Researchers from the University of North Carolina at Chapel Hill have found that deficiency of the vitamin in both mice and humans was associated with increased levels of the amino acid.
The preliminary findings could lead to new applications for the nutrient, most well known for its benefit to brain health.
Writing in this month's issue of the American Journal of Clinical Nutrition (vol 81, no 2, pp440-444), the researchers say that raised homocysteine concentrations can be caused by decreased methylation of homocysteine to form methionine, which occurs in folate deficiency.
But a parallel pathway exists for methylation of homocysteine, in which choline, by way of betaine, is the methyl donor.
Their tests appear to confirm that choline deficiency results in a decreased capacity to methylate homocysteine.
Mice were fed diets containing 0, 10, or 35 mmol choline in their diet for three weeks and then received oral methionine.
The researchers also examined eight men who were fed a diet providing 550 mg choline per day per 70 kg body weight for 10 days, followed by a diet providing almost no choline, until the subjects were clinically judged to be choline deficient.
A methionine load was administered at the end of each dietary phase.
Two hours after the methionine load, choline-deficient mice had plasma homocysteine concentrations twice those of choline-fed mice.
Four hours after the methionine load, clinically choline-depleted men had plasma homocysteine concentrations that were 35 per cent greater than those in control subjects.
Supplements of the amino acid L-arginine were also recently demonstrated to lower levels of homocysteine.