VITAMIN C AND MICRONUTRIENTS

PRESENTERS:
CHARUMATHI
Moderator: DEEPTI DIXIT
DR. MUTHULAKSHMI
DEEPTHAA
CHRISTY DIVAKAR
 VITAMIN C (ASCORBIC ACID)
BIOCHEMICAL ROLE:
It is important for synthesis of collagen at the
level of hydroxylation of lysine and proline in
procollagen.
It is also involved in neurotransmitter metabolism
(conversion of dopamine to norepinepherine and
tryptophan to serotonin).
It is also involved in cholesterol metabolism
(conversion of cholesterol to steriod hormones and
bile acids).
• It functions to maintain the iron and copper
atoms, cofactors of the metalloenzymes, in a
reduced state.
• It is important antioxidant( electron donor).
• It enhances nonheme iron absorption, the
transfer of iron from transferrin to ferritin, and
the formation of tetrahydrofolic acid and thus
can affect the cellular and immunological
functions of the hematopoietic system.
• It also has role in wound healing and bone formation.
DIETARY INTAKE:
0-6 months , 40mg
6-12months , 50mg
1-3years , 15mg
4-8years , 25mg
9-13years , 45mg
14-18years , 65-75mg
Dietary allowances during pregnancy and lactation are
85mg/day and 120mg/day.
• SOURCES: citrus fruits, fruit juices, peppers, berries,
melons, guava, kiwifruit, tomatoes, cauliflower,and
green leafy vegetables.
• Breast milk contains adequate level of vitamin c
• Vitamin c is destroyed by prolonged storage,
overcooking, and processing of foods.
• Absorption: It occurs in upper small intestine by an
active process or by simple diffusion when large
amounts are ingested. Its highest level found in
pituitary and adrenal glands.
 VITAMIN C DEFICIENCY
• Deficiency of vitamin c results in scurvy.
• In most cases of scurvy from north america and europe
have been reported in children with developmental and
behavioural disorders, especially autism spectrum
disorders, on highly restrictive diets.
• In scurvy, there is defective formation of connective
tissues and collagen in skin, cartilage,dentine and bone
and blood vessels, leading to fragility.
• In the long bones, osteoid is not deposited by
osteoblasts, the cortex is thin and trabeculae become
brittle and fracture easily.
 CLINICAL FEATURES
• Early manifestations are irritability, loss of appetite, low-
grade fever, musculoskeletal pain, and tenderness in the
legs.
• Followed by leg swelling most marked at the knees and
the ankles and pseudoparalysis. The infant might lie with
hips and knees semiflexed and feet rotated
outwards(frog like posture.)
• subperiosteal hemorrhages in the lower limbs .
• Scorbutic Rosary at costochondral junction and
depression of the sternum. It is sharper than rachitic
rosary.
SCORBITIC ROSARY
Frog like posture
• Gum changes manifests as bluish purple, spongy
swellings of the mucous membrane, especially over
upper incisors.
• Anemia in infants and young children with scurvy, is
related to impaired iron absorption and coexistent
hematopoietic nutrient defciencies, including iron,
vitamin B12 and folate.
• Hemorrhagic manifestations like petechiae, purpura
and ecchymoses at pressur points; epistaxis; gum
bleeding and perifollicular hemorrhages.
Inflamed marginal
gingiva Perifollicular hemorrhages
• Other findings are poor wound and fracture healing,
hyperkeratosis of hair follicles, arthralgia, and muscle weakness.
DIAGNOSIS:
X-RAY FINDINGS:
• Shaft of long bones have a ground glass appearance because of
trabecular atrophy.
• Cortex is thin and dense giving the appearance of pencil
outlining of the diaphysis and epiphysis.
• White line of frankel an irregular but thickened white line at the
metaphysis, represent the zone of well calcified cartilage.
• Epiphyseal centres of ossificatin also have a ground
glass appearance and are surrounded by a sclerotic
ring
• Zone of rarefaction under the white line at
metaphysis. This zone of rarefaction (Trummerfeld
zone), linear break in the bone that is proximal and
paralle t the white line, represent area of debris of
broken down bone trabeculae and connective tissue.
• A Pelkan spur is lateral prolongation of white line
and may be present at cortical ends.
• Epiphyseal separation can occur along the line of
destructio with either linear displacement or compression
of the epihysis against the shaft.
• Because of subperiosteal hemorrhages, during healing the
elevated periosteum becomes calcified and radiopaque,
sometimes gives a dumb-bell or club shape to the affected
bone.
MRI:
• Demonstrate both acute and healing subperiosteal
hematomas along with periostitis, metaphyseal changes
and heterogenous bone marrow signal intensity.
 BIOCHEMICAL TESTS:
• Plasma ascorbate concentration of <0.2 mg/dl usually is
considered deficient.
• Leukocyte concentration of ≤10µg/108 white blood cells
are considered deficient and indicate latent scurvy, even in
absence of clinical signs of deficiency.
• Saturation of the tissues with vitamin c can be estimated
from the urinary excretion of the vitamin after test dose of
ascorbic acid. In health children 80%of test dose appears in
urine within 3-5hours after parenteraal administration.
• Generalized nonspecific aminoaciduria is common.
 DIFFERENTIAL DIAGNOSIS
• Infectious or juvenile idiopathic arthritis,
osteomyelities, nonaccidental trauma(child
abuse), malignancy, acrodynia.
• Copper deficiency
• Henoch Schonlein purpura(Ig A vasculitis)
thrombocytopenic purpura or leukemia .
 TREATMENT
• Vitamin C supplements of 100-200mg/day orally or
parenterally .
• Improvement seen within 1week but treatment should
be continued for 3months for complete recovery.
• PREVENTION:
• Breastfeeding protects against vitamin C deficiency
throughout infancy.
• Children consuming heat treated milk or plant based
beverages should consume adequate vitamin c rich
foods.
• Dietary or medicinal supplements are
required in children on restrictive diets
deficient in vitamin C, severly malnourished
children and those with chronic debiliating
conditions( malignancies, neurological
disorders).
• Providing antenatal supplements of vitaminC
to smoking mothers.
 VITAMIN C TOXICITY
• Daily intake of <2g of vitamin c is generally
without adverse affects.
• Larger doses can cause gastrointestinal
problems such as abdominal pain and osmotic
diarrhea.
• Megadoses should be avoided in history of
urolithiasis or conditions like thalassemia and
hemochromatosis.
TRACE ELEMENTS
• Eleven 'major' elements constitute 99% of human body
weight: Hydrogen, gen, carbon, nitrogen, oxygen, sodium,
potassium, chlorine, calcium, phosphorus, sulfur and
magnesium. In addition, the body is composed of
numerous "trace" elements. The term trace elements
comprise an increasing number of compounds with
proven or putative essentiality for human nutrition. Each
of these contributes less than 0.01% of total body weight.
Their major functions are related to enzyme systems
where they act either as cofactor for metal-ion-activated
enzymes or as specific constituents of metallo-enzymes.
 ZINC
• Zinc is the second most common trace element in
the body after iron.
• It is an essential micronutrient with diverse but
critical physiological role being part of more than
200 enzymatic reactions.
• zinc regulates gene transcription and participates
in nucleic acid metabolism, protein synthesis and
thereby, cellular growth.
• Zinc is a major antioxidant being part of the enzyme
superoxide dismutase.
• Dietary sources:
Zinc is derived mainly from animal protein.
1. Liver
2. oyster
3. meat
4. fish
5. nuts
6. eggs are a rich source.
 ABSORPTION AND METABOLISM
• Zinc is absorbed throughout the
small intestine by a process of
facilitated diffusion.
• In the systemic circulation, the
major fraction of plasma zinc is
loosely bound to albumin.
• Almost 90% of total body zinc is
localized in bone and skeletal
muscle.
• Zinc status is regulated both at the
absorptive step and by intestinal
re-excretion.
• The major excretory route for
endogenous zinc is via the
intestinal tract; fecal losses are
increased in children with
intestinal diseases or diarrhea.
 DEFECIENCY
• Diets based on cereals/starch, plants and legumes are associated
with zinc deficiency, due to the presence of dietary phytic acid that
decreases the bioavailability of zinc.
• Infants, children, adolescents, pregnant and lactating women have
increased demand of zinc due to active growth and tissue synthesis.
Causes:
• malnutrition and malabsorption syndrome
• low dietary intake
• poor absorption due to intestinal disease.
• Excessive loss of zinc in stools can occur with recurrent or chronic
diarrhea.
• Severe zinc deficiency syndromes can occur in patients on
prolonged intravenous feeding
CLINICAL FEATURE
• Poor physical growth is an important feature of zinc
depletion in preschool and school-age children.
• Delayed sexual maturation and hypogonadism is a
prominent feature of zinc deficiency in adolescents.
• Other features include anemia, anorexia, diarrhea,
alopecia, dermatitis, impaired immune function,
poor wound healing and skeletal abnormalities.
• Acrodermatitis enteropathica is an autosomal
recessive disorder of severe zinc deficiency, caused
by impaired intestinal absorption due to defect in
intestinal zinc transporter protein. It presents in early
infancy, with vesicobullous, dry, scaly or eczematous
skin lesions chiefly in the periorificial (around the
mouth and perineum) and acral areas.
• Alopecia and eye changes, such as conjunctivitis,
blepharitis and photophobia, may be present.
• Chronic diarrhea, growth retardation, stomatitis, loss
of taste sense, irritability and delayed wound healing
are seen
 RDA
STATE REQUIREMENT

NORMAL CHILDREN 3.5 – 5.0 mg/day

ACQUIRED ZINC DEFICIENCY 0.5-1.0 mg/kg/day

(several weeks or months)

MALNOURISHED 2-4 mg/kg/day

1 mg of elemental zinc is available from 4.5mg zinc

sulfate or 3mg zinc acetate
 Toxicity
• Symptoms:
• Nausea
• vomiting
• loss of appetite
• abdominal cramps
• diarrhea,
.
 DIAGNOSIS
The diagnosis of zinc deficiency is based on the
combination of

o dietary history of chronic low zinc intake or

excessive intestinal losses,
o presence of clinical features compatible with
deficiency and
o low levels of zinc in plasma or hair
 COPPER
• Copper is a component of several metallo-
enzymes required for oxidative metabolism.
 Absorption and metabolism:
• Most of the ingested copper is absorbed in stomach
and small intestine, from where it is transported to
the liver and released into the systemic circulation
bound to ceruloplasmin, the main transport protein
for copper.

• STORAGE : liver and muscle.

• EXCRETION: through biliary secretions in the feces;

urinary excretion is minimal.
 SOURCES
o meats
o Liver
o Seafood
o nuts
o Seeds
o Additional copper may
enter the food chain
through pesticides and
contamination of water by
pipes and cooking utensils.
 RDA

• Infants: 200-220 µg/day

• Children (1-8 years): 340-440 µg/day
• Adolescents (9-18 years): 700-890 µg/day
• Adults: 900 µg/day
 DEFICIENCY
CAUSES
• malabsorption syndromes
• liver disease
• peritoneal dialysis
EFFECT
• Copper deficiency decreases the life span of the
erythrocyte and impairs mobilization of stored iron from
liver and bone marrow.
Features
 microcytic, hypochromic anemia unresponsive to iron
therapy
 depigmentation of hair
 Neutropenia
 neurological problems
 Osteoporosis
 Copper transport is disrupted in two human diseases:
Wilson disease and Menke disease. Both have defects in
copper transporting membrane
 Toxicity
Symptoms:
• Gastrointestinal distress (nausea, vomiting,
diarrhea)
• liver and kidney damage
• neurological symptoms.
 Selenium
• Selenium is a constituent of glutathione peroxidase, an
antioxidant in red blood cells and other tissues.
• function : Selenium also helps maintain normal immune function
and is a part of the enzyme type 1-deiodinase which converts
thyroxine to triiodothyronine.
Dietary sources :
 whole grain
 meat
 Egg
 Seafood
 garlic
 mushrooms.
 DEFICIENCY
Endemic selenium deficiency results
 Keshan disease:a form of
cardiomyopathy in young children
seen in some regions of China.
 In combination with iodine
deficiency, lack of selenium can
result in myxedematous endemic
cretinism, seen in certain parts of
Africa.
CAUSE OF DEFICIENCY
Selenium deficiency may be seen in
patients on total parenteral nutrition
Clinical feature
macrocytosis, brown hair and
whitening of nails.
 RDA

• Infants: 15-20 µg/day

• Children (1-8 years): 20-30
µg/day
• Adolescents (9-18 years): 40-55
µg/day
• Adults: 55 µg/day
 TOXICITY

Symptoms
• Garlic odor in breath
• hair and nail
brittleness
• gastrointestinal issues
• skin rashes
• neurological
abnormalities.
CHROMIUM
Chromium acts in glucose homeostasis potentiating insulin
action possibly by facilitating binding to its receptor.
FEATURES OF DEFICIENCY:
● Impaired glucose tolerance
● Peripheral neuropathy
● Encephalopathy
● Disturbed nitrogen and lipid metabolism
Recommended daily allowance for chromium:

AGE RDA
Birth to 6 months 0.2mcg
7-12 months 5.5 mcg
1-3 years 11 mcg
4-8 years 15 mcg
9-13 years 25 mcg
14-18 years 35 mcg
19-50 years 35 mcg
> 50 years 30 mcg
TOXICITY:
● Toxicity is unknown

DIETARY SOURCES:
● Meat
● Grains
● Fruits and Vegetables
IODINE

● Iodine present in small quantities in thyroid gland,is essential

for the formation of thyroid hormones,Thyroxine(T4) and
Triiodothyronine(T3).
SOURCES:
● Sea food (fish,sea weed,shrimp)
● Sea plants
● Sea water
● Dairy products (milk,yogurt)
Recommended daily allowance :

CRITERIA RDA(mcg/day)

Birth - 5 years 90

6-12 years 120

Adolescent &adults 150

Pregnancy and lactating 200

women
IODINE DEFICIENCY DISORDERS:

● Goitre is the earliest manifestation of iodine deficiency and is

an adaptive response to increase thyroid hormones production
under the influence of Increased TSH level but eventually leads
to decomposition in the form of hypothyroidism.

● Iodine deficiency disorder are the commonest cause of

MENTAL RETARDATION
Spectrum of iodine deficiency disorder:

CATEGORY DISORDERS

Fetus Abortion,stillbirth,congenit
al anomalies, endemic
cretinism,increased
Perinatal mortality

Neonate Neonatal Goitre,Endemic

mental retardation,
Neonatal hypothyroidism

Child,Adolescent Goitre,Impaired mental

function,subclinical
hypothyroidism
MANGANESE

● It acts as a enzyme Co- factor.

FEATURES OF DEFICIENCY:
● Hypercholestrolemia
● Weight loss
● Decreased clotting proteins
TOXICITY:
● Neurologic manifestation
● Cholestatic jaundice
DIETARY SOURCES:
● Nuts
● Meat
● Grains
● Tea
● Spinach
Iron,Fluorine

[Link] Divakar
 Distribution of Iron
• Total body iron content is 3 to 5 g;
• 75% of which is in blood, the rest is in liver,
bone marrow and muscles.
• Iron is present in almost all cell.
• Blood contains 14.5 g of Hb per 100 mL.
• About 75% of total iron is in hemoglobin, and
5% is in myoglobin and 15% in ferritin
 Requirement of Iron (ICMR)
• Daily allowance of iron for an adult Indian is
20 mg of iron, out of which about 1–2 mg is
absorbed.
• Children between 13–15 years need 20–30
mg/day.
• Pregnant women need 40mg/day.
 Sources of Iron
• Leafy vegetables (20 mg/100 g) are good
sources.
• Pulses (10 mg/100 g) and cereals (5 mg/100 g)
are less iron quantity.
• Liver (5 mg/100 g) and meat (2 mg/100 g).
• Jaggery is a good source for iron.
• Milk is a very poor source of iron, containing
lessthan 0.1 mg/100 mL.
 Factors Influencing Absorption of Iron
Ascorbic Acid
• Ferric ions are reduced with the help of gastric HCl, ascorbic
acid, cysteine and -SH groups of proteins. Therefore, these will
favor iron absorption.
Interfering Substances
• Iron absorption is decreased by phytic acid (in cereals) and
oxalic acid (in leafy vegetables) by forming insoluble iron salts.
Other Minerals
• Calcium, copper, lead and phosphates will inhibit iron
absorption.
 Summary of Iron Absorption
• Free iron in the intestines is reduced from the ferric (Fe3+) to the
ferrous (Fe2+) state on the luminal surface of intestinal enterocytes
and transported into the cells through the action of the divalent
metal transporter (DMT1).
• Intestinal uptake of heme iron occurs through the help of heme
carrier protein (HCP1).
• The iron is then released within the enterocytes by the enzyme
heme oxygenase.
• The iron can be temporarily stored within intestinal enterocytes
bound to ferritin.
• Iron is transported across the basolateral membrane of intestinal
enterocytes into the circulation, through the action of the transport
protein ferroportin (also called IREG1=iron-regulated gene 1).
• The synthesis of both DMT and ferroportin are
regulated by hepcidin.
• The enzyme hephaestin (a copper-containing
ferroxidase with homology to ceruloplasmin), which
oxidizes the ferrous form back to the ferric form.
• Once in the circulation, ferric form is maintained by
ceruloplasmin; and is bound to transferrin and
passes to liver.
• Ferritin is the storage form of iron
 Iron Deficiency Anemia
• This most common nutritional deficiency
disorder leaves about 30% of world population
anemic.
• About 70% of Indians have iron deficiency and
85% of pregnant women suffer from iron
deficiency anemia
 Causes for Iron Deficiency
• Nutritional deficiency of iron
• Hookworm infection
• Repeated pregnancies
• Chronic blood loss
• Nephrosis
• Lack of absorption
• Lead poisoning
 Clinical Manifestations
• When the level is lower than 10 g, body cells
lack oxygen and patient becomes uninterested
in surroundings (apathy).
• Prolonged iron deficiency causes atrophy of
gastric epithelium leading to achlorhydria
• Similar atrophy of epithelium in oral cavity and
esophagus causes dysphagia termed
Plummer- Wilson syndrome, which is a known
precancerous condition.
 Laboratory Findings
• Serum iron level:Itisdepressedinirondeficiency,
• Total iron binding capacity (TIBC): It is elevated
in hypochromic anemias
• Soluble transferrin receptor level (TfR):
The level of sTR is increased in iron-deficiency
anemia, hemolytic anemia and polycythemia.
Decreased values are seen in aplastic anemia and
chronic renal failure
 Treatment of Iron Deficiency
• Oral iron supplementation is the treatment of
choice.
• 100 mg of iron + 500 mg of folic acid are given to
pregnant women, and 20 mg of iron + 100 mg folic
acid to children.
• Iron tablets are usually given along with vitamin C,
to convert it into ferrous form, for easy absorption.
• Unabsorbed iron may generate free radicals and
so, it is advisable to give vitamin E (to prevent free
radical generation) along with iron.
 Iron Toxicity
• More than 50 mg of iron taken orally may
cause nausea, diarrhea and abdominal pain.
 FLUORIDE
• Fluoride is known to prevent caries.
• Caries is a Latin term, meaning “decay”.
• In the pits and fissures of premolar and molar teeth,
bacterial fermentation of residual food leads to acid
production.
• The acid removes enamel and dentine to expose the
pulp, leading to inflammation and toothache.
• Topical application of fluoride will result in a
fluoroapatite layer on the enamel, which protects
enamel from the decay by acid
 Safe limit and uses

• The safe limit of fluorine is about 1 ppm in

water.
• Fluoride ions enter the hydration shell
surrounding the apatite crystals and may
become incorporated into the crystal surface.
• The fluoroapatite makes the tooth surface
more resistant to plaque bacterial attack.
 Reference
• Op Ghai
• Nelson text book of paediatric
• Nutritional and child development by
Elizabeth
THANK YOU