Progress 09/01/05 to 02/28/09
Outputs
OUTPUTS: In 2008 and 2009, we shared information about our research project. How we shared information about the outcomes of our studies is presented in relation to the goals and objectives of our research project:1) Assess possible maternal depletion of lutein and zeaxanthin by comparing lutein and zeaxanthin in the plasma and diet of pregnant women with women who have never been pregnant and by comparing lutein and zeaxanthin. April 7, 200, a talk entitled Depletion of Maternal Stores of Lutein and Zeaxanthin During Pregnancy and Lactation was presented at the Experimental Biology meeting, Nutrition-Vitamin A, Carotenoids and Retinoids (Dietary and Metabolic Aspects). 2) Determine placental transfer of lutein and zeaxanthin into the preterm and full-term infants at the time of birth by measuring arterial and venous cord blood in term infants and mixed cord blood in preterm infants and maternal venous blood. April 7, 2008, a talk entitled Maternal Transfer of Lutein and Zeaxanthin into the Infant During Pregnancy was presented at the Experimental Biology meeting, Nutrition-Vitamin A, Carotenoids and Retinoids (Dietary and Metabolic Aspects). November 11, 2008, a talk entitled Maternal Transfer of Lutein and Zesxanthin into the Fetus: Implication for Age-Related Macular Degeneration, was presented at the Oregon Health & Science University, Heart Research Institute, Placenta Research Group. 3) In preterm infants, correlate the development of the retinopathy of prematurity with maternal and infant plasma concentrations of lutein and zeaxanthin, with maternal and infant dietary intakes of lutein and zeaxanthin (which for the infant will be human milk and/or formula) and with absorption of lutein and zeaxanthin. May 8, 2008, a talk entitled "Lutein and Zeaxanthin: Retinopathy of Prematurity and Macular Degeneration, was presented at the annual meeting of the Oregon Dietetic Association. 4) Measure over time the content of lutein and zeaxanthin in milk from lactating mothers and compare it with their dietary intakes and plasma concentrations. In a sub-sample of lactating women, give a lutein supplement to augment the milk concentration of lutein. April 18, 2009, a talk entitled Will Lutein Supplementation of Lactating Women Affect the Lutein Content of Milk and the Lutein Content of Maternal and Preterm Infant Plasma, was prepared but not presented because of illness at the Experimental Biology meeting, Nutrition-CARIG (Carotenoids). Our plan is to continue to share the data from these studies with colleagues through presentations at meetings and peer-reviewed publications. PARTICIPANTS: Principal Investigator William E. Connor, MD directed the study. Co-investigator Sonja L. Connor, MS, RD, LD was the study manager. She recruited subjects, collected and managed the data and supervised the study personnel. Rachel Van Dusen recruited subjects, collected and managed data, and analyzed dietary data. Nitza Bezzerides, BS, RD recruited subjects, collected and managed data, and analyzed dietary data. Sharon Dunham, RN recruited subjects in the OHSU Doernbecher Neonatal Intensive Care Center. YingYing Sun prepared milk and blood samples for analysis. Ying Ming Wang, MD performed the carotenoid analyses of the milk and blood samples. Collaborators included Richard Lowensohn, MD, Department of Obstetrics and Gynecology, Oregon Health & Science University, De-Ann Pillers, MD, PhD, Doernbecher Neonatal Care Center, Department of Pediatrics, Oregon Health & Science University and Earl Palmer, MD, Department of Ophthalmology, Casey Eye Institute, Oregon Health & Science University. TARGET AUDIENCES: Not relevant to this project. PROJECT MODIFICATIONS: Not relevant to this project.
Impacts
Women (22 never pregnant, 61 pregnant, 61 lactating) and infants (27 term, 67 preterm, 52 less than either 1,500 g or 31 weeks gestation) were studied. Never pregnant and pregnant women were similar in age (28 vs. 29 years), education (17 vs. 16 years), height (1.7 vs. 1.7 m), blood pressure (104/59 vs. 109/60 mmHg) and hemoglobin (13.2 vs. 12.0 g/dL). While plasma lutein/zeaxanthin were similar in the never pregnant (18.4/3.0 mcg/dL) and pregnant women (16.4/3.4 mcg/dL), they were significantly lower at 4 weeks lactation (10.4/2.1 mcg/dL). Plasma lutein/zeaxanthin were significantly lower in women who had given birth to three or more children compared to one or two children (10.3/2.3 vs. 15.4/3.1 mcg/dL). Dietary intakes were 2-3 mg/day (typical U.S. intake), which may have been insufficient to replace amounts transferred during multiple pregnancies/lactation. The suggested intake is 6-9 mg (5-9 servings of fruits and vegetables) for prevention of age-related macular degeneration. Cord blood lutein/zeaxanthin were 20 percent of maternal plasma indicating placental transfer from the mother to the fetus. Correlation of cord blood to maternal plasma lutein/zeaxanthin was 0.76/0.58. Lower fetal levels of lutein/zeaxanthin may be related to lower liproprotein levels of which HDL is the major transporter. Fetal HDL cholesterol was only 27% of maternal HDL cholesterol. Milk samples were obtained from 36 lactating women. Nineteen took a lutein supplement (12 mg/day) weeks 5-8. Plasma lutein at 4, 8 and 12 weeks was 10, 10 and 10 mcg/dL in the no supplement group and 11, 38 and 10 mcg/dL in the lutein supplement group. Breast milk lutein at 4, 8 and 12 weeks for women who did not receive the lutein supplement was 4.5, 3.8 and 4.5 mcg/dL (4 vs. 8 weeks p=0.64). Breast milk lutein at 4, 8 and 12 weeks in the supplement group was 3.1, 14.2 and 3.8 mcg/dL (4 vs. 8 weeks p=0.00). For Infants whose mothers did not receive the lutein supplement, the plasma lutein was 1.6 and 1.3 mcg/dL at 4 and 8 weeks; it increased from 1.7 to 10.8 mcg/dL in infants whose mothers received the lutein supplement. Plasma lutein and zeaxanthin at age 4 weeks were not different in preterm infants who developed retinopathy of prematurity (1.36/0.55 mcg/dL) and those who did not (1.48/0.43 mcg/dL). Cord blood lutein was 4.16 mcg/dL in term infants and 2.37 mcg/dL in preterm infants (p=0.02). Likewise, plasma lutein at 25-28 weeks gestation was 20.4 mcg/dL in mothers of term infants and 13.2 mcg/dL in mothers of preterm infants (p=0.01). At delivery plasma lutein was 18.7 mcg/dL in mothers of term infants and 10.3 mcg/dL in mothers of preterm infants (p=0.003). They were not different at 4 weeks postpartum (term 10.8 mcg/dL; preterm 10.1 mcg/dL. Conclusions: 1) Pregnancy and lactation may be a drain on body stores of lutein and zeaxanthin, 2) Dietary intakes may not be sufficient to replace lutein and zeaxanthin transferred during pregnancy, 3) Supplementation increased lutein in maternal plasma, breast milk and preterm plasma. The finding that plasma lutein and zeaxanthin levels were significantly lower in preterm vs. term infants and mothers needs further investigation.
Publications
- Connor, S.L., Bezerrides, E., Pillers D-A., and Connor, W.E. Will lutein supplementation of lactating women affect the lutein content of milk and the lutein content of maternal and preterm infant plasma Experimental Biology 2009, New Orleans, Nutrition-CARIG (Carotenoids) I.The FASEB Journal 2009;23:34.6
- Connor, W.E., Bezzerides, E., Wang, Y., and Connor, S.L. The depletion of maternal stores of lutein and zeaxanthin during pregnancy and lactation. Experimental Biology 2008, San Diego. Nutrition-Vitamin A, Carotenoids and Retinoids (Dietary and Metabolic Aspects). The FASEB Journal 2008;22:313.8.
- Connor, S.L., Connor, W.E., Bezzerides, E.A., Wang, Y. The maternal transfer of lutein and zeaxanthin into the fetus during pregnancy. Experimental Biology 2008, San Diego. Nutrition-Vitamin A, Carotenoids and Retinoids (Dietary and Metabolic Aspects). The FASEB Journal 2008;22:451.4.
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Progress 09/01/06 to 08/31/07
Outputs
Enrollment has proceeded as planned: 22 women who had never been pregnant, 53 pregnant women, 47 lactating women and 27 term and 34 preterm infants. Never pregnant and pregnant women were similar in age (28 vs. 29 years respectively), education (17 vs. 16 years), height (1.7 vs. 1.7 m), blood pressure (104/59 vs. 109/61 mmHg) and hemoglobin (13.2 vs. 12.2 g/dL). While plasma lutein and zeaxanthin concentrations were similar in the never pregnant (18.4/3.0 mcg/dL), pregnant (16.2/3.4 mcg/dL) and lactating (16.6/3.6 mcg/dL) groups, they were lower in women who had given birth to three or more children compared to women who had given birth to one or two children (plasma lutein, 10.5 vs. 15.8 mg/dL respectively, p< 0.01; plasma zeaxanthin 2.4 vs. 3.2 mcg/dL, p<0.03). Dietary intakes of lutein and zeaxanthin of never pregnant, pregnant and lactating women were similar to typical U.S. intakes (totaling 2 to 3 mg/day), but may have been insufficient to replace amounts
transferred during multiple pregnancies and lactation. Dietary intakes were considerably lower than the suggested intake of 6-9 mg for the prevention of age-related macular degeneration. Such an amount would be provided by the recommended daily intake of five to nine servings of fruits and vegetables. Plasma lutein and zeaxanthin concentrations of the fetus (cord blood) were twenty percent of maternal levels, indicative of placental transfer from the mother to the fetus. Lower concentrations of lutein and zeaxanthin in the fetus may be related to lower concentrations in lipoproteins, of which HDL is the major transporter of lutein and zeaxanthin (cord blood lutein and zeaxanthin were 28%of maternal lutein and zeaxanthin; cord blood HDL cholesterol was 27% of maternal HDL cholesterol). Milk samples were obtained from twenty-five lactating women at weeks 2, 4, 5, 6, 7, 8, 10 and 12 postpartum. Twelve women took a lutein supplement (12 mg/day) weeks 5-8. Plasma lutein at 4, 8 and 12
weeks was 10, 12 and 9 mcg/dL respectively in the no supplement group and 12, 38 and 11 mcg/dL in the lutein supplement group. Breast milk lutein concentrations at 4, 8 and 12 weeks for women who did not received the lutein supplement was 4, 4, and 5 mcg/dL. Breast milk lutein concentrations at 4, 8 and 12 weeks for the women who received the lutein supplement were 4, 16 and 4 mcg/dL. Preterm infant plasma lutein at 4 and 8 weeks was 1.6 and 1.5 mcg/dL in infants whose mothers did not receive the lutein supplement and 2.6 and 10.4 mcg/dL in preterm infants whose mothers received the lutein supplement. Summary of preliminary findings: 1) Lutein supplementation increased lutein in maternal plasma, breast milk and preterm infant plasma, 2) Because of placental and breast milk transfer, pregnancy and lactation may be a drain on body stores of lutein and zeaxanthin, 3) Current dietary intakes of lutein and zeaxanthin may not be sufficient to replace the amount that is transferred during
pregnancy and lactation.
Impacts
Since this was the second year of the three year study, there are no outcomes/impacts to report.
Publications
- No publications reported this period
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Progress 09/01/05 to 08/31/06
Outputs
Nine women who have never been pregnant, 30 pregnant women, 19 lactating women and 20 term and 16 preterm infants were enrolled. Plasma lutein was 18.2 (SD-8.5) mcg/dL (pregnant, n=24) vs. 13.4 (SD4.4) mcg/dL (never pregnant, n=9). Plasma zeaxanthin was 4.0 (SD 2.1)mcg/dL (pregnant) and 2.2 (SD 0.6) mcg/dL (never pregnant). Lutein and zeaxanthin are transported in lipoproteins, especially HDL, but also in LDL and VLDL. Total cholesterol, LDL, VLDL, HDL and triglyceride concentrations were higher in the pregnant women, an expansion of all of the lipoproteins (plasma cholesterol 23%, triglyceride 188%, VLDL 171%, LDL 17% and HDL 8%). Differences between pregnant and never pregnant women for plasma lutein (36%) and zeaxanthin (82%) were similar to differences in plasma lipids and lipoproteins. If amounts of lutein and zeaxanthin delivered to plasma from the diet and adipose tissue stores remain constant and lipoproteins increase, the actual amounts of lutein and
zeaxanthin could have been diluted. Instead, the expansion of their pools in the plasma was similar to the expansion of lipoprotein pools. The origin of this increase in lutein and zeaxanthin might have come from increased dietary sources, with pregnant women being encouraged to consume fruits and vegetables, or it could have been derived from adipose tissue stores. Lutein supplementation (12 mg/d for four weeks) to lactating women led to increased breast milk lutein (3.47 [SD 2.53] to 11.55 [SD 13.61] mcg/dl). Plasma lutein also increased (10.6 [SD 1.6] to 31.8 [SD 9.4] mcg/dL). While these data represent small numbers, the increase appears to be significant. In comparison, zeaxanthin did not increase (plasma - 2.6 [SD 0.8] to 2.6 [SD 1.0] mcg/dL); breast milk - 1.55 [SD 1.49] to 1.39 [SD 1.26]). Zeaxanthin was not a prominent part of the supplement so no change was expected. We have data on preterm twins who had blood drawn before and after their mother took the lutein supplement.
The plasma lutein value for one twin (insufficient amount for the other) was 1.82 mcg/dL before and 9.78 (SD 2.36) mcg/dl after lutein supplementation. The relationship between maternal and fetal plasma lutein and zeaxanthin is interesting. Maternal lutein was 460 percent higher than fetal lutein; zeaxanthin was 304 percent higher. Since fetal lutein and zeaxanthin are derived from maternal sources by placental transport, we can compare the lutein-zeaxanthin ratio (maternal to fetal). The ratio was 5.42 in maternal plasma vs. 3.58 in fetal plasma, which implies a different way of handling lutein or zeaxanthin in the fetus. The lower ratio in fetal plasma suggests there is preferential loss of lutein to the tissues or retention of zeaxanthin. Perhaps there is some meaning in this in that in chicks and quail there seems to be greater preference of the retina for zeaxanthin. This may also occur in the developing retina of the fetus since the retina would be deriving zeaxanthin via
transport from plasma lipoproteins, particularly HDL.
Impacts
Since this was the first year of the study, there are no outcomes/impacts to report.
Publications
- No publications reported this period
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