Vitamin A is a generic term for a large number of related
compounds. Retinol (an alcohol) and retinal (an aldehyde) are often referred
to as preformed vitamin A. Retinal can be converted by the body to retinoic
acid, the form of vitamin A known to affect gene
transcription. Retinol,
retinal, retinoic acid, and related compounds are known as retinoids.
Beta-carotene and other carotenoids that can be converted by the body
into retinol are referred to as provitamin A carotenoids. Hundreds of
different carotenoids are synthesized by plants, but only about 10% of
them are provitamin A carotenoids (1).
The following discussion will focus mainly on preformed vitamin A and
retinoic acid.
Vision
The retina is located
at the back of the eye. When light passes through the lens, it is sensed
by the retina and converted to a nerve impulse for interpretation by the
brain. Retinol is transported to the retina via the circulation and accumulates in retinal pigment epithelial cells (diagram).
Here, retinol is esterified to form a retinyl ester, which can be stored.
When needed, retinyl esters are broken apart (hydrolyzed) and isomerized
to form 11-cis-retinol, which can be oxidized
to form 11-cis-retinal. 11-cis-retinal can be shuttled across
the interphotoreceptor matrix to the rod cell where it binds to a protein
called opsin to form the visual pigment, rhodopsin (also known as visual purple). Rod
cells with rhodopsin can detect very small amounts of light, making them
important for night vision. Absorption of a photon of light catalyzes
the isomerization of 11-cis-retinal to all-trans-retinal and results
in its release. This isomerization triggers a cascade of events, leading
to the generation of an electrical signal to the optic nerve. The nerve
impulse generated by the optic nerve is conveyed to the brain where it
can be interpreted as vision. Once released, all-trans retinal is
converted to all-trans-retinol, which can be transported across
the interphotoreceptor matrix to the retinal epithelial cell, thereby completing
the visual cycle (2). Inadequate retinol
available to the retina results in impaired dark adaptation, known as
"night blindness."
Regulation of gene expression
Isomers of retinoic acid (RA) act as hormones to affect gene
expression and thereby influence numerous physiological processes.
All-trans-RA and 9-cis-RA are transported to the nucleus
of the cell bound to cytoplasmic retinoic acid-binding proteins (CRABP).
Within the nucleus, RA binds to retinoic acid receptor proteins (diagram).
Specifically, all-trans-RA binds to retinoic acid receptors (RAR) and 9-cis-RA binds to retinoid X receptors (RXR). RAR and RXR form RAR/RXR heterodimers; these heterodimers
bind to regulatory regions of the chromosome
called retinoic acid response elements (RARE). A dimer is a complex of
two protein molecules. Heterodimers are complexes of two different proteins,
while homodimers are complexes of two of the same protein. Binding of
all-trans-RA and 9-cis-RA to RAR and RXR respectively allows
the complex to regulate the rate of gene transcription,
thereby influencing the synthesis
of certain proteins. RXR may also form heterodimers
with thyroid hormone receptors (THR) or vitamin D receptors (VDR). In
this way, vitamin A, thyroid hormone, and vitamin
D may interact to influence gene transcription (3).
Through the stimulation and inhibition of transcription of specific genes,
retinoic acid plays a major role in cellular differentiation,
the specialization of cells for highly specific physiological
roles. Many of the physiological effects attributed to vitamin A appear
to result
from its role in cellular differentiation.
Immunity
Vitamin A is commonly known as the anti-infective vitamin,
because it is required for normal functioning of the immune system (4).
The skin and mucosal cells (cells that line the airways, digestive tract,
and urinary tract) function as a barrier and form the body's first line
of defense against infection. Retinol and its metabolites
are required to maintain the integrity and function of these cells (5).
Vitamin A and retinoic acid (RA) play a central role in the development
and differentiation
of white blood cells, such as lymphocytes, which
play critical roles in the immune response. Activation of T-lymphocytes,
the major regulatory cells of the immune system, appears to require all-trans-RA binding of RAR (3).
Growth and development
Both vitamin A excess and deficiency are known to cause
birth defects. Retinol and retinoic acid (RA) are essential for embryonic
development (4). During fetal development,
RA functions in limb development and formation of the heart, eyes, and
ears (6). Additionally, RA has been found
to regulate expression
of the gene for growth hormone.
Red blood cell production
Red blood cells, like all blood cells, are derived from
precursor cells called stem cells. Stem cells are dependent on
retinoids for normal differentiation
into red blood cells. Additionally, vitamin A appears to facilitate
the mobilization of iron from storage sites to the developing red blood
cell for incorporation into hemoglobin,
the oxygen carrier in red blood cells (2, 7).
Nutrient interactions
Zinc
Zinc
deficiency is thought to interfere with vitamin A metabolism
in several
ways: (1) zinc deficiency results in decreased synthesis of
retinol binding
protein (RBP), which transports retinol through the
circulation to tissues
(e.g., the retina) and also protects the organism against
potential toxicity of retinol; (2) zinc deficiency results in decreased
activity
of the enzyme that releases retinol from its storage form,
retinyl palmitate,
in the liver; and (3) zinc is required for the enzyme that
converts retinol
into retinal (8, 9). At present, the health
consequences of zinc deficiency on vitamin A nutritional status in humans
are unclear (10).
Iron
Vitamin A deficiency may exacerbate iron-deficiency anemia. Vitamin
A supplementation has beneficial effects on iron
deficiency anemia and improves iron nutritional status among children
and pregnant women. The combination of supplemental vitamin A and iron seems to reduce
anemia more effectively than either supplemental iron or vitamin A alone (11). Moreover, studies in rats have shown that iron deficiency alters plasma and liver levels of vitamin A (12, 13).
Vitamin A deficiency and vision
Vitamin A deficiency among children in developing nations
is the leading preventable cause of blindness (14).
The earliest evidence of vitamin A deficiency is impaired dark adaptation
or night blindness. Mild vitamin A deficiency may result in changes
in the conjunctiva (corner of the eye) called Bitot's spots. Severe
or prolonged vitamin A deficiency causes a condition called xerophthalmia
(dry eye), characterized by changes in the cells of the cornea (clear
covering of the eye) that ultimately result in corneal ulcers, scarring,
and blindness (4, 9).
Vitamin A deficiency can be considered a nutritionally
acquired immunodeficiency disease (15).
Even children who are only mildly deficient in vitamin A have a higher
incidence of respiratory disease and diarrhea as well as a higher rate
of mortality from infectious disease compared to children who consume sufficient
vitamin A (16). Vitamin A supplementation has been found to decrease both the severity and incidence of deaths related to diarrhea
and measles in developing countries, where vitamin A deficiency is common
(17). The onset of infection reduces blood retinol levels very rapidly. This
phenomenon is generally believed to be related to decreased synthesis
of retinol binding protein (RBP) by the liver. In this manner, infection
stimulates a vicious cycle, because inadequate vitamin A nutritional
status is related to increased severity and likelihood of death from
infectious disease (18).
However, a recent review of four studies concluded that vitamin A
supplementation is not beneficial in reducing the mother-to-child
transmission of HIV (19). One study found that HIV-infected
women who were vitamin A deficient were three to four times more likely
to transmit HIV to their infants (20).
The RDA for vitamin
A was revised by the Food and Nutrition Board (FNB) of the Institute
of Medicine in 2001. The latest RDA is based on the amount needed to
ensure adequate stores (four months) of vitamin A in the body to support normal reproductive
function, immune function, gene
expression, and vision (21).
The table below lists the RDA values in both micrograms (mcg) of
Retinol Activity Equivalents (RAE) and international units (IU). For
more information on these units, see the section on RAE.
| Recommended Dietary Allowance (RDA) for Vitamin A as Preformed Vitamin A (Retinol Activity Equivalents) | |||
| Life Stage | Age | Males: mcg/day (IU/day) | Females: mcg/day (IU/day) |
| Infants (AI) | 0-6 months | 400 (1,333 IU) | 400 (1,333 IU) |
| Infants (AI) | 7-12 months | 500 (1,667 IU) | 500 (1,667 IU) |
| Children | 1-3 years | 300 (1,000 IU) | 300 (1,000 IU) |
| Children | 4-8 years | 400 (1,333 IU) | 400 (1,333 IU) |
| Children | 9-13 years | 600 (2,000 IU) | 600 (2,000 IU) |
| Adolescents | 14-18 years | 900 (3,000 IU) | 700 (2,333 IU) |
| Adults | 19 years and older | 900 (3,000 IU) | 700 (2,333 IU) |
| Pregnancy | 18 years and younger | - | 750 (2,500 IU) |
| Pregnancy | 19 years and older | - | 770 (2,567 IU) |
| Breast-feeding | 18 years and younger | - | 1,200 (4,000 IU) |
| Breast-feeding | 19 years and older | - | 1,300 (4,333 IU) |
Cancer
Studies in cell culture and animal models have documented
the capacity for natural and synthetic retinoids to reduce carcinogenesis
significantly in skin, breast, liver, colon, prostate, and other sites
(2). However, the results of human studies
examining the relationship between the consumption of preformed vitamin
A and cancer are less clear.
At least ten prospective
studies have compared blood retinol levels at baseline among people
who subsequently developed lung cancer and those who did not. Only one
of those studies found a statistically significant inverse association
between serum retinol and lung cancer risk (22).
The results of the Beta-Carotene And Retinol Efficacy Trial (CARET)
suggest that high-dose supplementation of vitamin A and beta-carotene should
be avoided in people at high risk of lung cancer (23).
About 9,000 people (smokers and people with asbestos exposure) were
assigned a daily regimen of 25,000 IU of retinol and 30 milligrams of
beta-carotene, while a similar number of people were assigned a placebo.
After four years of follow-up, the incidence of lung cancer
was 28% higher
in the supplemented group compared to the placebo group. A
possible explanation for such a finding is that the oxidative
environment of the lung, created by smoke or asbestos exposure, gives
rise to unusual carotenoid cleavage products, which are involved in
carcinogenesis. Presently, it seems unlikely that increased
retinol intake decreases the risk of lung cancer, although the
effects
of retinol may be different for nonsmokers than for smokers (22).
Retinol and its metabolites
have been found to reduce the growth of breast cancer cells in vitro, but observational studies of dietary retinol intake in humans
have not confirmed this in vivo (24). The majority
of epidemiological
studies have failed to find significant associations between retinol
intake and breast cancer risk in women (25-28),
although one large prospective study found that total vitamin A
intake was inversely associated with the risk of breast cancer in
premenopausal
women with a family history of breast cancer (29).
Blood levels of retinol reflect the intake of both preformed vitamin
A and provitamin A carotenoids like beta-carotene. Although a case-control
study found serum retinol levels and serum antioxidant levels to be
inversely related to the risk of breast cancer (30),
two prospective studies did not observe significant associations
between blood retinol levels and subsequent risk of developing breast
cancer (31, 32). Presently, there is
little evidence in humans that increased intake of preformed vitamin
A or retinol reduces breast cancer risk.
Pharmacologic doses of retinoids (see also Upper Level)
Retinoids are used at pharmacologic doses to
treat several conditions, including retinitis pigmentosa, acute
promyelocytic leukemia, and various skin diseases. It is important to
note that treatment with high doses
of natural or synthetic retinoids overrides the body's own
control mechanisms; therefore, retinoid therapies are associated with
potential side effects and toxicities. Additionally,
all of the retinoid compounds have been found to cause birth
defects. Thus, women
who have a chance of becoming pregnant should avoid treatment
with these
medications. Retinoids tend to be very long acting: side
effects and
birth defects have been reported to occur months after
discontinuing
retinoid therapy (2). The retinoids discussed
below are prescription drugs and should not be used without medical
supervision.
Retinitis pigmentosa
Retinitis pigmentosa describes a broad spectrum of genetic
disorders that result in the progressive loss of photoreceptor cells
(rods and cones) in the eye's retina
(33). Early symptoms of retinitis pigmentosa
include impaired dark adaptation and night blindness, followed by the
progressive loss of peripheral and central vision over time. The results
of a randomized
controlled trial in more than 600 patients with common forms of
retinitis pigmentosa indicated that supplementation with 4,500 mcg (15,000
IU)/day of preformed vitamin A (retinol) significantly slowed the loss
of retinal function over a period of 4-6 years (34).
In contrast, supplementation with 400 IU/day of vitamin E increased
the loss of retinal function by a small but significant amount, suggesting
that patients with common forms of retinitis pigmentosa may benefit
from long-term vitamin A supplementation but should avoid vitamin E
supplementation at levels higher than those found in a typical multivitamin.
Up to 12 years of follow-up in these patients did not reveal any signs
of liver toxicity as a result of excess vitamin A intake (35).
High-dose vitamin A supplementation to slow the course of retinitis
pigmentosa requires medical supervision and must be discontinued if
there is a possibility of pregnancy (see Safety).
Acute promyelocytic leukemia
Normal differentiation
of myeloid stem cells in the bone marrow gives rise to platelets, red
blood cells, and white blood cells that are important for the immune
response. Altered differentiation of those stem cells results in the
proliferation of immature leukemic cells, giving rise to leukemia. A
mutation of the retinoic acid receptor (RAR) has been discovered in patients
with a specific type of leukemia called acute promyelocytic leukemia (APL).
Treatment with all-trans-retinoic acid or with high doses of all-trans-retinyl palmitate restores normal differentiation and leads to improvement
in some APL patients (2, 18).
Diseases of the skin
Both natural and synthetic retinoids have been used as
pharmacologic agents to treat disorders of the skin. Etretinate and
acitretin are retinoids that have been useful in the treatment of psoriasis,
while tretinoin (Retin-A) and isotretinoin (Accutane) have been used
successfully to treat severe acne. Retinoids most likely affect the
transcription of skin growth factors and their receptors (2). Use of pharmacological doses of retinoids by pregnant women causes birth defects (see Safety in pregnancy).
Different dietary sources
of vitamin A have different potencies. For example, beta-carotene is
less easily absorbed than retinol and must be converted to retinal and
retinol by the body. The most recent international standard of measure
for vitamin A is retinol activity equivalents (RAE), which represent
vitamin A activity as retinol. Two micrograms (mcg) of beta-carotene
in oil provided as a supplement can be converted by the body to 1 mcg
of retinol giving it an RAE ratio of 2:1. However, 12 mcg of beta-carotene
from foods are required to provide the body with 1 mcg of retinol, giving
dietary beta-carotene an RAE ratio of 12:1. Other provitamin A carotenoids
in foods are less easily absorbed than beta-carotene, resulting in RAE
ratios of 24:1. The RAE ratios for beta-carotene and other provitamin
A carotenoids are shown in the table below (21).
An older international standard, still commonly used, is the international
unit (IU). One IU is equivalent to 0.3 mcg of retinol.
| Retinol activity equivalents (RAE) ratios for beta-carotene and other provitamin A carotenoids | ||
| Quantity Consumed | Quantity Bioconverted to Retinol | RAE ratio |
| 1 mcg of dietary or supplemental vitamin A | 1 mcg of retinol* | 1:1 |
| 2 mcg of supplemental beta-carotene | 1 mcg of retinol | 2:1 |
| 12 mcg of dietary beta-carotene | 1 mcg of retinol | 12:1 |
| 24 mcg of dietary alpha-carotene | 1 mcg of retinol | 24:1 |
| 24 mcg of dietary beta-cryptoxanthin | 1 mcg of retinol | 24:1 |
Free retinol is not generally found in foods. Retinyl
palmitate, a precursor and storage form of retinol, is found in foods
from animals. Plants contain carotenoids, some of which are precursors
for vitamin A (e.g., alpha-carotene, beta-carotene, and beta-cryptoxanthin). Yellow and orange
vegetables contain significant quantities of carotenoids. Green vegetables
also contain carotenoids, though the pigment is masked by the green
pigment of chlorophyll (1). A number of good food sources of vitamin
A are listed in the table below along with their vitamin A content in micrograms of
retinol activity equivalents (mcg RAE). In those foods where retinol
activity comes mainly from provitamin A carotenoids, the carotenoid
content and the retinol activity equivalents are presented. You may
use the USDA
food composition database to check foods for their content
of several
different carotenoids, including lycopene, lutein, and
zeaxanthin. The vitamin A IU listings in the USDA database, however, do
not take into account bioavailability of the various carotenoids. To
obtain a more accurate estimate of the number of IUs of vitamin A in
carotenoid-containing foods, multiply the RAE by 3.33.
| Food | Serving | Vitamin A, RAE |
Vitamin A, IU | Retinol, mcg | Retinol, IU |
| Cod liver oil | 1 teaspoon | 1,350 mcg | 4,500 IU | 1,350 mcg | 4,500 IU |
| Fortified breakfast cereals | 1 serving | 150-230 mcg | 500-767 IU | 150-230 mcg | 500-767 IU |
| Egg | 1 large | 91 mcg | 303 IU | 89 mcg | 296 IU |
| Butter | 1 tablespoon | 97 mcg | 323 IU | 95 mcg | 317 IU |
| Whole milk | 1 cup (8 fl oz.) | 68 mcg | 227 IU | 68 mcg | 227 IU |
| 2% fat milk (vitamin A added) | 1 cup (8 fl oz) | 134 mcg | 447 IU | 134 mcg | 447 IU |
| Nonfat milk (vitamin A added) | 1 cup (8 fl oz.) | 149 mcg | 497 IU | 149 mcg | 497 IU |
| Sweet potato, canned | 1/2 cup, mashed | 555 mcg | 1,848 IU | 0 | 0 |
| Sweet potato, baked | 1/2 cup | 961 mcg | 3,203 IU | 0 | 0 |
| Pumpkin, canned | 1/2 cup | 953 mcg | 3,177 IU | 0 | 0 |
| Carrot (raw) | 1/2 cup, chopped | 538 mcg | 1,793 IU | 0 | 0 |
| Cantaloupe | 1/2 medium melon | 467 mcg | 1,555 IU | 0 | 0 |
| Mango | 1 fruit | 79 mcg | 263 IU | 0 | 0 |
| Spinach | 1/2 cup, cooked | 472 mcg | 1,572 IU | 0 | 0 |
| Broccoli | 1/2 cup, cooked | 60 mcg | 200 IU | 0 | 0 |
| Kale | 1/2 cup, cooked | 443 mcg | 1,475 IU | 0 | 0 |
| Collards | 1/2 cup, cooked | 386 mcg | 1,285 IU | 0 | 0 |
| Squash, butternut | 1/2 cup, cooked | 572 mcg | 1,907 IU | 0 | 0 |
Supplements
The principal forms of preformed vitamin A (retinol) in
supplements are retinyl palmitate and retinyl acetate. Beta-carotene
is also a common source of vitamin A in supplements, and many supplements
provide a combination of retinol and beta-carotene (36).
If a percentage of the total vitamin A content of a supplement comes
from beta-carotene, this information is included in the Supplement Facts
label under vitamin A (see example supplement
label). Most multivitamin supplements available in the U.S. provide
1,500 mcg (5,000 IU) of vitamin A, which is substantially more than the current
RDA for vitamin A. This is due to the fact that the
Daily Values (DV) used by the FDA for supplement labeling are based
on the RDA established in 1968 rather than the most recent RDA, and
multivitamin supplements typically provide 100% of the DV for most nutrients.
Because retinol intakes of 5,000 IU/day may be associated
with an increased risk of osteoporosis
in older adults (see Safety), some companies
have reduced the retinol content in their multivitamin supplements to
750 mcg (2,500 IU).
Toxicity
The condition caused by vitamin A toxicity is called
hypervitaminosis A. It is caused by overconsumption of preformed vitamin
A, not carotenoids. Preformed vitamin A is rapidly absorbed and slowly
cleared from the body. Therefore, toxicity from preformed vitamin A may result acutely from high-dose
exposure over a short period of time or chronically from a much lower
intake (2).
Acute vitamin A toxicity is relatively
rare, and symptoms include nausea, headache, fatigue, loss of
appetite,
dizziness, dry skin, desquamation, and cerebral edema. Signs
of chronic toxicity include dry itchy
skin, desquamation, loss of appetite, headache, cerebral
edema, and bone and joint pain. Also, symptoms of vitamin A toxicity in
infants include bulging fontanels.Severe cases
of hypervitaminosis A may result in liver damage, hemorrhage,
and coma. Generally, signs of toxicity are associated with
long-term
consumption of vitamin A in excess of ten times the RDA (8,000
to 10,000
mcg/day or 25,000 to 33,000 IU/day). However, more research is
necessary to determine if subclinical vitamin A toxicity is a concern
in certain populations (37). There is evidence that
some populations may be more susceptible to toxicity at lower doses,
including the elderly, chronic alcohol users, and some people with a
genetic predisposition to high cholesterol (8).
In January 2001, the Food and Nutrition Board (FNB) of the Institute
of Medicine set the tolerable upper intake level (UL)
of vitamin A intake for adults at 3,000 mcg (10,000 IU)/day of preformed
vitamin A (21).
| Tolerable Upper Intake Level (UL) for Preformed Vitamin A (Retinol) | |
| Age Group | UL in mcg/day (IU/day) |
| Infants 0-12 months | 600 (2,000 IU) |
| Children 1-3 years | 600 (2,000 IU) |
| Children 4-8 years | 900 (3,000 IU) |
| Children 9-13 years | 1,700 (5,667 IU) |
| Adolescents 14-18 years | 2,800 (9,333 IU) |
| Adults 19 years and older | 3,000 (10,000 IU) |
Although normal fetal development requires sufficient
vitamin A intake, consumption of excess preformed vitamin A (retinol)
during pregnancy is known to cause birth defects. No increase in the
risk of vitamin A-associated birth defects has been observed at doses
of preformed vitamin A from supplements below 3,000 mcg/day (10,000
IU/day) (21). Since a number of foods
in the U.S. are fortified with preformed vitamin A, pregnant women should
avoid multivitamin or prenatal supplements that contain more than 1,500
mcg (5,000 IU) of vitamin A. Vitamin
A from beta-carotene is not known to increase the risk of birth defects.
Etretinate and isotretinoin (Accutane), synthetic derivatives of retinol,
are known to cause serious birth defects and should not be taken during pregnancy
or if there is a possibility of becoming pregnant (38). Tretinoin (Retin-A),
another retinol derivative, is prescribed as a topical preparation that
is applied to the skin. Because of the potential for systemic absorption
of topical tretinoin, its use during pregnancy is not recommended.
Results of some studies indicate that vitamin A intake is not associated with detrimental effects on bone
mineral density (BMD) or fracture risk (39-41). However, results of some prospective studies suggest
that long-term intakes of preformed vitamin A in excess of 1,500 mcg/day
(5,000 IU/day) are associated with increased risk of osteoporotic
fracture and decreased BMD in older men and women (42-44).
Although this level of intake is greater than the RDA of 700-900 mcg/day
(2,300-3,000 IU/day), it is substantially lower than the UL
of 3,000 mcg/day (10,000 IU/day). Only excess intakes of preformed vitamin
A (retinol), not beta-carotene, were associated with adverse effects
on bone health. Although these observational studies cannot provide
the reason for the association between excess retinol intake and osteoporosis,
limited experimental data suggest that excess retinol may stimulate
bone resorption (45)
or interfere with the ability of vitamin D to maintain calcium balance
(46). In the U.S., retinol intakes in
excess of 5,000 IU/day can be easily attained by those who regularly
consume multivitamin supplements and/or fortified
foods, including some breakfast cereals. At the other end of the spectrum,
a significant number of elderly people have insufficient vitamin A intakes,
which have also been associated with decreased BMD. One study of elderly
men and women found that BMD was optimal at vitamin A intakes close
to the RDA (43). Until
supplements and fortified foods are reformulated to reflect the current
RDA for vitamin A, it makes sense to look for multivitamin supplements
that contain 2,500 IU of vitamin A or multivitamin supplements that
contain 5,000 IU of vitamin A, of which at least 50% comes from beta-carotene
(see example supplement label).
Drug Interactions
Chronic alcohol consumption results in depletion of liver
stores of vitamin A, and may contribute to alcohol-induced liver damage
(47). However, the liver toxicity of
preformed vitamin A (retinol) is enhanced by chronic alcohol consumption,
thus narrowing the therapeutic window for vitamin A supplementation
in alcoholics (48). Oral contraceptives
that contain estrogen and progestin increase retinol binding protein
(RBP) synthesis by the liver, increasing the export of RBP-retinol complex
in the blood. Whether this increases the dietary requirement of vitamin
A is not known. Retinoids or retinoid analogs,
including acitretin, all-trans-retinoic acid, bexarotene, etretinate
and isotretinoin (Accutane), should not be used in combination with
vitamin A supplements, because they may increase the risk of vitamin
A toxicity (36).
The RDA for vitamin A (2,300 IU/day for women
and 3,000
IU/day for men) is sufficient to support normal gene
expression, immune
function, and vision. However, following the Linus Pauling
Institute’s
recommendation to take a multivitamin/mineral supplement daily
could supply as much as 5,000 IU/day of vitamin A as retinol,
the amount
that has been associated with adverse effects on bone health
in older
adults. For this reason, we recommend taking a
multivitamin/multimineral
supplement that provides no more than 2,500 IU (750 mcg) of
preformed vitamin A (usually labeled vitamin A acetate or vitamin A
palmitate) and no more than 2,500 IU of additional vitamin A as
beta-carotene.
High potency vitamin A supplements should not be used without
medical
supervision due to the risk of toxicity.
Older adults (65 years and older)
Presently, there is little evidence that the
requirement
for vitamin A in older adults differs from that of younger
adults. Additionally,
vitamin A toxicity may occur at lower doses in older adults
than in
younger adults. Following the Linus Pauling Institute’s
recommendation
to take a multivitamin/mineral supplement daily could supply
as
much as 5,000 IU/day of retinol, the amount that has been
associated
with adverse effects on bone health in older adults. For this
reason,
we recommend taking a multivitamin/mineral
supplement that provides no more than 2,500 IU (750 mcg) of
preformed vitamin A (usually labeled vitamin A acetate or vitamin A
palmitate) and no more than 2,500 IU of additional vitamin A as
beta-carotene. High potency
vitamin A supplements should not be used without medical
supervision
due to the risk of toxicity.
Written in December 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in November 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in November 2007 by:
Robert M. Russell, M.D., Senior Scientist and Director
Jean Mayer USDA Human Nutrition Research on Aging
Tufts University
Robert M. Russell, M.D., Senior Scientist and Director
Jean Mayer USDA Human Nutrition Research on Aging
Tufts University
Copyright 2000-2012 Linus Pauling Institute
dikutip dari: http://lpi.oregonstate.edu/infocenter/vitamins/vitaminA/
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