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Exploitation and control of women's reproductive bodies
Published in Wendy A. Rogers, Jackie Leach Scully, Stacy M. Carter, Vikki A. Entwistle, Catherine Mills, The Routledge Handbook of Feminist Bioethics, 2022
As the maternal body is the focus of transgenerational epigenetics it offers a new target for biomedical interventions and surveillance. Transgenerational epigenetics suggests a link between maternal behavior and lifestyle during pregnancy and after birth, and the subsequent wellbeing of children in both early and adult life. Poor prenatal diet, prenatal exposure to domestic violence, exposure to maternal distress, Cesarean delivery, alcohol intake before conception and during pregnancy are all linked to epigenetic changes that may cause health problems in the offspring. In this field, the uterus is seen as a micro-environment in which new generations take shape for better and worse. Hence scientists, especially those who work in the developmental origins of health and disease (DOHAD), seek to find out how to control the maternal environment and behavior to advance the health of the offspring and next generations. Does this increasing focus on the “maternal effect” exert power over women to take on new responsibilities?
Life Course Approach to Prevention of Chronic Disease
Published in James M. Rippe, Lifestyle Medicine, 2019
Katherine A. Sauder, Dana Dabelea
A critical question for the field of developmental origins of health and disease relates to the role of postnatal life in mediating or modifying the long-term health risks conferred by various fetal exposures. Indeed, if specific associations between prenatal factors and offspring adiposity, vascular, or metabolic outcomes are observed, then examining the role of potentially modifiable postnatal mediators is valuable for considering interventions in children who are already delivered and have been exposed to adverse exposures in utero (Table 74.2).
Epigenetic Reprogramming in Early Embryo Development
Published in Cristina Camprubí, Joan Blanco, Epigenetics and Assisted Reproduction, 2018
From an evolutionary point of view, DNA methylation and other epigenetic marks (such as histone methylation, histone acetylation and de-acetylation) represent a more rapid response to environmental changes than evolution via genetic mutation, the way followed by natural selection (35). Not in vain, epigenetics is defined “as heritable but potentially reversible changes in gene expression caused by mechanisms other than changes in the underlying DNA sequence” (36). In fact, changes in gene expression derived from epigenetic modifications can occur in one organism during embryonic or fetal development, or during adulthood, and can persist through generations, as the classical examples used to explain the concept of Epigenetics usually refers: The alterations found as a consequence of the Dutch Famine of 1944–1945, explained by the so-called Developmental Origins of Health and Disease (DOHaD) hypothesis (37).
A new mathematical mixed effect model was used for analysing the influencing factors of hypoglycaemia of newborns from women with gestational diabetes mellitus
Published in Journal of Obstetrics and Gynaecology, 2022
Yin Ying, Lijun Bei, Lili Sun, Junhua Ye, Mengyan Xu
Since the 1990s, some epidemiological studies found that the nutritional status during pregnancy will have an important impact on the occurrence of cardiovascular, glucose metabolism, obesity, and other diseases in the newborn, that is, "the origin of the foetus of adult diseases theory". Many research results have confirmed this theory (Tian et al. 2006; Victora et al. 2008; Whincup et al. 2008). During the further study, it is confirmed that heredity, intrauterine environment, and other factors not only affect the intrauterine development of foetus, but also can cause functional and structural changes, leading to a series of diseases in adulthood. This theory also gradually transits and perfects into the DOHaD (Developmental Origins of Health and Disease) theory (Uauy et al. 2011; Wojtya 2011; Aisa et al. 2019), which indicates that we should pay much more attentions on nutrition during pregnancy in order to provide early prevention for chronic diseases that were bad for adult health and the future newborns.
Enhanced antioxidant capacity prevents epitranscriptomic and cardiac alterations in adult offspring gestationally-exposed to ENM
Published in Nanotoxicology, 2021
Amina Kunovac, Quincy A. Hathaway, Mark V. Pinti, Andrya J. Durr, Andrew D. Taylor, William T. Goldsmith, Krista L. Garner, Timothy R. Nurkiewicz, John M. Hollander
Maternal ENM exposure during gestation interferes with fetal development and has long-term consequences for offspring that persist into adulthood (Sun et al. 2013; Hougaard et al. 2015; Bommarito, Martin, and Fry 2017; Crispi, Miranda, and Gratacos 2018). The importance of the maternal environment are outlined by the developmental origins of health and disease (DOHaD) hypothesis and supported by an increasing number of studies (Swanson et al. 2009). The current study highlights how amplifying antioxidant capacity in the maternal environment can deter the maladaptive cardiovascular changes that persist into adulthood, regardless of the progeny’s genotype. Although transgenic expression provides a limitation to clinical uses of maternal antioxidant protection, we establish a basis for investigating other potential antioxidant protective strategies. One example is mitoquinone mesylate (MitoQ), a mitochondrial-targeted antioxidant that has shown promise in improving mitochondrial dysfunction, reducing hydrogen peroxide production, and enhancing antioxidant enzyme activity (Ribeiro Junior et al. 2018; Park et al. 2020). MitoQ also has the ability to prevent the long-term impacts of maternal cigarette smoke exposure on progeny by mitigating renal total ROS in the mothers and offspring at adulthood (Sukjamnong et al. 2018). Future investigations should aim to determine whether supplementation with antioxidant-boosting therapeutics during pregnancy can provide the same protective effect to progeny as maternal mPHGPx overexpression.
Infant blood lipids: a systematic review of predictive value and influential factors
Published in Expert Review of Cardiovascular Therapy, 2020
Isabella Theresa Felzer-Kim, Joseph R. Visker, D. P. Ferguson, J. L. Hauck
It is well known that low birth weight can have adverse consequences to physiology in adulthood [88]. The Developmental Origins of Health and Disease (DOHaD) hypothesis states that impairments in early life increase the risk for chronic disease in adulthood, specifically CVD. There appears to be an important link between extreme birth weight (either low or high) and adult coronary heart disease, stroke, and ischemic heart disease [89] [90]. Whether the link between birth weight and adult blood lipids is less clear and evidence suggests that low birth weight does associate with high TC and TRG in childhood and later life, but that other factors such as gender and adiposity are more relevant [91–96]. There is evidence of an inverse association between carotid atherosclerosis and birth weight [97] and metabolic syndrome is also more likely in individuals with low birth weight [98]. Thus, there may be a programming effect that implicates blood lipids as one of the mechanisms by which birth weight associates with adult cardiovascular risk, but other mechanisms may be contributory to enhanced atherosclerosis [99].