ii

List of Abbreviations
ADL X-Adrenoleukodystrophy
AGA Appropriate For Gestational Age
AIDS Acquired Immunodeficiency Syndrome
BMI Body Mass Index
BMR Basal Metabolic Rate
CF Cystic Fibrosis
CNS Central Nervous System
CTD Carnitine Transporter Deficiency
DHA Decosahexaenoic Acid
DRI Dietary Reference Intakes
ELBW Extremely Low Birth Weight
ELISA Enzyme Like Immunoassay
EPA Eicosapentaenoic Acid
FDA Food And Drug Administration
GERD Gastroesophageal Reflux Disease
GIT Gastrointestinal Tract
HCL Hydrochloric Acid
HFI Hereditary Fructose Intolerance
HHC Hereditary Hemochromatosis
HIV Human Immunodeficiency Virus
IBS Inflammatory Bowel Syndrome
IgE Immunoglobulin E
LBW Low Birth Weight
LCT Long Chain Triglycerides
LDL Low Density Lipoprotein
LGA Large For Gestational Age
MCT Medium Chain Triglycerides
NG Naso Gastric
NPO Nil Per Os
 NSP Nutrition Support Professionals
ORS Oral Rehydration Salts
ORT Oral Rehydration Therapy
PEM Protein Energy Malnutrition
PERT Pancreatic Enzyme Replacement Therapy
PPN Peripheral Parenteral Nutrition
PUD Peptic Ulcers Disease
RAST Radio Allergosorbent
RDA Recommended Dietary Allowance
SGA Small For Gestational Age
TPN Total Parenteral Nutrition
UNICEF United Nations International Children’s Emergency Fund
USDA United State Department Of Agriculture
VLBW Very Low Birth Weight
WHO World Health Organization

Introduction
Diet Therapy I module is designed to equip the learner with
knowledge, skills and attitude to enable them plan and execute
nutrition care to patients.
The prerequisite modules include; Human anatomy and
physiology, Principles of human nutrition, Introduction to
Microbiology and Communicable & non communicable diseases,
nutrition assessment and surveillance and basic critical
reasoning and patient documentation skills.
The module takes 60 contact hours: 33 hours for theory and 27
hours for practicals. Learners undertaking this module will have
both theory and practical assessments. The formative
assessment will be in the form of continuous assessment tests,
assignments, clinical and field assessments and
promotional/end of semester examination whereas summative
assessment will be done in form of final qualifying examination.
‘’Let food be thy medicine
and medicine be thy food’’
Hippocrates
 Competence
Plan and execute nutrition care to patients
Competence

Module Outcomes
Discuss the basic concepts of diet therapy
Discuss the need and role of special diet in management of
diseases and disorders
Apply diet planning in management of diseases and
disorders
Discuss drug and nutrient interaction in management of
diseases and disorders
Prepare therapeutic diets for various conditions

Module Learning Strategies

Lectures, individual and group assignments and
presentation, practicals, clinical exposure,
demonstrations, case studies, role playing etc.

Learning Logistics/Resources
LCDS, white boards, laptops, markers, diet therapy textbooks, flip charts,
student notebooks, food items for practicals, hospital facilities

Assessment
Formative Assessment (continuous assessment tests, individual
assignments and group assignments) - 40% and Summative Assessment
(end of semester examination) - 60% and final qualifying practical
examination).
TABLE OF CONTENTS
Acknowledgement ii
List of Abbreviations iii
Introduction iv
Competencev
Module Outcomes v
Module Learning Strategies v
Learning Logistics/Resources v
Assessment v
UNIT 1: INTRODUCTION TO DIET THERAPY 1
UNIT 2: BACKGROUND OF MEDICAL TERMINOLOGIES 9
UNIT 3: MEDICAL RECORDS 14
UNIT 4: NUTRITION CARE PROCESS 19
UNIT 5: DIET MODIFICATION 25
UNIT 6: NUTRITIONAL SUPPLEMENTS, FUNCTIONAL FOODS AND
NUTRACEUTICALS 35
UNIT 7: NUTRITION SUPPORT 40
UNIT 8 : DRUG-NUTRIENT INTERACTIONS 67
UNIT 9: DIET PLANNING 80
UNIT 10: INBORN ERRORS OF METABOLISM, FOOD ALLERGIES AND
FOOD INTOLERANCE 87
UNIT 11: NUTRITION THERAPY IN DISEASES OF INFANCY AND
CHILDHOOD 103
UNIT 12: GASTROINTESTINAL DISEASES AND DISORDERS 119
UNIT 13: WEIGHT MANAGEMENT 163
UNIT 14 EMERGING ISSUES IN NUTRITION AND DIETETICS 181
REFERENCES 182
UNIT 1: INTRODUCTION TO DIET THERAPY
___________________________________________________________________________
Unit Objectives
Define terms used in diet therapy
Explain the relationship between nutrition and infection
Describe nutrition care team and give roles of dieticians in nutrition care

Introduction to Diet Therapy

Diet therapy involves the management/treatment of a patient by the use of
a diet whose food selection and combination is made to fit the demands of
the disease or disorder being managed. It is a personalized eating program
designed to address a particular medical problem or to help one to restore
or maintain good health. It involves the modification of an existing dietary
lifestyle to promote optimum health.
It is the practical application of nutrition as a preventative or corrective
treatment of disease e.g. the intake of high levels of antioxidants and bio-
flavonoids that come from many fruits and vegetables which deters
oxidative stress in the body, may help to prevent many types of cancer. Or
an alternative dietary lifestyle plan may be developed for the purpose of
minimizing certain foods in order to reclaim health e.g. Limiting total fat in
the diet to 30 percent of total caloric daily intake may reduce the risk of
colon and breast cancer.

Why Study Diet Therapy

 The study of diet therapy helps us to understand the correct dietary
combinations necessary in supporting the patient’s healing and recovery
process.
 Helps us to know diets which may help to correct an imbalance or
supply necessary dietary nutrients when a pre-existing medical
condition exits.

1
 It helps to identify the range of food combinations used in diet
preparation to meet the needs of patients with diverse medical and
recovery needs.
Definition of terms

Diet: All food eaten or drank in a day.

Nutrient: This is the chemical components in food needed to maintain life
i.e. proteins, carbohydrates, lipids, vitamins, minerals, and water.
Nutrition: This is the science of food, the nutrients and other
substances therein, their action, interaction and balance in
relation to health and disease, and the processes by which one
ingests, digests, absorbs, transports, utilizes and excretes food
substances.
Normal diet: This refers to an adequate diet that provides the body with all the
nutrients necessary
for the growth and repair of tissues and the normal functioning of
the body organs. It is used for patients whose food intake is
unrestricted in kind and amount and who do not need additional
nutritional support. It can also be referred to as a regular diet.
Modified A modified diet is any diet altered to include or exclude certain
Diet: components,
such as calories, fat, vitamins and minerals. Diets are typically
modified for therapeutic reasons, including treatment of high
blood pressure, low body weight or vitamin and mineral
deficiencies.
Therapeutic A diet used as part of a treatment to hasten recovery from a
diets: disease or
clinical condition (such as an injury, nutritional deficiency, and
burns). It aims to eliminate, decrease, or increase certain
substances in the diet. They are also used to control health
conditions such as blood sugar levels. Therapeutic diet is
sometimes called a “special diet”.
Care Plan: Design (or scheme) of professional clinical activities developed to
implement and achieve treatment goals.
Nutritional this is the application of science and art of human nutrition in
care: helping people
select and obtain food for the primary purpose of nourishing their
bodies in health or disease throughout their life cycle.
Nutrition A formal statement of the nutrition goals and interventions
Care Plan: prescribed for an individual using the data obtained from a
nutrition assessment. The plan should include statements of
nutrition goals and monitoring/evaluation parameters, the most
appropriate route of administration of nutrition therapy, method
of nutrition access, anticipated duration of therapy, and training
and counseling goals and methods. It involves assessment,
diagnosis, intervention, and follow up plan.
Nutrition A component of medical treatment that includes oral, enteral,
Therapy: and parenteral nutrition.
Oral Nutrients taken by mouth
Nutrition:
Enteral This is a way of providing nutrition to the patients who are
nutrition: unable to consume an adequate oral intake but have at least a
partially functional GI tract. Enteral feeding and tube feeding are
used interchangeably.
Parenteral The intravenous administration of nutrients.
Nutrition:
Drug- An event that results from a physical, chemical, physiologic, or
Nutrient pathophysiologic relationship between a drug and nutrient
Interaction: status, nutrient(s), or food in general, which is clinically
significant if drug response is altered or nutrition status is
compromised.
Nutrition A comprehensive approach to diagnosing nutrition problems that
Assessment: use a combination of the following: medical, nutrition, and
medication histories; physical examination; anthropometric
measurements; and laboratory data.
Nutrition A process to identify an individual who may be malnourished or
Screening: at risk for malnutrition to determine if a detailed nutrition
assessment is indicated.
Nutrition An interdisciplinary group which may include
Support physicians, nurses, dietitians, pharmacists, and/or other
Service (or healthcare professionals with expertise in nutrition who manage
Team): the provision of nutrition support therapy.
Neonate: An infant during the first month of life.
Infant: Prenatal to 12 months of age.
Geriatric: An adult 65 years of age or greater.
Medical systematic documentation of a single patient's medical history
record: and care across time within one particular health care
provider's jurisdiction
Exchange A grouping of foods in which the carbohydrates, fats, proteins,
list: and calories are similar for the serving size listed.

Importance of diet therapy

It aims at accomplishing one or more of the following:
 Maintaining normal nutrition
 Correcting nutritional deficiency, e.g. high protein diet
 Effecting necessary changes in body weight as with low or high calorie
diets
 Adjusting to the body’s ability to use one or more nutrients e.g. diabetic
diet
 Giving rest to the body or an affected organ as with soft, low –calories
diet in six feedings, etc and help the organs rejuvenate.
 To treat and manage disease and restore health
 To prevent or delay complications of a disorder
 To alleviate symptoms of disease e.g. pain
Relationship Between Nutrition and Infection
 Undernutrition is not necessarily caused by a lack of food, and it is not
unique to poor populations. Even in rich nations, there are malnourished
people.
 Malnutrition is the primary cause of immunodeficiency worldwide, with
infants, children, adolescents, and the elderly most affected.
 There is a strong relationship between malnutrition and infection and
infant mortality, because poor nutrition leaves children underweight,
weakened, and vulnerable to infections, primarily because of epithelial
integrity and inflammation (Figure 1). Five infectious diseases—
pneumonia, diarrhoea, malaria, measles, and AIDS—account for more
than one-half of all deaths in children aged <5 years.

Figure 1: The relationship between malnutrition and infection.

Source: The Interaction between Nutrition and Infection Clin Infect Dis. 2008;
46(10):1582-1588. doi:10.1086/587658 Clin Infect Dis | © 2008 Infectious Diseases
Society of America

The Cycle of Malnutrition and Infection

Malnutrition can make a person more susceptible to infection, and infection
also contributes to malnutrition, which causes a vicious cycle as illustrated
in figure 2 below.
An inadequate dietary intake or poor nutrition status leads to:
 Weight loss
 Lowered immunity (i.e. decreased activity of the macrophages,
diminished inflammatory response and reduction in the capacity to
create specific antibodies).
 Mucosal damage
 Impaired growth and development
On the other hand, diseases cause impaired nutrition status in the
individuals. A sick person's nutrition status can further be aggravated by:
 Diarrhea
 Malabsorption
 Loss of appetite
 Diversion of nutrients for the immune response, and
 protein catabolism and increased urinary nitrogen loss resulting in
negative nitrogen balance
 Fever which increases both energy and micronutrient requirements
 Increased vitamin utilization and excretion
 Depletion of carbohydrate stores
These lead to nutrient losses, further damage to defense mechanisms and
reduced food intake. Malaria and influenza, for example, have mortality
rates proportionate to the degree of malnutrition. This is summarized in the
figure on the next page.
Figure 2. Malnutrition-infection Cycle.
Source: The Interaction between Nutrition and Infection Clin Infect Dis.
2008;46(10):1582-1588. doi:10.1086/587658 Clin Infect Dis | © 2008
Infectious Diseases Society of America
The Nutrition Care Team
Nutrition care is an organized group of activities allowing identification of
nutritional needs and provision of care to meet these needs. It can occur in
a variety of settings and populations, involving members of the
multidisciplinary team, as appropriate
Nutrition services are provided throughout the continuum of care: in acute
and ambulatory care, in skilled nursing and long-term care, in home health
agencies, and in community-based nutrition programs.
Nutrition care services include:
 Assessing the nutrition needs of individuals and groups and determining
resources and constraints in the practice setting
 Establishing priorities, goals, and objectives that meet nutrition needs
and are consistent with available resources and constraints
 Providing nutrition counselling in health and disease
 Developing, implementing, and managing nutrition care systems
 Evaluating, making changes in, and maintaining appropriate standards
of quality in food and nutrition care services.
Nutrition care team refers to members of the health care team who work
together to ensure that the nutritional needs of patients are met during
illness. They can also be referred to as Nutrition support professionals
(NSP). It involves all health care workers involved in direct patient care i.e.
it is multidisciplinary. Such as nurses, doctors, pharmacist and
dieticians/nutritionists. Physiotherapists, occupational therapists, speech
and language therapists may also be involved as needed. They may work
either independently or as part of a nutrition support team. The NSP can
work in a variety of settings, including hospitals, home-care agencies, long-
term care facilities, research facilities, and academia.
NSPs become so by caring for patients who require provision and
management of enteral and parenteral nutrition while utilizing approved
standards and guidelines to deliver that care. The NSP seeks out resources
and colleagues to share knowledge and experiences.
Roles of Nutrition Support Professionals
Multiple healthcare practitioners are involved in the delivery of nutrition
support. Their unique contributions are outlined below:
 Physicians
Nutrition support physicians lead the nutrition care implementation
structure in many institutions. Their roles depends on the area of
specialization but generally they take medical histories, perform physical
examination, diagnosis, provision of continuous care, management and
treatment of disease, prescribe diet orders e.g. NPO, fluid restriction and
collaborate with other health care providers. They supervise care provided
by dietitians, nurses and pharmacists, and engage in all aspects of direct
care of patients’ nutrition needs as indicated.
 Pharmacists
Nutrition support pharmacists compound the parenteral nutrition
formulation prescribed and provide direct patient care. Many pharmacists
also conduct research or participate in research activities. They can
integrate pharmaceutical treatment with diet, counsel patients about drug–
food interactions as they relate to drug bioavailability, and advise patients
about non-prescription nutrition products. Their knowledge of genetics,
molecular biology, and botany will likely be important as more products
marketed as “nutraceuticals” are approved.
 Nurses
The responsibilities of a nutrition support nurse vary with the practitioner’s
educational background, position and practice environment. The scope of
practice includes but is not limited to the following: directing patient care
including intravenous access; education of patients and caregivers and
participation in research activities.
The registered nurse coordinates patient care, works with the dietitian and
other health care team members to identify nutrition problems, and
reinforces the importance of nutrition interventions. The registered nurse
may also provide less complex nutrition care, such as counselling on
preventing chewing and swallowing difficulties or contributing to the
nutritional assessment.
 Dietitians
Nutrition support dietitians' primary roles are to conduct individualized
nutrition screening and assessment; develop and implement a nutrition
care plan; monitor the patient’s response to the nutrition care delivered;
and develop a transitional feeding care plan or termination of nutrition
support as appropriate.

Roles of Dieticians
 They promote healthy eating habits by developing health plans and
educating people about food.
 They help facilities, patients, and communities plan menus and
nutritional programs.
 They evaluate clientele to determine their dietary needs and restrictions.
 They consult with doctors and other healthcare professionals during the
diet-planning process.
 They oversee meal preparation and serving to make sure dietary needs
and food safety regulations are being met.
 They educate the public on healthy eating and diet monitoring and
provide clients with nutritional counselling and teach them the principles
of nutrition.
 They work with clients' families, informing them of how to implement new
diet plans at home.
 They serve as instructors in dietary courses and training programs.
UNIT 2: BACKGROUND OF MEDICAL TERMINOLOGIES
___________________________________________________________________________
Unit Objectives
Define medical terminology
Describe the components of medical terminologies
Identify common medical abbreviations and their meanings as used in
patient files in health facilities

Introduction to medical terminologies

Most medical terms are derived from Greek or Latin.
Basic elements of a medical word
a. Word root or root word
b. Combining form/vowel
c. Suffix
d. Prefix
Root Words
Refers to an organ or body part that is modified by prefixes or suffixes. The
word root is the foundation of the word. Medical words must have one or
more word roots. E.g. arthritis -arthr (which means joint) is the word root
and hepatitis - hepat (which means liver) is the word root. Others include;

Cardi-heart, pancreat- my/o – muscle

enter-intestine pancreas neur/o – nerve
gastr-stomach Acr/o - or/o – mouth
hemo-blood extremities ot/o – ear
hepat-liver angi/o – vessel pneum or
nephr-kidney cephal/o – head pulmon/o, - Lung

osteo- bone col/o - colon psych/o -mind

Dent-tooth cost/o – ribs rhin/o – nose

dermat-skin crani/o - skull splen/o – spleen

gastr-stomach cyst/o – sac thorac/o- chest

containing fluid
Suffixes
Suffix is the word part attached to the end of the word root to modify its
meaning. The suffix usually indicates the procedure, diagnosis or disease or
condition and symptoms. All medical terms must have a suffix. Suffixes are
prepositions or adverbs added to root words to modify their meaning.
Adjectives or nouns can also be used as suffixes to form compound words.
Diagnostic suffixes
Suffix Definition Examples

Ectasis Dilation of Bronchiectasis

Iasis Presence of Lithiasis

It is Inflammation of Hepatitis or appendicitis

Megaly Enlargement of Cardiomegaly

Oma Tumor of Hepatoma

Osis Condition Nephrosis

Pathy Disease Cardiopathy

Procedure suffixes
Suffix Definition Examples

Ectomy Removal of appendicectomy

Scopy Examination of gastroscopy

Stomy Opening Ileostomy

Tomy Incision lithotomy

Suffixes indicating symptoms

Suffix Definition Examples

Algia Pain Myalgia

Genic Originate Cardiogenic

Lysis Breakdown Lipolysis

Osis Increase Leukocytosis

Penia Decrease Leukopenia

Spasm Involuntary contraction Cardiospasm

Examples of a suffix change

Cardiologist (a physician specializing in the heart), cardiomyopathy (damage
to the heart muscle layer), cardiomegaly (enlargement of the heart)
Prefixes
It is added at the beginning of a root word and modifies words by indicating
location/position, number of times and colour. Not all medical terms have
prefixes.
Prefix Definition Examples

Dys Difficult, painful Dyspnea

Endo Within endocardium

Hemi semi Half hemiplegic

Hyper Above, excessive Hyperglycemia

Hypo Beneath, below, deficient Hypodermic

Para Beside, around, near, abnormal Parathyroid

Peri Around Perinatal

Prefix defining colours

cyan/o Blue
erythr/o Red
leuk/o White
melan/o Black
xanth/o Yellow

Other examples of prefixes includes

a - absence of without endo- within mal – bad
ab- away from epi- above, upon micro - small
dors- back hemi-half peri - surrounding, around
ante- before hyper-over, above, hypo- below, under,
increased decreased
anti- against intra- within, inside post - after
auto – self macro- large sub- under, less, below
dys- difficult, painful poly- many tachy – fast
ad- toward, in the inter-between, among super-above, excessive,
direction of beyond
Combining forms
Combination of a word root and a vowel. The combining vowel links the root
to the suffix or the root to another root.
o Gastr/o
(Word root)Gastr/o(combining vowel)
When a word has more than one root a combining vowel is used to link the root
to each other
o Osteoarthritis
(Word root)osteo/o (combining vowel)/arthr (word root)/it is(suffix)
o Leukocytopenia
(Prefix) leuk/o (combining vowel)/cyt (word root)/o (combing vowel)/penia
(suffix)

A combining vowel is used between a word root and a suffix that begins with a
consonant (not a vowel) e.g. Scleroderma- hardening of the skin

N/B: There are a few rules when using medical roots. Firstly, prefixes and
suffixes, primarily in Greek, but also in Latin, have a droppable -o-. As a
general rule, this -o- almost always acts as a joint-stem to connect two
consonantal roots, e.g. arthr- + -o- + logy = arthrology. But generally, the -o- is
dropped when connecting to a vowel-stem; e.g. arthr- + itis = arthritis, instead
of arthr-o-itis.
E.g. we can breakdown 'myocarditis' into three parts which will clarify the
meaning of this term.
Common medical abbreviation list
 c – with
 s – without
 a – before
 p – after
 po – by mouth
 prn – as needed
 NPO – nothing by mouth
 ASAP – as soon as possible
 ABG’s - arterial blood gases
 ac – before meals
 amb – ambulate or to walk
 BP – blood pressure
 BS – blood sugar
 CBC – complete blood count
 c/o – complaining of
 CXR – chest x-ray
 DNR – do not resuscitate
 EKG – electrocardiogram
 ER - emergency room
 GI – gastrointestinal
 ICU – intensive care unit
 PACU – post-anesthesia care unit
 PT - physical therapy
 Pt - patient
 SOB – shortness of breath
 VS – vital signs
 W/C – wheel chair
 wnl - within normal limits
 y/o – year old
 stat – immediately
 IV – intravenous (within a vein)
 q.d. – every day
 b.i.d. – two times a day
 t.i.d. – three times a day
 q.i.d – four times a day
 Rx – prescription
 Tx - treatment

UNIT 3: MEDICAL RECORDS

___________________________________________________________________________
Unit Objectives
Define medical records
Describe the types of medical records
Explain the components of medical records
Explain the importance of medical records
Visit a health facility to learn about types of medical records

Introduction to medical records

The terms medical record, health record, and medical chart are used
somewhat interchangeably to describe the systematic documentation of a
single patient's medical history and care across time within one particular
health care provider's jurisdiction. They are used in the management and
planning of health care facilities and services, for medical research and the
production of health care statistics.
Doctors, nurses and other health care professionals write up medical/health
records so that previous medical information is available when the patient
returns to the health care facility. The medical/health record must be available
because if it cannot be located, the patient may suffer because information,
which could be vital for their continuing care, is unavailable. If it cannot be
produced when needed for patient care it shows that the medical record system
is not working properly and confidence in the overall work of the
medical/health record service is affected.
Parts of a medical record:
1. Demographics/legal information i.e. non-medical information, identifying
numbers, addresses, contact information, religion, occupation, emergency
contacts etc.
2. Medical history – this encompasses:
- Surgical history – chronicle of surgery performed on the patient; may
include dates of surgery, operative reports, etc.
- Obstetric history – lists prior pregnancies and their outcomes;
complications of pregnancy
 - Medication and medical allergies – summary of the patient’s current and
previous medications and allergies to medications
- Family history – health status of immediate family members and causes
of death; diseases common in the family; important for predicting risk of
certain genetic or chronic diseases
- Social history – chronicle of human interactions; important relationships,
education, career and financial status, community and family support
- Habits – that impact health, such as tobacco use, alcohol intake,
recreational drug use, activity, and diet; may address sexual habits and
sexual preferences
- Immunization history – history of immunizations
- Growth chart and developmental history, including comparison to other
children of the same age and gender
- Addresses developmental milestones such as walking, talking, etc.
- Vital signs: body temperature, pulse rate (heart rate), blood pressure and
respiratory rate;
- Intake: medication, fluid, nutrition, water and blood, etc.;
- Output: blood, urine, excrement, vomitus, sweat, etc.;
- Observation of pupil size;
- Capability of four limbs of body.
3. Medical encounters this captures information such as
- Summary of an episode of care
- Outpatient or inpatient admission
- Chief complaint
- History of the present illness
- Physical exam
- Assessment and plan
4. Orders i.e. written orders by medical providers – physicians (residents or
attendings) and nurse practitioners; others with order writing privileges.
They must be signed. One can find diet orders, lab orders, medications,
enteral and parenteral orders
5. Progress notes - Daily updates entered into the medical record
documenting clinical changes, new information, results of tests. May be in
SOAP, narrative, or other formats. Generally entered by all members of the
health care team (doctors, nurses, physical therapists, dietitians,
pharmacists. They are kept in chronological order
6. Test results – these includes blood tests, radiology exams, pathology,
specialized testing etc.
7. Other information e.g. an informed consent form, radiologic images,
outputs from medical devices, vital signs etc.

Types of medical records

 Paper-based medical records
 Computer-based medical records
 Hybrid record (health care record exist in both paper and computer records)
Paper-based and electronic patient records generally are used in parallel to
support different tasks
Disadvantages of Paper-Based Medical Records
 Only one person can use the record at a time, unless multiple people are
crowding around the same record.
 Items can be easily lost or misfiled or can slip out of the record if not
securely fastened.
 The record itself can be misplaced or be in a different area of the facility
when needed
Advantages of Computer-Based Medical Records
 More than one person can use the record at a time.
 Information can be accessed in a variety of physical locations.
 Records can often be accessed from another city or state.
 Complete information is often available in emergency situations.
Organization of the Medical Record
i. Source-oriented records
 Traditional method of keeping patient records, used mainly in inpatient.
 Observations and data are kept according to the document source.
 Progress noted are written in paragraph format.
 separated sections by labeled dividers within the folder(each health cadre
with their own section, similar subject matters are kept together e.g.
progress notes, lab reports)
 forms and progress notes are filed in reverse chronological order
 separate sections are established for laboratory reports, x-ray films,
radiology reports
ii. Problem-oriented records
 It divides records into 4 bases: database, problem list, treatment plan,
progress notes.
 Organized by diagnosis or medical problem with each disease in separate
sections
 A number is assigned to each problem(problem number) with the
progress notes kept in SOAP format
SOAP stands for
Subjective: verbal expressions by the patient e.g. symptoms. The information
cannot be measured.
Objective: objective observations that can be measured (factors you can
see/hear/feel/smell) e.g. heart rate, temperature, lab work, x-ray
Assessment: diagnosis or condition the patient has
Plan: how to address the patients problem e.g. additional tests to rule
out/confirm diagnosis, treatment (medication/surgery), information for self-
care e.g. bed rest.
iii. Integrated record
 Organizes all paper forms in chronological order and mixes forms by
different department
 Uses reverse chronological order as it makes the recent information easier
to view.
Importance of medical records
 To document the course of the patient's illness and treatment
 To track the patient’s medical history and identify problems or patterns that
may help determine the course of health care
 To communicate between attending doctors and other health care
professionals providing care to the patient
 For the continuity of the care of the patient
 To enable physicians (and other health care providers) to provide quality
health care to their patients; facilitating patient safety improvements
 For research (subject to ethics committee approval, as required) of specific
diseases and treatment
 Investigation of complaints/Evidence of care: The record may become an
important piece of evidence in protecting the legal interests of the
patient/client, health care personnel, other personnel or public health
organization (PHO).
 Medical records are legal documents and may provide significant evidence in
regulatory, civil, criminal, or administrative matters when the patient care
provided by a physician is questioned
 The collection of health statistics
 Financial reimbursement
 The health care record may also be used for communication with external
health care providers, and statutory and regulatory bodies
 Planning audit activities
UNIT 4: NUTRITION CARE PROCESS
___________________________________________________________________________
Unit Objectives
Define nutrition care process
Describe the phases of nutrition care
Come up with a nutrition care plan for hypothetical cases

Nutrition care process

Definition of terms used in NCP;
1. Process is a series of connected steps or actions to achieve an outcome
and /or any activities that transform into outputs.
2. Process approach is the systematic identification and management of
activities and the interaction between activities.
3. Critical thinking integrates facts, informed opinions, active listening and
evaluations. It’s defined as transcending the boundaries of formal education
to explore a problem and form a hypothesis and a defensible conclusion.
Further characteristics of critical thinking to include the ability to do the
following; conceptualize, think rationally, think creatively, be inquiring and
think autonomously.
4. Decision making; is a critical process for choosing the best action to meet
a desired goal
5. Problem solving is the process of the following; problem identification,
solution formation, implementation, and evaluation of results.
6. Collaboration; is a process by which several individuals or groups with
shared concern are united to address an identified problem or need, leading
to the accomplishment of what each could not do separately.
The nutrition care process consist of four distinct, but interrelated and
connected steps;
 - Nutrition assessment – It is the first step of the nutrition care process.
Its purpose is to obtain adequate information in order to identify
nutrition-related problems. It is initiated by referral and / or screening
of individuals or groups for nutritional risk factors.
- Nutrition diagnosis – It is the second step in the nutrition care process,
and is the identification and labeling that describes an actual
occurrence, risk of, or potential for developing a nutritional problem that
dietetics professionals are responsible for treating independently
- Nutrition intervention – It is the third step of the nutrition care
process. An intervention is a specific set of activities and associated
materials used to address the problem. Nutrition interventions are
purposely planned actions designed with the intent of changing a
nutrition-related behavior, risk factor, environmental condition, or aspect
of health status for an individual, target group, or the community at
large.
- Nutrition monitoring and evaluation - Monitoring specifically refer to
the review and measurement of the patient/client/groups status at a
scheduled follow-up point with regard to the nutrition diagnosis,
intervention plans/goals, and outcomes. Evaluation is the systematic
comparison of current findings with previous status, intervention goals,
or a reference standard.
The nutrition care process does not restrict practice but acknowledges the
common dimensions of practice by the following;
a) Defining the common language that allows nutrition practice to be more
measurable
b) Creating a format that enables the process to generate quantitative and
qualitative data that can be analyzed and interpreted
c) Serving as the structure to validate nutrition care and showing how the
nutrition care that was provided does what it intends to do.

Nutritional care record

This is written documentation of the nutritional care process, including the
interventions and activities used to meet the nutritional objectives
“If it’s not documented, it didn’t happen.”
A medical record is a legal document.
Styles of nutrition care documentation
 ADIME (assessment, diagnosis, intervention, monitoring and evaluation)
 DAP (diagnosis, assessment, plan)
 DAR (data, action, response)
 PIE (problem, intervention, evaluation)
 PES (problem, etiology, symptoms)
 IER (intervention, evaluation, revision)
 HOAP (history, observation, assessment, plan)
 SAP (screen, assess, plan)
 SOAPIER (subjective, objective, analysis/assessment, plan, intervention,
evaluation, revisions)
 SOAP (subjective, objective, assessment, plan)
For the purpose of this module, we shall discuss two of the most commonly
used documentation styles.
SOAP style:
S: Subjective
 Info provided by patient, family, or other
 Pertinent socioeconomic, cultural info
 Level of physical activity
 Significant nutritional history: usual eating pattern, cooking, dining out
 Work schedule
O: Objective
 Factual, reproducible observations
 Diagnosis
 Height, age, weight—and weight gain/loss patterns
 Lab data
 Clinical data (nausea, diarrhea)
 Diet order
 Medications
 Estimation of nutritional needs
A: Assessment
 Nutrition diagnosis
 Interpretation of patient’s status based on subjective and objective info
 Evaluation of nutritional history
 Assessment of laboratory data and medications
 Assessment of diet order
 Assessment of patient’s comprehension and motivation
P: Plan
 Diagnostic studies needed
 Further workup, data needed
 Medical nutrition therapy goals
 Education plans
 Recommendations for nutritional care
SOAP style example:
• S: Patient works night shift, eats two meals a day, before and after his shift;
fried foods, burgers, ice cream, beers in restaurants. Does not add salt to
foods. Activity: Plays golf 1x month.
• O: 34 y.o. male s/p MI with history of htn, DM2, hyperlipidemia.
• Ht: 5 ft. 10 in; wt: 250 lb; BMI 36, Obesity II
• A: Excessive sodium intake (NI-5.10.2) related to frequent use of vending
foods as evidenced by diet history. Pt could benefit from increased activity
and gradual wt loss as recovery allows
• P: Provided basic education (E-1) on 3-4 gram sodium diet and wt
management guidelines
• Patient will return to outpatient nutrition clinic for lifestyle
intervention and counseling
ADIME style:
This style was developed to facilitate the nutrition care process.
A – Assessment: All data pertinent to clinical decision making, including diet
history, medical history, medications, physical assessment, lab values, current
diet order, estimated nutritional needs. Should include relevant data only
D – Diagnosis: Should include PES statement for nutrition diagnosis.
Patients may have more than one diagnosis, but try to choose the one or two
most pertinent, or the ones you mean to address
I – Intervention: What do you recommend or plan to do to address the
nutrition diagnoses?
 Recommend change in food-nutrient delivery (supplement, change in
diet, nutrition support, vitamin-mineral supplement) (NI)
 Nutrition education (E)
 Nutrition counseling (C)
 Coordination of nutrition care (RC)
ME – Monitoring and Evaluation: What will you monitor to determine if the
nutrition intervention was successful?
Generally based on the signs and symptoms
 Weight
 Intake
 Lab values
 Clinical symptoms
ADIME style example:
• A - 34 y.o. male s/p MI with history of htn, DM2, hyperlipidemia; ht: 5 ft. 10
in; wt: 250 lb; BMI 36, obesity II. Patient works night shift, eats two meals a
day, before and after his shift--fried foods, burgers, ice cream, beers in
restaurants. Does not add salt to foods. Activity: Plays golf 1x month.
• D - Excessive energy intake; excessive sodium intake related to frequent use
of restaurant foods as evidenced by diet history.
D - Excessive energy intake related to high intake of fat and restaurant foods
aeb BMI and diet history.
• I – Provided basic education on 3-4 gram sodium diet and wt. management
guidelines (nutrition education); pt to return to outpatient nutrition clinic
for lifestyle intervention.
• ME – Evaluate weight, blood pressure, diet history at outpatient visit
sodium intake; energy intake; fat intake. Re-check lipids in 3 months.
Students Question for practice

You were approached by a patient as an expert in

dietetics to give some nutrition advice on the problems
that had disturbed her for some time. Assuming that
after assessments were done, you obtained the
following information about the client;

Weight; 56

Height;160cm

24hour recall was done:

That the client consumed 500Kcal below

recommended amount per day

Irregular meal consumption

10Kg weight loss in the past ten months

Using the information given, write a nutrition care plan

for the patients that you can include in her medical file

(10 Marks)
UNIT 5: DIET MODIFICATION
___________________________________________________________________________
Unit Objectives
Define diet modification
State principles of diet modification
Elaborate the importance of diet modification
Identify factors influencing diet modification
Describe types of modified diets
State challenges of modified diets
Plan and prepare modified diets

Introduction to diet modification

Diet modification is not simply a matter of knowing what to eat and making the
rational choice to change dietary practices. Rather, diet and eating practices
should be considered as part of the situated lives of patients, requiring an
individualized approach that is responsive to the conditions in which each
patient is attempting to make a change.

Principles of diet modification

 To maintain good nutritional status
 To correct deficiencies
 To afford rest to the body/organs
 To metabolise the nutrients
 To make changes in the body weight when nessesary
Factors influencing diet modification
a. Nature of disease/illness and symptoms
b. Severity of disease or symptoms (condition of the patient)
c. Metabolic changes involved in the disease process and the nutritional
implications
 d. Nutritional status of the patient
e. The patient’s tolerance for food by mouth.
f. The factors in the diet which must be altered to overcome these
conditions.
g. Physiological state

Challenges of diet modification

Challenges that are common to patients include; self-discipline, knowledge,
coping with everyday stress, negotiating with family members and managing
the social significance of food.
a) Self-discipline- Patients feel the challenge of trying to resist food they want
to eat but know isn’t healthy, eat food they know healthy but didn’t enjoy
and reduce portion sizes.
b) Knowledge - Various knowledge-related challenges are reported by patients:
understanding what they should eat, understanding the link between their
diet and health conditions and employing techniques they learn from health
care professionals to count carbohydrates or monitor salt intake.
c) Coping with Everyday Stress -All patients have challenges related to
routine events (such as coordinating family schedules); being forced to eat
at particular times because of work; and avoiding convenience foods when
busy. Patients who experience higher levels of stress, or who have fewer
resources to cope with stress, have additional challenges that negatively
affect attempts to modify their diet.
d) Negotiating With Family Members -Considering the influence of spouses
and family members on meal planning and eating practices is important,
since “food and eating form a large part of the ‘normal’ but essential
activities of families, across cultures. Consequently, any type of dietary
modification involves some degree of negotiation with other members of the
household
e) Managing the Social Significance of Food -Many studies emphasized
patient reports that maintaining diet modification is especially difficult when
visiting or hosting friends and family members, and during holiday or social
occasions. Because of the central role of food in social gatherings, patients
often feel left out or separated, when they cannot consume special foods.
Modified/Therapeutic diets
It is a diet that is usually a modification of a regular/normal diet. It is part of
the treatment of a medical condition and is normally prescribed by a physician
and planned by a dietician. It is modified or tailored to fit the nutrition needs of
a particular person.
Common reasons therapeutic diets may be ordered:
1) To maintain nutritional status
2) To restore nutritional status
3) To correct nutritional status
4) To decrease calories for weight control
5) To provide extra calories for weight gain
6) To balance amounts of carbohydrates, fat and protein for control of diabetes
7) To provide a greater amount of a nutrient such as protein
8) To decrease the amount of a nutrient such as sodium
9) To exclude foods due to allergies or food intolerance
10) To provide texture modifications due to problems with chewing and/or
swallowing
Normal diet - is a regular diet, well balanced and adequate for nutrition. It is
the foundation of all diets, designed to provide adequate nutrition in persons
who do not require diet modification or restrictions. Individual requirements for
normal diets differ with age, gender, height, weight, activity level and different
physiological states. It is derived from foods from the basic food groups (water,
cereals and starch, vegetables, fruits, animal and plant proteins, fats and oils,
gars and sweets).
The advantages of using normal diet as the basis for therapeutic diets are
1. It emphasizes the similarity of psychological and social needs of those who
are well, even though there are quantitative and qualitative differences in
requirements, thus ensuring better acceptability.
2. Food preparation is simplified when the modified diet is based upon the
family pattern and the number of items requiring special preparation is
reduced to a minimum.
3. The calculated values for the basic plan are useful in finding out the effects
of addition or omission of certain foods. e.g.; if vegetables are restricted,
vitamin A or Vitamin C deficiency can occur.
The most common therapeutic diet adaptations include;
a) Change in consistency so as to provide soft or fluid (liquid) diets
b) Change in energy content to provide high calorie or calorie restricted or
calorie controlled diets
c) Change in content of one or more nutrients e.g. high or low protein, sodium
restricted diet or controlled diet , fat restricted or controlled diet
d) Change in the fibre content to provide high fibre or fibre restricted
e) Change in the frequency of feeding
f) Change in the mode of feeding
g) Exclusion of certain foods in confirmed and severe allergic conditions

Types of therapeutic diets

Therapeutic diets can be modified in terms of quality and quantity.
1. Qualitative
- Restriction of a nutrient e.g.; Sodium in hypertension
- Excess of a nutrient e.g.; Tuberculosis where increased protein and energy
are required
2. Quantitative
- Change in consistency e.g.; clear liquid diet
- Rearrangement of meals e.g.: Increasing frequency of meals
- Omission of foods e.g.: Allergy, which demands complete exclusion of the
allergic food.
Qualitative modification
i) Modification in Fiber
Diseases of the GIT generally require modification in fiber content.
i. Fiber restricted /low residue diet:
The diet excludes certain raw fruits, raw vegetables, wholegrains and nuts,
meat high in connective tissue. The diet is modified to meet the clients’ caloric,
protein, fat as well as vitamins and mineral requirements. It is designed to
prevent blockage of inflamed GIT and reduce the frequency and volume of fecal
matter while prolonging the intestinal transit time.
It is indicated in GIT disorders such as colitis, colostomy, inflammatory bowel
disease, diarrhoea, hemorroids, acute diverticulitis, partial intestinal
obstruction, pre-post-operative phase of the large bowel, post perineal
suturing.
ii. High Fiber diet:
This is designed to prevent constipation and slow development of hemorroids,
reduce colonic pressure and prevent segmentation. The diet also reduces
serum cholesterol levels, reduces transit time and can be used for control of
glucose absorption for diabetic patients and obese/overweight clients. In
addition, it reduces the risk of colon and rectum cancers. The indications
include GIT diseases, CVS diseases, diabetes mellitus, cancer prevention,
diverticular, and weight reduction.
ii) Modification in energy intake
a. High energy diet:
This is meant to provide an energy value above the total energy requirement
per day order to provide regeneration of glycogen stores and spare protein for
tissue regeneration. It involves addition of an extra 500 kcal of the RDA in
terms of butter, sugar, honey, and ghee. The indications include
hypethyroidism, wasting/cachexia, typhoid, severe malaria, HIV/AIDs,
prolonged degenerative diseases.
b. Calorie restricted diet:
These are prescribed for weight reduction, maintenance of normal glucose and
lipid levels. Should include complex carbohydrates and minimal fats. It is
indicated in overweight, obesity, hyperlipidemia, gout, gallbladder diseases.
iii) Fat Restricted Diet
This is designed for patient who experience symptoms of nutrient losses when
high fat foods are eaten. It minimises the side effects of fat malabsorption such
as diarrhoea, gas and cramping. The indications include; biliary tract diseases,
hepatic cirrhosis, pancreatic insufficiency, fat malabsorption syndromes,
overweight, obesity, CVDs and steatorrhea among others.
iv) High protein- high calorie diet
The diet is designed to maintain appositive nitrogen balance, promote normal
osmotic pressure, promote tissue body repair, prevent muscle atrophy in
chronic diseases and build and repair tissues in severe malnutrition. The
purpose is to help heal wounds, maintain or increase weight, promote growth,
decrease respiratory complications, resist infections and support the immune
system. The indications include; febrile states, cancer, wounds, burns, post-
surgery, pregnancy, lactation and infancy.
v) Low protein diet
This is usually a temporary indication to avoid breakdown of tissue protein
which can lead to undesirable levels of nitrogen constituents in the blood. The
calorie intake form carbohydrates must be sufficient to spare body proteins.
The indications include; hepatic coma, liver cirrhosis, acute and chronic renal
failure and glomerulonephritis.
vi) Low sodium diet
This involves reduction in salt and reduced intake of processed foods and
beverages, avoid frozen foods and fast foods. The purpose of the diet is to aid in
control of BP in salt sensitive people and to promote loss of excessive fluids in
oedema and in hypertension management. It is indicated in impaired liver
function, CVS diseases, cardiac failure, acute and chronic renal failure.
vii) Bland diet
This diet chemically, mechanically and thermally modified to avoid irritation to
the GIT. For instance, spices, stimulants and strong flavours that because
irritation are eliminated and food served at room temperature.
viii) Frequency and quantity of meals
The usual three meals a day may be replaced by more frequent but mall
quantity meals to reduce stress to the body. This is necessary in peptic ulcer
disease (PUD) demands increased frequency of meals to dilute the acid; weight
management; diabetes mellitus
ix) Exclusion of certain foods (allergens)
Products normally included in the diet may be eliminated; wheat products,
milk products due to allergies.

Qualitative modification
i) Clear liquid Diet
Clear liquid diet is a temporary diet (24-48 hrs) because it is nutritionally in
adequate, it is a diet of clear liquids without residue and is non – stimulating,
non-irritating and non-gas forming. Small amounts of fluids (usually 30-60 ml)
are served at frequent intervals (2 hrs)
Major purpose is to prevent dehydration and relieve thirst thus they majorly
water and have small amounts of electrolytes and calories
Characteristics
1. 400-500 kcal
2. 5-10 g protein
3. Negligible fat
4. 100-120 g of carbohydrates.
Indicators
 Preoperative patients e.g.: preparation for bowel surgery.
 Prior to colonoscopy examination.
 Post-operative patients e.g.: in the initial recovery phase after abdominal
surgery or after a period of intravenous feeding.
 Acute illness and infections as in acute Gastro Intestinal (GI) disturbances
such as acute gastroenteritis, when fluid and electrolyte replacement is
desired to compensate for losses from diarrhoea.
 As the first step in oral alimentation of a nutritionally debilitated person.
 Temporary food intolerance.
 To relieve thirst.
 To reduce colonic fecal matter.
 ii) Full fluid diet
It is designed to provide nourishment in liquid form to facilitate digestion and
optimal utilization of nutrients in acutely ill patients who are unable to chew or
swallow certain foods. It is used as transition between clear liquid diet and soft
regular diet, when the diet is used for a period exceeding 2-3 weeks protein
and calorie value are increased
Characteristics
 It is free from cellulose and irritating condiments and spices.
 Liquid at room temperature
 Provides 1500-2000 kcal/day
 35 g protein
 This should be given at 2-4 hr interval
 Large percentage is milk based
This diet can be properly planned and made nutritionally adequate for
maintenance requirements. If used for more than two days, then a high
protein, high calorie supplement may be necessary.
Indicators
 Most often used post operatively by patients progressing from clear liquids
to solid foods.
 Acute gastritis and infections.
 Following oral surgery or plastic surgery of face or neck area.
 In presence of chewing and swallowing dysfunction for acutely ill patients.
 Patients with oesophageal or stomach disorder who cannot tolerate solid
foods owing to anatomical irregularity
iii) Soft Diet
A soft diet is used as a transitional diet between full fluid and normal diet. It is
nutritionally adequate. It is soft in consistency, easy to chew, made up of
simple, easily digested foods, containing limited fibre and connecting tissues
and does not contain rich or highly flavoured foods.
The average soft diet supplies around 1800 kcal and 50 g protein. However, the
energy, protein and other nutrients are adjustable according to the individual’s
need, based on activity, height, weight, sex, age and disease condition. It can
be given as three meals a day with or without in between meal feedings.
Indicators
 Patients progressing from full fluid diet to general diet.
 Post- operative patients unable to tolerate general diet.
 Patients with mild GI problems.
 Weak patients or patients with inadequate dentition to handle all foods in a
general diet.
 Diarrhoea convalescence.
 Between acute illness and convalescence.
 Acute infections.
A soft diet can be modified as mechanical soft diet.
iv) Mechanical soft diet
Many people require a soft diet simply because they have no teeth and such a
diet is known as mechanical or a dental soft diet. It is not desirable to restrict
the patient to the food selection of the customary soft diet and the following
modifications to the normal diet may suffice.
 Vegetables may be chopped or diced before cooking
 Hard raw fruits and vegetables are to be avoided; tough skins and seeds to
be removed.
 Nuts and dried fruits may be used in chopped or powdered forms.
 Meat to be finely minced or ground.
 Soft breads and chapattis can be given.
Indicators
 In cases of limited chewing or swallowing.
 Patients who have undergone head and neck surgery.
 Dental problems.
 Anatomical oesophageal strictures.
 v) Cold semi liquid diets
This diet is given following tonsillectomy or throat surgery until a soft or
general diet may be swallowed without difficulty. It contains more of cold
beverages and luke warm preparations.
vi) Blenderized liquid diet
This is adopted in conditions of
 Inadequate oral control
 Oral surgery with dysphagia
 Wired jaws (blenderized foods can be consumed through small openings).
 Patients with reduced pharyngeal peristalisis.
Routine food is made into liquid pulp and can be prepared using a kitchen
blender.
UNIT 6: NUTRITIONAL SUPPLEMENTS, FUNCTIONAL FOODS AND
NUTRACEUTICALS
___________________________________________________________________________
Unit Objectives
Define nutrient supplements, describe their types and uses
Define functional foods, describe their types and uses
Define nutraceuticals, describe their types and uses
Visit pharmacies/chemists to learn about the common nutrient supplements,
functional foods and nutraceuticals they stock

Dietary supplements are defined as any product (other than tobacco) that is
intended to supplement the diet and contains one or more of the following: a
vitamin, mineral, herb or other botanical; an amino acid or metabolite; an
extract; or any combination of the previously mentioned items.
Fortified foods are enriched with vitamins and minerals, usually at a range up
to 100 percent of the Dietary Reference Intake (DRI, formally called the
Recommended Daily Allowance or RDA) for that nutrient. Often, these foods are
mandated by law to be fortified to a level that replaces nutrients lost during
processing, as in adding B vitamins to many baked goods.
Probiotics are defined as live microorganisms, as they are consumed in
adequate numbers to confer a health benefit on the host by adding on to the
beneficial microflora in the GIT. Lactic acid bacteria and bifidobacteria, the
most studied and widely employed bacteria within the probiotic field. They are
mainly used in production of dairy products such as yoghurt.
Prebiotics are non-digestible food ingredients that beneficially affect the host
by stimulating the growth and/or activity of one or a limited number of
bacteria in the colon, thus improving host health. Fructo-oligosaccharides and
content inulin, isomalto-oligosaccharides (IMO), polydextrose, lactulose and
resistant starch are considered the main prebiotic components.
Inulin and oligofrucose besides being prebiotics, have shown to increase
calcium absorption, thus improve both bone mineral content and bone mineral
density. Furthermore, they influence the formation of blood glucose, and
reduce the levels of cholesterol and serum lipids.
Functional foods are "any food or food ingredient that may provide a health
benefit beyond the traditional nutrients it contains". This is a tricky definition
because the term "traditional nutrients" refers only to vitamins and minerals.
The reason is that these are considered essential to the diet and/or correct a
classical nutrient deficiency disease; for instance, vitamin C corrects scurvy.
Hence, the vitamin D content in sardines, which alleviates rickets, is not an
example of a functional food, while soy, which contains soy protein associated
with a reduction in cardiovascular disease, is one because soy protein is not
considered to be essential.
Other functional foods include red grapes and cranberry juice (for the
oligomeric proanthocyanidins) and oat bran (for the fiber content), all with
health benefits attributed to "non-nutrient" compounds as classified by
standard agreement of the term.
Examples of functional foods:
1. Omega-3 enriched eggs. Functional Components: Omega-3 fatty acids e.g.
DHA; the fatty acid profile of the egg yolks is altered by changing the feed
the hens receive. Hens receive feed rich in omega-3s, typically from flaxseed,
fish oil or sea algae. The subsequent eggs the hens lay, contain increased
amounts of omega-3s, and decreased amounts of saturated fats. What they
do: May lower triglycerides, cholesterol, and reduce the risk for coronary
heart disease.
2. Oats – the functional components are ß-glucan and phytochemicals called
saponins. What they do: Reduce total and LDL cholesterol, may help lower
blood pressure. Foods: Whole oats, oatmeal, low fat granola, whole-oat
bread, other whole-oat products.
3. Fatty fish - the functional components are Omega-3 fatty acids (DHA and
EPA). What they do: Reduce triglycerides, reduce coronary heart disease.
Foods: Salmon, Tuna, Striped Bass, Halibut, Sardines, Trout, Flounder.
4. Fortified margarines - the functional components are plant Sterol and stanol
esters. What they do: Reduce total and LDL cholesterol for those persons
with elevated cholesterol. Foods: Fortified margarines such as Benecol, Take
Control, and SmartBalance. Replace your normal serving of margarine or
butter with fortified margarines.
5. Soy- the functional components are phytochemicals such as isoflavones and
genistein, and soy protein. What they do: May reduce total and LDL
cholesterol. Foods: Edamame, tofu, tempeh, miso, soynuts.
6. Tomatoes and tomato products - the functional component is the
phytochemical lycopene. What it does: The strongest evidence exists for
lycopene’s role in the reduction of prostate cancer, but it also may reduce
the risk of certain other cancers, and heart disease. Foods: Whole fresh or
canned tomatoes, crushed tomatoes, diced tomatoes, tomato paste, tomato
soup (low-salt), salsa, gazpacho.
7. Probiotics - the functional components are “Good for you” bacteria, typically
lactobacillus. What they do: Support gastrointestinal (GI) health, may boost
immunity. Foods: Yogurts supplemented with probiotics (look for a variety of
live active cultures), fermented vegetables, and fermented soy products (i.e.
tempeh).
8. Nuts - the functional components are monounsaturated fatty acids (healthy
fats) and vitamin E (antioxidant). What they do: May reduce the risk of
coronary heart disease. Foods: Walnuts, almonds, pecans, pistachios,
peanuts, cashews, hazelnuts, chestnuts, and Brazil nuts.
9. Grape Juice or Red Wine - the functional components is resveratrol. What
they do: Exhibit heart-healthy effects. Foods: 100% juice grape juice or
grape juice mixtures (i.e. Grape-Apple 100% juice mixtures); any variety of
red wine.
10. Leafy Greens - the functional components are phytochemicals such as
carotenoids, sulforaphanes, apigenin, and lutein/zeaxanthin. What they do:
Carotenoids block carcinogens from entering cells (cancer protective),
sulforaphanes and apigenin provide heart protection, lutein reduces
blindness in the elderly, and zeaxanthin enhances immune function. Foods:
Spinach, kale, collard greens, broccoli, broccoli rabe, broccoli sprouts,
arugula and other leafy greens
Nutraceuticals
Dr. Stephen De Felice coined the term ‘Nutraceutical’ and defined it as ‘food, or
parts of a food, that provide medical or health benefits, including the
prevention and treatment of disease’.
Another definition from the USDA is ‘diet supplement that delivers a
concentrated form of a perfumed bioactive agent from a food, presented in a
non-food matrix, and used to enhance health in dosages that exceed those that
could be obtained from normal –food’.
It include dietary supplements, those fortified foods that are enriched with
nutrients not natural to the food such as orange juice with added calcium,
functional foods and medical foods.
A nutraceutical is a product isolated or purified from foods that is generally
sold in medicinal forms not usually associated with foods. A nutraceutical is
demonstrated to have a physiological benefit or provide protection against
chronic disease.
They include;
 Minerals, vitamins and other dietary supplements
 Herbal products: garlic (allicin), ginger, echinacea, ginseng, liquorice,
onion, senna, turmeric (curcumin)
 Dietary enzymes: bromelain, papain
 Dietary fiber
 Hydrolyzed proteins
 Phytonutrients: resveratrol
 Carotenoids: lycopene
 Prebiotics
 Probiotics
Regulatory and perception issues
 Functional foods may carry either health claims, which are usually FDA
preapproved, or structure/function claims, depending on the most recent
regulations promulgated by FDA as a result of the Dietary Supplement
Health and Education Act of 1994. The FDA regulates medical foods
somewhat loosely within their own regulatory category.
 Health claims describe the relationship of diet to a disease, and only 11
health claims are approved by FDA. An example is, "Healthful diets with
adequate folate may reduce a woman's risk of having a child with a brain or
spinal cord defect.
 Structure/Function claims are statements of health-promoting or
nutritional benefit allowed on dietary supplement labels. They are not
allowed to mention disease conditions; they must describe the support or
maintenance of the normal functioning of the body. "Cranberry supports the
health of the urinary tract," is an example of a model structure/function
claim.
UNIT 7: NUTRITION SUPPORT
___________________________________________________________________________
Unit Objectives
Define terms used in nutrition support
Describe rationale of nutrition support
Describe the types of nutrition support
Explain the feeding routes used in nutrition support
Describe the complications of nutrition support
Visit a health facility to learn more about placing and handling of feeding tubes
and parenteral catheters and types of nutrition support formula.

Introduction to nutrition support

This refers to the provision of food and nutrients to the patient when the
conventional (oral) feeding methods are not adequate or cannot meet nutrition
needs. It includes Enteral and parenteral nutrition.
Enteral nutrition
The term enteral means “within or by the way of the GI tract”. Enteral
nutrition is a way of providing nutrition to the patients who are unable to
consume an adequate oral intake but have at least a partially functional GI
tract. Enteral feeding and tube feeding are used interchangeably.
It is a nutrition support therapy that involves provision of nutrients to the
gastrointestinal tract via a feeding tube, catheter, or stoma to maintain or
replete the patient’s nutritional reserves. It is the preferred route for the
provision of nutrition for patients who cannot meet their needs through
voluntary oral intake. Enteral nutrition may complement the diet or may be the
sole source of nutrition.
Enteral nutrition is provided by means of a feeding tube which is a medical
device used to provide nutrition to patients who cannot obtain nutrition by
mouth, are unable to swallow safely, or need nutritional supplementation. The
diameter of a feeding tube is approximately 0.33 millimeters. The feeding tubes
are classified by site of insertion and intended use. Enteral feeding involves the
use of liquid formula diets.
The aim is to provide adequate nutrition in order to prevent or reverse the
development of malnutrition in patients who are unable to ingest/derive
sufficient nutrients from ordinary foods despite having a functional
gastrointestinal tract (G.I.T).
Classification of Enteral feeding formula
Enteral feeding formula may be commercial preparations or blenderized
mixtures prepared from regular foods. In both, the nutrient composition must
be known or defined. Commercial preparations may be in liquid or in powder
form with instructions for reconstitution. Some formulas are nutritionally
complete and therefore can be used as the sole source of nutrients. Other
contains only specific nutrients and are thereby used as supplements to an
existing deficiency.
Enteral feeding formulas are basically classified into two groups based on the
form of the nutrients in the formula.
a) Intact formulas also referred to as polymeric diets. In these the
carbohydrates, protein and fats are in high molecular forms. Patients fed on
them should have full digestive capabilities. All slenderized mixtures
prepared from regular foods are in this category
b) Elemental/ hydrolysed formula also referred to as oligometric diet.
These are mainly commercial preparations in which nutrients are already
hydrolysed into lower molecular forms e.g. Carbohydrates into glucose,
fructose, malto-destrins, lactose etc., protein into mono-peptides and
dipeptides, fats into medium chain triglycerides and short chain
triglycerides. These feeds are of great benefit to patients with limited
digestive capacity.

NB: Enteral feeding formulas may also be classified according to the amounts
of the nutrients they contain. Standards feeds are designed for normal
requirements and provides1Kcal per ml with 15% of the total Kcal from protein
and 20% to 30% from fats. Calorie dense feeds may contain 2 Kcal per ml with
20% of the total Kcal from proteins and 25-35% from fats. The carbohydrate
content of these feeds should range from 45% - 55% of the total Kcal.
Some of the formulas may be disease specific, thereby carrying labels such as
low fat, lactose free, low sodium, low protein, sugar free etc.

Criteria for Formula Selection

There are a variety of enteral nutrition products on the market, many of which
have only subtle differences in composition. The following criteria should be
considered when selecting a formula:
i. Integrity of the patient’s gastrointestinal system
ii. Energy density: An energy density of 1 kcal/mL is considered standard.
Additional free water is usually necessary to meet fluid requirements.
Higher energy concentrations (1.5 to 2.0 kcal/mL) may be indicated when
fluid must be restricted or when feeding volumes sufficient to meet energy
requirements cannot be tolerated. Fluid-restricted, energy-dense
formulations should be considered for patients with acute respiratory
failure to prevent fluid accumulation and pulmonary edema.
iii. Osmolarity: It is the measure of the osmotically active particles per
kilogram of solvent in which the particles are dispersed. The size and
number of the nutrient particles in a solution defines its osmolality.
Products are available at isotonic osmolalities (300 mOsm/kg), moderate
osmolalities (400 mOsm/kg), and high osmolalities (700 mOsm/kg). The
main contributors to osmolality are sugars, free amino acids, and
electrolytes. Lipids are isotonic and therefore do not contribute to
osmolality. High-carbohydrate, amino acid–based, or peptide-based
formulas have moderate to high osmolality. Formula osmolality has not
been conclusively found to be a direct cause of diarrhea.
iv. Protein: Protein sources are intact proteins, peptides, or amino acids.
Generally, protein contributes 9% to 24% of total energy. High-nitrogen
formulas may not be well tolerated in patients with certain renal or
hepatic disorders. High-nitrogen concentrations can result in a higher
renal solute load and can predispose elderly patients to dehydration. One
gram of nitrogen requires 40 to 60 mL of water for excretion.
v. Fat: Fat sources are long-chain triglycerides (LCT) and Medium-chain
triglycerides (MCT). The fat content usually ranges from 3% to 35% of
energy for amino acid–based or peptide-based formulas and from 25% to
55% of energy for standard formulas. Fats do not contribute to osmolality.
Inclusion of MCT may be beneficial for patients who experience fat
malabsorption or maldigestion, since MCT do not require pancreatic
lipase for absorption, and intraluminal hydrolysis is more rapid and
complete than with LCT. The MCT do not supply essential fatty acids, and
they may cause complications for cirrhotic patients who have a limited
ability to oxidize MCT. The administration of MCT along with LCT
increases the total intestinal absorption of both types of fats, as compared
with the absorption of either fat administered alone.
vi. Carbohydrate: Carbohydrate is the most easily digested and absorbed
nutrient. Enzyme digestion is very efficient, as surface digestion is not
rate limiting (except with lactose). The transport process is the slowest
part of carbohydrate metabolism. Carbohydrate sources are
monosaccharides, oligosaccharides, and lactose. The carbohydrate
content of formulas ranges from 35% to 90% of energy. Longer
carbohydrate molecules exert less osmotic pressure, taste less sweet, and
require more digestion than do shorter ones. Glucose polymers are better
absorbed than free glucose and enhance absorption of calcium, zinc, and
magnesium in the jejunum. Some specialty formulas include fiber,
fructose, and/or fructo-oligosaccharides. Fructo-oligosaccharides occur
naturally in a variety of fruits and vegetables and provide sweetening at a
 lower cost than sucrose. Fructo-oligosaccharides are poorly absorbed by
the small intestine and fermented in the colon, where they promote the
growth of healthy species of bacteria.
vii. Lactose: Lactose is present in milk-based formulas and some blenderized
formulas. Most commercial formulas are lactose free. Due to the
presumed high incidence of secondary lactase deficiency in illness, lactose
is not present in most enteral formulas
viii. Residue: Milk-based formulas and other formulas with intact nutrients
are generally low residue. Blenderized and fiber-supplemented formulas
leave a moderate to high residue.
ix. Renal solute load: The main contributors to renal solute load are protein,
sodium, potassium, and chloride. Excessive solute burden on the kidneys
from an enteral formula can result in concomitant excess excretion of
water and dehydration. This can be significant factor with high-protein
formulas since urea is the excretion product of protein metabolism and
contributes heavily to solute load.
x. Fiber: Fiber is added to enteral formulas for a variety of potential health
benefits. Soluble fibers, such as guar gum, oat fiber, and pectin, are
fermented to short-chain fatty acids, which are easily absorbed by the
gastrointestinal mucosa
xi. Sodium and potassium: Select formula according to the patient’s
nutrition prescription and laboratory profile.
xii. Safety: A ready-to-use closed bag or system is recommended, as it is
more sterile and provides less risk for contamination than canned or
powdered products. Formulas that are made in a blender in the facility
are discouraged because they carry a greater risk of infection, require
careful handling, tend to clog tubes, and need a high volume to meet
nutrient needs.
xiii. Viscosity: Blenderized, high-fiber, and high-density formulas should not
be administered through tubes with a diameter smaller than ‘10 French’
unless a pump is used. Formulas may flow through an 8-French diameter
tube when a pump is used.
xiv. Vitamin K: Patients who are receiving enteral nutrition support while on
anticoagulant therapy should be monitored closely. Significant vitamin K
intake from enteral formulas can antagonize the effect of the
anticoagulant drug warfarin and result in treatment failure. Most enteral
 formulations contain modest amounts of vitamin K and provide daily
vitamin K intake similar to the average dietary intake from foods.
Consistent intake of an enteral formulation containing less than 100 mcg
of vitamin K per 1,000 kcal is not expected to cause warfarin resistance.
xv. Cost: Amino acid–based formulas and peptide-based formulas are usually
more expensive than synthetic formulas containing intact nutrients

Indications for enteral nutrition

Enteral nutrition support is required in the following situations where there is:
i) Decreased oral intake due to physical impairment as in; cerebral vascular
accidents, oralpharyngeal/oesophageal disorders, trauma and coma,
neurological disorders such as demyelinating diseases, and psychological
conditions such as anorexia nervosa, depression etc.
ii) Increased nutrients requirements such as in case of trauma, surgery,
burns, sepsis, cancer, malnutrition etc.
iii) Impaired gastrointestinal capabilities such as inflammatory bowel
syndrome, short bowel syndrome, malabsorption, fistulas, pancreatitis etc.
iv) Decreased oral intake, anticipated less than 50% of required nutrient intake
orally for 7-10 days as seen in severe dysphagia (difficulty swallowing),
metabolic stress, major bowel resections, low-output fistulas and coma.
v) Neurological disorders and psychological conditions
vi) Malnourished patients expected to be unable to eat > 5 Days
vii) Normally nourished patients expected to be unable to eat >5 days
viii) Adaptive phase of short bowel syndrome
ix) Following severe trauma or burns

Tube feeding routes (route of access)

The decision regarding the type of feeding route/tube depends on:
 The patient’s medical status
 The anticipated length of time that the tube feeding will be required.
 Degree of risk for aspiration
 Presence or absence of normal digestive processes
 Whether or not there is a planned surgical intervention
Tube feeding routes include;
1. Mechanically inserted tubes
Feeding tubes may be mechanically inserted as follows;
 Nasogastric; nasogastric feeding tube (NG-tube) is passed through the
nares (nostril), down the esophagus and into the stomach. This type of
feeding tube is generally used for short term feeding, usually less than a
month, though some infants and children may use an NG-tube longterm.
The primary advantage of the NG-tube is that it is temporary and relatively
non-invasive to place, meaning it can be removed or replaced at any time
without surgery. NG-tubes can have complications, particularly related to
accidental removal of the tube and nasal irritation.
 Nasojejunal; A Nasojejunal tube is similar to an NG-tube except that it is
threaded through the stomach and into the jejunum, the middle section of
the small intestine.
 Nasoduodenal tube may be placed into the duodenum, the first part of the
small intestine. ND and NJ - tubes are used for individuals who are unable
to tolerate feeding into the stomach, due to dysfunction of the stomach,
impaired gastric motility, severe reflux or vomiting. These types of tubes
must be placed in a hospital setting.
2. Surgically inserted tubes
Feeding tubes may also be surgically placed under general anaesthesia. For
example;
 Oesophagostomy; a surgical opening is made at the lower neck through
which a feeding tube is pushed into the stomach e.g. in case of neck
surgeries and cancer.
 Gastrostomy; A gastric feeding tube is a tube inserted through a small
incision in the abdomen into the stomach and is used for long-term enteral
 nutrition
 Jejunostomy; A jejunostomy feeding tube is a tube surgically or
endoscopically inserted through the abdomen and into the jejunum (the
second part of the small intestine).
Methods of Enteral Feeding Administration
There are three methods of tube feeding administration: continuous drip;
intermittent drip; and bolus. The method selection is individualized to patient
needs. One method can serve as a transition to another method if
hyperosmolarity is a factor
1. Continuous feeding/delivery/drip
Continuous feedings require that the enteral formula be administered at a
controlled rate with a pump over a 24-hour period. The pump should deliver the
controlled rate within 10% accuracy and be calibrated periodically to ensure
accuracy. It’s indicated for unstable critically ill patients, patients unable to
tolerate high-volume feedings, patients with malabsorption, and patients at
increased risk for aspiration.
Once a formula has been selected and a goal volume to meet estimated needs is
determined, the final rate, in milliliters per hour, is set by dividing the total daily
volume by the number of hours per day of administration (usually 18-24 hr)
Continuous drip can also be accompanied by the use of gravity: a roll bar clamp
on the tubing connecting the bad to the feeding tube adjusted to a drip rate.
This method is difficult to control with any degree of accuracy.
Advantages:
 Allows the lowest possible hourly feed rate to meet nutrient requirements
 Better gastrointestinal tolerance due to the lower feed rate
 Better control of blood glucose levels due to continuous carbohydrate
input
Disadvantages:
 Physical attachment to the feeding apparatus (may affect quality of life)
 Expense of equipment (pump and giving sets)
2. Intermittent or cyclic feeding/delivery
Intermittent or cyclic feedings are administered over an 8- to 20-hour period by
using a pump to control the rate of delivery. It involves infusion of 400 – 500 ml
of formula by gravity, over approx. 30 min – 1 hour 3 to 4 hourly/day
This method of tube feeding is most beneficial for patients who are progressing
from complete tube feeding support to oral feedings as discontinuation of
feedings during the day may help to stimulate the appetite. It is also beneficial
for ambulatory home-care patients who are unable to tolerate bolus feedings
because it allows freedom from the pump and equipment. Since this method of
delivery usually requires a higher infusion rate, monitoring for formula and
delivery tolerance is necessary. Formula and delivery intolerance can be avoided
by a gradual transitioning of the patient from continuous feeding to an
intermittent feeding schedule.
Advantages:
 Allows greater patient mobility (may improve quality of life)
 Allows breaks for physical activity, for administration of medications that are
incompatible with feeds, and to encourage oral intake if applicable.
 Useful in the transition from continuous to bolus feeding, or from tube
feeding to oral intake.
 Daytime feeds may reduce aspiration risk if it is difficult to maintain a 30°
elevation overnight
 Feeding during daytime only is more physiological and may therefore have
benefits such as helping to re-establish the diurnal cycle; promoting normal
gastrointestinal motility17 and promoting re-acidification of the stomach
(which protects against bacteria). There is no evidence for a benefit of ‘gut
rest’, however.
Disadvantages:
 Compared with continuous feeding, a higher infusion rate is required to
provide the same volume of feed. This may be less well-tolerated, with a
higher risk of problems such as reflux, aspiration, abdominal distension,
 diarrhoea and nausea.
3. Bolus formula delivery not requiring a pump
The syringe bolus-feeding method involves the delivery of 240 to 480 mL of
formula via a feeding tube over a 20- to 30-minute period, three to six times a
day, to meet estimated nutritional requirements. This method is usually
restricted to gastric feedings and may be contraindicated in patients who have
a high risk of aspiration, disorders of glucose metabolism, or fluid
management issues.
Advantages:
 Physiologically similar to a typical eating pattern
 Allows greater patient mobility
 Convenient for gastrostomy feeding
 Can be used to supplement oral intake
 Can be flexible to suit the patient’s lifestyle and improve quality of life
 May facilitate transition to oral intake
 Avoids the use of expensive equipment
Disadvantages:
 Large boluses may be poorly tolerated, especially in small bowel feeding
 Requires more nursing time compared with pump-controlled feeding
 Highest risk of aspiration, reflux, abdominal distension, diarrhoea and
nausea

Enteral Feeding Formula and Equipment Handling Guidelines

1. Formula handling
 Care should be taken to ensure that the tube feeds meet the patient’s
nutrient requirements
 Prescribe intervals and volumes of feeding should be adhered to
 Shake/stir mixtures before use.
 Bring formula to room temperature before feeding, but do not allow the
formula to remain unrefrigerated for more than 12 hours. Cold mixtures can
 cause diarrhea
 The hang time for formula in an open system should be less than 8 hours or
as specified by the manufacturer. Formula from a closed system is provided
in ready-to-hang, prefilled containers and may hang for 24 to 48 hours per
manufacturer’s guidelines. Discard any formula remaining in the container
after the hang time has expired.
 Opened, unused formula should be kept refrigerated for no longer than the
manufacturer’s specifications (usually 24-48 hours)
 In the absence of the refrigeration, quantities lasting only six to twelve hours
should be prepared
2. Formula delivery equipment guidelines
 Ensure proper placement of tube and feed at a slow constant rate
 Irrigate the tube every 4 hours with 20 to 30 mL of warm sterile water or
saline to ensure patency for continuous feeding. Also, irrigate the tube
before and after each intermittent feeding or medication administration.
 To reduce bacterial contamination, flush water through the bag and tube
every 8 hours before adding new formula when an open system is in
place.
 Avoid putting food and beverages into the tube (eg, juice, milk, and soda).
 Flush tube with purified sterile water or saline before and immediately
after the administration of medicines to avoid clogging the tube.
 To reduce the risk of contamination and infection, the feeding bag should
be properly labeled, and tubing should be changed every 24 hours or as
specified by the manufacturer

Gastrointestinal Complications of Tube Feeding

Gastro  Diarrhea
intestinal  Constipation
complications  Nausea/Vomiting
 Malabsoption/maldigestion
 Abdominal distention s
Mechanical  Tube placement
 Tube clogging
complications  Esophageal erosion
 Nasopharyngeal irritation
Metabolic  Fluid and electrolyte imbalance, trace element, vitamin and
complications mineral deficiencies, essential
 Hyperglycemia
 Tube feeding syndrome
 Hypernatremia (dehydration)
 Hyponatremia (over-hydration)
Pulmonary  Pulmonary aspiration
complication
Approaches for Management of Gastrointestinal Complications of Tube
Feeding
Problem Approaches
Diarrhea  Evaluate medication profile (eg, laxatives, stool softeners,
antibiotics, medications containing magnesium, or elixirs
containing sorbitol, such as acetaminophen or theophylline).
 Check for Clostridium difficile.
 Consider different formula
 Try soluble fiber–containing formula with guar gum, or add
soluble fiber to the medication regimen for patients with a low
risk for bowl ischemia or bowel dysmotility)
 Consider antidiarrheal medications such as loperamide,
diphenoxylate, or paregoric if C. difficile or other infectious
complications are ruled out.
 Use continuous infusion administration. Implement continuous
enteral feedings
 Check osmolarity of feeds (< 500mosl/l recommended/Try
isotonic or peptide-based formula.
 Check flow rate of feed
 Slow feeding rate
 Observe proper sanitation.
 Consider use of prebiotics and probiotics
Nausea,  Evaluate medication profile (eg, opiate analgesics or
gastroparesis/ anticholinergics).
delayed gastric  Consider low-fat or isotonic formula.
emptying  Reduce the rate of infusion by 20 to 25 mL/hour, or try small
bolus feedings of 50 to 100 mL
 Try motility medications such as a prokinetic agent (eg,
metoclopramide or erythromycin)
 Administer formula at room temperature
 Check and evaluate gastric residual volume prior to each bolus
feeding or every 4 hours for continuous feeding
 Check for fecal impaction.
 Try antiemetic medications if gastric residual volumes are
normal.
 Discontinue feeding until underlying condition is managed
 Change to polymeric feeds if on elemental diet
Hyperglycemia  Monitor blood glucose levels. The target glucose goal is 100 to
150 mg/dL for nondiabetic critically ill patients and 140 to 180
mg/dL for diabetic critically ill patients. The target glucose goal
for medically stable patients with diabetes is <140 mg/dL with
random blood glucose levels <180 mg/dL. Most critically ill
patients with diabetes require intravenous insulin to achieve the
 desired glucose range without increasing the risk for
hypoglycemia. More stringent targets may be appropriate in
stable patients with previously tight glycemic control. Less
stringent targets may be appropriate in patients with severe
comorbidities.
 Avoid overfeeding. Evaluate total energy compared to estimated
requirements
 Consult with physician regarding the need for intravenous
insulin administration in patients who experience persistent
hyperglycemia.
Dehydration  Use less concentrated formula.
 Supplement with additional water as needed.
Clogged tube  Check for proper tube size (viscous formulas should be
administered through a >10-French catheter).
 Flush tube with warm water (usually 20 to 30 mL) regularly and
before and after administration of medicines.
Constipation  Monitor hydration status.
 Add free water.
 Consider fiber-containing formula with extra free water (>1 mL
free water/kcal).
 Consider adding soluble or insoluble fiber medication with extra
free water.
 Increase physical activity if possible.
 If hydration is adequate and other causes are ruled out, consider
a stool softener (docusate sodium or docusate calcium),
emollients, or laxative.
Essential  Add 5 mL of safflower oil daily, or provide at least 4% of energy
fatty acid needs as linoleic acid
deficiency  Change formula to one that contains essential fatty acid.
Overhydratio  Check fluid input and output.
n,  A weight change of 0.2 kg/day or more reflects a change in
rapid/excessi extracellular fluid volume
ve weight  Consider fluid-restricted formula based on fluid/volume status
gain and medical issues.
Abdominal  Check gastric residual volume. If two consecutive measurements
distention are > 500 mL, decrease or hold feedings until possible causes are
assessed, or follow organization-specific protocols for gastric
residual volume targets and intervention strategies
 Check for constipation, fecal impaction, or obstruction.
 Place feeding tube in distal duodenum or proximal jejunum
Aspiration  Maintain the head of the patient’s bed at a 30˚ to 45˚ angle
risk during feedings
 Post-pyloric placement of the feeding tube tip at or below the
Ligament of Treitz may be beneficial for patients who are supine
or heavily sedated Consider the use of motility agents such as
 prokinetic medications (metoclopramide and erythromycin) or
narcotic agonists if clinically feasible.
 Implement continuous enteral feedings
Advantages of enteral nutrition
 There is stimulation of G.I hormones and consequent regulated metabolism
and utilisation of nutrients
 It ensures adequate nutrients supply to the mucosal wall, and protection
against atrophy of intestinal villi
 It offers physiological protection against ulcers due to its buffering effect from
gastric acids
 Intake easily/accurately monitored
 Provides nutrition when oral is not possible or adequate
 Costs less than parenteral nutrition
 Supplies readily available
 Reduces risks associated with disease state
 Decreases likelihood of bacterial translocation
N/B: Enteral nutrition therefore should be considered before attempting
parenteral nutrition for patients with a functional G.I.T unless where
contraindicated.

Disadvantages of enteral nutrition

 Complications from tube feeding, such as minor or major bleeding,
infections, tube problems or death
 May become agitated with the tube
 Feeding tube may limit where patient can receive care
 Can be dangerous if inserted into the airway instead of the food pipe.
 GI, metabolic, and mechanical complications—tube migration; increased risk
of bacterial contamination; tube obstruction; pneumothorax
 Costs more than oral diets
 Less “palatable/normal”
 Labor-intensive assessment, administration, tube patency and site care,
monitoring
Contraindications for enteral nutrition
Enteral nutrition support should be avoided in patients who do not have an
adequately functioning gastrointestinal tract or who are hemodynamically
unstable. Specific contraindications include:
 Intestinal obstruction that prohibits use of intestine
 Intractable vomiting
 Peritonitis
 Severe diarrhea
 High output of enterocutaneous fistula (greater than 500 Ml/day) between
the GI tract and the skin
 Severe acute pancreatitis
 Inability to gain access
 Short-bowel syndrome (less than 100 cm of small bowel remaining)
 Aggressive therapy not warranted
 Severe inflammatory bowel disease
 Upper gastrointestinal hemorrhage (caused by esophageal varices, portal
hypertension, or cirrhosis)
 Paralytic ileus
 A prognosis that does not warrant aggressive nutrition support
 Intestinal obstruction (depending on location)
 Shock
Parenteral nutrition
It is a form of nutrition support delivered directly into the systemic circulation
i.e. intravenously, bypassing the gastro-intestinal tract (GIT) and the first
circulation through the liver. The person receives nutritional formulae that
contain nutrients such as glucose, amino acids, lipids and added vitamins and
dietary minerals that is infused directly into the blood stream.
Its primary objective is to maintain or improve the nutritional and metabolic
status of patients who have temporary or permanent intestinal failure.
Key factors influencing the decision for parenteral nutrition
i) Anticipated time frame for the use of parenteral nutrition
ii) Total nutrient needs, which define the relative hyperosmality of the required
solution and whether it can be given through a peripheral vein or requires a
central vein
iii) Capacity to handle fluid volume
iv) Condition of peripheral veins. If the patient’s peripheral veins are in good
condition and nutrient needs are not high, peripheral parenteral nutrition
may be indicated. If nutrient needs are high and central access is required
for approximately 1-6 weeks, a percutaneously placed central venous
catheter is usually employed. For long term infusions, implanted vascular
devices are inserted using surgical or fluoroscopic techniques

Indications for Parenteral Nutrition

Parenteral nutrition is indicated for patients with inability to eat and absorb
nutrients via GI tract due to;
 Nonfunctioning G.I tract
 Disease of the small intestine
 Massive small bowel resection
 Radiation enteritis
 Chemotherapy reaction
 Bone marrow transplantation
 Intractable vomiting/diarrhoea
 Moderate to severe pancreatitis
 Severe malnutrition or 10 -15 % loss of body weight due to nonfunctioning
G.I tract
 Nil by mouth for more than 5 days for severely catabolic patients with or
without malnutrition.
 Fistula in the gastro intestinal tract
 Excessive nutritional needs which cannot be met by enteral feeding e.g. burn
 or multiple trauma
 Refusal to eat as in anorexia
Methods of parenteral nutrition
The methods used in PN depend on the person’s immediate medical and
nutrient needs, nutrition status and anticipated length of time on IV nutrition
support. They include:
1. Peripheral Parenteral Nutrition (PPN)
2. Total/Central Parenteral Nutrition (TPN)
The general decision to use PPN instead of TPN are based on comparative
energy demands anticipated time of use.
1. Peripheral Parenteral Nutrition
This involves the use of peripheral veins to provide a solution that meet
nutrient needs for infusion. It has lower dextrose (5% to 10% final
concentration) and amino acid (5% final concentration) concentration than
TPN.
It may provide full or partial nutritional requirements to patients. PPN can be
administered in to peripheral veins if solutions used have osmolality below 800
- 900mosm/l for a brief period of less than 14 days. Short catheters (cannulas)
and mid-way catheters are normally used. However, PPN administration is
possible for several weeks with fine bore catheter.
PPN may be used in patients with mild or moderate malnutrition to provide
partial or total nutrition support when they are not able to ingest adequate
calories orally or enterally or when central vein PN is not feasible. All in one
admixture are highly recommended compared to the single bottle system
during PPN.
2. Total/Central Parenteral Nutrition (TPN/CPN)
CPN is often referred to as “Total Parenteral Nutrition” since the entire nutrient
needs of the patient may be delivered by this route.
It requires a central venous system for long term infusions. The sites mainly
used are the Vena jugularis external, Vena jugularis internal, Vena subclavia,
Vena cephalica and Vena basilica for solutions with osmolarity above 800 - 900
mosm/l.
Fluid/volume requirements
The fluid requirement/allowance determines the volume of dextrose needed in
designing parenteral feeding regimes. Generally an adult patient needs 30-50ml
fluid per kg body weight/day. Extra fluid is added for abnormal fluid losses, e.g.
fever, stomal losses, diarrhoea, etc.
Electrolytes
In absence of any fluid or electrolyte abnormalities, a standard electrolyte
solution is usually recommended. However, electrolyte dosage should be
individualized and adjusted according to the patient’s diagnosis, serum
electrolyte concentration, renal function, and other modifying factors.
Vitamins and minerals
Multivitamin formulations containing both fat-soluble and water-soluble
vitamins may be incorporated into intravenous infusions. Patients with
increased vitamins requirements may be given multiples of the daily dosage.
Consequently, certain essential parenteral trace-element supplements may be
administered intravenously.

Metabolic complications of parenteral nutrition

Complication Causes Symptoms Treatments
Hyperglycemia  Trauma Elevated With persistent hyperglycemia,
 Infection blood provide insulin when necessary

 Diabetes glucose to maintain blood glucose levels

mellitus level of 100 to 150 mg/dL in

 Excessive critically ill patients.

dextrose In diabetic patients, the plasma

administration goal is 140 to 180 mg/dL for

 Corticosteroids the majority of critically ill

or patients and <140 mg/dL for

immunosuppre non-critically ill patients with

 ssive therapy random blood glucose targeting
levels <180 mg/dL. More
stringent targets may be
appropriate in stable patients
with previously tight glycemic
control. Less stringent targets
may be appropriate in patients
with severe comorbidities.
The rate of dextrose infusion in
parenteral nutrition (PN) should
not exceed 4 to 5 mg/kg per
min.
Hypoglycemia Sudden cessation Low blood If managed on insulin, decrease
of PN glucose insulin administration.
Excessive insulin level (<70 Give intravenous dextrose.
administration mg/dL) Avoid the abrupt cessation of
Headache PN. Studies show that
Sweating hypoglycemia is equally
Thirst prevalent in non-diabetic
Disorientati patients due to stress. Taper PN
on solution for 1 to 2 hours. If PN
Convulsions must be discontinued quickly,
Coma 10% dextrose should be infused
for 1 or 2 hours following PN
discontinuation. Check the
capillary blood glucose
concentration 30 min to 1 hour
after the discontinuation of PN
to identify rebound
hypoglycemia
Hyperglycemic Dehydration from Lethargy Discontinue PN.
hyperosmotic osmotic diuresis Stupor Initiate rate of half of the
syndrome (type 1 diabetes Convulsions estimated needs or
 mellitus) Blood approximately 150 to 200 g (or
Poor intake of glucose 100 g/day if severe
water (occurs in level >600 hyperglycemia) for the first 24
elderly patients mg/dL (6-7) hours until tolerance is
with type 2 Serum documented.
diabetes mellitus) osmolality Provide insulin to correct the
>350 blood glucose level.
mOsm/L Carbohydrate administration
should not exceed a rate of 4 to
5 mg/kg per min
Azotemia Dehydration High blood urea Increase
Renal insufficiency nitrogen level administration of
Excessive protein free fluid.
administration or Reduce amino
inadequate nonprotein acid dose.
energy Patients with
impaired renal or
hepatic disease
may require
dialysis.
Hypophosphat Alcoholism Anorexia Increase
emia Intractable vomiting Muscle weakness phosphorus in
Inadequate intake Paresthesias PN solution
Refeeding syndrome Long bone pain based on
Vitamin D deficiency Coma individual
Hyperparathyroidism Respiratory medical needs.
distress If refeeding
syndrome
occurs, modify
the amount of
energy provided
by carbohydrates
(15 to 20 kcal/kg
 per day) until
electrolytes are
stable.
Cholestasis Disuse of gastrointestinal Elevated total Reduce total
tract bilirubin level >2 energy provided.
Overfeeding mg/dL (1) Decrease
Long-term use of PN Elevated alkaline dextrose to <5
Excessive use of phosphatase level mg/kg per min.
intravenous fat emulsions and gamma- Decrease IVFE to
(IVFE) glutamyl <1 g/kg per day.
transpeptidase Consider cyclic
level PN infusion.
Steatosis Overfeeding Elevated Consider cyclic
(hepatic Essential fatty acid aminotransferase PN infusion.
accumulation) deficiency level Decrease total
energy provided.
Balance dextrose
energy with
energy from fat.
Decrease
dextrose to <5
mg/kg per min.
If essential fatty
acid deficiency
occurs, treat with
lipid infusions.
Hypomagnese Malabsorption Muscle weakness Increase Mg in
mia Massive small bowel Depression PN.
resection Apathy Provide
Acute pancreatitis Nausea additional
Prolonged nasogastric Vomiting intravenous
suction Irritability supplementation.
Intestinal fistula Vertigo If refeeding
 Vomiting Ataxia syndrome
Refeeding syndrome Muscle tremor occurs, modify
Hypocalcemia the delivery of
Hypoparathyroidis energy from
m carbohydrates
(15 to 20 kcal/kg
per day) until
electrolytes are
stable.
Hypermagnese Excessive Mg Drowsiness Decrease Mg in
mia administration Weakness PN
Renal insufficiency Nausea
Vomiting
Cardiac arrhythmia
Hypotension
Hyponatremia Fluid overload Decreased serum Evaluate free-
Excessive gastrointestinal Na levels and water intake and
loss osmolality total volume
Excessive urinary loss Irritability status
Adrenal insufficiency Confusion considering
Congestive heart failure Seizures disease state and
Syndrome of underlying
inappropriate antidiuretic causes. If the
hormone secretion volume is
excessive (e.g.,
free water,
intravenous
fluids), decrease
fluid intake
and/or adjust
free-water
volume. If the
volume is
 deficient,
increase water
and Na. Adjust
Na intake as
condition
dictates.
Hypernatremia Dehydration Increased serum Evaluate for
Excessive Na intake Na level dehydration or
Osmotic diuresis Convulsions deficit of water or
Hypoglycemia Irritability total volume.
Hypocalcemia Restlessness Increase free-
Head trauma Coma water or fluid
Antidiuretic hormone intake as
deficiency appropriate.
Evaluate
intravenous
sources and
consider
decreasing Na if
excessive.
Hyperphospha Renal insufficiency Elevated serum Decrease
temia Excessive phosphorous phosphorous level phosphorous in
administration PN.
Hypokalemia Inadequate K+ intake Ileus Consider
Diarrhea Cardiac arrhythmia additional
Intestinal fistula intravenous
Anabolism supplementation.
Metabolic alkalosis If refeeding
K+-wasting medications syndrome
Vomiting occurs, modify
Refeeding syndrome the delivery of
energy from
carbohydrates
 (15 to 20 kcal/kg
per day) until
electrolytes are
stable.
Hyperkalemia Renal insufficiency Cardiac arrhythmia Decrease K+ in
Excessive K+ Paresthesias PN (also consider
administration decreasing K+
Medication from other
(spironolactone) intravenous
sources).
Provide K+
binders and
antagonists.
K+ > 5.5 mEq
may warrant an
electrocardiogra
m
Hypocalcemia Hypoalbuminemia Paresthesias Increase Ca2+ in
Inadequate vitamin D Tetany PN. (Use caution
intake Muscular and follow
Hypoparathyroidism cramping/ spasms protocols to avoid
Inadequate Ca intake Ca2+–
Increased gastrointestinal phosphorus
losses precipitation.
Inadequate phosphorus Evaluate ionized
intake calcium level or
High protein dose adjusted total
Metabolic acidosis serum Ca2+ if
hypoalbuminemi
c prior to
increasing Ca2+
in PN.)
Ensure adequate
phosphorus (20
to 40 mmol) in
PN.
Evaluate protein
(>2 g/kg per day
associated with
increased urinary
excretion of
calcium).
Ensure adequate
acetate and Mg
in PN.
For critically ill
patients or
patients with
hypoalbuminemi
a it is preferable
to evaluate
ionized calcium
levels. Ionized
calcium is
unaffected by
changes in
serum albumin
levels and
provides a more
accurate
assessment of
calcium status in
critically ill and
patients receiving
specialized
nutrition support
 .
Hypercalcemia Excessive vitamin D Thirst Evaluate Ca2+ in
administration Polyuria PN.
Prolonged immobilization Decreased appetite Ensure adequate
Stress Nausea hydration.
Hyperparathyroidism Vomiting Provide
Malignancy Itching intravenous
Muscle weakness hydration using
0.9% sodium
chloride at 200 to
300 mL/hour
when calcium
>13 mg/dL.
After adequate
hydration,
furosemide can
be used to
increase renal
calcium
excretion.
Hypertriglyceri Overfeeding with dextrose Triglyceride level Reduce dose or
demia Rapid administration of >400 mg/dL lengthen the
IVFE >110 mg/kg per (1,3,10) IVFE infusion
hour (1) Impaired immune time.
Intravenous infusion of response Provide <30% of
propofol (Diprivan), which Pancreatitis (risk energy from
has the same lipid occurs when the IVFE, or provide
content as IVFE providing triglyceride level 1 g/kg per day
1.1 kcal/mL (11) exceeds 1000 and infuse slowly
mg/dL) (1) (no less than 8 to
10 hours).
Avoid excessive
dextrose
administration.
Advantages of parenteral feeding
 Ease of administration
 Easier correction of fluid and electrolyte disturbances
 Allows nutrition support when GI intolerance prevents oral or enteral
support
 Ease of administration
 Provides nutrients when less than 2 to 3 feet of small intestine remains

Disadvantages of parenteral feeding

 High financial cost
 Catheter-associated infections
 Fluid overload
 Hyperglycemia
 Catheter-associated thrombosis
 Hepatic dysfunction
 Promotes enterocyte atrophy leading to loss of gut barrier function
 Blood electrolyte abnormalities
 Additional nursing time for nonclinical activities
UNIT 8 : DRUG-NUTRIENT INTERACTIONS
___________________________________________________________________________
Unit Objectives
Define terms used in drug-nutrient interactions
Explain the effects of drugs on nutrients
Explain the effects of nutrients on drugs
Research on drugs commonly used in Kenya in managing Communicable and
Non-Communicable conditions of public health concern

Introduction to drug-nutrient interactions

The term food-drug interactions and drug- nutrient interactions are mostly
used interchangeably. Drug therapy plays an important role in disease
management and influence nutrient intake, absorption, metabolism and even
excretion. Food, nutrients or other components on the other hand may affect
the absorption, metabolism and excretion of drugs. Serious side effects may
occur if drugs interact with nutrients or other dietary components. It is
therefore necessary to understand their relationships and maximize their
utility by planning well.
Definition of terms
Drugs - WHO defines a drug as a substance or product that is used or
intended to be used to modify or explore physiological systems or pathological
state mainly for the benefit of the recipient. It is a simple chemical substance
that forms an ingredient of medicine that would cure a disease i.e. active
ingredient. They are used for the purpose of cure, prevention and relieve of
pain.
Medicine contains many substances that are used to deliver a drug e.g. a
stabilizer, water, preservative, emulsifier, colour etc. many drugs have the
potential to affect and be affected by nutrition.
By law drugs are divided into two categories i.e. prescription and over-the-
counter drugs.
a. Prescription drugs; these are drugs usually given to treat serious
conditions and may cause severe side effects. For these reasons, they are
sold by prescription only which ensures that a physician has evaluated
the patient’s medical condition and determined that the benefits of using
the medication outweighs the risks of incurring the side effects.
b. Over-the-counter (OTC) drugs; these are drugs that can generally be
used safely and effectively without medical supervision. People use them
to treat less serious illnesses that are easily self-diagnosed e.g.
analgesics such as aspirin, panadol, used to treat headache or antacids
to combat indigestion.
Law regulates labels on OTC drugs to make sure that they provide accurate
information about the drugs appropriate uses and dosage and potential side
effects. Prescription drugs considered safe enough for self-medication are
frequently switched to OTC status, sometimes smaller doses then are available.
Drug – nutrient interaction refers to an interaction resulting from a physical,
chemical, physiologic, or pathophysiologic relationship between a drug and a
nutrient, multiple nutrients, food in general, or nutritional status.
Pharmacology – study of drugs and their interactions with systems. In order
for a drug to achieve the pharmacologic action for which it is administered, it
must move from the site of administration through the blood stream and finally
to the target site of action. It is divided into pharmacokinetics and
pharmacodynamics.
Pharmacokinetics – it is the study of what the body does to the drug. The four
basic pharmacokinetic processes include absorption, distribution, metabolism
and excretion of the drug.
Pharmacodynamics - it is study of biochemical and physiologic effects of a
drug i.e. what the drug does to the body.
Absorption – process of movement of the drug from the site of administration
to the bloodstream and is dependent on route of administration, chemistry of
the drug and rate of gastric emptying.
Risk factors for food –drug interaction
 Long term and multiple use of drugs as in treatment of chronic diseases
 Old age due to increased exposure to drugs for treatment of chronic
conditions, decreased efficiency of nutrient absorption, poor compliance,
inefficiency in drug handling, increased variability in their response to
drugs, and the possibility of their drugs being more toxic. Many of the
elderly suffer from chronic diseases e.g. CVDs, diabetes etc. and have to
take several drugs for prolonged period, their food intake is often
inadequate, they take wrong drugs at times due to mental confusion, illness
or lack of drugs, thus they need assistance to avoid adverse drug-nutrient
interaction, their drugs are likely to be toxic, they respond to drugs with
greater variability and they are less capable of handling drugs sufficiently.
 Pregnancy, (for both mother and foetus), and infancy due to elevated
requirements for many nutrients. In addition, increased concentration of the
 transport proteins for most drugs results in increased drug concentration in
the foetus.
 Genetic variation in drug transporters, enzymes or receptors
 Impaired organ function
 Malnutrition. Protein alteration and changes in body composition secondary’
to malnutrition may affect drug disposition by altering protein binding and
volume of distribution. Also drug oxidation rate is impaired in severe
malnutrition and elimination protein-bound drugs are much faster due to
due to lack of protein-binding in plasma.
 Body composition distribution of fat soluble drugs is increased in the obese
and the elderly whose proportion of adipose tissue to lean body mass is
greater than in young individuals.
Effects of drugs on nutrients
Drugs can affect nutrients and conversely nutrition status in one of the
following ways:
1. Drugs altering appetite and food intake
2. Drugs influencing absorption of nutrients
3. Drugs influencing metabolism and excretion of nutrients
1. Drugs that alter appetite and food intake
Drugs which affect appetite and hence food intake are;
a) Anorexic drugs; there are drugs that reduce or depress appetite. These
drugs are used to manage conditions like obesity. It diminishes appetite in
obese subjects so that they will eat less food. It functions on the centers of
controlling appetite. Examples include;
i. Selective serotonin reuptake inhibitors (antidepressant) which
causes anorexia and weight loss. They include; Floxeone and Prozac
ii. Amphetamines; acts as a stimulant of the CNS and have the effects of
depressing desire for food thus leading to a marked loss of weight.
N/B- long-term use leads to addiction.
iii. Alcohol (abuse); this can lead to appetite loss, reduced food intake and
malnutrition. Anorexia which stems from effects of alcoholism e.g.
gastritis, hepatitis, pancreatitis, alcohol brain syndrome, drunkardness
and withdrawal syndrome.
b) Drugs affecting taste sensation and smell; these drugs bring about
alteration in taste sensitivity. The effects may be abnormal taste like
dysgeusia i.e. reduced ability of taste sensation or hypogeusia i.e.
unpleasant after taste or ageusia i.e. lack of taste sensation.
These effects on taste and smell are brought about by;
i. Radiotherapy; used to treat carcinoma of the mouth, tongue and
tonsillitis which damage the taste buds
ii. Chemotherapy; this involves the use of cancer chemotherapy
agents e.g. 5-fluorouracil which results in altered bitter and sour
taste and increased sweet sensitivity.
iii. Clofibrate which is a cholesterol binding agent in the GIT which
leads to decreased sensitivity.
N/B: Zinc deficiency also causes hypogeusia and dygeusia which can be
cured by supplementing the diet with zinc sulphate.
c) Drugs causing nausea and vomiting;
The common side effect of many drugs is nausea and vomiting. These drugs
include; Nitrofuradantin used for the treatment of urinary infection which
causes nausea and vomiting as well many drugs used in chemotherapy of
cancer. These drugs can be counteracted by taking anti-vomiting drugs.
d) Appetizers;
These drugs stimulate appetite and help in weight gain. They include;
i. Several tonics; these contain gastric stimulation and B-vitamins which are
prescribed by doctors to improve the appetite of patients suffering from
various diseases. These tonics normally improve the appetite and increase
the food intake of patients.
ii. Antihistamines; e.g. cyproheptadine
iii. Anti-anxiety drugs which leads to hyperphagia (excessive eating) e.g.
 Chlordiazepoxide hydrochloride (librium)
 Diazepam (valium)
 Alprazolam (xanax)
iv. Insulin; leads to hypoglycemia in Type II diabetes mellitus. If food is not
taken immediately, it leads to coma and death. If excess food is
consumed to avoid or treat hypoglycemia weight gain occurs.
v. Steroids (anabolic steroids) e .g testosterone promotes nitrogen
retention and increased lean body mass and subsequent weight gain.

2. Drugs that affect nutrient absorption;

Many drugs can affect the stomach and cause nausea, vomiting and
ulceration, bleeding, change in intestinal peristalsis or change in the intestinal
flora.
The drugs adversely affect the absorption of nutrients in the small intestines
because they alter motility of the GIT. Some effects may be due to the change
brought in the intestinal mucosa and lumen to the binding effects of drugs on
nutrients.
Many drugs may reduce the GIT transit time leading to greater loss of proteins,
fats and minerals in the feaces.
Medication can decrease or prevent nutrient absorption through the following
ways;
i) Chelation; this is the reaction between medication and minerals (metal ions)
reducing the amounts of minerals available for absorption e.g. Tetracycline
or ciprofloxacin which chelate calcium found in milk or in supplements as
well as magnesium, zinc or iron.
Therefore these minerals should be taken at least 2-4 hours apart from the
drugs. For short-term antibiotic use, it may be more practical to discontinue
the use of the dairy products i.e. milk and iron or calcium supplements.
ii) Adsorption; these decrease nutrient absorption e.g. Celestipol and Clofibrate
(anti-hyperlipidemic bile acid sequesterants ) which affect the secretion of
bile salts so as to reduce the absorption of fats and fat soluble vitamins.
These drugs are used to reduce fat absorption and o lower blood cholesterol
levels. Cholestyramine (Questeran) is used to treat diarrhoea and adsorbs fat
soluble vitamins as well as folic acid leading to reduction in their absorption.
iii) Transit time reduction; drugs can reduce nutrient absorption by reducing
the transit time in the GIT e.g. the use of laxatives which may cause
diarrhoea leading to losses of calcium and potassium.
Diarrhoea may also be induced by drugs containing sorbital (artificial
sweetener) or those that increase peristalsis e.g. gastric mucosa
protectant called Misoprosol.
iv) Changes in gastrointestinal environment; anti-secretory drugs e.g.
zantac (ranitidine) and Omeprazole are used to treat ulcers, inhibit
gastric acid secretion an draise gastric pH making it alkaline, this impairs
the absorption of vitamin B12 by reducing cleavage from its dietary source.
Drugs e.g. Cimetidine (Tagamate) reduces intrinsic factor secretion thus
reduce absorption of vitamin B12 and leads to its deficiency.
v) Damage to intestinal mucosa; the damage to the structure of the villi or
microvilli inhibit the production of brush border enzymes and intestinal
transport systems involved in nutrient absorption especially of iron and
calcium.
Examples of these drugs include;
 Colchine used in gout management
 Paramino salicylic acid which is an anti-TB drug which impairs
vitamin B12 absorption
 Salfasalazine an antibiotic for bacteria and antiprotozoal agent
pyrimethamine which are competitive inhibitors of folate transport
mechanism.
vi) Irritation of the GIT; non-steroidal anti-inflammatory drugs (NSAIDs) e.g.
acetylsalycylic acid (aspirin) and ibuprofen (brufen) causes stomach
irritation and sometimes the irritation is so severe that it can cause sudden
and serious gastric bleeding.
N/B- aspirin works better when taken alone than with food, however they tend
to irritate the GIT, but when taken with food, it reduces irritation or nausea.
Other ways in which drugs affects nutrient absorption;
i. Noticholinergic, antipsychotics and antihistamines slows down
peristalsis resulting in constipation
ii. Drugs like Ciprofloxacin an antibiotics can allow overgrowth of Clostridium
difficulie causing colitis which interfere with absorption.
iii. Monoamine oxidase inhibitors (MOI) which is an antidepressant alters
enzyme system activities which leads to hypertension if taken together with
food containing substance called tyramine e.g. organ meats, aged cheese,
wine and beer. These interfere with the enzyme system of the brain which
inactivates tyramine leading to hypertension and severe headache. It inhibits
the release of certain neurotransmitters with the following symptoms;

 Vomiting  Sweating
 Nausea  Palpitation
 Restlessness  Angina
 Dilated pupils  Fever.

3. Drugs that affect metabolism and excretion of nutrients;

a) Drugs that affect metabolism of nutrients
Drugs and nutrients can interact and therefore alter metabolism. A drug
increases metabolism of a nutrient causing it to pass through the body faster
resulting in increase in the requirements or cause vitamin antagonism by
blocking conversion of the vitamin i.e. structural analogs and interfere in the
function of the enzymes requiring the coenzyme of the vitamin.
Examples of these drugs that affect metabolism of nutrients;
i) Some cancer drugs function on the principle of structural analogs by
taking up the form of an anti-vitamin and affect its metabolism, it
 adversely affects the coenzyme of the vitamin concerned hence the cells
ceases to grow and it dies.
ii) Methotrexase drugs used to treat leukemia and arthritis is a folic acid
antagonist which works against one another therefore folate is lost. It
acts by blocking folate conversion and in turn inhibits cell DNA synthesis
which stops cell replication and the cell die. Leucoronic (folinic acid)
which is a reduced form of folic acid is used with high doses of
methotrexase to prevent anaemia and GIT damage. These thus rescue
cells (not cancer cells) from methotrexase damage by competing for the
same transport mechanism in the cells.
iii) Some malaria drugs bindsto and inhibit the enzyme dihydrofolate
reductase thus preventing the conversion of folic acid to its active form
which eventually leads to megaloblastic anaemia due to its deficiency.
iv) Isonicotinic hydrazine (INH) used to treat TB combines with vitamin
B6 and makes it unavailable. It acts by preventing the conversion of
pyridoxine (B6) to pyridoxal-5-phosphate (active form) and its deficiency
causes peripheral neuropathy. Supplements of pyridoxine can be
prescribed with INH.
v) Warfarin is an anticoagulant which is a structural analogue of vitamin
K. i.e. it resembles vitamin K in structure, therefore prevents the working
of vitamin K in blood clotting. It reduces the hepatic production of
vitamin K dependent clotting factors. It prevents the conversion of
vitamin K to its usable form.
Injection of vitamin K useable form will oppose the action of warfarin and
increases the production of clotting factors therefore a balance between the two
must be maintained.
b) Drugs that affect excretion of nutrients
Some drugs either increase or decrease the urinary excretion of nutrients.
Drugs can increase the excretion of a nutrient by interfering with nutrient
reabsorption by the kidneys e.g.
i) Diuretics e.g. larsix, Furosemide/bumetadine which increases the
excretion of potassium, sodium, magnesium, calcium and chloride in
urine by preventing its reabsorption in the kidneys. Supplements of
these needs to be prescribed in long term use.
ii) Chlorothiazide which causes hypocalcemia and increased excretion of
calcium in urine.
iii) Thiazide this increases the excretion of potassium and magnesium but
reduces the excretion of calcium by enhancing its renal
reabsorption.high doses of these drugs and calcium supplementantion
may result in hypercalcemia same applies to drugs that decrease
excretion of potassium which results in hyperkalemia.
iv) Corticosteroids; this decrease sodium excretion resulting in sodium and
water retention leading to oedema. These drugs increase calcium
excretion. Therefore prolonged use of them requires the use of vitamin D
supplements to prevent oesteoporosis especially in patient with asthma
and arthritis.
v) Antipsychotic drugs e.g. thorazine which increases excretion of vitamin
B2 leading to its deficiency in those with inadequate vitamin B 2 intake.
vi) Aspirin may alter the transport of folate by competing for sites on the
serum protein that transport folate and thus folate is excreted.
vii) D-Penicillamine used to treat heavy metal poisoning (such as lead
poisoning) wilson’s disease, cytinuria or rheumatoid arthritis besides
chelating with the intended metal such as lead or copper may also
chelated with other metals causing their excretion in the urine for
example, it increases the excretion of zinc through formation of a zinc-
penicillamine chelate.
viii) EDTA (ethylenediaminotetra-acetate) administered intravenously to treat
lead poisoning may also cause excessive urinary excretion of zinc
N/B: besides the active ingredients, medication may have other substances
that can affect nutrient metabolism e.g. sugar, sodium, alcohol, caffeine of
which if taken in large quantities may have other effects in the diet e.g.
antacids contain sodium and magnesium which tends to neutralize stomach
acid which is responsible for iron and calcium deficiencies.
Effects of nutrients on drugs
a) How nutrients affect drug absorption
This is through the influence on the stomach emptying rate, the level of
stomach acidity and direct interaction with dietary components.
i. Stomach emptying rate; drugs reach the small intestines more
quickly when the stomach is empty therefore taking medication with
meals may delay its absorption even though the total amounts may
not be lower e.g. aspirin works faster when taken on an empty
stomach although taking it with food is encouraged to reduce
irritation of the stomach .
Slow stomach emptying sometimes enhances drug absorption because the
drug absorption sites in the small intestines are less likely to be saturated.
Although slow drug absorption can be a problem if high drug concentrations
are needed for effectiveness.
ii. Stomach acidity; some drugs are better absorbed in an acid medium
whereas others are better absorbed under alkaline conditions e.g.
reduced stomach pH can reduce absorption of Ketoconazole
(antifungal) and Atazanavir (ARV) but increase absorption of Digoxin
(Lanoxin) for heart failure and Alendronate for treating oesteoporosis.
Some drugs can be damaged by acidity and are available in coated forms that
resist the stomach acidity.
iii. Binding between food components and drugs; some dietary
substances can bind to drugs and inhibit their absorption e.g.
a) Phytates in foods can bind to Digoxin.
b) High fibre diet can decrease the absorption of some Tricyclic
antidepressants due to the binding between fibre and drugs.
 c) Some minerals e.g. calcium can bind to some antibiotics
reducing the absorption of both the mineral and drug.
• Stimulating secretion of digestive juices
b) Nutrient effects on drug metabolism;
Some food components alter the activities of enzymes that metabolize drugs or
may counteract drug effects in other ways. E.g.
i. Some components of grape juice can inhibit or inactivate enzymes
that metabolize a number of different drugs such as calcium-channel
blockers and anti-anxiety agents e.g. diazepam, as a result reducing
enzyme action, increasing the blood levels of the drugs leading to
stronger physiological effects.
ii. Some nutrients acts as antagonists e.g. vitamin K with warfarin
altering the effects of the anticoagulant.
iii. High protein-low carbohydrate can enhance clearance of
carbidopa/levodopa and theophylline, a bronchodilator drug for
treating asthma and chronic obstructive pulmonary disease.
iv. Dietary carbohydrates and fat influence liver enzymes that metabolize
drugs. Presence of fat for example increases the activity of diazepam
(valium) by displacing the increasing its concentration.
v. Indoles in cruciferous vegetables (cabbages Brussels sprouts broccoli
cauliflower) can speed up the rate of the drug metabolism by
apparently inducing mixed function oxidase enzymes system in the
liver.
vi. Cooking methods may alter the rate of drugs metabolism for example
charcoal broiling increase hepatic drug metabolism through enzyme
induction.
c) Nutrient effects on drug excretion;
Inadequate excretion of medication can cause toxicity whereas excessive losses
may reduce the amount available for therapeutic effects. Some food
components influence drug excretion by altering the drug excretion through
altering the amount reabsorbed in the kidneys e.g.
 The amount of lithium (mood stabilizer) reabsorbed in the kidneys is
similar to the amounts of sodium that is reabsorbed. Consequently
dehydration and sodium depletion that promotes sodium reabsorption can
result in lithium retention on the other hand; a person with high sodium
intake will excrete more sodium in the urine and therefore more lithium.
Individuals using lithium are advised to maintain a consistent sodium
intake from day to day to maintain stable blood concentration of lithium.
 Urine acidity can affect drug excretion due to the effects of pH on the
compound’s ionic form. Medication e.g. Quinidine used to treat
arrhythmias is excreted more readily in acidic urine. Foods or drugs that
cause urine to become more alkaline may reduce Quinidine excretion and
raise the blood levels of the medication.
Situations that lead to serious drug — nutrient interactions occur when:
 Some drugs are taken with food
 Drugs are taken with nutrient supplements
 Drugs are taken with alcohol
 Drugs are used to achieve specific drug-nutrient interactions
 Drugs are taken in multiple drug regimens in which more than one drug
produces an adverse effect due to interaction with diet
 Drugs that cause nutrient depletion are taken for a long period.
Nutrient- drug mechanisms that influence nutritional status include those that
lead to:-
 Decreased intestinal absorption
 Increased renal excretion
 Competition or displacement of nutrients for carrier protein – sites
 Interference with synthesis of necessary enzymes coenzymes or carrier
 Hormonal effects on genetic systems
 Effects on the drug delivery system
 Components in drugs formation
UNIT 9: DIET PLANNING
___________________________________________________________________________
Unit Objectives
Define terms used in diet planning
Describe principles of diet planning
Explain the types of diet planning tools
Use food exchange lists in planning diets for various hypothetical cases

Diet planning
Principles of diet planning
 Adequacy in all nutrients - An adequate diet provides all nutrients to meet
the recommended nutrient intake of healthy people.
 Balance of foods and nutrients in the diet - This means not over
consuming any one food. The art of balance involves the use of enough but
not too much or too little of each type of the seven food groups for example
use some meat or meat alternatives for iron, use some milk or milk products
for calcium and save some space for other foods. The concept of balance
encompasses proportionality both between and among the groups.
 Nutrient density - This is the relative ratio obtained by dividing a food's
contribution to the needs for a nutrient by its contribution to calorie needs.
This is assessed by comparing the vitamin and mineral content of a food
with the amount of calories it provides. A food is nutrient dense if it
provides a large amount of nutrient for a relatively small amount of calories.
 Energy density - This is the amount of energy in kilocalories in a food
compared with its weight. Examples of energy dense foods are nuts, cookies,
and fried foods. Low energy density foods include fruits, vegetables and any
food that incorporates a lot of water during cooking. They contribute to
satiety without giving many calories.
 Moderation in the diet - This mainly refers to portion size. This requires
planning the entire day’s diet so as not to under/over consume any one
food. In planning the diets, the goal should be to moderate rather than
eliminate intake of some foods
 Variety in food choice - This means choosing a number of different foods
within any given food group rather than eating the same food daily. People
should vary their choices of food within each class of food from day to day.
This makes meals more interesting, helps to ensure a diet contains
sufficient nutrients as different foods in the same group contain different
arrays of nutrients and gives one the advantage of added bonus in fruits
and vegetables as each contain different phytochemicals
Diet planning tools
To achieve the dietary ideals outlined above with the six principles, there are
several tools used for diet planning. Some of the commonly used tools are:
i) Food guide pyramid
ii) Exchange lists
iii) Food composition tables
The food guide pyramid
The food pyramid translates the food guide into a graphic image. The broad
base of the pyramid displays water followed by cereals; rice, pasta, bread and
other foods made from grains. It also includes the roots and tubers. Fruits and
vegetables make the next layer. Dairy products such as milk and yoghurt are
included in the same tier as meats, poultry, eggs beans and nuts. The foods at
the top of the pyramid which include fats, oils, sugars and sweets are to be
consumed sparingly. As shown in figure 1 below.
Figure 3 Food Guide Pyramid.
Source: https://www.hsph.harvard.edu/news/magazine/centennial-food-guides-history/
food-guide-pyramid/Exchange lists

Food composition tables

These are tables of the chemical composition, energy, and nutrient yield of
foods, based on chemical analysis. They can provide information on chemical
forms of nutrients and the presence and amounts of interacting components,
and thus provide information on their bioavailability.
Food composition data acts as a guideline in assessment of nutrient intake to
determine nutrition adequacy and diet formulation. It also helps in determining
the relationships between disease outcome and nutrient intake.
All component values in a food composition table are given per 100 g edible
portion sizes. As shown in the figure 2 below.
Figure 4 Food Composition Table.
Source: Kenya Food Composition Tables - 2018

Food exchange list

A food exchange list is a simple grouping of common foods according to
generally equivalent nutritional values. This system is used for any situation
requiring caloric and food value control. All the foods listed together are
approximately equal in proteins, carbohydrates and fat value. Exchange lists
provide additional help in achieving kilocalorie control and moderation.
Originally developed for people with diabetes, exchange systems have proved so
useful that they are now in general use for diet planning.
Any food on a list can be exchanged or traded for any other food on that same
list without affecting a plan’s balance or total kilocalories. The system
organizes food into six exchange lists that includes;
1. Milk exchanges 4. Starch exchanges
2. Vegetable exchanges 5. Meat exchanges
3. Fruit exchanges 6. Fat exchanges
The number of kilocalories associated with each food is an average for the
group. The number of kilocalories is calculated given the number of grams of
carbohydrates, fats and proteins in a food (1g of carbohydrate/ protein yields 4
kcal; 1g of fat yields 9 kcal). To apply the system successfully, users must
become familiar with portion sizes. The table below shows exchanges for
carbohydrates, proteins, fat and energy values that pertain to each list

List Portion size per serving Amount (ml CHO Protein Fats Kcal/serving
or g)

Starch  1/3 cup arrowroots 30 g  15  2  Trace 80

 1/3 cup ugali  15  2
 1 slice bread  15  2
 1/3 cup cassava  15  2
 ½ cup cooked bananas  15  2
 ½ cup dried cooked beans  15  7
 ½ cup cooked rice  15  2
 ½ cup cooked pasta  15  2
 ½ cup sweet potatoes  15  2
 ½ cup porridge  15  2
 ½ cup Irish potatoes  15  2
 ½ chapatti  15  2

Milk  ½ cup fresh milk 240 ml  12  8  Trace  90

 Nonfat  ¼ cup ice cream  12  8  5  120
 Low fat 75 ml or one scoop  12  8  8  150
 Whole  1 cup yoghurt 

Meat  Size of matchbox meat 30 g -  7  3  55

 Lean  Palm size of fish  7  5  75
 Medium  A leg, thigh or breast  7  8  100
fat chicken  7  3  75
 High fat  2 tbsp peanut
 Egg  ½ cup fresh bean
 ½ cup omena

Vegetables  ½ cup cooked vegetable 100-150 g 5 2 - 25

 1 cup raw vegetable

Fruits  1 small apple, peach, Varies 15 - - 60

orange, apple or grape fruit
juice (pure juice)
 ¾ cup diced fruits

Fats  1 tsp margarine or oil - - 5 45

 10 large peanuts
 1/8 medium avocado
 1 slice bacon
 1 tbsp shredded coconut
 1 tbsp cream cheese
 1 tbsp salad dressing
 5 large olives
Sugar 1 tsp 5 20
Procedure for calculating diets using exchange lists
Suppose that 1,200 – calorie diet is to be planned with the following levels,
CHO 120g, protein 70g, and fat 50g. Data from tables provided (above) can be
used to use to calculate dietary plan.
1. Estimate the amounts of milk, vegetables and fruits to be included. The
amounts are dictated somewhat by the preferences of the clients but the
following are minimum levels that should ordinarily be included: Milk 2
exchanges for adults, 3-4 exchanges for children and for pregnant/lactating
mother; fruits – 2 exchanges; vegetables – 2 exchanges
2. Fill the carbohydrate, protein and fat values for the tentative amount of
milk, vegetables and fruit.
3. Determine the number of starch exchanges. Add up the CHO value of milk,
vegetables and fruit. Subtract this total from the total amount of CHO
prescribed. Then divide the remainder by 15 (the CHO value of one starch
exchange). Use the nearest whole number of starch exchanges. Fill in the
starch.
4. Total the CHO column. If the total deviates more than 3-4 from the
prescribed amount, adjust the amounts of vegetable, fruit and starch. No
diets should be planned with fractions of an exchange, since awkward
measures of food would sometimes be encountered.
5. Determine the number of meat exchanges. Add up the protein value of all
food so far calculated. Subtract this total from the amount of proteins
prescribed. Divide remainder by 7 (the protein value of one meat exchange).
Fill in the protein and fat values
6. Determine the number of fat exchange. Add up the fat value from the milk
and meat. Subtract this total from the amount of fat prescribed. Divide the
remainder by 5 (the fat content of one fat exchange). Fill in the fat value.
7. Check the entire diet for the accuracy of the computations. Divide the day’s
food allowances into a meal pattern suitable for the client. Example shown
below:
Sample day’s food allowances divided into a meal pattern

ListFoodMeasureCHO (g)Protein (g)Fat (g)Calories

Kcal1.Milk2 exchanges 2416203402.Vegetable2 exchanges104-

503.Fruits 3 exchanges 30

64--1204.Starch4 exchanges 60

1248
24-2805.Meat, Low fat6 exchanges 42183306.Fat 2 exchanges --
1090TOTAL12470481210
UNIT 10: INBORN ERRORS OF METABOLISM, FOOD ALLERGIES AND
FOOD INTOLERANCE
___________________________________________________________________________
Unit Objectives
Define terms used in the topic
Describe the types of inborn errors of metabolism and their management
Describe food allergies and intolerances and their management
Plan and prepare meals for managing food intolerances
Visit a health facility to learn on commercial formulations for managing inborn
errors of metabolism and allergies

Inborn Errors of Metabolism (IEM)

These are rare genetic (inherited) disorders usually caused by defects in
specific proteins (enzymes) that help break down (metabolize) parts of food.
Inborn errors of metabolism include inherited biochemical disorders in which a
specific enzyme defect interferes with the normal metabolism of protein, fat, or
carbohydrate. As a result of diminished or absent enzyme activity in these
disorders, certain compounds accumulate in the body to toxic levels and the
levels of others that the body normally makes may become deficient.
They are present at birth and not constituting a disease although persons with
cystinuria might develop renal stones. If they are not treated, these metabolic
disturbances can lead to a host of medical and developmental consequences
ranging from intellectual disability to severe cognitive impairment and even
death. Through early identification and initiation of treatment, many of the
adverse outcomes of IEM can be mitigated or prevented. For many IEM,
treatment strategies rely on the provision of specialized medical foods and
dietary supplements.
These conditions are also referred to as congenital metabolic disorders or
inherited metabolic disorders.
The most common inborn errors of metabolism are classified as follows;
a. Disorders of amino acids metabolism
b. Disorders of carbohydrate metabolism
c. Disorders of lipid metabolism
d. Disorders of mineral metabolism
e. Other inborn errors of metabolism e.g. albinism, cystic fibrosis and
hemophilia

Disorders of amino acid metabolism;

There are 50 known amino acid metabolic disorders in which there is a defect
in an enzyme system responsible for the intermediary metabolism of one of the
amino acids. They include;
i. Phenylketonuria due to increased phenylalanine in plasma
ii. Hypertyrosinemiadue to elevated tyrosine levels in blood
iii. Argininuria due to elevated Arginine levels
iv. Homocystinuria due to increased methionine as a result of cystathion
synthetase deficiency
v. Histidinemia due to high histidine levels in blood
vi. Marple syrup urine disease due to high levels of leucine, isoleucine
and valine and corresponding ketoacids
vii. Hypervalinemia due to high valine levels in blood
viii. Hyperlysinemia due to high levels of lysine and ammonia in blood.
These amino acids metabolic disorders may be treated using diet that has
reduced amounts of the amino acid concerned either by a low protein diet or a
formula diet based on a suitable mixture of amino acids.
The most common of these amino acids metabolic disorders are;
phenylketonuria and tyrosine disorders whereas others are rare and there are
limited experiences of their treatment.
 i. Phenylketonuria (pKu);
pKu is an autosomal recessive metabolic genetic disorder. It is a condition that
occurs due to a genetic deficiency of a liver enzyme known as phenylalanine
hydroxylase that converts essential amino acid phenylalanine to the amino
acid tyrosine.
It results in the accumulation of phenylalanine in blood and cerebrospinal fluid
as well as its phenyl pyruvic acid (pyruvate), phenyl lactic acid (lactate), phenyl
acetic acid (acetate) derivatives which become excess than normal. These
metabolites accumulate in the body damaging the developing nervous system
which may be severe and an irreversible illness. The derivatives are excreted
through urine as phenylketones and hence the name phenylketonuria. The
impairment in the metabolic pathway also prevents the liver synthesis of
tyrosine and tyrosine-derived compounds such as neurotransmitter
epinephrine /adrenaline, norepinephrine, thyroxine and melanine. Under
this condition, tyrosine becomes essential.

N/B: a better term for this condition is hyperphenylalaninemia since it can

exist without phenylketonuria.
If early diagnosis and effective treatment is began in time i.e. within the first
few weeks or months of life, the symptoms may be prevent or if already present
can be treated. If it is delayed, the mental retardation may never be
compensated.
Treatment of pKu;
This mainly involves diet therapy in the form of reduced phenylalanine intake.
If the daily intake of infant is reduced from normal of about 100mg/kg body
weight/day, to between 20-60mg/kg body weight/day, the child will grow
satisfactorily and the plasma phenylalanine concentration falls to between 30-
100mg/l.
Phenylalanine restriction should be started within 30-90 days of birth. This
diet need a continuance in use for six to eight years which results in significant
improvement in the intellectual of the child comparable to normal siblings.
Phenylalanine is present in all dietary proteins e.g. 2g milk contains 100mg.
Complete synthetic diets that are commercially available may be used. The
plasma concentration of pnenylalanine should be determined at frequent
intervals and the diet adjusted.
N/B: it is safe to stop dietary treatments at the age of 8 years so as to relieve
the child of severe emotional stress inevitable with artificial diets.
Maternal hyperphenylalalinemia during pregnancy results in offspring who
suffer from;
i. Mental retardation
ii. Microcephaly (small head)
iii. Congenital heart disease.
A majority of mothers with blood phenylalanine concentration above 20mg/l
during pregnancy have at least one mentally retarded child. Therefore if in
adult life, a girl who has pKu decides to have children, the risk of her child
having pKu should be pointed out if she becomes pregnant, she should return
to a low phenylalanine diet to avoid the risk of damage to the foetus or prior to
proposed conception.
It is essential that the diet is adequate in essential and non-essential amino
acid, fatty acids, calories, minerals, vitamins and trace elements according to
the age related requirements.
Aspartame which is an artificial sweetener is known to be hydrolysed into
phenylalanine in the GIT and should be avoided.
There is also need to provide tyrosine supplements to the patient as the diet is
phenylalanine restricted.
ii. Maple syrup urine disease (MSUD);
This is an inborn error of metabolism associated with elevated levels of
branched chain amino acids e.g. leucine, isoleucine and valine, which results
in impaired metabolism of amino acids due to impairment of branched chain
alpha-ketoacid dehydrogenase. It is a condition that gets its name from the
distinctive sweet odour of affected infants’ urine particularly prior to diagnosis
and during times of acute illness. The accumulation of the branched chain a.as
leads to serious medical problems associated with maple syrup urine disease.
N/B: if no prompt treatment, the patient will likely die of cerebral oedema.
Dietary management of MSUD
MSUD management involves a specially tailored metabolic formula; a modified
diet and lifestyle precautions e.g. avoid fatigue and infections as well as
consuming regular sufficient calories in proportions to physical stress.
Without sufficient calories, catabolism of muscles proteins will result in
metabolic crisis.
Those with MUSD must be hospitalized for intravenous infusion of sugar and
nasogatric drip-feeding of formula. A diet with carefully controlled levels of the
amino acids leucine, isoleucine and valine must be maintained at all times in
order to prevent a neurological damage.
Some patients with MSUD may also improve with administration of high doses
of thiamin, a cofactor of enzymes that causes the condition.
Liver transplantation is another treatment option that can completely and
permanently normalize metabolic function.
N/B: Research and write notes on the following
i. Hypertyrosinemiadue to elevated tyrosine levels in blood
ii. Argininuria due to elevated Arginine levels
iii. Homocystinuria due to increased methionine as a result of cystathion
synthetase deficiency
iv. Histidinemia due to high histidine levels in blood
v. Hypervalinemia due to high valine levels in blood
vi. Hyperlysinemia due to high levels of lysine

Carbohydrate metabolic disorders;

These include galactosemia and glycogen storage disease discussed below.
i. Galactosemia;
Galactosemia occurs due to deficient function of any of the enzymes (i.e.
galactokinase, galactose-1-phosphate uridyl transferase or UDP galacto-4-
epimerase).
Lactose is a principal carbohydrate and energy source for infants and young
children in milk. Galactose is a monosaccharide that is only found as a
component of lactose in natural foods and has a central metabolic role in
human nutrition. Galactose is formed by hydrolysis of lactose by enzyme
lactase in the intestines. Galactose must be converted in the liver to glucose
before it is used. If most of the untreated infants survive, retarded mental and
physical growth occurs.
Dietary management of galactosemia
The aim is to prevent or treat symptoms and provide adequate energy and
other nutrients to ensure normal growth and development of the infant.
Treatment involves the removal of all sources of lactose and galactose from the
diet. It should be started from the first week of life.
Human milk contains 7% lactose. This milk must be replaced by a formula low
in galactose. Soya proteins isolate formulas have been found to be suitable as it
contains only 1-4 mg galactose per 100ml in oligosaccharides forms which are
not hydrolyzed in the human intestines. As the child grows, solid foods are
added to the diet after proper scrutiny to avoid lactose containing foods.
N/B- fermented dairy products and aged cheese must be excluded from the
diet as the conversion of lactose to lactic acid is not complete in them.

ii. Glycogen storage disease; (GSD);

It is a carbohydrate inborn error of metabolism also called glycogenosis and
dextrinosis as a result of defects in the processing of glycogen synthesis or
breakdown within the muscles or liver and other cells resulting in the
accumulation of glycogen in the tissues.
There are two types;
i. Genetic
ii. Acquired
 Genetic GSD is an inborn error of metabolism due to genetically defective
enzymes involved in the processes.
 Acquired is due to intoxication.

Dietary management;
It involves frequent small meals of carbohydrates and corn starch to prevent
low blood sugar. Corn starch supplementation and high protein diet.

Lipid metabolic disorders (fatty acid metabolic disorder);

These include;
i. Carnitine transporter deficiency (CTD) - Carnitine is a non-protein
amino acid made from lysine in the body that helps transport long chain
fatty acids across the mitochondrial membrane for metabolism at the
times of excessive energy needs CTD is an inborn error of fatty acid
transport caused by a defect on this transporter. Individuals with CTD
cannot produce ketone bodies as energy due to interruption of fatty acid
oxidation.
ii. X- adrenoleukodystrophy (ADL) - This is a disease linked to the X-
chromosome which presents most commonly in male. It is a metabolic
disorder of very long chain saturated fatty acids e.g. cerotic acid (C26:0)
associated with impaired peroxisomal fatty acid beta oxidation leading to
its accumulation throughout the body which causes damage to the
myelin sheath of the nerves and the CNS.
N/B: This condition is characterized by normal development in early childhood
followed by rapid degeneration to a vegetative state and death.
Dietary treatment involves the use of Lorenzo’s oil. The oil is a supplement of
various unsaturated fatty acid mixture which inhibit the elongation of
saturated fatty acids.
Children with cerebral form of this condition requires stem cell transplant and
gene therapy if the condition is detected early in the clinical stages so as to
stop the demyelination in the cerebral form of the disease.
Mineral metabolic disorders;
i. Hemochromatosis (iron overload);
This is an inborn error of iron metabolism due to excessive iron absorption and
accumulation in the liver from many causes. The most common causes are;
a) Hereditary haemochromatosis (HHC) which is a genetic disorder and
b) Transfusional iron overload which can result from repeated blood
transfusion.
The organs commonly affected are the liver, heart and endocrine glands.

Consequences of hemochromatosis
 Cirrhosis of the liver due to iron deposits
 Diabetes due to selective iron deposits in the pancreatic islets beta cells
leading to functional failure and cell death
 Cardiomyopathy
 Arthritis from calcium pyrophosphate deposition in joints especially those of
the hands
 Testicular failure
 Bronzing of the skin- deep tan color due to insulin insufficiency resulting
from pancreatic damage which is the source of the nickname of the
condition as “Bronze diabetes”.
 Joint pain and bone pain
Treatment of hemochromatosis;
It involves regularly scheduled phlebotomies i.e. drawing of blood between 450-
500cc of whole blood until iron levels can be brought to within normal range or
use of chelating agents. These are drugs that bind iron in the blood stream and
thus enhance its elimination in urine and feaces.
Treatment of chronic iron overload requires subcutaneous injection over a
period of 8-12 hours daily especially for those receiving regular blood
transfusion to treat severe anemia and leukemia etc.
Avoidance of iron and vitamin C supplementation and alcoholic beverages is
required.

ii. Wilson’s disease;

This is a copper inborn error of metabolism. It is a genetic disorder in which
copper build up in the body, due to impaired excretion. It is an inherited
condition.
Due to deficiency of a protein required to transport copper into bile and
incorporate it into ceruloplasmin (enzyme) making it to accumulate in the
body.
This condition mainly affects;
 The liver resulting in; vomiting, weakness and tiredness, ascites, itchiness,
oedema, jaundice and portal hypertension
 The brain resulting in; tremors, muscle stiffness, trouble speaking,
personality changes, anxiety and seeing or hearing things that others do
not

Other organs affected include;

 Eyes; deposition of copper ring around the cornea and sunflower cataracts
i.e. browning or green pigmentation of the lens which can result in visual
loss
 Kidneys; it results in renal tubular acidosis which can lead to calcium
accumulation in the kidneys and weakening of bones due to calcium and
phosphate loss and amino aciduria- loss of amino acids needed for protein
synthesis.
 Heart; cardiomyopathy- weakness of the heart muscle, which can lead to
heart failure, cardiac arrhythmias (irregular heart beat- too fast or too slow)
 Thyroid gland; it can result in hypoparathyroidism leading to low calcium
levels, infertility and habitual abortion.
Treatment;
 Use of a diet low in copper containing foods with the avoidance of
mushrooms, nuts, chocolate, dried fruits, liver and shell fish.
 Use of drugs that enhance copper removal from the body while others
prevent its absorption from the diet and copper chelating drugs can be
used.
 Liver transplantation
 Use of Zinc therapy that reduce copper absorption.
Importance of dietary treatment of inborn errors of metabolism;
i. It prevents accumulation of toxic metabolites
ii. It helps in replacing nutrients that are deficient as a result of a defective
metabolic pathway.
iii. It provides a diet that supports normal growth and development and
maintenance of health

Food allergies
An allergy is an adverse immunologic reaction to food that develops when
there is contact between a foreign protein (allergen) and the body tissue that is
sensitive to it. It is a hypersensitivity to certain substances or conditions. It
involves the immune system reacting to some foods causing a rash, wheezing
or itching. This immune reaction due to consumption of food gives an
immediate reaction.
Allergic person produces antibodies (i.e. immunoglobulin E- IgE) which
combine with foreign material (allergen) e.g. food protein leading to an antigen-
antibody reaction with release of mediators e.g. histamine and
prostaglandins. The allergens are usually acid proteins or glycoproteins e.g.
cow’s milk, eggs, fish, soya beans, peanuts, wheat etc. These mediators injure
the body cells and cause illnesses. These illnesses are called allergies.
Incidences of food allergies are highest in the early stages of life and it tends to
decline with age.
Food allergies may be symptomatic or asymptomatic. Symptomatic allergy is
where the production of antibodies is also accompanied by symptoms whereas
in asymptomatic allergy the person only produces antibodies without having
the symptoms.
Symptoms of food allergies;
Depending on the location of the allergic reactions in the body, a symptomatic
allergy will exhibit different symptoms that include;
1. Cutaneous (skin); symptoms
Atopic dermatitis which this include;
 Allergic eczema is due to substances taken in internally. In mild
attacks, the face, neck, and back of the elbows or knees are affected
while in severe cases, rashes may cover the entire skin.
 Hives (urticaria) are temporary swellings that start below the skin
surface. Causes of most hives are foods and drugs.
2. Systemic (very anaphylactic dangerous);
 Mild itching  Slight fever
 Redness of skin  Urticaria
3. Gastrointestinal symptoms;
 Nausea  Abdominal pain
 Vomiting  Cramping
 Swelling of throat  Constipation/Diarrhoea
 Abdominal distention
(bloating)
The GIT symptoms may begin in the area first exposed like the mouth, gums,
lips, tongue and pharynx which may itch, swell and burn.
4. Respiratory symptoms;
 Inflamed nasal membrane  Sneezing
 Chest pain  Convulsion
 Hypertension  Wheezing
 Fever  Coughing etc.
 Nasal congestion
Diagnosis/detection of food allergies;
Methods used in detecting food allergies include;
1. Dietary history;
A very careful diet history must always be taken for people suspicious of being
allergic to certain foods. There are cases where the symptoms develop so
rapidly and dramatically almost immediately after eating the offending food. In
such a case the diagnosis is very simple to draw a conclusion.
A patient should note in a diary for two weeks all the foods eaten and the time
of meals. They should note all the disturbances by recording the nature and
intensity of the symptoms and their time of occurrence. The records can be
used to suggest a relationship between individuals certain foods and allergic
manifestation and other tests can be carried out before a conclusion is drawn.
2. Provocative food tests;
The patient is given a small activity on the suspected food in a made up dish.
The patient should not be aware of this. If there are typical symptoms at the
appropriate interval after the meal, then there is likelihood that the person is
allergic to the food. This should be repeated 2 or 3 times before conclusion is
drawn and all the results should be positive.
3. Laboratory test;
Several laboratory tests are used but the common ones are the skin test and
in vitro testing (RAST)
i. Skin testing; immediate skin testing to food allergies is done by the
prick testing method or puncture skin test (PST). Skin test is the
most useful technique with the most predictable results. A positive test
should be followed by a food challenge or provocative test.
ii. In vitro testing; the Radio Allergosobent Test (RAST) and a growing
number of Enzyme Like Immunoassays (ELISA) for detecting specific
antibodies have become widely available anti-IgE and enzyme linked
immunosorbent assay (ELISA). It uses an enzyme for testing suspected
foods.
4. Elimination diet;
These are based on skin tests and/or from the diet history or the
immunological test. The purpose of the diet is to eliminate symptoms and/or
objective physical or laboratory findings. The patients begin with the simple
elimination diet omitting only foods that are under suspicion. If this does not
provide relief from the symptoms, then a more restrictive elimination diet is
taken. If symptoms persist, the allergy probably is not food.
Management of food allergies;
1. Elimination of causative food; A positive food factor when identified
should be eliminated from the person’s diet. This is the most effective
treatment.
2. Substitution of alternative foods; appropriate substitution should be
made to boost the nutrient intake of the person/patient. E.g. For infants
who are not breastfed and are allergic to cow’s milk, casein hydrolysate
formulas are used. The patient’s nutritional adequacy must be achieved. If
one is allergic to citrus fruits, other sources of vitamin C must be included
in the diet.
3. Denaturation of proteins; sometimes if a protein is denatured by heat or
fermentation, it ceases to cause allergy like protein in plain milk can be
denatured by fermenting it to make it sour.
4. Use of drugs; drugs like adrenaline/epinephrine, aminophyllic and
corticoterad are useful for alleviation of the immediate symptoms of allergic
reactions.
5. Education; Persons who have allergies to foods should be educated about
cross-reactivity that is allergy to foods from the same group or botanical
family e.g. a person allergic to groundnuts may also be allergic to other
beans e.g. soya beans. Patients need to be educated to read labels and to
avoid those containing foods which they are allergic to. While eating out, it
is best to select foods which are free from the offending food.
For the allergies that may produce adverse reactions, the person should wear a
medical alert locket indicating the allergen(s) and carry an epinephrine kit
to be used if the offending food is eaten by mistake or unknowingly. The
injection of epinephrine can give great relief from an allergic reaction.

Food intolerance
This is a detrimental reaction, often delayed to a food, beverage, food additives
or compounds found in foods that produce symptoms in one or more body
organs and systems. It doesn’t involve the immune system, there is no allergic
reactions i.e. no response of immune system, it is never life threatening.
It can be caused by many foods. Symptoms come much slowly often hours
after consuming food. Symptoms result if one eats reasonable amounts of food
unlike allergy where a trace triggers it. Tolerance to food is highly an individual
reaction and needs to be treated as such.
Food intolerance can be classified as;
 Those due to absence of a specific chemical or enzyme needed to digest food
substance
 Those that result from the body’s inability to a absorb nutrients
 Those that occur due to reaction to naturally occurring chemicals in foods
e.g. salicylate sensitivity, drugs e.g. aspirin etc.

Factors that can cause food intolerance;

 Absence of enzymes to digest and metabolize food
 Reaction with some chemicals in food
 Irregular eating hours
 Quick gulping down of food and hence poor mastication
 Lack of rest
 Lack of rational schedule of work
 Irritable bowel syndrome. This chronic condition can cause cramping,
constipation and diarrhea.
 Food poisoning. Toxins such as bacteria in spoiled food can cause severe
digestive symptoms.
 Sensitivity to food additives. For example, sulfites used to preserve dried
fruit, canned goods and wine can trigger asthma attacks in sensitive people.
 Recurring stress or psychological factors. Sometimes the mere thought of a
food may make you sick. The reason is not fully understood.
General symptoms of food intolerance;
 Heart burn
 Flatulence
 Distention of the stomach/bloating
 Vomiting
 Nausea
 Diarrhoea

Types of food intolerance;

i. Hereditary fructose intolerance (HFI);
This is a condition that results from deficiency of enzyme aldolase B. When an
individual ingest fructose, sucrose and sorbitol, the enzymatic block at aldolase
B causes an accumulation of fructose-1-phosphate which affects
gluconeogenesis and regeneration of ATP.
Symptoms;
 Vomiting  Hepatomegaly
 Hypoglycemia  Hyperuricemia
 Jaundice  Potential kidney failure
 Hemorrhage  It can result in death in infants.
Management involves;
Change the diet to exclude foods causing the reaction i.e. use trial and
exclusion method.
ii. Lactose intolerance;
This is a common digestive problem where the body is unable to digest lactose
a type of sugar mainly found in milk and milk products (dairy products) due to
lack of enzyme lactase. Lactose pass into the large intestines undigested where
it is fermented by bacteria producing gases with the symptoms which may be
temporary or permanent.
They usually develop few hours after consuming food or drinks containing
lactose. They include;
 Flatulence (wind)
 Diarrhoea
 Bloated stomach and pain
 Stomach rumbling
 Feeling sick.
The severity of the symptoms depends on the amounts of lactose consumed.
Some people may drink a small glass of milk without triggering symptoms
while others may not even be able to have milk in their tea or coffee.
Dietary management;
i. Limit or avoid foods and drinks containing milk
ii. Use fermented dairy products e.g. yoghurt, mala etc.
iii. Addition of lactase substitutes with food/drinks in drops or tablet forms
to help improve the digestion of lactose.
iv. Give additional calcium and vitamin D supplements to keep the bones
strong and healthy if dairy products are omitted.
UNIT 11: NUTRITION THERAPY IN DISEASES OF INFANCY AND
CHILDHOOD
___________________________________________________________________________
Unit Objectives
Describe nutrition care of hospitalized children
Describe nutrition care of low birth weight children
Describe nutrition care of colic, functional infant vomiting and constipation in
children
Describe nutrition care of cleft lip and palate in children
Visit a health facility to learn on the care of LBW and hospitalized children

Hospitalized infants and children during and after illness

These categories of vulnerable groups are at a higher risk of malnutrition due
to their increased nutrient demand due to illness/medical conditions,
compromised environment and attendant care. Additionally, their nutrient
intake is affected by reduced appetite.
Goals of nutrition care of hospitalized infants and children
 To provide optimal nourishment to the child
 To help fight infections without depleting nutrient reserves of the child’s
body
 To reduce the risk of weight loss
 To reduce risk of micronutrient deficiencies during and after illness
Key issues and justification
Nutrition care and support is critically important during this period to enable
the child attain its potential development. Special attention must be paid to
mitigation of malnutrition in the mother and the child, as the effects on the
child of such malnutrition can result in severe and irreversible long-term
physical and mental retardation.
Policy guidelines, recommendations and key messages on infant and
young child feeding for practices for hospitalized infants and children
Policy guideline 1: Promote, protect and support breastfeeding in the best
interests of the vast majority of infants and health care; personnel should not
recommend formula feeding as an alternative to breastfeeding, unless there are
legitimate medical reasons to do so.
Recommendations and key messages
 Enable mothers to remain with their hospitalized infants and young
children and assist/support them to ensure continued breastfeeding and
adequate complementary feeding.
 Breastfeed more frequently during illness, including diarrhoea to help the
baby fight sickness, reduce weight loss and recover more quickly.
 Breastfeeding also provides comfort to your sick baby. If your baby refuses
to breastfeed, encourage your baby until s/he takes the breast again.
 For babies less than 6 months, give baby only breast milk, medicines and
fluids recommended by your doctor/health care provider.
 For babies older than 6 months, continue to breastfeed and provide more
frequent feeds and fluids.
 If your baby is too weak to suckle, express breast milk to give the baby. This
will help you to keep up your milk supply and prevent breast difficulties.
 After each illness, increase the frequency of breastfeeding to help your baby
regain health and weight.
 When you are sick, you can continue to breastfeed your baby.
 The mother may need extra food and support during this time.
 Replacement feeding using a specialized formula is only necessary: in rare
cases of metabolic disorders of the infant, such as galactosemia, maple
syrup urine disease and phenylketonuria; and in some cases of maternal
illness e.g. life-threatening illness, and when a mother makes an informed
decision not to breastfeed.
Policy guideline 2: Provide an adequate age-appropriate diet for hospitalized
children while continuing to promote breastfeeding for up to two years and
beyond and assess, refer and/or appropriately manage any child suspected of
special metabolic conditions or difficulty feeding.
Recommendations and key messages
 Provide information and support to mothers, fathers and caregivers on
feeding sick infants and young children.
 Promote and support the mother to breastfeed more frequently during and
after illness, including diarrhoea, to help your baby fight sickness, prevent
weight loss and recover more quickly.
 The baby needs more food and liquids while s/he is sick.
 If the child’s appetite is decreased, counsel the mother to encourage him or
her to eat small frequent meals.
 Encourage the mother to bring the child for weighing after an illness to
make sure he /she gains enough weight for full recovery.
 The mother may need extra food and support during this time.
 When the mother is sick, she will also need plenty of liquids
Strategies to encourage children to eat more
During an illness;
 Encourage the child to drink and to eat with lots of patience.
 Feed small amounts frequently.
 Give foods that the child likes most.
 Give a variety of nutrient-rich foods which are well prepared and
attractively served.
 Continue to breastfeed (often ill children breastfeed more frequently).
During recovery
 Give extra breastfeeds.
 Feed an extra meal.
 Give an extra amount.
 Use extra-rich foods.
  Feed with extra patience and love.
 Give a variety of nutrient-rich foods which are well prepared and
attractively served to stimulate appetite.

Low birth weight (LBW) and pre-term infants

Low birth weight (LBW) has been defined by the World Health Organization
(WHO) as weight at birth less than 2500g (2.5kg). LBW could be as a
consequence of pre-term birth (delivery before 37 completed weeks) or due to
small size for gestational age (SGA, defined as weight for gestation <10th
percentile) or both.
LBW thus defines a heterogeneous group of infants; some are born early, some
are born at term but are SGA, and some are both born early and SGA.
LBW infants are at higher risk of early growth retardation, infectious disease,
developmental delay, reduced chances of survival during infancy and
childhood, increased risk of obesity, diabetes and heart disease in later life.
Intrauterine growth restriction, defined as a slower than normal rate of fetal
growth, is usually responsible for SGA. Optimal maternal nutrition during
pregnancy reduces the chances of delivering a LBW baby.
Classification of weight by gestational age
1. Large for gestational age (LGA): >90th percentile (2 SD from mean birth
weight)
2. Appropriate for gestational age (AGA): 10th – 90th percentile (birth weight
length and head circumference in the normal
3. Small for gestational age (SGA): <10th percentile (≤-2SD below mean birth
weight and or length
Classification of low birth weight
1. Low Birth Weight (LBW): Birth weight < 2500 grams.
2. Very Low Birth Weight (VLBW): Birth weight < 1500 grams
3. Extremely Low Birth Weight (ELBW): Birth weight < 1000 gms and
greater than 750gms
4. Preterm born before 37 completed weeks of gestation
N/B: These guidelines focus on the feeding of clinically stable LBW infants.
Some of the questions and recommendations focus only on VBLW infants (birth
weight less than 1.5 kg). They do not specifically address the feeding of infants
with a birth weight less than 1.0 kg (ELBW), who are often clinically unstable
and may require parenteral nutrition. Further, the guidelines do not provide
separate recommendations for the two groups of LBW infants, preterm and
small for gestational age (SGA), because of lack of evidence.
Objective of nutrition care in LBW infants
To provide optimal nutrition support and care for low birth weight and pre-
term infants.
Key issues and justification
Preterm babies (born before 37 weeks gestation) tend to have more problems
than term babies who are small (less than 2.5 kg at birth) and require
specialized care due to prematurity. However, because the baby’s gestational
age is not always known, this guide refers to preterm babies and low birth
weight term babies collectively as “small babies.”
If the baby’s gestational age is known, use this, when possible, to guide
diagnosis and management decisions. Remember that the more preterm or the
smaller the baby is, the more likely the baby is to have problems.
A small baby:
May have a problem that is specific to small babies (e.g. Jaundice of
prematurity) but may also have any other problem that a full-size, term baby
can have (e.g. jaundice associated with sepsis);
Has a different resting posture than a term baby, and this is not necessarily an
indication of a problem (e.g. floppiness).
Small babies are prone to complications. These include:
 Feeding difficulty: Feeding difficulty is a common problem; as the baby
grows, feeding ability improves;
 Abnormal body temperature: Low body temperature (hypothermia) may be
caused by exposure to a cold environment (low ambient temperature, cold
surface, or draught), or the baby may be wet or under-dressed for age and
size. Elevated body temperature (hyperthermia) may be caused by exposure
to a warm environment (e.g. high ambient temperature, sun exposure, or
overheating by an incubator or radiant warmer). Hypothermia and
hyperthermia may also be signs of illness, such as sepsis. Kangaroo mother
care is the recommended method of maintaining a small baby’s body
temperature.
 Breathing difficulty, such as respiratory distress syndrome and apnea;
 Necrotizing enterocolitis;
 Jaundice of prematurity;
 Intraventricular bleeding;
 Anemia; to prevent iron deficiency anemia, give small babies an oral iron
preparation to give elemental iron 2 mg/kg body weight once daily from two
months of age up to 23 months of age);
 Low blood glucose.
Further reading: Review chapters in the National guidelines on essential
newborn care, the National Guidelines for Quality Obstetric and Perinatal Care
for general management instructions applicable to all newborn babies and
Feeding and Fluid Management of Small Babies in Management of Infant and
Young Child Nutrition manual
Failure to thrive
Failure to thrive is defined as decelerated or arrested physical growth (height
and weight measurements fall below the third or fifth percentile, or a
downward change in growth across two major growth percentiles) and is
associated with abnormal growth and development.
Causes of failure to thrive
Inadequate nutrition - If an infant is not offered enough food or is not willing
to eat enough food, or vomits repeatedly (such as with severe gastroesophageal
reflux), there will not be enough calories to support growth.
Diseases/illnesses - A child who is unable to absorb enough calories (such as
with severe allergies or a medical condition like cystic fibrosis) will also not
grow as expected. Any condition that causes a child to need more calories than
normally expected may also lead to failure to thrive.
Symptoms of failure to thrive
 Lack of appropriate weight gain
 Irritability
 Easily fatigued
 Excessive sleepiness
 Lack of age-appropriate social response (i.e., smile)
 Does not make vocal sounds
 Delayed motor development
 Learning and behavior difficulties later in childhood
Treatment for failure to thrive
Specific treatment for failure to thrive will be determined by your child's
physician based on:
 Your child's age, overall health, and medical history
 Extent of your child's symptoms
 Cause of the condition
 Your child's tolerance for specific medications, procedures, or therapies
 Expectations for the course of the condition
 Your opinion or preference
The individual issues involved in causing failure to thrive are almost always
complex. Treatment depends on the cause of the condition and may involve a
team of health care providers, including social workers, nutritionists, physical
therapists, geneticists, and other specialists
Colic
Colic is a condition marked by predictable periods of significant distress in an
otherwise well-fed, healthy baby. Babies with colic often cry more than three
hours a day, three days a week for three weeks or longer. Nothing you do to try
to help your baby during these episodes seems to bring any relief.
Symptoms
Fussing and crying are normal for infants, and a fussy baby doesn't necessarily
have colic. In an otherwise healthy, well-fed baby, signs of colic include:
 Predictable crying episodes. A baby who has colic often cries about the
same time every day, usually in the late afternoon or evening. Colic episodes
may last from a few minutes to three hours or more on any given day. Your
baby may have a bowel movement or pass gas near the end of the colic
episode.
 Intense or inconsolable crying. Colic crying is intense, sounds distressed
and is often high pitched. Your baby's face may flush, and he or she is
extremely difficult — if not impossible — to comfort.
 Crying that occurs for no apparent reason. It's normal for babies to cry
sometimes. But, crying usually means your baby needs something, such as
food or a clean diaper. Crying associated with colic occurs with no clear
cause.
 Posture changes. Curled up legs, clenched fists and tensed abdominal
muscles are common during colic episodes.
Colic is common. It usually starts a few weeks after birth and often improves
by age of 3 months.
Colic treatment
Colic improves on its own, often by age 3 months. Unfortunately, there are no
proven treatments that consistently help every baby. Treatments that have
been tried include:
 Gas-relief medications
 Probiotics. Probiotics are substances that help maintain the natural
balance of "good" bacteria in the digestive tract. Lactobacillus reuteri,
significantly decreased colic symptoms.
Tips for feeding your baby
If you think your baby may be hungry, try a feeding to ease fussiness. These
other feeding strategies may help, too:
 Hold your baby as upright as possible during feedings. Pause often
during feedings to burp your baby. Sometimes smaller, more-frequent
feedings are helpful. If you're breast-feeding, it may help to allow your baby
to feed at one breast until it's nearly empty before switching sides. This
provides your baby with rich, fatty hind milk, potentially more satisfying
than the lighter, thirst-quenching foremilk present at the start of a feeding.
 Consider changing your diet, if breast-feeding. A breast-feeding mother's
diet likely doesn't play a role in baby's colicky symptoms. However, in
families with a history of allergies, removing potential allergens from your
diet might uncover an unknown food allergy in your baby. Eliminating foods
most likely to cause allergy - such as dairy, peanuts, tree nuts, wheat, soy
and fish - for two weeks to see if the baby's symptoms improve may be
advised.
 Switch baby's formula. As with breast-feeding, your baby's formula isn't a
likely cause of his or her symptoms. But, changing to a type of formula
called hydrolysate infant formula might make a difference if your baby is
allergic to cow's milk or has a milk intolerance. The whole milk proteins in
these formulas are already broken down, which makes them easier to
digest. If an allergy or intolerance was causing your baby's symptoms, you
should see a response within two days of changing formula. If there's no
improvement, you can switch back to the original formula as the
hydrolysate formula is much more expensive than standard formula.
 Change bottles. There are a variety of bottles and nipples from which to
choose. Trying a different type of bottle or nipple could help ease some of
 your baby's symptoms. Bottles that have disposable, collapsible bags may
lessen the amount of air your baby swallows.
Functional infant vomiting
A functional disorder refers to a disorder or disease where the primary
abnormality is an altered physiological function (the way the body works),
rather than an identifiable structural or biochemical cause. It characterizes a
disorder that generally cannot be diagnosed in a traditional way; that is, as an
inflammatory, infectious, or structural abnormality that can be seen by
commonly used examination, x-ray, or blood test.
In this context, "functional" means that the symptoms occur within the
expected range of the body's behavior. (Examples: Shivering after a cold swim
is a symptom, but not due to disease. Or, a runner's leg cramp is very painful,
but the muscle is healthy).
Functional disorders are characterized by symptoms. Childhood functional
gastrointestinal disorders include a variable combination of often age-
dependent, chronic or recurrent symptoms not explained by structural or
biochemical abnormalities.

Symptoms include:
 Functional vomiting  Bloating
 Abdominal pain or bellyaches  Belching
 Abdominal distention  Nausea
 Nausea  Regurgitation
 Chronic diarrhea or constipation  Heartburn
 Fecal soiling  Food refusal

Childhood functional GI disorders, while distressing, are not dangerous when

symptoms and parental concerns are addressed appropriately. However, failed
diagnosis and inappropriate treatments may be the cause of needless physical
and emotional suffering.
Constipation
Constipation is a very common problem for children. Constipation means
passing hard stools (faeces), with difficulty, less often than normal.
Constipation in children or babies can mean any, or all, of the following:
a) Difficulty or straining when passing stools (faeces).
b) Pain when passing stools, sometimes with a tiny amount of blood in the
nappy or on the toilet paper, due to a small tear in the skin of the back
passage (anus).
c) Passing stools less often than normal. Generally, this is less than three
complete (proper) stools per week.
d) Stools that are hard and perhaps very large, or pellet-like and small, like
rabbit droppings.
Symptoms of constipation
 As well as less frequent, hard (and perhaps painful) stools, constipation can
cause:
 Tummy ache (abdominal pain).
 Poor appetite.
 Feeling 'off colour' (general malaise).
 Behavioral changes, such as being more irritable or unhappy.
 Fidgeting, restlessness and other signs that the child needs to go to the
toilet.
 Feeling sick (nausea).
Severe constipation can cause impaction (where a very large stool is stuck in
the rectum). This can cause further symptoms. In particular, this can cause a
child to soil their pants regularly with very soft faeces, or with faecal-stained
mucus. This is often mistaken by parents as diarrhoea.
Types of constipation in children and babies
 Idiopathic constipation. It is the most common. The word idiopathic
means of unknown cause. Various factors may be involved but many
children become constipated for no known reason, it may be;
o Short bouts of constipation. It is a mild constipation and it occurs for
a day or so. This may settle quickly, often without the need for
medical treatment.
o Long-term constipation. It occurs in about 1 in 3 children. The
problem becomes more long-term (persistent). It is also called chronic
idiopathic constipation.
 Constipation due to an underlying disease or condition. This is
uncommon. The constipation is said to be secondary to other problems.
Examples of conditions and problems that can cause constipation are:
o Some neurological conditions.
o An underactive thyroid gland (hypothyroidism).
o Cystic fibrosis.
o Rare diseases with abnormal development of the bowel, such as
Hirschsprung's disease.
o As a side-effect of certain medications that a child has to take for
another condition.
o Dietary factors that may play a part in constipation are - not eating
enough foods with fibre (the roughage part of the food that is not
digested and stays in the gut) and not having enough to drink. Stools
tend to become harder, drier, and more difficult to pass if there is
little fibre and fluid in the gut.
o Stool holding - This means the child has the feeling of needing the
toilet but resists it. The child holds on to the stool, trying to ignore the
desire to empty the bowels. The longer the child holds on, the bigger
the stool gets. Eventually the child has to go but the large stool is
more difficult to pass and often more painful. This may lead to a bit of
 a vicious cycle where the child is even more reluctant to open his or
her bowels the next time.
o Emotional problems - Constipation problems may be made worse with
upset due to change in surroundings or routine. Common examples
are moving house and starting nursery. Potty training may be a factor
if a child becomes scared of using the potty. Fears and phobias are
usually the underlying reasons for these problems
Treatment of constipation
Treatment of underlying causes - It may involve treating the underlying
condition (if that is possible) in addition to tackling the constipation.
Use of laxatives - Idiopathic constipation that has lasted for more than a few
days is usually treated with laxatives.
Diet - Dietary measures should not be used on their own to treat idiopathic
constipation, as it will be unlikely to solve the problem. However, it is still
important to get a child into a habit of eating a good balanced diet. This is to
include plenty of drinks (mainly water) and foods with fibre. This will help to
prevent a recurrence of constipation once it has cleared.
Eating foods with plenty of fibre and drinking plenty makes stools (faeces) that
are bulky but soft and easy to pass out. This advice applies to babies who are
complementary fed and to children. Foods which are high in fibre are fruit,
vegetables, cereals and whole meal bread.
Physical activity - Getting plenty of exercise is also thought to help.

Diarrhoea
Diarrhoea is the passage of 3 or more loose or liquid stools per day, or more
frequently than is normal for the individual. It is usually a symptom of
gastrointestinal infection, which can be caused by a variety of bacterial, viral
and parasitic organisms. Infection is spread through contaminated food or
drinking-water, or from person to person as a result of poor hygiene.
Severe diarrhoea leads to fluid loss, and may be life-threatening, particularly in
young children and people who are malnourished or have impaired immunity.
There are non-infectious causes of diarrhoea, but sepsis is the most common
cause during the newborn period.
Observe strict infection prevention practices at all times when caring for any
baby with diarrhea to prevent spreading one baby’s infection to other babies in
the newborn special care unit. Wear gloves when handling soiled napkins and
other items used to care for the baby, and carefully wash hands after handling
a baby with diarrhoea.
General management
 Allow the baby to begin breastfeeding. If the baby cannot be breastfed, give
expressed breast milk using an alternative feeding method.
 If the mother is giving the baby any food or fluid other than breast milk,
advise her to stop giving them.
 Give oral rehydration salt (ORS) for every diarrhoeal stool passed:
 If the baby is able to feed, have the mother breastfeed more often, or give
ORS 20 ml/kg body weight between breastfeeds using a cup.
 If the baby is not feeding well, insert a gastric tube, and give ORS 20 ml/kg
body weight by tube;
 If prepackaged ORS is not available, make ORS as follows:
o Use recently boiled and cooled water;
o To 1 litre of water, add:
o Sodium chloride 3.5 g;
o Trisodium citrate 2.9 g (or sodium bicarbonate 2.5 g);
o potassium chloride 1.5 g;
o Glucose (anhydrous) 20 g (or sucrose [common sugar] 40 g).
o If the baby has signs of dehydration or sepsis, establish an IV line,
and give IV fluid while allowing the baby to continue to breastfeed:
 o If there are signs of dehydration, increase the volume of fluid by 10%
of the baby’s body weight on the first day that the dehydration is
noted;
o If the baby receives a sufficient volume of fluid to meet rehydration
and maintenance requirements and to replace ongoing losses, the use
of ORS is not necessary;
 Assess the baby again in 12 hours:
 If the baby is still having diarrhoeal stools, continue the increased volume of
IV fluid for an additional 24 hours;
 If the baby has not had a diarrhoeal stool in the last 12 hours, adjust fluid
to maintenance volume according to the baby’s age.
 Determine the probable diagnosis.

Management of nosocomial diarrhoea

If the diarrhea developed while the baby was hospitalized and more than one
baby with diarrhea from the same ward is seen within a two-day period,
suspect a nosocomial infection.
 Isolate the baby from other babies, if possible.
 Treat for sepsis.
 Continue to provide general management for diarrhea.

Cleft lip and palate.

A cleft lip occurs when there is a split or opening in the lip. This opening can
be small or large enough to connect the upper lip and nose. A cleft palate
occurs when the roof of the mouth does not close properly during a baby’s
early development inside the womb.
Symptoms of Cleft Palate and Lip
In most cases, the split in the lip that is characteristic of a cleft is the most
noticeable sign of the defect. Milk may come out of your baby’s nose while
feeding because the barrier between the mouth and nose is abnormal. It’s also
possible for children with a cleft to have dental problems, such as missing
teeth or having extra teeth.
A cleft palate can also trigger frequent middle ear infections and problems with
the child’s Eustachian tubes. A child may also have problems with speech. This
is more common in cases of cleft palate than in cases of cleft lip. Speech
problems caused by a cleft are usually characterized by a nasal quality in the
voice.
Causes of Cleft Palate and Lip
Genetics can play a role in the development of clefts if one or both parents pass
down a gene that makes a cleft palate or lip more likely.
What a pregnant woman does during pregnancy can also increase the
likelihood that a child will have a cleft palate or lip. Factors that scientists
believe may cause a cleft to develop include:
 Cigarette smoking
 Drinking alcohol
 Taking illegal drugs
 Being diabetic
 Not getting enough prenatal vitamins, like folic acid

Treatment of cleft palate and lip

The treatment will depend on the severity of the condition. Treatment often
involves several surgeries to close the opening and reconstruct the face.
UNIT 12: GASTROINTESTINAL DISEASES AND DISORDERS
___________________________________________________________________________
Unit Objectives
Describe disorders of the GIT and their nutritional management
Describe disorders of GIT accessory (salivary glands) and their nutrition
management
Plan and prepare meals for management of GIT disorders

Introduction to gastrointestinal diseases and disorders

Digestive system problems are among the most common problems in health
care. Dietary habits and specific food types can play a significant role in the
onset, treatment and prevention of many gastrointestinal disorders.
Dietary and in other cases diet can also play a role in improving the patient’s
sense of wellbeing. Gastrointestinal disorders are divided into four categories
namely;
i) Diseases of the upper GIT
ii) Diseases of the stomach
iii) Diseases of the small intestines
iv) Diseases of the large intestines.

Diseases of the upper GIT;

These are disorders of the mouth and the oesophagus. These disorders
interfere with the intake of food through;
i) Reduce appetite
ii) Induce nausea and vomiting
iii) Evoke pain
iv) Produce obstruction
Diseases/ disorders of the upper GIT include;
a. Dental, medical and surgical conditions affecting the mouth;
These are conditions that would interfere with the chewing of food. They
manifest themselves through;
 Mouth ulcers or oral thrush
 Reduced saliva flow
 Dental caries
 HIV infection
 Mouth cancers
N/B: oral thrush is quite common in children.
Any inflammatory condition in the mouth may contribute to nutritional
disorders because of pain and difficulty in swallowing which may restrict the
intake of food. Without adjustment in the diet, people with these conditions
will find eating a problem and a difficult experience.
Dietary management;
Lesions that cause pain on chewing or swallowing require the modification of
the diet to make it fluid or semi fluid in consistency until the condition is
brought under control. A mechanically soft diet that eliminates food that
cannot be easily chewed and tenderly cooked or pureed food with reduced
seasonings should be used too.
b. Parotitis;
This is a condition of the salivary glands which is characterized by the
enlargement of the parotid glands which is associated with inadequate intake
of proteins. This inflammation may be due to;
 Virus of mumps
 Virus of parotitis
 Bacterial infection of the glands which tend to develop after an illness
 After a major surgical operation due to an oral infection.
Acute parotitis from any cause is often so severe that it makes chewing and
swallowing painful and difficult.
Dietary management;
Use of fluid diet until the inflammation subsides.
c. Dry mouth (Xerostomia);
Xerostomia is a condition that is caused by reduced saliva flow a side effect of
many medications and is associated with a number of diseases and disease
treatments. They include;
 Drugs such as antihistamines, antihypertensive agents, antidepressants,
decongestants and other medications can cause dry mouth.
 Poorly controlled diabetes
 Conditions that directly affect the functions of the salivary glands such as
Sjӧgrens syndrome
 Radiation therapy that treats head and neck cancers which often damage
salivary glands sometimes permanently leading to reduced saliva flow thus
dry mouth.
A reduction in salivary flow can impact health in the following ways;
 Interfere with speech
 Cause bad breath
 Make mouth infections and dental diseases more common
 Chewing and swallowing become more difficult
 Diminished taste sensation
 Make wearing of dentures uncomfortable and may cause ulcerations in the
areas where they contact the mouth.
 Reduced food intake thus increase malnutrition risks

Management of dry mouth;

 Take frequent sips of water or sugarless beverage
 Chew sugarless gum to help stimulate salivary flow
 Suck on ice cubes or frozen fruit juice bars (unless their coldness cause
discomfort).
 Avoid any foods e.g. toast, chips and crackers
 Avoid caffeine, alcohol and smoking which may dry the mouth
 Consume foods that have a high fluid content e.g. soups, stews, sauces etc
 Try over-the-counter saliva substitute especially just before meals and at
bed time
 Try rinsing the mouth with small amounts of vegetable oil or softened
margarine
 Pay attention to oral hygiene, brushing and flossing at least twice daily. Try
to brush immediately after each meal.
 Avoid alcohol- and detergent-containing mouth washes that may dry and
irritate the mouth
 If the dry mouth is due to medication, ask your physician about possible
intervention.

d. Dysphagia;
This is a term that means “difficulty in swallowing”. It is a condition that
results from;
i) Functional defect with the failure of onward movement of peristaltic wave
that is associated with neurological diseases, surgical procedures involving
the head and the neck.
ii) A blockage of adequate waves by inflammation or malignant diseases. These
blocks onward movement of food within the affected region either the throat
or the oesophagus.
This condition occurs in association with;
 Tonsolitis
 Surgery
 Ageing
 Nervous system diseases e.g. stroke that affects one side.
 
Types of dysphagia;
1. Oropharangeal dysphagia - this inhibits the transfer of food from the
mouth and pharynx to the oesophagus. It is often due to a neuromuscular
condition that upsets the swallowing reflux or impairs the mobility of the
tongue and other oral tissues.
The symptoms include;
 Inability to initiate swallowing
 Coughing during or after swallowing (due to aspiration)
 Nasal regurgitation
 Bad breath
 Gurgling noise after swallowing
 Hoarse or ‘wet’ voice or speech disorder
This condition is common in the elderly persons and frequently follows a
stroke.
2. Oesophageal dysphagia - This is a condition that interferes with the
passage of materials through the oesophageal lumen and into the stomach.
It is usually caused by an obstruction in the oesophagus or a motility
disorder. Obstruction can be caused by a stricture (abnormal narrowing),
tumor or compression of the oesophagus by surrounding tissues. The main
symptom is sensation of food “sticking” in the oesphagus after it is
swallowed.
The obstruction of the oesophagus can prevent passage of solid foods but
may not affect liquid foods motility disorders hinder passage of both solid
and liquids.

General warning signs of dysphagia

 Clearing of the throat frequently  Spoken or non-verbal
 A voice that sounds wet and expressions about fear of eating,
“gurgly” swallowing or chocking
 A delay in swallowing after food  Food or liquid falling out of the
has been chewed mouth
 Holding food or liquid in the  Food left in the mouth after
mouth swallowing it. swallowing or after finishing a
 Exaggerated movement of jaws, meal
lips or tongue  Coughing during or after a meal
 Tilting of the head back to eat or  Fatigue or exhaustion after or
drink during a meal.
 Swallowing several times of one  Significant weight loss over time
bite
Consequences of dysphagia
 Food that moves back into the throat may enter the trachea and pass on
into the lungs a condition known as aspiration which can cause bacterial
pneumonia.
 It may also cause chocking and airway obstruction.
 If it restricts food intake, malnutrition and weight loss may occur and may
lead to death.
 Individuals who cannot swallow liquids are at an increased risk of
dehydration.
N/B: aspiration mainly occurs at night.

Dietary management of dysphagia;

There are various levels of diet for managing dysphagia depending on the
patient’s swallowing ability and tolerance;
i) Level 1: Dysphagia pureed diet; foods should be pureed or well
mashed, homogenous and cohesive (single consistency) this diet is for
patients with moderate to severe dysphagia and poor oral or chewing
ability.
ii) Level 2: Dysphagia mechanically altered diet; foods should be moist,
cohesive and soft textured and should easily form bolus. This diet is for
 patients with mild to moderate dysphagia. Some chewing ability is
required.
iii) Level 3: Dysphagia advanced diet; food should be moist and bite-sized
pieces. When swallowed foods with mixed textures are included. This diet
is for patients with mild dysphagia and adequate chewing ability.
N/B: - in many cases, the most appropriate foods may be determined by trial
and error.
 A person’s swallowing ability can fluctuate over time, so the dietary plan
needs frequent reassessment. A consultation with a swallowing expert such
a speech and language therapist is often necessary.
 Consuming foods that have similar consistency (cohesive) can quickly
become monotonous. By using commercial thickeners and food molds,
pureed foods can be formed into attractive shapes, including a variety of
flavours and colours can also make a meal more appealing. Thickened
liquids are easier to swallow than thin liquids such as water or juice. To
increase viscosity of fluids, commercial starch thickeners can be stirred into
beverages and soups and broths.
 Some patients may be able to learn alternative feeding techniques to help
them compensate for their swallowing problems. E.g. changing the position
of the head and neck while eating and drinking to minimize swallowing
difficulties. It can involve the use of cups designed for dysphagia patients
which allow them to drink without tilting the head back.
 Tube feeding may be necessary if attempts to feed the patient orally are not
successful.
 Individuals with oropharangeal dysphagia can be taught exercises that
strengthen the jaws, tongue or larynx or they can learn new methods of
swallowing that allow them to consume a normal diet. These are often
taught by speech and language therapist.

e. Achalasia;
This is a condition that is uncommon with “a” meaning “without” and
“chalasia” meaning “relaxation”. It is a condition in which the lower few
centimeters of the oesophageal sphincter muscle (LES) fails to relax when
presented with food during the swallowing mechanism.
It is a primary oesophageal motility ailment characterized by absence of
oesophageal peristalsis and failure of the LES to relax upon swallowing i.e. the
oesophagus tends to relax in unison rather than peristaltically. This thus
brings about a functional obstruction at the oesophageal junction. Food is
therefore prevented from being transmitted into the stomach.
The musculature of the oesophagus is still capable of contracting and even
exhibit in-coordinated movements but it has lost the ability to conduct a
peristaltic wave especially in its lower part and has lost the ability to transmit a
signal to cause the “receptive relaxation” of the gastro-oesophageal sphincter as
food approaches this area during swallowing process.
Dietary management of achalasia;
A bland diet can be used to manage this condition.

f. Hiatal hernia;
Hiatal hernia is a condition in which there is an abnormal gap in the
diaphragm so that the upper portion of the stomach and other abdominal
organs protrude and slip into the chest cavity (i.e. the thorax).
Hiatus is an opening where the oesophagus is loosely attached to the stomach.
In middle age this attachment weakens so that thereafter the stomach and
oesophagus readily herniates. In most cases it is asymptomatic. It is found in
10% of all people more frequently, it is seen in women than in men.
This condition occurs mostly in;
 Obesity because of increased bulk of the abdominal contents which exerts
more pressure on the hiatus
 Pregnancy due to pressure exerted by the uterus on the abdominal organs
 Chronic coughs.
Hiatal hernias are mostly symptomless although they usually give rise to
symptoms only in so far as the cardiac sphincter of the stomach ceases to act
as a sphincter and allow acid of gastric juice to regurgitate into the
oesophagus. The patient complains of heartburn. The regurgitation of acid into
the oesophagus results in a condition known as reflux oesophagitis.
The main symptoms of reflux are;
 Heartburn which may be accompanied by regurgitation of acid fluid into
the mouth. The regurgitation of gastric juice is periodically after a meal
following;
o Bending
o Lifting
o Straining
 Severe pain
 Sensation of food sticking
 Chronic bleeding which can lead to iron deficiency anaemia
 Peptic ulceration of the oesophagus due to reflux of acid.

Management of hiatal hernia and reflux oesophagitis;

 Medical treatment to keep the patient free from the symptoms
 Weight reduction in the case of obesity through the use of a calorie reduced
diet as well as exercise
 Avoid wearing tight garments
 Those patients distressed by pain should sleep with a pillow under their
chest and the head of the bed should be raised by blocks.
 Patients are required not to take any solid foods before going to bed.
 Normal diets are usually tolerated although some patients omit certain
foods to which they are intolerant
 Small meals with mid-morning and midafternoon snacks should be used
than three large meals.
 No food should be taken several hours prior to bed time.
 If the pain is severe, liquid antacid particularly those containing topical
anesthetics in antacid gel is advisable. These should be taken at the onset
of pain and one top two hours thereafter.
 Anaemia due to bleeding should be treated with oral iron supplements
 If there is severe blood loss then blood transfusion may be needed.
g. Gastroesophageal Reflux Disease (GERD);
This is a condition in which the stomach’s acid contents back up into the
oesophagus causing discomfort and sometimes tissue damage. People who
suffer from GERD often refer to these symptoms as heartburn or acid
indigestion.
Causes of GERD - It results if the oesophageal sphincter muscle is weak or
relaxes inappropriately. Medical conditions that either interfere with the
sphincter function or prevent rapid clearance of acid from the oesophagus can
predispose a person to GERD.
Conditions associated with GERD include;
 Pregnancy- Pregnancy is the most predisposing condition with as many as
2
/3 of pregnant women reporting heartburn which usually worsen during
the third trimester.
 Obesity
 Asthma
 Hiatal hernia
 Some medication
 Nasogastric tubes can also result in reflux.
Consequences of GERD;
 If gastric juice remains in the oesophagus long enough to damage the
oesophagus lining, the resulting inflammation is called reflux oesophagitis.
 Severe and chronic inflammation may lead to oesophageal ulcers with
consequent bleeding
 Healing and scarring of ulcerated tissues may narrow the diameter of the
oesophagus causing oesophageal stricture.
 A slowly progressive dysphagia for solid foods sometimes results and
occasionally swallowing becomes painful.
 Pulmonary diseases can develop if gastric contents are aspirated into the
lungs.
 Chronic reflux is associated with Barret’s oesophagus a condition in which
oesophageal cells damaged by chronic exposure to stomach acid are
replaced by cells that resemble those in the stomach and intestines such
cellular changes increases the risk of developing oesophageal cancer.
 GERD can also damage tissues in the mouth, pharynx and larynx resulting
in eroded tooth enamel, sore throat and laryngitis.
Treatment of GERD;
The treatment of GERD objectives are to alleviate symptoms and facilitate the
healing of the damaged tissues.
Severe ulceration may require immediate acid suppressing medication,
whereas mild cases may be managed with dietary and lifestyle modifications.
Medications that suppress gastric acid secretion help the healing process by
reducing the damaging effects of acid on the oesophageal tissues. There is need
to use antisecretory agents and antacids which neutralize the gastric acids.
Antacids relieve heartburn but they have only short term effects and may
cause some nutrient deficiencies when used over a long time.
Lifestyle modifications include;
 Avoid eating bed time snacks or lying down after meals. Meals should be
consumed at least 3 hours before bed.
 Reduce night time reflux by elevating the head of the bed and using pillows
under the head and upper chest.
 Consume only small meals and drink liquids between meals so that the
stomach does not become distended which can exert pressure on the lower
oesophageal sphincter.
 Limit foods that weaken the lower oesophageal sphincter pressure e.g.
caffeinated beverages, chocolates, fatty foods etc.
 Avoid cigarette smoking and alcohol both relax the lower oesophageal
sphincter
 Avoid bending over and wearing tight-fitting garments since they can cause
pressure in the stomach to increasingly heightening the risk of reflux.
 During periods of oesophagitis, avoid foods and beverages that may irritate
the oesophagus e.g. citrus fruits and juices, tomato products, garlic, onions,
pepper, spicy foods, carbonated and very hot or very cold foods.
 Avoid using Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. aspirin
and ibuprofen which can damage the oesophageal mucosa.
N/B: food tolerance among patients with GERD can vary, health workers can
help patients to identify food intolerances by advising them to keep a record of
the food and beverages they consume as well as any resulting symptoms.

Diseases of the Stomach

The function of the stomach is to retain its contents i.e. the swallowed food
and then slowly release it into the small intestines. This is where food is mixed
with fluids i.e. acid and enzymes for further digestion downstream. Disorders of
the stomach range from indigestion to serious conditions that require surgical
resection. They are;
a. Dyspepsia
b. Gastritis
c. Peptic ulcers
d. Gastric Surgery

a. Dyspepsia
This is a condition derived from Greek words Dys meaning bad or impaired
while pepsis means digestion. It is indigestion or difficulty in digestion. It is a
symptom of illness rather than a disease itself.
It refers to general symptoms of indigestion in the upper abdominal region
which may include;
 Epigastric pain  Bloating (abdominal distention)
 Gnawing sensation.  Flatulence due to swallowed gas
 Early satiety with food
 Nausea and vomiting  Acid regurgitation
Types of dyspepsia;
There are two types;
i) Functional dyspepsia-This is indigestion without any structural
changes in any part of the alimentary canal. The symptoms are
psychological in origin or due to a particular food.
ii) Organic dyspepsia-This is indigestion that comes as a symptom of the
structures outside the alimentary canal e.g. gall bladder , pancreas,
chronic nephritis, cardiac failure etc.
Symptoms of dyspepsia;
 Reflux of highly acidic gastric fluids which occurs frequently and which may
cause irritation of the oesophagus causing painful inflammation (reflux
oesophagitis)
 Nausea and vomiting.
Management of dyspepsia;
There is need to do careful inquiry into the dietary history, social habits and
general physical examination of the patient.
If the cause is functional e.g.
i) Patient eating meals when excessively tired
ii) Has been smoking too excessively
iii) Taking too much alcohol
iv) Emotionally stressed
v) Overworking
vi) Over worrying
The patient should be assured that if he gives up such habits, his symptoms
will probably clear up rapidly.
The patient should;
 Have sufficient time to eat in a relaxed atmosphere
 Use a balanced diet  Chew properly (mastication)
 Follow a regular meal patter  Rest after meals
 Avoid emotional stress/tension
If dyspepsia is organic, the treatment of underlying disease or diseases may
alleviate the symptoms of dyspepsia.
How to avoid reflux in dyspepsia;
 Reduce gastric acidity by taking  Don’t lie down or exercise
antacids so as to prevent vigorous after eating
irritation  Limit fatty food intake
 Use foods that are least likely to  Avoid alcohol, caffeine, pepper,
irritate the affected oesophagus spices, fruits and fruit juices,
 Eat small frequent meals tomatoes and its products
 Eat high protein foods which act because they irritate the GIT.
as buffers  Avoid tightly fitting garments.
 Avoid liquids after or before  In severe cases, prescribed anti-
eating ulcer drugs can be used to
suppress the GIT secretions.
Treatment of nausea and vomiting;
Prolonged vomiting can be serious and dangerous because large amounts of
electrolytes and fluids are lost and this causes dehydration and nutrient
deficiencies.
To treat nausea and vomiting the following should be done;
 Encourage the patient to relax before eating and avoid over eating
 Eat small meals and avid fluid intake between meals to prevent distention of
the stomach
 Avoid the use of carbonated beverages
 Patients should identify food intolerance and aromas that precipitate
nausea so as to avoid them
 High fat and spiced foods should be avoided
 Patients should not lie down immediately after eating
 Avoid excess alcohol intake alcohol intake
 For vomiting, fluid and electrolytes should be replaced orally and if it is
intractable vomiting (that is not easily managed/controlled), IV fluids can be
used.

b. Gastritis
It is an inflammation of the stomach mucosa.
Causes of gastritis;
 Action of irritant foods on the gastric mucosa
 Excessive erosion of the mucosa by stomach’s own peptic secretions and by
bacterial inflammation.
N/B- the most frequent cause of gastritis is irritation of the mucosa by alcohol.
Gastritis can be acute or chronic;
A. Acute gastritis
This is gastritis that is caused by temporary inflammation of the gastric ucosa
that is usually self-limiting caused by the ingestion of infectious or corrosive
substances e.g.
 Aspirin  Metabolic alcoholism
 Food spoilage  Uraemia (elevated urea in blood)
 Radiation therapy
Causes of acute gastritis;
 Overeating  Shock
 Overuse of alcohol and  Jaundice
tobacco  Fever
 Chronic or excessive doses of  Renal failure
aspirin and other NSAID  Burns
 Trauma  Radiation therapy
 Surgery
Symptoms of acute gastritis;
 Nausea and vomiting  Malaise (general body weakness)
 Headaches  Hemorrhage
 Anorexia  Epigastric pain

Acute gastritis causes anemia, loss of nutrients and increased metabolism.

Dietary management of acute gastritis;
Aims of nutrition management of acute gastritis;
i) To relieve pain
ii) To manage dietary deficiencies
iii) To prevent dehydration

Dietary management involves

 Withhold food for 24-48 hours or longer depending on whether there is
bleeding or pain to allow the stomach to rest and heal
 Give fluids intravenously during this period so as to prevent loss of
electrolytes and fluids i.e. give 5% glucose in isotonic Nacl. If fluids given by
mouth cannot be retained and signs of dehydration appear, then IV fluids
should be given.
 Water with Nacl with or without the addition of glucose and fruit
juiceshould be given frequently in small amounts of 1000-1500ml/hour.
 Avoid seasoned foods.
 When the condition has improved, the patient is given small frequent feeds
of milk and gradually returns to normal diet within 1-2days.
 N/B-The treatment of this condition also involves stopping the drug and
sometimes washing out the stomach and giving alkalis e.g. maxolon and a
liquid diet for 24hours.
B. Chronic gastritis (atrophic gastritis);
This is a condition in which there is marked progressive and irreversible
atrophy of the gastric mucosa related to chronic inflammation, this causes loss
in mucosal cell functions. In atrophic gastritis, the stomach becomes atrophic
until no gastric gland activity remains. This causes all the essential digestive
functions of the stomach to be lost.
This condition may be due to an autoimmune reaction of the gastric mucosa
or caused by a long term infections mostly by Helicobacter pylori.
Chronic gastritis is a condition that is responsible for;
i) Failure of secretion of intrinsic factor for vitamin B 12 absorption leading
to pernicious anemia (macrocytic/megaloblastic anemia) which is a late
stage complication of chronic gastritis
ii) Achlorhydria which is failure of the stomach to secrete HCl and
hypochlorhydria which is abnormally low HCL production (ddiminished
acid secretion).
iii) The lack of acid medium required for iron absorption which leads to
severe iron deficiency anaemia.
iv) Lack of pepsin secretion and if it is secreted it doesn’t work because of
lack of HCL. Thus it affects protein digestion. This condition can lead to
malnutrition.

Symptoms of chronic gastritis;

 Mild anorexia  Early feeling of fullness/satiety
 Heart burn  Haemorrhage
 Nausea and severely repeated  Epigastric pain
vomiting  Pyloric obstruction related to
 Diarrhoea scarred tissues.
 Belching

Management of chronic gastritis;

Aims of management of chronic gastritis;
i) Resting of the chronically inflamed mucosa
ii) Restore nutrients loss
iii) Maintain adequate food and nutrient intake
Management of chronic gastritis involves;
i) Removal of underlying causes e.g. faulty eating habits, drinking alcohol
or smoking
ii) Drug administration e.g. antacids, anti-secretory agents and anti-ulcers
iii) Patients with pernicious anaemia require parenteral injections or nasal
sprays of vitamin B12 due to lack of intrinsic factor for absorption of the
vitamin
iv) Achlorhydria may require parenteral iron injection
v) Once the symptoms have disappeared, an ordinary diet can be used.
vi) Provide a relaxed environment for eating for the patient.
vii) Emphasize the use of adequate calories.
viii) Use a soft and a bland diet
ix) Eliminate foods that irritate the mucosa and those that stimulate gastric
acid secretion as well as individual intolerances.
Foods that stimulate the secretion of gastric acid include;
 Coffee  Peppermint
 Cloves  Tea
 Garlic  Fatty foods
 Chili powder  Alcohol.

c. Peptic ulcers Disease (PUD)

This is a disease due to hurry, worry and curry. It is a general term given to an
eroded mucosal lesion in the central position of the GIT. It is an open sore that
develops in the GIT mucosa. It is a condition that is caused by excess secretion
of or decreased mucosal resistance to hydrochloric acid.
The term peptic ulcers is used because it appears to develop from a loss of the
ability of the mucosa to withstand the digestive action of pepsin and HCL. In a
healthy individual, there is normally a balance between acid and pepsin
secretion. The mucous membrane is protected by mucus, production of
bicarbonate, removal of excess HCL by blood flow and rapid renewal and repair
of epithelial cell injury.
This condition affects those areas that come in contact with gastric juice e.g.
lower portion of the oesophagus leading to oesophageal ulcers, the stomach
leading to gastric ulcers and first part of the duodenum leading to duodenal
ulcers.
In patients with gastric ulcers, the secretion of gastric acid is often within the
normal limits whereas in duodenal ulcers nearly always they have a high
output of acid. Most ulcers are found at the duodenum (70%-90%). This occurs
at the age of between 20-30years. Oesophageal and gastric ulcers (30%-60%)
occurs at age of 45-60years. There is also a type of peptic ulcers called
marginal ulcers which occurs frequently whenever there is an abnormal
opening e.g. gastrojejunostomy that is made between the stomach and some
portion of intestines.
Causes of peptic ulcers;
i) It is most often caused by bacterial infection i.e. by Helicobacter
pylori which causes enteral gastritis where it tends to secrete enzymes
that depletes gastric mucus, making mucosal layer more susceptible to
erosion.
ii) Stressful life, nervous tension and strenuous activities;
N/B-Psychological stress does not cause ulcers per se, but it has effects on the
physiological processes and behaviours that may increase a person’s
vulnerability e.g.
 It may increase the secretion of HCL and pepsin
 It may promote more gastric emptying thus increasing the acid load at the
duodenum
 It brings about hormonal changes that impair immune response and wound
healing e.g. it stimulates the adrenal gland to secrete the hormone adrenalin
and noradrenalin into the blood stream causing an increase in metabolism
or increase the release of excessive amounts of gastric juice which contains
HCL and pepsin.
 It results in elevated levels of steroid hormones which reduce the epithelial
replacement and thus make the mucosa of the duodenum more prone to
erosion by HCL and pepsin.
iii) Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. aspirin which
damage the stomach lining.
iv) Disorders that cause excessive acid secretion.
v) Zollinger-Ellison syndrome which forms a tumor of the pancreas that
causes production of gastrin which stimulates production of excessive
gastric secretion by day and night.
vi) Hereditary factors where a high proportion of duodenal ulcers patients
belong to blood group O. It is believed that secretion of blood group A
and B substances into gastric juice have some protective effects. Close
relatives are more liable to develop peptic ulcers than are relatives of
normal people.
vii) Having irregular and inadequate mastication of food
viii) Potential irritants e.g. caffeine and alcohol which produce an
increase in the gastric acid secretion and thus damage the mucosa
ix) Defects in the pyloric sphincter resulting in reflux of the duodenal
contents to the stomach where the effects of bile salts reduce mucosal
resistance to NSAIDs e.g. aspirin and brufen.
x) Cigarette smoking where some tobacco products decrease bicarbonate
secretion, decrease mucosal blood flow and exacerbate inflammation.

Symptoms of peptic ulcers;

 Epigastric pain which occurs as deep hunger contractions 2-3 hours after
meals. This pain could be piercing or burning type which is relieved by
consumption of food and antacids. The pain is due HCL coming into contact
with exposed nerve endings.
 Low plasma protein levels due to loss or poor utilization of proteins and
thus delaying the healing of ulcers
 There is weight loss and iron deficiency anemia due to blood loss
 There is weight loss in gastric ulcers due to the food eaten not being
utilized and one tends to be choosy and have a poor appetite.
 There is weight gain in duodenal ulcers because the appetite is good as
one eats food to eliminate pain.
 Following the intake of large fluids, there is evidence of pain due to
hypermotility.
 There is discomfort and flatulence in the upper part of the abdomen
 Bleeding of the ulcers can also result in blood in vomit referred to as
haematemesis (blood in vomit).
 There is nausea and vomiting and anorexia in gastric ulcers and heart
burn and constipation in duodenal ulcers
 Melanoma occurs which is black stool due to bleeding.

Treatment of peptic ulcers;

Aims of treatment of peptic ulcers;
i) To relieve pain
ii) Bring healing to the ulcers
The general treatment involves;
a) Drugs;
This plays an important role and depends on the cause of the ulcers. These
drugs include;
i. Antacids that neutralize the acids e.g. aluminum hydroxide or
magnesium oxide
ii. Anticholinergic drugs to decrease acid secretion in the stomach e.g.
proton pump inhibitors
iii. Antispasmodic to reduce motility
iv. Antibiotics used to treat infections.
b) Dietary management;
The main objectives of dietary management are;
i. To maintain good nutritional status
ii. To promote healing
iii. To supply the nutrients needed to heal the ulcers i.e. proteins and
ascorbic acid
iv. To provide foods that give the patient satisfaction and comfort
v. To avoid mechanical, chemical and thermal irritation of the GIT.
vi. To prevent recurrence of the ulcers.
 Patients should avoid substances that increase acid secretion or irritate the
GIT lining e.g. alcohol, coffee, tea, chocolate, pepper although individual’s
tolerance may vary.
 Patients should take small frequent meals. They should avoid consumption
of food atleast two hours before bed times.
 Eat meals in a relaxed way
 Avoid spicy foods and fried foods
 Avoid overeating since it exposes gastric or duodenal mucosa to excessive
amounts of acids
 A light and bland diet is recommended.
 Avoid excessive acid production by starvation or fasting
 Eat slowly
 Avoid gas forming foods e.g. cabbages, pulses, onions, water melon etc.
Dietary recommendations;
i. Energy- consumption of food should be increased to overcome weight
loss and achieve ideal body weight in gastric ulcers. For weight gain
provide 30-35kcals/kgbwt/day, for weight loss, give
20-25kcals/kgbwt/day and for maintainace of ideal body weight give
25-30kcals/kgbwt/day.
ii. Proteins- if ulcer wounds are not healed on time, they get perforated;
they can also bleed; in order to heal it and help in the formation of new
tissues, adequate amounts of proteins are required.
N/B: milk is a good option since it neutralizes the acidic effects in the
gastric juice. But the intake should be restricted since high calcium intake
 can be hazardous for the inflamed mucosa in that it causes excessive
stimulation of gastric secretion. It should therefore be used in moderation.
Other protein sources including eggs, fish, cheese etc are preferred. Provide
between 1.2-1.5g/kgbwt/day which account for 10-15% of the total kcal.
iii. Fats- they help delay gastric emptying. It plays a role in inhibiting gastric
juice secretion ad thus reduce ulcers. 25-30g (5-6 teaspoons) of visible
fats can be given freely per day. They should include; oil, ghee, butter
etc. They should provide between 25-30% of the total kcals.
iv. Carbohydrates; these should provide between 55-65% of the total kcals
per day and should come from carbohydrates foods that are well cooked.
Soft foods should be consumed. Soluble fibre is more acceptable and
beneficial than insoluble fibre. Foods rich in soluble fibre are fruits and
vegetables. Give fruits that are alkaline and avoid citrus fruits and juices.
v. To accelerate the healing process, in addition to proteins there are
specific micronutrients e.g.
 Zinc that is essential for maintaining the immune system function
as a response to oxidative stress and to heal wounds.
 Selenium is needed to reduce infection complications and to
improve healing
 Vitamin A is needed to increase production of mucus in the GIT
thus protect it from acidity
 Vitamin C needed to eradicate Helicobacter pylori and to promote
healing of the ulcers
N/B: alcoholic beverages e.g. beer should be avoided because even in small
amounts it induces to near maximal gastric acid secretion without providing
any significant buffering capacity.
c) Rest;
Both physical and mental rests are important for patients in the management
of peptic ulcer. These provide complete relaxation of the mind and body and
control of emotional stress and thus help to relieve the patient.
d) Surgery;
Surgical procedures known as vagotomy are performed so as to reduce the
stimulation of gastric acid secretion thereby relieving the patient of the
symptoms associated with peptic ulcers. Although these results in rapid entry
of liquids or liquids and solids into the intestines resulting in abdominal
distension and pain.
e) Giving up smoking;
This is because some tobacco products decrease bicarbonate secretion,
decerese mucosal blood flow and increase inflammation.
Diseases of the Small Intestines;
The small intestines consist of the duodenum, jejunum and the ileum.
The functions of the small intestines are;
i. Complete digestion by enzymes secreted here
ii. Absorption of nutrients.
The duodenum is the absorptive site for; iron, calcium, folic acid, fat, some
sugar and amino acids. Jejunum is the absorptive site for sugar and amino
acids while the ileum is the absorptive site for vitamins and bile salts.
N/B: the functions of the intestines may be affected by organs surrounding it.
I.e. liver, pancreas, disturbance of motility, transport mechanism which
interfere with efficiency of the small intestines.
The disorders of the small intestines include;

a. Diarrhea and dysentery;

Diarrhea is characterized by the passage of loose watery unformed stool.
Dysentery is the passing of unformed stool with mucus and blood. These
conditions cause food to pass rapidly not allowing time for nutrients to be
absorbed thus leading to nutritional deficiencies. Diarrhea is a symptom not a
disease thus its treatment must be preceded by a careful investigation of the
cause.
Diarrhea can be acute or chronic. Acute diarrhea may occur due to ingestion
of contaminated food. It has a sudden onset and is accompanied by the
following symptoms;
 Abdominal pain/Cramps
 Weakness
 Fever
 Vomiting
If the attack of diarrhea or dysentery persists, it leads to chronic diarrhea
which is a diarrhea that persists for 2 weeks or even longer.
Types of diarrhoea;
i) Osmotic diarrhea-this is the passage of watery stool due to nutrient
malabsorption e.g. when sugars like sorbitol or fructose are poorly
absorbed, they attract water to the colon and increase water content in the
fecaes
ii) Secretory diarrhea-is due to the secretion of fluids by the intestines which
exceeds the amount that can be reabsorbed by the intestinal cells. It may be
caused by bacterial food poisoning, chemical substances and the
inflammation associated with some intestinal diseases
iii) Motility disorders diarrhea- this is diarrhea caused by accelerated transit
of the colonic residue reducing the contact time available for fluid
reabsorption.
Causes of diarrhea;
i. Tension due to exams or fear of facing an interview
ii. Excessive use of laxatives which become a habit for most people
iii. Diseases of the small intestines e.g. malabsorption syndrome, malnutrition,
vitamin A deficiency, niacin deficiency etc.
iv. Carcinoma of the colon and rectum
v. Overeating or eating foods difficult to digest
vi. Allergies to certain foods e.g. milk, eggs and sea foods.
vii. Antibiotics and some drugs.
N/B: most causes of diarrhea may be functional or organic. Functional
diarrhea results from neuromuscular over activity due to emotional states.
Organic diarrhea comes as a result of irritation or inflammation of the mucous
membrane of the bowel by bacterial, viral, protozoan, chemical or physical
agents especially by microbial food poisoning and feacal-oral infections e.g.
salmonella and shigella.
Diarrhea is the most common and dangerous ailment which small children
suffer from. It frequently causes dehydration through the passage of loose
watery stool with increased frequency. The number of stools varies from
several per day to one every few minutes.
Symptoms of dehydration;
 Severe thirst
 Very little output of urine
 Drying up of the smooth
 Loss of skin elasticity
Treatment of diarrhea;
 Drugs are unnecessary because they relieve symptoms only shortly and also
they interfere with the bowel’s protective function to rid the body of harmful
contents. Antibiotics are best if avoided unless there is a bacterial diagnosis
and the appropriate drug can be given.
 An effective preventive measure is to start Oral Rehydration Therapy (ORT)
which is based on the administration of correct oral fluids while allowing
food intake. This provides a balanced water and electrolyte replacement.
This can be administered not only in health facilities but also by
community-based health worker and by mothers and relatives with some
guidance.
 Rehydration with fluids improves appetite, allows better feeding and
continued weight gain.

WHO/UNICEF recommended ORT formula;

Sodium chloride 3.5g
Sodium bicarbonate 2.5g
Potassium chloride 1.5g
Glucose 20.0g
Water 1 litre

Management of diarrhea;
 At the first sign of diarrhea, a simple formula can be made at home using
1liter boiled and cooled water mixed with 20g glucose or 40g sugar with ½
 teaspoons of common salt, ½ teaspoon of sodium bicarbonate and a little
lemon juice (to provide potassium chloride) and the patient should be given
at least 4-6 glasses per day.
 After the patient has stabilized, he can be given water, coconut water, tea,
buttermilk and rice water (prepared by cooking rice in a lot of water and
draining the water to which salt is added to taste).
 If the patient is able to eat, he can be given ripe bananas, soft cooked rice,
curds, bread, mashed potatoes and arrow root biscuits.
 Breastfeeding of the infant should be continued throughout.
 Juices of oranges, buttermilk, or barley water with milk and sugar can be
given.
 Other natural remedies e.g. carrot soup, bananas, peeled apple, turmeric
powder, cultured milk, or sour milk and garlic can be used effectively.

Principles of dietary management of diarrhea;

i) The diet should be low in residue
ii) It should be bland with no spices and condiments.
iii) Plenty of fluids should be included to maintain electrolyte balance.
iv) Energy from easily assimilated carbohydrates should be given e.g. porridge
v) Proteins used should be easily digestible e.g. soft boiled eggs, skimmed
milk, but if the person has lactose intolerance, milk should be restricted.
vi) Fats are usually restricted because they are not easily absorbed and may
aggravate the diarrhea.
vii)Avoid spicy foods, strongly tea/coffee, carbonated beverages, fried foods and
fibrous fruits and vegetables.

b. Malabsorption syndrome;
Malabsorption is a general term that describes incomplete absorption of one or
more essential nutrients even though food is well digested. Malabsorption can
lead to nutrient deficiencies and weight loss and cause serious complications.
To digest and absorb we depend on normal digestive secretions and healthy
intestinal mucosa. Malabsorption can therefore be caused by several different
diseases that cause decreased absorbability by the mucosa.
Causes of malabsorption are;
 Increased motility of the GIT e.g. diarrhea
 Inadequate supply or absence of pancreatic or intestinal enzymes or bile
 Defects in the structure of the villi so that the area of absorbing surface is
reduced.
 Deficiency of mechanisms of amino acids transport e.g. in cystinuria
 Allergy i.e. injury of the mucosa of the small intestines due to sensitivity to
certain nutrients e.g. wheat gluten.
 Prolonged use of certain antibiotics
 Competition with bacteria and other biological agents for nutrients due to
deficiency of protective secretions e.g. HCL.
 Surgery used in the treatment of intestinal disorders that causes resection
resulting in the reduction in the absorptive surfaces.
 AIDS-related enteropathy
N/B: fat malabsorption may lead to formation of insoluble calcium and
magnesium soaps which are carried out of the body. And also formation of
oxalate stones in the kidneys as a result of fat malabsorption because oxalates
in foods bind calcium and are excreted out of the body (the stones are absorbed
and travel to the kidneys).
There are four types of malabsorption syndromes (sprue);
i) Nutritional sprue (in adults);
This is a sprue that is commonly known as idiopathic sprue, celiac disease (in
children) or gluten induced enteropathy. It results from toxic effects of gluten
present in certain types of grains especially wheat and rye. Gluten has a
fraction known as gliadin which is responsible for these toxic effects.
The stools are bulky, foamy and foul and have a high percentage of fat
(steatorrhea) and there are serious losses of nutrients because there is no
absorption of most essential nutrients.
If the patient is untreated, he or she may present many signs of malnutrition
which include;
 Weight loss  Pernicious anaemia due to the
 Protruding abdomen deficiency of vitamin B12 and
 Bone pain folate.
 Peripheral neuritis  Prolonged bleeding time (due to
 Muscle wasting inadequate blood coagulation
 Sore mouth due to lack of vitamin K)
 Increased fractures due to
demineralization

Dietary management;
Eliminate all sources of gluten in the diet which brings about remarkable
improvement within 2 weeks. Omit all products containing wheat, rye, oats or
barley. This diet must be continued indefinitely. The patients require much
counseling regarding the foods that they have to prepare them and how to
interpret labels.
N/B-do not use wheat flour in thickening soup even if very little.
ii) Tropical sprue;
This is a condition that frequently occurs in the tropics and can be treated with
antibacterial agents. It is believed that it is caused by inflammation of the
intestinal mucosa resulting from unidentified infectious agents (bacterium).
This condition causes atrophy of the jejunal villi like what is seen in gluten
enteropathy.
iii) Idiopathic steatorrhea (fat malabsorption);
This means excess fats in stool as a result of unknown causes. In its early
stages, the absorption of fats is more impaired than any other digestive
product. The fat appearing in stool is almost entirely in the form of soap rather
than undigested neutral fats (this shows that the problem is absorption not
digestion). The condition results in lack of absorption of very many important
nutrients.
Dietary Management;
 The management of this condition involves the use of low fat diet.
 When steatorrhea is severe, it is important to begin with a diet nearly fat
free as possible and to add small quantities of fat few days until the patients
limit of tolerance is reached.
 Food rich in fats should be restricted/ excluded at first. The best fat that is
tolerated is milk fat because it contains a high proportion of fatty acids of
medium chain length. MCT (medium chained triglyceride) are useful in the
treatment of steatorrhea because they are absorbed at the portal vein by
combining with albumin.
 Water miscible fat soluble vitamins can be used.
 Oxalate restricted diets should be used (avoiding foods e.g. spinach, tea and
nuts).
iv) Lactose intolerance;
This is a congenital lactase deficiency condition. It is a condition which is
present in small percentage of the infants born and those children with protein
energy malnutrition who are unable to digest lactose in milk.
This condition comes as a result of the failure of the mucosal cells of the small
intestines to produce enzyme lactase as a result lactose passes unchanged into
the large intestines where it is fermented by bacteria flora with the production
of loose stool containing lactic acid.
Acquired lactase deficiency is a condition whereby many individuals who had
adequate levels of lactase during infancy and preschool years lose some of
ability to digest lactose in his later years. This especially occurs in people who
consume large amounts of milk e.g. those with excessive use of milk in the diet
like peptic ulcers and in tube feeding.
Dietary management;
This involves the use of lactose free diet.
N/B: most children and adults with lactase deficiency can tolerate small
amounts of lactose therefore the diet should be adjusted to the individual’s
tolerance e.g. a child may tolerate ½ cup of milk at a time but have symptoms
of;
 Bloating
 Flatulence
 Cramps
 Diarrhea when he drinks greater amounts at each meal.
Some people tolerate amounts of lactose in cheese and in butter whereas
others tolerate fermented milk e.g. buttermilk, mala and yoghurt.
Where there is total absence of lactase (a rare occurrence), the diet must be
planned to eliminate all of lactose. Calcium supplements must be prescribed
for such dietary restrictions.
N/B: lactase cannot be induced in adults who have the enzymes but a
commercial preparation of lactase can be added to milk to convert the lactose
to sugars that can be absorbed.

c. Diverticular Disease;
Diverticula are small pouches or sacs which develop in the intestinal walls (it
can be in the oesophagus, stomach, small and large intestines) which bulge
out. They may be congenital in origin or acquired during life. They are found
mostly in the colon. This condition is associated with pressure on the intestinal
walls combined with weakness of supporting muscles of the intestines.
Aging and low fibre diet increases the risk of this condition.
The presence of diverticula is known as diverticulosis whereas the
inflammation of the sacs is known as diverticulitis this result due to
accumulation of feacal materials leading to infection.
N/B: a larger percentage of people (30%-60%) have diverticulosis but only 5% -
10% of them have diverticulitis.
Symptoms of diverticulitis;
 Abdominal pain  Flatulence
 Alternating periods of diarrhea  Abdominal distention
and constipation  Fever
 Dyspepsia  Bloody stool
Chronically inflamed diverticulitis results in chronically inflamed bowel with
narrowing of the lumen creating obstruction. The inflamed bowel segment can
stick to other pelvic organs forming a fistula (an abnormal opening between
organs).
Dietary management and treatment of diverticular;
i) Use a high fibre diet to stimulate GIT maintenance.
ii) Avoid food with needs e.g. berries, passion fruits and tomatoes that may
be trapped in the diverticular which may cause irritation
iii) Drink a lot of fluids especially water
iv) Drugs e.g. antibiotics can be used when there are signs of active
inflammations e.g. ampicillin, antispasmodic drugs can be used to
relieve pain.
v) Surgery which can be performed in a few cases because of obstruction
(especially in severe cases)

d. Crohn’s diseases (Chronic Regional Enteritis);

This is a chronic inflammatory bowel syndrome (IBS) which is mainly found in
the small intestines. It is a quite prevalent condition with no known cause.
Infectious agents are the major theoretical focus; it is thought to be an
autoimmune disease (whereby the body produces antibodies against itself).
In this condition the body produces an antibody that affects the bowel. It also
has some genetic influence so that there is inflammation and ulceration along
the tract causing granuloma tumors. This can affect the ileum and follow the
colon or the entire system; this may affect the joints, eyes and skin.
When fibrous tissues form in the intestines it reduces the absorptive ability
and may narrow the intestinal lumen causing obstruction. Sometimes the
intestines may rapture and cause infections to other organs.
This condition may cause the nutritional status of the patient to be affected
due to;
 Anorexia  Bleeding that may lead to anemia
 Weight loss and loss of serum proteins
 Fever essential for transport of nutrients
 Diarrhea  Deficiencies of minerals and
 Malabsorption vitamins and PEM.
 Abdominal pain
Treatment of Crohn’s disease;
This condition has no specific treatment; the following may be used;
 Surgery which involves the removal of the affected part can be used. This
can lead to “short bowel syndrome” which may further contribute to
malabsorption.
 Parenteral and enteral nutrition may be applied using easy to absorb
formulas.
 If patient tolerates; give an oral diet consisting of high calorie, high protein
diet, fat restricted depending on the on the patients tolerance with adequate
vitamins and minerals.
 Low fibre diet to avoid obstruction of the lumen should be given
 Identify lactose or any food intolerance so as to remove it from the diet.

e. Short bowel syndrome;

This condition occurs when the absorptive surface of the intestines is reduced
due to surgery e.g. up to 60% of the intestines. It could be due to;
 Ulcers  Crohn’s disease
 Cancer  Entangling of the intestines.
The length, location and the health status of the remaining intestines will
determine the degree to which nutrient absorption and metabolism is affected.
The length of time that has elapsed since resection also determines occurrence
of the symptoms of this condition. Up to 50% can be resected without serious
nutritional consequences.
Sometimes the intestines can regenerate and absorb nutrients efficiently i.e.
adaptation or it may begin to absorb nutrients that were not absorbed before. It
sometimes becomes thicker, longer and wider to be able to absorb the
nutrients. This adaptation normally occurs after 1-2years after the surgery.
This condition is characterized by three postsurgical phase namely;
i) First phase which lasts for 7-10 days after surgery where the patients
experience large fluid and electrolyte losses related to massive diarrhea.
ii) Second phase which occurs 1-3 months after surgery where majority of
adaption occurs. There is stabilization of diarrhea and a positive fluid
balance which can be achieved through oral intake. There is fat
malabsorption in this phase and deficiencies of nutrients e.g. calcium
and magnesium.
iii) Third phase is the phase of complete adaptation in which nutritional
requirements are met through an oral diet.
Some of the nutrients affected in this include: Ca, Mg, Vitamin A, D, E and K,
carbohydrates and proteins especially if the ileum is affected. Little bile will
also be absorbed thus reduce the body’s pool making it difficult to hydrolyze fat
thus its absorption.
Symptoms;
 Diarrhea
 Protein and fat malabsorption
 Anaemia due to blooed loss
 Calcium and magnesium reduction
 Causes the colon to receive a large volume of unabsorbed nutrients
Nutrition management;
 Nutrition therapy for short bowel syndrome is highly individualized
depending on the patient’s tolerance.
 Usually TPN is used as the primary sources of nutrients during the first two
phases.
 During the third phase; enteral nutrition is gradually introduced to
stimulate GTI.
 When diarrhea is controlled and tolerance of an oral feeding improves,
complete transition to an oral diet occurs.
 Tolerance of an oral diet is usually enhanced by restricting ;
o Fats
o Oxalates
o Concentrated sweets
 Calorie needs may be one and half to two times above normal in patients
who have had 50% or more of the GI removed.

General guidelines to slow the passage of food through the

gastrointestinal tract and thus reduce diarrhea include;
 Eat six to eight small meals daily
 Avoid fluids 1 hour before and after each meal.
 Avoid caffeine (coffee, tea and chocolate) and alcohol for the first year after
surgery then use sparingly
 Reduce fat to a minimum with a goal of less than 8 g per meal if eating six
meals per day. Label reading is very important to identify hidden sources of
fats.
 MCT (medium chain triglycerides) oil in doses of 15ml three to four times a
day may be used to supply additional calories.
 Use yoghurt and aged cheese that doesn’t have lactose. Lactose should be
limited to small amounts.
 Avoid foods and medication that contain mannitol and sorbital because they
have a laxative effect.
 Dilute fruit juices and soft drinks to 50% strength by adding water so as to
lower the osmolality
 Avoid acidic foods such as tomato products and citrus juices, if they cause
heart burns
 Avoid concentrated sweets because they are hyperosmotic and may promote
diarrhea
 After a baseline diet, restricted categories are reintroduced one at a time.
Patients who are unable to adapt need TPN permanently.

f. Cystic fibrosis (CF);

This is an inherited autosomal recessive trait condition characterized by
hypersecretion of abnormally thick mucus that obstructs exocrine glands and
ducts (it is normally classified as a respiratory or GI disorder). This condition
results in an abnormally high concentration of sodium in perspiration and low
water content in mucus.
CF affects the pancreas, intestinal tract, sweat glands, and lungs. In male it
causes infertility.
Symptoms;
 Thick mucus in the lungs that accumulates and clogs the air passage,
damages the epithelial tissues of the airways which leads to chronic
obstructive pulmonary disease (COPD) and frequent respiratory infections
which leads to increased metabolism and energy-nutrient needs.
 Pancreatic insufficiency caused by progressive clogging of panctreatic
enzymes leading to a bulky foul smelling, oily stools (steatorrhea),
progressive loss of insulin-producing beta cells in the islets of langerhans
resulting in diabetes mellitus.
 Malabsorption of undigested food nutrients, extensive malnutrition and
stunted growth
 Excessive sweating in hot weather that may lead to dehydration and
circulatory failure
 Biliary cirrhosis which is a chronic liver disease characterized by loss of
functional liver cells with fibrous and nodular regeneration caused by
progressive clogging of bile ducts producing biliary obstruction and
functional liver tissue degeneration.
 Inflammatory complications e.g. arthritis
 Gall bladder disease, peptic ulcers, GERD or episodes of partial intestinal
obstruction
 Delayed puberty and maturity probably due to chronic malnutrition (male
are typically infertile because the vas deferens fails to develop).

Nutritional management;
 The patient with CF should consume high calorie, high protein diet with no
fat restriction
 Proteins range from between 10%-20% of the RDA. To compensate for fat
malabsorption, about 35%-40% of the total kilocalories should come from
fats.
 Patients are encouraged to eat high calorie and high fat foods, eat frequent
small meals and snacks and supplement meals with milk shakes or liquid
dietary supplements.
 Supplemental tube feedings can help to improve nutrition status if energy
intakes are inadequate.
 There is need to use improved therapeutic products e.g. replacement of
pancreatic enzymes e.g. PERT(Pancreatic Enzyme Replacement Therapy) in
the form of capsules encased enteric coated microspheres “beads” that
correct maldigestion and support energy-nutrient growth needs.
 Enzyme dosage may need to be increased if malabsorption e.g. steatorrhea,
intestinal gas and abdominal pain. The risk of the deficiency depends on the
 degree of malabsorption of nutrients of greatest concern which include the
fat soluble vitamins, essential fatty acids and calcium.
 Multivitamin and fat soluble vitamin supplements are routinely
recommended.
 The liberal use of table salts and salty foods is encouraged to make up for
losses of sodium in sweat.

g. Dumping syndrome;
This is a disease of the small intestines that is a complication that
accompanies gastric surgery in which the pyloric sphincter is removed,
bypassed or disrupted. It is characterized by a group of symptoms resulting
from rapid gastric emptying.
There are nutritional problems that are experienced until the patient adapts to
the altered pyloric sphincter. There is also weight loss after gastric surgery that
is caused by;
 Diarrhea
 Steatorrhea
 Voluntary restriction of food intake to avoid symptoms
 Early satiety
 Restrictive diet
The work of the pyloric sphincter is to allow controlled amounts of food to move
from the stomach into the small intestines. When this sphincter is bypassed or
impaired, undigested food (hypertonic stomach contents) is rapidly “dumped”
into the duodenum or jejunum.
When the duodenum is bypassed, digestive activity that normally occurs there
is also bypassed. If the sphincter is bypassed, normally food moves quickly into
the jejunum even if the duodenum is intact. The undigested food in the
jejunum is hypertonic (i.e. higher osmolality than the fluids in the jejunum and
blood) which causes fluids to shift from the plasma and extracellular fluids into
the jejunum to dilute the high particle concentration.
Large volume of hypertonic fluid in the jejunum causes the following within
15minutes after eating;
 Nausea  Diarrhea
 Distention  Light headedness
 Crampy pain  Rapid heart beat
These results from fluid shift from the plasma and extracellular fluid to the
jejunum which causes a rapid decrease in circulating blood volume.
There is a secondary reaction called reactive hypoglycemia which may occur
hours later. This comes as a result of rapid absorption of carbohydrates which
causes a rapid rise in blood glucose levels which the body compensates by over
secreting insulin which causes a rapid drop in blood glucose levels with the
following symptoms;
 Dizziness  Syncope- fainting or ‘passing out’
 Perspiration due to insufficient blood supply
 Tachycardia-fast heart rate than to the brain resulting from
normal. More than 100 beats per sudden reduced heart rate and
minute blood pressure.
 Mental confusion
There is also maldigestion and malabsorption because of rapid transit time
which causes food not to have adequate exposure time to be with enzymes and
bile. There is also reduced gastric acid secretion which leads to bacterial
overgrowth in the stomach or small intestines which causes malabsorption of
fat, fat-soluble vitamins, folate, vitamin B12, calcium and iron.
The excretion of calories and nutrients produces weight loss and increased risk
of malnutrition.

Early dumping syndrome (within 15- Late dumping syndrome (1 hour

30 minutes after meals) to 3 hours after meals)

 Abdominal pain (cramping)  Anxiety

 Diarrhea  Confusion
  Dizziness  Headache

 Flushing (sweating)  Hunger

 Nausea and vomiting  Palpitation

 Rapid heartbeat  Sweating

 Weakness and feeling faint  Weakness and feeling faint

Nutrition management of dumping syndrome;

 Take small frequent meals i.e. 5-6 or more meals per day because the
holding capacity of the stomach is reduced.
 The patient should eat slowly and to chew food thoroughly
 Simple sugars need to be eliminated because they are quickly digested and
form a hyperosmolar solution in the jejunum that attracts water e.g. sugar,
gelatin, cookies, soft drinks, undiluted juices and other high sugar items
need to be avoided.
 Include moderate fat and high protein at each feeding because they are
digested more slowly than carbohydrates and do not increase osmolality.
 Total calories need to be adjusted accordingly to weight goals e.g.
o Weight gain may be indicated for patients undergoing gastric surgery for
cancer
o Weight loss may be indicated in patients who have gastric bypass
surgery to treat obesity.
 Avoid fluids with meals an hour before or after eating. Limit liquids to ½ to
1 cup.
 Lie down 20-30 minutes after eating to delay gastric emptying time (patients
with reflux should not lie down after meals).
 Eat foods high in pectin e.g. apples and guar gum e.g. oats so as to help to
slow gastric emptying, slow carbohydrate absorption and blunt the glycemic
response e.g. take 1 teaspoon pectin three times daily.
 Milk is restricted or eliminated based on tolerance. Lactose restricted milk
may be tolerated because lactose has been broken down to glucose an
galactose although these are simple sugars that may promote dumping.
 Parenteral injection of iron and vitamin B12 may be necessary due to iron
and vitamin B12 and folate deficiencies may occur secondary to decreased
intake, blood loss or impaired absorption.
 All food and beverages should be served at moderate temperature
 The diet can be liberalized to include limited amounts of concentrated
sweets, larger meal sizes and some liquids with meals as the remaining
portion of the stomach or duodenum hypertrophies to hold more food and
allow for more normal digestion.

Diseases of the Large Intestines;

a. Ulcerative colitis;
This is an inflammatory bowel disease of the large intestines which causes;
 Severe diarrhea  Anorexia
 Rectal bleeding thus blood loss  Electrolyte imbalance
and anaemia  Dehydration
 Abdominal crampy pain  Fever
 Weight loss
It is a condition characterized by presence of ulcers in the mucosa of the large
intestines. The ulcerations are most commonly situated in the rectum. The
condition has got no known cause though an autoimmune disorder is believed
to be its cause.
People with active ulcerative colitis fail to respond to medical therapy therefore
surgery is used to remove the part that has been affected.
Nutritional management of ulcerative colitis;
 In acute periods no dietary intervention are given but people may be given
bowel rest through the use of parenteral feeding (TPN).
 High protein of about 1.5g/kg body weight/day should be given.
 High calories of 3000kcals/day should be given.
 Low fibre and restricted fats should be used.
 Any foods that irritate the mucosa especially raw vegetables, spiced foods
should be eliminated.
 In case of lactose intolerance, milk and milk products may be eliminated
(use soya milk).
 The patient should be treated for anaemia with iron salts (orally), folic acid
and vitamin B12 parenterally.
Drugs used in the management of ulcerative colitis;
 Anti-inflammatory agents  Anti-diarrheal drugs
 Anti-infective agents  Analgesics.

b. Constipation;
This means the hardening of stools resulting in distention and difficulty in
evacuation of the intestinal contents (faeces). It is delay in passages of feaces.
Stools are sometimes accompanied by blood loss as the anal passage may be
damaged or scratched.
General causes of constipation;
 Lack of sleep and rest  Painful defeacation due to
 Irregular eating and elimination hemorrhoids hence psychological
habits aversion and avoidance to
 Faulty dietary habits such as eliminate feaces
including more refined and  Organic diseases e.g.
concentrated foods and very little diverticulosis
fibre  Ingestion of certain drugs
 Chronic use of laxatives  Changes in the surrounding
 Poor muscle tones e.g. in the old
persons or bed ridden patients

Treatment of constipation;
The principles of treatment of constipation are as follows;
i. Correction of faulty habits;
 The bowel should be moved at fixed hours of the day
 If the diet doesn’t contain adequate fibre, the patient should asked to
take foods rich in roughage
 He should be encouraged to drink enough water particularly in the
morning
 ii. Physical exercise;
The patient must be advised to take exercise for the development of the
abdominal muscles.
iii. Removal of other causes;
Mental worry and anxiety should be eliminated.
iv. Diet;
The diet should contain foods rich in fibre which includes;
 Whole cereals, whole legumes and mature vegetables
 Fruits rich in fibre and/or pectin e.g. guavas, apples and bananas
 Adequate amounts of water should be drunk.

c. Flatulence;
This is a disease of the large intestines which is a condition of having excessive
stomach or intestinal gas.
Sources of gas are;
o Swallowed air
o Production of gas in the intestines from food or by microbes
 Air swallowing (aerophagia) is a common cause of gas in the stomach. This
is air that is swallowed when eating or drinking. This gas is expelled
through belching. Residual gas after belching moves to the small intestines
and a small quantity travels to the large intestines and is expelled through
the rectum.
 Gas produced in the intestines is by the action of bacteria in the large
intestines that that break that break down undigested foods that human
beings can’t due to lack of specific digestive enzymes. This is gas is made of
odourless vapours i.e. CO3, O2, NH2 and sometimes methane (CH4).
 The unpleasant odour of flatulence is produced by bacteria in the large
intestines that release small amounts of gases that contain sulfur, H 2 and
 carbon dioxide after digestion of indigestible carbohydrates, fruits and
vegetables.
 In those patients with malabsorption syndrome, large amounts of
disaccharides pass into the colon and are fermented producing H 2 while
those with lactose-intolerance there is production of CH 4
 Foods that produce gas in one may not produce gas in another. Most foods
that produce gas contain carbohydrates, fats and proteins.

Management of flatulence;
 Change the diet
 Take medication
 Reduce the amounts of swallowed air by eating slowly.

UNIT 13: WEIGHT MANAGEMENT
___________________________________________________________________________

Unit Objectives
Define terms used in weight management
Describe overweight and obesity, their causes, health risks and nutrition management
Describe underweight, its causes and nutrition management
Plan and prepare meals for weight management

Introduction to weight management

Both overweight and underweight result from energy imbalances. Overweight
people have consumed more energy than they expend and the surplus is
banked as body fat. Underweight people have consumed too little food energy
to support their activities and so have depleted their body fat stores and some
of the lean tissue mass.
To reduce weight requires people to expend more than they consume; to gain
they need to take in more food energy than they expend. A body’s weight
reflects its composition i.e. the proportion of its bone, muscle, fat, fluid and
other tissues. All of these components can vary in quantity and quality. The
bones can be dense or porous, the muscles can be well developed or
underdeveloped, fat can be abundant or scarce etc. The most variable tissue is
body fat.
The most important criterion for determining how much a person should weigh
and how much body fat a person needs is not appearance but good health and
longevity.
Obesity; is a condition in which an excess of fats accumulate in the body in
some cases can be detected by visual inspection. It is a condition in which the
body’s weight is considerably greater than normal weight for age. It is fatness
with adverse degree that is defined as a body mass index greater than 30.
Obese; is person who is more than 20% above the normal ideal weight for his
or her age, sex and height.
Hyperplasic obesity is obesity due to increase in the number of new fat cells.
Commonly seen in children.
Hypertrophic obesity is obesity increase in the size of fat cells. Commonly
seen in adults. Overweight; is a weight that is above the normal that might be
explained by increased muscular development or excessive fatness. It is fatness
of moderate degree that is defined as a body mass index of between 25.0 and
29.9.
Overweight person; is a person whose weight is 10-20% above the normal or
ideal weight for his/her age, sex and height.
Underweight; this is a weight that is 10% or more below the normal or ideal
weight of his/her age, sex and height.
% weight loss= Usual weight-current weight x 100
Usual weight
Anorexia nervosa; is a psychiatric disease (anorexia-without appetite and
nervosa-of nervous origin) from a refusal to eat which often leads to severe
emaciation especially in women between 15-25years. It is a normal desire to
maintain a low body weight. It is associated with self-starvation to the extreme
and disturbed perception of body weight and shape.
Bulimia nervosa; is mental condition in which a person eats food and induces
vomiting (purging) so as to avoid the increase in weight. It is common in
adolescence who have phobia of being obese. A range of healthy body weights
has been identified using a common measure of weight and height known as
Body Mass Index (BMI). It is an index of a person’s weight in relation to
height. It often correlates with the degree of body fatness and disease risks.
BMI is determined by dividing weight in kilograms by square of the height in
meters. i.e. BMI=wt(kgs)/ht(m)2 .
Classification of BMI by WHO;
Classification BMI
Severely underweight <16
Underweight 16-18.5
Average/Normal 18.5-24.5
Overweight 25.0-29.9
Obese Class I 30.0-34.9
Obese Class II 35.0-39.9
Obese Class III (Morbid Obese) >40
Limitations of using BMI
 BMI values are most accurate in assessing the degree of obesity and are less
useful for evaluating non-obese people’s body fatness.
 It also fails to reveal the information in assessing disease risks and how
much of the weight is fat and where the fat is located.
For this knowledge, measures of body composition are needed.

Body Composition:
For many people being overweight compared with the standard means that
they are fat, which is not the case with athletes who have dense bones and
well-developed muscles, they may be overweight but carry little body fat. On
the other hand, inactive people may seem to have acceptable weights but still
carry too much body fat.
Distribution of fat on the body is even more critical than fatness alone.
There are two types of fat distribution in the body;
i) Visceral fat; these are fats that collects deep within the central
abdominal area i.e. the trunk of the body. This is a fat that is associated
with central obesity which is a risk factor for diabetes, stroke,
hypertension and coronary artery diseases. These increases the risk of
death.
The possible explanation for the increased risk of diseases associated
with this fat involves reduced adipokines a hormone released by visceral
adipose tissues which help regulate inflammation and energy metabolism
in the tissues. The reduced levels of this hormone results in increased
inflammation and insulin resistance which contributes to diabetes,
atherosclerosis and other chronic diseases. Weight loss restores
 adipokines levels and inflammation and insulin resistance are relieved
resulting in disease risk drop.
This fat creates the “Apple body shape”. This shape is more common in
men than in women and also common in post menopause women.
Smokers are also more likely to have central fats.
ii) Subcutaneous fat; these are fats found around the hips and thighs i.e.
the lower body. It creates the “Pear body shape”.
Smoking, alcohol intake and lack of physical activity contribute to central
obesity. Physical activity prevents abdominal fat accumulation.
Waist circumference is a good indicator of body fat distribution and central
obesity. Women with a waist circumference of greater than 35inches (88cm)
and men with a waist circumference of greater than 40inches (102cm) have a
higher risk of central obesity related health problems.
Skin-fold measurement is also used to estimate the amount of total body fats
and for assessment of the fat’s location. About a 1/3 of the fat in the body lies
deep beneath the skin, thus the thickness of the subcutaneous fat is assumed
to reflect total body fat. The total amount of body fat depends partly on the
person. I.e. a man with a BMI within normal range may have between 13-21%
body fat while a woman has between 23-31% body fat.
N/B: the higher percentage of body fat in women compared to men is normal
and necessary for reproduction; to support conception and foetal growth.
Many athletes have a lower percentage of body fat just enough to provide fuel;
insulate the body; assist in nerve impulse transmission and support normal
hormone activity; not so much as to burden the muscles. They have between 5-
10% body fat for men and 15-20% for women.
Body fat that is very low below normal leads to an individual becoming infertile,
developing depression, experiencing abnormal hunger regulation or being
unable to keep warm.

A. Obesity;
Obesity is excessive body fat. Excessive body fat accumulates when people take
in more food energy than they expend. There is a tendency to put on weight as
age advances.
Some of the reasons that lead to calorie intake in excess of needs;
 Family patterns of the rich; e.g. mothers often have a reputation of being a
good cook
 “Good appetite” which leads to likes of many rich foods and dislikes of fruits
and vegetables.
 Ignorance of calorie value of foods.
 Skipping of breakfast, frequent nibbling, coffee breaks with calorie rich
snacks.
 Patterns of living e.g. sedentary occupation and idleness riding to work or to
school, little exercise during leisure time and sleeping more often.
 Emotional outlet where one eats to overcome worry, boredom, loneliness or
grief
 Many social events with rich foods and frequently eating in restaurants.
 Lower metabolism with increasing age but failure to reduce intake.
 Influence by pressure of advertising of many high calorie foods.

Causes of obesity;
These are divided into two categories i.e. internal and external factors
1. Internal factors/Non-modifiable factors
These are include;
i. Hereditary factors; the genetic make-up of an individual influence the
body’s tendency to consume or store too much energy or to expend too
little. Obesity runs through families. Obesity in parents influences obesity
in children. If both parents are lean, the incidence of children being obese
are very low but if both parents are obese, the incidence of children being
obese is very high (i.e. 66-80% or 2-3times higher) and can remain so
throughout life.
 Genetic inheritance may make obesity likely; it will not develop unless given
a push by the environmental factors that encourage energy consumption
and discourage energy expenditure.
ii. Physiological factors within the internal environment; obesity may be
as a result of the inability to respond to hunger and appetite as well as
satiety sensation. There are various control systems that regulate feeding
are integrated in a region of the brain called the hypothalamus. This region
has numerous connections with other parts of the brain and with the
pituitary gland. This region has a greater density of blood vessels than any
other area of the brain and it can be readily influenced by the chemical
state of blood.
This region receives nerve impulses to interpret hunger and satiety
sensation which can be explained by four types of theories which include;
glucostatic theory, lipostatic theory, set point theory and fat cell theory.
iii. Hormonal or endocrine factors; obesity may also be caused by hormonal
imbalance. It frequently accompanies hypothyroidism, hypogonadism,
hypopituitarism etc.
In women obesity is associated with puberty and pregnancy and
menopause and people with much more lipoprotein lipase activity (it
hydrolyses triglycerides in blood into fatty acids and glycerol for
absorption into cells) in their fat cells than lean people. This activity
makes fat storage especially efficient.
People with defective Obesity Gene (ob) that code for hormone leptin (a
hormone produced by fat cells in proportion to the amounts of fat stored,
it suppresses appetite, increase energy expenditure and produce fat loss)
can cause suppression of leptin production, increased appetite and
decreased energy expenditure. Some of them also have leptin resistance.
Obese people have lower levels of hormone Adiponectin which is a
hormone that inhibits inflammation and protecting against insulin
resistance which makes obese people more likely to have insulin
resistance.
Obese people also have higher levels of Ghrelin a hormone which
promotes a positive energy balance by stimulating appetite and increasing
energy storage.
2. External/Modifiable factors
These are factors which are related to the environment, food and activity.
These factors can be controlled. They include;
i) Psychological factors/emotional factors; while most people eat to satisfy
hunger, others eat to satisfy stress and anger, intense reading etc.
ii) Social and cultural factors; some cultures will view a fat person as a
healthy person. People in upper social-economic strata seem to be more
obese mainly due to their food intake, luxurious lifestyles which involve
minimum activity.
Obesity mainly occurs in successful businessmen or civil servants. In young
children, obesity occurs due to changes in methods of feeding. In top class
executives, the main causes of obesity is the business lunches and the
accompanying alcohol.
iii) Activity; inactivity is the major cause of obesity in the modern society.
Obesity is unusual in those who follow occupations or recreations
demanding hard exercise. Obesity is common in those people whose lives
are largely sedentary. E.g. those who use motor vehicles for transport.
iv) Behavioral factors; obesity may be the result of gluttony which is a deadly
sin which comes due to an emotional disturbance caused by stress and
social environment and psychological factors operating on an individual
with some effects on the person’s body.
v) Overconsumption of calories; these may lead to an increase in a person’s
weight especially if the person is inactive. Too often it is assumed that obese
people simply eats tremendous amounts of food, however, obesity more
often results because of the little extra day by day. E.g. extra slice of bread
etc.
Early introduction of cereals and other baby foods before the baby is ready
will also contribute to overweight babies.
Health risks associated with obesity and overweight;
There are many and varied complications which range from premature deaths
to several fatal problems which impact on the quality of life e.g. mechanical
disabilities. Obesity is a risk factor for non-communicable diseases or lifestyle
diseases which include;
i) Cardiovascular diseases e.g. heart disease, high blood pressure and other
peripheral vascular diseases. The work of the heart is increased by the
extra mechanical work needed in moving the heavy body and by the
increased peripheral vascular resistance in the patients with hypertension
due to atherosclerosis in coronary artery.
ii) Diabetes mellitus; obesity is associated with type II diabetes mellitus
because of its association with insulin resistance i.e. the insulin will not get
into the cells so as to make them absorb glucose. If the fat increases
around the cells then the cells will be resistant to insulin and thus will not
absorb glucose from blood thus lead to elevated blood glucose levels.
iii) Some types of cancers; there are certain types of cancers that are
associated with overweight and obesity especially those that are hormone
dependent e.g. cervical cancer, ovarian cancer etc.
iv) Gout; this is a disease of the joints which is caused by increase in plasma
uric acid levels mostly in people who consume food with high purine.
v) Psychological problems; obesity creates emotional problems e.g. some
patients may develop a well-defined neurosis known as disturbance of
body image because the patients develop a distorted view of their own body
and are refuted (lied to) by the site of it in a mirror.
vi) Respiratory or pulmonary diseases; there is increased difficulty in
breathing due to stiffness of the thoracic cage as a result of accumulation of
adipose tissues in and around the ribs, abdomen and the diaphragm. This
may lead to carbon dioxide retention followed by somnolence
(sleepiness/drowsiness/long time sleep).
vii) Mechanical disability; this is because of the extra load on the legs
required to carry the heavy body.
viii) Accidents; obese people are often slow and cannot avoid accidents e.g.
on the road or in an industry.
ix) Reduced life expectancy/life span; complications associated with
obesity can lead to premature deaths.
x) Skin; excessive deposits of subcutaneous fats predisposes one to skin
diseases especially at the flexures e.g. infertigo below the breasts.
xi) Obstetric risks;

Treatment of obesity and overweight;

The treatment of obesity mainly involves weight loss. Weight loss programme
should include three key components;
i. Dietary management-control of energy intake
ii. Regular physical activity
iii. Control of behavioral problems i.e. lifestyle modification.

1. Dietary management of obesity and overweight;

Weight loss can only occur if a person has energy balance one needs to expend
more energy than is consumed.
Strategies for prevention and management of obese and overweight;
The following should be adhered to;
i) Focus on those elements of the environment that affect the weight status
of an individual, the community and the population at large.
ii) Teach the community of the risks associated with obesity and
overweight.
iii) Focus on a management protocol on those individuals with existing
obesity and overweight.
During dietary management, weight determination is important so as to know
the amount of weight to be reduced; this can be done by referring to height-
weight tables for different ages and sexes. The desirable weight is subtracted
from the present weight to give the excess weight that must be reduced in the
form of kilograms.
Calculate the energy requirements using the ideal weight and subtract
500kcals every day until the amounts of weight loss has been attained. E.g.
female ht 1.65m weighing 90kgs (ideal weight is 50-68kgs); 1.55m wt
85kgs (ideal weight 44.4-60kgs).
Determining energy needs;
i. Determine the BMR(kcals)
ii. Physical activity(kcals)
iii. Thermic effect(kcals)
iv. Total energy expenditure(kcals)
v. Subtract 500kcals to determine the kcals for weight loss.

The basic principles;

i. Calories; provide lesser calories than what the person requires.
ii. Proteins; a normal intake is essential i.e. about 1g/kg body weight/day
should be supplied by the diet.
iii. Fat; this is essential to give taste satiety to the diet. This supplies the
essential fatty acids as fat soluble vitamins about 4 teaspoons per day is
recommended.
iv. Carbohydrates; these should be supplied so that they contribute not
less than 70% of the total calories. Avoid simple carbohydrates e.g. those
present in table sugar, jams, squashes, syrups, cakes and fruit juices.
They should be avoided since they are quick sources of carbohydrates
and they do not contribute bulk to the diet.
The diet must supply a good amount of fibre which helps to achieve a
feeling of fullness with lesser amounts of calories.
v. Vitamins and minerals; include vitamins rich foods e.g. leafy vegetables,
fruits, fresh and whole grains and legumes so as to provide essential
vitamin and minerals for the body.
Practical suggestions for reducing weight;
i. Set the goal which is realistic e.g. to reduce the weight of obese person by
10kgs in 20 weeks.
ii. Adjust the rate of weight loss to one pound/1/2 kg per week
iii. Use the help of weighing machine and motivational techniques
iv. Learn calorie values of home dishes
v. Increase exercises to help get rid of water and resistant weight reduction.
vi. Avoid commercially available low calorie foods because they are not
better than home mad meals besides from buying expensive foods.
vii. Avoid a separate menu for you instead adapt your dietary needs from the
regularly prepared family diets.
viii. When eating away from home or in the company of guests take care and
avoid excess but do not get upset if you miss your plan.
ix. Avoid use of appetite depressants and such types of medication because
they may do more harm than good rather try natural methods.
x. Do not change your meal or snack pattern because you should not take
all your calories at one sitting.
xi. Do not think of any surgical methods because use of it may be harmful
although liposuction may be tried in extreme obesity.
xii. Grill, broil, boil, steam or bake foods instead of frying them.

Maintenance diet;
The reducing diet is to be maintained until desirable weight is obtained after
which a maintenance diet has to be formulated.
Maintenance tips;
i. After the gradual loss in weight and desirable weight attainment completed,
increase the intake of low calorie foods gradually.
ii. For a snack, prepare one with raw vegetables which are in season because
they supply bulk, large amounts of fibre and good amounts of vitamin B
complex and minerals.
iii. Learn to curb your appetite before going out to attend parties e.g. a large
glass of skim milk and an apple or a banana or a fried toast before leaving
for the occasion which will prevent you from overeating at the party.
iv. Do not eat absent mindedly. Concentrate on the food that you eat. Do not
eat while being disrupted by conversations, reading or watching TV.
v. Learn to become more mobile, depend less on others. Do your work, be
active, go for long walks, and develop a habit of exercising at least for ½ an
hour a day.
vi. Seasonings e.g. lemon juice, vinegar, spices especially peppers and herbs
may be used to give unique flavours to foods.
vii. Always make use of skimmed milk instead of whole milk because it has ½
free calories of whole milk and more proteins.
viii.Weigh yourself every week to keep check on the weight loss or gain
accordingly. Modify the maintenance diet in the corresponding week.
ix. Wear a dress which does proud to your figure
x. Do not be misled by any occasion by the common phrase “it does not harm
to eat just this once”
2. Exercise;
Low calorie diet with moderate exercise of walking should be the basis in which
the lifespan can be increased. A combination of exercise and diet give
considerably more flexibility for achieving a negative calorie balance and
accompanying fat loss than either exercise or diet alone.
Exercise is important to reduce body fat, tone up muscles and maintain the
decreased weight and help in the normal functioning of the brain’s feeding
control centers.
Examples of exercises are skipping, brisk or uphill walking, cycling, jogging
and swimming which expend many calories. The 1 st 12 minutes of vigorous
exercise are more effective in burning up body fats.
Example;
If there is need for a person to reduce 500kcals from the daily intake (i.e.
3500kcals/week) to reduce ½ kg /0.45kg/week.
If the client performed ½ hour of moderate exercise, he expends about 140-
150kcals/day (i.e. about 1000kcals/week). With this exercise the weekly
calorie restriction necessary to lose ½ kg/week would now be necessary to be
2500kcals/week instead of 3500kcals/week.
If the duration of the exercise is doubled to 1hour, to expend 300kcals, calorie
restriction of the diet would be about 200kcals/day or 1400kcals/week which
is quite manageable.
Advantages of exercise;
i) It can be used effectively by itself or in combination with mild dietary
restriction to bring the effective loss of body weight
ii) It helps in minimizing the instance of intense hunger and other
psychological stresses seen in similar programmes of weight reduction
solely achieved by diets.
iii) It enhances mobilization and breakdown of fat from the body’s adipose
deposits. This helps to protect the lean tissue(i.e. proteins) breakdown
which is first lost when the weight loss is achieved by diet alone.
3. Lifestyle modification in obesity and overweight
This involves behavior modifications which include;
1. Chain breaking; this involves breaking the link between behavior that
tend to occur together e.g. snacking on chips while watching TV. Make
eating a singular activity.
2. Stimulus control; alter the environment to minimize the stimulus for
eating e.g. storing food out of sight and avoiding the paths by the food
outlets.
Positive stimulus control include;
 Keep low fat snacks at hand to satisfy hunger and appetite
 Place walking shoes in a convenient visible location
 Slow the rate of eating to become mindful of your eating and to reduce
food intake
 Pausing during meals
 Chewing for a maximum number of times so as to slow the eating
process.
3. Cognitive structuring; this involves changing ones frame of mind
regarding eating. E.g. instead of using a difficult day as an excuse for
eating.
4. Self-monitoring; this involves monitoring the tracks which foods are
eaten “when”, “who one eats with”, which physical activities are
completed and records of body weight. This helps to understand more
about their habits and reveals patterns e.g. unconscious overeating that
may explain problem behaviours that lead to weight gain. Emotional
settings in which eating occur can be indicated.
5. Setting easy to achieve short term goals; these includes increasing the
number of minutes of walking on weekends
6. Stress management; these involves daily meditation, progressive
relaxation and visual imaginary exercise.
7. Social support; this involves organizing commercial support meetings
and classes. E.g. slim possible programme.

Other methods used in the management of obesity

1. Use of artificial sweeteners and ready to use diets (slimming diets);
synthetic sweeteners e.g. drops of tablets of saccharin or aspartame may be
used by the dieting person. Over use of these may cause so many
undesirable effects.
However, it is best to drink a beverage without any added sweetener,
natural or artificial so as to control calories.
One should be careful to evaluate nutritional value of ready to use diets
(slimming diets) which are available in the market. If possible, a well-
planned balanced diet prepared at home can be used instead of slimming
diets readily available in the market.
2. Liposuction; this is the surgical procedure involving removal of excess fats.
3. Gastric plication; this involves placing surgical staples across the upper
portion of the stomach to which its reservoir capacity of food is reduced or
sometimes gastric by-pass is performed.
4. Use of diet pills and hormones; these diminishes appetite which may
cause one to lose weight.
5. Use of diuretics; these may cause dehydration and potassium deficiency
6. Use of fad diets; these are commonly referred to as crash diets e.g. rice,
banana, ice cream, liquid protein diets, fasting diets or no carbohydrate diet
or ketogenic diets(fat). These diets are hazardous in the long run because it
involves the manipulation of the components of a normal balanced diet.

B. Underweight
This is weight that is 10% below the established standard i.e. BMI <18.5. A
person who is underweight is vulnerable to infections e.g. Tuberculosis and
other acute infections. A person who is underweight looks severely emaciated.
It is mostly related with diet inadequate in calories.
Causes of underweight;
i. Very active, nervous and people who obtain too little rest lose weight.
ii. Starvation- this occurs during famine condition due to inadequate intake of
proteins, during which the fatty tissues are used for energy purposes. This
results in marked emaciation, loss of hair and low blood pressure.
iii. Irregular eating habits and poor selection of food which can lead to
inadequate calorie intake
iv. Severe infection which may result in weight loss, high gastrointestinal
disturbances, hyperthyroidism, diabetes, cancer, malabsorption syndrome,
HIV/AIDS etc.
v. Psychological factors which may cause a person to overeat may also cause
a person to eat less e.g. anorexia nervosa where there is severe weight loss
due to some mental illness which may make a person to refuse to eat food.
It is therefore necessary to make special efforts for such persons to put on
weight until the desirable weight is attained.

Dietary management of underweight;

The cause of weight loss must first be removed and a high calorie, high
protein, high fat diet with liberal vitamin intake may be given. A well
balanced diet should be planned keeping in mind all the nutrients.
i) Calories; calorie requirements depends upon the activities. Excessive intake
of high calorie foods should be avoided because there might be digestive
disorders. An additional increase of 500kcals/day to the normal
requirements should be given (calculate using the ideal body weight of a
person of the same height). This will help gain about 1 pound or ½ kg or
0.45kgs/week.
ii) Proteins; about 1.2-1.5g/kg body weight/day should be given. This is
recommended for tissue building activity. High biological value proteins
should be included as they can be completely utilized by the body.
iii) Fat; fat content should be increased, it should be easily digestible. Fried
and excess oily foods are not recommended as they could cause diarrhea or
may reduce the appetite. High fat foods e.g. butter and cream help
increasing weight.
iv) Minerals and vitamins; a well-planned high calorie diet will provide liberal
amounts of vitamins and minerals thus supplements may not be required.
v) Carbohydrates; carbohydrate rich foods must form the basis of the diet.
Include dried fruits and nuts, cereals, pulses, tubers and cereal products
which are rich sources of energy. Initially intake should be less to counter
the balance. Frequent and small feeds should be given. Easily digestible
foods are best accepted.
vi) Fluids; liquids should be consumed after a meal since before meals would
prove to be an appetite suppressor. Enough fluids in fresh fruit juices and
soups should be consumed in order to avoid constipation.
vii)Exercise; this is also important for an effective weight gain programme
because it will stimulate their appetite thus improve the intake of calories
and helps improve muscle tone especially of the digestive system resulting
in better absorption and assimilation of the food which helps in weight gain.
Exercise also help to increase lean weight and prevent fat accumulation and
increase strength and endurance.
N/B: an underweight person must be emotionally sound in order to have a
good appetite.
Synthetic and carbonated beverages should be avoided because they reduce
the appetite.
Rules to be followed in the management of underweight;
i) An underweight person cannot initially adjust to a higher calorie intake
hence begin with the present diet and modify its quality or quantity until
the desired calorie intake is reached.
ii) Meal times should be attractive and pleasant as possible.
iii) Small frequent meals should be taken at least six meals are desirable. Mid-
morning and midafternoon snacks do not give better results because they
interfere with the next meals. Bed time snacks are more helpful.
iv) No food should be forced for eating; whatever food is appreciated by the
patient should be eaten. Mild coaxing may be helpful but if pushed by, no
result is achieved.
v) No topics about food and their importance should be discussed during meal
times especially if it undesirable for the person concerned.

Risks factors associated with underweight;

 Death (increased death rate)
 Reduced lifespan.
 Infertility
 Suppressed immunity
 Low bone mass
 Loss of menstrual flow (amenorrhea)
 Complications with pregnancy and surgery
 Slow recovery after illness
 Interference with normal growth and development in children and teens
UNIT 14 EMERGING ISSUES IN NUTRITION AND DIETETICS
___________________________________________________________________________
Unit Objectives
Research on emerging issues in diet therapy
Present and discuss emerging issues in class
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