Choline Bitartrate prevents fats from accumulating in liver, and is essential for the health of the nerves, kidneys and liver. The deficiency symptoms include fatty deposits in the liver, high blood pressure and cirrhosis of the liver.
Choline is an important lipotropic (fat emulsifier) involved in the biosynthesis of lecithin and the formation of the amino acid methionine. It aids in emulsifying cholesterol so it doesn't settle on the arterial walls. Abnormalities of the heart, such as heart palpitation, can occur as a result of Choline deficiency.
Choline deficiency in mice and humans is associated with increased plasma homocysteine concentration after a methionine load.
American Journal of Clinical Nutrition, Vol. 81, No. 2, 440-444, February 2005
Background: Elevated concentrations of homocysteine in blood may be an independent risk factor for the development of atherosclerosis. Elevated homocysteine concentrations can be caused by decreased methylation of homocysteine to form methionine, as occurs in folate deficiency. A parallel pathway exists for methylation of homocysteine, in which choline, by way of betaine, is the methyl donor. Objective: Our goal was to determine whether choline deficiency results in a decreased capacity to methylate homocysteine. Design: C57BL/6J mice were fed diets containing 0, 10, or 35 mmol choline/kg diet for 3 wk. We then administered an oral methionine load to the animals and measured plasma homocysteine concentrations. Also, in a pilot study, we examined 8 men who were fed a diet providing 550 mg choline/d per 70 kg body weight for 10 d, followed by a diet providing almost no choline, until the subjects were clinically judged to be choline deficient or for 42 d. A methionine load was administered at the end of each dietary phase. Results: 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% greater than those in men not choline depleted. Conclusion: These results suggest that choline, like folate, plays an important role in the metabolism of homocysteine in humans and that response to a methionine load may be useful when assessing choline nutriture.
Choline, when oxidized in the body to form betaine, provides a methyl group for the conversion of homocysteine to methionine by the enzyme, betaine-homocysteine methyltransferase (BHMT). Despite its relevance, the relationship of betaine and choline to homocysteine metabolism has been only lightly investigated in humans. Methodological problems make betaine and BHMT difficult to measure. One study found higher urinary excretion of betaine and its metabolites in patients with vascular disease and elevated homocysteine levels than in control subjects, suggesting that elevated blood homocysteine levels were not related to reduced intake of choline or betaine or diminished activity of BHMT. In preliminary studies, pharmacologic doses of betaine (1.7 to 6 grams/day) were found to reduce blood levels of homocysteine in a small number of patients with vascular disease and elevated homocysteine levels. Although further research is indicated, convincing evidence that increased dietary intake or blood levels of choline or betaine affect homocysteine levels in humans is presently lacking.