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Journal of Nutrition Vol. 116 No. 1 January 1986, pp. 50-58
Copyright © 1986 by American Society for Nutrition
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Choline, Phosphatidylcholine and Sphingomyelin in Human and Bovine Milk and Infant Formulas1

Steven H. Zeisel, Douglas Char and Nancy F. Sheard

Departments of Pediatrics and Pathology, Nutrient Metabolism Laboratory, Boston University School of Medicine, 85 E. Newton Street, Room M1002, Boston, MA 02118

Choline is a precursor for the biosynthesis of phosphatidylcholine (lecithin), sphingomyelin, and choline plasmalogens—all essential constituents of membranes. Choline is also needed to make acetylcholine, a major neurotransmitter. The major choline-containing compounds of human milk (unesterified choline, phosphatidylcholine, sphingomyelin) were measured in samples obtained from mothers of full-term infants. Unesterified choline concentrations were highest (> 600 nmol/ml) during the first week of lactation, but thereafter remained relatively constant at 70–200 nmol/ml. There was no difference among foremilk, middle milk and hind milk, nor was there a diurnal pattern of variation in unesterified choline concentrations. Milk phosphatidylcholine and sphingomyelin concentrations remained relatively constant throughout lactation (100–200 nmol/ml). Hind milk always contained more of these phospholipids than did foremilk or middle milk. There was no consistent diurnal pattern of variation in milk concentrations of phosphatidylcholine or sphingomyelin. Milk contained no phospholipase activity capable of forming free choline from phosphatidylcholine or sphingomyelin. Bovine milk contained approximately the same concentrations of choline, phosphatidylcholine and sphingomyelin as did human milk from mothers more than 15 d postpartum. The same was true of "humanized" infant formulas made from cow's milk. Soy protein-based formulas had much more unesterified choline (up to 650 nmol/ml) and much less sphingomyelin than did mature human milk.


KEY WORDS: • choline • phosphatidylcholine • sphingomyelin • milk • infant formula

1 This work was supported by a grant from the National Institutes of Child Health and Human Development (HD 16727) and a grant from the National Cancer Institute (CA 26731) of the National Institutes of Health.

Manuscript received 10 October 1984. Revision accepted 25 September 1985.




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