Abstract
Environmental exposures such as nutrition during life stages with high developmental plasticity—in particular, the in utero period, infancy, childhood, and puberty—may have long-lasting influences on risk of chronic diseases, including obesity-related conditions that manifest as early as childhood. Yet, specific mechanisms underlying these relationships remain unclear. Here, we consider the study of ‘omics mechanisms, including nutrigenomics, epigenetics/epigenomics, and metabolomics, within a life course epidemiological framework to accomplish three objectives. First, we carried out a scoping review of population-based literature with a focus on studies that include ‘omics analyses during three sensitive periods during early life: in utero, infancy, and childhood. We elected to conduct a scoping review because the application of multi-‘omics and/or precision nutrition in childhood obesity prevention and treatment is relatively recent, and identifying knowledge gaps can expedite future research. Second, concomitant with the literature review, we discuss the relevance and plausibility of biological mechanisms that may underlie early origins of childhood obesity identified by studies to date. Finally, we identify current research limitations and future opportunities for application of multi-‘omics in precision nutrition/health practice.
Highlights
After adjusting for potential confounders and cluster effects, paternal obesity was significantly associated with lower methylation levels at multiple human imprinted genes that are important in growth and development, including DMRs of maternally expressed gene 3 (MEG3), necdin (NDN), small nuclear ribonucleoprotein polypeptide N (SNRPN) and epsilon sarcoglycan/paternally expressed gene 10 (SGCE/PEG10)
We described studies that sought to identify biological mechanisms linking early nutrition to obesity during the in utero period, infancy, and childhood
The second research gap is that the majority of studies to date have considered single biological pathways, which overlooks the contribution of multiple mechanisms and interactions among them [124]
Summary
Recent data from Centers for Disease Control and Prevention (CDC) in the United States documented a prevalence of childhood obesity of 18.5% in 2015–2016, indicating nearly one in five children were obese [2,3,4,5]. These burgeoning trends have spurred widespread public health efforts to reduce and manage the childhood obesity pandemic [6,7], framed by the social-ecological approaches [8] that emphasize multiple levels of influence, ranging from individual and family to organizational and community/policy approaches, as well as social determinants of health [8]. This model highlights that environmental and hereditary factors have potential to influence disease risk at any stage of child development from
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