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Maternal iron nutriture as a critical modulator of fetal alcohol spectrum disorder risk in alcohol-exposed pregnancies

机译：母性铁保险保鲜作为胎儿醇谱紊乱风险的临界调节剂，含酒精妊娠

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摘要

Alcohol consumption during pregnancy places the fetus at risk for permanent physical, cognitive, and behavioral impairments, collectively termed fetal alcohol spectrum disorder (FASD). However, prenatal alcohol exposure (PAE) outcomes vary widely, and growing evidence suggests that maternal nutrition is a modifying factor. Certain nutrients, such as iron, may modulate FASD outcomes. Untreated gestational iron deficiency (ID) causes persistent neurodevelopmental deficits in the offspring that affect many of the same domains damaged by PAE. Although chronic alcohol consumption enhances iron uptake and elevates liver iron stores in adult alcoholics, alcohol-abusing premenopausal women often have low iron reserves due to menstruation, childbirth, and poor diet. Recent investigations show that low iron reserves during pregnancy are strongly associated with a worsening of several hallmark features in FASD including reduced growth and impaired associative learning. This review discusses recent clinical and animal model findings that maternal ID worsens fetal outcomes in response to PAE. It also discusses underlying mechanisms by which PAE disrupts maternal and fetal iron homeostasis. We suggest that alcohol-exposed ID pregnancies contribute to the severe end of the FASD spectrum.
机译：妊娠期间的酒精消耗将胎儿占永久性身体，认知和行为损伤的风险，集体称为胎儿酒精谱系障碍（FASD）。然而，产前酒精暴露（PAE）结果很大，并且越来越多的证据表明母体营养是一种改性因素。某些营养素，如铁，可以调节FASD结果。未经治疗的妊娠缺铁（ID）导致后代的持续神经发作缺陷，这些缺陷会影响PAE损坏的许多相同结构域。虽然慢性酒精消费增强了铸铁吸收，但升高了成人酗酒者中的肝脏铁储存，滥用酗酒女性往往由于月经，分娩和饮食贫困和饮食差而导致的铁储量低。最近的调查表明，怀孕期间的低铁储量与FASD中的几个标志特征恶化，包括减少增长和联合学习受损。本综述讨论了最近的临床和动物模型结果，母体ID响应于PAE而恶化胎儿结果。它还讨论了PAE破坏母亲和胎儿铁袜的潜在机制。我们表明酒精暴露的ID怀孕有助于FASD谱的严重结束。

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