Balanced diet / oral surgery courses

BALANCED DIET
Part-1
• INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandental.com

NUTRITIONAL REQUIREMENTS AND
DIETARY ASSESSMENT

Contents
• Introduction
• Energy and energy Requirements
• Essential dietary requirements (Function and Food Source)
-Proteins
-Carbohydrates
-Fat
-Water
-Vitamins-water soluble
-Fat soluble
-Minerals
• Malnutrition and Nutritional Assessment
-Clinical Examination
-Physical Examination
-Laboratory Assessment
-Specialized Procedures for Nutritional Assessment
• Dietary Reference Intakes & Recommended Dietary Allowances
• Factors altering Nutrient needswww.indiandental.com

BALANCED DIET- Part-2
Contents
• Nutrition’s influence on Mortality and morbidity
• Dietary Deficiency and excess
-Proteins
-Carbohydrates
-Fat
-Water
-Vitamins-water soluble
-Fat soluble
-Minerals
• NUTRITIONAL ABNORMALITIES
-Protein-energy malnutrition
-Anorexia nervosa and Bullemia
-Starvation
-Obesity
-Alcohol
• Effect of Nutrition on Dental health

INTRODUCTION
• Different cells of the body are continuously active at different
rates.For this activity ,energy and other neccessities are to be
supplied.All these are achieved through nutrition.
• Nutrition is a dynamic process and it involves supply of correct
amount of nutrients to the body for repair, growth and maintainance.
• Nutrients are substances that are not synthesized in the body in
sufficient amounts and therefore must be supplied by the diet.
• Nutrients are the substances which provide nutrition to the body and
include protein, fat, carbohydrate, vitamins, minerals and water.

ENERGY
• Food is necessary to provide the body with energy
• The SI unit of energy is the joule (J), and 1 kj = 0.239
kcal. The conversion factor of 4.2 kj, equivalent to 1 kcal,
is used in clinical nutrition.
• For weight to remain stable, energy intake must match
energy output.

Energy requirements
• There are two approaches to assessing energy
requirements for subjects who are weight stable and
close to energy balance:
• Assessment of energy intake
This can be estimated from dietary surveys and in the
past has been used to decide daily energy requirements
• Assessment of total energy expenditure.
Daily energy expenditure is the sum of:
-the basal metabolic rate (BMR)
-the thermic effect of food eaten
-occupational activities
-non-occupational activities

• Basal metabolic rate.
The BMR can be calculated by measuring oxygen
consumption and CO2 production, but it is more usually
taken from standardized tables that require knowledge
of the subject's age, weight and sex.
• Physical activity. The physical activity ratio (PAR) is
expressed as multiples of the BMR for both occupational
and non-occupational activities of varying intensities.
• Total daily energy expenditure
BMR X [Time in bed +(Time at work X PAR)+
(Non- occupational time x PAR)].

• Another method is to compare with a so called
'reference man'. For example, for India, a hypothetical
man, called the ICMR man (Indian Council of Medical
Research) has been imagined who represents the
'average' Indian in an 'average' Indian ambient
temperature.

• Energy requirements increase during the growing period,
with pregnancy and lactation, and sometimes following
infection or trauma.
• In the basal state, energy demands for resting muscle
are 20% of the total energy required, abdominal viscera
35-40%, brain 20% and heart 10%. There can be more
than a 50-fold increase in muscle energy demands
during exercise.

Balanced diet
• The term balanced diet means a diet
which is complete in all respects (i.e., it is
not lacking in any respect) at the same
time it contains no excess of any item that
may cause harm to the body.

Essential Dietary Requirements
PROTEINS
• Dietary protein consists of both essential and
nonessential amino acids that are required for protein
synthesis.
• Certain amino acids can also be used for energy and
gluconeogenesis.
• The nine essential amino acids are histidine, isoleucine,
leucine,lysine,methionine/cystine,phenylalanine/tyrosine,
threonine, tryptophan. and valine.

• When energy intake is inadequate, protein intake must
be increased, since ingested amino acids are diverted
into pathways of glucose synthesis and oxidation.
• The proteins containing all the essential amino acids are
called first class proteins.
• The proteins deficient in one or more essential amino
acids, are called second class proteins.
• The proteins of animal origin belong to the first class and
most of the vegetable proteins are of second class in
nature.

• A protein which is deficient in one essential amino acid
when mixed with another protein having that particular
amino acid in sufficient amount, the mixture becomes a
superior protein. This is called supplementary value of
proteins.
• Amino acids may be utilized to synthesize products other
than protein or urea. For example:
• haem requires glycine
• melanin and thyroid hormones require tyrosine
• nucleic acid bases require glutamine, aspartate and
glycine
• glutathione, which is part of the defence system against
free radicals, requires glutamate, cysteine and glycine.

• According to a recommendation of BMA (British Medical
Association) Committee of Nutrition, 11% of the total
calories should come from protein. As an example, a
person requires 2200 Kcal/day 11% of 2200 =242 K cal.
Now each gm of protein = 4 Kcal. 242 K cal can come
from 242 + 4 =60gms of protein approximately.
• The most widespread idea is. an adult requires 1 gm/kg/
day of food protein. Thus, if he (or she) weighs 65 kg,
the protein requirement is 65 gm/day.

The protein requirement increases in the following
conditions :
(i) Growing children.
• Infants require 3 to 5 gms of protein/kg/bodywt/day.
• Throughout the period of growth, (which completes
around 18th-year in the boys) greater proportion of
protein is required. Between 14th to 16th year in the
boys, when there is again a fresh spurt of growth,
heavier quantity of protein is to be given.
(ii) Lactation, pregnancy. The protein requirement is
about 1.5 gm/kg body wt/day.
(iii) Convalescence.

Protein rich foods
• Meat (20%), fish (20%), egg (15%), cow's milk (3.5%)
are some of the excellent sources of protein of high
biological value.
• Dal (about 20%), legumes (about 25%), rice(10%),
wheat (10%) are some examples of vegetable proteins.
• Because of the quantity consumed, rice and wheat have
assumed major importance as protein suppliers of Indian
diet. Because of the high percentage of proteins in dal,
dal is also a crucially important protein supplier in the
Indian dishes.
• Soya bean is another vegetable rich in protein but the
quality of protein in soya bean is low.

NITROGEN BALANCE
• Normally in an adult healthy individual the amount of
protein catabolised in the body is exactly replaced by the
proteins in the diet.
• This can be said as protein balance.
• But proteins are quantified by nitrogen; hence, the actual
term used is 'Nitrogen balance‘.
• Proteins, on an average contain 16% of nitrogen, i.e., 1
g of nitrogen is equivalent to 6.25 gms of protein.

• Nitrogen in the dietary proteins can be estimated, so also
the daily urinary nitrogen excretion. If the values are
same, the body is said to be in nitrogen balance,.
• Positive nitrogen balance is seen in growing children,
convalescent patients, pregnancy, etc. On the other
hand, negative nitrogen balance is seen in glucorticoid
excess, thyrotoxicosis, etc., and above all, in the cases
of protein malnutrition (less protein in diet).

Carbohydrates
• Carbohydrates are readily available in the diet,
providing 17 kj (4 kcal) per gram of energy (15.7 kj
(3.75 kcal) per gram monosaccharide equivalent).
• At least 55% of total calories should be derived from
carbohydrates.
• The brain requires about 100g/d of glucose for
fuel.;other tissues about 50g/d.
• Carbohydrate intake comprises the polysaccharide
starch, the disaccharides (mainly sucrose) and
monosaccharides (glucose and fructose).

FUNCTIONS
• Carbohydrates are essential for running the TCA cycle
and without the TCA cycle functioning properly, ketosis
will develop.
• Carbohydrates are cheaper energy giving food, so an
easy source of energy, particularly to the poor.
• Another important biochemical aspect of carbohydrate is
its protein sparing effect, i.e., it prevents breakdown of
body proteins and also provides materials for synthesis
of lipids as well as for some amino acids.

• Dietary fibre, which is largely non-starch
polysaccharide(NSP) increases faecal bulk and is helpful
in the treatment of constipation. Eg.Bran ,the fibre from
wheat.
• A high intake of dietary fibre reduces blood lipids.
• Pectins and gums have been added to food to slow
down monosaccharide absorption, particularly in type 2
diabetes.
• Association between a high-fibre diet and protection
against colonic adenomas or colonic cancer has been
found in various studies.www.indiandental.com

Food Sources of carbohydrates
• These are found in plenty in different cereals, roots,
tubers, fruits (i.e., all are of plant origin).
• Examples ; rice, wheat, maize, bajra, cane sugar,
potato, apple and in many other fruits and vegetable.

FAT
• Lipids include both the solid (fats) and the liquid (oil)
variety.
• These can be obtained from both animal and plant
sources.
• One advantage of lipid is its high energy content, i.e.,
unlike carbohydrate a small amount of lipid will give
plenty of energy.
• Dietary fat is chiefly in the form of triglycerides, which
are esters of glycerol and free fatty acids

• Unsaturated fatty acids are monounsaturated or
polyunsaturated.
• The hvdrogen molecules related to these double bonds
can be in the cis or the trans position, most natural fatty
acids in food being in the cis position.
• Trans fatty acid consumption and their intake should not,
on present evidence, increase more than the current
estimated average of 5 g per day or 2% of the dietary
energy.
• Trans fatty acids behave as if they were saturated fatty
acids, increasing circulating low-density lipoprotein (LDL)
cholesterol concentration, which in turn increases the
risk of cardiovascular disease.

• The essential fatty acids (EFAs) are linoleic and
α- linolenic acid, both of which are precursors of
prostaglandins
• Synthesis of triglycerides, sterols and
phospholipids is verv efficient, and even with
low-fat diets subcutaneous fat stores can be
normal.
• Dietary fat provides 37 kj {9 kcal) of energy per
gram.

• The n-6 polyunsaturated fatty acids (PUFA) ,are
components of membrane phospholipids, influencing
membrane fluidity and ion transport.
• They also have anti-arrhythmic, anti-thrombotic and anti-
inflammatory properties, all of which are potentially
helpful in preventing cardiovascular disease
.
• In addition, n-3 PUFA increase circulating high-density
lipoprotein (HDL) cholesterol and lower triglycerides,
both of which might reduce cardiovascular risk.

The current recommendations for fat intake
are as follows:
• saturated fatty acids should provide approximately
10% of the dietary energy
• cis-monounsaturated acids (mainly oleic acid) should
continue to provide approximately 12% of the dietary
energy
• cis-polyunsaturated acids should provide 6% of
dietary energy, and are derived from n-6 and n-3 poly-
unsaturated fatty acids, which should provide ~ 0.5%
of total energy intake
• total fat intake should be no more than 35% of the total
dietary energy, and restriction to 30% is desirable.www.indiandental.com

Cholestrol
• It is found in all animal products.
• Eggs are particularly rich in cholesterol, which is virtually
absent from plants.
• The average daily intake in the UK is 300-500 mg.
• Cholesterol is also synthesized and only very high or
low dietary intakes will significantly affect blood levels.

WATER
• For adults, 1 to 1.5 mL water per kcal of energy
expenditure is sufficient under usual conditions to allow
for normal variations in physical activity, sweating, and
solute load of the diet.
• Water losses include 50 to 100 mL/d in the feces, 500 to
1000 mL/d by evaporation or exhalation, and, depending
on the renal solute load, >1000 mL/d in the urine. If
external losses increase, intakes must increase
accordingly to avoid underhydration.

• Fever increases water losses by approximately 200 mL/d
per °C; diarrheal losses vary but may be as great as 5
L/d in severe diarrhea.
• Heavy sweating and vomiting also increase water
losses.
• When renal function is normal and solute intakes are
adequate, the kidneys can adjust to increased water
intake by excreting up to 18 I/d of excess water .
• However, obligatory urine outputs can compromise
hydration status when there is inadequate intake or
when losses increase in disease or kidney damage.

• Infants have high requirements for water because of
their large ratio of surface area to volume, the limited
capacity of the immature kidney to handle high renal
solute loads, and their inability to communicate their
thirst.
• Increased water needs during pregnancy are low,
perhaps an additional 30 mL/d.

• During lactation, milk production increases water
requirements so that approximately 1000 mL/d of
additional water is needed, or 1 mL for each mL of milk
produced.
• Special attention must be paid to the water needs of the
elderly, who have reduced total body water and blunted
thirst sensation, and may be taking diuretics.

VITAMINS
Vitamins can be defined as the complex organic
molecules without energy value but are essential for
growth and maintenance of a healthy body. These are
not formed in the body and must be supplied from
outside.
Vitamins are of two types :
• (i) Fat soluble vitamins—A, D, E, K,
• (ii) Water soluble vitamins—B complex and C.

VITAMIN-A
• Vitamin A (retinol) is part of the family of retinoids which
is present only in foods of animal origin.
• The richest food source is liver, but it is also found in
milk, butter, cheese, egg yolks and fish oils.
• Herbivores obtain the vitamin from provitamins-
carotenoid pigments.
• Beta-carotene is the main carotenoid found in green
vegetables, carrots and other yellow and red fruits.
• Other carotenoids, lycopene and lutein, are probably of
little quantitative importance as dietary precursors of
vitamin A

Function
Retinol is stored in the liver and is transported in plasma
bound to an α-globulin, retinol-binding protein (RBP).
Vitamin A has several functions:
• It forms visual pigments.
• Retinol and retinoic acid are involved in the control of cell
proliferation and differentiation.
Vitamin A also plays a role in
• Iron utilization
• Humoral immunity,
• T-cell-mediated immunity,
• Natural killer cell activity,
• Phagocytosis

VITAMIN-D
• A group of sterol compounds whose parent structure is
cholecalciferol (vitamin D3).
• Cholecalciferol is formed in the skin from 7-
dehydrocholesterol by exposure to UV-B radiation.
• A plant sterol, ergocalciferol, can be similarly converted
into vitamin D2, and has similar vitamin D activity.
• Maintains intracellular and extracellular concentrations
of calcium and phosphate by enhancing intestinal
absorption of the two ions and, in conjunction with
parathormone, promoting their mobilization from bone
mineral.

VITAMIN-E
• Vitamin E includes eight naturally occurring compounds
divided into tocopherols and tocotrienoles.
• The most active compound and the most widely
available in food is the natural isomer d- (or RRR) α-
tocopherol, which accounts for 90% of vitamin E in the
human body.
• Food Sources- Vegetables and seed oils, including
soya bean, saffron, sunflower, cereals and nuts, are the
main sources. Animal products are poor sources of the
vitamin.

• Vitamin E is absorbed with fat, transported in the blood
largely in low-density lipoproteins (LDL).
• An individual's vitamin E requirement depends on the
intake of polyunsaturated fatty acids (PUFAs).

FUNCTION
• The biological activity of vitamin E results principally from
its antioxidant properties.
• In biological membranes it contributes to membrane
stability.
• It protects cellular structures against damage from a
number of highly reactive oxygen species, including
hydrogen peroxide, superoxide and other oxygen
radicals.
• Vitamin E may also affect cell proliferation and growth

VITAMIN-K
• Vitamin K is found as phylloquinone (vitamin K1) in
green leafy vegetables, dairy products, rape seed and
soya bean oils.
• Intestinal bacteria can synthesize the other major form
of vitamin K, menaquinone (vitamin K2), in the terminal
ileum and colon.
• Vitamin K is absorbed in a similar manner to other fat-
soluble substances in the upper small gut.

FUNCTIONS
• Vitamin K is a cofactor necessary for the production not
only of blood clotting factors but also for proteins
necessary in the formation of bone.
• Bone osteoblasts contain three vitamin K-dependent
proteins, osteocalcin, matrix Gla protein and protein S,
which have a role in bone matrix formation.
• Osteocalcin contains three Gla residues which bind
tightly to the hydroxyapatite matrix depending on the
degree of carboxylation; this leads to bone
mineralization.
• There is, however, no convincing evidence that vitamin K
deficiency or antagonism affects bone other than rapidly
growing bone.

Thiamin- Vitamin B1
Function
• Thiamin diphosphate, often called thiamin
pyrophosphate {TPP), is an essential cofactor,
particularly in carbohydrate metabolism.
• Thiamin is found in many foodstuffs, including cereals,
grains, beans, nuts, as well as pork and duck. It is often
added to food (e.g. in cereals) in developed countries.
• Following absorption, thiamin is found in all body tissues,
the majority being in the liver. Body stores are small and
signs of deficiency quickly develop with inadequate
intake.

Riboflavin
• Riboflavin is widely distributed throughout all plant and
animal cells.
• Good food sources are dairy products, leafy
vegetables.
• Riboflavin is not destroyed appreciably by cooking, but is
destroyed by sunlight.
• Riboflavin is a flavoprotein that is a cofactor for many
oxidative reactions in the cell.

NIACIN
• The term niacin refers to nicotinic acid and nicotinamide
and biologically active derivatives.
• Nicotinic acid and nicotinamide; as precursors of two
coenzymes, nicotinamide adenine dinucleotide (NAD)
and NAD phosphate (NADP), which are important in
numerous oxidation and reduction reactions in the body.
• In addition NAD and NADP are active in adenine
diphosphate-ribose transfer reactions involved in DNA
repair and calcium mobilization.

• Niacin is found in many foodstuffs, including plants,
meat and fish. Niacin is lost by removing bran from
cereals but is added to processed cereals and white
bread in many countries.
• Niacin can be synthesized in humans from tryptophan,
60 mg of tryptophan being converted to 1 mg of niacin.
• The amount of niacin in food is given as the 'niacin
equivalent', which is equal to the amount of niacin plus
one-sixtieth of the tryptophan content. Eggs and cheese
contain tryptophan.

PYRIDOXINE (VITAMIN B6)
• Vitamin B6 refers to a family of compounds including
pyridoxine, pyridoxal, pyridoxamine, and their 5'-
phosphate derivatives.
Vitamin B6, is involved in
• 5'-Pyridoxal phosphate (PLP) is a cofactor for more than
100 enzymes involved in amino acid metabolism.
• Heme and neurotransmitter synthesis.
• Metabolism of glycogen, lipids, steroids, sphingoid
bases, and several vitamins, including the conversion of
tryptophan to niacin.

Folic acid
• It is found in plenty in green leafy vegetables and also
in liver, fish, kidney, etc.
• It acts as a coenzyme for one carbon atom transfer
mainly in amino acid metabolism and in DNA synthesis.

Vitamin B12 (Cyanocobalamine)
• It is available only from animal source as from liver,
kidney, meal and from egg, milk, fish, etc.
• It takes part in transmethylation and is essential for DNA
synthesis as in the developing RBCs .
• It is also required for myelin formation.
• Its deficiency leads to megalobastic anaemia and
subacute combined degeneration of the spinal cord.

BIOTIN
• Biotin is a water-soluble vitamin that plays a role in
gluconeogenesis and fatty acid synthesis and serves as
a CO2 carrier on the surface of both cytosolic and
mitochondrial carboxylase enzymes.
• The vitamin also functions in the catabolism of specific
amino acids (e.g., leucine).
• Excellent food sources of biotin include liver, soy,
beans, yeast, and yolks.
• However, egg white contains the protein avidin, which
strongly binds the vitamin and reduces its bioavailability.www.indiandental.com

Pantothenic Acid
• It is found in liver, kidney, meat, fish, egg, milk and milk
products, yeast, wheat bran, peas, vegetables, etc
• Daily requirement unknown.
• It is a prosthetic group in coenzyme A.

VITAMIN-C
• It is found in foods of plant origin, particularly citrus fruits and green
leafy vegetables.
• Total vitamin C is measured as the sum of ascorbic and
dehydroascorbic acid concentrations.
• Because of its reductant properties, it serves primarily as a biologic
antioxidant and free radical scavenger in aqueous environments.
• The biosynthesis of collagen, carnitine, bile acids, and
norepinephrine as well as proper functioning of the hepatic mixed-
function oxygenase system, all depend on these properties.
• Vitamin C in foodstuffs increases the intestinal
absorption of non-heme iron.

• It has been suggested that ascorbic acid in high dosage
(1-2 g daily) will prevent the common cold.
• Vitamin C supplements have also been advocated to
prevent atherosclerosis and cancer.
• Vitamin C deficiency is seen mainly in infants fed boiled
milk and in the elderly and single people who do not eat
vegetables.

Minerals
• Inorganic and organic combinations of essential
elements are active in many physiologic processes.
• They constitute the basic structure of bone and teeth.
• They help maintain the osmotic relations of the body
fluids.
• They regulate the acid-base equilibrium of the tissues.
• They form a part of some hormones.
• They are an integral part of some enzymes.
• They serve as activators of certain enzymatic reactions.
• They are an essential part of the oxygen carrying
pigments.

MINERALS
Copper
• The daily RNI of copper is 1.2 mg (19 umol).
• Shellfish, legumes, cereals and nuts are good dietary
sources.
• Copper is necessary for normal erythropoiesis as well as
for iron absorption which is mediated by
ceruloplasmin,which acts as a ferroxidase.
• Other metalloenzymes which require copper are
cytochrome c oxidase,superoxide dismutase,tyrosinase
and lysyl oxidase.

Zinc
• The daily RNI of zinc is 9.5 mg for men, 7 mg for
women and it is widely available in food.
• Zinc is an integral part of many enzymes like-Carbonic
anhydrase,lactic dehydrogenase and component of
some peptidases and is important for the digestion of
proteins in the gastointestinal tract.
• Zinc is essential for the synthesis of RNA and DNA.
• The best dietary sources are meat,whole grains and
legumes.
• Oysters are outstandingly rich in zinc, while white bread,
fats and sugar contain negligible amounts.www.indiandental.com

IODINE
• The daily RNI of iodine is 140 ug for men and women, and it is
found in milk, meat and seafoods.
• It exists in foodstuffs as inorganic iodides which are efficiently
absorbed. Iodine is a constituent of the thyroid hormones.
Fluoride
• In areas where the level of fluoride in drinking water is less than I
ppm. (0.7-1.2 mg/l.), dental caries is relatively more prevalent.
• Fluoridation of the water provides 1-2 mg daily, resulting in a
reduction of about 50% of tooth decay in children. There is little
fluoride in food except for seafish and tea providing 70% the daily
intake.
• Fluoride-containing toothpaste may add up to 2 mg a day.

Selenium
• Selenium is a component of several enzymes, most notably
glutathione peroxidase and super-oxide dismutase.
• These enzymes appear to prevent oxidative and free radical
damage of various cell structures.
• Evidence suggests that the antioxidant protection conveyed by
selenium operates in conjunction with vitamin E, since deficiency of
one seems to enhance damage induced by a deficiency of the
other.
• Selenium also participates in the enzymatic conversion of thyroxine
to its more active metabolite, tri-iodothyronine.
• Rich diet sources of selenium include seafood, muscle meat, and
cereals though the selenium content of cereal is determined by the
soil concentration.

Chromium
• Chromium potentiates the action of insulin in patients
with impaired glucose tolerance, presumably by
increasing insulin receptor mediated signaling.
• In addition, in some patients, improvement in blood lipid
profiles has been reported.
• Rich food sources of chromium include yeast, meat, and
grain products

Iron
• Participates in redox reactions in a number of
metalloproteins such as hemoglobin, myoglobin, and the
cytochrome enzymes.
• Blood is the tissue richest in iron.
• Primary storage form is ferritin.
• Intestinal absorption is 15-20%. for"heme" iron and 1-8%
for the iron contained in vegetables.
• Absorption of the Iatter form is enhanced by the ascorbic
acid in foodstuffs, by poultry, fish, or beef and by an iron-
deficient state.It is decreased by phytate and tannins.
• Foods rich in iron are meat,liver,whole meal
cereals,oatmeal,peas,beans and lentils.

Manganese
• A component of several metalloenzymes.
• Most manganese is in mitochondria, where it is a component of
manganese superoxide dismutase.
• It is necessary for the activation of phophatase and forms a part of
the enzyme arginase.
Molybdenum
• A cofactor in several enzymes, most prominently xanthine oxidase
and sulfite oxidase.

PHOSPHORUS
• The normal inorganic phosphate level of blood in adults ranges from
2-4mg/dl.
• Phosphate is the major anion of intracellular fluid.
• Many important reactions of phosphates are in relation to the
functions of adenosine diphosphate, adenosine
triphosphate,phosphocreatine and so forth.
• Phosphates are present in all natural foods, and dietary deficiency
has not been described.
• Patients taking large amounts of aluminium hydroxide can,
however, develop phosphate deficiency owing to binding in the gut
lumen. It can also be seen in total parenteral nutrition

Calcium
• It is found in many foodstuffs, with two-thirds of the
intake coming from milk and milk products, only 5% from
vegetables.
• Calcium absorption from the gastrointestinal tract is
vitamin D-dependent. Ninety-nine per cent of body
calcium is in the skeleton.
• Increased calcium is required in pregnancy and lactation,
when dietary intake must be increased.
• The serum calcium ion concentration is in the range of 9-
11mg/dl.

Calcium forms a major role in-
• The formation of bones and teeth
• Maintainance of skeletal structure
• Normal membrane permeability
• Normal heart rhythm and other neuromuscular
excitabiity.
• In coagulation of blood.

Sodium
• Most of the sodium is in extacellular fluid and plasma.
• The normal blood level is 147.8mEq./liter of plasma.
• One third of the total sodium ion concentration in the
body is in the skeleton.
• Sodium ions play an important role in the maintenance of
the acid-base equilibrium as well as of osmotic pressure.
• The bulk of basic metabolic energy expenditure is
concerned exclusively with the maintenance of proper
intracellular sodium concentration.i.e.,the sodium pump.

Potassium
• Most of the body potassium is intracellular.
• It is the predominant base in the cells.
• There is constant exchange of potassium between its
intracellular and extacellular phases.
• The requirement of potassium is greatest during periods
of rapid growth.
• About 90% of potassium is excreted in urine.
• The urinary excretion is influenced by Aldosterone which
controls the active tubular excretion of potassium.
• The normal plasma level is about 4mEq./liter of plasma.

MALNUTRITION AND NUTRITIONAL
ASSESSMENT
In clinical situations, nutritional assessment involves:
• (1) screening for malnutrition,
• (2) assessing the diet and other data to establish either
the absence or presence of malnutrition and its possible
causes,
• (3) planning for the most appropriate nutritional therapy

CLINICAL EVALUATION OF THE
MALNOURISHED PATIENT
THE PATIENT HISTORY
• The clinical nutritional history is based on understanding
the etiologies and pathophysiology of malnutrition and
should focus on changes in diet and body weight,
socioeconomic conditions, and symptoms unique to
each clinical setting.
• Social and economic conditions that may lead to poverty
and malnutrition include inadequate income,
homelessness, drug abuse, or chronic alcoholism.

On the general medical service, PCM may be an integral
part of the clinical presentation of-
• Chronic recurrent pancreatitis,
• renal failure,
• chronic liver disease,
• chronic obstructive pulmonary disease,
• disseminated cancer
• chronic infections such as AIDS or tuberculosis.

THE PHYSICAL EXAMINATION
• A variety of nutritional deficiencies can be identified by
examination of the patient's general appearance,
including skin, hair, nails, mucus membranes, and
neurologic system.
• Initially, a pinch of the posterior upper arm may reveal a
loss of subcutaneous fat in the malnourished patient.
• Hollowing of the temporal muscles, wasting of upper
arms and thigh muscles, plucked hair, and peripheral
edema are all consistent with protein deficiency.

Examination of the skin may reveal
• The papular keratitis ("goose bump rash") of vitamin A
deficiency,
• Perifollicular, hemorrhages of vitamin C deficiency,
• Ecchymoses of vitamin K deficiency,
• The "flaky paint" lower extremity rash of zinc deficiency,
• Hyperpigmentation of skin-exposed areas from niacin
deficiency,
• Seborrhea essential fatty acid deficiency,
• Spooning of nails in iron deficiency,and transverse nail
pigmentation in protein deficiency.

• The eye examination yields conjunctival pallor of
anemia, pericorneal and corneal opacities of severe
vitamin A deficiency ("Bitot spots) ,and nystagmus and
isolated ocular muscle paresis of thiamine deficiency.
• The oral examination may reveal
• Angular stomatitis and cheilosis of either riboflavin or
niacin deficiency.
• Glossitis with smooth and red tongue of riboflavin,
niacin, vitamin BI2, or pyridoxine deficiency.
• Hypertrophied bleeding gums of vitamin C deficiency.

• Examination of the neurologic system, particularly in
the setting of chronic alcohol abuse, may detect memory
loss with confabulation, a wide-based gait, and past
pointing, which, together with ophthalmoplegia and
peripheral neuropathy, constitute the Wernickc-korsakoff
syndrome of thiamine deficiency.
• Other neurologic causes of dementia include pellagra
due to niacin and/or tryptophan deficiency.
• Additional causes of peripheral neuropathy include
deficiencies of pyridoxine or vitamin E;
• Loss of distal vibratory and position sense is
characteristic of the subacute combined degeneration of
vitamin B12 deficiency.www.indiandental.com

• Arthropometry
• Measurements of subcutaneous fat and skeletal muscle
are important to determine the severity of PCM.
• Using specialized callipers and a tape measure,
anthropometry estimates body fat from the thickness of
the skin fold of the posterior mid-upper arm.
• Mid-arm muscle circumference is estimated by using the
equation:
Mid-arm muscle circumference = mid-upper
circumference (cm)- (Π X triceps skin-fold thickness)
(cm)

LABORATORY ASSESSMENT
• Selected use of laboratory tests, most of which are
widely available, is essential for characterizing and
quantifying malnutrition.
• Laboratory findings that are often attributed to chronic
disease may, in actuality, reflect the response to PCM or
selected, micronutrient deficiencies in the setting of
chronic illness.

Serum Visceral Proteins
• Serum albumin, which has a 2- to 3-week half-life, is a
sensitive but nonspecific measure of PCM.
• A normal serum albumin level in a well-hydrated patient
is inconsistent with PCM.
• In contrast, a low serum albumin level could reflect PCM,
but can also occur because of increased plasma volume
in an overhydrated patient,or because of chronic liver,
renal, or cardiopulmonary failure.

• The serum albumin level falls during the acute stress of
surgery, sepsis, or other acute inflammatory illness
because of a combination of increased circulating
extracellular volume and TNF-a-mediated inhibition of
albumin synthesis.
• Several shorter-lived visceral proteins can also be
measured to estimate the severity of PCM.
• These include transferrin (1-week half-life), prealbumin
or retinol-binding protein complex (2-day half-life), and
flbronectin (1-day half life).

Vitamins and Minerals Assays
• PCM is typically associated with low serum levels of
vitamin A, zinc, and magnesium.
• Abnormal digestion and absorption of dietary fat are
associated with deficiencies of fat-soluble vitamins A, D,
and E, whereas intestinal mucosal malabsorption (as in
celiac disease) is commonly associated with additional
deficiencies of iron and folic acid.
• Chronic alcoholism is frequently associated with
thiamine, folate, vitamin A, and zinc deficiencies .

Assessment of Immune Function
• PCM is associated with atrophy of thymic-dependent
lymphoid structures and reduced T cell-mediated
immunity.
• Conversely, B cell-mediated production of
immunoglobulins is usually unaffected.
• Total lymphocyte count (total white cell count x fraction
as lymphocytes) is often <1000/uL in PCM and may be
accompanied by anergy to common skin test antigens.

SPECIALIZED PROCEDURES FOR
NUTRITIONAL ASSESSMENT
Several specialized procedures are used to assess energy
and protein stores and energy expenditure in
malnourished patients. These procedures may be
employed during the initial nutritional assessment or may
serve as an index of the efficacy of nutritional support
during the treatment of malnourished patients.

Bioelectric Impedance Analysis-
• Bioelectric impedance analysis (BIA) is a simplified and
portable method for measurement of body fat, Fat free
mass(FFM), and total-body water.
• BIA is performed by measuring the electric conductivity
of a weak current between electrodes placed on the
dorsal surfaces of the hands and feet.
• The measurement reflects differences in the impedance
to electric current, which is greatest through fat and least
through water.
• Lean body mass can be calculated by subtracting fat
mass from body weight or by dividing total-body water by
0.73.

Energy Expenditure
• The three components of total energy expenditure
(TEE.) are basal energy expenditure (about 55 to 65%
of TEE), thermal effect of feeding (about 10% of TEE),
and activity energy expenditure (the remainder)
• For estimating TEE, can be calculated by the Harrison
and Benedict formula
• Or estimated at 25% kcal/kg of ideal body weight for
height, then modified by adding-
- 10% for digestion and metabolism of intravenous or
enteral feeding

-and an additional 12.5% for each degree of fever over
37 degree C
-as well as an additional multiplier commensurate with
the severity of illness (e.g., 25% for general surgery,
50% for sepsis, and 100% for extensive third-degree
burns).
• TEE can be measured at the bedside more precisely by
the gas-exchange method of indirect calorimetry using a
mobile metabolic cart.

Creatinine Excretion in the 24-h Urine-
• Creatinine, the metabolic product of skeletal muscle
creatine, is produced at a constant rate and in an
amount directly proportional to skeletal muscle mass.
• With steady day-to-day renal function, each gram of
creatinine in the 24-h urine collection represent 18.5 g of
fat-free skeletal muscle.
• Since skeletal muscle is the major component of FFM,
measurement of creatinine in the 24-h urine collection
can be used as a relative measure of this body
compartment during the initial assessment or to assess
the efficacy of nutritional support.

Urine nitrogen Excretion and Nitrogen Balance
• Nitrogen balance provides an index of protein gain or
loss: 1 g nitrogen is equivalent to 6.25 g protein.
• Nitrogen balance can be assessed by measuring the
difference between nitrogen consumed through the
mouth, enteral tube, or intravenous-sources and nitrogen
excreted in the urine, feces, and other intestinal sources.

DIETARY REFERENCE INTAKES AND
RECOMMENDED DIETARY
ALLOWANCES
• Human life and well-being can be maintained within a
fairly wide range for most nutrients.
• However, the capacity for adaptation is not infinite —
too much, as well as too little, intake of a nutrient may
have adverse effects or alter the health benefits
conferred by another nutrient.

• Therefore, benchmark recommendations on nutrient
intakes have been developed to guide clinical practice.
• These quantitative estimates of nutrient intakes are
collectively referred to as the dietarv reference intakes
(DRls)

• The DRIs supplant the recommended daily allowances
(RDAs).
• DRIs include the estimated average requirement (EAR)
for nutrients, as well as three other reference values
used for dietary planning for individuals: the RDA, the
adequate intake (AI), and the tolerable upper level (UL).
ESTIMATED AVERAGE REQUIREMENT
• The EAR is the amount of a nutrient estimated to be
adequate for half of the healthy individuals of a specific
age and sex.
• The types of evidence and criteria used to establish
nutrient requirements vary by nutrient, age, and
physiologic group.

• The EAR is not an effective estimate of nutrient
adequacy in individuals because it is a median
requirement for a group.
• 50% of individuals in a group fall below the requirement
and 50% fall above it.
• Thus, a person with a usual intake at the EAR has a
50% risk of an inadequate intake.

RECOMMENDED DIETARY ALLOWANCES
• The RDA is the average daily dietary intake level that
meets the nutrient requirement of nearly all healthy
persons of a specific sex, age, life stage, or physiologic
condition (such as pregnancy or lactation).
• The RDA is the nutrient-intake goal for planning diets of
individuals.
• The RDA is defined statistically as 2 standard deviations
above the EAR to ensure that the needs of any given
individual is met.
• The RDAs are used to formulate food guides, to create
food exchange lists for therapeutic diet planning,and as
a standard for describing the nutritional content of
processed foods and nutrient supplements.

• The nutrient content in a food is stated by weight or as a
percent of the daily value (DV), a variant of the RDA
that, for an adult, represents the highest RDA for an adult
consuming 2000kcal/d.
• The risk of dietary inadequacy increases as intake falls
further below the RDA. However, the RDA is an overly
generous criterion for evaluating nutrient adequacy. For
example, by definition the RDA exceeds the actual
requirements of all but about 2 to 3% of the population.
Therefore, many people whose intake falls below the
RDA may still be getting enough of the nutrient.

• ADEQUATE INTAKE –
• It is not possible to set an RDA for some nutrients that
do not have an established EAR.
• In this circumstance, the AI is based on observed, or
experimentally determined, approximations of nutrient
intakes in healthy people.
• In the DRIs established to date, AIs rather than RDAs
are proposed for infants up to age I year, as well as for
calcium, chromium, vitamin D, fluoride, manganese,
pantothenic acid, biotin, and choline for persons of all
ages.

TOLERABLE UPPER LEVELS OF NUTRIENT
INTAKE
• Excessive nutrient intake can disturb body functions and
cause acute, progressive, or permanent disabilities.
• The tolerable UL is the highest level of chronic nutrient
intake(usually daily) that is unlikely to pose a risk of
adverse health effects for most of the population.
• Data on the adverse health effects of large amounts of
many nutrients are unavailable or too limited to establish
a UL .
• Therefore, the lack of a UL does not mean that the risk
of adverse effects from high intake is nonexistent.

• Healthy individuals derive no established benefit from
consuming nutrient levels above the RDA or AL.
• Individual nutrients in foods that most people eat rarely
reach levels that exceed the UL. However, nutritional
supplements provide more concentrated amounts of
nutrients per dose and, as a result, pose a potential risk
of toxicity.
• Nutrient supplements are labelled with "suplement
facts" that express the amount of nutrient in absolute
units or is the percent of the DV provided per
recommended serving size.
• Total nutrient consumption, including both food and
supplements, should not exceed RDA levels.

FACTORS ALTERING NUTRIENT
NEEDS
The DRIs are affected by –
• Physiologic Factors-Age, sex. rate of growth, pregnancy,
lactation, physical activity,
• Composition of diet,
• Concomitant diseases and drugs.
When only slight differences exist between the
requirements for nutrient sufficiency and excess, dietary
planning becomes more difficult.

PHYSIOLOGIC FACTORS-
• Growth, strenuous physical activity, pregnancy, and
lactation increase needs for energy and several essential
nutrients.
• Energy needs rise during pregnancy, due to the
demands of fetal growth, and during lactation, because
of the increased energy required for milk production.
• Energy needs decrease with loss of lean body mass,
the major determinant of REE.
• Because both health and physical activity tend to decline
with age, energy needs in older persons, especially
those over 70 tend to be less than those of younger
persons. www.indiandental.com

DIETARY COMPOSITION
• Dietary composition affects the biologic availability and
utilization of nutrients. For example, the absorption of
iron may be impaired by high amounts of calcium or
lead;
• non-heme iron uptake may be impaired by the lack of
ascorbic acid and amino acids in the meal.

• Protein utilization by the body may be decreased when
essential amino acids are not present in sufficient
amounts. Animal foods, such as milk, eggs, and meat,
have high biologic values with most of the needed amino
acids present in adequate amounts.
• Plant proteins in corn (maize), soy, and wheat have
lower biologic values and must be combined with other
plant or animal proteins to achieve optimal utilization by
the body.

DISEASE
Imbalances in nutrient intakes are recognized as risk
factors for certain chronic degenerative diseases, such
as
• saturated fat and cholesterol in coronary artery disease;
• sodium in hypertension;
• obesity in hormone-dependent endometrial and breast
cancers;

• Ethanol in alcoholism. Since the etiology and
pathogenesis of these disorders are multifactorial, diet is
only one of many risk factors.
• Osteoporosis, for example, is associated with calcium
deficiency, as well as risk factors related to environment
(e.g., smoking, sedentary lifestyle), physiology (e.g.,
estrogen deficiency), genetic determinants (e.g.. defects
in collagen metabolism), and drug use (chronic steroids)

There are many ways to assess the adequacy of the
patient's habitual diet.
• These include a food guide, a food exchange list, a diet
history, or a food frequency questionnaire.
• A commonly used food guide for healthy persons is the
USDA's food pyramid, which is useful as a basis for
identifying inadequate intakes of essential nutrients, as
well as likely excesses in fat, saturated fat, sodium,
sugar, and alcohol .
• The guide can be adjusted by varying the number of
servings to provide for the needs of persons of different
ages and life cycle stages.

• Those who follow ethnic or unusual dietary patterns may
need extra instruction on how foods should be
categorized, as well as the appropriate portion sizes that
constitute a serving.
• The process of reviewing the guide with patients helps
them transition to healthier dietary patterns and identifies
food groups eaten in excess of recomendations or in
insufficient quantities.

• For those on therapeutic diets,assessment against food
exchange lists may be useful.
• These include, for example, the American Diabetes
Association food exchange lists for diabetes, or the
American Dietetic Association food exchange lists for
renal disease

DietaryPlanning
Fats, oils & sweets
USE SPARINGLY
Bread, cereal, rice
& pasta group
= 6 SERVINGS
Milk, yoghurt & cheese group
3 SERVINGS
Vegetable group
= 3 SERVINGS
Meat, poultry, fish, dry beans,
eggs, and nut group
= 2 SERVINGS
Calcium, vitamin D & B12
SUPPLEMENTS
F= Fibre
F
F
F
F
Water
= 8 SERVINGS
Fruit group
= 2 SERVINGS

References
• Harrisons,Principles of Internal Medicine,PartIV,Chapter
60,16th
Ed,Vol 1,Mc Graw-Hill Companies Inc,2005
• Kumar & Clark,Clinical medicine,Chapter 5,6th
Ed,Elsevier Saunders,2005
• Cecil,Textbook of Medicine,Part XVI,20th
Ed,W.B.Saunders Company,1996
• Davidson’s,Principles and Practice of Medicine,Chapter
4,15th
Ed,E. & S. Livingstone,1990

• Robins and Cotran,Pathologic Basis of Disease,Chapter9,7th
• Guyton & Hall,Textbook of Medical Physiology,Chapter 71,11th
• Shafer,Hine & Levy,Textbook of Oral Pathology,Chapter 12,4th
Ed,W.B.Saunders Company,1983
• S.K.Choudhary,Concise Medical Physiology,ChapterVII.16,2nd
Ed,New Central Book Agency(P)Ltd.,1996
• Anil Barar Singh & Mahapatra,Essentials of Medical
Physiology,Chapter 4,2nd
Ed,Current Books International,2003

Thank-You

BALANCED DIET
Part-2
Guided by
Dr Shirish S. Degwekar
Presented by
Sangeeta Malik

DIETARY DEFICIENCY AND EXCESS

Carbohydrate
• Carbohydrates are essential for running the TCA cycle
and without the TCA cycle functioning properly, ketosis
will develop.
• If the carbohydrate intake is less than 100g per day
ketosis is likely to occur.

Fat
• A high fat intake has been implicated in the causation of:
-cardiovascular disease
-cancer (e.g. breast, colon and prostate)
-obesity
-type 2 diabetes.

Essential fatty acid deficiency
• Essential fatty acid deficiency may accompany protein-
energy malnutrition (PEM), but it has been clearly-
defined as a clinical entity only in patients on long-term
parenteral nutrition given glucose, protein and no fat.
• Alopecia, thrombocytopenia, anaemia and a dermatitis
occur within weeks with an increased ratio of triene (n-9)
to tetraene (n-6) in plasma fatty acids.

VITAMIN-A Deficiency
• Follicular hyperkeratosis and night blindness are early
indicators.
• Conjunctival xerosis, keratomalacia, and de-
differentiation of rapidly proliferating epithelia indicate
more severe deficiency.
• Bitot spots (focal areas of the conjunctiva or cornea with
foamy appearance) are an indication of xerosis.
• Blindness, due to corneal destruction and retinal
dysfunction, ensues if left uncorrected.
• Increased susceptibility to infection is also a
consequence.

VITAMIN-A TOXICITY
 500,000 IU may cause acute toxicity: intracranial
hypertension, skin exfoliation and hepatocellular
necrosis.
 Chronic toxicity may occur with habitual daily intake of >
33,000 IU: alopecia, ataxia. dermatitis, cheilitis,
pseudotumor cerebri. hepatocellular necrosis, and
hyperlipidemia.

VITAMIN-A TOXICITY
 Daily ingestion of > 25,000 IU during early pregnancy
can be teratogenic.
 Excessive intake of most carotenoids causes a benign,
yellowish discoloration of the skin. Large doses of
canthaxanthin, a carotenoid, can induce retinopathy.

Assessment of status
• Retinol concentration in the plasma as well as vitamin A
concentrations in the milk and tears are reasonably
accurate measures.
• Toxicity best assessed by elevated levels of retinyl
esters in plasma.
• A quantitative measure of dark adaptation for night
vision or an electroretinogram are useful functional tests.

VITAMIN-B1 Deficiency
• Classic deficiency syndrome ("beriberi") described in
Asian populations consuming polished rice diet.
• Alcoholism and chronic renal dialysis are also common
precipitants. High carbohydrate intake increases need
for B1.
• Prolonged thiamine deficiency causes beriberi, which is
classically categorized as wet or dry .

• Wet beriberi
-Presents primarily with cardiovascular symptoms
-Patients present with an enlarged heart tachycardia,
high-output congestive heart failure, peripheral edema,
and peripheral neuritis.
• Dry beriberi
- Presents with a symmetric peripheral neuropathy of the
motor and sensory systems with diminished reflexes.
-The neuropathy affects the legs most markedly, and
patients have difficulty rising from a squatting position.

Wernicke's encephalopathy
Alcoholic patients with chronic thiamine deficiency may
also have central nervous system manifestations
consisting of -
• Horizontal nystagmus,
• Ophthalmoplegia (due to weakness of one or more
extraocular muscles),
• Cerebellar ataxia, and mental impairment.
When there is an additional loss of memory and a
confabulatory psychosis, the syndrome is known as
Wernicke'Korsakoff syndrome.

VITAMIN-B1 Toxicity
• Excess intake is largely excreted in the urine although
parenteral doses of > 400 mg/d are reported to cause
lethargy, ataxia, and reduced tone of the gastrointestinal
tract.
• The laboratory diagnosis of thiamine deficiency is
usually made by a functional enzymatic assay of
transketolase activity measured before and after the
addition of thiamine pyrophosphate.

RIBOFLAVIN DEFICIENCY
There is no definite deficiency, although many communities have
low dietary intakes. Studies in volunteers taking a low riboflavin
diet have produced:
• Angular stomatitis or cheilosis (fissuring at the corners of the
mouth) a red, inflamed tongue
• Seborrhoeic dermatitis, particularly involving the face (around the
nose) and the scrotum or vulva.
• Conjunctivitis with vascularization of the cornea and opacity of
the lens has also been described.
• It is probable, however, that many of the above features are due
to multiple deficiencies rather than the riboflavin itself.

Assessment of Status
• The most common assessment is determining the
activity coefficient of glutathione reductase in red blood
cells (the test is invalid for individuals with glucose-6-
phosphate dehydrogenase deficiency).
• Measurements of blood and urine concentrations are
less desirable methods.

NIACIN Deficiency
• Pellagra is the classic deficiency syndrome and often
affects populations where corn is the major source of
energy.
• Still endemic in parts of China, Africa, and India.
• Diarrhea, dementia (or associated symptoms of anxiety
or insomnia) and pigmented dermatitis that develops in
sun-exposed areas are tvpical.
• Glossitis, stomatitis, vaginitis, vertigo, and burning
dysesthesias are early signs.
• Seen also in carcinoid syndrome, which diverts
tryptophan to other synthetic pathways.

NIACIN Toxicity
• Human toxicity known largely through studies examining
hypolipidemic effects.
• Includes vasomotor phenomenon (flushing),
hyperglycemia, parenchymal liver damage, and
hyperuricemia.

ASSESSMENT OF STATUS
• Assessment is problematic: Blood levels of vitamin is
not reliable.
• Measurement of urinary excretion of the niacin
metabolites, N-methylnicotinamide and 2-pyridone are
thought to be the most effective means of assessment at
present.

Pyridoxine Deficiency
• Dietary deficiency is extremely rare.
• Some drugs (e.g. isoniazid, hydralazine and
penicillnmine) interact with pyridoxal phosphate,
producing B6 deficiency.
• The polyneuropathy occurring after isoniazid usually
responds to vitamin B6.
• Sideroblastic anaemia occasionally responds to vitamin
B6 .
• A polyneuropathy has occurred after high doses (> 200
mg) given over many months.
• Vitamin B6, is used for premenstrual tension: a daily

Pyridoxine Toxicity
• Chronic use with doses exceeding 200 mg/d (in adults)
may cause peripheral neuropathies and photosensitivity.

Assessment of status(Vit-B6)
• The plasma or erythrocyte PLP levels are most common.
• Urinary excretion of xanthurenic acid after an oral
tryptophan load or activity indices of RBC alanine or
aspartic acid transaminases (ALT and AST, respectively)
all are functional measures of enzyme activity.

Folic acid deficiency
• Folic acid deficiency produces megaloblastic anaemia.
• Women of childbearing age are the most likely
individuals to develop deficiency.
• The hemopoietic cells in the bone marrow develop
megaloblastic features, reflecting ineffective DNA
synthesis.

• The peripheral blood smear demonstrates
macroovalocytes and polymorphonuclear leukocytes
with an average of more than 3.5 nuclear lobes.
• Megaloblastic changes in the oral and gastrointestinal
epithelia often occur, producing glossitis and diarrhea,
respectively.
• Sulfasalazine and phenytoin inhibit absorption and
predispose to deficiency.

TOXICITY
• Doses >400 microgm/d may partially correct the anemia
of B12 deficiency and mask (and perhaps exacerbate)
the associated neuropathy.
• Doses >400 microgm also reported to lower seizure
threshold in individuals prone to seizures.
• Rarely parenteral administration is reported to cause
allergic phenomena, but are probably due to dispersion
agents.

• Serum folate measures short-term folate balance,
whereas RBC folate better reflects tissue status.
• Serum homocysteine rises early in deficiency but is
nonspecific since B12 deficiency or renal insufficiency
also may cause elevations.

Vit-B-12 Deficiency
• Its deficiency leads to megalobastic anaemia and
subacute combined degeneration of the spinal cord.
• Loss of vibratory and position sense
• Abnormal gait
• Dementia
• Impotence
• Loss of bladder and bowel control
• Increased homocysteine and increased methylmalonic
acid

Toxicity
• A few allergic reactions have been reported to crystalline
B12 preparations and are probably due to impurities, not
the vitamin.

• Serum, or plasma, concentrations are generally
accurate.
• Subtle deficiency with neurologic complications can best
be confirmed by measuring the concentration of serum
methylmalonic acid, which is a sensitive indicator of
cellular deficiency.

Biotin Deficiency
• In the adult, biotin deficiency results in mental changes
(depression, hallucinations), paresthesia, anorexia, and
nausea.
• A scaling, seborrheic, and erythematous rash may occur
around the eyes, nose, and mouth as well as on the
extremities.
• In infants, biotin deficiency presents as hypotonia.
lethargy, and apathy.
• In addition, the infant may develop alopecia and a
characteristic rash that includes the ears.

Biotin Toxicity
• Toxicity has not been reported in humans with doses as
high as 60 mg/d in children.
• The laboratory diagnosis of biotin deficiency can be
established based on a decreased Plasma and urinary
concentration.

Pantothenic Acid
• Its deficiency produces dermatitis, alopecia, enteritis,
fatigue, abdominal pain and vomiting, insomnia, and
paraesthesias of the extremities.
• Doses exceeding 10 g/d may induce diarrhea.
• Whole blood and urine concetrations of pantothenate are
indicators of status; serum levels are not accurate.

Vitamin-C Deficiency
• The classic deficiency syndrome is scurvy characterized by-
-fatigue, depression
-widespread abnormalities in connective tissues such
as- inflamed gingivae
petichiae
perifollicular hemorrhages
impaired wound healing
coiled hairs
bleeding into body cavities.
• In infants, defects in ossification and bone growth may occur.
• Tobacco smoking lowers plasma and leukocyte vitamin C levels.

Vitamin-C Toxicity
• Quantities exceeding 500 mg/d (in adults) sometimes
cause nausea and diarrhea.
• Acidification of the urine with supplementation, and the
potential for enhanced oxalate synthesis, have raised
concerns regarding nephrolithiasis, but this has yet to be
demonstrated.

• Plasma ascorbic acid is very low in obvious deficiency
and a vitamin C level of less than 11 umoI/L (0.2 mg per
100 mL) indicates vitamin C deficiency.
• The leucocyte-platelet layer (buffy coat) of centrifuged
blood corresponds to vitamin C concentrations in other
tissues.
• The normal level of leucocyte ascorbate is 1.1-2.8 pmol
per 106 cells.

VITAMIN-D Deficiency
• Rickets in childhood
• Osteomalacia in adults.
• Expansion of the epiphyseal growth plates and
replacement of normal bone with unmineralized bone
matrix are the cardinal features.
• Deformity of bone and pathologic fractures occur.
• Serum concentrations of calcium and phosphate may
decline.

VITAMIN-D TOXICITY
• Excess amounts result in abnormally high serum
concentrations of calcium and phosphate
• Metastatic calcifications
• Renal damage
• Altered mentation may ensue

• The serum concentration of the major circulating
metabolite, 25-hydroxy vitamin D, indicates systemic
status except in chronic renal failure, in which the
impairment of renal 1-hydroxylation results in
disassociation of the monohydroxy and dihydroxy
vitamin concentrations.
• Measuring the serum concentration of 1,25-dihydroxy
vitamin D is then necessary.

Vitamin-E Deficiency
• The first deficiency to be demonstrated was a haemolytic
anaemia described in premature infants. Infant
formulations now contain vitamin E.
• Deficiency is seen only in children with abetalipo-
proteinaemia and in patients on long-term parenteral
nutrition.
• The severe neurological deficit (gross ataxia) can be
prevented by vitamin E injection.
• Plasma or serum levels of α-tocopherol can be
measured and should be corrected for the level of
plasma lipids by expressing the value as per milligram of
plasma lipid or cholesterol.www.indiandental.com

VITAMIN-E TOXICITY
• High doses of vitamin E (>800 mg/d) may reduce platelet
aggregation and interfere with vitamin K metabolism and
are therefore contraindicated in patients taking warfarin.
• Nausea, flatulence, and diahorrhea have been reported
at doses >1 g/d.

Assessment of Status
• Plasma or serum concentration of α-tocopherol is most
commonly used.
• Additional accuracy is obtained by expressing this value
per mg of total plasma lipid.
• Red blood cell peroxide hemolysis test is not entirely
specific, but is useful functional measure of antioxidant
potential of cell membranes.

VITAMIN-K Deficiency
Deficiency syndrome is uncommon except in
• (I) breastfed new-borns, in whom it may cause
"hemorrhagic disease of the newborn“
• (2) adults with fat malabsorption or who are taking drugs
that interfere with vitamin K metabolism (e.g.. coumarin.
phenytoin. broad-spectrum antibiotics)
• (3) individuals taking large doses of vitamin E and
anticoagulant drugs. Excessive hemorrhage is usual
manifestation.

VITAMIN-K TOXICITY
• Rapid intravenous infusion of K has been associated
with dyspnea, flushing and cardiovascular collapse,
probably related to dispersing agents in the solution.
• Supplementation may interfere with coumarin-based
anticoagulation.
• Pregnant women taking large amounts the provitamin
menadione may deliver infants with hemolytic anemia,
hyperbilirubinemia and kernicterus.

• The prothrombin time is typically used as a measure of
functional K status;
• It is neither sensitive nor specific for vitamin K deficiency.
• Determination of under-carboxylated prothrombin in the
plasma is more accurate but less widely available.

Copper
Deficiency
• Menkes' kinky hair syndrome is a rare condition caused
by malabsorption of copper.
• Infants with this sex linked recessive abnormality
develop growth failure, mental retardation, bone lesions
and brittle hair.
• Anaemia and neutropenia also occur.
Toxicity-
• Nausea, vomiting, diarrhea, hepatic failure, tremor,
mental deterioration, hemolytic anemia, renal
dysfunction.

ZINC
Deficiency
• Growth retardation,
• reduced taste and smell,
• alopecia, dermatitis,
• diarrhea, immune dysfunction,
• failure to thrive, gonadal atrophy, congenital
malformations
Toxicity-
• General: Reduced copper absorption, gastritis, sweating,
fever, nausea, vomiting.
• Occupational: Respiratory distress, pulmonary fibrosis

Iodine Deficiency
• Iodine deficiency impairs brain development.
• Endemic goitre occurs in remote areas where the daily
intake is below 70 ug, and in those parts 1-5% of babies
are born with cretinism.
• In these areas, iodized oil should be given
intramuscularly to all reproductive women every 3-5
years.
• In developed countries, Salt is iodised and endemic
goitre has disappeared.www.indiandental.com

Excessive fluoride intake
• In areas where the water fluoride level is above 3 mg/L
can result in fluorosis, in which there is infiltration into the
enamel of the teeth, producing pitting and discoloration.

Selenium
• Clinical deficiency of selenium is rare except in areas
of China where Keshan disease, a selenium-responsive
cardiomyopathy, occurs.
• Selenium deficiency may also cause myopathy.
• Toxicity has been described with very high intakes.
General: Alopecia, nausea, vomiting, abnormal nails,
emotional lability, peripheral neuropathy, lassitude, garlic
odor to breath, dermatitis
Occupational: Lung and nasal carcinomas,liver necrosis,
pulmonary inflammation

Calcium
• Deficiency- is usually due to vitamin D deficiency and results in
reduced bone mass & osteoporosis.
• Toxicity- Renal insufficiency (milk-alkalai syndrome),
nephrolithiasis, impaired iron absorption
Phosphorous
• Deficiency-
Rickets (osteomalacia), proximal muscle weakness,rhabdomyolysis,
paresthesia,ataxia, seizure, confusion, heart failure,hemolysis,
acidosis
• Toxicity-
Hyperphosphatemia

Iron Deficiency-
• The most common micronutrient deficiency in the world.
• Women of childbearing age constitute the highest risk group
because of menstrual blood losses, pregnancy, and lactation.
• The classic deficiency syndrome is hypochromic microcytic anemia.
• Glossitis and koilonychia (spoon nails) are also observed.
• Easy fatigability often develops as an early symptom.
• In children, mild deficiency insufficient to cause anemia is
associated with behavioral disturbances and poor school
performance

Iron Toxicity
• Iron overload occurs when habitual dietary intake is
extremely high, intestinal absorption is excessive, or
repeated parenteral administration occurs.
• Excessive iron stores usually accumulate in
reticuloendothelial tissues and cause little damage
(hemosiderosis).
• If overload continues, iron eventually begins to
accumulate in tissues such as the liver, pancreas, heart,
and synovium; the result is hemochromatosis.

Manganese
• Deficiency-Impaired growth and skeletal development,
reproduction, lipid and carbohydrate metabolism; upper
body rash.
• Toxicity
General: Neurotoxicity, Parkinson-like Symptoms
Occupational: Encephalitis-like syndrome,Parkinson-like
syndrome, psychosis, pneumoconiosis

Molybdenum
• Deficiency-Severe neurologic abnormalities
• Toxicity-Reproductive and fetal abnormalities
Chromium
• Deficiency-Impaired glucose tolerance
• Toxicity-Occupational: renal failure, dermatitis,
pulmonary cancer

NUTRITIONAL ABNORMALITIES
• Protein-energy malnutrition
• Anorexia nervosa and Bullemia
• Starvation
• Obesity
• Alcohol

PROTEIN-ENERGY MALNUTRITION
(PEM)
• Protein-energy malnutrition (PEM) occurs when
inadequate protein and/or calories are ingested to meet
an individual's nutritional requirements.
• PEM may be primary, as a result of inadequate food
intake, or secondary, as a result of illness.

• In developing nations, PEM is most often primary and
affects predominantly infants and children.
• It is the most important nutritional disorder and one of
the developing world's most important health problems.
• In industrialized nations, PEM is most often secondary
to other diseases and affects both children and adults.

CAUSES OF PROTEIN-ENERGY
MALNUTRITION IN HOSPITALIZED PATIENTS

Children under 5 years may present with:
Marasmus
• Marasmus is the childhood form of starvation, which is
associated with obvious wasting.
• The child looks emaciated, there is obvious muscle
wasting and loss of body fat.
• There is no oedema.

• The hair is thin and dry.
• The child is not so apathetic or anorexic as
with kwashiorkor.
• Diarrhoea is frequently present and signs of infection
must be looked for carefully.

Kwashiorkor
• Occurs typically in a young child displaced
from breast-feeding by a new baby.
• It is often precipitated by infections such as measles,
malaria and diarrhoeal illnesses.
• The child is apathetic and lethargic with severe anorexia.
• There is generalized oedema with skin pigmentation and
thickening .
• The hair is dry, sparse and may become reddish or
yellow in colour.

• The abdomen is distended owing to hepatomegaly
and/or ascites.
• The serum albumin is always low.
• The exact cause is unknown, but theories related to diet
(low in protein, and high in carbohydrate) and free
radical damage in the presence of inadequate
antioxidant defences have been proposed.

• A recent classification of severe malnutrition by the
World Health Organization makes no distinction between
kwashiorkor and marasmus, because their approach to
treatment is similar.
• The World Health Organization (WHO) classification of
chronic undernutrition in children is based on standard
deviation (SD) scores.

• Thus, children with an SD score between -2 and -3
(between 3 and 2 standard deviation scores below the
median - corresponding to a value between 0.13 and 2.3
centile) can be regarded as being at moderate risk of
undernutrition, and below an SD score of -3, of severe
malnutrition.
• A low weight-for-height is a measure of thinness
(wasting when pathological), and a low height-for-age is
a measure of shortness (stunting when pathological).
• Those with oedema and clinical signs of severe
malnutrition are classified as having oedematous
malnutrition.

• Starvation in adults may lead to extreme loss of weight
depending upon the severity and duration.
• They may crave for food, are apathetic and complain of
cold and weakness with a loss of subcutaneous fat and
muscle wasting.
• Infections such as gastrointestinal or bronchopneumonia
are common. The WHO classification is based on body
mass index, with a value less than 18.5 kg/m2: indicating
malnutrition (severe malnutrition if less than 16.0 kg/m2)
• Severely malnourished adults and children are very
susceptible to respiratory and gastrointestinal infections,
leading to an increased mortality in these groups.www.indiandental.com

Treatment of severe PEM whether kwashiorkor or
marasmus, is in three phases.
• 1. Resuscitation consists of correction of dehydration,
electrolyte disturbances, acidosis, hypoglycaemia and
hypothermia and also treatment of infections.
• 2. Start of cure consists of refeeding, gradually working
up the calories to 150kcal/kg with protein about 1.5 g/kg.
The dietary formulas, are usually based on dried
skimmed milk mixed with some flour or sugar and some
oil and given 5 to 6 times a day. Potassium,
magnesium and a multi-vitamin mixture are also needed.

• 3. Nutritional rehabilitation. After about 3 weeks the child
should be obviously better.
• The child is stronger, mentally bright and has a good
appetite but is still underweight for his or her age.
• During this stage of rehabilitation and catch-up growth,
the child should be looked after in a convalescent home
or by the mother who should have been educated about
nutrition and helped to obtain extra food. The diet should
be based on nutritious combinations of local, familiar
foods.

Mild to moderate PEM (the underweight child)
• For every florid case of kwashiorkor or marasmus there
are likely to be 7 or 10 in the community with mild to
moderate PEM.
• The great importance of mild to moderate PEM is that
these children are growing up smaller than their potential
and they are very susceptible to gastroenteritis and
respiratory infections, which in turn can precipitate frank
malnutrition.
• Mild to moderate PEM is probably the major underlying
reason why the 1 to 4 year mortality in a developing
country can be 30 to 40 times higher than in Europe or
North America. Official statistics record most of these
deaths as due simply to infections

• In areas where kwashiorkor is the predominant florid
form of PEM, subclinical cases have reduced plasma
albumin and sometimes other biochemical signs of
protein deficiency ('prekwashiorkor').
• Sometimes a child is seen who has adapted to chronic
inadequate feeding by reduced linear growth but who
looks like a normal child a year or two younger. This is
known as nutritional dwarfism.

UNICEF has drawn world-wide attention to five relatively simple and
inexpensive methods, abbreviated as 'GOBIF', which they believe
could halve the present death rate of children in developing
countries;
• G for growth monitoring. The mother keeps the simple growth chart.
• O for oral rehydration. The UNICEF formula (NaCl 3.5 g, NaH CO3
2.5 g, KC1 1.5 g, glucose 20 g or sucrose 40 g and clean water to 1
litre) is saving many lives from gastroenteritis.
• B for breastfeeding.supplemented by food after 6 months.
• / for immunisation. A child can be protected against measles,
diphtheria, pertussis, tetanus, tuberculosis and poliomyelitis.
• F for family planning

Anorexia Nervosa and Bulimia
Anorexia nervosa is a chronic disorder characterized
behaviorally by self-induced weight loss, psychologically
by body-image and other perceptual disturbances, and
biologically by physiologic alterations (e.g., amenorrhea)
that result from nutritional depletion.
Bulimia, derived from the Greek meaning "ox-eating," is a
behavioral disorder characterized by episodes of
overeating (binging), usually followed by acts to "undo"
the threatened weight gain with self-induced vomiting,
cathartic or diuretic abuse (purging), fasting, or
excessive physical activity. Bulimia nervosa particularly
describes patients who binge and purge.

Compared to anorectics, bulimics have normal body weight
and tend to have less distortion of body image. Bulimics
are more aware that their behavior,'although secretive, is
aberrant, and they may therefore be more accepting of
treatment.

Diagnostic features of Anorexia Nervosa
• Refusal to maintain body weight at or above a minimally
normal weight for age and height. (This includes a failure
to achieve weight gain expected during a period of
growth leading to an abnormally low body weight.)
• Intense fear of weight gain or becoming fat.
• Distortion of body image (e.g., feeling fat despite an
objectively low weight or minimizing the seriousness of
low weight).
• Amenorrhea. (This criterion is met if menstrual periods
occur only following hormone—e.g., estrogen—
administration.) '

Common Characteristics of Anorexia Nervosa and Bullemia

TREATMENT.
There are two goals in the treatment of patients with
anorexia nervosa:
• Nutritional restitution with alleviation, of medical
complications, and modification of the psychological and
environmental factors that promote anorectic behavior.
• No single treatment is superior, and a multidisciplinary
approach involving medical, psychiatric/psychological,
and nutritional (dietitians, pharmacists) personnel is
needed.

TREATMENT OF BULLEMIC PATIENTS
• The goal of treatment is to help the patient overcome the
urge to overeat.
• The currently most favored psychotherapeutic approach
consists of cognitive-behavioral.
• Antidepressants have been reported to be successful in
decreasing the binge activity.
• One recent study also indicates that combined
treatment using cognitive-behavior and antidepressant
therapy is superior lo antidepressant treatment alone.

Starvation
• Starvation means lack of food.
• It may be absolute starvation when nothing is taken or
may be food starvation and in that case water and
electrolytes are taken.
• Continued starvation leads to death which is delayed in
case of food starvation, i.e., when water and electrolytes
are supplied to the individual.

Physiological changes during starvation :
• i) Body weight decreases progressively. The loss is
mostly from the loss of subcutaneous fat and water.
There is also contribution due to loss from muscles, liver,
gut, spleen, kidney, etc. There is a minimum loss from
the brain and the heart.
• (ii) Carbohydrate metabolism is affected first as the
body store of carbohydrate runs out very quickly. But a
low normal glucose level is maintained by
gluconeogenesis.

• (iii) Fat metabolism supplies energy for the most part of
the starvation period. There is catabolism of body fats,
which leads to ketoacidosis
• (iv) Protein catabolism also occurs. Initially there is a
slow breakdown but after the carbohydrate store is
depleted there is more protein breakdown for
gluconeogenesis.

• (v) Blood : There is only a slight lowering of blood sugar
level. Plasma proteins are reduced. Ketone bodies
increase, so also the K+.
• (vi) Urine : Urine becomes more acidic. Excretion of
ketone bodies increases. There is increase in urinary
excretion of nitrogen and also of NH4 salts. There is
excretion of creatine.

Obesity
• Obesity means.increased body weight in respect to the
height and frame size of an individual.
• It is calculated on the basis of body mass index {BMI).
BMI =Body weight in Kg /(Height in metre)2
The value is 25 to 30. A value more than 30 is taken
as obesity in male and more than 28.5 in female.
• Skin fold measurements
• Various body circumferences,particularly the ratio of
waist to hip circumference.

Two types of obesity are described :
• 1)Secondary, where the obesity is due to some
endocrinological or CNS disease, like hypothalamic
syndrome/Cushing's syndrome/hypothyroidism etc,
• 2) Primary, where obesity cannot be explained due to a
frankly recognizable (endocrinal, CNS ) disease. The
vast majority of the obese persons belong to the primary
category.

Dangers of obesity.

Treatment
A.Medical
• Energy input is reduced, either by short bouts of
starvation(provided the person has no diabetes prone to
ketosis or peptic ulcer) or incessant reduced food intake.
High calorie foods like fat, sugar etc. must be stopped.
So called soft drinks often contain high calories. Various
diet courses can be implemented to reduce obesity.
• Drugs for various reasons are not popular. Thyroxine
(almost obsolete) and amphetamine (a banned drug in
India, because of its addictive properties) were once very
popular . Amphetamine, by acting on the hypothalamus
reduces appetite and is thus an well known anorexant.

B. Surgical
• Various surgical procedures have developed to tackle
extreme obesity One commonly done is, small intestinal
bypass surgery, where jejunum is anastomosed with a
loop of ileum near its terminal (so that a good deal of
small intestine is by passed). Result is ultimately
speaking, diminished energy input. Very often the patient
becomes a chronic sufferer from various after effects of
the operation.
• Role of exercise in the treatment of obesity should be
emphasised. All obese persons should increase his (her)
energy output by increasing the physical exercise.

ALCOHOL
• Alcohol is a popular 'nutrient' consumed in large
quantities all over the world. In many countries, alcohol
consumption is becoming a major problem.
• Ethanol (ethyl alcohol) is oxidized to acetaldehyde which
is then converted to acetate, 90% in the liver
mitochondria. Acetate is released into the blood and
oxidized by peripheral tissues to carbon dioxide, fatty
acids and water.

• Ethanol itself produces 29.3 kj/g (8 kcal/g), but many
alcoholic drinks also contain sugar, which increases their
calorific value. For example, one pint of beer provides
1045 kj (250 kcal), so the heavy drinker will be unable to
lose weight if he or she continues to drink.

Effects of excess alcohol consumption
• Excess consumption of alcohol leads to two major
problems, both of which can be present in the same
patient:
• Alcohol dependence syndrome .
• Physical damage to various tissues.

• In general the effects of a given intake of alcohol seem
to be worse in women. The following figures are for men
and should be reduced by 50% for women:
• 160 g ethanol per day (20 single drinks) carries a high
risk.
• 80 g ethanol per day (10 single drinks) carries a medium
risk.
• 40 g ethanol per day (five single drinks) carries little risk.

Alcohol consumption in pregnancy
• Women are advised not to drink alcohol at all during
pregnancy because even small amounts of alcohol
consumed can lead to 'small babies'.
• The fetal alcohol syndrome is characterized by mental
retardation, dysmorphic features and growth impairment;
it occurs in fetuses of alcohol-dependent women.

Effect of nutrition on dental health

• Carbohydrate
Deficiency: Caries rate generally decreases when
carbohydrate intakes decreases.
Excess: Increased frequency of intake of all
carbohydrates (except fibre) is a causative risk factor for
caries
• Fats
Deficiency: Angular cheilosis; pallor of lips and oral
mucosa; sore, burning tongue; atrophy/denudation of
filliform papillae; increased risk of candidiasis; glossitis.
Excess: No direct effect but fats may coat teeth and
protect them against cariogenic challenge

• Protein
Deficiency: Defects in tooth composition, eruption
pattern & resistance to decay; increased susceptibitlity to
soft tissue infection poor healing/tissue regeneration.
• Water
Deficiency: Dehydration and fragility of of epithelial
tissue; decreased muscle strength for chewing;
xerostomia; burning tongue.

Vitamin A
• The salivary glands are affected, often with blockage of
the major ducts, resulting in some degree of xerostomia.
The relevance of this to the bilateral, asymptomatic
enlargement of the major salivary glands occasionally
observed in malnourished children.
• Atrophy of the major salivary glands is the major
outcome, and that the glandular enlargement may result
from oedema and blockage of the secretory ducts due to
retinol deficiency-induced metaplasia of the epithelial
cells.
• Hyperkeratosis of the oral mucosa is usually seen in
severe cases of vitamin A deficiency.www.indiandental.com

VITAMIN-B
• Oral signs of B-complex deficiencies include
fissuring of the lips and angular cheilosis,
changes in colour of the oral mucosa and
dorsum of the tongue ranging from pallor to
inflammatory redness, and atrophy of the lingual
papillae.

Riboflavin (vitamin B2) deficiency
• In the mild deficiency state there is a glossitis which
begins with soreness of the tip and/or the lateral margins
of the tongue.
• The dorsum of the tongue may show patchy, irregular
denudations, but in many cases there is a characteristic
granular appearance due to 'bloating' of the fungiform
papillae which project over the markedly atrophied
filiform papillae.
• The lesions extend backward over the dorsum of the
tongue.

• In severe cases the tongue may become glazed and
smooth, owing to complete atrophy of all papillae.
• In many cases the tongue has a magenta color which
can be easily distinguished from cyanosis.
• Paleness of the lips, especially at the angles of the
mouth, but not involving the moist areas of the buccal
mucosa, is the earliest sign of the deficiency disease.
• The pallor which usually continues for days, is followed
by cheilosis, which is evidenced by a maceration and
fissuring at the angles of the mouth.

• The fissures may be single or multiple.
• Later the macerated lesions develop a dry yellow crust
which can be removed without causing bleeding.
• The lips become unusually red and shiny because of a
desquamation of the epithelium.
• As the disease progresses, the angular cheilosis
spreads to the cheek.
• The fissures become deeper, bleed easily and are
painful when secondarily infected with oral and/or skin
microorganisms.
• Deep lesions leave scars on healing. The gingival
tissues are not involved.

NIACIN DEFICIENCY
• In pellagra, there is an extensive burning sensation
throughout the oral mucosa.
• The tip and lateral margins of the tongue are reddened,
swollen, and sore in the initial stages.
• Saliva is profuse.
• The lips may present with very painful cheilosis and
angular stomatitis.

• Atrophy of the fungiform papillae usually precedes that of
the filiform papillae resulting in a rather stippled
appearance, but in the typical chronic cases seen in
impoverished communities, virtually the entire dorsum of
the tongue is devoid of papillation, and is smooth and
beefy red although parts of the tongue may be covered
by a grey membrane of degenerating cells and micro-
organisms.
• Superimposed acute necrotizing ulcerative
gingivostomatitis or Vincents infection involving the
gingiva, tongue and oral mucosa is a common sequelae.

PYRIDOXINE
• The oral lesions of experimentally induced pyridoxine
deficiency bear a striking resemblance to pellagrous
stomatitis.
• In some people with angular cheilosis, pyridoxine
administration will effect a cure when riboflavin and
nicotinic acid will not.

FOLIC ACID
• Atrophy of the filiform and fungiform papillae of the
tongue in folic acid deficiency associated with protein-
energy malnutrition.
• In folic acid deficiency, the dorsum of the tongue may
appear smooth and shiny due to almost complete
disappearance of the filiform and fungiform papillae
• Earlier stages show loss of only the filiform papillae with
'bloating' of the fungiform papillae at the tip and lateral
margins of the tongue.
• Studies in the human suggest that folate deficiency
increases gingival exudate flow.

• The gingival flow is an early predictor of gingival
inflammation, and the reported increased flow rate in
folic acid deficiency may reflect the affect of the latter on
the rapidly proliferating junctional epithelial cells.
• This clinical finding may not, however, be specific to
folate deficiency since the integrity of the oral mucosal
epithelium is vulnerable to deficiencies of several other
nutrients.
• Another important oral feature of folic acid deficiency is
impaired keratinization with increased susceptibility to
oral infections as evidenced by severe gingivitis and
necrosis of oral mucosa.

Vitamin B12
• Glossitis
• Tongue is inflammed ,beefy Red in colour,either in
entirety or in patches scattered over the dorsum or
lateral borders.
• Small shallow ulcers resembling apthous ulcers occurs
on the tongue.
• Characteristically with glossitis,glossodynia and
glossopyrosis,there is gradual atrophy of the papillae of
the tongue that eventuates in a smooth or bald tongue
which is often referred to as Hunters glossitis or
Moeller’s glossitis. And is similar to bald tongue of
sandwith seen in pellagra.

• Loss or distortion of taste is also reported.
• The fiery red appearance of the tongue may undergo
periods of remmission, but recurrent attacks are
common.
• On occasion the inflammation and burning sensation
extend to involve the entire oral mucosa ,but more
frequently the rest of the mucosa exhibits only the pale
yellowish tinge noted on the skin.
• A nonspecific persistent or recurring stomatitis of
unexplained local origin may be an early clinical
manifestation of pernicious anaemia

VITAMIN-C
• Deficiency of vitamin C predominantly affects
mesenchymal cells so that, in oral tissues, fibroblasts,
osteoblasts, and odontoblasts as well as their products
are defective. The ability of cells to form epithelial and
vascular basement membrane is severely restricted in
avitaminosis C .

• Typical intraoral features of infantile scurvy include
swollen, bleeding gingivae devoid of the normal stippling
and the enlarged tissue may cover the clinical crowns of
the teeth
• The process starts in the interdental papilla area but
spreads to involve the marginal and attached gingivae,
breakdown of periodontal collagen fibres, and resorption
of the alveolar bone resulting in a widening of the
periodontal ligament.
• The-interdental and marginal gingiva is bright red with a
swollen, smooth, shiny surface. In developed scurvy the
gingiva becomes boggv, ulcerates and bleeds.
• The color changes to a violaceous red.

• In almost all cases of acute or chronic scurvy the
gingival ulcers show the typical organisms, and the
patients have the typical foul breath of persons-with
fusospirochetal stomatitis.
• In the severe chronic cases of scurvy, hemorrhages into
and swelling of the periodontal membranes occur,
followed by loss of bone and loosening of the teeth,
which eventually exfoliate.

VITAMIN-D
• Rickets is characterized by poor maturation and
calcification of bones and teeth. Developmental
abnormalities in the form of hypoplasia and
hypocalcification occur in the dentine and enamel, and
tooth eruption is quite often retarded.
VITAMIN-K
• Avitaminosis K is characterized by diminished
prothrombin level in blood and increased tendency to
haemorrhage and bruising. The latter may affect the
gingivae.

MINERALS
• Fluoride
Deficiency: Decreased resistance to caries.
Excess: Disturbed amelogenesis;
mottled/stained enamel; enamel hypoplasia
(fluorosis)
• Iron
Deficiency: Angular cheilosis; pallor of lips and
oral mucosa; sore, burning tongue;
atrophy/denudation of filliform papillae;
increased risk of candidiasis; glossitiswww.indiandental.com

• Calcium
Deficiency: Incomplete mineralisation of teeth; rickets;
osteomalacia; osteoporosis; excessive bone resorption &
bone fragility; increased tendency to haemorrhage;
increased tooth mobility & premature loss.
• Copper
Deficiency: Decreased trabeculae of alveolar bone;
decreased tissue vascularity; increased tissue fragility

• Zinc
Deficiency: Loss or distortion of taste & smell acuity; loss
of tongue sensation; delayed wound healing; impaired
keratinisation of epithelial cells; epithelial thickening;
atrophic oral mucosa, increased susceptibility to
periodontal disease, candidiasis, xerostomia & caries if
deficient during tooth formation.
• Magnesium
Deficiency: Alveolar bone fragility; gingival hypertrophy
• Phosphorus
Deficiency: Incomplete mineralisation of teeth;
increased susceptibility to caries if deficient during tooth
formation; increased susceptibility to periodontal
disease due to effects on alveolar bone.www.indiandental.com

NUTRITION'S INFLUENCE ON MORTALITY
AND MORBIDITY

THANK-YOU

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