Maternal ethanol use and selective fetal malnutrition.
Maternal ethanol ingestion may cause fetal injury, particularly impaired somatic and brain growth, by at least two mechanisms: (1) directly, by fetotoxicity from ethanol and/or acetaldehyde; (2) indirectly, by ethanol-induced placental injury and selective fatal malnutrition. There is ample evidence that ethanol and/or acetaldehyde is fetotoxic. In addition, alcoholics are frequently in a state of poor nutrition. However, regardless of maternal nutritional status, ethanol can be placentotoxic, impairing the normal transfer of essential fetal nutrients. Ethanol and/or acetaldehyde has been shown to inhibit placental uptake and/or transfer of amino acids, zinc, and glucose. These effects have been evaluated in animal models and in human tissue. Recent use of the isolated perfused human placental cotyledon has begun to delineate the pathophysiology of ethanol-induced placental injury.
Fisher
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Department of Pediatrics, North Shore University Hospital, Manhasset, New York 11030.
Karl
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PI
D000818:Animals; D000431:Ethanol / Q000097:blood; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000209:etiology*; D005317:Fetal Growth Retardation / Q000209:etiology*; D006801:Humans; D008431:Maternal-Fetal Exchange; D011247:Pregnancy
D000431:Ethanol