The Micronutrients of Balanced Meals



The Micronutrients of Balanced Meals


Vitamins, Minerals, and Phytochemicals





INTRODUCTION


As we become more knowledgeable about our vitamin and mineral needs, it is helpful to keep the history of that knowledge in perspective. Initially, food was recognized as the important element in health. One of the first major discoveries about the role of vitamins was that the use of lemons/limes offered protection against the dreaded scurvy that plagued ocean voyagers. Before this revelation, sailors often developed this severe vitamin C deficiency, which resulted in internal bleeding and death. The effect of toxic vitamin levels was noted when Arctic explorers died from ingesting polar bear liver, which has a high level of vitamin A.


It was not until the twentieth century that vitamins were chemically identified. Vitamins are now known to be organic substances that are genetically produced by plants, and many are also found in animal products. One retired scientist recalled being one of the first people asked to put vitamin C into pill form during the 1920s. He and his colleagues laughed at the foolishness of this idea at the time. We may no longer laugh about the importance of vitamins, but we cannot expect that all has been learned in one lifetime about the complexity of the body’s need for vitamins.


Minerals, the seeming equivalent of vitamins in the consumer’s eye, are inorganic substances that have some similarities to vitamins but also have many differences. The most notable difference is that minerals are elemental, which means that they do not break down. This characteristic of minerals prevents their destruction by heat and air—destruction to which vitamins are susceptible. All minerals are elements found in the chemical periodic table. In the saying “Ashes to ashes, dust to dust,” the ashes are the minerals found in the body.


Vitamins and minerals become available to body cells from foods we eat after the processes of digestion and absorption. Vitamins and minerals are integral to the function of metabolic enzymes at the cellular level for basic life processes (see Chapter 4).


Food is the ideal medium for intake of vitamins and minerals. For example, it has been found that individuals consuming salads and other raw vegetables tend to have improved serum levels of vitamin E and the water-soluble vitamins C and folic acid along with a form of vitamin A called carotenoid (Su and Arab, 2006). Nuts are another source of many nutrients needed by the body and have been noted to improve health status. They contain a variety of compounds that can lower risk of heart disease: phytosterols that interfere with intestinal cholesterol absorption, healthy fats and fiber that lower the body’s production of cholesterol, folate that lowers homocysteine levels (see Chapter 7), and magnesium and potassium with naturally low levels of sodium related to lowered blood pressure (see Dietary Approaches to Stop Hypertension [DASH] diet, Chapter 7). These nutrients and other trace minerals found in nuts contribute to healthy bones and lower insulin resistance and the risk of diabetes (see Chapter 5). Nuts are also a good source of protein, and are vital to a healthy vegetarian diet. No vitamin and mineral supplement can include all of the healthy nutrients found in nuts and other unprocessed foods.


A variety of foods best allows inclusion of all known nutrients for health. Plant-based foods are also a source of phytochemicals (substances in foods that are beneficial to health but are not vitamins or minerals). It is believed there are at least 100 phytochemicals yet to be identified in food. Low-processed foods in balanced meals with an emphasis on variety will likely meet all known requirements of the many nutrients needed for health. Inadequate intake of calcium and vitamin D from limited intake of milk is common. However, persons needing or electing to take additional amounts of vitamins and minerals through supplements need to do so with caution for two main reasons. One is the concern of excess or unintentionally inadequate intake of vitamins and minerals. Excess intake can easily occur with calcium from supplements. Health providers who recommend calcium supplementation need to first assess dietary intake. This is especially true if other sources of calcium are included in a person’s intake, such as with calcium-based antacids and calcium-fortified foods. Along this line, a person taking a multivitamin and mineral supplement may be under the illusion that good nutritional intake from foods is not important. For example, the magnesium and calcium content of common multivitamin preparations do not meet the Dietary Reference Intake (DRI) for these minerals. Actually, there are a variety of minerals that will not be found at 100% of the DRI in basic multivitamin-mineral supplements. This is due, in part, to the fact that minerals are bulky and cannot all fit into a pill that can be swallowed easily.


The other major concern with vitamin and mineral supplementation is the concern of potency and truth in advertising. Since the Dietary Supplement Health and Education Act of 1995 (DSHEA—pronounced D-shay) dietary supplements have been distinguished from drugs or food additives and have minimal regulation on quality. Vitamin and mineral supplements are not legally bound to provide the stated amounts listed on the labels unless a statement of potency guarantee is made (see later section). Furthermore, it is potentially very easy to take toxic doses from supplements, which is virtually impossible from food. An excess of one vitamin or mineral can compete with another; for example, zinc competes with copper, and vitamin E can inhibit the activity of vitamin K.


When vitamin and mineral supplements are used, they should usually be within 100% to 200% of the recommended amounts (see the table at the end of this book). Exceptions to these guidelines should be made only with a warranted medical condition and on the advice of a health care provider or registered dietitian. Many health conditions associated with the need for vitamins and minerals are better resolved through food because the human body is extremely complex and the nutrient composition of food best matches this need. Health care professionals are in a unique position to positively influence an individual’s nutrient intake. This chapter is aimed at increasing appreciation for the micronutrients in food that our bodies require.



WHAT ARE THE DIETARY REFERENCE INTAKES?


The U.S. Recommended Dietary Allowances (RDAs) and Canadian Recommended Nutrient Intake (RNIs) have been replaced with the Dietary Reference Intakes (DRIs), the term used collectively to describe four primary measures of recommended dietary intake. The updated DRIs are now used by both the United States and Canada. Nutrient intake amounting to less than the lower end of the range of the DRIs may lead to nutrient deficiency. Intake amounting to more than the upper limit may give rise to toxic effects, especially with trace minerals (Figure 3-1). The DRIs should not be confused with requirements for a specific individual because requirements vary considerably. Problems such as premature birth, inherited metabolic disorders, infections, chronic diseases, and the use of medications may require special dietary modifications. The specific reference values that constitute the DRIs are as follows:




Estimated Average Requirement (EAR): the amount of a nutrient estimated to meet half of healthy individuals’ needs based on life stage and gender.


Recommended Dietary Allowance (RDA): the average daily dietary intake level that meets the nutrient requirement of more than 97% of the healthy population in a particular life stage and gender group.


Adequate Intake (AI): a recommended intake of vitamins and minerals based on observations of nutrient intake by a group of healthy persons that is assumed to be adequate (when an RDA cannot be determined). The AI level is generally between the RDA level and the maximum safe amount.


Tolerable Upper Intake Level (UL): the highest level of daily nutrient intake that is likely to pose no risk of adverse health effects in almost all individuals in the general population. Intakes above the UL are associated with increased risk of adverse reactions. Derived from UL are two newer methods described as the Observed Safe Level (OSL) and Highest Observed Intake (HOI).



HOW ARE VITAMINS AND MINERALS BEST INCLUDED IN THE DIET?


Reliance on nonfortified (see section below) food sources for vitamins and minerals offers little risk of ingesting toxic amounts and provides a good balance of vitamins and minerals. The MyPyramid Food Guidance System (see Chapter 1) is a strategy to plan healthy meals. Although there is debate about how best to portray recommended intake for the majority of the population through MyPyramid, the general goals are still sound. The 2005 Dietary Guidelines were updated to specifically recommend three whole-grain servings or half of the daily grain intake, along with increased quantities of fruits and vegetables to the equivalent of image cups, and a minimum of 3 cups of milk daily; MyPyramid has been altered to better portray these guidelines for food choices.


The B vitamins (especially thiamin and niacin) are naturally found in whole grains and legumes. These foods also provide a wide array of minerals such as chromium and zinc. Vegetables and fruits supply a variety of vitamins, such as vitamin C, and minerals, such as potassium. The dark green, leafy vegetables are especially high in potassium, magnesium, and vitamins A (in the carotene form) and C, as well as the B vitamin, folate. Deep orange fruits and vegetables such as sweet potatoes, carrots, cantaloupe, and mango are very high in carotene. Citrus fruits (oranges, grapefruits, lemons, and limes) are very high in vitamin C. Milk and milk products are high in calcium and also provide the primary source of riboflavin. The addition of meat or other protein-rich foods further rounds out the nutritional needs, providing B vitamins and many minerals.



WHAT IS THE ROLE OF VITAMINS IN NUTRITION?


The body requires vitamins only in minute amounts, but proper growth and development and optimal health are impossible without them. Some vitamins may be synthesized by the body, but for the most part they must be supplied in the daily diet of normal healthy persons. Early attention was paid to the clear-cut manifestations of diseases caused by vitamin deficiencies (Figure 3-2).



Vitamins, although organic in nature, do not provide energy (kilocalories [kcalories or kcal]) However, they do help in the metabolism of the kcalorie-containing macronutrients: carbohydrate, protein, and fat. In this role, vitamins are thought to act as catalysts.


Vitamins are classified as body regulators because of the following functions:




WHAT IS THE DIFFERENCE BETWEEN FAT-SOLUBLE AND WATER-SOLUBLE VITAMINS?


Generally vitamins are classified into two groups: fat-soluble vitamins (vitamins A, D, E, and K) and water-soluble vitamins (B-complex vitamins and vitamin C). However, there are water-soluble forms of these vitamins that can be supplemented for persons with fat malabsorption, as found with cystic fibrosis, such as vitamin D3 and vitamin K3. The fat-soluble vitamins are stored in body fat and can reach toxic levels. This is why intake of fat-soluble vitamins should not exceed the Upper Limit of Safety (may be found at the back of the book). The one exception to this is vitamin D as currently stated; an updated DRI and Upper Limit of Safety is being reviewed and is expected to be at much higher levels than currently advised in the DRIs. Water-soluble vitamins are generally not stored in any significant amounts in the body, which means that they need to be included in the diet on a daily basis. Fat-soluble vitamins are generally more stable than water-soluble vitamins and are less prone to destruction by heat, air, and light. Deficiencies of fat-soluble vitamins in healthy individuals are less likely to occur than deficiencies of water-soluble vitamins.


The absorption of fat-soluble vitamins is enhanced by dietary fat. Individuals who are afflicted with malabsorption of fat or who consume an extremely small amount of fat are at higher risk for development of fat-soluble vitamin deficiencies. The same applies to use of a weight loss medication, orlistat, that is now available for over-the-counter sale. This medication interferes with the digestion of fat (see Chapter 4) and has the potential to contribute to deficiency of fat-soluble vitamins (Filippatos and colleagues, 2008).



FAT-SOLUBLE VITAMINS


Vitamin A


Vitamin A can be obtained in two forms. The precursor form is beta-carotene, simply referred to as carotene, which is turned into vitamin A in the liver. Carotene is found in abundance in dark green, leafy vegetables and deep-orange vegetables and fruits (except oranges—there are exceptions to every rule). The color of carotene is orange, which is why those foods high in carotene are of similar color and why a person’s skin can turn orange when these foods are eaten in abundance. This is usually innocuous, and orange skin color fades away once carotene foods are decreased in the diet. There are a variety of carotenoids, including lycopene, lutein, and zeaxanthin (also referred to as phytochemicals; see later section). Colorful fruits and vegetables contain a variety of carotenoids. Egg yolk is a highly bioavailable source of lutein and zeaxanthin.


The other form of vitamin A is the preformed version (retinol and retinyl palmitate as used in food fortification). Preformed vitamin A is found in animal products such as liver; milk fat as in whole milk, cream, and butter; and egg yolks. See Table 3-1 and Figure 3-3 for other specific food sources. Vitamin A is often added to foods in a process called fortification (see section below) and is found in supplements. Vitamin A in the preformed version is able to produce toxicity if ingested in large amounts, especially because it is readily stored in the body for up to 2 years. Some acne creams contain preformed vitamin A, which has been linked with birth defects; caution is advised for use of these creams among women of childbearing years.



Table 3-1


Fat-Soluble Vitamins*






































FUNCTIONS GOOD SOURCES SYMPTOMS OF DEFICIENCY SYMPTOMS OF TOXICITY
Vitamin A (Nomenclature: Preformed—Retinol, Retinal, Retinoic Acid; Precursor—Carotene)


Preformed vitamin A:
100% DRI:




Carotene:
100% DRI:




25% DRI:




Vitamin D (Nomenclature: Ergocalciferol [Vitamin D2], Cholecalciferol [Vitamin D3]; Precursors—Ergosterol [Plants], 7-Dehydrocholesterol [in Skin])


100% DRI:




25% DRI:




Vitamin E (Nomenclature: Tocopherol)


100% DRI:




25% DRI:




Vitamin K (Nomenclature: Menadione [Vitamin K3], Phylloquinone [Vitamin K1])


100% DRI:




25% DRI:



No toxicity known


image


image


DRI, Dietary Reference Intake.


*Amounts of foods listed meet the Dietary Reference Intake for adults ages 31 to 50 (largest amount used as reference) as rounded off to the nearest portion size to meet the DRI.


Data from USDA Composition of Foods, Handbook No. 8 Series, Washington, DC, 1976-1986, Agricultural Research Service, USDA; U.S. Department of Agriculture, Agricultural Research Service: USDA National Nutrient Database for Standard Reference, release 17; Davis J, Sherer K: Applied nutrition and diet therapy for nurses, ed 2, Philadelphia, 1994, Saunders; and Mahan KL, Escott-Stump S: Krause’s food, nutrition, and diet therapy, ed 12, Philadelphia, 2008, Saunders.



Retinol can be found in oil-based or water-based forms (water-miscible), emulsified, and in solid preparations. The non–oil-based forms of retinol are approximately 10 times as toxic as are oil-based preparations. This is due to increased absorption. The safe upper single dose of retinol in oil or liver seems to be approximately 4 to 6 mg/kg body weight. Chronic intake of 2 mg retinol per kilogram in oil-based preparations results in hypervitaminosis A, regardless of age (Myhre and colleagues, 2003). Food fortification with retinyl palmitate can lead to toxic levels of vitamin A in the body, called hypervitaminosis A.


Retinoids (vitamin A and its derivatives) circulate in the body predominantly attached to retinol-binding protein (RBP). This allows transport of retinol from liver stores to body tissues. There are wide variations in carotenoid usage from one person to another due to a variety of factors such as absorption differences from specific foods consumed, certain medicines used, genetic and physiologic factors, and nutritional status. Conversion of provitamin A carotenoids into vitamin A is not 100% efficient, and good protein status is needed (Borel and colleagues, 2005).


Vitamin A is important for healthy epithelial tissue (external skin and internal lining of the respiratory and gastrointestinal [GI] tract). Deficiency of vitamin A has long been known to increase the risk of infection and is associated with night blindness, as well as total blindness in many countries (see Chapter 14). It is now known that a good intake of vitamin A helps with bone growth, a healthy immune system, improved vision, and reproduction. Marginal vitamin A deficiency is common and can result in a form of iron deficiency. Marginal vitamin A intake by a breastfeeding mother can put the nursing offspring at risk for iron deficiency (Kelleher and Lonnerdal, 2005). It is beneficial for individuals with marginal vitamin A status to consume carotene-rich orange and green leafy vegetables with a low-fat diet. It has been shown this can normalize the body pool of vitamin A through increased absorption (Ribaya-Mercado and colleagues, 2007).


Toxicity of vitamin A has been linked with cheilosis (see Figure 3-4), altered lipids, and hypercalcemia (excess calcium in the blood). Although vitamin A deficiency impairs bone growth, hypervitaminosis A causes bones to lose their calcium and can lead to osteoporosis (see Chapter 13). It can also cause severe liver damage (Castaño, Etchart, and Sookoian, 2006). In one situation after ingestion of large doses of vitamin A, the symptoms included muscle soreness, hair loss, nail disorder, and ascites (fluid accumulation in the peritoneal cavity of the abdomen), and with deteriorating health, the person further developed renal insufficiency, encephalopathy (brain degeneration), failure to thrive, and ultimately required liver transplantation (Cheruvattath and colleagues, 2006). Hypervitaminosis A caused hypercalcemia to develop in a toddler who had been treated for autism with massive doses of vitamin A, 100,000 IU daily for 3 months followed by a daily dose of 150,000 IU the 3 following months. His symptoms included vomiting, headache, fever, and skin abnormalities (Kimmoun and colleagues, 2008). Cases of children overdosing on vitamin A via excess intake of chewable vitamins has been reported and found to take months to normalize serum levels (Lam and colleagues, 2006). Treatment of hypervitaminosis A may be helped by use of vitamin E supplementation. This was found in a study of rabbits, with 2 weeks of supplementation effectively lowering the serum vitamin A levels (St Claire, Kennett, and Besch-Williford, 2004).



Persons with cystic fibrosis and impaired pancreatic function are at risk of vitamin A deficiency because of fat malabsorption. However, avoidance of excess vitamin A intake is still important. One study of individuals with cystic fibrosis found that total preformed vitamin A intake exceeded the UL in the majority studied. Despite the fat malabsorption, the serum levels of vitamin A were found to be at levels for potential toxicity (Graham-Maar and colleagues, 2006).


Vitamin A in foods is measured in retinol equivalents (RE) or international units (IU). The use of international units indicates that both preformed vitamin A and carotenoids are measured; this is still a common method used in food composition tables and diet planning. Because the biologic activities of carotenoids and vitamin A are different, however, retinol equivalents began to be used. Simply put, numbers used in the IU system are about three times those expressed in the RE system. The DRI for vitamin A is expressed as micrograms (mcg), with 1 mcg being equal to 3.3 IU.



Vitamin D


With the advent of industrialization in the late nineteenth century and the resulting long hours of working in factories endured by many children, rickets (bowing of the legs caused by body weight on soft leg bones) (Figure 3-5) became common enough that public health measures for its prevention began. The preventive measure used was the practice of giving children cod-liver oil. After vitamin D was chemically isolated in 1935, it was eventually added to milk, which ultimately replaced cod-liver oil as a means of preventing rickets (1 teaspoon of cod-liver oil provides about 100% of the DRI for vitamin D and vitamin A). Milk is an appropriate food to fortify with vitamin D because this vitamin greatly enhances the absorption of calcium, of which milk is one of the best sources. Rickets is again on the upsurge because of reduced intakes of fortified milk, decreased exposure to ultraviolet B sunlight in urban settings, and children increasingly spending their time indoors.



Sunlight contributes to vitamin D levels by starting the conversion of a cholesterol-related vitamin D precursor in the skin to an active form. This conversion varies according to the length and intensity of sun exposure and the color of the skin, with lighter skin color increasing the production of vitamin D. Institutionalized elderly persons are at high risk for vitamin D deficiency because of negligible exposure to the sun and likely will benefit from supplementation. With aging, the ability of the body to produce vitamin D from sunlight exposure becomes impaired, and thus even community-dwelling elder persons require more vitamin D as reflected in a higher DRI after age 70.


Factors that influence vitamin D production in the skin include sunscreen use, skin pigmentation, time of day, season of the year, latitude, and aging. A total of 100 IU of vitamin D raises the blood level of 25-hydroxyvitamin D (25[OH]D) by 1 to 2 nmol/L (Cranney and colleagues, 2007). Thus children and adults who do not receive adequate vitamin D from sun exposure need at least 1000 IU/day vitamin D.


There are different forms of vitamin D, including 1,25-dihydroxyvitamin D3 (1,25[OH][2]D], simply known as vitamin D2, which is generally the form of vitamin D in vitamin supplements. The biomarker for vitamin D stores is the serum level of 25(OH)D, with the minimum goal of 80 nmol/L or 32 ng/mL for optimal health. The evidence now appears strong enough to advise a higher vitamin D intake than the current DRI guidelines (see back of book). Based on a study in Nebraska, it was found that to achieve optimal vitamin D status an expected intake would be almost 2000 IU/day (Lappe and colleagues, 2006). Evidence is growing that a minimum of 800 IU of vitamin D is required to meet goals of optimal vitamin D status.


However, the recognition of increased needs for vitamin D comes at a time when there is concern about the growing number of persons who do not even meet the minimum recommended vitamin D intake because of decreased intake of milk and fish. One microgram of vitamin D equals 40 IU in the diet.


Vitamin D has many physiologic roles beyond those related to bones, including regulating blood pressure and acting as a tumor suppressant. A study using data from the National Health and Nutrition Examination Survey (NHANES) found that although the mean levels of 25(OH)D were above the minimum goal, vitamin D levels were lower in women, persons 60 years of age and older, minorities, and persons with obesity, hypertension, diabetes mellitus, and elevated triglycerides. This was particularly true at the lowest levels of 25(OH)D (Martins and colleagues, 2007). There is evidence from a variety of studies that shows a 50% lower incidence of colon cancer with an intake of 1000 IU/day vitamin D or serum 25(OH)D levels greater than 33 ng/mL (82 nmol/L) and that this level of serum vitamin D is associated with reduced risk for a number of other cancers, including breast, lung, ovarian, prostate, and non-Hodgkin’s lymphoma. There is further evidence that vitamin D reduces the risk of autoimmune diseases, including multiple sclerosis (MS), a disease of the central nervous that is more prevalent in regions farther from the equator, and type 1 diabetes mellitus (see Chapter 8). Olympic skiers have noted a high rate of MS in their sport. Exposure to sunlight during early life or vitamin D supplementation has been related to reduced incidence of this condition. There also appears to be benefit for the primary forms of arthritis, type 2 diabetes mellitus, hypertension, and stroke (Grant, 2006).


Vitamin D deficiency leads to secondary hyperparathyroidism, increased bone turnover, bone loss, and when severe, osteomalacia (softening of the bones). Hypovitaminosis D (a condition of low vitamin D status) is associated with impaired neuromuscular function. All persons with persistent, nonspecific musculoskeletal pain are at high risk for severe hypovitaminosis D (the condition of vitamin D deficiency). Hypovitaminosis D is prevalent even in southern latitudes and should be taken into account in the evaluation of postmenopausal and male osteoporosis (Levis and colleagues, 2005).


Persons with renal (kidney) disease usually require supplementation because of impairment of the final steps of vitamin D synthesis (see Chapter 9). There is an increased risk of vitamin D deficiency in conditions of malabsorption of fat, such as with cystic fibrosis. In one study of this condition, despite a mean intake of 800 IU daily, optimal goals of 25(OH)D were not met (Rovner and colleagues, 2007). Prevalence of vitamin D deficiency in persons treated with medication for epilepsy has been found, especially with use of multiple medications, with indicators of adverse impact on bone health. Routine monitoring of serum 25(OH)D and vitamin D supplementation should be considered for individuals with epilepsy treated with medication (Nettekoven and colleagues, 2008).





Vitamin E


Vitamin E, also known as tocopherol, was initially recognized as essential for reproduction in rats. Vitamin E is transported in triglyceride (TG)-rich lipoproteins (see Chapter 7). One case of type 2 diabetes was found with both high levels of triglycerides and vitamin E (Girona and colleagues, 2008).


Vitamin E acts as an antioxidant (preventing cell damage from oxidation). In relatively recent years, vitamin E was routinely advised at the 400 IU level in medical practices for the goal of reduced cardiovascular disease related to the oxidative damage. However, no evidence was found for this expected protection, and instead there was evidence of increased incidence of disease and mortality. Consequently, vitamin E supplementation is no longer routinely advised. However, a genetic subgroup of persons with diabetes were found to benefit with 400 IU vitamin E supplementation significantly reducing cardiovascular events (Milman and colleagues, 2008).


Vitamin E is still important for overall health, when it comes from food sources in particular. Nuts and vegetable oils are rich in vitamin E and are protective against heart disease (see Chapter 7). A mere image cup of almonds provides 100% of the RDA for vitamin E.


Maternal intake of vitamin E during pregnancy is beneficial for growth and development of the fetus. One study found that infants whose mothers had low plasma alpha-tocopherol concentrations weighed less and had smaller head circumference. Higher levels of both maternal alpha-tocopherol and cord retinol concentrations were associated with improved growth (Masters and colleagues, 2007). There is some evidence that asthma among children may be also related to maternal diet during pregnancy due to inadequate vitamin E intake (Seaton, 2008). One form of vitamin E, gamma-tocopherol, has been shown to be more effective than alpha-tocopherol in reducing systemic inflammation. In a rat study large doses of the gamma form was found to inhibit inflammatory pathways that are related to allergic rhinitis and asthma (Wagner and colleagues, 2008). However, in another rat study large doses of vitamin E were associated with changes in the small intestine and inflammation (Gianello and colleagues, 2007). Thus too little or excess intake of vitamin E appears to be related to inflammation.


Known toxic effects from excess ingestion of vitamin E are limited primarily to premature infants and persons receiving anticoagulant medications such as Coumadin. This is due to potential complications of inadequate clotting of blood.





Vitamin K


Vitamin K is also known as phylloquinone. Recommendations for dietary vitamin K intake have been made on the basis of blood coagulation factors. Vitamin K was first recognized as an antihemorrhagic factor. Because vitamin K is essential for the formation of prothrombin (a clotting factor), defective blood coagulation is the main symptom of vitamin K deficiency. Vitamin K is also involved in other physiologic processes, including vascular function and bone metabolism. There are three forms of dietary vitamin K, known as K1, K2, and K3. Vitamin K is found in dietary sources such as dark green, leafy vegetables (see Table 3-1), and it is also synthesized by bacteria in the jejunum and ileum of the small intestine (see Chapter 4).


Vitamin K has a key function in the synthesis of at least two proteins involved in calcium and bone metabolism. Good vitamin K status has been found to increase bone mass in healthy peripubertal children (van Summeren and colleagues, 2008).


Vitamin K deficiency is most likely to occur in individuals receiving antibiotics over an extended period who are not able to absorb fat and who have a low intake of foods containing vitamin K. Persons receiving antibiotic therapy should be considered for vitamin K supplementation. Persons who take Coumadin to reduce the risk of blood clot formation need a consistent intake of vitamin K to maintain stable prothrombin rates. The combined use of Coumadin and gram-negative antibiotics results in high risk of hemorrhage; such treatment requires monitoring of the individual’s blood coagulation.


Deficiency of vitamin K is common among young infants. This is because of low levels of the vitamin K–synthesizing bacteria in the intestinal tract at birth. A parenteral vitamin K injection is recommended for newborn infants. Infant formulas are now routinely supplemented with this vitamin. Intracranial hemorrhage (ICH) is one outcome of vitamin K deficiency in early infancy. Signs of ICH related to vitamin K deficiency can occur at 1 to 2 months of age. This condition can cause convulsion, vomiting, and irritability with coma, fontanel bulging, and absence of pupil reaction. Infants with ICH are at high risk for developmental delay, epilepsy, blindness, and mortality.


Poor vitamin K status has been associated with a greater risk for hip fracture in older men and women. Oral anticoagulants, such as Coumadin, block the use of vitamin K. The vitamin K in spinach and broccoli (high vitamin K sources) appears to have poor bioavailability with a short-lived effect on blood clotting. Moderate intake is generally tolerated in conjunction with use of Coumadin.



WATER-SOLUBLE VITAMINS


The B vitamins are water-soluble vitamins required as coenzymes for enzymes essential for cell function. They have an essential role in maintaining function of the mitochondria (the furnaces of the cell); mitochondria are compromised by a deficiency of any B vitamin (Depeint and colleagues, 2006). Water-soluble vitamins are required in the diet because they cannot be synthesized by humans. The vitamin B complex refers to all water-soluble vitamins except ascorbic acid, also known as vitamin C (Table 3-2). Thiamin, or vitamin B1, is a water-soluble B complex vitamin that was first discovered in 1910 in the process of exploring how rice bran cured patients of beriberi (a condition involving inflammation of the nerves). Beriberi is classified as “dry” (neurologic) or “wet” (cardiovascular) and may include both forms in the same person.



Table 3-2


Water-Soluble Vitamins*























FUNCTIONS GOOD SOURCES SYMPTOMS OF DEFICIENCY SYMPTOMS OF TOXICITY
Vitamin B1 (Nomenclature: Thiamin)


100% DRI:




25% DRI



Rare with IV thiamin
Vitamin B2 (Nomenclature: Riboflavin)


100% DRI:




25% DRI:



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