Adequacy of Maternal Iron Status Protects against Behavioral, Neuroanatomical, and Growth Deficits in Fetal Alcohol Spectrum Disorders
| Autor: | Matthew E. Andrzejewski, Susan M. Smith, George R. Flentke, Tuan D. Tran, Echoleah S. Rufer, Megan M. Attridge |
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| Rok vydání: | 2012 |
| Předmět: |
lcsh:Medicine
Developmental and Pediatric Neurology Toxicology Pediatrics Cognition Child Development 0302 clinical medicine Pregnancy Risk Factors lcsh:Science Maternal-Fetal Exchange reproductive and urinary physiology 2. Zero hunger Teratology 0303 health sciences Multidisciplinary Brain Anemia Iron Deficiencies Animal Models Hematology Iron deficiency female genital diseases and pregnancy complications 3. Good health Infectious Diseases Fetal Alcohol Spectrum Disorders Prenatal Exposure Delayed Effects Medicine Female Public Health Alcohol Research Article Neglected Tropical Diseases Neurotoxicology medicine.medical_specialty Binge drinking Gravidity Binge Drinking 03 medical and health sciences Fetus Model Organisms medicine Animals Learning Iron Deficiency Anemia Psychiatry Biology Socioeconomic status Nutrition 030304 developmental biology Ethanol business.industry lcsh:R medicine.disease Nutritional Diseases Rats Associative learning Pregnancy Complications Disease Models Animal Malnutrition Animals Newborn Iron-deficiency anemia Rat lcsh:Q business Organism Development 030217 neurology & neurosurgery Developmental Biology |
| Zdroj: | PLoS ONE PLoS ONE, Vol 7, Iss 10, p e47499 (2012) |
| ISSN: | 1932-6203 |
| DOI: | 10.1371/journal.pone.0047499 |
| Popis: | Fetal alcohol spectrum disorders (FASD) are the leading non-genetic cause of neurodevelopmental disability in children. Although alcohol is clearly teratogenic, environmental factors such as gravidity and socioeconomic status significantly modify individual FASD risk despite equivalent alcohol intake. An explanation for this variability could inform FASD prevention. Here we show that the most common nutritional deficiency of pregnancy, iron deficiency without anemia (ID), is a potent and synergistic modifier of FASD risk. Using an established rat model of third trimester-equivalent binge drinking, we show that ID significantly interacts with alcohol to impair postnatal somatic growth, associative learning, and white matter formation, as compared with either insult separately. For the associative learning and myelination deficits, the ID-alcohol interaction was synergistic and the deficits persisted even after the offsprings' iron status had normalized. Importantly, the observed deficits in the ID-alcohol animals comprise key diagnostic criteria of FASD. Other neurobehaviors were normal, showing the ID-alcohol interaction was selective and did not reflect a generalized malnutrition. Importantly ID worsened FASD outcome even though the mothers lacked overt anemia; thus diagnostics that emphasize hematological markers will not identify pregnancies at-risk. This is the first direct demonstration that, as suggested by clinical studies, maternal iron status has a unique influence upon FASD outcome. While alcohol is unquestionably teratogenic, this ID-alcohol interaction likely represents a significant portion of FASD diagnoses because ID is more common in alcohol-abusing pregnancies than generally appreciated. Iron status may also underlie the associations between FASD and parity or socioeconomic status. We propose that increased attention to normalizing maternal iron status will substantially improve FASD outcome, even if maternal alcohol abuse continues. These findings offer novel insights into how alcohol damages the developing brain. |
| Databáze: | OpenAIRE |
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