WATER AND FAT SOLUBLE VITAMINS

WATER AND FAT SOLUBLE VITAMINS

 

Vitamins are nutrients required in tiny amounts for essential metabolic reactions in the body.

The term vitamin does not include other essential nutrients such as dietary minerals, essential fatty acids, or essential amino acids, nor does it encompass the large number of other nutrients that promote health but that are not essential for life.

 

 

Vitamins are bio-molecules that act both as catalysts and substrates in chemical reactions. When acting as a catalyst, vitamins are bound to enzymes and are called cofactors.

(For example, vitamin K forms part of the proteases involved in blood clotting.)

Vitamins also act as coenzymes to carry chemical groups between enzymes. (For example, folic acid carries various forms of carbon groups–methyl, formyl or methylene–in the cell.)/

Until the 1900s, vitamins were obtained solely through food intake. Many food sources contain different ratios of vitamins. Therefore, if the only source of vitamins is food, changes in diet will alter the types and amounts of vitamins ingested. However, as many vitamins can be stored by the body, short-term deficiencies (which, for example, could occur during a particular growing season) do not usually cause disease.

Vitamins have been produced as commodity chemicals and made widely available as inexpensive pills for several decades, allowing supplementation of the dietary intake.

 

 

WATER SOLUBLE VITAMINS

 

 

Difference from water soluble vitamins

Water soluble vitamins are included into coenzymes, don’t have provitamins, are not included into the membranes, and hypervitaminoses are not peculiar for them.

With exception of vitamin B₆ and B₁₂, they are readily excreted in urine without appreciable storage, so frequent consumption becomes necessary. They are generally nontoxic when present in excess of needs, although symptoms may be reported in people taking megadoses of niacin, vitamin C, or pyridoxine (vitamin B₆). All the B vitamins function as coenzymes or cofactors, assisting in the activity of important enzymes and allowing energy-producing reactions to proceed normally. As a result, any lack of water-soluble vitamins mostly affects growing or rapidly metabolizing tissues such as skin, blood, the digestive tract, and the nervous system. Water-soluble vitamins are easily lost with overcooking.

 

 

 

Thiamin (Vitamin B₁)

 

Role in human metabolic processes

Thiamine functions as the coenzyme thiamine pyrophosphate (TPP) in the metabolism of carbohydrates and branched-chain amino acids. Specifically the Mg2+-coordinated TPP participates in the formation of a-ketols (e.g. among hexose and pentose phosphates) as catalysed by transketolase and in the oxidation of a-keto acids (e.g. pyruvate, a-ketoglutarate, and branchedchain a-keto acids) by dehydrogenase complexes.

Hence, when there is insufficient thiamine, the overall decrease in carbohydrate metabolism and its interconnection with amino acid metabolism (via a-keto acids) has severe consequences, such as a decrease in the formation of acetylcholine for neural  function.

 

Biochemical indicators

Indicators used to estimate thiamine requirements are urinary excretion, erythrocyte transketolase activity coefficient, erythrocyte thiamine, blood pyruvate and lactate, and neurologic changes. The excretion rate of the vitamin and its metabolites reflects intake, and the validity of the assessment of thiamine nutriture is improved with load test. Erythrocyte transketolase activity coefficient reflects TPP levels and can indicate rare genetic defects. Erythrocyte thiamine is mainly a direct measure of TPP but when combined with high performance liquid chromatography (HPLC) separation can also provide a measure of thiamine and thiamine monophosphate.

Thiamine status has been assessed by measuring urinary thiamine excretion under basal conditions or after thiamine loading; transketolase activity; and free and phosphorylated forms in blood or serum. Although overlap with baseline values for urinary thiamine was found with oral doses below 1mg, a correlation of 0.86 between oral and excreted amounts was found by Bayliss et al.. The erythrocyte transketolase assay, in which an activity coefficient based on a TPP stimulation of the basal level is given, continues to be a main functional indicator, but some problems have been encountered.

Gans and Harper found a wide range of TPP effects when thiamine intakes were adequate (i.e. above 1.5 mg/day over a 3-day period). In some cases, the activity coefficient may appear normal after prolonged deficiency. This measure seemed poorly correlated with dietary intakes estimated for a group of English adolescents. Certainly, there are both interindividual and genetic factors affecting the transketolase. Baines and Davies  suggested that it is useful to determine erythrocyte TPP directly because the coenzyme is less susceptible to factors that influence enzyme activity; there are also methods for determining thiamine and its phosphate esters in whole blood.

 

Thiamin pyrophosphate (TPP)

 

Food Sources for Thiamin.

 

 

 

Sources include peas, pork, liver, and legumes. Most commonly, thiamin is found in whole grains and fortified grain products such as cereal, and enriched products like bread, pasta, rice, and tortillas.

The process of enrichment adds back nutrients that are lost when grains are processed. Among the nutrients added during the enrichment process are thiamin (B1), niacin (B3), riboflavin (B2), folate and iron.

 

 

 

 

 

 

Thiamin functions as the coenzyme thiamin pyrophosphate (TPP) in the metabolism of carbohydrate and in conduction of nerve impulses. Thiamin deficiency causes beri-beri, which is frequently seen in parts of the world where polished (white) rice or unenriched white flour are predominantly eaten.

 

 How much Thiamin.

The Recommended Dietary Allowance (RDA) for thiamin is 1.2 mg/day for adult males and 1.1 mg/day for adult females (Table 1). These values are closely tied to calorie expenditure.

 

Thiamin Deficiency.

Under-consumption of thiamin is rare in the United States due to wide availability of enriched grain products. However, low calorie diets as well as diets high in refined and processed carbohydrates may place one at risk for thiamin deficiency. Alcoholics are especially prone to thiamin deficiency because excess alcohol consumption often replaces food or meals. Symptoms of thiamin deficiency include: mental confusion, muscle weakness, wasting, water retention (edema), impaired growth, and the disease known as beriberi. Thiamin deficiency is currently not a problem in the United States.

 

 

 

There are three basic expressions of beriberi: childhood, wet, and dry. Childhood beriberi stunts growth in infants and children. Wet beriberi is the classic form, with swelling due to fluid retention (edema) in the lower limbs that spreads to the upper body, affecting the heart and leading to heart failure. Dry beriberi affects peripheral nerves, initially causing tingling or burning sensations in the lower limbs and progressing to nerve degeneration, muscle wasting, and weight loss.

Thiamine-deficiency disease in North America commonly occurs in people with heavy alcohol consumption and is called Wernicke-Korsakoff syndrome. It is caused by poor food intake and by decreased absorption and increased excretion caused by alcohol consumption.

 

 

 

 

Too much Thiamin.

No problems with overconsumption are known for thiamin.

 

Riboflavin (Vitamin B₂)

Riboflavin is stable when heated in ordinary cooking, unless the food is exposed to ultraviolet radiation (sunlight). To prevent riboflavin breakdown, riboflavin-rich foods such as milk, milk products, and cereals are packaged in opaque containers. Riboflavin is a component of two coenzymes—flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)—that act as hydrogen carriers when carbohydrates and fats are used to produce energy. It is helpful in maintaining good vision and healthy hair, skin and nails, and it is necessary for normal cell growth.

 

Role in human metabolic processes

 

Conversion of riboflavin to flavin mononucleotide (FMN) and then to the predominant flavin, flavin adenine dinucleotide (FAD), occurs before these flavins form complexes with numerous flavoprotein dehydrogenases and oxidases. The flavocoenzymes (FMN and FASD) participate in oxidation– reduction reactions in metabolic pathways and in energy production via the respiratory chain.

 

Food Sources for Riboflavin.

Sources include liver, eggs, dark green vegetables, legumes, whole and enriched grain products, and milk. Ultraviolet light is known to destroy riboflavin, which is why most milk is packaged in opaque containers instead of clear.

 

 

 

How much Riboflavin.

The Recommended Dietary Allowance (RDA) for riboflavin is 1.3 mg/day for adult males and 1.1 mg/day for adult females. Like thiamin, these values are closely tied to energy expenditure.

 

 

 

Deficiency

Riboflavin (vitamin B2) deficiency results in the condition of hypo- or ariboflavinosis, with sore throat; hyperaemia; oedema of the pharyngeal and oral mucous membranes; cheilosis; angular stomatitis; glossitis; seborrheic dermatitis; and normochromic, normocytic anaemia associated with pure red cell cytoplasia of the bone marrow. As riboflavin deficiency almost invariably occurs in combination with a deficiency of other B-complex vitamins, some of the symptoms (e.g. glossitis and dermatitis) may result from other complicating deficiencies. The major cause of hyporiboflavinosis is inadequate dietary intake as a result of limited food supply, which is sometimes exacerbated by poor food storage or processing. Children in developing countries will commonly demonstrate clinical signs of riboflavin deficiency during periods of the year when gastrointestinal infections are prevalent. Decreased assimilation of riboflavin also results from abnormal digestion, such as that which occurs with lactose intolerance. This condition is highest in African and Asian populations and can lead to a decreased intake of milk, as well as an abnormal absorption of the vitamin. Absorption of riboflavin is also affected in some other conditions, for example, tropical sprue, celiac disease, malignancy and resection of the small bowel, and decreased gastrointestinal passage time. In relatively rare cases, the cause of deficiency is inborn errors in which the genetic defect is in the formation of a flavoprotein (e.g. acyl-coenzyme A [coA] dehydrogenases). Also at risk are infants receiving phototherapy for neonatal jaundice and perhaps those with inadequate thyroid hormone. Some cases of riboflavin deficiency have been observed in Russian schoolchildren (Moscow) and south-east Asian schoolchildren (infected with hookworm).

Riboflavin deficiency causes a condition known as ariboflavinosis, which is marked by cheilosis (cracks at the corners of the mouth), oily scaling of the skin, and a red, sore tongue. In addition, cataracts may occur more frequently with riboflavin deficiency. A deficiency of this nutrient is usually a part of multinutrient deficiency and does not occur in isolation. In North America, it is mostly observed in alcoholics, elderly persons with low income or depression, and people with poor eating habits, particularly those who consume highly refined and fast foods and those who do not consume milk and milk products.

Toxicity

Riboflavin toxicity is not a problem because of limited intestinal absorption.

 

 

Unlike fat-soluble vitamins, water-soluble vitamins are easily lost during cooking and processing. The body does not store excess quantities of most water-soluble vitamins, so foods bearing them must be consumed frequently.

 

Niacin (Vitamin B₃, Nicotinamide, Nicotinic Acid.)

Niacin

 

 

 

Niacin exists in two forms, nicotinic acid and nicotinamide. Both forms are readily absorbed from the stomach and the small intestine. Niacin is stored in small amounts in the liver and transported to tissues, where it is converted to coenzyme forms. Any excess is excreted in urine. Niacin is one of the most stable of the B vitamins. It is resistant to heat and light, and to both acid and alkali environments. The human body is capable of converting the amino acid tryptophan to niacin wheeeded. However, when both tryptophan and niacin are deficient, tryptophan is used for protein synthesis.

 

 

Structure of NAD⁺

There are two coenzyme forms of niacin: nicotinamide adenine dinucleotide (NAD⁺) and nicotinamide adenine dinucleotide phophate (NADP⁺). They both help break down and utilize proteins, fats, and carbohydrates for energy. Niacin is essential for growth and is involved in hormone synthesis.

Pellagra results from a combined deficiency of niacin and tryptophan. Long-term deficiency leads to central nervous system dysfunction manifested as confusion, apathy, disorientation, and eventually coma and death. Pellagra is rarely seen in industrialized countries, where it may be observed in people with rare disorder of tryptophan metabolism (Hartnup’s disease), alcoholics, and those with diseases that affect food intake.

 

 

 

 

 

Food Sources for Niacin.

Sources include liver, fish, poultry, meat, peanuts, whole and enriched grain products.

How much Niacin.

The Recommended Dietary Allowance (RDA) for niacin is 16 mg/day for adult males and 14 mg/day for adult females. These values are closely tied to energy expenditure.

 

 

 

 

 

 

Niacin Deficiency.

Niacin deficiency is not a problem in the United States. However, it is known to occur with alcoholism, protein malnourishment, low calorie diets, and diets high in refined carbohydrates. Pellagra is the disease state that occurs as a result of severe niacin deficiency. Symptoms include cramps, nausea, mental confusion, and skin problems.

The main problem with the clinical use of niacin for dyslipidemia is the occurrence of skin flushing, even with moderate doses.

 

 

The skin features of pellagra (niacin deficiency) include desquamation, erythema, scaling, and keratosis of sun-exposed areas.

 

Recommended intake is expressed as milligrams of niacin equivalents (NE) to account for niacin synthesized from tryptophan. High doses taken orally as nicotinic acid at 1.5 to 2 grams per day can decrease cholesterol and triglyceride levels, and along with diet and exercise can slow or reverse the progression of heart disease.

 

The nicotinamide form of niacin in multivitamin and B-complex tablets do not work for this purpose. Supplementation should be under a physician’s guidance.

 

 

Biotin (Vitamin B₈)

Biotin

 

 

Biotin is a water soluble vitamin and a member of Vitamin B complex.  Also known as Vitamin H, Bios II, Co-enzyme R.  Its natural form is D-biotin.  It was isolated from liver in 1941 by Dr. Paul Gyorgy.

 

Function

·                     co-enzyme in wide variety of body metabolic reactions

·                     needed for production of energy from carbohydrates, fats and proteins

·                     needed for interconversions

·                     essential for maintenance of healthy skin, hair, sweat glands, nerves, bone marrow and glands producing sex hormones

Food source

·                     Brewer’s Yeast

·                     cheese

·                     eggs

·                     maize

·                     fish, fatty, white

·                     meats, especially pig liver and kidney

·                     milk

·                     oats

·                     wheat bran

·                     wheat germ

·                     wholemeal grains

·                     unpolished brown rice

·                     vegetables

·                     yoghurt

 

How much Biotin.

The Adequate Intake (AI) for Biotin is 30 mcg/day for adult males and females

Effective with

Increased intakes needed

·                     by newborn children being fed on dried milk

·                     during stress situations

·                     when on antibiotic therapy

USED FOR

·                     seborrheic dermatitis

·                     Leiner’s Disease

·                     alopecia (hair falling out in handfuls)

·                     scalp disease

·                     skin complaints

·                     preventing cot death (given to babies)

Destroyed by

·                     leaching into cooking

·                     drying of milk for baby foods

Symptoms of deficiency

In babies:

·                     dry scaling of the scalp and face

·                     persistent diarrhea

In adults:

·                     depression

·                     diminished reflexes

·                     fatigue

·                     hair loss

·                     increase in blood cholesterol levels

·                     loss of appetite

·                     muscular pains

·                     nausea

·                     pale, smooth tongue

·                     sleepiness

DEFICIENCY LEADS TO

·                     specific anemia

·                     deficiency may be induced by excessive intake of raw egg whites, which contain the protein Avidin which immobilizes Biotin

SYMPTOMS OF TOXICITY

·                     toxicity unknown

High quality Vitamin B (Biotin) can be purchased from Global Herbal Supplies

 

Biotin is the most stable of B vitamins. It is commonly found in two forms: the free vitamin and the protein-bound coenzyme form called biocytin. Biotin is absorbed in the small intestine, and it requires digestion by enzyme biotinidase, which is present in the small intestine. Biotin is synthesized by bacteria in the large intestine, but its absorption is questionable. Biotincontaining coenzymes participate in key reactions that produce energy from carbohydrate and synthesize fatty acids and protein.

Avidin is a protein in raw egg white, which can bind to the biotin in the stomach and decrease its absorption. Therefore, consumption of raw whites is of concern due to the risk of becoming biotin deficient. Cooking the egg white, however, destroys avidin. Deficiency may develop in infants born with a genetic defect that results in reduced levels of biotinidase. In the past, biotin deficiency was observed in infants fed biotin-deficient formula, so it is now added to infant formulas and other baby foods.

 

Vitamin B₆

 

Pyridoxal, pyridoxamine and pyridoxine are collectively known as vitamin B₆. All three compounds are efficiently converted to the biologically active form of vitamin B₆, pyridoxal phosphate. This conversion is catalyzed by the ATP requiring enzyme, pyridoxal kinase.

 

Vitamin B₆ is present in three forms: pyridoxal, pyridoxine, and pyridoxamine. All forms can be converted to the active vitamin-B₆ coenzyme in the body. Pyridoxal phosphate (PLP) is the predominant biologically active form. Vitamin B₆ is not stable in heat or in alkaline conditions, so cooking and food processing reduce its content in food. Both coenzyme and free forms are absorbed in the small intestine and transported to the liver, where they are phosphorylated and released into circulation, bound to albumin for transport to tissues. Vitamin B₆ is stored in the muscle and only excreted in urine when intake is excessive.

 

 

 

PLP participates in amino acid synthesis and the interconversion of some amino acids. It catalyzes a step in the synthesis of hemoglobin, which is needed to transport oxygen in blood. PLP helps maintain blood glucose levels by facilitating the release of glucose from liver and muscle glycogen. It also plays a role in the synthesis of many neurotransmitters important for brain function. This has led some physicians to prescribe megadoses of B₆ to patients with psychological problems such as depression and mood swings, and to some women for premenstrual syndrome (PMS). It is unclear, however, whether this therapy is effective. PLP participates in the conversion of the amino acid tryptophan to niacin and helps avoid niacin deficiency. Pyridoxine affects immune function, as it is essential for the formation of a type of white blood cell.

Populations at risk of vitamin-B₆ deficiency include alcoholics and elderly persons who consume an inadequate diet. Individuals taking medication to treat Parkinson’s disease or tuberculosis may take extra vitamin B₆ with physician supervision. Carpal tunnel syndrome, a nerve disorder of the wrist, has also been treated with large daily doses of B₆. However, data on its effectiveness are conflicting.

Folic Acid, Folate, Folacin (Vitamin B₉)

Folic Acid

 

 

Folacin or folate, as it is usually called, is the form of vitamin B₉ naturally present in foods, whereas folic acid is the synthetic form added to fortified foods and supplements. Both forms are absorbed in the small intestine and stored in the liver. The folic acid form, however, is more efficiently absorbed and available to the body. When consumed in excess of needs, both forms are excreted in urine and easily destroyed by heat, oxidation, and light.

 

Folic acid is a water soluble vitamin and is a member of the Vitamin B complex. Also known as Folacin, pteroyl-L-glutamic acid (PGA), vitamin Bc or vitamin M. Folic acid and its derivatives (mostly the tri and heptaglutamyl peptides) are widespread in nature. It is a specific growth factor for certain micro-organisms.  Found in yeast and liver in 1935.

All forms of this vitamin are readily converted to the coenzyme form called tetrahydrofolate (THFA), which plays a key role in transferring single-carbon methyl units during the synthesis of DNA and RNA, and in interconversions of amino acids. Folate also plays an important role in the synthesis of neurotransmitters. Meeting folate needs can improve mood and mental functions.

 Function

·                     involved in the formation of new cells

·                     involved in the metabolism of ribonucleic acids (RNA) and deoxyribonucleic acids (DNA), essential for protein synthesis, formation of blood and transmission of genetic code

·                     essential during pregnancy to reduce the risk of neural tube defects (birth defects affecting the brain and/or spinal cord)essential for the normal growth and development of the fetus

·                     involved in the biosynthesis of purines, serines and glycine

·                     involved in some functions associated with Vitamin B12

·                     necessary for building resistance to diseases in the thymus gland of new born babies and infants

·                     may reduce the risk of cervical dysplasia

·                     necessary for red blood cell production

Food Source

·                     bananas

·                     Brewers’s Yeast

·                     citrus fruits, peeled

·                     eggs

·                     fatty fish

·                     fresh nuts

·                     green leafy vegetables

·                     meats, especially pig liver and kidney

·                     milk

·                     oats

·                     pulses, such as lentils

·                     roasted nuts

·                     soy products, such as tofu

·                     unpolished brown rice

·                     wheat germ

·                     wheat bran

·                     wheat grains

Effective With

·                     B-Complex

·                     B12

·                     Biotin

·                     Pantothenic Acid

·                     Vitamin C

Increased Intakes Needed

·                     by alcohol drinkers

·                     by the elderly

·                     during pregnancy and breastfeeding

·                     if taking contraceptive pill

·                     if taking the drugs, Aspirin, Cholestyramine,  Isethionate, Isoniazid, Methotrexate,  Pentamidime, Phenytoin (may be neutralized), Primidone, Pyrimethamine, Triamterene,Trimethoprim

Used For

·                     malabsorption in geriatric patients

·                     megaloblastic anemia

·                     mental deterioration

·                     psychosis

·                     schizophrenia

Destroyed By

·                     leached into cooking water

·                     processing and cooking of vegetables, fruits and dairy products

·                     unstable to oxygen at high temperatures but protected by Vitamin C

Symptoms of Deficiency

·                     breathlessness

·                     fatigue

·                     irritability

·                     sleeplessness

·                     weakness

Deficiency Leads To

Various conditions relating to childbirth:

·                     abortion

·                     birth defects, such as neural tube defect which causes spina bifida

·                     hemorrhage following birth

·                     premature birth

·                     premature separation of the placenta from the uterus

·                     toxemia

As well as:

·                     megaloblastic anemia (red blood cells are large and uneven with a shortened life span)

·                     mild mental symptoms, such as forgetfulness and confusion

Symptoms of Toxicity

Folic Acid has a low toxicity but occasionally the following symptoms occur:

·                     abdominal distension

·                     flatulence (gas/wind)

·                     irritability

·                     loss of appetite

·                     nausea

·                     over-activity

·                     sleep disturbance

·                     symptoms of fever

·                     temperature rise

Long term high doses may cause Vitamin B12 losses from the body

 

Folate deficiency is one of the most common vitamin deficiencies. Early symptoms are nonspecific and include tiredness, irritability, and loss of appetite. Severe folate deficiency leads to macrocytic anemia, a condition in which cells in the bone marrow cannot divide normally and red blood cells remain in a large immature form called macrocytes. Large immature cells also appear along the length of the gastrointestinal tract, resulting in abdominal pain and diarrhea.

 

Pregnancy is a time of rapid cell multiplication and DNA synthesis, which increases the need for folate. Folate deficiency may lead to neural tube defects such as spina bifida (failure of the spine to close properly during the first month of pregnancy) and anencephaly (closure of the neural tube during fetal development, resulting in part of the cranium not being formed). Seventy percent of these defects could be avoided by adequate folate status before conception, and it is recommended that all women of childbearing age consume at least 400 micrograms (μg) of folic acid each day from fortified foods and supplements.

Other groups at risk of deficiency include elderly persons and persons suffering from alcohol abuse or taking certain prescription drugs.

 

Vitamin B₁₂

Vitamin B₁₂ is found in its free-vitamin form, called cyanocobalamin, and in two active coenzyme forms. Absorption of vitamin B₁₂ requires the presence of intrinsic factor, a protein synthesized by acid-producing cells of the stomach. The vitamin is absorbed in the terminal portion of the small intestine called the ileum. Most of body’s supply of vitamin B₁₂ is stored in the liver.

 

 

 

What makes Vitamin B12 important for the body?

There are a number of vital body functions that are aided by Vitamin B12. Not only is B12 involved in the metabolism of all the cells in the body, but it also helps to maintain the health of the nervous system. Vitamin B12 is required for synthesis of red blood cells and even for regulation and synthesis of fatty acids. It also helps production of energy and is extremely important for growth and development in children.

 

Food Source

 

Since Vitamin B12 is generally synthesized by bacteria, it is usually found in animal products like fish, egg and meat and certain dairy products as well. B12 is also found in some plant sources like algae and seaweed, but, these are not fit for human consumption and digestion. The good news, however, is that there are fortified foods being developed to meet the dietary needs of vegetarians.

 

 

 

 

Vitamin B12

 

 

Vitamin B₁₂ is defficiently conserved in the body, since most of it is secreted into bile and reabsorbed. This explains the slow development (about two years) of deficiency in people with reduced intake or absorption. Vitamin B₁₂ is stable when heated and slowly loses its activity when exposed to light, oxygen, and acid or alkaline environments.

 

Vitamin B₁₂ coenzymes help recycle folate coenzymes involved in the synthesis of DNA and RNA, and in the normal formation of red blood cells. Vitamin B₁₂ prevents degeneration of the myelin sheaths that cover nerves and help maintaiormal electrical conductivity through the nerves.

 

Vitamin-B₁₂ deficiency results in pernicious anemia, which is caused by a genetic problem in the production of intrinsic factor. When this occurs, folate function is impaired, leading to macrocytic anemia due to interference iormal DNA synthesis. Unlike folate deficiency, the anemia caused by vitamin-B₁₂ deficiency is accompanied by symptoms of nerve degeneration, which if left untreated can result in paralysis and death.

Since vitamin B₁₂ is well conserved in the body, it is difficult to become deficient from dietary factors alone, unless a person is a strict vegan and consumes a diet devoid of eggs and dairy for several years.

 

 

Deficiency is usually observed when B₁₂ absorption is hampered by disease or surgery to the stomach or ileum, damage to gastric mucosa by alcoholism, or prolonged use of anti-ulcer medications that affect secretion of intrinsic factor. Agerelated decrease in stomach-acid production also reduces absorption of B₁₂ in elderly persons. These groups are advised to consume fortified foods or take a supplemental form of vitamin B₁₂.

 

 

Choline

 

For many years, choline was not considered a vitamin because the body makes enough of it to meet its needs in most age groups. However, research now shows that choline production in the body is not enough to cover requirements. Choline is not considered a B vitamin because it does not have a coenzyme function and the amount in the body is much greater than other B vitamins. Choline not only helps maintain the structural integrity of membranes surrounding every cell in the body, but also can play a role ierve signaling, cholesterol transport, and energy metabolism. An “adequate intake” is 550 milligrams per day for men and 425 milligrams per day for women. Choline is widely found in foods, so it is unlikely that a dietary deficiency will occur.

 

Vitamin C (Ascorbic Acid)

Ascorbic Acid

 

In 1746, James Lind, a British physician, conducted the first nutrition experiment on human beings in an effort to find a cure for scurvy.

 

James Lind

 

James Lind (1716 – 1794),a British Royal Navy surgeon who, in 1774, identified that a quality in fruit prevented the disease of scurvy in what was the first recorded controlled experiment

However, it was not until nearly 200 years later that ascorbic acid, or vitamin C, was discovered. Vitamin C participates in many reactions by donating electrons as hydrogen atoms. In a reducing reaction, the electron in the hydrogen atom donated by vitamin C combines with other participating molecules, making vitamin C a reducing agent, essential to the activity of many enzymes. By neutralizing free radicals, vitamin C may reduce the risk of heart disease, certain forms of cancer, and cataracts.

Vitamin C is needed to form and maintain collagen, a fibrous protein that gives strength to connective tissues in skin, cartilage, bones, teeth, and joints. Collagen is also needed for the healing of wounds.

 

 

 When added to meals, vitamin C increases intestinal absorption of iron from plant-based foods. High concentration of vitamin C in white blood cells enables the immune system to function properly by providing protection against oxidative damage from free radicals generated during their action against bacterial, viral, or fungal infections.

 

 

 Vitamin C also recycles oxidized vitamin E for reuse in cells, and it helps folic acid convert to its active form, (THF). Vitamin C helps synthesize carnitine, adrenaline, epinephrine, the neurotransmitter serotonin, the thyroid hormone thyroxine, bile acids, and steroid hormones.

 

 

A deficiency of vitamin C causes widespread connective tissue changes throughout the body. Deficiencies may occur in people who eat few fruits and vegetables, follow restrictive diets, or abuse alcohol and drugs. Smokers also have lower vitamin-C status. Supplementation may be prescribed by physicians to speed the healing of bedsores, skin ulcers, fractures, burns, and after surgery. Research has shown that doses up to 1 gram per day may have small effects on duration and severity of the common cold, but not on the prevention of its occurrence.

 

 

Ascorbic acid

 

Ascorbic acid is required in the diet of only a few vertebrates — man, monkeys, the guinea pig, and certain fishes. Some insects and other invertebrates also require ascorbic acid, but most other higher animals and plants can synthesize ascorbic acid from glucose or other simple precursors. Ascorbic acid is not present in microorganisms, nor does it seem to be required.

Ascorbic acid is a strong reducing agent, readily losing hydrogen atoms to become dehydroascorbic acid, which also has vitamin C activity. However, vitamin activity is lost when the lactone ring of dehydroascorbic acid is hydrolyzed to yield diketogulonic acid.

 

Biological role of ascorbic acid:

 

–         acts as a cofactor in the en­zymatic hydroxylation of proline to hydroxyproline and in other hydroxylation reactions;

–         inhibits the oxidation of hemoglobin;

–         accelerates the oxidation of glucose in pentose phosphate pathway;

–         reduces the disulfide bonds to sulfhydryl bonds;

–         is necessary for hydroxylation of cholesterol;

–         takes part in metabolism of adrenaline;

–         is necessary for the metabolism of mineral elements (Fe, Ca);

– accelerates the synthesis of glycogen in liver.

While at sea in May 1747, Lind provided some crewmembers with two oranges and one lemon per day, in addition to normal rations, while others continued on cider, vinegar or seawater, along with their normal rations. In the history of science this is considered to be the first example of a controlled experiment comparing results on two populations of a factor applied to one group only with all other factors the same.

 

 

In the hypovitaminosis of vitamin C the disease scurvy is developed. Main clinical symptoms of scurvy: delicacy, vertigo, palpitation, tachycardia, pain in the area of heart, dyspnea, petechias, odontorrhagia, dedentition.

Ascorbic acid and products of its decomposition are excreted from the organism via kidneys. Iormal conditions 20-30 mg or 113,5-170,3 mkmol of ascorbic acid is excreted per day with urine.

In animal and plant tissues rather large concentrations of ascorbic acid are present, in comparison with other water-soluble vitamins; e.g., human blood plasma contains about 1 mg of ascorbic acid per 100 ml. Ascorbic acid is especially abundant in citrus fruits, tomatoes, currant, onion, garlic, cabbage, fruits of wild rose, needles of a pine-tree.

 

Sources of vitamin C

 

 

Vitamin C is obtained through the diet by the vast majority of the world’s population. The richest natural sources are fruits and vegetables, and of those, the camu camu fruit and the billygoat plum contain the highest concentration of the vitamin. It is also present  in some cuts of meat, especially liver. Vitamin C as ascorbic acid is the most widely takeutritional supplement and is available in a variety of forms from tablets and drink mixes to pure ascorbic acid crystals in capsules or as plain powder.

 

Plant sources

 

Rose hips are a particularly rich source of vitamin C Citrus fruits (orange, lemon, grapefruit, lime), tomatoes, and potatoes are good common sources of vitamin C. Other foods that are good sources of vitamin C include papaya, broccoli, brussels sprouts, black currants, strawberries, cauliflower, spinach, cantaloupe, kiwifruit, cranberries and red peppers. Ascorbic acid in food is largely destroyed by cooking.

Although the symptoms of scurvy in man can be prevented by as little as 20 mg of ascorbic acid per day, there are evidences that far larger amounts may be required for completely normal physiological function and well-being. Day necessity of vitain C: 50 – 70 mg. But in different diseases, pregnancy, in hard physical and mental work, in growing organism, after operations the day requirement of vitamin C increased.

 

Vitamin P (bioflavonoids)

This is the group of compounds (rutin, hesperedin, katecholamines) supporting the elasticity of capillaries, strengthen their walls and decrease the permeability.

Vitamin P takes part in the oxidative-reduction processes. It oppresses the activity of enzyme hyaluronidase protecting the hyaluronic acid which is necessary for elasticity of vessel walls.

 

Vitamin P or Bioflavonoids Rich  Sources

 

Vitamin P includes a number of substances that are normally found in the same foods as vitamin C. Several hundred bioflavonoids have now been identified from a wide variety of foods, especially citrus fruits, red and blue berries and grapes, onions, garlic and buckwheat. Their absorption into the body may be slow and is sometimes incomplete, but they can be stored in small amounts. A diet rich in fruit and vegetables, especially those that are red, blue or purple in color, can provide as much as one gram a day of these substances.

The bioflavonoids present in many foods appear to have slightly different actions. To make best use of their powerful anti-oxidant potential, eat as many different types as possible. Try drinking juices made from berries and grapes, especially black grapes, instead of tea and coffee. Consider taking some of the less palatable varieties, such as those from grape seeds, pine bark, in the form of food supplements.

The deficiency of vitamin P in organism results in the petechias (dot hemorrhages on skin).

Day necessity of vitamin P is not clear exactly (about 25-50 mg). In some diseases 1-2 g per day of vitamin P is administrated.

 

FAT SOLUBLE VITAMINS

The fat-soluble vitamins, A, D, E, and K, are stored in the body for long periods of time and generally pose a greater risk for toxicity when consumed in excess than water-soluble vitamins. Eating a normal, well-balanced diet will not lead to toxicity in otherwise healthy individuals. However, taking vitamin supplements that contain megadoses of vitamins A, D, E and K may lead to toxicity. The body only needs small amounts of any vitamin.

While diseases caused by a lack of fatsoluble vitamins are rare in the United States, symptoms of mild deficiency can develop without adequate amounts of vitamins in the diet. Additionally, some health problems may decrease the absorption of fat, and in turn, decrease the absorption of vitamins A, D, E and K.

 

 

Vitamin A

Each year about 250,000 children enter a world of permanent darkness.

The cause? Vitamin A deficiency. Extreme vitamin A deficiency is so damaging to corneas that blindness occurs. Although this could be prevented with just a few cents worth of vitamin A per year, there is little money for preventive health measures in areas of the world where food is scarce.

Vitamin A, also called retinol, has many functions in the body. In addition to helping the eyes adjust to light changes, vitamin A plays an important role in bone growth, tooth development, reproduction, cell division, gene expression, and regulation of the immune system. The skin, eyes, and mucous membranes of the mouth, nose, throat and lungs depend on vitamin A to remain moist. Vitamin A is also an important antioxidant that may play a role in the prevention of certain cancers.

 

Function

Vitamin A is a group of compounds that function to maintain skin and mucous membranes throughout the body. Specific activities depending on vitamin A are vision, bone growth, functioning of the immune system, and normal reproduction.

Our eyes depend on visual purple, technically called rhodopsin, to be able to adjust to light variations. Rhodopsin is formed from retinal, a vitamin A substance, and opsin, a protein. Without enough vitamin A, rhodopsin cannot be formed and the retina cannot easily respond to light changes. As a result, night blindness develops. Bone growth involves a process of remodeling that reshapes and enlarges the skeleton. Reshaping requires vitamin A to undo existing bone. Vitamin A maintains integrity of epithelial tissues throughout the body, providing protection against infections and assuring optimum function.

Hormonelike effects of vitamin A appear to be tied to cell synthesis for reproductive purposes.

 

Recommended Intake and Sources

Vitamin A is measured as retinol activity equivalents (RAE). The RDA, based on providing optimum storage of vitamin A in the liver, is 900 meg RAE for men and 700 meg RAE for women.1 RAE incorporates both the preformed, active forms of vitamin A called retinoids (found in animal foods) and the precursor forms of vitamin A called carotenoids (found in plant foods). The carotenoid beta carotene is the primary source of vitamin A from plant foods.

Because vitamin A (a fat-soluble vitamin) is stored in the body, daily doses are not necessary, but they are desirable. Deficiency of other nutrients affects the absorption and use of vitamin A. Nutrients are interdependent, and imbalances of specific nutrients affect the functioning of others.

Natural preformed vitamin A is found only in the fat of animal-related foods; these include whole milk, butter, liver, egg yolks, and fatty fish. Carotenoids are found in deep green, yellow, and orange fruits and vegetables. The best sources include broccoli, cantaloupe, sweet potatoes, carrots, tomatoes, and spinach. High consumption of carotenoids recently has been associated with decreased risk of certain cancers and other chronic diseases (see the Health Debate box, “Antioxidants: From Foods or Pills?”).

When fats are removed from animal-related foods, preformed vitamin A is also lost. To maintain traditional sources of the vitamin, low-fat, skim, and nonfat milks are fortified with vitamin A. Other fortified products include margarine (which often replaces butter, a natural source of vitamin A), and ready-to-eat cereal, a staple food product commonly fortified with many nutrients.

 

Deficiency

Vitamin A deficiency is either primary, caused by lack of dietary intake, or secondary, the result of chronic fat malabsorption. As liver storage becomes depleted, symptoms develop. The effects are closely tied to vitamin A functions. Ocularly, xerophthalmia incorporates a range of symptoms manifested by night blindness progressing to a hard, dry cornea (keratinization) or keratomalacia, resulting in complete blindness. The degeneration of the epithelial tissues protecting the eye itself leads to the effects of xerophthalmia. Compromised epithelial tissues also result in hair follicles developing white hard lumps of keratin (hyperderatosis), respiratory infections, diarrhea, and other GI disturbances. Overall, the immune system is endangered; for children especially, a minor illness or a bout of measles may be deadly. Growth is inhibited because of lack of vitamin A-dependent proteins for bone growth.

In the United States individuals experiencing chronic fat malabsorption are at risk for vitamin A deficiency and deficiencies of other fat-soluble vitamins.

These nutrients are incorporated into their overall medical nutrition therapy plans. Although marginal vitamin A deficiency is possible, overt deficiencies are rare. Deficiency is a health threat in parts of the world where food availability is limited.

 

 

Toxicity

Hypervitaminosis A occurs only from preformed vitamin A from either an acute or chronic intake of supplements. Most food sources of preformed A do not contain high enough levels to ever result in toxicity. The only exceptiooted is polar bear liver and the livers of other large animals. Explorers who feasted on polar bear liver developed hypervitaminosis A; in fact, the way we learned about the toxic effects of vitamin A was through their misfortune.10 Apparently, the livers of hibernating animals store an extraordinary quantity of vitamin A to provide sufficient amounts for a long winter without nourishment. When humans consume the preformed vitamin A of these livers, the quantity is toxic.

Toxicity does not occur from the carotenoid precursor in foods. If carotenoids are consumed in excess, either from foods or supplements, the skin takes on an orange hue, which dissipates when carotenoid consumption is reduced.

Immediate symptoms of vitamin A toxicity include blistered skin, weakness, anorexia, vomiting, headache, joint pain, irritability, and enlargement of the spleen and liver; long-term effects include bone abnormalities and liver damage

 

 

Vitamin D

 

With sufficient exposure to ultraviolet light or sunshine, the body can manufacture its own supply of vitamin D. The exposure of skin to ultraviolet light begins the conversion process of the vitamin D precursor 7-dehydrocholesterol (found in our skin) to cholecalciferol, the active form of vitamin D. Because the body can produce vitamin D, it is technically a hormone. However, when vitamin D is supplied by the diet, it is technically a vitamin. Regardless of how it is classified, vitamin D is a substance necessary for a variety of the body’s regulating processes as well as normal development of bones and teeth.

 

 

 

 

Function

Intestinal absorption of calcium and phosphorus depends on the action of vitamin D.

This vitamin also affects bone mineralization and mineral homeostasis by helping to regulate blood calcium levels.

Recommended Intake and Sources

The AI for vitamin D is 5 meg. The DR1 includes new AI recommendations for vitamin D for people ages 51 through 70; the suggested new level jumps from 5 meg (200 International Units [IU]) a day to 10 meg (400 IU). After age 70, the recommended levels jump again to 15 meg (600 IU). These levels reflect that older adults are less efficient at synthesizing vitamin D from sun exposure. If these amounts are not consumed from foods or obtained from sunlight, supplement use may be appropriate. Before beginning supplementation, a dietitian should be consulted; these amounts may already be contained in multivitamin mineral supplements formulated for individuals older than 51 years of age. The UL for vitamin D is 50 meg (2000 IU). The effects of intakes higher than the UL are discussed in the section on toxicity.

Vitamin D is available through body synthesis or from dietary sources.

Cholecalciferol, the active form of vitamin D, can be synthesized. Ultraviolet irradiation from sunlight affects the vitamin D precursor 7-dehydrocholesterol in our skin, and this cholesterol derivative is transformed by the liver and kidneys into cholecalciferol. The amount of vitamin D produced depends on length of exposure to ultraviolet irradiation, atmospheric conditions, and skin pigmentation.

Geographic regions and seasons that are particularly cloudy and rainy diminish the quantity of vitamin D synthesized. Darker skin pigmentation also reduces the effect of radiation on the skin, as does sunscreen and concealing clothing. Aging may lessen the amount of vitamin D to be formed from sunlight exposure.

The few sources of natural preformed vitamin D are the fat of the animalrelated foods of butter, egg yolks, fatty fish, and liver. Milk, although containing fat, is not a good source; it is, however, a good vehicle for vitamin D fortification because it contains calcium and phosphorus, which need vitamin D for absorption.

Because vegans consume no animal foods, they may require supplements or regular sunlight exposure to ensure formation of cholecalciferol. Appropriate guidance should be sought from a primary healthcare provider or dietitian.

 

Deficiency

A deficiency of vitamin D can lead to the disorders of rickets and osteomalacia.

 

 

Windswept deformity

 

 

Knock knee deformity (genu valgum)

 

Because of insufficient mineralization of bone and tooth matrix, rickets in children leads to malformed skeletons, characterized by bowed legs unable to bear body weight, oddly angled rib bones and chests, and abnormal tooth formation. In adults, osteomalacia, or bad bones, is characterized by soft bones that are at risk for fractures.

It has been thought that rickets occur rarely among well-nourished populations.

However, recent reports reveal the risk of rickets has increased among well-fed African American children of families following the dietary and dress customs of the Muslim faith.28 Other instances are documented in Alaska among breastfed African American and Alaska native children between the ages of 11 to 20 months. The increased risk for these children is caused by several factors, including darker pigmentation, use of heavier clothing by children that limits exposure of the skin to vitamin D synthesis, and limited consumption of dietary sources  of fortified vitamin D dairy products by children or women who are breastfeeding infants. Healthcare providers initially misdiagnosed cases of rickets among these children because the disease is more common in instances of famine, neglect, malabsorption, or restricted dietary intakes.

Among older adults who may have a diminished ability to produce vitamin D, osteomalacia may develop when marginal intakes of vitamin D or calcium exist for a number of years. Calcium absorption may also be affected by the aging process and contribute to osteomalacia risk. Older women are more at risk than men because of the effects of repeated pregnancies and lactation on bone density.

Symptoms of osteomalacia include weakness, rheumatic-like pain, and an awkward gait. Because bones are weakened, fractures of the spine, hips, and limbs may occur.

The use of sedatives and tranquilizers as well as anticonvulsant therapy in persons with epilepsy has also been associated with increases in the incidence of rickets and osteomalacia.

Another disorder of the skeleton is osteoporosis. Osteoporosis is a condition in which bone density is reduced and the remaining bone is brittle and breaks easily. Because vitamin D is crucial for absorption of calcium and the mineralization of bone, chronic vitamin D deficiency may be one of the risk factors of this disorder.

Outright deficiency of vitamin D is rare in the United States because milk and related food products are fortified. Deficiency is a concern when a lack of exposure to sunlight occurs as a result of (1) environmental limitations, (2) cultural clothing customs that conceal the body, or (3) the inability of older adults or persons with disabilities to get outdoors or to the store, resulting in malnourishment.

These conditions may require vigilance in the consumption of fortified dietary sources, or supplements may be appropriate.

Toxicity

High intakes of vitamin D can result in hypercalcemia (high blood levels of calcium) and hypercalciuria (high calcium level in urine), which affect kidneys and may cause cardiovascular damage. Toxicity symptoms occur when dietary intake of vitamin D is just above the UL of 50 meg or 2000 IU, making vitamin D the most toxic of vitamins.

 

 

Vitamin E

 

During the 1970s vitamin E supplements were a popular aphrodisiac. Male virility, in particular, was thought to be enhanced by taking extra vitamin E. There was only one problem. Vitamin E increased the libido of male rats, not of humans. Research conducted on rats about the effects of vitamin E noted that male rats were able to reproduce better with additional intake of vitamin E. Although research conducted on rats is often applicable to humans, in this instance the results could not be generalized to humans. However, vitamin E is an essential nutrient performing vital functions; we are still learning more about its role in relation to disease prevention.

 

Function

Vitamin E acts as an antioxidant, protecting polyunsaturated fatty acids and vitamin A in cell membranes from oxidative damage by being oxidized itself. This function is particularly important in protecting the integrity of lung and red blood cell membranes, which are exposed to large amounts of oxygen. Other antioxidative functions of vitamin E are performed as part of a system in conjunction with selenium and ascorbic acid (vitamin C).

 

 

 

Recommended Intake and Sources

 

Vitamin E is the name given to a family of compounds called tocopherols, which are found in plants. Alpha-tocopherol is the most widely occurring form of tocopherol and is also the most active. Vitamin E is measured in terms of alphatocopherol equivalents (a-TE). The RDA for vitamin E is 15 mg a-TE for men and women. (The older unit of measurement, International Units [IU], may still be in use on dietary supplements: one mg a-TE equals 1.49 IU). A positive relationship exists between dietary intake of polyunsaturated fats and vitamin E requirements.

As our dietary intake of polyunsaturated fats increases, we need more vitamin E to protect the integrity of these fats from oxidation.

For vitamin E to function as an antioxidant protecting against heart disease and possible reduced risk of prostate cancer, higher levels—30 to 70 mg a-TE (50 to 100 IU)—are recommended These amounts cannot be consumed through dietary means and suggests the use of supplements. These amounts are most often measured as IU. Although a number of studies support the use of vitamin E in this manner, use of vitamin E at these levels for antioxidant function is not part of the RDA recommendations.

 Some of the studies used levels of 400 to 800 IU. The optimum level is still being studied. Because no UL has been set yet, it is important to check with a primary healthcare provider before supplementing with vitamin E, especially if an individual has hypertension.

Vitamin E may increase the risk of stroke for those with hypertension. It is also contraindicated for individuals taking warfarin (Coumadin) or other medicines that inhibit blood clots because vitamin E may affect the efficacy of the medications.

The best sources of vitamin E are vegetable oils (e.g., corn, soy, safflower, and cottonseed) and margarine. Whole grains, seeds, nuts, wheat germ, and green leafy vegetables also provide adequate amounts of vitamin E. Processing of these foods may decrease the final vitamin E content.

 

Deficiency

A primary deficiency of vitamin E is rare.

Secondary deficiencies occur in premature infants and others who are unable to absorb fat normally. Some chronic fat absorption disorders in which deficiencies may occur are cystic fibrosis, biliary atresia, other disorders of the hepatobiliary system, or liver transport problems. Symptoms of vitamin E deficiency include neurologic disorders resulting from cell damage and anemia caused by hemolysis of red blood cells (hemolytic anemia).

 

Toxicity

There is no evidence of toxicity associated with excessive intake of vitamin E. Intakes of about 70 to 530 mg a-TE (100 to 800 IU) per day appear to be tolerated, but the value of such doses has not been determined. Megadoses of vitamin E can exacerbate the anticoagulant effect of drugs taken to reduce blood clotting; vitamin E supplementation is not recommended in persons who receive anticoagulant therapy, have a coagulation disorder, or have a vitamin К deficiency. A UL of 1000 mg a-TE has been set.

 

Vitamin К

 

Discovered by a Danish scientist, vitamin К was called koagulationsvitamin for its blood clotting properties. Later research revealed that vitamin К is several related compounds with similar functions in the body.

 

Function

 

Vitamin K’s main function is as a cofactor in the synthesis of blood clotting factors, including prothrombin. Protein formation in bone, kidney, and plasma also depends on the actions of vitamin K.

 

 

Recommended Intake and Sources

The AI for vitamin К is 120 meg for men and 90 meg for women. This amount provides for sufficient storage of vitamin К in the liver. Vitamin К actually consists of compounds in different forms in plant and animal tissues. All are converted by the liver to the biologically active form of menaquinone called vitamin K.

Vitamin К is available through dietary sources and can be synthesized by microflora in the jejunum and ileum of the digestive tract. From plants, vitamin К is consumed as phylloquinone; bacterial synthesis produces vitamin К homologues as forms of menaquinones. As noted, phylloquinone and vitamin К homologues are converted to the active form of menaquinone—vitamin К—by the liver.

Vitamin К is still an essential nutrient although bacteria residing in the intestinal tract can synthesize it. The key distinction is that bacteria hosted by the human body produce the vitamin. Additionally, not enough vitamin К is produced by the microflora to ensure adequate levels for total blood clotting needs; dietary intake is still required.

Primary food sources for vitamin К are dark green leafy vegetables. Lesser amounts are found in dairy products, cereals, meats, and fruits.

Deficiency

Deficiency of vitamin К inhibits blood coagulation. Deficiencies may be observed in clinical settings related to malabsorption disorders or medication interactions.

Long-term intensive antibiotic therapy destroys the intestinal microflora that produce vitamin K. As with the other fat-soluble vitamins, any barrier to absorption affects the quantity of fat-soluble vitamin absorbed.

Premature infants and newborns are unable to immediately produce vitamin K; their guts are too sterile, free from the microflora necessary to produce vitamin K. Hospitals in the United States routinely give newborns an intramuscular dose of vitamin К to prevent hemorrhagic disease.

Because vitamin К also has a role in bone metabolism, recent research is considering whether vitamin К has a function in the treatment of osteoporosis.” Although insufficient data exist to support vitamin К as a formal treatment component for osteoporosis, it does highlight the need to regularly consume at least the AI for vitamin K.

Toxicity

Consumption of foods containing vitamin К produces no problems of toxicity.

Certain medications may be affected by vitamin K. The effectiveness of anticoagulant medications such as warfarin (Coumadin) and other blood thinning drugs can be reduced by high intakes of vitamin К whether from foods or supplements.

Clients should be advised to moderate their consumption of foods containing vitamin K. Therapeutic administration of vitamin К in the menadione form has caused reactions ieonates, including hemolytic anemia and hyperbilirubinemia. Phylloquinone administration has been acceptable.

Vitamin К supplements should only be used if advised by a registered dietitian or primary healthcare provider. Because vitamin К has a role in blood clotting, excess amounts may decrease clotting time, thereby increasing the potential risk for stroke.