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Vitamin A
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The chemical name of vitamin A is retinol [3,
7-dimethyl-9-(2,6,6,
trimethyl-1-cyclohexen-1-yl)-2,4,6,8-natetraen-1-ol]. Retinol is also
found as retynyl (vitamin A) esters such as retinyl acetate and retinyl
palmitate. The major storage site of vitamin A in the body is in the
liver, primarily in the form of retinyl esters.
The best known function of vitamin A is in vision,
where it participates (as the metabolite retinal) in the visual cycle.
However, in the chemical form retinoic acid, vitamin A plays an
important role in control of gene expression. This function maintains
differentiation of epithelial cells such as skin, lung, and intestinal
tissue. Retinoic acid can be formed from retinol in the body, and shows
strong biological activity in some functions but not in vision.
Deficiencies: Night blindness is one
of the early signs of vitamin A deficiency, because of the role of
vitamin A in vision. Bacterial invasion and permanent scarring of the
cornea of the eye (xerophthalmia) is a symptom of more profound
deficiency, but this is due to a different mechanism, the lack of
vitamin A for control of gene expression. Profound vitamin A deficiency
also results in altered appearance and function of skin, lung, and
intestinal tissues. Children are most at risk of vitamin A deficiency
because they have not yet developed adequate vitamin A stores. It has
been estimated that 0.5 million children in the world become blind each
year, 70% of these due to vitamin A deficiency. Over half of these blind
children die from malnutrition and associated illnesses.
Diet recommendations: For adult
human males, the Recommended Dietary Allowance (RDA) is 1000 ug Retinyl
Equivalents (RE)/d; for adult females, 800 ug RE.
Food sources: The RDA can be met by
consuming dietary preformed vitamin A (retinyl esters) from liver, eggs
and fortified foods, and provitamin A carotenoids such as beta-carotene,
which are found in green leafy vegetables as well as in orange and red
fruits and vegetables.
Clinical uses: Synthetic retinoids
such as 13-cis retinoic acid (trade name Accutane, also known as
isotretinoin) are used to treat acne and skin wrinkling. Other
derivatives, such as 4-hydroxyphenylretinamide (4-HPR, Fenretinide), are
used to treat breast cancer. No one should consume vitamin A in
quantities exceeding the RDA without a doctor's advice because of the
dangers of toxicity.
Toxicity: Acute intake of extremely
high doses of vitamin A (>200 mg RE in adult humans) can cause nausea,
vomiting, headache, and increased cerebrospinal pressure. Symptoms are
generally transient. Chronic high intakes (e.g., >10x RDA) can cause
hair loss, bone and muscle pain, headache, liver damage, and increased
blood lipid concentrations. A particular danger in pregnant women is
teratogenesis (birth defects). On the other hand, carotenoids as a
source of vitamin A are not toxic, even with very high intakes.
Recent research: Studies focusing on
the role of retinoic acid isomers in the control of gene expression are
explaining effects of vitamin A in hitherto unexpected metabolic
pathways as well as in established functions. This role of vitamin A in
gene expression undoubtedly explains the anti-cancer and anti-acne
effects of vitamin A, for example. The presence of several nuclear
binding proteins for retinoic acid as well as numerous controls on the
metabolism and plasma transport of vitamin A provide an exquisite system
for controlling the effects of vitamin A.
For further information:
Ross, C. A. (1999) Vitamin A and retinoids. In:
Modern Nutrition in Health and Disease (Shils, M. E., Olson, J. A.,
Shike, M. & Ross, C. A., eds.), 9th ed., pp. 305-328. Williams & Wilkins,
Baltimore, MD.
Sporn, M. B., Roberts, A .B. & Goodman, D.S., eds.
(1994) The Retinoids, 2nd ed. Raven Press, New York, NY.
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Vitamin B-12 (cobalamin), stored in the liver, is a
cofactor for two coenzymes. Methyl-cobalamin catalyzes methyl group
transfer from a folic acid cofactor to form methionine; the
unmethylated folate cofactor then participates in single carbon
reactions for nucleic acid synthesis. Thus some B-12 and folic
deficiency symptoms are similar. The B-12 coenzyme
deoxyadenosylcobalamin catalyzes amino acid and fatty acid breakdown.
Deficiencies: Stages of deficiency
symptoms include Stage I (early deficiency), lower serum holoTC II
(<60 pg/mL); Stage II, lower serum vitamin B-12 (<300 pg/mL) and holoTC II (<40 pg/mL); Stage III, serum B-12 <200 and holoTC II <40 pg/mL,
neutrophil hypersegmentation, elevated serum and urinary methylmalonic
acid and homocysteine; and Stage IV (severest deficiency), also
megaloblastic, macrocytic anemia. Around Stage III (before anemia),
potentially irreversible demyelination of spinal cord, brain, and
optic and peripheral nerves produces peripheral neuropathy progressing
to subacute combined degeneration. Dementia, poor attention span, and
depression may be early symptoms.
The stomach secretes intrinsic factor that binds
B-12 and mediates its absorption at receptor sites in the ileum.
Inadequate intrinsic factor secretion occurs in pernicious anemia, an
autoimmune disease. In the elderly, atrophic gastritis is commonly
associated with B-12 malabsorption and deficiency. Because the
absorbed vitamin is secreted in bile and subsequently reabsorbed,
deficiency symptoms can take 20 years to develop from low intakes, e.g.,
in strict vegetarians. However, in malabsorption, deficiency occurs in
months or a few years because absorption from both the diet and
enterohepatic circulation is impaired.
Diet recommendations: The
Recommended Daily Allowances (RDAs) are (µg/day): 0.3 at age 0-6
months, 0.5 for 6-12 months, 0.7 for 1-3 years, 1.0 for 4-6 years, 1.4
for 7-10 years, 2.0 for adolescents and adults, 2.2 in pregnancy and
2.6 in lactation. Usual intakes are about 4-8 µg/d. Pregnant,
lactating, and long-term strict vegetarians should take supplements
providing the RDA.
Food sources: Vitamin B-12 is
found only in animal products. Excellent sources (>10 µg/100g) include
organ meats and bivalve mollusks such as clams and oysters. Moderate
amounts (1-10 µg/100g) are contained in egg yolks, muscle meats and
poultry, fish, fermented cheeses and dry milk. Milk and milk products
contain <1 µg/100g. There is no human-active form of B-12 in algae
such as nori and spirulina; the forms are all analogues.
Toxicity: No toxic effects have
been reported when up to 100 µg/day are consumed. Intramuscular
injections of 100 µg are usually given once/month to individuals who
cannot absorb the vitamin through their intestine, because of
pernicious anemia or other problems.
Recent research: Vitamin B-12
deficiency may increase the risk of neural tube defects in pregnant
women with a high risk of this condition. Vitamin B-12 deficiency may
be common in developing countries, perhaps due to malabsorption and
low intakes.
For further information:
Herbert, V. (1996) Vitamin B-12. In: Present
Knowledge in Nutrition (Ziegler, E. E. & Filer, L. J., Jr., eds.), 7th
ed., pp. 191-205. International Life Sciences Institute Press,
Washington, DC.
Allen, L. H. & Casterline, J. (1994) Vitamin B-12
deficiency in the elderly: diagnosis and requirements. Am. J. Clin.
Nutr. 60: 12-14.
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Vitamin B6
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The chemical name of vitamin B6
is pyridoxine hydrochloride; 2-methyl-3-hydroxy-4,5-bis (hydroxy-methyl)
pyridine. Other forms of vitamin B6
include pyridoxal, and pyridoxamine. In the body all three of these
compounds can be phosphorylated. About 70-80% of the vitamin B6
in the body is located in muscle bound to glycogen phosphorylase, an
enzyme involved in releasing glucose from glycogen. About 10% is located
in the liver; the remainder is distributed among the other tissues.
B6 is one of the
most versatile enzyme cofactors. It is involved in breaking more types
of chemical bonds than most cofactors. It is listed in Enzyme
Nomenclature as a component of approximately 120 enzymes including at
least one entry in 5 of the 6 major enzyme classes. Pyridoxal phosphate
is a cofactor in the metabolism of amino acids and neurotransmitters and
in the breakdown of glycogen. Pyridoxal phosphate can bind to steroid
hormone receptors and may have a role in regulating steroid hormone
action. Pyridoxal phosphate can be converted to pyridoxamine phosphate
which can also serve as an enzyme cofactor. 4-pyridoxic acid is the
major excretory product.
Deficiencies: Alterations in the
function of the nervous system evidenced by electroencephalography are
among the earliest symptoms of vitamin B-6 deficiency. Severe deficiency
may produce seizures, dermatitis, glossitis, cheilosis, angular
stomatitis and anemia. Frank deficiencies are rare, but subclinical
deficiencies may exist, especially in women and the elderly.
Diet recommendations: Adequate
Intakes (AI) have been set at 0.1 mg/d for infants up to 6 mo. and 0.3
mg/d for 6 mo. to 1 yr. Recommended Dietary Allowances (RDAs) (mg/d) for
children have been set at 0.5 (1-3 yr.), 0.6 (4-8 yr.), and 1.0 (9-13 yr.).
For men the RDAs (mg/d) are 1.3 (14-50 yr.) and 1.7 (51+ yr.). For women
the RDAs (mg/d) are 1.2 (14 - 18 yrs.), 1.3 (19-50 yr.), 1.5 (51+ yr.),
1.9 during pregnancy, and 2.0 during lactation.
Food sources: White meats (poultry,
fish, pork), bananas and whole grains are good sources of vitamin B6.
Clinical uses: Pyridoxine-dependent
seizures and some types of sideroblastic anemias respond to vitamin B6
supplementation. Vitamin B6 in conjunction with folate and vitamin B12
helps to lower plasma homocysteine, a risk factor for heart disease.
Vitamin B6 supplements may be required in conjunction with a number of
drugs which have the side-effect of altering vitamin B6 metabolism.
Increased concentrations of pyridoxal phosphate in plasma are used as
one of the criteria for diagnosing hypophosphatasia. Because vitamin B6
metabolism is altered in a variety of disease states, there have been
suggestions that vitamin B6 supplements may be beneficial in many other
conditions. However, convincing scientific support is not currently
available.
Recent research: Current studies
involve the bioavailability of pyridoxine glycosides, which can account
for a significant fraction of the vitamin B6 in some plant products;
improved methods of assessing vitamin B6 status and requirements; and
alterations in vitamin B6 metabolism in various pathological conditions,
particularly heart disease and homocysteine.
For further information:
Leklem, J. E. (1990) Vitamin B6. In: Handbook of
Vitamins (Machlin, L. J., ed.), 2nd ed., pp. 341 - 392, Marcel Dekker,
New York, NY
Committee on the Scientific Evaluation of Dietary
Reference Intakes, Institute of Medicine (1998) Dietary Reference
Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin
B12, Pantothenic acid, Biotin, and Choline. National Academy Press,
Washington, DC.
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Viatmin C
Vitamin C is also known as ascorbic acid, L-ascorbic
acid, dehydroascorbic acid and the antiscorbutic vitamin. Chemically, it
is called L-xyloascorbic acid and L-threo-hex-2-uronic acidy-lactone.
The very highest concentrations of vitamin C are found in the adrenal
and pituitary glands. High levels are also found in liver, leukocytes,
brain, kidney and pancreas. Most of the vitamin C is found in liver and
skeletal muscle because of their size relative to the rest of the body.
The best characterized function of vitamin C is in
the synthesis of collagen connective tissue protein at the level of
hydroxylation of prolyl and lysyl residues of procollagen. Vitamin C
also plays important roles in the synthesis of neurotransmitters,
steroid hormones, carnitine, conversion of cholesterol to bile acids,
tyrosine degradation and metal ion metabolism. This vitamin also may
enhance iron bioavailability. The role of ascorbic acid as a biological
reducing agent may be linked to its prevention of degenerative diseases,
such as cataracts, certain cancers and cardiovascular diseases.
Deficiencies: Severe ascorbic acid
deficiency results in clinical scurvy which is characterized by swollen,
bleeding gums, loosening of the teeth, capillary hemorrhaging, including
bleeding into joints, tender and painful extremities, poor wound healing,
weakness and fatigue, and psychological disturbances.
Clinical uses: The only established
use of vitamin C is in the prevention and treatment of scurvy. Studies
investigating possible effects on wound healing, blood pressure, colds
and immune function have been epidemiological in nature or have often
employed other antioxidants in addition to ascorbic acid. In most cases,
the results have been unremarkable, conflicting or inconsistent, but
research and interest continue in these areas.
Diet recommendations: The
Recommended Dietary Allowance (RDA) for adults is 60 mg/day in the US,
but may range from 30-75 mg/day in other Western countries. Intakes of
75-95 mg/day are recommended for pregnant and lactating women. The RDA
is 35 mg/day in infants and 40 mg/day in children, ages 1-3 yr. About 10
mg/day is required to prevent scurvy. Increased intake of vitamin C is
recommended for stress situations such as trauma, infection, strenuous
exercise, or elevated environmental temperatures. The requirement in
smokers may be 100 mg/day. Recent kinetic analyses suggest that intakes
of 150-200 mg/day, but below 400 mg/day, obtained from the diet, may
offer the most benefit in normal, healthy individuals.
Food sources: The best food sources
of vitamin C are citrus fruits, berries, melons, tomatoes, potatoes,
green peppers and leafy green vegetables. Vitamin C is sensitive to air,
heat and water, so it can easily be destroyed by prolonged storage,
overcooking and processing of foods.
Toxicity: Megadoses of vitamin C of
1000-2000 mg have commonly been associated with gastrointestinal
disturbances (nausea, abdominal cramps and diarrhea). In general,
megadoses of vitamin C should be avoided in individuals with a history
of renal stones due to oxalate formation or hemochromatosis or other
diseases related to excessive iron accumulation. Excess vitamin C may
predispose premature infants to hemolytic anemia due to the fragility of
their red blood cells. In healthy individuals, it appears that megadoses
of up to 1000 mg/day of vitamin C are well tolerated and not associated
with any consistent adverse effects. Concern of its pro-oxidant
properties is stimulating renewed interest in its potential long-term
toxicity.
Recent research: Work continues to
develop and define a useful functional test for vitamin C status, such
as activities of certain enzymes, white cell viability, or perhaps a
test related to the immune response. Investigations continue into
developing a better understanding of the role of vitamin C beyond
preventing vitamin C deficiency. Some examples are establishing optimal
or pharmacologic uses of the vitamin and discerning its role as an
antioxidant/pro-oxidant in human biology. Clinical studies also continue
to define the role of vitamin C in the prevention and treatment of
cataracts, certain cancers and other human diseases.
For Further Information:
Harris, J. R. (1996) Ascorbic Acid: Biochemistry and
Biomedical Cell Biology. Subcellular Biochemistry, vol. 25, Plenum
Press, NY.
Weber, P., Bendich, A. & Schalch, W. (1995) Vitamin C
and human health. A review of recent data relevant to human requirements.
Internat. J. Vit. Nutr. Res. 66: 19-30.
Rumsey, S. C. & Levine, M. (1998) Absorption,
transport and disposition of ascorbic acid in humans. J. Nutr. Biochem.
9: 116-130
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Vitamin D3
Vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol)
are stored in body fat. The vitamin D precursors produced in yeast and
plants (ergosterol) and animals (7-dehydrocholesterol) are converted to
vitamin D by exposure to ultraviolet light (290-315 nm). Vitamin D (either
vitamin D2 or vitamin D3) is metabolized in the liver to
25-hydroxyvitamin D and then to 1, 25-dihydroxyvitamin D in the kidney.
1, 25-Dihydroxyvitamin D is considered to be the biologically
functioning form of vitamin D. The major functions of vitamin D are to
increase the efficiency of intestinal calcium absorption and to mobilize
calcium stores from bone in order to maintain the serum calcium and
phosphorus concentrations within the normal physiological range.
Deficiencies: In humans, deficiency
symptoms include rickets in children, osteomalacia in adults, muscle
weakness, bony deformities, neuromuscular irritability causing muscle
spasms of the larynx (laryngospasm) and hands (carpopedal spasm),
generalized convulsions and tetany.
Clinical uses: Vitamin D is useful
for preventing and treating vitamin D-deficiency bone diseases (rickets
in children and osteomalacia in adults). 25-Hydroxyvitamin D3 is useful
for treating disorders, such as severe liver failure, in which vitamin D
cannot be metabolized to 25-hydroxyvitamin D. The active form of vitamin
D (1, 25-dihydroxyvitamin D3) and its analogs are useful for treating
metabolic bone disorders due to inborn and acquired disorders in the
metabolism of 1, 25-dihydroxyvitamin D2. These have recently been shown
to also be valuable in treating the skin disease psoriasis.
Diet recommendations: The Institute
of Medicine (IOM) for the National Academy of Sciences issued a report
in August 1997 regarding new dietary guidelines for vitamin D. After
careful review of the literature, the IOM concluded that it was not
possible to determine a recommended dietary allowance (RDA) for vitamin
D from the literature but rather to recommend an adequate intake (AI).
Based on the available literature and assuming some exposure to sunlight,
an AI for ages 0 - 50 years was set at 200 IU (5 mg)/day.
The IOM panel recognized that vitamin D insufficiency and deficiency are
prevalent in adults over the age of 50 years and set the AI for adults
51 - 70 years as 400 IU (10 mg)/day and for
adults > 71 years, 600 IU (15 mg)/day. There
was no compelling data to increase the vitamin D requirement either
during pregnancy or lactation. A Tolerable Upper Limit level for vitamin
D for ages 0 - 12 months was set at a limit of 1,000 IU (25
mg)/day. For older children and adults,
including pregnant and lactating women, the UL was set at 2,000 IU (50
mmg)/day.
Food sources: Good food sources are
milk properly fortified with vitamin D, fatty fish such as salmon and
mackerel, cod liver oil, fish liver oil, some breads and cereals, and
some egg yolks.
Toxicity: Excessive quantities of
vitamin D (in excess of 5,000-10,000 IU/day) can cause hypercalcemia,
hypercalciuria, kidney stones, and soft tissue calcifications.
Recent research: Epidemiological
evidence suggests that there may be a correlation with increased
exposure to sunlight with decreased risk of colon, breast and prostrate
cancer. Whether this is due to increased production of vitamin D in the
skin remains unknown. 1, 25-dihydroxyvitamin D3 is a potent
antiproliferative agent for tumor cells and normal cells that possess a
vitamin D receptor. 1,25-dihydroxyvitamin D3 also has been shown to be
of value in treating osteoporosis, especially in patients who are
calcium deficient.
For further information:
Holick, M. F. (1994) Vitamin D-new horizons for the
21st century. Am. J. Clin. Nutr. 60: 619-630.
DeLuca, H. F. (1988) The vitamin D story: a
collaborative effort of basic science and clinical medicine. FASEB J. 2:
224-236.
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Vitamin E
Vitamin E is an essential fat-soluble vitamin that
includes eight naturally occurring compounds in two classes designated
as tocopherols and tocotrienols. Each of these compounds exhibits
different biological activities. d-a-Tocopherol
has the highest biological activity and is the most widely available
form of vitamin E in food. The other isomers ( beta, delta, gamma), some
of which are more abundant in a typical Western diet, are less
biologically active than d-a-tocopherol. The
commercially available synthetic forms of vitamin E are comprised of
approximately an equal mixture of eight stereoisomeric forms of
a-tocopherol, usually in the esterified form
such as acetate or succinate. For practical purposes, 1 International
Unit (IU) of vitamin E represents 1 mg of the synthetic form, racemic
a-tocopherol acetate, while the natural form of d-a-tocopherol has a
biopotency of vitamin E equal to at least 1.49 IU, if not more. The most
widely accepted biological function of vitamin E is its antioxidant
properties. Vitamin E is the most effective chain-breaking,
lipid-soluble antioxidant in biological membranes, where it contributes
to membrane stability. It protects critical cellular structures against
damage from oxygen free radicals and reactive products of lipid
peroxidation.
Absorption of vitamin E is dependent upon the
digestion and absorption of fat. Free tocopherols are absorbed by a
non-saturable, passive process into the lymphatic circulation along with
fat. About 45% of an ordinary dose is absorbed into the lymph.
Deficiencies: The main signs of
severe deficiency in animals are reproductive failure, nutritional "muscular
dystrophy," hemolytic anemia, and neurological and immunological
abnormalities. The last three processes also have been identified in
humans. However, vitamin E deficiency occurs rarely in humans, having
been reported in only two situations: premature infants with very low
birth weight and patients who fail to absorb fat.
Diet recommendations: The
Recommended Dietary Allowance (RDA) for vitamin E is based primarily on
customary intakes from US food sources. The current RDA for males is 10
mg and 8 mg for females. However, the requirement for vitamin E
increases with higher intakes of polyunsaturated fatty acids (PUFA). The
recommended ratio of E/PUFA is 0.4 mg d-a-tocopherol
per gram of PUFA. In defining the ideal intake, factors to consider are
intake of other antioxidants, age, environmental pollutants, and
physical activity.
Food sources: Vegetables and seed
oils including soybean, safflower, and corn; sunflower seeds; nuts;
whole grains; and wheat germ are the main sources of the tocopherols.
Leafy vegetables also supply an appreciable amount of this nutrient.
However, animal products and most fruits and vegetables are generally
poor sources.
Toxicity: Vitamin E is relatively
safe compared to the fat-soluble vitamins. Few side effects from high
intakes of this vitamin have been reported, even at doses as high as
3200 mg daily. However, high vitamin E supplementation may be
contraindicated when a coagulation defect is present due to vitamin K
deficiency or in individuals receiving anticoagulant drugs.
Recent research: Vitamin E has been
shown to influence signal transduction pathways. This effect, however,
may not be mediated through its antioxidant properties. Evidence from in
vitro studies shows that vitamin E influences expression of adhesion
molecules on endothelial cells and monocyte adhesion to endothelial
cells. Vitamin E supplementation at a dose of 200 IU/day significantly
improved immune response in healthy elderly. High intake (³ 200 IU/ day)
and high serum vitamin E levels have been associated with reduced risk
for coronary heart disease in men and women, reduced risk of prostate
cancer and may slow progression of Alzheimer's disease.
For further information:
Meydani, M. (1995) Vitamin E. Lancet 345: 170-175.
Miller, R. D. & Hayes, K. C. (1982) Vitamin excess
and toxicity. In: Nutritional Toxicology (Hathcock, J. N., ed.) vol. 1,
pp. 81-133. Academic Press, New York, NY.
Meydani, S. N., Meydani, M., Blumberg, J. B., Leka,
L. S., Siber, G., Loszewski, R., Thompson, C., Pedrosa, M. C., Diamond,
R. D. & Stollar, B. D. (1997) Vitamin E supplementation enhances in vivo
immune response in healthy elderly: A dose-response study. JAMA. 277:
1380-1386.
Meydani, S. N., Wu, D., Santos, M. S. & Hayek, M. G.
(1995) Antioxidants and immune response in aged persons: Overview of
present evidence. Am. J. Clin. Nutr.; 62: 1463S-1462S.
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Vitamin K
Vitamin K is a coenzyme for a microsomal enzyme that
catalyzes the posttranslational conversion of specific glutamyl residues
to gamma-carboxyglutamyl (Gla) residues in a small number of proteins.
Several of the Gla-proteins are essential for blood clotting and its
regulation (coagulation factors II, VII, IX, and X; proteins C, S and
Z). Others have a role in the regulation of tissue mineralization (osteocalcin,
matrix Gla protein) and cell proliferation (gas6). Recently, additional
Gla proteins have been identified whose function is not well defined to
date. Phylloquinone (2-Me-3-polyisoprenyl-1,4-naphthoquinone) from
plants and a series of bacterial menaquinones
(2-Me-3-polyisoprenyl-1,4-naphthoquinone) are natural forms of the
vitamin.
Deficiencies: Historically, vitamin
K deficiency has been defined as a disruption of blood clotting due to
diminished Gla content of the vitamin K-dependent coagulation factors.
Infants are at risk for severe cerebral hemorrhage during the first
three to four months after birth, if they do not get enough vitamin K.
The reason for vitamin K deficiency in these children is usually
impaired fat absorption in conjunction with a low vitamin intake from
breastfeeding. (Human milk contains much less vitamin K than infant
formulas). In the US and many other countries newborn infants routinely
receive vitamin K. Bleeding due to the lack of vitamin K is very rare in
older children and adults, presumably, because vitamin K is produced by
intestinal bacteria and a small fraction is absorbed from ileum and
colon. Oral antibiotic treatment, in conjunction with low vitamin K
intake, can induce bleeding. Less than a few days' intake of vitamin K
is stored, most of it in liver and bone; in the absence of dietary or
intestinal vitamin K sources, symptoms appear rapidly.
Suboptimal vitamin K status which is far more common
than outright deficiency may contribute to the progression of
osteoporosis and atherosclerosis; research in these areas is promising
but preliminary. 4-hydroxy coumarins are vitamin K antagonists that
interfere with reactivation of the vitamin and suppress production of
mature Gla-proteins needed for coagulation. Some 4-hydroxy coumarins are
medically important anticoagulants, others are used as rodenticides.
Diet recommendations: The current
Recommended Dietary Allowances (RDAs) for vitamin K (µg/day) are: 5 at
age 0-6 months, 10 for 6-12 months, 15 for 1-3 years, 20 for 4-6 years,
30 for 7-10 years, 45 for 11-14 years, 55 for females 15-18 years, 60
for females 19-24 years, 65 for females 25 years and older, pregnant and
lactating women and males 15-18; 70 for males 19-24 years, and 80 for
males 25 years and older.
Past estimates of vitamin K intake were in the range
of a few hundred µg/day; current data suggest that a range of intake of
75-125 µg of phylloquinone is more accurate. Most Americans obtain
almost no menaquinones with their diet, but intakes may be very
significant for Asians consuming traditional foods. While it is likely
that some vitamin K (menaquinones) from bacterial production in the
lower intestines is absorbed, the amounts appear to be much less than
what is usually available from dietary sources.
Food Sources: Cooked dark green
vegetables, such as spinach, kale and broccoli, can provide more than
one RDA in a single serving. The bioavailability of vitamin K from
different food sources and the effect of food processing is
insufficiently known. A small amount of fat is needed for absorption.
Natto and similar fermented Asian soy foods also are excellent vitamin K
sources. Kiwi, cabbage, liver, soybean, canola and olive oils, including
margarine and mayonnaise made from these oils, contain 20-50 % of
current RDAs per serving.
Toxicity: Large amounts of
phylloquinone or menaquinones can be consumed over extended periods with
no toxic effects. Menadione (2-Me-1,4-naphthoquinone) is currently used
in animal feeds, but not in foods for human consumption, because it
causes hemolytic anemia, hyperbilirubinemia, and kernicterus in infants.
Recent Research: A number of reports
point to a relationship between vitamin K status and skeletal health of
the elderly. Another promising line of investigations concerns the role
of matrix Gla protein and other vitamin K-dependent proteins in the
control of arterial calcification. Definitive evidence is still lacking,
however, that increased vitamin K consumption decreases the incidence or
severity of osteoporosis or other diseases. Several prospective
population studies have been initiated, therefore, to investigate
whether increased vitamin K intakes may slow bone loss.
For Further Information:
Suttie, J. W. (1992) Vitamin K and human nutrition.
J. Am. Diet. Assoc. 92: 585-590.
Kohlmeier, M., Salomon, A., Saupe, J. & Shearer, M.
J. (1996) Transport of vitamin K to bone in humans. J. Nutr. 126:
1192S-1196S.
Booth, S. L., Pennington, J. A. T. & Sadowski, J. A.
(1996) Food sources and dietary intakes of vitamin K-1 (phylloquinone)
in the American diet. J. Am. Diet. Assoc. 96: 149-154.
Booth, S. L. & Suttie, J. W. (1998) Dietary intake
and adequacy of vitamin K. J. Nutr. 128: 785-788.
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