CH-13 Water-Soluble Vitamins – Wardlaw’s Perspectives in Nutrition : Chapter Notes

This document contains Chapters 13 to 14 Chapter 13 The Water-Soluble Vitamins Overview Chapter 13 covers the history, sources, chemistry, functions, metabolism, and requirements of the water-soluble vitamins (B-vitamins and vitamin C), choline, and some vitamin-like compounds. All of the B-vitamins (thiamin, riboflavin, niacin, pantothenic acid, biotin, vitamin B-6, folate, and vitamin B-12) have coenzyme forms that function in energy metabolism, protein and amino acid metabolism, some antioxidant systems, and many biosynthetic pathways. Although excesses of most of the water-soluble vitamins are readily excreted in the urine, vitamins B-6 and B-12 may lead to serious toxicity syndromes, and Upper Levels also have been set based on side effects for a few others. Besides their roles in metabolism, some water-soluble vitamins also participate in blood formation and bone health. Pharmacological uses of megadoses of some water-soluble vitamins, including vitamin B-6 and niacin, may help people with carpal tunnel syndrome, pregnancy-induced nausea, and elevated blood cholesterol. In addition to the water-soluble vitamins and choline, which have established Dietary Reference Intakes, the authors present two vitamin-like compounds (carnitine and taurine), which are synthesized by the body, but may be conditionally essential in some life stages or disease states. Although supplementation of folate and vitamin B-12 may be required during some life stages, overall, the authors emphasize the superiority of dietary sources over supplemental forms of most vitamins to achieve optimal health. Learning Objectives Identify the water-soluble vitamins. List important food sources for each water-soluble vitamin. Describe how each water-soluble vitamin is absorbed, transported, stored, and excreted. List the major functions of and deficiency symptoms for each water-soluble vitamin. Describe the toxicity symptoms from the excess consumption of certain water-soluble vitamins. Distinguish between vitamins and nonvitamins, such as carnitine and taurine. 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? Lecture Outline Water-Soluble Vitamin Overview General Essential organic compounds needed in small amounts for normal function, growth, and maintenance of body tissues General functions of vitamins (see Figure 13-1) Energy metabolism Thiamin Riboflavin Niacin Pantothenic Acid Biotin Vitamin B-12 Blood formation Vitamin B-6 Vitamin B-12 Folate Vitamin K Protein and amino acid metabolism Vitamin B-6 Folate Vitamin B-12 Vitamin C Choline Riboflavin Antioxidant defenses Vitamin E Vitamin C Carotenoids Riboflavin Gene expression Vitamin A Vitamin D Bone health Vitamin A Vitamin D Vitamin K Vitamin C Immune function Vitamin A Vitamin D Vitamin C Vitamin B-6 Water-soluble vitamins are not well-stored and pose low risk for toxicity, except for: Water-soluble vitamins are more easily destroyed than fat-soluble vitamins Heat Light Air Alkaline Tips for preserving the vitamin content of fruits and vegetables (see Table 13-1) Keep cool until eaten Refrigerate fruits and vegetables (except bananas, onions, potatoes, tomatoes, and unripe fruit) in moisture-proof, airtight containers or in the vegetable drawer Trim, peel, and cut fruits and vegetables minimally Microwave, steam, or stir-fry vegetables Minimize cooking time Avoid adding fats to vegetables during cooking if you plan to discard the liquid Do not add baking soda to vegetables to enhance green color Store canned and frozen fruits and vegetables carefully Eat canned and frozen foods within 12 months Coenzymes: A Common Role of B-Vitamins Coenzyme: small, organic molecules, type of cofactor Cofactor: substance that combines with an inactive form of an enzyme to activate it (e.g., metals, vitamins) Apoenzyme: inactive form of enzyme Holoenzyme: active form of enzyme (i.e., apoenzyme + cofactor) B-vitamin needs may increase with increased physical activity due to their role in energy metabolism, but increased food intake usually supplies requirements Examples of coenzyme forms of B-vitamins (see Table 13-2 and Figure 13-3) Thiamin pyrophosphate (thiamin) Flavin adenine dinucleotide (riboflavin) Flavin mononucleotide (riboflavin) Nicotinamide adenine dinucleotide (niacin) Nicotinamide adenine dinucleotide phosphate (niacin) Coenzyme A (pantothenic acid) N-carboxylbiotinyl lysine (biotin) Pyridoxyl phosphate (vitamin B-6) Tetrahydrofolic acid (folic acid) Methylcobalamin (vitamin B-12) In foods, B-vitamins exist as free vitamins and coenzymes, sometimes bound to proteins Digestion breaks down coenzymes and protein-bound vitamins to free vitamins Free vitamins are absorbed There is no benefit to consuming supplemental vitamins in coenzyme form over free form Enrichment and Fortification of Grains Milling of grains (refinement) removes germ, grain, and husk, which contain many vitamins and minerals (see Figure 13-5) Bread and cereal enrichment Thiamin Riboflavin Niacin Folic acid Iron Nutrients still low in enriched, refined grain products Vitamin B-6 Potassium Magnesium Zinc Fiber Phytochemicals Thiamin General Devastating effects of beriberi were seen in Asian countries where milled white (polished) rice is the staple food Also known as vitamin B-1 Chemistry Central carbon attached to 6-member nitrogen-containing ring and 5-member sulfur-containing ring Addition of two phosphate groups forms thiamin pyrophosphate (TPP), the coenzyme form of thiamin Thiamin in Foods Pork Sunflower seeds Legumes Whole and enriched grains and cereals Green peas Asparagus Organ meats Peanuts Mushrooms Some foods contain thiamin antagonists, which lower bioavailability of thiamin Some species of fresh fish and shellfish contain thiaminase enzymes; cooking inactivates them Coffee, tea, blueberries, red cabbage, Brussel sprouts, and beets contain compounds that inactivate thiamin Eating these foods has not been linked to thiamin deficiency Easily destroyed by cooking (heat) and alkaline Thiamin Needs and Upper Level RDA Adult men: 1.2 mg Adult women: 1.1 mg DV: 1.5 mg Average U.S. intake Men: 1.95 mg/d Women: 1.4 mg/d No UL has been set Absorption, Transport, Storage, and Excretion of Thiamin Absorption: in small intestine by sodium-dependent active absorption process Transport: by RBCs in its coenzyme form Storage: small reserves in muscles and liver Excretion: rapidly filtered by kidneys and excreted in urine Functions of Thiamin TPP is required for metabolism of carbohydrates and branched-chain amino acids Decarboxylation reactions: remove CO2 Pyruvate  acetyl CoA during the aerobic metabolism of glucose Alpha-ketoglutarate  succinyl CoA during citric acid cycle These reactions also require CoA (pantothenic acid), NAD (niacin), and FAD (riboflavin) Transketolase: enzyme in pentose phosphate pathway that forms DNA and RNA Thiamin Deficiency Develops after 14 days on thiamin-deficient diet Beriberi “I can’t, I can’t” in Sinhalese - leads to weakness due to impaired nervous, muscle, gastrointestinal, and cardiovascular function Symptoms, many due to disruption of glucose metabolism Peripheral neuropathy: numbness of extremities Weakness Muscle pain Muscle tenderness Enlargement of heart Difficulty breathing Edema Anorexia Weight loss Poor memory Confusion Wet beriberi: affects cardiovascular system, leading to congestive heart failure; also neurological symptoms Dry beriberi: nerve and muscular system Wernicke-Korsakoff Syndrome Mainly due to alcoholism Alcohol decreases thiamin absorption Alcohol increases urinary thiamin excretion Alcoholics consume poor-quality diet Symptoms Vision changes (e.g., double vision, crossed eyes, rapid eye movements) Ataxia: inability to coordinate voluntary muscle movement Confusion Apathy Riboflavin General Vitamin B-2 “Yellow enzyme” due to yellow-green fluorescence Chemistry: 3 linked 6-membered rings with a sugar alcohol attached to the middle ring Riboflavin in Foods Milk products Enriched white bread, rolls, and crackers Eggs Meat Liver Mushrooms Green leafy vegetables Broccoli Asparagus Susceptible to destruction by light; should be stored in plastic containers Riboflavin Needs and Upper Level RDA Adult men: 1.3 mg Adult women: 1.1 mg DV: 1.7 mg Average intake Men: 2.49 mg Women: 1.85 mg No UL has been set Absorption, Transport, Storage, and Excretion of Riboflavin Absorption Released from protein-bound form by HCl in stomach Free riboflavin absorbed by active transport or facilitated diffusion in the small intestine Transport: protein carriers Storage Converted to coenzyme forms mainly in small intestine, liver, heart, and kidneys Small amount stored in liver, kidneys, and heart Excretion: urine (excess may cause bright yellow urine that glows under black light) Functions of Riboflavin Coenzyme forms (flavins) participate in many oxidation/reduction reactions Flavin mononucleotide Flavin adenine dinucleotide (FAD is oxidized form, FADH2 is reduced form) Energy Metabolism Succinate  fumarate requires succinate dehydrogenase and FAD Beta-oxidation of fatty acids to acetyl CoA requires fatty acyl dehydrogenase and FAD FMN shuttles hydrogen atoms into the electron transport chain Other B-Vitamin Functions Tryptophan  niacin requires FAD Formation of PLP requires FMN Riboflavin participates in folate metabolism Antioxidant Function Synthesis of glutathione requires glutathione reductase and FAD Riboflavin Deficiency Ariboflavinosis Symptoms Inflammation of the throat, mouth (stomatitis), and tongue (glossitis) Cracking of tissue around the mouth (angular cheilitis) Moist, red, scaly skin (seborrheic dermatitis) Anemia Fatigue Confusion Headaches Difficult to separate from deficiencies of other B-vitamins Develops after 2 months of riboflavin-deficient diet Biochemical assessment Low riboflavin levels in RBCs Reduced activity of glutathione reductase High-risk populations Adolescent girls Elderly Cancer CVD Diabetes Alcoholism Malabsorption disorder Poor diet Long-term phenobarbital use increases breakdown of riboflavin and other nutrients in the liver Avoidance of milk or milk products Niacin General Pellagra is the only dietary deficiency disease to ever reach epidemic proportions in the U.S. (early 1900s in southeastern states) Vitamin B-3 Two forms Nicotinic acid (niacin) Nicotinamide (niacinamide) Two coenzyme forms Nicotinamide adenine dinucleotide (NAD+) Nicotinamide adenine dinucleotide phosphate (NADP+) Niacin in Foods Obtained from food as preformed niacin Poultry Meat Fish Enriched bread products Coffee and tea Mushrooms Wheat bran Peanuts Very heat stable Little cooking losses Synthesized by the body from tryptophan 60 mg tryptophan  1 mg niacin Also requires riboflavin and vitamin B-6 Protein is ~1% tryptophan To determine niacin derived from tryptophan, divide g protein/6 Amount of tryptophan in many foods has not yet been determined Niacin equivalents take into consideration preformed niacin and contribution of tryptophan Niacin Needs and Upper Level RDA Adult men: 16 mg/day Adult women: 14 mg/day Average intake Men: 31.2 mg/day Women: 20.8 mg/day DV: 20 mg UL: 35 mg (based on flushing; applies only to niacin supplements and fortified foods) Absorption, Transport, Storage, and Excretion of Niacin Absorption Nicotinic acid and nicotinamide are readily absorbed from stomach and small intestine by active transport and passive diffusion Bioavailability of niacin in low (30%) in some grains, especially corn (bound to protein) Soaking corn in lime water improves bioavailability of niacin Transport Freely transported via portal vein to liver Converted to coenzyme forms in all tissues Storage: liver Excretion: urine Functions of Riboflavin Coenzyme forms participate in 200+ oxidation/reduction reactions, especially those that produce ATP NAD+ is an electron and hydrogen acceptor; required for catabolism of carbohydrates, proteins, and fats NAD+ regenerated by pyruvate  lactate under anaerobic conditions In electron transport chain, NADH + H+ donates electrons and H+ Alcohol metabolism requires niacin coenzymes Synthetic pathways require NADPH + H+ (reduced form) Fatty acid synthesis Liver and mammary glands have high [NADPH + H+] Niacin Deficiency Pellagra (mal de la rosa, “red sickness”), once thought to be an infectious disease, was found to be a dietary deficiency Prevalent in areas with corn-based diets (low niacin bioavailability, low tryptophan content) Dr. Joseph Goldberger determined cause of pellagra Nicotinic acid was found to cure black tongue (similar to pellagra) in dogs Pellagra has been eradicated by enrichment of grains and protein-rich diets Symptoms Dermatitis (rough, red rash on skin exposed to sunlight) Diarrhea Dementia Death, if untreated High-risk populations Severe malabsorption Chronic alcoholism Hartnup disease (conversion of tryptophan  niacin is blocked) Pharmacological Use of Niacin 1 - 2 g/d nicotinic acid (60 x RDA; controlled time-release preparation) may be prescribed to increase HDL cholesterol and lower triglyceride levels In combination with diet, exercise, and other medications, nicotinic acid may lower risk of heart attack Side effects Flushing GI tract upset Liver damage Pantothenic Acid General “From every side” - supplied by a wide variety of foods Part of coenzyme A (combination of pantothenic acid, derivative of ADP, and part of cysteine) Sulfur atom (from cysteine) is functional end of CoA Pantothenic Acid in Foods Meat Milk Many vegetables Mushrooms Peanuts Egg yolks Yeast Broccoli Soy milk Unprocessed foods are better sources than processed foods (milling, refining, freezing, heating, and canning reduce pantothenic acid content) Pantothenic Acid Needs and Upper Level AI: 5 mg Average intake exceeds AI DV: 10 mg No UL has been set Absorption, Transport, Storage, and Excretion of Pantothenic Acid Absorption Released from CoA during digestion in small intestine Absorbed in small intestine Transport: bound to RBCs Storage: minimal, in CoA form Excretion: urine Functions of Pantothenic Acid CoA essential for formation of acetyl-CoA from metabolism of carbohydrate, protein, fat, and alcohol; enters citric acid cycle CoA is building block for fatty acids, cholesterol, bile acids, and steroid hormones Pantothenic acid forms acyl carrier protein, shuttles fatty acids through metabolic pathways to increase chain length CoA donates fatty acids to proteins Pantothenic Acid Deficiency Rare; only experimentally induced Symptoms Fatigue Headache Impaired muscle coordination GI tract disturbances Biotin General “Egg-white injury:” development of severe rash, fur loss, and paralysis in rats fed large amounts of egg whites Sources of Biotin: Food and Microbial Synthesis Two forms in food Free vitamin Biocytin: protein-bound form Food sources Whole grains Eggs Nuts Legumes Nutrient databases are incomplete with respect to biotin content of many foods Bacteria in the large intestine synthesize biotin; bioavailability from this source is unknown because most efficient absorption occurs in small intestine Biotin Needs and Upper Level AI: 30 µg DV: 300 µg No UL has been set Absorption, Transport, Storage, and Excretion of Biotin Absorption In small intestine, biotinidase releases biotin from biocytin and other biotin-dependent enzymes found in foods Free biotin absorbed in small intestine by sodium-dependent carrier Storage: small amounts in muscles, liver, and brain Excretion: urine, minor amount in bile Functions of Biotin Coenzyme for carboxylase enzymes that add CO2 to various compounds; required for metabolism of carbohydrates, proteins, and fats Pyruvate  oxaloacetate Catabolism of threonine, leucine, methionine, and isoleucine for energy Acetyl-CoA  malonyl CoA in fatty acid synthesis Biotin Deficiency Rare High-risk populations 1/112,000 infants has genetic defect that results in low biotinidase Ingestion of large amounts of raw egg whites (avidin binds biotin; denatured by cooking) Symptoms Skin rash Hair loss Convulsions Low muscle tone Impaired growth Vitamin B-6 General Vitamin B-6 coenzyme required for metabolism of amino acids Family of 3 compounds, all of which can by phosphorylated to become active coenzymes Pyridoxal Pyridoxine Pyridoxamine Pyridoxal phosphate (PLP) is primary vitamin B-6 coenzyme Vitamin B-6 in Foods Animal sources are most bioavailable Meat Fish Poultry Plant sources Whole grains (lost during refinement, not replaced by enrichment) Carrots Spinach Potatoes Bananas Avocados Fortified breakfast cereals Susceptible to destruction by heat and other processing Vitamin B-6 Needs and Upper Level RDA Adult men and women up to age 50: 1.3 mg Adult men > 50: 1.7 mg Adult women > 50: 1.5 mg DV: 2 mg Average intakes exceed RDA Men: 2.5 mg Women: 1.7 mg UL: 100 mg, based on development of nerve problems Absorption, Transport, Storage, and Excretion of Vitamin B-6 Absorption Coenzyme form normally converted to free vitamin form; but some absorbed as coenzyme Absorbed by passive diffusion Transport Free vitamin transported via portal vein to liver, where it is phosphorylated Phosphorylated form (mainly PLP) transported bound to albumin Storage: muscle tissue Excretion: urine Functions of Vitamin B-6 PLP is coenzyme in 100+ reactions, mostly involving nitrogen-containing compounds Metabolism Transamination reactions transfer amino groups to allow synthesis of non-essential amino acids Homocysteine  cysteine during methionine metabolism Release of glucose from glycogen; PLP helps maintain blood glucose Synthesis of Compounds In RBCs, PLP catalyzes a step in heme synthesis Neurotransmitter synthesis Tryptophan  serotonin Tyrosine  dopamine or norepinephrine Histidine  histamine Glutamic acid  gamma-aminobutyric acid (GABA) Vitamin formation Tryptophan  niacin Other functions Help support normal immune function Regulation of gene expression May help prevent colon cancer May help reduce inflammatory disease CVD Inflammatory bowel disease Diabetes Rheumatoid arthritis Vitamin B-6 Deficiency Rare Symptoms Seborrheic dermatitis Microcytic hypochromic anemia: small, pale RBCs that lack sufficient hemoglobin and have reduced O2-carrying capacity Convulsions Depression Confusion High-risk populations Poor diets Alcoholics: acetaldehyde decreases formation of PLP and may reduce its biological activity Use of L-DOPA for Parkinson’s disease Use of isoniazid for tuberculosis Use of theophylline for asthma Pharmacological Use of Vitamin B-6 Carpal tunnel syndrome: insufficient evidence Premenstrual syndrome: may be useful Nausea during pregnancy: insufficient evidence Folate General “Folium:” leaf Folate: various, naturally-occurring forms in foods Folic acid: synthetic form found in supplements and fortified foods Consists of three parts Pteridine Para-aminobenzoic acid (PABA) One or more molecules of glutamic acid Folate monoglutamate (folic acid) contains one glutamate molecule Polyglutamates have 3 or more glutamates; 90% of food sources Folate in Foods Liver Legumes Green leafy vegetables Avocados Oranges, orange juice, grapefruit juice Fortified grains and cereals Bread Milk (low content, but high consumption) Potatoes (low content, but high consumption) 50 - 90% destroyed by food processing and preparation Heat Oxidation UV light Vitamin C is protective Dietary Folate Equivalents Dietary folate equivalents (DFE) reflect differences in absorption from natural and synthetic sources 1 DFE = 1 µg food folate = 0.6 µg folic acid taken with food = 0.5 µg folic acid taken on an empty stomach DFE = µg food folate + (µg folic acid x 1.7) Folate Needs RDA: adults: 400 µg Average intake: Men: 628 DFE Women: 474 DFE DV: 400 µg Upper Level for Folate UL = 1000 µg; applies only to synthetic folic acid Excess folate may mask vitamin B-12 deficiency FDA limits folic acid in non-prescription vitamin supplements Absorption, Transport, Storage, and Excretion of Folate Absorption Polyglutamates must be hydrolyzed by folate conjugases in the absorptive cells of the GI tract to the monoglutamate form Monoglutamate form actively transported in small intestine Synthetic form without food has nearly 100% bioavailability Transport Via portal vein to liver, converted to polyglutamate form inside cells (traps inside cells) Some is released in blood and bile Folate in bile is reabsorbed via enterohepatic circulation (diminished in alcoholics) Storage: liver Excretion Urine Feces Functions of Folate Exchange of single carbon groups in metabolic pathways Central coenzyme form: tetrahydrofolic acid (THFA) DNA Synthesis Folate supplies methylene group to uracil to form thymine Synthesis of purines (adenine and guanine) Recycling of folate coenzyme requires vitamin B-12 coenzyme Cancer drug methotrexate is a folate antagonist; interferes with THFA metabolism in rapidly proliferating cells; may require supplemental folate to reduce toxic side effects Amino Acid Metabolism Transfers 1-carbon groups among amino acids Glycine  serine Histidine  glutamic acid Homocysteine  methionine (with vitamin B-12) Other Functions Formation of neurotransmitters; supplementation may enhance action of antidepressant medications Maintenance of normal blood pressure Reduced risk of colon cancer Folate Deficiency Fortification of the food supply has decreased the number of persons with low red blood cell folate (which measures long-term body stores) from 30% to > 1% High-risk populations Low intake Malabsorption (alcoholics, chronic GI diseases) Increased need (e.g., pregnancy increases needs to 600 µg) Compromised utilization (e.g., vitamin B-12 deficiency) Chemotherapy medications Anti-convulsant medications Consequences Megaloblastic (macrocytic) anemia: RBCs cannot divide normally to become mature red blood cells; large, immature RBCs Large, immature cells in the GI tract; decreased absorptive capacity leads to diarrhea Compromised immune function due to disruption of WBC synthesis Neural tube defects Clinical Perspective: Neural Tube Defects Defect in early development of the neural tube leads to: Spina bifida: spinal cord or spinal fluid bulge through the back Paralysis Incontinence Hydrocephalus Learning disabilities Anencephaly: absence of a brain; leads to death shortly after birth Neural tube forms and closes during the first 21 - 28 days after conception Ensuring good folate status among women of childbearing potential is important Folic acid fortification of refined cereals and grains began in 1998 Rates have decreased by 1/3 Rates vary by race and ethnicity Movement to double rate of fortification is countered by those who are concerned over the risk of masking vitamin B-12 deficiency Fortified foods supply 200 µg/d Vitamin B-12 General Animal products are the only reliable sources Contains cobalt as part of complex, multi-ring structure Two active coenzymes Methylcobalamin 5-deoxyadenosylcobalamin Research linking vitamin B-12 deficiency to pernicious anemia was worthy of 6 Nobel Prizes Vitamin B-12 in Foods Synthesized by microorganisms Grazing animals acquire vitamin B-12 through soil Bacteria synthesize vitamin B-12 in ruminant animals Meat (especially organ meats) Poultry Seafood Eggs Dairy products Fortified foods Algae and fermented soy products may contain vitamin B-12 analogs, which may not function as vitamin B-12 in the body Vitamin B-12 Needs and Upper Level RDA: 2.4 µg DV: 6 µg Average intake exceeds RDA, providing 2 to 3 years’ worth of storage in liver Men: 6.3 g Women: 4.6 g No UL has been set Absorption, Transport, Storage, and Excretion of Vitamin B-12 Absorption HCl and pepsin in gastric juice release vitamin B-12 from proteins In stomach, free vitamin B-12 binds to R-protein (from salivary glands) In small intestine, pancreatic protease enzymes (e.g., trypsin) release vitamin B-12 from R-protein Free vitamin combines with intrinsic factor (from parietal cells of stomach) Vitamin B-12/intrinsic factor complex travels to ileum Vitamin B-12/intrinsic factor complex is absorbed in the ileum (50% efficiency) Synthetic vitamin B-12 (crystalline form) is readily absorbed without R-protein and intrinsic factor Transport: bound to transcobalamin II Storage: liver can store enough vitamin B-12 to last several years Excretion Bile (reabsorbed by enterohepatic circulation) Little excreted in urine Functions of Vitamin B-12 Homocysteine  methionine requires methionine synthase and methylcobalamin (vitamin B-12 coenzyme) Methionine then forms S-adenosyl methionine (SAM), which serves as a methyl donor in many reactions (e.g., DNA and RNA regulation, myelin regulation, biosynthesis of many compounds) 5-methyl-tetrahydrofolate (folate coenzyme) donates methyl group to methylcobalamin to reform THFA Deficiency of vitamin B-12 or folate leads to decreased methionine and SAM synthesis, increased [homocysteine] Metabolism of fatty acids with odd numbered carbon chain requires methylmalonyl mutase and 5-deoxyadenosylcobalamine (vitamin B-12 coenzyme) Vitamin B-12 Deficiency Pernicious (“leading to death”) anemia can result from inadequate production of intrinsic factor Macrocytic (megaloblastic) Anemia Identical to anemia from folate deficiency Due to disruption of normal DNA and RBC synthesis Neurological Changes Paresthesia: burning, tingling, prickling, and numbness in the legs Mental problems: loss of concentration and memory, disorientation, dementia Loss of bowel and bladder control Visual disturbances GI tract problems: sore tongue, constipation Neurological complications often precede development of anemia Elevated Plasma Homocysteine Concentrations Risk factor for heart attack and stroke Associated with cognitive dysfunction Associated with osteoporotic fractures Supplementation with folate, B-12, and B-6 can lower blood homocysteine, but evidence that supplementation lowers risk for diseases associated with high blood homocysteine is weak Persons at Risk of Vitamin B-12 Deficiency Affects ~20% of older Americans Mostly due to atrophic gastritis Not severe enough to produce anemia, but may lead to neurological problems and elevated homocysteine Supplementation with crystalline vitamin B-12 improves vitamin status Malabsorption syndromes Monthly injections to bypass GI tract Use of vitamin B-12 nasal gel to bypass GI tract Very high oral doses (1 - 2 mg/d), some of which is passively absorbed Vegetarians Liver stores from previous omnivorous diet can delay onset for years Infants born to or breastfed by vegetarian or vegan mothers may develop anemia, neurological problems, diminished brain growth, degeneration of spinal cord, poor intellectual development; supplementation and use of fortified foods is advised Choline General Recognized as an essential nutrient in 1998 Synthesized in cells, but this alone cannot support needs Low dietary intakes can lead to liver and muscle damage Choline is not yet considered a B-vitamin No coenzyme form Higher concentrations in the body than B-vitamins Composed of phospholipids, such as phosphatidylcholine (lecithin) Choline in Foods Milk Eggs Chicken Beef Pork Lecithin added to foods during processing Nutrient content data is incomplete for many foods Choline Needs and Upper Level AI Adult men: 550 mg Adult women: 425 mg Average intake Men: 396 mg Women: 260 mg UL: 3.5 g based on fishy body odor, low blood pressure, vomiting, salivation, sweating, and GI tract effects Absorption, Transport, Storage, and Excretion of Choline Absorption: small intestine via transport proteins Transport: via portal vein to liver Storage: all tissue store some choline Excretion of Choline Some excreted in urine Most converted to betaine (methyl donor) Functions of Choline Component of phospholipids Precursor for acetylcholine, a neurotransmitter associated with attention, learning, memory, and muscle control Liver export of VLDL Methyl donor for homocysteine  methionine May protect against cardiovascular disease based on association of high intakes of choline with low [C-reactive protein], a marker of inflammation Choline Deficiency Liver and muscle damage observed in humans fed choline-deficient diets Vitamin C General Humans, guinea pigs, fruit bats, and some birds and fish are unique in their inability to synthesize vitamin C Ascorbic acid and dehydroascorbic acid (oxidized form) Electron donor for many body processes Vitamin C in Foods Citrus fruits Peppers Green vegetables Tomatoes Fortified fruit drinks Potatoes (due to high consumption) Least stable vitamin, easily lost in processing and cooking (up to 40%) Unstable when it comes in contact with iron, copper, and oxygen Acidity of juices reduces destruction of vitamin C Vitamin C Needs RDA Adult men: 90 mg Adult women: 75 mg DV: 60 mg Average intakes exceed RDA, but 40% of adults consume less than the EAR and 6% are deficient Smokers require 35 mg/d extra vitamin C Upper Level for Vitamin C 2 g based on adverse GI effects (e.g., bloating, stomach inflammation, diarrhea) High doses slightly increase risk of kidney stone formation and excess iron absorption in high-risk individuals High doses may give false results for blood in the stool Absorption, Transport, Storage, and Excretion of Vitamin C Absorption Ascorbic acid is absorbed in the small intestine by active transport Dehydroascorbic acid is absorbed in the small intestine by facilitated transport Absorption efficiency is 70 - 90% at recommended intakes, but declines as intakes increase above RDA Storage Highly concentrated in pituitary and adrenal glands, white blood cells, eyes, and brain Low concentrations in blood and saliva Excretion: urine Functions of Vitamin C Electron donor in oxidation/reduction reactions Cofactor role for several metalloenzymes (e.g., keeps iron in reduced ferrous form, allowing enzymes that require iron as a cofactor to remain active) Collagen Synthesis Major fibrous protein that gives strength to connective tissues, such as tendons and ligaments Found in bone, blood vessels, eyes, and skin Essential in wound healing 3 polypeptide chains wound into triple helix; vitamin C aids in the conversion of lysine to hydroxylysine and proline to hydroxyproline to hold collagen’s 3-D structure Synthesis of Other Vital Compounds Aids in biosynthesis by keeping iron or copper in metalloenzymes in reduced state (Fe2+ or Cu+) Tyrosine Thyroxine Carnitine Neurotransmitters (e.g., norepinephrine, epinephrine, serotonin) Conversion of cholesterol to bile acids Corticosteroids Aldosterone Antioxidant Activity Donates electrons to free radicals in vitro; theorized to act as antioxidant in water-based fluids Recycling of vitamin E Some research indicates that vitamin C increases oxidative stress (e.g., in diabetes) High concentrations in eye tissue and neutrophils (type of WBC) suggest that vitamin C does have antioxidant actions Iron Absorption With meals, vitamin C modestly facilitates intestinal absorption of non-heme iron by conversion from ferric to ferrous forms Counters action of food components that inhibit iron absorption Immune Function Highest concentration of vitamin C in WBCs, which may protect against oxidative damage Supplementation beyond RDA may is not recommended for improving immune function Vitamin C Deficiency Scurvy is due to impaired synthesis of collagen Fatigue Pinpoint hemorrhages Bleeding gums and joints Impaired wound healing Bone pain Fractures Diarrhea Psychological problems (e.g., depression) Fatal if untreated Vitamin C, Cancer, and Heart Disease Based on roles of vitamin C in antioxidant and immune functions Best evidence for prevention of cancers of mouth, esophagus, stomach, and lung, but healthy diet is advocated rather than vitamin C supplementation Many, but not all, studies suggest that good vitamin C status protects against heart disease, but clinical trials fail to provide evidence of the connection Vitamin C Intake above the RDA Little research exists to compare various levels of intake Above 100 mg/d, excess is generally excreted in urine 200 mg/d is suggested to be highest amount needed to maximize health benefits of vitamin C; can be obtained through consumption of fruits and vegetables Vitamin C and the Common Cold Doses up to 1000 mg/d Any benefit is modest (e.g., reduce cold duration by 1 day) Not enough evidence to suggest megadoses of vitamin C for prevention of common cold Vitamin-Like Compounds General Necessary to maintain normal body functions Can be synthesized in the body, but biosynthesis is at expense of other nutrients (e.g., amino acids) Needs increase during times of rapid tissue growth, but deficiencies do not exist in otherwise healthy adults Additional research is required to determine whether vitamin-like compounds are required in specific life stages or disease states Currently included in infant formulas Carnitine Needs are met from animal foods (meat and dairy products) and liver biosynthesis from lysine and methionine Average consumption: 100 - 300 mg/d Functions Transports fatty acids from cytosol to mitochondria for beta-oxidation Removal of excess organic acids produced by mitochondrial metabolism Removal of toxic compounds in people with inborn errors of metabolism Improvements in people with progressive muscle disease and heart muscle deterioration Research on use for weight loss or ergogenic aid is limited May be conditionally essential Recovery from disease Malnutrition Serious trauma Cirrhosis Kidney dialysis Preterm birth Taurine Synthesized from methionine and cysteine Abundant in muscle, platelets, and nerve tissue Attached to bile acids Dietary sources: animal products Average consumption: 2% of body weight Perspiration contains only 2/3 the sodium content of blood, but seems salty due to evaporation of water Symptoms Headache Nausea/vomiting Fatigue Muscle cramps Seizures, coma, death in severe cases Prevention/treatment Salting foods Sports drinks Excess Sodium and Upper Level UL: 2300 mg Persistent sodium intakes over the UL can increase the chance of developing high blood pressure, heart disease and stroke Additional concerns Increased calcium losses in urine (although not linked to osteoporosis risk) Increased risk of calcium oxalate kidney stones American Medical Association and World Health Organization call for 50% reduction in sodium content of processed and restaurant foods Reducing sodium intake to less than 240 mg/day will reduce prevalence of hypertension by at least 20% and reduce mortality from coronary heart disease and stroke Food labels help consumers identify sodium content of food Nutrition Facts panel Salt-free, sodium-free, low sodium Taste preferences adjust with low-sodium diet Table 14-6 provides tips for decreasing sodium intake Potassium (K) Potassium in Foods Unprocessed foods are best sources of potassium Fruits Vegetables Milk Whole grains Dried beans Meats Salt substitutes (potassium chloride) Food additives Potassium Needs AI: 4700 mg DV: 3500 mg Average potassium intakes range from 2408 - 3172 mg/day Absorption, Transport, Storage, Excretion of Potassium Absorption 90% absorption efficiency Absorbed in small and large intestines Transport: ion in body fluids Storage: 95% of potassium is found in cells Excretion: urine Functions of Potassium Fluid balance Transmission of nerve impulses Contraction of muscles High potassium decreases calcium excretion in urine High potassium suppresses renin-angiotensin system and promotes excretion of excess sodium and water Potassium Deficiency Hypokalemia is life-threatening Consequences Weakness Fatigue Constipation Arrhythmia Increased blood pressure Increased risk of stroke Increased risk of kidney stones Increased risk of bone loss Causes Losses via urine (e.g., due to diuretics) Losses via GI tract (e.g., excessive vomiting) Low dietary intake (e.g., eating disorders or alcoholism) Heavy perspiration Excess Potassium and Upper Level Hyperkalemia is also life-threatening Causes Not likely due to high dietary intake; excess would be excreted in urine Kidney disease impairs excretion Consequences Irregular heartbeat Cardiac arrest Intestinal upset Chloride (Cl) General Main anion in the extracellular fluid Chlorine (Cl2) is toxic Chloride in Foods Table salt Same foods that supply sodium Seaweed Olives Rye Lettuce Fruits Vegetables Salt substitutes Chloride Needs AI: 2300 mg, based on AI for sodium DV: 3400 mg Average daily consumption of 9 g of salt yields 5400 mg of chloride Absorption, Transport, Storage, and Excretion of Chloride Absorption Efficient absorption in small and large intestines Follows sodium absorption to balance ions in extracellular fluid Transport: ion in body fluids Storage: extracellular fluid, associated with sodium Excretion: urine Functions of Chloride Major anion in extracellular fluid; maintains extracellular fluid volume and balance Transmission of nerve impulses Component of HCl Immune response Acid-base balance Excretion of CO2 via lungs Chloride Deficiency Causes Unlikely due to high salt intake Frequent and lengthy bouts of vomiting coupled with nutrient-poor diet Consequences Weakness Anorexia Lethargy Disruption of acid-base balance Upper Level for Chloride UL: 3600 mg, based on UL for sodium Dietary chloride has been implicated along with sodium as a culprit for hypertension Clinical Perspective: Hypertension and Nutrition General 1 in 3 adults has hypertension Measurement of blood pressure Systolic: pressure in arteries when heart contracts Diastolic: pressure in arteries when heart relaxes Classifying blood pressure (see Table 14-7) Normal: <120/<80 Prehypertenion: 120 - 139/80 - 89 Hypertension, stage 1: 140 - 159/90 - 99 Hypertension, stage 2: ≥160/≥100 Causes of Hypertension Secondary hypertension (5 - 10% of cases) Kidney disease Liver disease Diabetes Primary hypertension Develops over a period of years as arteries narrow and harden (arteriosclerosis) Endothelial cells release vasoconstrictors in response to arterial damage Increased production of renin by kidneys, leading to increased angiotensin II, a powerful vasoconstrictor that triggers sodium and water retention Risk Factors for Hypertension Age: 90%+ over age 55 develop hypertension Race: African-Americans develop hypertension more often and at younger age than whites Obesity: increased fat mass adds blood vessels, increasing heart’s workload Diabetes: elevated insulin increases sodium retention; 65% of diabetics also have hypertension Effects of Hypertension Damage to arteries Heart attack Stroke Kidney failure Vision loss Lifestyle Modifications to Prevent and Treat Hypertension Modest weight loss (10 lbs.) for overweight person DASH eating plan: high in fruits, vegetables, low-fat dairy; low in sodium and saturated and total fat Moderate physical activity, particularly aerobic exercise Control alcohol intake Control sodium intake Minerals, Phytochemicals, and Hypertension Sodium Intersalt study: as urinary sodium excretion increases, blood pressure increases Salt sensitivity (only 25-50% of people experience high blood pressure with high salt intake, trial of sodium restriction is only way to determine salt sensitivity, African-Americans, overweight people, those with diabetes, and the elderly are more likely to be salt sensitive) High potassium, low sodium diet offers best protection against hypertension High calcium linked to lower blood pressure High magnesium linked to lower blood pressure High fiber linked to lower blood pressure Chocolate made from cocoa may have modest reductions in blood pressure due to flavanols that may improve insulin action, vascular function, and inhibit renin-angiotension system Caffeine temporarily increases blood pressure, but chronic intake is not associated with increased blood pressure The Dietary Approaches to Stop Hypertension (DASH) Diet Food plan Grains: 6 - 8 servings/day (emphasize whole grains) Vegetables: 4 -5 servings/day Fruits: 4 - 5 servings/day Fat-free or low-fat milk products: 2 - 3 servings/day Lean meats, poultry, and fish: 6 or less servings/week Nuts, seeds, and legumes: 4 - 5 servings/week Fats and oils: 2 - 3 servings/day Sweets and added sugars: 5 or less per week Nutrient goals Low in fat (27% of kcal) Low in saturated fat (6% of kcal) Moderate in protein (18% of kcal) Moderate in carbohydrates (55% of kcal) Low in cholesterol (150 mg/day) Low in sodium (2300 mg/d is effective, 1500 mg/day shows better reductions in blood pressure) High in potassium (4700 mg/day) High in calcium (1250 mg/day) High in magnesium (500 mg/day) High in fiber (30 g/day) Works as well as medications for those with hypertension Health benefits of DASH diet Reduced blood pressure Cancer prevention Heart disease prevention Drug Therapy for Hypertension Usually initiated when blood pressure exceeds 140 mmHg systolic and/or 90 mmHg diastolic on 3 or more occasions Diuretics: increase water and salt excretion; may increase potassium excretion (e.g., furosemide and hydrochlorothiazide) Beta-blockers: slow heart rate and decrease force of heart contraction (e.g., metropolol) Angiotensin-converting enzyme (ACE) inhibitors: reduce conversion of angiotensin I to angiotensin II in the lung, leading to vasodilation (e.g., captopril) Calcium channel blockers: prevent calcium from entering cells of heart and blood vessels, leading to vasodilation (e.g., nifedipine) Calcium (Ca) Calcium in Foods Dairy products are most bioavailable dietary source of calcium, provide ½ calcium in American diets Yeast breads, rolls, crackers Leafy greens (e.g., collards, kale, turnip greens), although bioavailability in some foods is limited by oxalic acid Broccoli Calcium-fortified foods (e.g., orange juice, breakfast cereals) Canned fish with bones Soybean curd made with calcium carbonate Calcium Needs RDA Based on promoting bone growth and maintenance Adults up to age 50: 1000 mg Women 50+ and men 70+: 1200 mg Adolescents: 1300 mg DV: 1000 mg Average intake is adequate for men, but inadequate for women and older men Calcium Supplements Helpful for those with restricted calorie intakes and those who avoid dairy products Made of calcium salts Calcium carbonate (40% calcium) Calcium citrate: better for those with low stomach acid Calcium gluconate (9% calcium) May contain vitamin D to boost calcium absorption Dose should be no more than 500 mg at a time Consuming with meals improves absorption due to higher acid concentration in stomach Calcium supplements should be used with care (below 1.5 g/day) Excessive use of calcium and vitamin D supplements is associated with calcium-alkali syndrome (milk-alkali syndrome) Hypercalcemia, can lead to kidney stones, high blood pressure, and kidney failure Evidence that calcium supplements may increase calcium deposits in coronary arteries Interactions with other minerals; do not take calcium supplements at the same time as other mineral supplements Zinc Iron Magnesium Contamination with lead Most likely in supplements made with bone meal or oyster shell Look for USP label to lessen risk of contamination Calcium Absorption, Transport, Storage, Regulation, and Excretion Absorption Most efficient in upper small intestine due to slightly acidic pH Occurs along length of intestinal tract via passive diffusion Absorption efficiency: 25 - 30% for healthy adults Factors that increase calcium absorption Active vitamin D hormone (in upper GI tract) Increased need (e.g., infancy, pregnancy), absorption increases to 75% Lactose and other sugars Protein Factors that decrease calcium absorption Age Phytic acid Oxalic acid Excessive phosphorus Polyphenols Vitamin D deficiency Diarrhea Fat malabsorption: fatty acids bind to calcium to form unabsorbable soaps Transport Free ionized calcium Bound to proteins Storage 99% in skeleton and teeth Small, regulated amount in blood Regulation Because of tight regulation, blood calcium is a poor indicator of calcium status When blood calcium is low, parathyroid gland releases parathyroid hormone (PTH): Works with calcitriol to increase kidney’s reabsorption of calcium Increases calcium absorption by increasing synthesis of calcitriol Works with calcitriol to increase release of calcium from bones When blood calcium is high, release of PTH falls Urinary calcium excretion increases Synthesis of calcitriol decreases, leading to decreased absorption of calcium Thyroid gland secretes calcitonin, which blocks calcium loss from bones Excretion Urine Skin Feces (intestinal secretions) Functions of Calcium Bone Development and Maintenance Calcium and phosphorus are main bone minerals, form hydroxyapatite, which imparts strength and resilience Collagen forms bone matrix, allows absorption of impact Compact (cortical) bone Outer, dense shell 75% of skeletal mass Spongy (trabecular) bone Inner, spongy network of rods, plates, and spines Abundant at ends of long bones, inside vertebrae, inside flat bones of pelvis Site of mineral exchange Remodeling: continuous building, breaking down, and replacing bone Repairs damaged and brittle areas Allows withdrawal of stored minerals Osteoblasts: bone building cells that produce collagen and add minerals to bone; most active during times of growth and stress (e.g., weight-bearing activity) Osteocytes: mature osteoblasts; take up and release minerals Osteoclasts: release acids and enzymes on the bone surface to dissolve bone; stimulated by PTH and 1,25 (OH)2 vitamin D; most active when dietary calcium is deficient From infancy through adolescence, osteoblast activity exceeds osteoclast activity During early adulthood, continuous remodeling takes place and some small increases in bone mass occur During middle age and older adulthood, osteoclast activity exceeds osteoblast activity Bone mass declines 25% with aging, or more for women with low estrogen (e.g., menopause, amenorrhea, oophorectomy) because estrogen inhibits osteoclast activity Other nutrients involved in bone metabolism Magnesium Potassium Sodium Fluoride Vitamin K Sulfur Blood Clotting: calcium ions participate in formation of fibrin Transmission of Nerve Impulses to Target Cells When nerve impulses reach a synapse, calcium ions from the extracellular fluid flow into the nerve Rise in calcium ions in the nerve triggers vesicles to release neurotransmitters, carrying a nerve impulse to the target cell If insufficient calcium is available, hypocalcemic tetany develops, in which muscles receive continual nerve stimulation, resulting in continuous, forceful muscle contraction without relaxation; usually caused by inadequate PTH release or action Muscle Contraction Nerve signal from the brain causes calcium ions to be released from muscle cells Increased calcium ions in muscle cells (with ATP) permits muscle contraction Active transport of calcium ions to intracellular storage allows muscle relaxation Cell Metabolism (calmodulin system) Each calmodulin bins 4 calcium ions Calcium-calmodulin complex activates many intracellular enzymes Potential Health Benefits of Calcium Bone health Protection against colon cancer Protection against some forms of kidney stones (but not calcium from supplements) Decreased blood pressure Upper Level for Calcium UL: 2500 mg, based on increased risk of kidney stones at higher intakes In some cases, high amounts of calcium can cause hypercalcemia Consequences of excessive blood calcium Calcification of kidneys and other organs Irritability Headache Kidney failure Kidney stones Decreased absorption of other minerals Clinical Perspective: Osteoporosis General Low calcium intake is most common cause; calcium is withdrawn from bone to maintain blood calcium levels Develops over many years Failure to maintain adequate bone mass first leads to osteopenia (low bone mass) Diagnosis of osteoporosis occurs when bone mass has declined to the extent that bone strength is compromised and bones are likely to break (e.g., hip, wrist, vertebrae) Kyphosis (dowager’s hump): compression fractures in vertebrae lead to loss of height 9 million adults suffer from osteoporosis; 43 million have low bone mass Ethnic/racial disparity African-Americans are least likely to develop osteoporosis Highest rates in Caucasian and Asian populations Risk factors for osteoporosis Family history Small, thin skeletal frame Low peak bone mass Advancing age Caucasian or Asian ancestry Postmenopausal Amenorrhea Oophorectomy: removal of ovaries Smoking Low calcium intake Vitamin D deficiency Low physical activity Excessive alcohol consumption Diseases that impair nutrient absorption, metabolism, or utilization of bone-forming nutrients or increase their excretion (e.g., cystic fibrosis, anorexia nervosa, type 1 diabetes mellitus, inflammatory bowel disease, celiac disease, multiple sclerosis, epilepsy) Some medications (e.g., glucocorticoids) Osteoporosis Diagnosis Dual energy X-ray absorptiometry (DEXA) bone scan measures ability of bone (spine, hips, and whole body) to block the path of radiation; compare with bone density of person at peak bone density Peripheral DEXA or ultrasound: measure bone density at one site (e.g., wrist or heel); faster than DEXA, but not as accurate Osteoporosis Prevention Consume ample calcium, vitamin D, phosphorus, magnesium, potassium, vitamin K, and protein Calcium-rich foods and supplements decrease bone turnover, increase bone density and reduce risk of fractures Physical activity, including weight-bearing activity; also improves balance and strength to reduce risk of falling Smoking cessation Limited alcohol intake Moderate intakes of caffeine, sodium, and protein to decrease calcium excretion Decrease of more than 1 ½ inches from pre-menopausal height is a sign of significant bone loss among postmenopausal women Five medical therapies used to slow bone loss at menopause: Estrogen: slows osteoclast activity, but may increase risk of CVD and certain cancers Bisphosphonates: bind to hydroxyapatite crystals and osteoclasts to slow bone resorption (e.g., alendronate and ibandronate) Selective estrogen receptor modulators (SERMS): increase utilization of existing estrogen to slow osteoclast activity (e.g., raloxifene) Calcitonin: inhibits osteoclast activity and bone resorption PTH: stimulates osteoblast activity and new bone formation Phosphorus (P) General Major component of bones and teeth Glowing material Required by every body cell Phosphorus in Foods Milk Cheese Meat Bakery products Cereals Bran Nuts Fish Food additives (may not be included in nutrient databases) Nutrients used for fortification Phosphorus Needs RDA: 700 mg DV: 1000 mg Average intake: 1190 - 1655 mg Absorption, Transport, Storage, and Excretion of Phosphorus Absorption Absorption efficiency up to 70% Mainly in upper small intestine by both active transport and diffusion Enhanced by 1,25 (OH)2 vitamin D Phosphorus in grains and legumes is not well absorbed due to binding by phytates, but leavening releases phosphorus Transport: phosphate ion Storage of Phosphorus 80% found in bones and teeth as a component of hydroxyapatite Extracellular fluid Body cells Excretion: urine Functions of Phosphorus Major component of bones and teeth Main intracellular anion (HPO42- or H2PO4-) Component of ATP and creatine phosphate Component of DNA and RNA Component of phospholipids in cell membranes Takes part in enzyme and cellular message systems (phosphorylation activates many hormones and enzymes) Regulation of acid-base balance Phosphorus Deficiency Rare Consequences Bone loss Decreased growth Poor tooth development Symptoms of rickets due to insufficient bone mineralization Anorexia Weight loss Weakness Irritability Stiff joints Bone pain High-risk populations Premature infants Alcoholics Older adults with nutrient-poor diets Chronic diarrhea or weight loss Frequent use of aluminum-containing antacids (bind phosphorus in small intestine) Toxicity and Upper Level for Phosphorus Rare Hyperphosphatemia is usually due to compromised kidney function Consequences: calcium-phosphorus deposits in body tissues UL: 3 - 4 g, based on development of high blood [P] Magnesium (Mg) Magnesium in Foods Component of chlorophyll; richest sources are plant foods Green leafy vegetables Broccoli Squash Beans Nuts Seeds Whole grains Chocolate Animal products supply some Mg Milk Meats Hard tap water Magnesium oxide (in supplements) is not well absorbed Magnesium Needs RDA Adult men (age 19 - 30): 400 mg Adult women (age 19 - 30): 310 mg Needs slightly increase beyond age 30 DV: 400 mg Average intakes: 267 – 349 mg/day Fewer than 25% pf adults meet the RDA Absorption, Transport, Storage, and Excretion of Magnesium Absorption 30 - 40% absorption efficiency, but may rise to 80% when intakes are low Small intestine by both passive and active transport Enhanced by1,25 (OH)2 vitamin D Storage Bones (about 50%) Other tissue (particularly muscle) Excretion: kidneys Functions of Magnesium Stabilizes ATP by binding phosphate groups Cofactor for more than 300 enzymes that utilize ATP Energy metabolism Muscle contraction Protein synthesis Required for activity of cellular sodium-potassium pump DNA and RNA synthesis Role in calcium metabolism, contributes to bone structure and mineralization Nerve transmission Heart and smooth muscle contraction Glucose and insulin metabolism Decreased blood pressure due to vasodilation Prevention of arrhythmias Protective against gallstone formation Magnesium Deficiency Consequences, likely due to impaired function of Na/K pump Irregular heartbeat Weakness Muscle spasms Disorientation Nausea Vomiting Seizures Decreased PTH release, resulting in low blood calcium Blunted action of 1,25 (OH)2 vitamin D Increased risk of metabolic syndrome Slow to develop due to body storage Causes Excessive GI tract losses (e.g., prolonged diarrhea or vomiting) Excessive urinary losses (e.g., use of diuretics) Alcoholism Poorly controlled diabetes Low dietary intake Heavy perspiration Upper Level for Magnesium UL: 350 mg from supplement and other nonfood sources (e.g., antacids or laxatives) Causes Excessive supplementation Chronic antacid or laxative use Kidney failure Consequences Weakness Nausea Slowed respiration Malaise, coma, death High-risk population: older adults, due to declines in kidney function Sulfur (S) Sources Protein-rich foods (component of methionine and cysteine) Preservative used to protect color of dried fruit and white wines Requirements No AI or RDA established because of ample consumption from protein foods No UL established, no toxicity symptoms Functions Synthesis of sulfur-containing compounds Stabilize protein structure Acid-base balance Instructor Manual for Wardlaw's Perspectives in Nutrition Carol Byrd-Bredbenner, Gaile Moe , Jacqueline Berning , Danita Kelley 9780078021411