Download Perspectives in Nutrition, 8th Edition

Perspectives in Nutrition, 8th Edition
Chapter 12 Outline: The Fat-Soluble Vitamins
After studying this chapter, you will be able to:
1.
2.
3.
4.
5.
Define the term vitamin and list 3 characteristics of vitamins as a group.
Classify the vitamins according to whether they are fat-soluble or water soluble.
List 3 important food sources for each fat-soluble vitamin.
List the major functions for each fat-soluble vitamin.
Describe the deficiency symptoms for each fat-soluble vitamin and state the conditions in which
deficiencies are likely to occur.
6. Describe the toxicity symptoms caused by excess consumption of certain fat-soluble vitamins.
7. Evaluate the use of vitamin and mineral supplements with respect to their potential benefits and
risks to health.
12.1
Vitamins: Essential Dietary Components
A.
General
1.
Vitamins: essential, organic substances needed in small amounts in the diet
a.
Fat-soluble vitamins: dissolve in organic solvents (e.g., ether, benzene)
b.
Water-soluble vitamins: dissolve in water
2.
Supply no energy
3.
Aid in growth, development, and maintenance of body tissues
4.
Essential in diet because they cannot be synthesized at all or in sufficient
amounts by the body to support needs
5.
Health declines when vitamins are deficient
6.
Resupplying vitamins alleviates deficiency symptoms
7.
Megadoses of some vitamins are useful as pharmacological agents
8.
Synthetic and natural forms of vitamins generally work equally well in the body
9.
Vitamins consumed in foods as part of a varied diet are more beneficial than
supplements
B.
Absorption of Vitamins
1.
Fat-soluble vitamins are absorbed with dietary fat
a.
Requirements for absorption
i.
Dietary fat
ii.
Bile
iii.
Pancreatic lipase
iv.
Absorptive capacity of intestinal cells
b.
Absorption efficiency of fat-soluble vitamins is 40 - 90% when
consumed in recommended amounts
2.
Water-soluble vitamins are absorbed in the small intestine independent of dietary
fat with 90 - 100% efficiency
C.
D.
E.
F.
12.2
Malabsorption of Vitamins
1.
Fat malabsorption (e.g., from GI tract disease or pancreatic disease) may cause
poor absorption of fat-soluble vitamins
2.
Alcohol abuse and some intestinal diseases may cause malabsorption of some Bvitamins
3.
Poor absorption increases vitamin requirements
Transport of Vitamins
1.
Fat-soluble vitamins are transported through lymphatic system and delivered to
bloodstream via chylomicrons and other blood lipoproteins
a.
Triglycerides are removed by cells as chylomicrons circulate
b.
Remnants, which include fat-soluble vitamins, are taken up by the liver
and repackaged as new lipoproteins for transport or stored in adipose
tissue or liver
2.
Water-soluble vitamins are delivered directly to the bloodstream and distributed
throughout the body
Storage of Vitamins in the Body
1.
Except for vitamin K, fat-soluble vitamins are not readily excreted, but are stored
in the liver and/or adipose tissue
2.
Except for vitamins B-6 and B-12, water-soluble vitamins are excreted readily
and poorly stored
3.
Vitamins should be consumed daily, but deficiency symptoms do not develop for
several weeks with inadequate consumption
Vitamin Toxicity
1.
Toxicity from vitamins A and D is most likely
2.
Toxicity usually results when intake exceeds 5 - 10 times DRI guidelines
3.
Balanced multivitamin and mineral supplements that supply less than 2X the
Daily Value are unlikely to cause toxicity
Vitamin A
A.
General
1.
Vitamin A (from consumption of beef liver) has been known to prevent night
blindness for >3500 years
2.
Vitamin A is a family of compounds
a.
Preformed retinoids: biologically active form of vitamin A; three forms
may be interconverted to some extent
i.
Retinol
ii.
Retinal
iii.
Retinoic acid
b.
Provitamin A carotenoids: must be converted to vitamin A
3.
Carotenoids: yellow/orange pigments in fruits and vegetables; some are
provitamins (converted to vitamin A)
a.
Alpha-carotene
b.
Beta-carotene
B.
C.
D.
c.
Beta-cryptoxanthin
Vitamin A in Foods (see Figure 12-3)
1.
Sources of retinoids
a.
Liver
b.
Fish and fish oils
c.
Fortified milk
d.
Eggs
e.
Margarine
2.
Sources of carotenoids
a.
Yellow/orange fruits and vegetables (e.g., carrots, spinach, winter
squash, sweet potatoes, mangoes, cantaloupe, peaches, apricots)
b.
Leafy green vegetables
c.
Broccoli
3.
70% of vitamin A in typical American diet comes from animal (preformed
vitamin A) sources
4.
Dietary vitamin A activity is expressed in Retinol Activity Equivalents (RAE)
a.
1 RAE = 1 µg retinol
b.
1 RAE = 12 µg beta-carotene
c.
1 RAE = 24 µg alpha-carotene or beta-cryptoxanthin
5.
Outdated units of measurement for vitamin A
a.
International units (IU)
b.
Retinol equivalents (RE): overestimate contribution of carotenoids to
vitamin A needs
i.
For preformed vitamin A, 1 RE (3.3 IU) =1 RAE
ii.
For provitamin A, assume 1 RE/2 = 1 RAE
Vitamin A Needs
1.
RDA
a.
Adult men: 900 µg
b.
Adult women: 700 µg
2.
DV: 5000 IU (1000 µg)
3.
No DRI available for carotenoids
4.
Average intake meets DRI
Absorption
1.
Preformed vitamin A in animal foods
a.
Retinol
b.
Retinyl esters (attached to fatty acid); must be cleaved by action of bile
and pancreatic lipase to have vitamin A activity
2.
Absorption of preformed vitamin A
a.
Takes place in the small intestine
b.
Up to 90% efficient
3.
Absorption of carotenoids
a.
Takes place in small intestine
b.
Absorption efficiency is lower than that of preformed vitamin A
E.
F.
G.
H.
Transport of Vitamin A
1.
Transport of retinoids
a.
After absorption, retinol is attached to a fatty acid to form a new retinyl
ester and packaged into chylomicrons
b.
Chylomicrons are absorbed into lymphatic vessels, which empty into the
bloodstream
2.
Transport of carotenoids
a.
Enzymatically split in intestinal cells or liver cells to form retinal and
retinoic acid
b.
Retinal is converted to retinol and can become a retinyl ester to enter
lymphatic circulation
c.
Carotenoids can also enter bloodstream directly
3.
Retinoids are released from liver into bloodstream bound to retinol-binding
protein, which binds to transthyretin (prealbumin)
4.
Carotenoids are released from liver into bloodstream as part of VLDL
5.
Retinoids bind to specific RBPs in cells
Storage of Vitamin A
1.
90% of body’s vitamin A stores are in the liver (enough to last for several
months)
2.
Small amounts of vitamin A are stored in adipose tissue, kidneys, bone marrow,
testicles, and eyes
Excretion of Vitamin A
1.
Minor amount lost in urine
2.
Kidney disease can lead to vitamin A toxicity because of impaired excretion
Functions of Vitamin A (Retinoids)
1.
Growth and Development
a.
Development of eyes, limbs, cardiovascular system, and nervous system
of embryo
b.
Lack of vitamin A in first trimester leads to birth defects or fetal death
c.
Retinoid acid is needed for production, structure, and normal function of
epithelial (mucous forming) cells in lungs, trachea, skin, GI tract, etc
2.
Cell Differentiation (see Figure 12-4)
a.
Retinoids bind to retinoid receptors in cell nucleus that regulate
formation of mRNA and subsequent gene expression, which directs cell
differentiation (process by which stem cells develop into specialized
cells)
i.
Retinoic acid receptor (RAR)
ii.
Retinoid X receptor (RXR)
b.
Especially involved in cell differentiation in the eyes
3.
Vision
a.
Retinal is needed in the retina to turn visual light into nerve signals to the
brain
b.
Rods: vision in dim light, black and white images, detection of motion
i.
ii.
I.
11-cis-retinal binds to opsin to form rhodopsin
Absorption of light catalyzes bleaching process: change in shape
of 11-cis-retinal to all-trans-retinal, separates from opsin
iii.
Ion permeability of photoreceptor cells
iv.
Initiation of signal to nerve cells that communicate with brain’s
visual center
v.
With exposure to bright light, rhodopsin is completely activated
and cannot respond to more light
vi.
Regeneration of 11-cis-retinal from all-trans-retinal and binding
with opsin restarts visual cycle
vii.
Some retinal is stored and not used for each visual cycle
viii.
Depletion of vitamin A pools leads to night blindness, wherein
the process of dark adaptation is impaired
ix.
Dark adaptation: [rhodopsin] in the eye increases in dark
conditions to allow vision in the dark
c.
Cones: vision in bright light, color vision
4.
Immune Function
a.
Increased incidence of infection is an early symptom of vitamin A
deficiency
b.
May be due to role of vitamin A in maintenance of epithelial cells, which
form a barrier against pathogens
c.
Vitamin A supplementation decreases severity of infections in vitamin A
deficient children
5.
Use of Vitamin A Analogs in Dermatology
a.
Retin-A (topical) and Accutane (oral)
b.
Used to treat acne and psoriasis or lessen damage from sun or UV
exposure
c.
Toxic effects are especially harmful to fetus; causes birth defects
Carotenoid Functions
1.
Some can be converted to vitamin A
2.
Reduced risk of eye disease
3.
Reduced risk of cancer
4.
Reduced risk of cardiovascular disease
5.
Beta-carotene may act as antioxidant, especially to protect eye tissues; diets high
in fruits and vegetables show more success than supplementation
6.
Possible role for beta-carotene in prevention of lung cancer: although diets high
in fruits and vegetables are associated with reduced risk of lung cancer,
supplementation actually increases risk of lung cancer in high-risk individuals
7.
Lutein and zeaxanthin may protect against age-related macular degeneration
(leads to deterioration of central vision)
8.
Lycopene may protect against prostate cancer
9.
J.
K.
Beta-carotene and lycopene may reduce risk of CVD, possibly by inhibiting
oxidation of LDL and cholesterol synthesis and increasing LDL receptor activity
in cells
10.
In all cases, diets high in carotenoid-rich fruits and vegetables are recommended
rather than carotenoid supplements
Vitamin A Deficiency Diseases
1.
Low risk for deficiency in North America, but vitamin A deficiency is a major
public health problem in developing countries
2.
Leading cause of non-accidental blindness worldwide
3.
At-risk populations in North America
a.
Poverty
b.
Older adults
c.
Alcoholism or liver disease (limits vitamin A storage)
d.
Severe fat malabsorption
e.
Premature infants (low stores of vitamin A)
4.
Effects on eyes
a.
Slowed regeneration of rhodophsin by rods in the retina leads to night
blindness
b.
Deterioration of mucous-forming cells leads to xerophthalmia:
progression of eye disease leading to blindness, including
i.
Conjunctival xerosis: dryness
ii.
Bitot’s spots: hardened epithelial cells on the eye
iii.
Keratomalacia: softening of the cornea
iv.
Scarring
c.
Follicular hyperkeratosis: keratinized cells replace normal epithelial
cells, leading to dry, roughened skin
d.
Impaired growth in children
Vitamin A Toxicity (hypervitaminosis A)
1.
Occurs with chronic intake (usually from supplements) of 5 - 10 times RDA for
retinoids
2.
UL: 3000 µg of retinoids (no UL for carotenoids)
3.
Types of hypervitaminonis A
a.
Acute:1 very large dose or several large doses over a few days (100 x
RDA)
i.
GI tract upset
ii.
Headache
iii.
Blurred vision
iv.
Poor muscle coordination
v.
Fatality for extremely large doses (e.g., 500 mg for children or
10 g for adults)
b.
Chronic: repeated intakes of at least 10 x RDA; most symptoms
disappear after supplementation ceases, but permanent damage may
occur to the liver, bones, and eyes
4.
12.3
i.
Joint pain
ii.
Loss of appetite
iii.
Skin disorders
iv.
Headache
v.
Reduced bone minerals
vi.
Liver damage
vii.
Double vision
viii.
Hemorrhage
ix.
Coma
c.
Teratogenic: toxic doses during pregnancy, usually from vitamin A
analogs used to treat skin conditions, but also possible from food sources
(e.g., liver, fortified breakfast cereals); pregnant women should limit
intake of vitamin A to 100% DV
i.
Birth defects, especially of head and neck, where neural crest
cells form in first trimester
ii.
Spontaneous abortion
Consuming excessive carotenoids does not lead to toxicity; may turn skin to
yellow/orange color (hypercarotenemia)
Vitamin D
A.
General
1.
In 1918, cod liver oil (source of vitamin D) was discovered as cure for rickets
2.
In the presence of sunlight, skin cells can synthesize sufficient vitamin D, which
makes vitamin D a “conditional vitamin” or prohormone (precursor to active
hormone)
a.
Skin produces vitamin D3 (cholecalciferol) from a derivative of
cholesterol
b.
Liver and kidneys add hydroxyl group to cholecalciferol to yield active
vitamin D (1,25 dihydroxy D3, or calcitriol)
B.
Vitamin D2 (Ergocalciferol) in Foods
1.
High sources
a.
Fatty fish (e.g., sardines, mackerel, salmon) and fish oils (e.g., cod liver
oil)
b.
Fortified milk [10 µg (400 IU)/quart]
c.
Fortified breakfast cereals
d.
Supplements
2.
Low sources
a.
Eggs
b.
Butter
c.
Liver
d.
Some brands of margarine
3.
Ergocalciferol (D3) has vitamin D activity in humans, but not as much as
cholecalciferol (D2)
C.
D.
E.
F.
G.
Vitamin D3 Formation in the Skin
1.
Occurs in the liver and kidneys
2.
This process provides 80 - 100% of vitamin D requirements for some people
3.
Required sun exposure varies by
a.
Time of day
b.
Geographic location
c.
Season
d.
Age: skin production decreases by 70% by age 70
e.
Skin color: melanin blocks UV light and prevents adequate D3 synthesis
f.
Use of sunscreen > SPF 8
4.
Expose hands, face, and arms to UV light at least 2 - 3 times per week for 10 - 15
minutes (longer for dark-skinned individuals)
5.
Prolonged skin exposure is unlikely to cause toxicity because excess previtamin
D3 in the skin is rapidly degraded
Vitamin D Needs
1.
AI
a.
Adult men and women up to age 51: 5 µg (200 IU)
b.
Adults ages 51 - 70: 10 µg (400 IU)
c.
Adults ages 71+: 15 µg (600 IU); may need 20 - 25 µg from fortified
foods and supplements to decrease bone loss and other chronic diseases
2.
DV: 10 µg
3.
Full-term infants are born with a supply of vitamin D, but American Academy of
Pediatrics recommends 5 µg (200 IU)/d supplements until weaned to good food
sources of vitamin D
Absorption of Vitamin D
1.
80% of vitamin D2 is incorporated with dietary fats into micelles in the small
intestine
2.
Absorbed by small intestine
3.
Packaged into chylomicrons for transport in lymph
4.
Fat malabsorption syndromes increase risk for vitamin D deficiency
Transport of Vitamin D
1.
Vitamin D2 and D3 are transported through bloodstream bound to a protein to the
adipose, liver, or kidney cells
2.
In liver, vitamin D is hydroxylated to 25-OH vitamin D3 (inactive form), which
may circulate in the blood for weeks
3.
In kidney, 25-OH vitamin D3 is hydroxylated to 1,25-dihydroxy vitamin D3
4.
Synthesis of 1,25(OH)2 vitamin D3 is tightly regulated by parathyroid gland and
kidneys in response to blood calcium levels
a.
Low [Ca]  increased 1,25(OH)2 synthesis
b.
High [Ca]  decreased 1,25(OH)2 synthesis
Storage of Vitamin D
1.
25-OH vitamin D3 circulates in bloodstream
2.
Adipose cells
H.
I.
J.
K.
Excretion of Vitamin D
1.
Lost in bile during digestion
2.
Small amount excreted in urine
Functions of Vitamin D
1.
Hormone-like functions that regulate body’s concentration of calcium and
phosphorus (see Figure 12-13)
a.
Promotes increased intestinal absorption of calcium and phosphorus from
foods to maintain blood levels of these minerals
b.
With PTH, enables release of calcium and phosphorus from the bone into
the blood
2.
Immune function
3.
Cellular metabolism, likely regulation of cell cycle
4.
Possible protection against cancer
5.
Possible protection against diabetes
6.
Possible protection against hypertension
Vitamin D Deficiency Diseases
1.
In children, deficiency leads to rickets: abnormal mineralization of skeleton
a.
Signs
i.
Enlarged head, joints, and ribcage
ii.
Deformed pelvis
iii.
Bowed legs
b.
At-risk populations
i.
Fat malabsorption
ii.
Dark skin pigmentation
iii.
Low milk intake
iv.
Minimal sun exposure
2.
In adults, deficiency leads to osteomalacia: soft bones
a.
Signs
i.
Poor calcification of newly synthesized bone
ii.
Hip, spine, and other fractures
b.
At-risk populations
i.
Kidney disease
ii.
Liver disease
iii.
Gallbladder disease
iv.
Intestinal disease
v.
Dark skin pigmentation
vi.
Limited UV exposure
3.
Those with low 25-OH vitamin D3 levels should take 20 - 25 µg/d of vitamin D
until normalized, then maintenance dose of 10 µg/d
Vitamin D Toxicity
1.
Only likely from excessive supplementation
2.
Vitamin D in skin is readily broken down
3.
UL: 50 µg (2000 IU)
4.
12.4
Consequences
a.
Overabsorption of calcium
b.
Hypercalcemia (high blood calcium)
c.
Calcium deposits in kidneys, heart, and lungs
d.
Anorexia
e.
Nausea/vomiting
f.
Bone demineralization
g.
Weakness
h.
Joint pain
i.
Disorientation
j.
Fatality
Vitamin E
A.
General
1.
Link between vegetable oil and normal reproduction in rats was first noted in
1922
2.
Vitamin E is a family of 8 compounds
a.
Alpha-tocopherol: most active form
b.
Beta- tocopherol
c.
Gamma- tocopherol: found in many vegetable oils, may have health
benefits, but not as active as alpha-tocopherol
d.
Delta- tocopherol
e.
Alpha-tocotrienol
f.
Beta- tocotrienol
g.
Gamma- tocotrienol
h.
Delta- tocotrienol
3.
Chemistry
a.
Long carbon tail that can exist in many isomeric forms
b.
Ringed structure
B.
Vitamin E in Foods
1.
Plant oils (e.g., cottonseed, canola, safflower, sunflower)
2.
Wheat germ
3.
Asparagus
4.
Peanuts
5.
Sunflower seeds
6.
Products made from plant oils (e.g., margarine, shortening, salad dressing)
7.
Vitamin E content of foods may vary due to harvesting, processing, storage, and
cooking (susceptible to destruction by oxygen, metals, light, and high
temperatures)
C.
Vitamin E Needs
1.
RDA (adult men and women): 15 mg, based on amount needed to prevent
hemolysis (breakdown of RBC membranes)
2.
DV: 30 IU
3.
4.
D.
E.
F.
G.
H.
Typical intakes are 2/3 RDA
Converting IU to mg
a.
For a synthetic source (e.g., supplements): 1 IU = 0.45 mg
b.
For a natural source (most potent), 1 IU = 0.67 mg
Absorption of Vitamin E
1.
Efficiency ranges from 20 - 70% depending on amount consumed and absorption
of dietary fat
2.
Incorporated into micelles with dietary fat in the small intestine; requires bile and
pancreatic enzymes
3.
Absorbed by small intestinal cells
4.
Incorporated into chylomicrons
Transport of Vitamin E
1.
Transported as part of chylomicrons in lymph, then bloodstream
2.
Triglycerides and some vitamin E are removed from chylomicrons by body cells,
chylomicron remnant remains
3.
Chylomicron remnant (containing vitamin E) is transported to liver
4.
Vitamin E is repackaged as VLDL, LDL, and HDL for delivery to body tissues
5.
No specific transport protein
Storage of Vitamin E
1.
Does not accumulate in liver
2.
Mostly stored in adipose tissue
Excretion of Vitamin E
1.
Bile (mostly)
2.
Urine
3.
Skin
Functions of Vitamin E
1.
Antioxidant
a.
Free radical: unstable compound with unpaired electron that acts as a
strong oxidizing agent; destructive to cell components (e.g., cell
membranes and DNA)
b.
In lipid-rich areas of the body, free radicals initiate lipid peroxidation
reactions that create lipid peroxyl radicals
c.
Vitamin E donates a hydrogen to lipid radicals to stop the oxidation
reaction, thus reducing oxidative stress
d.
Reduction in oxidative stress may lower risk for CVD, certain cancers,
cognitive decline, and impaired immune function
e.
Free radicals have some beneficial roles (e.g., immune function)
f.
Other antioxidant systems in the body
i.
Glutathione peroxidase: catalyzes breakdown of hydrogen
peroxides and lipid peroxides; requires selenium
ii.
Catalase: neutralizes free radicals in peroxisomes
iii.
Superoxide dismutase: eliminate superoxide radicals; requires
copper, zinc, and/or manganese
I.
J.
12.5
iv.
Carotenoids
v.
Vitamin C
vi.
Bilirubin
vii.
Uric acid
viii.
Ubiquinone
ix.
Lipoic acid
x.
Metal-binding proteins
2.
Interactions with other nutrients
a.
Due to the activity of selenium in the glutathione peroxidase pathway,
adequate selenium intake reduces vitamin E needs
b.
Vitamin C may aid in partial regeneration of vitamin E after vitamin E
donates a hydrogen to a free radical
Vitamin E Deficiency
1.
High-risk populations
a.
Fat malabsorption
b.
Smokers: smoking increases oxidative stress
c.
Preterm infants: born with limited stores of vitamin E, insufficient
intestinal absorption of vitamin E
2.
Consequences
a.
Hemolytic anemia: RBCs break down faster than they can be replaced
b.
Impaired immune function
c.
Neurological changes
Vitamin E Toxicity
1.
Consequences
a.
Hemorrhaging: insufficient clotting leads to excessive bleeding
b.
High intake of alpha-tocopherol may decrease gamma-tocopherol
activity; mixed isomer supplement preparations may be preferable
2.
High-risk populations
a.
Concurrent use of anticoagulant medications
3.
UL: 1000 mg (1500 IU) of alpha-tocopherol from natural sources or 1100 IU
from synthetic sources
Vitamin K
A.
General
1.
Vitamin K is a family of compounds known as quinones
a.
Phylloquinones (K1): from plant sources
b.
Menaquinones (K2): from fish oils and meats; synthesized by intestinal
bacteria
c.
Menadione: synthetic compound that can be converted to menaquinone
in body tissues
2.
Stable to heat processing
3.
Susceptible to destruction by light
B.
Vitamin K Sources
1.
2.
C.
D.
E.
F.
G.
H.
10% from bacterial synthesis in colon
90% from dietary sources
a.
Green leafy vegetables (e.g., kale, turnip greens, parsley, salad greens,
cabbage, spinach)
b.
Broccoli
c.
Peas
d.
Green beans
e.
Vegetable oils (e.g., soy, canola)
Vitamin K Needs
1.
AI, based on providing adequate vitamin K for blood clotting
a.
Adult women: 90 µg
b.
Adult men: 120 µg
2.
DV: 80 µg
Absorption of Vitamin K
1.
80% absorption efficiency
2.
Taken up by small intestine (requires bile and pancreatic enzymes), incorporated
into chylomicrons
3.
10% of needs are provided by colonic bacteria
Transport of Vitamin K
1.
Incorporated into VLDL and LDL
Storage of Vitamin K
1.
Liver
2.
Bone
Excretion of Vitamin K
1.
Bile
2.
Urine (minor)
Functions of Vitamin K
1.
Blood clotting (see Figure 12-20)
a.
Synthesis of clotting factors by the liver
b.
Conversion of preprothrombin to prothrombin (active blood-clotting
factor)
i.
CO2 added to glutamic acid to yield Gla protein (gammacarboxyglutamic acid)
ii.
Conversion also relies on calcium binding: Gla residues bind
calcium to form blood clots
c.
Anticoagulant medications (e.g., warfarin) inhibit reactivation of
prothrombin
d.
Consistent vitamin K intake and avoidance of vitamin K supplements are
necessary for individuals on anticoagulant therapies
2.
Bone metabolism: some vitamin K-dependent Gla proteins are synthesized in
bone
a.
Osteocalcium
b.
Matrix Gla protein
I.
J.
12.6
c.
Protein S
3.
Reduction of inflammation
Vitamin K Deficiency
1.
High-risk populations
a.
Prolonged antibiotic therapy
b.
Fat malabsorption
c.
Newborns: vitamin K stores are low at birth; vitamin K injections are
administered
d.
Megadoses of other fat-soluble vitamins
i.
Vitamin A inhibits intestinal absorption
ii.
Vitamin E decreases vitamin K-dependent clotting factors
2.
Consequences
a.
Hemorrhage
Vitamin K Toxicity
1.
No UL has been set
2.
Stored in liver and bone, but more readily excreted than other fat-soluble
vitamins
3.
High doses of menadione may result in hemolytic anemia, excess bilirubin in the
blood, and death
Dietary Supplements: Healthful or Harmful?
A.
40% of US adults regularly use vitamin/mineral supplements
B.
Reasons for use
1.
Reduced susceptibility to disease
2.
Compensate for dietary insufficiencies
3.
Protect against age-related changes
4.
Enhance well-being
C.
Dietary Supplement Health and Education Act (DSHEA): supplement is any product
intended to supplement the diet that contains one or more vitamins, minerals, amino
acids, herbs, botanicals, or plant extracts
1.
FDA does not have the authority or resources to closely monitor dietary
supplements unless they are dangerous or marketed using illegal claims
2.
Supplement manufacturers may not claim that supplements will prevent, treat, or
cure diseases
3.
Structure/function claims are allowed
4.
Claims that are not related to diseases are allowed
5.
Evidence is not always available to support claims
6.
Quality, purity, and consistency are not closely monitored by FDA, but voluntary
labeling with US Pharmacopeia symbol indicates that product meets established
industry standards for strength, quality, purity, packaging, labeling, solubility,
and storage life
D.
Dietary supplements are no substitute for a healthy diet
1.
Lack of fiber
2.
3.
4.
E.
F.
12.7
Lack of phytochemicals
Limited calcium content
Risk of toxicities and nutrient interactions
a.
Excessive zinc interferes with iron and copper absorption
b.
High folate masks vitamin B-12 deficiency
c.
Excessive vitamins A or D may result in toxicity symptoms
Some situations necessitate use of multivitamin/mineral supplements
1.
Iron supplements for women with excessive menstrual losses
2.
Iron and folate supplements for pregnant or breastfeeding women
3.
MVI for those with limited calorie intakes
4.
Calcium, iron, zinc, and vitamin B-12 for vegans
5.
Vitamin K for newborns
6.
Fluoride for infants and young children
7.
Vitamin D for those with limited sun exposure and low intake of fortified dairy
products
8.
Calcium and vitamin D for those with low dairy intake due to lactose intolerance
or milk allergies
9.
Specific vitamins or minerals for those with medical conditions that alter nutrient
metabolism
Guidelines for choosing MVI
1.
Nationally-recognized brand
2.
No more than 100% DV for nutrients listed
3.
Avoid exceeding UL for any nutrient from combination of supplements, foods,
and fortified foods
4.
Avoid superfluous ingredients (e.g., bee pollen, lecithin, hesperidin complex,
inositol, laetrile, pangamic acid, PABA)
Global Perspective: Vitamin A Deficiency
A.
100 - 140 million children worldwide suffer from vitamin A deficiency
B.
At-risk populations
1.
Children
a.
Leading cause of preventable blindness in children: 250,000 - 500,000
cases/year
b.
Increased death from infections
2.
Women of childbearing age
a.
Increased risk of HIV transmission from mother to fetus
b.
Maternal mortality
C.
Vitamin A Global Initiative: partnership among World Health Organization, United
Nations Children’s Fund, Canadian International Development Agency, US Agency for
International Development, and Micronutrient Initiative formed in 1998 to combat
vitamin A deficiency
1.
Promotes breastfeeding
2.
Promotes fortification of foods
3.
4.
5.
12.8
Provides educational programs to increase home gardening of vitamin A-rich
foods
Provides vitamin A supplements to at-risk populations - shown to decrease
vitamin A-related mortality by 15% in affected areas
Development of programs to increase production and access to nutrient-rich
foods
Expert Perspective: Vitamin D: “The Iceberg below the Surface”
A.
Vitamin D deficiency is reemerging as a global health concern for children and adults due
to low dietary intakes and limited UV light exposure
B.
Prevention of vitamin D-related bone disorders and maintenance of calcium homeostasis
are only the “tip of the iceberg” with regard to the role of vitamin D in the body
C.
Important roles in gene control and cell cycle regulation
1.
Diabetes
2.
Colon, prostate, and breast cancer
3.
CVD
4.
Autoimmune diseases (e.g., multiple sclerosis)
D.
Some scientists advocate higher vitamin D intake recommendations: 75 - 100 µg,
compared to current recommendations of 5 - 15 µg
E.
UL is currently set at 50 µg (2000 IU)