Estigations report no significant XR9576 chemical information association between maternal B12 status (measured atEstigations report

Estigations report no significant XR9576 chemical information association between maternal B12 status (measured at
Estigations report no significant association between maternal B12 status (measured at various time points during the prenatal period) and birth weight or IUGR [7, 8, 22]. We similarly found no association with birth weight. To our knowledge, we are the first to report on the association between maternal concentrations of vitamin B12 and offspring WG at age 3 years. Our finding of an inverse association between maternal B12 concentrations and WG could suggest that maternal B vitamins during the prenatal period have downstream effects on offspring body size, and these associations may, in part, drive the inverse relationship between childhood B12 concentrations and obesity [23].McCullough et al. Clinical Epigenetics (2016) 8:Page 7 ofPlasma PLP, the best single indicator of vitamin B6 status, is involved in many aspects of macronutrient metabolism and is known to decline during gestation [24]. Several studies report positive associations between maternal B6 supplementation and birth weight, including a recent meta-analysis where a 217-g difference (95 CI: 130?04; p = 0.009) was observed [24]. We observed a monotonic increase in birth weight with increasing maternal PLP concentration, but the effect was small and insignificant. We found no previous studies that examined the association between maternal PLP and offspring WG, and anthropometric data on children whose mothers received vitamin B6 supplements during pregnancy are not available. The concentrations of Hcy, a sulfur-containing amino acid, are tightly regulated by two enzymatic pathways: (1) Hcy can be remethylated to methionine by a pathway requiring folate and vitamin B12 as a methyl donor and co-factor, respectively, or (2) Hcy may be removed by transsulfuration, a pathway reliant on vitamin B6 [25]. Therefore, deficiencies of folate, vitamin B12, or vitamin B6 are likely to lead to increase Hcy. Blood concentrations of Hcy during pregnancy are variable: a slight decrease during early gestation; a nadir between 20 and 32 weeks; and subsequent rise after delivery [26]. Investigations of the association between maternal total Hcy and birth weight have yielded diverging results. Many, but not all [7], studies have observed an increased risk of LBW or IUGR in women with elevated levels of total Hcy [27, 28] and a recent meta-analysis showed that hyperhomocysteinaemia (>90th percentile) was associated with a 25 increased odds of being SGA (95 CI: 1.09, 1.44) [29]. While we found no statistically significant associations between Hcy and birth weight overall, we did observe a novel inverse association among male infants. No previous study had evaluated WG or BMI with prenatal maternal Hcy concentrations, and our study found no significant associations. The association between nutrients in the one-carbon pathway and offspring methylation are well-documented in animal models [30, 31], but studies among humans are limited. A cross-sectional study assessing maternal vitamin B12 status at the time of parturition found inverse associations with umbilical cord blood IGF2 DMR methylation [13]. Another study showed associations between plasma levels of Hcy and cord blood DNA methylation of 289 CpG sites [32]. A recent investigation of dietary nutrients showed maternal vitamin B2 intake was positively correlated with PLAGL1 DMR methylation in umbilical cord blood, although no association was found with B6 or B12 [15]. These investigations PubMed ID: were limited by cross-sectional data collection, s.