‫بسم هللا الرحمن الرحيم‬

Micronutrients
Vitamins and Minerals
Dr. Mahmoud Sirdah
 Classes of Nutrients
Macronutrients
1. Carbohydrate

2. Protein

3. Lipids

4. Water

Micronutrients
1. Vitamins

2. Minerals
 Vitamins and minerals are called micronutrients
because we only need them in very small amounts.

 That doesn’t mean they aren’t important; in fact

we can’t live without vitamins and minerals.

 we measured protein, carbohydrate and fat needs

in grams. However, Vitamins and minerals are
measured in milligrams (mg), micrograms (mcg)
and international units (IU).
 Vitamins
 A vitamin is an organic compound required as a nutrient
in tiny amounts by an organism.

 Vitamins serve crucial functions in almost all bodily

processes (immune, hormonal and nervous systems) and
must be obtained from food or supplements as our bodies
are unable to make vitamins.
 A compound is called a vitamin when it cannot be
synthesized in sufficient quantities by an organism, and
must be obtained from the diet.
 Thus, the term is conditional both on the circumstances
and the particular organism.
 For example, ascorbic acid functions as vitamin C for
some animals but not others, and vitamins D and K are
required in the human diet only in certain circumstances.
 Vitamins are classified in two categories:
• Water-soluble
• Fat-soluble

 Classification is based on whether or not the

vitamins can dissolve in water.
 Water-soluble vitamins include the B complex
of vitamins and vitamin C.
 The fat-soluble vitamins include vitamins A,
D, E and K
 The fat-soluble vitamins
 Because they are soluble in fat (lipids), these vitamins tend to
because stored in the body's fat tissues, fat deposits, and liver.

   This storage capability makes the fat-soluble vitamins

potentially toxins.

 Care should be exercised when taking the fat-soluble vitamins. 

The fat-soluble vitamins, especially vitamin A, should be
consumed with care because of their storage capabilities.

 They have the potential of building up to harmful levels. Even

though very few cases of vitamin toxicity have been reported,
concern has grown during recent years as the practice of taking
mega doses has become popular.
 Water-soluble vitamins
 In contrast to the fat-soluble vitamins, the water-soluble vitamins are not
easily stored by the body. They are often lost from foods during cooking or
are eliminated from the body.

 We don’t store water-soluble vitamins in your body very well so they need
to be replaced constantly through your diet. That is one of the reasons we
need to eat good foods every day, not just once in a while.

 With exception of vitamin B6 and B12, they are readily excreted in urine
without appreciable storage, so frequent consumption becomes necessary.

 They are generally nontoxic when present in excess of needs, although

symptoms may be reported in people taking mega doses of niacin, vitamin
C, or pyridoxine (vitamin B6).

 All the B vitamins function as coenzymes or cofactors, assisting in the

activity of important enzymes and allowing energy-producing reactions to
proceed normally. As a result, any lack of water-soluble vitamins mostly
affects growing or rapidly metabolizing tissues such as skin, blood, the
digestive tract, and the nervous system.
 Water-soluble vitamins
 The water-soluble vitamins include vitamins B1, B2, B3, B6,
B12 and vitamin Cas well as Folic acid and Biotin.

 Vitamin C has been in the spotlight for many years and is best
known for its ability to combat colds and its function as an
antioxidant.
 The B vitamins basically act as coenzymes and are involved
in the metabolism of fat, protein, and carbohydrates.

 The water-soluble vitamins are not normally stored in the

body in any significant amounts. Therefore, they must be
consumed in constant daily amounts to avoid depletion and
interference with normal metabolic functioning.
 Coenzymes and Cofactors
 Coenzymes and cofactors are any non-protein molecules (usually organic
molecules or metal ions) that are required by an enzyme for its activity.

 Enzymes may or may not have a nonprotein molecule attached to them.

Some enzymes contain covalently bound carbohydrate groups, which do
not affect the catalytic activity, but may influence enzyme stability or
solubility.

 Many enzymes have metal ions, while some others possess low weight
organic molecules; these are called cofactors /coenzymes, and are essential
for enzyme activity.
An organic cofactor is commonly known as coenzyme. Cofactors and
coenzymes may be covalently or noncovalently attached to the protein
molecule, called apoenzyme.

 Cofactors are often classified as inorganic substances that are required for,
or increase the rate of, catalysis.

 coenzymes are organic molecules that are required by certain enzymes to

carry out catalysis.
 Coenzymes and Cofactors
 cofactors /coenzymes bind to the active site of the enzyme
and participate in catalysis but are not considered substrates of
the reaction.
 An apoenzyme lacks catalytic activity in the absence of its specific
cofactor /coenzyme.
 When a cofactor is so tightly bound to the apoenzyme that it is difficult to
remove it without damaging the enzyme, the cofactor is often called a
prosthetic group.
Both coenzymes and cofactors generally contribute to enzyme activity as
well as stability. The complex of an apoenzyme and the cofactor is known
as holoenzyme.

 Coenzyme molecules are often Vitamins or are

made from vitamins
Inactive enzyme
Enzyme

Vitamin coenzyme

cofactor

Substrate

Active enzyme
 Vitamins Overview
 What is a vitamin?
 What are the two types of vitamins?
 Where do I get my vitamins?
 How much do I need?
 Why are the vitamins important?
• Associated diseases.
 Vitamins Overview
 The term vitamin is derived from the words:
vital and amine
because vitamins are required for life and were
originally thought to be amines.
 Although not all vitamins are amines, they are

organic compounds required by humans in small

amounts from the diet.
 An organic compound is considered a vitamin if a

lack of that compound in the diet results in overt

symptoms of deficiency.
 Vitamins Overview
 Vitamins are grouped by their biological and
chemical activity, not their structure.
 Thus, each "vitamin" may refer to several vitamer
compounds that all show the biological activity
associated with a particular vitamin.

 Vitamers are often inter-converted in the body.

 Such a set of chemicals are grouped under an

alphabetized vitamin "generic descriptor" title, such
as "vitamin A," which includes the retinoid
compounds (retinal, retinol , retinoic acid and many
carotenoids
Good Sources of Vitamins
Vitamin Pyramid
 Vitamins Bioavailability
Vitamins Bioavailability = amount available + amount absorbed
 Vitamins Bioavailability affected by
 Efficiency of digestion
 Nutrition status
 Other foods consumed at the same time
 Method of food preparation
 Source of nutrient
• synthetic, naturally occurring, fortified
 Reference Value Definitions
 Estimated Average Requirement (EAR)
• a daily nutrient intake value that is estimated to meet the
requirements of half the healthy individuals in a group
• intake at which the risk of inadequacy is 0.5 (50 percent) to
an individual
 Recommended Daily Allowance (RDA)
• the average daily intake level that is sufficient to meet the
nutrient requirement of nearly all (97-98%) healthy
individuals in a particular life stage and gender group
• the intake at which the risk of inadequacy is very small—
only 0.02 to 0.03 (2 to 3 percent)
 Tolerable Upper Limit (UL)
• highest level of a daily nutrient that is likely to pose no risk
of adverse health effects to almost all individuals
 Two Classifications of Vitamins

Water Soluble Fat Soluble

 Vitamin C  Vitamin A

 B Vitamins  Vitamin D
 Thiamin  Vitamin E
 Riboflavin  Vitamin K
 Niacin
 Pantothenic Acid
 Biotin
 Vitamin B6
 Folic Acid
 Vitamin B12
 Vitamin Comparisons

Fat Soluble Water Soluble

Vits A, D, E, K Vits B & C
Lymph then blood/protein Directly into blood Absorption
carrier
Long term Short term Storage

Less readily excreted – Kidneys detect and Excretion

remain in fat storage sites remove in urine

Likely Possible Toxicity

Regular intake Daily intake Requirements

 Fat Soluble Vitamin Functions

 Vitamin A

 Vitamin D

 Vitamin E

 Vitamin K
 Vitamin A Retinol
 Vitamin A is a generic term for a large number of
related compounds.
 Retinol (an alcohol) and retinal (an aldehyde) are
often referred to as preformed vitamin A.
 Retinal can be converted by the body to retinoic acid,
the form of vitamin A known to affect gene
transcription.
 Retinol, retinal, retinoic acid, and related compounds
are known as retinoids (Vitamer).
 Beta-carotene and other carotenoids that can be
converted by the body into retinol are referred to as
provitamin A carotenoids.
 Vitamin A
 Vital – promote growth and reproduction and
maintain health

 organic

 do not supply calories

 required in the diet in small amounts (micrograms or
milligrams per day) for the maintenance of normal
health and metabolic integrity
 Vitamin A
 Vitamin A was the first fat-soluble vitamin identified (in 1913).

 Vitamin A comprises the preformed retinoids (Retinol, retinal, retinoic

acid), plus the precursor forms, the provitamin A carotenoids.

 Preformed retinoids is a collective term for retinol, retinal, and

retinoic acid, all of which are biologically active.

 The provitamin A carotenoids include mainly beta-carotene,

which is converted to retinoids with varying degrees of efficiency.

 Retinoids are sensitive to heat, light, and oxidation by air. while

Beta-carotene is relatively more stable.

 There is some loss of vitamin A with cooking, but only after boiling
for a comparatively long period.
 Vitamin A
 Retinoids are converted to retinol in the
intestines and transported with dietary fat to the
liver, where it is stored.

 A special transport protein, retinolbinding

protein (RBP), transports vitamin A from the
liver to other tissues.

 Carotenoids are absorbed intact at a much lower

absorption rate than retinol. Of all the
carotenoids, beta-carotene has the highest
potential vitamin-A activity.
 Vitamin A functions
 The active forms of vitamin A have three
basic functions:
 vision,

 growth and development of tissues,

 immunity.

 Vision. Vitamin A combines with a

protein called opsin to form rhodopsin in
the rod cells of the retina. When vitamin
A is inadequate, the lack of rhodopsin
makes it difficult to see in dim light.
 Vision
Retinal is the key molecule involved in vision and responsible for
converting the energy in light photons into electrical impulses
in the retina

 The precursor of 11-cis-retinal is the alcohol all-trans-retinol

(Vitamin A). These molecules (11-cis-retinal or vitamin A)
cannot be synthesized by mammals and has to be acquired
through the diet.

 Precursors to Vitamin A are carotenes, which are found in

many vegetables including carrots. Perhaps this leads credence
to the old superstition that carrots help you see better in the
dark - indeed, it is known that a deficiency of Vitamin A leads
to night blindness and eventually damage to the retinal cells
involved in vision.
 Vision
 All-trans-retinol is converted to
11-cis-retinal.
 The photosensitive molecule
rhodopsin
involved in vision is called
rhodopsin, (also known as visual
purple) which consists of a large
protein (having a molecular
weight of around 38,000) called
opsin, joined to 11-cis-retinal.
 Opsin does not absorb visible
light, but when it is bonded with
11-cis-retinal to form rhodopsin,
the new molecule has a very
broad absorption band in the
visible region of the spectrum.
The rhodopsin cycle
 Vitamin A functions, continue
 Growth and development of tissues. Vitamin A is involved in
normal cell differentiation specially for epithelial tissue cells
of Cornea, skin, respiratory lining, GI tract lining
 Vitamin A supports male and female reproductive processes
and bone growth.

 Immunity. Vitamin A is essential for immune function and

vitamin-A deficiency is associated with decreased resistance
to infections.
• Respiratory infections and diarrhea 2-3X more likely in kids
with low Vitamin A.
• Bacteria and viruses more likely to invade unhealthy epithelial
tissue
 The severity of some infections, such as measles and diarrhea,
is reduced by vitamin-A supplementation among those who
suffer from vitamin-A deficiency.
 Vitamin A functions, continue
 It has been suggested that beta-carotene and other carotenoids (also
called phytochemicals) may function as antioxidants by
neutralizing free radicals.

 Free radicals are unstable, highly reactive molecules that damage

DNA, cause cell injury, and increase the risk of chronic disease.

 Beta-carotene has also been associated with reducing the risk of

lung cancer.

 Lutein and zeaxanthin, yellow carotenoid pigments in corn and dark

green leafy vegetables, may reduce the risk of macular
degeneration of cornea or retina (‫لشبكية‬CC‫لقرنية او ا‬CC‫ ا‬C‫بقع‬CC‫ ) ت‬and age-
related cataracts (‫زرق‬
‫الزرق‬CC‫لماء ا‬CC‫)ا‬.
 Lycopene, a red carotenoid pigment in tomatoes, may help reduce
the risk of prostrate cancer, cardiovascular disease, and skin
damage from sunlight.
 Repairs skin and promotes the growth of elastin e.g Retain A
Retin A is retinol that
Repairs skin and
promotes the growth
of elastin
 which foods are rich in vitamin A sources
(preformed and provitamin A precursors)?

 Provitamin A Carotenoids
 Preformed Retinoids • Dark greens
• Liver • Yellow-orange
• Fish • Carrots,
• Fish oils • kale ‫لفت‬
( ‫للف‬QQ‫)ا‬,
‫ت‬
• Fortified milk • spinach,
• Egg • squash,
• sweet potatoes,
• cantaloupe,
• peaches,
• broccoli,
• apricots
?which foods are rich in vitamin A

Essential Nutrient
Toxicity Sources People at risk Deficiency Functions Vitamin A
symptoms

Headache, Preformed Rare in United Poor growth, Vision in dim Preformed

vomiting, vitamin A: States but night blindness, light and color retinoids and
double vision, liver, fortified common in blindness, dry vision, cell provitamin A
hair loss, dry milk, fish liver preschool skin, differentiation carotinoids
mucous oils children living Xerophthalmia and growth,
membranes, Provitamin A: in poverty in (‫لملتحمة‬QQ‫)جفافا‬ immunity
bone and joint red, orange, developing
pain, fractures, dark green, and countries,
liver damage, yellow alcoholics
hemorrhage, vegetables,
coma, orange fruits
teratogenic
effects (‫مسخ او‬
‫ خلقي‬Q‫شوه‬QQQ‫)ت‬:
spontaneous
abortions, birth
defects.
 Vit A deficiency
 Dietary deficiency of vitamin A is rare in North America and
western Europe.

 it is the leading cause of blindness in children worldwide.

 Newborn and premature infants, the urban poor, older adults,

people with alcoholism or liver disease, and those with fat
malabsorption syndrome are all at increased risk.

 One of the earliest symptoms of vitamin-A deficiency is night blindness. It

is a temporary condition, but if left untreated it can cause permanent
blindness. This degeneration is called xerophthalmia ‫لملتحمة‬QQ‫))جفافا‬, and it
usually occurs in children after they are weaned.
 Symptoms of xerophthalmia include dryness of the cornea and
eye membranes due to lack of mucus production, which leaves
the eye vulnerable to surface dirt and bacterial infections.

 Vit A deficiency

 Vitamin-A deficiency can cause follicular hyperkeratosis

(‫لجلد‬QQ‫ر ا‬Q‫ع‬QQ‫ريباتش‬Q‫قرنج‬QQQ‫خامة و ت‬QQ‫)ض‬, a condition in which hair follicles become
plugged with keratin, giving a bumpy appearance and a rough, dry texture
to skin.

 In developing countries, the severity of infectious diseases such as measles

is often correlated to the degree of vitamin-A deficiency.

 Providing large doses of vitamin A reduces the risk of dying from these
infections.

 The age range of the target population for vitamin-A intervention programs
is usually from birth to seven years.

 Administration of high-potency doses in the range of 15,000 to 60,000

micrograms (μg) are distributed to young children in targeted areas of the
world to build up liver stores for up to six months. However, consumption
of adequate food sources is the most important long-term solution to
vitamin-A deficiency.
 Vit A Toxicity
None of the forms of vitamin are easily excreted, so toxicity is a risk for those
with kidney disease or as people age.

 Vitamin-A toxicity, called hypervitaminosis A,

 It can result from long-term supplementation of two to four times the
Recommended Daily Allowance (RDA) for preformed vitamin A.
 Excess intake of preformed vitamin A is a teratogen, meaning it can cause
birth defects.
 Birth defects associated with vitamin-A toxicity include:
 cleft palate (‫لحنك‬QQ‫نشقاقا‬Q‫)ا‬

 heart abnormalities

 brain malfunction.

 Acute excess intake during pregnancy can also cause spontaneous

abortions.
 Pregnant women should avoid prenatal supplements containing retinal, as
well as medications made from retinoids, such as Accutane and Retin-A.
 Prolonged and excessive consumption of carotene-rich foods can lead to
hypercarotenemia (Q‫لدم‬QQ‫زرنة ا‬Q‫رط ج‬QQQ‫)ف‬, a clinical condition characterized by
deep orange discoloration of the skin and increased carotene levels in the
blood. This condition is usually harmless.
 Vitamin D (Calciferol)
 Common Names: Vitamin D; Calciferol, Cholecalciferol, Ergocalciferol
 Forms: Calciferol, cholecalciferol, ergocalciferol, irradiated ergosterol
 Vitamin D plays a critical role in the body’s use of calcium and phosphorous. It
increases the amount of calcium absorbed from the small intestine and helps form and
maintain bones. Children especially need adequate amounts of vitamin D to develop
strong bones and healthy teeth.
 Vitamin D is Called a “conditional” vitamin.
 For most people in sunny regions , sun provides 80-100% of their needs of Vitamin D

Vitamin D2 (ergocalciferol) is
obtained from plants.
Vitamin D

• Vitamin D3 is cholecalciferol
derived from animal products
 Structures of Vitamin D
 There are different forms of vitamin D
 Vitamin D2 (ergocalciferol)
 vitamin D3 (cholecalciferol)
 provitamins
 Vitamin D is a generic term and indicates a molecule
of the general structure that contains the 4 fused rings
of steroid with differing side chain structures.
 Technically vitamin D is classified as a seco-steroid.
 Seco-steroids are those in which one of the rings has
been broken.
 in vitamin D, the 9,10 carbon-carbon bond of ring B
is broken, and it is indicated by the inclusion of
"9,10-seco" in the official nomenclature
 Vitamins D3 & D2
 Vitamin D2 (ergocalciferol) is obtained from plants.
 Vitamin D3 is cholecalciferol derived from animal products
 Vitamin D3 (cholecalciferol) can be produced
photochemically by the action of sunlight or ultraviolet light
from the precursor sterol 7-dehydrocholesterol which is
present in the epidermis or skin of most higher animals.

 Thus, it is important to appreciate that vitamin D3 can be

endogenously produced and that as long as the animal (or
human) has access on a regular basis to sunlight there is no
dietary requirement for this vitamin.

 Vitamin D2 = ergocalciferol (which is equivalently potent to

vitamin D3 in humans and many mammals) is produced
commercially by the irradiation of the plant sterol ergosterol
with ultraviolet light.
 Absorption of Vitamin D
 Vitamin D from foods is absorbed from the upper part of the
small intestine, along with dietary fat, and transported to the
liver.

 In the skin, ultraviolet (UV) radiation from the sun converts a

cholesterol derivative 7-dehydrocholesterol to cholecalciferol,
which enters the blood stream and is transported to the liver.

 In the liver, vitamin D is converted to calcidiol, an inactive

form that circulates in blood. Kidneys take up calcidiol and
convert it to an active hormone form of vitamin D called
calcitriol.

 People with chronic kidney failure have very low levels of

calcitriol and must be routinely treated with this form of the
vitamin.
 Vitamin D –

Skin Cholesterol Cholecalciferol

derivative
blood

blood Calcidiol
(inactive)

Calcitriol (Active hormone form of vitamin D)

5-15 min Sunlight/week

 Functions of Vitamin D
 The group known as the D vitamins are required for growth, especially bone
growth or "calcification".
 The best-known function of active vitamin D is to help regulate blood levels of
calcium and phosphorous. Vitamin D increases absorption of these minerals from
the gastrointestinal (GI) tract. In combination with parathyroid hormone, it
enhances their reabsorption from the kidneys and their mobilization from bones
into the blood.

 Vitamin D can be considered both a vitamin and a hormone.

 Vitamin D plays an important role in maintaining adequate blood levels of insulin
and may assist the metabolism of sugar.
 1,25 dihydroxycholecalciferol (DHCC), the most active form of vitamin D,
functions to:
» Increase the absorption of calcium from the intestines by stimulating the
synthesis of calcium-binding protein. This occurs in the brush border of the
intestinal mucosa.
» Increase the resorption ‫ارتشاف‬
( ) of calcium from bone.
» Increase serum calcium levels. Once this occurs calcium can then be
stored in the bones. Thus, even though it initially causes bone resorption,
the net effect is to increase calcium deposition in the bone
 Vitamin D helps maintain calcium levels even if dietary intakes are not optimal.
Calcitriol controls growth of normal cells and some cancer cells. Adequate
vitamin-D status has been linked to a reduced risk of developing breast, colon, and
prostrate cancers
 Primary sources of vitamin D
 The primary food sources of vitamin D are milk and
other dairy products fortified with vitamin D.
 Egg yolk
 Vitamin D is also found in oily fish as well as in cod
liver oil.
 Vegetables are usually low in vitamin D. Leafy dark
green vegetables and mushrooms are significant
sources of vitamin D from non-animal sources.
 In addition to the vitamin D provided by food, we
obtain vitamin D through our skin which makes
vitamin D in response to sunlight.
 Although about 10 substances have fat soluble vitamin D
activity, vitamins D2 (or ergocalciferol) and D3 (or
cholecalciferol) are the two most significant to humans.

 Vitamin D3 is found in our diet, while vitamin D2 occurs in

yeasts and fungi. Both can be formed from their respective
provitamins by ultraviolet irradiation; in man the provitamin
(7-dehydrocholesterol), which is found in skin, can be
converted by sunlight to vitamin D3 and thus is an important
source of the vitamin. Human beings can utilize both vitamins
D2 and D3.
 Vitamin D deficiency
 Children in particular need adequate amounts of
vitamin D to develop strong bones and healthy teeth.
 Symptoms of vitamin D deficiency in growing
children include rickets (‫لكساح‬QQ‫( )ا‬long, soft bowed
legs) and flattening of the back of the skull.

 Vitamin D deficiency in adults is called osteomalacia

(Q‫لعظام‬QQ‫لينا‬QQQ‫يناو ت‬QQ‫)ل‬, which leads to muscular weakness
and weak bones.
 rickets in children
Osteomalacia and osteoporosis in adults
Vitamin D
Deficiency: Children = Ricket’s Disease
Adults = Osteomalacia
Calcium absorption; Blood Calcium
= bone deficiency

Toxicity: 10x RDA

Calcium absorption; Blood Calcium
= Calcium deposits on soft tissue
eg kidney stones

RDA: 5 μg/dl 5 μg/dl (19-30 yrs)

 Vitamin D deficiency
 Long-term deficiency of vitamin D affects the skeletal system.
In children, vitamin-D deficiency leads to rickets, a condition
in which bones weaken and bow under pressure.

 In adults, vitamin-D deficiency causes osteomalacia, or "soft

bones," increasing the risk for fractures in hip, spine, and other
bones.

 Vitamin-D deficiency also contributes to osteoporosis(‫هشاشة‬

C‫لعظام‬CC‫)ا‬. In elderly persons, vitamin-D supplementation reduces
the risk of osteoporotic fractures.

 Infants are born with stores of vitamin D that last about six
months. Breast milk contains very little vitamin D, however,
and infants beyond six months of age who are exclusively
breastfed must obtain vitamin D via exposure to sunlight or a
supplement given under the guidance of a physician.
 Vitamin D deficiency
 Older adults are especially at risk for vitamin-D deficiency for several
reasons. The skin, liver, and kidneys lose their capacity to synthesize and
activate vitamin D with advancing age, and older adults typically drink
little or no milk, a major dietary source of vitamin D.

 Older adults also rarely venture outdoors, and when they do, they apply
sunscreen to exposed areas of the body, further contributing to the decline
in vitamin-D synthesis in the skin.

 Sunscreens with a sun protection factor (SPF) of 8 and above prevent

vitamin-D synthesis. Sunscreen should be applied only after enough time
has gone to provide sufficient vitamin-D synthesis.

 Exposure to the sun does not cause vitamin-D toxicity, and for most
people, exposing the hands, face, and arms on a clear summer day for
fifteen minutes a few times a week should provide sufficient Vitamin D.

 Dark-skinned people require longer sunlight exposure because melanin, a

skin pigment, is a natural sunscreen.
 Vitamin D deficiency
 Dietary recommendations assume that no
vitamin D is available from exposure to
sunlight. Thus, people who do not venture
outdoors or who live in northern or
predominantly cloudy climates need to pay
attention to dietary sources.

 Plants are poor sources of vitamin D, so strict

vegetarians must meet their vitamin-D needs
through exposure to sunlight, fortification, or
supplementation.
 Vitamin D toxicity
 Vitamin D is most likely to have toxic effects when consumed in excessive
amounts through supplementation.
 vitamin D is the most potentially toxic vitamin in human nutrition, with an
upper limit (UL) of 50 micrograms per day. We can obtain the vitamin in
an inactive form from food and sunlight exposure

 Excess vitamin D raises blood calcium levels, resulting in calcium

precipitation in soft tissues and stone formation in the kidneys, where
calcium becomes concentrated in an effort to excrete it.
 The adult DRI for vitamin D is 5 micrograms per day of cholecalciferol or
200 international units (IU) of vitamin D (1 microgram of calciferol equals
40 IU of vitamin D).

 However, because of vitamin D's potential toxicity, caution must be taken

not to consume too much. Excess Vitamin D intake may lead to vomiting,
diarrhea , kidney damage, high blood calcium levels, increased frequency
in urination, nausea, loss of appetite and weight loss, muscle weakness,
dizziness, calcification of heart, blood vessels and lungs; and possibly
death.
 symptoms reverse after overdosing is discontinued.
 Vitamin E
 vitamin-E was firstly associated with reproductive failure in rats in
1922
 Vitamin E comprises a family of eight naturally occurring
compounds:
• tocopherols (alpha-, beta-, gamma-, and delta-)
• tocotrienols (alpha-, beta-, gamma-, and delta-).
 The chemical name of vitamin E, is derived from toco, meaning
"related to childbirth.“
 The tocopherols, are a closely related group of biologically active
compounds. The active tocopherols are named in order of their
potency. Thus, alpha-tocopherol is the most active.

 alpha- tocopherol is the only one to have vitamin-E activity in the

human body. It is also the most common form of vitamin E in food.
 Vitamin E is highly susceptible to destruction by oxygen, metals,
light, and deep-fat frying. As a result, prolonged food storage lowers
the vitamin-E content of food.
Chemical structure of Vitamin E
 Overview of Vitamin E
 Unlike vitamins A and D, Vitamin E, is not
stored primarily in liver but instead stored
primarily within body fat.
 Virtually every tissue has some vitamin E
within cell membrane
 Absorption is dependent on the absorption of
dietary fat
 Absorption is dependent on bile and pancreatic
enzyme for absorption
 Much excreted via bile and urine
 Overview of Vitamin E
 The vitamin E α-Tocopherol is necessary for normal growth.
 The main function of alpha-tocopherol in humans appears to be that of an
antioxidant(protects cells from toxic compounds, heavy metals, radiation, and free
radicals).
 free radicals are formed primarily in the body during normal metabolism and
also upon exposure to environmental factors, such as cigarette smoke or
pollutants.
 Fats, which are an integral part of all cell membranes, are vulnerable to
destruction through oxidation by free radicals. 

 The fat-soluble vitamin E, alpha-tocopherol, is distinctively suitable to catch free

radicals and thus prevent a chain reaction of lipid destruction of cell membranes
and other fats of the tissues.

 The vitamin E α-Tocopherol enhances retinal development; protects vitamin A in

eyes protecting vitamins C, red blood cells and essential fatty acids from
destruction.
 Taking antioxidant supplements, vitamin E in particular, might help prevent
heart disease and cancer.

 Everybody needs E. This hard-working vitamin maintains a lot of our body's

tissues, like the ones in our eyes, skin and liver. It protects our lungs from
becoming damaged by polluted air.
 Overview of Vitamin E
 absorption of vitamin E requires adequate absorption
of dietary fat.
 the percentage of absorption declines as the amount
consumed is increased.
 Vitamin E is stored mainly in adipose tissue, while
some is stored in the muscle. The remaining vitamin
E is found in cell membranes in tissue.
 Vitamin E interrupts free-radical chain reactions by
getting oxidized, thus protecting cell membranes
from free-radical attack.
 oxidative stress is highly involved in the development
of cancer, arthritis, cataracts, heart disease, and in the
process of aging itself.
 Overview of Vitamin E
 Many of the anti-oxidant properties of Vitamin E have been
hypothesized to protect from chronic diseases (i.e. heart, lung
cancer, parkinsons, alzheimer’s,etc).
 However, it is not yet documented whether supplementation
with large doses of vitamin E offers protection against heart
disease and cancer beyond that provided by positive dietary
and lifestyle changes.
 Several other functions of alpha-tocopherol have been
identified that are not likely related to its antioxidant capacity.
 alpha-tocopherol is known to inhibit the activity of protein
kinase C, an important cell-signaling molecule.
 Alpha-tocopherol appears to also affect the expression and
activities of molecules and enzymes in immune and
inflammatory cells.
 Additionally, alpha-tocopherol has been shown to inhibit
platelet aggregation and to enhance vasodilatation !!!!!!!
 Sources of Vitamin E
 About 20% of vit E in the diet comes from veg. oils
 Fruits and veggies
 Fortified cereals and grain products
 Wheat germ oil
 Corn and soybean oil
 Nuts
 Seeds
 animal fat NOT good source - almost none there
 Destroyed easily by heat.
Sources Vitamin E
 Vitamin E deficiency
 Vitamin E deficiency has been observed in individuals with:
• severe malnutrition
• genetic defects affecting the alpha-tocopherol transfer
protein
• fat malabsorption syndromes
• children with liver diseases who have an impaired capacity
to absorb dietary fat and therefore fat-soluble vitamins,
may develop symptomatic vitamin E deficiency.
 Severe vitamin E deficiency results mainly in neurological
symptoms, including impaired balance and coordination
(ataxia), injury to the sensory nerves (peripheral neuropathy),
muscle weakness (myopathy), and damage to the retina of the
eye (pigmented retinopathy). For this reason, people who
develop peripheral neuropathy, ataxia, or retinitis pigmentosa
should be screened for vitamin E deficiency
 Vitamin E deficiency
 children who have born with severe vitamin E
deficiency and are not treated with vitamin E
rapidly develop neurological symptoms.
 While, individuals who develop
malabsorption of vitamin E in adulthood may
not develop neurological symptoms for 10-20
years.
 Vitamin E and disease prevention
 Cardiovascular disease
• Increased vitamin E consumption has been found to be associated with
decreased risk of myocardial infarction (heart attack) or death from
heart disease
 Cataracts
• Cataracts which appear to be formed by protein oxidation in the lens of
the eye; such oxidation may be prevented by antioxidants like alpha-
tocopherol.  Direct association was reported between vitamin E
consumption and the incidence and severity of cataracts. increased
vitamin E intake protects against cataract development.
 Immune Function
• Alpha-tocopherol has been shown to enhance specific aspects of the
immune response that appear to decline as people age .
 Cancer
• Many types of cancer are thought to result from oxidative damage to
DNA caused by free radical formulation . The ability of alpha-
tocopherol to neutralize free radicals formulated the hypothesis that
Vit E could help in the cancer prevention, however results are not yet
confirmed
 Safety and toxicity aspects of vit E

 RDA: 15 mg/dl (19-30 yrs)

 Few side effects have been noted in adults taking supplements
of less than 2,000 mg of alpha-tocopherol daily.

 However, most studies of toxicity or side effects of alpha-

tocopherol supplementation have lasted only a few weeks to a
few months, and side effects occurring as a result of long-term
alpha-tocopherol supplementation have not been adequately
studied.
 The most worrisome possibility is that of impaired blood
clotting, which may increase the likelihood of hemorrage in
some individuals.
 Therfore it is recommended to discontinuing high-dose
vitamin E supplementation one month before elective surgery
or teeth extraction to decrease the risk of hemorrhage
 Drug Interactions
 Use of vitamin E supplements may increase the risk of bleeding in
individuals taking anticoagulant drugs, such as warfarin (Coumadin);
antiplatelet drugs; and non-steroidal anti-inflammatory drugs (NSAIDs),
including aspirin, ibuprofen, and others.
 Also, individuals on anticoagulant therapy (blood thinners) or individuals
who are vitamin K deficient should not take alpha-tocopherol supplements
without close medical supervision because of the increased risk of
hemorrhage.

 A number of medications may decrease the absorption of vitamin E,

including cholestyramine (chol-less), colestipol (colestid), isoniazid (anti
T.B), mineral oil, orlistat (xenical antiobesity), sucralfate (ulsanic gastric
ulcer), and the fat substitute, olestra. Anticonvulsant drugs, such as
phenobarbital, phenytoin, or carbamazepine, may decrease plasma levels
of vitamin E.
 Vitamin K
 Was first discovered in 1929, by the Danish researcher Henrik
Dam.
 He noted that vitamin K played a critical role in blood
clotting, and he named it vitamin "K" for "Koagulation."
 Vitamin K is the clotmaster!
 Used by the liver for the formation of prothrombin
 There are two naturally occurring forms of vitamin K.
 Vitamin K comprises a family of compounds known as
quinones.
 These include phylloquinone from plants sources
 menaquinones from animal sources.
 Phylloquinone is the most biologically active form.
Menaquinones are also synthesized by bacteria in the
intestine and absorbed, contributing about 10 percent of total
vitamin-K needs.
 Vitamin-K absorption depends on normal consumption and
digestion of dietary fat. It is primarily stored in the liver.
Chemical structure of Vitamin K
 Overview of Vitamin K
 Vitamin K is found in green leafy vegetables and also, in small
amounts, in cereals, fruits, and meats.
 Bacteria in the intestines also produce vitamin K, so the absolute
dietary requirement is not known.
 This vitamin is needed for the formation of prothrombin , which is
required for the formation of blood clots.
 It is possible for people who regularly take antibiotics that destroy
the bacteria in the intestines (normal flora) to be at increased risk for
Vitamin k.
 A deficiency would cause an increase in bleeding and hemorrhages.
 Vitamin K appears to be relatively nontoxic, but high intakes of
synthetic forms may cause jaundice.
 Supplemental doses also interfere with anticoagulant drugs.
 People taking warfarin (a blood thinner) must be aware that vitamin
K or foods containing vitamin K may reduce the effectiveness of
their medication.
 Overview of Vitamin K
 Vitamin K has also been linked to bone density.
 People with low levels of vitamin K have lower bone density, which can be
improved with vitamin K supplementation.
 women obtaining a minimum of 110 micrograms of vitamin K are at
significantly lower hip fracture risk than women who have a lower intake.
 Different Studies also found a relationship between higher vitamin K intake
and reduced hip fracture risk.
 Vitamin K is found in so many foods, and with bacterial production in the
small intestine, it would seem difficult to not get enough.

 particularly children and young adults, does not obtain sufficient vitamin K.
 Newborn babies lack the intestinal bacteria to produce vitamin K and need a
supplement for the first week.
 Also, people with chronic diarrhea may be unable to absorb enough vitamin
K through the intestine. These groups of people need to take additional
Vitamin K to ensure a proper level in the body.
 Although a tolerable upper intake level has not been established for vitamin
K, excessive amounts can cause the breakdown of red blood cells and liver
damage. Large doses are not advised.
 Sources of Vitamin K
 Naturally produced by the bacteria in
the intestines,
 Good food sources of vitamin K are:
 green vegetables such as turnip ‫فت‬Q
( ‫ف‬QQ‫)ل‬, spinach,
‫ت‬
cauliflower (‫رنبيط‬QQ‫)ق‬, cabbage and broccoli, and
certain vegetables oils including soybean oil,
cottonseed oil, canola oil and olive oil.
 Animal foods, in general, contain limited
amounts of vitamin K.
 Deficiency vitamin K
 A primary deficiency of vitamin K is rare, but a secondary
deficiency may result from fat malabsorption syndrome.
 vitamin K deficiency results in impaired blood clotting,
usually demonstrated by laboratory tests that measure clotting
time. Symptoms include easy bleeding that may be manifested
as nosebleeds, bleeding gums, blood in the urine, blood in the
stool, or extremely heavy menstrual bleeding.
 In infants, vitamin K deficiency may result in life-threatening
bleeding within the skull (intracranial hemorrhage
 Prolonged use of antibiotics can destroy the intestinal bacteria
that produce vitamin K, precipitating deficiency in individuals
at risk.
 Newborn infants are born with a sterile intestinal tract and
those who are breastfed, may run the risk of vitamin-K
deficiency, since breast-milk production takes a few days to
establish and breast milk is naturally low in this vitamin.
 To prevent hemorrhaging, infants should receive injections of
vitamin K within six hours of birth.
 Toxicity vitamin K
 High doses of vitamin K can reduce the effectiveness
of anticoagulant drugs (Vit K antagonists) such as
warfarin (Coumadin), which is used to prevent blood
clotting. People taking these drugs should maintain a
consistent daily intake of vitamin K.
 Megadose supplements of vitamin A and E can pose
a risk to vitamin-K status. Vitamin A interferes with
absorption of vitamin K, and large doses of vitamin E
decrease vitamin K–dependent clotting factors, thus
promoting bleeding.
 Toxicity from food is rare, because the body excretes
vitamin K much more rapidly than other fat-soluble
vitamins.
 Water soluble vitamins

 Vitamins are essential micronutrients.

 vitamin elimination from the diet must result
in a more-or-less clearly defined deficiency
disease, and restoration must cure or prevent
that deficiency disease
 Water vs. Fat

Water Soluble Fat Soluble

 Vitamin C  Vitamin A

 B Vitamins  Vitamin D

• Thiamin  Vitamin E
• Riboflavin
 Vitamin K
• Niacin
• Pantothenic Acid
• Biotin
• Vitamin B6
• Folic Acid
• Vitamin B12
 Water Soluble Vitamin Functions

Water Soluble Vitamins

 Vitamin C Skin, bones,
infections
 B Vitamins

• Thiamin (B1)
• Riboflavin (B2)
• Niacin Release energy from
• Vitamin B6 MACROnutrients:
• Folic Acid
• Vitamin B12
• Pantothenic Acid
• Biotin
 Vitamin C (ascorbic acid)
 Our bodies need vitamin C to keep it in good working condition.
 vitamin C helps hold body cells together, aids in wound healing, assists in bone and
tooth formation, and strengthens the blood vessel walls.
 Vitamin C is also crucial to the functioning of our immune system, and it helps
improve the absorption and utilization of iron. (Enhances absorption of iron
(protects it from oxidation) – tip: take vitamins with orange juice)
 Our bodies cannot make vitamin C and our capacity to store vitamin C is limited.
 We must, therefore, take in some daily.
 Some conditions have been shown to increase vitamin C requirements:
• environmental stress,
• use of certain drugs (such as oral contraceptives),
• tissue healing of wounds,
• growth (children and pregnant women),
• fever and infection, and
• smoking.
 Megadoses of vitamin C can be help prevent or possibly even cure a case of the
common cold. Vitamin C also serves as a powerful antioxidant. It works
synergistically with vitamin E as a free-radical scavenger.

 Studies suggest that vitamin C may reduce the risk of certain cancers, heart disease
and cataracts. Recent studies also suggest that the combination of vitamins C and E
in high doses can help reduce the risk of developing Alzheimer’s disease.
 Functions of Vitamin C
 Vitamin C is required for the synthesis of collagen, an
important structural component of blood vessels, tendons,
ligaments, and bone.
 Vitamin C also plays an important role in the synthesis of the
Neurotransmitter, norepinephrine.
 Neurotransmitters are critical to brain function and are known
to affect mood.
 In addition, vitamin C is required for the synthesis of carnitine
(a small molecule that is essential for the transport of fat to
mitochondria for conversion to energy.
  Vitamin C is also a highly effective antioxidant.
 Even in small amounts vitamin C can protect proteins, lipids
(fats), carbohydrates, and DNA & RNA from damage by free
radicals that can be generated during normal metabolism as
well as through exposure to toxins and pollutants (e.g.
smoking).
 Vitamin C may also be able to regenerate or potentiate other
antioxidants such as vitamin E
 Functions of Vitamin C
 The argument over megadoses of vitamin C to
prevent or cure the common cold and other
disorders has not been resolved.
 Vitamin supplements will not necessarily
provide extra energy, clear up skin problems,
or prevent and cure the common cold, heart
disease, and cancer. Unlike scurvy, these
problems are not the result of a vitamin C
deficiency. What is known is that the only
disease a vitamin will cure is the one caused
by a deficiency of that vitamin.
 Sources of Vitamin C
 Eating vitamin C-rich foods is the best method to ensure an
adequate intake of this vitamin.
 While many common foods contain vitamin C, the best
food sources are citrus fruits. One orange, a kiwi fruit, cup
of grapefruit juice each supply enough vitamin C for one
day.
 Vitamin C can be found in fresh fruits and vegetables:
strawberries, peppers, tomatoes, leafy green vegetables and
potatoes.
 It is not found in meat or animal products.
 Vitamin C is present in some processed foods, too.
 Since ascorbic acid is an antioxidant, it doesn’t last long in
the presence of oxygen. This means that once you cut or
peel fruits and vegetables and expose them to air, the
vitamin C content will diminish.
Sources of Vitamin C
Vitamin C intake
UL Men
3000

2000 UL Women

Limited absorption and little increase in

blood concentration
200
Rec for Men Smokers
125 Rec for Women Smokers
110 Saturates Tissues
100 RDA Men
90
RDA Women
75
Supports metabolism
30
Prevents Scurvy
10
0
Stability in Overconsumpt Deficiency Major Common food
foods ion symptoms symptoms functions sources

Most unstable Nontoxic under Bleeding gums; Formation of Citrus fruits,

under heat, normal wounds don't collagen (a broccoli,
drying, storage; conditions; heal; bruise component of strawberries,
very soluble in rebound scurvy easily; dry, tissues), helps melon, green
water, leaches when high rough skin; hold them pepper,
out of some doses scurvy; sore together; tomatoes,
vegetables discontinued; joints and wound healing; dark green
during cooking; diarrhea, bones; maintaining vegetables,
alkalinity bloating, increased blood vessels, potatoes.
(baking soda) cramps; infections. bones, teeth;
destroys increased absorption of
vitamin C. incidence of iron, calcium,;
kidney stones. production of
brain
hormones,
immune
factors;
antioxidant.
 Vitamin C Deficiency
 Severe vitamin C deficiency has been known for many
centuries as the potentially fatal disease, Scurvy (‫ر او‬Q‫لحف‬QQ‫داء ا‬
‫ربوط‬Q‫السق‬QQ‫)ا‬.
 By the late 1700's the British navy was aware that scurvy could
be cured by eating oranges or lemons, even though vitamin C
would not be isolated until the early 1930's.
 Symptoms of scurvy include bleeding easily, hair and tooth
loss, joint pain and swelling. Such symptoms appear to be
related to the weakening of blood vessels, connective tissue,
and bone, which contain collagen.
 Early symptoms of scurvy such as fatigue may result from
diminished levels of carnitine , needed to derive energy from
fat, or decreased synthesis of the norepinephrine.
 Scurvy is rare in developed countries because it can be
prevented by as little as 10 mg of vitamin C daily . However,
recent cases have occurred in children and the elderly on very
restricted diets
 Safety & Toxicity of Vitamin C
 A number of possible problems with very
large doses of vitamin C have been
suggested, mainly based on in vitro
experiments, including genetic mutations ,
birth defects, kidney stone , increased
oxidative stress , excess iron absorption,
vitamin B-12 deficiency, and erosion of
dental enamel.
 However, none of these adverse health
effects have been confirmed, and there is
no reliable scientific evidence that large
amounts of vitamin C (up to 10 grams/day
in adults) are toxic or detrimental to
health.
 B vitamins (B-complex)
These vitamins are widely distributed in foods. Their
influence is felt in many parts of the body.
They function as coenzymes that help the body obtain

energy from food.

They also are important for normal appetite, good

vision, healthy skin, healthy nervous system and red

blood cell formation.
Beriberi, pellagra and pernicious anemia are three

well-known B-vitamin deficiencies.

These diseases are not a problem in the United States,

but occasionally they occur when people omit certain

foods or overeat certain foods at the expense of others.
 B vitamins (B-complex)
 B vitamins are needed for conversion of food
to energy.
 They do not provide the energy, that comes
from the macronutrients, but the B vitamins
are essential helpers.
 When you are deficient in any of the B
vitamins you will feel fatigued and some B
vitamin deficiencies will lead to anemia.
 B complex vitamins also help you withstand
stress, keep your cardiovascular system
healthy and will boost your immune system.
 B Vitamins

1. Thiamin (B1)
2. Riboflavin (B2)
3. Niacin Coenzymes:
4. Vitamin B6 Catalysts in
5. Folic Acid Biochemical Pathways
6. Vitamin B12
7. Pantothenic Acid
8. Biotin
 Thiamin (Vitamin B1)
 Thiamin (Vitamin B1) functions as the coenzyme thiamin pyrophosphate (TPP)
in the metabolism of carbohydrate. Thiamin is also needed for healthy muscles
and normal nervous system function and conduction of nerve impulses.
 A deficiency of thiamine will cause fatigue and decreased mental alertness. A
severe deficiency will cause a nervous system disorder called beriberi . People
with beriberi may have nerve damage in their hands and feet or heart damage.

Thiamin deficiency causes beriberi, which is frequently seen in parts of the world
where polished (white) rice or unenriched white flour are predominantly eaten.
 There are three basic expressions of beriberi : childhood, wet, and dry.
• Childhood beriberi stunts or inhibits growth in infants and children.
• Wet beriberi is the classic form, with swelling due to fluid retention
(edema) in the lower limbs that spreads to the upper body, affecting
the heart and leading to heart failure.
• Dry beriberi affects peripheral nerves, initially causing tingling or
burning sensations in the lower limbs and progressing to nerve
degeneration, muscle wasting and weight loss.
 Thiamine-deficiency disease in North America commonly occurs in people
with heavy alcohol consumption.
 It is caused by poor food intake and by decreased absorption and increased
excretion caused by alcohol consumption.
 Thiamin (Vitamin B1)
 Wernicke-Korsakoff syndrome is another thiamine deficiency
disorder. In this case, the brain and nervous system are
affected so that a person has nerve damage and impaired
mental ability. This disease is most commonly found in people
who drink lots of alcohol on a regular basis. Replacing the
deficient thiamine improves the symptoms.

 Thiamine is found in whole grains, legumes, lean meat, fish

and fortified breads and cereals.
 Fruits and vegetables contain smaller amounts of thiamine.
Your daily requirement for thiamine may be increased if you
eat a lot of sugar or in a heavy alcohol drinker.
 Riboflavin (Vitamin B2)
 Riboflavin (vitamin B2) is a component of two coenzymes—flavin
mononucleotide (FMN) and flavin adenine dinucleotide (FAD)—that act as
hydrogen carriers when carbohydrates and fats are used to produce energy.
 Riboflavin (vitamin B2) is helpful in maintaining good vision and healthy
hair, skin and nails, and it is necessary for normal cell growth.
 Riboflavin (vitamin B2) is stable when heated in ordinary cooking, unless
the food is exposed to ultraviolet radiation (sunlight). To prevent riboflavin
breakdown, riboflavin-rich foods such as milk, milk products, and cereals are
packaged in opaque containers.

 Riboflavin deficiency causes a condition known as ariboflavinosis

(Riboflavin deficiency ), which is marked by cheilosis (‫رشفتهما‬Q‫لشفتينو ح‬QQ‫شققا‬QQQ‫)ت‬
(cracked lips at the corners of the mouth), oily scaling of the skin, and a red,
sore tongue, ulcers in the mouth, dry skin and a sore throat.
 In addition, cataracts may occur more frequently with riboflavin deficiency.
 A deficiency of Riboflavin (vitamin B2) is usually a part of multinutrient
deficiency and does not occur in isolation.
 In North America, it is mostly observed in alcoholics, elderly persons with
low income or depression, and people with poor eating habits, particularly
those who consume highly refined and fast foods and those who do not
consume milk and milk products
 Sources of Riboflavin B2
 Riboflavin is easily obtained from a healthy
diet and can be found in dairy products,
legumes, green leafy vegetables and nuts.
 Riboflavin can be destroyed fairly easily by
light. This is the reason milk is sold in cartons
or opaque bottles. Riboflavin is also reduced
by alkaline conditions, so soaking legumes in
baking soda and water before cooking them
destroys some riboflavin.
 Niacin (Vitamin B3)
 Niacin (Vitamin B3) exists in two forms: nicotinic acid and
nicotinamide.
 There are two coenzyme forms of Niacin (Vitamin B3) :
• nicotinamide adenine dinucleotide (NAD+)
• nicotinamide adenine dinucleotide phosphate (NADP+).
• They (NAD+ and NADP+) both help break down and utilize proteins,
fats, and carbohydrates for energy.
 Niacin (Vitamin B3) is essential for growth and is involved in
hormone synthesis.
 Both forms are readily absorbed from the stomach and small intestine.
 Good sources for Niacin (Vitamin B3) are Protein, milk, fish,
chicken; whole grains
 Niacin is stored in small amounts in the Liver and transported to
tissues, where it is converted to coenzyme forms. Any excess is
excreted in urine.
 Niacin is one of the most stable of the B vitamins. It is resistant to heat
and light, and to both acid and alkali environments.
 Niacin (Vitamin B3) deficiency
 The human body is capable of converting
the a.a tryptophan to niacin when needed.
However, when both tryptophan and niacin
are deficient, tryptophan is used only for
protein synthesis.

 Pellagra (‫لجلد‬QQ‫خشنا‬QQQ‫لحصافاو ت‬QQ‫يالجرا او ا‬QQQ‫)ب‬

Diarrhea, Dermatitis, Dementia (‫رفاو خبل‬Q‫) خ‬,
Death results from a combined deficiency
of niacin and tryptophan.
 Long-term deficiency leads to CNS
dysfunction manifested as confusion,
apathy (lack of concern), disorientation,
and eventually coma and death.
 Pantothenic Acid (B5)
 Pantothenic acid is released from coenzyme A in food
in the small intestine. After absorption, it is transported
to tissues, where coenzyme A is resynthesized.
 Coenzyme A is essential for the formation of energy as
adenosine triphosphate (ATP) from carbohydrate,
protein, alcohol, and fat.
 Coenzyme A is also important in the synthesis of fatty
acids, cholesterol, steroids, and the neurotransmitter
acetylcholine, which is essential for transmission of
nerve impulses to muscles
Sources of Pantothenic acid B5
 Sources include: Liver, kidney, meats, egg yolk,
whole grains, legumes; also made by intestinal
bacteria.
 Deficiency syndrome are Uncommon due to
availability in most foods.
 Dietary deficiency occurs in conjunction with other
B-vitamin deficiencies. In studies, experimentally
induced deficiency in humans has resulted in
headache, fatigue, impaired muscle coordination,
abdominal cramps, and vomiting.
 Pantothenic acid is stable in moist heat. It is
destroyed by vinegar (acid), baking soda (alkali), and
dry heat. Significant losses occur during the
processing and refining of foods.
 Vitamin B6 (pyridoxal, pyridoxine, and pyridoxamine)

 Vitamin B6 is present in three forms: pyridoxal, pyridoxine, and

pyridoxamine.
 All forms can be converted to the active vitamin-B6 coenzyme in
the body.
 Pyridoxal phosphate (PLP) is the predominant biologically active
form.
 Vitamin B6 is not stable in heat or in alkaline conditions, so cooking
and food processing reduce its content in food.
 Both coenzyme ( Pyridoxal phosphate (PLP) and free forms
(pyridoxal, pyridoxine, and pyridoxamine) are absorbed in the small
intestine and transported to the liver, where they are phosphorylated
and released into circulation, bound to albumin for transport to
tissues.
 Vitamin B6 is stored in the muscle and only excreted in urine when
intake is excessive.
 Functions of Vit B6
 Pyridoxal phosphate (PLP) participates in amino acid
synthesis and the interconversion of some amino
acids.
 Pyridoxal phosphate (PLP) catalyzes a step in the
synthesis of Hb
 Pyridoxal phosphate (PLP) helps maintain blood
glucose levels by facilitating the release of glucose
from liver and muscle glycogen.
 Pyridoxal phosphate (PLP) also plays a role in the
synthesis of many neurotransmitters important for
brain function. This has led some physicians to
prescribe megadoses of B6 to patients with
psychological problems such as depression
 Sources and deficiency

 Meats, fish, chick, spinach, potatoes, bananas,

avocados, sunflower seeds, whole grains and
cereals, legumes, green, leafy vegetables.
 Dermatitis, anemia, convulsion , depression,
confusion , decline in immune function
 Biotin (Vitamin B8)
 Biotin is the most stable of B vitamins.
 It is commonly found in two forms: the free vitamin
and the protein-bound coenzyme form called
biocytin.
 Biotin is absorbed in the small intestine, and it
requires digestion by enzyme biotinidase, which is
present in the small intestine.
 Biotin is synthesized by bacteria in the large intestine
, but its absorption is questionable.
 Biotin containing coenzymes participate in key
reactions that produce energy from carbohydrate and
synthesize fatty acids and protein.
 Sources and deficiency
 Sources include: Liver, kidney, egg yolk, milk, most fresh
vegetables, Whole grains, nuts and seeds also made by
intestinal bacteria.
 Avidin is a protein in raw egg white, which can bind to the
biotin (B8) in the stomach and decrease its absorption.
Therefore, consumption of raw whites is of concern due to the
risk of becoming biotin deficient. Cooking the egg white,
however, destroys avidin.
 Deficiency may develop in infants born with a genetic defect
that results in reduced levels of biotinidase. In the past, biotin
deficiency was observed in infants fed biotin-deficient
formula, so it is now added to infant formulas and other baby
foods.
 deficiency uncommon under normal circumstances; fatigue;
loss of appetite, nausea, vomiting; depression; muscle pains;
anemia.
 infants: Dermatitis, convulsions, hair loss (alopecia),
neurological disorders, impaired growth
 Folic Acid, Folate, Folacin (Vitamin B9)
 Folacin or folate, as it is usually called, is the form of vitamin
B9 naturally present in foods, whereas folic acid is the
synthetic form added to fortified foods and supplements.
 Both forms are absorbed in the small intestine and stored in
the liver.
 The folic acid form, however, is more efficiently absorbed and
available to the body. When consumed in excess of needs,
both forms are excreted in urine and easily destroyed by heat,
oxidation, and light.
 All forms of this vitamin are readily converted to the
coenzyme form called tetrahydrofolate (THFA).
 tetrahydrofolate (THFA) plays a key role in the synthesis of
DNA and RNA, and in interconversions of amino acids.
 Folate also plays an important role in the synthesis of
neurotransmitters. Meeting folate needs can improve mood
and mental functions.
 Sources and deficiency Folic Acid, (Vitamin B9)
 Liver, kidney, dark green leafy vegetables, meats,
fish, whole grains, fortified grains and cereals,
legumes, citrus fruits.
 folate deficiency is one of the most common vit
deficiencies.
 Early symptoms are nonspecific and include
tiredness, irritability, and loss of appetite.
 Severe folate deficiency leads to macrocytic anemia,
a condition in which cells in the bone marrow cannot
divide normally and red blood cells remain in a large
immature form called macrocytes. Large immature
cells also appear along the length of the
gastrointestinal tract, resulting in abdominal pain and
diarrhea. Megaoblastic (macrocytic) anemia,
abdominal pain, diarrhea, birth defects
 Sources and deficiency Folic Acid, (Vitamin B9)
 Pregnancy is a time of rapid cell multiplication and DNA
synthesis, which increases the need for folate. Folate
deficiency may lead to neural tube defects such as spina bifida
(failure of the spine to close properly during the first month of
pregnancy) and anencephaly (closure of the neural tube during
fetal development, resulting in part of the cranium not being
formed).
 Seventy percent of these defects could be avoided by adequate
folate status before conception, and it is recommended that all
women of childbearing age consume at least 400 micrograms
(μg) of folic acid each day from fortified foods and
supplements. Other groups at risk of deficiency include elderly
persons and persons suffering from alcohol abuse or taking
certain prescription drugs.
 Vitamin B12 (cyanocobalamin)
 Vitamin B12 is found in its free-vitamin form, called
cyanocobalamin, and in two active coenzyme forms.
 Absorption of Vitamin B12 requires the presence of intrinsic
factor, a protein synthesized by acid-producing cells of the
stomach.
 Vitamin B12 is absorbed in the terminal portion of the small
intestine (the ileum).
 Most of body's supply of Vitamin B12 is stored in the liver.
 Vitamin B12 is efficiently conserved in the body, since most
of it is secreted into bile and reabsorbed. This explains the
slow development (about two years) of deficiency in people
with reduced intake or absorption.
 Vitamin B12 stable when heated and slowly loses its activity
when exposed to light, oxygen, and acid or alkaline
environments.
 Function of Vitamin B12 (cyanocobalamin)
 Vitamin B12 coenzymes help recycle folate coenzymes
involved in the synthesis of DNA and RNA, and in the normal
formation of red blood cells.
 Vitamin B12 prevents degeneration of the myelin sheaths that
cover nerves and help maintain normal electrical conductivity
through the nerves.
 Sources and deficiency
 Sources include: Meat, fish, poultry, ready-to-eat fortified breakfast
cereals, eggs, fermented dairy products (cheese, yogurt, etc).
 Vitamin-B12 deficiency results in pernicious anemia (‫وبيل‬QQ‫ لا‬Q‫م‬QQ‫قر لدا‬
QQQ‫) ف‬,
which is caused by a genetic problem in the production of intrinsic factor.
When this occurs, folate function is impaired, leading to macrocytic
anemia due to interference in normal DNA synthesis.
 Unlike folate deficiency, the anemia caused by vitamin-B12 deficiency is
accompanied by symptoms of nerve degeneration, which if left untreated
can result in paralysis (‫شلل‬
‫لشلل‬QQ‫ )ا‬and death.
 Since vitamin B12 is well conserved in the body, it is difficult to become
deficient from dietary factors alone, unless a person is a strict vegan and
consumes a diet devoid of eggs and dairy for several years.
 Deficiency is usually observed when B12 absorption is hindered by disease
or surgery to the stomach or ileum, damage to gastric mucosa by
alcoholism, or prolonged use of anti-ulcer medications that affect secretion
of intrinsic factor.
 Age-related decrease in stomach-acid production also reduces absorption
of B12 in elderly persons. These groups are advised to consume fortified
foods or take a supplemental form of vitamin B12