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Choline deficiency causes muscle damage and abnormal deposition of fat in the liver, which results in a condition called nonalcoholic fatty liver disease. Genetic predispositions and gender can influence individual variation in choline requirements and thus the susceptibility to choline deficiency-induced fatty liver disease. Choline is involved in the regulation of homocysteine concentration in the blood through its metabolite betaine. There is currently no convincing evidence that high choline intakes could benefit cardiovascular health through lowering blood homocysteine.
The need for choline is probably increased during pregnancy. It is not yet known whether periconceptual choline supplementation could confer protection against NTDs. Animal studies have shown that choline is essential for optimal brain development and influences cognitive function in later life. However, in humans, there is not enough evidence to assert that choline supplementation during pregnancy improves offspring’s cognitive performance or that it helps prevent cognitive decline in older people. De novo choline synthesis in humans is not sufficient to meet their metabolic needs.
Good dietary sources of choline include eggs, meat, poultry, fish, cruciferous vegetables, peanuts, and dairy products. Although choline is not by strict definition a vitamin, it is an essential nutrient. Despite the fact that humans can synthesize it in small amounts, choline must be consumed in the diet to maintain health. Cell signaling The choline-containing phospholipids, phosphatidylcholine and sphingomyelin, are precursors for the intracellular messenger molecules, diacylglycerol and ceramide. Nerve impulse transmission Choline is a precursor for acetylcholine, an important neurotransmitter synthesized by cholinergic neurons and involved in muscle control, circadian rhythm, memory, and many other neuronal functions. Fat and cholesterol consumed in the diet are transported to the liver by lipoproteins called chylomicrons.
Major source of methyl groups Choline may be oxidized in the liver and kidney to form a metabolite called betaine via a two-step enzymatic reaction. Homocysteine is methylated to form the essential amino acid methionine in two pathways. Osmoregulation The conversion of choline to betaine is irreversible. These signs of organ dysfunction resolved upon choline reintroduction in the diet. See Disease Prevention for more information on fatty liver diseases. Thus, the human requirement for choline is especially influenced by the relationship between choline and other methyl group donors such as folate and S-adenosylmethionine. A low intake of folate leads to an increased demand for choline-derived metabolite, betaine.