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Fetal Origins (fetal + origins)
Selected AbstractsFetal origins of developmental plasticity: Are fetal cues reliable predictors of future nutritional environments?AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 1 2005Christopher W. Kuzawa Evidence that fetal nutrition triggers permanent adjustments in a wide range of systems and health outcomes is stimulating interest in the evolutionary significance of these responses. This review evaluates the postnatal adaptive significance of fetal developmental plasticity from the perspective of life history theory and evolutionary models of energy partitioning. Birthweight is positively related to multiple metabolically costly postnatal functions, suggesting that the fetus has the capacity to distribute the burden of energy insufficiency when faced with a nutritionally challenging environment. Lowering total requirements may reduce the risk of negative energy balance, which disproportionately impacts functions that are not essential for survival but that are crucial for reproductive success. The long-term benefit of these metabolic adjustments is contingent upon the fetus having access to a cue that is predictive of its future nutritional environment, a problem complicated in a long-lived species by short-term ecologic fluctuations like seasonality. Evidence is reviewed suggesting that the flow of nutrients reaching the fetus provides an integrated signal of nutrition as experienced by recent matrilineal ancestors, which effectively limits the responsiveness to short-term ecologic fluctuations during any given pregnancy. This capacity for fetal nutrition to minimize the growth response to transient ecologic fluctuations is defined here as intergenerational "phenotypic inertia," and is hypothesized to allow the fetus to cut through the "noise" of seasonal or other stochastic influences to read the "signal" of longer-term ecologic trends. As a mode of adaptation, phenotypic inertia may help the organism cope with ecologic trends too gradual to be tracked by conventional developmental plasticity, but too rapid to be tracked by natural selection. From an applied perspective, if a trait like fetal growth is designed to minimize the effects of short-term fluctuations by integrating information across generations, public health interventions may be most effective if focused not on the individual but on the matriline. Am. J. Hum. Biol. 17:5,21, 2005. © 2004 Wiley-Liss, Inc. [source] Fetal and offspring arrhythmia following exposure to nicotine during pregnancyJOURNAL OF APPLIED TOXICOLOGY, Issue 1 2010Yu Feng Abstract Although recent studies have demonstrated prenatal nicotine can increase cardiovascular risk in the offspring, it is unknown whether exposure to nicotine during pregnancy also may be a risk for development of arrhythmia in the offspring. In addition, in previous studies of fetal arrhythmia affected by smoking, only two patterns, bradycardia and tachycardia, were observed. The present study examined acute effects of maternal nicotine on the fetal arrhythmia in utero, and chronic influence on offspring arrhythmia at adult stage following prenatal exposure to nicotine. Nicotine was administered to pregnant ewes and rats. In the fetal sheep, intravenous nicotine not only induced changes of fetal heart rate, but also caused cardiac cycle irregularity, single and multiple dropped cardiac cycles. Although maternal nicotine had no influence on fetal blood pH, lactic acid, hemocrit, Na+, K+ levels and plasma osmolality, fetal blood PO2 levels were significantly decreased following maternal nicotine in ewes. In offspring rats at 4,5 months after birth, prenatal exposure to nicotine significantly increased heart rate and premature ventricular contraction in restraint stress. In addition, arrhythmias induced by injection of nicotine were higher in the offspring prenatal exposure to nicotine in utero. The results provide new evidence that exposure to nicotine in pregnancy can cause fetal arrhythmia in various patterns besides tachycardia and bradycardia, the possible mechanisms for nicotine-induced fetal arrhythmia included in utero hypoxia. Importantly, following exposure to nicotine significantly increased risk of arrhythmia in the adult offspring. The finding offers new insight for development of cardiac rhythm problems in fetal origins. Copyright © 2009 John Wiley & Sons, Ltd. [source] Studies of twins: what can they tell us about the fetal origins of adult disease?PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 2005Ruth Morley Summary There has been much interest in evidence that people with lower birthweight have higher risk of adult cardiovascular disease, but the causal pathways underlying such observations are uncertain. Study of twins offers an opportunity to shed light on the underlying causal pathways, in particular by investigating the role of ,shared' factors vs. factors affecting each individual fetus. This involves comparing results of within-cohort vs. within-pair analyses. Twins share many factors during gestation but birthweight discordance (difference in birthweight within a twin pair) cannot be determined by these shared factors and must relate to factors affecting growth of each individual fetus. If associations seen in a cohort of twins remain in within-pair analyses, then factors specific to each individual must be involved in the underlying causal pathways. Conversely, if the relationships disappear or substantially diminish in within-pair analyses, then factors common to the pair must be involved. Comparison of findings in monozygotic vs. dizygotic twins may provide insights into the role of genetic factors, although issues related to chorionicity need to be taken into account. We tabulate published data and conclude that differences in methodology and analyses preclude informative meta-analysis, and that analysis of pooled data would provide more useful information. [source] The Walker Project: a longitudinal study of 48 000 children born 1952,1966 (aged 36,50 years in 2002) and their familiesPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 4 2004Gillian Libby Summary The Walker cohort is a database of over 48 000 birth records that has recently become available. It contains meticulously recorded details of pregnancy, labour, birth and care before discharge for babies born in hospital in Dundee, Scotland between 1952 and 1966. These babies accounted for 75% of all births in Dundee at this time. Over 34 000 (73%) of these subjects can be identified and this presents the opportunity to link this birth information with a large number of current health-outcome databases covering both primary and secondary care. Further, it allows linkage of records across siblings and over two and, in future, three generations. The number of birth records available and linkage to current databases make this a unique birth cohort with huge potential for the investigation of the fetal origins of adult disease. [source] The importance of the fetal origins of adult disease for geneticistsCLINICAL GENETICS, Issue 2 2007JG Hall The purpose of this paper is to summarize some of the newly recognized in utero factors that interact with gene expression to establish the structural and physiologic processes that will serve the individual long term. These may be common to all mammals and probably reflect evolutionary plasticity, which improves species survival. The concepts of programming, fetal-maternal microchimerism, growth factors, and transgenerational nutritional affects are explored. [source] | ||||||||||