54
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Pregnancy: An Underutilized Window of Opportunity to Improve Long-term Maternal and Infant Health—An Appeal for Continuous Family Care and Interdisciplinary Communication

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Physiologic adaptations during pregnancy unmask a woman’s predisposition to diseases. Complications are increasingly predicted by first-trimester algorithms, amplify a pre-existing maternal phenotype and accelerate risks for chronic diseases in the offspring up to adulthood (Barker hypothesis). Recent evidence suggests that vice versa, pregnancy diseases also indicate maternal and even grandparent’s risks for chronic diseases (reverse Barker hypothesis). Pub-Med and Embase were reviewed for Mesh terms “fetal programming” and “pregnancy complications combined with maternal disease” until January 2017. Studies linking pregnancy complications to future cardiovascular, metabolic, and thrombotic risks for mother and offspring were reviewed. Women with a history of miscarriage, fetal growth restriction, preeclampsia, preterm delivery, obesity, excessive gestational weight gain, gestational diabetes, subfertility, and thrombophilia more frequently demonstrate with echocardiographic abnormalities, higher fasting insulin, deviating lipids or clotting factors and show defective endothelial function. Thrombophilia hints to thrombotic risks in later life. Pregnancy abnormalities correlate with future cardiovascular and metabolic complications and earlier mortality. Conversely, women with a normal pregnancy have lower rates of subsequent diseases than the general female population creating the term: “Pregnancy as a window for future health.” Although the placenta works as a gatekeeper, many pregnancy complications may lead to sickness and earlier death in later life when the child becomes an adult. The epigenetic mechanisms and the mismatch between pre- and postnatal life have created the term “fetal origin of adult disease.” Up to now, the impact of cardiovascular, metabolic, or thrombotic risk profiles has been investigated separately for mother and child. In this manuscript, we strive to illustrate the consequences for both, fetus and mother within a cohesive perspective and thus try to demonstrate the complex interrelationship of genetics and epigenetics for long-term health of societies and future generations. Maternal–fetal medicine specialists should have a key role in the prevention of non-communicable diseases by implementing a framework for patient consultation and interdisciplinary networks. Health-care providers and policy makers should increasingly invest in a stratified primary prevention and follow-up to reduce the increasing number of manifest cardiovascular and metabolic diseases and to prevent waste of health-care resources.

          Related collections

          Most cited references165

          • Record: found
          • Abstract: not found
          • Article: not found

          The fetal and infant origins of adult disease.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The thrifty phenotype hypothesis.

            The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism. These changes include reduced capacity for insulin secretion and insulin resistance which, combined with effects of obesity, ageing and physical inactivity, are the most important factors in determining type 2 diabetes. Since the hypothesis was proposed, many studies world-wide have confirmed the initial epidemiological evidence, although the strength of the relationships has varied from one study to another. The relationship with insulin resistance is clear at all ages studied. Less clear is the relationship with insulin secretion. The relative contribution of genes and environment to these relationships remains a matter of debate. The contributions of maternal hyperglycaemia and the trajectory of postnatal growth need to be clarified.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Review: Sex and the human placenta: mediating differential strategies of fetal growth and survival.

              There are known sex specific differences in fetal and neonatal morbidity and mortality. There are also known differences in birthweight centile with males generally being larger than females at birth. These differences are generally ignored when studying obstetric complications of pregnancy and the mechanisms that confer these differences between the sexes are unknown. Current evidence suggests sex specific adaptation of the placenta may be central to the differences in fetal growth and survival. Our research examining pregnancies complicated by asthma has reported sexually dimorphic differences in fetal growth and survival with males adapting placental function to allow for continued growth in an adverse maternal environment while females reduce growth in an attempt to survive further maternal insults. We have reported sex differences in placental cytokine expression, insulin-like growth factor pathways and the placental response to cortisol in relation to the complication of asthma during pregnancy. More recently we have identified sex specific alterations in placental function in pregnancies complicated by preterm delivery which were associated with neonatal outcome and survival. We propose the sexually dimorphic differences in growth and survival of the fetus are mediated by the sex specific function of the human placenta. This review will present evidence supporting this hypothesis and will argue that to ignore the sex of the placenta is no longer sound scientific practice. Crown Copyright 2010. Published by Elsevier Ltd. All rights reserved.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Pediatr
                Front Pediatr
                Front. Pediatr.
                Frontiers in Pediatrics
                Frontiers Media S.A.
                2296-2360
                13 April 2017
                2017
                : 5
                : 69
                Affiliations
                [1] 1Center for Mother and Child, Philipps University , Marburg, Germany
                [2] 2Clara Angela Foundation , Witten, Germany
                [3] 3Center for Fetal Therapy, Johns Hopkins University , Baltimore, MD, USA
                Author notes

                Edited by: Ana Claudia Zenclussen, Otto-von-Guericke University Magdeburg, Germany

                Reviewed by: Patrick Shannon Ramsey, University of Texas Health Science Center at San Antonio, USA; Azadeh Farzin, Johns Hopkins University, USA

                *Correspondence: Birgit Arabin, bine.clara.angela@ 123456gmail.com

                Specialty section: This article was submitted to Obstetric and Pediatric Pharmacology, a section of the journal Frontiers in Pediatrics

                Article
                10.3389/fped.2017.00069
                5389980
                28451583
                39f8a156-26d1-4864-ad20-075138a1faf0
                Copyright © 2017 Arabin and Baschat.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 14 November 2016
                : 20 March 2017
                Page count
                Figures: 3, Tables: 4, Equations: 0, References: 211, Pages: 18, Words: 16032
                Categories
                Pediatrics
                Review

                fetal programming,cardiovascular diseases,metabolic diseases,pregnancy as a window for future health,preventive healthcare

                Comments

                Comment on this article