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Developmental origins of non-communicable disease: Implications for research and public health
Robert Barouki, Peter D Gluckman, Philippe Grandjean, Mark Hanson, Jerrold J Heindel
Environmental Health , 2012, DOI: 10.1186/1476-069x-11-42
Abstract: For many years biologists considered the developmental period to be controlled by a strict, hard-wired genetic program, and thus it was uncertain how it could be influenced by the environment. It is now clear that development is plastic, and that it allows the organism to respond to the surrounding environment, especially during early development when cells are differentiating and tissues are developing. This capacity is based on molecular pathways that lead to control of gene expression and induction of specific phenotypes in the absence of DNA sequence modification [1]. These pathways, as currently understood, include DNA methylation, histone covalent modification, and noncoding RNA expression. Such epigenetic modifications can be passed from one cell generation to the next and, in some cases, when germ cells are targeted, can be transgenerationally transmitted [2]. Furthermore, these changes can be cell, tissue, and sex specific, and time dependent. In many cases they may not be apparent during a latent period which may last from months to years or decades. Thus, each individual has one genome, but will hold multiple epigenomes.The ability to respond to environmental conditions can be evolutionarily advantageous by allowing fine-tuning of gene expression, likely through epigenetic mechanisms [3]. Thus, developmentally plastic processes allow the organism to adapt to changing environments in order to maintain or improve reproductive capability in part by sustaining health through the reproductive period. However, interference with these developmentally-adaptive processes may also have adverse consequences on some functions and disease risks later in life. Furthermore, these mechanisms are also sensitive to environmental stimuli other than the nutrients and physiological factors that are normative, in evolutionary terms, to the human environment. Indeed, drugs, industrial chemicals, tobacco smoke, and other environmental exposures can affect these same mechanisms l
Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis  [PDF]
F. Boubred,M. Saint-Faust,C. Buffat,I. Ligi,I. Grandvuillemin,U. Simeoni
International Journal of Nephrology , 2013, DOI: 10.1155/2013/346067
Abstract: Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the “early programming” of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a “factor of vulnerability” when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways. 1. Introduction Cardiovascular diseases ((CVD) hypertension, coronary disease and stroke, and heart failure) are one of the leading causes of mortality in industrialized countries, and the prevalence is increasing in emerging societies. All cardiovascular diseases account for 4.3 million deaths per year in the European Union, and the prevalence of chronic heart failure in the United States of America is approximately 6 million [1, 2]. In industrialized countries, hypertension (HT) affects 25% to 35% of the global population and reaches 60% to 70% of the population aged 60 or more. Hypertension is the principal risk factor of death worldwide [3]. It increases the severity of ischemic vascular diseases and, with obesity and type 2 diabetes, is one of the important risk factors for chronic kidney disease (CKD). Chronic kidney disease is defined as reduced glomerular filtration rate (GFR) up to end-stage renal disease (ESRD), proteinuria, or both. Prevalence of ESRD, estimated to be 0.5–2.5‰ worldwide, is increasing in several countries [4]. In turn, impaired renal factor favors the development of and amplifies the severity of CVD [5–7]. During the last two decades, it has been raised the concept of developmental programming of adult chronic
Developmental levels in adult's conceptions of health and disease
Reis, Joaquim C.;Fradique, Fernando S.;
Psicologia: Teoria e Pesquisa , 2010, DOI: 10.1590/S0102-37722010000300012
Abstract: a socio-cognitive developmental perspective suggests that conceptions regarding health and disease processes may present different levels of openness, flexibility, inclusiveness and differentiation, and thus can be ordered into different levels. we present a qualitative study on lay significations regarding health and disease processes, endorsed by 67 adults. the results show that these adults have different socio-cognitive developmental competences related to health and disease processes. for each dimension of significations of health and disease, it is possible to sequence lay person's conceptions developmentally. each level is distinct qualitatively, including responses characterized by a higher degree of differentiation, integration and complexity than the previous level. finally, the implications of this approach to clinical and educational methods are discussed.
The Roles of PPARs in the Fetal Origins of Metabolic Health and Disease
William D. Rees,Christopher J. McNeil,Christopher A. Maloney
PPAR Research , 2008, DOI: 10.1155/2008/459030
Abstract: Beyond the short-term effects on fertility, there is increasing evidence that obesity or the consumption of an inappropriate diet by the mother during pregnancy adversely affects the long-term health of her offspring. PPAR and RXR isotypes are widely expressed in reproductive tissues and in the developing fetus. Through their interactions with fatty acids, they may mediate adaptive responses to the changes in the maternal diet. In the maturing follicle, PPAR- has an important role in the granulosa cells that surround the maturing oocyte. After fertilisation, PPAR- and PPAR-/ are essential regulators of placentation and the subsequent development of key metabolic tissues such as skeletal muscle and adipose cells. Activation of PPAR- and PPAR-/ during fetal development has the potential to modify the growth and development of these tissues. PPAR- is expressed at low levels in the fetal liver, however, this expression may be important, as changes in the methylation of DNA in its promoter region are reported to take place during this period of development. This epigenetic modification then programmes subsequent expression. These findings suggest that two separate PPAR-dependent mechanisms may be involved in the fetal adaptations to the maternal diet, one, mediated by PPAR- and PPAR-/, regulating cell growth and differentiation; and another adapting long-term lipid metabolism via epigenetic changes in PPAR- to optimise postnatal survival.
Epigenomics – Grand Challenge: Much more than the Developmental Origins of Adult Health and Disease  [PDF]
Michael Edward Symonds
Frontiers in Genetics , 2010, DOI: 10.3389/fgene.2010.00001
Health Promotion and Disease Prevention Strategies in Older Adults with Intellectual and Developmental Disabilities  [PDF]
Eli Carmeli
Frontiers in Public Health , 2014, DOI: 10.3389/fpubh.2014.00031
Abstract: The rapid growth in the number of individuals living with intellectual and developmental disabilities (IDD) along with their increased longevity present challenges to those concerned about health and well-being of this unique population. While much is known about health promotion and disease prevention in the general geriatric population, far less is known about those in older adults with IDD. Effective and efficient health promotion and disease prevention strategies need to be developed and implemented for improving the health and quality of life of older adults living with IDD. This is considered to be challenging given the continued shrinkage in the overall health care and welfare system services due to the cut in the governmental budget in some of the western countries. The ideal health promotion and disease prevention strategies for older adults with IDD should be tailored to the individuals’ health risks, address primary and secondary disease prevention, and prevent avoidable impairments that cause premature institutionalization. Domains of intervention should include cognitive, mental and physical health, accommodations, workplace considerations, assistive technology, recreational activities, and nutrition.
Developmental Programming of Hypertension and Kidney Disease  [PDF]
Euming Chong,Ihor V. Yosypiv
International Journal of Nephrology , 2012, DOI: 10.1155/2012/760580
Abstract: A growing body of evidence supports the concept that changes in the intrauterine milieu during “sensitive” periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as “developmental programming” or “developmental origins of health and disease.” The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500?g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencing in utero environment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD. 1. Introduction Despite the availability of a number of treatment options for hypertension, cardiovascular, and renal disease, the prevalence, morbidity, and mortality of these diseases in children and adults remain very high [1]. Therefore, elucidation of the causality and pathogenesis of these diseases is critical. Studies by Widdowson and McCance in the 1960s demonstrated that acceleration or retardation of the rate of growth induced by malnutrition during early postnatal life in rats led to distinct and different effects on anatomical, physiological, and chemical development [2]. In the 1980s, studies by Barker demonstrated that systolic blood pressure in older children is inversely related to their birth weight [3]. Around the same time, Brenner hypothesized that early loss of nephron mass results in hyperfiltration of remaining nephrons leading to subsequent hypertension, proteinuria, and progressive kidney injury [4]. These and subsequent studies have provided initial evidence that a suboptimal in utero environment may predispose or “program” an individual to an increased risk of
Developmental programming of the metabolic syndrome - critical windows for intervention  [cached]
Mark H Vickers
World Journal of Diabetes , 2011, DOI: 10.4239/wjd.v2.i9.137
Abstract: Metabolic disease results from a complex interaction of many factors, including genetic, physiological, behavioral and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and the metabolic syndrome. Although the mechanisms are yet to be fully elucidated, this programming was generally considered an irreversible change in developmental trajectory. Recent work in animal models suggests that developmental programming of metabolic disorders is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This review will discuss critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal metabolic disorders following an adverse early life environment.
Maternal origins of developmental reproducibility  [PDF]
Mariela D. Petkova,Feng Liu,Thomas Gregor
Quantitative Biology , 2013,
Abstract: Cell fate decisions in multicellular organisms are precisely coordinated, leading to highly reproducible macroscopic outcomes of developmental processes. The origins of this reproducibility can be found at the molecular level during the earliest stages of development when spatial patterns of morphogen (form-generating) molecules emerge reproducibly. However, the initial conditions for these early stages are determined by the female during oogenesis, and it is unknown whether reproducibility is passed on to the zygote or whether it is reacquired by the zygote. Here we examine the earliest reproducible pattern in the Drosophila embryo, the Bicoid protein gradient. Using a unique combination of absolute molecule counting techniques, we show that it is generated from a highly controlled source of mRNA molecules that is reproducible from embryo to embryo to within ~8%. This occurs in a perfectly linear feed-forward process: changes in the female's gene dosage lead to proportional changes in the mRNA and protein counts in the embryo. In this setup, noise is kept low in the transition from one molecular species to another, allowing the female to precisely deposit the same absolute number of mRNA molecules in each embryo and therefore confer reproducibility to the Bicoid pattern. Our results indicate that the reproducibility of the morphological structures that emerge in the embryo originates during oogenesis when all initial patterning signals are controlled with precision similar to what we observe for the Bicoid pattern.
DNA methylation differences at growth related genes correlate with birth weight: a molecular signature linked to developmental origins of adult disease?
Nahid Turan, Mohamed F Ghalwash, Sunita Katari, Christos Coutifaris, Zoran Obradovic, Carmen Sapienza
BMC Medical Genomics , 2012, DOI: 10.1186/1755-8794-5-10
Abstract: We performed DNA methylation and transcript profiling on cord blood and placenta from newborns. We then used novel computational approaches to identify genes correlated with birth weight.We identified 23 genes whose methylation levels explain 70-87% of the variance in birth weight. Six of these (ANGPT4, APOE, CDK2, GRB10, OSBPL5 and REG1B) are associated with growth phenotypes in human or mouse models. Gene expression profiling explained a much smaller fraction of variance in birth weight than did DNA methylation. We further show that two genes, the transcriptional repressor MSX1 and the growth factor receptor adaptor protein GRB10, are correlated with transcriptional control of at least seven genes reported to be involved in fetal or placental growth, suggesting that we have identified important networks in growth control. GRB10 methylation is also correlated with genes involved in reactive oxygen species signaling, stress signaling and oxygen sensing and more recent data implicate GRB10 in insulin signaling.Single time point measurements of gene expression may reflect many factors unrelated to birth weight, while inter-individual differences in DNA methylation may represent a "molecular fossil record" of differences in birth weight-related gene expression. Finding these "unexpected" pathways may tell us something about the long-term association between low birth weight and adult disease, as well as which genes may be susceptible to environmental effects. These findings increase our understanding of the molecular mechanisms involved in human development and disease progression.One common non-disease phenotype that puts children at increased risk for multiple adverse outcomes is "low birth weight". Low birth weight is simply the transformation of the quantitative phenotype of birth weight into a discrete trait by truncation at the lowest decile of infant birth weights; i.e., a birth weight of less than 2,500 g. Low birth weight increases the risk of neonatal death b
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