Download chapter overview

10
THE WATER-SOLUBLE VITAMINS
CHAPTER OVERVIEW
Included as part of “The Vitamins and Minerals” section of the text, chapter 10 discusses
the water soluble vitamins. General properties of water soluble vitamins are reviewed, as are
enrichment and fortification. Each vitamin is outlined, defining or subscribing the functions,
chemical structure, deficiency disease or symptoms, recommended intake, food sources, potential
toxicities, and at-risk populations. Food sources are ranked by nutrient density. Other
information, including alternative sources of the nutrient, nutritional status evaluation, and
barriers to absorption or utilization, is also introduced to the learner. The author depicts the
important historical events associated with the discovery of the various water-soluble vitamins.
The Expert Opinion discusses choline in “Is There a Need for Choline in the Human Diet?”
Finally, The Nutrition Perspective, “Nutrition and Cancer,” explains what cancer is, mechanisms
of carcinogenesis, the role of environment, including food and nutrients/diet, in the promotion or
prevention of cancer.
CHAPTER OBJECTIVES
By the end of this chapter the student should be able to:
Identify the functions of water-soluble vitamins
Recognize important sources of these vitamins.
Describe the signs and symptoms of deficiency.
Classify the chemical and physical properties of the individual vitamins.
Identify the vitamins most likely to be toxic when ingested in large amounts
Explain the rationale for establishing the RDA.
Identify the vitamins that may be deficient in the American diet.
Recognize the important role of nutrients in possibly preventing cancer.
LECTURE NOTES
I. General Properties of the Water-Soluble Vitamins
A. Brief history
B. Coenzymes
1. Serve as carriers of specific ions or chemical groups
2. Bound to specific protein
C. Absorption and Excretion
D. Retention in Foods
1. Steaming
2. stir-frying
3. microwaving
4. simmering
II. B-Vitamin and Vitamin C Status of North Americans
A. Generally Good--Typical diets contain plentiful varied sources of these vitamins
B. Many foods are fortified with one or more of the water-soluble vitamins
III. Enrichment and Fortification of Foods with B-Vitamins
A. Enrichment
1. Milling process leads to loss of vitamins and minerals
2. Enrichment program began in 1940s in United States
3. Bread and cereal products are enriched with thiamin, riboflavin, niacin and folate
B. Fortification
1. Bread and cereal products are fortified with folate
C. Milling process and lack of additional fortification leave bread and cereal products with less
vitamin B6, magnesium, and zinc
IV. Thiamin
A. Structure and Nomenclature
B. Absorption, Transport, Metabolism, and Excretion of Thiamin
1. Absorbed mainly in jejunum by carrier-mediated system, requiring phosphorylation of
the vitamin and passive diffusion at higher concentration
2. Transported in blood and by red blood cells
3. Storage in body is negligible
4. Excess is quickly excreted in urine
C. Functions of Thiamin
1. Coenzyme form = thiamin pyrophosphate (TPP)
a. Biologically active part of several enzyme systems in metabolism of carbohydrates
and branched-chain amino acids
i. Functions in decarboxylation of alpha keto acids (conversion of pyruvate to
acetyl-CoA)
ii. Functions in action of transketolase (formation of five-carbon sugar components
of RNA and DNA)
D. Thiamin-Deficiency Diseases
1. Beriberi
a. “I can’t, I can’t.”
b. Types
i. Wet
ii. Dry
c. Clinical signs of Deficiency
Anorexia, weight loss, apathy, loss of short-term memory, confusion, irritability, and muscle
weakness, peripheral neuropathy
Edema with enlarged heart and congestive heart failure (wet)
Muscle wasting (dry)
2. Wernicke-Korsakoff Syndrome
a. Thiamin deficiency disease among heavy alcohol users
b. Alcohol diminishes thiamin absorption, increases thiamin excretion, and results in
individuals consuming a poor quality diet
c. Symptoms include:
i. ocular motor signs
ii. ataxia
iii. deranged mental functions
d. Not all alcoholics experience this syndrome-genetics may influence
E. Thiamin in Foods
1. Found in a wide variety of foods but in small amounts
2.
Foods high in nutrient density (mg/kcl)
a. pork products
b. sunflower seeds
c. legumes
d. wheat germ
e. watermelon
3. Overall, enriched, fortified, and whole grain products make greatest contribution to diet
F. Thiamin Needs
1. Activity of transketolase in red blood cells is regarded as the best test for thiamin status
2. DRI
a. RDA for thiamin for men and women ages 19-70+ is approximately 1.2 mg/day and
1.1 mg for day, respectively
b. No adverse effects with excess intake of thiamin from foods or supplements
i. No UL
G. North Americans at Risk for Thiamin Deficiency
1. Poor and elderly
2. Alcoholics
V. Riboflavin
A. Structure and Nomenclature
1. Component of two coenzymes
a. flavin mononucleotide (FMN)
b. flavin adenine dinucleotide (FAD)
2. Coenzyme forms are present in many foods; free form found in milk and enriched grain
products
B. Absorption, Transport, Metabolism, and Excretion of Riboflavin
1. In stomach, HCl releases riboflavin from its bound form
2. Absorption is via active or facilitated transport; at very high intakes, it is absorbed
passively
3. Transported by protein carriers in the blood
4. Converted to its coenzyme forms in most tissues, especially, small intestine, heart, liver,
kidney
5. Small amount stored in liver
6. Excess excreted in urine
C. Function of Riboflavin
1. Coenzyme in numerous oxidation-reduction reactions
2. FAD-containing enzymes
a. Succinate dehydrogenase accepts electrons from succinate to form fumarate in citric
acid cycle, electrons passed to ETC
b. Another enzyme participates in beta oxidation of fatty acids to acetyl-CoA
c. Another enzyme forms vitamin B6 coenzyme and converts tyrptophan to niacin
d. Metabolism of oxidized form of glutathione to reduced form of glutathione is
dependent on a FAD- requiring enzyme
i. Used to assess riboflavin status
3. FMN-containing enzymes
a. One enzyme shuttles hydrogen ions and electrons into electron transport chain
D. Riboflavin Deficiency
1.
Signs and symptoms of ariboflavinosis
a. Glossitis
b. Cheilosis
c. seborrheic dermatitis
d. stomatitis
e. inflammation of the throat
f. various eye and nervous disorders
g. confusion
2. Rarely seen among healthy individuals
a. Diseases such as cancer, cardiac disease, and diabetes are known to precipitate or
worsen riboflavin deficiency
E. Riboflavin in Foods
1. One quarter of riboflavin in our diets comes from milk products, three quarters from
enriched grain products
2. Nutrient dense sources
a. liver
b. mushrooms
c. spinach
d. broccoli
e. asparagus
f. low-fat milk
g. nonfat milk
h. cottage cheese
3. Ultraviolet radiation causes riboflavin to breakdown rapidly
a. Food Packaging Strategies
F. Riboflavin Needs
1. Assessment of riboflavin status
a. erythrocyte glutathione reductase
b. urinary riboflavin excretion
2. DRI
a. RDA for men is 1.3 mg/day and for women, is 1.1 mg/day
b. No adverse effects from consuming large amounts due to rapid excretion via urine
i. No UL
G. North Americans at Risk for Riboflavin Deficiency
1. Deficiency rare
2. Marginal intakes observed in those who do not consume milk or milk products
3. Alcoholics and long term users of phenobarbital at risk
VI. Niacin
A. Structure and Nomenclature
1. Two forms
a. nicotinic acid (niacin)
b. nicotinamide (niacinamide)
2. Coenzyme forms
a. nicotinamide adenine dinucleotide (NAD)
b. nicotinamide adenine dinucleotide phosphate (NADP)
B. Absorption, Transport, Metabolism, and Excretion of Niacin
1. Readily absorbed from the stomach and small intestine by active transport and passive
diffusion
2. Transported to liver, converted to NAD and NADP, and stored
3. Excess excreted via urine
C. Functions of Niacin
1. Coenzyme forms participate in oxidation-reduction reactions
2. Functions in at least 200 reactions in cellular metabolic pathways, especially those that
produce ATP
D. Niacin Deficiency: Pellagra
1. First record of deficiency by Casals in 1735
2. Since almost every metabolic pathway uses either NAD or NADP, niacin deficiency
results in widespread damage in body
3. Four Ds
a. Dementia
b. Diarrhea
c. Dermatitis
d. Death, if disease is not treated
4. Early symptoms include diminished appetite, weight loss and weakness
5. Both insufficient intake of protein and/or niacin can result in deficiency
E. Niacin in Foods
1. In U.S. diets, about 25% preformed niacin comes from mixed dishes which include meat,
fish, poultry and from poultry alone; another 11% comes from bread and bread products
through fortification
2. Number of milligrams of niacin supplied by dietary protein can be estimated by dividing
dietary protein (in grams) by 6
3. Heat stable, little lost in cooking
4. Most nutrient dense foods (mg/kcal)
a. mushrooms
b. wheat bran
c. fish
d. chicken
e. turkey
f. asparagus
g. peanuts
5. Soaking corn in an alkaline solution (calcium hydroxide in water) releases bound niacin,
making it more bioavailable; explains why native peoples of Mexico, Central America,
and South America and Spanish settlers to those areas did not suffer from pellagra
F. Niacin Needs
1. RDA for niacin is expressed as niacin equivalent (NE)
a. Accounts for niacin preformed from the diet and that synthesized from tryptophan
2. RDA for niacin for men of all ages is 16 NE/day and for women of all ages, 14 NE/day
3. Primary criterion used to establish RDA
a. Urinary excretion of N-methyl nicotinamide and other metabolites
4. Populations at risk for deficiency
a. individuals with Hartnup’s disease
b. alcoholics
c. those with diseases that greatly impair food intake
G. Pharmacologic Use and Toxicity of Niacin
1. Cholesterol reduction
a. Discover in 1955
b. Consuming 1.5 to 2.0 g of nicotinic acid per day can decrease LDL cholesterol and
increase HDL cholesterol
c. Adverse effects
i. flushing of skin
ii. itching
iii. nausea and vomiting
iv. liver damage
2. Range of doses produce side effects in individuals, therefore, megadoses require
physician supervision
3. UL for adults = 35 mg/day
VII.
Pantothenic Acid
A. Structure and Nomenclature
B. Functions of Pantothenic Acid
1. Essential part of acetyl-Coenzyme A (CoA)
a. Essential for metabolism of carbohydrate, protein, fat and alcohol
2. Part of the compound, acyl carrier protein
C. Pantothenic Acid in Foods
1. “Panothen” = “from every side”
2. Ample supply in foods
3. Common sources include: milk, meat, many vegetables
4. Nutrient dense sources of the vitamin (mg/kcal)
a. Mushrooms
b. Liver
c. Peanuts
d. Eggs
e. Yeast
f. Broccoli
g. Milk
D. Pantothenic Acid Needs
1. Adequate Intake = 5 mg/day
2. Primary criterion used to estimate AI
a. Amount needed to replace urinary excretion
3. Deficiency
a. May with alcoholism but this may be masked among other B vitamin deficiencies
4. No known toxicity, no UL
VIII. Biotin
A. Structure and Nomenclature
1. Found free (biotin) or bound to lysine (biocytin)
2. Biotin is absorbed in small intestine, biocytin is not
3.
IX.
Enzyme biotinidase in the small intestine cleaves bond linking biotin to protein releasing
biotin
a. Deficiency may occur in individuals with genetic defect leaving individual with little
biotinidase
B. Functions of Biotin
1. Essential cofactor for four carboxylase enzymes
a. Catalyzes carboxylation of acetyl-CoA to form malonyl-CoA (first step in elongation
of carbon chain to form fatty acid)
b. Carboxylation reaction involving addition of carbon dioxide to the three carbon
pyruvate to produce four carbon oxaloacetate (keeps citric acid cycle running
effectively)
c. Carboxylation reaction involving the breakdown of leucine
d. Carboxylation reaction involving threonine, methionine, and isoleucine to be
oxidized for energy via citric acid cycle
C. Sources of Biotin: Food and Microbial Synthesis
1. Content in foods determined only small number of foods—not included in most
composition tables
2. Widely distributed in foods with concentration varying
3. Likely that intestinal synthesis of biotin by bacteria supplies part of needs
4. Avidin
a. protein in raw eggs
b. Binds biotin and inhibits absorption
5. Deficiency Risk
a. Genetic defect
b. Alcoholics have reported to develop a deficiency from eating as little as 3 raw eggs
per day. Would typically be seen with consumption of 12-24.
D. Biotin Needs
1. Adequate Intake
a. adults = 30 ug/day
b. Extrapolated from exclusively breastfed infants
c. No UL
E. North Americans at Risk for Biotin Deficiency
1. Genetic defect in infants
2. Certain individuals with alcoholism
3. Omission of biotin from total parenteral nutrition formula
Vitamin B-6
A. Structure and Nomenclature
1. A family of three compounds that can be phosphorylated to the active vitamin
a. pyridoxal
b. pyridoxine
c. pyridoxamine
2. Primary coenzyme = pyridoxal phosphate (PLP)
B. Absorption, Metabolism, Excretion, and Storage of Vitamin B-6
1. Both phosphorylated and nonphosphorylated forms absorbed by passive diffusion in
small intestine
2. Transported to liver via portal vein where ultimately all three forms are phosphorylated
3. Mainly PLP is released to general circulation bound to albumin for transport
4. Muscle tissue is site of storage in body
C. Functions of Vitamin B-6
1. Amino Acid Metabolism
a. Functions as a decarboxylase
b. Participates in transamination reactions
c. Acts as a racemase for the interconversion of D- and L-amino acids
d. Can move sulfur groups from one amino acid to another (conversion of
homocysteine to cysteine)
2. Blood Cell Synthesis and Function
a. PLP catalyses first step in synthesis of heme
b. Pyridoxal participates in binding oxygen to hemoglobin; PLP lowers the oxygen
binding capacity
c. Necessary for synthesis of lymphocytes
3. Carbohydrate Metabolism
a. Provides carbon skeletons to produce glucose via gluconeogenesis
b. Part of enzyme which releases glucose from glycogen during glycogenolysis
4. Lipid Metabolism
a. PLP needed for synthesis of arachidonic acid from linoleic acid
b. PLP participates is formation of myelin
5. Neurotransmitter Synthesis
a. Involved in synthesis of neurotransmitters
i. Serotonin from tryptophan
ii. Dopamine (DOPA) and norepinephrine from tyrosine
iii. Histamine from histadine and gamma-aminobutyric acid (GABA)
6. Vitamin Formation
a. As PLP participates in conversion of tyrptophan to niacin
D. Vitamin B-6 Deficiency
1. Symptoms
a. seborrheic dermatitis
b. microcytic hypochromic anemia
c. depression
d. convulsion
e. confusion
2. Diminished immune function
E. Vitamin B-6 in Foods
1. Most nutrient dense sources (mg/kcal)
a. whole-wheat bread
b. peanut butter
c. garbanzo beans
d. raw carrots
e. cooked potatoes
f. chicken breast
g. water packed tuna
h. bananas
X.
i. avocados
2. Stored in muscle tissue of animals, meat, fish, poultry--good sources
3. Not stable under heat and alkaline conditions
4. Bioavailability = 75% (mixed diet)
F. Vitamin B-6 Needs
1. RDA is 1.3 mg/day for adults; for men and women over 50 years RDA is 1.7 mg/day and
1.5 mg/day respectively
2. Blood PLP concentration = Indicator used to estimate needs
G. Factors That Affect Vitamin B-6 Requirements
1. Medications
a. L-DOPA
b. Isoniazid
2. Alcohol
a. When alcohol is metabolized to acetaldehyde, acetaldehyde decreases formation of
PLP by cells and may compete with PLP for protein-binding sites
3. Pregnancy
a. Pregnant women with preeclampsia have lower blood concentrations of PLP and
proteinuria; unknown if supplementation with vitamin prevents problem
H. North Americans at Risk for B-6 Deficiency
1. Deficiency is rare but some elderly have shown signs of deficiency
I. Pharmacologic Use of Vitamin B-6 and Toxicity
1. Vitamin B-6 not recommended for treatment of carpal tunnel syndrome and PMS at this
time
2. Toxicity
a. Intakes of 2 to 6 mg per day for 2 months or longer as well as long term use of 200
mg/day or greater can lead to irreversible nerve damage
b. UL for adults = 100 mg/day
Folate
A. Structure and Nomenclature
1. Formerly known as folic acid or folacin
2. Three parts:
a. Pteridine
b. Para-amino benzoic acid
c. One or more molecules of glutamic acid or glutamate
B. Metabolism, Absorption, Storage, and Excretion of Folate
1. Folate polyglutamates are hydrolyzed by conjugases in small intestine
2. Monoglutamate form is actively transported across intestinal wall; very high doses are
absorbed passively
3. Travel to liver via portal vein and are changed back to polyglutamate form
4. Primarily stored in liver
5. Urinary excretion of folate = primarily metabolic products
6. Alcohol interferes with reabsorption by enterohepatic circulation
C. Functions of Folate
1. Metabolic Reactions
a. Basic coenzyme form is tetrahydorfolic acid (THFA)
b.
Crucial reaction of THFA is transfer of one-carbon methylene group to uridylate to
form thymidylate (essential component of DNA)
i. Methotrexate is a folic acid antagonist used to treat certain cancers, rheumatoid
arthritis, psoriasis, asthma, cirrhosis, and inflammatory bowel disease
ii. Typical sign effects of methotrexate therapy are the same as for a folate
deficiency (hair loss and diarrhea)
iii. Individuals taking methotrexate need to follow a high folate diet or take a folate
supplement so as to reduce toxic side effects of drug
c. Formation of neurotransmitters in the brain
2. Other Functions
a. Important in interconversions of amino acids
i. Glycine to serine
ii. Histadine to glutamate
iii. Homocysteine to methonine
D. Folate Deficiency
1. Generally results from a low intake, inadequate absorption, increased requirement,
compromised utilization or excessive excretion
2. Megaloblastic Anemia
a. One of first major folate-deficiency signs to appear is changes in early phases of red
blood cell synthesis
i. Without folate, precursor cell in bone arrow cannot divide normally because
they cannot for new DNA
ii. Cells grow larger and remain so as megaloblasts and retain their nuclei
b. Symptoms of folate deficiency
i. inflammation of tongue and mouth
ii. abnormal pigmentation of skin
iii. diarrhea
iv. poor growth
v. depression and mental confusion
vi. problems with nerve function
3. Neural Tube Defects
1. Maternal deficiency of folate and a genetic predisposition linked to development of
neural tube defects
2. Defects
a. spina bifida
b. anencephaly
3. Neural tube closure occurs begins about 21 days after conception and is complete by
day 28
4. Women with varied diets may not consume adequate folate to prevent neural tube
defects (400 ug/day) unless sources of synthetic folic acid are consumed (many
breakfast cereals, e.g.)
E. Folate in Foods
1. Biologically availability varies with source of vitamin
2. Best sources (amount and availability)
a. Liver
b. fortified breakfast cereals and other grain products
c. legumes and vegetables
3.
Most nutrient dense sources (mg/kcal)
a. spinach and other dark leafy greens
b. asparagus
c. broccoli
d. orange juice
e. wheat germ
f. liver
g. sunflower seeds
h. cauliflower
i. cabbage
F. Folate Needs and Dietary Folate Equivalents
1. Dietary folate equivalents (DFE) used to express needs
2. DFE reflect difference in absorption of food folate and synthetic folic acid
a. Folic acid consumed as a supplement is about 100% bioavailable
b. Folic acid consumed with food (fortified cereals) is slightly less bioavailable than a
supplement
c. Naturally-occurring folate is less well absorbed
3. RDA for men and women is 400 ug/day
4. To estimate DFE:
a. Determine how much of day’s food comes from food folate and from synthetic folate
added to foods
b. In doubt, assume all folate in diet is derived from food except that coming from
breakfast cereals and refined grain products
c. Include any folate from supplements in synthetic folate added to foods
d. Multiply total synthetic folate intake by 1.7 and add that value to total food folate
G. North Americans at Risk for Folate Deficiency
1. Deficiencies sometimes appear in pregnant women
2. Young women
3. Elderly
4. Persons with alcoholism
5. Those taking one or more of long list of medications (e.g., methotrexate, isoniazid)
6. Smokers
H. Toxicity of Folate
1. FDA regulates potency of folate supplements because consuming excessive amounts of
folate can mask vitamin B-12 deficiency
a. 400 ug when no age is listed on supplement label
b. Up to100 ug for infants
c. Up to 300 ug for children
d. Up to 400 ug for adults
e. Prenatal vitamin supplements can contain 800 ug
f. UL for synthetic folate = 1 ug
XI. Vitamin B-12
A. Structure and Nomenclature
1. Free vitamin = cyanocobalamin
2. Coenzymes
B.
C.
D.
E.
F.
a. Methylcobalamin
b. 5-deoxyadenosylcobalamin
3. Synthesized by bacteria, fungi, and algae
4. Only reliable source for humans is animal foods
Absorption, Transport, and Storage of Vitamin B-12
1. Vitamin is released from proteins in stomach by HCl and pepsin
2. Free B-12 binds to R – protein which originates in salivary glands in mouth and is
swallowed
3. Intrinsic factor is released from parietal cells in stomach and travels to small intestine
4. Trypsin from pancreas releases R-protein
5. Vitamin B-12-intrinsic factor complex formed
6. Vitamin B-12 is absorbed in ileum
7. Transferred to a transport protein (transcobalamin II) within ileum cell
8. Vitamin-protein complex enters portal blood and travels to liver where it is stored
9. Failure in any links found in absorptive process reduces absorption to 2% or less
10. Therapies for those with B-12 absorption defects
a. Monthly injections of vitamin B-12 (bypasses GI tract)
b. Use of B-12 nasal gel (does not require intrinsic factor)
c. Weekly ingestion of B-12 megadoses (allows absorption by passive diffusion)
Functions of Vitamin B-12
1. Metabolism of 3-carbon fatty acids for entry into citric acid cycle (methylmalonyl CoA
mutase)
2. Maintenance of methionine stores and synthesis of DNA (methionine synthase)
3. Normal RBC formation
4.
Maintains myelin sheath that insulates nerve fibers
Vitamin B-12 Deficiency: Pernicious Anemia
1. Anemia that results from inability to absorb sufficient vitamin B-12
2. Associated with nerve degeneration, resulting in eventual paralysis and death
Vitamin B-12 in Foods
1. Sources
a. Meat
b. Poultry
c. Seafood
d. Eggs
2. Most nutrient dense sources (mg/kcal)
a. organ meats
b. seafood
c. beef
d. eggs
e. hot dog
f. ham
Vitamin B-12 Needs
1. RDA for adult men and women of all age is 2.4 ug/day
2. Those older than 51 years are advised to select foods fortified with vitamin B-12 and/or
take a supplement
G. North Americans at Risk for Vitamin B-12 Deficiency
1. Individuals with malabsorption syndromes of any kind
2. Vegans
3. Elderly with poor absorptive capacity
4. Individuals consuming excess vitamin C
5. Failure to thrive infants
7. Red blood cells look like folate deficiency (except B-12 deficiency can result in nerve
destruction)
8. Symptoms
a. painful tongue
b. weakness
c. weight loss
d. indigestion
e. diarrhea
f. parathesia
XII.
Choline
A. Structure and Nomenclature
B. Absorption, Metabolism, Excretion
1. Absorbed in small intestine via transport proteins
2. Taken up by liver via portal vein
3. All tissues contain choline
4. Some choline excreted in urine; however, most excess converted to betaine
C. Functions of Choline
1. Precursor for acetylcholine
2. Precursor of phospholipids (phosphatidylcholine)
3. Liver export of VLDL is associated with choline action
4. Precursor for methyl donor betaine
D. Choline in Foods
1. Widely distributed in foods mostly in form of phosphatidylcholine in membranes
2. Rich Sources: Milk, liver, eggs, peanuts
3. Lecithin (food additive)
4. Can be synthesized from serine
E. Choline Deficiency
1. Only one published study examining effect of inadequate dietary intake of choline
a. Male subjects maintained on choline deficient total parenteral formula
b. Developed fatty livers and liver damage
F. Choline Needs
1. Adequate Intake for men 19 years and older is 550 mg/day; women 19 years and older,
the AI is 425 mg/day
a. Based on choline intake to maintain liver function as assessed by alanine
aminotransferase concentration in blood
2. UL for adults = 3.5 mg/day based on development of fishy body odor and low blood
pressure
G. Expert Opinion: “Is There a Need for Choline in the Human Diet?”
XIII. Vitamin C
A. Structure and Nomenclature
1. Vitamin C refers to its reduced form, ascorbic acid; its oxidized form is called
dehydroascorbic acid
2. Two forms are interchangeable and biologically active
B. Absorption, Metabolism, Storage, and Excretion of Vitamin C
1. Absorption occurs in small intestine via active transport at low GI concentrations or
simple diffusion at high GI concentrations
2. Excretion by kidneys increases as dietary intake increases
3. Total body pool varies over wide range, 300 mg up to 2.0 grams
C. Functions of Vitamin C
1. Nonspecific reducing agent (donates electrons)
2. Collagen Synthesis
a. Post-translational hydroxylation of peptide bound proline and lysine
b. Scurvy associated with deterioration of elastic tissues
3. Antioxidant Activity
a. Can both donate and accept hydrogen atoms readily
b. Protective water-soluble antioxidant in intracellular and extracellular environment by
quenching a variety of reactive oxygen species and reactive nitrogen species
c. Scavenger for reactive oxygen species and reactive nitrogen species in lungs,
leukocytes, and stomach
d. Protects against lipid peroxidation
e. In smokers, helps prevent damage by oxidative stress
4. Iron Absorption
a. Facilitates nonheme iron absorption in small intestine
b. Counters the action of certain food components that inhibit iron absorption
5. Synthesis of Other Vital Cell Components
a. Participates in two separate steps of carnitine biosynthesis
b. Biosynthesis of norepinephrine and epinephrine
c. Biosynthesis of thyroxine
d. Conversion of tyrptophan to serotonine and cholesterol to bile acids
e. Biosynthesis of corticosteroids and aldosterone
f. Tyrosine metabolism
6. Immune Function
a. High concentration in leukocytes provides protection against oxidative damage
associated with cellular respiration
b. Amount of vitamin C in neutrophils is used as index for establishing RDA
7. Cancer Prevention
a. No compelling evidence yet that vitamin C reduces in vivo DNA oxidative damage
D. Vitamin C Deficiency: Scurvy
1. Appears after 20 to 40 days on a vitamin C deficient diet
2. Prevents normal synthesis of collagen, thus causing widespread and significant changes
in connective tissue throughout the body
3. Early signs and symptoms
a. Fatigue
b. pinpoint hemorrhages (petechiae) around hair follicles on back of arms and legs
c. bleeding in gums and joints
d. impaired wound healing
e. bone pain
f. fractures
4. Associated with poverty
E. Vitamin C in Foods
1. Good sources
a. citrus fruits
b. potatoes
c. green vegetables
2. Most nutrient dense foods (mg/kcal)
a. green peppers
b. cauliflower
c. broccoli
d. strawberries
e. papayas
f. romaine lettuces
g. oranges
h. spinach
3. Vitamin C - very unstable when in contact with heat, iron, copper, and oxygen
F. Vitamin C Needs
1. RDA for vitamin C for adult men 19 years and older is 90 mg/day; for adult women 19
years and older, 75 mg/day
2. Smoking causes oxidative stress requirement increases 35 mg/day
G. North Americans at Risk for Vitamin C Deficiency
1. Alcoholics and those addicted to drugs
2. Elderly men consuming few fruits and vegetables
3. People exposed to cigarette smoke
H. Toxicity of Vitamin C
1. Principal adverse effects
a. Gastrointestinal disturbances (nausea, abdominal cramps, osmotic diarrhea)
b. Conflicting data as to whether megadoses of vitamin C cause increase in uric acid
excretion
2. UL = 2 g/day, based on osmotic diarrhea and gastrointestinal disturbances
XIV. Vitamin –like Compounds
A. Introductory Information
1. Carnitine, inositol, taurine and lipoic acid are necessary for normal metabolism in body
2. Can be synthesizes by body but biosynthesis often occurs at expense of other nutrients,
e.g., amino acids
3. More research is needed to clarify whether deficiencies may arise in certain disease states
and whether the compounds should be included in infant formulas and total parenteral
solutions
B. Carnitine
1. Can be synthesized in liver from lysine and methonine
2. Human needs are met from food and biosynthesis
3. Carnitine transports fatty acids from cytosol into mitochondria within cell and aids in
removing excess organic acids from the mitochondria
4.
5.
Meat and dairy products are main sources of carnitine; almost absent from plant foods
May be conditionally essential nutrient in times of recovery from disease, serious trauma,
or preterm birth
6. Has displayed pharmaceutical usefulness in removal of compounds that can build up to
toxic amounts with inborn errors of metabolism
C. Inositol
1. Of nine possible isomers, only one, myo-inositol, has nutritional implications for humans
2. Structure is related to glucose from which is synthesized in body
3. Much of inositol in body occurs in phosphorylated forms
4. Is incorporated into phospholipids in cell membrane, which are important precursors of
the eicosanoids
5. Both free and phosphorylated forms found in animal foods as well as some plant foods
6. Metabolism of inositol is altered by hyperglycemia (inhibits inositol transport)
7. Abnormal metabolism observed in multiple sclerosis, kidney failure, certain cancers
D. Taurine
1. Synthesized from methionine and cysteine
2. Abundant in muscle, platelets and nerve tissue
3. Mechanism of action not well understood, but involved in many vital functions
4. Only found in animal foods, but no cases of deficiencies reported among Vegans
5. Supplementation may be useful to children with cystic fibrosis as well as preterm infants;
both exhibit improved fat absorption
E. Lipoic Acid
1. Functions in reactions involving loss of carbon dioxide from a substrate (pyruvate
converted to acetyl-CoA)
2. Is a redox agent
3. Not necessary to obtain from outside sources
4. Rich Dietary Sources: Meats, liver, yeast
XV.
Bogus Vitamins
A. Para amino benzoic acid (PABA)
B. Laetrile
C. Bioflavonoids
D. Pangamic acid
XVI. Nutrition in Perspective: Nutrition and Cancer
A. What is Cancer?
1. Abnormal and uncontrollable cell division
2. Types of Cancer
a. Carcinomas
b. Sarcomas
c. Leukemias
d. Lymphomas
B. Mechanisms of Cancer
1. Oncogenes and Other Genes
2. Cancer Initiation, Promotion and Progression
C. Is Cancer Environmental or Hereditary?
D. Diet and Cancer
E. Cancer Warning Signs
ACTIVITIES, EXERCISES, AND ASSIGNMENTS (Additional Activities in
Text)
1.
Assign students to visit local health food stores, pharmacies, or supermarkets to determine the
various types of vitamin supplements on sale, their potency, price, and amount contributed to the
diet.
2.
What promotions are used to market these products?
3.
Do any of the supplements carry health warnings?
4.
Interview a store manager to ascertain which products are best sellers. Are single vitamins or
multivitamins more popular with the clients?
5.
Are there any “nonvitamins” being marketed as supplements?
6.
Select several popular magazines and body and fitness publications that are available at local
newsstands and bookstores. Provide a display of the various advertising techniques used to promote
vitamin supplements. Point out any deceptive or misleading statements regarding the products. Do
any come with a money-back guarantee?
7.
Videotape several current TV commercials for vitamin supplements. Show tapes to the class to
generate discussion and criticism. What population and age groups are they aimed at? What kinds of
gimmicks are used to sell the products? Are any promises made about the effectiveness of the
vitamins?
8.
Assign students to survey common supermarket items for evidence of vitamin fortification. What
products are being fortified and at what level? Compare costs to similar nonfortified products.
9.
Using the printouts from previous assignments have students assess their intake of the various
water-soluble vitamins. Have students select the groups of foods that contribute most of the Bvitamins and vitamin C to their diet. Did the student follow the Daily Food Guide? If not, what food
groups were deficient?
ANNOTATED REFERENCES AND READINGS (Annotated References in
Text)
Archer MC (1996): Cancer and Diet. In Ziegler EE and Filer LJ (eds.), Present Knowledge in
Nutrition, 7th ed., International Life Sciences Institute, Washington, DC pp. 456-463.
Butterworth CE and Bendich A: Folic Acid and the Prevention of Birth Defects, Ann. Rev. Nutr.,
16:73-97, 1996.
Driskell JA: Vitamin B6 Requirements for Humans, Nutr. Res. 14:293-324, 1994.
Folate Supplements Prevent Recurrence of Neural Tube Defects, Nutrition Reviews 50:22, 1992.
FDA Dietary Supplement Task Force, Nutrition Reviews 50:25, 1992.
Folate Supplements and Neural Tube Defects, Nutrition Reviews 50:25, 1992.
Vitamin B6 and Immune Function in the Elderly and HIV-seropositive subjects, Nutrition Reviews
50:145, 1992
Metz, J: Cobalamin deficiency and the pathogenesis of nervous system disease, Annual Review of
Nutrition 12:59, 1992.
Byers, T and G Perry: Dietary Carotenes, vitamin C, and vitamin B as protective antioxidants in
human cancers, Annual Review of Nutrition 12:139, 1992.
Kant, AK and G Block: Dietary vitamin B-6 intake and food sources in US population: NHANESII,
1976-1980: The American Journal of Clinical Nutrition 52:707, 1990.
Bailey, L: Evaluation of a new RDA for folate, Journal of the American Dietetic Association
92:463, 1992.
Bender, MM and others: Trends in prevalence and magnitude of vitamin and mineral supplement
usage and correlation with health status, Journal of the American Dietetic Association 92:1096,
1992.
MEDIA RESOURCES
Video:
1.
Vitamins I, II, III. Audio-Visual Department, The Pennsylvania State University, University Park,
PA 16803.
2.
Water-soluble Vitamins. Teaching Aids, Inc., PO Box 1798, Costa Mesa, CA 92626-0798.
Films:
1.
The Great Vitamin C Debate: to Dose or Megadose. Nutrition Today Society, Inc., Education
Service, PO Box 1829, Annapolis, MD 21404.
2.
Vitamins, what do they do? Alfred Higgins Production; Los Angeles, CA.
Slides:
Deficiency Disorders: How to Diagnose Nutrition Disorders in Daily Practice. Nutrition Today, Inc.,
Education Services, PO Box 1829, Annapolis, MD 21404.