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

Abstract

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.

Association of essential trace metals in maternal hair with the risk of neural tube defects in offspring

“…Zinc deficiency has been widely reported to be associated with NTD risk (Carrillo‐Ponce Mde et al, ; Golalipour et al, ; Dey et al, ). Because the hair Zn concentration in this population was at a comparable level to previous studies (Chojnacka et al, ; Wu et al, ; Gellein et al, ; Hsieh et al, ), we considered that there was no Zn deficiency in study participants.…”

“…Essential trace metals (ETMs), as important nutrients from various food types, play an important role in embryonic development (Hostetler et al, 2003). In the human body, some of them have been associated with NTD risk, e.g., zinc (Zn) (Dey et al, 2010), iron (Fe) (Shaw et al, 1999), copper (Cu) (Cengiz et al, 2004), and manganese (Mn) (Liu et al, 2013). However, the association between maternal intake of ETMs and the risk of NTDs has not been comprehensively studied among a large population.…”

The Continuing Challenge of Understanding, Preventing, and Treating Neural Tube Defects

“…This evidence has led to a small PONTI Study (Prevention of NTDs by Inositol), in conjunction with FA for women with a previous NTD-affected pregnancy. Expansion of studies to additional micronutrients—for instance vitamin B12 or zinc, low levels of which appear associated with NTD risk in humans (78, 79)—carry the possibility of defining which genetic risk factors may be best targeted by therapies beyond FA. Human epidemiological studies have uncovered a number of risk factors and animal models provide a largely untapped resource for defining which gene mutations may be most susceptible to these environmental influences and the mechanistic basis for their interaction.…”

Gestational marginal zinc deficiency impaired fetal neural progenitor cell proliferation by disrupting the ERK1/2 signaling pathway

“…It was recently estimated that 15%-20% of the global population is at risk of inadequate dietary zinc intake [1]. Global incidence of stunting is associated with dietary zinc intake [1] and zinc supplementation during pregnancy can prevent congenital malformations including neural tube defects resulting from inadequate intake [2,3], or impaired absorption in the case of acrodermititis enteropathica [4]. Subtler effects of prenatal zinc supplementation include improved function of the autonomic nervous system later in life [5].…”