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OCR for page 350
TABLE 1 Dietary Reference Intakes for Manganese by
Life Stage Group
DRI values (mg/day)
AIa ULb
males females
Life stage group
NDc
0 through 6 mo 0.003 0.003
7 through 12 mo 0.6 0.6 ND
1 through 3 y 1.2 1.2 2
4 through 8 y 1.5 1.5 3
9 through 13 y 1.9 1.6 6
14 through 18 y 2.2 1.6 9
19 through 30 y 2.3 1.8 11
31 through 50 y 2.3 1.8 11
51 through 70 y 2.3 1.8 11
> 70 y 2.3 1.8 11
Pregnancy
£ 18 y 2.0 9
19 through 50 y 2.0 11
Lactation
£ 18 y 2.6 9
19 through 50 y 2.6 11
a AI = Adequate Intake.
b UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents
total intake from food, water, and supplements.
c ND = Not determinable. This value is not determinable due to the lack of data of
adverse effects in this age group and concern regarding the lack of ability to handle
excess amounts. Source of intake should only be from food to prevent high levels of
intake.
OCR for page 351
PART III: MANGANESE 351
MANGANESE
M
anganese is involved in the formation of bone and in specific reac-
tions related to amino acid, cholesterol, and carbohydrate metabo-
lism. Manganese metalloenzymes include arginase, glutamine syn-
thetase, phosphoenolpyruvate decarboxylase, and manganese superoxide
dismutase.
Since data were insufficient to set an Estimated Average Requirement (EAR)
and thus calculate a Recommended Dietary Allowance (RDA) for manganese,
an Adequate Intake (AI) was instead developed. The AIs for manganese are
based on intakes in healthy individuals, using the median manganese intakes
reported from the Food and Drug Administration’s (FDA’s) Total Diet Study
(1991–1997). The Tolerable Upper Intake Level (UL) is based on elevated blood
manganese concentrations and neurotoxicity as the critical adverse effects. DRI
values are listed by life stage group in Table 1.
The highest contributors of manganese to the diet are grains, beverages
(tea), and vegetables. Although a manganese deficiency may contribute to one
or more clinical symptoms, a clinical deficiency has not been clearly associated
with poor dietary intakes of healthy individuals. Neurotoxicity of orally in-
gested manganese at relatively low doses is controversial, but evidence suggests
that elevated blood manganese levels and neurotoxicity are possible.
MANGANESE AND THE BODY
Function
Manganese is an essential nutrient involved in the formation of bone and in
specific reactions related to amino acid, cholesterol, and carbohydrate metabo-
lism. Manganese metalloenzymes include arginase, glutamine synthetase, phos-
phoenolpyruvate decarboxylase, and manganese superoxide dismutase.
Absorption, Metabolism, Storage, and Excretion
Only a small percentage of dietary manganese is absorbed by the body. Some
studies indicate that manganese is absorbed via active transport mechanisms,
while other studies suggest that passive diffusion via a nonsaturable process
occurs. Much of absorbed manganese is excreted very rapidly into the gut via
the bile, and only a small amount is retained.
Manganese is taken up from the blood by the liver and transported to ex-
OCR for page 352
DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
352
trahepatic tissues by transferrin and possibly a2-macroglobulin and albumin.
Excretion primarily occurs in the feces. Urinary excretion of manganese is low
and has not been found to be sensitive to dietary intake. Therefore, the poten-
tial risk for manganese toxicity is highest when bile excretion is low, such as in
the neonate or in liver disease.
DETERMINING DRIS
Determining Requirements
Since data were insufficient to set an EAR and thus calculate an RDA for manga-
nese, an AI was instead developed. The AIs for manganese are based on intakes
in healthy individuals, using the median manganese intake from the FDA’s Total
Diet Study (1991–1997).
Special Considerations
Gender: Men have been shown to absorb significantly less manganese com-
pared to women. This may be related to iron status, as men generally have
higher serum ferritin concentrations than do women (see “Dietary Interactions”).
Criteria for Determining Manganese Requirements,
by Life Stage Group
Life stage group Criterion
0 through 6 mo Average manganese intake from human milk
7 through 12 mo Extrapolation from adult AI
1 through > 70 y Median manganese intake from the Total Diet Study
Pregnancy
£ 18 y Extrapolation from adolescent female AI based on body weight
19 through 50 y Extrapolation from adult female AI based on body weight
Lactation
< 18 y through 50 y Median manganese intake from the Total Diet Study
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 healthy
people. Members of the general population should not routinely exceed the
UL. This value is based on elevated blood manganese and neurotoxicity as the
critical adverse effects and represents intake from food, water, and supplements.
OCR for page 353
PART III: MANGANESE 353
Based on the Total Diet Study, the highest dietary manganese intake at the
95th percentile was 6.3 mg/day, which was the level consumed by men aged 31
to 50 years. Data from the Third National Health and Nutrition Examination
Survey (NHANES III, 1988–1994) indicated that the highest supplemental in-
take of manganese at the 95th percentile was approximately 5 mg/day, which
was consumed by adults, including pregnant women. The risk of an adverse
effect resulting from excess intake of manganese from food and supplements
appears to be low at these intakes.
DIETARY SOURCES
Foods
Based on the Total Diet Study, grain products contributed 37 percent of dietary
manganese, while beverages (tea) and vegetables contributed 20 and 18 per-
cent, respectively, to the adult male diet.
Dietary Supplements
According to U.S. data from the 1986 National Health Interview Survey (NHIS),
12 percent of adults consumed supplements that contained manganese. Based
on data from NHANES III, the median supplemental intake of manganese was
2.4 mg/day for those adults who took supplements, an amount similar to the
average dietary manganese intake.
Bioavailability
Several factors may affect the bioavailability of manganese (see “Dietary Interac-
tions”).
Dietary Interactions
There is evidence that manganese may interact with certain other nutrients and
dietary substances (see Table 2).
INADEQUATE INTAKE AND DEFICIENCY
Although a manganese deficiency may contribute to one or more clinical symp-
toms, a clinical deficiency has not been clearly associated with poor dietary
intakes of healthy individuals. In limited studies on induced manganese deple-
tion in humans, subjects developed scaly dermatitis and hypocholesterolemia.
Studies in various animal species observed signs and symptoms of deficiency,
including impaired growth and skeletal development, impaired reproductive
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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS
354
TABLE 2 Potential Interactions with Other Dietary Substances
Substance Potential Interaction Notes
SUBSTANCES THAT AFFECT MANGANESE
Calcium Calcium may reduce In one study, adding calcium to human milk reduced
manganese absorption. the absorption of manganese from 4.9 percent to 3.0
percent.
Iron Iron status may affect Low ferritin concentrations are associated with
manganese absorption: low increased manganese absorption, thereby having a
serum ferritin concentration gender effect on manganese bioavailability (because
may increase manganese women tend to have lower ferritin concentrations
absorption. compared with men).
Phytate Phytate may decrease In a study of infant formula, the soy-based formula
manganese absorption. without phytate produced manganese absorption of
1.6 percent, whereas a formula with phytate produced
an absorption of 0.7 percent.
function, impaired glucose tolerance, and alterations in carbohydrate and lipid
metabolism.
EXCESS INTAKE
Manganese toxicity, which causes central nervous system effects similar to those
of Parkinson’s disease, is a well-recognized occupational hazard for people who
inhale manganese dust. The totality of evidence in animals and humans sup-
ports a causal association between elevated blood manganese concentrations
and neurotoxicity.
Special Considerations
Individuals susceptible to adverse effects: People with chronic liver disease
may be distinctly susceptible to the adverse effects of excess manganese intake,
probably because elimination of manganese in bile is impaired. Also, manga-
nese in drinking water and supplements may be more bioavailable than food
manganese. Therefore, individuals who take manganese supplements, particu-
larly those who already consume large amounts of manganese from diets high
in plant products, should take extra caution.
Plasma manganese concentrations can become elevated in infants with
choleostatic liver disease who are given supplemental manganese in total
parenteral nutrition (TPN).
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PART III: MANGANESE 355
KEY POINTS FOR MANGANESE
Manganese is an essential nutrient involved in the formation of
3
bone and in specific reactions related to amino acid,
cholesterol, and carbohydrate metabolism.
Since data were insufficient to set an EAR and thus calculate
3
an RDA for manganese, an AI was instead developed.
The AIs for manganese are based on the intakes of healthy
3
individuals, using median manganese intakes reported from the
FDA’s Total Diet Study. The UL is based on elevated blood
manganese concentrations and neurotoxicity as the critical
adverse effects.
The risk of an adverse effect resulting from excess intake of
3
manganese from food and supplements appears to be low.
The highest contributors of manganese to the diet are grain
3
products, beverages (tea), and vegetables.
Although a manganese deficiency may contribute to one or
3
more clinical symptoms, a clinical deficiency has not been
clearly associated with poor dietary intakes of healthy
individuals. In limited studies on induced manganese depletion
in humans, subjects developed scaly dermatitis and
hypocholesterolemia.
Manganese toxicity, which causes central nervous system
3
effects similar to those of Parkinson’s disease, is a well-
recognized occupational hazard for people who inhale
manganese dust. Neurotoxicity of orally ingested manganese
at relatively low doses is more controversial, but evidence
suggests that elevated blood manganese levels and
neurotoxicity are possible.
Plasma manganese concentrations can become elevated in
3
infants with choleostatic liver disease who are given
supplemental manganese in total parenteral nutrition.
