scholarly journals Sex-Specific Placental Responses in Fetal Development

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3422-3434 ◽  
Author(s):  
Cheryl S. Rosenfeld

The placenta is an ephemeral but critical organ for the survival of all eutherian mammals and marsupials. It is the primary messenger system between the mother and fetus, where communicational signals, nutrients, waste, gases, and extrinsic factors are exchanged. Although the placenta may buffer the fetus from various environmental insults, placental dysfunction might also contribute to detrimental developmental origins of adult health and disease effects. The placenta of one sex over the other might possess greater ability to respond and buffer against environmental insults. Given the potential role of the placenta in effecting the lifetime health of the offspring, it is not surprising that there has been a resurging interest in this organ, including the Human Placental Project launched by the National Institutes of Child Health and Human Development. In this review, we will compare embryological development of the laboratory mouse and human chorioallantoic placentae. Next, evidence that various species, including humans, exhibit normal sex-dependent structural and functional placental differences will be examined followed by how in utero environmental changes (nutritional state, stress, and exposure to environmental chemicals) might interact with fetal sex to affect this organ. Recent data also suggest that paternal state impacts placental function in a sex-dependent manner. The research to date linking placental maladaptive responses and later developmental origins of adult health and disease effects will be explored. Finally, we will focus on how sex chromosomes and epimutations may contribute to sex-dependent differences in placental function, the unanswered questions, and future directions that warrant further consideration.

2016 ◽  
Vol 8 (1) ◽  
pp. 8-29 ◽  
Author(s):  
C. S. Rosenfeld

Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.


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.


Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3416-3421 ◽  
Author(s):  
Jerrold J. Heindel ◽  
John Balbus ◽  
Linda Birnbaum ◽  
Marie Noel Brune-Drisse ◽  
Philippe Grandjean ◽  
...  

Abstract There are now robust data supporting the Developmental Origins of Health and Disease (DOHaD) paradigm. This includes human and animal data focusing on nutrition or environmental chemicals during development. However, the term DOHaD has not been generally accepted as the official term to be used when one is concerned with understanding the pathophysiological basis for how environmental influences acting during early development influence the risk of later noncommunicable diseases. Similarly, there is no global research or public health program built around the DOHaD paradigm that encompasses all aspects of environment. To better inform the global health efforts aimed at addressing the growing epidemic of chronic noncommunicable diseases of environmental origin, we propose a two-pronged approach: first, to make it clear that the current concept of DOHaD comprehensively includes a range of environmental factors and their relevance to disease occurrence not just throughout the life span but potentially across several generations; and second, to initiate the discussion of how adoption of DOHaD can promote a more realistic, accurate, and integrative approach to understanding environmental disruption of developmental programming and better inform clinical and policy interventions. (Endocrinology 156: 3416–3421, 2015)


2007 ◽  
Vol 137 (4) ◽  
pp. 1073-1075 ◽  
Author(s):  
Emanuel Lebenthal ◽  
Dennis M. Bier

2008 ◽  
Vol 102 (2) ◽  
pp. 82-89 ◽  
Author(s):  
I. Caroline McMillen ◽  
Severence M. MacLaughlin ◽  
Beverly S. Muhlhausler ◽  
Sheridan Gentili ◽  
Jaime L. Duffield ◽  
...  

2019 ◽  
Vol 10 (6) ◽  
pp. 608-615 ◽  
Author(s):  
Douglas Lopes Almeida ◽  
Audrei Pavanello ◽  
Lucas Paulo Saavedra ◽  
Tais Susane Pereira ◽  
Marialba Avezum Alves de Castro-Prado ◽  
...  

AbstractEarly-life chronic exposure to environmental contaminants, such as bisphenol-A, particulate matter air pollution, organophosphorus pesticides, and pharmaceutical drugs, among others, may affect central tissues, such as the hypothalamus, and peripheral tissues, such as the endocrine pancreas, causing inflammation and apoptosis with severe implications to the metabolism. The Developmental Origins of Health and Disease (DOHaD) concept articulates events in developmental phases of life, such as intrauterine, lactation, and adolescence, to later-life metabolism and health. These developmental phases are more susceptible to environmental changes, such as those caused by environmental contaminants, which may predispose individuals to obesity, metabolic syndrome, and chronic noncommunicable diseases later in life. Alterations in the epigenome are explored as an underlying mechanism to the programming effects on metabolism, as the expression of key genes related with central and peripheral metabolic functions may be altered in response to environmental disturbances. Studies show that environmental contaminants may affect gene expressions in mammals, especially when exposed to during the developmental phases of life, leading to metabolic disorders in adulthood. In this review, we discuss the current obesity epidemics, the DOHaD concept, pollutants’ toxicology, environmental control, and the role of environmental contaminants in the central and peripheral programming of obesity and metabolic syndrome. Improving environmental monitoring may directly affect the quality of life of the population and help protect the future generations from metabolic diseases.


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