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

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#REDIRECT Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease
 
==Introduction==
 
==Introduction==
 
[[File:Normal distribution curve.jpg|thumb|Normal distribution curve (red)]]
 
[[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, 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.  
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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.  
  
 
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.  
 
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 research has now shifted from birth weight emphasis to that of the early postnatal infant growth. (More? [[Postnatal - Growth Charts]])
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Go to [[Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease|Developmental Origins of Health and Disease]]
 
 
{{Template:Abnormality Links}} | [[Birth-Weight]]
 
 
 
== Some Recent Findings ==
 
{|
 
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* '''Delivery of a small for gestational age infant and greater maternal risk of ischemic heart disease'''<ref name="PMID22431995"><pubmed>22431995</pubmed>| [http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033047 PLoS One.]</ref> "Delivery of a small for gestational age (SGA) infant has been associated with increased maternal risk of ischemic heart disease (IHD). ...Risk of maternal IHD was evaluated in a population based cross-sectional study of 6,608 women with a prior live term birth who participated in the National Health and Nutrition Examination Survey (1999-2006), a probability sample of the U.S. population....Giving birth to a SGA infant is strongly and independently associated with IHD and a potential risk factor that precedes IHD by decades. A pregnancy that produces a SGA infant may induce long-term cardiovascular changes that increase risk for IHD." (Note this paper refers to a '''Maternal''' not Neonatal Risk).
 
* '''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]])
 
* '''The fetal origins hypothesis—10 years on (2005)'''<ref><pubmed>15891207</pubmed></ref>"In 1995 David Barker wrote: “The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease.”1 Now, 10 years later, the importance of events before birth for lifetime health has been confirmed in many populations."
 
|}
 
 
 
[[Talk:Abnormal_Development_-_Fetal_Origins_Hypothesis|Recent References]] | [[#References|References]]
 
 
 
==Barker Hypothesis==
 
There were some key papers by David Barker that initially studied UK birth weight data that gave rise to this area of research.<ref><pubmed>2252919</pubmed></ref><ref><pubmed>1573367</pubmed></ref><ref><pubmed>9158287</pubmed></ref>
 
 
 
“The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease.”
 
 
 
See also '''Fetal origins of adult disease-the hypothesis revisited.'''<ref><pubmed>10417093</pubmed>| [http://bmj.com/cgi/content/full/319/7204/245?view=full&pmid=10417093 BMJ]</ref>
 
 
 
* The hypothesis that adult disease has fetal origins is plausible, but much supportive evidence is flawed by incomplete and incorrect statistical interpretation.
 
* When size in early life is related to later health outcomes only after adjustment for current size, it is probably the change in size between these points (postnatal centile crossing) rather than fetal biology that is implicated.
 
* Even when birth size is directly related to later outcome, some studies fail to explore whether this is partly or wholly explained by postnatal rather that prenatal factors.
 
* These considerations are critical to understanding the biology and timing of "programming," the direction of future research, and future public health interventions.
 
 
 
==Fetal Growth Articles==
 
'''Fetal growth.'''<ref><pubmed>10813572</pubmed></ref> "Recent epidemiological and experimental studies show that abnormal fetal growth can lead to serious complications, including stillbirth, perinatal morbidity and disorders extending well beyond the neonatal period. It is now clear that the intrauterine milieu is as important as genetic endowment in shaping the future health of the conceptus. Maternal characteristics such as weight, height, parity and ethnic group need to be adjusted for, and pathological factors such as smoking excluded, to establish appropriate standards and improve the distinction between what is normal and abnormal. Currently, the aetiology of growth restriction is not well understood and preventative measures are ineffective. Elective delivery remains the principal management option, which emphasizes the need for better screening techniques for the timely detection of intrauterine growth failure."
 
 
 
'''Fetal growth and long-term consequences in animal models of growth retardation.'''<ref><pubmed>9989859</pubmed></ref> "Perturbations of the maternal environment involve an abnormal intrauterine milieu for the developing fetus. The altered fuel supply (depends on substrate availability, placental transport of nutrients and uteroplacental blood flow) from mother to fetus induces alterations in the development of the fetal endocrine pancreas and adaptations of the fetal metabolism to the altered intrauterine environment, resulting in intrauterine growth retardation. The alterations induced by maternal diabetes or maternal malnutrition (protein-calorie or protein deprivation) have consequences for the offspring, persisting into adulthood and into the next generation."
 
 
 
==Diabetes==
 
 
 
'''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."
 
 
 
==Cardiovascular==
 
 
 
== Neural Effects ==
 
The hypothesis proposes influences cause permanent changes in embryo/fetus, low birth weight, predisposition to chronic disease in adult life.
 
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 (<nowiki><2500 g)</nowiki> with controls, show impairment in neuro developmental tests up to age 11.
 
 
 
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<ref><pubmed>11517097</pubmed></ref> Note the commment made by Emeritus Professor P Pharaoh "One caveat that should be borne in mind, concerns the tests that are used to assess cognitive function. What do these tests actually measure? Ideally they measure innate mental ability, whatever that is, at a point in time.")
 
 
 
In contrast, a recent study of only '''postnatal growth''' (to 3 years of age) identified "Slower infant weight gain was not associated with poorer neurodevelopmental outcomes in healthy, term-born 3-year-old children."<ref><pubmed>18762504</pubmed></ref>
 
 
 
== 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/>
 
 
 
===Reviews===
 
<pubmed>21684471</pubmed>
 
<pubmed>20872047</pubmed>
 
<pubmed>20840260</pubmed>
 
<pubmed>20687308</pubmed>
 
<pubmed>20394764</pubmed>
 
<pubmed>20134170</pubmed>
 
<pubmed>19711246</pubmed>
 
 
 
===Articles===
 
 
 
<pubmed>20145229</pubmed>
 
 
 
===Search Pubmed===
 
 
 
'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=search&term=barker%20hypothesis barker hypothesis] | [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=search&term=fetal%20origins%20hypothesis fetal origins hypothesis] | [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=search&term=fetal%20programming%20hypothesis fetal programming hypothesis] |
 
 
 
 
 
{{Template:Glossary}}
 
 
 
{{Template:Footer}}
 
 
 
[[Category:Statistics]] [[Category:Birth]] [[Category:Human Fetus]] [[Category:Postnatal]]
 

Revision as of 13:23, 25 February 2014

  1. REDIRECT Abnormal_Development_-_Developmental_Origins_of_Health_and_Disease

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