Association between lower hair zinc levels and Neural Tube Defects

Srinivas, M; Gupta, DK; Rathi, Satyajeet S.; Grover, J.K; Vats, Vikrant; Sharma, Jyotsna; Mitra, Debdeep

doi:10.1007/bf02723245

Cited by 42 publications

(19 citation statements)

References 20 publications

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“…The group of 18 women used to estimate dietary folate intake was small, but comparison of our data with the National Survey [40] gave values almost identical to ours (Table IV).…”

Section: Strengths and Limitations Of The Studysupporting

confidence: 77%

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Survey of total folate intake at conception and assessment of impact of fortification

Nichols

Curtis

Rayman

2008

Journal of Nutritional & Environmental Medicine

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Background. In view of plans for dietary fortification with folic acid, there is a need to reassess the advice being given in primary care. Patients and professionals may assume that fortification will make preconceptional folic acid supplementation unnecessary, but this is unlikely to be correct. Aim. To calculate the intake of total folic acid and folate at conception and to estimate the impact of fortification on the incidence of neural tube defect (NTD) conceptions.Design. An in-depth investigation of dietary folate intake of 18 women and a survey of preconception supplementation in a group of 130 women, including an assessment of the probable impact of mandatory fortification. Method. Dietary folate intake of six infertile women and 12 age-matched fertile controls was assessed using a 7-day weighed diet diary. Mean values for this group were used as an estimate of local dietary folate intake. Questionnaires about periconceptional intake of supplements that included folic acid in their formulation were given to newly pregnant women attending district midwife clinics, a series of women attending an assisted conception unit and a self-help group of lesbians who were either pregnant or planning a pregnancy. Results. Of the 18 women in the dietary study there was suboptimal dietary folate intake in all infertile subjects and in eight of 12 controls. An approximate value for the combined intake of dietary folate and folic acid in the larger survey (n5130) was calculated. We estimated that UK dietary fortification will double the number of pregnancies with adequate total folate intake. From previous data on folic acid intake and NTD births we estimate that this will prevent 226-343 conceptions per year in the UK from developing NTD malformations. Conclusions. Fortification should prevent approximately 226-343 conceptions a year from developing NTDs, but 45% of women will still have an inadequate total folate intake, unless supplementation levels improve.

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“…The group of 18 women used to estimate dietary folate intake was small, but comparison of our data with the National Survey [40] gave values almost identical to ours (Table IV).…”

Section: Strengths and Limitations Of The Studysupporting

confidence: 77%

“…Justification of .700 mg /day as a standard for optimal TFI is based on the assumption that optimal lowering of homcysteine reduces the risk of NTD to near zero for most women [31,32], but 20-30% of women may need .4000 mg /day or may have a NTD aetiology that does not respond to any dose of FA [35,36,40].…”

Section: Strengths and Limitations Of The Studymentioning

confidence: 99%

Survey of total folate intake at conception and assessment of impact of fortification

Nichols

Curtis

Rayman

2008

Journal of Nutritional & Environmental Medicine

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“…Results of a study in Turkey showed newborn serum zinc and selenium to be low in NTDs compared to normal controls (26). An Indian study that evaluated maternal and newborn hair zinc levels in association with NTDs found that the hair zinc levels in both mothers and newborns were significantly low compared to normal controls and recommended a follow-up study with zinc supplementation in the periconceptional period and outcome in the subsequent pregnancy (27). …”

Section: Discussionmentioning

confidence: 99%

Maternal and Neonatal Serum Zinc Level and Its Relationship with Neural Tube Defects

Dey

Shahidullah

Mannan

et al. 2010

J Health Popul Nutr

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Neural tube defect (NTD) is a multi-factorial disorder in which nutritional, genetic and environmental factors are involved. Among the nutritional factors, low level of serum zinc has been reported from different parts of the world. This hospital-based case-control study was conducted with the objective of finding the relationship between serum zinc level in newborns and their mothers and NTDs in a Bangladeshi population. The study was conducted during August 2006–July 2007 at the Bangabandhu Sheikh Mujib Medical University (BSMMU) in Dhaka. In total, 32 mothers and their newborns with NTDs were included as cases and another 32 mothers with their normal babies were included as controls. Concentration of serum zinc was determined by pyro-coated graphite furnace atomic absorption spectrophotometer (GF-AAS). The mean age of the case and control mothers was 25.28 years and 24.34 years respectively. The mean gestational age of the case newborns was 36.59 weeks and that of the control newborns was 37.75 weeks. The mean serum zinc level of the case and control mothers was 610.2 μg/L and 883.0 μg/L respectively (p<0.01). The mean serum zinc level of the case and control newborns was 723 μg/L and 1,046 μg/L respectively (p<0.01). In both case and control groups, the serum zinc level of the newborns positively correlated with that of the mothers. The serum zinc levels of the mothers and newborns negatively correlated with NTDs. Mothers with serum zinc level lower than normal were 7.66 [95% confidence interval (CI) 2.5-23.28] times more likely to have NTDs compared to the normal zinc level of mothers. After adjusting for the zinc level of the newborns, parity, and age of the mothers, this risk reduced 1.61 times [confidence interval (CI) 95% 0.24-8.77]. On the other hand, the low serum zinc level of the newborns was 7.22 times more associated with NTDs compared to the newborns with the normal serum zinc level, which was statistically significant (p=0.001). After adjusting for other factors, such as maternal age and parity, newborns with the low serum zinc level was found to be 9.186 times more likely to be associated with NTDs compared to newborns with normal serum zinc level. Based on the findings, it may be concluded that the low serum zinc levels of newborns may be associated with NTDs. To confirm these findings, a further study with a larger sample-size is recommended. Moreover, a follow-up study with zinc supplementation to pregnant women and its impact on NTDs is also recommended.

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“…Zn is critical for many processes involved in CNS development, such as neurogenesis, neuronal migration, and synaptogenesis and its deficiency could interfere with neurophysiological development (22)(23)(24). In humans, mild maternal Zn deficiency, assessed by serum and hair Zn, is associated with an increased frequency of neural tube defects, which may subsequently impair brain development (25). Zn deprivation in immature animals has been demonstrated to impair behavior, including learning, attention, and memory (26) similar to the effects of prenatal ethanol exposure.…”

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confidence: 99%

Prenatal Zinc Treatment at the Time of Acute Ethanol Exposure Limits Spatial Memory Impairments in Mouse Offspring

2006

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Zinc (Zn) treatment given together with acute ethanol in early pregnancy has previously been demonstrated to protect against physical birth abnormalities in mice. The current study examined whether this Zn treatment (s.c. injection) can also prevent the more subtle cognitive impairments caused by ethanol exposure in early pregnancy. Pregnant C57BL/6J dams were injected with saline (0.85% wt/vol NaCl) or 25% ethanol (0.015 mL/g body weight) intraperitoneally at 0 and 4 h on gestational d (GD) 8. ZnSO 4 (2.5 g Zn/g at 0 h) treatment was administered by s.c. injection immediately following ethanol treatment. Offspring were randomly selected from litters for each of the three treatment groups and were tested at 55 and 70 d of age using a cross-maze water escape task for spatial learning and memory impairments consecutively. No differences were observed between treatments for the spatial learning task. However, young adult mice exposed to ethanol in utero demonstrated impaired spatial memory, with a decrease in correct trials and increased escape latency and incorrect entry measurements, compared with salinetreated controls. In comparison, offspring given s.c. Zn treatment at the time of ethanol exposure were not cognitively impaired, performing at the same level as control mice in the cross-maze escape task. These findings indicate that critically timed Zn administration can limit spatial memory impairments caused by ethanol exposure in early pregnancy. T he teratogenic nature of ethanol has been well documented in humans and experimental animals (1-3). Consumption of ethanol during pregnancy can produce an array of physical abnormalities, including prenatal and/or postnatal growth deficiency and craniofacial dysmorphology (4). However, cognitive and behavioral impairments, such as deficits in attention, learning, and memory (5) are much more commonly observed in children exposed prenatally to ethanol and hence are more significant and costly to both the individual and community. These outcomes result from diverse maternal drinking patterns, ranging from the episodic ЉbingeЉ of large quantities of ethanol over a short time period to chronic ethanol intake.The mechanisms involved in ethanol-related abnormalities are unclear. Although it is likely that many factors are involved, several lines of evidence support fetal Zn deficiency as a major contributing factor to ethanol teratogenicity. First, an adequate supply of Zn to the fetus is critical during pregnancy (6). In rodents, there are similarities in fetal outcome between prenatal Zn deficiency and prenatal ethanol exposure. These include increased fetal resorptions, low birth weight, and birth abnormalities (7-10). These effects are potentiated during organogenesis (GD 7-12 in rodents, weeks 3-9 in humans), a period during early pregnancy critical for development and cell differentiation.Second, studies in rats (11) and in our laboratory using mice demonstrate that acute ethanol exposure in early pregnancy causes fetal Zn deficiency via the induction of ...

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Association between lower hair zinc levels and Neural Tube Defects

Cited by 42 publications

References 20 publications

Survey of total folate intake at conception and assessment of impact of fortification

Survey of total folate intake at conception and assessment of impact of fortification

Maternal and Neonatal Serum Zinc Level and Its Relationship with Neural Tube Defects

Prenatal Zinc Treatment at the Time of Acute Ethanol Exposure Limits Spatial Memory Impairments in Mouse Offspring

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