Plasma cholesterol levels usually range between 50 and 100 mg/dl at birth, with the cholesterol approximately equally distributed between low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Plasma cholesterol increases rapidly over the first days after birth, predominantly due to an increase in cholesterol with LDL, irrespective of whether the infant is breast fed or fed with infant formulas. With continued feeding, plasma cholesterol becomes progressively, and significantly, higher in infants who are breast fed compared to those fed low-cholesterol, polyunsaturated fatty acid-rich infant formula. Studies in the developing young of other species have suggested that up-regulation of cholesterol synthesis, or turnover and excretion, at stages when these pathways are acquiring functional maturity may have lasting effects on cholesterol metabolism. The information available, however, indicates the diet-related differences in plasma cholesterol of the more mature human newborn are temporal in nature and probably not of significance to adult cardiovascular disease. Infants born early in the third trimester of gestation, however, are at risk for marked elevations in plasma cholesterol, with stimulation of endogenous cholesterol biosynthesis, as a result of the intravenous nutrition required to sustain life. Whether this has long-term consequences for this group of infants is unknown. There is presently no reason to advocate diet modification to alter the plasma cholesterol of normal infants under the age of 2 years.
ABSTRACT. Plasma cholesterol concentrations increase after birth. Whether this is due to increased cholesterol synthesis has not been reported. Additionally, it is not known if formulas, which lack cholesterol, result in higher rates of cholesterol synthesis than feeding breast milk. To address this, plasma lathosterol (quantitated by gas chromatography), a potential indicator of cholesterol synthesis, was measured in term infants at birth (cord) and 4 d of age fed either formula or breast milk (n = 6 each), normal adults (n = 6) at the expected nadir and peak of the diurnal rhythm (1700 h and 0830 h), and cholestyramine-treated hypercholesterolemic adults (n = 6). Plasma cholesterol and apo B increased, and apo A1 (measured by immunoprecipitation) did not change over the first 4 d of life. The increase in plasma cholesterol was greater in the formulafed infants compared with breast-fed infants. The plasma lathosterol concentrations (pmol/L) and the lathostero1:cholesterol ratios (10' x mmol lathosterol/mol cholesterol) decreased from birth to 4 d of age by 12 and 36%, respectively, in the breast-fed infants and by 20 and 46%, respectively, in formula-fed infants. The infant plasma lathosterol concentrations, however, were not different from normal adult levels 11700 h: 5.50 + 1.52 (SD); 0830 h: 6.18 f 1-80], but were lower than those of cholestyramine-treated adults (20.48 f 13.41). Sterol ratios of infants were higher than those of normal adults (1700 h: 112.5 + 26.0; 0830 h: 129.4 f 42.2), but not different from those of cholestyramine-treated adults (322.9 + 168.4). These data show that the evaluation in plasma cholesterol between birth and d 4 of age is not accompanied by increased plasma lathosterol levels, suggesting no increase in cholesterol synthesis. Further, infants fed formula do not have greater plasma lathosterol levels than breast-fed infants.
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