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Vitamin D deficiency during pregnancy has been associated with poor foetal growth and neonatal birth anthropometry. However, the associations were inconsistent and could be confounded by neonatal vitamin D status and genetic factors. Until recently, limited studies have concomitantly examined the effect of maternal and neonatal vitamin D deficiency and vitamin D-related single nucleotide polymorphisms (SNPs) on neonatal birth anthropometry. This study aims to examine the independent and combined effects of maternal and neonatal vitamin D deficiency and vitamin-D-related SNPs on neonatal birth anthropometry. This cross-sectional study included 217 mother–neonate dyads recruited from Hospital Serdang, Selangor, Malaysia, between 2015 and 2017. Plasma 25-hydroxyvitamin D (25OHD) concentration was measured in maternal and umbilical cord blood using ultra-high-performance liquid chromatography (UHPLC). Maternal and neonatal vitamin D Receptor (VDR) SNP (rs2228570) genotypes were determined using high-resolution melting (HRM). Group-specific component (GC) SNPs (rs4588 and rs7041) genotypes were determined using restriction fragment length polymorphism. Our results showed that: (1) maternal vitamin D deficiency (25OHD < 30 nmol/L) was inversely associated with birth weight, head circumference and crown–heel length; (2) neonatal SNPs, VDR rs2228570 and GC rs4588, were significantly associated with birth weight and head circumference, respectively; and (3) a potential interaction was observed between maternal VDR rs2228570 with maternal vitamin D deficiency on head circumference. These findings suggest that the underlying mechanisms of vitamin D on foetal growth are likely to be localised in the maternal compartment, mediated through the placenta, rather than through cellular mechanisms within the foetus. Further large-scale studies are warranted to validate and extend these findings.

Parkinson’s disease (PD) is the most prevalent brain motor disorder and is frequently regarded as an idiopathic and sporadic disease due to its unclear etiology. Although the pathological mechanisms of PD have already been investigated at various omics levels, no disease-modifying drugs are currently available. At the moment, treatments can only provide symptomatic relief to control or improve motor symptoms. Parkinson’s disease is a multifactorial disease, the development and progression of which are influenced by multiple factors, including the genetic markups and the environment. As an indispensable component of our daily life, nutrition is considered one of the most robust environmental factors affecting our health. Consequently, depending on our dietary habits, nutrition can either induce or reduce our susceptibility to PD. Epigenetic mechanisms regulate gene expression through DNA methylation, histone modifications, and non-coding RNAs (ncRNAs) activity. Accumulating evidence from nutriepigenomics studies has reported altered epigenetic mechanisms in clinical and pre-clinical PD models, and the potential role of nutrition in modifying the changes. In addition, through nutrigenetics and nutrigenomics studies, the diet-gene, and gene-diet interactions concerning PD development and progression have been investigated. Herein, current findings on the roles of nutrition in epigenetic mechanisms underpinning PD development and progression are discussed. Recent advancements in the multi-omics approach in PD nutrition research are also underlined. The ability of nutrients to influence epigenetic mechanisms and the availability of multi-omics applications compel the immediate use of personalized nutrition as adjuvant therapy for PD.

Background: The microbiota plays a key role in early immunity maturation that affects infant health and is associated with the development of non-communicable diseases and allergies in later life. Objective: The MYBIOTA is a prospective mother-infant cohort study in Malaysia aiming to determine the association between gut microbiota with infant health (temperament, gastrointestinal disorders, eczema, asthma, and developmental delays) in Selangor, Malaysia. Methods: Pregnant mothers will be enrolled in their first trimester of pregnancy, and follow-ups will be done for infants during their first year of life. Maternal-infant biological samples (blood, feces, saliva, urine, and breast milk), anthropometric, dietary, and clinical information will be collected at different time points from early pregnancy to 12 months postpartum. Discussion: This study could provide a better understanding of the colonization and development of the gut microbiome during early life and its impact on infant health. Clinical trial registration: https://clinicaltrials.gov/, identifier NCT04919265.

Introduction: This study was carried out to quantify the selected bioactive compounds (i.e., chlorogenic acids, caffeine, and N-methylpyridinium) in instant coffee and to analyze its correlation with the gastric release effect of the HGT-1 cell line. Methods: Selected bioactive compounds in regular (REG), low sugar (LS), low fat (LF), white coffee (WC), white coffee low acid (WCA), decaffeinated (DC), and instant black coffee (BC) were quantified using HPLCDAD (high-performance liquid chromatography diode array detection) system and flow cytometry analysis for its gastric release effect when treated with HGT-1 cell. Results: The HPLC data showed the content of caffeine (60,212 ± 212 µg/ml) and chlorogenic acid (35,779 ± 3027 µg/ml) were significantly high in BC while the lowest caffeine value was found in DC coffee. Chlorogenic acid in other instant coffee samples showed insignificant content distinctions. As for N-methylpyridinium (NMP), the highest content was found in BC (565 µg/ml) and the lowest value was detected in WC (52 µg/ml) coffee. Gastric release activity by HGT-1 cells was significantly higher in DC and REG coffee treatment. Pearson correlation showed no significant correlation between the quantitative data and gastric release activity by HGT-1 cells. Conclusion: The selected bioactive compounds contained in instant coffees were unable to stimulate gastric release.

Background/objectives: Low early pregnancy serum 25-hydroxy vitamin D (25[OH]D) levels can increase gestational diabetes mellitus (GDM) risk, although inconsistent findings related to that association have been reported. This study examined the association of serum vitamin D with GDM and the possible influencers on this association. Subjects/methods: This study included 259 pregnant women within the Seremban Cohort Study (SECOST). Blood samples at < 14 weeks of gestation were drawn to determine serum 25(OH)D levels. GDM diagnosis was made at 24 to 32 weeks of gestation using a standard procedure. Association between serum vitamin D and GDM was tested using binary logistic regression. Results: Nearly all women (90%) had mild (68.3%) or severe (32.2%) vitamin D deficiency (VDD). Non-GDM women with mild VDD had a significantly higher mean vitamin D intake than GDM women with mild VDD (t = 2.04, p < 0.05). Women with higher early pregnancy serum vitamin D levels had a greater risk of GDM. However, this significant association was only identified among those with a family history of type 2 diabetes mellitus (T2DM) and in women with a body mass index indicating overweight or obese status. Conclusions: The high prevalence of VDD in this sample of pregnant women underscores the need for effective preventive public health strategies. Further investigation of this unexpected association between serum vitamin D level and GDM risk in predominantly VDD pregnant women and the potential effects of adiposity and family history of T2DM on that association is warranted.

This study aimed to optimise and validate a simple and efficient sample preparation and extraction method for the quantification of 25-hydroxyvitamin D (25OHD) in the maternal plasma sample. Different sample preparation methods and precipitation reagentto sample ratio used by previous studies were compared. An ultrahigh performance liquid chromatography method was developed and validated for simultaneous quantification of 25OHD2 and 25OHD3. The chromatographic separation was achieved using the COSMOCORE 2.6Cholester Column and methanol and 0.1% formic acid (79:21, %v/v) as mobile phase at a flow rate of 0.3 mL/min and diode array detection at 264 nm. The results demonstrated that a recovery of approximately 100% could be achieved by extracting samples using 1 mL of hexane, vortex for 10s and a total number of three extraction steps. The precipitation reagentto-sample ratio of 2.8 was optimum for the quantification of 25OHD2 and 25OHD3 in a pooled maternal sample. The value obtained for validation parameters meets the criteria of the Recommendations and Acceptance Criteria for Bioanalytical Method Validation by the Food and Drug Administration. The results showed that this method could be applied for routine quantification of 25OHD, particularly in the maternal plasma sample.

Introduction Folic acid (0.4 mg) taken prior to and during early pregnancy reduces the risk of neural tube defects (NTDs). Because these birth defects occur early in pregnancy, before women may know they are pregnant, many countries have mandated the addition of folic acid to food staples. In countries where fortification is not possible, and weekly iron folic acid programmes exist to reduce anaemia, the WHO recommends that 2.8 mg (7×0.4 mg) folic acid be given instead of the current weekly practice of 0.4 mg. Currently, there is a lack of evidence to support if the 2.8 mg folic acid per week dose is sufficient to raise erythrocyte folate concentrations to a level associated with a reduced risk of a NTD-affected pregnancy. We aim to conduct a three-arm randomised controlled trial to determine the effect of weekly folic acid with iron on erythrocyte folate, a biomarker of NTD risk. Methods and analysis We will recruit non-pregnant women (n=300; 18–45 years) from Selangor, Malaysia. Women will be randomised to receive either 2.8, 0.4 or 0.0 (placebo) mg folic acid with 60 mg iron weekly for 16 weeks, followed by a 4-week washout period. The primary outcome will be erythrocyte folate concentration at 16 weeks and the mean concentration will be compared between randomised treatment groups (intention-to-treat) using a linear regression model adjusting for the baseline measure. Ethics and dissemination Ethical approval was obtained from the University of British Columbia (H18-00768) and Universiti Putra Malaysia (JKEUPM-2018-255). The results of this trial will be presented at scientific conferences and published in peer-reviewed journals.

A total of 201 patients with major depressive disorder from four hospitals in Malaysia were followed up for 5 years to determine the prognostic factors of recurrent major depressive disorder that could potentially contribute to improving the management of MDD patients. For each individual patient, at the time of recruitment as part of a case-control study, information was collected on recent threatening life events, personality and social and occupational functioning, while blood samples were collected to genotype single nucleotide polymorphisms of vitamin D receptor (VDR), zinc transporter-3 (ZnT3), dopamine transporter-1 (DAT1), brain-derived neurotropic factor (BDNF), serotonin receptor 1A (HT1A) and 2A (HT2A) genes. Kaplan-Meier and Cox-regression were used to estimate hazard functions for recurrence of major depressive disorder. Individuals with severe MDD in previous major depressive episodes had five and a half times higher hazard of developing recurrence compared to mild and moderate MDD (HR = 5.565, 95% CI = 1.631–18.994, p = 0.006). Individuals who scored higher on social avoidance had three and a half times higher hazard of recurrence of MDD (HR = 3.525, 95% CI = 1.349–9.209; p = 0.010). There was significant interaction between ApaI +64978C>A single nucleotide polymorphism and severity. The hazard ratio increased by 6.4 times from mild and moderate to severe MDD for A/A genotype while that for C/A genotype increased by 11.3 times. Social avoidance and severity of depression at first episode were prognostic of recurrence. Screening for personality factors at first encounter with MDD patients needs to be considered as part of the clinical practice. For those at risk of recurrence in relation to social avoidance, the psychological intervention prescribed should be customized to focus on this modifiable factor. Prompt and appropriate management of severe MDD is recommended to reduce risk of recurrence.

Background: Vitamin D deficiency (VDD) has been related to vitamin D binding protein (GC) gene polymorphism, demographics and lifestyle factors in different populations. However, previous studies only focused on demographic and lifestyle factors or genetic factors alone. Therefore, this cross-sectional study aimed to assess the association between GC gene polymorphism, demographics and lifestyle factors with VDD among Malaysian pregnant women. Method: Information on demographic characteristics, dietary vitamin D intake from supplement and food, time spent outdoors, skin type and clothing were collected using a questionnaire. Plasma total 25-hydroxyvitamin D (25OHD) levels were measured using an Ultra-High-Performance Liquid Chromatography (UHPLC). Maternal GC single nucleotide polymorphisms (SNPs) (rs4588 and rs7041) were determined using restriction fragment length polymorphism (RFLP) technique. Results: Results showed that 50.2% of pregnant women were vitamin D deficient (25OHD < 30 nmol/L). VDD (25OHD < 30 nmol/L) was significantly associated with age, veiled clothing, maternal vitamin D intakes from both food and supplements, and GC rs7041(and GC diplotypes). In contrast to previous studies that reported for non-pregnant population, a significant positive association was found between CC genotype for SNP GC rs7041, GC 1s-1s and GC If-2 with risk of VDD (25OHD < 30 nmol/L). Conclusions: The high prevalence of maternal VDD found in this study suggests the need for urgent development and implementation of vitamin D supplementation or fortification strategies to reduce VDD among pregnant women. The discrepancy in the association between GC rs7041 gene polymorphism and VDD reflects the variation in the factors associated with VDD in pregnancy compared to non-pregnant state.

Introduction: 25-hydroxyvitamin D (25OHD) is the principal biomarker of vitamin D status. In circulation, 25OHD is primarily bound to vitamin D binding protein (VDBP), leaving a small proportion bound to albumin and as free form. Previous studies have suggested that free 25OHD is better correlated with health outcomes. However, in pregnancy where VDBP level is extremely elevated, the correlations between free 25OHD with health outcomes are far from conclusive. Here we show the associations of maternal and cord total, free and bioavailable 25OHD con-currently with neonatal anthropometric measurements in healthy pregnant mothers-neonates pairs. Method: Total 25OHD level was measured by using chemiluminescent immunoassay. Free and bioavailable 25OHD were calculated using published mathematical models. Results: The results showed that birth weight and head circumference were negatively associated with maternal total 25OHD but not significantly associated with free and bioavailable 25OHD. There were no significant associations between cord total, free and bioavailable 25OHD with any of the neonatal anthropometric measurements. Conclusion: The outcomes of this study should encourage further research in a larger sample size. Notably, future research could lead to the establishment of causative relationships and plausible mechanisms between maternal and cord 25OHD with neonatal anthropometric measurements.

Docosahexaenoic acid (DHA) is an essential component for brain and visual acuity development during foetal and early postnatal life. A newly released directive under the European Commission stipulates DHA as a mandatory ingredient in infant formula. This poses challenges to manufacturers in preserving the stability and bioavailability of DHA at levels akin to human breast milk. The aims of this study were (a) to investigate the bioavailability of microencapsulated omega-3 DHA formulations in healthy toddlers compared with high DHA fish oil for a one-month period and (b) to assess the effect of DHA supplementation on children’s sleep and cry patterns. Sixty toddlers were randomly allocated to four groups: 1. unfortified formula, 2. unfortified formula plus high DHA tuna oil, 3. fortified formula with dairy-based microencapsulated high DHA tuna oil powder, and 4. fortified formula with allergenic-free microencapsulated high DHA tuna oil powder. Bioavailability was assessed from both blood and faecal fatty acid levels. The results showed an enhanced bioavailability with significantly greater concentrations of blood DHA levels in formulas with microencapsulated powders. There were no significant effects of treatment on sleep and cry patterns. Application and delivery of microencapsulated DHA tuna oil powder in toddlers’ formula provided better bioavailability of the active DHA.

Introduction Weekly iron-folic acid (IFA) supplements are recommended for all menstruating women in countries where anaemia prevalence is >20%. Anaemia caused by folate deficiency is low worldwide, and the need to include folic acid is in question. Including folic acid might reduce the risk of a neural tube defect (NTD) should a woman become pregnant. Most weekly supplements contain 0.4 mg folic acid; however, WHO recommends 2.8 mg because it is seven times the daily dose effective in reducing NTDs. There is a reluctance to switch to supplements containing 2.8 mg of folic acid because of a lack of evidence that this dose would prevent NTDs. Our aim was to investigate the effect of two doses of folic acid, compared with placebo, on red blood cell (RBC) folate, a biomarker of NTD risk. Methods We conducted a three-arm double-blind efficacy trial in Malaysia. Non-pregnant women (n=331) were randomised to receive 60 mg iron and either 0, 0.4, or 2.8 mg folic acid once weekly for 16 weeks. Results At 16 weeks, women receiving 0.4 mg and 2.8 mg folic acid per week had a higher mean RBC folate than those receiving 0 mg (mean difference (95% CI) 84 (54 to 113) and 355 (316 to 394) nmol/L, respectively). Women receiving 2.8 mg folic acid had a 271 (234 to 309) nmol/L greater mean RBC folate than those receiving 0.4 mg. Moreover, women in the 2.8 mg group were seven times (RR 7.3, 95% CI 3.9 to 13.7; p[removed]748 nmol/L, a concentration associated with a low risk of NTD, compared with the 0.4 mg group. Conclusion Weekly IFA supplements containing 2.8 mg folic acid increases RBC folate more than those containing 0.4 mg. Increased availability and access to the 2.8 mg formulation is needed. Trail registration number This trial is registered with the Australian New Zealand Clinical Trial Registry (ACTRN12619000818134).