Chapter 52. Diet, Nutrition, and Adolescence

females are shown in Table 52.1.



Table 52.1 Recommended Energy Intakes for Adolescents



In a group of normally growing teenagers followed longitudinally, Beal noted that actual energy intake for some teens fell outside the range of the RDA ( 8). Thus, even

when using the parameter for calculating calories best supported by data (kilocalorie per centimeter height), the margin of error is considerable. Nevertheless,

kilocalorie per centimeter height may represent the best way to calculate individual energy requirements of adolescents at the present time.

A review of studies of energy intake of children and adolescents in the United States shows that girls appear to consume their peak caloric intake, about 2550 kcal, at

the time of menarche (around 12 years). This peak demand is followed by a slow decline. In boys, caloric intake appears to parallel the adolescent growth spurt,

increasing until age 16 years to approximately 3400 kcal and then decreasing by 500 kcal by age 19 years ( 9).

The most accepted way of assessing adequacy of energy intake is to evaluate growth and body composition. The normal variability of pubertal growth patterns makes

ideal weight during puberty an untenable concept. A common practice is to plot height and weight on the National Center for Health Statistics (NCHS) growth chart

with the percentiles for each age group ( 10). This plot tells us the position of that teenager relative to the NCHS sample. Growth data gathered in the NCHS survey

published in 1973 form the basis for the growth charts currently used in the United States ( 11) (see Appendix Table III-A-12-d and Table III-A-12-e). If multiple

measurements over time are available, any significant changes in rates of linear growth or body mass can be detected by percentile shifts. However, the teenager in

the 90th percentile for height may or may not be appropriately in the 90th percentile for weight. For example, a male at the 90th percentile weight-for-height with a

triceps skinfold in the lower percentiles would be muscular. Another teenager in the 90th percentile weight-for-height with a triceps skinfold in the 95th percentile

would be classified as obese (survey data summarized in Appendix Tables III-A-14-a-1 through 4).

To determine appropriate weight-for-height for an adolescent and assess whether he or she has excess or deficient energy intake, the height and weight of youths

12–17 years, United States (11) tables (Appendix Table III-A-14-c-1-b, Table III-A-14-c-2-b, Table III-A-14-d-1-b , Table III-A-14-d-2-b, and Table III-A-15.) are often

used clinically. The data are problematic (such as sample size, lack of references to sexual maturity, ethnic differences, etc.), although the tables separate the

percentiles of weight by age, sex, and height, providing a range of weights for a particular height and age. With the additional information gained from triceps

percentiles (Appendix Table III-A-14-b-1 and Table III-A-14-b-2), overweight (triceps skinfold >95th percentile) or underweight (triceps skinfold <25th percentile) can

be assessed.

The National Center for Health data have been analyzed in such a sophisticated way that accurate assessment of growth and simple measures of body composition

are available to measure the impact of energy excess or scarcity on the growing teenager. However, the effects of marginal energy deficits have a subtle effect on

growth. The work of Dreizen et al. ( 12) is one of the few studies in the United States of the long-term effect of chronic mild malnutrition on growth. The net effect over

time was a diminished rate of growth during late childhood and adolescence and delay of puberty by 2 years, but ultimately, this group of malnourished youths in

southeastern United States reached heights and weights similar to those of a comparison group. Keeping in mind the great variation in timing and intensity of growth

seen in adolescents, we must emphasize the large variation in caloric intake in this group.

Physical activity also contributes significantly to the total energy requirement of an individual, as does previous growth and nutritional status. When considering the

energy requirements of adolescents, the importance of individual variation from one adolescent to another must be recognized in making nutritional recommendations.

Table 52.2 presents energy expenditure, expressed in three different body weights, for different activities ( 13). The different activities have highly variable energy

costs and can be used to guide dietary advice or weight management.



Table 52.2 Energy Expenditure of Selected Activities (calories expended/min activity)



Protein

As with energy recommendations, protein needs for an adolescent are more useful when physiologic age is emphasized over chronologic age. Using the RDA for

protein related to height is probably the most useful method for determining protein needs for adolescents ( 5). For adolescent males, the daily protein

recommendations are 0.29, 0.34, and 0.33 g/cm height for the age groups 11 to 14, 15 to 18, and 19 to 24 years, respectively. For adolescent females, the daily

recommendations are 0.29, 0.27, and 0.28 g/cm height for the age groups 11 to 14, 15 to 18, and 19 to 24 years, respectively. The protein requirement is determined

by the amount needed for maintenance plus that needed for growth of new tissue, which during adolescence may represent a substantial portion of the total need.

Unfortunately, data on either of these determinants of requirements are lacking for adolescents and have been interpolated from results of studies involving infants

and adults (5, 14).

The RDA for daily protein intake for adolescents ranges from 44 to 59 g ( 5). Peak intakes of protein coincide with the peak energy intake. The proportion of total

energy intake represented by protein remains fairly constant, between 12 and 14%, throughout childhood and adolescence ( 9).

Results of studies show that average intakes of protein in adolescents exceed the recommended levels ( 9, 15, 16). Although it appears that most adolescents in the

United States have sufficient protein intake, some teenagers who restrict food intake because of a desire to lose weight, eating disorders such as anorexia nervosa

and bulimia, or socioeconomic problems, may be at risk of poor protein intake. Without adequate caloric intake, protein is used in gluconeogenesis and is unavailable

for tissue synthesis. Heald and Hunt demonstrated that in the rapidly growing adolescent, protein metabolism is particularly sensitive to caloric restriction ( 17).

Anthropometric measurements generally are a simple way to assess protein status. Height, weight, and midarm circumference measurements (used to assess lean



body mass) can be used as growth indicators. Midarm circumference measurements and arm muscle area between the 25th and 75th percentiles probably indicate

good nutritional status (18).

Biochemical assessments of protein nutriture include creatinine/height index and serum concentrations of certain proteins: albumin, transferrin, prealbumin, and

retinol-binding protein ( 19, 20, 21 and 22). Determinations of prealbumin and retinol-binding protein are the most sensitive indicators of changes in diet that may

indicate subclinical malnutrition ( 22). A detailed evaluation of assessment procedures is given in Chapter 56.

Minerals

Because of the adolescent growth spurt, the need for three minerals is of particular importance: calcium to sustain increased skeletal mass, iron to aid expansion of

red cell and muscle mass, and zinc to generate new skeletal and muscle tissues. In addition to significant increases in need, intake of these nutrients has been shown

to be below the recommended levels for adolescents ( 15, 16, 23, 24 and 25).

Boys take in more calcium than do girls and are closer to achieving the recommended intakes ( 26). Daily iron intakes reported by the Ten State Nutrition Survey were

relatively lower. Most (80%) girls 10 to 16 years of age were below the recommended 18 mg of iron per day ( 15). Some evidence shows an association between low

concentrations of zinc in hair and poor growth. An analysis of food intake suggests poor eating habits ( 27). The full extent of zinc deficiency and its adverse effect on

puberty needs more inquiry.

Calcium

With approximately 99% of total-body calcium in the skeleton ( 28), the adolescent growth spurt associated with increased skeletal length and mass obviously has a

significant impact on dietary requirements for calcium. Skeletal growth during adolescence accounts for approximately 45% of the adult skeletal mass. Because the

absolute amount of calcium in the skeleton of a boy in the 95th percentile for height and that for a boy in the 5th percentile for height will differ by 36%, the calcium

needs of these two boys will differ sharply because of the difference in skeletal size. The problem is compounded further by the normal differences in pubertal

development, making age and sex alone poor predictors of individual calcium needs. Lastly, growth of skeletal mass and gains in height and muscle mass continue

until the third decade of life ( 29, 30 and 31). Table 52.3 shows the average increments of body calcium for adolescence and the daily increments of body calcium at

the peak of the growth spurt. At the peak of growth, daily deposition of calcium is approximately twice the average increment during the adolescent period. The daily

peak increment of calcium during the growth spurt is greater, occurs later, and lasts longer in boys than in girls ( 28).



Table 52.3 Daily Increments in Body Content Due to Growth



The amount of calcium absorbed from different dietary sources varies. During peak periods of growth in adolescence, the average calcium retention is approximately

300 mg/day. Because the lower range of absorption is approximately 30%, a minimum of 900 mg/day of calcium would be necessary during active skeletal growth

(32).

A wide difference exists in the daily allowances of calcium recommended by two expert committees. The WHO recommends intakes of 600 to 700 mg/day for 11- to

15-year-old adolescents and 500 to 600 mg/day for 16- to 19-year-old adolescents ( 30). The National Institutes of Health Consensus Conference recommended 1200

to 1500 mg/day for adolescents and young adults (11–24 years) ( 33). The Food and Nutrition Board's 1997 dietary reference intake value for ages 9 through 18 years

is 1300 mg/day (33a) (see Appendix Table II-A-2-b-1; see also Chapter 7). These differences in recommended intakes show that the amounts of dietary calcium

needed to sustain growth and to provide maintenance require further study.

Establishing requirements for the teenage group is difficult because many individuals can achieve equilibrium on a wide range of dietary intakes. A large error is likely

in calculating calcium balance because of errors in measuring intakes and excretions, individual differences in rate of biologic maturation; and effects on calcium

metabolism of protein, vitamin D, phosphorus, fiber ( 31), caffeine, and sucrose (32).

Surveys in the United States reveal that adolescent girls are less likely to meet the recommended levels of calcium than are teenage boys ( 15, 16, 23). In addition,

preliminary evidence suggests that adolescent females may need more calcium to reach optimal bone mass. In a recent study, 1500 mg/day of calcium was needed

for maximal calcium retention in a small group of 14-year-old girls ( 34).

Data from retrospective studies indicate that low calcium intakes during adolescence are associated with lower bone densities in women ( 35, 36). In a recent study,

bone density was correlated with calcium intake in a group of boys and girls 2 to 16 years of age. Those ingesting more than 1000 mg/day of calcium had greater

bone density than those ingesting less. Most serum determinations of calcium, phosphate, magnesium, alkaline phosphate, parathyroid hormone, 25-hydroxyvitamin

D and 1,25-dihydroxyvitamin D levels were normal and not correlated with bone mineral status ( 37). Decreased bone density may increase the risk of osteoporosis in

later life (38, 39). Teen mothers who breast-feed may also be at risk for poor calcium balance. Lactating adolescents who consumed about 900 mg/day of calcium had

a 10% decline in bone mineral content. Lactating teen mothers who consumed 1600 mg of calcium remained in calcium balance ( 40).

Iron

Iron deficiency is found in all races, both sexes, and all socioeconomic groups (see Chapter 10 and Chapter 88). Teenagers require additional iron to synthesize

substantial amounts of new myoglobin and hemoglobin. As puberty is initiated, boys accumulate more lean body mass than girls. In fact, at the end of puberty, boys

have twice the lean body mass of girls. Thus, Hepner calculated that for each additional kilogram of added tissue, males require 42 mg iron/kg body weight, compared

with 31 mg iron/kg body weight for girls ( 41). In addition to the described sex differences, the normal biologic differences in body size make a tremendous difference in

iron requirements. For example, a boy in the 97th percentile for body weight requires twice as much iron as a boy in the 3rd percentile.

Dietary intake of iron must suffice to account for losses in feces, urine, skin, and menstruation, as well as to provide for expansion of red cell volume and for tissue

growth in adolescence. The NRC recommends an additional 2 mg/day for males during the pubertal growth spurt (between ages 10 and 17 years), for a total of 12

mg/day of iron (5). With menarche, the adolescent girl has additional iron loss from menstruation. The NRC recommends an additional 5 mg/day for females, starting

with the pubertal growth spurt and menstruation, which begins at approximately 11 to 14 years. The iron recommendation for adolescent females is 15 mg/day ( 5).

In a comprehensive review of iron requirements, Bowering et al. could find only one report on a controlled study with adolescents ( 42). In the iron balance study of six

adolescent girls, Schlaphoff and Johnson found that 0.62 to 1.82 mg/day (mean, 1.0 mg/day) was retained, which included iron required to replace menstrual losses

(43). Assuming a rate of 10% absorption, they recommended a daily intake of 12 to 13 mg iron. Similar balance data are not available for boys. Finally, the amount of

iron available in the American diet is estimated at 6 mg/1000 calories. Therefore, teenage girls whose caloric intake varies between 2000 and 2400 calories may find

it difficult to ingest 15 mg of iron from dietary sources alone. Bioavailability of dietary iron is critical in iron nutrition. Diets high in lean meat and ascorbic acid and low

in phytate cover the iron requirements of most nonpregnant women (44).



In the Ten State Nutrition Survey, between 5 and 10% of teenagers had hemoglobin or hematocrit levels below normal ( 15). Analysis of data from the Health and

Nutrition Examination Survey (HANES) II showed the highest prevalence of impaired iron status (ferritin model) was in teenagers—14.2% of the 15- to 19-year-old

females and 12.1% of the 11- to 14-year-old males (45). The results of other studies vary ( 46, 47), generally reporting more iron deficiency than iron deficiency

anemia in adolescents.

Results of several large surveys—the Ten State Nutrition Survey ( 48), the HANES I (47), and the HANES II (49)—have shown a racial difference in hemoglobin level

in adolescents. Blacks have approximately 1 g less hemoglobin than whites, which apparently is unrelated to socioeconomic level, education, diet, or obesity ( 50).

These differences have led many authors to recommend race-specifia standards in screening for anemia ( 48, 51, 52, 53, 54 and 55). Although use of different

standards for hemoglobin concentration has been proposed, the biochemical basis for the racial difference in hemoglobin is unknown. The factors affecting

hemoglobin differences, including genetic, socioeconomic, and dietary, are complex. At the present time, no data indicate that iron needs of black and white

adolescents are different. Clearly, the standards for “normal” values used in any study determine the amount of iron deficiency or anemia in any population.

Measurements of hematocrit and hemoglobin, the most widely used screening procedures for anemia, are relatively insensitive indicators. The diagnosis of iron

deficiency can be made by using the serum ferritin level, which provides the most accurate assessment of iron stores. The true nature of iron deficiency anemia in

adolescents awaits more sophisticated studies.

Adolescent athletes may be at risk of iron deficiency caused by red blood cell destruction, increased need for red blood cell and tissue synthesis during puberty, or

poor dietary intake (53, 54). Many (34–44%) teenage female runners have been found to be iron deficient, as assessed by low iron stores ( 53, 54). This deficiency is

associated with abnormal gastrointestinal bleeding ( 54).

Sports anemia may also be common; increased destruction of erythrocytes and a transient drop in hemoglobin concentration in the adolescent athlete results from an

acute stress-response to exercise training. However, because the causes and treatments of sports anemia remain controversial, no basis currently exists for

recommending iron supplementation for this transient condition ( 55, 56).

Zinc

Zinc affects protein synthesis and is essential for growth. Zinc is particularly important in adolescence because of the rapid rate of growth and sexual maturation.

Table 52.3 reveals that during the adolescent growth spurt, zinc retention in both males and females is much higher than the average for the adolescent period. This

striking increase in zinc retention is related to the increase of lean body mass during this period ( 57).

The 1989 RDAs (5) reduced the daily zinc intake to 12 mg for adolescent females on the basis of their lower body weight. The recommendation for males remained at

15 mg/day.

Zinc deficiency has been associated with growth retardation and hypogonadism in adolescents ( 58, 59); zinc supplementation resulted in accelerated growth and

sexual maturation (58, 60). Poor dietary zinc sources and inhibition of zinc absorption by phytates in high-cereal diets contributed to the evolution of zinc deficiency

and were major factors in growth retardation and delayed sexual maturation ( 59).

Evidence that adolescents undergoing rapid growth may be highly susceptible to inadequate dietary zinc is provided by Butrimovitz and Purdy ( 61). These

investigators found low plasma zinc concentrations during infancy and puberty, both periods of rapid growth. For adolescent girls and boys, plasma zinc levels were

lowest at the ages when puberty was expected to occur.

Mild zinc deficiency has been reported in the United States. Hambidge et al. studied zinc status in apparently healthy children in Denver and found an association

between low growth percentiles, diminished taste acuity, and low hair zinc levels ( 62). Apparently, marginal zinc status may be a health problem in American children.

Adolescents undergoing rapid growth are at risk for inadequate zinc levels. Young pregnant teenagers may be particularly susceptible to zinc deficiency, because of

the rapid cell division and growth of the developing fetus as well as continued growth of the biologically immature teenager. These teenagers should be encouraged to

include such zinc-rich foods in their daily intake as poultry, lean meats, lowfat and nonfat dairy products, legumes, and grain products, particularly whole grains ( 63).

Vitamins

Data on vitamin requirements for adolescents are even more limited than those for mineral requirements. The vitamin requirements for youth are interpolated from

data on infant and adult allowances; few data are derived directly from studies on adolescents. Emphasis should be placed on vitamins necessary for the additional

nutrient requirements of the pubertal growth spurt.

Vitamin A is required for vision, growth, cellular differentiation and proliferation, reproduction, and immune system integrity. Vitamin A levels and intake in adolescents

are considerably below the recommended amount (15, 16, 64, 65). Vitamin D is involved in maintaining homeostasis of calcium and phosphorus in the mineralization

of bone. No controlled studies exist on vitamin D requirements for adolescents.

Vitamin C is essential for collagen synthesis, and intakes in adolescents are often below the recommended levels ( 66, 67). Added to the unknown demands of growth

and changes in vitamin C status because of smoking ( 68, 69) and oral contraceptive use ( 70), some teenagers may have problems with vitamin C adequacy.

Because of its role in DNA synthesis, folate is important during periods of increased cell replication and growth. Folate status may be at risk in some adolescents,

particularly those from low-income populations ( 71) and pregnant teenagers (72). The recent association of folate deficiency with neurotubal defects emphasizes the

importance of adequate folate intake in teenage girls ( 73). The FDA has recently mandated fortification of standard enriched grain products with folate. Dietary intakes

and serum folate levels have indicated poor folate status in adolescent girls ( 74, 75 and 76) and boys (76).

Adolescents appear to have increased need for vitamin B 12, which is required for rapid cell growth, particularly during the growth spurt. Vitamin B 6 is involved in a

large number of enzyme systems associated with nitrogen metabolism. The rapid growth of muscle mass, particularly in boys, makes vitamin B 6 adequacy important

during puberty. Riboflavin, niacin, and thiamin are involved in energy metabolism and thus are also important during puberty.



SPECIAL NUTRITIONAL PROBLEMS

Effect of Nutrition during Adolescence on Adult Morbidity and Mortality

Prospective studies of adults who are overweight or obese generally show increased morbidity and mortality. Does any of the risk in morbidity and mortality result

from obesity originating during childhood or adolescence? (For discussion of adolescent obesity see Chapter 63.) Or does the risk result from adult obesity? What

about thinness during the juvenile period as a predictor of disease or increased mortality during maturity in adults? Is promotion of growth in height and weight during

childhood and adolescence consistent with optimal adult health? The answers to these questions have significant implications for health professionals advising

adolescents on nutritional matters. This discussion only applies to populations in which food supplies are adequate and available.

Many studies associate obesity in adults with increased morbidity and mortality from a variety of clinical disorders. As Bray indicates, cardiovascular disease,

hypertension, diabetes mellitus, gallbladder disease, osteoarthritis, and colon cancer are major coconditions seen more frequently in obese adults ( 77). Bray goes on

to say that in adults whose BMI exceeds 30 kg/m2, more than 50% of all-cause mortality among those in the United States aged 20 to 74 years can be attributed to

overweight.

Until recently, little was known about the effect of overweight during adolescence as a predictor of disease in adults. Subjects from the Harvard Growth Study

(1922–1935) were followed for 55 years. They were then classified as overweight or lean. Morbidity and mortality data from this cohort clearly predicted additional

health risks for adults who were overweight adolescents compared with those who were lean. The risk of death from all causes and of coronary heart disease is

elevated in men who were overweight as adolescents. Men have a higher risk of atherosclerotic cerebrovascular disease and colon cancer. In contrast, in women

overweight as adolescents, all cause or cause-specific mortality is not increased in adulthood.



Other studies have shown a risk of increased morbidity from coronary heart disease and atherosclerosis in men and women who were overweight as teenagers.

Morbidity from colorectal cancer and gout was elevated in men overweight during adolescence. Arthritis was significantly higher in women who were overweight as

adolescents. These risks were strongly predicted by overweight during adolescence, compared with adult-onset obesity ( 78). This concept is further supported by

other long-term studies (79, 80).

There are no population studies on the effect of thinness during adolescence on adult morbidity and mortality. Waaler suggests that the excess morbidity and

mortality associated with short stature and low weight may result from poor nutrition during growth ( 81). The one model that may give clues to the effect of thinness on

adult health is anorexia or bulimia. These disorders are most common in adolescent girls when bone growth is at its peak. Once puberty is complete, very little bone

growth occurs. Osteopenia is a common complication of anorexia nervosa during adolescence ( 82). The concern is raised that osteopenia developed by anorectic

girls may not be reversible. Thus, osteoporosis may be the eventual outcome of this undernutrition during adolescence. Further research will determine whether this is

true.

Brain mass is reduced in anorexia nervosa. Cognitive defects have been described during the acute phase of this disorder. Reduction in brain mass is important as it

occurs during brain development. Long-term follow-up is necessary to determine whether these deficits result in significant brain malfunction as an adult.

The state of nutrition during adolescence is important in determining morbidity and mortality during adult life. How much and what kind of food is enough for growth

compatible with optimal adult health? Is maximal growth the same as optimal growth? These important questions must await the results of more research.

Eating Disorders

As mentioned above, two major eating disorders, anorexia nervosa and bulimia (or bulimia nervosa), may pose major problems in adolescence ( 83, 84 and 85) (see

also Chapter 93). Most eating disorder patients develop the problem during adolescence. Some of the psychologic changes in adolescence may make it difficult to

distinguish an adolescent with “normal” eating habits from one with an eating disorder. Adolescents may use food as a means of experimenting, gaining control, or

establishing themselves as individuals. Dissatisfaction with body weight, fear of obesity (resulting in unhealthy eating behavior), and preoccupation with dieting are

common among today's youth, particularly adolescent girls ( 86, 87, 88 and 89). Mellin et al. ( 90) found a high prevalence of disordered eating, particularly dieting; fear

of fatness; and binge eating in a group of middle-class predominantly white girls and adolescents. Additional studies suggest that unhealthy weight-control behaviors

occur in adolescents of other ethnic/racial subgroups ( 88, 91) and in adolescents with chronic illness ( 92).

Adolescents with eating disorders should be evaluated and treated by an interdisciplinary team of professionals with expertise in treating adolescents ( 93, 94).

Interdisciplinary treatment should be appropriate for the teenager's developmental needs. Recent findings from a group of over 33,000 adolescents suggest that

frequent dieting and eating-disordered behaviors should not be viewed in isolation. These eating-disordered behaviors occur in a broader social context of adolescent

health and risk-taking behavior ( 95).

Pregnancy

Nutritional care of the pregnant adolescent must consider the health of both mother and infant. Knowledge of the role of nutrients is vital, as is consideration of the

principles of adolescent growth and development. Physiologically, the adolescent is at risk if she has not completed her growth ( 96, 97, 98 and 99). Individual

variability is great, but most growth occurs before menarche. Linear growth in the adolescent female typically is not completed until approximately 4 years after the

onset of menarche. Although the rate of growth after menarche has decelerated considerably, growth allowances should still be considered.

Gynecologic age (the difference between chronologic age and age at menarche) can give some indication of physiologic maturity and growth potential. A young

adolescent (gynecologic age, 2 years or less) who becomes pregnant may still be growing. Her own needs for growth and development, along with the extra demands

of fetal growth, make the nutrient requirements of this young teen higher than those of a pregnant adult ( 96, 100) (see also Chapter 50).

The few studies that have focused on the energy needs of pregnant teenagers generally report that the teenagers frequently do not achieve the caloric intake

recommended by the NRC (5). Naeye hypothesized that optimal weight gains for fetal survival may be higher in young teenagers because mother and infant compete

for nutrients (101). Recent findings appear to support such a competition ( 102, 103 and 104). Results of further studies ( 104, 105, 106, 107 and 108) suggest that

optimal weight gains for adolescents during pregnancy, particularly for girls who are biologically immature ( 104), are greater than the adult recommendations.

The Institute of Medicine (109) recommends (by prepregnancy weight-for-height) that young adolescents strive for weight gains at the upper end of the ranges

suggested for adults. Young adolescents (<2 years postmenarche) may deliver smaller infants for a given weight gain than do older women ( 109, 110). Inadequate

weight gain during pregnancy has been associated with low-birth-weight infants ( 111) and preterm delivery in pregnant teens ( 112). Inadequate weight gain during

early stages of adolescent pregnancy was associated with significant deficits in infant birth weight and increased risk of low-birth-weight and small-for-gestational-age

infants (112, 113 and 114).

Recent studies have found that adolescents deliver a disproportionate number of very low birth weight infants ( 115) and low-birth-weight infants, compared with adult

mothers (116). In addition, low-birth-weight infants of teen mothers were associated with higher neonatal mortality ( 116). Teenagers who smoke may be at increased

risk of low prenatal weight gain and reduced infant birth weight ( 107, 117).

Preliminary data from our research using anthropometric measurements as predictors of low-birth-weight outcome in pregnant teenagers suggest that mothers of

low-birth-weight infants tend to exhibit prenatal depletion of fat reserves (estimated from triceps skinfold measurements and from calculating arm fat area), while

mothers of normal-birth-weight infants accumulate fat (118). In addition, prenatal protein stores of mothers of low-birth-weight infants changed little, whereas mothers

delivering normal-birth-weight infants gained protein stores (estimated from midarm circumference measurements and arm muscle area calculations). Scholl et al.

(104) found that despite weight gain and accumulation of fat stores during pregnancy, growing adolescents delivered infants with lower birth weights than those of

nongrowing teenagers and adult women. Estimates of energy requirements indicate that sedentary adolescents needed at least 2400 to 2600 kcal/day. Physically

active or rapidly growing adolescents needed additional energy, perhaps 50 kcal/kg pregnant body weight/day ( 119).

The issue of protein requirements for the pregnant adolescent is complex. Using careful nitrogen balance studies on pregnant teenagers, King et al. presented the

best experimental data on which to base protein recommendations ( 120). Their data suggested greater nitrogen retention than was previously reported. In addition,

maternal lean tissue of these adolescents increased during pregnancy, particularly during the last half of pregnancy.

Iron deficiency anemia in pregnancy has been associated with increased risk of preterm delivery and low birth weight ( 121, 122 and 123). The recommended intake of

iron for pregnant adolescents is 30 mg/day, which is twice the recommendation for the nonpregnant teenage girl ( 5).

Zinc metabolism is an important consideration during pregnancy. Data from a study of a small group of teenagers ( 124) are consistent with results of studies in adults,

indicating that prenatal iron supplementation impairs zinc retention. However, these adolescents did not show lower serum zinc concentrations during the second and

third trimesters, as observed in adults, implying differences in zinc metabolism between adolescent and adult pregnancy ( 124). Prenatal zinc supplementation in

low-income teenagers was associated with improved pregnancy outcome and reduced numbers of premature births, compared with a placebo group ( 125).

On the basis of recent data, it appears pregnant teenagers, particularly those who may still be in their own growth phase, do have increased needs for nutrients

during pregnancy. The pregnant adolescent needs an additional 300 calories and 14 to 16 more grams of protein daily, which can be supplied by addition of foods

such as those shown on Table 52.4 (126).



Table 52.4 Foods to Increase Calories and Protein for the Pregnant Adolescent



Vegetarian Diets

During a time of increased independence and decision making and greater influence by peers and role models, adolescents may use food as part of the process of

individuation. Because nutritional needs are high, vegetarian teenagers may be particularly at risk for nutritional deficiencies, especially at the time of the growth spurt

(see also Chapter 106).

Growing adolescents who are vegetarians may have problems meeting their energy requirements because of the high-bulk content of vegetarian food patterns. In

addition, vegetarian diets that are low in animal products are low in fat content ( 127, 128). Without sufficient energy intake, protein is used as an energy source and

thus is unavailable for tissue synthesis and growth. Hence, protein quality, protein quantity, and energy intake of the individual must be assessed. Other nutrients of

concern for the teenage vegetarian, particularly the strict vegetarian (who excludes all foods of animal origin), include calcium, iron, zinc, and vitamins D and B 12 (127,

128, 129, 130 and 131).

Conscious effort and careful planning are necessary to ensure adequacy of these nutrients. Supplements may be necessary to meet the recommended allowances.

The vegetarian should carefully plan a diet from a variety of foods. Protein complementation (combining different plant foods so that low essential amino acids from

one protein source are complemented by essential amino acids from another protein source, resulting in a complete protein) can ensure that the qualitative aspects of

protein adequacy are met. Evaluation of the quantitative aspects of protein adequacy of the vegetarian is also necessary. The RDA for total protein intake during

adolescence ranges from 44 to 59 g/day (5), providing energy requirements are met.

Vegetarian adolescents can generally meet their nutritional requirements for growth if they consume well-planned diets ( 129, 132). Vegetarian food guides for

adolescents are available in such sources as reports by Marino and King ( 133), the University of California's Creative Eater's Handbook (134), Messina and Messina

(130), and Johnston and Haddad ( 135). Haddad has developed daily dietary patterns for vegetarians at three different energy levels ( 136).

CHAPTER REFERENCES

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.



Marshall WA, Tanner JM. Arch Dis Child 1969;44:291–303.

Marshall WA, Tanner JM. Arch Dis Child 1970;45:13–23.

Tanner JM. Growth and endocrinology of the adolescent. In: Gardner LI, ed. Endocrine and genetic diseases of children and adolescents. 2nd ed. Philadelphia: WB Saunders, 1975.

Tanner JM. Growth and adolescence. 2nd ed. Oxford: Blackwell Scientific, 1952.

Food and Nutrition Board, National Research Council. Recommended dietary allowances. 10th ed. Washington, DC: National Academy Press, 1989.

Wait B, Blair R, Roberts LJ. Am J Clin Nutr 1969;22:1383–96.

Widdowson EM. Medical Research Council special report series no. 257. London: His Majesty Stationery Office, 1947.

Beal VA. Nutritional intake. In: McCammon RW, ed. Human growth and development. Springfield, IL: Charles C Thomas, 1970.

Heald FP, Remmell PS, Mayer J. Caloric, protein and fat intake in children and adolescents. In: Heald FP, ed. Adolescent nutrition and growth. New York: Appleton-Century-Crofts, 1969.

National Center for Health Statistics. NCHS growth charts, 1976. Monthly vital statistics report 25(3) suppl. (HRA) 76-1120. Rockville, MD: National Center for Health, 1976.

National Center for Health Statistics. Vital Health Stat (11) 1973;124.

Dreizen S, Spirakis CN, Stone RE. J Pediatr 1967;70:256–63.

McArdle WD, Katch FI, Katch VL. Exercise physiology. Energy, nutrition, and human performance. Philadelphia: Lea & Febiger, 1991.

Johnson JA. Ann NY Acad Sci 1958;69:881–901.

Center for Disease Control. Ten State Nutrition Survey in the United States, 1968–1970. Atlanta, GA: Health Services and Mental Health Administration, 1972.

National Center for Health Statistics. Caloric and selected nutrient values for persons 1–74 years of age. First Health and Examination Survey, 1971–1974, DHEW publ. (PHS) 79-1657.

Hyattsville, MD: National Center for Health, 1979.

Heald FP, Hunt SM. J Pediatr 1965;66:1035–41.

Frisancho AR. Am J Clin Nutr 1974;27:1052–8.

Jensen TG, Englert D, Dudrick SJ. Nutritional assessment. A manual for practitioners. Norwalk, CT: Appleton-Century-Crofts, 1983.

Ingenbleek Y, Van Den Schrieck HG, De Nayer P, et al. Clin Chim Acta 1975;63:61–7.

Ingenbleek Y, De Visscher M, De Nayer P. Lancet 1972;2:106–9.

Shetty PS, Watrasiewicz KE, Jung RT, et al. Lancet 1979;2:230–2.

Irwin MI, Kienholz EW. J Nutr 1973;103:1019–95.

Henkin RI. Trace elements in nutrition. New York: Marcel Dekker, 1971.

Committee on Nutrition, American Academy of Pediatrics. Pediatrics 1978;62:826–34.

Garn SM, Wagner B. The adolescent growth of the skeletal mass and its implications to mineral requirements. In: Heald FP, ed. Adolescent nutrition and growth. New York:

Appleton-Century-Crofts, 1969.

Roche AF, Roberts J, Hamill PV. Vital Health Stat (11) 1978;167:1–98.

Forbes GB. Nutritional requirements in adolescence. In: Suskind RM, ed. Textbook of pediatric nutrition. New York: Raven Press, 1981.

Greenwood CT, Richardson DP. World Rev Nutr Diet 1979;33:1–41.

World Health Organization. Handbook on human nutritional requirements. Monograph series no. 61. Geneva: WHO, 1974.

Schuette SA, Linksweiler HM. Calcium. In: Present knowledge of nutrition. 5th ed. Washington, DC: Nutrition Foundation, 1984.

Hollinbery PW, Massey LK. (Abstract 1280) Fed Proc 1986;45:375.

Optimal calcium intake. NIH consensus statement. Bethesda, MD: National Institutes of Health, 1994.



33a. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, DC: National Academy Press, 1997.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.



Matkovic V, Fontana D, Tominac C, et al. (Abstract 168) J Bone Miner Res 1986;(Suppl 1).

Sandler RB, Slemenda CW, LaPorte RE, et al. Am J Clin Nutr 1985;42:270–4.

Anderson JJB, Tylavsky FA, Lacey JM, et al. (Abstract 1841) Fed Proc 1987;46:632.

Chan GM. Am J Dis Child 1991;145:631–4.

Heaney RP, Gallagher JC, Johnston CC, et al. Am J Clin Nutr 1982;36(Suppl):986–1013.

Allen LH. Nutr Today 1986;21:6–10.

Chan GM, McMurry M, Westover K, et al. Am J Clin Nutr 1987;46:319–23.

Hepner RE. Nutrient requirements in adolescence. Cambridge: MIT Press, 1976.

Bowering J, Sanchez AM, Irwin MI. J Nutr 1976;106:985–1074.

Schlaphoff D, Johnson FA. J Nutr 1949;39:67–82.

Hulten L, Gramatkovski E, Gleerup A, et al. Eur J Clin Nutr 1995;49:794–808.

Expert Scientific Working Group. Am J Clin Nutr 1985;42:1318–1330.

National Academy of Sciences, Food and Nutrition Board. Iron nutriture in adolescence. DHEW publ. no. (HSA) 77-5100. Washington DC: U.S. Department of Health, Education and Welfare,

1976.

Johnson CL, Abraham S. Hemoglobin and selected iron- related findings of persons 1-74 years of age: United States, 1971–74. DHEW publication no. 46. Washington, DC: U.S. Department of

Health, Education and Welfare, 1979.

Garn SM, Smith NJ, Clark DC. J Natl Med Assoc 1975;67:91–6.

Yip R, Johnson C, Dallman PR. Am J Clin Nutr 1984;39:427–36.

Dallman PR, Barr GD, Allen CM, et al. Am J Clin Nutr 1978;31:377–80.

Owen GM, Yanochik-Owen A. Am J Public Health 1977;67:865–6.

Daniel WA Jr. Nutritional requirements of adolescents. In: Winick M, ed. Adolescent nutrition. New York: John Wiley & Sons, 1982.

Brown RT, McIntosh SM, Seabolt VR, et al. J Adolesc Health Care 1985;6:349–52.

Nickerson HJ, Holubets MC, Weiler BR, et al. J Pediatr 1989;114:657–63.

Sports and Cardiovascular Nutritionists (SCAN) Dietetic Practice Group. Sports nutrition. In: Marcus JB, ed. A guide for the professional working with active people. Chicago: American Dietetic

Association, 1986.

Position of the American Dietetic Association. J Am Diet Assoc 1987;87:933–9.

Sandstead HH. Am J Clin Nutr 1973;26:1251–60.



58.

59.

60.

61.

62.

63.

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

81.

82.

83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

93.

94.

95.

96.

97.

98.

99.

100.

101.

102.

103.

104.

105.

106.

107.

108.

109.

110.

111.

112.

113.

114.

115.

116.

117.

118.

119.

120.

121.

122.

123.

124.

125.

126.

127.

128.

129.

130.

131.

132.

133.

134.

135.

136.



Prasad AS, Miale A Jr, Farid Z, et al. J Lab Clin Med 1963;61:537–49.

Sandstead HH, Prasad AS, Schulert AR, et al. Am J Clin Nutr 1967;20:422–42.

Prasad AS, Halsted JA, Nadimi M. Am J Med 1961;31:532–46.

Butrimovitz GP, Purdy WC. Am J Clin Nutr 1978;31:1409–12.

Hambidge KM, Hambidge C, Jacobs M, et al. Pediatr Res 1972;6:868–74.

Moser-Veillon PB. J Am Diet Assoc 1990;90:1089–93.

Canada National Survey. Nutrition. A national priority. Ottawa: Department of National Health and Welfare, 1973.

Schorr BC, Sanjur D, Erickson EC. J Am Diet Assoc 1972;61:415–20.

Huenemann RL, Shapiro LR, Hampton MC, et al. J Am Diet Assoc 1968;53:17–24.

Nelson M. Dietary practices of adolescents. In: Winick M, ed. Adolescent nutrition. New York: John Wiley & Sons, 1982.

Pelletier O. Am J Clin Nutr 1970;23:520–4.

Schectman G, Byrd JC, Gruchow HW. Am J Public Health 1989;79:158–62.

Rivers JM. Am J Clin Nutr 1975;28:550–4.

Daniel WA Jr, Gaines EG, Bennett DL. Am J Clin Nutr 1975;28:363–70.

Vande Mark MS, Wright AC. J Am Diet Assoc 1972;61:511–6.

Anon. MMWR 1991;40:513–6.

Kirksey A, Keaton K, Abernathy RP, et al. Am J Clin Nutr 1978;31:946–54.

Reiter LA, Boylan LM, Driskell J, et al. J Am Diet Assoc 1987;87:1065–7.

Clark AJ, Mossholder S, Gates R. Am J Clin Nutr 1987;46:302–6.

Bray GA. J Endocrinol Metab Clin North Am 1996;25:907–19.

Must A, Jacques PF, Dallal GE, et al. N Engl J Med 1992;327:1350–5.

Nieto J, Szklo M, Comstock GW. Am J Epidemiol 1992;136:201–13.

Hoffman MD, Kromhount D, de Lezenne Coulander C. The impact of body mass index of 78,612 18 year old Dutch men on 32 year mortalities from all causes. J Clin Epidemiol

1988;41:749–56.

Waaler HT. Acta Med Scand Suppl 1984;64:1–56.

Katzman DK, Zipursky RB. Ann NY Acad Sci 1997;817:127–37.

Committee on Diet and Health, Food and Nutrition Board, National Research Council. Diet and health. Implications for reducing chronic disease risk. Washington, DC: National Academy Press,

1989.

Nussbaum MP. Anorexia nervosa. In: McAnarney ER, Kreipe RE, Orr DP, Comerci GD. Textbook of adolescent medicine. Philadelphia: WB Saunders, 1992.

Adams LB, Shafer MAB. J Nutr Educ 1988;20:307–13.

Moore DC. Am J Dis Child 1988;142:1114–8.

Moses N, Banilivy MM, Lifshitz F. Pediatrics 1989;83:393–8.

Emmons L. J Am Diet Assoc 1992;92:306–12.

Casper RC, Offer D. Am J Clin Nutr (Abstract 6) 1989;49(Suppl):1128–9.

Mellin LM, Irwin CE, Scully S. J Am Diet Assoc 1992;92:851–3.

Story M, French SA, Resnick MD, et al. Int J Eating Disord 1995;18:173–9.

Neumark-Sztainer D, Story M, Resnick MD, et al. Arch Pediatr Adolesc Med 1995;149:1330–5.

Kreipe RE, Golden NH, Katzman DK, et al. J Adolesc Health Care 1995;16:476–9.

Rees JM. J Am Diet Assoc 1996;96:22–3.

French SA, Story M, Downes B, et al. Am J Public Health 1995;85:695–701.

Jacobson MS, Heald FP. Nutritional risks of adolescent pregnancy and their management. In: McAnarney ER, ed. Premature adolescent pregnancy and parenthood. New York: Grune &

Stratton, 1983.

Rees JM, Worthington-Roberts B. Adolescence, nutrition, and pregnancy interrelationships. In: Mahan LK, Rees JM, eds. Nutrition in adolescence. St. Louis: Times Mirror/Mosby College

Publishing, 1984.

Gutierrez Y, King JC. Pediatr Ann 1993;22:99–108.

Position of The American Dietetic Association. J Am Diet Assoc 1994;94:449–50.

Gong EJ. Weight issues and management. In: Story M, ed. Nutrition management of the pregnant adolescent. A practical reference guide. March of Dimes Birth Defects Foundation.

Washington, DC: U.S. Department of Health and Human Services, U.S. Department of Agriculture, 1990.

Naeye RL. Pediatrics 1981;67:146–50.

Scholl TO, Hediger ML, Ances IG. Am J Clin Nutr 1990;51:790–3.

Scholl TO, Hediger ML. J Am College Nutr 1993;12:101–7.

Scholl TO, Hediger ML, Schall JI, et al. Am J Clin Nutr 1994;60:183–8.

Frisancho AR, Matos J, Flegel P. Am J Clin Nutr 1983;38:739–46.

Meserole LP, Worthington-Roberts BS, Rees JM, et al. J Adolesc Health Care 1984;5:21–7.

Hediger ML, Scholl TO, Ances IG, et al. Am J Clin Nutr 1990;52:793–9.

Rees JM, Engelbert-Fenton KA, Gong EJ, et al. Am J Clin Nutr 1992;56:868–73.

Subcommittee on Nutritional Status and Weight Gain During Pregnancy, Food and Nutrition Board. Institute of Medicine. National Academy of Sciences. Summary. Nutrition during pregnancy.

Part I. Weight gain. Washington, DC: National Academy Press, 1990.

Committee to Study the Prevention of Low Birthweight, Division of Health Promotion and Disease Prevention, Institute of Medicine. Preventing low birthweight. Washington, DC: National

Academy Press, 1985.

Eastman NJ, Jackson E. Obstet Gynecol Surv 1968;23:1003–25.

Hediger ML, Scholl TO, Belsky DH, et al. Obstet Gynecol 1989;74:6–12.

Scholl TO, Hediger ML, Ances IG, et al. Obstet Gynecol 1990;75:948–53.

Scholl TO, Hediger ML, Khoo CS, et al. J Clin Epidemiol 1991;44:423–8.

Miller HS, Lesser KB, Reed KL. Obstet Gynecol 1996;87:83–8.

Rees JM, Lederman SA, Kiely JL. Pediatrics 1996;98:1161–6.

Muscati SK, Mackey MA, Newsom B. J Nutr Educ 1988;20:299–306.

Maso MJ, Gong EJ, Jacobson MS, et al. J Adolesc Health Care 1988;9:188–93.

Blackburn ML, Calloway DH. J Am Diet Assoc 1974;65:24–30.

King JC, Calloway DH, Margen S. J Nutr 1973;103:772–5.

Rosso P. Nutrition and metabolism in pregnancy. Mother and fetus. New York: Oxford University Press, 1990.

Scholl TO, Hediger ML, Fischer RL, et al. Am J Clin Nutr 1992;55:985–8.

Scholl TO, Hediger ML. Am J Clin Nutr 1994;59(Suppl):492S–501S.

Dawson EB, Albers J, McGanity WJ. Am J Clin Nutr 1989;50:848–52.

Cherry FF, Sandstead HH, Rojas P, et al. Am J Clin Nutr 1989;50:945–54.

Pennington JAT. Bowes and Church's food values of portions commonly used. 15th ed. New York: Harper & Row, 1989.

Raper NR, Hill MM. Nutr Rev 1974;32(Suppl):29–33.

MacLean WC Jr, Graham GG. Am J Dis Child 1980;134:513–9.

Jacobs C, Dwyer JT. Am J Clin Nutr 1988;48:811–8.

Messina M, Messina V. The dietitian's guide to vegetarian diets. Issues and applications. Gaithersburg, MD: Aspen Publishers, 1996.

Carruth BR. J Curr Adolesc Med 1980;2:44–7.

Position of The American Dietetic Association. J Am Diet Assoc 1993;93:1317–9.

Marino DD, King JC. Pediatr Clin North Am 1980;27:125–39.

University of California. The creative eater's handbook. Better nutrition through vegetarian eating. Berkeley: University Student Health Service, 1982.

Johnston PK, Haddad EH. Vegetarian and other dietary practices. In: Rickert VI, ed. Adolescent nutrition: assessment and management. New York: Chapman & Hall, 1996.

Haddad EH. Am J Clin Nutr 1994;59(Suppl):1248S–54S.



Chapter 53. Nutrition in the Elderly

Modern Nutrition in Health and Disease



Chapter 53. Nutrition in the Elderly

LYNNE M. AUSMAN and ROBERT M. RUSSELL

Theories of Aging

Dietary Restriction Experiments with Animal Models

Factors Affecting Nutritional Status

Nutritional Requirements

Energy

Protein

Carbohydrate

Fat

Fiber

Fluid

Vitamins

Minerals

Nutritional Status

Dietary Intake

Nutritional Evaluation

Review of Studies of Institutional and Free-Living Elderly Populations

Drug-Nutrient Interaction

Alcohol and Nutritional Status in the Elderly

Chapter References

Selected Readings



Currently, 25 million Americans are over the age of 65; by the year 2030, 57 million will be 65 or older. The increasing numbers of elderly and aged, especially in

Western societies, present challenges to those concerned with their physical and emotional well-being. An understanding of the role of both early and later nutrition in

slowing or modulating the aging process and in providing adequate nutriture for the elderly is important. Further, nutrient needs may change with aging, and the

interaction of drugs and nutrients may play a major role in the nutrient needs of some elderly persons. A thorough and comprehensive review of all aspects of

nutrition, aging, and the elderly can be found in the work of Munro and Danford ( 1).



THEORIES OF AGING

Aging is a gradual process taking place over many decades. Most theories of aging relate to impaired DNA replication and loss of viability of the cell and hence of the

body's organs. The most common theories of aging relate to one or more of the following: immunologic breakdown, cellular proliferation, basal metabolic rate, rate of

DNA repair, free radical damage, and/or rate of protein synthesis and catabolism. One classification of general theories of aging is shown in Table 53.1.



Table 53.1 Selected Theories of Aging



Dietary Restriction Experiments with Animal Models

Animal studies yield the strongest evidence that diet plays a major role in longevity and the aging process ( 2). The most consistent finding from experimental rodent

studies is that moderate dietary restriction markedly extends the life span of experimental animals, compared with control animals fed ad libitum. Dietary restriction

also decreases the incidence of several chronic diseases such as glomerulonephritis, atherosclerosis, and tumors.

Dietary restriction by selective removal of individual macronutrients (fat, carbohydrate, or protein) has also been carried out. However, without a concomitant decrease

in energy intake, little extension of life span has been found. Dietary excess of protein or fat, however, (a) increases the incidence of tumors and certain organ

pathologies and (b) shortens the time of appearance of several physical, biochemical, and immunologic indices of early maturational development and aging.

The severity, age of initiation, and duration of the dietary perturbation are important in determining the eventual response to the dietary restriction. Many other factors,

including the species and strain of laboratory animal used, are important variables in determining the outcome of these experiments. Individual micronutrients also

have effects on life span and modulate the mechanisms of aging, at least to some extent. For example, increased levels of dietary antioxidants (ascorbic acid,

a-tocopherol, carotenoids) may partially decrease cellular free-radical concentrations ( 3). It is yet unclear whether any of these changes are related to the mechanism

of aging.



FACTORS AFFECTING NUTRITIONAL STATUS

The elderly are a more diverse population than any other age group; individuals have widely varying capabilities and levels of functioning. On the whole, elderly

persons are more likely than younger adults to be in marginal nutritional health and thus to be at higher risk for frank nutritional deficiency in times of stress or health

care problems. Physical, social, and emotional problems may interfere with appetite or affect the ability to purchase, prepare, and consume an adequate diet ( 4).

These factors include whether or not a person lives alone, how many daily meals are eaten, who does the cooking and shopping and any physical impediments that

would make this impossible, problems in chewing and denture use, adequate income to purchase appropriate foods, and alcohol and medication use.



NUTRITIONAL REQUIREMENTS

A decline in organ function normally accompanies the aging process, especially in the older elderly (i.e., those above 80 years old). Many of these changes in normal

function might reasonably be expected to influence nutrient needs of the individual ( 5, 6 and 7) (Table 53.2).



Table 53.2 Changes in Organ Function with Aging That May Influence Nutrient Status



Energy

Several studies have documented decreased energy needs in the elderly. In the Baltimore Longitudinal Study of Aging, energy intakes of a sample of males

decreased from 11.3 MJ (2700 kcal) per day at age 30 years to 8.8 MJ (2100 kcal) per day for those about 80 years. Two-thirds of this reduction was attributable to

decreased physical activity, and the remainder to decreased basal metabolism ( 8). These findings have generally been supported by other studies. In NHANES III

(preliminary), young men and women, aged 20 to 29, consumed 12.6 and 8.2 MJ (3025 and 1957 kcal), whereas men and women aged 50 to 59 consumed 9.8 and

6.8 MJ (2341 and 1629 kcal), and those 80+ consumed 7.4 and 5.6 MJ (1776 and 1329 kcal), respectively.

The recommended energy intake from the 1989 Recommended Dietary Allowances (RDAs) is 9.6 MJ (2300 kcal) for the reference 77-kg elderly male and 7.9 MJ

(1900 kcal) for the reference 65-kg female 51 years of age and older ( 9), both similar to the mean energy intake of the 50- to 59-year-old age group (see Appendix

Table II-A-2-a-1). The RDAs and estimated intakes based on population studies both appear to underestimate total energy expenditure (TEE) for men, derived from

using the excretion of administered 2H 218 to estimate the usual energy consumption of healthy elderly people. The TEE for men, aged 68 years, was 11.3 MJ (2700

kcal) (10) and for women, aged 74 years, was 7.6 MJ (1800 kcal) (11). The discrepancy between the RDA and the TEE for men could suggest that the small group

studied in the TEE experiment was not an accurate subsample of the total population or that individuals actually are consuming more than they record. In either case,

this higher TEE is not a recommendation for elderly men to consume more calories.

Protein

High-protein diets may be less well digested and absorbed in the elderly, judged by a minor increase in fecal nitrogen content in response to a protein load ( 12).

However, little quantitative information is available regarding absorptive changes in the elderly for amino acids and peptides in more usual amounts.

The current RDA for protein (0.8 g/kg/day) is adequate for the elderly when excessive energy intakes are observed (i.e., ³167 kJ (40 kcal/kg) per day) ( 13) (see

Appendix Table II-A-2-a-2). However, when an energy intake more usual for the elderly is used (e.g., 125 kJ (30 kcal/kg) per day), nitrogen balance is not attained in

more than half of elderly subjects (14). The degree of adaptation of the individual to the lower energy or lower protein intake before the actual experimental trial began

may account for many of the discrepancies in nitrogen needs reported in the literature ( 15). Furthermore, whereas 0.92 g/kg/day was needed to maintain nitrogen

balance and tissue protein stores in sedentary elderly persons ( 16), possibly less suffices if resistance training is part of the daily routine ( 17). The average protein

consumption among free-living elderly persons in Boston was 1.05 g/kg/day in one study, with no evidence that lower intakes were correlated with protein-energy

malnutrition (18). On the whole, a daily intake of 1 g/kg (and probably less) meets the needs of this population ( 1).

Carbohydrate

Carbohydrate absorption (mannitol, xylose, 3- O-methyl glucose) may be slightly impaired with advanced aging, although decreased renal function may interfere with

interpretation of “absorption” test results based on urinary excretion ( 19, 20 and 21). In one study in elderly persons 65 to 89 years of age, breath hydrogen was

measured in response to a 100- to 200-g carbohydrate challenge to estimate carbohydrate malabsorption ( 22). At the highest carbohydrate load, 80% had increased

breath hydrogen. The increased breath hydrogen found in most elderly persons could result from carbohydrate malabsorption with age, increased bacterial enzyme

activity in the small bowel, or both. Lactase activity decreases with age (especially in early life), but other brush border hydrolase activities appear to remain fairly

constant (23 and 24). The diminished lactase activity with age may create only a minor problem because most lactose-intolerant individuals can tolerate the lactose

present (12.5 g) in a glass of milk ( 25). Furthermore, in a double-blind study of healthy elderly persons given either lactose-containing or lactose-free products, about

30% of both groups showed bloating and discomfort associated with lactose intolerance. Although the elderly tend to avoid consumption of milk products (which are

excellent sources of riboflavin, vitamin D, and calcium), the perceived bloating and discomfort may not be due to lactose intolerance. Therefore, the true prevalence of

lactose intolerance in the elderly is difficult to define.

There is no RDA for dietary carbohydrate. However, the United States Department of Agriculture (USDA), American Heart Association, and American Cancer Society,

among others, recommend a dietary carbohydrate component of 55 to 60% of calories, with an increase in the proportion of complex carbohydrates to simple sugars.

Fat

Fat digestion and absorption in the elderly is equivalent to that of young adults when measured at normal consumption levels (100 g) ( 21, 22, 23, 24, 25 and 26). At

higher dietary levels (120 g/day), the elderly showed slightly less fat absorption than did the young adults ( 11), and institutionalized elderly persons may absorb even

less (27). Although not too common, fat malabsorption in the elderly, when found, is most often due to bacterial overgrowth of the small intestine, causing

deconjugation of bile salts. However, most bacterial overgrowth in hypochlorhydric subjects is not associated with clinical malabsorption of fat or carbohydrate,

despite the presence of positive indicators such as abnormal 14[C]-D-xylose absorption (28). Chylomicron appearance in blood after a 100-g fat meal is somewhat

slower in elderly persons than in young adults; however, an observed difference in gastric emptying times might explain this apparently slower lipid hydrolysis and

uptake (29).

There is no RDA for total fat. However, it is widely felt that a prudent diet with 30% or less of calories as fat (less than 10% saturated, 10 to 15% monounsaturated,

and no more than 10% polyunsaturated fatty acids) may be just as important in the elderly as in young adults for preventing or ameliorating chronic diseases such as

heart disease or cancer. At the same time, these amounts of polyunsaturated fat are consistent with a diet providing adequate amounts of essential fatty acids (linoleic

and linolenic acid) ( 9).

Fiber

Little is known about dietary fiber requirements of either adults or elderly persons. However, the various classes of dietary fiber (see Chapter 43) found in a mixed diet

have different mechanical and metabolic effects in the gastrointestinal tract. In population studies, increased consumption of dietary fiber is correlated with decreased

rates of heart disease and cancer. Fiber is also included in a treatment regimen for a variety of diseases that particularly affect the elderly—constipation, hemorrhoids,

diverticulosis, hiatal hernia, varicose veins, diabetes mellitus, hyperlipidemia, and obesity ( 30). Without evidence to the contrary, recommendations for fiber

consumption for the elderly would be the same as for the adult, about 25 g/day, the recommended “Daily Value” on the new food label.

Fluid

Fluid balance is as important in the elderly as in other age groups. Nevertheless, it deserves particular attention because dehydration often goes unrecognized in the

elderly. Indeed, a recent study indicated that dehydration was responsible for 6.7% of hospitalizations ( 31). Poor fluid balance may be due to both inadequate (lower

then normal) intake and excessive losses ( 32). Chronically ill, immobilized, or demented patients and those with bladder control problems often fail to drink sufficient

fluids. On the other hand, several clinical conditions such as fever, diarrhea, malabsorption, vomiting, and hemorrhage lead to excessive losses. Therapy with certain

diuretics and laxative or hypertonic intravenous solutions also contribute to the problem. In the absence of severe clinical problems, consumption of 30 mL/kg/day is