Vitamin K
In the early 1900's, research was conducted on the cause of pellagra. A US government investigator, Joseph Goldberger, took his study to a Jackson, Mississippi, orphanage, where many of the children had the disease. The symptoms disappeared when the children were fed high protein diets of meat, beans, and eggs. His conclusion was that pellagra was caused by a protein deficiency. By 1930, researchers had isolated the real cause of pellagra as that of niacin. It is now known that the body can produce the niacin it requires from the amino acid tryptophan, even such when foods as meat, beans, and eggs do not contain significant levels of niacin, thus explaining the reason pellagra improved with a protein diet.
Using chickens, studies in the 1920"s and 30's in Denmark revealed that blood clotting was slow after certain restricted diets. Through further research, it was found that a special fat soluble vitamin was the cause. By 1940, Dr. Henrik Dam had isolated the vitamin and named it Vitamin K for "koagulationsvitamin," the Danish spelling for the vitamin responsible for clotting.
There are three notable forms of Vitamin K, K1 (phytonadione/phylloquinone/phytonactone), K2 (menaquinones), which can be formed by natural bacteria in the intestines, and K3 (menadione), the most active synthetic form of the preparations K3-K7. Absorption of K1 is from the gut (duodenum and jejunum) via the lymphatic system. Conditions that impair lipid absorption will also impair the absorption of Vitamin K, especially antibiotics. In their effort to rid foreign bacteria, antibiotics destroy the normal intestinal flora needed for Vitamin K synthesis, causing a deficiency of the vitamin. Since it is produced in the intestines, it cannot qualify as an official vitamin. Excretion of absorbed Vitamin K occurs mainly in the feces (30-40%), but there is some excreted in the urine (15%) as well.
Vitamin K has a common basic structure that acts as a cofactor for the enzymes essential for normal blood-clotting, namely, in forming the blood clotting chemical "prothrombin" (coagulation factor II). In the liver, Vitamin K plays an important role in the actions of other factors (VII, IX, X), along with proteins C, S, and Z, in addition to its role with prothrombin. Although these proteins are "synthetic," in the absence of K, they become inactive. In the presence of K, prothrombin is converted to thrombin, an active enzyme which, in turn, converts fibrogen to fibrin to form a blood clot.
Vitamin K is most commonly known for its routine use for the newborn. A healthy newborn has low plasma prothrombin levels, but levels in premature infants may be inadequate to prevent hemorrhage. Newborns are customarily given 0.5-1.0 mg. of Vitamin K by injection. Preterm infants are given 1 mg. or more. If needed, the dose is repeated a week later.
Phytonadione (K1) is an analogue of Vitamin K; but it has the quickest onset of action, the most prolonged duration, and is the most potent of all the Vitamin K forms. It is also safer than menadione (K3) to use on newborns. K3 is the only one that could cause toxicity, causing hemolytic anemia. Hemolytic anemia happens when the RBC's die more quickly than the body can reproduce. In addition, it speeds liver damage, producing jaundice, deafness, and severe neurological problems, including retardation in infants. There is no record that the other two forms have produced toxic levels. Care must be taken with IV injections of Vitamin K, since they can cause facial flushing, excessive perspirations, chest tightness, cyanosis, vascular collapse, and shock as well as anaphylaxis.
The drug warfarin (Coumadin) is the most recognized medication that counteracts the effects of Vitamin K. On the other hand, Vitamin K does not reverse overdoses of the injectable anticoagulant, heparin. Those taking warfarin should avoid foods that contain such coumarin derivatives as tonka beans, melilot, sweet clover and sweet woodruff -- which is not a problem for most.
Trauma, physical dehabilitation, kidney failure, and prolonged use of broad spectrum antibiotics often cause a Vitamin K deficiency. Malabsorption syndromes also contribute deficiency for the same reason. Another reason for a Vitamin K deficiency is the excess intake of fat soluble vitamins (A, D, and E).
Breastfed infants, especially those delivered at home, may be especially prone to Vitamin K deficiency. An intake of 5 mcg., in the form of phylloquinone or menaquinone, per day is recommended for the first six months of life, and 10 mcg. during the second six months. Breast milk is considered the poorest source of Vitamin K. The recommended amount in infant formulas is 4 mcg. of Vitamin K/100 kcal. Vitamin K sometimes appears on baby food and formula labels as the additive "phytonadione."
Vitamin K proteins that depend on Vitamin K are found in bone, kidney, and other tissues and is known to play a significant role in the calcification of bone. It promotes proper blood clotting after cuts, scrapes, or surgeries, preventing internal bleeding and hemorrhaging.
The best sources, outside of supplements, are found in green, leafy vegetables; in some legumes; and in some oils. However, many oils lose much of their vitamin content through processing. Most of the Vitamin K is found in the outer leaves of the leafy vegetables, with lower amounts on the inside; but climate and soil conditions affect its content in foods. The RDA is 1 mcg. per kg. of body weight per day for older children and adults, with 300-500 mcg. considered to be an adequate supply and, certainly, no more than 500 mcg. of synthetic Vitamin K is ever recommended. It is not usually included in a multivitamin, as there is an abundance occurring naturally.
Summary:
Vitamin K Complex:
Names include: Vitamin K, antihemorrhagic factor/vitamin.
Forms include: Vitamin K1/vitamin K1(20)/phytonadione, Vitamin K2, Vitamin K2(0), Vitamin K2(5), Vitamin K2(10), Vitamin K2(15), Vitamin K2(20), Vitamin K2 (25), Vitamin K2(30), Vitamin K2(35), Vitamin K2(40), Vitamin K2(45), Vitamin K2(50), menaquinone, Vitamin K3/menodoine/menaphthone, Vitamin K4/menadiol, Vitamin K5, Vitamin K6, Vitamin K7, Vitamin K8, Vitamin K9, Vitamin K9(H), Vitamin K-S(II), Vitamin MK, Vitamin MK2, Vitamin MK3, Vitamin MK4, Vitamin MK5, Vitamin MK6, Vitamin MK7, Vitamin MK8, Vitamin MK9, Vitamin MK10.
Deficiency symptoms include: decreased clotting, nosebleeds, increased blood pressure, hemorrages, diarrhea.
Toxicity symptoms include: These are noted in the following ONLY: K3, K4, K5, K6, K7, K8, K9, K9(H), K-S(II): flushing, sweating, chest constrictions, severe neural symptoms, increased bilirubin in blood, red blood cell breakdown, anemia, yellowing of skin.
Inhibitors include: anticoagulants, x-rays, radiation, frozen foods, aspirin and substitutes, air pollution, mineral oil, antibiotics, neomycin, sweating, food processing, frozen foods, laxatives.
Helpers include: Vitamin H3 and intestinal bacteria.
Note: Counteracts the blood thinner, Dicumarol.
Vitamin K1 is a specific form of Vitamin K. Other names include: K-Ject, Konakion, Mephyton, Mono-Kay. Its forms are: Vitamin K1/ phytonadione, Vitamin K1 oxide, Vitamin K1(20), Naphthalendione.
Vitamin K2 is a specific form of Vitamin K. Its forms are: menaquinone/vitamins K2(0), K2(5), K2(10), K2(15), K2(20), K2(25), K2(3), K2(35), K2(40), K2(45), K245(H), K2(50), K2(55), K2(60), K2(65).
Vitamin K3 is a specific form of Vitamin K. Its form is menodoine/menaphthone.
Vitamin K3H2 is a specific form of Vitamin K3, but it does not have all the properties of Vitamin K. Its form is naphthalenediol.
Vitamin K4 is a specific form of Vitamin K. Its forms are: mendiol diacetate, menadiol dibutyrate, menadiol diphosphate (tetrasodium salt), menadiol disulfate.
