Choline and choline-related nutrients in regular and preterm infant growth.

BACKGROUND: Choline is an essential nutrient, with increased requirements during development. It forms the headgroup of phosphatidylcholine and sphingomyelin in all membranes and many secretions. Phosphatidylcholine is linked to cell signaling as a phosphocholine donor to synthesize sphingomyelin from ceramide, a trigger of apoptosis, and is the major carrier of arachidonic and docosahexaenoic acid in plasma. Acetylcholine is important for neurodevelopment and the placental storage form for fetal choline supply. Betaine, a choline metabolite, functions as osmolyte and methyl donor. Their concentrations are all tightly regulated in tissues. CLINCAL IMPACT: During the fetal growth spurt at 24-34-week postmenstrual age, plasma choline is higher than beyond 34 weeks, and threefold higher than in pregnant women [45 (36-60) µmol/L vs. 14 (10-17) µmol/L]. The rapid decrease in plasma choline after premature birth suggests an untimely reduction in choline supply, as cellular uptake is proportional to plasma concentration. Supply via breast milk, with phosphocholine and α-glycerophosphocholine as its major choline components, does not prevent such postnatal decrease. Moreover, high amounts of liver PC are secreted via bile, causing rapid hepatic choline turnover via the enterohepatic cycle, and deficiency in case of pancreatic phospholipase A2 deficiency or intestinal resection. Choline deficiency causes hepatic damage and choline accretion at the expense of the lungs and other tissues.
CONCLUSION: Choline deficiency may contribute to the impaired lean body mass growth and pulmonary and neurocognitive development of preterm infants despite adequate macronutrient supply and weight gain. In this context, a reconsideration of current recommendations for choline supply to preterm infants is required.