VITAMIN

Micronutrient deficience
 Larut Air : Vitamin C, Thiamin (B1), Riboflavin (B2), Niacin (B3),
Panthotenic acid, Biotin, Folic acid, B12, B6
 Larut Lemak : Vitamin A, Vitamin D, Vitamin E, Vitamin K

Makromineral : Calcium, Phosphorous, Magnesium, Sodium, Potassium,

chloride
Mikromineral : Iron, Zinc, Copper,, Selenium, Chromium, Iodine, Manganese,
Fluoride.

Vitamin C
Also known as ascorbic acid or ascorbate
The best food sources of vitamin C include asparagus, papaya, oranges, orange
juice, cantaloupe, cauliflower, broccoli, Brussels sprouts, green peppers,
grapefruit, grapefruit juice, kale, lemons, and strawberries

Function : Collagen Synthesis, Carnitine Synthesis, Tyrosine Synthesis and

Catabolism, Neurotransmitter Synthesis, Microsomal Metabolism, Antioxidant
Activity, pro oxidant activity.

Vitamin C interacts mainly with two minerals :

 iron
 copper.

The interaction between iron and vitamin C is related not only to the vitamin’s
effect on intestinal absorption of non heme iron but also to the distribution of
iron in the blood

Individuals at risk deficiency :

 Elderly
 Alkohlism
 Smoking

 The RDA for adult men and women is 90 mg and 75 mg

 During pregnancy and lactation recommendations for vitamin C
increase to 100 mg and 120 mg
 Cigarette smokers for an increased vitamin C requirement based on
studies showing that smoking accelerates depletion of the body’s
ascorbate pool.
 Current recommendations for smokers suggest an added 35 mg

Deficient vitamin C
 Deficiency vitamin C intakes result in the deficiency condition known
as scurvy.
 Scurvy is typically manifested when the total body vitamin C pools fall
below about 300 mg and plasma vitamin C concentrations drop to <0.2
mg/dL
 Scurvy may be characterized by a multitude of signs and symptoms,
many of which are thought to result from impaired hydroxyproline and
hydroxylysine synthesis needed for collagen formation.

Signs and symptoms :

 bleeding gums,
  Petechiae,
 ublingual hemorrhages,
 easy bruising (ecchymoses and purpurae),
 impaired wound and fracture healing,
 joint pain (arthralgia),
 loose and decaying teeth,
 hyperkeratosis of hair follicles, especially on the arms, legs, and
buttocks
Scurvy is fatal if untreated.

The four Hs :
 hemorrhagic signs,
 hyperkeratosis of hair follicles,
 hypochondriasis (psychological manifestation),
 hematologic abnormalities (associated with impaired iron
 absorption)—

Plasma concentrations of vitamin C below 0.2 mg/dL is deficient

Treatment should be initiated with vitamin C 100 mg threetimes daily.

 An initial intravenous dose of 60 to 100 mg of vitamin C may be given.

 Children may be given 100 to 200 mg/ day either orally or parenterally

Konsumsi per Hari

 Daily intakes of up to 2 g vitamin C are routinely consumed without
adverse effects
 The most common side effect with ingestion of large amounts (2 g) of
the vitaminC is gastrointestinal problems characterized by abdominal
pain and osmotic diarrhea.
 The unabsorbed vitamin C in the intestinal tract that is metabolized by
bacteria within the colon is what promotes the osmotic diarrhea
 These side effects include increased risk of kidney stones and iron
toxicity for those with renal disease
 Because vitamin C is metabolized in the body to oxalate and because
calcium oxalate is a common constituent of kidney stones etiologic
factor in nephrolithiasis.
Thiamin
Individual at risk :
 Elderly
 Alkoholism
 Malabsorption (some gastrointestinal tract cancers, biliary disease,
inflammatory bowel diseases )
 Congestive heart failure (low intakes and increased urinary thiamin
losses secondary to diuretic use )

Wernicke’s encephalopathy or Wernicke-Korsakoff syndrome, a

neuropsychological complication
Wernicke’s encephalopathy is characterized by ophthalmoplegia (paralysis of the
ocular muscles), nystagmus (constant, involuntary eyeball movement), ataxia
(impaired muscle coordination), loss of recent memory, and confusion
 Thiamin deficiency, or beriberi (beri means “weakness”).

 One of the first symptoms of thiamin deficiency is a loss

of appetite (anorexia) and thus weight loss.

 As the deficiency worsens, cardiovascular system involvement (such as

hypertrophy and altered heart rate) and neurological symptoms (such as apathy,
confusion, decreased short-term memory, and irritability) appear
 Dry beriberi, found predominantly in older adults, is thought to result from a
chronic low thiamin intake
 Dry beriberi is characterized by muscle weakness and wasting, especially in
the lower extremities, and peripheral neuropathy.
 Neuropathy consists of symmetrical sensory and motor nerve conduction
problems mostly affecting the distal parts of the limbs (i.e., the ankles, feet, wrists,
and hands).
 Wet beriberi results in more extensive cardiovascular system involvement
than dry beriberi
 Cardiomegaly (enlarged heart), rapid heart beat (tachycardia), rightside heart
failure with secondary respiratory involvement, and peripheral edema are common
symptoms along with peripheral neuropathy.
 Acute beriberi is associated with anorexia, vomiting, lactic acidosis (the lack
of thiamin, which is needed to convert pyruvate to acetyl CoA, causes pyruvate to be
converted to lactic acid; the lactic acid then accumulates, causing acidosis), altered
heart rate, and cardiomegaly.
 Urinary thiamin excretion decreases with decreased
thiamin status; excretion also is correlated with intake
 Urinary thiamin excretion <40 μg or <27 μg/g suggests thiamin deficiency.
Management of deficiency :
 Parenteral Thiamin Doses in the 50- to 100-mg range are initially administered
intravenously or intramuscularly to replenish cellular thiamin stores (particularly
liver

Excessive thiamin (100 times recommendations) administered intravenously or

intramuscularly, however, has been associated with headache, convulsions, cardiac
arrhythmia, and anaphylactic shock, among other signs
 Riboflavin (B2)

 Riboflavin consists of flavin (isoalloxazine ring), to which is attached a

ribitol
(sugar alcohol) side chain.
Individual at risk :
 Alkholism
 Heart failure
 Hypermetabolic condition
 Sources

 Riboflavin is found in a wide variety of foods, but

especially those of animal origin.
 Milk and milk products such as cheeses are thought to
contribute most dietary riboflavin.
 Eggs, meat, and legumes also provide riboflavin in
significant quantities
 Green vegetables like spinach provide fairly good
riboflavin content.
 Fruits and cereal grains are minor contributors of dietary
riboflavin.
Function

 electron transport chain

 oxidative decarboxylation of pyruvate and α-ketoglutarate
 Succinate dehydrogenase
 In fatty acid oxidation, fatty acyl CoA dehydrogenase requires FAD
 As a coenzyme for an oxidase such as xanthine oxidase,
 Sphinganine oxidase
 vitamin B6 metabolism (pyridoxine phosphate oxidase)
 Synthesis of an active form of folate,
 Synthesis of niacin from tryptophan
 choline catabolism,
 neurotransmitters (such as dopamine)
 Riboflavin

 The current RDAs for riboflavin for adult men and women
are 1.3 mg/day and 1.1 mg/day, respectively;
 With pregnancy and lactation, recommendations for daily riboflavin intake
increase to 1.4 mg and 1.6 mg

Management of deficiency:
 supplementation or therapy with riboflavin is warranted, oral administration
of 5 to 10 times the RDA usually is satisfactory
 Niacin (B3)

 The term niacin (vitamin B3) is considered a generic term for nicotinic acid
and nicotinamide (also called niacinamide).

 The best sources of niacin include fish such as tuna and halibut, and meats
such as beef, chicken, turkey, and pork,among others.
 Enriched cereals and bread products, whole grains, fortified cereals, seeds,
and legumes also contain appreciable amounts of niacin
Function

 NAD and NADP coenzymes, NADPH is generated from NADP by reduction

glycolysis oxidative decarboxylation of pyruvate
 oxidation of acetyl CoA in the TCA cycle
 β-oxidation of fatty acids
 oxidation of ethanol
 fatty acid synthesis
 cholesterol and steroid hormone synthesis
 oxidation of glutamate
 synthesis of deoxyribonucleotides (precursors of DNA)
 regeneration of glutathione, vitamin C, and thioredoxin
 Folate metabolism
 Niacin

 The RDAs for niacin (as niacin equivalents) for adult men
and women are 16 mg/day and 14 mg/day, respectively.
 With pregnancy and lactation, the RDA for niacin increases to 18 mg and 17
mg niacin equivalents, respectively
 Deficiency
 Classical deficiency of niacin results in a condition known as pellagra.
 The four Ds—dermatitis, dementia, diarrhea, and death—are often
used as a mnemonic device for remembering signs of pellagra.
 The dermatitis is similar to sunburn at first and appears on areas exposed to
sun, such as the face and neck, and on extremities such as the back of the hands,
wrists, elbows, knees, and feet.
 Neurological manifestations include headache, apathy, loss of memory,
peripheral neuritis, paralysis of extremities, and dementia or delirium
 Gastrointestinal manifestations include glossitis, cheilosis, stomatitis, nausea,
vomiting, and diarrhea or constipation.
 If untreated, death occurs.
 Risk of deficieny

 Alkoholism
 Malabsorptive conditions (chronic diarrhea, inflammatory bowel
diseases, some cancers)
 Tuberculosis patients
The antituberculosis drug isoniazid, for example, binds with vitamin B6 as PLP and
thereby reduces PLP-dependent kynureninase activity required for niacin synthesis.
 Niacin

 Urinary excretion of <0.8 mg/day of N' methyl

nicotinamide is considered suggestive of niacin deficiency.
 Urinary excretion of <0.5mmg N' methyl nicotinamide/1 g creatinine also
has been suggested as indicative of poor (deficient) niacin status
 Folate

 Folate refers to the reduced form of the vitamin found

naturally in foods and in biological tissues.
 The Latin word folium means “leaf,”
 Good food sources of folate include mushrooms and green vegetables such
as spinach, brussels sprouts, broccoli, asparagus, and turnip greens, okra, among
others, as well as peanuts, legumes (especially lima, pinto, and kidney beans),
lentils, fruits (especially strawberries and oranges) and their juices, and liver.
 Sources

 Raw foods typically are higher in folate than cooked foods

because of folate losses incurred with cooking.
 Fortification of flours, grains, and cereals with folic acid (140 μg folic acid
per 100 g of product)
 Function

 THF functions in the body as a coenzyme in both the mitochondria and

cytoplasm
 Folate is involved in the metabolism of several amino acids, including
histidine, serine, glycine, and methionine.
 Purine and Pyrimidine Synthesis/Nucleotide Metabolism
 DNA synthesis
DEFICIENCY: MEGALOBLASTIC MACROCYTIC ANEMIA
 Marginal folate deficiency results in megaloblastic macrocytic anemia.
 The deficiency is characterized initially (within a month if the diet is devoid
of folate) by low plasma folate.
 Red blood cell folate concentrations diminish after about 3 to 4 months of
low
folate intake.
 After approximately 4 to 5 months, bone marrow cells and other rapidly
dividing cells become megaloblastic
 Mean cell volume (MCV) increases, and hypersegmentation (increased
lobes) of white blood cells (neutrophils) occurs, along with decreased blood cell
counts
 People with folate deficiency may exhibit fatigue, weakness, headaches,
irritability, difficulty concentrating, shortness of breath, and palpitations
 Folate
 The RDA for adults for folate is 400 μg dietary folate
equivalents (DFE) per day
 Folate requirements are estimated at 320 μg per day
 Folate status is most often assessed by measuring folate concentrations in the
plasma, serum, or red blood cells.
 Serum or plasma folate levels reflect recent dietary intake; thus, true
deficiency must be interpreted through repeated measures of serum or plasma folate.
 Serum folate concentrations <6.8 ng/mL typically suggest
deficiency
 Cobalamin (B12)

 The best sources of the cobalamins are meat and meat products, poultry, fish,
shellfish (especially clams and oysters) and eggs (especially the yolk)
 The cobalamins in these products are predominantly adenosyl- and
hydroxocobalamin.

 Risk of deficiency : elderly, strict vegetarian, disorder

affecting stomach and ileum
 Cobalamin

 Diminished hydrochloric acid release (achlorhydria) also decreases release of the

vitamin bound to food, causing malabsorption of the vitamin.
 People with a decreased absorptive surface in the ileum, such as occurs with
ileal resection, celiac and tropical sprue, ileitis (inflammation of the ileum) also
malabsorb the vitamin and are at risk for deficiency.
 People with Zollinger-Ellison syndrome produce excessive quantities of gastric
acid, which results in increased acid release both into the stomach and passed into
the small intestine with the chyme.
 The increased acid in the small intestine lowers the intestinal pH and is
thought to impair the release of the B12 from the R-protein and the binding of the
vitamin to IF
 In addition, people with parasitic infections such as tapeworms may develop
a vitamin B12 deficiency because the parasite uses the vitamin, and consequently its
availability to the infected person is limited.

 Prolonged use of some medications, such as H2 blockers and proton pump

inhibitors used to treat people with ulcers or gastroesophageal reflux disease
(GERD), also is associated with diminished absorption of vitamin B12
 Deficiency of vitamin B12, like that of folate, results in megaloblastic macrocytic
anemia.
 Manifestations of vitamin B12 deficiency occur in stages.
 Initially, serum vitamin B12 concentrations diminish; serum B12 concentrations,
however, may remain normal until stores of the vitamin become depleted.
 Second, cell concentrations of the vitamin diminish.
 Third, DNA synthesis decreases and serum homocysteine and
methylmalonic acid concentrations increase.
 Finally, morphological and functional changes occur in blood cells and in
precursor blood cells in bone marrow resulting in a macrocytic megaloblastic (large
immature cell) anemia.
 Most deficiency signs and symptoms are of neurologic and
hematologic origin;
 some signs and symptoms include skin pallor, fatigue, shortness of
breath, palpitations, insomnia, tingling and numbness (paresthesia) in extremities,
abnormal gait, loss of concentration, memory loss, disorientation, swelling of
myelinated fibers, and possibly dementia.
 Neurological problems occur in about 75% to 90% of
deficient people
 Oral vitamin B12 in amounts of at least 6 to 9 μg and possibly up to
300 μg appears to be necessary to correct deficiency in the elderly

 Treating pernicious anemia or deficiency secondary to malabsorption often

requires monthly intramuscular injection of the vitamin in amounts of 500 to 1,000
μg [6] or oral ingestion of pharmacologic amounts (2 mg) of the vitamin [31].
 Vitamin B12 nasal sprays also are available.
 Nascobal ®, for example, provides the vitamin as cyanocobalamin (500
μg/spray) in a nasal spray that is beneficial to people with malabsorptive disorders
such as inflammatory bowel disease or those with pernicious anemia.
 Fat Soluble Vitamin
Vitamin A
 vitamin A is generally used to refer to a group of compounds that
possess the biological activity of all-trans retinol.

 The retinoids are structurally similar and include retinol, retinal,

retinoic acid, and retinyl ester

 Elected signs and symptoms of deficiency include xerophthalmia, anorexia,

retarded growth, increased susceptibility to infections, obstruction and enlargement
of hair follicles, and keratinization of epithelial (mucous) cells of the skin with
accompanying failure of normal differentiation.
 Vitamin
A
 Vitamin A is recognized as being essential for vision as well as for cellular
differentiation, growth, reproduction, bone development, and immune system
actions.
 The RDAs for vitamin A for adult men and women are 900 and 700 μg RAE,
respectively
 During pregnancy and lactation, the RDAs for vitamin A for adult women
are higher at 770 and 1,300 μg, respectively.
 A daily tolerable upper intake level (UL) for adults of 3,000 μg has
been established for preformed vitamin A
 Conditions and populations associated with increased need for vitamin A
include people with malabsorptive disorders such as steatorrhea (excessive fat in the
feces) or pancreatic, liver, or gallbladder diseases.
 People with chronic nephritis, acute protein deficiency, intestinal parasites,
or acute infections may also become vitamin A–deficiency
 Both retinoids (often called preformed vitamin A or simply vitamin A)
and carotenoids are found naturally in foods.
 Vitamin A is found primarily in selected foods of animal origin, especially
liver and dairy products (including whole milk, cheese, and butter) as well as fish
such as tuna, sardines, and herring.
 Some products, such as margarine, also may be fortified with vitamin
A.
 The highest concentrations of preformed vitamin A are found in liver
and fish liver oils, lower levels are present in milk and eggs
 Carotenoids are synthesized by a wide variety of plants and thus are found
naturally in many fruits and vegetables  yellow, orange, and red (brightly colored)
fruits and vegetables such as carrots, watermelon, papayas, tomatoes
 Vitamin D

 Dietary vitamin D is provided primarily by foods of animal origin, especially

liver, beef, and eggs (mainly the yolk); dairy products such as milk, cheese, and
butter; and some saltwater fish, including herring, salmon, tuna, and sardines.
 In the United States, selected foods, such as milk, yogurt, cheese, and
margarine as well as some orange juice, breads, and cereals, are fortified with
vitamin D.
Metabolism of vitamin D
 Function

 Calcium homeostasis
 The local presence of the calcitriol (1,25-[OH]2 D3) within the tissues
appears to regulate cell growth, differentiation, and proliferative activity in a variety
of different tissues.
 Vitamin D is also purported to have a role in regulating blood pressure and
preventing autoimmune disorders.
 Vitamin D

 In infants and children, vitamin D deficiency results in rickets, which is

characterized by seizures as well as growth retardation and failure of bone to
mineralize.
 In vitamin D–deficient infants, epiphyseal cartilage continues to grow and
enlarge without replacement by bone matrix and minerals.
 These effects are especially visible at the wrists, ankles, and knees, all of
which enlarge.
 In addition, long bones of the legs bow and knees knock as weight-bearing
activity such as walking begins.
 The spine becomes curvedpelvic and thoracic deform
 In adults, deprivation of vitamin D leads to mineralization
defects called osteomalacia.
 The defect results from changes in calcium and phosphorus absorption and
excretion.
 For example, with vitamin D deficiency, less calcium is absorbed
 Adequate Intake (AI) for vitamin D of 5 μg or 200 IU daily for infants over 6
months, children, adolescents and for adults age 19 to 50 years, including women
who are pregnant or lactating
 Newer studies suggest the requirement may be at least 500 IU (12.5 μg) and
that an intake >1,000 IU (25 μg) vitamin D may be needed by some (especially those
without sun exposure)
 This amount (1,000 IU) of the vitamin is thought to be obtainable by
exposure to sunlight for about 5 to 15 minutes between about 10 a.m. and 3 p.m.
during spring, summer, and fall
Vit E
 Vitamin E

 The RDA for vitamin E for adult men and women (including during
pregnancy for women) is 15 mg α-tocopherol
 During lactation, women require slightly higher vitamin E intake, with an
RDA of 19 mg
Some symptoms of vitamin E deficiency :
 skeletal muscle pain (myopathy) and weakness,
 hemolytic anemia,
 degenerative neurological problems, including peripheral neuropathy cerebellar
ataxia, loss of vibratory sense, and loss of coordination of limbs
 Vit K

 The naturally occurring forms of vitamin K are phylloquinone (2- methyl 3-

phytyl 1,4- naphthoquinone), isolated from green plants, and menaquinones, which
generally are synthesized by bacteria.
 RDA men 120 μg , Women  90 μg

The population groups that appear to be most at risk for a vitamin K

deficiency are :
 newborn infants
 people with severe gastrointestinal malabsorptive disorders
 people being treated chronically with antibiotics
 Vitamin K

Newborns are particularly at risk because :

 their food is limited to milk, which is low in vitamin K; their stores of the vitamin
are low because inadequate amounts cross the placenta; and
 their intestinal tract is not yet populated by vitamin K–synthesizing
bacteria.

Supplementation with vitamin K is considered advisable for all newborns; currently,

intramuscular injection of 0.5 to 1 mg phylloquinone shortly after birth is
recommended for all infants
 People consuming vitamin K–poor diets and on prolonged sulfa and
antibiotic drug therapy are at risk for vitamin K deficiency owing to the coupled
effects of low dietary intake and antibiotic-induced destruction of gastrointestinal
bacteria that manufacture the vitamin and contribute a source of vitamin K

 Function : activates blood clotting factors ( II,VII.IX, X)

 Severe vitamin K deficiency is associated with bleeding episodes

(hemorrhage) caused by prolonged prothrombin time.