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American Journal of Clinical Nutrition, Vol. 71, No. 1, 300S-306s, January 2000
© 2000 American Society for Clinical Nutrition


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Effects of gestational alcohol exposure on the fatty acid composition of umbilical cord serum in humans1,2,3

Yvonne M Denkins, James Woods, Janice E Whitty, John H Hannigan, Sue S Martier, Robert J Sokol and Norman Salem, Jr

1 From the National Institute on Alcoholism and Alcohol Abuse (NIAAA), Laboratory of Membrane Biochemistry and Biophysics, Division of Intramural Clinical and Biological Research, Rockville, MD, and the Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI.

This study examined the effects of maternal periconceptional alcohol intake on polyunsaturated fatty acid (PUFA) concentrations in human neonates. The area percentage of each fatty acid in cord blood serum from 12 infants born to control women (who consumed <2 mL absolute ethanol/d) was compared with that of 9 infants born to women whose periconceptional alcohol intake averaged >=30 mL absolute ethanol/d. Periconceptional alcohol use was associated with a 30% increase in the proportion of docosahexaenoic acid (22:6n-3) in cord blood (3.0% of total lipid in control infants compared with 3.9% in alcohol-exposed infants; P < 0.01). The rise in the proportion of 22:6n-3 was responsible for increases in the ratio of n-3 to n-6 fatty acids and the ratio of long-chain n-3 to n-6 fatty acids (P < 0.055). Examination of the lipid-class fatty acid profile indicated that serum lipid alterations were localized to the cholesterol esters; 22:6n-3 in the cholesterol esters of alcohol-exposed infants increased 54% (P < 0.011) and arachidonic acid increased 55% (P < 0.005). The relative fatty acyl composition of maternal serum showed a significant increase in 18:0 fatty acids in the alcohol-exposed group (25%, P < 0.005) but there were no changes in the other fatty acids. The increase in the proportion of 22:6n-3 was unexpected but is consistent with the hypothesis that this essential lipid may be conserved selectively. These results imply that the lifelong neurobehavioral and sensory dysfunction in fetal alcohol syndrome and other alcohol-related neurodevelopmental disorders may be due in part to PUFA dysregulation.

Key Words: Docosahexaenoic acid • DHA • polyunsaturated fatty acids • PUFAs • lipids • ethanol • alcohol in pregnancy • gestational alcohol exposure • neonate • fetus • umbilical cord serum




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