Conditions such as the metabolic syndrome, type 2 diabetes and CHD all tend to have peak prevalence in middle-aged and older individuals but assessments of cardiometabolic risk in childhood and adolescence are important to define early causal factors and characterise preventive measures. Typically, researchers investigating prospective cohort studies have relied on the thesis that cardiovascular risk factors, such as dyslipidaemia, hypertension and obesity, track from childhood into adult life. The present review summarises some of the evidence that these factors, when measured in childhood, may be of value in assessing the risk of adult cardiometabolic disease, and as such proceeds to describe some of the methods for assessing cardiometabolic risk in children.
Highlights
Pregnancy and birth cohorts have been utilised extensively to investigate the developmental origins of health and disease, in relation to understanding the aetiology of obesity and related cardiometabolic disorders
The resulting developmental origins of health and disease (DOHaD) paradigm proposed that a range of metabolic, immunological and physiological adaptations to suboptimal antenatal
The growing global burden of obesity is affecting all regions of the world, and associated cardiometabolic disorders are among the greatest threats to human health
Summary
Pregnancy and birth cohorts have been utilised extensively to investigate the developmental origins of health and disease, in relation to understanding the aetiology of obesity and related cardiometabolic disorders. Following earlier speculation that this may reflect maternal/infant nutrition at critical stages of development, David Barker’s team went on to report evidence that lower birth weight was an independent risk factor for later CHD and the metabolic syndrome. In this context, low birth weight represents a tangible, albeit multifactorial, reflection of a suboptimal in utero environment. Maternal environmental influences which have been studied include nutritional status (in the periconceptional period[3,4] and during pregnancy[5,6]), physical activity, pharmacological agents (prescribed and illicit), patterns of microbial diversity, smoking and pollutants Some of these have been shown to have epigenetic effects on diverse aspects of fetal development. This suggests that early life effects (potentially through obesity and hyperglycaemia during pregnancy) could be an important factor in the rising obesity rates being observed worldwide
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