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TABLE 1 Dietary Reference Intakes for Vitamin D by
Life Stage Group
DRI values (mg/day)
AIa,b,c ULd
Life stage groupe
0 through 6 mo 5 25
7 through 12 mo 5 25
1 through 3 y 5 50
4 through 8 y 5 50
9 through 13 y 5 50
14 through 18 y 5 50
19 through 30 y 5 50
31 through 50 y 5 50
51 through 70 y 10 50
> 70 y 15 50
Pregnancy
£ 18 y 5 50
19 through 50 y 5 50
Lactation
£ 18 y 5 50
19 through 50 y 5 50
a AI = Adequate Intake.
cholecalciferol. 1mg cholecalciferol = 40 IU vitamin D.
bAs
c In the absence of adequate exposure to sunlight.
d UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents
total intake from food, water, and supplements.
e All groups except Pregnancy and Lactation represent males and females.
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PART III: VITAMIN D 225
VITAMIN D
V
itamin D (calciferol) is involved in bone health and is naturally found in
very few foods. Synthesized in the skin through exposure to ultraviolet
B rays in sunlight, its major biological function is to aid in the absorp-
tion of calcium and phosphorus, thereby helping maintain normal serum levels
of these minerals. Vitamin D also functions as an antiproliferation and
prodifferentiation hormone, but the exact role it plays is not yet known.
The AIs for vitamin D are based on serum 25-hydroxyvitamin D [25(OH)D],
which is the form that represents vitamin D storage. The Tolerable Upper In-
take Level (UL) was derived using studies of the effect of vitamin D intake on
serum calcium concentrations (to prevent hypercalcemia) in humans. Since
data were inadequate to determine an Estimated Average Requirement (EAR)
and thus calculate a Recommended Dietary Allowance (RDA) for vitamin D, an
Adequate Intake (AI) was instead developed. DRI values are listed by life stage
group in Table 1.
Foods naturally rich in vitamin D include the flesh of fatty fish, some fish-
liver oils, and eggs from hens fed vitamin D. Fortified milk products and break-
fast cereals are also good sources of vitamin D. Vitamin D deficiency can impair
normal bone metabolism, which may lead to rickets in children or osteomala-
cia (undermineralized bone) or osteoporosis (porous bones) in adults. In con-
trast, excess vitamin D intake can cause high blood calcium, high urinary cal-
cium, and the calcification of soft tissues, such as blood vessels and certain
organs.
VITAMIN D AND THE BODY
Function
The primary function of vitamin D in the body is to aid in the intestinal absorp-
tion of calcium and phosphorus, thereby helping maintain normal serum levels
of these minerals in the body. Other roles in cellular metabolism involve
antiproliferation and prodifferentiation actions.
Vitamin D is fat-soluble and occurs in many forms, but the two dietary
forms are vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). Vitamin
D2 originates from the yeast and plant sterol, ergosterol; vitamin D3 originates
from 7-dehydrocholesterol, a precursor of cholesterol, when synthesized in the
skin. Vitamin D2 and vitamin D3 are similarly metabolized. Vitamin D without a
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
226
subscript represents either vitamins D2 or D3, or both, and is biologically inert.
The biologically active hormone form of vitamin D is 1,25-dihydroxyvitamin D
[1,25(OH)2D].
Absorption, Metabolism, Storage, and Excretion
Vitamin D is either synthesized in the skin through exposure to ultraviolet B
rays in sunlight or ingested as dietary vitamin D. After absorption of dietary fat-
soluble vitamin D in the small intestine, it is incorporated into the chylomicron
fraction and absorbed through the lymphatic system.
Whether from the skin or from the lymphatic system, vitamin D accumu-
lates in the liver, where it is hydroxylated to 25-hydroxyvitamin D [25(OH)D]
and then enters the circulation. The circulating 25(OH)D concentration is a
good indicator of vitamin D status. In order to have biological activity at physi-
ological concentrations, 25(OH)D must be hydroxylated to 1,25(OH)2D. This
conversion occurs in the kidneys and is tightly regulated by parathyroid hor-
mone in response to serum calcium and phosphorus levels. Vitamin D is ab-
sorbed in the small intestine and is principally excreted in the bile after metabo-
lites are inactivated. A variety of vitamin D metabolites are excreted by the
kidney into the urine.
DETERMINING DRIS
Determining Requirements
Because sufficient data were not available to establish an EAR and thus calculate
an RDA, an AI was instead developed. The AIs for vitamin D are based on
serum 25(OH)D concentrations; they assume that no vitamin D is available
from sun-mediated cutaneous synthesis. The AI is the intake value that appears
to be needed to maintain (in a defined group of healthy individuals with limited
but uncertain sun exposure and stores) serum 25-hydroxyvitamin D concen-
trations above a defined amount. The latter is that concentration below which
vitamin D deficiency rickets or osteomalacia occurs. When consumed by an
individual, the AI is sufficient to minimize the risk of low serum 25(OH)D.
Because human milk contains very little vitamin D, breast-fed infants who
are not exposed to sunlight are unlikely to obtain adequate amounts of vitamin
D from mother’s milk to satisfy their needs beyond early infancy. Therefore, the
AI for infants aged 0 through 12 months does not assume vitamin D synthesis
from sunlight exposure and is based on the lowest dietary intake associated
with adequate serum 25(OH)D concentrations.
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PART III: VITAMIN D 227
Accurate estimates of vitamin D intakes in the United States are lacking, in
part because the vitamin D composition of fortified foods highly varies and also
because many surveys do not include estimates of vitamin D intake.
Special Considerations
Older adults: Older adults, especially those who live in northern industrialized
cities of the world, are more prone to developing vitamin D deficiency.
Infants: Whether fed human milk or formula, infants have the same require-
ments for dietary vitamin D if they have not been exposed to sunlight. Most
standard infant formulas contain enough vitamin D to meet needs, but because
human milk has very little vitamin D, breast-fed infants who are not exposed to
sunlight are unlikely to obtain adequate amounts of vitamin D from mother’s
milk to satisfy their needs beyond early infancy.
For infants who live in far-northern latitudes or whose sunlight exposure is
restricted, a minimal intake of 2.5 mg (100 IU)/day of vitamin D will likely
prevent rickets. However, at this intake and in the absence of sunlight, many
infants will have serum 25(OH)D concentrations within the range that is often
observed in cases of rickets. For this reason, and assuming that infants are not
obtaining any vitamin D from sunlight, an AI of at least 5 mg (200 IU)/day is
recommended.
Criteria for Determining Vitamin D Requirements,
by Life Stage Group
Life stage group Criterion
For all life stage groups Serum 25(OH)D
The UL
The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient
intake that is likely to pose no risk of adverse effects for almost all people.
Members of the general population should not routinely exceed the UL. The
DRI for vitamin D was derived using studies of the effect of vitamin D intake on
serum calcium concentrations (to prevent hypercalcemia) in humans and rep-
resents total intake from food, water, and supplements.
Because milk is fortified to contain 10 mg (400 IU)/quart of vitamin D in
the United States and 8.8 mg (352 IU)/liter of vitamin D in Canada, people with
high milk intakes also may have relatively high vitamin D intakes. The 1986
National Health Interview Survey (NHIS) estimated that the 95th percentile of
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
228
intake by users of vitamin D supplements was 20 µg (800 IU)/day for men and
17.2 µg(686) IU/day for women. For most people, vitamin D intake from food
and supplements is unlikely to exceed the UL. However, people who are at the
upper end of the ranges for both sources of intake, particularly those who use
many supplements and those with high intakes of fish or fortified milk, may be
at risk for vitamin D toxicity.
Special Considerations
Granulomatous diseases: The UL for vitamin D only applies to health indi-
viduals and does not apply to people with granulomatous diseases (such as
sarcoidosis, tuberculosis, and histoplasmosis). Granulomatous diseases are char-
acterized by hypercalcemia or hypercalciuria, or both, in individuals with nor-
mal or less-than-normal vitamin D intakes or with exposure to sunlight (see
“Inadequate Intake and Deficiency”).
SOURCES OF VITAMIN D
Sunlight
Exposure to ultraviolet B rays through sunlight is a primary way by which hu-
mans obtain vitamin D. However, several factors can limit the skin’s synthesis of
vitamin D, including the use of sunscreen, increased levels of skin melanin, the
distance one is from the Equator, the time of day, and the season of the year.
Above and below latitudes of approximately 40 degrees N and 40 degrees S,
vitamin D3 in the skin is absent during most of the 3–4 winter months. The far-
northern and southern latitudes extend this period for up to 6 months.
Foods
Vitamin D naturally occurs in very few foods, mainly in the flesh of fatty fish,
some fish-liver oils, and eggs from hens fed vitamin D. Most people’s dietary
intake of vitamin D comes from foods fortified with vitamin D. In Canada, all
milks and margarines must be fortified. In the United States, milk products,
breakfast cereals, and some fruit juices are fortified.
Dietary Supplements
In the 1986 NHIS, the use of vitamin D supplements was reported in more than
one-third of children 2 to 6 years of age, more than one-fourth of women, and
almost one-fifth of men. The median supplement dose was the same for all
users: 10 µg (400 IU).
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PART III: VITAMIN D 229
Bioavailability
This information was not provided at the time the DRI values for this nutrient
were set.
Dietary interactions
There is evidence that vitamin D may interact with certain other nutrients and
dietary substances (see Table 2).
TABLE 2 Potential Interactions with Other Dietary Substances
Substance Potential Interaction Notes
SUBSTANCES THAT AFFECT VITAMIN D
Magnesium Magnesium deficiency may Individuals with hypocalcemia and magnesium
affect the body’s response to deficiency are resistant to pharmacological doses of
vitamin D, 1,a-hydroxyvitamin D, and 1,25-
pharmacological vitamin D.
dihydroxyvitamin D.
INADEQUATE INTAKE AND DEFICIENCY
Vitamin D deficiency results in the inadequate bone mineralization or deminer-
alization of the skeleton. The potential effects of vitamin D deficiency include
the following:
• Rickets (in children)
• Osteomalacia (in adults)
• Elevated serum parathyroid hormone
• Decreased serum phosphorus
• Elevated serum alkaline phosphatase
• Osteoporosis (porous bones)
Epidemiological studies have found an association between vitamin D defi-
ciency and an increased risk of colon, breast, and prostate cancer in people who
live at higher latitudes. However, additional studies are needed to further ex-
plore this association.
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
230
Special Considerations
Older adults: As adults age, their ability to synthesize vitamin D in the skin
significantly decreases. Adults over the age of 65 years produce four times less
vitamin D in the skin compared with adults aged 20 to 30 years.
Sunlight and skin pigmentation: The major source of vitamin D for humans
is the exposure of the skin to sunlight, which initiates the conversion of 7-
dehydrocholesterol to previtamin D3 in the skin. An increase in skin melanin
pigmentation or the topical use of sunscreen reduces the production of vitamin
D3 in the skin.
Malabsorption disorders: Conditions that cause fat malabsorption, such as se-
vere liver failure, Crohn’s disease, Whipple’s disease, and celiac sprue, are asso-
ciated with vitamin D deficiency because people with these conditions are un-
able to absorb vitamin D.
Medications: Glucocorticoids inhibit vitamin D–dependent intestinal calcium
absorption and therefore can cause osteopenia. Individuals on glucocorticoid
therapy may require supplemental vitamin D to maintain normal serum levels
of 25(OH)D. Medications used to control seizures, such as phenobarbital and
dilantin, can alter the metabolism and circulating half-life of vitamin D. People
taking these medications (particularly those without exposure to sunlight) may
require supplemental vitamin D.
EXCESS INTAKE
Excess intake of vitamin D can cause hypervitaminosis D, which is character-
ized by a considerable increase in the serum levels of 25(OH)D (to 400–1,250
nmol/L). The adverse effects of hypervitaminosis D are probably largely medi-
ated via hypercalcemia. The potential effects of the hypercalcemia associated
with hypervitaminosis D include the following:
• Polyuria
• Polydipsia
• Hypercalciuria
• Calcification of soft tissues (including the kidneys, blood vessels, heart,
and lungs)
• Anorexia
• Nausea
• Vomiting
• Reduced renal function
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PART III: VITAMIN D 231
There is no evidence that vitamin D obtained through sun exposure can con-
tribute to vitamin D toxicity because there is a limit to the amount of vitamin D3
formed. Once this amount is reached, the previtamin and vitamin D3 remaining
in the skin are destroyed with continued sunlight exposure.
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
232
KEY POINTS FOR VITAMIN D
Vitamin D (calciferol) is involved in bone health. It aids in the
3
absorption of calcium and phosphorus, thereby helping
maintain normal serum levels of these minerals.
Vitamin D is either synthesized in the skin through exposure to
3
ultraviolet B rays in sunlight or ingested as dietary vitamin D.
As adults age, their ability to synthesize vitamin D in the skin
significantly decreases.
Since data were inadequate to determine an EAR and thus
3
calculate an RDA for vitamin D, an AI was instead developed.
The AIs for vitamin D are based on serum 25(OH)D, which is
3
the form that represents vitamin D storage.
The UL was derived using studies of the effect of vitamin D
3
intake on serum calcium concentrations (to prevent
hypercalcemia) in humans.
For most people, dietary vitamin D intake is unlikely to exceed
3
the UL.
Most standard infant formulas contain enough vitamin D to
3
meet needs, but because human milk has very little vitamin D,
breast-fed infants who are not exposed to sunlight are unlikely
to obtain adequate amounts of vitamin D from mother’s milk to
satisfy their needs beyond early infancy.
Exposure to ultraviolet B rays through sunlight is a primary way
3
by which humans obtain vitamin D. However, several factors
can limit the skin’s synthesis of vitamin D, including the use of
sunscreen, increased levels of skin melanin, the distance one is
from the Equator, the time of day, and the season of the year.
Vitamin D naturally occurs in very few foods, mainly in the flesh
3
of fatty fish, some fish-liver oils, and eggs from hens fed
vitamin D. In Canada, all milks and margarines must be
fortified. In the United States, milk products, breakfast cereals,
and some fruit juices are fortified.
Vitamin D deficiency can impair normal bone metabolism,
3
which may lead to rickets in children and osteomalacia in
adults. It is also implicated in osteoporosis in adults.
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PART III: VITAMIN D 233
Older adults, especially those who live in northern
3
industrialized cities of the world, are more prone to developing
vitamin D deficiency.
There is no evidence that vitamin D obtained through sun
3
exposure can contribute to vitamin D toxicity.
Excess intake of vitamin D can cause hypervitaminosis D, the
3
effects of which include hypercalcemia, hypercalciuria, and
calcification of soft tissues, such as blood vessels and certain
organs.
