Dietary Reference Intakes based on daTocopherol

Infants (0-12 months) EAR

Children (1-8 years) Boys (9-18 years) Girls (9-18 years) Men (19-50 years) Women (19-50 years) Men (51-70+ years) Women (51-70+ years) Pregnancy Lactation RD A

Children (1-8 years) Boys (9-18 years) Girls (9-19 years) Men (19-50 years) Women (19-50 years) Men (51-70+ years) Women (51-70+ years) Pregnancy Lactation UL Infants

0.6mg/kg Vday

5-6 mglday 9-12 mg/day 9-12 mg/day 12 mglday 12 mg/day 12 mg/day 12 mg/day 12 mglday 16 mglday

6-7 mg/day 11-15 mglday 11-15 mglday 15 mglday 15 mg/day 15 mg/day 15 mglday 15 mglday 19 mg/day

Children

Not established (Do not give supplements; use only food and formula for sources.)

200 mg/day (1-3 years) up to 600 mg/day (9-13 years)

Phytonadione (VitaminK-i; phylloquinone)
Addition cf the geranylgeranyl chait1

Adolescents Adults (19+ years) Pregnancy Lactation

4 Vitamin K Family (38)

800 mg/day 1000 mg/day 800-1000 mg/day 800-1000 mg/day

itamin K was discovered by accident by Dan-¡h scientists who, using a special fat-free diet igned to determine whether chickens syn-;esize cholesterol, observed that the animals iveloped a hemorrhagic condition character-by a prolonged clotting time. The condi-jon could be cured by an organic factor found fresh cabbage, ether extract of alfalfa, pulled fish meal, cereals, or hog livers. It was ed Vitamin K for koagulation vitamin. may be the only vitamin that humans

Figure 8.23. Formation of menoquinone form of vitamin K.

receive in significant amounts from their intestinal bacterial, and there is some question regarding this commonly held assumption. Because of this source, it has been very difficult to establish a recommended daily allowance. An estimated safe intake was established for this vitamin for the first time with the 1989 RDA tables. With the release of the Dietary Reference Intakes, there is an adequate intake, but no RDA.

3.4.1 Chemistry. There are two series for this vitamin (Fig. 8.23). The vitamin K^ series is mostly obtained from green plants, whereas the K2 series is the product of bacteria. The active vitamin is in the K? series. Menadione has sometimes been referred to as vitamin K^

Several steps

Vilamin K2H2

Vitamin K Base

co2-

Figure 8.24. Outline of vitamin K in carboxylation of glutamic acid.

Vitamin K2(20)

Vitamnn K oxide y-Carboxyglutamate

Figure 8.24. Outline of vitamin K in carboxylation of glutamic acid.

The common commercial form is called phy-tonadione in the United States Pharmacopeia and phylloquinone by Chemical Abstracts.

3.4.2 Vitamin K Uptake and Metabolism. Dietary vitamin Kx and the pharmaceutical form, phytonadione or vitamin K1(20) must be converted to the K2 series known as menoquinones. The most common of these is menoquinone-4 or K2(20), This conversion to the K2 series occurs in the liver and possibly the intestinal flora. It involves removing the phytyl chain producing the intermediate men-adione. Menadione sometimes is prescribed when there is impaired uptake of lipids from the intestine. There is little storage reserve in the liver, and a deficiency can result when dietary intake of vitamin K is restricted or absorption is impaired.

Dietary vitamin K and supplements are processed similarly as with the other fat-soluble vitamins. Bile salts are required for emul-sification and formation of mixed micelles. They travel to the liver on chylomicrons along with vitamins A and E.

3.4.3 Vitamin K Biochemistry and Deficiency. Deficiencies of this vitamin lead to serious hemorrhaging. The vitamin is required for formation of proteins that complex calcium. This is done by functioning as a coen-in the y-carboxylation of glutamic acid (Fig. 8.24). Vitamin K2 is reduced to the hy-droquinone. After several steps, a complex oxidation occurs, resulting in the "vitamin K base" that is an integral part of the carboxylation step. In a key step, the vitamin K oxide is reduced to the original vitamin K2. It is this final reduction that is inhibited by the couma-din anticoagulants widely used by patients susceptible to stroke, pulmonary embolism, phlebitis, and coronary thrombosis. This interaction between the coumadin anticoagulants and the regeneration of vitamin K2 is the reason that patients on coumadin must monitor their vitamin K intake both from vitamin supplements and diet. This usually is done by regularly scheduled determinations of prothrombin time.

The carboxylation reaction is required for production of several clotting proteins includ-

ingprothrombin, protein C, protein S, and factors VII, IX, and X. It is also required for y-carboxylation of osteocalcin, an important calcium-binding protein found in the matrix of bone and required for proper deposition of calcium onto bone. This latter finding has led to several studies to determine whether patients prescribed Coumadin anticoagulants are at increased risk for osteoporosis and fractures (39-42). All of these studies indicate that vi-supplementation might be beneficial for the prevention of osteoporosis. If vitamin K helps prevent osteoporosis, then it would appear that patients on anticoagulant therapy would be at increased risk for bone fractures. There is some indication of this, but it is not conclusive. Nevertheless, some calcium supplements have both vitamins D and K added to their formulation.

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