Abnormal Development - Environmental
Introduction
Materal effects should really be called environmental (in contrast to genetic) removing the association of mother with the deleterious agent. Accepting this caveat, there are several maternal effects from lifestyle, environment and nutrition that can be prevented or decreased by change which is not an option for genetic effects.
Infections, collectively grouped under the acronym TORCH for Toxoplasmosis, Other organisms (parvovirus, HIV, Epstein-Barr, herpes 6 and 8, varicella, syphilis, enterovirus) , Rubella, Cytomegalovirus and Hepatitis. See related pages on Maternal Hyperthermia and Bacterial infections.
Maternal diet the best characterised is the role of low folic acid and Neural Tube Defects (NTDs) see also Abnormal neural development and Neural Tube Defects and the sample environmental effects listed below.
Maternal drugs effects either prescription drugs (therapeutic chemicals/agents, thalidomide limb development), non-prescription drugs (smoking), and illegal drugs (Cannabis/Marijuana, Methamphetamine/Amphetamine, Cocaine, Heroin, Lysergic Acid Diethylamide)
Environment (smoking, chemical, heavy metals) and maternal endocrine function (maternal diabetes, thyroid development) and maternal stress.
Different environmental effects can act individually or in combination on the same developing system. For example, neural development can be impacted upon by alcohol (fetal alcohol syndrome), viral infection (rubella) and/or inadequate dietry folate intake (neural tube defects). These effects may also not be seen as a direct effect on a system or systems but result in a reduced birth weight and the potential postnatal developmental effects.
Finally, when studying this topic remember the concept of "critical periods" of development that will affect the overall impact of the above listed factors. This can be extended to the potential differences between prenatal and postnatal effects, for example with infections and outcomes.
Some Recent Findings
- Environmental factors in axial skeletal dysmorphogenesis[1] "Approximately 1 in 1000 live births is afflicted with an axial skeletal defect. Although many of the known human teratogens can produce axial skeletal defects, the etiology of over half of the observed defects is unknown."
- The temporal dynamics of vertebrate limb development, teratogenesis and evolution.[2] "Recent genetic and functional analysis of vertebrate limb development begins to reveal how the functions of particular genes and regulatory hierarchies can drastically change over time. The temporal and spatial interplay of the two instructive signalling centres are part of a larger signalling system that orchestrates limb bud morphogenesis in a rather self-regulatory manner. It appears that mesenchymal cells are specified early and subsequently, the progenitors for the different skeletal elements are expanded and determined progressively during outgrowth. Mutations and teratogens that disrupt distal progression of limb development most often cause death of the early-specified progenitors rather than altering their fates."
- Predicting human developmental toxicity of pharmaceuticals using human embryonic stem cells and metabolomics.[3] "Teratogens, substances that may cause fetal abnormalities during development, are responsible for a significant number of birth defects. Animal models used to predict teratogenicity often do not faithfully correlate to human response. Here, we seek to develop a more predictive developmental toxicity model based on an in vitro method that utilizes both human embryonic stem (hES) cells and metabolomics to discover biomarkers of developmental toxicity."
References
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Articles
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Cite this page: Hill, M.A. (2024, May 13) Embryology Abnormal Development - Environmental. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Environmental
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G