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Maternal Consumption (maternal + consumption)
Selected AbstractsMaternal consumption of dairy products during pregnancy and lactation, and the development of cow's milk antibodies in the offspringACTA PAEDIATRICA, Issue 6 2005Maijaliisa Erkkola Abstract Objective: To assess whether the maternal consumption of milk and milk products affects development of cow's milk (CM) antibodies in infants. Design: A randomized pilot trial using food frequency questionnaires (mothers) and food records (infants). Setting: Families with a newborn infant with increased HLA-DQB1-conferred risk of type 1 diabetes and at least one first-degree relative affected by type 1 diabetes from 16 hospitals in Finland between April 1995 and November 1997. Subjects and intervention: Infants randomized to receive a hydrolysed formula when breast milk was not available during their first 6,8 mo (n=112). Of these, 13 dropped out by the age of 3 mo and two were excluded due to incomplete CM antibody data. Results: Maternal milk protein intake from cheese during pregnancy was inversely related to IgA-class antibody titres to beta-lactoglobulin (BLG) and casein (CAS) at 3 mo, and to IgA antibody titres to BLG at 6 mo. Maternal consumption of raw milk products during lactation was positively related to the development of IgA antibody titres to CAS at 6 mo, and inversely correlated to IgG antibody titres to bovine serum albumin (BSA) and IgA antibody titres to CAS at 2 y. Maternal cheese consumption was inversely related to the IgG antibody titres to CM formula and CAS and to the IgA antibody titres to CAS in early infancy. Conclusions: Few associations were established between maternal CM protein intake and CM protein antibody levels in the infants. The milk and milk products taken by the mother differed in their impact on the emerging CM antibody response in the offspring. [source] Prenatal Alcohol Exposure Alters Biobehavioral Reactivity to Pain in NewbornsALCOHOLISM, Issue 4 2010Tim F. Oberlander Objectives:, To examine biobehavioral responses to an acute pain event in a Cape Town, South Africa, cohort consisting of 28 Cape Colored (mixed ancestry) newborns (n = 14) heavily exposed to alcohol during pregnancy (exposed), and born to abstainers (n = 14) or light (,0.5 oz absolute alcohol/d) drinkers (controls). Methods:, Mothers were recruited during the third trimester of pregnancy. Newborn data were collected on postpartum day 3 in the maternity obstetrical unit where the infant had been delivered. Heavy prenatal alcohol exposure was defined as maternal consumption of at least 14 drinks/wk or at least 1 incident of binge drinking/mo. Acute stress-related biobehavioral markers [salivary cortisol, heart rate (HR), respiratory sinus arrhythmia (RSA), spectral measures of heart rate variability (HRV), and videotaped facial actions] were collected thrice during a heel lance blood collection (baseline, lance, and recovery). After a feeding and nap, newborns were administered an abbreviated Brazelton Neonatal Behavioral Assessment Scale. Results:, There were no between-group differences in maternal age, marital status, parity, gravidity, depression, anxiety, pregnancy smoking, maternal education, or infant gestational age at birth (all ps > 0.15). In both groups, HR increased with the heel lance and decreased during the postlance period. The alcohol-exposed group had lower mean HR than controls throughout, and showed no change in RSA over time. Cortisol levels showed no change over time in controls but decreased over time in exposed infants. Although facial action analyses revealed no group differences in response to the heel lance, behavioral responses assessed on the Brazelton Neonatal Scale showed less arousal in the exposed group. Conclusions:, Both cardiac autonomic and hypothalamic,pituitary,adrenal stress reactivity measures suggest a blunted response to an acute noxious event in alcohol-exposed newborns. This is supported by results on the Brazelton Neonatal Scale indicating reduced behavioral arousal in the exposed group. To our knowledge, these data provide the first biobehavioral examination of early pain reactivity in alcohol-exposed newborns and have important implications for understanding neuro-/biobehavioral effects of prenatal alcohol exposure in the newborn period. [source] Effects of Ethanol on Mouse Embryonic Stem CellsALCOHOLISM, Issue 12 2009Alla Arzumanyan Background:, Fetal alcohol syndrome (FAS) reflects a constellation of congenital abnormalities caused by excess maternal consumption of alcohol. It is likely that interference with embryonic development plays a role in the pathogenesis of the disorder. Ethanol-induced apoptosis has been suggested as a causal factor in the genesis of FAS. Mouse embryonic stem (mES) cells are pluripotent cells that differentiate in vitro to cell aggregates termed embryoid bodies (EBs), wherein differentiation capacity and gene expression profile are similar to those of the early embryo. Methods:, To investigate the effects of ethanol during differentiation, mES cells were cultured on a gelatin surface in the presence of leukemia inhibitory factor which maintains adherent undifferentiated cells or in suspension to promote formation of EBs. All cells were treated (1,6 days) with 80 mM ethanol. The pluripotency and differentiation of mES cells were evaluated by western blotting of stage-specific embryonic antigen (SSEA-1), transcription factors Oct-3/4, Sox-2, and Nanog, using alkaline phosphatase staining. Apoptosis (early to late stages) was assessed by fluorescence-activated cell sorting using TdT-mediated biotin,dUTP nick-end labelling assay and fluorescein isothiocyanate-Annexin V/propidium iodide staining. Results:, Ethanol increased apoptosis during in vitro differentiation of mES cells to EBs, whereas undifferentiated cells were not affected. Ethanol exposure also interfered with pluripotency marker patterns causing an upregulation of SSEA-1 under self-renewal conditions. In EBs, ethanol delayed the downregulation of SSEA-1 and affected the regulation of transcription factors during differentiation. Conclusion:, Our findings suggest that ethanol may contribute to the pathogenesis of FAS by triggering apoptotic pathways during differentiation of embryonic stem cells and deregulating early stages of embryogenesis. [source] Consumption of vegetables, fruit, and antioxidants during pregnancy and wheeze and eczema in infantsALLERGY, Issue 6 2010Y. Miyake To cite this article: Miyake Y, Sasaki S, Tanaka K, Hirota Y. Consumption of vegetables, fruit, and antioxidants during pregnancy and wheeze and eczema in infants. Allergy 2010; 65: 758,765. Abstract Background:, Two previous cohort studies showed inverse relationships between maternal vitamin E and zinc intake during pregnancy and the risk of wheeze and/or asthma in the offspring. We investigated the association between maternal intake of vegetables, fruit, and selected antioxidants during pregnancy and the risk of wheeze and eczema in the offspring aged 16,24 months. Methods:, Subjects were 763 Japanese mother,child pairs. Data on maternal intake during pregnancy were assessed with a diet history questionnaire. Data on symptoms of wheeze and eczema were based on criteria of the International Study of Asthma and Allergies in Childhood. Results:, Higher maternal intake of green and yellow vegetables, citrus fruit, and ,-carotene during pregnancy was significantly associated with a reduced risk of eczema, but not wheeze, in the offspring {adjusted odds ratios (ORs) between extreme quartiles [95% confidence intervals (CIs)] = 0.41 (0.24,0.71), 0.53 (0.30,0.93), and 0.52 (0.30,0.89), respectively}. Maternal vitamin E consumption during pregnancy was significantly inversely related to the risk of infantile wheeze, but not eczema [adjusted OR (95% CI) = 0.54 (0.32,0.90)]. No statistically significant exposure,response associations were observed between maternal intake of total vegetables, vegetables other than green and yellow vegetables, total fruit, apples, ,-carotene, vitamin C, or zinc and the risk of wheeze or eczema in the children. Conclusions:, Higher maternal consumption of green and yellow vegetables, citrus fruit, and ,-carotene during pregnancy may be protective against the development of eczema in the offspring. Higher maternal vitamin E intake during pregnancy may reduce the risk of infantile wheeze. [source] Maternal consumption of dairy products during pregnancy and lactation, and the development of cow's milk antibodies in the offspringACTA PAEDIATRICA, Issue 6 2005Maijaliisa Erkkola Abstract Objective: To assess whether the maternal consumption of milk and milk products affects development of cow's milk (CM) antibodies in infants. Design: A randomized pilot trial using food frequency questionnaires (mothers) and food records (infants). Setting: Families with a newborn infant with increased HLA-DQB1-conferred risk of type 1 diabetes and at least one first-degree relative affected by type 1 diabetes from 16 hospitals in Finland between April 1995 and November 1997. Subjects and intervention: Infants randomized to receive a hydrolysed formula when breast milk was not available during their first 6,8 mo (n=112). Of these, 13 dropped out by the age of 3 mo and two were excluded due to incomplete CM antibody data. Results: Maternal milk protein intake from cheese during pregnancy was inversely related to IgA-class antibody titres to beta-lactoglobulin (BLG) and casein (CAS) at 3 mo, and to IgA antibody titres to BLG at 6 mo. Maternal consumption of raw milk products during lactation was positively related to the development of IgA antibody titres to CAS at 6 mo, and inversely correlated to IgG antibody titres to bovine serum albumin (BSA) and IgA antibody titres to CAS at 2 y. Maternal cheese consumption was inversely related to the IgG antibody titres to CM formula and CAS and to the IgA antibody titres to CAS in early infancy. Conclusions: Few associations were established between maternal CM protein intake and CM protein antibody levels in the infants. The milk and milk products taken by the mother differed in their impact on the emerging CM antibody response in the offspring. [source] |