scholarly journals Fetal origins of adult disease: strength of effects and biological basis

2002 ◽  
Vol 31 (6) ◽  
pp. 1235-1239 ◽  
Author(s):  
DJP Barker ◽  
JG Eriksson ◽  
T Forsén ◽  
C Osmond
1999 ◽  
Vol 81 (1) ◽  
pp. 5-6 ◽  
Author(s):  
Simon C. Langley-Evans
Keyword(s):  

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.


BMJ ◽  
2001 ◽  
Vol 322 (7283) ◽  
pp. 375-376 ◽  
Author(s):  
R. Robinson
Keyword(s):  

2012 ◽  
Vol 3 (8) ◽  
pp. 1-7 ◽  
Author(s):  
Jens Christoffer Skogen ◽  
Simon Øverland

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Stephanie E. Hallows ◽  
Timothy R. H. Regnault ◽  
Dean H. Betts

Placental insufficiency, maternal malnutrition, and other causes of intrauterine growth restriction (IUGR) can significantly affect short-term growth and long-term health. Following IUGR, there is an increased risk for cardiovascular disease and Type 2 Diabetes. The etiology of these diseases is beginning to be elucidated, and premature aging or cellular senescence through increased oxidative stress and DNA damage to telomeric ends may be initiators of these disease processes. This paper will explore the areas where telomere and telomerase biology can have significant effects on various tissues in the body in IUGR outcomes.


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