APP1IHI

r#'r
]IUIRIIIII]I
llietlheraru

Our Lady of Fatima University

Fatima College of Medicine
Department of Biochemistry and Nutrition
 TABLE OF GONTENTS
TOPIC PAGE
I APPLIED NUTR]TION - INTRODUCTION 1-27

il FOOD EXCHANGE 28-43

ilt INFANT NUTRITION 4,/-52

IV EATING DISORDERS AND OBESITY 53-67

V
NUTRITION IN PREGNANCY ANO 68-82
LACTATION
DIET THERAPY IN GASTROINTESTINAL
VI 83-93
DISEASES
DIET THERAPY IN DISEASES OF LIVER
vil AND PANCREAS 9,f - 105
DIET THERAPY IN FEVER AND
vlil 't06 - 122
INFECTIOUS DISEASES
MEDICAL NUTRITION iHERAPY IN
tx 123 -'t34
CARDIOVASCULAR DISEASES
MEDICAL NUTRITION THERAPY IN
x KIDNEY DISEASES 135 - 145
DIET THERAPY IN S=LECTED
XI
METABOLIq DTSEASES 146 - {60
DIETARY MANAGEMEN'IN_SURGICAL
xil CONDITIONS 161 - 171
xilt MEDICAL NUTRITION IN CANCER
PATIENTS 171 - 187

xlv CRITICALLY III PATIENTS 188-198

xv PROBLEM SOLVING 199 - 202

 APPLIED NUTRITION - INTRODUCTION

Nutrition has played a significant role in your life, even from before your
birth, although you may not always have been aware of it. And it will continue to
affect you in major ways, depending on the foods you selecl.

Everyday you make food choices that influence your body's health for
better or for worse. Each day's choices may benefit or harm your heafth only a
little, but when these choices are repeated over years and decades, the rewards
or consequences become ma.ior. That being the case, close attention to good
eating habits now can bring health benelits later. Conversely, carelessness about
food choices from youth onwards can contribute lo many chronic diseases
prevalent in later life, including heart disease and cancet.

- People decide whal to eat, when to eat, and even whether to eat in highly
personal on behavioral and social motives rather than on
ways, often based
awareness of nutrition's importance to heahh.

FACTORS THAT AFFECT FOOD GHOICES:

1. Personal preference you like the food

-
The number one reason people choose foods is taste - they like certain
flavors like sweetness of sugar and the savoriness of salt.

2. Habit - the food is familiar; you always eat them

Peode sometimes select foods out of habit. Ex. They eat cereal every
morning because they have always eaten cereal for breaKast

3. Ethnic heritage or tradition - people eat the foods they grew up eating. Every
country, and in fact every region of a country, has its own typical foods and
ways of combining them into meals.

4. Social interactions - Mosl people enjoy companionship while eating. Meals are
social events and the sharing of tood is part of hospitality.

5. Availability, convenience and economy - people eat foods that are accessible,
quick and easy to prepare and within their financial means

6. Positive and negative associations - people tend to like foods with happy
associations.

7. Emotional comfort - some people cannot eat when they are emotionally upset;
others may eat in response to a variety of emotional stimuli. Eating in
response to ernotions can easily lead to overeating and obesity.
8. Values food choices may reflect people's religious beliefs, political views or
-
environmental concerns. Ex. Christians forego eating meat during Lent.

9. Body weight and image - people select certain foods and supplements that
they believe will improve their physical appearance and avoid those that they
believe might be detrimental.

'10. Nutrition and health benefits

-
many consumers make food choices that will
benefit health. Food manufacturers and restaurant chefs have responded to
scientific findings linking health with nutrition by offering an abundant
seleclion of health-promoting foods and beverages.

DEFINITION OF TERMS

NUTRITION -it is the science of foods and the nutrients and other substances
that they contain, their actions within the body and interaction and balance in
relation to health and diseases.
Nutrition includes the processes by which organisms ingest, digest,
absorb, transport, utilize and excrete food substances for maintenance of its
functions and for grolvth and renewal of its components.
Nutrition is best defined as the utilization of toods by living organisms.

-
FOOD it constitutes all solid and liquid materials which when taken into the
body serves to nourish , build, repair and supply energy or regulate body
processes.

NUTRIENTS - are chemical substances in food that nourish the body by

providing energy, materials for building body parts and factors that regulate
necessary chemical processes in the body.

ESSENTIAL NUTRIENT - it is a substance which the body cannot synthesize in

sufticient arnounts to meet the demands of the body and therefore must be
supplied in the diet.

The study of human nutrition can be divided into three areas:

1) undernutrition - a deficiency of calories or one or more essential

nutrients; a state of physical health resulting from long-standing dietary
practices that do nol meet the needs of the body.

2) overnutrition - resuhs form long-standing dietary practices that are

excessive of the normal needs of the body.

3i ideal or optimal nutrition - adequate intake and utilization of essential

nutrients, with reserves for energy and ability to fight diseases.
 NUTRITIONAL STATUS (NUTRTTURE) _
is rhe condition of the body resulting
rrom the consumption and utilization of nutrients.

fqALTH.-.jt is the state of comptete physicat, mentat and sociat welt_being and
not merely the absence of disease.

MALNUTRITION - it is a pathological state resulting from

a relatjve lack or
absolute deficiency or excess of one or more or tre isseniiar
nii-rr"nt.. rn"ru
are four types of malnutrition:

1) Undernutrition
2) Speciric nutrient deficiency
3) Overnutrition
4) Nutrient imbalance

DIET THERAPY - it is the science that deals with the use

of foods.to hetp in the
recovery from specmc diseases.

THERAPEUTIC DIET - it is a normat

_diel that is ji""u"".'
quantitativet moditied to help in the recou"ry trorn
quatitativety and/or
" "p""m"
I9.l$L -9llt -
nu rents necessary
it is an adequare diet that furnishes rhe body w h a the
for the gro*h and repair of tissues ani the normar
functioning of the organs. The body's needs.are vury
O"nnie. ft i""Os protein for
building and repairing body tissue; carbohydrates
and fat" lo, pro-u-iJng n."t
energy; vitamins which are indisnensable ln regulating
OoOy fln"tiln"; "nO
tor making bones and teeth strong, majntainin; the pi#ii."aroi'"r ,nin.r"f"
Jtuids and.regutatng body procestes. water, itrictr tnu u"ov
'also included in the adequate diel. For optimum
i" J"".niiliiI'"u"ry i"
t
thal supplies lhe nutrients in @rrect amounts and proportionl
""lit --'
, tn" U"Oll ,r.t
-- nave"ar,
fooO

Modifications of a normal diet

1. change in caloric content

2. change in protein conten{
3. change in carbohydrate content
4. change in fat content
5. change in consistency
6. chang€ in salt content
7, change in the number and frequency of meals
8. omission of certain foods

3
lndications for increasinq the caloric content of diet:

1. groMh
2. pregnancy/laciation
3. convalescence
4. marasmus/kwashiorkor
5. Hyperthyroidism
6. Fever/lnfections

lndications for increasing the protein content of a diet would be the same as
those mentioned for caloric increase, including some diseases as nephrosis,
acute glomerulonephritis, acute hepatitis, surgical conditions and others.

Ways of increasing the caloric conlent of a diet:

1) Serve jelly and jam along with bread and butter or marga;ine; butter
breakfast toast when it is hot because more butter can be used.
2)Add sugar to fruit juice or milk; a teaspoon (tsp) of sugar gives about 16
calories
3) Serve gravy on meat and potatoes
4) Serve mayonnaise, oil and salad dressings whenever possible with
sandwiches, salad and vegetables.
5) Along with breaKast egg, seNe bacon, ham or sausage
6) Add ice crearn or whipped cream to desserts and milk beverages
7) Serue cream soups instead of clear bouillon

CALORIE ALLOWANCE

Calories are needed to keep the body warm and to furnish energy for
biological cell work, e.g. mechanical work of muscle contraction, chemical work
of synthesis and osmotic work as in active transport mechanisms. lt is possible to
estimale roughly the calories required by a person in health and in disease.
App€tite is a good checking device provided by nature, and in most normally
active persons it regulates the weight with surprising accuracy. However, the
appetile cannot be trusted nor depended upon in diseases and in obesity.

The averag€ adult afebrile Filipino patient at bed rest with minor injury or
illness can maintain caloric balance by an intake of about 1600 Cal. per day.
Severe injury or illness will increase the needs. ln diseases wherein there is a
tendency to kf,se protein, the administration of 50 to 100 per cent more calories
than the calculated requirement has, at times, made it possible to maintain
nitrogen equilibrium. For ambulatory patients, the factors for determining caloric
requiremenls are their levels of activity and the appropriateness of their present
weights-
 For practical purposes, the energy requirement of an individual may be
determined by eilher (1) calculating the number of Calories per kilogram per day
or (2) calculating the per cent increase over basal demands. Students of Applied
Nutrition are encouraged to use the second method because it allows
appreciation of the various factors that demand the utilization ot energy.
Determinations are made based on desirable body weight.

Steps involved in the determination of the energy requirement of an individual:

'1) Determine desirable body weight (DBW) from available tables or by

using the Thannhauseas method:

Height in cm mrnus 100 = KDBW (DBW in kg)

Subtract l0% for Filipinos and other nationals of smaller frames

2) Determine BMR: 1 Cau hr /KDBW x 24 hrs.

3) Determine co.rected BMR (CBMR) for sleep by deducting

1o%/KDBWhr of sleep from the calculated BMR

4) Determine energy for physical activity (PA). Coope/s method is based

on a fixed p€r cent of the BMR as follows:

B€d patient = 10 % of corrected BMR

Sedentary activity = 30 Yo
activity
Light = 5O Yo
Moderate activity = 75 o/o
Heavyactivily = 100 %

5) Determine energy for SDA (specific dynamic action) of foods:

6 to 10 % of (GBMR + Physical activity)

6) cBMR + PA + SDA = TER [fotal Energy Requirement)

7) Translate TER into grams of CHON (Protein), CHO (carbohydrates)
and Fat per day based on the dietary prescription and on the
respective physiological value

Sample computation: A Filipino construction worker, 35 yeaIs of age, 5 feet 6

inches tall, engaged in heavy activity:

Nutrient distribution in % of TER: Protein = 15 % CHO = 60 % Fal= 25 Yo

1) DBW: 5 Feet,6 inches = 66 inches x 2.54 cm = 167.64 cm

167.64 mirus 100 = 67.64 kS - 10 7o = 60.88 o.61 kS. 5

 2)BMR: 1 x 24 hrs x 61 kg = 1464 6"'ot."
3) Calculate for cBMR (corrected BMR) by deducting 1o%/KDBW /hr of sleep
from the calculated BMR: e.g. slept for 8 hours

= l0% x 61 (KDBW) x I = 48.8 or49 Calories

.1464
CBMR = - 49 = 1415 Calories

3) Physical activity (PA): CBMR x 100 % = '1415 Calories

4) SDA: (1a15 + 1415)x 10% = 283 Calories

5) TER='1415 + 1415 r 283 =3113 Cal

To transtate the TER into grams of prolein, carbohydrate and fai:

3113x 15% = llTgrams of protein per day

4

31'13 x 60% = 467 grams of CHO per day

4

3113 x 25o/o = 86 grams of fat per day

o

. Grams of each nutrient per day may be rounded off.

THE DIET PRESCRIPTION

The diet prescription in nutrition serves the same purpose as the drug prescrip-
tion in medicine. lt designales the type, amount, frequency and route of food
ingestion just as the drug prescription identifies the drug name, dosage,
frequency and route of administration. The diet prescription includes the daily
caloric requirements based on the individual's desirable body weight and normal
activity plus the amounts and forms of needed protein, fat, carbohydrate,
mineralq vitamins and other substances such as fiber and fluids.

PROTEIN ALLOWANCE

Functions of proteins:
- maintenance of groMh
- regulation of body processes
- source of heat and energy
- contribules to numerous essential body secretions
- maintains normal osmolic relations among body fluids 6
TIte recommended daily allowances for protein are as follows:

-lnfants(0-2yrs) 3.0 - 2.5 gm/KDBW

- Chibren ( 2- '!0 yrs) 2.0 gm/KDBW
- Adolescents ( 11 - 19 yrs) = '1.5 gm/KDBW
- Adults '1.0 gm/KDBW

RENI for proteins: 10 - 15 % of TER or TCR

The bed patient who requires more than 10 days hospitalization; the patient
losing protein from burns, exudates, ascites or renal diseases, and the patient
who is not forming sufficient protein in hepatic disease will require an increase of
protein. Therefore, optimum rather than adequate protein levels are
recommended. Severe depletion of body protein can lead to prolonged
convalescence, poor wound healing, and increase in complications after surgery,
like anemia, and increased susceptibility to infections.

Protein foods of high biological value are usually the most expensive, e-g. meat,
eggs, fresh milk and poultry. Thus, there is often a tendency among the low
income groups lo consume less animal protein than the recommended amount.
Studies in the Food Nutrition Research lnstitute have led to the description of the
typical Filipino diet as high in carbohydrate, marginal in protein and low in
fat. The traditional Filipino diet of rice and fish exemplilles amino acid
supplementalion, where the limiting amino acid in rice which is lysine, is
supplemented by fish.

CARBOHYORATE ALLOWANCE

Functions of carbohydrates:
- provide fuelfor energy
- protein sparer
- allorrvs normal fat metabolism
- maintains functional integrity of the CNS
- precuFor of nucleic acid, connective tissue matrix
- facilitates excretion of chemical and bacterialtoxins
- aid in normal elimination of wasle materials
- promote groMh of coliform bacteria in the GIT

The allowance recommended for carbohydrate is 4 - 6 gms per KDBW per day
or roughly 50 - 70 % of the TER (average of 600/o). lt is the major source of
energy and if the amount of carbohydrate is insufficient to meet the energy
demands, the organism will utilize fat as the next fuel of priority which could lead
to ketoacidosis. lt is also a protein sparer, e.9., less protein is utilized for energy if
adequate carbohydrate is present to supply the energy needs. lts cellulose
content promoles regular bowel movement, thereby relieving constipation.
FAT ALLOWANCE

Functions of Fats:
- provide energy
- serve as shock absorber
- protection for nerves
- strenglhens membrane structure
- body insulator
- Protein sparer
- carrier of fat-soluble vitamins
- lubricant for GIT

Fat provides I calories for every gram oxidized, more than twice that provided by
the sarne amount of either carbohydrate or protein which gives only 4 calories. lt
is therefore a very good source of energy without bulk. The allowance (RENI) for
fat is I - 2 grams per KDBW or roughly 20 30 % of TER per day for all ag€
-
groups, except for infants which is 30 40 % following the FAO/WHO
-
reco{nmendation.

Recommended Energy and Nutrient lntake (RENI)

- The revised edition of the dietary standards is changed from RDA to

REM to emphasize that the standards are in lerms of nutrients, and
not foods or diets. RENIS are defined as levels of intake of energy and
nutrients which, on the basis of cunent scientific kno$,/ledge, are
considered adequate for the maintenance of health and well being of
nearly all healthy persons in the population.

MINERALS

- lhey are inorganic elements occurring in nature. Allhough minerals make

up only a small proportion of body tissue, they are essential for groMh and
normal functioning. About 4 o/o of the body weight is made up of minerals. These
elements remain largely as ash when plant or animal tissues are burned.
Calcium and phosphorus account for 3/. of the mineral elements in the body.

- Many of the essential minerals are widely distributed in foods, and most
peopb eating a mixed diet are likely to receive adequate intakes.The amounts
required vary from grams per day for sodium and calcium, through milligrams per
day (e.9. iron, zinc), to micrograms per day for the trace elements.

General functions ot minerals:

t. Structural - hard skeletal structures contain more of Ca, Mg and Phosphorus.

2. Aci+base balance
I
 a) Sodium - major extracellular cation
b) Chloride - major enracellular anion
c) Potassium - major intracellular cation
d) Bicarbonate - major intracellular anion

Neuromuscular irritability - normal generation and conduction of nerve

impulses - Ca, Mg, Na, K

4_ Cofactor in enzyme catalysis

a) Chloride in amylase
b) Zinc in carbonic anhydrase
c) Copper in cytochrome oxidase
d) lron in cytochromes
5. As constituents of hormones and olher compounds involved in regulatory
functions:
a) iodine - required lo produce thyroxine
b) lron - required in the synthesis of hemoglobin
c) Chromium - involved in the production of insulin
d) Copper - an integral part of cytochrome oxidase
e) Selenium - a component of glutathione peroxidase
f) Cobalt - a constituent of vitamin B12
g) Sulfur - a component of the amino acids cysteine and methionine
h) Phosphorus - a constituent of the sugar phosphate linkage in DNA and
RNA

Classification of minerals accordino to their function:

"Paqe48O)Function Minerals
Structural function Calcium, maonesium, Dhosohate
lnvolved in membrane funclion Sodium, potassium
Function as prosthetic aroups in Cobaft, copper, iron, molybdenum,
enzYmes selenium. zinc
Regulatory role or role in hormone Calcium, chromium, iodine,
action magnesium, manganese, sodium,
potassium
Known lo be essential, but function Silicon, vanadium, nickel, tin
unknown
Have effects in the body but Fluoride, lithium
essentiality is not established
May occur in toods and known to be Aluminum, arsenic, antimony,
toxic in excess boron, bromine, cadmium, lead,
mercury, silver. strontium

s
 Minerals are divided into two groups:
A. Macrominerals
-Catjons: Calcium, magnesium, sodium, potassium
- Anions - chloride, phosphorus, sulfur

B. Microminerals or trace elements

- Cations - lron, zjnc, ,manganese, copper,
cobalt, nickel, selentum,
molybdenum, chromium, silicon, tin, vanadium -
- Anions - lodlne and Fluoride

CALCIUM - it is the most abundant mineral in the body;

most abundant cation in
the human body; 1.5 _ 2% of body weighf '

Functions; - catcium phosphate in the form of hydroxyapatite

is the principal
component of the hard structures of bones and teeth'
- Required in the conversion of prothromUin
to iirromUin'in olooO
coagulation
- increases the permeability of cell membranes
- activates a number of enzymes including
lipase
- Neuromuscular iffitability
Hypocalcemia _ increase neuromuscular iritabilitv
Hypercalcemia _ decrease neuromuscur"i iriit"uiriry

- required in the absorption of Vit 812

- mediates excitation and contraction of muscle fibers
- hetps in the transmission of nerveimfui";;- '-- -
RDA: Adult- 800 rng/day; pregnancy and tactation _
.. 12OO mg/day
Calcium deficiencv causes:
- Rickets - in chitdrcn
- Osteornalacia in adults
- . Osteoporosis _- usually it is an asymptomatic disorder and
its presence
rs usually not detected until a fracture
oc"u" ,uny V*rs ui.i its onset.
PHOSPHORUS - it accounts fo|l % of body weight.
About 85% is inorqanic
combined with catcium as the insotubte
U"n*'""i'ii""if,. r"
"pifit" "i z,i.-- -"" '-""
bones, the proportion ot calcium to phosdm."i"
-
RDA: same as calcium

Functions: - phosphorus is a constituent.of the

sugar phosphate linkage in the
structure of DNA and RNA
- Phospholipids are constituents of cell membranes.
thus
regulating the transport of soiutes in anO ort
_
- phosphorytation is a key reaction in
oiif,.
,"nv rn"tuooii"-pili.""""
""ff
- Phosphorus compounds are essentiat f- tf," aLrr*""""J
controlled rel€ase of energy
't0
 - lnorganic phosphates in lhe body fluids constitute an important
buffer system (acid/base balance)
- bone and teeth formation

MAGNESIUM - adult body contains about 20 - 35 grams of magnesium. 60% is

present as phosphates and carbonates at the surfaces of bones.
The ratio of magnesium to calcium is about 3 :1

Functions: - Magnesium is a catalyst for various biologic reactions

- lnvolved in neuromuscular transmission
- Acts as a direct muscle depressant
- has effect on the cardiac conduction system
- antagonizes the effect of calcium in the CVS and CNS
RDA: Men - 350 mg/day
Wornen - 3o0 mg/day
Pregnancy and lactation - 450 mg/day

Deficiency: Hypornagnesemia - increase neuromuscular irritability;

manifested by weakness, muscle tremor, paresthesias, convulsive
seizures, cardiac arrhythmia, depression and delirium

SULFUR - lt is a component of the amino acids cysteine, cystine and

methionine; and once built into a protein strand, cysteine can link to
another by way of sulfur-sulfur bridges. The bridges stabilize the
protein structure
- Skin, hair, and nails contain some of the body's more rigid proteins
and these have high sulfur contents.

RDA: There is no recommended intake for sulfur because most of lhe

required dietary sulfur is provided by the dietary protein.. No
deficiencies are known. Only if a person lacks protein to the point of
severe deficiency will he lack the sulfur-containing amino acids.

SODIUM - major extracellular cation

- related to hypertension

Functions: - Water balance - Sodium acts like the other electrolytes,

especially potassium, in the intracellular fluids to maintain
proper osnotic and water balance.
- Acid/base balarrce - Sodium balances the acidic chloride and
bicarbonaie ions
-Transmission of nerve impuls€s - together with potassium,
sodium crea{es electrical charges on the nerve cell
rn€mbrane which passes impulses along the nerves.
11
 - Contraction of muscles - Sodium has a relaxing effect on
muscle conlractions, working to balance those ions that
stimulate muscle contraction-
- Glucose absorplion and cell permeability - exchange of sodium
and potassium across cell walls make the cell membrane
more p€rmeable to other substances.

RDA: No RDA has been set for sodium because there is no shortage in the
diet. lntakes of 1,100 to 3,300 mg per day ate considered safe and
adequate for normal adults.

POTASSIUM - maior inlracellular cation

- deficiency is usually a complication of diuretic drugs
- excess is related to renal failure

Functions - Potassium maintains osmotic pressure, water balan6e and

acid/base balance
- Potassium influences the transmission of nerve impulses and the
contraction of muscles, including the heart
- Energy metabolism - Potassium is a catalyst for reactions taking
place in the cell
- Glycogen synthesis and protein synthesis - Potassium bound to
phosphate is required for the conversion of glucose to
glycogen; it is also needed for the synthesis of muscle proteins
- Blood pressure - Potassium contributes to the maintenance of
normal blood pressure

RDA: No RDA has been set for potassium because it is abundant in the food
supply so deficiency does not occur under normal circumstances.

The followinq mav cause potassium deficiencv (hvpokalemia)

- use of diuretics
- severe vomiting, diarrhea, laxative
- some forms of chronic renal diseases
- diabetic acidosis
- severe protein-calode malnutrition
- adrenal gland abnormalities

The followino mav cause hiqh ootassium levels in the blood

(hyperkalemia):
- kidney failure
- abnormal adrenal function
- severe dehydration
- increase in potassium intake as with excessive use of
potassiurn supplements
't2
CHLORIDE - malor extracellular anion where it is found mostly in association
with sodium
- important in the regulation of acid/base balance, osmotic pressure
and water balance
- in the stomach, chloride is part of hydrochloric acid, which
- maintains the strong acidity of the stomach. One of the most serious
consequences of vomiting is the loss of acid from the stomach, which
upsets the acid/base balance

RDA: No RDA has been set for chloride. lt is never naturally lacking in the
diet. lt abounds in foods as part of sodium chloride and other salts.

IRON - lt usually occurs in foods in the ferric form bound to protein or organic
acids. Before absorption can occur, the iron must be reduced to the
ferrous form (a process that is enhanced by ascorbic acid). .
- 20 - 25 Vo - slored in the liver and spleen

Functions of iron:
- As a component of tEmoglobin and myoglobin, it is required for
02 and CO2 transport.
- As a component of cytochromes and nonheme iron proteins, it is
required for oxidative phosphorylation.
- As a component of the essential lysosomal enzyme myeloperoxidase, it
is required for proper phagocytosis and killing of bacteria by neutrophils.

RDA: Normal adult males - 10 mg/day

Menstruating females - 15 mg/day
' Pregnancy and lactation - 30 mg/day
Children: 1 -3yrs= 8 mg/day
4-6yrs=9mg/day
7-9yrs=11mg/day
10 - 12 yrs ='13 mg/day

The best known symptom of iron deficiency is a microcytic, hypochromic

anemia. lron deficiency is also associated with decreased immunocompetence.

IODINE - 70 - 80% of the iodine in adults is concentrated in the thyroid gland,

where it is involved in the biosynthesis ofthe thyroid hormones
triiodotl'ryroft ine and tlryroxine.

Functions: - required for the synthesis of thyroid hormoneswhich function in

regulating the basal metabolic rate of adults and the growth and
development ot children.
- required for the efficient synthesis of proteins by ribosomes

RDA: Adults - 10o- 150 micrograms per day

Children - 90 micrograms per day 13
lodine deticiency is one of the major health problems in the Philippines. The
richest food sources of iodine are seafoods.

ZINC - second to iron as the most abundant trace elemenl

Functions: - it is a cofactor for many enzymes. Over 300 zinc metalloenzymes

have been described to date.including a number of regulatory
proteins and both RNA and DNA polymerases.
- it is present in gustin, a salivary polypeptide that appears to be
necessary for normal development of taste buds
- it is necessary for the binding of steroid hormone receptors and
other transcription factors lo DNA
- it is absolutely required for normal spermatogenesis, fetal growth
and embryonicdeveloPment
- it stabilizes membrane structure by preventing lipid peroxidation and
reducing free radical formation
- it is necessary for Vit A metabolism

RDA: 10 - '15 mg/day

Manifestations of zinc deficiencv:

- Zinc deficiencies in children are usually marked by poor groMh

and impairment of sexual development.(dwarfism and hypogonadism)
- ln both children and adults, zinc deficiency results in poor wound
healing
- decreased taste acuity o. taste sensation
, - night blindness due to impaired Vit A metabolism

Zinc is a relatively nontoxic element. However, it can be toxic if consumed

in large enough quantities. Toxicity from ingestion of zinc can occur from
misuse ot supplements. Acute zinc toxicity after oral ingestion can cause
vomiting fever and respiratory distress- Chronic large doses of zinc may
depress immune function and cause hypochromic anemia as a result of
copPer deticiencY.

COPPER - the body contains around 50 to '120 mg of copper. High concentra-

tions are found in the liver, brain, heart, spleen, kidney and blood

Functions:1) it is a cofactor of several metalloenzymes including cytochrome c

oxidase, dopamine-Fhydroxylase, superoxide dismutase, lysyl
oxidase, A
vdesaturase, among others.

tySILgIlCASg is necessary for the conversion of certain lysine residues in

collagen and elastin to allystne, which is n€eded for cross-linking.

14
 AlgsglUlesg is responsible for converting stearic acid to oleic acid. This
may be responsible for the fact that dietary stearic acid does not have the
cholesterol-raising property of the other saturated fatty acids.

2) the copper-containing enzyme ferroxidase is necessary for

conversion of iron from the terrous state (in which form it is
absorbed) to the ferric state (in which form it can bind to the plasma
protein transferrin)

Excess intake of either copper or zinc interferes with the absorption of the
other.

RDA:1.5-3mg/day
Manifestations of cooper deficiencv includes:

- demineralization of bones I due to defects in elastin and

- fragility of large arteriesformation I collagen fomation
- leucop€nia
- anemia - due to defecl in iron metabolism (ferroxidase)
- hypercholesterolemia - may be related to increases in the ratio of
saturated to monounsaturated fatty acids due to reduced activity of
A e desaturase.

Diseases associaled with abnormalities in copper metabolism:

1) Menkes' syndrome - Kinky or Steely hair syndrome

- a relatively rare X-linked hereditary disease associated with a
defect in copper transport

a Wilson's disease - an autosomal recessive disease associated with

abnormal accumulation of copper in various tissues.

CHROMIUM - it functions primarily as a component of glucose tolerance tactor

(GTF), a naturally occurring coordination complex between
chromium, nicotinic acid, and the amino acids glycine, glutamate,
cysteine, or glutathione. GTF potentiates the effecls of insulin by
facilitating its binding to cell receptor sites.

- the chief symptom of chromium deficiency is impaired glucose

tolerance, as a result ofthe decreased insulin effectiveness.

- RDA: 50 - 200 micrograms for a normal adult

15
SELENIUM -functions primarily in the metalloenzyme glutathione
it
peroxidase, which destroys peroxides in the cytosol. Both selenium and
Vil E appear to be necessary for efficient scavenging of peroxides-
- Selenocysteine is also found in the deiodinase enzymes which
mediate the deiodination of thyroxine to the more active triiodothyronine.

- Selenium deficiency affects the heart (Keshan's disease). A severe

deficiency can cause heart failure; a chronic, mild deficiency enlarges
the heart and impairs its function.
- High doses of selenium are toxic, causing loss of hair and nails,
lesions of the skin and nervous system, and possibly damage to the
teeth.
- RDA: 31 micrograms/day

FLUORIDE - it is known to strengthen bones and teeth. When bones and teeth
become calcilied, lirsi a crystal called hydroryapatite ss forme.d from
calcium and phosphorus- Then fluoride replaces the hydroxyl positions of
the crystal, rendering it insoluble in water and resistant to decay.
15
- Drinking water is the usual source of fluoride. Where fluoride is lacking
in the water supply, the incidenc€ of dental decay is very high.
Fluoridation of community waler where needed, to raise its fluoride
concentration to Ipart per million, is thus an important health
measure. lf this can not be done, fluoride-containing toothpastes can
be used or fluoride tablets are also available.

- RDA: An adequate intake for fluoride (on the basis of protection

against dentalcarries) has been set as 3.'1 - 3.8 mg/day in adult
' females and males, respectively.

- An intake of 10 mg/day for prolonged periods results in mottled and

pitted defects in tooth enamel and brittle bone (skelelal fluorosis).

MANGANESE it is a component of pyruvate carborylase and probably other

-
metalloenzymes as well like hydrolases, decarborylases, and
transferases.lt is a cofactor for glycoprotein and proteoglycan
synthesis
- it is required for normal bone groMh and development, normal
lipid metabolism, reproduction and regulation of nervous irritability.

MOLYBDENUM -
it is a component of xanthine oxidase. Excess molybdenum
causes goutlike symptoms in human beings.
- it interferes with copper metabolism by diminishing the efficiency of
copper
- deficiency may result in skeletal and brain lesions
- minimum daily requirernent is estimated to b€ 25 micrograms per day

COBALT it is a constituent of vitamin 812 '16

-
VITAMINS- they are a group of chemically unrelated organic nutrients
thal are
ess€ntial in small quantities for normal metabolism, -groMh and physical
wellbeing. These nutrienls must. be.obtained througtiOi"t sin"e
iney.re
eithe[ not synthesized in our bodies or are syn"tnesleJ in- inadequate
amounls. Our bodies use vitamins to make substances that
participants in many of the chemical reactions in our are vital
cells, reactions
essential for the proper functioning of the cells.

Two maior qroups of vitamins:

A. WateFsoluble vitamins - B mmplex vitamins and Vit C; fhey function mainty

as enzyme cofaclors.

B. Fat-soluble vitamins - Vitamins A,D,E,K; these are hydrophobic

compounds
that can-be absorbed efficien y only when there is normal faiaUioiption.
f_ifre
other liFids, they are transported in the btood in lipoproteins oritti-OLA
to
specmc binding proteins.

VITAMIN B-l - Thiarnine, Anti-beriberi vitamin, Anti-neuritic vitamin

- most aclive coenzyme form: Tpp (thiamine diphosphate
. or
pyrophosphate
- RDA_ is direc y proportional to caloric or carbohydrate
intake
(1 - 1.5 mg/1000 Catories)

Thiamine acts as coenzvme in:

-, 1) Decarboxylation of pyruvate to acetyl CoA

2) Decarborylation of o-ketoglutarate !o succinyl CoA _
Krebs cvcle
3) Transketolase reacfion of the HMp shunt
4) metabolism of nerve lissues _ TTp _.morale vilamin"
Thiamine triphosphate CfTp) has a role in nerve conduction:
it
phosphorytates, and so activates, a chtoride
channei ilih";;rvu
membrane.

Thiamine deficiencv can result in 3 distinct svndromes:

1. Beriberi -
a chronic peripheral neurjtis which may or mav not be
associated with heart failure and edema
2. Shoshin beriberi ar acute pemicious (fulminating) Lriberi_
heart failure
metabolic abnormatities predominate. witn6ut
^ .and
J-
ferip;"r;i;;;i;
werntcKe encephalopathy with Korsakoff psychosis _ associated
especially with alcohol and narcotic abuie

Deficiencv manifestations (Beriberi)

?) Severe muscle weakness
- skeletal and cardiac muscles
acidosis
2) lactic
fi
 3) pentosemia/pentosqria
4) neurological symptoms
5) decreased 02 uptake by brain tissue

To determine the slatus of thiamine in the body, the enzyme to be

assayed is ervthrocvte transketolase.

VITAMIN B-2 - Riboflavin, Lactoflavin

- coenzyme forms: FMN , FAD
- General function: coenzyme for oxidation/reduction reactions;
coenzyme for hydrogen transfer reactions
- RDA: 1.2 - 1.7 mg/day for the normal adult
2.O - 2.5 mglday lor pregnant and lactating women

Riboflavin acts as coenzvme in:

1) Krebs cycle - succinate dehydrogenase step

2) decarborylation of pyruvate to acetyl CoA
3) decarboxylation of o-ketoglutarate to succinyl CoA
4) conversion of tryplophan to niacin

Deficiency manifestations of riboflavin

1) cheilosis or angular stomatitis

2) glossitls - magenta tongue
3) seborrheic dermatitis
4) corneal vascularization
5) photophobia

To d€termine the status of riboflavin in the body, the enzyme lo be

assayedis@.

VITAMIN B-3 - Niacin, nicotinic acid, Pellagra-preventive factor

- it is not strictly a vitamin since it can be synthesized in the body
from Tryptophan
- coenzyme forms: NAD/NADH, NADP/NADPH
- General function: coenzyme for oxidation/reduction reactions
- should not be given in latge doses to patients with allergies
- RDA: '13 - 19 mg/day

Niacin acls as coenzYme in:

1) Krebs cycle -
malate dehydrogenase, isocitrate dehydrog€nase,
q-ketoglutarate dehdyrogenase
2) oxidative deamination of glutamic acid - glutamate dehydr*un"""
.,
u
 3) Glycolysis - glyceraldehyde-3-Po4 dehydrogenase
4. Pyruvate to acetyl CoA - Pyruvate dehydrogenase
5) Pyruvate to lactate and vice versa
6) HMP shunt - NADP/NADPH

Deficiency manifestations of Niacin = Pellaora

1) dermatitis - Casal's necklace, Gloves and stockings lesions

2) diarrhea
3) dementia

lMAUlN_E$ - Pyridoxine, Pyridoxal, Pyridoxamine

- Amino acid metabolism vitamin
- Most active coenzyme form - pyridoxat phosphate
: Should be given in large doses to patients with tuberculogis
receiving INH therapy
- RDA is directly proportional to protein intake
- Enzyme assayed to determine the status of Vit BO in the body -
erythrocyte aminotransferases,

Functions of Vitamin 86:

1) amino group carrier in transamination

2) coenzyme for heme synthesis - d-ALA synthetase
3) coenzyme in the conversion of Trp to niacin
4) coenzyme in the conversion of Trp to serotonin
5) coenzyme in the decarboxylation of Glu to GABA
6) cofactor of glycogen phosphorylase

Deficiency manifestations of Vit 86

1) Microcytic, hypochromic anemia

a Pellaqra-like symptoms: diarhea, dermatitis, dementia
3)GlT manifestations - nausea, vomiting, abdominal pain, diarrhea
4) convulsive seizures
5) oxalaie stone formation
6) acrodynia in rats

VITAt'illN B-5 - Pantothenic acid; "Everywhere vitamin"

- it is an essenlial component of coenzyme A
- 3forms Acetyl CoA, Succinyl CoA, Acyl carrier protein
- RDA: ln the absence of any information indicating toxicity, daily doses
up to 100 mg do not seem unreasonable as part of a preventive
recirnen for healthy people.

'19
 Functions of Pantothenic acid:

A. as acetyl CoA, it is involved in:

1) Krebs cycle
2) cholesterol and steroid synthesis
3) synthesis of acetylcholine
4) activation of the branched-chain amino acids
5) activation of fatty acids

B. as Succinyl CoA, it is involved in heme synthesis

C. as ACP (acyl carrier protein), it is required in the biosynthesis of fatty

acids (extramitochondrial lipogenesis)

Deficiencv manifestations of Pantothenic acid

1) easy fatigability
2) atrophy of the adtenal glands
3) microcytic, hypochromic anemia

vlTAMlN B-7: BloTlN, Anti-eggwhite injury factor

- Coenzyme form is called biocytin
- abundint in liver and eggyolk. Raw egg white contains a protein called
AVlDlN, which combines very tightly with biotin, preventing its
absotption and inducing biotin deficiency
- RDA fot adults: 300 micrograms/day

Functions of Biotin: lt is the coenzyme for CO: lixation reactions or

carboxylation reactions which includes the following:

1) conversion of pyruvate to oxaloacetate - pyruvate carboxylase

2) fixation of CO at carbon 6 of purine
3j conversion of acetyl CoA to malonyl CoA - fatty acid biosynthesis
4) conversion of Propionyl CoA to methylmalonyl CoA - Beta-oxidation of
odd-numbered fatty acids

Deficiencv manifestations of Biotin

1) ln man - early loss of hair; early graying ofthe hair; fine,. scaly
'desquamation of the skin; muscle pains; depression; hallucinations
2) ln rais - "spectacte-eyed appearance, "kangaroo posture", retarded
groyvth, loss of hair, loss of muscular control

VITAMIN B-9 - FoLIC ACID, PGA (Ptetoylglutamic acid)

Active form: Tetrahydrofolate C|HFA or FHr)
-Activation of folic acid requires vitamin C
-RDA: 400 micrograms/day
m
--
 Functions of folic acid: THFA serves as carrier of one-carbon units
namely methyl, methylene, methenyl, formyl, and formimino which are
involved in the following biochemical reactions

1) Ns-methyl THFA - most abundant form of folic acid in the blood; it has
an important role in the methylation of homocysteine to methionine
involving methylcobalamin as cofactor

2) Ns,N1o-methylene THFA - involved in the formation of lhymidylate, a

necessary precursor of DNA synthesis and eMhrocyte formation-

3) Nlo-formyl THFA - source of carbon 2 of the purine nucleus

4) N5-formimino THFA - involved in histidine catabolism
5) N1o-hydrorymethyl THFA - involved in thymine synthesis

The participation of folic acid in purine and dTMP synthesis appears to be

metabolically its most significant function. Therefore, lhe most pronounced effect
of folate deticiency is inhibition of DNA synthesis due to decreased availability of
purines and dTMP.

Deficiencv rnanifestations of folic acid:

1) macrocytic or megaloblastic anemia

2) Pancytopenia
3) grolvth failure
4) Glossitis and GIT disturbances
5) ln rats - achrornotrichia (abcence of normal pigmentation of the hair)

vlTAMlN B-12 - Cobalamin, Antipernicious anemia factor, Extrinsic factor of

Castle, EMhrocyte maturation factor
- Coenzyme form: s'{eoryadenosylcobalamin
- Not found in fruits and vegetables; only found in foods of animal origin
so strict veg€tarians may develop deiiciency
- Becornes deficient if patient undergoes lotal gaslrectomy because
intrinsic factor from the stomach is needed for its absorption
- Methylcobalamin - most abundant form in the blood
- RDA: 5 to 50 micrograms/day

Functions of Vitaqin 812

1) required for RBC maturation - erythrocyte maturation factor

2) needed in the conversion of homocysteine to methionine
3) involved in nucleic acid synthesis possibly in the methylation of uridine
to thymine
4) involved in the activation of amino acids for protein synthesis

21
 Deliciencv manifestations of Vit B12
1) Pernicious anemia - megaloblastic or macrocytic type of anemia with
accompanying degenerative lesions of the posterior and lateral columns
of the spinal cord
2) Mucosal atrophy and glossitis, stomatitis and pharyngitis

VITAMIN C - ASCORBIC ACID; Anti-scorbutic vitamin; anticarcinogenic vil

- drying vegetables usually result in loss of vitamin C content
- smoking causes lower serum levels of vit C
- oral contraceptives and corticosteroids lower serum levels of vit C.
- RDA: '100 mg/day (although many nutritional researches now regard
this amount as too little for optimal health. The need for Vit C varies
consid€rably from one individual to another. Exposure to infection,
tobacco srnoke, environmental pollutants, various drugs, surgery,
bums, trauma, alcohol and other "slresses' may increase need for vit
C; so may pregnancy and advancing age.

Functions of Vitamin C

1) Collagen synthesis - Hydroxylation of proline and lysine

2) reduction of ferric to ferrous ion - facilitates absorption and utilization of
iron; also involved in the mobilization of iron from its storage form.
3) conversion of folic acid lo active THFA
4) Hydroxylation of cholesterol to cholic acid
5) Plays an important role in the reaction of the body to physiologic stress
6) potentiates the immune system
7) lowers incidence of blood clot formation in veins
8) necessary for bone formation since bone tissue has an organic matrix
' containing collagen
9) helps prevenl the formation of various cancer-causing substances,
principally the nitrosamines, within the body.

At least t g.am of vitamin C has been sho$/n to block the nitrosamine

formation in the human body.

Deficiencv manifestations of Vit C - refened to as Scurw

1) Gums are spongy, tender and easily bleed leading to infections,

loosening of teeth and falling of teeth
2) Poo{ wound healing
3) Decreased ability to combat infections
4) lmpairrnent of groMh of both bones and teeth.
5) Skin changes - roughening ot skin because of hyperkeratotic papules.
6) Petechial, subcutaneous, subperiosteal, and internal hemorrhages
7) swelling of the costochondraliunctions - scorbutic rosary
8) easy fatigability, weakness, aching in the bones and joints of the
extremiiies
9) anernia 22
FAT€OLUBLE VITAMINS:

VITAMIN A - Anti-infective vitamin; anticarcinogenic vitamin

- Beta-carolene is the best precursor
- Corwersion of carotenes lo vit A takes place in the liver and intestinal
cells.
- RDA: 525 RE/day for adult males, 450 Rgday for adult females
1 RE = 'l ug of retinol, 6 ug of beta-carotene

Functions of Vit A

1) Component of rhodopsin which is necessary for dark vision

2) Maintenance of the integrity of the epithelial tissues
3) Maintains moisture and smoothness of skin
4) Role in grcwth - failure of skeletal growth appears to retlect a defective
synthesis of chondroitin sulfate
5) Role in reFoduction - deficiency causes atrophy of the germinal
epithelium in males
6) Development of bones and teeth
7) Control of cell differentiation and tumover

Manifestations of Vit A deficiencv

A. Eye manifestations
- earliest manifestation - nyctalopia or night blindness
- Photophobia
- xerosis coniunctivae - Bitot's spots
- xerosis cornea - may lead to corneal ulcers. The whole cornea
may be transformed to a soft, jellylike mass - keEtomalacia
- blindness may result from opacities affecling the whole cornea or
from perforation of the cornea which results in the collapse of
the eyeball.
- xerophthalmia - generalized dryness ofthe ocular tissues

B. Skin manifestations - dryness and scaliness causing "toad skin"

C. Cessation of groMh
D Sterility in males due to atrophy of the germinal epithelium
E. Epithelial cells dries up and undergoes keratinization
- increased susceptibility to infection of the respiratory tract
- cells of the kidney medulla may cornify and renal calculi forms
- ducts of glands may become blocked and the glands atrophy

Hvpervitaminosis A - Manifested by painful joints, periosteal thickening of long

bones, bss o{ hair, headache, weakness, loss of appetite, hepatosplenomegaly,
serious liver damage may occur.
llIAUllLq - Anti-rachitjc vitamin, "sunshine vitamin"
- Vit D3 can be synthesized in the body from cholesterol
- Hydroxylation of vit D3 in the liver converts it to 2s-hydtory-
cholecalciferol (Calcidiol), the major form of vit D in the circulation and
the major storage form in the liver.
- Further hydroxylation of calcidiol in the kidneys converts it to 1,25-
dihydroxycholecalciferol (calcitriol), the most active form of vit D
- FAO/WHO recommends 5 ug/day which covers the needs of adults
regardless of exposure to sunlight.

Functions of Vit D

1) increases absorption of calcium and phosphorus in the intestines.

2) increases mobilization of calcium from the bones
3) increases kidney tubular reabsorption of phosphate
4) plays a role in citrate metabolism. Citrate is involved in the mobilization
of minerals from bone tissues and removal of calcium flom ihe blood.

Manifestations of vit D deficiencv

A. Rickets -Vit D deficiency in children: characterized by inadequate

calcification of cartilage and bone so bones become soft and pliable.
- bowlegs and knock-knees
- rachitic rosary - swelling of the costochondral junctions
- contracted pelvis
- delayed closure of fontanelles
- detayed tmth eruption
- caput quadratum
' - Harrison's groove

B. Osteomalacia - Vit D deliciency in adults. There is softening and

weakening of the bones and this may lead to deformities and easy
fracturability. Serum calcium is reduced - this leads to tetany

Hvpervitaminosis D - manifested by anorexia, weakness, headactre, digestive

disturbances, nausea, and polyuria. There is increased urinary excretion of
cahium and phosphates which may lead to urinary lithiasis. The hypercalcemia
and hyperphosphatemia may lead to metastatic calcitication.

VITAMIN E - ?nti-sterilit vitamin" (for rodents only) - because vit E deficiency

in rodenls results in resorption of fetuses and testicular atrophy.
-Precursors are called tocopherols
-RDA: The intake ot PUFA (polyunsaturated fatty acids) is the single
most important factor in the determination of the requirements for vit E
under normal circumslances The safe level of intake for vit E in adults
is 12 mg/day.
24
 Functions of vitamin E:

'1) Anti-oxidant property - most striking chemical property

- anticarcinog€nic effecl
- anti-aging or reiuvenating effect
- inhibits damage to lung tissue trom oxidants in the air
- protects PUFA from oxidative destruction thereby preventing
formation of radicals
- spares or protects vit A and carotenes from oxidative destruction

2) Maintains inlegrity of the RBC membrane

3) Maintains integrity of muscles
4) Together with selenium, vit E prevents liver necrosis
5i Gonadal and reproductive functions - in rodents only

Clinical manifestations of vit E deficiencv

1) megaloblastic anemia - due to increased hemolysis of red blood cells

. 2) muscular dystrophy - degenerative changes in the muscles
3) changes leading to degeneration of nerve cells which could be brought
about by toxic action of fatty acid peroxides
4) ln animals - testicular degeneration in males leading to permanenl
sterility; failure of gestation in females

YIIAUIILK - Anti-hemorrhagic vit; coagulation vitamin

- 3 forms: Phylloquinone from plants; farnoquinone from animal
sources: menadione - synthetic form
- can be synthesized by normal intestinal bacterialflora

Functions of Vit K

1) Cofactor in the gamma-carboxylation of glutamic acid residues in the

synthesis of blood clotting faclors ll (prothrombin), Vll, lX and X
2) Component o{ the electron transport chain in the form of coenzyme Q
3) Antidote to anticoagulant drugs such as Dicumarol
4) lmportant in the synthesis of bone calcium-binding proteins These two
proteins, osteocalcin and bone matrix Gla protein, contain
gammacarborygLlutamate

Deficiency manifestations of vitamin K will lead to hemorrhage due to

d€tective formation of clotting factors.
HOUSE DIETS

All hospitals and institutions engaged in feeding the sick have specific, basic
routine diets designed tor uniformity and convenience of service. These are
called "house diets" and are based on the foundation of an adequate diet,
which in turn is formulated from the Recommended Energy and Nutrient lntakes
(RENI). These recommendalions, however, apply to normal, healthy individuals
and are not designed to meet the needs of acutely or chronically ill, injured or
convatescent patients. Therefore, house diets should be carried a step further to
cover the increased metabolic demands created by stress or illness. The house
diet is supplied in three meals each day.

FULL DIET oT REGULAR DIET

This is a basic adequate diet of approximately 2,000 - 2,500 Calories and

includes the basic four food groups, namely, meat, milk, cereals/bread, fruits and
vegetables. Additional foods or more of the same foods such as butter or fortified
margarine, d€sserts, salad dressing, crackers and sugar are added to increase
calories and make the diet more palatable. There are no particular food
restrictions. However, foods which may cause digestive dislurbances such as
cooked cabbage and fried pork, are used with discrelion.

lndications: For afebrile patients in general, when no contraindication is present

and/or when no diagnosis is established yet; for ambulatory or bed patients
whose condition does not require a modified diet.

SOFT DIET
'ihis is an adequate diet characterized by being moderately low in cellulose and
connective tissue, e.9., lruits and vegetables with low tiber content and meat with
little or no tough connective tissues. Thorough cooking, cufting, mashing,
pureeing and removal of skin and seeds from fruits and vegetables and of gristle
and elastin from meats increase digestibility. Soft diet is planned for conditions
where mechanical ease in eating or digestion, or both, is desired plus supplying a
diet low in residue. A soft diet can Include many foods if they are mashed,
pureed, combined with sauce or gravy, or moked in soups.

Recommended for soft diets

-
Beverages - milk and milk products, coffee, tea, carbonated
beverages, fruit juices, fruil drinks, cocoa
-
Desserts - cakes, cookies, pies, pudding, ice cream, sherbet, gelatin,
fruit ice and frozen pops
-
Fruits - allfruit juices; cooked or canned fruit; soft fruits such as melon
and peaches; sections of banana, grapefruit and orange
without membrane
26
 - Meats and meal substitutes - all lean, tender meats; poultry; llsh;
eggs; crisp bacon; milk-flavored cheeses; creamy peanul butter; plain
or flavored Yogurt
- Breads and cereals - white, refined wheat or light rye breads; soft rolls
and crackers; cooked or ready to eat cereals
- vegetables - all vegetable iuices; cooked vegetables as tolerated
- soups - soups made with allowed foods
- miscellaneous - spaghetti, macaroni and other pasta; hard candies;
plain chocolate candies; marshmallows

-
Not recommended for soft diels alcoholic beverages; all sweets and desserts
Containing nuts, coconut or dried fruits; highly seasoned salad dressings; strong-
smelling or highly seasoned meats or fish; yogurt with nuts or dried frults: fried
eggs, potato chips and fried potatoes; raw and fried vegetables; highly seasoned
soups: whole kernel corn; whole{rain breads or crackers with seeds.

lndications: For patients with poor denture, oral lesions, after oral iurgery, fevet
and mild infeaions, gastritis, diarrhea. The soft diet is part of the post-surgical
progression diet from clear liquid to full liquid, then advancing to soft solids and
iinally regular foods. The diet is individualized to meet the needs of the patient
and varies from smooth, creamy foods to foods that are slightly crispy.

LIQUID DIET - Full liquid diet and clear or restricted liquid diet

Full liquid diet - it contains food that are liquid at room temperature or could be
liquefied at room temperature. lt is a diet consisting of all beverages allowed on
clear liquid diets with addition of milk, ice cream, yogurt, and liquid nutritional
supplements (e.g.,ensure, Boost). Examples are milk beverages, ice cream,
.' strained fruit juices, chocolate, tea, coffee with cream and sugar, clear soups,
strained cream soups, and strained vegetable souPs. lt is considered adequate
for maintenance requirements.

clear or restricted liquid diet - diet consisting of liquids that contribute minimal
residue to the gastrointestinal tract; it is frequently ordered for post-operative
patients to furnish nongas-forming fluid and nourishment. lt is an inadequate diet
composed chiefly of water and carbohydrates, therefore, it is used only for a very
short time. lt is served at frequent intervals to supply the tissues with fluid and to
relieve thirst. Examples: tea, coffee, broth, carbonated beverages, strained fruit
juices or fruit juices without pulp

lndications: For acute infections; during acute gastrointestinal distress like

diarrhea, vomiting; during gastrointestinal medical testing such as colonoscopy;
fever; after oral surg€ry, before and after surgery.

27
 FOOD EXCHANGE LIST

Thg Food Exchangq list is a fosd classificalion method wherein different

foods are plAqed iQ!9 Iogd gtggp" bas,ed on their chemical composition. For

example, eggs and cheese are high in protein and are therefore classified under

the meat group. This exchange list was created for diabetics by the American

Diabetic Association & the American Dietetic Association to track calories,

carbohydrates, proteins, and fat. Efchang-e lisis facilitate cqloie cantol and

provid€s an underslanding of how much carbohydrate, fat, and prqtein are in

egqh lood group. Following this can be a healthy, balanced way of eating for

most people.

C€mmon foods are divided into six lists,or groups called exchanges. Food

is classified into 6 groups: vegetables, fruit, milk, starch (rice), meavmeat

substitutes, and fat. All foods within a list have similar caloric value, so that each

S6rving has about the same amount of carbohydrate, protein, fat and overall

kilocalories. They have a similar chemical makeups, (similar amounls of

macronutienls) and are helpful in maintaining a varied diet. Any food within the

same category can be exchanged/traded for another food in that group, in th€

right portion size. The Daily Food Guide specifies how many servings of foods

from each group people need io consume to meet their nutrient requirements . A

p€rson wishing to avoid over consuming calories musl pay attention to serving

sizes. To measure your food you will need a teaspoon, a lablespoon, an 8-oz
cgffee qrp and a prepared matchbox size 5x3y2x2y2. Most foods are measured

after they are cmked .

LIST 1 - VEGETABLE EXCHANGES

>> "A" Vegetables <<

Contain negligible carbohydrate, protein and calorie if one exchange or

less is used, two exchanges of 'A" vegetables equals one exchange of "8"

vegetables. Use one cup of cooked vegetable or raw vegetable as desired.

Abitsuelas (Baquio beans) Lettuce '

Aceloas (Chinese cabbaoe) Malunooav (Morinoa)
Aluobati (Malabar soinach) leaves' Mushroom
AmDalava (Bitter oourd). leaves & fruit Mustasa (Mustard) leaves
Banana blossoms Okra (Ladies finqers)
Cabbaoe Onion bulb
Camote (Sweet ootato) leaves ' PaDava. qreen
Cauliflower Patola (Loofah. Luffa)
Cucumber Petsav (Chinese white cabbaoe) '
Eooolanl Saluvot (Jute) leaves ''
Garlic leaves ' Savote (Chavote) fruit '. leaves
Himbabao Siqarilvas Minoed beans)
Kanokono(Water soinach)' Souash- flower & leaves
Katurav (Corkwood tree flowers) Strino beans. leaves '
Kintsav (Chinese Celerv) Tomato '
Labanos (Radish) lJoo (Bottle oourd)
Labono (Bamboo shoot)
' These vegelables are rich sources offiber.
'? These veqetables are rich sources ot
pro Vitamin A.

Vegetables are important sources of minerals and vitamins. tnclude two to

three servings, one of which should be dark green or yellow. Dark green and

deep yellow vegetables are amoflg the best sources of pro-vitamin A such as

beta-carotene. Sorne vegetables such as cauliflower, cabbage, green, peppers,

turnips and lomatoes contain vitamin C. Green leafy vegetables such as

kangkong, kamole, malunggay, and saluyot, contain calcium and iron; and

29
cabbage, carrots, spinach and tomatoes are good sources of vitamin 86. Turnips

and tomatoes also contain potassium. Spinach is a good source of zinc while

green beans and tomatoes provide magnesium.

>> '8" Vegetables <<

l' ! gms carbohydrates

1 Exchange { 1 gm protein ] to
""to,i."
L osmfat
-t
bles or 1 cup raw vegetables.
Use 72 cup ol cooked veqetables bles.
Banana, heart Paayap (Cow pea)- Sitaw (Yardlong) beans,
fruit
Bataw (hyacinth bean) Patani (Lima) bean, Sitsaro (Sweet peas)
pods
Carrot ' Remolatsa (Suoar beel) Souash. fruil
Kadios (Pigeon pea), Singkamas, bunga (Yam Toge sprout (Mung bean)
fresh bean)
Kamansi (Breadfruit) ' Ubod (Coconut shoot)
' These vegetables aae rich sources of fiber.
2
These vegetables are rjch sources of pro Vitamin A.

LtsT2-FRqTTEXCHANGES

f 10gms carbohydrates -l
1 Exchange J o gm protein L 40 calories
I ogmfat
L, I

Fruits are important for their carbohydrate, vitamin, mineral, and fiber

contents. lnclude at least two to three exchanges daily in the diet, one of which

should be rich in vitamin C-

Canned Fruits
Fruit cockiail 3 tablespoons Pineapple, crushed 3 tablespoons
Peach halves 1 rZ halves Pineapple, sliced 3 tablesDoons
Canned Fruil Juices
Pineapple Grape
Orangel Y2 cuq Y. cuq
Fruit
Pineaogle Yz cu0
These huits are soorces of vitamin C. lnclude at least one exchange in the diet daily.
 Dried Frui',s
4 (2 cm dia.
Champoy, salted Prunes seedless 3 pieces
each)
Mango chips
2(2xBcm Ralsins seedles 2 tablesppons
each)
Others
Buko (young coconut) Y. cuP Buko water 'I cup
Fresh Fruits Servinq Size Fresh Fruils Servino Size
Anonas (Custard 5( 2 cm dia.)
|lz medium Lychees
aDDle)3
/z ol8 cm dia. Mabolo (Velvet apple % or 6 cm dia.
Apple |
or 1 (6cm dia.) or velvet oersimmon)
'lY. olgx5 Macopa (Maiay apple 3 (4 cm dia.
Balimbing (Starf ruit)1 1
cm or Wax iamboo) each)
Atis (Suar-apple or Manggo ripe 23 1 med slice ripe
1 small
sweelsoo) 3
Bavabas (Guava) 'P 'I medium Manqosteen 3 (6 cm dia.)
'll2 ol 12 x 10
Chico (Sapodilla) 2l medium Marang (Johey oak)
cm
Dalanghila (King or
2 medium Melon (Cantaloupe) Yr Pc
Mandarin oranoe 3
1 3 Pakwan (Watermelon) 1 slice, 12\7
Datites (Dates) Y2 cuq
cm
23
'1 slice, 20x5x2
Duhat (Black plum) 20 pcs Papaya, ripe
cm
.l
segment of
Durian Pear 1
1 (6 cm dia.)
6Y" x 4Y" cm
1 3 1 slice, 10 x 6%
Gtepes 1? pcs Pineapple
x'lY" cm
3
Guyabano (Soursop) Y2 oc Rambutan 8 (3 cm dia.)
Saba (Cardava 'I (10 x 4 cm)
Kaimito (Star apple) Y. Pc
banana)
Kamachile (Sweet
7 pods Santol t 1 pc, medium
tamarind)3
Sinigwelas (Spanish
Kasoy (Cashewf 'l (7 x 6% cm) 5 pcs, medium
olum) 3
Lakatan (Cavendish
banana)
1(9x3cm) Strawberry 1'3
1 cup

Langka (Jackfruit) 3 segments (6

Suha (Pomelo)3 2 segments
riD€ cm dia.)
Lansooes 7 10 pcs Tamarind 2 pcs, medium
Latundan banana 1 (9x 3 cm) Tiesa "'P- Y2 gc

?
These fruits are good sources of fiber. 'dia- diameter
These frurts are lood sources of provilamin A.
'These ln its are sources of vitamin C. lnclude at leasl ooe exchange in the diet daily.
 Bananas, oranges and dried fruits are sources of potassium. Bananas

contain magnesium and vitamin 86. Frujts may be used fresh, dried, canned,

frozen or cooked. Some fresh fruit juices like Kalamansi (Philippine lemon),

dayap and lemon may be rated as "free food" when used as flavoring, sauce or

when diluted and sweetened with artificial sweeteners. Fruits may cause a

temporary increase in blood sugars, thus meal plans for patients with diabetes

mellitus allow no more than 5 exchanges a day.

The natural sweetness of fruit is not contraindicated for diabetes. Some

physicians and dietitians prefer to use whole fruits rather than juice in diets for

patients with diab€tes because lhe latter have a greater glycemic effect.

Fruit juice consisls of unfermented but fermentable liquid obtained from

native fresh fruil, with nothing added or subtracted. Fruit juice is also

commercially available in the form of fruit juice drink and fruit juice concentrate.

Fruit drink is a ready-to{rink beverage prepared by mixing water with fruit

.concentrate and into which sugar and citric acid may be added to adjust the

soluble solid content and acidity of the product. The main ingredient consists of

fruit juice concentrate, essential oils, essences of extracts, with or without added

sugar. concentrated fruit juice is the fruit juice which is concentrated by the

removal of part of water but not dried.

 List3-MILKEXCHANGES

-{f
12 gms carlcohydrates
proteins I
'l Exchange 8 gms I 170 calories
WHOLE MILK L 10 gms fat )
'12 gmscarbohydrates
1 Exchange 8-gms proteins 125 calories
LOW FAT MILK { 5 gms fat )

1 Exchange
VERY LOW FAT MILK {
12 gms carbohydrates
8 gms protgrl]s
09mf4 l 80 calories

Milk is an excellent source of prolein and calcium. lt also a good.source of

phosphorous, some of the B-complex vitamins, and vitamins A and D Milk also

contains some magnesium. The milk allowance in the meal plan can be used as

a drink, added to cereals, or mixed with coffee or tea and other foods

Food Servrnq Sr'ze

Wnote litiltc. tS2S* Fat conient)
Milk. evaoorated. undiluted Y2 cuo
Milk. evaporated, Jilled, undiluted Y" cuo
Milk, fresh, carabao's ' 1 cuD {olus 2 oms fat)
Milk, fresh, co\,\,'s 1 cuD (Dlus 2 qms fat)
Milk. oowdered. whole 4 Tbso or |l. cuD
Reduced Fat Milk: (2% Fat content)
SoYmilk /" cup
Low Fat tltilk: {1% Fat content}
Lite Lov/ Fat Milk I tetra-pack
Milk. Dowdered. non-fat 4 TbsD or % cup
Skimmed (Non-Fawery Low Fat Milk) (0-0.5% Fat content)
Buttermilk: liouid ' 7" cu!
Lono life skimmed milk l cuD
Powdered Y, cuo
Yoqhurt Y2 cup
Equivalent to 1 cup cov/s milk plus 2 exchanges ol fal ot 112 cup evaporated milk PIus 2
exchanges of tat.
'1 Buttermilk refe6 to pasteurized skim milk that has been sourced by lactic acid producing
bacteria.

33
 List ! - RrcqEIclANGES
f23 gms cqrbohydrates
1 Exchange { 2 gms proteins roo""ro,i""
L osmfat )
'l Exchange % cup rice (well packed) or equivalent

Rice, other cereals and products made from these are the ma.ior

sources of carbohydrate which is the cheapest source of calories. ln

addition, whole grains or enriched rice and cereals are good sources of

iron, thiamin and riboflavin, whole grain products have more fiber than

products made from relined flours.

Rice and Rice Producb

1. Rice
Rice. cooked 7zcup, well-packed
2, Rice Products
Bibinoka 1 slice (1/4 of 15cm dia.,2cm thick
Biko lslice(10x5x1cm
Espasol
I 2(11 x2-112x 1-112 cm each
Kalamay: latik 1(4x6x2cm)
Kutsinla 1 (6 cm dia. x 2-112 cm)
Palitaw 4 7-112 x 4 x 0.3 cm each)
Puto: bumbonq 2 (1 x2 x'l cm each)
Puto: Puti 1 slice (+1/2 x 3 x 3-1/2 cm)
Saoin-saDin l slice{5x3x4cmeach)
Tikov '1 slice (10 x 3 x 1-112 cm)
These foods aae good sources of fiber-

Rice Equivalenb
l- gread
Pan Americano 2 slices Pan de Sal 1 Dc.
Pan de Limon 1 pc. Rolls (tor 1 pc.
hamburoer)
Whole wheat bread 2 slic.es
2. Corn
Binatoq Y. cvg boiled I
Corn. 'l pc
BabY corn l cup Mais.maha I 1 slice4x4Y2cm
 Rice Equivalents
3. Rootcrops
Gabi 'I oc10X6cm Patatas (Dotato) 1Dc7X6cm
Kamole (sweet 'I pc'l0X6cm Suman 1pc7 %X3Xz
Dolato) cm
Kamoteno kahov 1oc5/.X4/.cm Ube 1 cuD. cubed
4- Noodles
Bihon, mike l cup Sotanohon '1cuo
Macaroni 1 cup SDaohetti 1 cup
5. Other cereals
Drv (flake & Duff varietv l.l cuo Oatmeal l cup
Luoaw I cup
6. Bakery Products
Biskolso 2 Dcs Mamon 2 Dcs
Cookies. assorted 5 pcs Pasensiva 22 ocs
Ensavmada 1pc Saltine 10-Dcs
Hooia 'l Y" rcund Soda crackers 8 Dcs
Ladv finqers 5 ocs Soonoe cake 'lslice5X5cm

List 5 r IIEAT ExctlANgFs

f ogm
prcleins I F
carbohydrates
l Exchange -{ I gms 68 calories
L fat
4 sms
_t

Foods high in p{otein (except milk) compose the meat and fish exchange
.,
list. These foods include meat, fish, eggs, poultry, and legumes. ln addition to

p{otein majority of the foods in the list are also good sources of iron, zinc, and

other &complex vitamins. Those from animal origin are particularly rich in

vitamin 812. Seafoods, nuts, legumes and soybeans are good sources of

magnesium, zinc and iron. Organ meats like liver as well as egg, clams,

soybeans and nuts are rich in iron. Foods from animal sources contain

cholesterol, the richest sources of which are egg yolk, liver, kidney, brains,

sweetbreads and fish roe while smaller amounts are found in meat. Foods from

planl sources contain negligible cholesterol.

 The food is measured without bones or fat after it is cooked. The

matchbox (mbx), which is 5 X 3 % X 2 y. cm, is used as reference size to

measure I exchange of medt, fish and poultry.

Food Servinq Size Food Servinq Size

Cottage Cheese Meat, lean pork
Y2 cuq 1 slice, mbx size
and beef
lmported Cheese I
slice (2 Y. cm Corned beef
3 Tbsps
cube or 30 qms)
Native Cheese Cold cuts 1 slice, 4 Y2X 1
1 pc (4x4cm)
/. cm
Tokwa Frankfurters 1pc12X1Y2
1pc.6cm cm
Abitsuelas (Baguio Vienna sausage
1 cup cooked 3 pcs
beans)
Beans lnternalorgan
(qarbansos) Y" cooked Y" cuq
Glulen 'l mbx size Fish, Very Small % cup fresh,
(Dilis) Y. cuD dtied
Kasoy, roasted Fish, Small
Y. cuq
(Tawilis, Tamban) 2 pcs ('l2cm)
Monggo (mung Fish, Medium
bean)
1 cup cooked (Galunaoono) I pc (15 cm)
Peanuls, boiled 1 cup, wilh shell Fish, larqe 1 slice. mbx size
Peanuls, roasled Y, cu0 Fish meat 1 slice, mbx size
Veoemeat 1 mbx size Alamang, fresh Y2 cUD
Chicken Egg Crab, lobster,
lmedium Y2 cuq
salmon, tuna
Quail Egg Shrimps 2 medium or 6
6 pcs
small
',/2
Chicken breast or small Tulya (clam)
leo
Y" cuq meal
 LLsr 6--EAT EXGHAT!9ES
f o gm carbohydrates l
-l
ssmsfat )I
Uoteins
'I Exchange o gm 45 calories
L
Fat is a concentrated source of energy. Each gram of fat provides almost

2y2 Iimes as much energy as an equal weight of either carbohydrate ot protein.

Fats may be or plant origin and may be liquid or solid. Margarine, butter and

cream contain some vitamins in addtion to fat. Peanut butter is particulary a good

source of magnesium, potassium and zinc and contains protein.

Fats may be classified into polyunsaturated, monosaturated or saturated.

The fats found in animal source except fish consist mainly of saturated fatty acids

while vegetables oils except coconut oil contain more of unsaturated fatty acids.

Coconut oils are unique in that they have shorter chain length fatty acids

and the only vegetable oil that has 15-20 % medium chain triglycerides (MCT)

such as those found in animal sources. MCT is digested, absorbed and

transported easily and oxidized rapidly as source of energy and has very low

tendecy to be deposited in adipose and other tissues. Some vegetable oils,

particulary oilve oil and peanut oil are good sources of monosaturated fatty acids.

The role of unsaturated (poly and mono) faity acids in lowering plasma

cholesterd level has been demonstrated in patients with diabetes,

atherosclerosis and hyperlimidemia. However, excessive intake of

polyunsaturated fats is not recommend as they may lower HDL cholesterol,

cornmonly known as "good cholesterol".

One Exchang€ of meat and lish when fried or sauteed will absorb
approximately one exchange of fat.
Food Seruinq Size Food Servirq Srze
Saturated Fats Polvunsaturated Fats
Bacon 1 striD Oil (corn, marine,
Butter or marqarine 1 Tso soybean, rapesed- 'I Tsp
Coconut. orated 2 TbsDs canola)
Coconut, cream/milk 1 Tbso Monounsaturated Fats
Latik 2 Tso Avocado % medium
Mayonnaise/ Sandwich Butong pakwan 'l Tbsp (edible
1 Tbsp oorlionl
soread
Shortening (lard or Peanut Butter 2 TsDs
1 Tsp
cooking oil) Piti nut 5 ocs
Sitsaron 2 (5X3 cm) Peanut oil. olive oil 1 TsD
Whipping cream, 'l Tbsp
heaW/liqht

i TAALEOF COIII'OSTTION OF FOOD FXCHANG

LIST FOOD MEASURE cHo PRO FAT CALORIE
(oms) (qmsl (omsl
t-A Veo A 'I cuD
t-B VeoB' 7. cuo cooked 'l 16
Fruil Varies 10't 40
t Mitk' l cuD ",. ; 't2 8 10 170
IV Rice Y2 cuo gacked 23 2 100
Meat Matchbox or 8- 4 68
equivalent
Fat 1 tsp 45
'WHOLE MILK was used in this table

DrEr PRESGBlPTroN
Make a dLiet prescription for your diabetic Filipino patient whose height is 5'6" and

works as the Dean of the College of Business Administration.

TER = 2094 cal, CHO 314 qms, PRO = 105 qms, FAT: 46 qms
List Food Exchanqes'- cHo PRO FAT Calorie
t-A Veo A 1
t-B Vea B 6 (1) (2) (3)
Fruil 2 ut (5)
t Mitk 1 (6) (7) (8) (e)
IV Rice not (11) (12) (13)
Meat (14) h5) ft6) (17)
Fat ft8' (19) (20)
Tolal (21) (22) (23) (24)
 Complete each row by multiplying the number of exchanges with the

expected gms of CHO, PRO and FAT in each ot the food groups.

TER = 2094 cal, CHO = 314 qms. PRO = 105 qms, FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
l-A Veq A 1
t-B Veq B 6 6x3 6x1 6 x.16
Fruil 2 2x'lO 2x40
l Mitk 1 1 x'12 1xg 1 x 10 'I x 170
IV Rice (10) (11) n2') I tJt
Meat fl4t 05) (16) (17'
Fat n8) n9, (20)
Total (21) (22) (23) (24)

:hese values and the fol

't ER 2094 cal, CHO 314 qms, PRO 105 qms, FAT 46 gms
= = = =
List Food Exchanqes cHo PRO FAT Calorie
t-A Veq A 1
t-B Veo B 6 '18 6 96
Fruit 2 20 80
t Mitk 1 't2 8 10 170
IV Rice (10J (11) (12) (13)
Meat ( 14) fi5) n 6') h7)
Fat fi8) (1s) (20)
Total (21) (22) (23) (24)

Having partially completed the table above, follow the following steps:

Stgp 1; Figure out number of exchanges for Carbohydrate-containing food

groups

- Follow this order:*

. Vegetable
. Fruit
. Mitk
-Always begin with Carbohydrate-containing food groups

Step 2: Add all of the carbohydrates you have used so far for veggie, fruit, & milk

exchanges to get Rice Exchanges,

 TER = 2094 cal, CHO = 314 Sms, PRO = '105 qms, FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veq A 'l
t-B Vea B 6 18 6
Fruit 2 20 80
t Mitk 1 \12 8 10 170
50

This result (50) you subtract from the prescribed carbohydrate which is

314. 314 - 50 = 264

The result (264) is then diyided !y 2 (because there are 23 gms of

carbohyd rate in rice, remember?).

2U I Z3 = 't1 47 o, 'li Rice exchanges.

The dividend is the # of rice exchanges (11). put this vatue (1.1) in the

Rice row and complete that row as what you did with the previous rows.

TER = 2094 cal, CHO = 314 sms, PRO = 105 qms, FAT = 46 qms
List Food Exchanges cHo PRO FAT Calorie
t-A Veq A 1
t-B Veq B 6 '18 6 96
Fruil 2 20 80
It Mitk 1 12 8 10 170
Rice 11" 11 X23 11X2 11X 100
Meat (14) (1s) (16) (17)
Fat fl8' (19) (20)
Total Q1) (22) (23) (24)

u these values and oet the fol

:ER = 2094 cal, CHO = 314 gms, PRO = tos sms, FAT 46 qm-
=
List Food Exchanqes cHo PRO FAT Calode
t-A Veo A 1
t-B Veq B 6 18 o 96
Fruit 2 20 80
l Mitk 1 12 10 I 170
IV Rice 't1 253 1100
Meat (14) (15) fi6) fi7)
Fat n8) fi9) (20)
Tolal (21) (22) (23) Q4)
Step 3: To get lvleat ExcLanqlrs, add grams of protein used thus far for veggie,

milk and rice exchang€s.

TER = 2094 cal. CHO = 314 qms. PRO = 105 qms. FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veo A 1
l-B Veq B 6 18 (6 96
Fruit 2 20 80
I't Mitk 1 12 8 10 170
Rice 11 253 \22 1'100

This result (36) you subtract from the prescribed protein which is 105.

't05- 36 = 69 gms

The result (69) is then qivided by_q (bec there are 8 gms of protein in

meat, remernber?). 69 / 8 = 8.6 or 9 Meat exchanges.

The dividend is the # of meat exchanges (9). Put this value (9) in the

Meat rov/ and complete that row as what you did with the previous rows.

TER = 2094 cat, CHO = 314 qms, pRO = 105 qms, FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
l-A Veo A 1
l-B Veq B 6 '18 6 96
Fruit 2 20 80
t Mitk 1 12 8 10 '170
Rice 1'l 253 22 1100
Meat 9' 9x8 9x4 9xOL
Fat (181 ft9t (20)
Total (21) Q2) (23) (24'

47
M ult these values and oet the tollow
-ER
= 2094 cal. CHO = 314 qms. PRO = 105 oms, FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veq A 1

t-B Veq B 6 18 6 96
Fruit 2 20 80
t Mirk 1 12 8 10 't70
Rice 1'l 253 22 1100
Meat I 72 36 612
Fat 0 8) (19) (20)
Total (21) e2) (24)

Step 4: To get Fat Exchanges, add grams of fat used so far from rice and meat
exchanges.

TER = 2094 cal, CHO = 314 gms, PRo = 105 sms, FAT = 46 sms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veq A 1
t-B Veq B 6 18 6
Fruit 2 20 (- 80
t Mitk 12 8 10 170
Rice 'l'l 253 22 1100
Meat I 72 r36
612
46

This result (46) you subtract from the prescribed FAT which is 46.

46_46:Ogm
The result (0) is then divided by 5 (bec there are 5 gms of FAT in FAT,

rernember?). 0/5=0Fatexchanges.
The dividend is the # of Fat exchanges (0). Put this value (0) in the Fat

row and complete that rowas what you did with the previous rows.
 TER = 2094 cal, CHO = 314 qms, PRO = 105 qms. FAT = 46 qms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veq A I
l-B Veq B 6 18 6 96
Fruit 2 20 80
t Mitk 1 12 I '10 170
Rice 11 253 22 '1100
Meat I 72 612
VI Fat o. 0x5 0x45
Total (21) (22) (23) (24)

M ulti lhese values and qet the tol

I -ER = 2094 ca|. CHO = 314 qms, PRo = 105 qms, FAT = 46 gms
List Food Exchanqes cHo PRO FAT Calorie
t-A Veo A 'l
t-B Veq B 6 18 6
Fruit 2 20 80
It Mitk 1 12 '10 170
IV Rice 1'l 253 1100
Meat I 72 36 612
Fat o 0 0
Total e1) (22) (23) (24)

Nc'w total each column to determine if the computations you made are

near to the values you were targetting for.

{-IER = 20s4 cal, CHO = 314 gms, PRO = 105 sms, FAT = 46 oms P
List Food Exchanoes cHo PRO FAT Calori\
t-A Veo A I
t-B Veq B 6 18 6 96
I Fruit 2 20 80
t Mitk 1 12 B 10 170

I
Rice 11 253 22 1100
Meat I 72 JO 612
Fat 0 \0 \0
Total 108 46 20T8-:
-303
RESURCES:
htto:/
^/ww.cwu.edu/.../The%20Exchanqe%2osvstem%20-%20Clem.ppt
htto://www.bokarius.com/patholoqv/Nutrition2.ppt
htto://online-felmealolan.triood.com/foodex. html#'l
htto://www.diabetic.com.ph/cateoorv/lifestvle-chanqes/food-exchanqe-lisu

43
 INFANT NUTRITION
lnfant nutrition has become increasingly important through the years with
the realization that there are certain peculiarities of nutrition in early life.
These are:

'l) Growth is extremely rapid and as a result nutritional requirements are

higher than the adult relative to body size.
2) His surface area is relatively larger, therefore, heat and water loss via
the skin is greater.
3) He has hardly any teeth, thus, his sources of nutrition are limited.

Other important facts related to infant nutrition which have surfaced are:

1) lnfants from developing and developed countries grew at'the same

rate until six months of age when there is a flattening ot the groMh
curve of infants from developing countries.
2) lnfant mortality is highest in developing countries and the Philippines is
no exception. The causes of infant mortality in this country are related
in ofte way or another to malnutrition. Studies show that malnutrition
has a synergistic effect on infection and vice versa.
3) Normal brain groMh and development is associated with good
nutriotion from the last trimester of gestational age to six months from
term.

During infancy, attitudes toward foods and the whole eating process begin
to take shap€. lf parents and caregivers practice good nutrition and are
flexible, they can lead an infant into lifelong healthful food habits.

BASIC CONCEPTS ON INFANT NUTRITION

The infant requires food for:

1) Total energy expenditure: 50% for basal metabolism, 25% for

random activity, 12% for groMh, 3% for specific dynamic action
of food, 10% lost in feces and urine. The sources of calories are
fats, proteins and carbohydrates.
2) Maintendnce of internal environment.
3) Cell growth and repair.
INFANT NUTRITIONAL NEEDS

lnfants' nutritional needs vary as they grow, and those differ from
adult needs in both amount and propoftion. lnitaially' human milk or infant
formula (generally using heat{reated cow's milk as a base) supplies needed
nutrients. Solid foods are not needed until around 6 months. Even after solid
foods are added, the basis of an infant's diet is still human milk or infant
formula.

PRENATAL

During the last two months of intrauterine life' the fetus receives most of
its birth slo{es of vitamins A and D, iron, iodine, Brz and folic acid. Significant
amounts of calcium are also deposited Stores of iron in the full-term infant
are usually sufficient until the third and fifth month of life and iron-containing
foods are given at about that time to replenish his stores.

POSTNATAL

During postnatal life, the infant receives nutrition from breastfeeding,

artiflcial feeding, non-milk preparations and supplementary diet

Calories
- This is based on Estimated Energy Requirements:

89 kcal x weight of infant (kg) + 75 + 0-3 months

89 kcal x weight of infant (kg) + 44 (_ 4-6 months
89 kcal x weight on infant (kg) -78 E-+ 7-12 months

- The infant's high caloric needs are primarily driven by rapid

groMh. and high metabolic rate. The high metabolic rate is
caused in part by the ratio of the infant's body surface to its
weight. More body surface allows more heat loss from the
skin; the body must use extra calories to replace that heat.
Carbohydrate

- Needs in infancy are 60 g per day at 0 to 6 months and 95 g per

day at 7- 12 months.

- These needs are based on the typical intakes of human milk for
breastfed infants and their eventual use of solid foods.

Protein
- I
Needs in infancy are about g per day for younger infants and
about l4 g per day for older infants.

- About half of total protein intake should come from essential

amino acids.

- As with carbohydrate, protein needs are easily satisfied by either

human milk or infant formula.

- Protein intake should not greatly exceed the standard because

excess nitrogen and minerals from high-protein diets would
likewise exceed the ability of lhe infant's kidneys to eliminate
the waste products of protein metabolism.

Fat

lnfants need about 30 g of fat per day.

Essential fatty acids should make up about 15% day of total fat
intake (about 5 g per day)

Fats are important part of the infant's diet because they are
vital in the development of the nervous system.

As a concentrated source of caloies, fat also helps resolve the

potential problem of the infant's high calorie needs and small
stomach capacity

Arachidonic acid (AA) and docosahexaenoic acid (DHA) are two

long-cha.in fatty acids that have very important roles in infant
development

46
Vitamins of Special lnterest
- Vitamin K is routinely glven by injection to all infants at birth.

- Formula-fed infants receive the rest of the vitamins they need

from the formula.

- Breastfed infants are to be given vitamin D supplement (2OO lU

per day) until they are weaned.

- lnfants whose mothers are total vegetarians should receive

vitamin B'12 in supplement form.

Minerals of Special lnterest

- lnfanls are born with some stores of iron.

- By the time birth weight doubles (4_6 months of age), iron stores
are generally depleted if not otherwise part of the diet.

- Formula-fed infants should be given iron_fortified formula from

birth.

- Breastfed infants al about 6 months of age need solid foods lo

supply extra iron.

- Fluoride supplements are recommended for infanls after 6 months

of age to aid in tooth development.

- Adequate amounts of zinc and iodide are needed to support

groMh.

Water

An infant needs about 3 cups 97OO to 8OO ml) of water per day.
lnfants typically consume enough human milk or formula to
supply this amount.

ln hot climates, supplemental water may be given to avojd

dehydratiofl.
 Breastfeeding
The superiority of breastmilk for infant feeding is unquestioned and the
important reasons are:

1) Human milk produces softer and smaller curds that are better digested by the
infant.
2) The host resistance factors in colostrums protect the infant from infection in
the early months of life.
3) The lower solute toad of human milk is just enough to meet the needs of the
infant without compromising th€ excretory capability of the infant kidneys'
4) Better acceptance and tolerance.
5) Easy accessibility.
6) Psychological benefits for both mother and child.
The g{eater concentration of casein in whole cow's milk is responsible
for the formation of larg€ and poorly dig€sted curds in the stomach The
higher concentration of whey in human milk results in better digested curds

The higher lactose content of human milk favors infant nutrition

because:

1) lt increases absorption of calcium and magnesium

2) lt increases absorption of protein
3) lt favors intestinal production of riboflavin and pyridoxine
4) lt increases nitrogen retention
5) lt decreases intestinal pH resulting in a stool flora that is fermentative rather
than putrefactive
6) lt contributes to galactolipid synthesis which is important for the developing
central nervous system

Artificial Feeding
When b,reastfeeding cannot be utilized, formula feeding will have to be
given. The Feparations used for this purpose are the following:

1) Evaporated full cream milk

2) Evaporated filled rnilk

4a
3) Powdered milk: full cream milk or non-fat milk
4) Sweetened condensed milk
5) Non-milk preparations: soy-based or meat-based for babies who are allergic
to milk proteins

Although sweetened condensed milk is popular with the low-income

group because it is cheaper and it keeps better without refrigeration, most of
the calories come from carbohydrates. The child is jeopardized further if the
mother dilutes it to neutralize the sweetness. Condensed milk is not
recomrnended for infant feedrng due to the inherent drawbacks just
mentioned. lf it has to be used, it should be used with the full awareness of
itsshortcomings. Other sources of protein will have to be. used in
combination to make up for its inadequacy.

Evaporated milk is a concentrated sterilized milk preparation in which

th€ milk fat may be retained (full cream) or may be substituted with coconut
oil and corn oil (filled milk). Full cream milk is better than filled milk since milk
fat has a higher percentage of essential fatty acids.

Powdered milk is the other form in which milk is supplied. The

information on the constituents of the milk as written on the can should be
read lo know at what dilution an isocaloric formula (67 cal/1ooml) is
produced.
,

Th€ non-milk preparations which are soy-based or mealbased are

not routinely used except by babies who developed allergy to the proteins of
both animal and human milk.

FEEDING TECHNIQUE

As the irfant ingests either formula or human milk, he swallows a lot

of air so it is important to burp him after either 10 minutes of feeding or after
.l-2
ounces (30-60 ml) of milk have been consumed from a bottle, and again
at th€ end of the feeding.

49
 Generally, the infant's appetite is a better guide than standardized
recommendation concerning feeding amounts.

Once fed, placing the infant on its back is recommended. The reason
why an infant should not be placed on its stomach is because this sleeping
position has been linked to sudden infant death syndrome (SIDS).

Supplementary Diet
Bakwin says that the optimum time to introduce semisolid food to the
child is when the oral musculature is ready to receive it which is generaliy
between three and five monlhs of
age. FNRI recommends that
supplementary diet be started at four months of age. ln deprived
circumstances, it is recommended that it be started later but not later than six
months of age.

RECOGNIZING THE INFANT'S READINESS FOR SOLID FOODS

How does one know it is time to introduce solid foods? lnfant size can
serye as a rough indicator of readiness - reaching a weight of at least 13
lbq6 kg) is a preliminary sign of readiness for solid foods. Another
physiologicl cue is frequency of feeding, such as consuming more than 32
ounces (1L) of formula daily or breastfeeding more than 8-10 times within 24
hours. Underlying these noticeable signals are several developmental
factors:

1. Nutritional need

- Before the infant is 6 months old, nutritional needs can generally be

met with human milk and/or formula.

- After 6 monlhs of age, many infants need the additional calories

supplied by solid foods.

2. Physiological capabilities

- As the infant ages, the ability to digest and metabolize a wider range
of food components improves
 - Before about 3 months of age, an infant's digestive tract cannot
readily digest starch.

- Kidney function is quite limited until about 4-6 weeks of age.

3. Physical ability

- These are the three physical markers that can indicate if a child is
ready for solid foods:
*
the disappearance of extrusjon reflex
* head
and neck control
- ability to sit up wilh support

- The above markers usually occur around 4-6 months of age, but they
vary with each infant.

4. Allergy prevention
- An infant's intestinal tract is "leaky" - whole proteins can readily be
absorbed from birth until 4-5 months of age.

- if lhe infant is exposed too early to some kinds of proteins -

particularly those in cow's milk and egg whites - the infant may be
predisposed to future allergies and other health problems like
.' diabetes.

- lt is best to minimize the number of different types of proteins in an

infant's diet , especially after the first 3 months

The ideal supplementary diet is one that will supply sufficient calories
and proteins to the infant. The flattening of the groMh curve of many Filipino
infants at six months as previously mentioned is explained on the basis of
faulty supplementary feeding. Supplementary diets are generally of the
carbohydrate variery, i.e., lugaw, mashed potatoes or camotes, biscuits, and
the like. lt is also introduced late. The poor quality of the a(ificial milk
substituted for breastmilk when the infant is artificially fed contributes in no
small measure to the malnourished condition.
 Vitamin and Mineral Supplementation
Theoretically, one need not give vitamin supplements to a breastfed
infnt whose mother is adequately nourished. This is also true with formula-fed
infants since most of these formulas are enriched with vitamins. ln premature
infants whose birth slores are not as adequate as that of the full-term
newborns, supplementation can be started at two weeks of age onwards.

The most common mineral supplemented in infancy is iron.

Normally, birth stores are not depleted until three months of age. lron
supplements, 1 mg/kg, are given at this time. These are introduced earlier in
premature infants.

References:

Wardlaw, G.M. and Smith, A.M. 2007. Contemporary Nutrition. lJpdated 6th
Edltlon. N,lcGraw-Hill Companies, lnc.

Whitney, E.N., Cataldo, C.8., DeBruyne, L.K. and Rolfes, S.R. 2001,
Nutition for Heatth and Heatth Care, ld
Edition. Wadaworth,
Thomson Learning, lnc.

, Wardlaw, G.M. '1999. Perspective in Nutition, 4th Edition. The McGraw-Hill

Companies, lnc.

Coulston, A.M., Rock, C.L., and Monsen, E.R. 2001. Nutrition in the
Prevention and Treatment of Disease. Academic Press
 Eating Disorderc and Obesity
rlTRODUCTION

Eating disorders represent extremes in nutrition. These extremes

ofunder- and
rremutrition can exist within the same person, as in anorexia nervosa,
binge-

=ting/purging type, where an individual severery resrricts daily caroric intake whire
*riodically consuming extremery large amounts of food- Anemarivery, the extremes
can
E iound by defnitiorl, as in anorexia nervosa, resiricting type, and
bing€-€ating
lsoader.

NERVOSA
^IIOREXIA
Anorexia nervosa was tirst noled in the scientifc community in the
late l7th
€ntury and first appeared in lhe DSM_lll in 1980 as a diagnostic entity.
By the DSMIV-
TR definition there are iour key attribures. The fearure, is a refusar to maintain a
"ore
rinirnally normal body weight for age and height. Vvhile
there is vanability across
ndviduals by body type, ethnicity,and gender tor what is a .minimally
acceptable
Gilht," it is generally detined as weighing less than g5% of expecled weight ,or height,

:r at or below a body mass index (BMr) of i7.5 kg/m2. The

secood criterion describes
r! intense fear of geining weighl despite being underweight. The third requires a
lgortion in rhe way rhat body weight ard shape are viewed
or a deniar of lhe
s€riJusness of the cond;tion. Finally, among postmenarcheal
females, menstruat cycles
flJst have been absent tor al least 3 months. lf women are on
hormonal birth confrol,
a retrospective account of menstrual cyclicity is recommended,
olherwise ihis crlterion
amot be assessed- This criterion would also not apply lo men, but they
typically

53
 4erience lqvered teslosterone levels accompanied by a diminished sex
drive and
:rd funclioning.

There are two subtypes of anorexia

neryosa. The restricling type is classilied
by
lE sfict use of caloaic reslriciion and excessive exercise
as a means of controlling their

-ght rhe binge-eating/purging subtype describes

those who engage in binge eating
t happropriate compensalory measures,
such as vomiting or misuse of laxalives,
IrEtics, or enemas_ Those with the anorexia nervosa,
binge eating /purging subtype
t-r nom perso,ns with bulimia nervoGa who
binge and purge because of their
aletn€ly low body weight and amenonhea. Thuq
a diagnosis of anoiexia nervosa
*sedes a diagnosis of bulimia nervosa.
Almost every physicar system is negativery
impacled by anorexia nervosa; rhis
is
t le starvation and, when present, the effects purging.
of Resulting abnormalities
dde bradycardia, afihythmia, hypothyroidism,
lortr bone density, constipation,
rtrtrty, ad pednalal cornplications- Despite the gravity of
their symptoms, those with
rlervosa do not tylicafy comprain
of their a;lments and deny the seriousness
-exia o,
1}i physical and psychological states. paradoxically,
excessive exercise and
are observed in anorexia nervosa,
Vvhen excessive movement subsides
taiig.ue sets in, this may indicate
severe deFession, eleclrolyte imbalance,
or
dehydration Ca.diac furciioning may
also be poor at that point. For these
along with high rales of suieide, anorexia
nervosa is considered the deadtiest
disorder-

g
BULIMIA NERVOSA

The core features o{ bulimia nervosa are bing€ eating and subsequent use of

irappropriate coflrp€nsatory behaviors. These behaviors are used in an attempt to

ailain a lolv body weight or prevent weight gain. As with anorexia nervosa, there is

urdue influence of weight and shape on self-€valuation and self-concept. Diagnosis

requires that the binge-eating episodes and inappropriate compensatory behaviors

cur at least twice per week for at least 3 months. There are two subtypes of bulimia

r€rvosa: pwghg type and nonpurging typ€. Purging behaviors most ofien consist of

rc.niting, used in 8&-9flo of cases 0),lolbvled by laxatjve abuse. Many persons with

hrimia nervosa become skilled at inducing vomiting so that they no longer need to use

lheir fingers of another instrument and can vomit at will- Four @mmon signs associated

rith vomiting include "Russell's sign,' sflollen cheeks associated with parotid gland
enlagement, dental enamel erosion, and recedinggums. Laxative abuse is commonly

asociated with pedpheral edema and bloating. Constipation results when laxalives

dlse is discor{inued, but it generally resolves in less than a month with exercise and

gradual increasesin fluids and iber- Both vomiUng and laxalive use are asso"irt"O ritt
ebclrolyte imbalance, tatigue, heart anhythmias, and gastrointestinal problems, such as

g€stroesophageal reflu( disease (GERD).Most persons wilh bulimia nervosa have a

Bilrl in lhe healthy weight range, with sorne in the overweight and obese ranges.

lndividuals with bulimia nervosa feel free of their binge iood after purging and

consequ€ntty experience Fychologicd relief (if only temporarily), but, in reality, many of

*le calories from their binge episodes are absorbed and metabolized. They may also
restricl b€tween binge episodes and exercise, but not to the exlentthat is observed wilh

prexia ne.vosa, bingeeatingy'purging subtype

EANNG DISORDER - NOT OTHERWISE SPECIFIED

There are many torms of disordered eating that are serious and cause

Fychological and physical distress thal do not fit the diagnostic criteria for bulimia
iervosa or anorexia nervosa- These are captured in the ED-NOS category- The most

sorninent of these is bingseating disord€r, which will beconsidered for inclusion as its

*yr diagnosis for the next edition of the DSM. Two other disorders also gaining more

dentio.l are night eating syndrome and purging clisorder. Each of lhese is described

b€*o,v.

Eng*Eating Disord€,t
The hallmark of binge-eating disorder is eating large amounts of tood,

Gompanied by a loss of control. Addilionally, at least three of five of the following

si;ns must be present during bingeeating edsodes: (1) ealing more rapidly than
rsmaf (2) ealing untia uncomfortably tull; (3) eating when not physically hungry: (4)

eating alone due to embarrassment; and (5) feeling dtsgusted, depressed, or markedly

grilty after an episode.

Diagnosis requires lhat distress regarding the binge eating must be present, and

tE episodes must occur, on average, at least lwice per week ior 6 months (7).

Most inciivljuals with binge-eating disorder are overweight or obese, and many

tesent primarily for weight loss. Persons urith bulimia nervosa typbally restrict more
srsistently betwe€n binges than do peBons with binge-eating disorder, but in

C)oralory studies those with bulimia n€rvosa consume more energy during binges lhan

56
lnse $th binge-eating disorder. Persons with binge-eating disorder typically engage in

tinge eating in additjon to eating nomal to large-sized meals throughout the day. This

general pattem of overeating coupled with the lack of compensatory behaviors

contributes to weight gain.

Eight Eating Syndrome

Night eating syndrome did not rec€ive much research or clinical attention uniil

fte 199os. The following diagnostic criteria were reached by consensus at the First

hemational Night Ealing Symposium in 2oo8 (5)- First, the daily pattem of eating must
guff greatly increased intake in the evening and/or night time, as manifested by one or

Uh of the follorr/ing: (a) at least 25% of food intake is consumed afler the evening meal

rdlor (b) at leag tr/vo eating episodes occur upon awakening during the night per

Ek. Second, the clinical picture is characterized by at least three of five of the

baq ing fealures: (a) lack of desire to eat in lhe moming and,lor breakfast is omitted on

hr or more momings per week; (b) the presence of a strong urge to eat between

fner and bedtime and/or during the night (c) sleep onset andor sleep maintenance

rrsomnia are present four or more nighls per week; (d) presence of a belief that one

rrrst eat in order to get to sleep; and (e) mood is tequently depressed and/or mood
Esens in the eveningL Diagnosis requires that tbe night eating behaviors must be

resent for at leasl 3 months, and lhere must be distress or impairment of functioning

fesent in relation to the night eating.

htrging Disorder

PurginE drsorder is generally defined as lhe regular occurTence of inappropriale

.D.npensatory behaviors (e.9., vomiling, laxative use, or diurelic misuse) in the absence

t regular binge-eating episodes and with a body weightgreater than 8570 of that
ryled (7). The ftequency used for the purging criterion has varied between greater

lEn once per week to grealer than t\uice per week. Some studies have also included

-rdue influence of weight and shape on self-evaluation.

TREATMENT

Much progress has been made in treating bulimia nervosa, binge eating disorder,

rd night ealing syndrome. However, treatments for anorexia nervos€i that have long-

E(m effuctiveness are still sorely lacking. These treatnents typically involve a
Itidisciplinary team of professionals, including physicians, dietitians, psychologists,

rd, in some cases, art therapists and occupational therapists. lnterventions include

dr group and individual keatments- Therapeutic meals are included where patients

re challenged to eat nutritionally balanced meals and snacks at regular intervals each

lay, typically every 3-4 h- Patienls are encouraged to gain approximately 1-2 lbtoveek,

t an initid intake of about 1,500 kcauday (30-.40 kcal/k9/day), increasing up to 7H0

rcaukg/day (11). Liquid meal supplements are often used to help patients reach this

lo€f. Patients must be carefully monitored afier meals, particularly in the bathroom and

roorf,s, to prevent purging

'ldr
Bulirnia nervosa can typically be treated on an outpalient basis, but persisient or

cry severe cases require residential or partial teatment.

Psychotherapy

The most effec{ive outpatient psychotherapy approach for eating disorders is

cognitive behavioral therapy (CBT). A 2G.session course of treatment is effective for

bulimia nervosa and bingeeating disorder (/2,1.

lnterpersonal psychotherapy has been tested by several groups of researchers

and applied successfully to bulimia nervosa and binge-ealing disorder. Anoreia

nervosa has not responded as robustly as bulimia nervosa and bingseating disorder-

As persons with eating disord€rs lypicahv experience inlerpersonal or social

dystunclion, interpersonal therapy for $ting disorders focus on ho, t these social defcits

contribule to binge eating and purging behaviors-

Psychotopic M edi c ations

Antid€pressanls are widely prescribed for the treatment ot €aling disorders for two

reasons: they are etreclive in reducing binge-ealing and purging behaviors, and they

inprove comorbid mmd and anxiety symptoms. Unffiunately, they have not been

sl -ro{rn to reduce the core symptom of anorexia nervosa, i-e- , refusal 1o maintain a
helthy body weight. Thus, there are cunently no efficacious medications used tor the
treatment or maintenance of anorexia nervosa. Ho\rvever, antidepressants may still

relieve cdnorbid depression or anxiety, when present Tricyclic antidepressants,

rnonoamine oxidase inhibitors (MAOls), and seledive serotonin reuptake inhibitors

(SSRls) have all sho.n etfcacl over placebos in reducing binge eating and purging

(73,14). SSRIS are nou/ most commonly used, with typical reduclions ol 45-€5% in

binge eating The gSRl, sertraline, has also been shown to reduce evening hyperphagia

and noclumal inglestions significantly among those with night eating syndrome.

59
Topiramate successtully decreases binge eating and purging as compared to placebo

beatment and is associated with weighl loss: however, cognitjve sid€ effects may be

irtolerable for some users- Sibutramine efiectively reduces binge eating and produces

r€ight loss among those with binge-e€ting disorder, but blood pressure should be
rpnilored, particula.ly in those with hyperlension- Buproprion is not indicated for those

with ealing disorders as it has been associated with increased risk of seizures.

OBESITY

Ether increased body weight, as expressed in the body mass index [BW (kgyHt (m)2],

c waist circurnterence can be used to assess the degree of obesity, and both indices

llave been rising steadily as the epidemic of obesity has spread over the past 20 years

(t5) Although obesity results from an imbalance between energy inlake and

ependiture, it is the connections between these two componenls of the frst law of

tErmodynamics that can provide lhe dues about hour we should understand, prevent,

fld ireat this problem.

Definition of Obesity

bdy Nass lndex

A normal BMI is between 18.5 and 24.9 kg,lm2. A BMI between 25 and 29.9 is

operalionally defined as overweight, and individuals with BMI >30 are obese, afler

ding inlo consideration other factors such as muscle builders, who have a high BMl,

l+|ich may not be li€ most appropriate measure of weigtlt status due to muscle- BMI

*o provides the risk meaure for obesity (?5).

60
Centnt Adiposily

Risk for disease increases with a higher waist circumference. ln the United

Slates, a waist of more than 40 in. in men and more than 35 in. in women is a high_risk

category, but most of lhe rest of the wortd uses considerably lower cut-points (g0 cm

[31.5 in.l for wonren and 90-94 cm [35.5-37 in_] for men). When BMt and waist
circumference were used lo predict the risk of hyperlension, dyslipidemia, and the

rnetabolic syndrome, the rraist cjrcumGrence was shown to be a better prediclor than

tre BMI (75).

Etiology

Energyt lmbalance

I.'re become obese because, over an extended p€riod ot time, we ingest more carbon_

ad nitogen-containing compounds from food than we expend for energy. Voluntary

c^,ereating (by subjecting individuals to repeated ingestion of energy exceeding daily

energy needs) can increase body weight.

Wben ihese individuals stop overeating, they invariably lose most or all of the excess

Eight. The use of overeating protocols to study the consequences of food ingestion
has shom the impo.tance of genetic faclors in the pattem of weight gain

Dref

&ny asp€cts of the diet may contritute to obesity_ portion size and consumption of

tigh-tructose com sfup (HFCS) in beverages have all been implicated in the current

*esily epidemic- Consumption ol sofl drinks predicled future weight gain in children

rld adufts.
FAT INTAKE

A high-fat diet provides high energy density (i-e., more calories for the same weight of

bod), which makes overconsumption more likely. Differences in the siorage capacity for
yarious macronutrients may also be involved. The capacity to sto.e glucose as glycogen

h tile liver and muscle is limited, so glucose must be continually replenished. ln

contrast, lat stores contiain more than 1 OO times as many calories

6 in the daity intake of fat. This difference in slorage capaciiy makes eating
ca.bohydrates a more important physiologic need that may lead to overeating when

detary carbohydra{e is limited and carbohydrate oxidation cannot be reduced

srjffciently.

GLYCEMIC INDEX

The raie at which glucose is absorbed can be expressed as the glycemicindex

{Gl). The Gl is a way of describing the ease with which starches are digested in the

intestine with the release of glucose that can be readily absorbed. A food with a high Gl

6 readily digesH and produces a large and rapid increase in plasma glucose levels.

Conyersety, a food wilh a lo\i/ Gl is digested more sbwly and is associated with a

dorer and lo/ver increase in glucose levels- Foods with a high Gl suppress food intake

t:ss than foods with a low Gl. Foods with a low Gl include whole tuits and vegetableg

trat terd to have fber (but not iuices) pfus legumes and whole wheat. Potatoes, white

!i:e, and white bread have a high Gl,

62
FREOUET'ICY OF EATIiIG

The relatimship between the frequency of meals and the development of obesity

b not kDown- l-lov/ever, the fequency of ealing does affect lipid and glucose
rnetabolism. (t6)

RESTRAINED EATING

A pattem of conscious limitation of food intake is called 'restrained' eating. lt is a

conrnon practice in many, it not most, middle-aged women of normal weight. Higher

reslraint scores in wornen are associated with lo\r/e, body weights. Grealer increas€s in

r€slraint were conelated rrith greater \.'reight loss but also with a higher risk of lapses,

b6s of control, and overealing.

PHYSIOLOGIC FACTORS

The cJiscovery of leptin in 1994 opened a new window on lhe control of food intake and

body \rveight, The response ot teptindetcient chidren to teptin indicates the critical role

th6t ihis peptid€ days in the control of energy balance

TREATMENT

DIETS LOW IN FAT AND LOW IN ENERGY DENSITY

A variety of diets, induding lo^r-H ioods, lorFcarbohydrate food, or a balanced

r€duction of all rnacronutrienls, have been used to trcat obesity-

LOIIY4ARBOHYDRATE DIETS

Several conlrolled lrials showed more weight loss with a lcl\ carbohydrate diet

olan the control diet in the frst 6 months but no difference at 12 months. ln two head{o

h€ad coaparisons of four popular diets, the averag€ weight loss at 6 and 12 months
yas the same (17). fhe best predictor of weight loss for each of the diets was the

cgfee of adherence to the diet (t8).

PORTION-CONTROLLED DIETS

Po.tion control is one dietary strategy with promising long-term results- A trial in diab€tic

3dients using portion-conlrolled diets as part of the lifestyle intervention (Look AHEAD

ftogram) found more weight loss lhan a lifestyle intervention in another large clinical

lbl in prediabetic patients that did not include portion control (tg).

8f,tavi or,todifi cation and Lifestyt e tnfEryentions

Behavioral modification in lifestyle programs has been an importarf part of

Erograms for weighl loss for more than a quarter of a century- Weight losses have been

n the 5-10o/o range. Behavior modificalion has a number of components. First, it is a

sfdegy designed to help people understand their eating behavior, from the tiggers that

start it to the location, speed, and type of eating, through the consequences of eating

td the rewards that can change it. ln addition, it consists of slrategies to help people

&velrp-, assertive behavior, learn cognitive techniques for handling their intemal
Cscussions, and ways of dealing with strsqs (2O).

Exercise

Exercise is important for maintainiflg weight loss, but when used alone has not

td those who do not shows a qitical role of exercise- More than 200 min/week

trwides lrxjch more likelihood of maintaining \ryeight loss lhan loner levels of exercise.
using a pedometer a svs counting of steps. Working torr,ard 10,000 sleps per day is a

Fod qoal,
tdications
At present only two medications are approved for long term ireatmenl, namely

lhJtramine and orlistal O, 22), but seve|^al others are approved for short-term use.

rcRADRENERGIC DRUGS

Pbentermine, dielhylpropion, phenmeirazine, and phendimetrazine are approved

t the FDA for short-term use, usually considered to be up to 12 weeks. All of lhese

n€s probably work by blocking reuptake of norepinephrine into neurons. Phentermine

E among the most widely prescribed appetite suppressants.

SAUTRAMINE

Sibulramine significantly reduces the uptake of norepinephrine, serotonin, and

Jeamine by the pregranglionic nerve endings and produces dosedependent weight

lEs. The m4or drawback has been the small increase of blood pressure in some
s!]€'lis.(22)

ORLISTAT

Orlislat blocks intestinal lipase and thus enhances tecal loss of fat- Orlistat

&cks lriglyceride digestion and reduces lhe absorption of cholesterol from the

riestjne: this accounts in part tor the reduced plasma cholesterol tound in palients

!€ated with this dfug (24.

9rgery
Surgical intewention for obesity has become ever more popular (23). The

Siredish Obese Subrec{s Study offered a gastrointestinal operalion for obese patients.

The control group comprised obese patients who were treated with the best

{ematives. Weight loss for many patienls exceeded 50 kg; thos€ thal were grealer

ia.l 5O7o loss of excess weight were considered a success- There was a graded effect

d u/eight change, measured at 2 years and 10 years after the operation, on HDL
dohsterd, lriglycerides, systolic and diastolic blood pressure, insulin,'and glucose.

E$apolating fiom the degree of improvernent in these comorbidities among the

dients who l6t weight, it c€nnot be long betore this operaled group will show a

saatistically signilicant improvement in longevity resulting from a treatment aimed

specifically at reducing the mass of body lat. To maintain successtul weight loss afier

bblric surg€ry requires that calorie intake remains low. Failure rates, that is, weight

r€g4n or inad€quate initial weight bss, can occur in up to 40% ot some series indicating

tp importance ot commitment to the goals of bariatric surgery - maintaining weight

bs

66
If,Ff,RENCf,S
- .{mrdcan P*chiatric -qlsiarid DiagnGtic ad Statistrcal Mdual of Menhl Dsordetg4th ed, t€st rcv.). Am€flcan
+hidric Associatroo- IYalhingtoD, DC, 2000.
:2000 Crrltels fs ltseas Codol Gmrlh CharG fo. lhe Urired St ts Auilablc at \\as!.cdc.got7gro\\1bcbnv. ttst

: Snd*nrd AJ, Gme WJ, WollT HG The night-€alng sla&ow: A patl€m ot food iiiake rDotr8 cqiah obe* paliols. Am J
Ed 155: lq7t E6.
. Bi*dled G, Flsrholbr, J, Sud$dd J. d sl. Bcrlalio.al ard D MduiDe chrtacle.t$ics ofth€ niglt-€iliDg sladrctte
-*t{ 1999: 282:657-661
: Allisd (C, LDdgro JD, O'R€zrd.n JP, ea al hopo6.d diaCrEtic cri!6ia ftr ligrtl cnting slt&otne. Int J Ert Dsdd 2009
\r u, Epub ahe.ld o{prinL
r -{lis." KC, Ahinr RS. O'Rwdoll lP, er aL Neuro€rdosim profir€s a-rsocidd wirh cEsy itrtlke, sleep, ard sl'ess in $e
€ari.g s}r&onq .l Clin Endo.. Mebb 2m5l 90:621+6217.
-h
- xel PK PEging dis{.d€': $brh6$otd vlriant cr full-dr€.}oid eati4 dis.rd€t? l't J Ea. D's{fd 20f; 40:589-591-
t Xal Pr, Wolfc BE, uddle RA. DcYo$g KP, Jin€iso'! DC. Clinical fcatdes ad Phtsiol i@l rcsponlc !o . lest o€al in
Fghsdisrder.Bl bolimi..('vo6a Atch Gc! Psychialy 2m7l6l: I05E-1066- 9. HuJsJd JL Hnipi E, Pop€ HG, X€ssl€t RC.
:L p.6d.M ond co.relates of @rhg disord€rs in lh€ NaliqEl Como(bidily Surr'c,a Epli@tie Biol Ps''lhialry 2007; 61i348-
5t
{ R-ed CSW, Me{reg6 AM, Stun\a.d AJ The gltl €athg qn(home h fie gcnsal pQularion .nd anooS Pcl_.?<atiic
&ny wgay pdi€rni Id J Ed Dissd l99t 22:6tu9
- L Halni KA. !{@Bod oI effeaia rwo6r ir iryd;dl ald pdrar hosPildizdim s€ttinei In: Yaget I PsG PS, cds.
EF.l M ual of Eding Dso.dqs AlMiqd Pstchisaic Publshns W6hitrstoq DC, 2007, pp. I l3-l25.
a F irblrn CG, Marclls MD, W s GT. CogFitit+b€halidd theqy 16 tinge cdeg &d hrlimin !c.r'oe.: l coqrclie.siv€
tut da'ud. ln: Fairhrn CC, Wil$D GT, ods BiDgc EattrB: Na.urc, Ass€$sncn! ,n'd T'...Der( Cuiro.d PrGi NcwYdk
9qt, pp. 36l-:10l-
,l Hit hel Jq Slefer Xl, Roeiig JL Md€dtbt of brJimir a€t! o6a h Ylss J. Po*os PS, cds- Clioicd MDurl of Fitirg
I MitcheH Jq Derdn Ml, dc Zwar M, Crow SJ, Pct€s.n CB. Psrrcholfrqapy fd birse c?titg diso'd('. Bi'8+Frti's
)sdq: Clitri@l Folldd,oo6.d lEa&Dq . Guilfod Prcs+ Ner{ Yqt! 2008, pp. 5t-69.
'i. &!), &d O6.sity. Hl'rllr . PtBn Tdow', Ni, 2007.
GA. Thc Me*abolic S}o&dee
J CIh Endoqi'd Mctab 20ol; t9: 25t]t25t9.
5 Bray GA Mcdical cBs€qus'c€s ofobesiry
:t Sfaklng Kl+ ArDrr E, Wcasnrt PO, d al. Dynamics offd cclttmo*, in huDaE Ndue 20081451:783-787-
1t Qder CI. C5o$ Mq Flerrl KM Hish body nNi.dd fa lCF nnosg US.n &6 ad adol.sccrb, 2t103-2006. IAMA
s:2D:2401-241)5.
,t Finlelslei! EA Ficbelkqtr lC, Wlng G- Slrle-l€rel €slrD{t.s of Ral nedicrl eeoditures dibutabh ro ob.sity. Ot€s
ts 2004: 12:18 24.
i Rob€rrs SB, Pi-SBls FX, Dreher M, €t nl. Plrysiolos. of fd rcpl&crlor aDd f.t red.ddr: effecB of di€rry flt dd f.t
jdjl!r!. d eFry rcguldion, Ndr Rlv 1998;56 (5 PI2):S2!HI; $s$ssion S-9.
:1. hGliglf MI- Gleaso.IA- GriftI JI. Seftet HP, Scba€ls EI. Cosparisor ofl}s AltriDs, OEish, Wcisht Waldt€ir a'd
Zdc dt€e fd wighr lo6s rnd hcd diseasc d* r€duction: a rad@izcd Bial. JAMA 2005; 293:4!53.
:2 Rrrlq D, Pidsal & Li SII Cri6i C, lir DC- tns tdm pturm.colhcf,qy fn oHy ad @oTcisln: Dpdat d ne{t-
rb:is. BMJ 2007: 335: I l9l-l 199.
- Blf,hllau H, Avidoi Y, BnIlMaldE,lslsgl MD, P('rcs W, Fatub3ch r! Sclo€ll€s K. Briatric sl4ery: a stsleDatio
tiicw ed fteb-aDa\ra. JAMA 20G4; 292: t724-1737.

67
 PREGNANCY AND LACTATION

Maternal diets during pregnancy need to provide energy and nutrients for

the mother as well as for felal groMh.l Adequate nutrition at this stage cannot be

overly emphasized because numerous studies have shown the disadvantages

otherwise.

Lessons on Maternal Undernutrition from History

History shows, through the advent of famines, the effect of poor maternal

nutrition on the health of future babies. ln 1945 during the Dutch famine, there

was generatized undernutrition. During this time, most of the pregnant women

and tifty percent of non-pregnant women thrived only on less than 1000 calories

and 3O-4O grams of protein daily. This resulted to an average 250 grams drop
in

neonatal birth weights, an increase in prematurity rates with no observed

increase in stillbirths nor neonatal deaths. ln Leningrad, Germany in 1941-1942,

the most acute famine struck. With inadequate food supplies, women become

chronically undernourished. This resulted to a mean birth weight decrease

of
50G60O grams and a prematurity rale of 4'lo/o. From the Asian perspective,
the
1959-1961 Chinese iamine affecting all provinces in China, particularly the
Wuhu region ofAnhui province, saw birlh rates decreased by approximately
80%

1
chen& Dibley, zhan& zeng and yao. Assessm€nt of dietary intake among pregnant
women in a rurar
areaofwestern China. BMC pubtic Health 2009,9:222

68
for the years 1960 and 1961.'? This famine followed on the heels of immense

social and economic upheaval called the Great Leap Forward.

Maternal Underntrition and Poor Maternal and lnfant outcomes

lnadequate intakes of specific nutrients in pregnancy have been reported

to lead to a variety of poor maternal and infant oulcomes.l Severe protein and

energy shortages brought about by the Dutch famine of 1944-1945 showed that

persons born after exposure to the famine in late and mid gestation had lighter,

shorter and smaller heads, and their molhers weighed less at the last prenatal

visit compared with those unexposed.3 Yasmin et al (200'l), found that low birth

weight (LBW) is associated with an increased risk of neonatal morbidity and

mortality.'

Long Term Effects of Maternal Undernutrition on lnfanfs Adult Life

Lumey ('1992) demonslraled clear effects on reproductive outcomes in the

generation following the Dutch famine exposure in utero: lower birthweights for

offspJings of mothers exposed to famine during their first and second trimester in

uteio compared with those of mothers not exposed to famine.5 The decrease in

birthweight was in part due to slower fetal growth rate, in part to shorter

gestation. This LBW and postnalal groMh retardation have adverse long-term

t s. ct"ir,xu, wang, Yu, Fang, zhang zh€n& Gu, Feng, sham, and He. Rates of adult schizophrenia
following prenatal €xposure to the Chinese famine of 1959 1961. Journal of th€ American Medical
Association. 2OO5;294:557_562.
3
Lussana Painter, Ocke, Buller, Bossuyt, and Roseboom. Prenatal exposure to th€ Dutch famine is
associated with a preference for fatty foods and a more atherogenic iipid profile- American Journal of
Clinical Nutrition 2008;8&1648 -52.
a
Yasmin, Osrin, Paul, & Costello. Neonatal mortality of low-birth'weiSht infants in Eangladesh. Sulletjn of
the World Health Organi2ation, 2001, 79:608-614
5
lum€y, LH. Decreased birthweiShtt in infants after maternal in utero exposure to the Dutch famine of
1944'1945. Paediatric and Perinatal Epidemiology.l99. 6(2):24G53.

69
 effects on physical and cognitive development of the infant.l Barker et al (2002)

found that the risk for hypertension, chronic heart disease and type ll diabetes

fell with increasing birthweight.6 Lussana et al (2008) established that maternal

undernutrition during gestation increases the offspring's plasma chotesterol

concentration by inducing a preference for high{at food and a reduclion in

physical activity.2 Epidemiologic studies have shown that small size at birth is

associated with an increased risk of cardiovascular disease and its biological risk

factors, including type 2 diabetes, hypertension, hypercholesterolemia, and

coronary artery disease (CAD).1

Maternal Undernutrition and Cognitive Development

As to cognitive developrnent, Hoek et al (1998) summarized that early

prenatal famine was specifically and robusfly associated with each of three

condilions: (1) congenital anomalies of the central nervous system, (2)

schizophrenia, and (3) schizophrenia spectrum personality disorders.T The

.,greatest increase in the risk of schizophrenia spectrum disorder_ schizophrenia

plus spectrum personality disorder- occurred among males born during the Dutch

famine in lhe famine cities in December j94S (relative risk [RR] = 2.7). Susser et

al (1996)found that those conceived at the height of the Dutch famine showed a

twofold and statistically significant increase in the risk for schizophrenia (RR =

2.0, p < .0'l) in both men (RR = 1.9, p = O.O5) and women (RR = 2.2, p = 0.04).E

6
Barker, Ericsson, forsen & Osmond- Fetalorigins ofadutt disease: str€nAth of effects and biotogicat basis.
lnternational Journal of Epidemiobgy.2OO2;311235-9.
7 Hoek, Brown, grsser- The Dutch famine and schizophrenia spectrrrm disorders. Social
Psychiatry and Psychiatric Ettd€miotogy. 1998;33:373-379. Abstra€t
3
Susser, Neugebauer, Ho€k, Brown, tin, tatlov'tz, Gorman. khhophrenia att€r prenatal famine: further
evidence. Archives in General Psychiatry. 1996;53:25-31. Abstract.

]a
This finding was replicated in the study of St. Clair et al (2005) on the risk of

schizophrenia in later life as an effecl of the Chinese famine in 1959-1961.2 Hoek

et al (1996) found that prenatal nutritional deficiency was associated with a

e
greater risk of schizoid personality disorder in men at age 18 years

Effect of Maternal Undernutition During the Early Gestational Period

An early insult to maternal nutrition during the early gestation is far

reaching on the offspring's future adult well being as seen !n studies on the

effects of the Dutch famine: a more atherog€nic plasma lipid profile; increased

amounts of abdominal obesity in femate offsprings; lower plasma fibrinogen and

factor Vll concentrations; increased stress responsiveness and increased risk for

breast cancer in female offsprings; an earlier onset of CAD and a three-fold

I J2 13 1t 15
increase in cardiovascular disease.l0J

Effect of Maternal Undernutrition During the Mid Gestational Pedod

People exposed to famine during mid gesiation develop more obstructive

'puknonary disease and microalbuminuria.l3

e
Hoek, Susser, Buck, Lumey, Lin, Gorman. Schiroid personalitv disorder after prenatal €xposure to
f amine. Am€rican Journal of Psychiatry. 1995;153:1637-1639. Abstract.
10
Roseboom, van der Meulen, osmond, Barker, Rav€lli, and Bleker. Plasma lipid profiles in adults after
prenatal exposr re to the Dutch famine. American lournaiof ClinicalNutrition.20OO,T2:1101-6'
1I navelli, van Der Meulen,Osmond, Barker, Sleker. Obesitv at the age of 50 y in men end women
exposedto famin€ prenatallY. American lournalof Clinical Nutrition 1999.7o(s):8116.
t2 Roseboorn, uan der Meulen, Ravelli, osmond, Barker, Bleker' Plasma fibrinogen and factor Vll
con€entrations in adults after prenatal exposur€ to famine. Erltish Journal of
HaematoloSy. zmo.11l(1;t tzii. nbstract.
r3
Roseboom, d€ Root, Painter. The Dutch famine and its lonS_term consequences for adult health. €arlY
Human Development- mO6. 82(8I:485-91. Abstract.
to puinter,
de looii, Bossuyt, simmers, osmond, Barker, Bleker, Roseboom Early onset of€oronary artery
d:sease atrer prenatal exposure to the Dutch fam;ne American Journal of Clinical Nutrition.2006.
P.4l2l:322 7.
The Dutch Famine Binh Cohort Study: Hungerwinter Study http://www.dutchfamin€.nl/index htm
15

71
 Malernal Undernutrition and Diabetes

Maternal undernulrilion at any stage of g€stalion caused persons exposed

to have impaired glucose tolerance, probably because of an insulin secretion

defect.16'17

The Current Picture

Maternal undernutrition is not a thing of the past but still exists in this day

and age as shown in a 2009 study by Cheng et al of pregnant women in their

third trimester in two rural counties in western China- There was a low dietary

intake for most nutrients, especially for nutrients crucial in pregndncy such as

iron, zinc, riboflavin and folate.l Sukchan et al (2010) found inadequate nutrient

intake among pregnanl women in the deep south of Thailand: carbohydrate by

86.8010, protein 59.2%, fal 78.0%, calories 83.5%, calcium 55.0%, phosphorus

29.5o/o, iron 45-2%, thiamine 85.0%, riboflavin 19.2%, retinol 3.8Vo, niacin 43.2o/o,

vitamin C O8%, folic acid O.0% and iodine 0.87o inadequale.ls

., Guirindob wrote in 2006 that the Food Consumption Survey conducted by

the Food and Nutrition Research lnstilule of the Department of Science and

Technology (FNRI-DOST) as a component of the National Nutrition Survey

revealed that the food intake of Filipino pregnant and breastfeeding women was

less than what is required based on the Recommended Energy and Nutrient

16D€
Rooij, Paint€r, Phillips, Osmond, Michelr Godsland, Eossuyt, Bleker, Roseboom. tmpaired insulin
secretioo after prenatalexposure iothe Dutch famine. Diabet€s Care.2006.29{8}i1897 901.
17
Ravelli, van der Meulen, Michels, Osmond, Barker, Hales, Bleker. Glucose tolerance in adults after
prenatal exposure to famine, Lancet. 199a. 351{9097)r173-7. Abstract.
t" Suk"h"n, tirb.uetrakrrl,
ChonSsuvivatwong, songwathaha, So.nsrivichaL and Kuning. tnact€quacy of
nutrients intake amont pregnant women in the Deep South ofThailand. BMC Pubti€ Heatth 2O1O 10:572
 lntakes (RENI).1e Based on said survey results, the dietary pattern of pregnant

and b'reast feeding women is a rice-fish-vegetable combination. When the daily

food intake was computed to equivalent nutrients, it is alarming thdt except for

niacin, all other nutrients are below the RENI.

Nutrition must be a great concern for individuals especially women to

accomplish one of the goals of womanhood: that is lo give birth to a healthy child.

This needs plan and preparation so in order to have a healthy child nutrition is a

great factor to be consider.

Having discussed all these, we can summarize that good maternal

nutrition results in: lower incidence of abortion and miscarriage, fewer stillborn

and premature infants and infants with congenital malformations, fewer

complications during pregnancy (toxemias and anemias) and delivery (prolonged

labor, premature separation of placenta and hemorrhage), healthier full term

babies, and reduced infant mortality and morbidity rates.2o

The fetus is not a parasite. From early hislory lo current times, every culture

has had myths about diet in pregnancy and one of the more common pregnancy

myths is that the fetus is a parasite - capable of drawing whatever nutrienls it

needs from the mother at the expense of her health. This fallacy is refuted

because of the following arguments: there would be no such thing as a small or

poorly nourished newborn (the fetus receives an adequate supply

of nutrients

tt cuirindola, M.O. pregnancy and BreastfeedinS pinoy: Women Low in Energy and Nutrjent
tntake.
NAMD. WP- Jan,Dec 2006.
')o tagua, Claudio. Chapfian and Ha . Nutrition and cliet therapy reference dictionary
+th tdition. usA.
7996. ?252
 only if the mother's intake is sufficient lo maintain her own health); studies

identified deticiencies of vitamin 812, thiamine, iodine, folate, zinc and other

nutrients in newborns but not in their mothers; and infants born to women who

consumed excessive levels of vitamin or mineral supplements during pregnancy

are more likely to display signs of nutrient overdose than are the molhers.2l

DIET DURING PREGNANCY

Energy: Resting energy expenditure increases during pregnancy because of the

expendilure of the fetus and placenta and the increased workload on the heart

and lungs. lt is also needed to support weight gLain primarjly in the second and

third trimesters. According to Barba and Cabrera, the revised Required Energy

and Nutrient lntake (REN|) ot 2002 by the FNRI requires an additionat 3OO kcat

over and above the non-pregnant state during the 2nd and 3d trimesler.22 lFor a
summary of all the requirements, see tables at the end of lhis lecture guide.)

Calories: Total energy cost plus maintenance (additional work of maternal heart
''and uterus and the sleady rise in basal metabolism)
amounts to approximately

80000 cal. The energy cost of pregnancy ten is about 300 calories a day. Energy

intake should 36 calories per kilogram of pregnanl weight per day or 71 grams

per day.

Proteins; According to Guirindola, among pregnant women, energy and protein

intake is only 78.4 percent and 84.7 percent adequate, respectively.ie Food

Nutrition research lnstitute (FNRD of the philippines suggests increase of 14 yo jn

a
Brown. Nutrition Now. n'h Edn. thomson. gngapore. zoo5. page 295.
'z2 Barba and Cabrera. Recommended energy and nutrient inta*es for Fitidnos mO2. Asia pac, Ctin Nutr
2oo8;17 (S2):3994Oa.

74
 protein intake of pregnant woman over non pregnant
state (from 5B mg among
non-gravids to 66 mg protein in pregnant women).22 Additional protejns
provide
for the increase in maternal tjssue and for the groMh of fetus especjally
during
second and third trimesters. Two thirds of proteins should be of
animal origin of
the highest biological values (meal, eggs, cheese, poultry and fish).

Protein inadequacjes may lead to nutritional edema. Some research

workers believe that a diet low in protejn may cause toxemja of pregnancy.
Other
disorders may indicate anemia, poor muscle lone of uterus, abortion
lowered
resistance to infection and insufficient laclation.

Calcium, Phosphorus and Vitamin D: Guirindola wrote lhat calcium

intake was
less lhan 80% adequate for Filipino pregnant women.ie Calcium
is one of lhe
most important elements of the diet for the pregnant woman. Adequate
supply of
Vitamin D is essential for utilization of calcium and phosphorus
necessary for the
calcification of fetal bones and teelh, as well as for the gravid
woman,s own
FNRI recommends a 7yo increase in calcium for the pregnant
.,needs. woman
(from 750 mg of non pregnant state to 8OO mg in the pregnant
woman), but the
same phosphorus (700 m9) and vitamin D (5 pg) requirements
for both the
pregnanl wornan and th€ non gravid state.22

lron: Guirindola noted that iron, the nutrient specifically important

for malernal
blood volume and iron stores of the baby, is only 2g.8 percent
adequate for
pregnant women based on RENl.re There is
an increased need for iron to supply
the growing fetus. rron is slored in river for use during first
three to six months of
life. During second half of pregnancy, the molher requires grams
6 of iron daily to
increase her own blood volume and transfer necessary iron to placenta and

fetus. FNRI recommends a 26% increase in iron requirement during the 2nd

trimester and a 4'l yo during the 3'd trimester over the non-pregnant state.22 From

27 mg of iron in the non pregnant state (and l"rtrimesler) to 34 mg in the 2nd

trimester and 38 mg in 3'd trimester. Hemoglobin production also requires an

adequate supply of protein to furnish essential amino acids, sufficient calories to

protect the protein from catabolic degradatjon and iron and other minerals such

as copper, zinc, tolic acid, vitamin B-'12 and other cofactors involved in synthesis

of heme and globin. lron deficiency can lead to fatigue, increased susceptibility

to infections, increased risk of preterm delivery and increased incidence of low

birth weight. The iron from animal products, such as meat, is most easily

absorbed. Good sources include lean red meat, poultry and fish. Other options

include iron-fortified breaKast cereals, nuts and dried fruit. Pairing iron-rich food

from plant sources and supplements with a food or drink high in vitamin C would

pnhance absorption.

lodine: This mineral is of special importance in pregnancy to meet the added

demands placed upon the metabolism by the thyroid gland, to meet the needs for

fetal developrnent and to provide for the deficiency in iodine due lo urinary loss

during pregnancy. Maternal iodine deficiency has been associated with a number

of adverse effects on the infant brain resulting in a continuum of effects

depending on the d€gree of iodine deficiency, from lowered lQ to severe mental

retardation.a The thyroid gland uses iodine to make thyroid hormones, which in

'?3 nenner, n. Dietary dine: why Are so Many Moth€rs Not Getting Enough? Environm€ntal Heahh
Persp€ctives 2010. 118{10}A438-442.

16
turn direct brain development. lnsufficient iodine is considered the leading cause

of preventable mental relardation in the world, and iodine deficiency in pregnant

women has b€en estimated to result in the loss of some 1G-15 lQ points at the

global population level. The RENI for pregnant woman is 200 pg compared to

'l50pg for lhe non gravid woman.22 An inadequate iodine may result in goiter in

the mother, especially the adolescent. The child may have goiter also, or, in lhe

case of severe iodine deficiency, the child may develop cretinism.

Vitamins: According to Guirindola the mean riboflavin intake of Filipino pregnant

women does not meet one-half of the requirements of pregnant women at 48.'l

percent while intake of vitamin A, thiamin and ascorbic acid is less than 80% of

adequate levels.le FNRI recommends the following: a 60yo increase in Vitamin A

over that of the non-pregnant state (from 500 to 800 pg RE), 14% increase in

ascorbic acid (from 70 among non-gravids to 80 mg Vit C in pregnant women),

27o/o increase in thiamine (from 1.1 among non-gravids to 1.4 mg thiamin in

pregnant women) 5570 increase in riboflavin (from 1. 1 mg among non-gravids to

'1.7 mg riboflavin in pregnant women), and 29o/o increase in niacin (from 14 mg

among non-gravids to 18 mg niacin equivalent in pregnant women1.22 There is

strong evidence that maternal vitamin A status during the embryonic and fetal

periods is important for normal cardiac development.za Retinoic acid, the

biolosically active form of vitamin A, is an important signaling molecule during

fetal cardiovascular development. A state of both deficiency and excess has

'?a Christian and siewart. Maternal Micronutrient Deficiency, Fetal Development, and the Risk ofchronic
Disease. Journal of Nutrition. 140:437-"445, 2010.

77
been associated with congenital malformalions in both human and animal

studies. Folic acid requiremenls are markedly increased during pregnancy

because it is a period of rapid cell multiplicatjon and DNA synthesis Evidence of

folate depletion including megaloblastic anemia is common. Thus' RENI for folic

acid is an additional 20opg per day, bringing the total requirement to 600tjg per

day.22 This normally cannot be met by diet alone. Folic acid supplementation is

recommended.

DIET DURING LACTATION

Lactation - term used for the breast milk production in mothers after the

birth of a baby. Lactation starts following delivery of a baby and the preparation

of effective lactation starts during pregnancy. During breastfeeding, an adequate

and wellbatanced diet is needed for continuous milk supply to give all the

nutritional needs of the baby exclusively for six months and onwards. A nutrition

shortage for mother is more like to reduce the quantity of milk than the quality of

.the milk for baby.

Energy: According to Barba and Cabrera, the revised Required Energy and

Nutrient lntake (RENI) of 2002 by the FNRI requires an additional 500 kcal over

and above lhe non-pregnanl state during the 'l"t and 2nd 6months of lactation-22

Calories: The production if milk by maternal organism demands an extra 600 to

8OO cal above the normal intake. The energy mst in producing 100 mL of milk is

120 cal which translate 10 an extra 1,020 cal spent in producing 850 mL of milk a

day.

78
 l
Proteins: Lactation makes large demands on human nitrogen stores. The food

intake of the nursing molher must contain sufficient protein to supply both the

maternal needs and the essential amino acids to be transferred through her
breast milk to the baby. Human milk contains 12 mg/mL of protein. The amount
l

of protein in 850 mL is 10 g. lf the protein in the mother's diet is inadequate both l

to meet her body maintenance needs and to provide the protein for the milk

secreted, a loss of maternal body tissue will result. The protein content of the

milk will not be reduced. FNRI recommends an increase of 407o in protein intake

during the 'l"t Omonths of lactation and 31yo increase during the 2nd €months of

lactation by a nursing mother over that of the nonJactaling woman

z

Galcium, Phosphorus and vitamin D: FNRI recommends the same calcium

(75O mg), phosphorus (700 mg) and Vitamin D (5 pg) requirements for both the

pregnant woman and the non gravid state.2z

lron: Sorne lactatinq women tend to become anemic unless the iron allowance in

their diet is mainlained at the same level as during pregnancy. Dudng lactation

there is loss of iron which, if considered on an annual basis, is probably similar

in quanlity to that lost in the menstrual flow. FNRI recommends the same iron

requirement for both non pregnant and lactating mother during the first 6months

of lactation (27 mg lron) while women in the 2nd 6 months of lactation have'l1o/o

increase in iron requirements over that of non-pregnant state (from 27 mg of non-

pregnant state to 30 mg iron of pregnant state).22

79
 lodine: A 33% increase in iodine is required in laclatjng
mothers compared to
non-lactating state (1sopg for the non lactating
woman to 200 pg in lactating
mothers).22

Vitamins: FNRI recommends the following: 807o increase

in Vitamin A
requirements in the lactating mother (from 5OO pg RE
of nonjactating to 9OO pg
RE of lactating mother), a S0% increase in Vitamin
C during the .lst6 months of
lactation then a 43yo increase during the 2nd 6 months
of lactation over the non_
lactating state (from 70 mg Vitamin C in the nonlactating
state to 10S mg during
'l"tomonths of laclation, then
100 mg during 2nd 6 months of lactation); 36%
increase in thiamine (1.1 mg of non_lactating state to
1.S mg in the taciat,ng
state); same requirement for riboflavin ( 1.7 mg);
21yo inctease in niacin (from 14
mg niacin equivalent in the nonlactating state to .17
mg in lactating state); and a
25olo increase in folic acid (from 4OO pg of non_lactating
state to SOO pg folic acid
in the lactating state).z Breasl milk reflects the
mother,s intake of waler sotuble
vitamins and not the fat soluble vitamins. This is
exemplified in infants nursed by
mothers who have thiamine deficiency, the babies
develop infantile berjberi.

EO
 :"??;9i<.> E3F R,i

. -_::.,-.:.,1 9;-:,;,kk: :;: r.s

I E
F99FFis FFAFFcE

tl aBSEE= 3 AAaaAAE

6z
:E

'i
ii

E
:€

!
SAEFsgfi g*tf;EeE g5s sH
t
E

t
El
EI
EI
el
:l
I!
EI
E
E€ 3:3
a:l. - , E!
r i,:Fj.; e .-:,::: F:9; E!_E"CE5=
3!i i! --:at-i
nl ! -- i* :3 e e B 3 * i: a: : * fi 3 FF; I S E; *.
rl

*8ar ba ccabr energy and nutrient intakes for Filipinos 2002. Asia PacJ Clin
NUtT 2O0E;l7 7 s4 39q404.
ls2

81
 , P ae o.!oo..l
-@r-

ec o$soa
- -
? -F4
l
l

h6 tsi nfF o(crr-

l9
i"
i 9c .i-
ls
)

i-a
;r.:e -?

, iiI iEe
tiEt
e'l €38 ffc;Ea
. !lE Ld '

oi o{
PI 'L'
,! 6,
R c9

.sl 6 00

a-=* €
9.!A Ar-- C
9.
:rc-;.-, 9:=-4s
a;
! f 5 3----- =

'Barba and Cabrera. Recommend€d eneaSy and n utri Filipinos 2002. r Pac I Clin
Nutr 2OO8;17 (s2):399404.

82
 DIETARY MANAGEMENT OF
GASTROINTESTINAL DISEASES
DIARRHEA

Diarrhea is probably the most common manifestation of a malfunctioning

intestinal tract. lt is characterized by an increase in frequency and liquidity of
stools. lt can result from a variety of diseases or conditions (eg. celiac disease,
lBD, ostomies, following radiation of the pelvis, short bowel syndrome) and is
categorized by its origin as either osmotic with malabsorption and steatorrhea.
secretory from a change in electrolyte transport, or inflammatory, resulting from
enlerocyte damage. Diarrhea, based on its etiology, can also be classified as
functional or organic.

Some of the major causes of functional diarrhea are overeating or eating

the wrong foods, fermentation caused by incomplete digestion of starch,
putrefaction in the intestinal tract, nervous irritability, endocrine disturbance, and
diarrhea associated with diseases such as sprue and pellagra. Adolescents may
have loose bowel movements preceding the excitement of a dance or school
game. ln children, fright may cause diarrhea.

Organic diarrhea may be caused by external poisons, bacterial and

protozoan invasion, and may accompany certain djseases such as amoebic
dysentery, bacillary dysentery or Shig€llosis, typhoid fever, viral hepatitis, chronic
ulceratve colitis, regional ileitis and enteritis or by enzyme deflciency like lactose
intolerance.

Principles of Dietary Management

Liberal Fluid lntake. Large amounts of fluid may be lost and should be replaced
immediately to prevent dehydration, especially in susceptible age groups as the
very young or elderly persons.

Electrolytes. Losses of sodium and potassium and other electrolytes account for
the profound weakness associated with severe diarrhea. potassjum loss, in
particular, is detrimental as potassium is necessary for normal muscle tone of
the
GlT. Anorexia, vomiting, listlessness and muscle weakness may occur unless
losses are replaced by a ljberal intake of fluids such as fruit juices that are high jn
potassium.

a3
 Since 1971 , WHO and UNICEF began to promote the use of a standard
formulation for the preparation of oral rehydration solutions, widely regarded as
the physiologically most appropriate single formulation for world-wide use. lt
consists of the following active ingredients mixed in dry form for making one litre
of solution:

Glucose,anhydrous 20.09
Sodium chloride 3.5 g
Sodium bicarbonate 2.5 g
Potassiumchloride 1.5 g

Total weight 27 .5 g

Locally, it is distributed in packet by the DOH as Oresol.

Oral rehydrating solution ( ORS ), in the absence of oresol, may be prepared at

home as follows:

% tsp crude rock salt dissolved in 1 glass of

'1 tablespoon ( tbsp ) sugar boiled water or tea

Food is withheh for the first 12 - 24 houts to rest the clT. tf the fluid and
electrol!,te loss is critical, intravenous fluids may be given. As soon as possible,
foods should be given by mouth to provide calories not possible to obtain in
intravenous parenteral feedings. Simple foods are served first, such as broth,
qiuel, dry toast and tea. The amount of food allowed gradually proceeds to low
fiber diet which is high in calorie level, protein concentrales such as dry skim milk
powder can be added to milk, beverages and deserts, and carbohydrates such
as glucose and lactose can be added to beverage. Emulsified fats like butter and
cream may be added to foods as tolerated. ln the beginning, only fruit and
veg€tables juices will be included, then creamed vegetables soup and finally,
selected whole cooked foods. The return to normal is gradual. pectin has a value
in the treatment of diarrhea and is included in diets for children. Scraped raw
apple or liberal amounts of banana powder or applesauce in thin rice gruel or
vegetable broth may be given as tolerated for their pectin content.

A recent review article in the Journal pediatrics, Lactobacillus Therapy for

Acute lnbctious Diarrhea in Children: A Meta-analysis, offers a new treatment.

84
 The article states that Lactobacillus is safe and effective as treatment for
children with acute infectious diarrhea. One common way to give Lactobacillus is
to just feed a child yogurt with live and active cultures, which means that the
yogurt contains Lactobacillus bulgaricus and Streptococcus lhermophilus. Some
brands of yogurt also contain Lactobacillus acidophilus. Although most brands of
yogurt do not list the amount of live and active cultures on the label.

ATONIC CONSTIPATION

This is also called " lazy bowel " because of the loss of rectal sensibility;
lhe rectum is full of feces but the urge to defecate is lacking. lt is often observed
in older people whose body process are slowing down; it also occurs in obese
individuals, following operations and during pregnancy as well as fevers.
lnadequate diet, irregular meals, insufUcient liquids and fiber. and failure to
establish a regular time for defecation are the most important causes of atonic
constipation.

Dietary Management

The current trend in treatment is to develop regularity of habit through

boweltraining program and establish good health habits; regular meals, high
fiber and adequate fluids and exercise.

Recommendations emphasize on the use of high tlber foods, rather that

fiber supplements. Not only do high fiber foods contain phytonutrients, thought to
be protective against chronic disease, but many high fiber foods (eg, fruits and
vegetables) also contain water.

Fluid intake is also important in the treatment of constipation. The most

recent DRI recommends a total water intake for adults of 3-4 L per day from both
food and beverages,

SPASTIC CONSTIPATION

Atso known as lrritable Colon syndrome, it is caused by overstimulation of

the intestinal nerve ending which results in irregular contraction of the bowel.
 There is uncoordinated sigmoidal mobility and
loss of rectal sensibility. There is
abdominal pain, belching, heartburn, flatuience, palpitation
anJ ne-niou"ness.
Dietary Management

A low fiber diet is recommended so as not to irritate the

membrane of the jntestinal tract. Smooth non _ mucous
irritating tooOs sucn as mitt,
eggs, refined bread and cereats. butter, oil, -meal,
finety ground Rsi]pourtry ano
simple desserts are included in the diet. Large
airount of i"i'ur. inoi""t"O tor.
calorie and lubricating effect. Vitamin supplements
are lnctuaeO e-specially if the
restricted diet is prolonged. The return to normal
diet is gradual.

GASTRITIS

The term gastritis should be reserved for histoloqicallv

inflammation of the gastric mucosa. The etiotogic -l;i'nl documented
factors io"g""triti"
broad and heterogenous. Gastritis has been
classified U""ul "ori tl_" "ru
(acute vs chronic), histologic features,
"our.u
and anatomic distribution of ot proposed
pathogenic mechanism.

ACUTE GASTRITIS

.Acute gastritis is an inflammation of the gastric mucosa,

sometjmes violent in onset bul the term js sudden and
oft-en apptieJ ro*'aiv
discomfort. Atacks very often folow di"tay i;;;;;u;;n]", "tor""f,
overeating eating too fast or eating when .u"h
specific foods to which the individuat is
tired o, rpa"r, or eatjng ".
of
"rn"anuf,r
sensitive. Too ,u"i, iloiJ, roo"""o,
seasoned foods may atso be contributing
lld. ligtttvstaphytococci fr"i"r"'iilituo io"o"
or drugs tike saticylates uno
:onl:inils
anolher factor. ",irnoniri "ir'oiide can be
Medical Care

Administer medical theraov as needed,

depending on the cause and the
findings.No specific' therapy io, u",it" g""i,iil,"."x"ept
l:lholosicat
cases .exi.t"
caused by H pytoti.Administer fluids ;;;]roii;;' ;s
ror.
required,
particutarly if the patjent is vomiting. ""d

86
 Discontinue the use of drugs known to cause gastritis (eg, NSAlDs,
alcohol). A long-term prospective study found that patients with arthiitis who were
older than 65 years and regularly took low-dose aspirin were at an increased risk
for dyspepsia severe enough to necessitate the discontinuation of NSA|Ds. This
suggests that better management of NSAID use shoutd be discussed with older
patients in order to reduce NSAID-associated upper cl events.

Dietary Management

The initial treatment is to get rid of the offending substance as soon as

possible. lt may be necessary lo empty the stomach by jnduced vomiting, lavage
or both. lrrigation of the colon and the administration of a laxative may also be of
value in hastening the cleansing process.

To allow the stomach to rest and heal, food is usually withheld !o( 24lo 48
hours. Fluids are given int@venoqsly. Following the fast period, low fiber liquid
foods are given as toleraled. Milk, toast, cereal and cream soup fed at intervals
of one hour. Stimulating broths and highly seasoned foods should be avoided.
The amount of food and the number of feeding are increased according to the
patient's tolerance until he or she is eating a full regular diet.

Nutitional tips to help reduce symptoms:

. Foods containing flavonoids, like apples, celery, cranberries (including

craoberry juicel onions, garlic, and tea may inhibit the groMh of H pylori
. Eat antioxidant foods, including fruits (such as blueberries, cherries, and
tomatoes), and vegetables (such as squash and bell peppers).
. Eat foods high in B-vitamins and calcium, such as almonds, beans, whole
grains (if no allergy), dark leafy greens (such as splnach and kale), and sea
vegetables.
. Avoid refined foods, such as white breads, pastas, and sugar.
. Eat fewer red meats and more lean meats, cold_water fish, tofu (soy, if no
allergy) or beans for protein.
. Use healthy oils, such as olive oil or vegetable oil.
. Reduce or eliminale trans-fetty acjds, found in commercially baked goods

87
 such as cookies, crackers, cakes, French fries, onion rings,
donuts,
processed foods, and margarine.
Avoid beverages that may irritate the stomach lining or increase
acid
production including coffee (with or without caffeine),
alcohol, and carbonated
beverages.
Drjnk 6 - 8 glasses of filtered water dajly.
Exercise at least 30 minutes daily, S days a week.
ldentlfy and eliminate food allergies.

Probiotic supplement (containing Lactobacillus acidophilus .10

), S _ billion
CFUs (colony forming units) a day probiotics or,,friendly,,
- bacteria may hetp
maintain a balance in the digestive system between good
and harmful
bacteria such as H. pyloi. probiotics may help suppress H. pyloi
infection
and may also help reduce side effects from taking antibiotics:
ihe treatment
for an H. pyloi infeclion. Some probiotic supplements may need
to be
retrig€rated for best results.

CHRONIC GASTRIT'S

The same dietary indiscretions ljsted for acute gastritis

seem to be
frequent causes of chronic gastrjtis. The illness oflen preceies
ttre OJvetopment
of .organic gastric lesions such as ulcer and can.cer. The
chief manifestation is
pain which maybe mjld at tjmes but severe
and cutting at intervals.
Erosions, ulcerations, changes an the blood vessels
-
surface cells can be via endoscopy.
and destruction of
These then can be conerated wittr cnemicat,
histological and clinical findings to help make definite
diagnosis.

Medical Care

Treatment of chronic gastrjtis,can be directed to a

,
when it is known. ln other situations tn wnictr gist;t'is specific etiologic agent,
invotvement of a systemic disease, js
f.ir""Jit" g".tri"
treatment targei;oto ii,e pim-Ji, oise"se

.. .. . Until recenfly, specific recommendalions

rimired to peptic urcer
tor H pylori eradication were
disease. However, at the 1997 Dige;iiv; H;;it ]iiti"tiuu

88
 (DHl) lnternationar update conference on.H pytoriherd
in the united states, the
recommendations for H pvtori restjng and
infection is not easitv cuied an4. risesr"n 6as
t,;;r";i;;; -";;;
"nlll iJn"uo u pytori
snow-n fol, ,uttiorug
therapy H pybri are bacteria that infect the mucosal
bacterial. infections, therapy incrudes antimicrobiar
surface. As with other
rs sensitive. The antjbiotics that have prouun
ug"ni" lo ,h i"r, ii" bacterium
ufr"""tiu" ii"irjJ"#nti rorny"in,
amoxicittin, metronjdazote. tetracvctine, rr.i"nJ""".
antibiotic agents have been poor, ranging- ""0 from oy" to i"re*iatl'witn single
es"Zi'. i4Jiorn"r"py i"
associated with the rapid devetopmenl oj antiUiotic
metron jdazole and clarithromycjn.
i".Li"n".,'""ip""i"f lV to

Dietary Management

diet should be adequate in calories and nutrition

. .The
consistency.
and soft in
Highry seasoned foods are to be avoided
and riquids during mears
should be restricted lo bare minimum as excess
of it tends to cause discomfort.
Frequenl small meals eaten regularly and chewed
antacid th€rapy are the mainstay of treatment.
in.r"lf ,tl-r.iur""c *itt

PEPTIC ULCER

An eroded lesion in the gastric mucosa or duodenal mucosa

..
pepliq ulcer. Duodenal is termed
ulcer are much rnore common in"" g;"i;;ro"*,
both kinds occur in the male more frequenfly ano
than i" f""ral"li.r"ffy p*pl"
i"
who are naturally tense, hardworking, workaholic,
anA cnronic worfer.,
An acidic environment is believed to be the principle
cause of peptic ulcer.
Normally, the mucosa of the stomach is protected
frorn tie- strJngry aciOi"
digestive juices by the mucus secreted by glands
from th" fo,""l' to
the upper duodenum. The duodenum is "Jopf,"gu"
also protected Uf tn-J-pancreatic
secretjons, which contains rarge quantities
of sodium ui"uruon"L ti,lt'n"utr"t,r"
the hydrochloric acid in the gastric juice. ln the
alkaline ,,
inactivated and cannot digest the duodenal "nu,ror_"-ni. OuO,,n
rnu"o"".Jiu ,-u""o"n'*t'y'in"
and duodenal acidily gets too high and why g""tri"
the mucosa to"u" it" ,l.i"t"n"" to
have j"""
normal gastric acidity are not clear but manytheories
"rgn"""O.

89
 lvlost duodenal ulcers occur within
3 cm of pylorus, at a point where the
gastric acidity is high. The following observations may
pathogenesis of the diseasel help explain the

1) lncreased capacity to secrete acid in response

because of a greater number of parietal
to gastrin
cells. va"imj
secretion has been found to be twice that "liJ
of persons witho-ui
duodenal ulcer disease.
2) Increased sensitivily of parietal cells to gastrin
3) Hypersecretion of gastrin in response to
meals
4) Decreased abjlity to jnhibjt gastrin realised
when the acidity of
the gastric content drops too low.
5) lncreased nocturnal gastric secretion.
6i Rapid entry of acidified chime into the
duodenum; it cannot be
neutralized rapidly enough.

All of these abnormal functions resufts in

an increased acid load to the
duodenum and development of a duodenal ulcer.

GASTRIC ULCER

, Most gastric ulcers are found in the atrium

of
'uf the stomach. Their
pathogenesis seems to be different
from tfrat ot auoOenaf c"rlril"U"r","n
possible pathological processes:
"*
1) Gastritis or inflammation of the antrum
or pyloric gland areas
tends to occur wjth gastric ulcer and ,!i, U" ""-or"*,"",
condition.
2) Chronic backward diffusion of H+ ions after the normat gastric
mucosal barrier is disrupted results in gross -
^
3) A disturbance in antroduodenal motil-ity can
muc"""l d";;;;.
from the duodenum to reflux back inro ""r""-i,J"""ia.
ir," .torl"n-*1""r. fl'r]v
break the mucosal barrier and cause gastritis.
The damaged

90
 mucosa then becomes susceptible to peptic ulceration. Other
agents that break the barrier are salicylates and alcohol.

Although chronic ulcer usually follows a typical course and produces

characteristic symptors, occasionally the symptoms are either non-existent or
indefinite, and hemorrhag€ or perforation maybe the first sign of the illness.

Predisposing Factors

Faculty dietary habits, excessive smoking, excessive aspirin and

excessive drinking of coffee and cola drinks are associated with an increased risk
of developing an ulcer.

Rushing through meals, improper selection of food and irregular mealtime

are poor eating habits that set the stage for ulcer development.

Heredity, physical stress, emotional conflicts, psychic trauma are

additional factors that can possibly contribule to ulcer formation. ( Explain the
possible role of stress in ulcerogenesis ).

Treatment of Peptic Ulcer

The objectives of treatments are:

- Relief of pain
- Healing of the ulcer
' - Reduction of the tendency to recuffence

The accepted medjcal treatment js directed towards the neutralization of

acids and the reduction of acid secretion by the stomach. By elevating the pH
of gastric contents, the proteolytic activity of peptin and the damaging effect of
acid are reduced. ln addition, therapy aims to preserve the resistance of
epithelium to tl€ destructive action of gastric iuice. These are achieve by the
use of antacids to neutralized the excess acidity, antispasmodics to inhibil
motitity and relieve pain, anticholjnergics to inhibit acid secretjon like H2
receplor antagonist (Cimelidine ) and proton pump inhibitor ( Omeprazole ).
H.pylori is treated with Metronidazole in combination with broad spectrum
antibiotics.

91
 Dietary Management

1) Adequate calorie to maintain DBW

2) High protein
- To promote healing
- To buffer the acids
- To replace nitrogen lost from the ulcer
3) Adequate carbohydrates to provide energy
and spare protein
4't High fat, preferably unsaturated, to inhibiigastric
secretion and motility
via cholecystokinin
5) Small frequent meals
- To afford rest to the organ
- To maintain constant neutralization of the acid
- To minimize distention of the stomach, thus minimize
gastrin
secrelion and HCI secretion
6) Fiber reslricted to reduce motility
7) Avoidance of gastric secretagogues, e.g., caffeine
containing
beverages and alcohol.
8) Avoidance of foods known to be gas_formers like cooked
cabbage,
Baked beanq milk, onions, fried foods, spiced
.because of the wide variation in
foods and orange juice.But

tesred, individuar torerance seems toslltJ:T.il[ff:;:::X,",,ff

individual response.
:t#L"1:
9) Avoidance of NSAIDS like salicylates as well as steroids
and other
drugs known to afiect GIT mucosa negatively.

Regardless of the regimen prescribed, careful

counseling of the patient is
essential. The emphasis should be on foods that
are allowed, not on foods to
avoid.

Eating meals in a pleasant environment wjth a

calm, happy frame of mind
should be given equal importance. Rest before
uft"r'rnuli'"uJn to, u t"*
minutes is conducive to qreater meal enjoyment. "nO fooO
chewed and eaten srowry rather than in haste. ihe patientnr"
stroutA i.
properry
,o rong
".truri"n

92
 term habits of eating his meals regularly and to practice moderation in eating as
well as in other activities. ln other words, a change in lifestyle is recommended to
complement dietary management.

References:

Nix, S. m05. Williams'Basic Nutrition and Diet Therapy, Vol t. Mosby, tnc.

Delegge, MO, M.H. 2008. Nutrition and Gastrointestinal Disease. Humana press

Buchman, Allan. 2006. Clinical Nutition in Gastrointestinat Dlsease. SLACK

lncorporated

lannelli, Ni1D, V.l. 2006. New Treatment for Diarrhea. http://About.com.pediatrics

93
 NUTRITION IN PATIENTS WIT}I DISEASES
OF THE LIVER AND
THE PANCREAS

PATIENTS WTH LIVER DISEASE

The river is a fundamentar organ for maintenance of meiaboric

homeostasis and therefore, when the liver,s
ability to mainlain homeo$asis is
compronised, it can be expected that signmcant
meraboric abnormarities wil
result. Palients with lhe end_stage liver disease
of cinhosis frequenfly exhibit
significarit marnutrition, and the proper medicar
management of the cinhotic
palient focuses, in large part, on nutritional
aspecls of therapy.

NUTRITIONAL CONSEQUENCES OF LIVER

INJURY

Acute Liver tnjury

.' Regardless of cause, acute liver injury is

often associated with anorexia,
nausea, and vomiting. When the liver injury
is due to alcohol, these symptoms
may be exacerbated by concomitant alcoholic
aa$rifis. Thus, acute liver injury
is likely to decrease the oral intake of ,ood,
but if the illness is short-lived and
sef-rimited' nutritionar consequences are
minimar. Both arcohoric and
nonalcoholic acute liver injury may cause
fasting hypoglycemia. This has been
attribuled to depleted live, glycogen reserves
and a block in gluconeogenesis
from arnino acids.

94
 Chronic Liver tnjury

Nutritional complications are frequent when

hepatic function becomes
impaired in chronic liver injury, particularly
cinhosis. Regardless of etiology,
cirrhosis is likery to cause patients to have abnormar anthropometric
measuremenls (i.e., muscle wasting) and to
be anergic lo common antigens on
skin testing ( 6). Circulating levels of bolh fat_
and water_soluble vitamins are
lo\,\, in a high percentage of patients
with alcoholic cinhosis. Low serum tevels
of
fat-soluble vitamins are more charac{eristic
of nonalcoholic cirhosis (7)_ These
nutritional deficiencies arise as a result of
one or more of the following fac{ors:
inadequate dietary inlake, maldigestion,
malabsorption, and derective
metabolism.

Dietaty lntake

lnadequate intake of protein is common,

., especially among alcoholica
with cirrhosis. Changes in mental status thal result ,rom hepatic
encepharopathy may arso contribute
to the poor intake of patients with
advanced liver disease. Hepatic coma
in turn is likely to result in hospitalization,
rryhich may itself exac€rbate nutritional deficiencies in these patients.

Mald ige stion and Matab soryiion

Decreased bile salt secretion and pool

size have been demonstrated in
patients wirh cifftrosis (8). rn
righl of the rore of bire salts in ,ar
dig€stion,

95
 contraclion of the bire sah poor wourd be
expected to impair micelre ,ormation
and lead to abnormalities of fat assimilation, especially
in patients with
underlying pancreatic in-suftic,ency. Steatorrhea
in tum causes deficiencies in
fat-soluble vitamins, with clinicat manifestations
such as night blindness,
osteoporosis, and easy bruisability or hemorrhage.

Metabolic Changes

A number of defects in protein metabolism have been

noted in patients
with chronic liver failure:

. Decreased hepatic synthesis of export proteins (albumin,

coagutation
factors), decreased urea synthesis ( 9), and
decreased metabotism of
arornatic arnino acids.

. Decreased synthesis of plasma proteins which leads to

hypoalbuminemia and exacerbate the formation
of ascites in patients
with portal hypertension.

Oepressed levels of coagulation fac{ors may predispose

these
patients to the risk of gastrointestinat
(Gl) hemorhage.

Failure to detoxify ammonia and the abnormal

amino acid profile of
palients with cinhosis may in part increase
the likelihood of hepatic
encephalopathy.

96
 NUTRITIONAL THERAPY IN LIVER DISORDERS

Protein and Amino Acids

To the extent that patients with liver injury, either acute

or chronic, are in
negative nitrogen balance, it has been assurned that river
regeneration wilr be
delayed and that muscre wasting wifl be accererated.
However, when feeding
protein or administering amino acids, one musl
be aware of lhe precarious
balance between the need to reslore protein intake and
the potential risk of
precipitating hepatic encepharopathy. positive
nitrogen barance can be
attained in patienls wiih chronic liver iniury (cinhosis)
with daity amounts of
dietary prorein (0.74 g/kg) simirar to thal required by
normar individuars
(10,11,12r.

Catbohydntes

cirfiotic patients are prone to deverop diabetes. As noted

above, insurin
resisrance appea* to account for this abnormarity
of grucose homeostasis. rn
patients with portal hypertension complicated
by portosystemic shunling, an
alteration in insulin melabolism may contdbute
to this resistance.

Oepleted body stores of poiassium and elevated levels of growth

horrnone are pfobabry arso significant. As in other patients with diabetes,
nutritional managemenl plays an important role
in therapy.

97
 Specilically, providing calories as complex
carbohydrates effectively
reduces insulin requiremenls. lncreasing intake
of complex carbohydrate may
arso be ot benetit in hepatic encepharopathy
because the nonabsorbabre fiber
found in such foods decreases colonic transit
time and lowers colonic pH.
lndeed, the ef{icacy of lactulose, one of the
mainstays in treatrnent of hepatic
encephalopathy, has been related lo these same
effects (1g).

Lipids

Fat accumulation in the tiver is strikingly

afiected by the amount and type
of dietary trigtycerides. With atcohol, the
more triglycerides in the diet, the
more
fat accumutates in the liver (14), at least
down to a level of 1oolo of total energy.
B€low that, fat accumulates even when
dietary fat is exremely lwt (Z%),
probably because of stimulation
of lipogenesis.

Dietary phospholipids also have striking

., effects on liver slrudure and
function. rndeed, in primates, chronic ethanorconsumption
resurts in a decrease
in liver phosphoripids and phosphatidyrchorine (pc)
revers; both can be
corected by pC supplementation (1S).

Fat-Soluble Vitamins

Poor dietary intake, together with changes

in bile salt metabolism and
pancreatic function, rncreases
the likelihood of fat_soluble vitamin dericiency
in
patients with both alcoholic and
nonalcoholic cirrhosis.Vitamin A. Iis

98
 reconmended that the diet of the nonalcoholic
with cirhosis be supplemented
with 5000 to 15,OOO tU vitamin A.

ln patients with alcoholic cinhosis, caulion must

bb exercised in this
respect because microsomal induction may
increase the toxicity of this vitamin,
and elhanol can potentiate liver damage caused
by excessive vilamin A (17).
Although b"calotene, the precursor of vitamin
A, is ress toxic, sfudies in
primates have shown that its toxic
effects are also enhan@d by alcohol (1g).
Furthermore, b.carotene increases the risk of pulmonary
€ncer in smokers, an
effect relaled to a concomltant consumption
of alcohol. Thus, vitamin A or b-
carotene supplementation must be used cautiously
in alcoholics.

vitamin D supprementation of the diet with vitamin

D may fairto hart the
progression of osteoporosis and osteopenia.
Ho\ rever, there appears to be no
hazard in re@mmending ingestion o, additional
25-OH D 3 (1OO to 3OO nmol
[aG-120 pgyday] when patients comprain of bone pain or demonstrate
pathologic fractures ( 19).

Vitamin E. ln children with biliary atresia

and cholestasis, vitamin E
deficienry may be associaled with a number
of neurologic atterations. Although
such infanb and children may benefit from
supplemenlation, replelion o, vitamin
E stores in adults with liver injury has
no proven ctinical benefit.

99
 Mtamin K. Deficiency of vitamin K leads to easy bruisability
and, at
times, to overt bleeding from esophageal varices or hemorrhoids.
When the
prothrombin time is lengthdned, parenteral supplemenfation
of vitamin K (10
mg/day for 3 days) wil serve to discriminate between vitamin
K deficiency and
failure of the liver to synthesize normal coagulation faclors;
after vltamin K, an
abnomal prothrombin time is corrected in the former setting but
not in the latter.

Water-Soluhle Vitamins and Trace Minerats

Deficiencies of water-soluble vitamins (folic acid, thiamin,

and pyridoxine)
are most likely lo occur in the malncurished alcoholic
with advanced iiver injury.
Patients with Wilson's disease and those with chronic
cholestasis (e.g., pnmary
biliary c;rhosis) have excessive copper accumulation in
the liver. Although
chelation of copper by penicilamine is highiy effective,
it is arso advantageous
to reduce the intake of foods rich in this mineral. Foods
rich in copper include
chccolate, shelmsh, and liver. Zinc deficiency occurs in
alcoholics with liver
injury.

ACUTE PANCREATITIS

Depenoing on the population, alcohol abuse and

biliary tract disease
cause acute pancreatitis in 75 to g5% of patients. ln
addition to these common
causes of acute pancreatilis, other factors have been
implicated in the
pathogenesis of acute pancreatitis, such
as metaboric, traumatic, operative,

'100
intectious, and pharmacologic etiologies. Patients with acute pancreatitis

typically present with acule abdominal pain and elevation of pancreatic

enzymes in the serum; amylase is the enzyme most commonly measured.

Clinica, Assessment and Prediction of Need for Speciatized Nutritional

Treahnenl

Mild acute intertitial pancrestitis is characterized by abdominal pain,

nausea, vomiting. anorexia, and low or no mortality (<20lo). Although local

eomplicaiions such as third-space losses leading to hypovolemia and systemic

complications such as respiratory or renal failure may occur in interstitial

pancreatitis, they are uncommon, and reso;ution of symptoms and reeovery

occurs in several days. ln these patients, simple supportive medical treatment

suffices, and parenteral nutrition is rarely needed. However, in severe

necrotizing pancreatitis, characterized by end-organ failure, the mortality rate

may approximate 30% if lhe necrotic tissue is infected (16). These patients

need paienteral nutrition instituted as soon as their seve.e pancreatitis is

recognized, because a prclonged, complicated clinical course is extremely

likely.

Treatment

Food and drink are lvithheld from all patients with acute pancreatitis. ln

addition, in moderate-to-severe attacks of pancreatitis, gastric contents are

101
aspirated from the stomach through a nasogastric tube. Most patients have mild

pancreatitis and are treated for several days with supportive care including pain

control, intravenous fluids, and nothing by mouth. Most patients eat within 5 to 7

days and do not require parenleral nutrition. ln contrast, patienls with moderate-

to-severe pancreatitis require nutritional support as a routine part of medical

management, to prevent inanition because they rapidly become nutritionally

depleted. However, total parenteral nutrition (TPN) does not affect the outcome

of attacks (15). Although resting energy expenditure in patients with

uncomplicated acute pancreatilis (measured by indirect calorimeiry) is no

greater than predic'.ed, 82% of patients hemodynamic features observed in

sepsis. ln addition, if pseudocysls, abscesses, or fistulas develop, a protracted

course with increased metabolic ne€ds should be anticipated; nulritional

complications are mcst likely to arise in this setting.

ln moderate-to-severe acute pancreaiitis, parenteral nutrition is initialcd

as soon as the cardiorespiralory systems are stable. Nutritional support shouid

rnclude (a) hypertonic dextrose; (b) solution of crystalline amino acids; (c) fat
emulsion to prevent fatty acid deficiency (except in patients with hyperlipidemia-

induced pancreatitis); (d) daily requirements of electrolytes, vitamins, and trace

elements; (e) insulin to control hyperglycemia; and (f) proton pump inhibitors

(omeprazole) or H 2 blockers to reduce gastric acid secretion. After paraMic

ileus has subsided and in patients requiring surgery, oral low-fat feedings

should be used instead of the parenteral route. The oral route, rather than TpN,

102
 should be used whenever possible, to eliminate the potential complications of

TPN.

TPN has the advantage of maintaining ,,pancrealic resl', better than

enteral nutrition. However, enleral feedings have a number of advantages over

TPN: maintenance of intestinal integrity and the gut mucosal barrier, which may

decrease the risk of bacterial lranslocation and subsequent septic compiications

of acute pancreatitis, lower cost, and elimination of complications related to

parenteral nutrltion. The farther down the upper gastrointestinal tract an

elemental diet is infused, the less stimulation of pancreetic exocrine secretion,

becauce the normal cephalic, gastric, and intestinal (more potent) phases of

pancrealic stimulation are bypassed. Unfc,riurraiely, lo date no prospective

randomized trials have assessed the effect of early enteral nulrition on the

course and outcome of acute pancreatitis.

Refeeding

The criteria we use to initiate oral feedings are (a) absence of

abdomlnal pain and tenderness, (b) reduction of amylase levels to near-normal

levels, and (c) absence of complications. We begin feeding patients by giving

100 to 300 mL of liquids containing no calories every 4 hours for the tiIst 24

hours. lf this diet is tolerated, oral feeding is advanced to giving the same

volume of liquids containing nutrients. Subsequenfly, if patients continue lo do

well, feedings are changed gradually over 3 to 4 days to soff, and finally solid,

103
 foods. All diets contain more ihan SO% carbohyd€te calories, and the total

caloric content is gradually jncreased from 160 to 640 kcal per meal.

CHRONIC PANCREATITIS

Most patients who develop chronic pancreatitis are alcoholics, who may

have nutritional deficiencies secondary to alcoholism. However, about 20olo of

patients wilh chronic pancreatitis in our population have idiopathic chronic
pancreatitis. Olher causes of chronic pancreatitis are much less common.
Some conditions give rise to exocine insufficiency and malabsorption and

malnutrition wilhout causing chronic pancreatitis, such as trypsinqgen or

enterokinase deticienry or colipase or lipase deficiency, but these
conditions
afe rare.

Dudng early chronic pancreatitis !n palients with abdominal pain

but no
a lo\ .fat, low-proiein, high_carboh)drate diet is indicated. ln dogs
.steatorrhea,
with Drofound exocrine pancreatic insufficiency, a diet co,ttaining a high
proportion ol tat (43 and 47%) along with sufticient lipotytic
activ.rty (bacteriat or
porcine lipase) decreases steatorhea by increasing
the coefticient of fat
absorption ( 20).

't04
RETERDNCES

1. Borgstrdm B, Erlanson C. Gastroenterology 19'18,'1513824.

2. Borgstritm B, Erlanson-Albertsson C, Wielock F. J Lipid Res 1979;20:805 16.
3. Westergaard H, Dietschy JM. J Clin lnvest 1976;58:97-108.
4. Lock L, Weiner IM. Fed Proc 1963:22:133+8.
5. Carey MC. The enterohepatic circulation. In: Arias IM, Popper H, Schacter D,
Shafritz DA, eds. The liver: biology and pathobiology. New York: Raven Press,
1982:42945.
6. Mccullogh Al, Mullen KD, Smanik EJ, et al. Gastro€nterol Clin North Am
1989;18:619-43.
7. Mezey E. Liver and biliary system. ln: Paige DM, ed. Clinical nutdtion. 2nd ed. St.
Louis: CV Mosby, 1988;186-97.
8. Vhlachevic ZR, Buhac I, Farrar JJ, et al. Castroenterology 1971;60:491-8.
9. Rudman D, DiFulco TJ, Galambos JT, et al. J Clin lnvest 1973;52:2242-9-
10. Mullen KD, Denne SC, McCullough AJ, et al. Hepatology 1986;o:622 .3C.
11. Swart GR, Van DenBerg JWO. Wahime$ JLD, et al. Clin Sci 1988;75:101 7.
12. Gabuzda GJ, Shear L. Am J Clin Nutr 1970:,23.479-84.
13. Ccllins JP., et al. Arch Intem Med \970;126:608-14.
14. Conn HO. Am J Md 1970:299:394404.
15. Oweo OE, Tnpp VE, Reichard GA. J Clin Invest 1983;72: l82l-32.
16 Merli M, Riggio O, Romiti A, et al. Hepatology 1990;12:106-12.
17. Schneeweiss B, Graninger W, Ferenci P, et al. Hepatology 1990;1 1:387 93.
lE. Jhongiani SS, Nanakram A, Holmes R, et al. ,\m J CliD Nutr 1986;44:323-9.
19. Shanbhogue PJK" Bistrian BR, Jenkins RL, et al. JPEN J Parenter Enteral
Nutrl987;1 l:305-{.
20.Matos C, Porayko MK, Francisco-Ziller N, DiCecco S. Nutition and chronic liver
disease. J Clin Gastroentercl2002. 351391-397.
.21., Carvalho L, Parise ER. Evaluation of nutritional status of nonhospitalized patients
withliver cirrhosis. Arq Gastroentercl 2006: 43:269 274.
22. Plauth M, Cabre E, fuggio O, et al. ESPEN guidelines on enteral nutrition: Liver
disease.Clin NutI 2006; 25:285-294.
23. Nakaya Y, Okita K, Suzuki K, et al. BC-\A-enriched snack improves nutritional
state ofcirrhosis. Nutririon 200'7:, 23tl 13-120.
24. Cordoba J, Lopez-Hellin J, Planas M, et al. Normal p.ctein diet for episodic hepatic
enceohalopathy: results ofa randomized study. J Hepatol 2004; 41:38 43.
25. Blonde-Cynober F, Aussel C, Cynob:r L. Abrormalities in branched-chail arrino
acid metabolism in cirrhosis: :iifluence of hormonal and nutritional facto$ and
directions for future research. Clin Nutr 1999; l8:5 13.

105
 DIET THERAPY IN INFECTIOUS DISEASES AND
FEVER
lnfectious diseases make up eight of the top ten leading causes of
morbidity in the philippines from 2000_2005. i Based on the same time pe'od,
pulmonary and gastrointestinal diseases take
up the top four leading causes of
morbidity in the country while pulmonary causes are within
the top ten causes of
mortarity. Poverty, marnutrition, poor education on hygiene
and sanitation, and
inferior health care syslem in some parts of lhe
country have contributed much to
the situation. Studies have shown how it is possible to
influence the body,s
susc€ptibility to disease through diet. Bacterial infections
such as typhoid fever.
luberculosis, pneumonia and malaria cause severe
and prolonged loss of
rjtrogen as a result chiefly of the toxjc destruction of intracellular
protein. With
anorexia, which results in a decreased food intake
during fever and ir,fection,
proiein intake is bound to be lowered, with furthe.
loss of nitrogen.

., When diets inadequate in protein are fed, it is very

likely that towered
res;stance to jnfection wili develop. This will interfere
with the production of
antibodies which play an important role in both
natural and acquired immunity. lt
has been founC to decrease the phagocytic activity
of white blood cells
lnadequate synthesis of haemoglobin as a result
of low protein intake leads io
anemia which increases further the assault on
the already compromised immune
syslem.

'106
Metabolic effects of fever:

1) lncreased melabolic rate

- for every one degree rjse in temperature above lhe

normal (Celsius) the metabolic rate is increased by approximately

13%.

2) lncreased protein catabolism - especially excessive ein typhoid fever, mataria,

typhus and others. The end products of protein calabolism excreled as urea

places a heavy burden upon the kidneys.

3) Decreased glycogen stores and adipose tissues

4) Loss of body fluids and electrolytes especially sodium and potassium

5) Decreased gastrointestinal motility that affects absorption of nulrients.

Diet in infections and fever

1) lncreased calorie intake - to meet lhe demand of increased metabotic rate.

"Starving a feved' leads to prolonged convalescence and acute deficiency

diseases.

2) lncreased prote;n - 50-100o/o increase of the recommended daiv allowance io

correot negative balance that arises from the increased tissue catabolism. ln

typhoid fever, for example, as much as one-half to three-fourth F,ound of muscle

is catabolised a day.

3) lncreased carbohydrate - to provide energv, spare body proteins from being

utilized for energy, replenish depleted glycogen stores and prevent ketosis.

4) Fat intake should be noimal or adequate, to help increase the caloric ccntent

of the diet without too much bulk

107
5) Liberal fluids and salts - to compensate for water and salt loss from overt
perspiration and insensible loss and to permit adequate volume of urine for

excreting metabolic wastes.

6) Vjtamin supplementation - especially the B vitamins which are part of the co-

enzymes which are involved in metabolism. Thiamine, riboflavin, niacin and

pyridoxine in particular are increased automatically whenever the caloric conlent

of the diet is increased.

The critical role of iron in host and pathogen biology

Among the 40 or so nutrients essential lo human health, iron plays the

most critical role in relation to lhe host's interactions with pathogens: 'l) iron is a

highly abundant element, but it is highly insoluble ai physioloqical pH and in the

oxidalive conditions of life, hence difficult to acquire; 2) iron has very usefLtl redox

characteristics that have resulted in its incorporaticn in a very wide range of

enzyme and oxygen transport systems; 3) these salne redox charect--ristcs also

fnake ftee iro,r potentialiy very harmful because of the generation of free radicals;

4) humans have evolved a range of transport, sequestration, and siorage

systems for iron (e.9., transferrin, lactoferrin, ferritin, haptoglobin, hemopexin)

that appear well adapted to prevent iron causing localized tissue damage; 5)

these systems are up-regulated by the acJte-phase response to infection

causing a Cepletion of iron in the systemic circulation down -10 " mol/L

(teleologically interpreted as a detense mechanism by depriving pathogens of

iron); 6) both in vitro and in vivo (small animal) experiments ctearly demonstrate

108
 that addition of iron (in various forms including as heme) overcomes the
bacteriostatic and bacteriocidal effects of iron-binding proteins; 7) in response

to these human adaptations, bacteria, in particular, have evolved an astonishing

range of siderophores and related iron acquisition molecules with very strong

iron-binding capabilities 1e.j., tO t' mol/L for enterobactin); 8) in many bacteria,

the so called "islands cf high pathogenicity" within their genome are enriched

in iron acquisition genes; and g) microorganisms acquired specialist methods for

iron retrieval before they could colonize humans. These factors combine to place

iron at the center of the hostpathogen battleground for nutrients and suggest that

optimizing iron status may involve a very delicate balance; a deticit of iron will

impair host function (including lrnmunity), bui an excess may favor the gro\,,rlh

and pathogenicity of microorganisms.2

TUEERCULOSIS

Pufunonary tubercuicsis (PTB) is one of ihe oidest diseases, afflicting the

.human race since ancient times.3 Before the advent of antituberculosis

chemotherapy, a diet rich in calories, proieins, fats, minerals, and vilamins was

generaliy considered to be an importanl, if not essential factor in trealment oi

tuberculosis (fB).4 Thus, the isolation of streptomycin Ain 1944, a drug with

antimycobacteriai activily, was a nilestone in therapy.3 The introduclion of

specific aitituberculosis drugs has so radically altered the management of the

disease that the role of diet should be considered in the ljght of the advances in

treatment.a Presently, > 90% of PTB cases can be cured with the currenfly

available drugs.3

109
 Only 5% to 10% of individuals exposed to M. fuberculosls develop TB, and

up to 70% of those who do develop the disease are male. Men seem to be more

affected than women, with a male/female ratio of 1.9i0.6 for the worldwide case

notification rate. This excess of male PTB cases is seen in all regions of the

world, and in almosl all countries, at least in non-Hlv-infected patienls. lt is also

seen in adults of all ages, but does not seem to apply to chibren and young

adolescents. This led to the question if TB was associated'with a sex-specifir;

genetic architecture. The first major locus identified by genome-wide linkage

analyses was recently mapped to 8ql2-q13, which houses at least 6ne major

gene that confers predisposition to PTB in adults with a dominanl mode of

inheritance. Trying to prove that PTB is X-linked, there was a strong association

found betwecn the rs3764880 allele A (Met) and susceptibility to TB and this was

restricied to men.5

The Philippines ranks ninth on the list of 22 high-burden TB counlries in

tne world, according to the World Health Organization's (WHO's) Global TB

Report 2009. it is the sixth greatest cause of morbidity and mortality in the
6
country.1 We have come a long way fron a TB death rate of 92.l in 1960 to a

42.5 in 20O5.?

The host protective immune mechanism of infection wilh Mycobacteium

tuberculosis depends critically on the interaction and cooperatien between

monocyte-macrophages and T-lymphocytes and their cytokines; malnutrition can

lead to secondary immunodeficiency resulting from alteration in the individual

protective function, hence increasing the host's susceptibility to infection.a

110
Nutritional Management of Tuberculosig

1) High calorie - TB results in anorexia, cachexia and generalized weakness.

Nutritional deficiencies are generally associated with increased risk for and

severity of tuberculosis by adversely affecting immunity. 35 - 40 kcal per

kilogram of lBW.

2) High Protein - Patients with pulmonary tuberculosis use a larger proportion

of proteins from oral feeding for oxidation ( hence for energy production) in

conlrast to malnourished and normally nourished healthy subjects. Such failure

to channel food protein into endogenous protein synthesis has b'een termed
"Anabolic block" - one of the mechanisms for wasting in luberculosis and other

inflammatory status.a Prolein intake would thus restore nitrogen balance, promote

adequate immune response to infection and prevent lr,asting of muscle. This

translates to 1.2 : 1.5 g/ kg body weight or 15% of energy of total daily intake cr

75 - 100 g per day will be sufticient.

.3) High Carbohydrate: To provide energy and to spare prctein

4) Micronutrients: 50-150% of RDA for mineral & multiviramins supplement.

lncrease A,C,E vitarnins to reduce oxidalive stress brought by the disease &

treatnent. Mineral & multivitamins supplement are advised because it is unlikely

that a person with TB will be able to meet the increased requirements for

vitamins and minerals with diet alone (due to a poor apl,etite).

Micronutrients defrciency is considered to be the most frequent cause of

secondary immunodeficiency and infection related morbidity including

tuberculosis.a

111
Zinc and TB. Plasma zinc concentrations are lower in patjents with tuberculosis,

with gradual improvemenl during treatment. This signifies decreased

requirements for zinc as the patient gets better health-wise.8 Zinc deficiency

results in decreased phagocytosis and leads to a reduced number of circulating

T-cells; in vilro cellular killing by macrophages was reduced and rapidly restored

after zinc supplementation. Zinc has an essential role in vitamin A metabolism so

that its deficiency impairs the synthesis of retinal binding proteins and reduces

plasma retinal concentration. An adequate supply of zinc may also limit free

radical membrane damage during inflammation.a e Zinc supplementation

improved the effecliveness of the antituberculosis drugs in the first 2 months

during which active bacilli are killed.6 Although zinc supplementation did not

produce increased sputum-snrear or culture conversion in a study population that

included H|V-infected patients.l0

Vitamin A and IB. Vitamin A inhibits multiplication of virutent bacilli in cultlred

human macrophages; it plays a vital role in lymphocyte proliferation and in

maintaining the funciion of epithelial ti$ues; it is essential for normal functioning

of T and B lymphocytes, macrophage aclivity, and generation of antibody

response. Likewise, the presence of infection can compromise vitamin A status

through: 'l) excretion in the urine in patients with fever, acute infection including

pneumonia. This js berause during the acute phase response, leakage of

proalbumin through the vascular endolhelium occurs; and production of retinal

binding proteins and prealbumin by liver is reduced; 2) increased requirement

brought about by its increased rate of excretion and melabolism.a

112
 Vitamin D and IB, Vitamin D binds to nuclear receptors resulting in the
generation of the oxidative burst responsible for the intracellular

antimycobacterial activity: vitamin D recej:tor polymorphisms provide differential

protection toward TB; vitamin D supplementation enhances immunity to

mycobacteria among exposed adults; low serum vilamin D is found in patients

with pulmonary TB.rr

Cholesterol Diet and IB- A cholesterol-rich diet enhances the bacteriologic

improvement during the intensive phase of short-course therapy for pulmonary

tuberculosis - lt accelerates the sterilizalion rate of the sputum culture.

Cholesterol constitutes up to 30% of the total lipid content in the cell membrane,

and participates in ihe fluidity of this slructure. Consequenfly, cholesterol is

involved in the activity of membrane-bound enzymes and membrane functions

such as phagoc)rlcsis and cell gtowth. Hence, cholesterol content in the cell

membrane of human lymphocy-ies is impor-iani for thei. cylotoxic function. ll

participates in the differentiation and proliferation cycles that convert tymphocytes

into cytotoxic celis. A clear derangement of the abilliy of the macrophage to

phagocytise mycobacteria was observed when experimental animals were

depleted of cholesterol. All of these findings are important in pat;ents with

pulmonary tuberculosis, since activated lymphccyte subsets. such as CD4+,

CD8+, and Yb T celis, recruit macrophages and release molecules, such as

interferon-Y and tumor necrosis tactor-o, that render them more efficient in killing

mycobacteria. ln addition, cytotoxic lymphocytes (either CD4+ or CD8+) undergo

phagocytosis of macrophages that have already internalized mycobacteria.3

 Dietary cholesterol replenishes metabolic pools (eg, cell membranes),
transformed into other products such as hormones and vitamins A and D, or

catabolized through bile salts, hence, replenishment of metabolic pools occurred

faster in those patients eating a cholesterol-rich diet.3

Studies have yielded inconsistent findings regarding serum or plasma

calcium concentration during tuberculosis. A study in Africa has relaled

4
hypocalcemia to moderate lo e)tensive radiographic disease

MALARIA

Malaria is a recurrent infection caused by a protozoa 6f the genus

plasmodium and transmitted by the anopheles mosquito. lt is characterized by

intermittent fever, preceded by severe chills and followed by profuse sweating,

anemia and debility.

Epidemiology: At risk of malaria: 3.3 billion peopte- half of world,s population,

rvhich calculates tc nearly 1 million deaths/ year. lt is the Bth leading cause of

-,morbidity in the Philippines.r

-fop
ten (10) provinces in te,,ns of the number of malaria cases were:

l.Palawan 3.Sulo 5.lsabela 7 Sultan Kudarat g.Surigao del Sur

2.Tawltaw; 4.Sarangani 6.Cagayan S.Agusan del Ncrte lO.Zambales

Vitamin status of the host and its effect on prasmodium development

Vitamin C & E. An infection wilh Plasmodium causes an immune response

resulting in the activation of macrophages leading to the production and release

of reactive oxygen species (ROS). The vitamins C (L-ascorbic acid) and E (o-

tocopherol) play pivotal roles in protecticn against oxidative stress. lt was

114
postulated that the increased concentrations of both vitamins io Plasmodium-

infected cells is the consequence of the increased ox'dative stress when the

immune system is activated by the malaria infection. This simultaneous increase

in concentration of both vitamins in eMhrocytes apparently offered an enhanced

protection against lipid peroxidation where lipid peroxides are detoxified by

vitamin E which itself is then reduced by the water-soluble ascorbale.

lnterestingly, vitamin E or vitamin C deficiencies have a protective effect in

malaria patients apparently because the lack of this antioxidant renders the

parasites more vulnerable to the damage by ROS. lt was also postilated that

ascorbic acid not only acts as an antioxidant but also has strong pro-oxidant

features resulting in the generalion of free radicals in the presence of oxygen and

free transition metals.l2

Vitamin A. There is evidence that P-carotene and vitamin A have proteclive

ef,ects against malaria. Malsria infection seems to be accompanied by

dccreases of vitamin A concentrations in the serurn trom > 120 mmol/L to < 70

pmol/L. Providing vitamin A supplements partially protected against malaria

rnfection, parlicularly in ;mmunologically nai've patients, with one study showing

o/o
-7O lo'::er parasite densities among subjects. This was suggested to be

mediated bv an increased clearance of parasitized erythrocytes (upregulation of

the phagocytotic receptor CD36) and a reduce,l pro-inflammalory cytokine

response (downregulation of cytokines such as TNFo by binding of g-cis-retinoic

acid to the peroxisome proliferator-activated receptor y (PPARY) or retinoid-x-

receptor), which is generally high in malaria patients. l2

115
 Vitamin D3. Vilamin D3 exerts immunomodulatory functions, whjch are mediated

through its receptor - vitamin D3 receptor (VDR) belonging to the family of

nuclear hormone receptord. lt has been shown that VDR is expressed in antigen_

presenting cells (e.9. macrophages and dendritic cells) and expression

is

inducible in lymphocytes. One way in which vitamin D3 might affect plasmodium

is through its involvement in phosphotipid melabolism and signalling pathways.

Vitamin D3 and analogues have pronounced inhibitory effects on p. fal.iparum

eMhrocytic late stage development possibly because the phospholipid
biosynthesis pathways of lhe parasite is affected by these compounds.i2

Dietary management of Malada

1) High Calorie because of the high metabolic rate during the attack

2) High protein due to protein destruction by rhe prolozoa

3) High carbohydrate to replenish depleted reserves

4) Moderate fats to reduce the workload of the impaired ljver

s),Liberal fiuids and salts to restore salt and

'.^/ater balance, to elimjnate toxins

6) Vitamin supplements are ;ndicated especially the B_vitamins because of the

inciease in calories.

syrnpt.ns a Eft*is of rotaria Nuftitional app.oach

Libera, lluids & satts_

116
 TYPHOID FEVER

Typhoid Fever is an acute illness associated with fever caused by the

Salmonellae fyphj bacterid. The infection is transmitted through food and drinks

contaminated by the bacteria. public health immunization programs have greafly

reduced the incidence, while the use of antibiotics has shortened the course of

the disease from what used to be a chronic fever lo one of short duration.

However the lenglh of convalescence is tc a large extent still dependent upon

nutritional therapy.

Peyer's patches (ulceration of the intestinal tret) and diarrhea are early
involvements and may interfere with absorption. ln addition, if not controlled in

the early stages, there are often extensive changes in the liver, with

complicatjons in the gallbladder and bile passages.

During the height of fever the metabolic r?te may iicrease 50% above the

nonnal. The protein destruction is great, appioximating ihiee times ihai which

occurs during normal health. The symptoms associated with typhoid are poor

;rppetite, headaches, generalized aches and pains, fever, and lelhaigy.

The main objectives of diet therapy are: 1) to maintain adequate nutrition.

2) to maintain water and electrolyte balance, and 3) lo provide enough proteins.

Dietary modifications of Typhoid Fever

Small meals should be given at frequent intervals. As the condition

improves larger meals may be given.

Energy: ln fevers the basal metabolic rate (BMR) increases, thus enhancing the

energy needs. Restlessness also increases the energy expenditure. Therefore, it

is recommended to increase the energy intake. But initially, a patient may be able

to consume only 1000 - 1200 kcal/day. But it should be gradually increased with

recovery and improved tolerance.13 ''

Protein: A high protein diet is advised. For an adult with typhoid, about 1009m

or more of protein is prescribed. Protein intake should be increased with the use

of foods such as milk and eggs. Large quantities of milk form the basis of the

diet. Three lo six eggs daily, served soft boiled or in soft custards, are well

tolerated. The milk and eggs provide calories, proteins, minerals and

vitamins. l3 la

Carbohydrates: A liberal intake of carbohydrales is suggested to meet the

increased energy intake. The glycogen stores are replenished by a liberal intake

of carbohydraies. Well cooked, easily digestible carbohydrates like starches,

glucose, honey and cane sugar, should be included as they are easily digested
1314
and are well absorberl by the bocly

Dietary fibre: A low fibre diet is advised, in order not to traumatize the inflamed
r314
bowels to precipitate hemorrhage or peferation.

Fats: Fats are required mainly to increase ihe energy intake. ln case diarrhoea is

present, fats need to bc restricted. lt is the quality of fat that is nrore important

than the qu3ntity. Emulsified fats such as butter, cream and milk fat are easily

digested.
13 'a

Minerals: There is excessive loss of electrolytes like sodium, potassium and

chloride due to increased sweating. Salty soups, broths, fruit juices and milk help
13Ja
compensale the loss.

114
Vitamins: lnfection and fevers increase the requirement for vitamin A, B and C.

Moreover, the use of antibiotics and drugs interferes with the synthesis of vitamin

B in the intestines. So, vitamin supplements may have to be given along with
r31a
other medicines.

Fluids: ln order to compensate for the losses through the sweat and also to

ensure adequate volume of urine for excreting waste, a liberal intake of fluids is

very essential. A daily intake of 3--4 litres is desirable. Fluids may be taken as

water, tea, milk, juices and soups. 13'o

RHEUMATIC FEVER

Rheumatic fever is one of the leading causes of chronic iliness in

children,especially the underprivileged. lt is characterized by high fever, painful

swelling of joints similar to those of early rheumatoid arthritis, and inflammation of

the heart muscle and valves. lt tras often been said to be a disease that "licks the

joints but bites the heart". An antecedent history of moderate to severe sore

throat or upper respiratory infection involving streptacoccus organisms usualiy

precede thg disease. Penicillin remains the mainstay of therapy. The use of

steroids sho,tens the period of acutc illness, lessens its severity and decreases

the likelihood of cardiac involvement.

Diet and nutritional management of Rheumatic Fever

lne full liquid diet for acute infections is satisfactory Curing the acute
phase of rheumatic fever. Progression from liquid to soft then regular diet

depends on the rate of patient's rehabililalion. Caloric intake should be

increased because of increased metabolic rate and protein increased to correct

119
 negative nitrogen balance. The intake of ascorbic
acid should be increased as
an antistress factor. lron supplement js recommended
due to the presence of
anemia but sodium should be restricted to about
1,OOO mg per day when steroids

are used because of the sodium_retaining property

of the drug to avoid edema.

CHOLERA

Cholera is an infection of the intestines by Cholera vibrio organrsms

transmitted through contaminated foods and drinks. lt is characterized by
sudden and massive diarrhea usually with vomiting
leading to a rapid loss of
water and electrolytes wilh consequent dehydration,
hypovolemia anc, shock .
Death may occur in hours. lntravenous rehycjration
with salts and glucose plus
antibiotics to combat the infection have saved
lives of infected individuals.
Dietary Management of Cholera:

A. lntravenous feeding with salts and glucose

to rehydrate the patier:t
B. Oral solutions of salt and glucose foilows the inlravenous
route; glucose
.' aids in the absotption of sodium and water

Dietary Profile;
.a)
High catoie 4) Restricted fat
2) High protein 5) Liberal fluids and satts
3) High carbohydrale 6) Vitamin supplements

Eir/tpHySEMA

Emphysema is a pathologic over distenfion of the lung alveoli brought

about by a number of causes, e.g. asthma, bronchitis,
infection, smoking and
others. Although changes in the rung and purmonary
vessers are irreversibre, it is

120
possible to give the patient considerable relief and increase the functioning

capacity of the lung. Treatment is designed to correct or diminish conditjons

causing the disability , i.6. it is directed at combating infection, bronchospasm,

bronchial over secretion and impaired pulmonary ventilation and circulation. Bed

rest should be allowed only when necessary. The patient should be ambulant

and active within lhe limits of his abilities, but exertion which increases dyspnea

should be strictly avoided. Nutritional rehabilitation is an important part of

management-

Recent studies have revealed that frequent cured meat consumption was

associated independently with an obstruclive pattern of lung function and

increased odds of COPD.15 And among dietary factors considered, only low

protein intake was associaled wth airway obstruction.l6

Typical symptoms are shortness of breath, tissue wasting and weight loss

and abdominal distress.

Diet Therapy in Emphysema

1) High calorie to combat iissue wasting and weight loss

2) Small frequent feedings of concentrated foods due to shortness of breath

3) Soft foods which are easy to masticate because of the difficulty in chewing

4) High protein to correct nsgative nitrogen balance

5) High vitamin supplements

t
http://www.doh.gov.ph/kp/statistics/morbiditV.html
'zPrentice. lron Metabolism, Malaria, and Other tnfections: What ts All the FLrss About?
Symposium: lnfant and Young Child lron Deficiency and lron Deficiency Anemia in
Developing Countries-The Critical Role of Research to Guide policy and programs. J.
Nutr. 138: 2537-2541, 2008.

121
r P6rez-Guzmdn, Vargas, Quiffonez, Bazavilvazo and Aguilar. A Cholesterol-Rich Diet
Accelerates Bacteriologic Sterilization in Pulmonary Tuberculosis. Chest 2005;127;643-
651
4
Gupta, Gupta, Atreja, Verma, and Vishvkarma. Tuberculosis and nutrition. Lung lndia.
2009 lan-Mar; 26(1):9-16.
'Neyrolles O, Quintana-Murci L (2009) Sexual lnequality in Tuberculosis. PLoS Med
6(12): e1000199.
6
http://www.usaid-gov/ou r_work/global_health/idltubercu losis/countries/asia/
philippines_profile.html
'3 http://www.doh.gov.ph/health_picture.html
Manary, Hotz, Krebs, Gibson, Westcott, Arnold, Broadhead and Hambidge. Dietary
Phytate Reduction lmproves Zinc Absorption in Malawian Children Recovering from
Tuberculosis but Not in Well Children. J- Nutr. 130: 2959-2964, 2000.
" Karyadi, West, Schultink, Nelwan, Gross, Amin, Dolmans, Schlebusch, van der Meer. A
double-biind, placebo-controlled study of vitamin A and zinc supplementation in
persons with tuberculosis in lndoiesia: effgcts on clinical response and nutritional
status. Am I Clin Nutr 2OO2;75:72O-7.
'o Range, Andersen, Magnussen, Mugomela and Friis. The effect of micronutrient
supplementation on treatment outcome in patients wiih pulmonary tuberculosis: a
randomized controlled trial in Mwarza, Tanzania. Tropical Medicine and lnternational
Health. volume 10 nc 9 pp 826-832 september 2005
" Friis, Range, Pederscn, MOlgaard, Changalucha, Krarup, Magnussen, Sobo.g, and
Andersen. Hypovitaminosis D ls Common among Pulmonary Tuberculosis Patients in
Tanzania but ls Nct Explained by tlre Acute Phase Response. J. Nutr. 138: 2414 2480,
2008
1'?Mrlller anC Kappes. Vitamin and co-factor biosynthesis pathways in Plosmodium and
other apicomplexan parasites. Ttends Porositol.2OOl Mat.h ;23131:1.12 127.
" http://doctor.ndtv.com/topicdetails/ndtv/tid/538lDieta.y management for
typhoid.html
'o http://www.dietnut.inlcD-9.html
'5 Jiang, Paik, Hankinson, and Barr. Cured Meat Consumption. Lung Function, and
Chronic Obstructive Pulmonary Diseas. among LJnited States Adults. Am J Respir Cflt
Care l'4ed Vol 115. pp 198 804,2OO/
16
Lee, Sim, suh, Ryu, Shin, Koh, Kim, Park, Yoon, Lee, Chang, and the Korean Academy
of Tuberculosis and Respiratory Diseases. Diet and Airway Obstruction: A Cross Sectional
Study from the Se.ond Xorean National Health and Nutrition Examination Survey. The
Korean Journal of lnternal Medicine Vol. 25, No. 2, June 2010

122
 DIETARY MANAGEMENT OF CARDIOVASCULAR DISEASES
Cardiovascular disease, including coronary heart disease, strokes and
diseases of other arteries, is a major cause of early death and disability. For
many years the major markers of disease risk have been well recognized: these
include high blood cholesterol levels and smoking. But it has also been
recognized that these markers do not account for all the cardiovascular risks.
Furthermore, treatments that are highly effective in altering these markers, for
instance, the "statin" drugs used to lower cholesterol, do not remove risk entirely;
typically they reduce it by 30% or less. These observations have prompted a
search for other, perhaps more subtle, indicators of risk of carciiovascular
disease. Over the past few years, a number of such risk markers have emerged.
These include subtle alterations of types of fats in the bloodstream other than
cholesterol, factors associated with inflammation and with clotting, lowered
resistance io oxidative stress and impaired functioning of the blood vessels. ln
addition, it has been recognized that experiences in early life, even before birth,
may influence later disease risk. Although these so-called ,emerging,and ,novel'
risk markers are now becoming clear, we know litfle about how they may be
altered to reduce risk of cardiovascular disease. ln particular, we know littte of
how they may be influenced by the diet, although the rapid changes in risk of
cardiovascular disease that occurred throughout the twentieth century suggests
that features of our lifestyle such as diet may play a fundamental role.
- Cardiovascular disease includes arterial disease affecting the blood
supp!.i to ihe heart or to ihe brain, or to the peripheral regions of the body.
- Cardiovascular diseases account for over half of all deaths in middle age
.' and one{hird of all deaths in old age in most developed countries
, Ccronary heari disease is a condition in which the walls of the arler'es
supplying the blood to the heart muscles (coronary e;teries) become
thickened. This thickening cause by the development of lesions in the
arterial wall is called atherosclerosis; the lesions are called plaoues. lt can
restrict the supply of blood to the he?rt rnuscje (the myocardium) and may
manifest to the patient as chest pain on exertion (angina) or
breathlessness on e;ertion. Iviore seriously, if the cap covering the plaque
rupt'.]res, exposing the contents to the circulation, the blood may cloi and
obstruct the flow completely, resulting in a myocardial infarction or heart
attack.
- CHD is also known as ischemic heart disease
- Cerebrovascular Disease involves interruption of the blood supply to part
of the brain and may result in a stroke or a transient ischemic attack.
- There are two types of stroke. The most common type of stroke in
Western countries is ischemic stroke, in which there js a blockage in the

a a'\
 blood supply to the brain and the other main type is called hemorrhagic
stroke, where there is rupture of a blood vessel supplying the brain. High
blood pressure (hypertension is a major risk factor for the latter.
- Peripheral Vascular Disease involves atherosclerotic plaques narrowjng
the arteries supplying other regions apart from the myocardium and brain.
- A common form involves narrowing ofthe arteries supplying blood to the
legs.
- The result may be pain on exercise (claudication).
, ln more severe cases, impaired blood supply leads to death of leg tissues
which require amputation.
, Pathogenesis: Cardiovascular disease whether affecting the coronary,
cerebral or peripheral arteries, share a common pathophysiology involving
atherosclerosis and thrombosis (clotting).

NUTRIENTS KNOWN TO AFFECT CARDIOVASCULAR DISEASES

' A high intake of dietary fats strongly influences the risk of devetoping
cardiovascular disease (CVD).

Saturated fatty acids commonly found in dairy products and meat rajse
cholesterol levels. Moreovef, studies have also shown trans fatty 3cids,
found in industrially hardened oils, increase the risk of coronary heart
disease. While they have been eliminaied from spreads in many parts of the
wcrld, trans fatty acids are still found in deep-fiied fast foods and baked
goods.

', The most eftective replacement for saturated fatty acids in th_- diet are
polyunsatlrated fatty acids (PUFAS) which can lower the risk of developing
cardiovascular disease. ln particular, they are found in scybean and
sunflower oils as well as in fatty fish and plant foods. polyunsaturated fatty
acids have many positi'/e effects, notably on blood pressure, heart function,
blood clotting, and inflammatory mechanisms.

Cholesierol, which is an essential component of cell membranes and

certain hormones, is produced by the liver, but it is also present in dairy
products, meat and eggs. A high amount of a certain type of cholesterol (Low
Density Lipoprotein or LDL) in the blood can lead to its deposition in the
arteries that can restrict blood flow and may cause heart problems. lt is not
clear lvhether dietary.cholesterol is associated with cardiovascular disease,
but it is recommended to avoid excessive intake. Cholesterol is not, in fact,
required in the diet because it is produced by the liver in sufficient amounts.

- Although fatty acids are generally grouped according to the degree of

unsaturation (number of double bonds), it should be noted that their

124
 chemjcal and biochemical properties are also dependent upon chain
length. For example, not all saturates raise blood cholesterol level and
they do so to different extents. Saturates with chain length of 18:O (stearic)
and above and l0:0 (caprjc) and below have essentially no effect on blood
cholesterol. Only 12:0 (lauric), 14:O (myristic). and 16:0 (patmitic) raise
serum cholesterol with the order of effectiveness being 14:0>12:0>16:0.
-Polyunsaturates of the omega-3 and omega-6 families are referred to as
n-3 and n-6 polyunsaturates.

* Dietary fiber is also a major factor in reducing total

cholesteroi in the
blood and LDL cholesterol in particular. Eating a diet high in flber and
wholegrain cereals can reduce the risk of coronary heart diselse.
* An intake of 0.8 mg of folic acid could possibly
reduce the risk of
coronary heart disease (reduced blood supply to the heart muscld) by 16%
and the risk of stroke by 24%. Flavonoids, compounds that occur in a variety
of foods such as tea, onions and apples, could also possibly reduce the risk
of ccronary heart disease. There is jnsufficient evidence to support the theory
that antioxidants such as Vitamin E, Vitamin C or b_carotene might reduce
the risk of cardiovascular diseases (CVD).
- A high intake of salt (sodium) has been linked
to high blood pressure, a
major risk factor for stroke and coronary heart disease.

There is convincing evidence that a reduction in the daily intake of sodium

(by 50 mmol, i.e about 1.2g) across the world would lead io reduction in the
-,
numbeJ_of deaths resulting fro.nt strokes and coronary heart disease (by
. a)oui 22oA and 16% respectively)

FOOO ITEMS KNOWN TO AFFECT CARDIOVASCULAR DISEASES

Fruits and vegetables consumption has been widely associated with good
health. Recent studies show a protcctive effect against coronary heart disJase,
stroke and high blood pressure.

Fish consumption also reduces the risk of coronary heart disease. The benefiis
are most evidenf in high risk groups. For these groups, consuming 40,609 of fish
per day would lead to a 50% reduction in the number of deathJ from coronary
heart disease.

Nuts are high in unsaturated fatty acids and low in saturated fats, which
contribute to lowering cholesterol levels. Several animal experiments have
suggested thal isoflavones, present in soy producb, may provide protection
against coronary heart disease.

125
 chemical and biochemical properties are also dependent upon chain
length. For example, not all saturates raise blood cholesterol level and
they do so to different extents. Saturates with chain length of 18:0 (stearic)
and above and 10:0 (capric) and below have essentially no effect on blood
cholesterol. Only'12:0 (lauric), 14:0 (myristic), and 16:0 (palmitic) raise
serum cholesterolwith the order of etfectiveness being 14:0>12:0>16:0.
-Polyunsaturates of the omega-3 and omega-6 families are referred to as
n-3 and n-6 polyunsaturates.

' Dietary fiber is also a major factor in reducing total cholesterol in the
blood and LDL cholesterol in particular. Eating a diet high in fiber and
wholegrain cereals can reduce the risk of coronary heart disease.
* An intake of 0.8 mg of folic acid could possibly reduce the risk of
coronary heart disease (reduced blood supply to the heart muscle) by 16%
and the risk of stroke hy 24o/o. Flavonoids, compounds thal occur in a variety
of foods such as tea, onions and apples, could also possibly reduce the risk
of corc,nary heart disease. There is insufficient evidence to support the theory
that antioxidants such as Vitamin E, Vitamin C or b-carotene might reduce
the risk of cardiovascular diseases (CVD).

" A high intake of salt (sodium) has been linked to high blood pressure, a
major risk factor for stroke and coronary heart disease.

There is convincing evidence that a reduction in the daily intake of sodium

(by 50 mmol, i.e about 1.29) across the world would lead to reduction in the
number of deaths resulting from strokes and coronary heart disease (by
:aboul22Yo and 16% respectivel),)

FOOD ITEMS KNOII'N TO AFFECT CARDIOVASCULAR DISEASES

Fruits and vegetables consumption has been widely associated with good
health. Recent studies show a protective efi'ect against coronary heart disease,
stroke and high blood pressure.

Fish consumption also redL,ces the risk of coronary heart disease. The benefits
are most evident in high risk groups Forthese groups, consuming 40-609 offish
per day would lead to a 50% reduction in the number of deaths from coronary
heart disease.

Nuts are high in unsaturated fatty acids and low in saturated fats, which
contribute to lowering cholesterol levels. Several animal experiments have
suggested that isoflavones, present in soy products, may provide protection
against coronary heaft disease.
Alcohol can have both a damaging and protective role in the development of
cardiovascular disease. Despite convincing evidence that low to moderate
alcohol consumption reduces the risk of coronary heart disease, consumption
should be limited because of the risk of other cardiovascular diseases and
health problems.

Coffee beans contain a substance called cafestol. which can raise the level of
cholesterol in the blood and may increase the risk of coronary heart disease.
The amount of cafestol in the cup depends on the brewing method: zero for
paper-filtered drip coffee and high for unfiltered coffee.

CARDIOVASCULAR DISEASE PREVENTION

1. Limit intake cf saturated fats to less than 10% of daily energy intake for most
people, and to less than 7% for high-risk groups. Products commonly used for
cooking, such as hydrogenated fats or coconut and palm oil, contain saturated
fatty acids. Limiting the amount of saturated fatty acids consumed can be
accomplished by restricting the intake of fat from dairy and meat sourDes,
avoiding the use of hydrogenated oils in cooking, and ensuring a regular intake
of fish (once or twice per wedk). A diet comprising of a total fat intake of up to
35% does not increase the risk of unhealthy weight gain in physically active
people who consume a lot of fruits, vegetables, legumes and wholegrain
cereals.

2. Fruit and vegetable (berries, green leafy vegetables and legumes) irrtake of
400 to 500 g is daily recommended to reduce the risk of coronary heart disease,
stroke and high blood pressure. This daily consumption provides an adequate
amount of potassium, which lowers blood pressure and is protectjve against
$troke and cardiac arMhmias. Other beneficial effects are due to
phllonutrients and fibe, contained in fruits and vegetables. lndeed, fiber that is
aiso found in wholegrain cereals helps protect against coronary heart disease
and lowers blood pressure.

3. Salt (sodium chloride) intake restriction ro less than 5 g per generally hetps to
reduce the risk of coronary heart disease and stroke. Restricting salt intake
even more, to1.7g of sodium per day, may provide additional benefits _cuch as
helping to reduce blood pressure.

ESSENTIAL HYPERTENSION (CARDIOVASCULAR HYPERTENSION}

This is a disorder of unknown origin characterized primarily by an elevated

blood pressure associated wrth generalized arteriolar vasoconstriction. The
cause is obscure. ln man, heredity has been emphasized as an important

127
predisposing factor. lt has also been reported that those populations ingesting
larger amounts of sodium chloride have more hypertensive disease.

It may be present for many years without symptoms or signs other than an
elevated blood pressure. ln others, patient may complain of fatigue,
neryousness, dizziness, palpitation, insomnia, weakness and headaches at some
time in the course of the disorder.

Medical Management

This involves offering reassurance to the patient and judicious use of

hypolensive drugs either singly or in combination plus diuretics when indicated.
An important part of management is a change in lifestyle of the patient
concerning such habits as smoking and drinking and various stress-related
activities.

Dietary Management

CALORIE. This is decreased in obese and overweight patients; even patients

with normal weight will find relief from most of the synlptoms when their vreight is
brought down to about 10% below their desirable body weight.

PROTEIN. Adequate to maintain nitrogen equilrbrium.

CARBOHYDRATE. This is decreased since it is the major source of energy.

FAL This is decreased to 25yo of the energy requirement; more of the

polyunsaturated fats are reccmmended.

SOD/U/tt. This is decreased to a reasonable level (See Sodium-restricted Diets)

according to the degree of hypertension.

FRUITS AND VEGETABLES. These should be increased to suppty vitamins

anci minerals and flber.

- Vegetarians, in general, have lower blood pressure levels ancj a io\/er

incidence of hypertension and other cardiovascular diseases. Experts postulate
that a typical vegetarian's diet contains rnore potassium, complex carbohydrates,
polyunsaturated fat, flber, calcium, magnesium, vitamin C and vitamin A, all of
which may have a favorable influence on blood pressure

- A highjiber diet has been shown to be effective in preventing and

treating many forms of cardiovascular disease, including hypertension.
The types of dietary fiber is important. Of the greatest benefit to hypertension are
the water soluble gel-forming fibers such as oat bran, apple pectin, psyllium
seeds, and guar gum. These fibers, in addition to be of benefit against

124
hypertension, are also useful to reduce cholesterol levels, promote weight loss
and chelate out heavy metals.

- Sucrose, common table sugar, elevates blood pressure. Underlying

mechanism is not clearly understood. lt is possible that sugar increases the
production of adrenaline, which in turn, increases blood vessel constriction and
sodium retention.

- ln an NIH sponsored research called "Dietary Approaches to Stop

Hypertension (DASH)," researchers tested the effects of nutrients in food on
blood pressure. The results showed that elevated blood pressures were reduced
by an eating plan that emphasized fruits, vegetables, and low-fat dairy foods and
was low in saturated fat, total fat, and cholesterol. The DASH diet included whole
grains, poultry, fish, and nuts. lt employed reduced amounts of fats, red meats,
sweets, and sugared beverages.

- Furthermore, in a clinical study, reseai.chers also looked into the effect of

reduced dietarv intake of sodium. Results showed that it lowered blood pressure
and the biggest blood pressure-lowering benefits weie for those eating diet at the
lowest sodium level (1,500 mg/day).

i'YOCAROIAL INFARCTION

Myocardial infarction or "heart attack" occurs v/hen there is a decrease in

coronary blood flow following a thrombotic occlusion or spasm of a coronary
artery previously narrowed by atheroscierosis. This causes oxygen deprivation
(ischemia) of the heart tissues producing necrosis and consequenfly death
of the
arfected tissues. lt is characteiized by chest pain, res essness, pallor, cold
clamrny perspiration and decreased carotid purse. The chest pain is dascribed
as tight, heavy, and sometimes squeezing in character that often radiates
to the
neck, lower jaw, shoulder and the arms. The attack usually occurs
after severe
physical exertion, severe emotional stress, excitement, exposure
to cold wind, or
digestion of a heavy meal.

Risk factors include cigarette smoking, chronic alcoholisn, and excessi,,e

intake of saturated fats and coffee. Excessive carbohydrate intake ai,d
lack oi
dietary fibers have been arso impricated as risk factors. Aside from these,
rack of
physical exercise, severe emotional stress especially in individuals
wilh Type A
personality, sex, age and famjlial predisposition have also been
found out to be
related to its cause.

129
hypertension, are also useful to reduce cholesterol levels, promote weight loss
and chelate out heavy metals.

- Sucrose, common table sugar, elevates blood pressure. Underlying

mechanism is not clearly understood. lt is possible that sugar increases the
production of adrenaline, which in turn, increases blood vessel constriction and
sodium retention.

- ln an NIH sponsored research called "Dietary Approaches to Stop

Hypertension (DASH)," researchers tested the effects of nutrients in food on
blood pressure. The results showed that elevated blood pressures were reduced
by an eating plan that emphasized fruits, vegetables, and low-fat dairy foods and
was low in iaturated fat, total fat, and cholesterol The DASH diet included whole
grains, poultry, fish, and nuts. lt employed reduced amounts of fats, red meats I

sweets, and sugared beverages.

- Furthermore, in a clinical study, researchers alsc looked into the effect of

reduced dietary intake of sodiurn. Results showed that it lowered blood pressure
and the biggest blood pressurelowering beneflts were for those eating diet at the
lowest sodium level (1,500 mg/day)

MLoIA8elAllxEABcILqN
Myocardial infarction o!'"heart attack" occurs when thele is a decrease in
coronary blood flow following a thrombotic occlusion or spasm of a coronary
artery previously nartowed by alherosclercsjs. This causes oxygen deprivation
(ische'ria) of the heart tissues producing necrosis and consequently death of the
affected tissues. lt is characterized by chest pain, restlessness, pallor' cold
ilammy perspiration and decreased carotid pulse The chest pain is described
as tight. heavy, and sometimes squeezing in character ihat often radiates to the
neck, lower jaw, shoulder and the arms. The attack usually occurs after severe
physical exertion, severe emotional stress, excitement, exposure to cold wino, or
digestion of a heavy meal.

Risk factors include cigarette smoking, chronic alcoholism and excessive

intake of saturated fars and coffee. Excessive carbohydrate intake and lack of
dietary fibers have been also implicated as risk factors Aside from these, lack of
physical exercise, severe emotional stress especially in individuals with Type A
personality, sex, age and familial predisposition have also been found out to be
related to its cause.

130
 I

Diet Therapy in Myocardial lnfarction ,

After a heart attack, patients are given nothing by mouth or just sips of
cool water. This is supplemented by parenteral dextrose solutions for the first 24
hours. Then for the 2nd and 3'd hospital day, patient is allowed low-fat liquid diets
that supply 500-800 kcal and '1000-1500 mt. of liquid given in small frequent
feedings. Extremes of temperature can cause arrhythmia, so food is given at
room temperature. Caffeine is strictly prohibited due to its stimulating effects on
the heart.

The patient then progresses to soft diet after three days. This diet has the
following characteristics:

1. 1000-1200 kcal io limit the metabolic demands of digestion and

absorption and to initiate weight loss for obese patients;
2. Easily digested meals given in 5-6 small feedings especia,ly in patients
who are dyspneic or has angina:
3. Less than 30% of calories as total fat; saturated fat is limited to less
than 10%;
4. Cholesterol is restricted to 300 rng. or less;
5. Sodium restriction of 2000 mg. or less and fluid restriction paiticularly
in rhose who have edema:
6. Foods that are gas-producing are avoided.

During the rehabilitation phase the diet before leaving the hospital should
be the basis for the diet to be give ai home. Diet must be based on the weight
., status and the blood lipid levels. ln patienls who are obese, an exercise regimen
must be instituted.

*
- DievNutrition is the key ingredient of a cardiac r-ehabjlitation program. A
carefully designed dievnutrition plan can prevent a heart attack
and/cr to avoid its
recurrence. The key is to eat whole foods and a predominanfly vegetarian diet,
consisting mostly of fresh vegetables and fruits, whole grains and nuts and
seeds.

coNGEsflvE H EAErlA!! UBE

As heart failijre progresses,reduced blood flow impairs the function of all
organs. Reduced blood flow to the kidneys triggers the retention of fluid, further
stressing the heart and compounding the stagnation of fluid in the body.
Peripheral, pulmonary and hepatic edema may develop may develop as the
person becomes increasingly "congested: with excess fluids

'131
 Diet therapy in CHF patjents is almost the same in post-myocardial
infarction patients; however, sodium and fluid restriction is more severe than
those in post Ml patients. The usual sodium restriction in CHF allows 500 mg per
day.

FOOD SELECTION GUIDE FOR MI AND CHF

Food GrouD Allowed Avoided

Vegetable all, prepared without fat buttered, creamed, fried in

or with allowed fats only restricted fats, or cooked with
fatty meat.

Fruit all. When usinS avocado

adjust fat allowance

Milk skim or non-fat only allothers

Meat, fish or use oftenj lean fish fresh
Substituie or froien or canned in water,
tomato olcustard; chicken
without skin and fat. Use
occasionally; very lean,
well trimried cuts of beef,
veal, pork; crab meat,
shrimps without head.
fatty me6ts, fish roe and
internal orSans; sausages,
cold cuts; canned or froz€n
meats; fatty poul'Lry with
skin, tripe, sweetbreads;
lobsiers, crab roe ialigul),
shrimp heads, oyster,
clams.

eggs, whole, up to 3-4

perweek, maY be cooked
in allowed fat;whites as
desired.

skim milk or low fat cheese, whole milk cheese.

dried peas, be;ns, lentils;
"vegemeat" tokwa, taho and
other bean products,

Fats in prescribed amounts: corn, butter, coconut meat, milk,

soybean, olive, sesame, and oil in excess of
peanut and cottonseed oils, allowance; hydrogenated

132
 coconut oil, in amount to vegetable oils like margarine
yield a P/S ratio of 1:1. and "mantika". animal fats
like lard, salt, pork, bacon,
meat and chicken drippings.

Eeverage coffee (not more than 5 soda fountain bevera8es like

cups, black), tee, carbonated milk shake, malted milk and
beverages chocolate drinks

5c'ups soups made with skim cream soups, fatty broth s.

milk;fat-free broths
made from meat or
chicken stock or
Concentrates

Miscellaneous non-dairy cream substitutes, sauces and gravies with

seasonjngs and spices in
moderation; sauce rnade
wiih allowed fats and skim
milk, v;negar, pickles,
mustard, catsup, banana
restricted fats or milk;
Popcornr French fries cr
potalo chips; br,tter dipped
foods, packed dinners or
"instant foods" oi unknown
fat content.

*
.Q10. (CoelO) is an essential component of the metabotic
Coenzyme
processes. involved in energy producticn. lndividuals with cardiovascular disease
(in"]rd]lS- hypertension, angina and congestive heart failure) onen are Oericient
rn loetu and requrre jncreased tjssue levels of Coe1O. Clinical
studjes have
indicated that CoQIO is of considerable benefit in the treatmenioi nlpertension
aiid other cardiovascular disease.

SOOIUM-RESTRICTEO DIETS

Levels of Sodium Restriction

Sodium-restricted diets are used for the prevention. control. and

elimination of edema in many pathologic conditions, and occasronally for
the
alleviation of hypertension. Since sodium is the ion of jmportance, it is
incorrect
to designate a diet as salt-free, salt-poor, or low sall. Moreover, to call a diet
low-
sodium or sodium-restricted is misleading, since any amount of sodium below
the

133
 normal intake would satisfy such a description,
but would not necessaflly be at
therapeutic levets. Sodium_restricted diets
shoutd U" pru""r,Oil-ii-t""lr" ,
milligrams of sodium, e.g., 600 mg sodium diet.

The normal diet contains about 3 to 6 gm of

sodium daily, although a
liberal intake of salty food results in considerably
higher soOium'tevets. fne
normal diet may be modified for its sodium
contents as follows:
MILD SODIUM RESTRICTTON (2400 mg. or 1
tsp crude rock salt/day)
Some salt may be used in cooking but no
salty foods are permitted; no salt is
used at the table. This level is used as a
mainienance dieiin r."n",
diseases. ""rOi" "lno
MODERATE SODTUM RESTRTCTION (12//.
mg or % Ep crude rocksatt/day)
No salt in cooking; permits sljgh y higher protein
level if needed. as in
pregnancy, may include measured amount
of salt, or salled bread and butter.
SfR/Cf SODrUnt RESTRTCTTON (600 ng. or,l tsp crude
rock satr/day)
No salt used in cooking; careful selection of foods
in measured amounts; regular
milk. This levej may be used for congestive heart
failure; i" r."""1
diseases with edema, c:irrhosis of the llver. "|"*r."iy

References:
Joint WHO/FAO Expert Consultation on Diet,
Nutrition and The prcvention ol
Chronic Diseases.2002. WHO Technical Report
Series.
Gropper,S.S., Smith, J.L., and Groff, J.L.2OO9.
Advanced Nutition at,.l Human
Metabolism, ith Edition. Wa.lsworth Cengage
Learning
Frayn, K. And Stanner, S. 2OOS. CATIDjOVASCULAR
DISEASE Diet, Nutrition
Rkk fectors; The Repoft of the British Founaation
1:d Fme.:.Sing
Blackwell pubtishing
rai* rorce.

Whitney, E.N., Catatdo, C.8., DeBruyne, L.K.,

and Rotfes, S.R.2001. Nurrtion
For Health and Health Care, fd Edition Wadsworth
Thomso" r""r"f"g
http://www. holisticon line. com/remedies/Hearuhypert_vitamins

134
 ftedical utrition Therapy in Kidney Dlsease

I'ITRODUCTION

The prevabnce of cfiFonic kidney disease (CKD) is nlsing w n a rise in the aging

poFilatbn 6 \,ydl as fiofi an increase tn the Feva,erEe of conorbidities associated

wi&] CKD {1, 2). Diabetes, hypertensio',i, and p.i.?a.y kidc€y dis€ases acco{int for

most cf lhe kitney iailure seeo in this 6unt-v Diabetes is the leading cause of end-

stage renal disease (ESRD). Medical nutrition lhempy is a yital part of the managern€nt

for th€ CKD potieflt population. Nuiritiff iherapy is correhted to ti}e siage of CKD as

nutrient needs cllar€e as CKD progresses to ESRD. Patients who begin renal

replacement therapy (either dialysis or transplantation) )vith compromised nutnlional

status have a higher rnorttdity and mortality than those who are adequately nounshed.

B€cause ot Ulis, FrtiqJlar attenlicn ta nuL.iticn in the earlier stiages of CKD is sucjal

f3j- Frimary nufiiional goals for the management oi the early stages of CK-D include:

l. Prevent proteirF-energy malnutriton

2. Minimize the buildup of uremic toxins and associated symptoms

3. Delay the progression of the disease

4. Prevent secondary hyperparathyroidism and conlrol acidosis

5. Treat any compli:alions resulling trom litestyle issues

STAGES OF CHRONIC KIDNEY DISEASE

The National Kidney Foundation (NKF) Kidney Disease Outcome euality lnitialives

(lCDOQl) has deined CKD as described in Table belo\r/- Clinical practice guidelines

classify cKD inlo five slages bas€d on kidney function indicated by gromerurar lirlrarion

rate (GFR) and evidenc€ of kidney damage.

lt'l.J!J

{." -r};l nrt."

:t* '.;ril:i .r.-:. i ', i:( I -rr:r i 'ir:! .t,:f I

:;';: l

I.n:\ ,'\ a;i i, :: sirr:s

I -Il l:.t'l:r .t-!r I .tr. I .rlri l .:r:L t -!:! I

',. . .r.- ,.r..,r ,.',..,,,iJ,,.JJ

,ir : ri .i . r . . , , l n..,. tl
.

'

tJo
Definition of Chronic Kidney Disease Criteria

J. Kidney Damage for > or equal to 3 mo, as deined by slruclural or functional

abnormalities of the kidney, with or without decreased GFR, manifest by erlher

Pathological abnormalities: or

Markers of kidney damage, including abnormalities lhe of the

blood or urine, or abnomalities in imaging lests

2. GFR < 60 mumin/1.73 m2 fot > cr equal to 3 mo, with or without kidney
damage.

DIET PRESCRIP]ION IN CKD STAGES I-4

-Protc,n,
. Recommendation for protein intake in CKD ,qtages 1-3 is 0.7S glkglday

which is close to the 0_8 g/kg/day necessary for the non-CKD population (7). B€tr;luse

typical consumption is much higher, this constitutes a significant reduction for the
average individual Of the 0.75 g&g/day, at least 50% shoutd be of h;gh biolcAical value

(HBV) providing all of the essenlial amino acids needed for protein synthesis. F,s ti.:e

indiyidual progresses to siages 4 and 5 protein restriction becomes more slringent

leveling out at 0.6 g/kgday (4).

137
 Energy. ln general, calorie needs sre similar to the general population and

should be cbnelated to energy expenditure to maintain a healthy weight. However, it

has been shown that CKD patients tend lo consume less than the 30-35 kcavkg

re@mmended in slages 4 and 5 (5,6). lnadequate energy ;ntakes not only lead to

malnutrition but will decrease any positive benefit afforded by a low-protein diet-

Minerals and tyafer_ Sodium intake can range trom 1 lo 4 glday depending on

blood pressure, ffuid balance, and the presence of congestive heart tailure and olher

diseases- Fluid intake is closely linked with urine oltput and is not restricted unless

oliguria is present (4). Potassium resiric.tion in CKD stages 1-4 is genera{y not

neca;sary unless urine output decreases to less than .1000 ml/day or seru!-fl level is

high {7). ln the earlier stages (1-3) of CKD, dietary restriction of phosphorous is
ef,eciive in controllir,g serurn levels. As kidney funclion declines fu.ther, phosphate-

binding medications are needed along with diet therapy ic maintain recommended
serum levels. ln the earlier stages ot CKD, calcium ievels should be mainlained wilhin

normal lab value ranges with a calcium intake not lo exceed 2O0O mgr'day due to the

risk of vasc lar calcification and bone dis€ase (8).

MEDICAL NUTRITIOT,I THERAPY FOR HEMODIALYSIS

Nutrient needs change when a patient reaches ESRD (end-stage renal disease) and

begins regular hemodialysis treatment, and malnutrition becomes a siglnificant concern.

The presence of comorbid conditions such as diabetes, chrcnic inflammalion, and

cardiovascular disease affect oral intake and contribule to declining nutritional slatus

138
(9r. Hemodralysis patents shc'l , evidence of chronic rnframmation with elevated levels

of C-reaclive protein (tO). Chronic inflammation has been found to be associated with

decreased oral intake (tu, Additionally, depression and social and economic issues

iactor into a patient's overall well-being and nutntional status. Allhough ulburnin
""a-
is used as a marker for chronic inflammation, it is also used as an important marker of

protein inlake and nulritional status in the dialysis patienl along with bcdy weighl (12).

Palients with serum albumins of less than 3.5 g/dl have a mortality rate 1.38 times
higher lhan those above 3.5 gidl (?3). The goal is ior albumin to reach 4.0 g/dL (r2)-

Potassium, Sodlum, and F/urd Most hernodialysis patients who are anuric ot

oligunc with a urine output of less than 1000 ml/day will become hyperkalemic without

Fotassium restriction. A reduced daily intake of 2500 mg potass;um is usually sufficient

to prevenl hyperkalemia in most hemodialysis pa$ents (7 7.). As kidney function declines,

th€ gyt comp€rlsates and becomes more efficient at removing potassium through the

stool contribuling lo pota$ium balance (2J. Nevertheless, individual differences

will exist, therelore 40 mglkg of ideal body weigh: or standard body weight is

recommended Along with dielary excess and conslipalion, hyp3rkalemia may also

resull from inadequate dialysis, metauolic acidosis, 3nd certain medications (10).

Phosphorous, Cabium, PTH, and Vitamin D. Controlling the balance between

phosphorous, calcium, PTH, and vitiamin D is crucial in the prevention of secondary

139
hyperparathyroidrsm. Excessive dietary intake ol phosphorous contributes to
hyperphosphatemta, elevated calcium phosphaie product, and high circulaling levels of

PTH, which in tum can lead to renal osteodystrophy and sofl tissue and vascular
c€.lcif!tr2,lion (14). ln addition to protein foods, other examples of high phosphorous
foods include dairy products, dried beans, beer, nuls, chocolate, and colas. Given the

risk of vascular calcification, in persons uadergoing hemodialysis, calcium intake should

not exceed 2000 mg/day.

V,tamins and Other M,?lerais, Because vitamins A and E accumulale in kidney failure,

lhese are not supplemented over usual reouirements. Losses of vilamins 86, 812, and

folate ocrur with dialysis so they are supplemented. Mtamin C is nol supplemented

above the RDA, as excessive levels arc assocjated with the formation of oxalate kidney

stones. Low zanc t9./9ls have been associated with decreased iaste acuity so inc is

ofren supplemented. Lastly iron deficiency is common in dialysis patients duc lo the use

of synthetic eryihropoietin and chronic blood loss, lv iron is more effective than oral iron
in replacement.

140
I}.ry Rd{EE.a,isr Nlllri.lr I.rrn r tu ,\.r!tb d Ftd}sd;rt!4a
lilr*icnr O:ii1. Rr=,rmarcrLrlrtr t'...\,iiijr'n'
lrarxl.:lyrir
I

t I S.'ltF .!!-i*c rfi::hll "r7.l lli*h

hio'"ag;!:* r.-r&']
Eocr:r) En.,lt
ir tc*t'\g
r'l&l|1 i{,{t !. L{ i,lt-* .il)-15 l,!Jrl,
Sor!fun :ral drrrl St{rt'nl ;rd t}ulrJ
>r1r gFrttr l. I t. tfuri o..irttll :.i t Nr inil: t. tl'r,d
< rrr rryEl r{' I l, frli! .$|tr' r I S !i: rsd I J.-i l. Iult
lii \e rnJ I L llt$d
rr' mglr* Ig\\ .r ,ili\\
S{lN-r :lI$ n;,j r,( '. ll r'+ll'! !$i\ { sfl\\
I'xl; v;.lBltTaal
!l*gr*-$ura rrl-+ lF
Zin';
luo-9gJ 11:

\irBntn f" I i :ttp

(X)-l:{t 1l:c
Thi:rmrn I l-i I t,i
itrtrrtiar *t
B;'ri'
Flat(,th.crr .1\ d
l$is.iE
Fol|. i.id l4lL l{tl} t(ll

1J ir1
\'iwniD C
iibe!iu;'h: lg\r- ,r{l &nr r.l!ar: SS$_ s6rJJ trrll -Ir}a
(.lnsirir laq d-.&i* {tiqr;r:.{*r:*r- p{,r.. !r€.J .ri,t,
F.,:bil,.,r f t,i,

1+1
MEDICAL NUTRITION THERAPY IN PERITONEAL DIALYSIS

Energy and Prolerin. Energy requirements in peritoneal dialysis are similar to

hemodialysis. Energy needs should be individualized to achieve or maintain desirable

body weight, including the calories from dexlrose in the dialysate solulion. pD palients

can absorb up to a third oflheir tolal energy requirement trom the dialysate (tS.). protein

intake musl compensate for the ,oss of protein in pD etfuent. Typically, between 5 and

15 g are lost daily, mostly as albumin (75.).

Potassium and Sodium. Most patients will remain in potassium balance with 3-
4 g of polassium daily, which is misistent with an unrestricted diet. Sodium is also

easily cleared on PD. Patients @nsuming gxcess sodium !!ill need to use higher
dextrose dialysate exchanges to remove excess fluid retaihed as a resuit of incniased

scdium intake. Frequent use of high deldrose exchanges ?an damage the peritoneal

membrane affecling its ultrafittralion caFabilities. This practice c€n atso aggravate
existing diabetes, hypertriglyceriden,ia, and hypercholesterolemia and contribute to

overweight and obesity from the absorption of dextrose calories. Sodium intake should

be individualized but rcmain belween 2 and

4 g/day to mainiain adequate fluid balance (t6).

Cholestercl and Tnglyceides. pD patients are at risk for hyperlipidemia due to

weight gain and absorption of dextrose from the dialysate. patients should be taught

142
ho/t, to limit sugars, saturated futs, and cholesterol bui wiihout compromising protein

in!€ke (15).

ACUTE RENAL FAILURE

Acuie renal failure (ARF) is associated with alterations in protein, carbohydrate,

and lipid metabolism as well as disturbances in fluid and electrolyte and acitrase

balanee (16). These metab€lic chaflges, wlrile associated with the utemic state, are also

the result of the calabolism of critical illness, a

complication of sepsis, trauma, or nruitiple organ latlure (14). Proiein

recommendations will differ based on wheiher the patient is receiving d'alysis. For those

not treated wlth dialysis, no less than 0.8 g/kg/day is iecommended with an upper limit

ot 1.2 gkg;day (16). Mote oftel than not patients are treated with dialysis. The
recomnendation of 1.2-1-5 g/kg.lday is sin ilar to that of the critically ill patient (10). The

hypeicatabJlism of critical illness and ARF cannot be ove:-come by increasing protein

intake. lntakes greater than 1.5 g/kg/day sho\.v no beneft and may actually aggravate

ihe uremia Protein provided should be a mixture of essenlial and nonesser'lial amino

acids. The goal is to provide adequate calories to minimize protein catrbolism without
overfe€ding: 25-35 kcal/kg/day can be used to estimale -'nergy needs (77). Fluid needs

are dependent on level ot renal funclion and the patient's fluid status. ln general, ur,ne

output plus 500 ml for insensible losses (e.9., through skin, sweat, stool) is a good

guideline. Electrolytes are individualized based on lab values and the mode of nuttition

143
support (t7). Palients can be ied orally, enterally, or parenterally based on the severity

of illness,

8, OTHER KIDNEY.RELATED CONDITIONS

UTls represent a major health problem and occur when bacteria (primarily Eschenbhra

cali ot E. colD adhere to the uroepithelial cells that line the bladder, kidney, or urethra

and then muttiply. Bacterial adhesion to uroepithelial cells requires the production of a

set of slruc{ures calledpfimbriae on ihe cell walls of the colonizing bac{eria. Cranberry
juice consumption leads to siqnifcant reductions in the numbers of both bacteria and

whiie blood cells i'l the urine over lhe 6.mG.siudy period. Recent cJinical studies have

confi[med its usefulness tor the prevention of UTt. The active agents are
proanthocyacidins which prevent baclerial adhesion to the urinary tract. lthile other

fruits and vegetabl€s contain proanthocyanins, only ihe cranberry, and its close relalive

lhe blueberry, have lhe abilily io prevenl p-imbriae exgression and bacterial adhesion

lo uroepithelial cells (18). Hoy./eyer, consumer and researcher understanding of how

cranberries affect human health remains difficult to determine in part because of the

large range of product formulations and the differences in the amount of cranberry juice

as{ually present in these beveragcs

144
REFEREI{CES
I Coftsd, A. Cko.dc ti&r€) dis4e Clincjan R6v 2{Xr7; 9137,53
2 Aelo -rA, Bansal VK. Medi€l rllririd lhdap_! in.h'o'!c liidrq fliluc iDlegrrirg.lirical pradie aidclirs J An Diet
Ass?0O4: IO4r4O1- 149.
:l- Wclls C. Optimzirg mridor in patisE sro chrdii. liery dsN. N?lrcio$ NGirgJ 2003; i 2:637 t'57
4 Nalnb.] KjdDe! FoudatiD Ki&e_v Di*i\i Ourco.ne qBfilv Itritiariys (X-/mQl) 2002 Ali,able ar
tn:rtih6rngi!.ofessiDals/KDoQyguid€lin6 c[(v!(l. hub. rst e6scd Apr;16,201l.
5.talind }ltlIrelgm B, CullctoflB, cr sl GuidllinB k thc s€naacmett of dlroikkidtr€y disije CtuEdian l\lcdical
Aslociati@ lo6nd 2008: I 79:1 l5.l I 162
6. Fedje l. Mdlis it Ndrilion rum8cnrcnl in dlt srag6 of ch.onic kidley dis€3se. In:B).han cny L, Wiesa K, gls A
Clirical Guide to Nutritim Cde i6 Kid.€t Dsse ADeriq. DeJdic Associ?tio4 CbicaSo, ll.2004, pp 21 28
7. NalioMl KidrE Fdrdrtid Kidne' Dasea-se Outcomc Qulity Initiatives (K[,O{]D,21)00. Alailable at
wll* tidn€y.ors/rfesliorrls/KDoQUsuideliB trpdntes/nut_a24.tdml.
8. Cwpari I. Ayesi CM- E dsl rEquiftftenls iD p.risls $it[ cksjc lidn€j' di$se J Rtu.l NtrlI 200:!, 14:l ]l,l ?6.
9. &r.row€s JD, Datotr S, Beksr"rd J, L€yin NW. Paltglt! recei.ing d.ir{annelEmodia\srs \ri[' lo\r rs high lqcls
ofnrnriiiEl risk haie d€{rcraed c.bidity. JAm Di.r Ass 2u)5: IO5:56F72_
10. M;tch E l,lrhr S. Hadbo{ r otNutririd md lhc K;(G}.-_. Ljppircofl \yllia6 ad Witritr! Phibdclpti! 2002
I l- Bisc.&d R, Sh6l N. Ndlitiol ]nsMgclmt oltbe rddt banodialy6is potidrt In:btun{fry la Wi6m (, sls A Clmrcar
Grid. to Nutilid Cd. i. Kihct Di.ea!. Afrsic Die.etic Asociiri{.. Ct\tcrgo, lL,2004, pp. 4l-55.
12 Ndir'tl Kid'5J FomdntioD KidEy Di$se Oulcone Quality ltritiative G/DOQII
2fiX)- Aiiilr$le
at $ae lddoey.6glprct€ssj@alyKDoQvgddelin€s_qdar€shut_dr3.htDl. tz51 accesed op n pnl 6, 20 I L
ll. carbe Mccllloogh XP, Asao Y' CiGbds N, Mtrad BJ, Pifa TB. lc&c' Ds@eOlrofres QrnliS lniriarnr
C,
(XDOQD ad rbe Dialys's Odcon6 ed Pncti@ Parrds Srdy (DOPPS): Nrditio suidolixB, irdicaroA, and practices. Am l
Krdn€y Das 2004.44:3!41.
14 Tlrc PU, Prie D, B€cl L FdcdLDde C Ndr &srpi€s f.. sec.odary h)"e.-raarb@idis J Rcn?l Nur 20{ttl
l6:E7-99 'ncDic
15. M.Cd L. Nulililr.l
'm'ge4en of$c a(Itrh pEil()Hl din\s,s pdid( lu DrLh&FcFy L, Wi€ser K, ei.ls. A Cliniql
Gnde b N'ltt[od Circ ;, K;i$rcv Diece Anericao Dictdic A.q;qtq Cniogp, n- 2U)4, pp. 57-69.
16. Bi.kfdd A, S.nd2 SR. Nqtrition trua8tmfrt in .cu!e.enal failurc. In: RyiaRrcrry Lwiesn I( €ds A Clinial Cuid€ 10
NuEiIiod Cde b Kidcv Ds.as&- AlFi@ DiddiicAs-so.i.tioa Chic.go. IL, 20Ot, p 29-tl .
!7. Kalida Ri.n&ds Ir- Pus€ll R Gonq R. Nut itional manag€dsd of lh€ patxr, sirh ncde rddl tailure. RenntNulr Fo.u
2UEj24.1 12-
i 6- \i'ilson T CJebsir'jutd.ili4tu or bdlili Ix ',Yli*xt T, Tcr,pl€ NJ,.ds B.ldaAe topnrs o,r Heatrh od iili.iriol
tlllll'@ fts, Torol4 Nl, 20Ol. pp- 51 62

145
 DIET THERAPY IN SELECTED METABOLIC DISEASES

DIABETES MELLITUS

Diabetes is a group of metabolic diseases characterized by hyperglycemia

resulting from defects in insulin secretion, insulin action, or both. The chronic

hyperglycemia of diabetes is associated wilh long-term damage, dysfunclion and

failure of different organs, especially the eyes, kidneys, nerves, heart, and blood

vesseb.l Diabetes is a chronic illness that requires continuing medical care and

patient self-managemenl education to prevent acute complications and to reduce

the risk of long-term complications.2

The classification of diabetes includes four clinical classes:3

. Type 1 diabetes (resuits from p-cell destruction, usually leading io absolute

insulin deficiency)

. Type 2 diabetes (ranging from predominantly insulin resistance v/iti.r relati.,/e

,insulir deficiency to predominantly an insulin secretory defect with insulin

resistance).

. Other specilic types of diabetes due to other causes, e.9., genetic defects in p-

cell function, genetic defects in insulin action, diseases of the exocrine pancreas

(such as cystic fibrosis), and. drug or chemical-induced (such as in the treatment

of HIV/AIDS or after organ transplantation).

. Gestational diabetes. mellitus (GDM) (diabetes diagnosed during pregnancy

that is not clearly overt diabetes)

TYPE 1 DIABETES. lmmune-mediated diabetes. This form of diabetes, which

accounts for only 5-10% of those with diabetes, previously encompassed by the

146
terms insulin dependent diabetes, type 1 diabetes, or juvenile_onset diabetes,

results from a cellula[-mediated autoimmune destruction of the B-cells of the

pancreas. ln this form of diabetes, the rate of p-cell destruction is quite variable,

being rapid in some individuals (mainly infants and children) and slow in others

(mainly adults). ldiopathic diabetes. Some forms of type 1 diabetes have no

known etiologies. Some of these patients have permanent insulinopenia and are

prone to ketoacidosis, but have no evidence of autoimmunily. Although only a

minority of patients with type 1 diabetes fall into this category, of those who do,

most are of African or Asian anceslry.1

TYPF 2 DIABETES MELTTUS (T2DM)_ T2DM is a comptex heterogeneous

group of metabolic conditions characterized by increased levels of blood glucose

due to impaired insulin action and/or secretion. physiologically, lhe pancreatic g_

celis constantly synthesize insulin, regardless of blocd glucose levels. lnsulin is

stored within vacuoles and releascd once triggered by an elevation of ihe blood

gkrcose level. lnsulin is the key hormone concerning the regulation of glucose

uptake f'om blood into most cells, including skeletal muscle ce!ls and adipocytes.

lnsulin is also the major signal for ccnversion of glucose to glycogen for internal

storage in liver and skeletal muscle cells. A drop in the blood glucose level
results in decrease of insulin release from B-cells and in increase of glucagon

release from o-cells, whjch stimulates glycogen to glucose conversion. Following

an overnight fast, glucose is largely produced by glycogenolysis and

gluconeogenesis.a

There are three key defects in lhe onset of hyperglycemia in T2DM:

increased hepatic glucose production, diminished insulin secretion and impaired

147
insulin action. lnsulin resislance refers to a suppressed or delayed response to

insulin and is generally a post-receptor phenomenon, due to a defect in cells that

respond to insulin, rather than on insulin production. lnsulin resistance in muscle

and liver, together with B-cell failure, are pivotal pathophysiologic defects in

T2DM. lt is now recognized that p-cell failure occurs much earlier and is more

severe than previously thoughl. Subjects in the upper tertile of impaired glucose

tolerance (lGT) are maximally or near-maximally insulin resistant and have lost

over 80o/o of their p-cell function. ln addition to muscle, liver and p-cells, the fat

cell (accelerated lipolysis), the gastrointestinal tract (incretin

deficiency/tes;stance), lhe o-cell (hyperglucagonemia), the kidney (,ncreased

glucose reabsorption) anC the brain (insulin resistance) all play important roles in

the development of gluccse intolerance in type 2 diabetic individuals.3

Glycemic lndex, lnsulinemic lndex, Glycemic Load. The term 'gtycemic index'

is noy,/ used to describe the rate and extent of the rise in blood glucose following

a meal.s lt is defined as the incremental area under the 2 h blood glucose

response curve (IAUC) after uonsuming a test food compared to the

corresponding area after a carbohydrate equivalenl amount of a reference food

(either glucose or white bread).5 Per gram of 3arbohydrale, foods with a high

Glycenric index produce a higher peak in postprandial blood glucose and a

greater overall blood glucose response during the first 2 h after consumption than

do foods with a low Glycemic lndex.6 Expanding the theory of clycemic lndex lo

the postprandial insulin levels evoked by foods, the lnsulinemic lndex of foods

can also be determined from the corresponding incremental blood insulin areas.

Because insuljn is the hormone that maintains blood glucose homeostasis, a

148
food or diet high in lnsulinemic lndex could induce a higher degree of

postprandial insulin concentration and thus result in higher insulin demand in the

long term. Glycemic load, on the other hand, is a concept thal summarizes both

Glycemic lndex and the carbohydrate content and is considered to represent the

overall glycemic effects of a food. The Glycemic load of a typical serving of food

is the product of the amount of available carbohydi'ate in that serving and the

Glycemic lndex of the food. The higher the Glycemic load' the greater the

expected elevation in blood glucose and in the insulinogenic effect of lhe food

The tong-term consumption of a diet with a relatively high Oycemic lcad

(adjusted for total energy) is associated with an increased risk of type 2 diabetes

and coronary heart disease.5

Medical Nutrition ]'herapy in Diabetes

Medical nutrition therapy (MNT) is important in preventing diabetes,

managing existing diabetes, and preventing, or at least slowing, the rate of

, development of diabetes complications. lt is' th3refore, important at all levels cf

d;abctes prevenlion.T

General recommendation3

. lndividuals who have prediabetes or diabetes should receive individualized

MNT as needed to achieve treatment goals, preferably provided by a registered

dietitian familiar with the components of diabetes MNT.

Energy balance, overweight, and obesity3

o In overweight and obese insulin-resistant individuals, modest weight loss has

been shown to reduce insulin resistance. Thus, weight loss is recommended for

all overweight or obese individuals who have or are at risk for diabetes
149
. For weighl loss, either low-carbohydrate, low-fat calorie-restricted, or

l\4editerranean diets may be effective in the short term (up to 2 years).

. For patienls on low-cdrbohydrate diets mooitor lipid profiles, renalfunction, and

protein intake (in those with nephropathy) and adjust hypoglycaemic therapy as

needed.

. Physical activity and behavior modiflcation are important componenls of weight

loss programs and are most helpful in maintenance of weight loss.

Recommendations for primary prevention of diabetes3

. Among individuals at high risk for developing type 2 diabetas, structured

programs that emphasize lifestyle changes that include moderate weight loss

(7% of body weight) and regular physical activ:ty (150 min^/veek), with dietary

strategies including reduced calories and reduced intake of dietary fat, can

reduce the risk for developing diabetes and are therefore recommended.

. lndividuals at high iisk for type 2 diabetes should be encouraged to achieve ihe

U.S. Department cf Agriculture (USDA) recommendation for dietary fiber (14 g

fiber/1,000 kcal) and foods containing whole grains (one-half of grain intake).

The presence of fiber causes glucose to be absorbed more slowly through

the following mechanisms: it reduces the rate of qastric emptying, so food enters

the small intestine more slowly; once the digesta reaches the small intestine the

higher viscosity caused by sJiuble fibres, especially gums, slows the diffusion of

nutrients to the gut wall; presence of intact remnants of plant cell walls may also

inhibit the access of digestive enzymes lo starch, thereby slowing its digestion.s

150
ReCommendatiOns ot{ft CrOnutrientS in diabetes
m2asg",nanr:

. The best mix of carbohydrate, protein, and fat may be adjusted to meet the

metabolic goals and individual preferences of the person with diabetes.

. Monitoring carbohydrate, whether by carbohydrate counting, choices, or

experrence-based estimation, remains a key strategy in achieving glycemic

control

. For individuals with diabetes, the use of the glycemic index and glycemic load

may provide a modest additional benefit for glycemic control over thal observed

when lotal carbohydrate is considered alone.

. Saturated fat intake should be <7% of total calories.

. Reducing intake of frans fat lowers LDL cholesterol and incraases HDL

cholesterol; therefore, intake of fans far should be minirnized.

Other nutrition recommendations3

. lf adults with diabetes choose to use alcohol, daily intake shculd be limited to a

moderate amount (one drink per day or less for adult women and two d.inks per

.day or less for aduli. men).

. Routine supplemertation with antioxidants, such as vitamins E and C and

carolene, is not advised because of lack of evidence of efficacy and concer,l

related to long-term safety.

. lndividualized meal planning should include optimization of food choices to

meet recommended daily allowance (RDA)/dietary reference intake (DRl) ror all

micronutrienls.
3
Physical activity

. People with diabetes should be advised to perform at least 150 min/week of

moderate-intensity aerobic physical activity (50-70% of maximum heart rale).

151
. ln the absence of contraindications, people with type 2 diabetes should be

encouraged to perform resistance lraining three times per week.

HYPERTHYROIDISM

Hyperthyroidism is a hypermetabolic state resulting from excess thyroid

hormone. Hyperthyroidism affects 2yo of women and O.2o/o of men in lheir

lifetime Toxic multinodular goiter usually occurs in women >55 yr old and is

more common than Graves' disease in the elderly. Disorder of carbohydrate

metabolism (with abnormal blood sugar curves and increased glucose

melabolism), increased protein metabolism, calcium imbalance, disorder of

creatine metabolism and depressed serum cholesterol are frequently present.

There are also changes !n the liver and destruction of the muscle cell. The

ccndition is also refeiied to as exophthalmic goiter, thyrotoxicosis, Basedow's

disease or Grave's disease.

Symptoms: hyperactivit-v, irritability, dysphoria; heat intolerance and sweating;

palpitations, fatigue and weakness; weight loss with increased appelite; diarrhea;

polyuria; oligomenorrhea and loss of libido; Sig::s: tachycardia; atrial fibrillation in

the elderly; tremor; goiter; warm, moist skin; rnuscle weakness, picximal

myopathy; lid retraction or lag; gynecomastia.

Nutritional managsment of Hyperthyroidism

Since all metabolic processes in the body are accelerated, a high calorie

diet is indicated to prevent lhe destruction of body tissue and a rapid loss of

weight.

Calories. The increase of calories over normal allowances should be in

accordance with the elevation of the metabolic rale. ln mild cases, the increase

152
 may be from 15 25o/o above the normal allowance, while in severe cases an

increase of 50-75% is required. A diet containing 4500_5000 kcal or more rs

frequently prescribed and consumed, since these patients exhibit a ravenous

appetite.

Protein. Hyperthyroidism is characterized by negalive nitrogen balance and a

decrease in muscle mass. Therefore, lhe protein allowance should be liberal _

sufficient to meet the increased need for nitrogen. By supplying sufficient

calories through carbohydrates and fats, an allowance of .lO0 gms of protein will

usually be adequate to maintain nilrogen balance.

Carbohydrate. Carbohydrate intake should be increased to compensate for the

disturbance in carbohydrate metabolism and supply an excellenl source of easily

assimilated focd enetgy. The increase in carbohydrates will spare the proteins in

the diet.

Fat. Fat is increased to take care cf the energy balance that c,annot be covered

by carbohydrate and protein.

Minerals and v;iamins. The diet should be abundant in all essential food

nutrients. Supplements, especially B vitanrins, should be a regular part of any

diet program to meet the greafly increased demand.

lodine. lodine administration plays a significant role in the lreatment of Grave,s

disease. lodine is an essential component of the thyroid hormone thyroxine, the

active principle of the thyroid gland. ln hyperthyrojdism, administration of iodine

in large doses (polassium jodide) will increase the storage of thyroid hormone

and prevent its release. Consequenfly its effects on hyperthyroidism are striking

153
even if only temporary. lt is normally used only for a short period of time in

conjunction with antithyroid drugs and before surgery or other therapy.

Foods to avoid: Dairy products, sea salt and iodized salt, seafood and eggs.

Stimulants like tea, coffee, alcohol, nicotine, and soft drinks should also be

avoided because they increase the metabolic rate.

Foods that help; Brussels sprouts, cauliflower, peaches, pears, cabbage,

turnips, spinach and soybeans.

HYPOTHYROIDISM & IiIYXEDEMA

Hypothyroidism is an endocrine condition characterized by the deficient

activity and lessened secretion of thyroxine or triiodothyronine, or both, which are

th thyroid gland hormones. lt is common, affecting over 1% of the general

population and about sc/i) of individuals over age 60 years. lodine deficiency
remains the mosl common cause of hypothyroidism worldwide. ln areas of iodine

sufficiency, autoimmune disease (Hashimoto's thyrojditis) and jatrogenic causes

(treatment of hyperthyroidism) are most common. Thyroid hormone deficiency

affecis almosl all body functions. The degree of severity ranges from mild and

unrecognized hypothyroid states to strikinq myxedema. The fluid retention seen

i" myxedema !s caused by tne interstitial accumulation of hydrophilic

mucopolysaccharides, which leads to lymphedema. Hyponatrernia is the result of

impaired renal tubular sodium reabsorpticn due to reducticns in Na*-K*-ATpase.

A seminal study by Haddow et al showed a 7-point reduction in

intelligence quotient in children aged 7 to I years whose mothers had SCH at

pregnancy compared with the children of euthyroid mothers.s

154
 I

Symptoms. Tiredness, weakness; dry skin; feeling cold; hair loss; difficulty

concentrating and poor memory; constipation; weight gain with poor appetite;

dyspnea; hoarse voice; menorrhagia (later oligomenorrhea or amenorrhea),

paresthesia; impaired hearing.lo

Signs. Dry coarse skjn; cool peripheral extremilies; puffy face, hands, and feet

(myxedema); diffuse alopecia; bradycardia; peripheral edema; del3yed tendon

reflex relaxation; carpaltunnel syndrome; serous cavity effusions.

Treatment. Levothyroxine (thyroxine; T4) is the treatment of choice. lt is partially

converted in the body to T:, the active thyroid hormone. Hypothyroid patients

who are taking thyroxine replacement typically have serum T3 levels that are

lower than normal, owing to their lack of thyroidal T3 secretion.

Dietary Management of Hypothyroidism and Myxedema

Because most of the patients suffering with myxedema are overweight, a

low-calorie diet is indicated. The calories should be redilced ;n accordance with

.the low metabolic rate and the degree of overweight. Along with a balanced diet,

eating the following foods may heip to support thyroid health:

Fiber. Help prevent weight gain or prcmote u/eigtrt loss, helps control insulin

levels in the bloodstream, aids in digestion and elimination (solves constipation),

and helps control appetite. Fiber is available from a variety of food sources

including frij;ts, vegetables, gluten-free whole grains and legumes.

Selenium. Selenium is essential in converting Ta to T3. Selenium-rich foods

include chicken, salmon, onions, and garlic.

Tyrosine. Tyrosine is one of the components of thyroxine. Eat foods rich in

tyrosine: animal proteins, dairy products, almonds and bananas.

 lodine. lodine is the other component of thyroxine. lodine rich foods include
seaweed, iodized sali and seafood

The following foods should be avoided or minimized: Goitroqenic Foods.

Soy products; Cruciferous vegetables like broccoli, turnips and cabbage;

Mustard; Peaches; Peanuts; Radishes; Strawberries; Walnuts. Gluten. Gluten

can trigger an autoimmune response in many people, because it mimics the .

structure of the thyroid gland, resulting in the body attacking the thyrojd gland.

Glulen can be found in wheat, rye, barley and oats. lt is also present in many

processed foods like soy sauce and muslard. Fluoride and Chloiine. Fluoride

and chlorine found in most tap water may block iodine receptors in the thyroid.

Drink bottled water.

GOUT

Gout is a disorder of pilrine metaboiisrn, in which excess of uric acid

appears in the blood, and th-- sodium urates are deposited as tophi in the small

.,jornts and the surrounding tissues, their most common site in chronic gout is the

helj)( of the ear. When crystals form in the joints, it cau,qes recurring attacks of

joint inflammation (arthritis). An abnormality in handling uric acid can cause

attacks of painful arthritis (gout attack), kidney stones, and blockage of the

kidney-filtering tubules with uric acid crystals, teading to kidney failure. The state

of elevated levels of uric acid in the blood without symptoms is referred to as

asymptomatic hyperurieemia. Asymptomatic hyperuricemia is considered a

precursor state to the development of gout.

Risk FactoB. ln addition to an inherited abnormalily in handling uric acid, other

risk factors for developing gout include: Obesity, excessive weiqht

156
gain (especjally in youth); moderate to heavy alcohot jntake; high blood pressure;

abnormal kidney function; certain drugs, such as thiazide diurelics, low-dose

aspirin, niacin, cyclosporine, pyrazinamide and ethambutol; certain diseases

(leukemias, lymphomas, and hemoglobin disorders); chronic conditions such as

diabetes, high levels of fat and cholesterol in the blood (hyperlipidemia), and

narrowing of the arteries (arteriosclerosis); family history of gout; very low-

calorie diets; African race, men age 40-50 yrs old.

Dietary Management of Gout

From a practical point of view, it is almosl impossible to plan a cliet devoid

of purine, since all foods have some traces of nucleoprotein from which purines

are derived. However, a nurnber of foods are almost purine-free. lt must

however be emphasized that purines are also synthesized in the body, hence it is

unlikely that avoidance of foods high in purine content will significantly decrease

the acid poo!. However, sjnce puijne meiabolism is deranged, restriction oi foods

conta;ning nucleoproteins, which give rise to purines, is indicated. Excessive use

of fats should be avoided , si[ce fals are believed to prevent the normal excretion

of urates. Calories should be maintained with carbonydrates, which have a

tendency to increase uric acid secretion.

Acute Stage - Rigid restriction of foods containing purines. Diet is composed of

foods high in carbohydrates, moderate in protein and low in fats. Fluids such as

water or fruit juice (up to 3 Liters a day) should be forced to assist in excretion of

uric acid and to minimize risks of calculi formation. Sodium bicarbonate or

Trisodium citrate can be given to alkalinize the urine and increase solubility of

157
uric acid in the urine. Sodium restricted patjents would require potassjum salt of

carbonate and citrate instead.

lnterval Stage - Dietary management during intervals between attacks is used,

along with uricosuric drugs (such as probenecid), to achieve negatjve acid

balance and controlthe urate deposits and serum uric acid level. Pateints are

recommended to take adjusted normal adequate diet to achieve their ideal

weight. The diet should be moderate in protein (60 to 70 gms), increased in

carbohydrate and relatively low in fat, and should exclude foods of high purine

contents such as liver, kidney, sweetbreads, meat extracts, s..noe,l meat,

anchovies, sardines and leguminous vegetables. ln severe advanced cases, a

further restriction of purine intake and the limitation of protein intake 50 to 75

grams daily (in the form of plant and dairy protein products as much as possible)

may be helpful. Protein intake is limited because it has been shown that

endogenous usr:c acid biosynthesis may be accelerated in b<.rth normal and

gouty patients by high intake of proteins. i!4ost of the proteins in the therapeutic

diet come from cheese, eggs and milk, which are low in nucleoproteins. -luids

should be adjusted to proouce a normal urinary output (2000m1).

Alcohol. Mild to mcderate use of alcohol in patients with gout will not necessarily

induce an attack. However, iactic acid, which appears during metabolism of

ethanol, has a demonstrable effect on the metabolisn't oi uric acid. lt results in

the renal retention of urate.

Obesity. For patients desirous of weight management programs, weight loss

should not be drastic but should occur gradually over a period of several months.

The rationale behind this is to avoid the development of ketonemia which occurs

158
as a consequence of a sudden reduction if calories resulting in a metabolic state

comparable to fasting. Ketonemia is recognized as a precjpitating factor for acut

gouty attacks. Weight reduction should be deferred until the serum uric acid

concentration has been brought under control.

Low-purine diet. The normal diet contains from 600 to 1000mg purines daily. ln

cases of severe or advanced gout, the purine content of the daily det is restricteC

to approximately 100 to 150mg. Fat is kept to 40% of the caloric intake.

Although controversial, the following groupings are observed:

FOOD GROUPS ACCORDING TO PURINE CONTENT

Group 1: High Purine Content (100 to 1000 mg of purine nitrogen pe l00 gms
of food) *Ihese foods should be omitted from the diet of patients who nave gout

in the acute and remission stages. Anchovies, Bouillon, Bra;ns, Broth, Gravy,
L4ackerel, Meat extracts, Mincemint, Mussels, Sardines, Heed, Herring, Kidney,

Liver, Scallops, Sweetbreads, Yeasts (baker's and brewer's)

Group 2: Moderate Purine Content (9 to 10C mg of purine per 100 gms of food)

MEAT and FISH: (except those in group 1) Fish, Poultry, Meat, Shellfish

VEGETABLES: Asparagus, Beans(shell), Lentils, Mushrooms, peas, Spinach

One serving to (2 to 3 oz) of meat. fish or fowl or 1 serving (1/2 cup)

vegetable from this group is allowed each day or five days a week during

remissions.

Group 3: Negligible Pitrine Content. Bread(enriched white and crackers),

Butter or Fortifled margarine, Cake and cookies, Carbonated beverages, Cereal

beverages, Cereal and Cereal products, Herbs, lce Cream, Milk, Macaroni

products, Noodles, Nuts, Oil, Olives, Pickles, Cheese, Chocolate. Coffee,

159
Condiments, Cornbread, cream, Custard, Eggs, Fats, Fruit, Gelatin desserts,

popcorn, Puddings, Relishes, Rice, Salt, Sugar and sweets, Tea,

* Foods in this
Vegetables(except those in Group 2), Vinegar, White Sauce.

group can be used daily

'American Diabetes Association. Diagnosis and classification of Diabetes Mellitus- Diabetes

care. 2011; 34(1): s62-59.
I
American Diabetes fusociation. Standards of Medical Care in Diabetes-2009. Diabetes Care.
Volume 32, S!pplement 1.lanuary 2009.
rAmer:can Diabetes Association. Standards of MedicalCare in Diabetes-2011. Diabetes Care.
2011; 34(1): S11-61.
o
Teixeira-Lemos, Nunes, Teixeira, Reis. Regular physical exercise training assists in preventing
type 2 diabetes development: focus on its anticxidant and anti_inflammatory properties.
Cardiovascular Diabetology 2011, 10:12
'Lin MHA" wu Mc, Lu 5, tin l.Glycemic index, glycemrc load and insulinenic index of chinese
st:rchy foods. World J Gastroenterol2010; 16(39)t 4973-4979
6
Foster-Poweil, Holt, and Brand-Miller. international table ot glycemic index and glycemic load
values: 2002. Am J Clin Nutr 2002;76:5-56
7
American Diabetes Asso€iation. Nutrition Recom;nenCttions and lnterventions for Diabetes,
Diabetes Care. Volume 31, Supplement 1, January 2oo8.
3
Molecular Basis of Human Nutrition. Sandeis and Ernery. 2003. P55
" Fatourechi. Snbclinical Hypothyroidism: An tlpdate for Primary Care Physicians. Mayo Clin Pro€.
2009j84(1):65 71.
'oweetman andlameson. chapter 335: Disorders oftheThyroid Gland in Harrison's Principles of
lnternal Medici.e. 17'h ECn. Fauci, Braunwald, Kasper, Hauser, Longo, lameson and Loscalzo
editors. McGraw-H'll Companies. 2003. L,SA.

160
 DIETARY MANAGEMENT IN SURGICAL CONDITIONS
Nutritional care before and after surgery plays an important role in the
success of the operation as well as in the welfare and comfort of the patient.
The advantages of bringing the patient to an adequate nutritional status
before surgery are:

1) lt shortens the period of disability

2) lt improves the healing process
3) lt lessens complications
4) It reduces mortality

Metabolic Changes in Surgery

1) Cessation of peristalsis
2) Rapid protein catabolisrn ---.> loss of nitrogen ---+ weight loss
3) lncreased glucose in the blood (traumatic diabetes )
4) lncreased utilization of adipose tissues
5) Dehydration due to blood loss, water loss, potassium loss
6) Calcium loss
7) lncreased ascorbic acid utilization in response tc stress
8) Anernia from iron and vitamin B-12 deficiency

ln normal subjects, the body's characteristic response to starvation is to

turn to body fat for energy suppiy, thus conserving lean body mass. But
When trauriia, i.e., surgery, sepsis or major iiiness occurs the body shifts to
protein as the energy source probably in part mediated by increased output of
catecholamines and glucocorticoid which are stress hormones. This results in
marked increase in urinary nitrogen excretion to as much as 15 - 25 grams per
day, mainly coming from the breakdown of skeletal muscle protein which leads
to rapid muscle wasting.

Each gram of urinary nitrogen loss equals:

. 6.25 grams of muscle protein catabolized
. Loss of 30 grams of lean body mass
. Loss of 70 ml of blooci plasma
. Loss of 25 - 50 ml of whole blood

Diets ln Surgery
'1) Preoperative Diet
2) Postoperative Diet

to I
Factors that determine the preoperative diet:

1) Type of surgery ( minor / major )

2) Emergency / Elective
3) Metabolic circumstances before surgery

Preoperative Diet

The major nutritional problems during the preoperative period are

undernutrition and overnutrition. Both the undernourished and the
obese patients present special needs.
The undernourished patient, because of a lack of the major nutrients
necessary for recovery, is at a higher risk in surgery than a patient of normal
weight. Protein deficiency is most common among these patients. Low protein
storage may predispose the patient to shock, less detoxification of the
anesthetic agent by the liver, increased edema at the incision site, anci
Cecreased antibody formation. The last factor increases the risk of infection.
lntravenous feeding of solutions that are more concentrated in nutrients prior to
surgery is one way to replenish. This assumes that surgery can be postponed
tor a time. Aggressive oral nutntion, although more time consuming, can
accomplish the same goals.

Obese patients are at higher hea'th risk in surgery than those of normal
weight. Excess fats complicate surgery, puts a slrain on the heart, increases
the risk of infection and respiratory problems, and delays healing. The risks of
dehiscence and evisceration are greater in the obese patient. Pre-existi g
conditions such as hypertensicn and diabetes mellitus, which are prevalent in
obese pcisons also increase risks. There is no quick way for an obese person
to safely lose weight prior to surgery.

lf time permlts, a low-calorie diet, high in the essential nutrients should

be attempted. Starvation cr fad diets are obviously not recommended
preoperatively. Conversely, a reduction diet after surgery is i,ot in the patient's
best interest ,^rhen thc need for all the nutrients is high. lf weight loss is
needeil, a low-calorie diet should not be instituted until healing is complete.

Dietary considerations for an adequately nourished patient prior to

surgery are also important. The special nutritional needs of surgical
intervention should be met. The preoperative diet of these persons should be
rich in carbohydrates, protein, minerals, vitamins and fluids. Thjs diet will assist
 in a rapid recovery as it promotes wound healing and decreases the risk of
infections and other complications.

lf a patient has a pre-existing conditions - for example, diabetes - the

blood sugar should be stabilized before surgery. Other problems such as
anemia, dehydration, acidosis, or electrolyte imbalances should be corrected
before the procedure.

ln general, preoperative diet has

1 ) H igh ca lorie - to fortify the patient to withsta nd the stress of surgery

2) High protein
- to promote faster wound healing
- to make up for the nitrogen loss during surgery
- to increase resislance to infection
- to promole hemoglobin regeneraticn
- to hasten the return of muscular strengih
3) High carbohydrates
- To provide ertra energy for the increased metabolism
- To spare body proteins
- To promote glycogen stores in the liver
- To prevent ketosis
4) Adequate fat - to contribute to ihe total caloric requirement witholtt too
much bulk
5) lncreased vitamins: Ascorbic acid, Vitamin K and the Vitamin B-
complex members---+ for wound healing, to prevent hemorrhage, and
for carbohydrate and protein meiabolisnl
6) lncreased rrinerals specially phosphorus and potassium, sodium and
chloride +for electrolyte balance, tc make up for loss due to
breakdown of body tissues, and to make up for losses via urine and
sweat; iron due to anemia
7) Increased flu ids ---| to restore sa lt and water balance if there was
vomiting, diarrhea, dieresis

Postoperative Diet

The type of surgery determines the postoperative diet. For example, a

patient who had a major stomach operation, e.g., partial gastrectomy will have a
different diet from one who underwent limb amputation.

163
 Although some surgeons may be very specific about the postoperative
orders for their patients, there are some general principles applicable to all
patients who have undergone surgery.

CALORIES AND PROTE /VS, For the etective surgicat patient the energy
requirement postoperatively will increase by only 1O percent provided there are
no complications. However, if the surgery was preceded by multiple fractures or
trauma, the energy requirement will increase 10 to 25 percent.

Moderate or severe tissue damage caused by injury or surgery leads to an

increased excretion of nitrogen and often to considerable loss of body protein.
Sepsis, fever, infection and trauma accelerale nitrogen loss further. Under the
conditions mentioned the body shifts from carbohydrate to protein as the energy
source resulting in an increased urinary nitrogen loss. if there are exudates or
discharges, seen in cases of peritonitis cr open wounds, much nitrogen will be
lost daily. ln general, the caloric requirement for most postoperative patients is
35 to 45 cal. per kg desirable body weight per day, and the protein intake should
be 1 .0 to '1.5 g per kg DBW per day.

Depletion of body protein is very serious. lt causes edema, inhibits wound

healing, makes the body more vulnerable to infection, renders the liver rnore
liable to toxic damage, impecjes regeneration of haemoglobin, prevents
resumption of normal gastrointestinal activity and delays the return of muscular
strength. lt is largely responsible for postoperative weakness and slow recovery.

VITAMINS. Ascorbic acid deiiciency :s associated with the delay of wound

healing. lt is required for the synthesis of collagen precursors and collagen, and
i000 mg or more daiiy rnay be required in extreme conditions.

Vitamin A deficiency may also interfere with wound healing; the vitamin is
necessary for normal epithelializatjon. lt aiso helps prevent gastric stress
ulceration.

Vitamin K deficiency results in hypoprothrombinemia witn a resultant

defect in clotting. Thiamine, riboflavin and niacin provides essential coenzyme
factors to metabolize carbohydrates and protein and can be rapidly depleted
after major trauma. The requirement for thiamine is doubled in hypermetabolic
states such as fever, trauma or hyperthyroidism.

A healthy person having minor surgery usually does not require vitamin
supplementation. Patients fasting longer than four days before or after surgery
and those having major surgery, especially if poorly prepared for it, usually
requires therapeutic doses of vitamins.

164
MINERALS, There is evidence that the administration of zinc helps the process
of wound healing in palients who have low serum zinc levels. Although its
specific role in wound.healing is unclear, zinc seems necessary for amino acid
metabolism and synthesis of collagen precursors.

FLUIDS. lrnmediately following an operation the patient should be supplied with

sufficient fluids to maintain normal water and electrolyte balance. At this time,
the patient may experience more or less difficulty with the intake of large
quantities of water by mouth, and fluids are usually administered intravenously.
ln many instances, fluids can be given by mouth as soon as the patient has
recovered from the anesthesia.

FOODS. The introduction of food following surgery will depend upon the
condition of the patient's gastrointestinal tract. As soon as bowel qounds return
after the operation, the patient should be given a clear liquid diet for a few
meals. Tlren a ful! liquid diet can be given for a day or so followed by soft diet
and progressing tc a full diet generally on the fifth or sixth postoperative day. To
meet calorie, protein and carbohydrate needs, generous amount of high quality
protein food such as milk, meat and eggs and simple carbohydrate food are
needed.

FEEDING THE PATIENT IMMEDIATELY AFTER THE OPERATION

Since a patient usuallv cannot tolerate solid food immediately after an

operation, it is withheld anywhere from a few hours to two or three days. A
feeding that is too early rnay nauseate the patient and cause vomiting and
possible aspiration. This results in further fluid and electrolyte losses,
discomfort, and potential pneumonia. The follovving oufline ljsts the vanous
types of dietary support that can be used during this short part of the
postoperative period.

1. No food by mouth (NPO)

2. lntravenous feeding: blood transfusion, fluios and electrolytes, 5%
dextrose, vitamin and mineral supplements, protei;,sparing solutions
(with or without ;ntralipid), cmbinations of aoove
3. Oral feeding: routine hospital progressive liquid diets vlith or without
supplement, liquid-protein supplements with or without nonprotein
calories, combinations of above
4. A combination of oral and intravenous feedings

Although solids foods are withheld from patients immediately after an

operation, most hospitals provide patients with oral feedings afler their
intestinal functions return to normal (as earlv as 24 hours after the operation)
165
 The feedings consist of routine hospital proqressive diel. This
stepwise
postoperative feeding may cover one to three days
depending on the patient's
tolerance, strength, and type of operation or trauma.

The diet transition shown below may be used as a pattern guide

or
postoperatively:

NpO / lntravenous feeding

A=l.V. leeding I ice chips / sips of waler <7
\> LV feeding / clear fluid diet
d=t V teeding t fu tiqujd diet >
\> LV feeding / soft diet
<?
Full diet =>
5% Dexhose in Lactate-Ringer,s solutjon is frequenfly used for LV.
feeding;
amino acid solutions are usually added to the l.V feeding during
the first three
days or so. As a general rule of thumb, the maintenancelluid is
l OOml per 100
cal. of energy requiremerrt per day.

Special attention should be given to patients who rnay have prolonged

recovery with difftculty eating and tolerating oral nutritjon, such
as patients with
advanced age or those who require extensive abdominal surgery procedures.
Many surgical procedures can affect the patient,s abitity tJ
cheiv, swa ow,
digest and absorb nutrients and can also be associated with prolonged
physical irnmobiiity Therefore carefur consideration
shourd be given to the
postoper?tive management of these patients in
order to minimiz! the risk of
developing undernutrition and to support the recovery process.

DIETARY MANAGEi-,:ENT FOR RECOVERY

When a patient can tolerate regular hospiialfoods, the

health team
should pran and prescribe an 3ppropriate diet. Experts in
nutrition have tried
for.a number of years to develop a postoperatjve diet that
will provide patients
with an optimal amount of nutrients. ln general, the followjng
djet prescription
should satisfy most clinical aonditions that jnvolve trauma.

1. 40-50 kcal/kg body wejght/d

2. 12o/o-15% of lotal calories as protein
3. Wellbalanced intakes of the established RDAS/DRls
4. Carefully monitored intakes of vitamins A, K, C, Brzj foljc acid:
and the
minerals, iron and zinc

166
 ed as Essen

Protein Vitamin C Vitamin B Vltamin K lron Zinc

Complex'
Complete: '1. Thiamin green leafy liver shellfish
milk citrus fruits pork vegetablesi heart (especially
eggs sweet and oysters fruits eggs oysters)
meat hot pepper organ cereals raisins dairy
fish greens meats meats prunes products
poultry skawberries enriched whole eggs
bread and wheat whole grain
cereals erlriched cereals
cereals
and bread
lncomplete: 2. Riboflavin apricots, dried
vegetables brocolli milk, nrilk red meats
grains tomatoes ProductS oysters
nuts and cantaloupe organ meats pork
seeds muscle meats almonds
oYsters
enriched
bread anC
cereals

3. Nia.rn
liver
tuna, peanuts
peanut butter
peas
pork
enriched bread
and cereals

* Othe,-s
not li3ted of this group wi be supptied if these three B vitamins in tfre Ciet
are adequale
t Best source
Sr.nfield. P and Hui, Y H 20A9. Oiet fheapy,
Set lnsltuctianat Appntaches dr Editian.
Jones and Banlen Pubtshers n.

167
 TONSILLECTOMY

Fo owtng a tonsillectomy, very cold and very mild _ flavoured foods bring
comfort to the patient and offer the most protection against bleeding of the
surgical area.

For the first 24-hour postoperative period these foods are recommended:

Cold milk
Milk beverage like matted milk and eggnogs
Chocolate and vanilla ice cream
Fruit juice

Warm fluids and food rnay be started by the second day and cautiously
replaced by hot foods as healing progresses.

GASTRIC SURGERY

The metabolic changes folloy./ing subtotal gastrectomy are:

1) Absence of hydrochloric acid and peosin

2) Defective mixing of food with digestive juices leads to impairment of fat
utilization
3) lmpairment of prolein digestion
4) lncreased intestinal motility
., 5) Less absorption of iron that leads to hypochromic anemia
6) Absence of gastric juice and the lntrjnsic Faoior ol Casfle (a glycoprotein)
that binds vitamin Bl2 for normal absorption results in a macrocytic anemia
unless the vitamin is given parenterally.

DUMPING SYNDROME

The dumping syndrome is a complex physiological response to the

presence of undigested food in the jejunum. After food is swallowed,
ir is
"dumped' into ihe jejunum abo.tt 10 to 15 minutes afler i,rgesticn instead
of
being gradually released in small amounts, and it does not have the benefit
of
the stomach's participatibn in the digestive process.

It is
characterized by abdominal fullness, nausea, and at times, crampy
abdominal pain followed by diarrhea within 15 minutes after eating. Others
feel
watm, dizzy, weak and faint; their pulses race and they break into cold sweat
which are unmistakable signs of shock.

168
 Rapid entry of ingested nutrients into the jejunum and their subsequent
hydrolysis lead to a hypertonic intestinal content. Thls hypedonic material is
rapidly diluted by fluid drawn from the plasma which leads to a sharp drop in
circulating blood volume. Drop in blood volume, decrease in cardiac output and
perhaps dilatation of the jejunum lead to a sympathetic vasomotor response
producing sweating, tachycardia, electrocardiographic changes and weakness.
Serotonin, a vasoconstrictor and vasoactive kinins, histamine and prostaglandin
are thought to be released because of the hyperosmolarity of the jejunal chyma.
These substances cause the cramping, hypermotility and diaffhea of the
dumping syndrome.

Symptoms of hypoglycemia, such as weakness, perspiration, hunger"

nausea, anxiety and tremors, can occrrr from one to two hours after the meal is
ingested. The hypoglycemia is due to the rapid digestion and absorption of the
food, especially carbohydrate that has been dumped into the duodenum. The
glucose rapidly enters the blood streams and causes a postprandial elevation in
blood glucose and an overproduction of insulin which results later in
hypoglycemia.

Dietary Management

Postgastrectomy patients frequeniiy do not eat enough and become

underweight, malncurished and fntstrated. The object of nutritional care is to
restore nutritional status and pleasant leaving for the pdttent.

Protein and fats are better tcierated ihan carbohydrates because ihey are
more slowly hydrolyzed into osrnotically active particles. Simple carbohydrates
.'like dextrose, sucrose and lactose, are rapidly hydrolyzed and should Le limited,
but complex carbonydrates such as starch can be included. Liq'rids enter the
jejunum rapidl/, and for th3t reason should only bc taken between meals,
without food.

Basically, the diet is moderate in fat (30-4C percent of calories), low in

simple carbohydrates and lrigh in protein (20 percent of calories), with the
purpose cf achieving or maintaining tne optimal weight and nutritional status of
the patient.

Milk in small amounts is apt to be tolerated better than in a large amounts,

although some patients may not tolerate it at all. Dried skim milk or casern
hydrolysates may be used and be well tolerated.

169
RECTAL SURGERY

Following rectal surgery such as hemorrhoidectomy, nutritional care

should be directed toward maintaining an intake that will allow wound repair,
prevent frequent stool so that the wound can heal and prevent infeciion of the
wound by feces. A minimal residue diel and the use of constipating drugs are
indicated. Starting from a clear liquid diet progressing to fu liquid diet (omitting
milk ) then to low residue diet until wound is healed and patient can tolerate a
full diet.( Milk, potatoes, egg, cheese, butter, lard are known to produce bulky
stools).

BURNS

Thermal injury has a tremendous impact on metabolism because of

prolonged, intense neuroendocrine stirnulation. Extensive burns can double or
triple the REE and urinary nitrogen losses, producing a loss of 15009 per day of
lean tissue and a median survival of 7-10 days without nuiritional support. lf
infecticn cievelops, the nitrogen lcsses are even greater. ln addition to losses of
protein, fluids and electrolytes especially potassium and sodtum chloride are losl
through exudation. The increase jn metabolic demands following thermal injury
is proportional to the extent of the ungrafted body surface. The principal
mediators of burn hypermetabolism are catecholamines, which return to
baseiine only when skin coverage is complete.

ln the average adult with burr,s over 50 percer)t of the body surface area
(BSA) the hourly fluid loss may be more than .1U times greater than normal. The
initial consideration in treatment is fluid and electroly.te replacement. Seven to
ten liters per day rnaybe needed. The provision of adequate fluid and electrolyte
is paramount for taintaining circulatory volumc and preventing renal failure.
Because of the large areas of raw flesh exposed, prevention of infection is the
second most consideratior:.

Nutritional Care

1) High Calorie
- to meet the demands of increased metabolism and to insure optimum
ulilization of protein for tissue repair.

ln addition to estimated maintenance needs ( females, 22 kcallkgldayl

males,25 kcal/kg/day), these patients require 40 kcat per percentage point
of burned total body sudace area.
170
 2) High Protein
- to correct negative nitrogen balance
- to promote wound healing
- to increase resistance to infection

Protein is increased from the normal 0.8 g/kg/day to approximately

2.5 glkglday in severely burned patients

3) High carbohydrate
- to provide the needed calorie and spare body protein
During the hypermetabolic phase of burn injury ( 0-14 days ), the ability
to metabolize fat is restricted, so a diet that derives calories primarily from
carbohydrales is preferred.

4) Fat is moderately increased to contribute to the total caloric

requirement.

5) Vitamins are increased

- to promote wound healing
- to promote prcper utilization of protein and carbohydrates
6) Fluids and electrolytes are increased.

The burn paiient should elso be given supplemental arginine,

nucleotides, and omega-3 polyunsaturated fat to st:mulate and mainiain
imrnunocompetence.

REFERENCES:

Doherty, G.M. 2010. Current Diagnosis and Treatment: Surgery, 13th Edition.
McCraw-Hill Companies, lnc.

Stanfield, P. and Hui, Y.H. 2009. Diet Therapy,self lnstructional Approaches,

sth Edition. Jones and Bartlett Publishers, !nc

Marian, M., Russell, l\.4.K. and Shikora, S.A. 2008. Clinical Nutrition for
Surgical Patients. Jones and Bartlett Publishers, lnc.

'171
 CANCER and NUTRITION
Quick Overview:
CANCER - a wide anay of disease conditions characterized by:
. UnregulatedcellgroMh.
. Subsequent multiplication and spread

Mortality in the US
. The total number of deaths from cancer is 2nd only to cardiovascular
disease
. Striking changes in the past 70 years have been dramatic conceming
the rnortality rates in canc€r.

Despite overall redudion of mortslity rates from cancer

. '1.3 million new cases diagnosed e.rery year (US, 2003, excluding skin

cancer)
. 43% of men and 39% of women will be diagnosed with cancer in their
lifetime
. Lung, colorectal, breast, and prostate cancers alone will accouni tor
more than % of the 550,000+ cancer-related deaths each year
. 80o/o suff\9r ftom malnutrition during the course of their illness
,
Effects of Cancer on Nutritional Status
Siqnilicance of malnutrition in cancer
. Associated with longer hospitalization
. Reduced responses to anti-cancer therapies
. lncreased complications from anti-cancer therapies
. Worsened functional performance status
. Decreased survival

lnvoluntary weight loss of more than 10% in the canc€r patient should
faise concem
. Especially it it is rapid (< 6 months)
. Becomes an independent risk factor for survival

172
 CANCER and NUTR|T|ON
Quick Overview:
CANCER- ofdisease conditions characterized by;
a wide array
. Unregulatedcellgrowth.
. Subsequent multiplicatjon and spread

irortality in the US
. The total number of deaths from cancer is 2d only to cardiovascular
disease
. Striking changes in the past 70 years have been dramatic conceming
the mortality rates in cancer.

Despite overall reduction of mortslity rates from cancen

. 1.3 million new cases diagnosed every year (US, 2003, excluding skin
can4er)
. 43% of men and 39o/o of women will be diagnosed with cancer in their
lifetime
. Lung, colorectal, breast, and prostate cancers alone will account for
more than % of the 550,000+ cancer-related deaths each year
. 80% sutfer fiom malnulrition during the course of lheir ifiness

Effects of Cancer on Nutritional Statu3

Significance of malnutriti6n in cancer
. Associated with longer hospitalization
. Reduced responses to anti-cancer therapies
. lncreased complications from anti-cancer thgrapies
. Worsened functional performance status
. Decreased su.vival

lnvoluntary weight loss of more than 10% in the cancer patient should
raise concem
. Especially if it is rapid (< 6 months)
. Becomes an independent risk factorfor survival

172
 Malignancies induca adverse changes in nuiriiional statug
. multifactorial
. Usually assessed through unexplained and involuntary weight loss
1. Loss of appetite (anorexia)
- presence of cancer in the body (state of illness)
- inFeciion associated with the CA
- side effect of therapy (surgery, radiation, chemotherapy, meds)
- psychosocial strains that can affect the patient mentally
2. lmpaired nutrient intake
- specific cancers that obstrucuprevent tood intake
- malabsorption of nulrients
- pain associated with eatng
- in specitic OA conditions
3. Metabolic alterations due to tumor-induced changes that increase
basal metabolic rate.

Alterations of Merabolism in Cancer

Cancer affects how all nutrients and focd stuffs are utilized in our bcdies
. Carbohydrates
. Proteins
.' . Lipids
. Minerals, Vitamins, Hormones

Cancer also induces cytokines, neuropeptides, neurotransmitters, tumor-

derived factors and other mediators which also play roles in metabohc
function.
1 . Glucose lntolerance and hyperglycemia have been fiequenfly noted in
patients with cancer.
. lncreased endogenous glucose production
. lncreased resistance to both exogenous and endogenous insulin
. lnadequate ansulin release
Non-specifc factors
. Weight loss . Bed rest . Sepsis

173
 Wastetul metabolic cycles, such as the CORI CYCLE, contribute
altered
glucose in patients \,with cancer. Gluconeogenesis via
the Cori cycle yields a
net loss of energy. lf this anaerobic glycolysis by tumor cells is substantial
and release of lactate is increased, large amounts would be wasted in
this
futile cycle. Studies have shown that Cori cycje activity is increased
with
canc€r patients who are malnourished versus properly nourished cancer
patients.
2. Patienls with cancer and weight loss lose the natural ability to preserve
Iean body mass
. Prolein lumover rates in the whole body increase, resulting in impaired
protein synthesis
. h,luscle protein catabolism increases rapidly with advancing stdges
of
disease and weight lcss
. These derangements are not reversed by parenteral nutrition ln
maftlourished patienis with malignancies.

3 distjnct pathways involved in the increase of proteolysis in patients

wiih
CA:
1. Lysosomal energy-dependent proteolysis
2. Calcium-independent proteases
3. Ubiquitin-proteascme dependent pathway
- predominant pathway of muscle loss in CA
- effeDtive CA therapy reverses n:uscle loss

3. Depletion of adipose tissue and lipid stores is commonly seen

in
patients with cancer who have lost weight.
Anorexia and impaired
nutrient intake contribute to this loss of fat; howcver, an imbalance
between ltpogenesis and lipolysrs hes been suggested
. Decreased food intake
. Stress response to illness which stimulates adrenal medulla to increase
catecholamines
. lnsulin resistance
. Lipotic factors from tumors or myeloid tissue (LirF)

't74
Cancer and Changes of Taste and Appetite
The proinflammatory cytokines and rEuropeptides outlined earlier
contribute to diminished appetite among patients with cancer. Up to 50% of
CA patients experience unpleasant alterations oJ taste and smell.
. compounds anorexia
. further limits caloric intake
Chemotherapeutic agents have been linked to changes in taste
( cisplatin,carboplatin, cyclophosphamide, doxorubicin, tfluorouracil,
levamisote, and methotrexate). Delivery of nutrition can be impaired
depending on types of CA (head/neck, gasto-intestinal, etc ).

lmportance of Nutrition in the Cancer Patient

. Diets design€d to address the issues outlined above is KEY to
successful treatrnent ol CA.
. Providing the CA patient with a proper diet is just as important as the
cancer treatments.
. Nutrition requirements must be created depending on the type ot
cancei involved.
Ma ln utrition
- Condition that results from taking an lnbalanced diet in which certain
nutrients are taken in excess, lacking, or in the wrong propc{icns
- Common prtblem in cancer oatients often coexisting with significant
weight loss (loss > 10% body weight in 6 mos) + 1 morbidity t mortality
J quality of life
- Most closely associated with cancers of the GIT + cancers in the
head and neck.
. Cacnexia
Progressive wasting syndrome evidenced by weakness and a marked anJ
progressive loss of body.weight, fat, and muscle
lmmediate cause ol death in 2G40% of CA patients
Due to:
Cytokines with direct catabolic effect (e.9. TNF-cr, lL-1, lL-6, INF-I)
Altered fat, protein, carbohydrate metabolism.

175
Goals of Nutrition Therapy
. Prevent or reverse nutrient deficiency
. Preserve lean body'mass
. Help patient better tolerete treatment
' lvlaintain strength and energy
. Protect immune function + decreasing nsk of infeciion
. Aid in recovery and healing
. Maximize the quality of life

Nutritional Management of Patients t\ith Specmc Cancers

. Head and Neck Cancers
. GIT Cancers
Esophageal CA Pancreatic CA
Gastr:c CA ColoreotalCA

Cancers of the Head and Neck

. Mostly squamous cell carcinoma (90%)
. Risk Factors:

' Chroqic alcoholinlake + Malnutrition

. Smoking
. Sun exposure
. Occupational carcinogens (e.9. nickel, chromium)
. Tumor obstruction of food passage -)
. Signiflcant weight loss
. Malnulrition
. 5 year survival rate: 52%

Effects of Treatmeni
.Radiation

Mucositis
Loss ot taslo
Xerostomia

176
 .Surgery

Difficulty in chewing and swallowing

1 risk of chronic aspiration
.Chemotherapy

Systemic effects
Anorexia
Alteralions in taste
Nausea and Vomiting
Early satiety
Dianhea
Constipation
Nutlitional Support
. ln relation to surgery:
Many have ei'iteral lubes placed prophylactically telore undergoing
surgery
Percutaneous endoscopic gastrostciiies for tube feeding
Enteralfeeding immediatety pcstop allows healing of operative
wounds and in)provement of swaliolving
With dsk of chronic aspiration, the tip of tube is placed in the small
bowel instead of the stomach and nr{rients are supplied via slow
dnp.

Depending on the degree of dysphagia:

Mild to moderate dysphagia
. Foods with pleasant aroma
. Foods with high caloric content
Sig'rificant dysphagia
. Endoscopic gastrostomy tubes for feedings }4rday.

. GIT tu.:roB can cause;

Obstruction
Nausea and Vomiting
lmpaired Digestion
Malabsorption
Marked alterations in the normal metabolism
 . Treatment can result in:
Gastric paresis
Alterations in digestion
Malabsorption
Hyperglyc€mia
Hyperlipidemia
Hepatic encephalopathy
Anastomotic leaks
Fluid and electrolyte imbalance
Dumping syndrome
Vitamin and mineial deficiency

Esophageal Cancer
o Most common histologic type worldwide is squamous cell carcinoma
. Oecurs in the upper2/3
. Associated with tobacco and alcohol use
o l',lost prevalent in USA, adenocarcinoma
. GERD
. Barrett s esophaqus
C/M: progressjve dysphagia (present in 90%) -+ malnutrition + significant
,veight loss
o 5 year survival: 11yo
o Effects of Treatment
- Surgery
- Total or distal esophagectomy
- Bilateral vagotomy
- Proximal gastrectomy
- Complications:
Anastomotic ieak
Stricture
Dysinotility
Eady satiety
Regurgitation
Vomiting
Dianhea
Steatorrhea

178
 - Radiation
Esophagitis (normally resolves, but may result in strictures, fistulas, or
perforations)

- Chemotherapy
Systemic effects (e.9. anorexia, alterations jn taste. nausea and
vomiting. early satiety, dianhea, constipation)

. Nutritional Suppott
Since the distal GIT is functional, enteral nutrition should be advocated over
TPN in th. absence of contraindjcations

Mild dysphagia
- Well-planned meals and liquid tormulas

Moderate to severe dysphagia

- Special oral or enteralfeedings

Following resumption of oral intake:

Frequent small meals wjth high carbohydrales and adequate in protein
and fat

ln the presence of post-cp stictures:

Tube-fed iiquid fom,jlas

Gastric Cat:cer
o Most comrnon histologic type is adenocarcinoma
o Risk faclors include diet ol processed food high tn preservatives
and
nilrosamtnes
o c/M:
. Weightloss . Anorexie
. Abdominal pain Weakness
o 5 vear survival rate in USA
. Stage 1: 43%
. Stage 4: 20%
o Effects of Treatment
- Surgery
Early satiety > weight loss
Dumping syndrome
Rapid entry of food into the small bowel _> lt jnsulin response )
hypoolycemia -.> catecholamine discharge + sweating + lachycardia +
faintness

179
 I Fat malabsorption ) Fat-soluble vilamin deticiency
r Deticiencies in lron and calcium
I J Gastric acidity + .t lntrinsic factor + J R protein )
lnability to absorb Vit. 812 ) Pemicious anemia
Nutritional Support
r Frequent small meals (5-6x/day)
r Diet:
r High protein
r Adequate fat
r Low simple carbohydrates
r Calorically dense
r Low in insoluble liber (because of early satiety and
decreased transit time)
r Vitamin and Mineral Deficiency
Oral administration of lron + Vitamin supplements
Monthly injection of 100p9 of Vit.Brz

I Lactose intole!"ance is treated by consuming lactas+trested milk

and Yogurt
I Vvith weight loss and dumping despite znti-dumping diet,
noctumal enteral teeding via jejunum

' Pancteatic Cancer

- An aggressive disease that is usually no longer curative at the time
of dr39nosis
- Most common location is the head oi the pancreas

Associated with
. Chronic alcol,ol intake
. Smoking
. NIDDM
. Chronac pancreatitis
. Peptic ulcer disease
. Lynch syndrome
. Diet high in fat and meat
5 year survival; 20%

180
o Clinical Manifestations:
Abdominal pain
Nausea and vomiting due to duodenal obstruction
Bile insufficiency due to tumor mass effects + reduced fat and
fat-soluble vitamin absorption
Weight loss
Digestjve enzyme deficiency with pancreatic duct obstruction _+
malabsorption J weight loss
Anorexia
o Effec{s of Tleatm€I
Surgery: Whipple's procedurc/pancreaticoduodenectomy, only cure, but
only 20olo resectable
. Malabsorption
. Early satiety
. Rapid transrt of food
. Dianhea
. Dumping
. Anorexia
. Marginat ulceration
. Bile reflux gastrilis
' Decreased glucose tolerance
. Deficiency of exogine secretions
o Nutdtional Support
o Adequate amounts of pancreatic enzyme prepaftltions
with all meals
o Aim is to provide sufttcient amounts of calories and
nutrients to compensate malabsorption
o Give oligosaccharides rather than long_chain
carbohydrates [Do not require pancreatic enzymes for
hydrolysisl
o Frequent small meals to combat early satiety
o lf nutritional demands are not met. noctumal enteral
feeding through jejunostomy tube

181
Colorecial Cancer
' . Risk factors include a high calorie diet low in fber and high in animal
fat
. Results in little to no weight loss
. 5 year survival: 6iolo
. Treated surgically with adjuvant 5FU chemotherapy
. Effects of Treatment

' Surgery
. Transient diantlea (usually no nutritional problems)
. Watery diarrhea due to inflow of bile salts into the colon with
resection of the right colon including ihe ileocecal valve
. Divers;on colitis. an inflammatory process resulting in abdominal
cramping and mucoid or bloody dianhea
. Chemothirapy
. Systemic eftects (e.g. anorexb, alterations in tasle, nausea and
vomiting, €iady satiety, dianhea, constipation)

. Nutritional Support
. ;nfusion oI salt solution crntaining short chain fatty acids (e g.
butync acid) into rectai remnant to promote healing
Nuiritional Management of Specific Symptonts

Sid€ ef{ed Dietary manipulation

Consume smalland frequent meals, lYhcn appetite is best.
Serve fooci rn manageable portians. The sight of la.ge
portions is orf putting.
Eat srowly, chew welland relax between courses and after

Eat anythinq rhat ;s particularly fancied.

Do not coirsume large quantitiee of liquids before or
du'ing meals
A shon rv.lk be{ore a meal may help app:rite
lf alcohol is allowed small .luantities before or during a
meal can stimulate apPette.
Avoid exposure to cookins smells durins food

Choose foods full offlavour and aroma-

Use seasonings (e.9. vina;grette), herbs (e.s. basil,
oregano, sanic), spices (e.9. curry, pepper, sweet
paprika), lemon juice to enhance Ravour.
Lemon juice in water before {ood may be help{ul.
Marinating food in wine. beer, cider or lruitjuice may also

182
 Changes in taste Avoid any tood wlrh an unpleasant rasre.
Allow hot food to cool before eatr'ng since high
temperature enhances unpleasanr taste.
lt.meat tastes unpleasant, consume other sources of high
biological value proteins. Try to rnarjnate meat or

lfyou erperierce a metallic raste. a small portion ot temon

luice in water belore eatins may help.
Xerogtomia (dry Moisten me:ls by adding sauces, seasoninss, gravy,
mouth) cream or evsporated milk.
Avoid gr;lling or lrying as cooking methods and preler
others that maintain moisture (e.9. pressure cooki^g.
steaming, boiling).
Avoid drylrough foods (e.g. toasts, Uscuits, crackers,
cereal bars, crisps).
Sip liquids during meals.
Preler sharp'tasdng foods {e.9. those Ravou.ed with
lemon, grape{iuit and fiubarb).

pain{ul .
Sore or Eat so{t, moist foods.
mouth a Avoid very dry or rough-rexured foods (3ee above).
a Avoid salty or spicy foods.
Avoid orange, grapefruit and lemon juice, as wetl as

Ways of restiding nausea and voniting

. A,void drinking Jluids with meals. Consurne small sips of fluids or with a
straw aod pref€rably between m€als or 40-,60 min b€fore or aft€r th€m.
. Cold dink: rn3y b.e bettcr r.clcrsteC than Fiarm/hot cnce.
. Carbonated drinks or ica .ubes mly alleviate th€ sense of nausea.
. Consumption of cr3ckers, lolt -fat cereel bars, pretzels or toast may restrict
nausea, esp€cially during the rnorning.
. Foods thatcommonly cause dyspepsia, such es fatty orfried food3,.offee,
foods rich in spices or condimonts and alsovegetables with a st ong odour,
such es onions, garlic and cruciferous vegetabtes, should be generally
avoided.
. Cold foods and those with a mild odour are better tolerated.
. Small and frequent meals prevent stornach distension. as weii as th€ fpel_
rn9 of empttness, wfiich otten aggravates nausea.
. Avoil smelling {ood during preparerion/cooking.
. Avoid going to bed straight after consurning food_

Effects of Chemotherapy
. The mechanism for chemotherapy associated toxicities affectrng nutrition
depend upon the drugs administered and their site of location

. Chemotherapeutic agents adversely affect dietary intake

183
 . Some ot this drugs produces:
Anorexia - causes an abnormality in taste
Mucosal ulceration - presenting as mucositis, cheilosis, glossitis,
stomatitis
Esophagitis - painfully interfere with ingestion of nutriments
Nausea, vomiting and dianhea - caused by neoplastic drugs
Constipation or Adynamic ileus may also occur
Sodium and water retention, nitrogen and calcium loss - caused by
corticosteroids

. Chemotherapeutic agents may also have a pronounced damaging effects

on bone marrow and renal tubules as well as hepatic, cardiac, pulmonary
and nerve cells.

. Negative nitrogen balance - nitrogen equilibrium before starting

vinblastin, cisplatin and bleomycin changed lo negative balance, protein
tumover, synthesis and catabolism decreased by 23, 34 and 30%.
resPectively.

Dietary lnfluences on Toxicity and Efficacy

. Protein and Amino Acids
Protein-caloric malnutritjon is associated with increased methotrexate toxicity
because of reduced drug clearance.
Casein-based diets enhanced the gastrointestinal toxicity and weight loss of
methotrexate while soy concenfates or peptide-based diets offered
sig|liiicant protection.

. ConditionallyEssentialNutients
Arginine, N-3 Fatty.{cids and RNA
Effect is to enhance the immune response that result to fewer wound
compli.atons and infections and a shorler hospitalization stay.

Effects of Radiaiion Therapy

. Central Nervous System
Tumors ofthe nervous system can produce somnolence, lethargy, confusion
and initability which can lead to decreased oral intake.
lncreased ICP can cause headache, nausea and vomiting.
. Head and Neck
l\rucosal surfaces of the head and neck are sensitive to radiation, and
treatment induced reactions often result in severe nutritional sequelae.
Symptoms which occur acutely may include sore throat, pain on swallowing,
dry mouth and lack of appetite.

184
 . Thorax
Radiation given to organs in the thorax such as lung' mediastinum or
esophagu; may acutay create dysphagia because of local irritation to the
mucosa of the pharynx and esophagus

. Abdomen-Pelvis
Stomach can tolerate radiation remarkably well.
AsvmDtomatic radiation gastritis accompanied by hyperemia edema'
microscopic hemorrhages and exudation may occur after
approximately 2 weeks of radtatlon

Enteral Feeding
. Liquid leedings thmugh tube going to stomach or small intestine
. Best if Gl system is functioning normally, but c€nnot eat enough
Ex, Cancer in head and neck

Enteral Methods
. Nasogastric (NG) feeding - Tube passed down nose and into stomach
Used for radiotherapy to mouth or throat

. Percutaneous endoscopic gastrostomy (PEG) and radiologically

inserted gastrostomy (RlG) - Tube passed into stomach through skin
and muscle of abdomen
Support needed for more than a few w€eks
. Percutaneous endoscopic jejunostomy (PEJ) -Tube passgd through ski4
and muscle of abdomen into jejunum

Total Parenteral Nutrition Feeding

. Nutntion is given intravenously
' Thrcugh central or PICC liire
. Used if enteral is not Possible
. Can be given even if Gl is not tunctioning properly

lnfection and TPN

. Fourfold risk of infection in patients given chemotherapy and TPN
. Associated leukopenia and depressed immunity
. Evidence in neonates that use of lntralipid is associated with increased
intection rates.

't 85
Home Nutritlonal SuPPort
. Long-term TPN can be lilesaving and life sustaining for prolonged
periods for select cancer patients
Massive inteslinal resection
Severe radiation enteritis
Major radiation-induced unresectable stenosiswith cured malignancy
. Patients with metastatic disease who have failed all therapy limited -
benefit; only 15% suNive longerthan'1 year'

Megesterol Acetone
. {Jsed to treat metastatic endometrial and breast cancers
Synthetic progestational agenl
lmoroves appetite and weight
Tested in adult cancer patients in both hormone sensitive/insensitive
tumors as an anticachcctic agent
Daily dcsages varied from '160-1500 mg/day
No possible survival benefit, but fat accurnulation was indicated
Head and neck carEer
. Patients that failed standard antiturnor therapy
. Between chemotherapy cycles
. ln conjunction with cytokine INF-a and lL-2
. Deily doses as lov.' as 60 n:g

Medroxyprogesterone acetate, Cyproheptadine

. Tested as appetite stimulant
. Failed to prevent weight loss in advanced cancer

Cannabinoids
. Marijuana and dronabinol
. Enhances appetite and induces weight gain
. Dronabinol is FDA approved
Chemotherapy: nausea and vomrtting
HIV patients: anorexia with weight loss
. Several states have deciiminalized use foi cancer patients

186
REFERENCES
Lopez AD. Ann NY Acad Sci 1990;609:58-74. 4. Doll R. Am J Epidemiol
1991t'134:67H8.

Heymsfield SB, McManus C, Smith J, et al. Am J Clin Nutr '1982;36:68G-90.

Veterans Atfairs Total Parenteral Nutrition Cooperative Study Group. N Engl J

lvled l991 :325:525-32. L

Ollenschlager G, Viell B, Thomas W, et al. Cancer Res 1991;121:249-59.

Goodwin WJ, Byers PM. Med Clin Nuiih Am 1993,77:597- 610. L

LanzottiVJ, Thomas DR, Boyle LE Cancer 1977;39:303-13.

Senie R, Rosen PP, Rhodes P, et al. Ann lntern Med 1992;1'16:26-32.115.

Brennan MF, PisieB PW Posner M, et al. Ann Surg 1994:220:436-4.1..

Donaldson SS, Wesley MN, Dewys WD, et al. Am J Dis Child

1981;135:'1107-12.

Cole P, Rody B. Cancer 1996;78:204H.16. Bailar JC lll, Gomik HL. N Engl

J M€d 1997;336: I 569-74.

Spom MB. Lancet 1996;347:1377-81. A. Ames BN, Goid LS, Vvillet WE.
Proc NatlAcad Sci IJSA 1995;92:5258-65.

LanzottiVJ, Thomas DR, Boyle LE. Cancer 1977i39:303-13.

Senie R, Rosen PP, Rhodes P, et al. Ann lntem Med 1992;116:26-32.

 CriticallY lll Patient
Learning Obiectives
At the end of the topic students must be able to:
1. Define critically ill patient and metabolic stress
2. List the three phases of the stress response
3. Discuss the metabolic alterations in critical illness
4. Discuss the causes and consequences of malnutriiion in critically ill patients
5. Discuss Specialized Nutrition Support
6. Discuss the evidence-based clinical practice guidelines fo' nutrition support in
adult critically-ill patients

Course Outline:
l. Definition of terms
ll. Stress response
lll. Metabolic alterations in critical illness
A. Hyperglycemia and insulin resistance
P. Protein catabolism
C. Negative nitrogen balance
lV. Malnutrition in critically ill patients
A. Causes
B. Consequences
V. Specialized Nuirition SuPPort
A. Enteral Nutrition
1 . Roules
2. Advantages

4. Contraindications
5. fypes
6. ComPonents
7. complicaticiis
B. Parentera! Nutrition
1. lndications
2 Types
3. ComPonents
4. complications

Clinical practice evidence-baseC guidelines for nutrition support in adult

critically-ill patients (ASPEN 2009)
l. Definition of Terms:

Critically lll Patient:

- a patient cared for in an ICU environment who has an urgent or life-threatening
complication (high baseline mortality rate).
- does not include patients with elective surgery who also are cared for in some
lCUs but have a low baseline mortality rate (<5%).
- they are mechanically ventilated patients.
- includes victims of trauma (gunshot wounds, slabbing, motor vehicle accidents);
closed head iniury (from falls); burns; severe inflammations such as in
pancreatitis, cancer; sepsis; hypoxic iniury as seen in acute renal failure; and
necrosis of tissues as in gangrene or after major surgery.

Metabolic stress is the hypermetabolic, catabolic response to acute injury or

disease.

ll. The Stress Response

The stress response is a piogression thrcugh 3 phases:

1. Ebb phase - encompasses the immediate period after injury (2 - 48
hrs); characterized by shock resulting in hypovolemia and J O, availability
to tissues. J in blood volume results in J cardiac output and urinary output.
- The goal of therapy is to restore blood flow to organs, maintain
oxygenation to alltissues, and stop all hemorrhaging.
2. Flow phase - encompasses the classic signs and symptoms of
meiaooiic stress: hypermetabolisrn, catabolism, altered immune and
hormonal response
''
3. Final adaptation phase or recovery phase - indicates a
resolution ofthe stress with areturn to anabolism and normal
melabolic rate.

lll. Metab^lic alterations in critical iilnesg

- Critical illness is generally recognized as a hypermetabolic state with caiabolic

response to acute injury or disease and with energy expenditure (EE) being
proportional to :he amcunt of stress.

- Characteristic of critical illness is the so-called "diabetes of stress" with

hyperglycemia and insulin resistance.

- Most striking metabolic feature of critical illness is protein catabolism and net
negative nitrogen balance- major mediators are the catabolic hormones
gluiagon, epinephrine and cortisol and the reduced anabolic influence of groMh
hormone, insulin and testosterone.

'189
A, Hyperglycemia and insulin resistance
This is brought about by:
- Hepatic gluconeogenesis (from amino acids and lactate) increases mainly due
to the action of catabolic hormones such as glucagon, epinephrine and cortilol.
- The normal suppressive action of exogenous glucose and insulin on hepatic
gluconeogenesis is decreased.
- Peripheral glucose utilization in insulin-dependent tissues (muscle and fat) is
decreased.

B. Protein catabolism
Sustained hypercatabolism can result to:
- Substantial loss of lean body mass (LBNil)
- lvluscle weakness
- Decreased immune function

- The increased catecholamines and cortisol levels in stress states stimulate

lipolysis in peripheral adipose tissues

C. Negative nitrogen balance

-.a consistent sign during metabolic stress; brought about bysubstantial
nitrogen loss and compiications that accompany skeletal muscle catabolism
which includes:
1. lmmunosuppression
2. lncreased infection rates
3. Delayed or impaired wound healing
4. lncreased mortality

Summary of major metabolic ahnormalities in ,,stress response":

.' 1. lncreased catabolic hormones (cortisoi, glucagon and catecholamines)
2. Decreased anabolic hormones (groMh hormone and testosterone)
3. Marked increase in metabolic rate
4. Susiained increase in body temperature
5. Marked increase in glucose demands and liver gluconeogenesis
6. Rapid skeletal muscle breakdown with amino acid uied as energy
source
7. Lack of ketos;s, indicating that fat is not the major calorie source
8. Unresponsiveness of catabolism to nutrient intake

lV. Malnutrition in critically ill patients:

A. Causes of malnutrition in critically ill patients:

1. lmpaired intake
2. lmpaired digestion and absorption
3. Altered nutritional requirements
4. Excess nutrient losses
> Up to 43 % of patients in ICU are malnourished (Gisher et al, 2000)

'190
B. Consequences of malnutrition
1. Weight loss
2. Weakness and fatigue
3. lmpaired ventilatory drive
4. Depression/apathy
5. Poor wound healing
6. lmpaired immune function

V. Specialized Nutrition SuPPort

Why feed the critically ill patient?

- Provide nutritional substrates to meet protein and energy requirements
- Help protect vital organs and reduce breakdcwn of skeletal muscle
- Provicie nutrients needed for repair and healing of wounds and injuries
- Maintain gut barrier function
- Modulate stress response and improve outcolne
- Decrease comPlications

Specialized Nutrition Support (SNS)

- biven to patients who are unable to maintain their nutritionai status using oral
diets, supplements, or appetite stimulants.
- lt refers to administration of nuirients with therapeutic intent. This includes the
provision of total enteral and parenteral nutrition suppon ancj. the provision of
iherapeutic nutrients to maintain cr restore health (ASPEN 2002)

Benetils of nutrition support in critically-ill patients

- lmproved wound heaiing
- Decreased cataL'olic response to injury
- lirrproved gastrointestinai structure and functiorr
- lmproved clinical outcomc
-reduction rn comPlicalion rates
-reduction in length of stay in the hospital
-accompanying cost savings

A. Enteral Nutrition
- From the Greek word "enteron" ot "intestine"
- Feeding thru the gastrointestinal tract via a tube, catheter or sto'na that delivers
nutrients distalto (or beyond) the oral cavity (ASPEN 2005)
- Used interchangeably with "enteral feeding' and "tube feeding"
- lt is recommended that enteral feeds commence within 24 - 48 hours in
hemodynamically stable patients following admission to ICU'
- lt is the preferred route over parenteral route

191
'1. Routes of Enteral feeding

a. Nasogastric feeding - nose to stomach' most commonly used route'

-- -easie-st
to acnieve; easiest to maintain; least expenslve
b. Orogastric feeding - motrth to stomach more difficult
or
c. Nasointestinal teeoing - noseG ouodenum iejunum;
- '6;il;v; ;;; in cases of:
malntain li li useo to bvpass the stomach
1) gastroparesis
2) gastric outlet obstruction
3) previous ga"tr'" suri;ry pre"ludes feeding into the stomach
y'*"*i-tf,iu'tit"
a. r""'iiin iit skin: surgical gastrostomv or surgical
" ga"tiic t"eoing oi percutaneous iejunal
leiunostomy; ptrcutaneo'J
ieeding f6r long-term enteral feeding'
-
2. Advantages of enteral nutition support
over parenteral nutrition:
-
Cost-eftectiveness
n"Ou""O rate of infectious and metabolic complications
-
C"l"tiu"
"""" "nd
safety of administration
-
lmoroved wound healing
-
Reduced surgical interventions
preseNes gut mucosal integrity
_
maintenance of gastrointestin;l function or

3. lndications for Enteral feeding feed themselves

I Ji.ii,ii:ti,i"-"i" *no t'r," " frincticning Gl tract but cannot
adeouatelv:
'""n"]'"p'"ii.nt" who are mentally incapacitated due to confusion' dementia or
neLroiooicai,iiff icu:iies
. - Patienis with swallowing d'/s{unction
- Patients with disorders 6i in" upp"' GIT that can be bypassed
by

inserting a leeding tube below the dyslunction to ingest

-'F"iil"i" *in irn'palrea oig€stive flnction and 'vho are unable
hydrolyzed formulas orallY' are beginning
- Patients who have unoergone inlestinal resections and
enteralfeeding periods esp the
- Patients who have little or no appetite for exrended
malnounshed.
- Patients irr coma
- Patients on mechar:ical ventilators

4. Contraindications for Enteral feeding tract

]: il;;i;';irh ;;iious medicat "onditio-n" that affecr the sastrointestinal
such as:
- Diffuse Peritonitis
contents from passing thru
- lntestinal obstruction that prevents intestinal
the intestines
treatment
- rniiaJatre uomiting not responding to medical
192
 - Paralytic ileus that prevents gastrointestinal contents from passing thru
the GIT
- Intractable diarrhea that can not be conkolled with medications.
- Gastrointestinal ischemia (insufflcient blood flow to Gl tissues.

5. Types of enteral feed

- Most enteral feeds are a mixture of fat, CHO, protein, vitamins, minerals, water,
electrolytes and fibre in proportions that mimic a balanced diet, or a diet designed
for a specific disease or medical condition.
- Some enteral feeds (e.g. Pulmocare) provide a greater percentage of calories
as fat (less CHO means less COz produced, thereby assisting ventilatory
weaning in some patienls.
- Other specialized feeds provide elemental solutions of amino acids or peptides
- For patients with short-bowel syndrome, malabsorption or severe inflammalory
bowel disease.

roximate combinations of nulraents in entera

teral feeds
E ld e rlv/fra il Normal Seosis
Prctein 8-10q 10-16 16-20 q
Carbohvdrate 700 Cal 1000 Cal 1200 Cal
Fat 700 Cal 1000 Cal 1200 Cal
l"otal calories 1400 2000 2400
(non-nitrcoen)
Total volume 2.5 liters 2.5 liters 3.0 liters

6. Components of enteral feeds:

. a. Protein - usually derived from soy or caseii.l; usual amount = 1O - 15o/o

of kcal; high protein formulas contain 25% of kcal. Some formulas are
supplemented with specialized amino acids such as glutamine or
arginine.
b. Carbohydratc - includes monosaccharides, oligosaccharides, dextrins
and maltodextrins; lactose flee formulas; suc;ose rarely used
Fiber is added to improve bowelfunction.
c, Lipid usually include corn and soy oil which are long and medium
-
chain faty acids. i'lewer producls contain omega-3-fatty acids from fish
a;d plant sources.
d, Vitamins & minerals - for stress and wound healing
e. lmmunonutrients - nutrients that modulate immunosystem functions:
i. Glutamine - Most abundant amino acid in the body; accounts for
60% of the intracellular amino acid pool.
- Considered to be conditionally essential because deficiency can
occur raPidlY after injury.
- Used as energy source after the stress response since it is
released from cells to undergo gluconeogenesis in the liver for use

193
 as energy. it is the primary fuel source for rapidly dividing cells like
epithelial cells during healing.
- Component of glutathione (antioxidant)
- Used as a substrate for metabolism by leucocytes and
enterocytes, it ban therefore augment lymphocyte and macrophage
function.
- lt has anticatabolic and anabolic properties and is the rate-limiting
agent for new Protein synthesis

ii. Arginine
- A conditionally essential amino acid whose level decreases after
major lrauma and wounds.
- Enhances immune function - improves T cell function
- Role in wound healing - increase tissue collagen content;
enhances collagen and total protein deposition at the wound site
- Stimulates the release of hormones including insulin, prolactin and
groMh hormone
- Needed for nitric oxide production which regl!lates blooC flow
- Studies have shown that arginine supplementation in patients with
sepsis is associated with higher mortality Therefore, Arginine is
NoT recommended in critically iil patier'ts with severe sepsis
(ESPEN 2006)

7. Complications of enteral feeding

a. Mechanical complications - tube misplacement; clogged, twisted cr

kinked feeding tubes

'
b. Gastrointestinal complications - Diarrhea, abdominal discomfort,
nausea and vomiting
c. Metabolic complications - hyperglvcemia, fluid and electrolyte
imbalances
d. Aspiration - paiients whc are sedated, who have an endotracheal tube
or who have difficulty swallcwing are at risk for aspiration To.avoid
aspiration, the patient's head must be elevated higher than his
stomach or al an angle of about 45 degrees during feeding.
e. Tube feeding syndron'ie - hyperosmolar-nonketotic dehydration;
develops in patients with insufficient fluid intake. prevented by giving
sufflcient fluid (about 1ml/kcal) with the feeding

B. Parenteral Nutrition
- Sometimes called central venous nutrition (CVN) or lntravenous
hyperalimentation (lVH)
- Should be used only when the enteral route is either not possible or cannol
provide sufficienl nutrient input.

'194
 I

lndications for Parenteral nutrition

'1.
- indicated in those clinical situations where the patient is unable to meet
nutritional needs either by an oral diet or thru the use of EN such as:
- lnability to digest and absorb nutrients such as in malabsorption
- Massive bowel resection or short bowel syndrome
- lntractable vomiting
- Gl tract obstruction
- lmpaired ct motitity
- Abdominal trauma, injury or infection
- Severe pancreatitis
- Poslsurgery - if bowel function is likely to be disturbed

2. Types of parenteral nutrition

a. Total parenteral nutrition

- .The distingujshing fearure of TpN (total parenteral nutrition) is
administration of concentrated macronutrients, vitamins, minerals and
electrolytes into a l6rge central vein so that the volume of blood flow is
sufficient to irnmediately dilute the concenlrated parenteral solutions.

b. Peripheral parenteral nutrition (ppN) and peripheral venous

nutrition (PVN)
- Refer to the administration of large_volume, dilute solutions of nutrients
into a vein in the arm or back of the i]and.
- lrritating to the small veins and peripheral access is difficult to maintain
for more than a few days.
- Provides insufficient calories for many patients

3, C6nrponenis of Parenterai Nutrition

- iontains a balanced mixture of proiein, CHO and lipid, together with water,
vitamins, minerals and electrolytes.

a. Protein included in pN in the form of individual amino acids in

-
amounts coi,sislent with the recommendaticns of the VVHO and FAO;
balanced solution of essential (40%) and non_essential (60%) amino
aclds.
- Protein requirements usually range from 0.g g/kg for normal adults to
g/kg for patients with burns, kauml or heating wounds
J:5_!o_] 9
(ASPEN 2002).
- Protein restrictions are occasionally needed for patients with renal
failure who are not receiving dialysis.
b. Carbohydrate - primary function of dHO is to serve as energy source
- Dextrose monohydrate is used - provides 3.4 kcal/g
- Mjnimum CHO intake 130 g/day. Approximatety IOO q of CHO is
-
required daily to allow for protein sparing.
 - Excessive CHO may contribute to hyperglycemia and excessive CO2
production which may jeopardize respiratory status and result in
difficulty weaning from mechanical ventilation.
c. Lipid in PN - an emulsion of soybean or safflower oil
- Provides essential fatty acids and a concentrated source of energy.
- Common clinical practice is to provide a minimum of 10% of kcal
requirements as lipid but may provide 20 to 30% of total kcal.
- Reduces the need for energy from dextrose and lowers the risk of
hyperglycemia in glucose-intolerant patients.
d. Fluids and electrolytes in PN
- Daily fluid needs appioximate 30 to 40 ml per kg of body weight in
young adults and 30 ml/kg BW in older adults (for a daily average
of 1500 - 2500 mlfor most people)
- Electrolytes added to PN inituOi: tta., K., cl, Ca'-, Mg'*, and P3'.
Blood tests to monitor electrolyte status must be done daily until
patient has stabilized.
e. Vitamins and Minerals in PN
- All water-soluble Vitamins are supplied, as well as Vitamirr A,D,E;
Vitamin K is often omitted and must be added separately.
- Trace minerals added include Zinc, copper, chromium, seleitium, and
manganese. lron is excluded because it alters the stability cf other
components.

4. Complications of TPN
a. Technieal complications:
-
1) Catheter-relatecj injury related to insertion (hemothorax,
pneumothorax, air embolism, subclavian artery injury, etc.)
, 2\ Sepsis secondary to contaminalion of central venous catheter
.- -
b- Metabolic complications glucose abnormalitids (hyperglycemia),
electrolyte disturbances, vitamin deficiencies, etc.
c. GIT related - gut mucosal atrophy, hepatobiliary dysfunction.

vl. Clinical practice evidence-based guidelines for nutrition support in adult

critically-ill patients (ASPEN 20C9)

1. Use of PN versus EN
- Use of EN over PN is strongly recommended oecause:
- EN compared lo PN is associated with a reduction ;,r the number of infectious
complications, lower rncidence of hyperglycemia, and cost savings.

2. Early versus delayed nutrient intake - EN within 24-48 hrs following

admission to ICU is recommended. Early EN improves nutritional intake and is
associated with reduction in mortality and reduction in infectious complications.

196
 I
3. lmmune-enhancing diets
EN with Glutamine --Use of glutamine in PN is strongly recommended, but not
recommended in critically-ill patients receiving EN.
- Effects of PN with glutamine:
a) Reduction in mortality
b) Reduction in length of stay in the hospital
c) Reduction in infectious comolications
- Dose of glutamine = 0.2 - O.57 gm/kg/day

EN with Arginine - studies noted the lack of a treatment effect with respect to
.o*rllty infections. Given the possible harm in septic patients and the
costs, its use is not recommended for critically-ill patients'
increased "n-O

EN with Fish oils (OXEPA - fish oil, borage oil, antioxidants): Recommended in
patients with acute lung injury (ALl) and acute respiratory.distress syndrome
iARDS;; no evidence ofl treatment effect in septic patients withcut lung.injury'

Noled effects in patients with ALI and ARDS:

- Significant reduction in mortality
- Lower incidence of newly acquircd pneumonia
- Signiflcant reduction in ICU length of stay
- Significant reductiorr in ventilated days
- Signiflcant reduction in new organ failures

4. ProteintFeptides in EN
-VJhen initiating enteral feeds, the use of whole protein formulas (polymeric)
insiead of pepticie-based formulas is recommendeC

s..Fiber in EN - no sufficient data to support the routine use of fiber (pectin or

soy polysaccharides) in enteral feeding formulas.

6. Motility agents - metoclopramide; they have a physiologic effect on Gl

-may
motility a;d improve tolerai.e to EN; recommended in patients who
exper;ence feed intolerance (high gastric residuals, en]esis).

7. Enteral feeding via the small bowel compared with gastric feeding
- Small bowel fe.ding was a:sociated with significant reduction in infections
(pneumonia) when con:pared wiih gastric feeding; specially recommended for
patients at hign risk for regurgitation and aspiration (nursed in supine position)
and those who are not tolerating adequate amounts of EN delivered into the
stomach.
- Small bowel feeding improves calorie and protein intake

8. Body position
- Recohmendation: Patients receiving EN should have the head of the bed
elevated to 45 degrees (semirecumbent position).

't97
 a

- This position is associated with a significant decrease in the incidence of

ventilation-associated pneumonia.

9. PN in combination with EN - studies showed a trend towards harm. There

was increase in mortality which could not be explained by overfeeding.

10. Blood sugar control

- lntensive insulin therapy to control blood sugar level between 4.4 - 6.1 mmol/L
should be considered in all critically-ill patients.
- associated with lower incidence of sepsis, reduction in ventilator days,
and reduced ICU and hospital mortality.

'l'1. Vitamins and minerals - recommendeC for critically-ill palients.

198
 PROBLEM-SOLVING IN APPLIED NUTRITION

PROBLEM 1

vears old' 5 feet T inches tall engaged

in
A Filipino government employee, 32
l.l5r"t "p-t''v"i*r .aiuity; *itt' an average of 7 hours of sleep per night'

Nutrient distribution in % of TER:

ili'lilviili.i" =;sih F^t" = zoo Protein = 15 %

show your computations:

Determine each of the following and

1. Desirable body weight in kg'

needs (BMR)
2. Energy to meet his basic metabolic

3. corrected BMR for sleep

4 Energy for his Physical aciivity

5. Energy to cover for SDA (use 10%)

6. Total energy requirement per day

7. Grams of carbohydrates Per CaY

8. Grams cf fats Per day

' 9. Grams of Protein Per day
at the back of this page:
SHOW COMPUTATIONS BELOW ant'j

199
 PROBLEM II

Determine your own TER per day based on the following data:

1 .
Your Desirable body weight (DBW) based on your height (use Thannhauser's
method)
2. Your physical activity is considered l!qt{.

3. Nutrientdistribution: CHO=60'/o Fals=25% Protein=15%

Determine each of lhe following and show your computations:

1. Desirable body weight

2. Energy to meet your basal metabolic needs (BMR)

3. corrected BMR for sleep (use your average sleeping hours/night) .-

4. Energy for your physical aciivity

5. Energy lo cover the SDA of your foods

6. Your TER per day _

7. Grams of carbohydrates per day

8. Grams of fats per day

. 9. Grams of protein per Cay

SHOW YOUR COMPUTATIONS BELOW:

200
PROBLEM lll: FOOD EXCHANGE LIST

adult diabetic is as follows:

The dietary prescription for an
Fat=44gms
TER= 1600Cal CHO=24Ogms Protein=60gms
given below
exchanges for Vegetable A and B' milk and sugar are
Number for 1o tht nutbered questions
that
Given these data, suppry tne mrssrn!."n"*""
;;;il;;i;Juv;";rtls:1i-lll!s relsltlglc!]g
FAT EnergY
FOOD #of cHo CHON
(kcal)
(sm) (sm) (sm)
exchanges

Vegetable A 'l (3)

(1) (2\
Vegetable B 1 .(5)
4 (4)
Fruit (7) (1) (e)
1
(6)
Milk (1 1)
2 (10)
Sugar (15)
Rice ('t2) (r_3) tr+l (1e)
(17) (18)
Meat (16) (22)
(21)
Fat (20)

BELOW;
SHOW YOUR COMPLITATIONS

201
 PROBLEM IV

WiththedataobtainedinProblemlll,plana.dietforadayusingthetablebelow.
i""t''ng"" into o. 't l"t""t
i"rj,ljiui"'l'6"'v:. "
Dividing a d"Y"'
btut"n t
"t"h"ngt" Supper
No of Breakfast Lunch Mid PM snack
Exchange
group exchanges

CHo grouP
- Vegetable A
Vegetable B --
-
Fruit

Mirk

Sugar

Rice

L4eat and meat

substitutes

Fai grp -

into a Day's Meal

Translating a Day's Exchanges
Afternoon snack Supper
Breakfast Lunch