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Nutrition for infants, children, and adolescents should maintain current weight and support normal growth and development. Growth during infancy is rapid, critical for neurocognitive development, and has the highest energy and nutrient requirements relative to body size than any other period of growth. It is followed by growth during childhood, when 60% of total growth occurs, and finally by puberty. Nutrition and growth during the 1st 3 yr of life predict adult stature and some health outcomes. The major risk period for growth stunting (impaired linear growth) is between 4 and 24 mo of age. Therefore, it is critical to identify nutrient deficiencies promptly and to address them aggressively early in life, because missing them can impart lasting adverse effects on later growth and development.
Dietary intake should provide energy requirements as well as the essential macronutrient and micronutrient needs for sustaining the function of multiple vital processes. Nutrient deficiencies can limit growth, impair immune function, affect neurodevelopment, and increase morbidity and mortality. Worldwide, malnutrition and undernutrition are the leading causes of acquired immunodeficiency, and a major factor underlying morbidity and mortality in children <5 yr of age.
The transition in food supply and type of nutrition chosen in many developing countries, coincident with population change, from traditional to Western diet has resulted in increased life expectancy and adult stature. Unfortunately, the Western diet in these populations is also frequently accompanied by decreased physical activity and, in parallel, decreases in the incidence and prevalence of communicable (infectious) diseases along with increases in the incidence and prevalence of noncommunicable diseases such as type 2 diabetes, cardiovascular (CV) disease, obesity, inflammatory bowel disease (IBD), and certain cancers. Consequently, it is important to view the impact of nutrition on health from various perspectives: to prevent deficiency, to promote adequacy, and to prevent or reduce the risk for acquiring diseases associated with excess intakes, such as obesity, diabetes, and CV disease.
Advances in our understanding of the roles of some nutrients such as vitamin D, polyunsaturated fatty acids (PUFAs), and fiber have changed our focus from recommendations about preventing deficiency to recommendations about nutritional intake associated with optimal health. The 2006 World Health Organization (WHO) growth charts, which now are recommended for all children until age 2 yr , are not only descriptive but also proscriptive on how children with adequate nutrition and health care should grow. Therefore, identifying and providing appropriate and adequate nutrition in infancy and childhood are critical to supporting normal growth and development as well as providing the foundation for lifelong health and well-being.
The dietary reference intake (DRI) established by the Food and Nutrition Board of the U.S. Institutes of Medicine (IOM) provides guidance on the nutrient needs for individuals and groups across different life stages and by gender (see Tables 55.1 to 55.4 ).
Key concepts on DRI concepts include the estimated average requirement (EAR) , the recommended dietary allowance (RDA), and the tolerable upper limit of intake (UL) ( Fig. 55.1 ). The EAR is the average level of daily nutrient intake that is estimated to meet the requirements for 50% of the population, assuming normal distribution. The RDA is an estimate of the daily average nutrient intake that meets the nutritional needs of >97% of the individuals in a population, and it can be used as a guideline for individuals to avoid deficiency. When an EAR cannot be derived, an RDA cannot be calculated; therefore, an adequate intake (AI) is developed as a guideline for individuals based on the best available data and scientific consensus. The UL denotes the highest average daily intake with no associated adverse health effects for almost all individuals in a particular group. Fig. 55.2 shows the relationships among EAR, RDA, and UL.
Energy includes both food intake and metabolic expenditure. Deficits and excesses of energy intake yield undesirable health consequences. Inadequate energy intake can lead to growth faltering, catabolism of body tissues, and inability to provide adequate energy substrate. Excess energy intakes can increase the risk for obesity. Adequacy of energy intake in adults is associated with maintenance of a healthy weight. The three components of energy expenditure in adults are the basal metabolic rate (BMR), thermal effect of food (e.g., energy required for digestion and absorption), and energy for physical activity. In children, additional energy intake is required to support growth and development.
Estimated energy requirement (EER) is the average dietary energy intake predicted to maintain energy balance in a healthy individual and takes into account age, gender, weight, stature, and level of physical activity ( Table 55.1 ). The 2015–2020 Dietary Guidelines for Americans refer to the 2008 Physical Activity Guidelines for Americans. These guidelines recommend ≥60 min of moderate- or vigorous-intensity aerobic physical daily for children and adolescents. This activity should include vigorous intensity physical activity at least 3 days per week. In addition, as part of their ≥60 min of daily physical activity, children and adolescents are advised to incorporate muscle- and bone-strengthening activity for ≥3 days a week, to maintain a healthy weight and to prevent or delay progression of chronic noncommunicable diseases such as obesity and CV disease.
INFANTS AND YOUNG CHILDREN: EER (kcal/day) = TEE + ED | |
0-3 mo | EER = (89 × weight [kg] − 100) + 175 |
4-6 mo | EER = (89 × weight [kg] − 100) + 56 |
7-12 mo | EER = (89 × weight [kg] − 100) + 22 |
13-36 mo | EER = (89 × weight [kg] − 100) + 20 |
CHILDREN AND ADOLESCENTS 3-18 yr: EER (kcal/day) = TEE + ED | |
Boys | |
3-8 yr | EER = 88.5 − (61.9 × age [yr] + PA × [(26.7 × weight [kg] + (903 × height [m])] + 20 |
9-18 yr | EER = 88.5 − (61.9 × age [yr] + PA × [(26.7 × weight [kg] + (903 × height [m])] + 25 |
Girls | |
3-8 yr | EER = 135.3 − (30.8 × age [yr] + PA [(10 × weight [kg] + (934 × height [m])] + 20 |
9-18 yr | EER = 135.3 − (30.8 × age [yr] + PA [(10 × weight [kg] + (934 × height [m])] + 25 |
The EER was determined based on empirical research in healthy persons at different levels of physical activity, including levels different from recommended levels. They do not necessarily apply to children with acute or chronic diseases. EER is estimated by equations that account for total energy expenditure (TEE) and energy deposition (ED) for healthy growth. EERs for infants, relative to body weight, are approximately twice those for adults because of the increased metabolic rate and requirements for weight maintenance and tissue accretion (growth).
Dietary nutrients that provide energy include fats (approximately 9 kcal/g), carbohydrates (4 kcal/g), and protein (4 kcal/g). These nutrients are called macronutrients . If alcohol is consumed, it also contributes to energy intake (7 kcal/g). The EER does not specify the relative energy contributions of macronutrients. Once the minimal intake of each macronutrient is attained (e.g., sufficient protein intake to meet specific amino acid requirements, sufficient fat intake to meet linoleic acid and α-linolenic acid needs for brain development), the remainder of the intake is used to meet energy requirements, with some degree of freedom and interchangeability among fat, carbohydrate, and protein. This argument forms the basis for the acceptable macronutrient distribution ranges (AMDRs) , expressed as a function of total energy intake ( Table 55.2 ).
AMDA (% OF ENERGY) | ||
---|---|---|
Macronutrient | Age 1-3 yr | Age 4-18 yr |
Fat | 30-40 | 25-35 |
ω6 PUFAs (linoleic acid) | 5-10 | 5-10 |
ω3 PUFAs (α-linolenic acid) | 0.6-1.2 | 0.6-1.2 |
Carbohydrate | 45-65 | 45-65 |
Protein | 5-20 | 10-30 |
Fat is the most calorically dense macronutrient, providing approximately 9 kcal/g. For infants, human milk and formula are the main dietary sources of fat, whereas older children obtain fat from animal products, vegetable oils, and margarine. The AMDR for fats is 30–40% of total energy intake for children 1-3 yr and 25–35% for children 4-18 yr of age. In addition to being energy dense, fats provide essential fatty acids that have body structural and functional roles (e.g., cholesterol moieties are precursors for cell membranes, hormones, and bile acids). Fat intake facilitates absorption of fat-soluble vitamins (vitamins A, D, E, and K). Both roles are relevant to neurologic and ocular development ( Table 55.3 ).
FUNCTION | LIFE STAGE GROUP | RDA OR AI * (g/day) | SELECTED FOOD SOURCES | ADVERSE EFFECTS OF EXCESSIVE CONSUMPTION |
---|---|---|---|---|
TOTAL DIGESTIBLE CARBOHYDRATE | ||||
RDA based on its role as the primary energy source for the brain AMDR based on its role as a source of kcal to maintain body weight |
Infants | Major types: starches and sugars, grains, and vegetables (corn, pasta, rice, potatoes, and breads) are sources of starch. Natural sugars are found in fruits and juices. Sources of added sugars: soft drinks, candy, fruit drinks, desserts, syrups, and sweeteners † |
No defined intake level for potential adverse effects of total digestible carbohydrate is identified, but the upper end of the AMDR was based on decreasing risk of chronic disease and providing adequate intake of other nutrients. It is suggested that the maximal intake of added sugars be limited to providing no more than 10% of energy. |
|
0-6 mo | 60 * | |||
7-12 mo | 95 * | |||
Children | ||||
>1 yr | 130 | |||
Pregnancy | ||||
≤18 yr | 175 | |||
19-30 yr | 175 | |||
TOTAL FIBER | ||||
Improves laxation, reduces risk of coronary artery (heart) disease, assists in maintaining normal blood glucose levels | Infants | Includes dietary fiber naturally present in grains (e.g., oats, wheat, unmilled rice) and functional fiber synthesized or isolated from plants or animals and shown to be of benefit to health | Dietary fiber can have variable compositions; therefore it is difficult to link a specific source of fiber with a particular adverse effect, especially when phytate is also present in the natural fiber source. As part of an overall healthy diet, a high intake of dietary fiber will not produce deleterious effects in healthy persons. Occasional adverse GI symptoms are observed when consuming some isolated or synthetic fibers, but serious chronic adverse effects have not been observed because of the bulky nature of fibers. Excess consumption is likely to be self-limiting; therefore, UL was not set for individual functional fibers. |
|
0-6 mo | ND | |||
7-12 mo | ND | |||
Children | ||||
1-3 yr | 190 * | |||
4-8 yr | 25 * | |||
Males | ||||
9-13 yr | 31 * | |||
14-18 yr | 38 * | |||
19-21 yr | 38 * | |||
Females | ||||
9-13 yr | 26 * | |||
14-18 yr | 26 * | |||
19-21 yr | 25 * | |||
Pregnancy | ||||
≤18 yr | 28 * | |||
19-21 yr | 28 * | |||
TOTAL FAT | ||||
Energy source When found in foods, is a source of ω3 and ω6 PUFAs Facilitates absorption of fat-soluble vitamins |
Infants | Infants: Human milk or infant formula Older children: Butter, margarine, vegetable oils, whole milk, visible fat on meat and poultry products, invisible fat in fish, shellfish, some plant products such as seeds and nuts, bakery products |
UL is not set because there is no defined intake of fat at which adverse effects occur. High fat intake will lead to obesity. Upper end of AMDR is also based on reducing risk of chronic disease and providing adequate intake of other nutrients. † Low fat intake (with high carbohydrate) has been shown to increase plasma triacylglycerol concentrations and decrease HDL cholesterol. |
|
0-6 mo | 31 * | |||
7-12 mo 1-18 yr |
30 * Insufficient evidence to determine AI or EAR; see AMDR, Table 55.2 . |
|||
ω6 POLYUNSATURATED FATTY ACIDS | ||||
Essential component of structural membrane lipids, involved with cell signaling Precursor of eicosanoids Required for normal skin function |
Infants | Nuts, seeds; vegetable oils such as soybean, safflower, corn oil | There is no defined intake of ω6 level at which adverse effects occur. Upper end of AMDR is based on the lack of evidence that demonstrates long-term safety and human in vitro studies that show increased free radical formation and lipid peroxidation with higher amounts of ω6 fatty acids. Lipid peroxidation is thought to be a component of atherosclerotic plaques. |
|
0-6 mo | 4.4 * | |||
7-12 mo | 4.6 * | |||
Children | ||||
1-3 yr | 7 * | |||
4-8 yr | 10 * | |||
Males | ||||
9-13 yr | 12 * | |||
14-18 yr | 16 * | |||
19-21 yr | 17 * | |||
Females | ||||
9-13 yr | 10 * | |||
14-18 yr | 11 * | |||
19-21 yr | 12 * | |||
Pregnancy | ||||
≤18 yr | 13 * | |||
19-21 yr | 13 * | |||
Lactation | ||||
≤18 yr | 13 * | |||
19-21 yr | 13 * | |||
ω3 POLYUNSATURATED FATTY ACIDS | ||||
Involved with neurologic development and growth Precursor of eicosanoids |
Infants | Vegetable oils, e.g., soybean, canola, flax seed oil; fish oils, fatty fish, walnuts; † smaller amounts in meats and eggs | No defined intake levels for potential adverse effects of ω3 PUFAs are identified. Upper end of AMDR is based on maintaining appropriate balance with ω6 fatty acids and the lack of evidence that demonstrates long-term safety, along with human in vitro studies that show increased free radical formation and lipid peroxidation with higher amounts of PUFAs. Because the longer-chain n -3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are biologically more potent than their precursor, linolenic acid, much of the work on adverse effects of this group of fatty acids has been on DHA and EPA. Lipid peroxidation is thought to be a component in the development of atherosclerotic plaques. |
|
0-6 mo | 0.5 * | |||
7-12 mo | 0.5 * | |||
Children | ||||
1-3 yr | 0.7 * | |||
4-8 yr | 0.9 * | |||
Males | ||||
9-13 yr | 1.2 * | |||
14-18 yr | 1.6 * | |||
19-21 yr | 1.6 * | |||
Females | ||||
9-13 yr | 1.0 * | |||
14-18 yr | 1.1 * | |||
19-21 yr | 1.1 * | |||
Pregnancy | ||||
≤18 yr | 1.4 * | |||
19-21 yr | 1.4 * | |||
Lactation | ||||
≤18 yr | 1.3 * | |||
19-21 yr | 1.3 * | |||
SATURATED AND TRANS FATTY ACIDS | ||||
The body can synthesize its needs for saturated fatty acids from other sources. | No dietary requirement | Saturated fatty acids are present in animal fats (meat fats and butter fat), and coconut and palm kernel oils. Trans fat: stick margarines, foods containing hydrogenated or partially hydrogenated vegetable shortenings |
There is an incremental increase in plasma total and LDL cholesterol concentrations with increased intake of saturated or trans fatty acids; therefore, saturated fat intake should be limited to <10% with no trans fat. † ‡ | |
CHOLESTEROL | ||||
No dietary requirement | Sources: liver, eggs, foods that contain eggs, e.g., cheesecake, custard pie | |||
PROTEIN AND AMINO ACIDS ‡ | ||||
Major structural component of all cells in the body Functions as enzymes, in membranes, as transport carriers, and as some hormones During digestion and absorption, dietary protein is broken down to amino acids, which become the building blocks of these structural and functional compounds. Nine indispensable amino acids must be provided in the diet; the body can make the other amino acids needed to synthesize specific structures from other amino acids. |
Infants | Proteins from animal sources, e.g., meat, poultry, fish, eggs, milk, cheese, yogurt, provide all 9 indispensable amino acids in adequate amounts and are considered “complete protein.” Protein from plants, legumes, grains, nuts, seeds, and vegetables tend to be deficient in ≥1 of the indispensable amino acids and are called “incomplete protein.” Vegan diets adequate in total protein content can be “complete” by combining sources of incomplete protein, which lack different indispensable amino acids. |
No defined intake levels for potential adverse effects of protein are identified. Upper end of AMDR was based on complementing AMDR for carbohydrate and fat for the various age-groups. Lower end of AMDR is set at approximately the RDA. |
|
0-6 mo | 9.1 * | |||
7-12 mo | 11.0 | |||
Children | ||||
1-3 yr | 13 | |||
4-8 yr | 19 | |||
Males | ||||
9-13 yr | 34 | |||
14-18 yr | 52 | |||
≥19 yr | 56 | |||
Females | ||||
9-13 yr | 34 | |||
≥14 yr | 46 | |||
≤18 yr | ||||
19-21 yr | 71 |
† 2015–2020 Dietary Guidelines for Americans. US Department of Health and Human Services. https://health.gov/dietaryguidelines/2015/ .
‡ Based on 1.5 g/kg/day for infants, 1.1 g/kg/day for 1-3 yr, 0.95 g/kg/day for 4-13 yr, 0.85 g/kg/day for 14-18 yr, 0.8 g/kg/day for adults, and 1.1 g/kg/day for pregnant (using pre-pregnancy weight) and lactating women.
Triglycerides are the most common form of dietary fat and are composed of 1 glycerol molecule with 3 fatty acids. Triglycerides are found in animal and vegetable fats. Simple sugars (i.e., refined grains and high sugar drinks) are converted to triglycerides in the liver. Elevated serum triglycerides are a risk factor for CV disease and metabolic syndrome. Decreasing simple sugars and increasing complex carbohydrate intake reduces serum triglyceride levels.
Dietary saturated fatty acids (found primarily in animal fat and dairy products), trans fats (found in hydrogenated margarines and oils), and cholesterol increase the low-density lipoprotein (LDL) fraction of serum cholesterol, which is a risk factor for the development of atherosclerosis ( Fig. 55.3 ). Autopsy studies demonstrate that atherosclerosis begins early in childhood, even in infancy. Therefore, dietary advice to optimize CV health should be given starting from age 2 yr, when sufficient fat intake to sustain growth and brain development is less of a concern.
Because saturated and monounsaturated fats can be synthesized endogenously to support adequate structural and physiologic requirements, there is no AI or RDA set for these dietary components. Trans fats, a by-product of the hydrogenation of vegetables oils to form margarine, have no known health benefits in humans. Trans fats do not have an AI or RDA defined. In fact, trans fats behave like saturated fats. An UL has not been set for cholesterol, saturated, or trans fats because there is a continuous positive linear association between intake of these fats and increased risk for CV disease, without a threshold level. Diets low in saturated fats and cholesterol without trans fats are therefore preferred.
Efforts continue to reduce or eliminate trans fats from the diet. For optimal CV health in the general population, rather than limiting fat intake, advice should focus in most cases on changing the type of fat consumed. With respect to preventing obesity, all types of fatty acids have the same energy content and can contribute to increasing the risk for obesity. The current 2015–2020 Dietary Guidelines for Americans no longer restrict how much energy should come from fat intake, but continue to recommend that <10% of total daily calories come from saturated fat, with no trans fat intake. Furthermore, these guidelines do not specify limits on dietary cholesterol intake, because there is no clear strong evidence of the relationship between dietary and blood cholesterol.
Humans are incapable of synthesizing the precursor omega (ω) 3 (α-linolenic acid; ALA) and ω6 (linoleic acid; LA) PUFAs and depend on diet for these 2 essential fatty acids (EFAs). Safflower and sunflower oil are good sources of linoleic acid. Walnut and flaxseed oil are good sources of ALA. Essential fatty acid deficiency with LA is associated with desquamating skin rashes, alopecia, thrombocytopenia, impaired immunity, and growth deficits but is rare in the general population. EFAs are enzymatically elongated and desaturated into longer-chain fatty acids; ALA can be converted to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) ω3 PUFAs. LA is converted to arachidonic acid (ARA). Long-chain PUFAs such as DHA and ARA have a variety of cellular structural and functional roles; they influence membrane fluidity and function in gene expression and modulate the inflammatory response. ARA and DHA are present in breast milk, often supplemented in infant formulas, and are required for normal growth and development. DHA is present in the retina and is involved in the visual evoked response in infants.
The conversion of ALA to EPA and DHA and of LA to ARA is influenced by many factors, including type and amounts of dietary fats, and by enzymatic substrate affinity among competing ω3, ω6, ω9, saturated, and trans fatty acids. Approximately 0.5% of dietary ALA is converted to DHA, and 5% of ALA intake is converted to EPA; therefore, dietary intake of longer-chain PUFAs is an important determinant of serum and tissue long-chain PUFA status. The biologic activity and health benefits of ALA are thought to be derived from the longer-chain PUFA products EPA and DHA. Consistent with these findings of limited conversion of ALA to EPA and DHA, and that EPA and DHA appear to confer the biologic role and health benefits, the dietary reference intake (DRI) stipulates that up to 10% of the AI for ω3 PUFA (ALA being the major dietary constituent) can be replaced by DHA and EPA to support normal neural development and growth.
The ratio of dietary intake of each type of PUFA influences their relative amounts in different tissue compartments. A dietary ω6:ω3 PUFA ratio of 4-5 : 1 may be beneficial in reducing risk of disease and may be associated with improved health outcomes, compared with the current 15-30 : 1 ratio observed in U.S. diets.
Protein and amino acids have structural and functional roles in every cell in the body. Dietary protein intake is required to replenish the turnover of protein and to meet amino acid needs for growth. Dietary protein also provides approximately 4 kcal/g as an energy substrate when intake is in excess of needs, or during periods of catabolism. Inadequate energy intake or inadequate protein intake increases catabolism of body protein reservoirs (i.e., lean body mass) for energy and free amino acids required to support normal physiologic function. Nitrogen from protein turnover is excreted in urine, stool, and other bodily excretions. Increased protein intake may be required for rare hypermetabolic states, such as extensive burn injury. Protein-energy malnutrition, although relatively rare in the noninstitutionalized U.S. population, is more common in the developing world. Protein-energy malnutrition impairs brain, immune system, and intestinal mucosal functions (see Chapter 59 ).
The DRI for protein is provided in Table 55.3 . According to the 2015–2020 Dietary Guidelines for Americans, the average intake of protein from poultry, meat, eggs, nuts, seeds, and soy products are close to the recommended amounts for all ages. Protein intake is higher than recommended amounts in adolescent males (mostly from meats, poultry, and eggs). Intake of seafood protein is low across all age and sex groups. An UL for protein has not been set. Some athletes may have increased protein needs, of approximately 2 g/kg/day, to prevent loss of fat-free mass or lean body mass. Certain conditions may require a modest increase in protein intake, including conditions with high protein turnover, inflammatory conditions, or postsurgical states, as well as with cystic fibrosis, critical illnesses, burn injuries, compensated liver disease, and bariatric surgery (e.g., laparoscopic sleeve gastrectomy and Roux-en- Y gastric bypass). Intake of protein or specific amino acids needs to be limited in some health conditions, such as renal disease and decompensated liver disease, and metabolic diseases such as phenylketonuria and maple syrup urine disease, in which specific amino acids can be toxic.
The amino acid content of dietary protein is also important. Certain amino acids are indispensable , and humans depend on dietary sources to meet adequacy and prevent deficiency. Certain amino acids are termed conditional essential/indispensable , meaning they become essential in patients affected by some diseases or during a certain life stage, such as with cysteine, tyrosine, and arginine in newborns because of enzyme immaturity ( Table 55.4 ). Human milk contains both the indispensable and conditionally indispensable amino acids and therefore meets the protein requirements for infants. Breast milk is considered the optimal protein source for infants and is the reference amino acid composition by which biologic quality is determined for infants. If a single amino acid in a food protein source is low or absent but is required to support normal metabolism, that specific amino acid becomes the limiting nutrient in that food. For soy-based infant formula, supplementing the formula with the limiting amino acid (methionine) is necessary. Certain amino acid–like substances, such as creatinine, are used by some athletes and may enhance performance. Such supplementation should be monitored for potential side effects.
INDISPENSABLE | DISPENSABLE | CONDITIONALLY INDISPENSABLE * | PRECURSORS OF CONDITIONALLY INDISPENSABLE |
---|---|---|---|
Histidine † Isoleucine Leucine Lysine Methionine Phenylalanine Threonine Tryptophan Valine |
Alanine Aspartic acid Asparagine Glutamic acid Serine |
Arginine Cysteine Glutamine Glycine Proline Tyrosine |
Glutamine/glutamate, aspartate Methionine, serine Glutamic acid/ammonia Serine, choline Glutamate Phenylalanine |
* Conditionally indispensable is defined as requiring a dietary source when endogenous synthesis cannot meet metabolic need.
† Although histidine is considered indispensable, unlike the other 8 indispensable amino acids, it does not fulfill the criteria of reducing protein deposition and inducing negative nitrogen balance promptly on removal from the diet.
To ensure appropriate growth and to promote satiety, children should consume the recommended amount of protein. Specific recommendations for appropriate dietary protein sources to meet indispensable amino acid requirements are available for groups adopting specific diets, such as vegetarians and vegans. Inclusion of legumes and corn, as well as the use of a variety of food sources to provide all of the required amino acids is a strategy advocated for vegetarians and vegans (see Chapter 56 ).
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