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Open AccessJournal ArticleDOI

Developmental origins of health and disease: current knowledge and potential mechanisms.

TLDR
A summary of current research that supports the concept of DOHaD, as well as potential mechanisms and interactions that explain how nutrition in utero and during early childhood influences lifelong health are presented.
Abstract
Epidemiologic and clinical research has provided a large body of evidence supporting the developmental origins of health and disease (DOHaD), but there has been a relative dearth of mechanistic studies in humans due to the complexity of working with large, longitudinal cohorts. Nonetheless, animal models of undernutrition have provided substantial evidence for the potential epigenetic, metabolic, and endocrine mechanisms behind DOHaD. Furthermore, recent research has explored the interaction between the environment and the gastrointestinal system by investigating how the gut microbial ecology may impact the capacity for nutrient processing and absorption in a manner that may limit growth. This review presents a summary of current research that supports the concept of DOHaD, as well as potential mechanisms and interactions that explain how nutrition in utero and during early childhood influences lifelong health.

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Role of the microbiome in human development.

TL;DR: The role of the microbiome in human development, including evolutionary considerations, and the maternal/fetal relationships, contributions to nutrition and growth are reviewed.
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Cadmium: Toxic effects on placental and embryonic development.

TL;DR: An understanding of how cadmium exposure contributes to placental and fetal development is necessary for the development of prevention and control strategies for fetal development defects caused by cad mium exposure during pregnancy.
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Gestational Diabetes Mellitus: A Harbinger of the Vicious Cycle of Diabetes.

TL;DR: Current preclinical models of GDM are discussed to better understand the underlying pathophysiology of the disease and the timely need to increase the scientific toolbox to identify strategies to prevent and treat GDM, thereby advancing clinical care.
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Epigenetics and the Developmental Origins of Health and Disease: Parental environment signalling to the epigenome, critical time windows and sculpting the adult phenotype

TL;DR: An overview of the epigenetic changes in response to maternal environment during the vulnerability time windows, gametogenesis, early development, placentation and foetal growth, and postnatal period is described.
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The good, the bad, and the ugly of pregnancy nutrients and developmental programming of adult disease.

TL;DR: Evidence from animal models for nutritional programming of human disease is summarized, for the common mechanisms underlying nutritional programming, and potential nutritional interventions used as reprogramming strategies are discussed.
References
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Journal ArticleDOI

Translating the Histone Code

TL;DR: It is proposed that this epigenetic marking system represents a fundamental regulatory mechanism that has an impact on most, if not all, chromatin-templated processes, with far-reaching consequences for cell fate decisions and both normal and pathological development.
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Prediction of Coronary Heart Disease Using Risk Factor Categories

TL;DR: A simple coronary disease prediction algorithm was developed using categorical variables, which allows physicians to predict multivariate CHD risk in patients without overt CHD.
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Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis.

TL;DR: It is proposed that one of the major long-term consequences of inadequate early nutrition is impaired development of the endocrine pancreas and a greatly increased susceptibility to the development of Type 2 diabetes.
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Fetal and infant growth and impaired glucose tolerance at age 64.

TL;DR: Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes and reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction.
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Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales.

TL;DR: Although the rise in ischaemic heart disease in England and Wales has been associated with increasing prosperity, mortality rates are highest in the least affluent areas.
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