scholarly journals Fetal growth restriction: adaptations and consequences

Reproduction ◽  
2001 ◽  
pp. 195-204 ◽  
Author(s):  
IC McMillen ◽  
MB Adams ◽  
JT Ross ◽  
CL Coulter ◽  
G Simonetta ◽  
...  

A range of pathophysiological factors can result in a perturbation or restriction of fetal growth, and the cardiovascular, neuroendocrine and metabolic adaptations of the fetus to these stimuli will depend on their nature, timing and intensity. The critical importance of these physiological adaptations for both immediate survival and long-term health outcomes has provided an impetus for experimental studies of the nature and consequences of specific fetal adaptations to a poor intrauterine environment. This review summarizes data from recent studies that have focused on the responses of the fetal cardiovascular, sympathoadrenal, hypothalamo-pituitary-adrenal and renin-angiotensin systems to experimental restriction of placental function in the sheep and discusses the consequences of these adaptations for fetal, neonatal and adult health.

Author(s):  
Damian H. Adams ◽  
Adam Gerace ◽  
Michael J. Davies ◽  
Sheryl de Lacey

Abstract Donor-conceived neonates have poorer birth outcomes, including low birth weight and preterm delivery that are associated with poorer long-term health in adulthood through the developmental origins of health and disease (DOHaD) theory. The aim of this study was to conduct the first investigation of the adult health outcomes of donor-conceived people. An online health survey was completed by 272 donor sperm-conceived adults and 877 spontaneously conceived adults from around the world. Donor and spontaneously conceived groups were matched for age, sex, height, smoking, alcohol consumption, exercise, own fertility and maternal smoking. Donor sperm-conceived adults had significantly higher reports of being diagnosed with type 1 diabetes (P = 0.031), thyroid disease (P = 0.031), acute bronchitis (P = 0.008), environmental allergies (P = 0.046), sleep apnoea (P = 0.037) and having ear tubes/grommets surgically implanted (P = 0.046). This is the first study to investigate the health outcomes of adult donor sperm-conceived people. Donor sperm-conceived adults self-reported elevated frequencies of various health conditions. The outcomes are consistent with birth defect data from donor sperm treatment and are consistent with the DOHaD linking perturbed early growth and chronic disease in adulthood.


Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3450
Author(s):  
Violet N. L. Oosterwijk ◽  
Joyce M. Molenaar ◽  
Lily A. van Bilsen ◽  
Jessica C. Kiefte-de Jong

Ramadan is one of the five pillars of Islam, during which fasting is obligatory for all healthy individuals. Although pregnant women are exempt from this Islamic law, the majority nevertheless choose to fast. This review aims to identify the effects of Ramadan fasting on the offspring of Muslim mothers, particularly on fetal growth, birth indices, cognitive effects and long-term effects. A systematic literature search was conducted until March 2020 in Web of Science, Pubmed, Cochrane Library, Embase and Google Scholar. Studies were evaluated based on a pre-defined quality score ranging from 0 (low quality) to 10 (high quality), and 43 articles were included. The study quality ranged from 2 to 9 with a mean quality score of 5.4. Only 3 studies had a high quality score (>7), of which one found a lower birth weight among fasting women. Few medium quality studies found a significant negative effect on fetal growth or birth indices. The quality of articles that investigated cognitive and long-term effects was poor. The association between Ramadan fasting and health outcomes of offspring is not supported by strong evidence. To further elucidate the effects of Ramadan fasting, larger prospective and retrospective studies with novel designs are needed.


2016 ◽  
Vol 28 (4pt2) ◽  
pp. 1333-1346 ◽  
Author(s):  
Steven R. H. Beach ◽  
Gene H. Brody ◽  
Allen W. Barton ◽  
Robert A. Philibert

AbstractIn the current manuscript, we provide an overview of a research program at the University of Georgia's Center for Family Research designed to expand upon rapid and ongoing developments in the fields of genetics and epigenetics. By placing those developments in the context of translational research on family and community determinants of health and well-being among rural African Americans, we hope to identify novel, modifiable environments and biological processes. In the first section of the article, we review our earlier work on genotypic variation effects on the association between family context and mental and physical health outcomes as well as differential responses to family-based intervention. We then transition to discuss our more recent research on the association of family and community environments with epigenetic processes. In this second section of the article, we begin by briefly reviewing terminology and basic considerations before describing evidence that early environments may influence epigenetic motifs that potentially serve as mediators of long-term effects of early family and community environments on longer term health outcomes. We also provide evidence that genotype may sometimes influence epigenetic outcomes. Finally, we describe our recent efforts to use genome-wide characterization of epigenetic patterns to better understand the biological impact of protective parenting on long-term shifts in inflammatory processes and its potential implications for young adult health. As will be clear, research on epigenetics as a mediator of the connections between family/community processes and a range of health outcomes is still in its infancy, but the potential to develop important insights regarding mechanisms linking modifiable environments to biological processes and long-term health outcomes already is coming into view.


2019 ◽  
Vol 10 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Aya Sasaki ◽  
Stephen G. Matthews

AbstractMaternal adversity and fetal glucocorticoid exposure has long-term effects on cardiovascular, metabolic and behavioral systems in offspring that can persist throughout the lifespan. These data, along with other environmental exposure data, implicate epigenetic modifications as potential mechanisms for long-term effects of maternal exposures on adverse health outcomes in offspring. Advances in microarray, sequencing and bioinformatic approaches have enabled recent studies to examine the genome-wide epigenetic response to maternal adversity. Studies of maternal exposures to xenobiotics such as arsenic and smoking have been performed at birth to examine fetal epigenomic signatures in cord blood relating to adult health outcomes. However, there have been no epigenomic studies examining these effects in animal models. On the other hand, to date, only a few studies of the effects of maternal psychosocial stress have been performed in human infants, and the majority of animal studies have examined epigenomic outcomes in adulthood. In terms of maternal exposure to excess glucocorticoids by synthetic glucocorticoid treatment, there has been no epigenetic study performed in humans and only a few studies undertaken in animal models. This review emphasizes the importance of examining biomarkers of exposure to adversity throughout development to identify individuals at risk and to target interventions. Thus, research performed at birth will be reviewed. In addition, potential subject characteristics associated with epigenetic modifications, technical considerations, the selection of target tissues and combining human studies with animal models will be discussed in relation to the design of experiments in this field of study.


2001 ◽  
Vol 90 (4) ◽  
pp. 1593-1599 ◽  
Author(s):  
Judith A. Neubauer

This mini-review summarizes the physiological adaptations to and pathophysiological consequences of intermittent hypoxia with special emphasis given to the pathophysiology associated with obstructive sleep apnea. Intermittent hypoxia is an effective stimulus for evoking the respiratory, cardiovascular, and metabolic adaptations normally associated with continuous chronic hypoxia. These adaptations are thought by some to be beneficial in that they may provide protection against disease as well as improve exercise performance in athletes. The long-term consequences of chronic intermittent hypoxia may have detrimental effects, including hypertension, cerebral and coronary vascular problems, developmental and neurocognitive deficits, and neurodegeneration due to the cumulative effects of persistent bouts of hypoxia. Emphasis is placed on reviewing the available data on intermittent hypoxia, making extensions from applicable information from acute and chronic hypoxia studies, and pointing out major gaps in information linking the genomic and cellular responses to intermittent hypoxia with physiological or pathophysiological responses.


Reproduction ◽  
2004 ◽  
Vol 127 (5) ◽  
pp. 515-526 ◽  
Author(s):  
A L Fowden ◽  
A J Forhead

Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmedin uteroduring critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual fetal tissues, they have a central role in intrauterine programming. Hormones such as insulin, insulin-like growth factors, thyroxine and the glucocorticoids act as nutritional and maturational signals and adapt fetal development to prevailing intrauterine conditions, thereby maximizing the chances of survival bothin uteroand at birth. However, these adaptations may have long-term sequelae. Of the hormones known to control fetal development, it is the glucocorticoids that are most likely to cause tissue programmingin utero. They are growth inhibitory and affect the development of all the tissues and organ systems most at risk of postnatal pathophysiology when fetal growth is impaired. Their concentrationsin uteroare also elevated by all the nutritional and other challenges known to have programming effects. Glucocorticoids act at cellular and molecular levels to alter cell function by changing the expression of receptors, enzymes, ion channels and transporters. They also alter various growth factors, cytoarchitectural proteins, binding proteins and components of the intracellular signalling pathways. Glucocorticoids act, directly, on genes and, indirectly, through changes in the bioavailability of other hormones. These glucocorticoid-induced endocrine changes may be transient or persist into postnatal life with consequences for tissue growth and development both before and after birth. In the long term, prenatal glucocorticoid exposure can permanently reset endocrine systems, such as the somatotrophic and hypothalamic–pituitary–adrenal axes, which, in turn, may contribute to the pathogenesis of adult disease. Endocrine changes may, therefore, be both the cause and the consequence of intrauterine programming.


2017 ◽  
Vol 8 (4) ◽  
pp. 388-402 ◽  
Author(s):  
M. Chen ◽  
L. K. Heilbronn

Concerns have been raised about the health and development of children conceived by assisted reproductive technologies (ART) since 1978. Controversially, ART has been linked with adverse obstetric and perinatal outcomes, an increased risk of birth defects, cancers, and growth and development disorders. Emerging evidence suggests that ART treatment may also predispose individuals to an increased risk of chronic ageing related diseases such as obesity, type 2 diabetes and cardiovascular disease. This review will summarize the available evidence on the short-term and long-term health outcomes of ART singletons, as multiple pregnancies after multiple embryos transfer, are associated with low birth weight and preterm delivery, which can separately increase risk of adverse postnatal outcomes, and impact long-term health. We will also examine the potential factors that may contribute to these health risks, and discuss underlying mechanisms, including epigenetic changes that may occur during the preimplantation period and reprogram development in utero, and adult health, later in life. Lastly, this review will consider the future directions with the view to optimize the long-term health of ART children.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Richard Xu ◽  
Xiumei Hong ◽  
Boyang Zhang ◽  
Wanyu Huang ◽  
Wenpin Hou ◽  
...  

Abstract Background Maternal smoking affects more than half a million pregnancies each year in the US and is known to result in fetal growth restriction as measured by lower birthweight and its associated long-term consequences. Maternal smoking also has been linked to altered fetal DNA methylation (DNAm). However, what remains largely unexplored is whether these DNAm alterations are merely markers of smoking exposure or if they also have implications for health outcomes. This study tested the hypothesis that fetal DNAm mediates the effect of maternal smoking on newborn birthweight. Methods This study included mother–newborn pairs from a US predominantly urban, low-income multi-ethnic birth cohort. DNAm in cord blood were determined using the Illumina Infinium MethylationEPIC BeadChip. After standard quality control and normalization procedures, an epigenome-wide association study (EWAS) of maternal smoking was performed using linear regression models, controlling for maternal age, education, race, parity, pre-pregnancy body mass index, alcohol consumption, gestational age, maternal pregestational/gestational diabetes, child sex, cord blood cell compositions and batch effects. To quantify the degree to which cord DNAm mediates the smoking-birthweight association, the VanderWeele-Vansteelandt approach for single mediator and structural equational model for multiple mediators were used, adjusting for pertinent covariates. Results The study included 954 mother–newborn pairs. Among mothers, 165 (17.3%) ever smoked before or during pregnancy. Newborns with smoking exposure had on average 258 g lower birthweight than newborns without exposure (P < 0.001). Using a false discovery rate (FDR) < 0.05 as the significance cutoff, the EWAS identified 38 differentially methylated CpG sites associated with maternal smoking. Of those, 17 CpG sites were mapped to previously reported genes: GFI1, AHRR, CYP1A1, and CNTNAP2; 8 of those, located in the first three genes, were Bonferroni significantly associated with newborn birthweight and mediated the smoking-birthweight association. The combined mediation effect of the three genes explained 67.8% of the smoking-birthweight association. Conclusions Our study not only lends further support that maternal smoking alters fetal DNAm in a multiethnic population, but also suggests that fetal DNAm substantially mediates the maternal smoking–birthweight association. Our findings, if further validated, indicate that DNAm modification is likely an important pathway by which maternal smoking impairs fetal growth and, perhaps, even long-term health outcomes.


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