scholarly journals Folic acid supplementation and dietary folate intake, and risk of preeclampsia

2015 ◽  
Vol 69 (10) ◽  
pp. 1145-1150 ◽  
Author(s):  
Y Wang ◽  
N Zhao ◽  
J Qiu ◽  
X He ◽  
M Zhou ◽  
...  
2019 ◽  
Vol 23 (11) ◽  
pp. 1965-1973
Author(s):  
Huaqi Guo ◽  
Baohong Mao ◽  
Meng Wang ◽  
Qing Liu ◽  
Liping Yang ◽  
...  

AbstractObjective:To investigate the hypothesis that folic acid supplementation and dietary folate intake before conception and during pregnancy reduce the risk of small for gestational age (SGA) and to examine the joint effect of folic acid supplementation and dietary folate intake on the risk of SGA.Design:Participants were interviewed by trained study interviewers using a standardized and structured questionnaire. Information on birth outcomes and maternal complications was abstracted from medical records and dietary information was collected via a semi-quantitative FFQ before conception and during pregnancy.Setting:A birth cohort data analysis using the 2010–2012 Gansu Provincial Maternity and Child Care Hospital.Participants:Women (n 8758) and their children enrolled in the study.Results:Folic acid supplementation was associated with a reduced risk of SGA (OR = 0·72, 95 % CI 0·60, 0·86), with the reduced risk seen mainly for SGA at ≥37 weeks of gestational age (OR = 0·70, 95 % CI 0·58, 0·85) and nulliparous SGA (OR = 0·67, 95 % CI 0·54, 0·84). There was no significant association between dietary folate intake and SGA risk.Conclusions:Our study suggested that folic acid supplementation was associated with a reduced risk of SGA and the risk varied by preterm status and parity.


2021 ◽  
Author(s):  
LiPing Yang ◽  
Wenjuan Wang ◽  
Baohong Mao ◽  
Jie Qiu ◽  
Huaqi Guo ◽  
...  

Abstract ObjectivesTo investigate the independent and collective effects of maternal folic acid supplementation or dietary folate intake upon the risk of low birth weight (LBW), and to further comprehensively examine the joint associations of folic acid supplementation and dietary folate intake with LBW by various clinical subtypes.DesignParticipants were recruited in Gansu Provincial Maternity and Child Care Hospital. A standardized and structured questionnaire was distributed to collect demographic factors, reproductive and medical history, occupational and residential history, physical activity and diet. Data on pregnancy-related complications and birth outcomes were extracted from medical records. Unconditional logistic regression models were used to estimate odds ratio (OR) and 95% confidence interval (95%CI) for single and joint associations of folic acid supplementation and dietary folate intake with LBW. SettingA birth cohort data analysis using the 2010–2012 Gansu Provincial Maternity and Child Care Hospital in Lanzhou, China.Participants9231 pregnant women and their children were enrolled in the study. ResultsCompared to non-users, folic acid supplementation was associated with a reduced risk of LBW (OR: 0.80, 95%CI: 0.66-0.97), and the reduced risk was mainly seen for term-LBW (OR: 0.59, 95%CI: 0.41-0.85), and multiparous-LBW (OR: 0.72, 95%CI: 0.54-0.94). For dietary folate intake, there were no significant associations with LBW, and there was no interaction of folic acid supplement and dietary folate intake on LBW.ConclusionsOur study results indicated that folic acid supplementation was associated with a reduced risk of LBW, and there was not interaction of folic acid supplement and dietary folate intake on LBW.


PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0187996 ◽  
Author(s):  
Baohong Mao ◽  
Jie Qiu ◽  
Nan Zhao ◽  
Yawen Shao ◽  
Wei Dai ◽  
...  

2015 ◽  
Vol 55 (4) ◽  
pp. 1411-1422 ◽  
Author(s):  
Xiaohui Liu ◽  
Ling Lv ◽  
Hanru Zhang ◽  
Nan Zhao ◽  
Jie Qiu ◽  
...  

2019 ◽  
Vol 57 (6) ◽  
pp. 678-686
Author(s):  
Vivienne J. Mendonca

Background: Orofacial clefts are the most common congenital anomaly worldwide. Cleft etiology appears to be multifactorial, with genetic and environmental components. Although periconceptional folic acid supplementation has been shown to be protective for neural tube defects, current evidence for its role in cleft prevention is mixed with few studies from low- and middle-income countries. Aim: To investigate the association between periconceptional folic acid intake and incidence of nonsyndromic orofacial clefts among infants in Bangalore, India. Methods: A hospital-based case–control study (106 cases, 212 controls) utilizing a questionnaire to collect data on prenatal supplements, dietary folate, and potentially confounding factors. Multivariate logistic regression analysis was used to assess relationships between folic acid supplementation and all nonsyndromic clefts, and in separate analyses for cleft lip and/or palate (CL/P) and cleft palate (CP), adjusting for statistically significant variables. Results: A statistically significant protective association was found for separate folic acid supplements (not combined with iron or multivitamins) taken in the periconceptional period and all clefts combined (adjusted odds ratio [OR]: 0.62, 95% confidence interval [CI], 0.45-0.86) and CL/P (adjusted OR: 0.57; 95% CI, 0.38-0.86). Higher levels of dietary folate were found to be associated with a reduced risk for all clefts (adjusted OR: 0.98, 95% CI, 0.96-0.99), CL/P (adjusted OR: 0.98, 95% CI, 0.96-0.99), and CP (adjusted OR: 0.96, 95% CI, 0.93-0.99). Conclusion: This study provides limited evidence for a protective association of periconceptional folic acid supplementation with nonsyndromic orofacial clefts. The low proportion of mothers taking folic acid supplements in the periconceptional period highlights the need for increased education and awareness regarding prenatal nutrition.


2011 ◽  
Vol 105 (9) ◽  
pp. 1294-1302 ◽  
Author(s):  
Ta-Fu Chen ◽  
Ming-Jang Chiu ◽  
Chou-Tz Huang ◽  
Ming-Chi Tang ◽  
Sue-Jane Wang ◽  
...  

Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of β-amyloid(25–35)(Aβ) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aβ peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aβ injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aβ peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aβ-injected rats enriched brain folate levels and reduced mtDNA4834deletion in the hippocampal and medullary regions compared with corresponding tissues of Aβ+FD rats (P < 0·05). Aβ+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aβ+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834deletions, particularly, in the hippocampus. Upon Aβ challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.


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