Choline is an important component of phospholipids, functions in lipid metabolism and is also able to form the neurotransmitter acetylcholine. Choline can be derived from the diet, but is also synthesised endogenously. The synthesis of choline requires methylation and this is provided by the S-adenosylmethionine (SAM) an intermediate in the methionine to homocysteine pathway. For every molecule of choline, three molecules of methionine are utilised and three molecules of homocysteine are formed. Homocysteine is damaging to cells and tissues and so it important that cellular levels are kept low through conversion of homocysteine back to methionine. This can be achieved through methylation of homocysteine using 5-methyltetrahydrofolate and the enzyme methylenetetrahydrofolate reductase, which require the co-factors folic acid and vitamin B12, respectively. Alternatively the homocysteine can be converted back to methionine through the betaine pathway using betaine as a source of methylation (figure 1).
Figure 1. The homocysteine pathway including the synthesis of choline from phosphatidylcholine via methylation with s-adenosylmethionine.
When the vitamin B12 status of the individuals is poor, flux through the betaine pathway increases. However, betaine is formed from choline, and an increase flux through the betaine pathway therefore increase demand for choline, which in turn increases the production of homocysteine from methionine. Inadequate vitamin B12 or choline in the diet may therefore disrupt the methionine homocysteine pathway and lead to a buildup of homocysteine in cells and tissues. Maternal demand for choline increases during pregnancy and a poor choline status is associated with detrimental foetal development that may have long term effects of mental abilities. Because vitamin B12 deficiency causes an increased reliance on an adequate choline status researchers have assessed the links between choline and vitamin B12 during pregnancy. For example, in one study1 the researchers investigated whether poor vitamin B12 status leads to low plasma choline and altered choline biomarkers in pregnant women.
When the researchers analysed the blood of the pregnant women for vitamin B12 and choline, they found that as pregnancy duration increased, the number of women with deficient (<148 pmol/L) or marginal (148-220 pmol/L) total plasma vitamin B12 concentrations increased. Deficiency or marginal status of vitamin B12 affected between 3 to 9 % of non-pregnant women, 10 to 20 % of women at 16 weeks gestation, and 23 to 35 % of women at 35 weeks of gestation. Those women at 35 weeks of gestation who had had deficient or marginal vitamin B12 concentrations in plasma had lower choline, betaine and dimethylglycine (a metabolite of betaine) concentrations compared to those women with adequate vitamin B12 concentrations in plasma (>220 pmol/L). All the women in this study were replete in folate which meant that this did not affect the results of the study. These result taken as a whole show a relationship between the vitamin B12 concentrations of pregnant women and their choline status.
Dr Robert Barrington’s Nutritional Recommendation: Vitamin B12 is produced by microorganisms and is present only is products of animal origin. Therefore vegans who do not consume animal products cannot obtain the vitamin B12 the require for optimal metabolic regulation. Although some plant cobalamins have been identified, these are thought to not be absorbed or utilised as a source of vitamin B12 in humans. It is therefore important for those who may be at risk of vitamin B12 deficiency though avoidance of animal products consume a vitamin B12 supplement especially if they may become pregnant. As choline deficiency may cause poor foetal development, it is important to maintain an optimal vitamin B12 and choline status during pregnancy.
RdB
