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,**,2
* Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile;
Retina Foundation of the Southwest, Dallas, TX; and
** London School of Hygiene and Tropical Medicine, London, United Kingdom
2To whom correspondence should be addressed. E-mail: uauy{at}uchile.cl.
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ABSTRACT |
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 TOP ABSTRACT Nomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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KEY WORDS: • infant nutrition • complementary foods • dietary lipids
Lipids have traditionally been considered a part of the dietary energy supply. The total amount of fat that could be tolerated and digested by infants and young children has been the main preoccupation whereas the composition of dietary fat has received little attention. Interest in the quality of dietary lipid supply in early childhood as a major determinant of growth, infant development and long-term health is presently growing. Thus, the selection of dietary lipids during the first years of life is now considered to be of critical importance (1–4). Fats enhance the taste and acceptability of foods, and lipid components largely determine the texture, flavor and aroma of foods. In addition they slow gastric emptying and intestinal motility, affecting satiety. Dietary lipids provide essential fatty acids (EFA)2 and facilitate the absorption of lipid-soluble vitamins (4,5). Lipids are the main energy source in the infant diet, thus necessary for normal growth and physical activity. Lipids provide around half (45–55%) of the energy in human milk, and a similar proportion is found in most artificial infant formulas. They constitute the major energy stores in the body; the energy content of adipose tissue on a wet weight basis is seven- to eightfold higher than that of tissue containing glycogen or protein because the latter substrates are in a hydrated state.
Over the past decades interest has focused on the role of essential lipids in central nervous system development and of fatty acids and cholesterol in lipoprotein metabolism throughout the life cycle. Lipids are also structural components of all tissues and are indispensable for cell and plasma membrane synthesis. The brain, retina and other neural tissues are particularly rich in long-chain PUFA (LCPUFA). Some LCPUFA derived from the (n-6) and (n-3) EFA are precursors for eicosanoid production (prostaglandins, prostacyclins, thromboxanes and leukotrienes). These autocrine and paracrine mediators are powerful regulators of numerous cell and tissue functions (e.g., thrombocyte aggregation, inflammatory reactions and leukocyte functions, vasoconstriction and vasodilatation, blood pressure, bronchial constriction and uterine contractility).
Dietary lipids affect cholesterol metabolism at an early age and may be associated with cardiovascular morbidity and mortality in later life. Lipid supply, particularly EFA and LCPUFA, have also been shown to affect neural development and function (6–10). Evidence indicates that specific fatty acids exert their effect by modifying the physical properties or membranes, including membrane-related transport systems, ion channels, enzymatic activity, receptor function and various signal transduction pathways. More recently the role of specific fatty acids in determining levels of gene expression for key transcription factors, peroxisome proliferator-activated receptors (PPAR) and retinoic acid receptors has renewed the interest in better defining the role of these critical nutrients in the regulation of lipid metabolism, energy partitioning, insulin sensitivity, adipocyte development and neural function across the lifespan (6–10).
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Nomenclature used to characterize dietary lipids |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Fatty acids are classified by chain length as short (<8 carbon), medium (8–11 carbons), intermediate (12–15 carbons) and long chain (
16 carbons). Based on their number of double bonds, they are classified as saturated, monounsaturated (1 double bond) or polyunsaturated (2 or more double bonds). The nomenclature indicates the total number of carbon atoms, number of double bonds and position of the terminal double bond. Thus stearic acid, 18:0, is a saturated carbon chain with 18 carbons and no double bonds, and oleic acid, 18:1(n-9), is a monounsaturated fatty acid with 18 carbons and 1 double bond in the (n-9) position. The position of the double bond is indicated by the carbon at which the double bond occurs; standardized nomenclature (International Union of Pure and Applied Chemistry) numbering starts from the carboxyl terminus or delta carbon; traditional or common nomenclature starts from the methyl or n- terminus (also called omega carbon). Most metabolic activity affecting fatty acids such as oxidation, desaturation and elongation affects the carboxyl end of the chain, thus changing the carbon position number relative to the delta terminus. Conversely the n- or omega terminus is rarely affected by metabolic activity and has the advantage of providing a stable base carbon position for numbering purpose. Thus, an omega-6 fatty acid, also termed (n-6) fatty acid [such as linoleic acid (LA), 18:2(n-6)] remains a member of the (n-6) family independent of its metabolism (4,9,10).
Fatty acids that are chemically identical in terms of number of carbon atoms and unsaturation may present double bonds as cis and trans isomers that have major differences in physical and biological characteristics. Animals and plants almost entirely use fatty acids with cis double bonds for metabolic and structural purposes. Cis isomers have both hydrogen atoms of the doubly bonded carbons in the same plane of symmetry, thus the molecule is bent and both acyl carbon chains may rotate using the double bond as an axis, allowing them to become more flexible and fluid. For example, the introduction of one double bond to stearic acid, 18:0, forming oleic acid, cis-18:1(n-9), takes the melting point from 
60°C to 16°C. On the contrary if the double bond is in the trans configuration forming elaidic acid, trans-18:1(n-9), the melting point is 56°C. Trans-isomeric fatty acids are formed naturally primarily by rumen bacteria (forestomach of grass-eating animals) and by chemical hydrogenation of fatty acids, which makes the fat hard and less susceptible to rancid oxidation. Trans fatty acids have a straight carbon chain with a tertiary structure similar to saturated fatty acids (10).
Triacylglycerols are the main form of storage of fat in the adipose tissue. They also transport fatty acids in plasma in the form of hepatic VLDL and gut-derived chylomicrons. Phospholipids and cholesterol are indispensable components of the lipid bilayer in cell membranes, providing the interface with the aqueous environment both in plasma and in the intracellular space. The type of phospholipids, cholesterol content and fatty acid composition of phospholipids are tissue specific and to a large extent define membrane properties. Phospholipids and cholesterol play a key role in lipoprotein synthesis and metabolism. They form lipoproteins that permit the circulation of nonpolar lipids in a bipolar solvent such as plasma. Cholesterol is synthesized by all living cells because it is required for membrane renewal and formation as the cell grows or divides. Cholesterol is a necessary precursor for steroid hormone and bile acids synthesis (4).
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Lipid absorption and metabolism |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Long-chain fatty acids, monoacylglycerols and diacylglycerols after being absorbed are reassembled into triacylglycerols and packed together with phospholipids, cholesterol, cholesterol esters, lipid-soluble vitamins and apoproteins B48 and E to form chylomicrons. These are secreted into the lacteal lymphatic ducts, reaching the venous system via the lymphatic thoracic duct. Short- and medium-chain fatty acids are less dependent on bile acid emulsification because of their greater solubility in a water phase; after absorption they are transported directly into the portal venous system and to the liver. Chylomicrons lose their triacylglycerol content as they progress through the circulation. They are hydrolyzed by lipoprotein lipase (LPL) present in the vascular endothelial cells, and free fatty acids are taken up in the periphery by muscle and adipose tissue.
The quality of the fat consumed modulates the activity of LPL and the clearance of chylomicrons. Unsaturated fatty acids result in chylomicrons of larger particle size that are cleared more effectively by LPL because of its greater affinity for unsaturated fatty acids. Diets rich in (n-6) and (n-3) LCPUFA can significantly reduce postprandial lipemia. Leftover particles (chylomicron remnants) are taken up primarily by the liver by LDL receptors and chylomicron remnant receptors. The liver secretes triacylglycerol-rich VLDL containing apoproteins B 100 and E, which serve as the transport system to the periphery. VLDL is also subject to the action of LPL, which liberates free fatty acids for tissue energy metabolism or adipose tissue storage.
Triacylglycerol synthesis in the liver depends primarily on the balance between fatty acid uptake and oxidation; there is very limited de novo fatty acid synthesis. Saturated fatty acids increase plasma VLDL whereas they are reduced by unsaturated fatty acids and particularly by (n-3) LCPUFA, as present in fish oil. These fatty acids enhance the rate of lipolysis and also decrease hepatic VLDL synthesis. As VLDL loses it triacylglycerol content, it forms intermediate-density lipoproteins, which can be taken up by the liver or depleted further in triacylglycerol content while increasing its cholesterol content, forming LDL.
The formation and removal of LDL by hepatic receptors are also affected by type of fat consumed. LDL is taken up primarily by the liver (70%); the rest is taken up by other organs and peripheral tissue. Dietary saturated fatty acids, especially C12, C14 and C16 (lauric, myristic and palmitic acids, respectively) suppress LDL receptor activity and LDL removal whereas unsaturated fatty acids, especially LA, enhance receptor activity. LDL may be modified by peroxidation, enhanced by PUFA and proxidants (e.g., iron or copper) and inhibited by antioxidants (e.g., ascorbic acid and 
-tocopherol). Modified LDL is rapidly removed from the plasma by macrophages and scavenger cells present in all tissues, including vessel walls. Vascular lipid deposition is enhanced by a high plasma concentration of LDL and reduced by a high plasma concentration of HDL.
Disc-shaped nascent HDL formed by the liver and to a certain degree by all tissues contains apoprotein AI and AII. They contain low amounts of triacylglycerol and high amounts of phospholipid and thus are dense. Cholesterol from peripheral tissues, including vessel walls, is taken up by HDL. High HDL concentrations protect against vascular cholesterol deposition and the development of atherosclerosis (15–21).
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Metabolism of EFA |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Lipids in infant nutrition |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Human milk provides a fat-energy ratio (FER) of 50%. Most of the fat is provided as saturated and monounsaturated fatty acids and a relatively high cholesterol intake of 100–150 mg/d. Formula-fed infants receive a similar FER but in contrast receive a much lower cholesterol intake, 25–60 mg/d. A mix of vegetable oils (corn, soy, safflower, olive or sunflower) is added to most formulas. The oleic acid or LA content will depend on the oil source. The use of vegetable oils in the infant diet is based on availability, nutritional properties and relative costs.
The need to include LA, the parent (n-6) EFA, has been recognized for over 40 y. More recently the need to provide -linolenic acid [(LNA), 18:3(n-3)] as a source of the (n-3) EFA found in retinal and nervous system development has been recognized. A possible need for long-chain fatty acids (>18-carbon chain length) derived from EFA has recently been established. The (n-6) PUFA are abundant in commonly used vegetable oils whereas (n-3) PUFA are relatively low except in soy, canola and linseed oils (Table 1). Presently, most formulas are designed to provide a similar fatty acid composition to that found in mature human milk from omnivorous women. This precision is necessary, because the fatty acid composition of human milk will vary based on the maternal diet. The EFA content of human milk, especially the LCPUFA content, will change according to the maternal diet. Cholesterol has not been routinely added to formula except in experimental products used in clinical research. The beneficial effects of cholesterol supplementation of artificial formula have not been established (10,25–28).
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EFA needs for growth and development |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Hansen et al. (31) firmly established that LA is essential for normal infant nutrition in a clinical and biochemical study of 428 infants fed cow’s milk–based formulations with different types of fat. Daily LA intake of study infants ranged from 10 mg/kg when a fully skim milk–based preparation was fed to 800 mg/kg when a corn and coconut oil–based preparation was fed. Hansen et al. observed dryness, desquamation and thickening of the skin and growth faltering as frequent manifestations of LA deficiency in young infants. More subtle clinical symptoms appear in (n-3) EFA deficiency. They include skin changes unresponsive to LA supplementation, abnormal visual function and peripheral neuropathy. The nervous system manifestations of (n-3) deficit are likely caused by an insufficiency of the specific metabolic derivative of LNA, namely DHA. Indeed, the high concentrations of DHA in cerebral cortex and retina support its role in neural and visual function (32).
Studies of several animal species and recent evidence from humans have established that brain phospholipid AA and DHA decrease whereas (n-9) and (n-7) monopolyunsaturated and PUFA increase when LA and LNA or only (n-3) fatty acids are deficient in the diet. Typically, cells deficient in (n-3) fatty acids have decreased DHA and increased levels of the end product of (n-6) metabolism, DPA. Within the subcellular organelles, synaptosomes and mitochondria seem to be more sensitive to a low dietary (n-3) supply as evidenced by the relative abundance of DHA and the changes in composition of these organelles in response to dietary deprivation (33).
The evidence indicates that in early life 18(n-3) precursors are not sufficiently converted to DHA to allow for biochemical and functional normalcy (23,24). Thus, not only LA and LNA but DHA and AA are now considered necessary nutrients for normal eye and brain development in the human.
The role of LCPUFA derived from EFA in prevention of disease mediated by eicosanoid is also being increasingly recognized (34,35). The LCPUFA AA, eicosapentaenoic acid [(EPA) 20:5(n-3)] and DHA are important membrane components and precursors of potent bioactive oxygenated products. Eicosanoids such as prostaglandins, leukotrienes and epoxides derived from AA and EPA are required in numerous physiologic processes. Blood pressure, vascular reactivity, inflammation, platelet aggregation, immune function, allergy and cytokine release are all modulated by dietary AA and EPA intake (Fig. 2.) A myriad of clinical correlates associated with LCPUFA intake have been observed (34,36).
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Lipids as an energy source for growth and development |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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9 kcal/g compared with 4 kcal/g for carbohydrates and protein. Fat contributes 35% of the energy required and 90% of the energy retained during the first 6 mo of life in a healthy infant. Infants can form saturated and monounsaturated lipids de novo for tissue deposition but the capacity for endogenous synthesis is limited. Endogenous lipid synthesis is an energy-demanding process. The synthesis of fat from glucose requires 25% of the energy from glucose for the cost of fat synthesis whereas the storage of fat from preformed fatty acids requires only 1–4% of the energy in the fat. The isoenergetic supply of fat relative to carbohydrate leads to a greater weight and fat gain and a lower energy expenditure in infants. Medium-chain triacylglycerols provide less energy than do long-chain triacylglycerols. Medium-chain triacylglycerols contain 8–10 carbon atoms and are easily absorbed and thus serve to treat fat malabsorption. However, because of their shorter chain length, their energy content is only 7.5–8.0 kcal/g fat. Medium-chain triacylglycerols are very rapidly oxidized and have a higher thermogenic effect; they enter the mitochondria and are metabolized directly by a carnitine independent system. Fat increases the palatability and caloric density of the diet and usually enhances total energy intake. Obese children who consume high fat diets tend to have a greater weight gain whereas infants who consume low fat diets (fat content < 25% of total energy intake) commonly fail to thrive (4,41,42).
The energy cost of growth is an important component (20–30%) of total energy requirements for the first 6 mo of life, progressively dropping its significance to <5% at age12 mo. Weight gain is a sensitive indicator of overall dietary adequacy for the first years of life. If the diet supplies adequate energy and essential nutrients, there is no convincing evidence that a dietary fat intake of 30% of energy adversely affects the growth and development of healthy children living in a clean environment. A review of studies from Europe and North America found little evidence of adverse effects of low dietary fat on growth of young children 6–36 mo of age (43–49). Percentage of dietary fat was not correlated with energy intake, growth velocity or energy density of the diet between ages 6 and 12 mo whereas energy density was positively associated with energy intake and weight gain. Dietary energy density, nutrient density and feeding frequency may be more important than dietary fat content in determining intake and growth of young children. No association between fat intake and growth was detected in infants aged 7–13 mo, children aged 2–5 y or children aged 3–5 y (50–52).
In the STRIP trial, moderately restricted fat intake (25–30% of energy) was not associated with compromised infant growth between 7 and 36 mo (53). A similar intervention with a fat intake of 30–35% in French infants aged 7 mo also did not result in impaired growth between ages 7 and 13 mo (54). A number of studies found lower energy intakes with low fat diets but no differences in growth. If the diet records accurately reflect habitual intake, these findings raise the possibility of decreased physical activity in infants and young toddlers adapted to low fat diets. Several studies on secular trends, migration and vegetarian diets link dietary fat restriction to slower growth. Unfortunately, these studies are confounded by inadequacies in total energy and micronutrient intake (55). Some investigators have reported lower vitamin and mineral intakes in association with low fat diets (56,57). A cohort of 500 Canadian preschoolers was stratified according to fat intake: <30%, 30–40% or >40% of energy from fat between ages 3 and 6 y. Low fat intake was associated with inadequate intake of fat-soluble vitamins. For children habitually on low fat diets, the odds ratio for underweight for age at age 6 y was 2.3 (58).
The relationship between dietary fat intake and body fat in children has been examined in a number of studies. Unfortunately, the commonly used measurement of skinfold thickness is not the most sensitive predictor of body fat. The effect of dietary fat on growth of 140 children in New Zealand was examined at ages 2, 4, 6 and 8 y (59). Median percent dietary fat intake fell from 44% at 3 mo to 36% at 6 mo and remained at a similar level until 8 y. At each age interval no differences in height, weight or skinfold thickness were observed among children consuming <30%, 30–34.9% and >34.9% of dietary energy as fat. Maffeis et al. (60) recorded a diet history and measured the skinfold thickness of 82 prepubertal Italian children. Mean fat intake was 36.6% in obese children and 33.8% in nonobese children. Percent dietary fat was weakly correlated with body fat mass (%). Gazzaniga and Burns (61) studied 48 lean and obese American children and reported that the obese children consumed higher proportions of total energy as fat. Percent fat mass was positively correlated with dietary fat intake independent of total energy intake. Fisher and Birch (62) found that children who preferred high-fat snacks consumed a high percentage of total energy as fat and had high triceps skinfold measurements. Ricketts (63) obtained diet records, preference ratings of high and low fat snack foods and skinfold measurements on 88 American children, aged 9–12 y. Mean percent dietary fat was 34%. Children who preferred the high fat snacks had high dietary fat intakes. High fat food preference was associated with higher body mass index and triceps skinfold measurements. These studies suggest that children establish food preferences at an early age. In summary, data from industrialized countries suggest that if diet supplies adequate energy and essential nutrients, a dietary fat intake of 30% of energy is adequate for normal growth and development of healthy children.
Prentice and Paul (64) described the total fat intake of the Gambian infants over their first 17 mo, showing relatively little change in intake on an absolute basis and therefore a marked decline per kilogram of body weight. Fat intake was highest in the first 3 mo and was provided almost entirely by human milk; as infancy progressed, an increased intake of cereal- and groundnut-based foods containing little fat replaced the gradual decline in human milk (Table 2). The percent energy from fat was initially >50% and declined to 30% by 17 mo. Once infants were fully weaned at around 2 y, both fat intake and fat percent energy fell very substantially, the latter being only 15%. Dietary fat was provided chiefly by groundnuts, but cereals were also important because relatively large quantities were eaten (Fig. 3). The few fat-rich foods were those containing oil, but these expensive items were not frequently used. Data on total fat intake including specific fatty acid intake of Gambian compared with British children are provided in Table 3. LCPUFA intakes expressed per unit of boy weight drop significantly in Gambian children after 12 mo. Higher total energy and saturated fat intake of British children is clearly evident from these results.
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The coexistence of early stunting with the progressive increase in urban obesity in Latin America creates a dilemma for complementary feedings programs. The need to improve growth beyond providing increased energy supply is suggested by the analysis. The association of improved growth with animal fat and protein suggests that micronutrients (e.g., vitamin A, zinc and iron) or other essential components [essential amino acids or (n-6) and (n-3) fatty acids] may be limiting the growth of Latin American children.
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Cholesterol in the infant diet |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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Short-term human studies have been in part confounded by diversity in solid food weaning regimens as well as varied composition of fatty acid components of the early diet; the latter are now known to affect circulating lipoprotein cholesterol species (69). Mean plasma total cholesterol by age 4 mo in human milk–fed infants reached 4.65 mmol/L whereas cholesterol values in formula-fed infants tended to remain <1.29 mmol/L. In a study by Carlson et al. (70), infants receiving predominantly an LA-enriched oil blend exhibited a mean cholesterol concentration of 2.84 mmol/L. A separate group of infants in that study receiving predominantly oleic acid had a mean cholesterol concentration of 3.44 mmol/L; moreover, infants fed human milk and oleic acid–enriched formula had relatively higher HDL cholesterol and apoproteins A-I and A-II than did the infants fed predominantly LA-enriched formula. The ratio of LDL+VLDL cholesterol to HDL cholesterol was lowest for infants receiving the oleic acid–predominant formula. Using a similar oleic acid–predominant formula, Darmady et al. (71) reported a mean value of 3.85 mmol/L at age 4 mo compared with 5.07 mmol/L in a parallel breast-fed group. Most of those infants then received an uncontrolled mixed diet and cow’s milk, with no evident differences in plasma cholesterol levels by 12 mo that were dependent of the type of early feeding they had received.
We (72) assessed the effect of feeding a controlled lipid diet on plasma cholesterol lipoprotein fractions. We used a prospective randomized diet-controlled study in matched populations of Caucasian normal growing infants from birth to age 12 mo followed by free access to food from age 12 to 24 mo. The experimental approach was based on the comparison of oleic acid– and LA-predominant diets (both low in cholesterol) compared with human milk (oleic acid predominant and high in cholesterol). Study subjects were enrolled from a population of 68 healthy infants from highly motivated families followed in a single private practice office in North Dallas. The two formulas provided each infant 15–25 mg cholesterol/d depending on intake volume. After being weaned, the two formula groups received a selection of predefined solid foods and oil supplementation, provided by the investigators, to maintain a daily fatty acid intake resembling that of the initially assigned infant formula but with a lower total fat content (35% of total energy).
As solid foods were introduced, the decrease in fat energy from the formula-only feeding was adjusted to preserve the relative fatty acid composition by using either oleic acid–enriched (High-Oleic group) or LA-enriched (High-Linoleic group) oil supplements (California Fats & Oils, Richmond, CA). For the remainder of the study, the selected foods together with either oleic acid– or LA-rich safflower oil supplements provided a daily intake of individual fatty acids that paralleled the assigned preweaning diets. A third group, fed human milk, was weaned at a mean age of 6.2 mo (range 4–8.5 mo) and after weaning until age 12 mo received a mixed diet resembling human milk in its cholesterol (150–200 mg/d, i.e., 1 egg yolk equivalent) and oleic acid content. This was accomplished by using added egg yolk and the same formula as for the High-Oleic group. The selected solid foods and oil supplements given to all infants after weaning were designed to maintain the fatty acid and cholesterol intake of the assigned diet group. Postweaning, all infants received, as a function of increasing age, 110–120 kcal/(kg · d) and 2.5–3.0 g protein/(kg · d), which was customary for this population. The diets provided vitamins and minerals to meet or exceed the Recommended Dietary Allowances according to age.
As a result of weaning, the percentage of energy delivered as fat decreased in all groups from 50% (to age 4 mo) to 35% (from ages 4 to 12 mo). Our study showed significant effects of exclusive human milk feeding on lipoprotein-cholesterol concentrations at age 4 mo. At ages 9 and 12 mo, while maintaining cholesterol and fatty acid intakes to mimic human milk, this group had concentrations that were not different from those of the High-Oleic formula group (low cholesterol). The High-Linoleic formula group (also low cholesterol) had lower total and LDL cholesterol throughout the study. Thus our data suggest that the specific fatty acid intake plays a predominant role in determining total and LDL cholesterol. We cannot discard a role for high dietary cholesterol associated with exclusive human milk feeding during the first 4 mo of life, because at this time the human milk–fed group had significantly higher total and LDL cholesterol than did the High-Oleic group.
In summary, measurements of serum lipoprotein concentrations and LDL receptor activity in infants suggest that it is the fatty acid content rather than the cholesterol in the diet that regulates cholesterol homeostasis. The regulation of endogenous cholesterol synthesis in infants appears to be regulated similarly to that of adult humans (73,74).
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Safety concerns for edible fats used in complementary feeding products |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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5%. (Carlos Castillo, unpublished data, 1984). The trans fatty acid content of hydrogenated fish oil was extremely high, on the order of 30%, raising serious concerns about long-term safety given the effects of trans acids on lipoprotein metabolism. Diets high in trans fatty acids increase LDL cholesterol, reduce HDL cholesterol and possibly increase lipoprotein(a). All of these changes increase atherogenicity. Trans fatty acids formed during hydrogenation have other problems. They are not substrates for LCPUFA formation and thus increase the need for EFA. For example if all-cis-18:2(n-6) is replaced by cis-trans-18:2(n-6), it does not work as an EFA. The impairment of LCPUFA synthesis by trans fatty acids should be considered in view of the importance of LCPUFA availability for infant growth and development. Furthermore, a reduction of postnatal growth was observed in animals exposed to high levels of trans fatty acids. The extent of EFA deficiency in developing countries is virtually unknown, especially because the clinical manifestations occur only in extreme deficiency. Thus, this problem may go unreported despite the potential effects in central nervous system development.
Improvement of the quality of the energy supply of infants in developing countries is urgently needed to avoid inducing problems in later life. Low price and shelf-life stability of hydrogenated fats has been the reason for their inclusion in complementary foods and other products given to children. However, this needs to be balanced against the possible long-term adverse effects of this type of fat. The European Union set an upper limit of 4% of total fat for the trans fatty acid content of foods for infants and young children. Children of low socioeconomic status should be given food products that meet long-term safety standards and are not just the cheapest source of energy available.
The issue of chemical composition is as relevant for lipid sources as it is to protein. Fats are structural components of tissues, especially neural tissues; (n-3) and (n-6) fatty acids are essential and must be provided by the diet. In most developing countries, fats included in foods, even those given to young children, are by-products of one of many industrial processes. For example, consider coconut oil, partially or fully hydrogenated fish oil and hydrogenated vegetable fats of low cost such as cotton oil. Coconut oil has a high content of saturated fatty acids with intermediate chain length (lauric acid and myristic acid); these fatty acids are well absorbed but contribute to raising LDL cholesterol. Human milk has relatively low concentrations of lauric (5–7%) and myristic acids (6–8%). Some countries have placed limits on dietary intakes of lauric and myristic acids to prevent adverse long-term effects (64).
Another safety issue in fats and oils used for complementary feeding in developing countries is the need to avoid the use of rapeseed oil with high concentrations of erucic acid. Erucic acid is a long-chain monounsaturated fatty acid [trans-22:1(n-9)] found in high amounts in some types of rapeseed oil. Absorbed erucic acid is oxidized slowly and accumulates in myocardium, causing myocardial lipidosis and functional abnormalities in myocardial mitochondria. These side effects are observed at high but not at low (<1% of dietary fatty acids) levels of intake. Canada has developed low erucic acid rapeseed oil seeds under the registered trade name "canola" (75,76). If this is not monitored, toxicity from erucic acid may occur, again virtually impossible to diagnose clinically. If rapeseed oil is to be used it should be derived from genetically low erucic acid varieties. Unfortunately these oil seeds revert to erucic acid–producing phenotypes with an increasing content of this fatty acid. Thus, certified low erucic acid seeds should be purchased every year. These seeds may be costly and farmers in developing countries may not use them unless forced by appropriate quality control measures.
Other components of vegetable oils may have adverse effects for infants and young children. Unsaponifiable ingredients in sesame seed oil have been reported to cause allergic reactions, and cyclopropenoids in cotton seed oil impair EFA desaturation. Therefore, the use of both oils in the production of infant foods has been prohibited in Europe.
Another critical safety issue is the stability of oils in terms of lipid peroxidation, noticed as rancidity by smell and taste. Highly unsaturated oils such as fish oil or vegetable oils used in human foods or as animal feed require substantial amounts of synthetic antioxidants to preserve their structure and prevent rancidity. Most legislation authorizes the use of up to 0.1% butylated hydroxytoluene, butylated hydroxyanisole, tert-butylhydroquinone and propyl or octyl gallate as total antioxidant. This is in accordance with Codex, despite some existing concerns with the safety of synthetic antioxidants, which have led some countries to restrict their use (77). A specific issue in the use of processed fish oil for animal feed is the safety concern of ethoxyquine or its mixtures used as an antioxidant in the product. Ethoxyquine is a highly efficient antioxidant and anticombustion agent but is prohibited in human food products. The consumption of poultry or other animals fed fish meal or fish oil containing ethoxyquine is a safety issue that has not been addressed by present regulatory efforts. Research is underway to find alternative antioxidants to replace ethoxyquine at reasonable prices.
Safety problems may be associated with how oils are dispensed. Large tin or plastic barrels used in developing countries to reduce costs may facilitate adulteration of products and promote peroxidation given the large volume and the long time until the total product is sold. A recent study in marasmic children demonstrated altered antioxidant defense systems and increased lipid peroxidation, suggesting an increased risk of oxidative damage in malnourished infants (78). Bottled oil ready for consumer purchase is undoubtedly safer but is also more expensive. Soft plastic containers made with phthalic acid as plasticizer can also create safety problems because this agent is fat soluble and a known carcinogen; rigid plastics or glass bottles are preferable (79). Tetrapak brick containers have recently been introduced in some countries in the Americas. This container prevents rancidity because exposure to light and oxygen are prevented by the metallic component of the packaging material and the nitrogen used to displace air in the container.
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Recommendations and conclusions |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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30–35% of energy (Table 4). 6–10% of energy and the remaining fat energy should come from monounsaturated fatty acids.
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Lipids are important determinants of growth and body composition, necessary for absorption of fat-soluble vitamins, a key dietary determinant of prostanoid metabolism and related functions, a structural component of cell membranes in all vital organs and a source of EFA required for normal neurodevelopment.
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FOOTNOTES |
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3 AA, arachidonic acid; DHA, docosahexaenoic acid; DPA, docosapentaenoic acid; EFA, essential fatty acid; FER, fat-energy ratio; LA, linoleic acid; LNA, -linolenic acid; LCPUFA, long-chain polyunsaturated fatty acid; LPL, lipoprotein lipase.
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LITERATURE CITED |
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TOPABSTRACTNomenclature used to...Lipid absorption and metabolismMetabolism of EFALipids in infant nutritionEFA needs for growth...Lipids as an energy...Cholesterol in the infant...Safety concerns for edible...Recommendations and conclusionsLITERATURE CITED |
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