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Chapter 1 - The Neuroendocrinology of Pregnancy
- from Section I - Hormones in the Physiology and Pharmacology of Pregnancy
- Edited by Felice Petraglia, Università degli Studi, Florence, Mariarosaria Di Tommaso, Università degli Studi, Florence, Federico Mecacci, Università degli Studi, Florence
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- Hormones and Pregnancy
- Published online:
- 09 November 2022
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- 13 October 2022, pp 1-12
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Summary
The neuroendocrine system in pregnancy involves highly complex maternal, fetal, and placental mechanisms, which are critical for the maintenance of pregnancy, the timing of parturition, fetal growth, and protection from adverse fetal programming. The brain and placenta are both central organs in the responses to stress, and the maternal, fetal, and placental hypothalamus-pituitary-adrenal (HPA) axes play a significant role in controlling some of the adaptive mechanisms during pregnancy. The secretion of maternal and fetal HPA axis hormones increases throughout pregnancy. Corticotropin-releasing hormone (CRH) represents the main regulator of the axis as, when released from the hypothalamus, it stimulates adrenocorticotropic hormone (ACTH) release from the anterior pituitary and consequently cortisol secretion from the adrenal cortex. However, the major source of maternal circulating CRH in human pregnancy is the placenta. Indeed, the placenta, may be considered a neuroendocrine organ rich in neurohormones, neuropeptides, and neurosteroids. Stress-related hormones, such as CRH, urocortins, oxytocin, and prolactin, are key placental neuroendocrine factors mediating both endocrine (metabolism, immune function, cardiovascular changes) and paracrine (uterine contractility, local hormone production) mechanisms involved in term and pre-term birth. Aberrations in neurohormones secretion, as an adaptive response of the feto-placental unit to adverse environmental conditions, may contribute to the development of gestational disorders, such as hypertensive disorders of pregnancy, intrauterine growth restriction, and gestational diabetes.
Chapter 17 - Hormones in Pregnancy and the Developmental Origins of Health and Disease
- from Section II - Hormones and Gestational Disorders
- Edited by Felice Petraglia, Università degli Studi, Florence, Mariarosaria Di Tommaso, Università degli Studi, Florence, Federico Mecacci, Università degli Studi, Florence
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- Hormones and Pregnancy
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- 09 November 2022
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- 13 October 2022, pp 189-198
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The Developmental Origins of Health and Disease (DOHaD), also termed developmental programming, refers to adaptations during development that predispose an individual or a population towards later life noncommunicable disease (NCD) conditions or chronic diseases. The developmental trajectory of an individual is determined broadly by the interaction between that individual’s genes and the environment. “Environment” in this sense may include maternal or paternal factors, influences such as nutritional status before or during pregnancy, stress and exposure to contaminants, drugs or alcohol; and maternal diseases of pregnancy that influence transport of substrates and nutrients across the placenta (e.g., preeclampsia, placental insufficiency); and pre-term birth; factors that occur before or around the time of conception, during gestation or in the period after birth; the so-called First 1,000 Days. The interactions between genes and environment determine not only the developmental processes of the fetus and placenta leading to short term morbidity (low birth weight) and mortality, but also long term morbidity of multiple systems including neurodevelopmental disorders such as learning difficulties, poor developmental trajectories and cognitive development, mental health and behavioral disorders in children, and metabolic disorders such as obesity and diabetes. In later life, developmental programming contributes to heart disease such as hypertension and coronary heart disease, type II diabetes, obesity, immune, behavioral, and neurological disorders.
The mechanisms underlying developmental programming can result from structural changes in tissues or organs, effects on germ cells or stem cells, alterations in the microbiome, or in core inflammatory and immunological processes. There are clear sex differences in these responses, strong intergenerational effects, and variable vulnerability across the life course. Many adjustments occur as adaptive fetal responses to adversity or stress, such as hypoxemia or inappropriate nutrient supply, to ensure survival. The placenta plays a critical role in developmental programming, both in regulating the impact of maternal influences on the fetus, and through its direct impact on fetal development.
Early life risk and resiliency factors and their influences on developmental outcomes and disease pathways: a rapid evidence review of systematic reviews and meta-analyses
- Ayah Abdul-Hussein, Ayesha Kareem, Shrankhala Tewari, Julie Bergeron, Laurent Briollais, John R. G. Challis, Sandra T. Davidge, Claudio Delrieux, Isabel Fortier, Daniel Goldowitz, Pablo Nepomnaschy, Ashley Wazana, Kristin L. Connor
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- Journal of Developmental Origins of Health and Disease / Volume 12 / Issue 3 / June 2021
- Published online by Cambridge University Press:
- 04 August 2020, pp. 357-372
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The Developmental Origins of Health and Disease (DOHaD) framework aims to understand how environmental exposures in early life shape lifecycle health. Our understanding and the ability to prevent poor health outcomes and enrich for resiliency remain limited, in part, because exposure–outcome relationships are complex and poorly defined. We, therefore, aimed to determine the major DOHaD risk and resilience factors. A systematic approach with a 3-level screening process was used to conduct our Rapid Evidence Review following the established guidelines. Scientific databases using DOHaD-related keywords were searched to capture articles between January 1, 2009 and April 19, 2019. A final total of 56 systematic reviews/meta-analyses were obtained. Studies were categorized into domains based on primary exposures and outcomes investigated. Primary summary statistics and extracted data from the studies are presented in Graphical Overview for Evidence Reviews diagrams. There was substantial heterogeneity within and between studies. While global trends showed an increase in DOHaD publications over the last decade, the majority of data reported were from high-income countries. Articles were categorized under six exposure domains: Early Life Nutrition, Maternal/Paternal Health, Maternal/Paternal Psychological Exposure, Toxicants/Environment, Social Determinants, and Others. Studies examining social determinants of health and paternal influences were underrepresented. Only 23% of the articles explored resiliency factors. We synthesized major evidence on relationships between early life exposures and developmental and health outcomes, identifying risk and resiliency factors that influence later life health. Our findings provide insight into important trends and gaps in knowledge within many exposures and outcome domains.
13 - The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
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- By Deborah M. Sloboda, University of Western Australia, John P. Newnham, University of Western Australia, Timothy J. M. Moss, University of Western Australia, John R. G. Challis, University of Toronto
- Edited by Peter Gluckman, University of Auckland, Mark Hanson, University of Southampton
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- Developmental Origins of Health and Disease
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- 08 August 2009
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- 20 April 2006, pp 191-205
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Introduction
A clear relationship exists between intrauterine development and predisposition to postnatal disease. It is now understood that pre- and periconceptional nutritional status, glucocorticoid exposure and immediate postnatal development including catch-up growth may all contribute to these influences of early development on later-life disease. Barker and colleagues have described in detail the potential influence that an adverse intrauterine environment could play in the risk of developing particular diseases later in life (Barker 1994a, 1994b, 1995). It has been proposed that resetting of endocrine axes controlling growth and development could be one pathway for the developmental programming of later health and wellbeing. The fetal hypothalamic–pituitary–adrenal (HPA) axis in particular is highly vulnerable to changes in the intrauterine environment. Fetal HPA axis activity increases with gestation in most species and contributes to increased fetal levels of circulating glucocorticoids (Fowden et al. 1998). Even subtle changes in the intrauterine environment can disrupt the delicate balance of fetal HPA development and glucocorticoid production and can therefore alter long-term HPA activity and function. HPA hyperactivity has been demonstrated in animals after prenatal undernutrition (Lingas et al. 1999), prenatal stress (Takahashi and Kalin 1991) and maternal synthetic glucocorticoid administration (Uno et al. 1990, Sloboda et al. 2000).
Programming of the fetal HPA axis during development appears to play a central role in the link between fetal growth and long-term disease in adulthood. Prenatal programming of HPA axis function may increase the risk of developing cardiovascular and metabolic diseases.
4 - Fetal HPA activation, preterm birth and postnatal programming
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- By Deborah M. Sloboda, Timothy J. M. Moss, John P. Newnham, School of Women's and Infants' Health and the Women and Infants Research Foundation, University of Western Australia, Western Australia, John R. G. Challis, Departments of Physiology, and Obstetrics and Gynaecology, University of Toronto, CIHR Group in Fetal and Neonatal Health and Development, CIHR Institute of Human Development, Child and Youth Health, Canada
- Edited by Michael L. Power, American College of Obstetricians and Gynecologists, Washington DC, Jay Schulkin, American College of Obstetricians and Gynecologists, Washington DC
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- Birth, Distress and Disease
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- 16 October 2009
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- 28 July 2005, pp 114-141
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Summary
Activation of the fetal hypothalamic—pituitary—adrenal (HPA) axis in late gestation is a common characteristic across species resulting in increased output of fetal glucocorticoids, contributing to mechanisms associated with the onset of parturition and maturation of organ systems required for extrauterine survival. The fetus responds to an adverse intrauterine environment with precocious HPA activation, and premature upregulation of critical genes at each level along the axis. Thus in utero the fetus may be exposed inappropriately to sustained elevations of glucocorticoids. In addition, fetal glucocorticoid concentrations may be elevated in circumstances of maternal stress, particularly in association with diminished activity of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) activity, or after maternal administration of synthetic glucocorticoids. Animal studies have demonstrated that glucocorticoid administration in late gestation results in intrauterine growth restriction (IUGR) and significant alterations in metabolic and HPA axis function and regulation.
These associations among elevated fetal glucocorticoid concentrations and growth and development may underlie the increased incidence of spontaneous preterm labor in small-for-gestational-age babies. They possibly contribute to mechanisms by which aberrant development in utero predisposes to different pathophysiologies in later life. Over the last 10–15 years epidemiological studies have shown that a suboptimal intrauterine environment is associated with an increased risk of developing cardiovascular disease, hypertension, type 2 diabetes and ‘syndrome X’ (metabolic syndrome).