Vitamins /orthodontic courses by Indian dental academy

VITAMINS
INDIAN DENTAL ACADEMY
LEADER IN CONTINUING Education
www.indiandentalacademy.com

Contents
Definition
History
Introduction
Vitamins
 Classification
 Types, functions, deficiency disorders
 Hypervitaminosis
 Nutrient interactions
 Dietary sources
 RDA

 Clinical considerations
 Commercially available
supplements
 Conclusion

Definition:
“Vitamins may be regarded as organic compounds
required in the diet in small amounts to perform specific
biological functions for normal maintenance of optimum
growth and health of the organism.”

History:
Hopkins coined the term ‘accessory factors’ to the
unknown and essential nutrients present in natural
foods.
Funk (1913) : coined the term Vitamin ( Greek: vita:
life)
The usage of A, B, C to the vitamins was introduced
in 1915 by McCollum and Davis

Introduction:
• Vitamins when are not synthesized in adequate amounts by
the body or has to obtained by diet or from a Provitamin.
• They are needed in Milligram to Microgram quantities
• These are required to maintain appropriate metabolic
reactions

Classification:
There are about 15 vitamins, essential for humans.
Fat soluble/ Lipid soluble:
Vitamin A, Vitamin D, Vitamin E, Vitamin K
Water soluble:
Vitamin B ( B1, B2, Niacin, B6, B12, Biotin, Panthothenic acid)
Vitamin C

VITAMIN A

Forms of Vitamin A:
• Retinol
• Retinal
• Retinoic acid
• Beta carotene ( Provitamin A)

Functions of Vitamin A:
• Vision
(color sensitive: porphyropsin - red
idopsin – green
cyanopsin - blue)
Retinol , retinoic acid Regulate protein synthesis
synthesis of transferrin
Essential for maintaining healthy epithelial tissue
Maintenance of immune function
Carotenoids function as antioxidants

Visual Cycle/Wald’s visual cycle:

Dietary source:
Liver, kidney, egg yolk, milk, fish liver oils
carrots, spinach, pumpkin, mango, papaya
RDA :
Men –900 mcg/day
Women-700 mcg/day
Children- 770 mcg/day
Pregnancy:770mcg/day

Nutrient Interactions:
Zinc:
1) Zinc deficiency results in decreased synthesis of retinol binding
protein (RBP), which transports retinol through the circulation
to tissues .
2) Zinc deficiency results in decreased activity of the enzyme that
releases retinol from its storage form, retinyl palmitate, in the
liver.
3) Zinc is required for the enzyme that converts retinol into retinal

Iron
Vitamin A deficiency may exacerbate iron deficiency anemia.
 Vitamin A supplementation has been shown to have beneficial
effects on iron deficiency anemia and improve iron nutritional
status.
 The combination of vitamin A and iron seems to reduce anemia
more effectively than either iron or vitamin A alone

Vit A deficiency:
Night blindness(nyctalopia)
Xerophthalmia
keratomalacia/Bitots spots
on growth, reproduction, skin and epithelial cells

Hypervitaminosis A
It is caused by overconsumption of preformed vitamin A,
not carotenoids. Preformed vitamin A is rapidly absorbed
and slowly cleared from the body, so toxicity may result
acutely from high-dose exposure over a short period of
time. Vitamin A toxicity is relatively rare.
Dermatitis, enlargement of liver,
skeletal decalcification,
joint pains
constant headache

Diagnostic Tests:
 Relative dose measurement( RDR)
( measure the increase in plasma retinol after administration of
retinyl palmitate / dehydroretinol)
 Conjuctival impression cytology- (CIC) Evaluation of the
morphology of corneal cells

Vitamin D
Vitamin D is a fat-soluble vitamin that is essential for
maintaining normal calcium metabolism , resembles
sterols in structure and functions as hormone
Types:
Vitamin D3 (cholecalciferol)
Vitamin D2 (ergocalciferol), which also has vitamin D
activity in humans.

History:
Augus (1931) isolated Vit D and named it as Calciferol

Formation

Absorption, transport and storage
in small intestine lymph enters the circulation bound to
plasma alpha 2 globulin and distributed throughout the body
Stored in liver and other tissues

•Functions of Vit D
Calcitriol (1,25 DHCC) is biologically active form of
Vit D
regulates plasma levels of calcium and phosphate
Blood Pressure Regulation
1,25(OH)2D decreases the expression of the gene encoding
renin through its interaction with the VDR .

• Insulin Secretion
Animal studies have shown that 1,25(OH)2D plays a role
insulin secretion under conditions of increased insulin
demand
• Immunity
Cell Differentiation

Vit D as a hormone :
Vit D3 (cholecalciferol) is synthesized in skin by UV rays of
sunlight
Biologically active form of Vit D, calcitriol is produced in
kidney
Synthesis of RNA
Calcitriol synthesis is self regulated by feed back mechanism
Along with parathyroid hormone and calcitonin to regulate ca
and phosphate level

Calcitriol has action on target organs.
Action is similar to steroid hormones binds to receptor on
the cytosol and acts on DNA to stimulate synthesis of
calcium binding protein.

Dietary source :
Fish, fish liver oil, egg yolk
exposure of skin to sunlight
RDA:
Men – 400 IU/ day
Women- 200 IU/day
Children-200 IU/day
Pregnancy: 200 IU/day

Deficiency of Vit D:
in strict vegetarians, chronic alcoholics, liver/kidney
diseases, insufficient exposure to sunlight
Osteomalacia ( osteon- bone, malakia- softness)
- diffuse bone pain, muscle weakness, numbness of
extremities, spasms of hand and feet
Treatment:
oral supplements of Vit D, Ca, Phosphorus.

Rickets: (wrickken- twist)
bone pain or tenderness
skeletal deformities bowlegs,
pigeon chest ,bumps" in the rib
cage ("rachitic rosary”)
dental deformities
delayed formation of teeth
defects in the structure of teeth
painful teeth, aggravated by sweets,
or by cold/hot food or drinks
increased incidence dental caries

Hypervitaminosis of Vit D
Hypercalcemia
Hyperphosphatemia, anorexia, nausea, vomiting, diarrhoea
Metastatic calcifications in kidneys, arteries, bronchi

Diagnostic Tests
Estimation of the levels of 1, 25 dihydroxycholecalciferol in
serum (less than 20-25 nmol/L)

Vitamin E / Tocopheral
describes a family of eight antioxidants, four tocopherols, alpha-,
beta-, gamma- and delta-, and four tocotrienols (also alpha-, beta-,
gamma- and delta-).
Alpha-tocopherol is the only form of vitamin E that is actively
maintained in the human body and is therefore, the form of vitamin
E found in the largest quantities in the blood and tissue

Sources: vegetable oils , almonds, sweet potato
Daily requirement:
Man: 10mg
Woman: 8mg
Infants and children: 3-7 mg
Pregnancy: 15 mg/day

Absorption:
is released from food fats and absorbed from small intestine
These are carried in chylomicrons to the liver , incoporated into
VLDL, LDL and stored in muscles and adipose tissue

Functions:
As an Antioxidant.
 maintaining the integrity of cell membranes throughout the
body, alpha-tocopherol also protects the fats in low density
lipoproteins (LDLs) from oxidation.
 Alpha-tocopherol is known to inhibit the activity of protein kinase C,
an important cell signaling molecule, as well as to affect the
expression and activity of immune and inflammatory cells.
 inhibit platelet aggregation and to enhance vasodilation .

Drug interactions of Vit E
Individuals on anticoagulant therapy (blood thinners) or
individuals who are vitamin K deficient should not take
alpha-tocopherol supplements, of the increased risk of
hemorrhage .
A number of medications may decrease the absorption of
vitamin E, including cholestyramine, , isoniazid, mineral oil,
orlistat, sucralfate.
Anticonvulsant drugs such as phenobarbitol, phenytoin, or
carbamazepine may decrease plasma levels of vitamin E.

Deficiency of Vit E:
In newborn infants :
Erythrocyte fragility
Haemolytic anemia
Edema
Thrombocytosis
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)

Detection of deficiency:
Erythrocytes hemolysis test
Hypervitaminosis E
Headache, dizziness, fatigue, blurring of vision, dermatitis,
acne, prolonged clotting time and rise in serum cholesterol ,
lipids

Vit K: ( German- Koagulation)
it is the only fat soluble vitamin, essential for production of
blood clotting factors.
Dam (1939) isolated Vit K1
Doisy isolated Vit K2

Types:
Naphthoquinone derivatives .
Vit k1 (phylloquinone) present in plants
Vit K2 (menaquinone) produced by intestinal bacteria
Vit K3 (menadione) is a synthetic form

Absorption, transport and storage:
absorption takes place along with fat and is dependent on
bile salts.
Stored in liver

Functions:
Clotting: binding to ca ions requires activation of 7 vitk
dependent clotting factors- factor prothrombin, 8, 9,
10 , protein C, protein S
Bone mineralization
Cell growth: Gas6 is a vitamin K-dependent protein . It
has been found throughout the nervous system, as
well in the heart, lungs, stomach, kidneys, and
cartilage. It may also play important roles in the
developing and aging nervous system.

Dietary source:
Cabbage, cauliflower, tomatoes
egg yolk, meat liver, diary products
RDA
Men -120mcg/day
Women-90 mcg/day
Children – 60 mcg/day
Pregnancy: 75 mcg/day

Deficiency symptoms:
The blood clotting time is increased easy bruising and bleeding
that may be manifested as nosebleeds, bleeding gums, blood in
the urine, blood in the stool, tarry black stools, or extremely
heavy menstrual bleeding. In infants, vitamin K deficiency may
result in life-threatening bleeding within the skull (intracranial
hemorrhage)
Hypervitaminosis K
produces hemolytic anemia and jaundice in infants

Antagonists to Vitamin K:
Certain oral anticoagulants, like warfarin, are known to be
antagonists of vitamin K.
The anticoagulant effect of vitamin K antagonists (e.g.,
warfarin) may be inhibited by very high dietary or
supplemental vitamin K intake. It is generally recommended
that individuals using warfarin try to consume the AI for
vitamin K (90-120 mcg) .

Diagnostic test
Direct measurement of Vit K in blood
Prothrombin time

Nutrient Interactions:
Large doses of vitamin A and vitamin E have been found to
antagonize vitamin K. Excess vitamin A appears to interfere
with vitamin K absorption,
Anticonvulsants, rifampin, and isoniazid can interfere with
fetal vitamin K synthesis and place the newborn at increased
risk of vitamin K deficiency .
Prolonged use of broad spectrum antibiotics may decrease
vitamin K synthesis by intestinal bacteria.
Cholestyramine, mineral oil, and the fat substitute olestra
may decrease vitamin K absorption

Water soluble Vitamins

Vit C ( Ascorbic acid)
Zilva (1917- 27) first showed that the antiscorbutic factor
possess reducing property and present in lemon juice
Ascorbic acid is synthesized from glucose via uronic acid
pathway
In humans due to deficiency of L-gulonolactone oxidase

•Functions of Vit C:
Collagen formation
acts as a coenzyme in hydroxylation of proline and
lysine while protocollagen is collagen
Hydroxylysine and Hydroxyproline are essential for the
collagen cross linking and the strength of the fiber.
Hence necessary for maintenance of normal
connective tissue and wound healing process.
Bone formation
Iron and Hemoglobulin metabolism

Tryptophan, tryosine, cholesterol, folic acid
metabolism
synthesis of corticosteroid hormone
sparing action of other vitamins
cellular respiration
immunologic function
preventive action on cataract

Dietary source:
citrus fruits, goosebery, tomatoes, potatoes
high content of vit C is found in adrenal gland, gonads
RDA:
Men-90mg/day
Women-75 mg/day
Children-45mg/day
Pregnancy-85mg/day

Deficiency of Vit C
Scurvy: bleeding , bruising easily, hair and tooth loss,
joint pain and swelling. ( be related to the weakening of
blood vessels, connective tissue, and bone, which
contain collagen)
Mega doses: (1-4g/day)
ascorbic acid is not toxic, but dehydroascorbic acid is toxic.
Oxalate is a major metabolite of Vit C. it has been implicted in
formation of Kidney stones

Drug Interactions:
Estrogen-containing contraceptives are known to lower
vitamin C levels in plasma and white blood cells.
Aspirin can lower vitamin C levels if taken frequently
Large doses of vitamin C may block the action of warfarin,
requiring an increase in dose to maintain its effectiveness
have their prothrombin time monitored by the clinician
following their anticoagulant therapy.

Vitamin B1 (Thiamine)
anti beri-beri/ antineuritic Vitamin
Isolated in the 1930's, thiamin was one of the first organic
compounds to be recognized as Vitamin. Thiamin occurs in the
human body as free Thiamin and its phosphorylated forms:
Thiamin monophosphate (TMP),
Thiamin triphosphate (TTP)
Thiamin pyrophosphate (TPP), which is also known as thiamin
diphosphate.
Jansen and Donath (1926) isolated Vit B1 from rice
polishings

Functions of Vit B1:
Thiamin pyrophosphate (TPP) is a required coenzyme .
TPP plays a role in transmission of nerve impulse
(it is required for acetylcholine synthesis and ion translocation of
neural tissue)
TTP is concentrated in nerve and muscle cells
Impaired formation of TTP may play a role in the neurologic
symptoms of severe thiamin deficiency

Dietary sources:
cereals, pulses, oil seeds, pork, liver, heart, kidney,
milk
RDA:
Men-1.2mg/day
Women-1.1mg/day
Children- 0.9 mg/day
Pregnancy- 1.4mg/day

Deficiency of Vit B1:
excessive loss of thiamin from the body, consumption of anti-
thiamin factors in food, or a combination of factors.
Certain plants contain ATF, which react with thiamin to form a
product that is oxidized in the body, rendering it inactive.
Consuming large amounts of tea and coffee

Deficiency symptoms:
In adults 2 types : Wet beri-beri
Dry beri- beri
Infantile beri-beri
Symptoms:
loss of appetite, weakness ,constipation
mental depression
peripheral neuropathy
Wernicke-Korsakoff syndrome: which is
characterized by confusion, mental changes, abnormal eye
movements, and unsteadiness that can progress to severe
memory loss.

Biochemical changes that occur in Vit B1
deficiency:
Carbohydrate metabolism is impaired
Accumulation of pyruvate in tissues is harmful
Pyruvate normally does not cross the BBR but in
deficiency alterations occurs and permitting entry of
Pyruvate in brain directly. Which leads to Polyneuritis
Impairment in nerve transmission
Transketolase activity in erythrocytes is decreasedwww.indiandentalacademy.com

Drug interactions
Reduced blood levels of thiamin have been reported in
individuals with epilepsy taking phenytoin, for long periods
of time .
5-Fluorouracil, a drug used in cancer therapy, inhibits the
phosphorylation of thiamin to thiamin pyrophosphate (TPP)
Diuretics, especially furosemide , may increase the risk of
thiamin deficiency in individuals with marginal thiamin
intake due to increased urinary excretion of thiamin .

Antagonists:
o Pyrimethiamine
o Oxythiamine

Vitamin B2/ Riboflavin
Riboflavin is found as an integral component of the coenzymes,
Flavin adenine dinucleotide (FAD)
Flavin mononucleotide (FMN)
Coenzymes derived from riboflavin are also called flavins.
Enzymes that use a flavin coenzyme are called flavoproteins.

Sources: yeast, liver, milk, cheese, legumes, green leafy
vegetables.
RDA
Adult man: 1.7 mg
Woman : 1.3 mg
infants and children: 0.7- 1.6 mg

Biochemical functions:
Flavin coenzymes participate in redox reactions in numerous
metabolic pathways .
Flavins are critical for the metabolism of carbohydrates, fats,
and proteins.
FAD is part of the electron transport (respiratory) chain,
which is central to energy production. In conjunction with
cytochrome P-450, flavins also participate in the metabolism
of drugs and toxins .

Riboflavin deficiency:
Cheilosis
Glossitis/ magenta colored inflammation of the tongue
Seborrheic dermatitis with thickening and atrophy of skin at
nasolabial folds, ears, forehead
Corneal vascularization
Continued intake of chlorpromazine may produce deficiency by
inhibiting the conversion of riboflavin to FMN

Detection of riboflavin deficiency:
Estimation of erythrocyte glutathione reductase activity
Urinary riboflavin estimated fluorometrically
Antagonists:
Galactoflavin
Dichlororiboflavin
Isoriboflavin

Toxicity
No toxic or adverse effects of high riboflavin intake in
humans are known.
Studies in cell culture indicate that excess riboflavin may
increase the risk of DNA strand breaks in the presence of
chromium (IV), a known carcinogen . This may be of
concern to workers exposed to chrome, but no data in
humans is available. High dose riboflavin therapy has been
found to intensify urine color to a bright yellow (flavinuria),
but this is a harmless side effect.

Niacin/ Vitamin B3
The term niacin refers to nicotinic acid and
nicotinamide, which are both used by the body to
form the coenzymes,
nicotinamide adenine dinucleotide (NAD)
nicotinamide adenine dinucleotide phospate (NADP).
(Neither form is related to the nicotine found in
tobacco)

Functions
NAD functions most often in reactions involving the
degradation of carbohydrates, fats, proteins, and alcohol to
produce energy.
NADP functions more often in biosynthetic (anabolic)
reactions, such as in the synthesis of fatty acids and
cholesterol .

Causes of deficiency
 Carcinoid syndrome, a condition of increased secretion of
serotonin and other catecholamines by carcinoid tumors,
may also result in pellagra due to increased utilization of
dietary tryptophan for serotonin rather than niacin synthesis.
Prolonged treatment with the anti-tuberculosis drug,
Isoniazid, has also resulted in niacin deficiency

Sources: Yeast, liver, cereals, fish, prawns
RDA:
Men: 19mg
Woman: 15mg
Infants and children: 8-14mg

Deficiency of Niacin:
Pellagra ( seen among people depending mainly
on maize /jowar)
Symptoms: glossitis
fissuring of lips
exfoliative dermatitis- red, itchy, dry ,
pigmented , desquamated skin , hands, wrists,
knees
Diarrhea
Dementia with cerebral and spinal
lesions, irritability and anxiety

Detection of niacin deficiency:
Estimation of urinary niacin derivatives by Spectrophotometrically

Pyridoxine / Vit B6:
first isolated in the 1930's. There are six forms of vitamin B6:
pyridoxal (PL), pyridoxine (PN), pyridoxamine (PM)
their phosphate derivatives:
pyridoxal 5'-phosphate (PLP)
pyridoxine 5'-phosphate (PNP)
pridoxamine 5'-phospate (PMP).
PLP is the active coenzyme form, and has the most importance
in human metabolism .

Sources: yeast, liver, cereal, egg yolk, meat
RDA
Men 1.7 mg/day
Infants and children: 0.3 – 1.6 mg
Pregnanacy: 2.4 mcg/day

Functions of Vit B6
PLP functions as a coenzyme that catalyzes the release of
glucose stored in the muscle as glycogen.
PLP is also a coenzyme for reactions used to generate glucose
from amino acids, a process known as gluconeogenesis.
Nervous system function
Red blood cell formation and function
synthesis of niacin from tryptophan, Nucleic acid synthesis

Drugs interactions
 medications, isoniazid , penicillamine, and antiparkinsonism
drugs, including L-dopa, form complexes with vitamin B6,
creating a functional deficiency.
 High doses of vitamin B6 have been found to decrease the
efficacy of the anticonvulsants, phenobarbitol and phenytoin,
and L-dopa .
Antagonists:
Deoxypyridoxine

Deficiency Vit B6:
Causes: Alcoholics
epileptic convulsive seizures , microcytic anemia, peripheral
neuropathy
seborrheic dermatitis
depression
demyelination, polyneuritis
symptoms of pellagra

Vitamin B12
Vitamin B12 is the largest and most complex of all the
vitamins. It is unique among vitamins in that it contains a
metal ion, cobalt. For this reason cobalamin is the term used
to refer to compounds having B12 activity.
Methylcobalamin and 5-deoxyadenosyl cobalamin are the
forms of vitamin B12 used in the human body . The form of
cobalamin used in most supplements cyanocobalamine

Dietary sources: Fortified
milk, meat, poultry, fish
RDA:
Men-2.4mcg/day
Women-2.4mcg/day
Children-0.9mcg/day
Pregnancy-2.6mcg/day

Deficiency causes:
Absorption of vitamin B12 from food requires normal function
of the stomach, pancreas, and small intestine. Stomach acid
and enzymes free vitamin B12 from food, allowing it to bind
to other proteins, known as R proteins .
Pernicious anemia
 food-bound vitamin B12 malabsorption.
Surgical resection of stomach or parts of small intestine

Deficiency of Vit B12
Megaloblastic anemia
Neurologic symptoms
Gastrointestinal symptoms

Diagnostic tests
• Measurement of serum B12 by Microbiological or
Radioligand assay
• Measurement of urine or serum Methylmalonic acid or
total homocysteine
• Schillings Test

Toxicity
No toxic or adverse effects
 Doses as high as 1 mg (1000 mcg) daily by mouth or 1 mg
monthly by intramuscular (IM) injection have been used to
treat pernicious anemia, without significant side effects.
When high doses of vitamin B12 are given orally only a small
percentage can be absorbed, which may explain its low
toxicity

Drug Interactions:
Proton pump inhibitors ( omeprazole and lansoprazole) has
been found to decrease blood vitamin B12 levels
H2-receptor antagonists ( Tagamet, Pepsid, Zantac)
cholestyramine , chloramphenicol, neomycin ,colchicine
Metformin decreases vitamin B12 absorption by tying up free
calcium required for absorption of the IF- B12 complex.
Nitrous oxide inhibits both vitamin B12 dependent enzymes

Folic acid:
The terms folic acid and folate are often used interchangeably
 Folic acid, the most stable form
 Naturally occurring folates exist in many chemical forms.
Folates are found in foods as well as in metabolically active
forms, in the human body .
 forms found in food are referred to as "folates",

Dietary sources
Green leafy vegetables (foliage) , Citrus fruit juices,
legumes, and fortified cereals are also excellent sources.
RDA
Men- 800 mcg/day
Women- 600 mcg/day

Functions
One-carbon metabolism
Nucleic acid metabolism
Amino acid metabolism

Nutrient Interactions
Vitamin B12 and vitamin B6
The metabolism of homocysteine has 2 pathways
methionine from homocysteine, and is dependent on a folate
coenzyme and a vitamin B12-dependent
converts homocysteine to another amino acid, cysteine, and
requires two vitamin B6-dependent enzymes. Thus, the
amount of homocysteine in the blood is regulated by three
vitamins: folic acid, vitamin B12, and vitamin B6.

Folic acid Antagonists
Aminopterin
Amethopterin
Trimethoprim
Methotrexate

Deficiency causes:
alcoholism, cancer, low dietary intake
Symptoms:
Increased blood levels of Homocysteine
Megaloblastic anemia

Biotin (Vitamin H)
 Biotin is required by all organisms but can only be
synthesized by bacteria, yeasts, molds, algae, and some plant
species .
Dietary sources:
Eggyolk, liver, and yeast are rich sources of biotin
RDA
Men- 30 mcg/day
Women-30 mcg/day
Children-20 mcg/day
Pregnancy-30 mcg/daywww.indiandentalacademy.com

Functions:
In its physiologically active form biotin is attached at the
active site of four important enzymes, known as
carboxylases. Each carboxylase catalyzes an essential
metabolic reaction
Acetyl-CoA carboxylase
Pyruvate carboxylase
Methylcrotonyl-CoA carboxylase
Propionyl-CoA carboxylase
Histone biotinylation

Deficiency causes:
prolonged intravenous feeding without biotin
supplementation and consumption of raw egg white for a
prolonged period . (Avidin is a protein found in egg white,
which binds biotin and prevents its absorption.)
Cooking egg white denatures avidin, rendering it susceptible
to digestion, and unable to prevent the absorption of dietary
biotin.

Symptoms:
hair loss , scaly red rash around the eyes, nose, mouth, and
genital area.
Neurologic symptoms-depression, lethargy, hallucination,
and numbness and tingling of the extremities. The
characteristic facial rash, together with an unusual facial fat
distribution, have been termed the "biotin deficient face”
Individuals with hereditary disorders of biotin metabolism
impaired immune system function, including increased
susceptibility to bacterial and fungal infections

Nutrient interactions
The anticonvulsants, carbamazepine, inhibit biotin
absorption in the small intestine. Phenobarbital, phentyoin,
and carbamazepine appear to increase urinary excretion of
biotin.
valproic acid, has been associated with decreased biotinidase
activity in children
Long-term treatment with sulfa drugs or other antibiotics
may decrease bacterial synthesis of biotin
Pantothenic acid have the potential to compete with biotin
for intestinal and cellular uptake due to their similar
structures

Toxicity
Oral biotin supplementation has been well-tolerated in doses
up to 200 mg/day in people with hereditary disorders of
biotin metabolism
one case report of life-threatening eosinophilic
pleuropericardial effusion in an elderly woman who took a
combination of 10 mg/day of biotin and 300 mg/day of
pantothenic acid for two months

Panthothenic acid
• In Greek the word Pantothenic means- from everywhere
• known as vitamin B5
• found throughout living cells in the form of coenzyme A
Dietary sources: liver, meat, peanuts, legumes, honey
It is absorbed from intestines and excreted in Urine
RDA:
Men, women- 5mg/day
Children- 4mg/day
Pregnancy-6mg/day

Functions
CoA is required for chemical reactions that generate energy
from food (fat, carbohydrates, and proteins). The synthesis
of essential fats, cholesterol, and steroid hormones requires
CoA.
 Heme, a component of hemoglobin synthesis.
Metabolism of a number of drugs and toxins
The acyl-carrier protein requires pantothenic acid (Both CoA
and the acyl-carrier protein are required for the synthesis of
fatty acids)

Drug interactions
Oral contraceptives containing estrogen and progestin may
increase the requirement for pantothenic acid

Deficiency
headache, fatigue, insomnia, intestinal disturbances, and
numbness and tingling of their hands and feet .
 In a more recent study, participants fed only a pantothenic
acid free diet did not develop clinical signs of deficiency.
Homopantothenate is a pantothenic acid antagonist

Toxicity:
The only adverse effect noted was diarrhea resulting from
very high intakes of 10 to 20 grams/day of calcium D-
pantothenate

Clinical uses of some of the vitamins
Vit D:
Osteoporosis- a prospective cohort study showed that daily
consumption of 600IU/day reduced the risk of osteoporotic
hip fracture by 37% in postmenopausal women
Cancer- induces cell differentiation
Autoimmune diseases: immune modulator
Hypertension: RCT have shown to reduce systolic blood
pressure in elderly women by 9%( 1600IU& 800mg of
ca/day)

Vitamin E
CVS: observational studies have shown that increased
consumption of Vit E reduced the risk of MI
Cataracts
Cancer
Dementia
Vit K
Osteoporosis: discovery of Vit k dependent proteins in bone

Vit C
Cancer
Cataract
Common cold
Vit A
Cancer
Acne
Psoriasis, retinitis pigmentosa

Panthothenic Acid
Wound healing:
pantothenol ointment to the skin have been shown to
accelerate the closure of skin wounds and increase the
strength of scar tissue in animals.
High cholesterol
A pantothenic acid derivative called pantethine has been
reported by a number of investigators to have a cholesterol
lowering effect

Commercially available nutrient
supplements
Becosules capsules ( b1- 10mg, b2- 10mg, b6-3mg,
niacinamide-50mg, folic acid- 1.5mg)
Cebion ( ascorbic acid 250 mg)
Shel cal (cal carb-625mg, vit D 125IU)
Evion ( vit E acetate 100, 400, 600mg)
Kinetone (vit A 2000IU, D3-200IU, b1-2mg, Vit C-50mg)

Bibliography
Principles of Biochemistry- Lehninger
Biochemistry- 2nd
edition-U. Satyanarayana
Biochemistry illustrated – Peter N. Campbell
Harper’s Biochemistry- 25th
edition- Robert K. Murray
Clinical Periodontology- 10th
edition- Carranza’s
Dental management of Medically compromised patients – 6th
edition – James. W. Little
Nutrition and Periodontal Disease-
Dent Clin N Am 49 (2005) 595-610

Vitamins /orthodontic courses by Indian dental academy

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