Nutrition, One-Carbon Metabolism and Neural Tube Defects: A Review

Abstract

Neural tube defects (NTDs) are a group of severe congenital malformations, induced by the combined effects of genes and the environment. The most valuable finding so far has been the protective effect of folic acid supplementation against NTDs. However, many women do not take folic acid supplements until they are pregnant, which is too late to prevent NTDs effectively. Long-term intake of folic acid–fortified food is a good choice to solve this problem, and mandatory folic acid fortification should be further promoted, especially in Europe, Asia and Africa. Vitamin B2, vitamin B-6, vitamin B-12, choline, betaine and n-3 polyunsaturated fatty acids (PUFAs) can also reduce the NTD risk by interacting with the one-carbon metabolism pathway. This suggest that multivitamin B combined with choline, betaine and n-3 PUFAs supplementation may have a better protective effect against NTDs than folic acid alone. Genetic polymorphisms involved in one-carbon metabolism are associated with NTD risk, and gene screening for women of childbearing age prior to pregnancy may help prevent NTDs induced by the risk allele. In addition, the consumption of alcohol, tea and coffee, and low intakes of fruit and vegetable are also associated with the increased risk of NTDs, and should be avoided by women of childbearing age.

Estimates of global and regional prevalence of neural tube defects for 2015: a systematic analysis

“…Apart from methodological influences, the estimated prevalence of NTDs can be influenced in populations by underlying risks due to genetic (such as MTHFR mutations among women of specific race and ethnicity), environmental, and nutrition differences, [17][18][19] as well as factors such as access to diagnostic services. 20 To date, there has not been a standard approach for estimating NTD prevalence and presenting global and regional estimates.…”

Metabolic switching and cell fate decisions: implications for pluripotency, reprogramming and development

“…Energy-generating pathways are highly dynamic and metabolic fluxes vary dramatically across different cell types and tissues in response to developmental signals [6], nutritional status [7], environmental signals [8] and disease pathogenesis [9]. Metabolic flux is finely tuned to maximize function in different cell types and is linked to cell identity just as gene expression, epigenetics and morphology are.…”

Diet and Lifestyle Role in Homocysteine Metabolism in Turner Syndrome

“…This may be partly due to caffeine and partly to the presence of chlorogenic acid [29] that may also contribute to the effect on levels of tHcy [30]. Alcohol consumption can reduce the level of S-adenosylmethionine (the major methyl donor) and the activity of 5-methyltetrahydrofolate-homocysteine methyltransferase (the enzyme catalyzing the remethylation of Hcy to methionine)| [31]. Habitual smoking is independently associated with hyperhomocysteinemia [32].…”