Nutrient Composition for Fortified Complementary Foods

Calcium, Magnesium, Phosphorus and Vitamin D Fortification of

Complementary Foods1,2
Steven A. Abrams*3 and Stephanie A. Atkinson
*U.S. Department of Agriculture/Agricultural Research Service, Childrens Nutrition Research Center,
Department of Pediatrics, Baylor College of Medicine and Texas Childrens Hospital, Houston, TX 77030;
and Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
ABSTRACT Provision of the bone minerals and vitamin D as fortificants in food or as dietary supplements
designed for older infants and toddlers in Latin America is likely to be beneficial and safe. Currently available data
are inadequate to establish the precise amounts of these nutrients that would be required for such a supplement.
These amounts would vary according to the local base diet. However, reasonable estimates can be made on the
basis of current dietary recommendations as well as existing data on bioavailability and customary intake. The
strongest case can be made for calcium and vitamin D supplementation. Because excessive dietary calcium can
reduce zinc absorption as a result of interactive effects within the intestine, an appropriate ratio of calcium to zinc
should be used, even if this means adding zinc as a fortificant or supplement. Magnesium supplementation may
be appropriate in some circumstances but it cannot be routinely advocated at present. It is unlikely that
phosphorus supplementation is needed for most population groups because of the relatively high usual dietary
phosphorus intakes, primarily from phosphate salts added to carbonated beverages and as food preservatives. J.
Nutr. 133: 2994S2999S, 2003.
KEY WORDS:
iron zinc

human nutrition bone mineral metabolism

infants young children

Provision of calcium, magnesium, phosphorus and vitamin

D as part of complementary foods should be considered to
incorporate an adequate supply of these nutrients into the
context of the diet as a whole. Several factors must be considered in order to determine the appropriate amount and form
of nutrients to provide in each case. These factors include the
amount of the nutrient needed to prevent overt deficiency
diseases, such as rickets, as well as the cost and form of the
fortified nutrients that will yield the highest bioavailability. In
addition, consideration should be given to the safety of adding
these minerals, especially in terms of evaluating potentially
adverse nutrient interactions such as those that can occur
between calcium and iron.

rickets

mineral fortification of foods

There is a paucity of experimental evidence available from

which to derive the daily recommended intakes for the
amount of calcium needed by older infants and toddlers.
Moreover, there are virtually no published data regarding
phosphorus, vitamin D or magnesium requirements in this age
group. Given the absence of experimental data specific to this
age group, current recommended dietary reference intakes are
usually interpolated from studies conducted on older children.
Calcium requirements in older infants and toddlers
Accretion. Determining dietary calcium requirements requires the evaluation of the total amount of calcium needed by
the skeleton during the ages of interest. The classic method
used to determine this is the analysis of cadavers for total
calcium content. These analyses were mostly performed more
than 50 y ago. Although the chemical analysis was likely to be
accurate, uncertainties regarding the cause of death and the
health status of the individuals involved, as well as the fact
that very few infants were analyzed, render this an unreliable
source of information on which to base dietary recommendations (1).
In the past 30 y, various radiological and densitometric
methods have been used to determine calcium and bone
accretion during childhood. These have ranged from the use of
metacarpal morphometry in the early 1970s (2) to more recent
analyses using techniques such as dual-energy X-ray absorptiometry (3).
In general, despite the disparity of techniques and popula-

1
Presented as part of the technical consultation Nutrient Composition for
Fortified Complementary Foods held at the Pan American Health Organization,
Washington, D.C., October 4 5, 2001. This conference was sponsored by the
Pan American Health Organization and the World Health Organization. Guest
editors for the supplement publication were Chessa K. Lutter, Pan American
Health Organization, Washington, D.C.; Kathryn G. Dewey, University of California, Davis; and Jorge L. Rosado, School of Natural Sciences, University of
Queretaro, Mexico.
2
This work is a publication of the U.S. Department of Agriculture (USDA)/
Agricultural Research Service (ARS) Childrens Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine and Texas Childrens Hospital,
Houston, TX. This project has been funded in part with federal funds from the
USDA/ARS under Cooperative Agreement number 58 6250-6 001. Contents of
this publication do not necessarily reflect the views or policies of the USDA, nor
does mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government.
3
To whom correspondence should be addressed.
E-mail: sabrams@bcm.tmc.edu.

0022-3166/03 $3.00 2003 American Society for Nutritional Sciences.

2994S

CALCIUM AND BONE MINERALS IN COMPLEMENTARY FOODS

tion studies, estimates of calcium accretion by the skeleton in

childhood are reasonably consistent. Typically, mean calcium
accretion is 80 mg/d during the 1st y of life, rising slightly to
100 mg/d during the 2nd y of life (4). There may be some
differences in typical accretion rates of calcium in comparing
breast-fed with formula-fed infants (5), with higher values
occurring in formula-fed infants; however, these differences
have not been well characterized and there is no evidence that
they are functionally significant. Of interest is that the rate of
calcium accretion (80 100 mg/d) in infancy appears to remain
fairly consistent throughout early childhood; it probably does
not increase substantially until after age 4 5 y and rises much
more rapidly during puberty (3,6), when it can reach levels as
high as 300 400 mg/d (7).
Intake. An Adequate Intake (AI) guideline, rather than a
Recommended Dietary Allowance (RDA), for calcium intakes
was set by the recent Dietary References Intake Panel of the
Food and Nutrition Board of the National Academy of Sciences (7). The AI for infants was derived on the basis of
expected usual calcium intakes of breast-fed infants during the
1st y of life. It is useful to review the AI of infants aged 6 12
mo and extend this information to what is known about the
2nd y of life.
Breast-feeding is the preferred feeding method for virtually
all infants in the 1st y of life. Rickets or calcium deficiency
should not occur in vitamin Dreplete, breast-fed, full-term
infants aged 712 mo who have an age-appropriate solid food
intake that includes calcium-containing foods. Typical human
milk intakes in infants aged 712 mo are 500 700 mL/d, with
a calcium concentration of 200 220 mg/L. This leads to an
estimated total calcium intake of 130 mg/d from human milk
(7,8). There are few studies on calcium intakes from solid food
in this age group, but a value of 140 mg/d for formula-fed
infants has been reported (5,9). Adding these two calcium
intakes led to the published AI value of 270 mg/d for infants
aged 712 mo (7). However, this value is far below the mean
observed calcium intake of 703 mg/d for this age group that has
been reported in dietary surveys in the United States (7).
Undoubtedly, this difference reflects the use of adapted formulas and whole cows milk to provide 500 600 mg/d of
calcium at usual intakes of older infants.
During the 2nd y of life, solid foods become a greater part
of most childrens diets. From dietary survey data, mean observed intakes in this age group were 766 mg/d whereas the
current recommended intake is 500 mg/d (7). At this age,
however, most children in the U.S. survey were probably
receiving whole cows milk as their milk source, leading to the
relatively high calcium intake.
Although calcium intake may be low in Latin American
children because of lower dairy product intake, this is not
always the case. For example, in toddlers in Mexico, Murphy
et al. (10) found adequate calcium intakes (mean 735 199
mg/d). This is far greater than the mean calcium intake of
220 mg/d found in children in Egypt and Kenya. The higher
calcium intake in the Mexican children likely was due to the
consumption of both dairy products and lime-treated tortillas
in parts of Latin America (10,11). Absorption of calcium from
this diet may be low because of poor bioavailability of calcium
from the lime-treated tortillas (12).
The relatively high calcium intakes reported by Murphy et
al. (10) may not occur among the poorer populations of Latin
America. Wyatt and Tejas (13) recently reported large economic differences related to the calcium intakes of children
aged 4 6 y in southern Mexico. In the children in the poorest
areas, mean calcium intake was only 272 mg/d, primarily
coming from corn tortillas. This increased to more acceptable

2995S

intakes of 625 mg/d in medium-income families that were due

to the increased availability of dairy products in families with
a higher socioeconomic status.
In Mexico City a mean calcium intake of 516 mg/d was
reported for children aged 15 y (14). In this group, 25% of the
children had calcium intakes of 361 mg/d, which was associated with higher blood lead levels. This contrasts with a 25th
percentile value of 599 mg/d for children aged 13 y (649 mg/d
for children aged 4 8 y) in the United States (7), suggesting
a much greater prevalence of very low calcium intakes in
Mexico compared with the United States.
Absorption. There is a general consensus that calcium is
well absorbed from human milk, with values for net calcium
retention of 50% of intake (1,9). Calcium absorption values
from infant formulas are highly variable because of the various
carbohydrate, protein and mineral sources of these formulas.
Although it is generally stated that calcium bioavailability is
lower from formulas than from human milk, this may not
always be the case. Early findings may have been related to the
greater concentration of calcium in infant formulas than in
human milk (1,7). In general, however, values of 30 40%
absorption are typical for cows milk based infant formulas or
whole cows milk (15,16). The efficiency of calcium absorption
from any food source is likely to depend more on the total
amount added and its interaction with other food components
such as vitamin D, phytate, oxalate and dietary fiber than on
the relative solubility of the type of calcium salt added as a
fortificant (17). However, if calcium intake is low, then each
of these factors significantly affects the efficiency of calcium
absorption (18).
Effects of deficiency. It is not easy to clinically identify
deficiencies of bone minerals in most children unless they are
severe enough to cause recurrent fractures or rickets. The most
common disease associated with severe bone mineral deficiency in very small children is nutritional rickets. Although
classically, nutritional rickets is caused by vitamin D deficiency, in some children very low calcium intakes may be
partially or even primarily responsible for development of the
disease (19,20).
Ideally, a calcium intake level below which rickets is likely
to occur could be identified. Unfortunately, it is not possible to
do this with any certainty. Some suggestions regarding dangerously low intakes can be found in studies of calciumdeficiency rickets in Africa and Asia. For example, Egyptian
children aged 12 y who had mean calcium intakes of 290
mg/d with adequate vitamin D status did not develop rickets
(21). In contrast, in the same study 20 children mostly breastfed with low vitamin D status and calcium intakes averaging
310 mg/d developed rickets. These results suggest that in the
presence of adequate vitamin D, 300 mg/d of calcium is
enough to ensure that rickets will not occur. Among black
South Africans, biochemical abnormalities associated with
rickets occurred in children aged 712 y with calcium intakes
of 125 mg/d but not in those with intakes of 337 mg/d. Neither
the children with rickets nor the control children were vitamin D deficient (22).
There is strong support for the suggestion that a calcium
intake of less than 300 mg/d may pose a risk for the development of rickets notwithstanding normal vitamin D status
(23). In Nigeria, children with calcium intakes of 200 mg/d
were reported to develop rickets despite normal vitamin D
levels (24). Many children with similar dietary calcium intakes
do not develop rickets in Nigeria. It is likely that crucial subtle
differences in calcium bioavailability, genetic factors or other
environmental conditions may contribute to the development
of rickets at low calcium intakes (20).

2996S

SUPPLEMENT

Taken together, these data indicate that even without

significant vitamin D deficiency, a calcium intake of 300
mg/d is adequate to prevent overt rickets in most small children and intakes below that, especially below 200 mg/d, pose
a substantial risk of rickets. The minimum intake of calcium to
prevent rickets in children with low or marginal vitamin D
status is not known but is likely much higher on the basis of
substantially lower calcium absorption in that circumstance.
Recommended intakes. Given this confused data set, it
should not be surprising that it has been relatively difficult to
set clear guidelines for calcium intake in the 1st 2 y of life. In
general, recommendations have been based either on usual
dietary intakes or on balance data from older children. Some
intake guidelines specify whether they were based on (although not necessarily only intended for) human milkfed
infants whereas others do not make this distinction. Currently
in the United States, the calcium AI for infants aged 712 mo
is 270 mg/d and for infants aged 1236 mo is 500 mg/d. For
infants fed adapted cows milk based formulas, the recommendation is that mineral intake be increased because of the
assumption that the calcium is not as bioavailable as that of
human milk (7). A recommended intake of 335 mg/d is
derived for infants ages 712 mo. In the United Kingdom, the
recommended pattern of intakes is opposite that of the United
States. The recommended calcium intake for infants aged
712 mo is 525 mg/d and for infants aged 1223 mo it
decreases to 350 mg/d (8).
Although it is lower than the United Kingdom value, there
are no data to indicate that the Food and Nutrition Boards AI
of 270 mg/d for infants ages 712 mo leads to bone demineralization or rickets. Calcium intake of 130 mg from human
milk and 50% calcium retention leads to a total of 65 mg/d of
calcium retained from human milk. If the other 140 mg of
dietary calcium comes from solid food, using an estimate for
calcium retention of 20 25% from solid food (7) leads to a
calculated additional 28 35 mg/d of retained calcium. These
totals are consistent with the 80 100 mg/d accretion value for
calcium during infancy.
In the 2nd y of life, 20 30% of cows milk calcium is likely
to be retained. Based on a cows milk calcium intake of 500
mg/d, milk intake alone would meet the 100-mg/d accretion
requirement. However, for breast-fed children aged 12 mo
with a human-milk intake of 400 500 mL/d, the net calcium
intake from human milk might be only 100 mg/d. Assuming
50% retention of calcium from human milk, then 50 mg/d of
retained calcium would need to come from solid foods. This
would require at least 250 mg/d of calcium (based on 20%
retention), or a total calcium intake of 350 mg/d. This value is
consistent with the United Kingdom recommendations and
somewhat lower than the U.S. recommendations, which were
based on 20% retention of the total intake of dietary calcium.
From these calculations, it is apparent that infants who
receive human milk without additional calcium sources and
infants who are inappropriately weaned to juices or other
noncalcium-containing beverages cannot readily meet the100mg/d calcium accretion level. It is not surprising then that
rickets occurs in these infants in the 2nd y of life, especially
when inadequate vitamin D status would lead to impaired
calcium absorption below critical levels.
Safety of calcium fortification. The addition of mineral
salts as fortificants in foods poses the potential risk of reducing
the bioavailability of the native minerals in the food by changing their intestinal solubility or by competing for uptake at
absorption sites that may occur between minerals with similar
physical and chemical properties. The potential for such mineralmineral interactions, such as between calcium and iron or

calcium and zinc, has been studied primarily in relation to

single mineral supplements to the diet rather than as fortificants in foods.
Calcium supplements decrease the absorption of iron contained within food when they are coingested or taken close
together (25,26). However, in the context of whole diets, a
series of human and animal studies has shown at least partial
adaptation to this effect without prolonged inhibition of iron
absorption or the development of abnormalities of iron status
(27,28). In two randomized studies, there were no detrimental
effects on iron absorption or status in infants fed calcium- and
phosphorus-fortified formulas to age 9 mo (29), or in children
fed calcium-fortified breakfast cereal (30). Thus, to date, no
evidence indicates that calcium intake should be restricted to
enhance iron status (30,31).
A negative effect of high intakes of calcium and phosphorus
(even from milk) on zinc absorption has been demonstrated in
adults (32,33) and premature infants (34) as well as in animal
models of human nutrition (35,36). The potential mechanisms
by which calcium interferes with zinc absorption include competition for a divalent cation channel across the brush border
membrane (36) or calcium-stimulated excess loss of endogenous zinc (33).
Indirect evidence of such an interaction is found in studies
that demonstrate a better zinc status (as measured by hair zinc
concentrations) both in premature (37) and term (38) infants
fed human milk compared with formula, the latter having a
higher calcium (and zinc) content. The ratio of calcium to
zinc that could affect such an interaction ranged from 20:1
(by weight) (36) to 50:1 (33). The interaction of calcium
and zinc may be of particular relevance to infants and children, for whom rapid growth including catch-up growth, or
recurrent diarrhea or infections may result in a greater need for
zinc.
If the diet is only marginally adequate in zinc as a result of
limited selection of zinc-containing foods with reasonable
bioavailability (such as those low in phytate content or of
animal origin), a high calcium intake may further compromise
zinc status in infants and children at risk of marginal zinc
status, such as premature infants, children recovering from
growth failure and children with persistent diarrhea. Because
29% of the zinc content of the body is found in the bone
mineral and as part of enzymes involved in bone turnover and
collagen degradation, zinc status is an important factor for
bone health (39). For the aforementioned target populations,
optimal dietary ratios of calcium to zinc should be determined.
In addition, there should be close monitoring of the effects of
calcium supplementation on zinc absorption or status in a
supplemented population.
In contrast to the above examples of antagonistic mineral
mineral interactions, the competition between lead and calcium for absorption is such that increased calcium intake may
ameliorate lead toxicity. In Mexico City an inverse relationship was recently reported between calcium intake and blood
lead levels in 200 children aged 13 mo to 5 y (14).
Fortification recommendations. Provision of additional
calcium by fortification of foods commonly fed to older infants
and toddlers has become increasingly common. The rationale
for this is related to optimizing peak bone mass as well as
preventing rickets. Many children in Latin America likely
have low milk calcium intakes and need supplemental calcium
from solid foods. It is reasonable for a fortified food to provide
100 200 mg/d of calcium. This could be provided as 100 mg of
calcium per 30-g serving of complementary food. This amount
is safe, would effectively help prevent calcium deficiency conditions and could be readily incorporated into the products.

CALCIUM AND BONE MINERALS IN COMPLEMENTARY FOODS

Identification of the optimal source and form of calcium is

not considered here. However, recent data strongly indicate
that the form of calcium used is not crucial to bioavailability,
although few data in children are available (40).

Magnesium requirements in older infants and toddlers

Accretion and balance. Few data are relevant to magnesium requirements in children of this age. Analysis of cadaver
data has led to an estimate of 10 mg/d of magnesium accretion by the skeleton in older infants and toddlers. Taking
childhood as a whole, a net magnesium accretion of 4 mg/d
has been calculated (7).
The amount of dietary magnesium needed to maintain this
level of accretion is poorly defined. Human milk provides
20 30 mg/d of magnesium depending on intake level. Solid
foods provided to older infants may typically provide 55
mg/d of magnesium. Based on these data, a magnesium intake
of 75 mg/d was set as the AI for infants ages 712 mo in the
United States (7). For children ages 12 y, data from older
children was interpolated to younger age groups (41) and an
RDA of 80 mg/d was established by the Food and Nutrition
Board (7).
Deficiency conditions. Although severe magnesium depletion has numerous readily apparent cardiovascular and neurological symptoms, it is much more difficult to identify early or
marginal deficiency (42). The inability to adequately form
bone related to vitamin D and parathyroid insufficiency as well
as lack of magnesium for bone mineralization may be among
the most important results of magnesium deficiency in small
children. Serum magnesium cannot be directly related to
magnesium status in children of any age and, thus, reliable
information on the incidence of magnesium deficiency in
children is not available.
Intake. Green leafy vegetables, unpolished grains and nuts
are high in magnesium. Dairy products, meat and eggs contain
lower amounts of magnesium. Although magnesium intakes
may be slightly below optimal values, a severe deficiency in
small children is uncommon. Murphy et al. (10) found mean
intakes of about 250 mg/d in toddlers in Mexico, consistent
with values in the United States. Similar values were seen in
Kenya and Egypt, although the calcium intake was low in
these countries. The RDA of 80 mg/d for children ages 13 y
is at the first percentile level of U.S. intakes (7). Although
excess magnesium consumed as a supplement can undoubtedly
lead to diarrhea (43) and, at very high levels, to neurological
and cardiac toxicity (44), this is very unlikely to occur with
food fortification strategies providing relatively small amounts
of magnesium.
Recommendations. Magnesium does not appear to be severely limiting in most diets in Latin America. However,
provision of calcium supplementation of foods without magnesium is highly controversial. A ratio of 4:1 or lower (by
weight) of calcium to magnesium has been advocated (45).
Although the overall risk and benefit of this addition cannot
be evaluated at this time, the addition of 40 60 mg/d of
magnesium to a supplement (as a food fortificant) is very
unlikely to have side effects. Until further data are available
demonstrating low magnesium intakes or inadequate magnesium status, the addition of magnesium to a complementary
food supplement would be a safe but not a necessary step and
cannot yet be advocated. Further research is needed to identify
the magnesium needs of small children.

2997S

Phosphorus requirements in older infants and toddlers

As with magnesium, few data are relevant to the phosphorus needs of weaning infants and toddlers. Estimates of phosphorus accretion suggest that 50 60 mg/d is accreted during
the 2nd y of life. Based on dietary and balance data, the AI of
275 mg/d was set for phosphorus for infants aged 712 mo (200
mg from solid foods and 75 mg from human milk) (7). For
children aged 13 y, an RDA of 460 mg/d was established
based on a factorial approach using tissue accretion to set an
Estimated Average Requirement.
Intake. Principal dietary sources of phosphorus in older
infants and toddlers include cows milk (or infant formula),
meat and some soda beverages. Because of the ubiquity of
these foods, intakes of phosphorus are generally high relative
to requirements even for toddlers. Despite calcium intakes of
220 mg/d in Africa, the intake of phosphorus in toddlers was
500 mg/d. The intake of phosphorus also exceeded the
calcium intake in toddlers in Mexico (10). The functional
consequence of these high intakes, especially in the presence
of low calcium intakes, remains a topic of considerable controversy (46). High phosphorus intakes have been suggested to
contribute to hypocalcemia and fractures in children, but
further controlled studies are needed to evaluate these relationships (47). Establishment of dietary phosphorus intake
recommendations on the basis of an optimal calcium-to-phosphorus ratio, usually 1.52.0:1 on a molar basis, is also an
unproven but common practice.
Recommendations. It is unlikely that the diets of most
weaning children need to be fortified with phosphorus. Phosphorus intake could be limiting in breast-fed older infants with
very restricted solid food intake. When complementary food is
expected to be the sole source of nutrients other than human
milk, phosphorus should be included because it is a necessary
component for bone and tissue growth. If phosphorus fortification of complimentary foods is undertaken, 75100 mg/d
would be reasonable based on the limited available data and
the limited potential usefulness of maintaining an appropriate
calcium-to-phosphorus ratio. However, fortification of phosphorus should only be undertaken where clearly needed, as
most children are more likely to have excess than inadequate
phosphorus intake.
Vitamin D requirements in older infants and toddlers
Sources. Vitamin D is required for calcium absorption and
is also involved in maintaining bone mineral homeostasis and
regulating renal calcium excretion. Severe vitamin D deficiency is the primary etiology of most cases of nutritional
rickets. Vitamin D is primarily derived naturally from cutaneous synthesis with exposure to ultraviolet radiation from sunlight. For populations with limited sun exposure because of
environment, clothing or housing conditions, vitamin D is
usually available in fortified milk because only a few foods,
such as liver, contain significant amounts. All cows milk in
the United States is fortified with vitamin D at a level of 2.5
g/240 mL (100 IU/240 mL). Relatively few other foods are
fortified with vitamin D, although many breakfast cereals
provide 1 g/serving. Relatively little vitamin D is present
in human milk except when high dose supplementation of the
lactating mothers diet occurs (48).
Prevalence and causes of deficiency. There are few data
regarding vitamin D intake, serum levels of 25-hydroxyvitamin D or vitamin D deficient rickets incidence in Latin
America. It is likely that dietary intake is relatively low for
most small children. Murphy et al. (10) reported mean intakes

2998S

SUPPLEMENT

of 0.53 0.45 g/d of vitamin D among schoolchildren in

Mexico.
Most vitamin D in the Latin America population is likely
the result of sunshine exposure and resultant UV-B conversion
in the skin of provitamin D to vitamin D. Vitamin D status
and sunshine exposure cannot be assumed to be adequate
throughout the Americas. In Ushuaia in Southern Argentina,
plasma 25-hydroxyvitamin D concentrations (the best measure of vitamin D status) were suboptimal in both light- and
dark-skinned children in winter (49). Approximately 70% of
children had plasma 25-hydroxyvitamin D concentrations
30 nmol/L during the winter. Vitamin D status was greater
in light-skinned than in dark-skinned children only during the
summer. Increased urbanization with resultant decreased time
spent outdoors and increased air pollution may also contribute
to lower sunshine exposure in children. In general, skin absorption of UV-B is related to melanin and is therefore lower
in darker-skinned populations. In Houston Texas, we found
lower plasma 25-hydroxyvitamin D concentrations at all seasons in Mexican-American children than in Caucasian children (50). There was no functional effect of this difference
because both groups had similar rates of calcium absorption
and bone mineral content. Two of the 16 Mexican-American
girls had 25-hydroxyvitamin D concentrations 40 nmol/L
and no concentration was 30 nmol/L.
The importance of fortification of vitamin D through the
diet is increasingly recognized for breast-fed infants. In many
cases the vitamin D deficiency will be subclinical but identifiable by a plasma biochemical profile of low plasma 25hydroxyvitamin D (30 nmol/L), high parathyroid hormone
and low or subnormal calcium (52). Infants identified with
such a biochemical profile normalized their status when supplemented with vitamin D for 1 mo with no signs of hypercalcemia (51). Data from a European study demonstrated
greater preadolescent bone mass in children who received
vitamin D fortification in infancy than in children who did not
(52).
Although rickets is not widely reported in Latin America,
it may be present in high risk areas. A much higher incidence
of rickets was reported in southern than in northern areas of
Argentina, associated with an up to 52% incidence of very low
(20 nmol/L) 25-hydroxyvitamin D concentrations in southern Argentina compared with a 9% incidence in Buenos Aires
(53).
In the United States there has been a dramatic recent
increase in the incidence of rickets, primarily in AfricanAmerican infants and toddlers (54). Many of these were
breast-fed and essentially none had received supplemental
vitamin D. This problem may worsen in the United States and
Canada as the frequency of breast-feeding beyond age 1 y
increases. Other factors leading to lower vitamin D status, such
as less time outdoors and increased sunscreen use, may make
vitamin D deficient rickets become more prevalent. It is of
note that at least in the United States, rickets occurs in
children of all socioeconomic classes.
Recommendations. The routine provision of vitamin D
supplementation for all breast-fed infants is controversial. Although rickets is apparently uncommon in Latin America,
increased breast-feeding, urbanization, the presence of air pollution, use of sunscreens and lack of cows milkvitamin D
fortification place infants and small children at risk for inadequate vitamin D status. It is reasonable to consider adding a
small amount of vitamin D to any complementary food if this
is technically feasible. A level of 12 g/d would be consistent
with other fortification strategies. This level would be safe
based on the Tolerable Upper Intake Level of 25 g/d estab-

lished by the Food and Nutrition Board for infants aged 12

mo (7).
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and sulfur. In: Nutrition of Normal Infants. (Fomon S. J., ed.) pp. 192218.
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2. Garn, S. M. (1972) The course of bone gain and the phases of bone
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a young multiethnic female population. Am. J. Clin. Nutr. 65: 724 731.
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mineral intakes of toddlers: predicted prevalence of inadequacy in village populations in Egypt, Kenya, and Mexico. Am. J. Clin. Nutr. 56: 565572.
11. Murphy, S. P., Calloway, D. H. & Beaton, G. H. (1995) Schoolchildren
have similar predicted prevalences of inadequate intakes as toddlers in village
populations in Egypt, Kenya, and Mexico. Eur. J. Clin. Nutr. 49: 647 657.
12. Wyatt, C. J., Hernandez, M. E. & Mendez, R. O. (1996) Dialyzable
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