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Published on: August 5, 2017
Fetal Alcohol Spectrum Disorder and Iron Homeostasis
Regan Bradley1, Koffi L Lakpa2, Michael Burd1
1School of Medicine, University of North Dakota, Grand Forks, ND 58201, USA.
Insights
Gestational iron deficiency worsens fetal alcohol spectrum disorder (FASD) outcomes. This review examines how iron impacts CNS development and links iron deficiency to increased FASD severity in animal and human studies.
Area of Science:
- Neuroscience
- Developmental Biology
- Public Health
Background:
- Prenatal alcohol exposure causes fetal alcohol spectrum disorder (FASD), a condition with varied effects.
- Maternal nutrition, particularly iron status, can influence FASD's phenotypic variability.
- Iron is vital for central nervous system (CNS) development and function.
Purpose of the Study:
- To review the relationship between iron deficiency and FASD.
- To explore pathophysiologic mechanisms linking iron homeostasis and prenatal alcohol exposure.
- To understand iron's role in modifying FASD severity.
Main Methods:
- Review of small animal studies.
- Review of human studies.
- Analysis of pathophysiologic mechanisms.
Main Results:
- Gestational iron deficiency alters CNS development.
- Iron deficiency may contribute to neurodevelopmental impairment in FASD.
- Data suggest iron deficiency exacerbates FASD severity.
Conclusions:
- Iron deficiency is linked to increased FASD severity.
- Iron homeostasis and prenatal alcohol exposure share mechanistic links.
- Understanding this relationship can inform prevention and intervention strategies.
Abstract:
Prenatal alcohol exposure results in a spectrum of behavioral, cognitive, and morphological abnormalities collectively referred to as fetal alcohol spectrum disorder (FASD). FASD presents with significant phenotypic variability and may be modified by gestational variables such as maternal nutritional status. Iron serves a critical function in the development of and processes within central nervous system (CNS) structures. Gestational iron deficiency alters CNS development and may contribute to neurodevelopmental impairment in FASD. This review explores the relationship between iron deficiency and fetal alcohol spectrum disorder as described in small animal and human studies. Consideration is given to the pathophysiologic mechanisms linking iron homeostasis and prenatal alcohol exposure. Existing data suggest that iron deficiency contributes to the severity of FASD and provide a mechanistic explanation linking these two conditions.
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