vitamin.pptx

For 4th Year Pharmacy students
VITAMINS (A,D,E,K,C)
Background
Sources
Functions
Deficiency
Recommended intake
30-Mar-22 Vitamins by Y.G for 4th Year Pharmacy students 1

Lesson objectives
At the end of completing the lesson, learners are expected to:
• Describe the different types of vitamins, & their metabolism
• Describe the functions of vitamins in the body
• Enumerate the food sources of vitamins
• Describe the clinical manifestations of specific vitamin deficiencies
• List their RDAs

Introduction
• The name vitamin is derived from ‘Vita’ meaning
life, and ‘amin’ since all types of vitamins
contained the chemical structure of an amine
• Are organic compounds needed in small amounts
in the diet of higher animals for growth,
maintenance of health and reproduction
• Discovered at the turn of this century due to the
fact the vitamins appeared in foods and the human
body in small amounts and the advancement of
technology

Cont…
• Some vitamins are highly stored in the liver
and get released to their functional sites when
needed, and are called hormones (A & D)
• Most vitamins are synthesized in the body
• Small amount of Vitamins K (Phylloquinone)
& B12 are synthesized by intestinal
microflora
• Other vitamins like pyridoxine (B6), vitamin
D are synthesized from their precursor in the
body
• Presently, there are 13 essential vitamins

Cont…
• The role of vitamins is to serve as helpers to the cell
machinery that make possible the process by which
other nutrients are digested, absorbed, and
metabolized, or built into the body structures
• Vitamins are not oxidized themselves (unlike energy
nutrients), but some help to liberate energy in a form
that the human body can use
• Most vitamins occur in food as precursors or
provitamins that are chemically changed to one or
more active forms in the body
• Classified on the basis of their solubility as water-
soluble & lipid soluble

Characteristics
Water soluble
B-groups and C
Lipid soluble
Vitamins A D E K
Solubility Water soluble Soluble in organic
compounds
Storage Usually not stored Has storage form
Absorption Directly
Needs lipids via the
lymphatic system
Transport in the
blood Freely Requires carrier protein
Deficiency
Occurs during acute
shortage No deficiency in acute shortage
Fat mal-absorption
Syndrome Not affected Affected
Mega dose intake Toxicity Unlikely Toxicity Likely

Vitamin A
• Three different forms of vitamin A are active in the
body: retinol, retinal, and retinoic acid.
Functions
•Regulates cellular differentiation
• Embryonic Epithelial (e.g. conjunctiva, tracts)
• Immune stem cells
• Hematopoietic
• Visual system, reproduction

Functions…
o Aids in treatment of many eye disorders
o Used as immune enhancer in viral disease (50% decrease
in mortality from measles)
o Essential for normal function of retina
o May act as Co-factor in enzyme system
o Necessary for bone growth, teeth development
o Has anti oxidant effect (pro vitamin A)

Food sources
Plant sources(Pro-vitamin A carotenoids )
 Vitamin A is generally found in green leafy
vegetables, yellow orange fruits).
 Green leafy vegetables (e.g., spinach,
young leafs from various sources), yellow
vegetables (e.g., pumpkins, and carrots),
and yellow and orange, no citrus fruits
(e.g., mango, and papaya).

Food sources
Animal sources (Preformed vitamin A )
 Human milk, glandular meats, liver and fish,
liver, oils, egg yolk, whole milk and dairy
products.

For infants BF is the source of vitamin

Digestion and Absorption
• Digestion & absorption
• Vitamin A requires digestion
• Retinol bound to fatty acid esters
• Retinyl esters & carotenes often complexed with
protein(pepsin )
• Emulsification of fat globules(bile)
• Retinol absorbed via protein carrier
• Carotenoids absorbed via transporters & passive diffusion

Bioavailability
• Foods containing provitamin A carotenoids tend to have less
biologically available vitamin A but are more affordable
than animal products.

Absorption
• Retinol 70-90% as long as the meal has 10% fat
• B-carotene 20-50% (but can be as low as 5% in uncooked
and non heat processed vegetable juice )
• Fiber intake and excessive vitamin E intake diminish
carotenoid absorption
• Much B-carotene converted to retinal & retinol in intestinal
mucosa

Recommended nutrient intake
• 500 g RE for women (or 1667 IU)
• 600 g RE for men (or 2000 IU)
• 1 g all-trans retinol = 1 RE
• 6 g -carotene = 1 RE
• Vitamin A activity equivalent to 1µg of all-trans retinol or 6µg of β-
carotene
• 12 g other provitamin A carotenoids = 1 RE
• 1 IU=0.300 g
• 1 IU of β-carotene = 0.6µg β-carotene

Upper Level
• 3000 ug/day of preformed vitamin A for adults
• Equivalent to 10,000 IU/day

Storage
• Vitamin A (retinol) is stored as retinyl esters (primarily
retinyl palmitate, but also retinyl stearate, oleate, and
linoleate) in the liver
• About 80% to 95% of the retinol is stored in the liver in
called stellate cells(also known as Ito cells).
• Retinoic acid does not accumulate in appreciable
amounts in the liver or other tissues.
• Adequate liver stores of vitamin A (minimum 20 μg
vitamin A per g liver)
• Plasma vitamin A concentrations remain fairly
constant over a wide range of dietary intakes.

Excretion
• Urinary excretion of vitamin A metabolites accounts
for up to about 60% of vitamin A excretion
• About 40% of vitamin A metabolites are excreted in
the feces

Interactions with other nutrients
• Vitamin A or carotenoids interact with vitamins
E and K.
• Excess dietary vitamin A intake interferes with
vitamin K absorption.
• High β-carotene intake, in turn, may decrease
plasma vitamin E concentrations.
• Vitamin A deficiency is associated with
decreased iron incorporation into red blood
cells and diminished mobilization of iron from
stores

Vitamin A deficiency
Definition
• WHO defines : Tissue concentrations of vitamin A low
enough to have adverse health consequences even if
there is no evidence of clinical xerophthalmia.
• VAD can occur in any age
• Affects mostly children between 5 months and 6 years, but
more before 3 years of age.
• Women of reproductive age (especially during pregnancy and
lactation).

Risk factors for VAD
• Low intake of vitamin A containing diet
• Seasonal vitamin A consumption
• Periods of general food shortage
• Food habits and taboos

Morbidity and mortality
• Infectious diseases depress circulating retinol and
contribute to vitamin A depletion, hence:
 There is increased morbidity from diarrhoeal diseases,
respiratory infection and measles.
 Measles mortality associated with VAD is increased up
to 50 percent.
 Improving vitamin A status can reduce child mortality by
23-34%.
 A lack of vitamin A can affect iron metabolism .

Clinical consequences of VAD
• Xerophthalmia (dryness and ulceration of the
conjunctiva and cornea): Mild to severe
• Lack of tear secretion
• Corneal blindness and disability
• Anemia
• Stunted growth
• Impaired immunity
• Increased severity of infection: (e.g. measles,
diarrhea, or malaria)
• Mortality

clinical significance of vitamin deficiency

Bitot’s Spot

Keratomalacia

VAD Reflect a Gradient of Health Consequences
Adapted from: KP West Jr J Nutr2002;132:2857S 27
30-Mar-22 Vitamins by Y.G for 4th Year Pharmacy students

Vitamin A Deficiency control programs
Issues
• When is vitamin A deficiency a public health
problem?
• Most micronutrient deficiencies are ‘hard to see’
• Best assessed by clinical and biochemical
measurements

Indicators for VAD as a public health problem
Clinical Indicators:
– Night blindness > 1.0%
– Bitot’s spot > 0.5%
– Corneal Ulceration >0.01%
– Xeropthalmia >0.05%
Low serum retinol (< 70 µmol/l)
– Moderate 10-20%
– Severe > 20%
29

Vitamin A Deficiency control....
Strategies:
• Breast milk: source of Vit A (mother’s status)
• Food diversification: Vitamin A rich foods
• Supplementation: mothers, infants & children
• Food fortification
30

Toxicity
• Excess in intake of vitamin A produces a toxic
syndrome called hypervitaminosis.
• Amounts exceeding 7.5mg /day should be avoided
• Birth Defects Excessive vitamin A poses a teratogenic
risk.
• High intakes(10,000 IU of supplemental vitamin A
daily) before the seventh week of pregnancy appear to
be the most damaging.

What is the Ethiopian Situation
• The national prevalence of Bitot's spots and night-blindness
among children were 1.7% and 0.8% respectively.
• The prevalence of subclinical deficiency was found 37.7%
among children (Demissie et al., 2010).
• According to profiles analysis, in Ethiopia 32% of child deaths
are attributable to vitamin A deficiency
(Ethiopian/PROFILES/Team&AED/Linkages., 2005).

Vitamin D
-The D vitamins are group of sterols that have a hormone
like function.
- There are two forms of vitamin D
a. Vitamin D2 (ergocalciferol)
b. Vitamin D3 (cholecalciferol)
- Ergesterole and 7 dehaydrocholesterol are the
provitamins forms of vitamin D

The role of vitamin D
• Maintain normal blood levels of calcium and
phosphate
• Reduced excretion of calcium by stimulating
resorption in the distal renal tubules
• Modulates the transcription of cell cycle proteins
• Increased intestinal absorption of calcium
• Decreased mobilization of bone mineral

Food sources
 Occur naturally in fatty fish ,liver, egg yolk
Can be synthesized from Cholesterol-like precursor
underneath the skin via exposure to UV B (7-
dehydrocholesterol)
Plant sources, mushrooms can synthesize
Can be found in its pre-formed forms in the diet (either D3-
Cholecalciferol or D2- ergocalciferol forms).

Synthesis of D from Sunlight Exposure
• 10 min of summer sun or 40 min winter sun on hands
and face for 10 g of D(Western countries)
• Elders may not have much sunlight exposure

Absorption
• Vitamin D3 (cholecalciferol) from the diet is absorbed
from a micelle, in association with fat and with the
aid of bile salts, by passive diffusion into the
intestinal cell.
• The largest amount of vitamin D is absorbed in the
distal small intestine.

Endogenous vitamin D
• Cholecalciferol diffuses from the skin into the blood.
• It is transported in the blood by an α-2 globulin
vitamin D–binding protein (DBP), also called
transcalciferin, that is synthesized in the liver.

Transport
• Chylomicrons transport about 40% of the cholecalciferol in the
blood.
• Chylomicron remnants deliver the vitamin to the liver.
• Cholecalciferol, which slowly diffuses from the skin into the
blood, is picked up for transport by DBP.
• The vitamin D bound to DBP travels primarily to the liver but
may be picked up by other tissues, especially muscle and
adipose tissue, before hepatic uptake.

Storage
• Most of the 25-OH D3 synthesized in the liver is secreted into the
blood and transported by DBP
• Little 25-OH D3 remains in the liver
• Blood is the largest pool
• a half-life of about 10 days to 3 weeks
• blood and muscle (for 25-OH D 3) and adipose tissue (for cholecalciferol).

Interactions
• Ca
• P
• Vitamin K
• Vitamins D and K are both fat-soluble vitamins and play a
central role in calcium metabolism
• Vitamin D promotes the production of vitamin K-dependent
proteins, which require vitamin K for carboxylation in order
to function properly

Metabolism & Excretion
• Undergoes different side-chain reactions when in excess
• Mostly excreted in bile

Recommended Nutrient Intakes
• Infants – age 50 5 g or 200 IU
• Adults 51 – 65 y 10 g or 400 IU
• Adults > 65 y 15 g or 600 IU
• 1 IU = 0.025 g
• Recent questions about whether these
recommendations are high enough for older
people??

Recommended Dietary Allowances (2010)
• Infants – age 70 15 g or 600 IU
• Adults > 70 y 20 g or 800 IU
• 1 IU = 0.025 g

Upper Levels (USA)
• > 1 yr 50 g (2000 IU)/d
• Infants < 1 yr 25 g (1000 IU)/d

Assessment
• Not routinely measured in blood
• 25-OH D3 is index of vitamin D status
• <10-12 ng/mL indicates deficiency
• >150 ng/mL indicates possible toxicity

Populations at risk for Vit. D deficiency
Infants
Exclusively breastfed, Limited UVB exposure
Adolescents
Rapid growth of the skeleton
Elderly
Limited metabolism of Vitamin D
Reduced response of target tissues (e.g., bone)
Reduced skin exposure

Vitamin D Deficiency disorders
Rickets and osteomalacia
• Rickets occurs in children, whose bones are still
growing.
• Osteomalacia occurs in adults who have formed
bones.
• Mostly rickets and osteomalacia are not common in
tropical countries however, reported in some large,
densely populated cities.
• Osteomalacia is most common in women who have
had many children ( maternal depletion).

Vitamin D deficiency

Bone Samples

Deficiency con’t…

Prevention of Vitamin D Deficiency
Rickets
• Adequate amounts of sunlight exposure
• Vitamin D and calcium supplements (Cod liver oil (saltwater fish
oil), milk, etc)
• Nutrition education should be provided regarding the needs for
calcium and vitamin D.
Osteomalacia
• The body should be exposed to adequate sunlight
• Supplementation especially for pregnant and lactating mothers
• Nutrition education

Vitamin K
 Are found in different forms
• K1 – Phylloquinone – from plants
• K2 – Menaquinones – synthesized by bacteria
• K3- Menadione(synthesized in the body)

Food sources
It is also found in liver, fish, egg yolk
Primarily from plants – broccoli, kale, cabbage, lettuce
Soy and rapeseed oil are rich sources; peanut and corn
are not
Bacteria in the colon provide menaquinone
Menaquinones also may be found in a few foods such as
liver, fermented cheeses, and soybean products
Exposure of the vitamin to light and heat can result in
significant vitamin K destruction

Function
• Post translational carboxylation of glutamate to
form -carboxyglutamate
• 4 of 13 factors for blood coagulation
• Binds calcium

Osteocalcin
• Secreted by osteoblasts during bone matrix formation
• Osteocalcin ~15-20% of noncollagen protein in bone
• Without vitaminK,the bones produce an abnormal protein
that cannot bind to the minerals that normally form
bones, resulting inlow bone density
• Long-term vitamin K deficiency caused bone
crystallization problems in animals

Nutrient Interactions
• Excess VA interferes with K absorption
• Excess E also antagonizes – perhaps through absorption or
metabolism

Recommended Intakes
• RNI for Adults
• Men – 65 g/d
• Women – 55 g/day

Deficiency
• Normal diet contains 300-500 ug vitamin K per day
• “At-risk” groups
• Newborn infants – injection at birth recommended
(0.5-1 mg im.)
• People who have been injured or are treated
chronically with antibiotics
• Fat malabsorption
• Antibiotics kill the vitamin K-producing bacteria
in the intestine
• Anticoagulant drugs interfere with vitamin K
metabolism and activity.

Deficiency and toxicity
Clinical indication
• Hyphothrombia (delayed clotting time )
• Causes hemorrhage diseases in new born infants
• Toxicity
• Prolonged administration of large doses of vitamin K
can produce hemolytic anemia

Deficiency
• Has been suggested that subclinical vitamin K
deficiency may be involved in pathogenesis of
mineral loss from bone

Sign of Clinical deficiency

Assessment
• Measurement of prothrombin time
• Normal is 11-14 seconds
• Major bleeding associated with >25
• Plama prothrombin concentrations in the normal
range suggest adequate K status

Vitamin E
• Forms: Tocopherols, Tocoterols
It is stable to high TO and acids.
Oxidation takes place readily in the presence of rancid
fats or lead and iron salts.

Function
 The major function of vitamin E is to act as natural
antioxidant by scavenging free radicals
 Vitamin E prevents the oxidation of the
polyunsaturated fatty acids
 It protects RBC’s from hemolysis.
It decreases the risk of myocardial infraction .
 It prevents the oxidation of vitamin A
Suppression of tumor growth and cell proliferation

Food sources
• Widely distributed, especially oils from plants
• Vitamin E correlates with level of PUFA
• Wheat bran & germ – tocotrienols
• Butter, milk and egg-yolk
• Animal products—little E—stored in fat
• Limiting fat may limit vitamin E

Absorption
• Need bile and pancreatic juice
• Dietary lipid improves absorption of E
• Absorption – 20-50%
• Absorption <10% from 200 mg dose
• Absorbed passively in jejunum
• Incorporated into chylomicrons; transported via
lymph

Transport & Storage
• Tocopherol in RBC membrane
• Transported to tissues by LDLs & protects LDLs
from oxidation
• Binds to specific proteins within cell
• Most stored in adipose tissue
• Adipose tissue E levels vary with intake

Excretion
• Major route of excretion for absorbed α-tocopherol is through
the bile

Recommended Intakes
• RNI
• Men – 10 mg/d a-TE
• Women – 7.5 mg/d
• Smokers have increased free-radical burden but
not known if vitamin E requirements need
adjustment

Vitamin E Deficiency
• With deficient intake of vitamin E the cells are more
vulnerable to oxidative attack and damage.
Hemolytic anemia: when adequate vitamin E is not
available, the lipid membranes of RBCs are exposed to
oxidation of their structural poly unsaturated fatty acids.
• The membranes are broken, the contents lost and the
cells destroyed. The continued loss of RBCs leads to
anemia called hemolytic anemia.
• Premature infants are especially vulnerable b/c that is
the period when vitamin E stores are normally built
up.

Clinical indication
Protect against the developments of heart diseases
Toxcity
 the least toxic of all fat soluble vitamins
No toxicity has been observed at doses of
300mg/day

Vitamin C (Ascorbic acid )
• Humans cannot synthesize – Most mammals
synthesize from glucose(l-gulonolactone oxidase)
• Simple 6-carbon structure

Function
• Has antioxidant effect
• Increase iron absorption from food
• Contributes for Hgb synthesis
• Amino acid metabolism and hormone

Collagen Synthesis
• Hydroxylation of proline to hydroxyproline & lysine to
hydroxylysine
• Ascorbate needed to reduce ferric iron back to ferrous
• Supports cross-linking of collagen
• Important for wound healing

Neurotransmitter Synthesis
• Affects formation of norepinephrine by dopamine
monoxygenase
• Hydroxylation of tryptophan for synthesis of serotonin

Antioxidant Activity
• Antioxidant that reverses oxidation
• Free radicals attack nucleic acids in DNA, PUFA in
phospholipids, and proteins in cells
• Ascorbate can interact w/oxidants before they initiate
damage

Vitamin C & Disease
• Cardiovascular Disease
• In some animals, vitamin C regulates cholesterol
metabolism to bile acids – not completely clear in humans
• Low vitamin C status may increase oxidation of LDLs
• Cataracts – oxidative damage to the proteins in the lens – C
may protect

Ascorbate–Nutrient Interactions
• Increases iron absorption by reducing to Fe2+ and/or by
forming soluble complex
• Increases the absorption of heavy metals by forming chelates
• High vitamin C intakes may have a negative impact on copper

Digestion and Absorption
• Vitamin C does not require digestion prior to being absorbed into intestinal
cells
• Absorbed primarily by active transport
• Absorption 98% at low intakes (<20 mg)
• Absorption may drop to ~16% with 12 g
• Pectin and zinc may impair absorption
• High iron in intestine – oxidative destruction
• Transported free in plasma
• Vitamin C highest in adrenal and pituitary glands
• Higher in tissues than in plasma

Excretion
• 25% excreted in urine as oxalic acid
• Ascorbate tends to be conserved if body pool is less than 1500
mg

Food sources
• Ascorbate is found in many fruits and vegetables.
• Vegetables such as cabbage, bean , kale, red and green peppers,
peas, potatoes and tomatoes may be more important sources of
vitamin C than fruits.
• Citrus products are most commonly cited as significant sources of
the vitamin.

Dietary sources of vitamin C and limitations
The vitamin C content of food is strongly influenced
by:
o Transport to market ( excessive bruising)
o Shelf life
o Time of storage
o Cooking practices and
o Chlorination of water
o Blanching reduces loss (inactivate ascorbate oxydase)
o Low PH preserves Vit.C
o Exposure to copper, iron and alkaline media destroys the
vitamin.

Recommended Intakes
• Adults
• Men – 45 mg/day
• Women – 45 mg/day
• Smokers may need additional
• Passive smoke also lowers ascorbate
• Little increase in plasma with intakes above 200 mg/d

Pregnant and lactating women
• During pregnancy there is a moderate increased need for
vitamin C, particularly during the last trimester.
• An extra 10 mg/day throughout pregnancy meet the extra
needs of the growing fetus in the last trimester.
• An extra 25 mg/day require during lactation

Scurvy
• Intakes < 10 mg/d
Manifestation
• Muscle weakness , swollen gum , loss of teeth,
painful joints
• Impaired wound healing
• Anaemia

Toxicity
• Daily intakes of up to 2 g vitamin C are routinely consumed
without adverse effects
• Vitamin C absorption is saturable and dose dependent, more
vitamin C is absorbed
• The most common side effect with ingestion of large amounts
(2 g) of the vitamin is gastrointestinal problems characterized
by abdominal pain and osmotic diarrhea.
• Kidney stone

END

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