Methyl donor micronutrients, hypothalamic development and programming for metabolic disease

Kubant, Ruslan; Cho, Clara E.; Pannia, Emanuela; Hammoud, Rola; Yang, Neil Victor; Simonian, Rebecca; Anderson, G. Harvey

doi:10.1016/j.neubiorev.2023.105512

Cited by 4 publications

(1 citation statement)

References 96 publications

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“…Folic acid is required for neural cell proliferation, migration, differentiation, vesicular transport, and synaptic plasticity, and its role in preventing neural tube defects and neurodevelopmental disorders is widely accepted [47,75]. During pregnancy, the demand for folic acid increases by around 50%, leading to the recommendation of supplementation of 400-800 µg for all women of childbearing age from two months before to three months after conception [76,77].…”

Section: Maternal Nutritionmentioning

confidence: 99%

Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment

Lubrano,

Parisi,

Cetin

2024

Antioxidants

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During intrauterine life, external stimuli including maternal nutrition, lifestyle, socioeconomic conditions, anxiety, stress, and air pollution can significantly impact fetal development. The human brain structures begin to form in the early weeks of gestation and continue to grow and mature throughout pregnancy. This review aims to assess, based on the latest research, the impact of environmental factors on fetal and neonatal brain development, showing that oxidative stress and inflammation are implied as a common factor for most of the stressors. Environmental insults can induce a maternal inflammatory state and modify nutrient supply to the fetus, possibly through epigenetic mechanisms, leading to significant consequences for brain morphogenesis and neurological outcomes. These risk factors are often synergic and mutually reinforcing. Fetal growth restriction and preterm birth represent paradigms of intrauterine reduced nutrient supply and inflammation, respectively. These mechanisms can lead to an increase in free radicals and, consequently, oxidative stress, with well-known adverse effects on the offspring’s neurodevelopment. Therefore, a healthy intrauterine environment is a critical factor in supporting normal fetal brain development. Hence, healthcare professionals and clinicians should implement effective interventions to prevent and reduce modifiable risk factors associated with an increased inflammatory state and decreased nutrient supply during pregnancy.

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Section: Maternal Nutritionmentioning

confidence: 99%

Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment

Lubrano,

Parisi,

Cetin

2024

Antioxidants

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Bidirectional causality between micronutrients and mental illness: Mendelian randomization studies

Wu,

Jiang,

Liang

et al. 2025

Journal of Affective Disorders

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Exposure to prenatal excess or imbalanced micronutrients leads to long‐term perturbations in one‐carbon metabolism, trimethylamine‐N‐oxide and DNA methylation in Wistar rat offspring

Shelp,

Dong,

Orlov

et al. 2024

The FASEB Journal

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Prenatal multivitamins, including folic acid, are commonly consumed in excess, whereas choline, an essential nutrient and an important source of labile methyl groups, is underconsumed. Here, we characterized profiles of one‐carbon metabolism and related pathways and patterns of DNA methylation in offspring exposed to excess or imbalanced micronutrients prenatally. Pregnant Wistar rats were fed either recommended 1× vitamins (RV), high 10× vitamins (HV), high 10× folic acid with recommended choline (HFolRC), or high 10× folic acid with no choline (HFolNC). Offspring were weaned to a high‐fat diet for 12 weeks. Circulating metabolites were analyzed with a focus on the hypothalamus, an area known to be under epigenetic regulation. HV, HFolRC, and HFolNC males had higher body weight (BW) and lower plasma choline and methionine consistent with lower hypothalamic S‐adenosylmethionine (SAM):S‐adenosylhomocysteine (SAH) and global DNA methylation compared with RV. HV and HFolNC females had higher BW and lower plasma 5‐methyltetrahydrofolate and methionine consistent with lower hypothalamic global DNA methylation compared with RV. Plasma dimethylglycine (DMG) and methionine were higher as with hypothalamic SAM:SAH and global DNA methylation in HFolRC females without changes in BW compared with RV. Plasma trimethylamine and trimethylamine‐N‐oxide were higher in males but lower in females from HFolRC compared with RV. Network modeling revealed a link between the folate‐dependent pathway and SAH, with most connections through DMG. Final BW was negatively correlated with choline, DMG, and global DNA methylation. In conclusion, prenatal intake of excess or imbalanced micronutrients induces distinct metabolic and epigenetic perturbations in offspring that reflect long‐term nutritional programming of health.

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Methyl donor micronutrients, hypothalamic development and programming for metabolic disease

Cited by 4 publications

References 96 publications

Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment

Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment

Bidirectional causality between micronutrients and mental illness: Mendelian randomization studies

Exposure to prenatal excess or imbalanced micronutrients leads to long‐term perturbations in one‐carbon metabolism, trimethylamine‐N‐oxide and DNA methylation in Wistar rat offspring

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