Difference between revisions of "Abnormal Development - Fetal Origins Hypothesis"

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#REDIRECT [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease]]
 
 
 
 
 
==Introduction==
 
==Introduction==
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[[File:Normal distribution curve.jpg|thumb|Normal distribution curve (red)]]
  
Maternal derived abnormalities relate to lifestyle, environment and nutrition and while some of these directly effect embryonic development, there is also growing evidence that some effects are more subtle and relate to later life health events. This theory is based on the early statistical analysis carried out by Barker of low birth weight data collected in the early 1900's in the south east of England which he then compared with these same babies later health outcomes. The theory was therefore originally called the "Barker Hypothesis" and has recently been renamed as "fetal origins" or "programming".
 
 
There have also been some issues relating to how the data is both collected and analyzed. (see Lucas reference)
 
 
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== Some Recent Findings ==
 
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* '''Fetal origins of adult diabetes'''<ref><pubmed>20840260</pubmed></ref> "According to the fetal origin of adult diseases hypothesis, the intrauterine environment through developmental plasticity may permanently influence long-term health and disease. Therefore, intrauterine growth restriction (IUGR), due either to maternal, placental, or genetic factors, may permanently alter the endocrine-metabolic status of the fetus, driving an insulin resistance state that can promote survival at the short term but that facilitates the development of type 2 diabetes mellitus and metabolic syndrome in adult life, especially when the intrauterine nutrient restriction is followed by a postnatal obesogenic environment."
 
* '''Perinatal Risk Factors for Diabetes in Later Life'''<ref><pubmed>19066311</pubmed></ref> "Low birth weight is consistently associated with an increased risk of non-insulin dependent diabetes mellitus in adulthood, but the individual contributions from poor fetal growth and preterm birth are not known. ....Our results suggest that the association between low birth weight and diabetes is due to factors associated with both poor fetal growth and short gestational age."
 
* '''Persistent epigenetic differences associated with prenatal exposure to famine in humans'''<ref><pubmed>18955703</pubmed></ref> "Here we show that individuals who were prenatally exposed to famine during the Dutch Hunger Winter in 1944-45 had, 6 decades later, less DNA methylation of the imprinted IGF2 gene compared with their unexposed, same-sex siblings. The association was specific for periconceptional exposure, reinforcing that very early mammalian development is a crucial period for establishing and maintaining epigenetic marks."  (More? see also [[Molecular Development - Epigenetics]])
 
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==Barker Hypothesis==
 
There were some key papers that initially studied UK birth weight data by Barker that gave rise to this area of research.<ref><pubmed>2252919</pubmed></ref><ref><pubmed>1573367</pubmed></ref><ref><pubmed>9158287</pubmed></ref>
 
 
== Environmental influences originate in utero ==
 
Hypothesis proposes influences cause permanent changes in embryo/fetus, low birth weight, predisposition to chronic disease in adult life.
 
 
<nowiki>Malnutrition in utero affects brain development, "low birth weight" or intrauterine growth restricted babies fare less well on measures of mental development in later life studies compared low birth weight babies (<2500 g) with controls, show impairment in neuro developmental tests up to age 11 </nowiki>
 
 
Intelligence is a combination of genetic and environmental influences (relative contributions of which are not yet established) and may vary over lifespan.
 
 
Modified Text from: Arch Dis Child 2001;85:189-196
 
 
== NCBI Bookshelf ==
 
Resources available from online textbooks freely available at National Library of Medicine (USA), National Center for Biotechnology Information.
 
 
'''Health Services/Technology Assessment Text (HSTAT)'''
 
 
[http://www.ncbi.nlm.nih.gov:80/books/bv.fcgi?db=Books&rid=hstat1a.table.31829 Evidence table 3. Studies Evaluating Association of LBW and Cerebral Palsy and Neurological Outcomes Part I]
 
 
[http://www.ncbi.nlm.nih.gov:80/books/bv.fcgi?db=Books&rid=hstat1a.table.31838 Evidence table 5B. Studies Evaluating Association of LBW of Audiology Outcomes Part II]
 
 
== Birth Terms ==
 
* Premature infant
 
** An infant born before 37 weeks of estimated gestational age
 
* Low birth weight
 
** <nowiki>Birth weight < 2,500 g (5 lb, 8 oz) </nowiki>
 
* Very low birth weight
 
** <nowiki>Birth weight < 1,500 g (3 lb, 5 oz) </nowiki>
 
* Extremely low birth weight
 
** <nowiki>Birth weight < 1,000 g (2 lb, 3 oz) </nowiki>
 
 
== References ==
 
<references/>
 
 
===Search Pubmed===
 
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=search&term=fetal+origins+hypothesis Search Pubmed - fetal origins hypothesis]
 
  
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This and also previously Fetal Origins Hypothesis, now called [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease|Developmental Origins of Health and Disease]]" (DOHAD) is based on the early statistical analysis carried out by Barker of low birth weight data collected in the early 1900's in the south east of England which he then compared with these same babies later health outcomes. The theory was therefore originally called the "Barker Hypothesis" and has recently been renamed as "fetal origins" or "programming". Several origins have been suggested including: fetal undernutrition, endocrine (increased cortisol exposure), genetic susceptibility and accelerated postnatal growth.
  
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More recently, discussion has occurred relating to how the data is both collected and analyzed, suggesting perhaps a smaller effect than original research suggested (see Lucas reference). Statistical methodology aside, these studies long-term periods of accurate data collection and we may have to wait some time for this research to develop.
  
[[Category:Human Fetus]] [[Category:Postnatal]]
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Go to [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease|Developmental Origins of Health and Disease]]

Latest revision as of 13:24, 25 February 2014

Introduction

Normal distribution curve (red)


This and also previously Fetal Origins Hypothesis, now called Developmental Origins of Health and Disease" (DOHAD) is based on the early statistical analysis carried out by Barker of low birth weight data collected in the early 1900's in the south east of England which he then compared with these same babies later health outcomes. The theory was therefore originally called the "Barker Hypothesis" and has recently been renamed as "fetal origins" or "programming". Several origins have been suggested including: fetal undernutrition, endocrine (increased cortisol exposure), genetic susceptibility and accelerated postnatal growth.

More recently, discussion has occurred relating to how the data is both collected and analyzed, suggesting perhaps a smaller effect than original research suggested (see Lucas reference). Statistical methodology aside, these studies long-term periods of accurate data collection and we may have to wait some time for this research to develop.

Go to Developmental Origins of Health and Disease