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1
Gilbert, Jeffrey S., and Mark J. Nijland. "Sex differences in the developmental origins of hypertension and cardiorenal disease." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 6 (December 2008): R1941—R1952. http://dx.doi.org/10.1152/ajpregu.90724.2008.
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The “developmental origins of health and disease” (DOHAD) hypothesis derives from clinical observations, indicating long-term health consequences for persons of low birth weight. There is growing evidence, primarily from animal studies, that supports the idea that processes put in motion during development that contribute to DOHAD do not necessarily reflect as significantly compromised growth and altered birth weight. Throughout the body of work investigating the DOHAD hypothesis, several themes have emerged; the importance of the placenta, the presence of critical periods of vulnerability, the involvement of the kidney in programmed hypertension, the presence of sex differences in the progression and development of adult diseases. Despite compelling findings in recent studies, much remains unclear regarding the impact of biological sex in the progression of human diseases, in general, and in the mechanisms underlying developmentally programmed responses, in particular. Although the contribution of biological sex to DOHAD is increasingly recognized, it also appears that it may exert distinctly different influences during fetal and adult life. The mechanisms by which biological sex contributes to these processes remains nebulous at present; nevertheless, several intriguing mechanistic candidates have been proposed ranging from differences in the amounts of sex hormones (e.g., estrogens, androgens) to recently described sexual dimorphism in the transcriptome of a variety of mammalian tissues. Recognizing the influences of biological sex or sex hormones on DOHAD uniquely situates research in this area to provide significant insights into the development and progression of many diseases, recent examples of which are the subject of this review.
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Rosenfeld, C. S. "Homage to the ‘H’ in developmental origins of health and disease." Journal of Developmental Origins of Health and Disease 8, no. 1 (August 31, 2016): 8–29. http://dx.doi.org/10.1017/s2040174416000465.
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Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.
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Intapad, Suttira, Norma B. Ojeda, John Henry Dasinger, and Barbara T. Alexander. "Sex Differences in the Developmental Origins of Cardiovascular Disease." Physiology 29, no. 2 (March 2014): 122–32. http://dx.doi.org/10.1152/physiol.00045.2013.
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The Developmental Origins of Health and Disease (DOHaD) proposes that adverse events during early life program an increased risk for cardiovascular disease. Experimental models provide proof of concept but also indicate that insults during early life program sex differences in adult blood pressure and cardiovascular risk. This review will highlight the potential mechanisms that contribute to the etiology of sex differences in the developmental programming of cardiovascular disease.
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Thompson, Michael D., and Brian J. DeBosch. "Maternal Fructose Diet-Induced Developmental Programming." Nutrients 13, no. 9 (September 20, 2021): 3278. http://dx.doi.org/10.3390/nu13093278.
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Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.
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Islam, Ariful. "Prenatal PUFA undernutrition and risk of adult psychiatric disorders." Bangladesh Journal of Medical Science 15, no. 3 (November 3, 2016): 313–19. http://dx.doi.org/10.3329/bjms.v15i3.21775.
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The developing fetus requires significant amounts of poly unsaturated fatty acids (PUFAs/ FAs) to maintain its normal cellular growth and integrity. Suboptimal intrauterine conditions, including poor PUFAs nutrition, during critical periods of growth may lead to lifelong changes in the bodys organs and tissues, thus providing a physiological basis for adultonset disease. However, the Developmental Origins of Health and Disease (DOHaD) model provide a structure to assess the effect of early nutrition and growth on long-term health. Epidemiological statistics shows that when pregnant mothers experienced malnutrition or famine (e.g. the Dutch Hunger Winter of 1944-1945 and the Chinese famine of 1959-1961), the risk of developing metabolic and psychiatric disease in their children increased. The theory of DOHaD is well referenced in the understanding of adult metabolic diseases, but less so in the field of psychiatric disorders. As PUFAs play critical roles in brain development, considerable effort has been taken in elucidating their function in the pathogenesis of neuropsychiatric disorders.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.313-319
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Magalhães, Elizabeth, Maria Méio, and Maria Moreira. "Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 41, no. 04 (April 2019): 256–63. http://dx.doi.org/10.1055/s-0039-1683904.
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AbstractThe hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify the fetal programming. The present nonsystematic review intended to summarize historical and current references that indicated that developmental origins of health and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic pathways. The purpose is to highlight the potential implications of growth factors and adipokines in “developmental programming”, which could interfere in the development by controlling fetal growth patterns. These changes affect the structure and the functional capacity of various organs, including the brain, the kidneys, and the pancreas. These investigations may improve the approach to optimizing antenatal as well as perinatal care aimed to protect newborns against long-term chronic diseases.
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Hsu, Chien-Ning, and You-Lin Tain. "Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target?" Antioxidants 10, no. 2 (February 5, 2021): 247. http://dx.doi.org/10.3390/antiox10020247.
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The cardiovascular system can be programmed by a diversity of early-life insults, leading to cardiovascular disease (CVD) in adulthood. This notion is now termed developmental origins of health and disease (DOHaD). Emerging evidence indicates hydrogen sulfide (H2S), a crucial regulator of cardiovascular homeostasis, plays a pathogenetic role in CVD of developmental origins. Conversely, early H2S-based interventions have proved beneficial in preventing adult-onset CVD in animal studies via reversing programming processes by so-called reprogramming. The focus of this review will first summarize the current knowledge on H2S implicated in cardiovascular programming. This will be followed by supporting evidence for the links between H2S signaling and underlying mechanisms of cardiovascular programming, such as oxidative stress, nitric oxide deficiency, dysregulated nutrient-sensing signals, activation of the renin–angiotensin system, and gut microbiota dysbiosis. It will also provide an overview from animal models regarding how H2S-based reprogramming interventions, such as precursors of H2S and H2S donors, may prevent CVD of developmental origins. A better understanding of cardiovascular programming and recent advances in H2S-based interventions might provide the answers to bring down the global burden of CVD.
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Bianco-Miotto, T., J. M. Craig, Y. P. Gasser, S. J. van Dijk, and S. E. Ozanne. "Epigenetics and DOHaD: from basics to birth and beyond." Journal of Developmental Origins of Health and Disease 8, no. 5 (September 11, 2017): 513–19. http://dx.doi.org/10.1017/s2040174417000733.
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Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.
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Ernst, Jana, Katharina Gert, Frank Bernhard Kraus, Ulrike Elisabeth Rolle-Kampczyk, Martin Wabitsch, Faramarz Dehghani, and Kristina Schaedlich. "Androstenedione changes steroidogenic activity of SGBS cells." Endocrine Connections 9, no. 7 (July 2020): 587–98. http://dx.doi.org/10.1530/ec-19-0549.
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The rapid increase of obesity during the last decades and its future prospects are alarming. Besides the general discussed causes of obesity, the ‘Developmental Origins of Health and Disease’ (DOHaD) hypothesis received more attention in recent years. This hypothesis postulates an adverse influence during early development that programs the unborn child for metabolic dysfunctions later in life. Childhood obesity – an as much increasing problem – can be predisposed by maternal overweight and diabetes. Both, obesity and hyperinsulinemia are major causes of female hyperandrogenemia. As predicted by the DOHaD hypothesis and shown in animal models, developmental androgen excess can lead to metabolic abnormalities in offspring. In this study, we investigated, if androgen exposure adversely affects the adipogenic differentiation of preadipocytes and the endocrine function of adult adipocytes. The human SGBS preadipocyte model was used to affirm the de novo biosynthesis of steroid hormones under normal adipogenesis conditions. Normal adipogenesis was paralleled by an increase of corticosteroids and androgens, whereas estrogen remained at a steady level. Treatment with androstenedione had no effect on SGBS proliferation and differentiation, but adult adipocytes exhibited a significant higher accumulation of triglycerides. Progesterone (up to 2-fold), testosterone (up to 38-fold) and cortisone (up to 1.4-fold) – but not cortisol – were elevated by androstenedione administration in adult adipocytes. Estrogen was not altered. Data suggest that androgen does not negatively influence adipogenic differentiation, but steroidogenic function of SGBS adipocytes.
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Dumesic, Daniel A., Luis R. Hoyos, Gregorio D. Chazenbalk, Rajanigandha Naik, Vasantha Padmanabhan, and David H. Abbott. "Mechanisms of intergenerational transmission of polycystic ovary syndrome." Reproduction 159, no. 1 (January 2020): R1—R13. http://dx.doi.org/10.1530/rep-19-0197.
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Developmental origins of adult disease (DoHAD) refers to critical gestational ages during human fetal development and beyond when the endocrine metabolic status of the mother can permanently program the physiology and/or morphology of the fetus, modifying its susceptibility to disease after birth. The aim of this review is to address how DoHAD plays an important role in the phenotypic expression of polycystic ovary syndrome (PCOS), the most common endocrinopathy of women characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. Clinical studies of PCOS women are integrated with findings from relevant animal models to show how intergenerational transmission of these central components of PCOS are programmed through an altered maternal endocrine–metabolic environment that adversely affects the female fetus and long-term offspring health. Prenatal testosterone treatment in monkeys and sheep have been particularly crucial in our understanding of developmental programming of PCOS because organ system differentiation in these species, as in humans, occurs during fetal life. These animal models, along with altricial rodents, produce permanent PCOS-like phenotypes variably characterized by LH hypersecretion from reduced steroid-negative feedback, hyperandrogenism, ovulatory dysfunction, increased adiposity, impaired glucose-insulin homeostasis and other metabolic abnormalities. The review concludes that DoHAD underlies the phenotypic expression of PCOS through an altered maternal endocrine–metabolic environment that can induce epigenetic modifications of fetal genetic susceptibility to PCOS after birth. It calls for improved maternal endocrine–metabolic health of PCOS women to lower their risks of pregnancy-related complications and to potentially reduce intergenerational susceptibility to PCOS and its metabolic derangements in offspring.
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Guarner-Lans, Verónica, Abril Ramírez-Higuera, María Esther Rubio-Ruiz, Vicente Castrejón-Téllez, María Elena Soto, and Israel Pérez-Torres. "Early Programming of Adult Systemic Essential Hypertension." International Journal of Molecular Sciences 21, no. 4 (February 11, 2020): 1203. http://dx.doi.org/10.3390/ijms21041203.
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Cardiovascular diseases are being included in the study of developmental origins of health and disease (DOHaD) and essential systemic hypertension has also been added to this field. Epigenetic modifications are one of the main mechanisms leading to early programming of disease. Different environmental factors occurring during critical windows in the early stages of life may leave epigenetic cues, which may be involved in the programming of hypertension when individuals reach adulthood. Such environmental factors include pre-term birth, low weight at birth, altered programming of different organs such as the blood vessels and the kidney, and living in disadvantageous conditions in the programming of hypertension. Mechanisms behind these factors that impact on the programming include undernutrition, oxidative stress, inflammation, emotional stress, and changes in the microbiota. These factors and their underlying causes acting at the vascular level will be discussed in this paper. We also explore the establishment of epigenetic cues that may lead to hypertension at the vascular level such as DNA methylation, histone modifications (methylation and acetylation), and the role of microRNAs in the endothelial cells and blood vessel smooth muscle which participate in hypertension. Since epigenetic changes are reversible, the knowledge of this type of markers could be useful in the field of prevention, diagnosis or epigenetic drugs as a therapeutic approach to hypertension.
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Tu’akoi, S., M. H. Vickers, K. Tairea, Y. Y. M. Aung, N. Tamarua-Herman, M. ’Ofanoa, and J. L. Bay. "The significance of DOHaD for Small Island Developing States." Journal of Developmental Origins of Health and Disease 9, no. 5 (July 12, 2018): 487–91. http://dx.doi.org/10.1017/s2040174418000466.
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AbstractSmall Island Developing States (SIDS) are island nations that experience specific social, economic and environmental vulnerabilities associated with small populations, isolation and limited resources. Globally, SIDS exhibit exceptionally high rates of non-communicable disease (NCD) risk and incidence. Despite this, there is a lack of context-specific research within SIDS focused on life course approaches to NCD prevention, particularly the impact of the early-life environment on later disease risk as defined by the Developmental Origins of Health and Disease (DOHaD) framework. Given that globalization has contributed to significant nutritional transitions in these populations, the DOHaD paradigm is highly relevant. SIDS in the Pacific region have the highest rates of NCD risk and incidence globally. Transitions from traditional foods grown locally to reliance on importation of Western-style processed foods high in fat and sugar are common. The Cook Islands is one Pacific SIDS that reports this transition, alongside rising overweight/obesity rates, currently 91%/72%, in the adult population. However, research on early-life NCD prevention within this context, as in many low- and middle-income countries, is scarce. Although traditional research emphasizes the need for large sample sizes, this is rarely possible in the smaller SIDS. In these vulnerable, high priority countries, consideration should be given to utilizing ‘small’ sample sizes that encompass a high proportion of the total population. This may enable contextually relevant research, crucial to inform NCD prevention strategies that can contribute to improving health and well-being for these at-risk communities.
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Fleming, Tom P., Congshan Sun, Oleg Denisenko, Laura Caetano, Anan Aljahdali, Joanna M. Gould, and Pooja Khurana. "Environmental Exposures around Conception: Developmental Pathways Leading to Lifetime Disease Risk." International Journal of Environmental Research and Public Health 18, no. 17 (September 6, 2021): 9380. http://dx.doi.org/10.3390/ijerph18179380.
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Environment around conception can influence the developmental programme with lasting effects on gestational and postnatal phenotype and with consequences for adult health and disease risk. Peri-conception exposure comprises a crucial part of the ‘Developmental Origins of Health and Disease’ (DOHaD) concept. In this review, we consider the effects of maternal undernutrition experienced during the peri-conception period in select human models and in a mouse experimental model of protein restriction. Human datasets indicate that macronutrient deprivation around conception affect the epigenome, with enduring effects on cardiometabolic and neurological health. The mouse model, comprising maternal low protein diet exclusively during the peri-conception period, has revealed a stepwise progression in altered developmental programming following induction through maternal metabolite deficiency. This progression includes differential effects in extra-embryonic and embryonic cell lineages and tissues, leading to maladaptation in the growth trajectory and increased chronic disease comorbidities. The timeline embraces an array of mechanisms across nutrient sensing and signalling, cellular, metabolic, epigenetic and physiological processes with a coordinating role for mTORC1 signalling proposed. Early embryos appear active participants in environmental sensing to optimise the developmental programme for survival but with the trade-off of later disease. Similar adverse health outcomes may derive from other peri-conception environmental experiences, including maternal overnutrition, micronutrient availability, pollutant exposure and assisted reproductive treatments (ART) and support the need for preconception health before pregnancy.
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Behere, Rishikesh V., Gopikrishna Deshpande, Souvik Kumar Bandyopadhyay, and Chittaranjan Yajnik. "Maternal vitamin B12, folate during pregnancy and neurocognitive outcomes in young adults of the Pune Maternal Nutrition Study (PMNS) prospective birth cohort: study protocol." BMJ Open 11, no. 9 (September 2021): e046242. http://dx.doi.org/10.1136/bmjopen-2020-046242.
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IntroductionThe Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that intrauterine and early life exposures significantly influence fetal development and risk for disease in later life. Evidence from prospective birth cohorts suggests a role for maternal B12 and folate in influencing neurocognitive outcomes in the offspring. In the Indian setting, B12 deficiency is common during the pregnancy while rates of folate deficiency are lower. The long-term influences of maternal nutrition during the pregnancy on adult neurocognitive outcomes have not been examined. The Pune Maternal Nutrition Study (PMNS) is a preconceptional birth cohort into its 24th year and is considered a unique resource to study the DOHaD hypothesis. We found an association between maternal B12 status in pregnancy and child’s neurocognitive status at 9 years of age. We now plan to assess neurocognitive function and MRI measurements of brain structural–functional connectivity at young adult age to study its association with maternal nutritional exposures during the pregnancy.Methods and analysisAs part of ongoing prospective follow-up in young adults of the PMNS at the Diabetes Unit, KEM Hospital Research Center, Pune India, the following measurements will be done: neurocognitive performance (Standardised Tests of Intelligence, Verbal and Visual Memory, Attention and Executive Functions), temperament (Adult Temperament Questionnaire), psychopathology (Brief Symptom Inventory and Clinical Interview on Mini Neuropsychiatric Interview 7.0). Brain MRI for structural T1, resting-state functional connectivity and diffusion tensor imaging will be performed on a subset of the cohort (selected based on exposure to a lower or higher maternal B12 status at 18 weeks of pregnancy).Ethics and disseminationThe study is approved by Institutional ethics committee of KEM Hospital Research Center, Pune. The results will be shared at national and international scientific conferences and published in peer-reviewed scientific journals.Trial registration numberNCT03096028
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Fall, Caroline H. D., and Kalyanaraman Kumaran. "Metabolic programming in early life in humans." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1770 (February 25, 2019): 20180123. http://dx.doi.org/10.1098/rstb.2018.0123.
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An association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently ‘programmes’ organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomized trials of maternal nutritional interventions during pregnancy have so far had limited follow-up of the offspring. Moreover, interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high-risk individuals in mid-life, DOHaD concepts offer a ‘primordial’ preventive strategy to reduce disease in future generations by improving fetal and infant development. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.
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Haugen, A. C., T. T. Schug, G. Collman, and J. J. Heindel. "Evolution of DOHaD: the impact of environmental health sciences." Journal of Developmental Origins of Health and Disease 6, no. 2 (December 4, 2014): 55–64. http://dx.doi.org/10.1017/s2040174414000580.
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Environmental exposures have a significant influence on the chronic health conditions plaguing children and adults. Although the Developmental Origins of Health and Disease (DOHaD) paradigm historically has focused on nutrition, an expanding body of research specifically communicates the effects of chemical exposures on early-life development and the propagation of non-communicable disease across the lifespan. This paper provides an overview of 20 years of research efforts aimed at identifying critical windows of susceptibility to environmental exposures and the signaling changes and epigenetic influences associated with disease progression. DOHaD grants funded by the National Institute of Environmental Health Sciences (NIEHS) in 1991, 2001 and 2011 are identified by grant-analysis software, and each portfolio is analyzed for exposures, disease endpoints, windows of exposure, study design and impact on the field based on publication data. Results show that the 1991 and 2001 portfolios comprised metals, PCBs and air pollutants; however, by 2011, the portfolio has evolved to include or expand the variety of endocrine disruptors, pesticides/persistent organic pollutants and metals. An assortment of brain-health endpoints is most targeted across the portfolios, whereas reproduction and cancer increase steadily over the same time period, and new endpoints like obesity are introduced by 2011. With mounting evidence connecting early-life exposures to later-life disease, we conclude that it is critical to expand the original DOHaD concept to include environmental chemical exposures, and to continue a research agenda that emphasizes defining sensitive windows of exposure and the mechanisms that cause disease.
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Rosenfeld, Cheryl S., Angela B. Javurek, Sarah A. Johnson, Zhentian Lei, Lloyd W. Sumner, and Rex A. Hess. "Seminal fluid metabolome and epididymal changes after antibiotic treatment in mice." Reproduction 156, no. 1 (July 2018): 1–10. http://dx.doi.org/10.1530/rep-18-0072.
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Paternal environment can induce detrimental developmental origins of health and disease (DOHaD) effects in resulting offspring and even future descendants. Such paternal-induced DOHaD effects might originate from alterations in a possible seminal fluid microbiome (SFM) and composite metabolome. Seminal vesicles secrete a slightly basic product enriched with fructose and other carbohydrates, providing an ideal habitat for microorganisms. Past studies confirm the existence of a SFM that is influenced by genetic and nutritional status. Herein, we sought to determine whether treatment of male mice with a combination of antibiotics designed to target SFM induces metabolic alterations in seminal vesicle gland secretions (seminal fluid) and histopathological changes in testes and epididymides. Adult (10- to 12-week-old) National Institutes of Health (NIH) Swiss males (n = 10 per group) were treated with Clindamycin 0.06 mg/kg day, Unasyn (ampicillin/sulbactam) 40 mg/kg day and Baytril (enrofloxacin) 50 mg/kg day designed to target the primary bacteria within the SFM or saline vehicle alone. Fourteen-day antibiotic treatment of males induced metabolomic changes in seminal vesicles with inosine, xanthine and l-glutamic acid decreased but d-fructose increased in glandular secretions. While spermatogenesis was not affected in treated males, increased number of epididymal tubules showed cribriform growth in this group (7 antibiotic-treated males: 3 saline control males; P = 0.01). Antibiotic-treated males showed more severe cribriform cysts. Current findings suggest antibiotic treatment of male mice results in seminal fluid metabolome and epididymal histopathological alterations. It remains to be determined whether such changes compromise male reproductive function or lead to DOHaD effects in resulting offspring.
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Gotoh, Takafumi. "Potential of the application of epigenetics in animal production." Animal Production Science 55, no. 2 (2015): 145. http://dx.doi.org/10.1071/an14467.
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Our many current environmental challenges, including worldwide abnormal weather, global warming, and pollution, necessitate a new and innovative strategy for animal production for the next generation. This strategy should incorporate not only higher-efficiency production, but also advanced biological concepts and multi-functional agricultural techniques, into environmentally friendly systems. Recent research has discovered a unique phenomenon referred to as ‘foetal and neonatal programming’, which is based on ‘the developmental origins of health and disease (DOHaD)’ concept. These studies have shown that alterations in foetal and early postnatal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology and metabolism of affected animals during adult life. Ruminants fill an important ecological niche that capitalises on the symbiotic relationship between fibre-fermenting ruminal microbes and the mammalian demand for usable nutrients. The timing of the perturbation in maternal nutrient availability plays an important role in determining the effect that the foetal and neonatal programming will have on the developing placenta or foetus and offspring performance. Developmental programming through nutritional manipulations may help the ruminant, as an effective grass–protein converter, fulfil its production potential.
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El Hajj, Nady, Eberhard Schneider, Harald Lehnen, and Thomas Haaf. "Epigenetics and life-long consequences of an adverse nutritional and diabetic intrauterine environment." REPRODUCTION 148, no. 6 (December 2014): R111—R120. http://dx.doi.org/10.1530/rep-14-0334.
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The phenomenon that adverse environmental exposures in early life are associated with increased susceptibilities for many adult, particularly metabolic diseases, is now referred to as ‘developmental origins of health and disease (DOHAD)’ or ‘Barker’ hypothesis. Fetal overnutrition and undernutrition have similar long-lasting effects on the setting of the neuroendocrine control systems, energy homeostasis, and metabolism, leading to life-long increased morbidity. There are sensitive time windows during early development, where environmental cues can program persistent epigenetic modifications which are generally assumed to mediate these gene–environment interactions. Most of our current knowledge on fetal programing comes from animal models and epidemiological studies in humans, in particular the Dutch famine birth cohort. In industrialized countries, there is more concern about adverse long-term consequences of fetal overnutrition, i.e. by exposure to gestational diabetes mellitus and/or maternal obesity which affect 10–20% of pregnancies. Epigenetic changes due to maternal diabetes/obesity may predispose the offspring to develop metabolic disease later in life and, thus, transmit the adverse environmental exposure to the next generation. This vicious cycle could contribute significantly to the worldwide metabolic disease epidemics. In this review article, we focus on the epigenetics of an adverse intrauterine environment, in particular gestational diabetes, and its implications for the prevention of complex disease.
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Klein, Caroline Peres, Juliana Bender Hoppe, André Brum Saccomori, Bernardo Gindri dos Santos, Pauline Maciel August, Isadora Peres Klein, Mariana Scortegagna Crestani, et al. "Protective effect of maternal exercise against amyloid-β neurotoxicity in the male rat offspring’s cerebellum." Journal of Developmental Origins of Health and Disease 11, no. 5 (June 23, 2020): 521–32. http://dx.doi.org/10.1017/s2040174420000562.
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AbstractThe Developmental Origins of Health and Disease (DOHaD) states that intrauterine maternal environment influences postnatal life by programming offspring’s metabolism. Intrauterine milieu induced by exercise during pregnancy promotes long-lasting benefits to the offspring’s health and seems to offer some resistance against chronic diseases in adult life. Alzheimer’s disease is a public health concern with limited treatment options. In the present study, we assessed the potential of maternal exercise during pregnancy in long-term programming of young adult male rat offspring’s cerebellar metabolism in conferring neuroprotection against amyloid-β (Aβ) neurotoxicity. Female Wistar rats were submitted to a swimming protocol 1 week prior mating and throughout pregnancy (five sessions/a week lasting 30 min). Aβ oligomers were infused bilaterally in the brain ventricles of 60-day-old male offspring. Fourteen days after surgery, we measured parameters related to redox state, mitochondrial function, and the immunocontent of proteins related to synaptic function. We found that maternal exercise during pregnancy attenuated several parameters in the offspring’s male rat cerebellum, such as the reactive species rise, the increase of inducible nitric oxide synthase immunocontent and tau phosphorylation induced by Aβ oligomers, increased mitochondrial fission indicated by dynamin-related protein 1 (DRP1), and protein oxidation identified by carbonylation. Strikingly, we find that maternal exercise promotes changes in the rat offspring’s cerebellum that are still evident in young adult life. These favorable neurochemical changes in offspring’s cerebellum induced by maternal exercise may contribute to a protective phenotype against Aβ-induced neurotoxicity in young adult male rat offspring.
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Zeng, Zhijun, Karolin F. Meyer, Khosbayar Lkhagvadorj, Wierd Kooistra, Marjan Reinders-Luinge, Xijin Xu, Xia Huo, Juan Song, Torsten Plösch, and Machteld N. Hylkema. "Prenatal smoke effect on mouse offspring Igf1 promoter methylation from fetal stage to adulthood is organ and sex specific." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 3 (March 1, 2020): L549—L561. http://dx.doi.org/10.1152/ajplung.00293.2019.
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Prenatal smoke exposure (PSE) is associated with reduced birth weight, impaired fetal development, and increased risk for diseases later in life. Changes in DNA methylation may be involved, as multiple large-scale epigenome-wide association studies showed that PSE is robustly associated with DNA methylation changes in blood among offspring in early life. Insulin-like growth factor-1 (IGF1) is important in growth, differentiation, and repair processes after injury. However, no studies investigated the organ-specific persistence of PSE-induced methylation change of Igf1 into adulthood. Based on our previous studies on the PSE effect on Igf1 promoter methylation in fetal and neonatal mouse offspring, we now have extended our studies to adulthood. Our data show that basal Igf1 promoter methylation generally increased in the lung but decreased in the liver (except for 2 persistent CpG sites in both organs) across three different developmental stages. PSE changed Igf1 promoter methylation in all three developmental stages, which was organ and sex specific. The PSE effect was less pronounced in adult offspring compared with the fetal and neonatal stages. In addition, the PSE effect in the adult stage was more pronounced in the lung compared with the liver. For most CpG sites, an inverse correlation was found for promoter methylation and mRNA expression when the data of all three stages were combined. This was more prominent in the liver. Our findings provide additional evidence for sex- and organ-dependent prenatal programming, which supports the developmental origins of health and disease (DOHaD) hypothesis.
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Barker, Mary, Caroline H. Fall, Clive Osmond, Cyrus Cooper, Tom P. Fleming, Kent L. Thornburg, and Graham J. Burton. "David James Purslove Barker. 29 June 1938—27 August 2013." Biographical Memoirs of Fellows of the Royal Society 67 (August 7, 2019): 29–57. http://dx.doi.org/10.1098/rsbm.2019.0021.
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Professor David James Purslove Barker was a physician and one of the most influential medical scientists of our time. His fetal programming hypothesis (known as the Barker Hypothesis) transformed thinking about what causes chronic diseases that are the scourge of modern society: cancer, cardiovascular disease and diabetes. The Barker Hypothesis proposed that the environment of the fetus and infant determined by maternal nutrition and exposure to infection subsequently predisposes the pathologies of later life. He challenged the idea that chronic diseases result from a combination of bad genes and unhealthy adult lifestyle. The environment of the fetus and infant, he suggested, permanently set or ‘programmed’ the body's metabolism and growth, and thereby pathologies of old age. His initially controversial, but now widely accepted, ideas have produced an explosion of research worldwide into the complex processes of nutrition and growth during intrauterine and early post-natal life and how these cause adult diseases. His discoveries created a new field of research, developmental origins of health and disease (DOHaD), influencing global scientific thinking. David believed that ‘the poorer health of people in lower socio-economic groups or living in impoverished places was linked to past and present neglect of the welfare of mothers and babies’. Tackling the epidemics of diabetes and heart disease in the Western world and in developing countries would require, he said, a shift in focus to prioritize the health and nutrition of adolescent girls, pregnant women and infants. This focus has subsequently been enshrined in global health policies and priorities.
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Salinas, Irving, Niharika Sinha, and Aritro Sen. "Androgen-induced epigenetic modulations in the ovary." Journal of Endocrinology 249, no. 3 (June 2021): R53—R64. http://dx.doi.org/10.1530/joe-20-0578.
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In recent years, androgens have emerged as critical regulators of female reproduction and women’s health in general. While high levels of androgens in women are associated with polycystic ovary syndrome (PCOS), recent evidence suggests that a certain amount of direct androgen action through androgen receptor is also essential for normal ovarian function. Moreover, prenatal androgen exposure has been reported to cause developmental reprogramming of the fetus that manifests into adult pathologies, supporting the Developmental Origins of Health and Disease (DOHaD) hypothesis. Therefore, it has become imperative to understand the underlying mechanism of androgen actions and its downstream effects under normal and pathophysiological conditions. Over the years, there has been a lot of studies on androgen receptor function as a transcriptional regulator in the nucleus as well as androgen-induced rapid extra-nuclear signaling. Conversely, new evidence suggests that androgen actions may also be mediated through epigenetic modulation involving both the nuclear and extra-nuclear androgen signaling. This review focuses on androgen-induced epigenetic modifications in female reproduction, specifically in the ovary, and discusses emerging concepts, latest perceptions, and highlight the areas that need further investigation.
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Zheng, Jia, Xinhua Xiao, Qian Zhang, and Miao Yu. "DNA methylation: the pivotal interaction between early-life nutrition and glucose metabolism in later life." British Journal of Nutrition 112, no. 11 (October 20, 2014): 1850–57. http://dx.doi.org/10.1017/s0007114514002827.
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Traditionally, it has been widely acknowledged that genes together with adult lifestyle factors determine the risk of developing some metabolic diseases such as insulin resistance, obesity and diabetes mellitus in later life. However, there is now substantial evidence that prenatal and early-postnatal nutrition play a critical role in determining susceptibility to these diseases in later life. Maternal nutrition has historically been a key determinant for offspring health, and gestation is the critical time window that can affect the growth and development of offspring. The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that exposures during early life play a critical role in determining the risk of developing metabolic diseases in adulthood. Currently, there are substantial epidemiological studies and experimental animal models that have demonstrated that nutritional disturbances during the critical periods of early-life development can significantly have an impact on the predisposition to developing some metabolic diseases in later life. The hypothesis that epigenetic mechanisms may link imbalanced early-life nutrition with altered disease risk has been widely accepted in recent years. Epigenetics can be defined as the study of heritable changes in gene expression that do not involve alterations in the DNA sequence. Epigenetic processes play a significant role in regulating tissue-specific gene expression, and hence alterations in these processes may induce long-term changes in gene function and metabolism that persist throughout the life course. The present review focuses on how nutrition in early life can alter the epigenome, produce different phenotypes and alter disease susceptibilities, especially for impaired glucose metabolism.
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Dal Magro, B. M., V. Stone, C. P. Klein, R. M. Maurmann, A. B. Saccomori, B. G. dos Santos, P. M. August, et al. "Developmental programming: intrauterine caloric restriction promotes upregulation of mitochondrial sirtuin with mild effects on oxidative parameters in the ovaries and testes of offspring." Reproduction, Fertility and Development 32, no. 8 (2020): 763. http://dx.doi.org/10.1071/rd19384.
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According to the developmental origins of health and disease (DOHaD) hypothesis, changes in the maternal environment are known to reprogram the metabolic response of offspring. Known for its redox modulation, caloric restriction extends the lifespan of some species, which contributes to diminished cellular damage. Little is known about the effects of gestational caloric restriction, in terms of antioxidant parameters and molecular mechanisms of action, on the reproductive organs of offspring. This study assessed the effects of moderate (20%) caloric restriction on redox status parameters, molecular expression of sirtuin (SIRT) 1 and SIRT3 and histopathological markers in the ovaries and testes of adult rats that were subjected to gestational caloric restriction. Although enzyme activity was increased, ovaries from female pups contained high levels of oxidants, whereas testes from male pups had decreased antioxidant enzyme defences, as evidenced by diminished glyoxalase I activity and reduced glutathione content. Expression of SIRT3, a deacetylase enzyme related to cellular bioenergetics, was increased in both ovaries and testes. Previous studies have suggested that, in ovaries, diminished antioxidant metabolism can lead to premature ovarian failure. Unfortunately, there is little information regarding the redox profile in the testis. This study is the first to assess the redox network in both ovaries and testes, suggesting that, although intrauterine caloric restriction improves molecular mechanisms, it has a negative effect on the antioxidant network and redox status of reproductive organs of young adult rats.
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Zhou, Liyuan, Lin Kang, Xinhua Xiao, Lijing Jia, Qian Zhang, and Mingqun Deng. "“Gut Microbiota-Circadian Clock Axis” in Deciphering the Mechanism Linking Early-Life Nutritional Environment and Abnormal Glucose Metabolism." International Journal of Endocrinology 2019 (August 27, 2019): 1–9. http://dx.doi.org/10.1155/2019/5893028.
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The prevalence of diabetes mellitus (DM) has been increasing dramatically worldwide, but the pathogenesis is still unknown. A growing amount of evidence suggests that an abnormal developmental environment in early life increases the risk of developing metabolic diseases in adult life, which is referred to as the “metabolic memory” and the Developmental Origins of Health and Disease (DOHaD) hypothesis. The mechanism of “metabolic memory” has become a hot topic in the field of DM worldwide and could be a key to understanding the pathogenesis of DM. In recent years, several large cohort studies have shown that shift workers have a higher risk of developing type 2 diabetes mellitus (T2DM) and worse control of blood glucose levels. Furthermore, a maternal high-fat diet could lead to metabolic disorders and abnormal expression of clock genes and clock-controlled genes in offspring. Thus, disorders of circadian rhythm might play a pivotal role in glucose metabolic disturbances, especially in terms of early adverse nutritional environments and the development of metabolic diseases in later life. In addition, as a peripheral clock, the gut microbiota has its own circadian rhythm that fluctuates with periodic feeding and has been widely recognized for its significant role in metabolism. In light of the important roles of the gut microbiota and circadian clock in metabolic health and their interconnected regulatory relationship, we propose that the “gut microbiota-circadian clock axis” might be a novel and crucial mechanism to decipher “metabolic memory.” The “gut microbiota-circadian clock axis” is expected to facilitate the future development of a novel target for the prevention and intervention of diabetes during the early stage of life.
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Csaba, György. "Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State." Current Genomics 20, no. 6 (January 2, 2019): 409–18. http://dx.doi.org/10.2174/1389202920666191116113524.
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Hormonal imprinting takes place perinatally at the first encounter between the developing hormone receptor and its target hormone. This process is needed for the normal function of the receptor- hormone pair and its effect is life-long. However, in this critical period, when the developmental window is open, related molecules (members of the same hormone family, synthetic hormones and hormone-like molecules, endocrine disruptors) also can be bound by the receptor, causing life-long faulty imprinting. In this case, the receptors’ binding capacity changes and alterations are caused at adult age in the sexual and behavioral sphere, in the brain and bones, inclination to diseases and manifestation of diseases, etc. Hereby, faulty hormonal imprinting is the basis of metabolic and immunological imprinting as well as the developmental origin of health and disease (DOHaD). Although the perinatal period is the most critical for faulty imprinting, there are other critical periods as weaning and adolescence, when the original imprinting can be modified or new imprintings develop. Hormonal imprinting is an epigenetic process, without changing the base sequence of DNA, it is inherited in the cell line of the imprinted cells and also transgenerationally (up to 1000 generations in unicellulars and up to the 3rd generation in mammals are justified). Considering the enormously growing number and amount of faulty imprinters (endocrine disruptors) and the hereditary character of faulty imprinting, this latter is threatening the whole human endocrine system.
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Singer, Dominique. "Aktuelle Aspekte der perinatologischen Versorgung." Zeitschrift für Geburtshilfe und Neonatologie 224, no. 01 (February 2020): 5. http://dx.doi.org/10.1055/a-0969-3480.
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Liebe Leserinnen und Leser,in den soeben angebrochenen „20er Jahren“ des 21. Jahrhunderts werden Fragen der perinatologischen Versorgung vermutlich eine zunehmende Rolle spielen: nicht nur wegen der strukturellen und personellen Engpässe, mit denen sich Perinatalzentren hierzulande allerorten konfrontiert sehen; sondern auch wegen der sich mehrenden Erkenntnisse zu den „Developmental Origins of Adult Disease“ (DOAD), die – einmal im gesellschaftlichen Bewusstsein angekommen – diesem Lebensabschnitt hoffentlich mehr politisches Gewicht verleihen werden. In der vorliegenden Ausgabe der Zeitschrift für Geburtshilfe und Neonatologie (ZGN) stehen unter anderem Aspekte der perinatologischen Versorgung – sowohl seitens der Mütter als auch seitens der Neu- und Frühgeborenen – im Fokus.
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Ruggeri, Elena, Saúl Lira-Albarrán, Edward J. Grow, Xiaowei Liu, Royce Harner, Emin Maltepe, Miguel Ramalho-Santos, Annemarie Donjacour, and Paolo Rinaudo. "Sex-specific epigenetic profile of inner cell mass of mice conceived in vivo or by IVF." Molecular Human Reproduction 26, no. 11 (October 3, 2020): 866–78. http://dx.doi.org/10.1093/molehr/gaaa064.
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Abstract The preimplantation stage of development is exquisitely sensitive to environmental stresses, and changes occurring during this developmental phase may have long-term health effects. Animal studies indicate that IVF offspring display metabolic alterations, including hypertension, glucose intolerance and cardiac hypertrophy, often in a sexual dimorphic fashion. The detailed nature of epigenetic changes following in-vitro culture is, however, unknown. This study was performed to evaluate the epigenetic (using whole-genome bisulfite sequencing (WGBS) and assay for transposase-accessible chromatin using sequencing (ATAC-seq)) and transcriptomic changes (using RNA-seq) occurring in the inner cell mass (ICM) of male or female mouse embryos generated in vivo or by IVF. We found that the ICM of IVF embryos, compared to the in-vivo ICM, differed in 3% of differentially methylated regions (DMRs), of which 0.1% were located on CpG islands. ATAC-seq revealed that 293 regions were more accessible and 101 were less accessible in IVF embryos, while RNA-seq revealed that 21 genes were differentially regulated in IVF embryos. Functional enrichment analysis revealed that stress signalling (STAT and NF-kB signalling), developmental processes and cardiac hypertrophy signalling showed consistent changes in WGBS and ATAC-seq platforms. In contrast, male and female embryos showed minimal changes. Male ICM had an increased number of significantly hyper-methylated DMRs, while only 27 regions showed different chromatin accessibility and only one gene was differentially expressed. In summary, this study provides the first comprehensive analysis of DNA methylation, chromatin accessibility and RNA expression changes induced by IVF in male and female ICMs. This dataset can be of value to all researchers interested in the developmental origin of health and disease (DOHaD) hypothesis and might lead to a better understanding of how early embryonic manipulation may affect adult health.
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Heindel, Jerrold J., John Balbus, Linda Birnbaum, Marie Noel Brune-Drisse, Philippe Grandjean, Kimberly Gray, Philip J. Landrigan, et al. "Developmental Origins of Health and Disease: Integrating Environmental Influences." Endocrinology 156, no. 10 (July 21, 2015): 3416–21. http://dx.doi.org/10.1210/en.2015-1394.
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Abstract There are now robust data supporting the Developmental Origins of Health and Disease (DOHaD) paradigm. This includes human and animal data focusing on nutrition or environmental chemicals during development. However, the term DOHaD has not been generally accepted as the official term to be used when one is concerned with understanding the pathophysiological basis for how environmental influences acting during early development influence the risk of later noncommunicable diseases. Similarly, there is no global research or public health program built around the DOHaD paradigm that encompasses all aspects of environment. To better inform the global health efforts aimed at addressing the growing epidemic of chronic noncommunicable diseases of environmental origin, we propose a two-pronged approach: first, to make it clear that the current concept of DOHaD comprehensively includes a range of environmental factors and their relevance to disease occurrence not just throughout the life span but potentially across several generations; and second, to initiate the discussion of how adoption of DOHaD can promote a more realistic, accurate, and integrative approach to understanding environmental disruption of developmental programming and better inform clinical and policy interventions. (Endocrinology 156: 3416–3421, 2015)
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Silveira, Patrícia P., André K. Portella, Marcelo Z. Goldani, and Marco A. Barbieri. "Developmental origins of health and disease (DOHaD)." Jornal de Pediatria 83, no. 6 (November 30, 2007): 494–504. http://dx.doi.org/10.2223/jped.1728.
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Lecoutre, Simon, Barbara Deracinois, Christine Laborie, Delphine Eberlé, Céline Guinez, Polina E. Panchenko, Jean Lesage, et al. "Depot- and sex-specific effects of maternal obesity in offspring’s adipose tissue." Journal of Endocrinology 230, no. 1 (July 2016): 39–53. http://dx.doi.org/10.1530/joe-16-0037.
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According to the Developmental Origin of Health and Disease (DOHaD) concept, alterations of nutrient supply in the fetus or neonate result in long-term programming of individual body weight (BW) setpoint. In particular, maternal obesity, excessive nutrition, and accelerated growth in neonates have been shown to sensitize offspring to obesity. The white adipose tissue may represent a prime target of metabolic programming induced by maternal obesity. In order to unravel the underlying mechanisms, we have developed a rat model of maternal obesity using a high-fat (HF) diet (containing 60% lipids) before and during gestation and lactation. At birth, newborns from obese dams (called HF) were normotrophs. However, HF neonates exhibited a rapid weight gain during lactation, a key period of adipose tissue development in rodents. In males, increased BW at weaning (+30%) persists until 3months of age. Nine-month-old HF male offspring was normoglycemic but showed mild glucose intolerance, hyperinsulinemia, and hypercorticosteronemia. Despite no difference in BW and energy intake, HF adult male offspring was predisposed to fat accumulation showing increased visceral (gonadal and perirenal) depots weights and hyperleptinemia. However, only perirenal adipose tissue depot exhibited marked adipocyte hypertrophy and hyperplasia with elevated lipogenic (i.e. sterol-regulated element binding protein 1 (Srebp1), fatty acid synthase (Fas), and leptin) and diminished adipogenic (i.e. peroxisome proliferator-activated receptor gamma (Pparγ), 11β-hydroxysteroid dehydrogenase type 1 (11β-Hds1)) mRNA levels. By contrast, very few metabolic variations were observed in HF female offspring. Thus, maternal obesity and accelerated growth during lactation program offspring for higher adiposity via transcriptional alterations of visceral adipose tissue in a depot- and sex-specific manner.
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Gluckman, P. D., M. A. Hanson, and T. Buklijas. "A conceptual framework for the developmental origins of health and disease." Journal of Developmental Origins of Health and Disease 1, no. 1 (December 9, 2009): 6–18. http://dx.doi.org/10.1017/s2040174409990171.
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In the last decades, the developmental origins of health and disease (DOHaD) have emerged as a vigorous field combining experimental, clinical, epidemiological and public health research. Its goal is to understand how events in early life shape later morbidity risk, especially of non-communicable chronic diseases. As these diseases become the major cause of morbidity and mortality worldwide, research arising from DOHaD is likely to gain significance to public health and economic development. But action may be hindered by the lack of a firm mechanistic explanation and of a conceptual basis, especially regarding the evolutionary significance of the DOHaD phenomenon. In this article, we provide a succinct historical review of the research into the relationship between development and later disease, consider the evolutionary and developmental significance and discuss the underlying mechanisms of the DOHaD phenomenon. DOHaD should be viewed as a part of a broader biological mechanism of plasticity by which organisms, in response to cues such as nutrition or hormones, adapt their phenotype to environment. These responses may be divided into those for immediate benefit and those aimed at prediction of a future environment: disease occurs in the mismatch between predicted and realized future. The likely mechanisms that enable plasticity involve epigenetic processes, affecting the expression of genes associated with regulatory pathways. There is now evidence that epigenetic marks may be inherited and so contribute to non-genomic heritable disease risk. We end by discussing the global significance of the DOHaD phenomenon and its potential applications for public health purposes.
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Lacagnina, Salvatore. "The Developmental Origins of Health and Disease (DOHaD)." American Journal of Lifestyle Medicine 14, no. 1 (October 11, 2019): 47–50. http://dx.doi.org/10.1177/1559827619879694.
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For years many have believed that genetic heritage defined one’s destiny, if an individual would grow to be healthy, or if he or she would suffer from chronic illness or cancer. Recent scientific evidence and the field of epigenetics has proven this to be untrue. Certainly, the DNA sequence and the genetic code are fixed; but the field of epigenetics has shown how methylation and other chemical modifications of the genome directly influence the production of proteins that can alter the phenotype of an organism. This article will lay out the supporting research, the details on how the internal and external environments influence genetic function, and will allow the reader to develop an action plan necessary to influence the genetic code, with the goal of then moving the individual toward optimal health. These research details will enable health care professionals in every field of medicine to work with patients on positively influencing the genetic output in order to improve the quality of life and longevity.
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SATA, Fumihiro. "Developmental Origins of Health and Disease (DOHaD) and Epidemiology." Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 71, no. 1 (2016): 41–46. http://dx.doi.org/10.1265/jjh.71.41.
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Fukunaga, Hisanori. "Mitochondrial DNA Copy Number and Developmental Origins of Health and Disease (DOHaD)." International Journal of Molecular Sciences 22, no. 12 (June 21, 2021): 6634. http://dx.doi.org/10.3390/ijms22126634.
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Mitochondrial dysfunction is known to contribute to mitochondrial diseases, as well as to a variety of aging-based pathologies. Mitochondria have their own genomes (mitochondrial DNA (mtDNA)) and the abnormalities, such as point mutations, deletions, and copy number variations, are involved in mitochondrial dysfunction. In recent years, several epidemiological studies and animal experiments have supported the Developmental Origin of Health and Disease (DOHaD) theory, which states that the environment during fetal life influences the predisposition to disease and the risk of morbidity in adulthood. Mitochondria play a central role in energy production, as well as in various cellular functions, such as apoptosis, lipid metabolism, and calcium metabolism. In terms of the DOHaD theory, mtDNA copy number may be a mediator of health and disease. This paper summarizes the results of recent epidemiological studies on the relationship between environmental factors and mtDNA copy number during pregnancy from the perspective of DOHaD theory. The results of these studies suggest a hypothesis that mtDNA copy number may reflect environmental influences during fetal life and possibly serve as a surrogate marker of health risks in adulthood.
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Kajee, N., E. Sobngwi, A. Macnab, and A. S. Daar. "The Developmental Origins of Health and Disease and Sustainable Development Goals: mapping the way forward." Journal of Developmental Origins of Health and Disease 9, no. 1 (August 14, 2017): 5–9. http://dx.doi.org/10.1017/s2040174417000630.
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In this paper, meant to stimulate debate, we argue that there is considerable benefit in approaching together the implementation of two seemingly separate recent developments. First, on the global development agenda, we have the United Nations General Assembly’s 2015 finalized list of 17 Sustainable Development Goals (SDGs). Several of the SDGs are related to health. Second, the field of Developmental Origins of Health and Disease (DOHaD) has garnered enough compelling evidence demonstrating that early exposures in life affect not only future health, but that the effects of that exposure can be transmitted across generations – necessitating that we begin to focus on prevention. We argue that implementing the SDGs and DOHaD together will be beneficial in several ways; and will require attending to multiple, complex and multidisciplinary approaches as we reach the point of translating science to policy to impact. Here, we begin by providing the context for our work and making the case for a mutually reinforcing, synergistic approach to implementing SDGs and DOHaD, particularly in Africa. To do this, we initiate discussion via an early mapping of some of the overlapping considerations between SDGs and DOHaD.
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Mohammed, N., R. Nuruddin, and A. Shoukat Ali. "Pakistan Developmental Origins of Health and Disease (DOHaD) Society: addressing the ‘DO’ component of DOHaD." Journal of Developmental Origins of Health and Disease 10, no. 02 (September 3, 2018): 141–43. http://dx.doi.org/10.1017/s2040174418000636.
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AbstractAdverse intrauterine environment could serve as an important stimulus for postnatal altered health status and for increased susceptibility to long-term non-communicable diseases (NCDs). The notion is now recognized as the Developmental Origins of Health and Disease (DOHaD), which was first proposed by Sir David Barker. Since then, several scientific disciplines have strived to measure the magnitude of the early fetal programming and later risk of diseases. Pakistan, with striking figures of morbidity and mortality from NCDs, is currently tackling with double burden of diseases and requires planned efforts to counteract the threat of NCDs. Considering the growing needs and available evidences, Pakistan DOHaD Society was officially instigated in September 2016. The Society aims to explicitly address the association of life in utero with future health and disease and to endorse early screening and interventions to reduce the burden of NCDs, mental health issues and learning disorders along the life course. It has shown significant progress toward investigating the influence of adverse in utero environment such as diabetes, maternal under-nutrition and pre-eclampsia on fetal programming under two major research lines, that is, cardiovascular and cerebrovascular programming. The Society has been successful in disseminating its research findings through several esteemed international scientific conferences. Pakistan DOHaD Society encourages scientific community for collaborative research aimed at improving the quality of life during early childhood, adolescence and adulthood through provision of appropriate pre-pregnancy and antenatal interventions targeted to address at-risk in utero conditions.
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FUKUOKA, Hideoki, and Fumihiro SATA. "Molecular Mechanism of Developmental Origins of Health and Disease (DOHaD)." Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 71, no. 3 (2016): 185–87. http://dx.doi.org/10.1265/jjh.71.185.
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Bourque, Stephane L., and Sandra T. Davidge. "Developmental programming of cardiovascular function: a translational perspective." Clinical Science 134, no. 22 (November 2020): 3023–46. http://dx.doi.org/10.1042/cs20191210.
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Abstract The developmental origins of health and disease (DOHaD) is a concept linking pre- and early postnatal exposures to environmental influences with long-term health outcomes and susceptibility to disease. It has provided a new perspective on the etiology and evolution of chronic disease risk, and as such is a classic example of a paradigm shift. What first emerged as the ‘fetal origins of disease’, the evolution of the DOHaD conceptual framework is a storied one in which preclinical studies played an important role. With its potential clinical applications of DOHaD, there is increasing desire to leverage this growing body of preclinical work to improve health outcomes in populations all over the world. In this review, we provide a perspective on the values and limitations of preclinical research, and the challenges that impede its translation. The review focuses largely on the developmental programming of cardiovascular function and begins with a brief discussion on the emergence of the ‘Barker hypothesis’, and its subsequent evolution into the more-encompassing DOHaD framework. We then discuss some fundamental pathophysiological processes by which developmental programming may occur, and attempt to define these as ‘instigator’ and ‘effector’ mechanisms, according to their role in early adversity. We conclude with a brief discussion of some notable challenges that hinder the translation of this preclinical work.
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Goyal, Dipali, Sean W. Limesand, and Ravi Goyal. "Epigenetic responses and the developmental origins of health and disease." Journal of Endocrinology 242, no. 1 (July 2019): T105—T119. http://dx.doi.org/10.1530/joe-19-0009.
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Maternal and paternal factors influence offspring development and program its genome for successful postnatal life. Based on the stressors during gestation, the pregnant female prepares the fetus for the outside environment. This preparation is achieved by changing the epigenome of the fetus and is referred to as ‘developmental programming’. For instance, nutritional insufficiency in utero will lead to programming events that prepare the fetus to cope up with nutrient scarcity following birth; however, offspring may not face nutrient scarcity following birth. This discrepancy between predicted and exposed postnatal environments are perceived as ‘stress’ by the offspring and may result in cardiovascular and metabolic disorders. Thus, this developmental programming may be both beneficial as well as harmful depending on the prenatal vs postnatal environment. Over the past three decades, accumulating evidence supports the hypothesis of Developmental Origin of Health and Disease (DOHaD) by the programming of the fetal phenotype without altering the genotype per se. These heritable modifications in gene expression occur through DNA methylation, histone modification and noncoding RNA-associated gene activation or silencing, and all are defined as epigenetic modifications. In the present review, we will summarize the evidence supporting epigenetic regulation as a significant component in DOHaD.
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Suzuki, K. "The developing world of DOHaD." Journal of Developmental Origins of Health and Disease 9, no. 3 (September 5, 2017): 266–69. http://dx.doi.org/10.1017/s2040174417000691.
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Since its debut in a ground-breaking report by Barker and Osmond in 1986, the concept of the Developmental Origins of Health and Disease (DOHaD) has been further developed in several aspects. Its methodology and conclusions relating to proposed origins and outcomes of early life events have been developing and spreading internationally. Indeed, the DOHaD concept now seems to have influenced many fields of research. This article aims to briefly review why the DOHaD concept is important in biomedical science, how it has developed, is currently developing, and how it should develop in future.
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Almeida, Douglas Lopes, Audrei Pavanello, Lucas Paulo Saavedra, Tais Susane Pereira, Marialba Avezum Alves de Castro-Prado, and Paulo Cezar de Freitas Mathias. "Environmental monitoring and the developmental origins of health and disease." Journal of Developmental Origins of Health and Disease 10, no. 6 (May 27, 2019): 608–15. http://dx.doi.org/10.1017/s2040174419000151.
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AbstractEarly-life chronic exposure to environmental contaminants, such as bisphenol-A, particulate matter air pollution, organophosphorus pesticides, and pharmaceutical drugs, among others, may affect central tissues, such as the hypothalamus, and peripheral tissues, such as the endocrine pancreas, causing inflammation and apoptosis with severe implications to the metabolism. The Developmental Origins of Health and Disease (DOHaD) concept articulates events in developmental phases of life, such as intrauterine, lactation, and adolescence, to later-life metabolism and health. These developmental phases are more susceptible to environmental changes, such as those caused by environmental contaminants, which may predispose individuals to obesity, metabolic syndrome, and chronic noncommunicable diseases later in life. Alterations in the epigenome are explored as an underlying mechanism to the programming effects on metabolism, as the expression of key genes related with central and peripheral metabolic functions may be altered in response to environmental disturbances. Studies show that environmental contaminants may affect gene expressions in mammals, especially when exposed to during the developmental phases of life, leading to metabolic disorders in adulthood. In this review, we discuss the current obesity epidemics, the DOHaD concept, pollutants’ toxicology, environmental control, and the role of environmental contaminants in the central and peripheral programming of obesity and metabolic syndrome. Improving environmental monitoring may directly affect the quality of life of the population and help protect the future generations from metabolic diseases.
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FUKUOKA, Hideoki. "DOHaD (Developmental Origins of Health and Disease) and Birth Cohort Research." Journal of Nutritional Science and Vitaminology 61, Supplement (2015): S2—S4. http://dx.doi.org/10.3177/jnsv.61.s2.
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Gage, Suzanne H., Marcus R. Munafò, and George Davey Smith. "Causal Inference in Developmental Origins of Health and Disease (DOHaD) Research." Annual Review of Psychology 67, no. 1 (January 4, 2016): 567–85. http://dx.doi.org/10.1146/annurev-psych-122414-033352.
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Hivert, M. F., W. Perng, S. M. Watkins, C. S. Newgard, L. C. Kenny, B. S. Kristal, M. E. Patti, et al. "Metabolomics in the developmental origins of obesity and its cardiometabolic consequences." Journal of Developmental Origins of Health and Disease 6, no. 2 (January 29, 2015): 65–78. http://dx.doi.org/10.1017/s204017441500001x.
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In this review, we discuss the potential role of metabolomics to enhance understanding of obesity-related developmental origins of health and disease (DOHaD). We first provide an overview of common techniques and analytical approaches to help interested investigators dive into this relatively novel field. Next, we describe how metabolomics may capture exposures that are notoriously difficult to quantify, and help to further refine phenotypes associated with excess adiposity and related metabolic sequelae over the life course. Together, these data can ultimately help to elucidate mechanisms that underlie fetal metabolic programming. Finally, we review current gaps in knowledge and identify areas where the field of metabolomics is likely to provide insights into mechanisms linked to DOHaD in human populations.
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McKerracher, L., T. Moffat, M. Barker, D. Williams, and D. M. Sloboda. "Translating the Developmental Origins of Health and Disease concept to improve the nutritional environment for our next generations: a call for a reflexive, positive, multi-level approach." Journal of Developmental Origins of Health and Disease 10, no. 4 (December 17, 2018): 420–28. http://dx.doi.org/10.1017/s2040174418001034.
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AbstractEvidence supporting the Developmental Origins of Health and Disease (DOHaD) hypothesis indicates that improving early life environments can reduce non-communicable disease risks and improve health over the lifecourse. A widespread understanding of this evidence may help to reshape structures, guidelines and individual behaviors to better the developmental conditions for the next generations. Yet, few efforts have yet been made to translate the DOHaD concept beyond the research community. To understand why, and to identify priorities for DOHaD Knowledge Translation (KT) programs, we review here a portion of published descriptions of DOHaD KT efforts and critiques thereof. We focus on KT targeting people equipped to apply DOHaD knowledge to their everyday home or work lives. We identified 17 reports of direct-to-public DOHaD KT that met our inclusion criteria. Relevant KT programs have been or are being initiated in nine countries, most focusing on secondary school students or care-workers-in-training; few target parents-to-be. Early indicators suggest that such programs can empower participants. Main critiques of DOHaD KT suggest it may overburden mothers with responsibility for children’s health and health environments, minimizing the roles of other people and institutions. Simultaneously, though, many mothers-to-be seek reliable guidance on prenatal health and nutrition, and would likely benefit from engagement with DOHaD KT. We thus recommend emphasizing solidarity, and bringing together people likely to one day become parents (youth), people planning pregnancies, expecting couples, care workers and policymakers into empowering conversation about DOHaD and about the importance and complexity of early life environments.
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Sergeyev, O. V., and A. I. Nikitin. "Developmental origins of health and disease (DOHaD) and paternal origins of health and disease (POHaD). Multigenerational inheritance." Obstetrics, Gynecology and Reproduction 13, no. 4 (January 16, 2020): 326–36. http://dx.doi.org/10.17749/2313-7347.2019.13.4.326-336.
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This review addresses the concept of ontogenetic origin of health and disease (DOHaD) and the new concept of paternal origin of health and disease (POHaD). These concepts are based on scientific evidence that environmental factors impacting mother or father can play a role in reprogramming the health of their off springs throughout their life span. Moreover, the changes that have arisen can be transmitted through generations via diverse epigenetic mechanisms. Terms, such as epigenetics (a kind of “driver” for these concepts), epigenetic inheritance (including Intergenerational Inheritance – from generation to the next generation and Transgenerational Inheritance – through generations), epigenetic changes caused by the environment (Environmental Epigenetics) are discussed. Vulnerable periods towards epigenetic changes (Windows of Susceptibility) that occur in male germ cells responsible for epigenetic inheritance are considered. Epigenetic epidemiological studies in the field of reproductology are described; their advantages and disadvantages are discussed. These studies can serve as the basis for obtaining new knowledge about the causes of epigenetic variations in germ cells that occur in health and upon exposure to environmental factors as well as the inherited phenotypic outcomes.
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Ideraabdullah, Folami Y., Anthony M. Belenchia, Cheryl S. Rosenfeld, Seth W. Kullman, Megan Knuth, Debabrata Mahapatra, Michael Bereman, Edward D. Levin, and Catherine A. Peterson. "Maternal vitamin D deficiency and developmental origins of health and disease (DOHaD)." Journal of Endocrinology 241, no. 2 (May 2019): R65—R80. http://dx.doi.org/10.1530/joe-18-0541.
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Vitamin D is an essential nutrient that is metabolized in the body to generate an active metabolite (1,25(OH)2D) with hormone-like activity and highly diverse roles in cellular function. Vitamin D deficiency (VDD) is a prevalent but easily preventable nutritional disturbance. Emerging evidence demonstrates the importance of sufficient vitamin D concentrations during fetal life with deficiencies leading to long-term effects into adulthood. Here, we provide a detailed review and perspective of evidence for the role of maternal VDD in offspring long-term health, particularly as it relates to developmental origins of health and disease (DOHaD). We focus on the roles in neurobehavioral and cardiometabolic disorders in humans and highlight recent findings from zebrafish and rodent models that probe potential mechanisms linking early life VDD to later life health outcomes. Moreover, we explore evidence implicating epigenetic mechanisms as a mediator of this link. Gaps in our current understanding of how maternal VDD might result in deleterious offspring outcomes later in life are also addressed.
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Simmons, Rebecca A. "Developmental Origins of Adult Disease." Pediatric Clinics of North America 56, no. 3 (June 2009): 449–66. http://dx.doi.org/10.1016/j.pcl.2009.03.004.
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