Abnormal Development - Fetal Origins Hypothesis
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)
Some Recent Findings
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) 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."
Heijmans BT, Tobi EW, Stein AD, Putter H, Blauw GJ, Susser ES, Slagboom PE, Lumey LH. 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]
"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])
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.
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
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
Resources available from online textbooks freely available at National Library of Medicine (USA), National Center for Biotechnology Information.
Health Services/Technology Assessment Text (HSTAT)
- Premature infant
- An infant born before 37 weeks of estimated gestational age
- Low birth weight
- Birth weight < 2,500 g (5 lb, 8 oz)
- Very low birth weight
- Birth weight < 1,500 g (3 lb, 5 oz)
- Extremely low birth weight
- Birth weight < 1,000 g (2 lb, 3 oz)
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Cite this page: Hill, M.A. (2021, December 3) Embryology Abnormal Development - Fetal Origins Hypothesis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Fetal_Origins_Hypothesis
- © Dr Mark Hill 2021, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G