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TABLE 1 Dietary Reference Intakes for Selenium by Life
Stage Group
DRI values (mg/day)
EARa RDAb AIc ULd
Life stage groupe
0 through 6 mo 15 45
7 through 12 mo 20 60
1 through 3 y 17 20 90
4 through 8 y 23 30 150
9 through 13 y 35 40 280
14 through 18 y 45 55 400
19 through 30 y 45 55 400
31 through 50 y 45 55 400
51 through 70 y 45 55 400
> 70 y 45 55 400
Pregnancy
£ 18 y 49 60 400
19 through 50 y 49 60 400
Lactation
£ 18 y 59 70 400
19 through 50 y 59 70 400
a EAR = Estimated Average Requirement.
b RDA = Recommended Dietary Allowance.
c AI = Adequate Intake.
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: SELENIUM 381
SELENIUM
S
elenium is an antioxidant nutrient involved in the defense against oxida-
tive stress. Selenoproteins regulate thyroid hormone actions and the re-
dox status of vitamin C and other molecules. Most selenium found in
animal tissue is in the form of selenomethionine (the major dietary form of
selenium) or selenocysteine, both of which are well absorbed.
The method used to estimate the requirements for selenium relates to the
intake needed to maximize the activity of the plasma selenoprotein glutathione
peroxidase, an oxidant defense enzyme. The Tolerable Upper Intake Level (UL)
is based on the adverse effect of selenosis, and pertains to intakes from food and
supplements. Although some studies indicate a potential anticancer effect of
selenium, the data were inadequate to set dietary selenium requirements based
on this potential effect. DRI values are listed by life stage group in Table 1.
Food sources of selenium include meat, seafood, grains, dairy products,
fruits, and vegetables, and the major dietary forms of selenium appear to be
highly bioavailable. However, the selenium content of foods greatly varies de-
pending on the selenium content of the soil where the animal was raised or
where the plant was grown. Neither selenium deficiency nor toxicity appears to
be common in U.S. and Canadian populations.
SELENIUM AND THE BODY
Function
Selenium functions through selenoproteins, several of which defend against
oxidative stress; and as such, it plays a role as a dietary antioxidant. Although
the function of all selenoproteins has not yet been characterized, selenium has
been found to regulate both thyroid hormone actions and the redox status of
vitamin C and other molecules.
Absorption, Metabolism, Storage, and Excretion
Most dietary selenium is in the form of selenomethionine (the major dietary
form of selenium) or selenocysteine, both of which are well absorbed. Other
forms of selenium include selenate and selenite, which are not major dietary
constituents, but are commonly used in fortified foods and dietary supplements.
Two pools of reserve selenium are present in the body. The first is as
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
382
selenomethionine, which is not known to have a physiological function sepa-
rate from that of methionine. The second reserve pool is the selenium found in
liver glutathione peroxidase.
Ingested selenite, selenate, and selenocysteine are all metabolized directly
to selenide, the reduced form of selenium. Selenomethionine can also be me-
tabolized to selenide. Selenide can be metabolized to a precursor of other reac-
tions or be converted into an excretory metabolite. Selenium is excreted mainly
through the urine. The breath may also contain volatile metabolites when large
amounts of selenium are being excreted.
DETERMINING DRIS
Determining Requirements
The adult requirements for selenium are based on the criterion of maximizing
plasma glutathione peroxidase activity, as assessed by plateau concentration of
plasma selenoproteins. Although some studies indicate a potential anticancer
effect of selenium, the data were inadequate to set dietary selenium require-
ments based on this potential effect. Further large-scale trials are necessary.
Criteria for Determining Selenium Requirements,
by Life Stage Group
Life stage group Criterion
0 through 6 mo Human milk content
7 through 12 mo Human milk + solid food
1 through 18 y Extrapolation from adult
19 through 30 y Maximizing plasma glutathione peroxidase activity
31 through >70 y Extrapolation of plasma glutathione peroxidase activity
from 19 through 30 y
Pregnancy
£ 18 y through 50 y Age-specific requirement + saturation of fetal selenoprotein
Lactation
£ 18 y through 50 y Age-specific requirement + human milk content requirement
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
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PART III: SELENIUM 383
UL for selenium is based on selenosis as the adverse effect and represents total
intake from food, water, and supplements. The most frequently reported fea-
tures of selenosis (chronic toxicity) are hair and nail brittleness and loss and
thus were selected as the critical endpoints on which to base a UL.
The extensive food distribution systems in Canada and the U.S. ensure
that individuals do not eat diets that originate solely from one locality. This
moderates the selenium content of diets, even in high-selenium areas. The risk
of selenium intake above the UL for U.S. and Canadian populations appears to
be small, and there is no known seleniferous area in the United States and
Canada with recognized cases of selenosis.
DIETARY SOURCES
Foods
Dietary sources of selenium include meat, seafood, cereals and grains, dairy
products, and fruits and vegetables. (Drinking water does not supply nutrition-
ally significant amounts of selenium.)
However, the selenium content of food can greatly vary depending on the
selenium content of the soil where the animal was raised or where the plant was
grown. Food animals in the United States and Canada usually have controlled
diets to which selenium is added, and thus, the amounts found in muscle meats,
milk, and eggs are more consistent than for plant-based foods.
Dietary intake of selenium in the United States and Canada varies by geo-
graphical origin, based on the selenium content of the soil and meat content of
the diet. This variation is buffered by a large food-distribution system, in which
the extensive transport of food throughout North America prevents decreased
intakes in people living in low-selenium areas. Although the food distribution
systems in the United States and Canada ensure a mix of plant- and animal-
based foods originating from a broad range of soil selenium conditions, local
foods (e.g., from farmers’ markets) may considerably vary from the mean val-
ues in food composition databases.
The content of selenium in plants depends on the availability of the ele-
ment in the soil where the plant was grown. Unlike plants, animals require
selenium, and so meat and seafood are reliable dietary sources of selenium.
Therefore, the lowest selenium intakes are in populations that eat vegetarian
diets comprising plants grown in low-selenium areas.
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
384
Dietary Supplements
Selenium is widely available in a variety of supplements and multivitamin prepa-
rations. In the 1986 National Health Interview Survey (NHIS), 9 percent of all
adults reported the use of supplements containing selenium.
Bioavailability
Most dietary selenium is highly bioavailable, although its bioavailability from
fortified foods and supplements is lower than for naturally occurring dietary
forms of selenium.
Dietary Interactions
This information was not provided at the time the DRI values for this nutrient
were set.
INADEQUATE INTAKE AND DEFICIENCY
Selenium deficiency in otherwise well-nourished individuals is not likely to
cause overt symptoms. However, selenium deficiency may lead to biochemical
changes that can predispose a person to illness associated with other stresses,
such as:
• Keshan disease, a cardiomyopathy found only in selenium-deficient
children that appears to be triggered by an additional stress, possibly an
infection or chemical exposure
• Kashin-Beck disease, an endemic disease of cartilage that occurs in
preadolescence or adolescence, has been reported in some of the low-
selenium areas of Asia, although the pathogenesis remains uncertain
EXCESS INTAKE
The limited data available on humans suggest that chronic toxicities from inor-
ganic and organic forms of selenium have similar clinical features, but differ in
the rapidity of onset and the relationship to tissue selenium concentrations.
Inorganic selenium can cause toxicity at tissue levels of selenium that are much
lower than those seen with similar intakes of dietary selenium as
selenomethionine. The signs and symptoms of chronic selenosis, or selenium
toxicity, are the following:
• Hair and nail brittleness and loss (most frequently reported symptoms)
• Gastrointestinal disturbances
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PART III: SELENIUM 385
• Skin rash
• Garlic breath odor
• Fatigue
• Irritability
• Nervous system abnormalities
Special Considerations
Soil variations: There are high-selenium regions in the United States, such as
western South Dakota and eastern Wyoming, but the U.S. Department of Agri-
culture has identified them and proscribed their use for raising animals for
food. No evidence of selenosis has been found in these areas of high selenium
content, even in the subjects consuming the most selenium.
KEY POINTS FOR SELENIUM
Selenium functions through selenoproteins, several of which
3
defend against oxidative stress and as such, plays a role as a
dietary antioxidant.
The requirements for selenium are based on the criterion of
3
maximizing plasma glutathione peroxidase activity. The UL is
based on the critical endpoints of hair and nail brittleness and
loss.
Although some studies indicate a potential anticancer effect of
3
selenium, the data were inadequate to set dietary selenium
requirements based on this potential effect.
Food sources of selenium include meat, seafood, cereals and
3
grains, dairy products, and fruits and vegetables.
The lowest selenium intakes are in populations that eat
3
vegetarian diets comprising plants grown in low-selenium
geographic areas.
The selenium content of foods can greatly vary depending on
3
the selenium content of the soil where the animal was raised or
where the plant was grown.
Selenium deficiency in otherwise well-nourished individuals is
3
not likely to cause overt symptoms.
The limited data available on humans suggest that chronic
3
toxicities from inorganic and organic forms of selenium have
similar clinical features but differ in rapidity of onset and
relationship to tissue selenium concentrations.
