OBJECTIVE: Our purpose was to investigate, in a prospective way, whether the altered essential fatty acid status observed in pregnancy-induced hypertension is a consequence of the disease or may contribute to its cause. STUDY DESIGN: Pregnant women healthy at the start of the study were asked to give a blood sample before 16 weeks, at 22 weeks, and at 32 weeks of gestation. After delivery a blood sample from the umbilical vein, a piece of the umbilical cord, and a maternal blood sample were collected. Fatty acid compositions were determined of the phospholipids isolated from plasma and umbilical arterial and venous vessel walls. The nutrient intake of the pregnant women was assessed by use of the dietary history method and food frequency questionnaires. The results of each woman with pregnancy-induced hypertension were compared with the results of three matched healthy controls. RESULTS: During pregnancy (16 to 32 weeks) no significant differences were observed in nutrient intake and maternal plasma fatty acid composition between the group with pregnancy-induced hypertension (n = 52) and the control group (n = 156). After delivery the relative amounts of 18:2(n-6) and 18:3(n-3) in maternal plasma were significantly lower in pregnancy-induced hypertension than in normal pregnancy. This was associated with significantly higher levels of (n-6) long-chain polyenes and cervonic acid (22:6[n-3]). In comparison with the situation at 32 weeks, the postpartum cervonic acid status increased in pregnancy-induced hypertension, whereas it decreased in normal pregnancy. The cervonic acid levels in umbilical plasma phospholipids were significantly higher after pregnancy-induced hypertension than after normal pregnancy. No significant differences were observed for the fatty acid content in umbilical vessel walls. CONCLUSION: The results indicate that the altered essential fatty acid status in pregnancy-induced hypertension is a late phenomenon and is therefore unlikely to have contributed to the pathogenesis of pregnancy-induced hypertension. Moreover, the neonatal essential fatty acid status is not negatively affected by pregnancy-induced hypertension.
OBJECTIVE: Our purpose was to investigate, in a prospective way, whether the altered essential fatty acid status observed in pregnancy-induced hypertension is a consequence of the disease or may contribute to its cause. STUDY DESIGN: Pregnant women healthy at the start of the study were asked to give a blood sample before 16 weeks, at 22 weeks, and at 32 weeks of gestation. After delivery a blood sample from the umbilical vein, a piece of the umbilical cord, and a maternal blood sample were collected. Fatty acid compositions were determined of the phospholipids isolated from plasma and umbilical arterial and venous vessel walls. The nutrient intake of the pregnant women was assessed by use of the dietary history method and food frequency questionnaires. The results of each woman with pregnancy-induced hypertension were compared with the results of three matched healthy controls. RESULTS: During pregnancy (16 to 32 weeks) no significant differences were observed in nutrient intake and maternal plasma fatty acid composition between the group with pregnancy-induced hypertension (n = 52) and the control group (n = 156). After delivery the relative amounts of 18:2(n-6) and 18:3(n-3) in maternal plasma were significantly lower in pregnancy-induced hypertension than in normal pregnancy. This was associated with significantly higher levels of (n-6) long-chain polyenes and cervonic acid (22:6[n-3]). In comparison with the situation at 32 weeks, the postpartum cervonic acid status increased in pregnancy-induced hypertension, whereas it decreased in normal pregnancy. The cervonic acid levels in umbilical plasma phospholipids were significantly higher after pregnancy-induced hypertension than after normal pregnancy. No significant differences were observed for the fatty acid content in umbilical vessel walls. CONCLUSION: The results indicate that the altered essential fatty acid status in pregnancy-induced hypertension is a late phenomenon and is therefore unlikely to have contributed to the pathogenesis of pregnancy-induced hypertension. Moreover, the neonatal essential fatty acid status is not negatively affected by pregnancy-induced hypertension.
Authors: Nisha S Wadhwani; Ankita S Narang; Savita S Mehendale; Girija N Wagh; Sanjay A Gupte; Sadhana R Joshi Journal: Lipids Date: 2015-12-01 Impact factor: 1.880
Authors: Wai-Yee Lim; Mary Chong; Philip C Calder; Kenneth Kwek; Yap-Seng Chong; Peter D Gluckman; Keith M Godfrey; Seang-Mei Saw; An Pan Journal: Medicine (Baltimore) Date: 2015-03 Impact factor: 1.889