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

From Embryology
 
(37 intermediate revisions by 2 users not shown)
Line 1: Line 1:
 +
#REDIRECT [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease]]
 
==Introduction==
 
==Introduction==
 +
[[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)
+
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.
  
{{Template:Abnormality Links}}
+
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.
  
== Some Recent Findings ==
+
Go to [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease|Developmental Origins of Health and Disease]]
[http://www.ncbi.nlm.nih.gov/pubmed/19066311 Perinatal Risk Factors for Diabetes in Later Life]. Kaijser M, Edstedt Bonamy AK, Akre O, Cnattingius S, Granath F, Norman M, Ekbom A. Diabetes. 2008 Dec 9.
 
 
 
"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."
 
 
 
This next '''PLoS One''' paper explores the effects of Low Birth Weight (LBW) and the postnatal development of muscle mass in function in young adult men. It identifies fundamental changes in at least one muscle signaling pathway.
 
 
 
Jensen CB, Martin-Gronert MS, Storgaard H, Madsbad S, Vaag A, et al. (2008) [http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003738 Altered PI3-Kinase/Akt Signalling in Skeletal Muscle of Young Men with Low Birth Weight.] PLoS ONE 3(11): e3738. doi:10.1371/journal.pone.0003738
 
 
 
"We conclude that altered insulin activation of the PI3K/Akt but not the MAPK pathway precedes and may contribute to development of whole-body insulin resistance and type 2 diabetes in men with LBW."
 
 
 
[http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=18955703&dopt=Abstract He][http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=18955703&dopt=Abstract ijmans BT, Tobi EW, Stein AD, Putter H, Blauw GJ, Susser ES, Slagboom PE, Lumey LH.]<nowiki> Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci U S A. 2008 Oct 27. [Epub ahead of print] </nowiki>
 
 
 
"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 [../MolDev/epigenetic.htm Epigenetics])
 
 
 
[http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16352854 Alexander BT.] Fetal programming of hypertension. Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R1-R10.
 
 
 
== 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/>
 

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