Journal of the American College of Nutrition, Vol. 17, No. 4, 303-305 (1998)
Published by the American College of Nutrition
Fat and Calcium Absorption in Infancy Revisited
Kathleen J. Motil, MD, PhD
Children’s Nutrition Research Center, Houston, TX
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INTRODUCTION
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The bioengineering of milk for formula-fed infants had its beginnings in the late 19th century, when the practice of pediatrics was in its infancy [1]. At that time, physicians recognized that the protein and fat components of cow milk were difficult for the infant to digest. They argued that artificial milk feedings had to be individualized, based on the infant’s tolerance of the milk, by giving certain percentages of each nutrient, rather than adjusting total milk volume. The blossoming interest in the premature infant paved the way for further studies on the scientific modification of infant formulas. In the 1940s, reports described the premature infant’s difficulty in absorbing human and cow milk fat [2] and documented that feeding half-skimmed milk resulted in a reduction of fecal fat while maintaining adequate weight gain in the infant [3]. In addition, investigators noted that fats containing predominantly unsaturated fatty acids such as olive oil and soybean oil were absorbed more completely than was milk fat [4] and that saturated long-chain fatty acids, such as palmitic, were absorbed to a greater degree when the fatty acid was present in the sn-2 position of the monoglyceride [5]. Others showed that triglycerides containing short- and medium-chain fatty acids resulted in an improvement in fat absorption [6], particularly in the premature infant [7].
Against this historical perspective, the article by Nelson et al in this issue of the Journal of the American College of Nutrition once again highlights the importance of understanding the developmental aspects of intestinal absorption in the infant at a time when the safety and efficacy of infant formulas are taken for granted. Although some components of fat absorption are not fully developed in infancy [8], the absorptive capacity of the infant is remarkable, considering the amount of fat relative to body weight that an infant consumes. Dietary fat intake averages 6.5 g/kg/day or approximately 45% of the infant’s total daily energy intake. Much of this fat is hydrolyzed in the stomach by lingual and gastric lipases. Intragastric hydrolysis facilitates the emulsification of fat from large globules to small droplets, a process which continues throughout the intestinal tract. Monoglycerides and free fatty acids that arise from intragastric hydrolysis enter the duodenum, where they stimulate the release of cholecystokinin, which in turn stimulates the release of biliary secretions and pancreatic enzymes. Bile salts emulsify the products of fat digestion and pancreatic lipase and colipase hydrolyze undigested long-chain triglycerides, resulting in the formation of 2-monoglycerides and free fatty acids. The monoglycerides and free fatty acids, as well as phospholipids, cholesterol, fat-soluble vitamins, and bile salts, form micellar aggregates which permit their transport from the intestinal lumen into the mucosal cell.
In their study, Nelson et al documented that the coefficient of fat absorption was reduced when palm olein was provided as a major constituent (45%) of the fat blend of a readily available infant formula. Today, infant formulas are comprised of a mixture of several oils, including corn, coconut, soy, canola, sunflower, safflower, and(or) palm oil. The fatty acid content of each of these fat sources is variable [9], with coconut oil being higher in short-chain (8% by weight) and medium-chain (68% by weight) fatty acids, and the remainder of the fat sources being higher in long-chain fatty acids. Palmitic acid, the major saturated long-chain fatty acid, comprises 10% or less of total fatty acids in each of these oils with the exception of palm oil, in which it comprises approximately 41% of total fatty acids (Table 1). Stearic acid, another saturated, long-chain fatty acid, comprises less than 5% of total fatty acids in these oils. With the exception of coconut and palm oil, the unsaturated long-chain fatty acids, oleic and linoleic, are the major constituents of the fat sources used in infant formulas. Among the long-chain fatty acids, unsaturated fatty acids are absorbed more readily than are saturated fatty acids. Absorption of saturated fatty acids, such as palmitic, is related to the position of the fatty acid on the triglyceride molecule [10]. In this case, the 2-monoglyceride of palmitic acid is well absorbed, whereas free palmitic acid and palmitic acid in the sn-1 or sn-3 position of the monoglyceride are not.
In the study conducted by Nelson et al, palm olein, a lower melting fraction of palm oil, contains palmitic acid predominately in the sn-1 and sn-3 position, thereby providing an explanation for the poorer performance of the formula containing this fat source. Nelson et al also showed previously that the reduction in fat absorption was evident even in the presence of generous amounts of medium-chain fatty acids in the formula containing palm olein [11]. Although medium-chain triglycerides may be absorbed directly into intestinal mucosal cells without prior hydrolysis, most are rapidly digested in the duodenum and absorbed directly into the cell without micellar formation, thereby providing a readily available source of dietary fat. In the latter study, however, the addition of medium-chain triglycerides did not compensate for the effects of palm olein on intestinal fat absorption.
Nelson et al were careful to point out that the clinical relevance of these observations is uncertain, particularly in view of the observation that coefficients of fat absorption less than 15% are considered to be within the normal functional capacity of the infant’s intestinal tract. The coefficient of fat absorption, expressed as the percentage of dietary fat absorbed by the intestine after accounting for fecal fat loss, is less in younger than in older infants. As a point of reference, the excretion of human milk fat ranges from 8% to 13% of dietary intake in the newborn infant, whereas the excretion of cow milk fat ranges from 20% to 50% [8]. A mixture of 50% cow milk fat, 25% corn oil, and 25% coconut oil results in an average fat excretion of 15%. In the older infant, human milk fat excretion averages 5% of dietary intake, whereas cow milk fat excretion ranges from 15% to 30%. This range can be reduced to less than 12% if vegetable or oleo oils partially replace cow milk fat. As a rule of thumb, fecal fat loss greater than 2 g/kg/d, which is equivalent to 15% or more of dietary energy intake, is consistent with clinically significant fat malabsorption [12]. In the study by Nelson et al, the coefficients of absorption for both formula groups (with and without palm olein) were within the normal range for infants. The 8% difference in the absorption of dietary fat between the two formula groups, which is equivalent to 5 kcal/kg/d, is unlikely to cause dietary energy insufficiency in the infant. As the authors point out, the infant is able to adapt readily by increasing the amount of milk consumed to meet its daily energy needs when intestinal fat malabsorption of this magnitude prevails.
The bioavailability of dietary calcium bears an important relationship to intestinal fat absorption in the infant [13]. The release of calcium from food is initiated in the stomach by hydrochloric acid and in the upper gastrointestinal tract by pancreatic enzymes. Soluble calcium is present at the highest concentrations in the duodenum and upper jejunum. Calcium absorption occurs by active and passive processes. Active transport occurs in the duodenum and proximal jejunum via a calcium binding protein that is regulated by vitamin D. Passive absorption occurs throughout the small bowel via movement down a concentration gradient, presumably through a paracellular route. Vitamin D, mono- and disaccharides, and ascorbic acid facilitate calcium absorption, whereas phytate, fiber, oxalate, and high concentrations of phosphorus inhibit calcium absorption.
In their study, Nelson et al documented that the absorption of dietary calcium was reduced in infants who consumed a formula rich in palm olein and that the magnitude of fecal calcium loss paralleled fecal fat loss, supporting the hypothesis that calcium absorption is reduced in the presence of steatorrhea because of soap formation [14]. Although calcium absorption, as a proportion of dietary intake, decreases as calcium intake increases, the similarity of the formulas with respect to calcium concentrations and the volume of formula consumed by the two groups of infants did not account for the differences in fecal calcium losses between the two formulas. Once again, the authors cautioned against the possibility of adverse consequences on bone mineral metabolism because calcium homeostasis is a highly regulated biologic process and the adaptability of the infant to variations in dietary nutrient availability is remarkable. If daily calcium needs are estimated by the factorial method to be approximately 100 mg/day during the first 4 months of life [13], this amount was readily available to both groups of infants, regardless of the fatty acid composition of their formula.
In summary, the article by Nelson et al in this issue of the J Am Coll Nutr reiterates an important and well-known principle of gastrointestinal physiology in infancy. It is clear that the developmental aspects of the absorptive capacity of the infant’s intestinal tract are specific for the types of fats most suitable for optimal nutrition during infancy. Furthermore, the fact that nutrients in foods exist in physical-chemical complexes implies that nutrient interactions are likely to occur. These issues must be given careful consideration when modifying the composition of the formulas and foods provided to infants. We must be certain that the nutritional needs for normal growth and development are met over the long term for the infant’s overall health and well-being.
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ACKNOWLEDGMENTS
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This work is a publication of the USDA/ARS Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, and Texas Children’s Hospital, Houston, TX, and has been funded in part with federal funds from the U.S. Department of Agriculture, Agricultural Research Service, under Cooperative Agreement number 58-6250-6-001. The contents of this publication do not necessarily reflect the views or policies of the U.S. Department of Agriculture, nor does mention of trade names, commercial products or organizations imply endorsement by the U.S. Government.
Received February 1, 1998.
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INTRODUCTION
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