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This document contains Chapters 11 to 12 Chapter 11 Nutrition, Exercise, and Sports Overview In Chapter 11, students will learn about the many benefits of exercise. The characteristics of a sound fitness program are laid out, including mode, duration, frequency, intensity, and progression. The metabolic pathways that supply energy to exercising muscle are explained, including ATP, phosphocreatine, and the breakdown of glucose, fat, and protein. Dietary recommendations for athletes regarding energy and fluid needs, vitamin and mineral requirements, and macronutrient distribution are discussed. Furthermore, guidelines for food and fluid consumption before, during, and after exercise are outlined. In general, athletes are advised to consume a moderate- to high-carbohydrate, low-fat diet with just enough protein to meet requirements. Athletes should be discouraged from using protein or amino acid supplements. Popular ergogenic aids are reviewed. The authors emphasize that a well-planned athletic training regimen with a healthy and varied diet and adequate hydration are the best methods for optimizing athletic performance. Learning Objectives Explain the benefits of physical activity. Design a fitness plan. Discuss the energy sources for muscles and human performance. Describe how the body responds to physical activity. Apply the principles of sports nutrition to create diet plans for athletes. Describe the fluid needs of athletes and how to avoid dehydration and hyponatremia. Describe how the composition of food or fluid consumed before, during, and after exercise training sessions can affect performance. Explain the role of ergogenic aids and describe their effect on athletic performance. Teaching Strategies, Activities, Demonstrations, and Assignments 1. Assign students the Take Action activity, “How Physically Fit Are You?” They should complete the measurements and the interpretations. Use this as a springboard for discussing current fitness levels. 2. Assign students the Take Action activity, “Meeting the Protein Needs of an Athlete: A Case Study.” 3. Have students look at their carbohydrate intake (in grams) from their nutrition assessment they did earlier in the semester. Ask them to list extra foods, high in carbohydrate and low in fat, they would need to eat to increase their intake to 600 grams per day, as a triathlete might eat. Have them list the servings they would choose and the amount of carbohydrate in each serving to ultimately sum to 600 grams. 4. Ask students to record their fluid intake in ounces or cups for one day. They shouldn't include milk. Have them total the amount they consumed in one day. Use this as a springboard for discussing fluid intake for sport. 5. Have students go to grocery stores, sports shops, or nutrition centers and look at commercial sports drink prices. In class, together with students, formulate these homemade sports drinks: A. Drink 1: Use 2 tablespoons sugar, 1/10 teaspoon salt, 1/16 of a teaspoon potassium chloride, to every quart of water. Flavor it with lemon or lime juice. B. Drink 2: Mix 1/2 cup water, 1/2 cup nonfat dry milk powder, 1/4 cup glucose polymer (can purchase in stores specializing in sports merchandise), 3 cups skim milk, 1 teaspoon flavoring for palatability (cherry, vanilla, or chocolate extract) Purchase a commercial sports drink or two and allow each student to taste and compare homemade and commercial sports drinks. Discuss the cost: benefit of purchasing versus making sports drink. Use this activity as a springboard to discuss fluid intake for athletes. 6. Have students write research papers on the relationship between proposed ergogenic aids and performance. Students can work in groups or individually. Have each student or group choose one substance to research. Table 11-11 can be used as a guide. Have students present their findings to the class. 7. Ask students to calculate 2% of their body weight. They should also weigh themselves before and after a period of exercise. Have them calculate how much fluid they should have to prevent losing more than 2% of their body weight. 8. Have students design a nutritious meal plan for a pre-game and post-game event as well as suggestions on food and fluid intake during an event. Lecture Outline Benefits of Fitness Summary of benefits Reduces blood pressure Increases cardiovascular function and improves blood lipid profile Increases flexibility and balance Improves sleep Aids in weight loss/weight control Reduces risk of colon, prostate, and breast cancer Reduced stress and improves self-image Improves blood glucose regulation Improves immune function Strengthens bones and joints Increases muscle mass and strength Improves GI tract peristalsis Healthy People 2020 objectives related to exercise Reduce the proportion of adults engaging in no leisure-time physical activity Increase the proportion of adults who meet current federal physical activity guidelines for aerobic and muscle-strengthening activity Goals from Physical Activity Guidelines for Americans Adults should be physically active For substantial health benefits, each week adults should engage in 150 minutes of moderate-intensity aerobic physical activity, or 75 minutes of vigorous aerobic activity, or an equivalent combination. For more health benefits, each day adults should double these exercise times. Adults should perform muscle-strengthening activities 2 or more days each week. Characteristics of a Good Fitness Program Mode: type of exercise performed Aerobic exercise: uses large muscle groups, can be maintained continuously, and is rhythmic in nature; causes heart and lungs to work harder than at rest Resistance exercise (i.e., strength training): activities that use muscular strength to move a weight or work against a resistant load Flexibility exercise: moving a joint through its entire range of motion Duration: amount of time spent in physical activity At least 30 min/day (not counting warm-up/cool-down) Benefits seen with both continuous or segmented sessions Frequency: number of times the activity is performed weekly Daily aerobic activity for best fitness For cardiovascular fitness, perform aerobic activity 3 - 5 times/week For weight control, perform aerobic activity 5 - 6 times/week To achieve muscular fitness, perform resistance exercises 2 - 3 times/week To achieve flexibility, perform flexibility exercises 2 - 3/week Intensity: level of effort required; difficulty Levels of intensity Low-intensity: very mild increased heart rate Moderate-intensity: increases breathing, sweating, and heartbeat, but permits conversation Vigorous-intensity: significantly increases breathing, sweating, and heart rate, making it difficult to carry on conversation Defining intensity Age-predicted maximum heart rate Max HR = 220 - age Target zone: 60 - 90% max HR May be affected by medications Rating of Perceived Exertion scale (RPE Scale) Ranges from 6 - 20 For fitness, aim for 12 - 15 (moderate intensity) Because it is subjective, ratings vary with fitness level Oxygen consumption (VO2max) Energy needs dictate amount of oxygen used by body cells Treadmill test to measure oxygen consumption during exercise (ml/min) Point at which subject can no longer increase O2 use as workload increases is deemed VO2max Metabolic equivalents (METs) 1 MET = 1 kcal/kg/hr (approximately resting energy expenditure) Progression: increase in duration, frequency, and intensity over time Initiation phase: first 3 - 6 weeks of an exercise program; adaptation to program Improvement phase: next 5 - 6 months; intensity and duration increased until no further physical gains are achieved Maintenance phase: evaluation of fitness goals; maintain achievements Consistency Make exercise part of daily routine Best times vary by individual With tight schedules, exercise can occur in short segments Variety Boredom may cause abandonment of fitness program Exercise different muscle groups for overall fitness Keeps exercise interesting and fun Helps individuals maintain program See Figure 11-4 for the Physical Activity Pyramid Achievement and Maintenance of Fitness Consult healthcare provider before starting a new fitness program Men over age 40 Women over age 50 Previously inactive Existing health conditions Assess and record baseline fitness scores to allow future measurement of progress Start with short intervals and lower end of target HR zone; work up to total of 30 min/day After achieving 30 min/day, focus on other goals, work up to higher level of MHR target zone Warm-up: 5 - 10 minutes of low-intensity exercise Gradual Sufficient to increase muscle and body temperature Cool-down: 5 - 10 minutes of low-intensity exercise Gradual Allow body to recover slowly Energy Sources for Muscle Use ATP: Immediately Usable Energy ATP ADP + Pi, energy is released for cell functions (e.g., muscle contraction) Resting muscle cell contains only enough ATP to keep muscle working maximally for 1 - 2 seconds Additional ATP comes from phosphocreatine and metabolism of macronutrients Phosphocreatine: Initial Resupply of Muscle ATP PCr: high-energy compound created from ATP and creatine that is stored in small amounts in muscle cells Creatine: organic molecule made from glycine, arginine, and methionine As ADP accumulates in exercising muscle, enzyme is activated to transfer high-energy Pi from PCr to ADP to reform ATP Without additional input, PCr could maintain maximal muscle contractions for about 10 seconds With energy from metabolism of glucose and fatty acids, PCr is major source of energy for events up to 1 minute Carbohydrate: Major Fuel for Short-Term, High-Intensity, and Medium-Term Exercise Anaerobic Pathway Glycolysis of glucose pyruvate requires no oxygen, yields 2 ATP With limited oxygen supply or intense physical activity, pyruvate accumulates in muscle and is converted to lactate Carbohydrate is sole source of fuel for glycolysis Glycolysis supplies majority of energy required for 30 seconds - 120 seconds Fast way to resupply ATP 2 disadvantages of anaerobic pathway Cannot sustain ATP production for long Only yields 5% potential energy from muscle glycogen Accumulation of lactate increases acidity, limits further glycolysis by inhibiting enzyme activity, leads to loss of K+ from muscle cells; contributes to fatigue Lactate is released into blood, used for energy (heart and other muscle cells) or recycled to glucose (liver and kidneys; requires energy) Aerobic Pathway When adequate O2 is available (moderate- to low-intensity physical activity), pyruvate is shuttled to mitochondria and metabolized to CO2 and H2O Aerobic pathway is slower than anaerobic pathway, but supplies more energy and can be sustained for hours Major contribution to energy needs for physical activity lasting from 2 minutes to 3 hours or more Muscle Glycogen versus Blood Glucose as Muscle Fuel Glycogen is temporary storage of glucose Liver glycogen (100 g) used to maintain blood glucose levels Muscle glycogen (400 g) supplies glucose to working muscle Glycogen may be broken down to glucose and metabolized by anaerobic and aerobic pathways Glycogen is primary source of glucose for ATP during fairly intense activity up to 2 hours in duration For short events (1 hr/day, requires moderate to high carbohydrate intake (see Table 11-5) Goal is to prevent fatigue and load muscles and liver with glycogen Low intensity: 3 - 5 g/kg/day Moderate intensity lasting about 1 hr/day: 5 - 7 g/kg/day Several hours of exercise/day: 6 - 10 g/kg/day Extreme activity lasting 4 to 5 hours: 8 – 12 g/kg/day Boosting Glycogen Stores Muscle glycogen is first source of glucose for exercising muscle During endurance activities > 90 min, muscle glycogen is depleted and high-intensity exercise cannot be maintained Glycogen depletion also occurs over several days of heavy training if glycogen breakdown exceeds replacement Carbohydrate (glycogen) loading involves both exercise and diet Taper training intensity and duration 6 days before competition Consume normal mixed diet for first 3 days, high-carbohydrate diet for last 3 days before competition May increase muscle glycogen stores 50 - 85% over typical conditions Difficult for athletes with several days of competitive events or who don’t wish to alter training regimen before competition Other carbohydrate loading strategies, some as short as 1 day in duration can increase muscle glycogen above typical levels Carbohydrate loading works for athletes competing in continuous, intense aerobic events >60 minutes duration or shorter events taking place more than once in a 24-hour period Not effective for shorter races, may harm performance due to muscle stiffness and heaviness caused by increased water storage with glycogen stores Experiment with carbohydrate loading during training Fat Needs 15 - 25% total kcal Emphasize unsaturated fats; limit saturated and trans fats Protein Needs Recommendations Non-athletes: 0.8 g/kg/day Strength-trained athletes, muscle maintenance phase: 1.0 - 1.2 g/kg/day Strength-trained athletes, muscle mass gain phase: 1.5 - 1.7 g/kg/day Moderate-intensity endurance athletes: 1.2 – 1.4 g/kg/day High-intensity endurance athletes: 1.7 g/kg/day Higher protein needed for repair and gain of muscle tissue, not energy needs Consuming protein in excess of needs results in increased use of amino acids for energy and may be accompanied by insufficient carbohydrate intake, increased urine production, and poor hydration Supplements are not necessary; protein needs may be met by varied diet (unless calorie-restricted) Vitamin and Mineral Needs In general, vitamin and mineral needs are the same or slightly higher than requirements for sedentary adults, but needs are met by increased food intake Calorie-restricted diets (1200 kcal/day or less) or vegetarian diets may require vitamin and mineral supplementation and/or use of fortified foods Iron Deficiency and Impaired Performance Iron contributes to RBC production, O2 transport, and energy production Deficiency results in fatigue and poor athletic performance Risk for iron deficiency Menstrual losses among females Low-energy or vegetarian diets Gastrointestinal bleeding resulting from intense workouts Sports anemia: exercise causes blood volume to expand at start of training regimen, which dilutes blood Not detrimental to performance Difficult to differentiate between sports anemia and true anemia True anemia Defined as reduced blood hemoglobin and hematocrit levels Affects up to 15% of males and 30% of female athletes Frequent monitoring of iron status and dietary intake is advised Iron supplements may be advisable, but toxic effects are possible Cause of anemia should be investigated Calcium Intake and the Female Athlete Triad Risk for low calcium intake Female athletes Calorie restriction Low intake of milk and other dairy products Female athlete triad Menstrual disorders Low energy availability Low bone mineral density Regular menstruation is needed to maintain bone mineral density Irregular menstrual periods or amenorrhea increase risk for bone fractures during training and competition and osteoporosis in the long term Goals of treatment for female athlete triad Control and manage diet Restore normal hormone levels and menstruation Monitor and treat injuries or other medical complications Possibly reduce training (10 - 20%) Increase energy intake for weight gain (2 - 5%) May require counseling to reassure that weight gain will improve performance and stamina Calcium supplementation Fluid Needs for Active Individuals General Fluid needs are higher for athletes than for sedentary adults to replace fluid lost in sweat Sweat losses during prolonged exercise range from 3- 8 c/hr; highest in hot weather or with heavy equipment Dehydration leads to decreased endurance, strength, and overall performance Heat-related illness Heat exhaustion: first stage of heat-related illness Depletion of blood volume Increased body temperature, leading to profuse sweating, headache, dizziness, nausea, vomiting, muscle weakness, visual disturbances, flushing of skin Treat by moving to cool environment, removal of excess clothing, sponging with cool water, replacing fluids as tolerated, immediate medical attention Heat cramps: frequent complication of heat exhaustion Cramps are contractions of skeletal muscles lasting 1 - 3 minutes, moves down muscle, excruciating pain Results from large sweat losses from exercising for several hours in hot climate and consuming large volume of water without replacing sodium losses Prevention involves warming up with moderate-intensity exercise, adequate salt intake before activity, avoidance of dehydration Heatstroke: internal body temperature reaches 104° or higher Exertional heatstroke results from high blood flow to exercising muscles, which overloads body’s cooling capacity Blood circulation is reduced Nervous system damage may result Death rate is 10% of cases Sweating ceases - skin feels hot and dry Other symptoms include nausea, confusion, irritability, poor coordination, seizures, rapid heart rate, vomiting, diarrhea, and coma Treatment includes cooling with ice packs or cold water, immediate medical attention Prevention includes monitoring for rapid changes (≥ 2%) in body weight, fluid and sodium replacement, avoidance of exercise in hot, humid conditions Fluid Intake and Replacement Strategies Before exercise, ensure optimal fluid status Freely drink beverages during the 24 hours preceding an event, even if not thirsty Drink 2 - 3 cups of fluid 2 - 3 hours before exercise to allow time for adequate hydration and excretion of excess fluid Drink 1 - 1.5 cups of fluid 10 - 15 minutes prior to exercise, especially for endurance events During exercise, limit fluid losses to 1 hr, fluid replacement beverages should contain 4 - 8% carbohydrates to maintain blood glucose and 0.5 - 0.7 g Na/l Urine should be no darker than color of lemonade (see Figure 11-14) Thirst is not a reliable indicator of an athlete’s need to replace fluid during exercise After exercise Drink 3 cups of water/1 lbs. weight loss Restore weight before next exercise period Water Intoxication Water intoxication caused by overdrinking before, during, or after exercise without also replacing sodium losses Prevention: consume beverages with sodium (~100 mg sodium/8 oz) and only drink to replace fluid losses (not more) Sports Drinks Athletes of all ages who consume only water for fluid replacement during exercise, even for short-term exercise, risk diluting the blood, increasing urine output, and decreasing drive to drink For exercise >60 min, sports drinks offer distinct advantages over plain water Carbohydrates supply glucose to muscles to prevent glycogen depletion Electrolytes maintain blood volume, enhance absorption of water and carbohydrates from the intestine, and stimulate thirst Avoid alcohol, which increases urine output and reduces fluid retention Avoid carbonated beverages, which decrease drive to drink and lead to feeling of fullness Avoid high caffeine intake (>500 mg/day), which increases urine output Avoid drinks with high sugar content (>10%), which are not quickly absorbed Food and Fluid Intake Before, During, and After Exercise Pre-exercise Meal Benefits Prevents hunger before and during exercise Maintains optimal blood glucose for exercising muscles Improves performance over fasted state Prevents glycogen depletion Composition High in carbohydrate Non-greasy, low-fat (delays gastric emptying), non-gas producing Easily digested Timing 3.5 - 4 hours before event, meal may contain up to 4 g/kg carbohydrate and 26% kcal from fat Closer to event, decrease carbohydrate (to 1 g/kg) and fat content Commercial liquid formulas provide high carbohydrate meal and are rapidly digested (also see Table 11-9) Within 10 - 15 minutes of long event, drink 8 - 12 oz water or other fluid Fueling During Exercise Benefits Improved athletic performance for events >60 minutes Prevents glycogen depletion Prevents hypoglycemia, which contributes to physical and mental fatigue Composition Consume 30 - 60 g of carbohydrate per hour; experiment during training Sports drinks provide fluid, electrolytes, and carbohydrates Carbohydrate gels: 25 g carbohydrate/serving Sports drinks: 14 g carbohydrate/8 oz serving Energy bars: 2 - 45 g carbohydrate/serving Choose up to 10 g protein, 4 g fat, and 5 g fiber Also contain vitamins and minerals Should be accompanied by fluid Recovery Meals 1 – 1.5 g carbohydrate/kg should be consumed 30 minutes after exercise and again at 2-hour intervals for up to 6 hours after exercise Glycogen resynthesis is greatest immediately after exercise when muscles are highly sensitive to insulin. Factors for rapid recovery of muscle glycogen are: Availability of adequate carbohydrate Ingestion of carbohydrate soon after exercise High glycemic load carbohydrates Consuming a small amount of protein (10-20g) with carbohydrates during the recovery period immediately after exercise may help repair and synthesis of muscle proteins Fluids and electrolytes replenish lost fluids as quickly as possible Global Perspective: Gene Doping and the Wide World of Sports Practice of using gene therapy to artificially enhance athletic performance Scientists are developing tests to detect whether an athlete’s DNA has been altered using gene doping Ergogenic Aids to Enhance Athletic Performance Ergogenic aid: nutritional, psychological, pharmacological, mechanical, or physical substance or treatment intended to improve exercise performance Most are ineffective Only a few ergogenic aids are supported by science Sufficient water and electrolytes Abundant carbohydrates Healthy, varied diet Caffeine Protein and amino acid supplements are unnecessary; requirements can be met by foods Nutrient supplements should be used only to meet specific dietary shortcomings Athletes should focus on training and proper nutrition rather than ergogenic aids to enhance athletic performance Table 11-11 evaluates popular ergogenic aids Useful in some circumstances Creatine Sodium bicarbonate Caffeine Not Effective Beta-hydroxy-beta-methylbutyric acid (HMB) Glutamine Branched chain amino acids Glucosamine Dangerous/illegal substances/practices Anabolic steroids Growth hormone Blood doping Gamma hydroxybutyric acid (GHB) National Collegiate Athletic Association’s Committee on Competitive Safeguards and Medical Aspects of Sports regulates dispensing of supplements by athletic departments Permissible Vitamins and minerals Energy bars (up to 30% protein) Sports drinks Meal replacement drinks Non-permissible Amino acids Creatine Glycerol HMB L-carnitine Protein powders
Chapter 12 The Fat-Soluble Vitamins Overview In Chapter 12, students will learn about the history, sources, chemistry, functions, metabolism, and requirements of each of the four fat-soluble vitamins - A, D, E, and K. In the section about vitamin A, the differences between retinoids and carotenoids are described and their roles in vision receive the most attention. Vitamin D is involved in bone metabolism and calcium homeostasis, but emerging research highlights the role of vitamin D in cell cycle regulation and gene expression. The contribution of vitamin E to the body’s antioxidant systems is reviewed. Vitamin K is involved mainly in blood clotting, but also takes part in bone metabolism. Throughout the chapter, the authors emphasize that a varied diet is preferred to supplements when it comes to deriving benefits from vitamins. Learning Objectives Define the term vitamin and list 3 characteristics of vitamins as a group. Classify the vitamins according to whether they are fat soluble or water soluble. List 3 important food sources for each fat-soluble vitamin. List the major functions for each fat-soluble vitamin. Describe the deficiency symptoms for each fat-soluble vitamin and state the conditions in which deficiencies are likely to occur. Describe the toxicity symptoms caused by excess consumption of certain fat-soluble vitamins. Evaluate the use of vitamin and mineral supplements with respect to their potential benefits and risks to health. Teaching Strategies, Activities, Demonstrations, and Assignments Ask students to bring to class the vitamin supplements they use, or you can provide a variety of brands (brand names and generic). Ask students to evaluate them using the guideline that no vitamin should be present in amounts greater than 150% of the USRDA. Divide the supplements into those that meet the guidelines and those that exceed them. Discuss the implications of consuming vitamins in too-high quantities. Next, compare the cost of name brands to generic ones. Have students determine how much money they would save by purchasing generic brands. Do this as a general class activity. Make a list of generic brands on the board and their prices and a similar list in a column next to it of the name brands. Do a price comparison. Lastly, discuss situations and conditions that would warrant the use of supplemental vitamins. Most vitamins have an interesting history. Have each student prepare a background report on the discovery and isolation of one vitamin. These could be handed in and graded or presented as oral reports. During class discussion, have students describe various food preparation and storage techniques that should be used to preserve the water-soluble vitamin content of fruits and vegetables. Fortified foods have become increasingly common in the U.S. Ask students to survey cereal products found in the supermarket and compare the vitamin content in at least eight. Which cereal would they choose if they wanted to get the most vitamin nutrition? Have students write the name of each vitamin on an index card. On the back, they will list one to three key functions of that vitamin; food sources; deficiency name, if appropriate; deficiency symptoms; and toxicity symptoms. Have students study these index cards in pairs until they can recall the information about each vitamin. Before class, write the name of each vitamin on a piece of paper, index card, or "post-it." If you use paper or an index card, remember to take stickpins or tape to class to fasten the card/paper on students' backs. Secure one card/paper/post-it on the back of each student. Have students circulate throughout the room asking other student’s questions about the vitamin posted on their back. Only yes and no questions are permitted, for example, "Am I involved in blood clotting?" and "Are green vegetables good food sources of me?" Only two questions can be asked of any person. After asking two questions of a person, students must move to someone else. Continue the game until everyone correctly identifies the vitamin they are. Place posters with names of vitamins and minerals around the room. Give students index cards describing symptoms of deficiencies and excesses. Have them match symptom cards with the appropriate vitamin or mineral. Assign students to prepare a skit based on a job interview. Ask the “vitamin applicant” what they can do for “the company,” how they work, etc. Post lists of foods around the room. Have students determine the key vitamin(s) present in each group of foods. Bring several recipes to class. Ask students to evaluate the ingredients---what are the phytochemicals in this recipe? Have students complete the Take Action activity “Does your fat-soluble vitamin intake add up?” Use this to fuel discussion on how to get enough vitamins A, D, E, & K in your diet through food alone. Lecture Outline Vitamins: Essential Dietary Components General Vitamins: essential, organic substances needed in small amounts in the diet Fat-soluble vitamins: dissolve in organic solvents (e.g., ether, benzene) Water-soluble vitamins: dissolve in water Supply no energy Aid in growth, development, and maintenance of body tissues Essential in diet because they cannot be synthesized at all or in sufficient amounts by the body to support needs Health declines when vitamins are deficient Resupplying vitamins alleviates deficiency symptoms Megadoses of some vitamins are useful as pharmacological agents Synthetic and natural forms of vitamins generally work equally well in the body Vitamins consumed in foods as part of a varied diet are more beneficial than supplements Absorption of Vitamins Fat-soluble vitamins are absorbed with dietary fat Requirements for absorption Dietary fat Bile Pancreatic lipase Adequate intestinal absorption Absorption efficiency of fat-soluble vitamins is 40 - 90% when consumed in recommended amounts Water-soluble vitamins are absorbed in the small intestine independent of dietary fat with 90 - 100% efficiency Malabsorption of Vitamins Fat malabsorption (e.g., from GI tract disease or pancreatic disease) may cause poor absorption of fat-soluble vitamins Alcohol abuse and some intestinal diseases may cause malabsorption of some B-vitamins Poor absorption increases need for vitamin supplements Transport of Vitamins Fat-soluble vitamins are transported through lymphatic system and delivered to bloodstream via chylomicrons and other blood lipoproteins Triglycerides are removed by cells as chylomicrons circulate Remnants, which include fat-soluble vitamins, are taken up by the liver and repackaged as new lipoproteins for transport or stored in adipose tissue or liver Water-soluble vitamins are delivered directly to the bloodstream and distributed throughout the body Storage of Vitamins in the Body Except for vitamin K, fat-soluble vitamins are not readily excreted, but are stored in the liver and/or adipose tissue Except for vitamins B-6 and B-12, water-soluble vitamins are excreted readily and have limited storage Vitamins should be consumed daily, but deficiency symptoms do not develop for several weeks with inadequate consumption Vitamin Toxicity Toxicity from vitamins A and D is most likely Toxicity usually results when intake exceeds 5 - 10 times DRI guidelines Balanced multivitamin and mineral supplements that supply less than 2X the Daily Value are unlikely to cause toxicity Vitamin A General Vitamin A (from consumption of beef liver) has been known to prevent night blindness Vitamin A is a family of compounds Preformed retinoids: biologically active form of vitamin A; three forms may be interconverted to some extent Retinol Retinal Retinoic acid Provitamin A carotenoids: must be converted to vitamin A Chemistry Retinyl esters reversibly convert into retinol Retinol reversibly converts into retinal Beta carotone converts into retinal Retinal irreversibly converts into retinoic acid Tail of vitamin A varies from cis to trans configuration Carotenoids: yellow/orange pigments in fruits and vegetables; some are provitamins (converted to vitamin A) Alpha-carotene Beta-carotene Beta-cryptoxanthin Vitamin A in Foods (see Figure 12-3) Sources of retinoids Liver Fish and fish oils Fortified milk Eggs Margarine (fortified) Sources of carotenoids Yellow/orange fruits and vegetables (e.g., carrots, spinach, winter squash, sweet potatoes, mangoes, cantaloupe, peaches, apricots) Leafy green vegetables Broccoli 70% of vitamin A in typical American diet comes from animal (preformed vitamin A) sources Dietary vitamin A activity is expressed in Retinol Activity Equivalents (RAE) 1 RAE = 1 µg retinol 1 RAE = 12 µg beta-carotene 1 RAE = 24 µg alpha-carotene or beta-cryptoxanthin Outdated units of measurement for vitamin A International units (IU) Retinol equivalents (RE): overestimate contribution of carotenoids to vitamin A needs For preformed vitamin A, 1 RE (3.3 IU) =1 RAE For provitamin A, assume 1 RE/2 = 1 RAE Vitamin A Needs RDA Adult men: 900 µg RAE Adult women: 700 µg RAE DV: 5000 IU (1000 µg) No DRI available for carotenoids Average intake meets DRI Absorption, Transport, Storage, and Excretion of Vitamin A Preformed vitamin A in animal foods Retinol Retinyl esters (attached to fatty acid); must be cleaved by action of bile and pancreatic lipase to have vitamin A activity Dietary carotenoids attached to proteins are split off by digestive enzymes Absorption of preformed vitamin A Takes place in the small intestine via specific carrier proteins Up to 90% efficient Absorption of carotenoids Takes place in small intestine via passive diffusion Absorption rates range from 5-60% of intake Transport of retinoids After absorption, retinol is attached to a fatty acid to form a new retinyl ester and packaged into chylomicrons Chylomicrons are absorbed into lymphatic vessels, which empty into the bloodstream Transport of carotenoids Enzymatically split in intestinal cells to form retinal and retinoic acid Retinal is converted to retinol and can become a retinyl ester to enter lymphatic circulation as part of a chylomicron Retinoic acid can enter the bloodstream directly for transport to liver Carotenoids can also enter bloodstream directly Storage of Vitamin A 90% of body’s vitamin A stores are in the liver (enough to last for several months) Small amounts of vitamin A are stored in adipose tissue, kidneys, bone marrow, testicles, and eyes Retinoids are released from liver into bloodstream bound to retinol-binding protein (RBP), which binds to transthyretin (prealbumin) Synthesis of RBP depends on having adequate amounts of retinol, protein, and zinc Carotenoids are released from liver into bloodstream as part of lipoproteins Retinoids bind to specific RBPs in cells Excretion of Vitamin A Not readily excreted, but primary means of excretion is via urine Carotenoids excreted via bile that is eliminated with feces Functions of Vitamin A (Retinoids) Growth and Development Development of eyes, limbs, cardiovascular system, and nervous system of embryo Lack of vitamin A in first trimester leads to birth defects or fetal death Retinoid acid is needed for production, structure, and normal function of epithelial (mucous forming) cells in lungs, trachea, skin, GI tract, etc. Cell Differentiation (see Figure 12-4) Retinoids bind to retinoid receptors in cell nucleus that regulate formation of mRNA and subsequent gene expression, which directs cell differentiation (process by which stem cells develop into specialized cells) Retinoic acid receptor (RAR) Retinoid X receptor (RXR) Especially involved in cell differentiation in the eyes Vision Retinal is needed in the retina to turn visual light into nerve signals to the brain Rods: vision in dim light, black and white images, detection of motion 11-cis-retinal binds to opsin to form rhodopsin Absorption of light catalyzes bleaching process: change in shape of 11-cis-retinal to all-trans-retinal, separates from opsin Ion permeability of photoreceptor cells Initiation of signal to nerve cells that communicate with brain’s visual center With exposure to bright light, rhodopsin is completely activated and cannot respond to more light Regeneration of 11-cis-retinal from all-trans-retinal and binding with opsin restarts visual cycle Some retinal is stored and not used for each visual cycle Depletion of vitamin A pools leads to night blindness, wherein the process of dark adaptation is impaired Dark adaptation: [rhodopsin] in the eye increases in dark conditions to allow vision in the dark Cones: vision in bright light, color vision Immune Function Increased incidence of infection is an early symptom of vitamin A deficiency May be due to role of vitamin A in maintenance of epithelial cells, which form a barrier against pathogens Vitamin A supplementation decreases severity of infections in vitamin A deficient children Use of Vitamin A Analogs in Dermatology Retin-A (topical) and Accutane (oral) Used to treat acne and psoriasis or lessen damage from sun or UV exposure Toxic effects are especially harmful to fetus; causes birth defects Carotenoid Functions Some can be converted to vitamin A Reduced risk of eye disease Reduced risk of cancer Reduced risk of cardiovascular disease Beta-carotene may act as antioxidant, especially to protect eye tissues; diets high in fruits and vegetables show more success than supplementation Possible role for beta-carotene in prevention of lung cancer: although diets high in fruits and vegetables are associated with reduced risk of lung cancer, supplementation actually increases risk of lung cancer in high-risk individuals Lutein and zeaxanthin may protect against age-related macular degeneration (leads to deterioration of central vision) Lycopene may protect against prostate cancer Beta-carotene and lycopene may reduce risk of CVD, possibly by inhibiting oxidation of LDL and cholesterol synthesis and increasing LDL receptor activity in cells In all cases, diets high in carotenoid-rich fruits and vegetables are recommended rather than carotenoid supplements Vitamin A Deficiency Diseases Low risk for deficiency in North America, but vitamin A deficiency is a major public health problem in developing countries Leading cause of non-accidental blindness worldwide At-risk populations in North America Poverty Older adults Alcoholism or liver disease (limits vitamin A storage) Severe fat malabsorption Premature infants (low stores of vitamin A) Effects on eyes Slowed regeneration of rhodopsin by rods in the retina leads to night blindness Deterioration of mucous-forming cells leads to xerophthalmia: progression of eye disease leading to blindness, including Conjunctival xerosis: dryness Bitot’s spots: hardened epithelial cells on the eye Keratomalacia: softening of the cornea Scarring Follicular hyperkeratosis: keratinized cells replace normal epithelial cells, leading to dry, roughened skin Impaired growth in children Vitamin A Toxicity Also called hypervitaminosis A Occurs with chronic intake (usually from supplements) of 5 - 10 times RDA for retinoids UL: 3000 µg of retinoids (no UL for carotenoids) Types of hypervitaminosis A Acute: 1 very large dose or several large doses over a few days (100 x RDA) GI tract upset Headache Blurred vision Poor muscle coordination Fatality for extremely large doses (e.g., 500 mg for children or 10 g for adults) Chronic: repeated intakes of at least 10 x RDA; most symptoms disappear after supplementation ceases, but permanent damage may occur to the liver, bones, and eyes Joint pain Loss of appetite Skin disorders Headache Reduced bone minerals Liver damage Double vision Hemorrhage Coma Teratogenic: toxic doses during pregnancy, usually from vitamin A analogs used to treat skin conditions, but also possible from food sources (e.g., liver, fortified breakfast cereals); pregnant women should limit intake of preformed vitamin A to 100% DV Birth defects, especially of head and neck, where neural crest cells form in first trimester Spontaneous abortion Consuming excessive carotenoids does not lead to toxicity; may turn skin to yellow/orange color (hypercarotenemia) Global Perspective: Vitamin A Deficiency 250 million preschool children worldwide suffer from vitamin A deficiency At-risk populations Children Leading cause of preventable blindness in children: 250,000 - 500,000 cases/year Increased death from infections Women of childbearing age Increased risk of HIV transmission from mother to fetus Maternal mortality Vitamin A Global Initiative: partnership among World Health Organization, United Nations Children’s Fund, Canadian International Development Agency, US Agency for International Development, and Micronutrient Initiative formed in 1998 to combat vitamin A deficiency Promotes breastfeeding Promotes fortification of foods Provides educational programs to increase home gardening of vitamin-A-rich foods Provides vitamin A supplements to at-risk populations - shown to decrease vitamin A-related mortality by 15% in affected areas Development of programs to increase production and access to nutrient-rich foods Vitamin D General In 1918, cod liver oil (source of vitamin D) was discovered as cure for rickets In the presence of sunlight, skin cells can synthesize sufficient vitamin D from a derivative of cholesterol Vitamin D is a “conditional vitamin” or prohormone (precursor to active hormone) Vitamin D2 (Ergocalciferol) in Foods High sources Fatty fish (e.g., sardines, mackerel, salmon) and fish oils (e.g., cod liver oil) Fortified milk [10 µg (400 IU)/quart] Fortified breakfast cereals Supplements Low sources Eggs Butter Liver Some brands of margarine Ergocalciferol (D2) has vitamin D activity in humans, but not as much as vitamin D3 formed in the body Vitamin D3 Formation in the Skin 7-dehydrocholesterol in skin is exposed to sunlight 1 ring in chemical structure of 7-dehydrocholesterol transforms into vitamin D3 (cholecalciferol) Vitamin D3 enters the bloodstream, is transported to liver and kidneys, undergoes conversion to its bioactive form, calcitriol This process provides 80 - 100% of vitamin D requirements for some people Required sun exposure varies by Time of day Geographic location Season Age: skin production decreases by 70% by age 70 Skin color: melanin blocks UV light and prevents adequate D3 synthesis Use of sunscreen > SPF 8 Expose hands, face, and arms to UV light at least 2 - 3 times per week for 10 - 15 minutes (longer for dark-skinned individuals) Prolonged skin exposure is unlikely to cause toxicity because excess previtamin D3 in the skin is rapidly degraded Vitamin D Needs RDA Based on minimal sun exposure Individuals ages 1 to 70: 15 µg (600 IU) Adults ages 70+: 20 µg (800 IU) DV: 10 µg Full-term infants are born with a supply of vitamin D, but American Academy of Pediatrics recommends 10 µg (400 IU)/d supplements until weaned to good food sources of vitamin D Absorption, Transport, Storage, and Excretion of Vitamin D Absorption 80% of vitamin D2 is incorporated with dietary fats into micelles in the small intestine Absorbed by small intestine Packaged into chylomicrons for transport in lymph Fat malabsorption syndromes increase risk for vitamin D deficiency Transport Vitamin D2 and D3 are transported through bloodstream bound to vitamin-D-binding protein to the adipose, muscle, liver, or kidney cells In liver, vitamin D is hydroxylated to 25-OH vitamin D3 (inactive form), which may circulate in the blood for weeks In kidney, 25-OH vitamin D3 is hydroxylated to 1,25-dihydroxy vitamin D3 (calcitriol; active form of vitamin D) Synthesis of 1,25(OH)2 vitamin D3 is tightly regulated by parathyroid gland and kidneys in response to blood calcium levels Low [Ca] increased 1,25(OH)2 synthesis High [Ca] decreased 1,25(OH)2 synthesis Storage 25-OH vitamin D3 circulates in bloodstream Adipose cells Excretion Lost in bile during digestion Small amount excreted in urine Functions of Vitamin D Hormone-like functions that regulate body’s concentration of calcium and phosphorus (see Figure 12-14) Promotes increased intestinal absorption of calcium and phosphorus from foods to maintain blood levels of these minerals With PTH, enables release of calcium and phosphorus from the bone into the blood Immune function Secretion of several hormones Cellular metabolism, likely regulation of cell cycle Possible protection against cancer Possible protection against diabetes Possible protection against hypertension Vitamin D Deficiency Diseases In children, deficiency leads to rickets: abnormal mineralization of skeleton Signs Enlarged head, joints, and ribcage Deformed pelvis Bowed legs At-risk populations Fat malabsorption Dark skin pigmentation Low milk intake Minimal sun exposure In adults, deficiency leads to osteomalacia: soft bones Signs Poor calcification of newly synthesized bone Hip, spine, and other fractures At-risk populations Kidney disease Liver disease Gallbladder disease Intestinal disease Dark skin pigmentation Limited UV exposure Those with low 25-OH vitamin D3 levels should take 20 - 25 µg/d of vitamin D until normalized, then maintenance dose of 10 µg/d Vitamin D Toxicity Only likely from excessive supplementation Vitamin D in skin is readily broken down UL Infants and children up to 8 years of age: 1000-3000 IU Ages 9+: 4000 IU Consequences Overabsorption of calcium Hypercalcemia (high blood calcium) Calcium deposits in kidneys, heart, and lungs Anorexia Nausea/vomiting Bone demineralization Weakness Joint pain Disorientation Fatality Current vitamin D concerns Low intakes of vitamin D coupled with behaviors that limit UV-light exposure have resulted in widespread inadequate vitamin D status 2010 IOM recommendations are based on promoting calcium homeostasis and preventing bone disorders Other known roles of vitamin D Gene control Cell cycle regulation Decreases risk of diabetes Decreases risk of colon, prostate, and breast cancer Decreases risk of CVD Decreases risk of autoimmune diseases Estimated that the body requires 3000 to 4000 IU (75 – 100 g)/day Typical inputs provide 2400 IU/d or less Oral intake of 1000 to 4000 IU/d may be necessary for those with limited sun exposure Vitamin E General Link between vegetable oil and normal reproduction in rats was first noted in 1922 Vitamin E is a family of 8 compounds Alpha-tocopherol: most active form Beta- tocopherol Gamma- tocopherol: found in many vegetable oils, may have health benefits, but not as active as alpha-tocopherol Delta- tocopherol Alpha-tocotrienol Beta- tocotrienol Gamma- tocotrienol Delta- tocotrienol Chemistry Long carbon tail that can exist in many isomeric forms Ringed structure Vitamin E in Foods Plant oils (e.g., cottonseed, canola, safflower, sunflower) Wheat germ Peanuts Sunflower seeds Products made from plant oils (e.g., margarine, shortening, salad dressing) Vitamin E content of foods may vary due to harvesting, processing, storage, and cooking (susceptible to destruction by oxygen, metals, light, and high temperatures) Vitamin E Needs RDA (adult men and women): 15 mg, based on amount needed to prevent hemolysis (breakdown of RBC membranes) DV: 30 IU Typical intakes are 2/3 RDA Converting IU to mg For a synthetic source (e.g., supplements): 1 IU = 0.45 mg For a natural source (most potent), 1 IU = 0.67 mg Absorption, Transport, Storage, and Excretion of Vitamin E Absorption Efficiency ranges from 20 - 70% depending on amount consumed and absorption of dietary fat Incorporated into micelles with dietary fat in the small intestine; requires bile and pancreatic enzymes Absorbed by small intestinal cells Incorporated into chylomicrons Transport Transported as part of chylomicrons in lymph, then bloodstream Triglycerides and some vitamin E are removed from chylomicrons by body cells, chylomicron remnant remains Chylomicron remnant (containing vitamin E) is transported to liver Vitamin E is repackaged as VLDL, LDL, and HDL for delivery to body tissues No specific transport protein Storage of Does not accumulate in liver About 90% is stored in adipose tissue Excretion Bile (mostly) Urine Skin Functions of Vitamin E Antioxidant Free radical: unstable compound with unpaired electron that acts as a strong oxidizing agent; destructive to cell components (e.g., cell membranes and DNA) Free radicals have some beneficial roles (e.g., immune function) Body protects itself by regulating free radical activity with antioxidants Antioxidant systems in the body Vitamin E Vitamin C Glutathione peroxidase: catalyzes breakdown of hydrogen peroxides and lipid peroxides; requires selenium Catalase: neutralizes free radicals in peroxisomes Superoxide dismutase: eliminate superoxide radicals; requires copper, zinc, and/or manganese Carotenoids Bilirubin Uric acid Ubiquinone Lipoic acid Metal-binding proteins In lipid-rich areas of the body, free radicals initiate lipid peroxidation reactions that create lipid peroxyl radicals Vitamin E donates a hydrogen to lipid radicals to stop the oxidation reaction, thus reducing oxidative stress Reduction in oxidative stress may lower risk for CVD, certain cancers, cognitive decline, and impaired immune function Interactions with other nutrients Due to the activity of selenium in the glutathione peroxidase pathway, adequate selenium intake reduces vitamin E needs Vitamin C aids in the regeneration of vitamin E after vitamin E donates a hydrogen to a free radical Vitamin E Deficiency High-risk populations Fat malabsorption Smokers: smoking increases oxidative stress Preterm infants: born with limited stores of vitamin E, insufficient intestinal absorption of vitamin E Consequences Hemolytic anemia: RBCs break down faster than they can be replaced Impaired immune function Neurological changes Vitamin E Toxicity Consequences Hemorrhaging: insufficient clotting leads to excessive bleeding High intake of alpha-tocopherol may decrease gamma-tocopherol activity; mixed isomer supplement preparations may be preferable High-risk populations Concurrent use of anticoagulant medications UL: 1000 mg (1500 IU) of alpha-tocopherol from natural sources or 1100 IU from synthetic sources Vitamin K General Vitamin K is a family of compounds known as quinones Phylloquinones (K1): from plant sources Menaquinones (K2): from fish oils and meats; synthesized by intestinal bacteria Menadione: synthetic compound that can be converted to menaquinone in body tissues Vitamin K Sources 10% from bacterial synthesis in colon 90% from dietary sources Green leafy vegetables (e.g., kale, turnip greens, parsley, salad greens, cabbage, spinach) Broccoli Peas Green beans Vegetable oils (e.g., soy, canola) Stable to heat processing Susceptible to destruction by light Vitamin K Needs AI, based on providing adequate vitamin K for blood clotting Adult women: 90 µg Adult men: 120 µg DV: 80 µg Absorption, Transport, Storage, and Excretion of Vitamin K Absorption 80% absorption efficiency Taken up by small intestine (requires bile and pancreatic enzymes), incorporated into chylomicrons Transport Incorporated into VLDL for storage in the liver or carried by HDL and LDL Storage Liver Bone Excretion Bile Urine (minor) Functions of Vitamin K Blood clotting (see Figure 12-21) Synthesis of clotting factors by the liver Conversion of preprothrombin to prothrombin (active blood-clotting factor) CO2 added to glutamic acid to yield Gla protein (gamma-carboxyglutamic acid) Conversion also relies on calcium binding: Gla residues bind calcium to form blood clots Anticoagulant medications (e.g., warfarin) inhibit reactivation of prothrombin Consistent vitamin K intake and avoidance of vitamin K supplements are necessary for individuals on anticoagulant therapies Bone metabolism: some vitamin K-dependent Gla proteins are synthesized in bone Osteocalcium Matrix Gla protein Protein S Vitamin K Deficiency High-risk populations Fat malabsorption Newborns: vitamin K stores are low at birth; vitamin K injections are administered Megadoses of other fat-soluble vitamins Vitamin A inhibits intestinal absorption Vitamin E decreases vitamin K-dependent clotting factors Consequences Hemorrhage Vitamin K Toxicity No UL has been set Stored in liver and bone, but more readily excreted than other fat-soluble vitamins Injections of menadione may result in hemolytic anemia, excess bilirubin in the blood, and death Dietary Supplements: Healthful or Harmful? 40% of US adults regularly use vitamin/mineral supplements Reasons for use Enhance or maintain overall well-being Health specific sites (bones, heart, eyes) Dietary Supplement Health and Education Act (DSHEA): supplement is any product intended to supplement the diet that contains one or more vitamins, minerals, amino acids, herbs, botanicals, or plant extracts FDA does not have the authority or resources to closely monitor dietary supplements unless they are dangerous or marketed using illegal claims Supplement manufacturers may not claim that supplements will prevent, treat, or cure diseases Structure/function claims are allowed Claims that are not related to diseases are allowed Evidence is not always available to support claims Quality, purity, and consistency are not closely monitored by FDA, but voluntary labeling with US Pharmacopeia symbol indicates that product meets established industry standards for strength, quality, purity, packaging, labeling, solubility, and storage life Dietary supplements are no substitute for a healthy diet Lack of fiber Lack of phytochemicals Limited calcium content Risk of toxicities and nutrient interactions Excessive zinc interferes with iron and copper absorption High folate masks vitamin B-12 deficiency Excessive vitamins A or D may result in toxicity symptoms Some situations necessitate use of multivitamin/mineral supplements Iron supplements for women with excessive menstrual losses Iron and folate supplements for pregnant or breastfeeding women MVI for those with limited calorie intakes Calcium, iron, zinc, vitamin D, and vitamin B-12 for vegans Vitamin K for newborns Fluoride for infants and young children Vitamin D for those with limited sun exposure and low intake of fortified dairy products Calcium and vitamin D for those with low dairy intake due to lactose intolerance or milk allergies Specific vitamins or minerals for those with medical conditions that alter nutrient metabolism Guidelines for choosing MVI Nationally-recognized brand No more than 100% DV for nutrients listed Avoid exceeding UL for any nutrient from combination of supplements, foods, and fortified foods Avoid superfluous ingredients (e.g., bee pollen, lecithin, hesperidin complex, inositol, laetrile, pangamic acid, PABA) Instructor Manual for Wardlaw's Perspectives in Nutrition Carol Byrd-Bredbenner, Gaile Moe , Jacqueline Berning , Danita Kelley 9780078021411
