Beschreibung:
<jats:p>Objective. Alcohol influences the intake and metabolism of several nutrients including long-chain polyunsaturated fatty acids (LC-PUFAs). The LC-PUFAs docosahexaenoic acid (DHA) and arachidonic acid (AA) are particularly crucial for intrauterine growth and brain development. We hypothesized that alcohol consumption adversely affects LC-PUFA levels in pregnant women and their newborn infants.</jats:p>
<jats:p>Methods. Pregnant black women (N = 208) presenting at a core city antenatal clinic were screened and recruited. Shortly before delivery, maternal plasma was collected. After delivery, umbilical arteries and veins were dissected from the cords, total lipids were extracted from the vessel tissues and maternal plasma, and fatty acid levels were assayed by gas chromatography. For statistical analysis, subjects were categorized according to absolute alcohol intake per day (AAD) and absolute alcohol intake per drinking day (AADD) around the time of conception, with smoking and other potential confounders included in the analyses.</jats:p>
<jats:p>Results. Significant differences in fatty acid composition of total lipid extracts were detected in umbilical cord vessels among the AADD groups: abstainers (AADD = 0), moderate drinkers (AADD &lt; 130 g), and heavy drinkers (AADD ≥ 130 g). DHA and AA content in the arterial umbilical vessel wall was ∼14% and ∼10% higher in the moderate (n = 127) and heavy (n = 32) alcohol groups, respectively, than in abstainers (n = 49). A small, nonsignificant increase (∼3%) was seen in the umbilical vein for AA but not for DHA. Alcohol intake was positively correlated to both DHA and AA concentrations in the arterial vessel wall but to neither in the venous wall nor maternal plasma. Maternal plasma DHA was positively correlated with both umbilical arteries and vein DHA, but there were no significant correlations for AA between maternal plasma and either umbilical vessel.</jats:p>
<jats:p>Conclusions. Our findings indicate that alcohol intake during pregnancy is associated with altered DHA and AA status in fetal tissues. Although differences may be due to either metabolism and/or distribution, it is most likely a result of a direct influence of alcohol on fetal metabolism.</jats:p>