Dietitians Lecture Note 2017

DIETETIC INTERNSHIP PROGRAMME
A COMPREHENSIVE LECTURE
NOTE
FOR
INTERNS
UNTH, ITUKU/OZALLA, ENUGU
STATE.
2016/2017 SESSION.
1
Nutrition and Dietetics Interns Lecture Note 2016/2017
TABLE OF CONTENTS
Cover page 1
Table of contents 2
Menu planning, nutrition supplementation and celiac disease, by Dtns. Olebu Justina
and Nwachukwu Chioma 3
Anatomy and Physiology by Ms Ekechukwu, Frances A. 18
Overweight and Obesity by Rev. Sr. Odinakachukwu Nwosu 30
Nutrition counseling and geriatric nutrition, by Dtn. Mbomi 55
Diabetes mellitus and oncology, by Dtn Dr. Nnadi Ihuoma M. 67
Protein energy malnutrition, hydration for children and paediatric weight management,
by Dtn. Onwuka-kalu Nkeiru 83
Hygiene and Chronic renal failure by Dtn. Okwy-Nweke 94
Food Processing, energy expenditure and Energy Conservation, by Dtn. Afieroho

Mercy C. 102
Health and safety practices in the hospital, Hypertension, microwave and safety
by Dtn. Okwara C.C. 114
Nutrition in pregnancy & lactation, Medical nutrition therapy clinics & talks,
and Breastfeeding by Dtn. Onyia Blessing. 139
Billing and Costing, Nutrition Care Process, Nutrition in HIV/AIDS and,

Vegetarian Nutrition, by Dtn. Vivian Okoyeh 154
Coronary Heart Disease, bariatric surgery and micronutrient deficiency

by Dtn. Igbanugo Vivian 206
Nutritional Genomics and nutrition in critical care, by Dtn. Enuka Hannah C. 221
Cardiovascular diseases: Angina Pectoris, Myocardial Infraction &

Hypertensive Heart Disease by Dtn. Ajaebili Ngozi A. 255
Medical nutrition therapy in liver disease by Dtn. Onoja Ifeoma 272
Hepatic Encephalopathy, Disorders of lipid metabolism, enteral and parenteral feeding,

by Dtn. Ugwuanyi, Modesta C. 292
Acute Renal Failure, Obesity, Case Studies, by Dtn Azurunwa Chigozie A. 313
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MENU PLANNING
NUTRITION SUPPLEMENTATION
CELIAC DISEASE
BY
DTN OLEBU JUSTINA

&
DTN. NWACHUKWU CHIOMA.
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MENU PLANNING
The food service industry has long recognized the importance of accuracy in describing its
product in menus based on ethical grounds and from the stand point of customer’s satisfaction.
Every food service operator is very much aware that the success is based upon providing
customer’s satisfaction. A key stone in this effort is the accurate representation of the products
served. The ultimate responsibility for accuracy in representing a menu rest with the menu
planner’s knowledge and creativity.
The menu is the main consideration in the managerial operation of a food service system. All
aspects of the operation of a food service business depend on the menu. The menu is the single
most important document in food service business. Purchasing, product sales, cost accounting,
labour management, even the kitchen layout and equipment selection of a new facility, all are
based on the menu.
The menu provides a list of food items available for selection by a customer; it serves as the
primary control of the food service operation and is the core common to all function of the
system. It is a sales tool for food service operations.
An additional function of the menu is consumer education. For example, the menu is a valuable
tool for teaching children proper dietary habits through the school lunch program and for
instructing hospital patients on modified diets. Menu may be presented in many different forms
ranging from printed copy or other visual means to orally present type by a wait person. Menus
that are not frequently changed maybe printed in qualities for use over a definite period of time.
Things to consider when writing menus are:
1. Kind of menu
2. The meal the menu will cover
3. Clientele
4. Menu structure
5. Menu balance
6. Portion size
7. Production capacity and production availability
8. Probability and budget.
Types of menu
a) Static menu
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b) Cycle menu
c) Market menu
d) Non-selective menu
e) A la carte
Static menu: offers the same items every day. It is used in establishments where the clientele
changes daily or where there are enough items listed on the menu to offer variety.
Disadvantages of static menu
 Lacks flexibility, variety and has restrictive food chores
 Limited menu information
 Clients gets familiar to the menu
Advantages
 Saves cost and time
 Simplify meal planning or shopping
Cycle menu: rotation of different menus within a fixed period of time in sequence. It can be
defined as carefully planned menus which are rotated according to definite patterns. It varies
from two to several weeks. Example a seven day cycle menu will have a different menu
everyday for a week and will repeat each week. This type of menu is mostly used in schools and
hospitals, used for on-site food service and volume catering.
Advantages of cycle menu
 Minimizing menu planning time: it saves substantial time in the long run because the
need for planning weekly menu would be eliminated.
 Co-ordinating preparation
 Reducing repetition of menu items
 Promoting standardization of preparation procedures
 Increasing labour efficiency due to improved coordination and organization planned in
the menus
 Simplifying purchasing
 Enhance acceptance of menu item by clients
 Taking advantages of purchasing seasonal variation of foods
 Improving inventory control and cost control
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 Offer variety without putting too much strain on the kitchen
 Maximizing utilization of equipment potentially resulting in reduction of energy
expenditures.
Disadvantages
 Drafting a cycle menu is initially time consuming, but saves substantial time in the long
run since the need for planning the weekly would be eliminated.
 It incorporates variety into food prepatation.
Market menu: planned each day according to food availability and “best buys”.
A la carte: each food item is offered and priced separately. The customer marked selections
from the various courses and side dishes to make up a meal. A’la carte is also used to refer to
cooking to order.
Selective and non selective menus
Selective menu:
Advantages
 Patient satisfaction could be improved, since there is a positive psychological impact
when the patient chooses specific foods.
 Menu variety could be increased, which could minimize special food orders.
 Special diet orders by physicians could be limited because special diet could be ordered
only as a therapeutic measure, rather than to cater to a special patient.
 Knowledge of favourite menu items could be improved and used in the future menu
planning, patient contact would be fostered if the direction of food service director
offered written guidance in marking the daily menu selection.
 Food waste could be reduced if menus were carefully tallied.
The disadvantage inherent in the selection of menus is labour intensive and increase food service
cost.
Advantages of non selective menu.
 Food and labour costs would be minimized
 Demand on skill and quality of labour would be decreased due to the reduction in number
and types of foods to be prepared
 Time requird for meal preparation and service would be reduced. Which would generally
enable the food reach the patient at a more optimum temperature.
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 Storage and preparation areas required would be reduced.
 Quantity and types of equipment required would be minimized
 Quantity of supervision required would be decreased
 Food waste would be minimized with the non selective menu, since closer control on all
aspects of food service could be maintained.
Nutritional factors
Nutrient adequacy is a very vital factor in drafting menu, to ensure nutritional adequacy, menu
should be drawn considering:-
The number of servings of vegetables and fruits that will supply sufficient vitamins and minerals.
Floor or more servings of fruits and vegetables should be incorporated daily into the menu. All
food groups should be represented adequately the cereal and legume meat and meat products,
mills and dairy products etc.
Factors that can enhance acceptability of food:-
1) Try a new menu item at least three times so that it will become familiar to the clients and
not be regarded as foreign.
2) Maintain variety in foods served during the week and throughout the menu cycle.
3) Vary menu combinations of food according to colour, shape, taste, texture and
temperature.
4) Avoid serving more than two starches in one meal (fried plantain/pasta/rice/potato chips)
Factors to increase labour efficiency
1) Incorporate at least one menu item that can be prepared the day before.
2) Distribute the planning of menu items according to the skill of employees scheduled.
3) Plan menu items to utilize equipment efficiently.
Factors to maintain cost control
i. Minimize the use of expensive vegetable, this is dependent on the budget, the expensive
vegetables could be included a maximum of once weekly.
ii. Check menus in advance to take advantage of specials (quantity purchased as storage
permits and if there is sufficient money available)
iii. Specify portion sizes directly on the menu, including the number of scoops to be utilized
THE MEAL THE MENU WILL COVER
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Menus usually cover breakfast, lunch and dinner. It is not worthy that foods for lunch and
dinner may be interchanged depending on your clients’ lifestyle.
Clientele
 Who are you feeding? Hospital patients require nutritionally adequate meals, modified to
suite their disease conditions. Travelers’ restaurant might offer fast food items and
optional take-out service.
 Consider ethnic traditions, religious and regional preference, temperature and time of the
year,
 Consider the amount the customer will be willing to pay or able to spend on the meal.
Menu balance (taste, texture, colour, nutrition).
Taste: balance spicy with bland and vice versa
 Do not repeat foods in the meal
 Do not serve similar tastes together
 Do not serve more than one fried food in the same meal (fried potatoes and fried plantain)
Texture: - applies to the softness of firmness of foods their feel in the mouth. Foods with similar
textures should not be combined balance soft food with crisp foods- serve only one starch at a
time. Do not serve too many mashed or pureed food in the same menu, the same day.
Colour: put bright-couloured food in menu, serve foods with a variety of colour and shapes.
Colourful vegetables are always used in livening up cereals tubers, meat fish and poultry which
tend to be mostly white or brown.
o Choose foods with colour contrast
o Do not serve dark and all light foods
Portion size
A good balance of the amounts of different foods affects:-
 Plate appearance and appeal
 Portion control
 Food cost control
PRODUCTION CAPABILITY AND FOOD AVAILABILITY
Equipment: is the menu producible with the existing equipment? Will a new menu item
interfere with production of any other item? Does this menu distribute preparation evenly over
other equipment?
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 Production skills: - what is the professional skill level of your employees? Do any menu
items require special skills offer items that the cooks are able to prepare. Do not put items
on time menu that are above the skill level of the staff, is the work load spread among
employees to make maximum advantage of the man hours available?
Profitability and budget

Can the menu be produced within the budget guidelines set by management, is the menu
profitable?
High cost of food may result from the following:-
 Unbusiness-like purchasing
 Careless store room operations
 Extravagant cooking
 Neglect of left-over: complete utilization of foods must be planned into menus
 Too much food wasted in dustbins
 Too large servings
 Pilferage and theft.
Food availability: use foods in season. Foods that are out of season are more expensive.
Use foods locally available.
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NUTRITION SUPPLEMENTATION
The position of the ADA that the near nutritional strategy for promoting optimal health and
reducing the risk of chronic disease is to wisely chooses a wide variety of nutrient rich foods.
Additional nutrients for fortified foods and supplements can help some people meet their
nutritional needs as specified by science based nutrition standards such as DRI (Hasler et al.,
2009).
In making this statement, the ADA puts food first but leaves the door open for those with
specific nutrient needs, identified through assessment by a dietetic or health professional, to be
nutritionally supplemented.
Traditionally, one thinks of vitamins and minerals, fibre and protein as nutrient supplements
generally in pill, capsule, or liquid form. The DRIs are standards used with most adults.
However, food fortification is another form of nutrient supplementation. The level of fortified
foods (such as “energy bars or sport drinks”) in the market place puts another layer of potential
nutrient since is the mixture with traditional supplements. These traditional supplements such as
herbals and other natural dietary “enhancers” are also added to the array of supplements
available to consumers.
Americans frequently do not meet the dietary recommendations for promoting optimal health.
Several segments of the adult population fall into high-risk groups who are unlikely to meet their
nutrient needs because of life stage (e.g pregnancy), alcohol or drug dependency, food insecurity,
chronic illness, recovery from illness, or choosing a nutritionally restrictive diet or lifestyle
(ADA, 2008). Other special persons with special needs include those with food allergies or
intolerances that eliminate major food groups, persons using prescription drugs or therapies that
change the way the body uses nutrients, those with disabilities that limit their ability to enjoy a
varied diet, and those who are just unable or unwilling because of time or energy to prepare or
consume a nutritionally adequate diets. These adults potentially need a nutritional supplement.
Dietary supplementation
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Is common practice among Americans particularly among those at risk or diagnosed with clinical
conditions such as cancer, CVD, DM or HTN.
Consumers and health professionals should be aware that there is limited information in the
effects of dietary supplements taken concurrently with prescriptions and over-the-counter
medications. Historically, dietetics professionals should focus their assessment, care plan, and
counseling on diet or food related recommendations.
Dietary supplementation have been officially defined under the dietary supplement Health and
Education Act (DSHEA) of 1994 as products intended to supplement the diet that contain one or
more of the following ingredients: a vitamin, mineral, herbs or other botanical amino acid,
concentrate, metabolite, constituent, extract, or combinations of these ingredients.
Dietary supplements are intended for ingestion in pill, capsule, tablet, or liquid form and are not
to be represented for use as a conventional food or as the sole item of a meal or diet. They should
be labeled as a Dietary supplement and carry the dietary supplement facts label. They must also
be differentiated from drugs, cosmetics, and foods. The degree is dependent upon the location,
extent and duration of the disease. The diagnosis is confirmed by evidence of malabsorption.
Once gluten is removed from the diet, there is a gradual improvement in symptoms over a period
of weeks to months. Initially there is a relief of symptoms and later the return of intestinal
mucosa to near normal condition. Gluten-sensitive enteropathy should be considered a chronic
disease that is controlled by diet. Failure to respond to a gluten-free diet is not common but it
may occur. The most common reason for lack of response is the wrong diagnosis or failure to
strictly adhere to the diet. Others include secondary lactose deficiency. Concurrent disease, such
as pancreatic insuffiency, jejunal or ileal ulceration, or rarely, intestinal lymphoma.
Collagenous sprue is an extremely rare entity and is characterized by a lack of response to

dietary therapy.
Supplementation, food fortification and dietary diversification- a three prolonged

approach to reducing hidden hunger.
Hunger has been automatically associated with not having enough to eat by us. However, not
having enough to eat is mainly part of the problem of hunger, what experts refer to as “Hidden
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hunger” attracts less attention because it does not produce dramatic images yet while it has gone
largely unnoticed, it has assumed dramatic properties. Two billion people are now affected by it
almost a third of the world’s population. This hidden form of malnutrition is caused by a
deficiency of vital micronutrients (vitamins, minerals and trace elements) in the body. These
micronutrients are essential to the mental and physical development of both children and adults.
Vitamin A-deficient infants, for eg are at risk of infection, visual impairment and high mortality
rates.
Anaemia caused by an iron deficiency impends the ability of school-age children to learn and
reduces adults’ ability to work.
The symptoms of vitamin and mineral deficiencies are still largely ignored in national health
system and in bilateral development co-operation despite the fact that hidden hunger not only
impacts on health but also comes at a high economic price.
Deficiencies of vitamin A, iodine and iron are the three forms of malnutrition prioritized by the
international community. Zinc deficiency is also being targeted. These problems are particularly
widespread and have serious consequences. The human body needs mainly very small amounts
of micronutrients but it cannot produce them itself; they have to be supplied through the diet.
Individuals become deficient in micronutrients when they do not have enough to eat or when diet
is insufficiently varied or unbalanced. A micronutrients deficiency often goes hand in hand with
undernutrition and can have many causes: families may be generally poor or their spending
patterns may be in appropriate, meaning that they are unable to buy food that is sufficiently rich
in vitamins and minerals, to grow it, or to include it in their diet. Once individuals have a
deficiency, they become more prone to illness and less able to perform well at work, rapidly
establishing a link between malnutrition and poverty.
Evidence -based solutions of reducing hidden hunger. At risk groups include women of child-
bearing age, newborns and infants, and the sick and elderly. They also include those in
emergency situations, such as refugees or displaced persons, who do not have reliable access to
adequate nutrition.
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There are three main types of intervention to prevent and combat vitamin and mineral
deficiencies which can be deployed individually or in combinations:
1. Short – term supplementation
2. Medium – term food fortifications and
3. A long –term focus on balance nutrition (dietary diversification)
Supplementation
It talks about filling the gap. Food supplements are highly concentrated vitamins and minerals
produced by pharmaceutical manufacturers in the form of capsules, tablets or injections and
administered as part of health care or specific nutrition campaigns. Medical staff working for
national health services supported by organizations such as UNICEF distributes vitamin capsules
and iodine and iron tablets widely to infants, women of child-bearing age and women who have
given birth without prior assessment of their individual needs. The World Bank estimates that the
per capital cost per unit is low: a dose of Vit A for example is estimated to cost between USDI
and USD 2.5 per capita. The greatest cost-benefit effect comes for giving supplementary vitamin
A to children under the age of 2, because the damage caused by micronutrients deficiency in the
early years of life is irreversible. The United Nations scaling up nutrition represented by
individual’s first thousand days of life; starting from conception. However, older people,
displaced persons and refugees may also suffer specific deficiencies.
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CELIAC DISEASE
Celiac disease can be defined as a chronic disease in which the gliadin protein fraction of gluten
causes a mucosal lesion of the small intestinal that impairs nutrient absorption. The term celiac is
derived from the Greek (koiliakos, abdominal) and was introduced in the 19 th century in a
translation of what is generally regarded as an ancient Greek description of the disease by
Aretaeus of Cappadocia. Celiac disease is also termed gluten sensitive enteropathy. In children, it
is termed celiac disease and celiac sprue in adult. Other names include nontropical sprue and
endemic sprue. The disease damages primarily the mucosa of the small intestine especially the
duodenum and proximal jejunum.
Celiac disease is one of the most common intestinal diseases to cause malabsorption in
childhood.
Symptoms often begin during the second six months of life after wheat containing foods are
added to the diet. The affected child gradually becomes irritable and unwell, experience loss of
appetite and begins to pass frequent foul bulky stools. Vomitting is common; weight gain slows
down during the time. Diminished body weight is seen in almost all patients especially in those
with prolonged active disease; short stature is also common in children. Other symptoms include
pain and discomfort in the digestive tract, chronic constipation and diarrhea, anaemia and
fatigue. The growth problems are related more closely to inadequate caloric and protein intake
than to the severity of the malabsorption.
Factors that trigger symptoms include:
1. Surgery
2. Pregnancy
3. Infection and
4. Emotional stress
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Diagnosis
Blood: Serological blood tests are the first line investigation required to make a diagnosis of
celiac disease.
Endoscopy/gastroscopy and biopsy
Investigations to measure bone density may be performed at diagnosis such as dual energy X-ray
absorptiometry (DXA) scanning, identify risk of fracture and need for bone protection
medication. Biopsy in adult reveals a flat mucosal surface with absence or severe blunting of
normal intestinal villi.
Biopsy in children shows atrophy of intestinal mucosa, and the typical clinical findings are those
of malnutrition. Histologic examination confirms loss of normal villous structure. The result of
these changes is usually diarrhea and steatorrhea, flatulence, abdominal distention, weight loss,
and weakness also occur.
Extraintestinal symptoms may result from anaemia and metabolic bone disease such as
osteomalacia, malabsorption of protein, fat and fat soluble vitamins, vitamin B 12, folate, iron,
calcium and other nutrients can occur.
Celiac disease is also associated with bacterial overgrowth of small intestine which can worsen
malabsorption or cause malabsorption despite adherence to treatment.
Goals of Dietary management
1) Control gluten intake.
2) Provide all nutrients in quantities adequate to ensure that needs are met for growth,
development and activity.
Dietary guidelines should be designed using catch-up growth, energy and protein
recommendation. When catch-up growth has occurred, a gluten-controlled diet that reflects
normal energy and nutrient needs should be recommended.
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Nutritional Inadequacy
If gluten-free diet is not nutritionally inadequate, prior to initiation of dietary treatment, nutrient
deficiencies may be seen as a result of fat malabsorption and inadequate intake. Water miscible
preparations of fat-soluble vitamins and a daily vitamin supplement may be indicated to convert
these deficiencies in children. If the patient is also lactose intolerant and is not able to consume
or tolerate adequate amounts of lactose treated dairy products, calcium supplementation to meet
requirements may be indicated. Vitamin and supplementation may also be needed initially for
patients with metabolic bone disease. Iron, folate or vitamin B 12 supplementation maybe
necessary for patients with anaemia. Increased absorption of nutrients occurs with dietary
treatment, even if the recovery of intestinal mucosa may not be seen for a few months, so
supplements may not be needed for more than a few months. If diarrhea has been severe,
electrolyte supplementation might be needed for the first few days of therapy. With severe
malabsorption, calcium and magnesium blood levels may be low and thus may need to be
corrected by supplementation.
Dietary Recommendations
1. Use of gluten – controlled diet.
2. Temporary tolerance to lactose is common and temporary intolerance to fat is sometimes seen.
3. Some control of dietary fat should be considered because unabsorbed long – chain fatty acid
which may produce diarrhoea.
With control of symptoms, milk and milk products should again be added to the diet and the
level of fat can be increased. The widespread use of emulsifiers, thickness, or other additives
derived from gluten containing grains in commercially processed foods further complicates strict
adherence to gluten-free diet.
It is important for patients to read food labels carefully and to avoid products that lost ingredients
that cannot be verified as gluten free by the manufacturer. The unintentional consumption of
gluten is the most common cause of reoccurrence of symptoms. Other reasons patient may fail to
maintain a strict gluten-free diet are boredom with the taste of alternatives to wheat, breads,
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crackers and pasta and the limited availability of appropriate foods when eating away from
home.
Initially a high kilocaloric and high protein diet should be recommended, especially if weight
loss and specific deficiencies owing to malabsorption are pronounced.
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ANATOMY AND PHYSIOLOGY
BY
MS EKECHUKWU, FRANCES A.
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Outline
 Pancreas
 Kidney
 Liver
 Heart
 GIT
PANCREASE
Description: It is a pale yellowish gland placed in epigastria left hypochondriac region of the
abdominal cavity, it is about 18cm long and weighs about 60g. It consists of a head which is
enlarged and attached to the curve of the duodenum, then a body lying behind the body of the
stomach and a narrowed end where it ends as the tail reaching the spleen and in front of the
kidney.
Structure: The pancreas consists of a number of loblues made of small aveoli made up of
secretory cells (these are smaller cells). These loblues are drained by tiny ducts which unit with
each other to form the many pancreatic duct which passes into the duodenum at its midpoint
joining with the bile duct to form the ampullar of the bile duct. The opening is guided by the
sphincter of Oddi.
Another structure with the pancreas is called the islets of Langerhans, these are cells distributed
throughout the substance of the pancreas. Their secretion is poured directly into the bloodstream
consisting of the hormone insulin necessary for proper absorption of glucose.
Function: The pancreas secrets pancreatic juice necessary for chemical digestion of food.
Kidney
Description: The human body has two kidneys. They are bean shaped. The length is about 10cm
long. They are located on each side of the spinal column at the lowest level of the rib cage. They
weigh q50-180g each. It is said that the kidney contains about one million (1,000,000) tiny
microscopic nephrons (filters). Each nephron consist of glomerulus (a small bunch of small
blood vessels) and a tubule ( a long tin winding tube) to connect the glomerulus to the pelvis of
the kidney from where the urine runs through both ureters to the bladder where it collects and the
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urine is discharged via the urethra coming out through the urinary orifice. The best function of
the kidney is the production of urine.
About solitaries of blood flows through the kidneys each every day. From this, the glormeruli
produce about 9liters of filtrates. The filtrates contain substance essential to the blood such as
protein, water and minerals. These are reabsorbed while the filtrates runs through the tubules
what is left is waste and it is excreted in the urine usually about 1.5-2 liters.
Functions:
1. Regulation of the amount of many substances contained in the body e.g. K+, Na+, H+,
Mg+, Water, and Phosphate.
2. Excretion of waste product in the urine such as end product of protein metabolism e.g.
Urea, uric acid, creatinine, sodium.
3. Metabolism functions (a). Production or synthesis of vitamin D (b). Production or
synthesis of erythropoietin (c) Production or synthesis of rennin (d) Hormone Depression.
4. Production or synthesive site for the production of 1-2-5-, dihydroxy vitamin D this is the
most active metabolic of the vitamin which acts on the intestine to increase calcium
absorption, it maintains normal mineralization of bones.
5. Production or synthesis of Erythropoietin. Erythropoietin acts on the bone marrow to
increase the production of red blood cells.
6. Renin is released from the kidney in response to a blood pressure of sodium deficiency.
When the kidney becomes impaired by disease, disturbances in various functions occurs,
excretory products begins to increase in the blood in various amounts. E.g. creatinnine,
urea and sodium.
The failing kidney cannot compensate for large fluctuations in salt intake and large metabolic
demands. As renal failure progress to severe ureamia, you begin to experience nausea, vomiting
from accumulation of urea and creatinine, there is tiredness, and breathlessness on exhaustion
may arise from anaemia. At the terminal stages of renal diseases, many parts begin to develop
features of water intoxication.
ANATOMY OF THE LIVER

Description: The liver is the largest gland in the body. It is situate at the upper part of the
abdominal cavity mostly in the right hypochondriac region extending to the epigastric and left
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hypochondriac regions respectively. It weighs about 1.36kg (3pounds 50oz). it has an upper and
anterior surface which is smooth and curved corresponding with the under surface of the
diaphragm and a posterior surface which is irregular when viewed or rough.
Organs in relation: Superiorly, it is related to the diaphragm, posteriorly it is related to
diaphragm, esophagus, the gall bladder, vertebral column, aorta and inferior vena cava. Laterally
it is related to the lower ribs and the diaphragm.
Structure: The liver is enclosed in a thin fibrous capsule and covered incompletely by a fold of
peritoneum.
Lobes: The liver has four lobes, the right lobe which is the largest containing a fissure or
opening for the inferior vena cava. The left lobe is smaller and wedge shaped. The left lobe is
separated from the right lobe by a ligament called falciform ligament. The quadrate lobe is on the
posterior surface of the liver. It is square in outline. The caudate lobe is situated in the posterior
surface of the liver and it is like tail in appearance.
Portal fissure: It is an opening liver in the posterior surface of the where structures enter and
leave the liver. The structures are the portal vein with food nutrients carrying blood from the
digestive tract, spleen and pancreas.
The hepatic artery carries arterial blood to supply the liver with oxygenated blood. The nerve
fibers which are the sympathetic and parasympathetic. The hepatic ducts carrying bile to the gall
bladder, lymph vessels draining lymph from the liver substance, then the hepatic veins right and
left draining venous blood from the liver.
Intra-Lobular Structure of the Liver or Minute Structure of the Liver
When the liver is viewed microscopically, reveals tiny lobules that make up the liver substance.
The lobules are formed by cubical shaped cells arranged in columns radiating from a central
vein. Between the columns there are blood vessels known as Sinusoids which contain a mixture
of blood from the tiny bunches of the portal vein and hepatic artery. This arrangement makes it
possible for the liver veins to come intact both oxygenated blood and blood full of food nutrients.
Central veins from all the lobular drains blood eventually from the liver uniting with each other
to form the hepatic vein. The hepatic veins drain the whole blood from the liver and empty into
the inferior vena cava.
Production of Bile: Bile is produced in the liver cells in a fine bile capillaries. Bile passes from
the liver to the gall bladder through the bile duct.
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NB: The sphincter of oddi is the common opening for bile duct and pancreatic duct is the
duodenum.
ANATOMY AND PHYSIOLOGY OF THE HEART
The heart is hollow muscular organ and it is located in the thoracic cavity mostly in the medial
and between the two lungs. It is cone shaped or inverted cone shaped. The length is about 10cm
and weighs about 270g and the size makes about the owners fist.
Organs in Association
Superioly: Great blood vessels
Inferiorly: The Diaphragm
Posteriorly: the esophagus, trachea, left and right bronchus and thoracic and descending Aorta.
Laterally: The two lungs
Anteriorly: The Sternum, the ribs and the intercostals muscles.
Structure: The heart consists of three main layer of tissue, the pericardium, the myocardium.
The Pericardium
This is the outer covering of the heart. It consists of an outer fibrous pericaerdium and an inner
serous pericardium. The outer fibrous pericardium is made up of fibrous tissue hence the name.
Functions: It prevent over distension of the heart as it is filled with blood. The inner serous
pericardium is made up of serous membrane, it has two smooth layers.
1. The parietal layer
2. Visceral layer.
The visceral layer is attached to the heart while the parietal layer is attached to the fibrous sac.
The serious membrane secrets a fluid known as the serious fluid.
Functions of the serous fluid:
It prevents friction of the space between the 2 layers known as potential space.
The Myocardium
This is the middle layer of the heart and is composed of special muscular tissue known as cardic
muscles.
The Myocardium is thickest towards the apex(top) and thins out towards the base. It is not
under the control of will. And once an impulse starts it may spread to the whole heart without
any interruption.
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The Endocardium
This is the inner lining of the heart and consists of flattened epithelial cells known as the
endothelium.
Functions of Endocardium:
These cells provide smooth surface for the heart.
Interior of the Heart
The heart is divided into right and left side by a muscular tissue known as the septum. The sides
are further divided into two by valves thus the heart is divided into four chambers. The upper
chamber constitutes of the atria and the lower chambers constitutes of the ventricles. The
chambers of the heart are right and Left atrium and right and left ventricles. The tricuspid valve
which is made up of three flasps separate the right atrium from the right ventricles and the
bicuspid valves which is made up of 2 flasps separate the left atrium from the left ventricle.
Functions:
The valve prevents flow of blood from the ventricles to the atriums. There are fine structures
attached to the ventricular surface of the valves known as Chordae Tendinae.
They help to support the heart thus preventing backflow from ventricle to atria.
Blood flow through the heart
The Superior and inferior Vena cava carrying impure blood empties their content into the right
atrium of the heart. The blood passes through the Atrio-ventricular valve or Triscuspid valve
into the right ventricle.
The blood is pumped into the pulmonary artery through the pulmonary valve. From the
pulmonary artery, it goes to the lungs. On reaching the Lungs, it is divided into left and right
pulmonary arteries and each joins the corresponding lung. In the lungs, exchange of gasses takes
place after which the blood becomes oxygenated and is carried back to the left atrium of the
heart by the pulmonary veins. From the left atrium, the blood passes to the left ventricle through
the mitral valve or bicuspid valve. The blood then goes to the aorta, through the aortic valve and
from the Aorta, it joins the general circulation. Therefore the right side of the heart deals with
impure or deoxygenated blood while the left side deals with pure or oxygenated blood.
Note: All veins carry deoxygenated blood except the pulmonary vein. While all arteries carry
oxygenated except the pulmonary artery.
23
The Conducting system of the Heart
There 3 areas involves
1. Cardiac Impulse
2. Cardiac Circle
3. Nervous control of the heart.
Spread of cardiac impulse: There are specialized cells situated between the heart muscles
referred to as neuro-muscular cells. These cells provide the conducting impulse which starts the
contraction of the heart muscle.
Sinuatrial Node is a mass of specialized cells which lies just around where the superior vena
cava enters the right atrium. Each heart beat originates from sinuatrial node even though the 2
atria are on the two separate chambers. The due to the arrangement of the heart muscle.
Hence the two atria contracts at the same time for any blood in them through the respective
atrioventricular valve into the ventricles. During this time, the muscle ring around the
pulmonary veins and venacava close preventing backflow of blood from the atria into them.
The atrioventricular node and atrioventricular bundle which is also referred to as bundle of his.
The cardiac impulse stops at the fibrous septum as this is non-conducting but the only
conducting septum is atrioventricular node which lies near the atrioventricular valve.
Cardiac impulse which passes into the atrioventricular bundle soon spreads through the
ventricles. This spread is possible because within the myocardium of the ventricles the bundle
and the fibres form a network of fibres known as the purkinge. The atrioventricular bundle and
the purkinge fibres convey the impulse of contraction to the ventricle thus blood is forced from
the ventricles upwards into the Aorta and pulmonary artery respectively.
Cardiac Bundle
The heart beats continuously for the whole of the person’s life. There are cycle of events
referred to as the cardiac cycle which occurs about 70 – 74 times per minute.
The complete cardiac cycle lasts for about 0.8 seconds. It consists of atrial systole, ventricular
systole and cardiac diastole. The atrial systole: as the superior and inferior vena cava pour
venous blood into the right atrium, the four pulmonary veins at the same time pour their content
into the left atrium. Atrial systole is the contraction of the atria as the sinuatrial nodes transmits
Impulse of contraction throughout the arteries. It last for 0.1 sec.
24
The ventricular: is the contraction of the ventricles as the wave of contractions spread through
the bundle of his and purkinge fibres. Blood is pushed through the pulmonary artery and the
Aorta respectively and last for 0.3 sec.
Cardiac Diastole: This is a resting phase, it follows after the contraction of the ventricles, the
heart rests. It last for 0.4sec after which the cycle begins again. The whole cardiac cycle takes
about 0.8sec to complete.
The Nervous Control
The cardiac center is located in the medulla oblongata. From this centre, nervous influence
reaches the heart through the autonomic nervous system.
The sympathetic nerves and vague or parasympathetic nerve which slows down the rate and
force of the heart beat as it influences the sinuatrial node. The sympathetic nerves tend to speed
up rate and force of heart beat. This could be evidenced in exercise when the heart beats faster to
meet the demand of the body tissue.
Blood supply to the heart is through the branches of coronary artery which is the first artery
that arises from the Aorta.
Venous drainage is through the coronary sinus to the atrium.
Functions of the heart
The heart is pumping organ of the body, thus making it possible for the constant circulation
throughout the body.
***Assignment, (a) Draw a diagram illustrating the conducting system of the heart.
(a) The period of one cardiac diastole.
ANATOMY AND PHYSIOLOGY OF GIT
Digestive System
The digestive system is the system that deals with food. It is either called the digestive system or
the alimentary tract. Common activities involved are ingestion, digestion, absorption and
elimination. The digestive system comprises of mouth esophagus, the stomach, Duodenum,
intestines, rectum and Anus. They make up the alimentary tract. U8nder the digestive system,
we have the accessory organs; they are the liver, pancreas, salivary glands and biliary tract.
Mouth or Oral cavity: The mouth is the beginning of the Alimentary tract. It is a cavity
bounded by muscles and bones.
25
Anteriorly - Bounded by muscles of the lip
Posteriorly – Continues as the oral pharynx
Laterally – bounded by the muscles of the cheek
Superiorly _bounded by the hard and soft palate
Inferiorly _ bounded by the tongue and soft tissue of floor of the mouth.
The whole cavity is lined throughout with mucous membrance consisting of stratified squamous
epithelim.
Structure within the mouth
1. Palate: The palate is divided into hard and soft palate. The hard palate is formed by the
bones of the maxillae and palatal bones and is most anterior while the soft palate is muscular
most posteriorly joining with the walls of the pharynx.
2. Uvula: it is fold of muscle covered with mucous membrane. It hangs from the soft palate
originating from the uvula are the anterior and posterior fauces. In between the fauces is a
collection of lymphoid tissue called the oral tonsil.
3. Tongue: The tongue occupies the floor of the mouth in base and is connected to the
hypoid bone.
Structure of the Tongue: The tongue is a muscular organ. Its superior surface is covered by
stratified squamous epithelium and with numerous papillae. These papillae contain nerve
endings of the sense of taste called taste buds.
Functions of the Tongue:
1. It helps in mastication of food – it helps to roll.
2. It helps in the act of swallowing
3. It is an organ of speech
4. It is an organ of taste because of the taste buds
***READ UP THE TEETH

The Alimentary tract.
The esophagus also known as gullet is a tube extending from the oropharynx in the neck to the
stomach in the abdominal cavity. It is about 19 inches or 20cm long.
Position; As it continues to the pharynx, it lies mainly in the median plain. It lies behind the
trachea and the heart and in front of the vertebral column. To enter the abdominal cavity, it
26
pierces the central tendon of the diaphragm at the level of 10th throracic vertebra curving
upwards to join the stomach.
Structure: the esophagus consists of four layers of tissue. A muscular layer consisting of
longitudenal fibres and circular fibres. The longitudinal fibres are outermost while the circular
fibres are innermost, encirculating the walls of the esophagus. The next layer is the sub mucous
layer. This is next to the muscular layer consisting of areola tissue, blood vessels, lymph vessels
and nerves which are autonomic nervous system. Mucous layer is the inner lining and it consists
of stratified mucous epithelium with mucous secretory gland that open unto the surface.
The Blood Supply: Branches from the thoracic and gastric.
Venous return; Azygos Vein, left and right gastric vein.
Nerve supply: Sympathetic and parasympathetic nerve.
The Stomach: This is the most dilated portion or part of the alimentary tract.
It is a J-Shaped organ located in the epigastric umbilical and left hypochondria region of the
abdomen.
Organs in relation to the stomach.
Posteriorly: it is related to the abdominal Aorta, the inferior vena cava, diaphragm, pancreas,
spleen and vertebral column.
Anteriorly: It is related to left lobe of the liver and anterior abdominal wall.
Superiorly: Diaphragm.
Inferiorly: Transverse Colon and small intestine
Structure: The stomach begins at the cardiac orifice where the esophagus joins it. Towards the
tail end, it joins with the duodenum at the pyloric orifice.
Parts of the Stomach
It is described as having two curvatures. The lesser curvature is short and lies at the posterior
curvature of the stomach curving up before the pyloric sphincter to complete the “J”-shape. The
greater curvature is at the anterior surface of the stomach curving upwards and downwards
towards the pyloric sphincter.
Stomach Portion:
The first portion of the stomach is called the fondus that represents the part of the stomach above
and to the left of the cardiac orifice. The body represents the main portion of the stomach.
Toward the end, the pyloric antrum represents the lower portion of the stomach. At the pyloric
27
antrum, there is a pyloric sphincter (a little portion of the muscle and guides the opening between
the pyloric antrum and the duodenum).
Coverings of the Stomach
The stomach consists of four (4) layers of tissue, the outer serious layer called peritoneum, the
muscular layer lying to the serious layer consisting of longitudinal fibres. The next layer is sub-
mucous layer which is the inner one made up of areolar tissues, blood vessels, nerves and
lymphatic layer. The innermost layer is the mucous membrane, it lines the stomach and it is
thrown into folds by rugae. The mucous surface is greatly increased and two arrangements, the
first being the circular folds. When the stomach is empty, it folds into the rugae; but when it is
full, the rugae straitens out (The rugae appear when the stomach is empty) giving the line a
smooth surface. The mucous membrane consists of columnar squamous epithelium with goblet
cells and also numerous secreting gastric glands which secrete gastric juice. Enzymes are
contained in the gastric juice which begins the digestion of protein foods.
***Read – Blood supply and nerve supply
The Small Intestine
This is a continuation of the stomach starting from the pyloric sphincter to the ileocolic valve
where it joins the large intestine. The small intestine is about 21 feet long and it is surrounded by
the large intestine.
Parts of the small Intestine
1. Duodenum: This is about 10inc long and it is C-shaped curving around the head of the
pancreas (First Portion) at its mid point. There is a common opening for the pancreatic
duct and bile duct and this opening is guided by the sphincter of Oddi.
2. Jejunum: This is the middle part of the small intestine and measures about 8 feet in
length.
3. Ileum: This is the tail end of the small intestine and it is about 12ft long. The ileum
joins the large intestine at the ileocolic valve. The ileocolic valve controls backflow of
materials from the ileum to the large intestine. (Read up the structure).
Large Intestine:
The large intestine begins at the caecum located in the right iliac fossa and ends at the rectum
and canal located in the pelvic. It is about 5ft long. Its lumen being larger than that of the small
intestine. It forms an arc around the small intestine.
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Parts of the Large Intestine.
The large intestine is divided into many parts:
1. Caecum: It is about 5 inches long and dilated with a blind end inferiorly and superiorly
it continues as the ascending colon. The ileum joins it at the ileocolic valve. The
Vermiform Appendix is attached to the Caecum.
2. The ascending Colon starts from the caecum passing upwards the liver. It bends acutely
to the left at the right colic flexure or hepatic flexure. It continues as the transverse
colon.
3. The transverse colon passes in the umbilical region in a loop extending transversely
across the abdominal cavity in front of the duodenum and the stomach the spleen and
bending acutely at the left colic flexure or spleenic flexure to continue as the descending
colon.
4. The descending colon passes from the end of the transverse colon down to the left side
of the abdominal cavity into the pelvic cavity to become the pelvic colon.
5. The pelvic colon extends from the descending colon just a loop and continues as the
rectum.
6. Rectum: it extends from the pelvic colon. It is lightly dilated and it is about 5 inches
long. It ends at the anus.
7. The Anus Canal: it extends from rectum and it is about 1 inch long and terminates at
the exterior. Two sphincters internal and external control the anus. The internal
sphincter consisting of smooth muscle fibres, is under the autonomic nervous system.
The external sphincter consists of stratified muscle; it is under the voluntary muscle.
***(Read up Structure of the large Intestine.)
29
OVERWEIGHT AND OBESITY
BY
REV. SR. ODINAKACHUKWU NWOSU
30
Being overweight or obese is a common condition especially
where food supplies are plentiful and lifestyle is sedentary. As much as 64% of the United
States, 55% of Nigeria and 50% Kenya adult population is considered either overweight or
obese, and this percentage has increased over the last four decades.
Obesity and overweight are the leading preventable cause of death worldwide with increasing
prevalence in adults and children, and authorities view it as one of the most serious public health
problems of the 21st century (Barness et al., 2007).
Obesity
An Overview
Overweight and obesity are both chronic conditions that are the result of an energy imbalance
over a period of time. The cause of this energy imbalance can be due to a combination of several
different factors and varies from one person to another. Individual behaviors, environmental
factors, and genetics all contribute to the complexity of the obesity epidemic.
Energy Imbalance
31
What is it?
Energy balance can be compared to a scale.
An energy imbalance arises when the number of calories consumed is not equal to the number
of calories used by the body.
Weight gain usually involves the combination of consuming too many calories and not
expending enough through physical activity.
Energy Imbalance
Effects in the Body

Excess energy is stored in fat cells, which enlarge or multiply.
Enlargement of fat cells is known as hypertrophy, whereas multiplication of fat cells is known as
hyperplasia.
With time, excesses in energy storage lead to obesity.
Fat Cell Enlargement

Hypertrophy
Enlarged fat cells produce the clinical problems associated with obesity, due to the following:
 The weight or mass of the extra fat
32
 The increased secretion of free fatty acids and peptides from enlarged fat cells.
Weight Classifications
With a BMI of: You are considered:
Below 18.5 Underweight
18.5 - 24.9 Healthy Weight
25.0 - 29.9 Overweight
30 or higher Obese
A Review
Body mass index (BMI) is a mathematical ratio which is calculated as weight (kg)/ height
squared (m2). It is used to describe an individual’s relative weight for height, and is significantly
correlated with total body fat content. BMI is intended for those 20 years of age and older.
BMI CLASSIFICATION
<18.5 Underweight
18.5 – 24.9 Normal weight
25.0 – 29.9 Overweight
30.0 – 34.9 Class I obesity
35.0 – 39.9 Class II obesity
≥40 Class III obesity
Mortality and Morbidity Associated with Obesity

The effects of excess weight on mortality and morbidity have been recognized for more than
2,000 years. It was Hippocrates who recognized that “sudden death is more common in those
who are naturally fat than in the lean.”
Today, obesity is increasing rapidly. Research shows that many factors related to obesity
influence mortality and morbidity.
Weight, Fat Distribution, and Activity
33
The following factors have
been shown to increase mortality in
individuals:
Excess body weight

Regional fat distribution
Weight gain patterns
Sedentary Lifestyle
Excess Body Weight
Mortality associated with excess body weight increases as the degree of obesity and overweight
increases.
It is estimated that 280,000 to 325,000 deaths a year can be attributed to obesity in the United
States, more than 80% of these deaths occur among individuals with a BMI greater than 30
kg/m2.
Regional Fat Distribution

Regional fat distribution can contribute to mortality. This was first noted in the beginning of the
20th century. Obese individuals with an android (or apple) distribution of body fat are at a greater
risk for diabetes and heart disease than were those with a gynoid distribution (pear).
Android fat distribution results in higher free fatty acid levels, higher glucose and insulin levels
and reduced HDL levels. It also results in higher blood pressure and inflammatory markers.
Weight Gain
In addition to overweight and central fatness, the amount of weight gain after ages 18 to 20 also
predicts mortality.
34
The Nurses’ Health Study and the Health Professionals Follow-up Study showed that a marked
increase in mortality from heart disease is associated with increasing degrees of weight gain.
Sedentary Lifestyle
Sedentary lifestyle is another important component in the relationship of excess mortality to
obesity. A sedentary lifestyle increases the risk of death at all levels of BMI.
Unfit men in the BMI range of less than 25 kg/m 2 had a significantly higher risk than men with a
high level of cardiovascular fitness. Obese men with a high level of fitness had risks of death that
were not different from fit men with normal body fat.
Associated with Obesity
Overweight affects several diseases, although its degree of contribution varies from one disease
to another.
Additionally, the risk of developing a disease often differs by ethnic group, and by gender within
a given ethnic group.
Morbidity Associated with Obesity
 Obstructive sleep apnea
Endometrial, prostate
 Osteoarthritis
 Cardiovascular disorders
and breast cancers
 Gastrointestinal disorders
Complications of pregnancy
 Metabolic disorders Menstrual irregularities
Psychological disorders
CAUSES OF OVERWEIGHT AND OBESITY
Obesity is a complex multifactorial chronic disease developing from interactive influences of
numerous factors which include:
 Genetic Factors
 Age and Sex
 Dietary Pattern
 Physical Activity
 Socio Economic Factors
35
 Emotional Factors
 Prosperity and Civilization
What about children?
When children are overweight, they are more likely to be overweight and obese as adults.
How can children avoid being obese?

This starts as soon as we are born….
Healthy Starts
Before we are born
Mothers who:
 Normal BMI during pregnancy
 Eat healthy and exercise moderately
 Gain 11.5-16 kg
 Prenatal care
When we are babies
Study shows babies weaned before 4 months gained more weight than recommended.
According to WHO: Breastfeed for at least 6 months exclusively and beyond if possible.
Childhood Obesity
Rates of childhood obesity are alarming. Problem is worldwide. Estimated in 2010 42 million
children under age 5 are considered overweight. Tripled in past 30 years.
Age 6-11 6.5% to 19.6%
Age 12-19 5.0% to 18.1%
Childhood Obesity
Genetic Link
Multifactorial condition related to sedentary lifestyle, too much good intake and choice of
foods actually alter genetic make-up, creating higher risk of obesity.
Behavioral
Children will more likely choose healthier foods if they are offered to them at young ages and in
the home Environment.
In homes where healthy food is not available or the food choices are not healthy. Obesity can
occur.
36
Childhood Obesity
Why does this matter?
 Premature death
 Developing heart disease at younger ages
 Developing diabetes type 2 at younger ages
 What can be done?
 Childhood obesity is preventable
 Role of the schools
 Role of health care professionals
Nutrition
Nutrition counts!
Nutrition is everything! Healthy foods, fruits, vegetables, legumes…a colorful diet is best!
Low sugar, low fat
Play an hour a day!
What can Schools do to help?
 Create “healthy” eating policy during school hours. Meaning…no junk food
 Provide healthy snacks for children to have or purchase…local fruits and vegetables that
children like to eat
 Have an exercise activity every day during school hours of at least 20 minutes
 Use activities as a “reward” rather than food
Reducing Childhood Obesity
Takes collaborative effort from everyone
From Nursing:
 Advocate for healthy eating
 Advocate obtaining nutritious food
 Advocate for exercise…one hour a day to play
 Advocate for health promoting exercise
 Educate the public
WHO Strategy
WHO Strategy for preventing overweight and obesity
37
Adopted by World Health Assembly in 2004 and WHO Global Strategy on Diet, Physical
Activity and Health
Four objectives
 Reduce risk factors of chronic disease
 Increase awareness and understanding
 Implement global, regional, national policies actions plans
 Monitor science and promote research
Let’s talk about each one…

Reduce risk factors for chronic disease
To reduce, there needs to be more exercise and better eating habits
Increase awareness and understanding
To understand the influence of diet and why physical activity makes a difference
And the last two…
To develop and implement global, regional, national policies and action plans
Work to improve diets and definition of physical activity
Monitor Science and promote research
On how diet affects the body, how to influences
How much physical activity is best for most
Evidence
Where is the evidence?
The Global Strategy on Diet, Physical Activity and Health has determined:
When threats to health are addressed, people can remain health into their 80’s and 90’s
Risk reduction…even modest has sustainable benefits.
Healthy living with not smoking is considered effective in reducing threats of non-communicable
disease.
Something as simple as eating fruits and vegetables can save millions of lives; according to
WHO, 2002:
Low fruit and vegetable intake.
2.7 million lives could be saved with enough fruits and vegetables.
Fruits and Vegetables
38
WHO states:
Fruits and vegetables need to be part of the daily diet to prevent disease such as obesity and non-
communicable disease. The statistics are startling;
Lack of enough fruits and vegetables cause
 19% of GI deaths
 31% of Ischemic heart disease
 11% of stroke
How much fruit is enough?
WHO recommends at least 400 gms of fruit and vegetables each day…
This will prevent chronic disease related to overweight and obesity
 Heart disease
 Diabetes
 Cancers
Essential Understandings
It is well known that obesity is preventable. It is caused by eating more than we need…so how
can we prevent obesity?
Each of us can…according to WHO
 Have a balance of energy and healthy weight
 Limit how much fat we eat…we need to eat some but not too much.
 Increase fruits and vegetables
 Limit sugars
 Increase exercise to at least 30-60 minutes per day on most days!
RECOMMENDATION
The best approach to weight loss strategies and management include;
 Proper diets and good food habits
 Increased level of activity in the forms of regular exercise
 Strict behavioural change to favour weight reduction
WEIGHT MANAGEMENT STRATEGIES: MEDICAL AND NUTRITIONAL THERAPY

What is Successful Weight Loss?
39
Common definition: Lose at least 10% of starting weight and keep it off at least one year.
What is the Goal of Obesity Treatment?
Specifically, the goal of obesity treatment should be refocused from weight loss alone, which is
often aimed at appearance, to weight management, achieving the best weight possible in the
context of overall health. –FTC Panel, Commercial Weight Loss Products and Programs
What Consumers Stand To Gain and Lose, 1997.
Who Should Consider A Weight Management Intervention?

Persons with a BMI of >30
Persons with a BMI between 25-29.9 OR a high-risk waist circumference, and two or more risk
factors
Persons who are ready to change
Obesity-Associated Risk Factors: 3 or More = ↑ Risk
 Hypertension
 Cigarette smoking
 High low-density lipoprotein cholesterol
 Low high-density lipoprotein cholesterol
 Impaired fasting glucose
 Family history of early cardiovascular disease
 Age (male ≥ 45 years, female ≥ 55 years)
Other Obesity-Associated Risk Factors
 Osteoarthritis
 Gallstones
 Stress incontinence
 Gynecological abnormalities
How Much and How Fast?

 NIH guidelines recommend a weight loss of .5 to 1 pound/week for persons with a BMI
of 27-35 and 1-2 pounds a week for those with a BMI>35 kg/m2
40
 Allow 6 months to achieve 10% weight loss
 After 6 months, focus should shift to weight maintenance for 6 months
 Following this, weight loss efforts may resume (NIH, 1998)
Weight Loss Goals
R.4.0. Individualized goals of weight loss therapy should be to reduce body weight at an optimal
rate of 1-2 lbs per week for the first 6 months and to achieve an initial weight loss goal of up to
10% from baseline.
These goals are realistic, achievable, and sustainable, strong and imperative.
Rates of Weight Loss Vary

Men will lose weight faster than women of similar size, due to higher LBM and RMR
A heavier person (who has higher energy needs) will lose weight faster than a smaller person on
the same caloric regimen
Modest Weight Loss and Health: Diabetes Prevention
A 7% weight loss (mean 15 pounds) through diet and exercise in high risk individuals was
associated with a 58% reduction of diabetes incidence in the Diabetes Prevention Program DPP
Research Group. N Engl J Med. 2002 Feb 7;346(6):393-403.
An average 7.7 pound weight loss was associated with a 58% reduction in diabetes incidence in
high risk individuals in the Finnish Diabetes Prevention study. FDPS Group. N Engl J Med
344:1343–1350, 2001.
Modest Weight Loss and Health: Hypertension
Weight loss of as little as 4.5 kg (10 pounds) will improve or prevent hypertension in a large
segment of overweight persons. Seventh Report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
http://www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.
Clinically significant long-term reductions in blood pressure and reduced risk for hypertension
can be achieved with modest weight loss and increased physical activity. American Dietetic
Association Evidence Analysis Library, Hypertension and hyperlipidemia.
http://www.adaevidencelibrary.org/
Modest Weight Loss and Health: Hyperlipidemia
41
The ATP-III guidelines recommend a 10% weight loss in overweight persons with
hyperlipidemia. http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf
A weight loss of ≥2.25 kg was associated with a 40-50% reduction in cardiovascular risk factors
in the Framingham Offspring Study (BP, triglyceride, TC, FBS, HDL) Karason K et al. Int J
Obes Relat Metab Disord 1999; 23:948-56.
Modest Weight Loss and Health: Diabetes
Calorie restriction and weight loss improves insulin sensitivity and glycemic control in obese
patients with Type 2 diabetes. Henry RR et al. J Clin Endocrinol Metab 1985; 61:917-25; Kelly
DE et al. J Clin Endocrinol MEtab 1993;77:1287-93.
A 5% weight loss can decrease FBG, insulin, A1C concentrations and medication requirements.
Wing RR et al. Arch Intern Med 1987; 147:1749-53.
Setting Weight Management Goals
Many severely overweight persons have unrealistic expectations in setting weight loss goals
(Blackburn, 1998)
Even modest weight loss may produce significant improvements in health
For some persons (especially those with BMI of 25-29.9) weight maintenance may be a goal
Evaluation of Body Wt
Body mass index (BMI) and waist circumference should be used to classify overweight and
obesity, estimate risk for disease, and to identify treatment options.
BMI and waist circumference are highly correlated to obesity or fat mass and risk of other
diseases (NHLBI report). Fair, Imperative
Estimation of Energy Needs
Estimated energy needs should be based on RMR. If possible, RMR should be measured (e.g.,
indirect calorimetry).
If RMR cannot be measured, then the Mifflin-St. Jeor equation using actual weight is the most
accurate for estimating RMR for overweight and obese individuals. Strong, Conditional
Readiness to Change: A Brief Assessment
 Has the individual sought weight loss on his/her own initiative?
 What has led the patient to seek weight loss now?
 What are the patient’s stress level and mood?
 Does the individual have an eating disorder?
42
Readiness to Change: A Brief Assessment
Does the individual understand the requirements of treatment and believe that he/she can fulfill
them?
How much weight does the patient expect to lose?
NIH Recommended Interventions
 Dietary therapy
 Physical activity
 Behavior therapy
 Pharmacotherapy
 Bariatric surgery
Comprehensive Wt Mgt Program
Weight loss and weight maintenance therapy should be based on a comprehensive weight
management program including diet, physical activity, and behavior therapy. The combination
therapy is more successful than using any one intervention alone. Strong, Imperative
Dietary Interventions
Optimal Length of Wt Mgt Therapy
Medical Nutrition Therapy for weight loss should last at least 6 months or until weight loss goals
are achieved, with implementation of a weight maintenance program after that time.
Greater frequency of contacts between the patient and practitioner may lead to more successful
weight loss and maintenance.
Strong, Imperative
Goals of Weight Management (NIH)
Achievement of healthy body weight (or close to desired BMI)
Select a realistic goal—no more than 1 to 1.5 lb/week
Prevent loss of LBM, especially from heart and brain
Support psychosocial factors
Reduced Calorie Diets
An individualized reduced calorie diet is the basis of the dietary component of a comprehensive
weight management program.
43
Reducing dietary fat and/or carbohydrates is a practical way to create a caloric deficit of 500 –
1000 kcals below estimated energy needs and should result in a weight loss of 1 – 2 lbs per
week.
Strong, Imperative
Balanced Energy-Restricted Diet
Is the most widely-prescribed method of weight reduction?
Should be nutritionally adequate except for energy.
Energy level varies with individual’s size, sex, and activity, ranging from 800 kcals to 1500 kcals
(NIH, 1998)
Should be relatively high in carbohydrate (50-55% of total kcals)
CHO sources should be fruits, vegetables, whole grains
Include generous protein (15-25% of kcals) for increased satiety and to assure adequate supply
Fat < 30% of kcals
Increased fiber to improve satiety (NIH, 1998)
Alcohol and high-sugar foods should be limited to limit excess energy
Use of non-nutritive sweeteners and fat replacements may improve the palatability of the diet
Vitamins and mineral supplements may be needed in programs that provide <1200 kcals for
women or 1800 kcals for men (NIH, 1998)
Exchange System Diets
Allow flexibility in making food choices while limiting total caloric intake
Provides framework for healthy balance of nutrients
May be too complex or restrictive for some clients
Nutrition Education
Nutrition education should be individualized and included as part of the diet component of a
comprehensive weight management program.
Short term studies show that nutrition education (e.g. reading nutrition labels, recipe
modification, cooking classes) increases knowledge and may lead to improved food choices.
Fair, Imperative
Eating Frequency and Patterns
44
Total caloric intake should be distributed throughout the day, with the consumption of 4 to 5
meals/snacks per day including breakfast.
Consumption of greater energy intake during the day may be preferable to evening consumption.
Fair, Imperative
Portion Control
Portion control should be included as part of a comprehensive weight management program.
Portion control at meals and snacks results in reduced energy intake and weight loss.
Fair, Imperative
Meal Replacements
For people who have difficulty with self selection and/or portion control, meal replacements
(e.g., liquid meals, meal bars, calorie-controlled packaged meals) may be used as part of the diet
component of a comprehensive weight management program.
Substituting one or two daily meals or snacks with meal replacements is a successful weight loss
and weight maintenance strategy.
Strong, Conditional
Low Glycemic Index Diets
A low glycemic index diet is not recommended for weight loss or weight maintenance as part of
a comprehensive weight management program, since it has not been shown to be effective in
these areas.
Strong, Imperative
Low fat Dairy Foods
In order to meet current nutritional recommendations, incorporate 3-4 servings of low fat dairy
foods a day as part of the diet component of a comprehensive weight management program.
Research suggests that calcium intake lower than recommended levels is associated with
increased body weight. However, the effect of dairy and/or calcium at or above recommended
levels on weight management is unclear.
Fair, Imperative
Low Carbohydrate Diets
45
Having patients focus on reducing carbohydrates rather than reducing calories and/or fat may be
a short term strategy for some individuals.
Research indicates that focusing on reducing carbohydrate intake (<35% of kcals from
carbohydrates) results in reduced energy intake.
Consumption of a low-carbohydrate diet is associated with a greater weight and fat loss than
traditional reduced calorie diets during the first 6 months, but these differences are not significant
after 1 year.
Fair, Conditional
Very Low Calorie Diets (VLCD)
Diets providing 200-800 kcals/day
Hypocaloric but relatively rich in protein (.8-1.5 g/kg/day)
Designed to include adequate vitamins, minerals, electrolytes, and EFAs
Completely replace usual meal intake
Usually given for 12-16 weeks
Usually reserved for those with BMI>30; or 27-30 with risk factors
Protein Sparing Modified Fast (PSMF)
 Uses real food
 Contains 1.5 g protein/kg IBW as lean meat, fish and poultry
 May include low-carbohydrate vegetables
 Only fat is that present in the protein sources
 Commercial VLCD Liquid Diets
 Contain 33-70 g of protein, 30-45 g CHO, small amount of fat
 Provides 400-800 kcals
 Patients lose 20 kg in 12 to 16 weeks
VLCDs
Cardiac complications a concern
Risks include potassium loss as well as body protein (higher in the less obese)
Requires close medical supervision and monitoring of serum electrolytes
But VLCDs may be a more effective method of weight loss for some
(Anderson et al Am J Clin Nutr 74;579:2001)
Dietary Therapy: NIH Guidelines
46
Very low calorie diets (VLCDs) should not be used routinely for weight loss therapy because
they require special monitoring and supplementation
LCDs may be just as effective
Behavioral Therapy in Weight Management
Behavioral Therapy: NIH Guidelines
 Self-monitoring
 Stress management
 Stimulus control
 Problem-solving
 Contingency management
 Cognitive restructuring
 Social support
Behavior Therapy in Wt Mgt
A comprehensive weight management program should make maximum use of multiple strategies
for behavior therapy (e.g. self monitoring, stress management, stimulus control, problem solving,
contingency management, cognitive restructuring, and social support).
Behavior therapy in addition to diet and physical activity leads to additional weight loss.
Continued behavioral interventions may be necessary to prevent a return to baseline weight.
Strong, Imperative
 Self Monitoring
 Records of place and time of food intake
 Accompanying thoughts and feelings
 Helps identify the physical and emotional settings in which eating occurs
 Provides feedback on progress and puts responsibility on the patient
 Problem Solving
 Process for defining the eating or weight problem
 Generating possible solutions; evaluating the solutions, choosing the best one
 Trialing the new behavior, evaluating outcome and generating alternatives
 Stimulus Control
Modification of:
47
 The settings or the chain of events that precede eating
 The kinds of foods consumed
 The consequences of eating
 Become mindful of satiety cues
 Put fork down between bites
 Pausing during meals
Cognitive Restructuring
Teaches patients to identify, challenge, and correct negative thoughts
Positive self-talk
Behavior Modification
Most effective in mildly obese (20-40% overweight)
Patients can maintain losses of 20-25 pounds
Longer programs more successful
Many patients regain the weight they lost over time
Weight Loss Medications
Pharmacological Therapy NIH Guidelines
Should be used only in the context of a program that includes lifestyle changes
If lifestyle changes do not promote weight loss after 6 months, drugs should be considered
Limited to those with BMI ≥30; or ≥27 with risk factors
Wt Loss Medications
R.14.0 FDA-approved weight loss medications may be part of a comprehensive weight
management program.
Dietitians should collaborate with other members of the health care team regarding the use of
FDA-approved weight loss medications for people who meet the NHLBI criteria.
Research indicates that pharmacotherapy may enhance weight loss in some overweight and
obese adults.
Strong, Imperative
Catecholaminergic Drugs
Appetite suppressants
Act on the brain, increasing the availability of norepinephrine
Schedule II anorexic agents
48
 High potential for abuse
 Include amphetamine, phenmetrazine HCl
 Not recommended for weight management
Schedule III agents
 Some potential for abuse
 Include benzphetamine HCl, phendimetrazine tartrate
Catecholaminergic Drugs
Schedule IV agents
Includes diethypropion HCl, manzindol HCl, phentermine HCl, phentermine resin
Low potential for abuse
Can raise blood pressure, so prescribed with caution in patients with hypertension
Serotonin Reuptake Inhibitors
 Includes sibutramine (Meridia)
 Inhibits the reuptake of serotonin and norepinephrine
 Initially developed to treat depression
 Use caution in hypertension, CHD, arrhythmias, CHF
 Orlistat (Xenical)
 Lipase inhibitor
 Acts directly on the gastrointestinal tract to inhibit fat absorption
 Associated with reduced LDL-C and increased HDL; improved glycemic control,
reduced blood pressure
 Some concern about fat soluble vitamins
 Side effects: oily spotting, fecal urgency, flatus with discharge
 FDA Approves Reduced Dose of Orlistat for Over the Counter
 Over the counter dose of orlistat, a lipase inhibitor
 Half the dose of prescription form (Xenical)
 The only FDA-approved over the counter wt mgt drug
 Available summer 2007
 Serotoninergic Agents
 Increase serotonin levels in the brain
49
 Fenfluramine hydrochloride and dexfenfluramine HCl (Fen-Phen) were removed
from the market in 1997 due to association with heart valve disease and pulmonary
hypertension
Pharmacological Obesity Treatments
Weight loss of about 1 lb/week can be expected
Most weight loss will occur within the first 6 months of therapy
Significant weight maintenance as long as the drug treatment is continued
Most patients regain weight if medication is stopped
Pharmacological Obesity Treatments
Weight-loss medications lead to an additional weight loss of 5 to 22 pounds more than with
non-drug obesity treatments
Two to 20 kg total loss, usually during first 6 months of treatment
When drugs are discontinued, weight regain occurs
Physical Activity and Weight Management
Physical Activity
Physical activity should be part of a comprehensive weight management program. Physical
activity level should be assessed and individualized long-term goals established to
accumulate at least 30 minutes or more of moderate intensity physical activity on most, and
preferably, all days of the week, unless medically contraindicated.
Physical activity contributes to weight loss, may decrease abdominal fat, and may help with
maintenance of weight loss.
Strong, Imperative
Physical Activity: NIH Guidelines
 Physical activity increases energy expenditure and plays an integral role in weight
maintenance
 Reduces the risk of heart disease more than weight loss alone
 Reduces body fat, prevents decrease in muscle mass during weight loss
 All adults: goal of 30 minutes or more of moderate-intensity physical activity on most
and preferably all days.
Role of Physical Activity in Weight Management
50
 Physical activity usually will not lead to a greater weight loss over diet alone in a 6-
month period (NIH, 2000)
 Physical activity is most helpful in preventing weight regain
 Physical activity also is beneficial in reducing risk for heart disease and diabetes
beyond the effect of weight loss
 Exercise helps balance the loss of LBM and reduction in RMR caused by hypocaloric
diets
 A combination of aerobic exercise and resistance training is recommended
 Even when weight loss does not occur, loss of body fat often does
 May require 2 months to see loss of weight through exercise
U.S. Dietary Guidelines 2005
 Suggest 60 minutes of moderate-vigorous activity on most days of the week to prevent
weight gain in adulthood
 To sustain weight loss in adulthood: at least 60-90 minutes of daily moderate-intensity
physical activity
 Achieve physical fitness by including cardiovascular conditioning, stretching exercises
for flexibility, and resistance exercises or calisthenics for muscle strength and endurance.
Other Benefits:
 Improved sense of well-being
 Relief of boredom
 Sense of control
 Relief from depression
Bariatric Surgery
Dietitians should collaborate with other members of the health care team regarding the
appropriateness of bariatric surgery for people who have not achieved weight loss goals with less
invasive weight loss methods and who meet the NHLBI criteria.
Separate ADA evidence based guidelines are being developed on nutrition care in bariatric
surgery.
51
Strong, Imperative
Bariatric Surgery: NIH Guidelines
 Option for well-informed and motivated patients with clinically severe obesity (BMI≥40
or BMI ≥35 with serious co-morbid conditions
 Candidates for Bariatric Surgery
 BMI of 40 or more—about 100 pounds overweight for men and 80 pounds for women
 BMI between 35 and 39.9 and a serious obesity-related health problem such as type 2
diabetes, heart disease, or severe sleep apnea
 Willingness to make associated lifestyle changes
Bariatric Surgery Options
 Restrictive
 Malabsorptive
 Combination restrictive/malabsorptive
 Restrictive Procedures
Adjustable gastric banding (AGB) a hollow band made of silicone rubber is placed around the
stomach near its upper end, creating a small pouch and a narrow passage into the rest of the
stomach
Vertical banded gastroplasty. VBG uses both a band and staples to create a small stomach
pouch (not often used today)
Restrictive Surgery: Adjustable Gastric Band
Diet After Surgery

After restrictive surgeries, patients can only eat ½ cup to 1 cup of food at a time
Foods often must be soft and chewed thoroughly
Patients who eat too fast or the wrong kinds of food may have vomiting
Restrictive Procedures: Advantages
52
 Don’t interfere with
the normal digestive
process
 Easier to perform and
generally safer than
malabsorptive
surgeries
 AGB often done
laparoscopically
 Can be reversed if necessary
Restrictive Procedures: Disadvantages
 Generally results in less weight loss
 Patients generally lose about half of their excess body weight in the first year after
restrictive procedures
 Only 20% keep weight off over 10 years, though there is evidence that AGB is more
effective than VBG
Restrictive/Malabsorptive Procedures
53
Roux-en-Y gastric bypass (RGB) is the most common.
The surgeon creates a small stomach pouch to restrict food intake. Next, a Y-shaped section of
the small intestine is attached to the pouch to allow food to bypass the lower stomach, the
duodenum and the first portion of the jejunum.
This reduces the amount of calories and nutrients the body absorbs.
Restrictive/Malabsorptive: Roux en Y
Restrictive/Malabsorptive Procedures: Advantages
 Patients lose weight quickly and continue to lose 18-24 months after the procedure.
 With RGB, many patients maintain a weight loss of 60 to 70 percent of their excess
weight for 10 years or more.
Restrictive/Malabsorptive Procedures: Disadvantages
 More difficult to perform
 More likely to result in long-term nutritional deficiencies (calcium, iron)
 Greater risk of dumping syndrome
 Increased likelihood of complications including hernia (decreased with laparoscopic
procedures)
Weight Management—Children
Goals: Weight maintenance or slowing of gains
Grow into weight
If severely obese, lose no more than 1 lb monthly to reach desired adult weight for height
Weight Management in Children
At risk at BMI 85% to 95%ile; obese at 95%
Review parents’ history—height, weight, etc.
Weight management in children is a family affair
Weight Management in Children
Overweight children should try to achieve weight maintenance or slowing of the rate of weight
gain, not weight loss
Depends on age and degree of overweight
Once adult height is achieved, weight loss is necessary to improve health
Summary
54
Even modest weight loss can produce improvements in overall health in persons who are
overweight (lipids, BG, insulin, blood pressure)
Most persons will need sustained, long-term lifestyle interventions to achieve significant weight
loss.
55
NUTRITION COUNSELING
GERIATRIC NUTRITION
BY
DTN MBOMI
56
NUTRITION COUNSELLING
Counseling is a process of communication between a client and a counselor, which is
aimed at assisting the client to know and solve his or her problems. The counsellor works
together with the client to identify his problems and possible solution to these problems. The
primary function of counselling is to help people think clearly when feelings are present.
Counselling helps people to change as they lean to think things through for themselves and make
their own decisions.
A GOOD COUNSELLOR
A counsellor is a person who is professionally qualified or trained to give counsel. A
good counsellor should be knowledgeable, friendly, respectful and patient. He should also have
good communication skills and should know is limitations. He should be accessible and available
for his clients. A good counsellor should also be able to empathize and show high level of
confidentiality.
COUNSELLING SKILLS/TECHNIQUES BASIC SKILLS
1. Listening: This is the most important skill in counselling. It is a process of “hearing” the
other person. This means listening with interest, indicating that the counsellor
understands what the client is saying. There are three aspects of listening. It could be
through the use of words, phrases and metaphor to convey feeling. It may not be words
itself, but timing, accent, volume etc. It may also be non-verbal like use of body
languages or facial expression, gestures, body position and movement or touch in relation
to the counsellor. Also nodding of heads, leaning towards the other, making eye contact,
could be used. All these are known as “attending behaviours” communication is 55%
body language, 38% tone and 7% words.
2. Empathy: This involves placing oneself in another person’s situation, yetcontrolling
ones emotions. The counsellor shows that he understands the client’s worlds and feelings
and expresses that understanding.
3. Effective questioning: Counselors should use questions to help their client state their
feelings and fears. They could use open-ended questions or closed-ended questions.
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Open-ended questions- These are questions that the client cannot easily answer with “Yes” or
“No” eg why is that important to you” or “what are your reasons for saying that?, “how do you
feel”.
The purpose of open-ended questions is:
- To begin an interview
- To encourage client elaboration
- To elicit specific examples
- To motivate client to communicate
Close-ended questions: These are questions the other can easily answer with a “Yes” or “No” or
one or two-word responses. Eg. Do you give your baby pap?, have you taken your breakfast?.
Close-ended questions is used to:
- To obtain specific information
- To narrow the topic of discussion
- To interrupt an over-talkative client
4. Non-judgmental:In counseling, counselors should not judge the client so that he will
feel safe. He should accept the client’s feelings and fears and encourage emotional outlet.
5. Paraphrasing: This means rephrasing the content of the client’s message.
Eg. Client: I know I have not been feeding my baby exclusively.
Counsellor: it sounds like you know you should feed your baby exclusively.
Paraphrasing is used:
- To convey that you are understanding
- To encourage him to elaborate
- Help the client to simplify and focus on what he said.
This is used when a counsellor notices that the clientis in a decision making conflict.
- When the client presents a lot of matters that are confusing.
- When you have a hypothesis about what is going on with the client.
6. Reflection: This is a verbal response to the client’s emotion.
Eg.Client: This my baby eats two must, I don’t think I can continue with exclusive
breastfeeding.
Counsellor: You are feeling as if you cannot do exclusive breastfeeding.
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Reflection is used to
- Help client feel understood
- Express more feelings
- Manage feelings
The counsellor should be skilled in recognizing and distinguishing the different emotions
exhibited by the client.
7. Challenge: Sometimes, counselors can challenge or confront the client with fallacies in
her stories. He will do it in such a way that the client sees it as a positive act, not blame or
judge.
Eg. Client: I am tired of this baby’s sickness and there is no one to run to.
Counsellor: No one?
Client: I have always been a failure
Counsellor:Always?
8. Summary: This means condensing the client’s messages.
- The purpose of summary is to lay emphasis on most critical issues and interrupt excessive
rambling
- To identify a common theme or pattern
- To tie together multiple elements in clients messages
9. Motivation:Counsellors should motivate their clients to workout realistic plans and act
on them. He should not try to change the client, but helps him to become more
authentically himself.
STAGES OF COUNSELLING
The three stages of counselling are:
i. Assessment
ii. Analysis
iii. Action
STAGE ONE: INTRODUCTION/ASSESSMENT
This first stage in counselling process starts with introduction and has to do with
relationship building. The counsellor tries to establish rapport with the client and ensures
confidentiality. He starts by asking informal or friendly questions like “How are you? Or how do
you feel?” At this first stage of counselling, the counsellor takes the client’spersonal history
59
(social, economical,religions etc). He accesses the emotional status of his client, trying to explore
his problems and feelings and allows expression of emotional reactions. The time consumed in
this stage depends on the client’s knowledge, his specific or personal concern and the content of
the counselling.
THE SECOND STAGE OF COUNSELLING: ANALYSIS
This is the stage of information gathering and analysis.The counsellor tries to find out
what the problem is like. He solicits information about what the client already knows, the
discusses actions that have already been taken by the client and demonstrated concern and
support for the client. He discusses the client’s feelings and fears, and helps him to establish a
plan of action. The counsellorcorrects misconception, explains accurately the workout strategies
and provides useful information through discussions. Behavioral changes are also made were
necessary.
THE THIRD AND LAST STAGE OF COUNSELLING: ACTION
Through the discussion, a good counsellor would have gotten hold of the client’s
problems. He now asks the client to accept his problems and move towards control. The
counsellor works with the client to prepare and put plans of actions into practice. He recognizes
and praises the client where he did well, and also offers practical help where necessary. Home
work or assignment may be given to the client to maintain the relationship. He summaries the
discussion and provides agenda for future relationship i.e. appointment. The counsellor stresses
that the appointment continues until the client is able to cope.
RECOMMENDATION
The primary function of counselling is to help people think clearly about their feelings
and actions. This helps them to change as they learn to think things through for themselves and
make their own decision.
The counsellor should listen with interest so that the client feels heard and understood.
He should not judge, so that the client feels safe and respected.
- Accept the client’s feelings so that he feels not judged.
- Do not argue so that he will not be defensive or confrontational.
- Think about the client and empathize so that he gets the best care.
- Ask questions so that he will develop his own thinking.
- Do not belittle him and his feelings so that he will not withdraw or attack.
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- Do not avoid painful areas so that he will not be frustrated.
- Do not force or push him to do something but let him find out what works best for him
within his own ability.
If you decisde to solve the problem for him, he will become dependent.
NUTRITION AND AGING PROCESS (GERIATRIC NUTRITION)
Aging is a process of growing older. It actually begins at conception and ends at death. It
encompasses the whole of life with different stages. (Young age, middle age and older age). At
all these stages, basic human nutritional needs continue but in changing patterns as we grow
older. Aging starts once growth is complete at the age of 25years. It occurs at individual and
unique gene-controlled rate.
Initially at the beginning of aging, a lot of people may not notice that it has started and it causes
no problem. Later on, these processes speed up and physiological changes become apparent. At
the age of 25years, growth seizes and aging starts. At the stage 25-45years physical growth is no
longer marked by increasing number of cells and body size of replication, growing new cells to
replace old ones to maintain body structure and function, increase learning. Energy needs
decrease 2% of the total daily need after each decade as we grow older. This is because of the
decline in skeletal muscle mass and strength. A condition called SARCOPENIA. Metabolic rate
drops due to decline in physical activities.
Around 30 and 40years, physical activities drop and body fat may begin to increase. At the stage,
blood lipid levels should be monitored to recognize only risk of heart diseases that respond to
intervention.
At middle adult stage (45-65yrs) cell replication rate begins to slow down and gradual cell loss
begins. Physical activities decrease the more, lowering metabolism further resulting to atrophy of
the muscles. The body becomes less efficient in nutrient absorption and utilization.
As we get older (65-85yrs), degeneration in body composition continues and the body may find
it difficult to digest, absorb or utilize nutrients. There is also an interaction between the aging
process and chronic diseases at this older age which may also influence nutrient intake and
utilization. The oxidative cell damage by free radical influences the aging process and this
damage may affect both physiological and mental process.
61
CHANGES THAT OCCUR DURING AGING PROCESS
As we get older from 25years, physical growth gradually declines. Loss of body cells begins and
the body tries to replace them by growing new cells depending on the nutrient available. The
gradual loss of cells at the older age leads to a reduction in the metabolism in the remaining cells,
which leads to a gradual reduction in the performance capacity of most organ systems due to loss
of muscle mass and strength (atrophy).
These changes-both physical and mental, vary from individual to individual and can occur
rapidly in one organ system and slowly in another.
As aging continues from 70yrs and above, in general, lean body mass continues to decline and
accelerates in later life. Example, by the age of 70yrs the liver loses about 25% of its weight, the
kidney about 28% and the skeletal muscle diminishes by almost half, when compared with
young adults. As a result of the aging process, the functional unit of the kidney (nephrons) is lost
as a result of the aging and the effect of high protein intake. Lack of physical activities also
contributed to the loss of skeletal muscles. These gradual losses of cellular units in organs results
in overall reduction in the body’s reserve capacity, thus older adults are less able to respond to
environmental changes, physical stress or conditions of diseases and infections.
EFFECTS OF THESE CHANGES ON FOOD INTAKE AND UTILIZATION

1. The secretion of certain digestive juices is reduced. This can lead to indigestion of some
nutrients and mal-absorption of some important nutrients. Lack of gastric acid can lead to
unwanted bacterial growths.
2. These changes both physical and mental can influence sensory perception of taste smell,
vision and hearings although these responses are highly individualized. These senses
affect appetite and the enjoyment of food and may determine the amount of food
consumed.
3. These changes may often lead to loss of independence and loss of self esteem all of
which can affect food intake.
4. Malnutrition- Inadequate nutrient intake may result to various disease conditions which
will influence aging process.
5. Loss of teeth affects food intake.
62
FACTORS THAT AFFECT AGING PROCESS
1. Genetic-make up (Biological).
2. Dietary habit I(Malnutrition).
3. Lifestyle (Alcohol, smoking).
4. Lack of physical activity.
5. Pollution.
6. Oxidative stress.
7. General functional decline as the result of aging.
TYPES OF AGING
1. Natural aging: As a result of genetic and typical environmental influence.
2. Graceful or successful aging: This occurs when individuals slow down the number
and the rate of aging changes through positive living, healthy diet, and avoidance of
poisons (smoking, alcohol, tobacco, drugs).
NUTRITIONAL REQUIREMENT OF ELDERLY PEOPLE

At old age, individual situations and needs vary widely and must be individually assessed
because each has been exposed to a unique set of genetic and environmental influences.
Generally, there is a fall in energy requirement with age and an increased requirement for
vitamin D for the house bound.
However, it can be extremely difficult for elderly people to have a diet that is nutritionally
adequate when there is loss of appetite, pain or disability.
ENERGY REQUIREMENT
Reduction of energy requirement because:
1. There are changes in body composition and functions which leads to reduction in basal
metabolic rate.
2. Activity declines with age, so less energy is expanded.
The reduction in energy need means that the diet has to be of a higher nutritional quality to
meet requirement for other nutrients while the energy intake is reduced.
63
Studies indicate that a diet limited in Kcalories but adequate in protein, vitamins and minerals
may actually help us to live longer. This may prevent the deposition of unwanted body fat.
Individual energy need varies widely body size and physical activity. Average energy estimate
for the elderly is about 1800kcal/day, more or less.
However, in many older people, the average energy intake is 1400-1600kcal and such low
calorie diets are likely to be limiting in protein and important vitamins and minerals. The
simplest criterion for judging adequacy of kcalories intake is maintenance of body weight.
A variety of physiological changes and increased use of multiple prescribed medications reduce
food intake in many elderly people. To meet energy need, older adults need enough complex
carbohydrate (50-55%) diet rich in fiber such as legumes and cereals and limited fats.
FATS
Some fat is needed as a source of energy, essential fatty acids and to help the absorption of fat
soluble vitamins. The fat intake should be limited to 30% and should be mostly plant fats (poly
unsaturated fat and mono-unsaturated fat). Digestion and absorption of fat may be delayed in
elderly people, so large quantities of fat should be avoided. However, there should be enough fat
to enhance palatability, appetite and serve as a concentrated form of energy. Some of the sick
elderly people lose a lot of weight, so in some very frail and elderly, fat may be increased to
about 35% to prevent unwanted weight loss. When elderly people eat a diet that is inadequate in
many nutrients, they will become under weight and will lack the metabolic reserve they require
to respond to infection and stress. To ensure an adequate energy intake, all elderly people should
require 1.5kcal per/kg Bw/day irrespective of their activity level. A low BMI in old age is
associated with increased risk of mortality and morbidity.
CARBOHYDRATE (ENERGY)
The brain relies on glucose as the energy source to do its function. Under normal circumstances,
glucose is the only source of energy used by the brain cells. Diabetes and poor glucose tolerance
seem to have adverse effect on brain function in elderly individuals. The use of snacks (mid-
morning snacks) by older adults to maintain stable blood glucose level may support optimal
brain function. Carbohydrate should supply 50-55% of total calorie and should be mainly from
complex carbohydrate with fiber.
64
PRTOTEIN NEEDS
The current RDA of protein for adult is 0.8g/kg Bw, but in some cases, intake of 1.0-1.2/kg may
be needed to ensure preservation of muscle mass. This is because;
1. The amount of muscle present in a predicator of functional ability and the capacity for
self-care.
2. Muscle serves as a store for amino acids to meet emergency requirement during illness or
injury.
Healthy elderly with protein intake below 1.0kg/Bw are more likely to have a lower immune
response.
Debilitating elderly individuals may require intakes of up to 1.6g/kg along with additional
Kcalorie to adequately replace body stores.
Protein should supply from 15-20% of the daily kilocalorie. Healthy adults do not need
supplemental amino acid preparation because they can get enough from food combination.
Debilitating elderly people may need supplements containing good-quality protein but should be
used only by the advice of a professional (Dietitian). The quality as well as the quantity of
protein given should be considered.
WATER REQUIREMENT
Changes in the hypothalamus, affects thirst mechanism so that the older people do not get thirsty.
This affects their fluid intake and dehydration can easily occur. Body water serve as the medium
for dilation of medications and dehydration increases the risk of adverse drug reactions. Older
adults should take not less than 1500ml-2000mls of water daily.
VITAMIN REQUIREMENT
B complex vitamins are particularly important for energy metabolism and brain functions. It
helps delay aging of the brain and nervous system. The antioxidant vitamins A, C and E may
help prevent degenerative changes in the brain and nervous tissues. Vitamin E prevents the
oxidation of cholesterol that damage vessels supplying blood to the brain (body). Vitamin B6 is
necessary for the synthesis of various neuro-transmitters eg dopamine, and low level of this will
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result in the less of muscle control and tremor. It will also affect memory and reasoning. Folate
also plays several roles in brain function and red blood formation.
Vitamin D- This may be a problem for elderly who spent most of their time indoors and do not
eat vitamin D fortified foods. With healthy diet, all there nutrients can be obtained and individual
counseling should stress on good food sources.
MINERAL REQUIREMENT
It may be difficult to meet calcium need for elderly people but with a well balanced nutrition all
other minerals (potassium, iron, zinc, phosphorous, magnesium etc) needed may be supplied.
The very sick ones may need supplements.
NUTRIENT SUPPLEMENTS
Healthy adults may not need nutrient supplements as long as they are on healthy diet. However,
elderly people may benefit from prudent use of individualized assessed supplementation. It is
important to note that nutritional supplements should add to, not replace food and older people
should be properly guided as to their choice of supplements.
THE GOAL OF NUTRITION INTERVENTION

1. Ensure optimum nutritional status through a well-balanced diet that offers a wide variety
of food choices and moderation in fat.
2. Improve their functional abilities to maximize their opportunities to live independently or
to perform self-are.
3. The overall goal is to add quality of life to these elderly people, helping them to cope
with the pain and chronic diseases that may accompany aging.
Optimum nutritional status helps prevent or delay biological aging and the effect of existing
chronic diseases.
CHALLENGES IN MEETING NUTRITIONAL NEEDS IN THE ELDERLY

Nutritional requirements are influenced by;
1. Biological changes of aging that affect organ function and body composition.
2. Physical disability.
3. Poverty.
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4. Chronic illness.
5. Inadequate food intake due to oral problem, difficulty in swallowing and lack or poor
teeth.
6. Psychological problem such as isolation, boredom and apathy.
7. Effect of multiple medications.
CAUSES OF UNWANTED WEIGHT-LOSS IN ELDERLY PEOPLE

1. Poverty- lack of resources to obtain food.
2. Chronic diseases; this influences energy need and food intake.
3. Congestive heart failure and pulmonary disease can elevate energy requirement and lead
to continuing weight loss.
4. Certain drugs like digoxin can lead to cardiac cachexia related to both increased energy
need and low food intake.
5. Loss of taste is a common side effect of many prescribed drugs.
6. Changes in the hypothalamus by the aging process also decrease appetite and food intake.
7. Fear of obesity and its consequences may reduce food intake.
8. Loss of interest in life and depression reduces eating in some older adults.
9. Increased use or abuse of alcohol reduces food intake.
10. Physical disability affects the purchase of food and may lead to inadequate food intake.
11. Poor secretion of saliva may result to swallowing difficulty and may reduce food intake.
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DIABETES MELLITUS
ONCOLOGY
BY
DTN DR. NNADI I.M
68
DIABETES MELLITUS
Introduction
According to Lam (2002) diabetes mellitus is a metabolic disorder characterized by a
congenital (juvenile-onset or Type I diabetes mellitus) or acquired (adult-onset or Type ll
diabetes mellitus) inability to transport sugar from the bloodstream into cells. Once sugar is
inside the cells, that glucose is used to generate the energy for normal cellular function. The
disease results when glucose transport channels on cell membranes are insensitive to the effects
of insulin or when there are too few channels or when the quantity of insulin produced by the
pancreas is inadequate to activate the number of glucose channels needed to maintain normal
cellular metabolism. A diabetic therefore, has elevated glucose in the bloodstream where most of
it cannot be absorbed and utilized, causing inadequate glucose within the cells for energy. As a
result, cells attempt to derive energy from alternative metabolic pathways, such as fat breakdown
(Lam, 2002).
Diabetes mellitus may present with characteristic symptoms such as thirst, polyuria,
blurring of vision and weight loss. In its severe forms, ketoacidosis or a non-ketotic
hyperosmolar state may develop and lead to coma and in absence of effective treatment, death.
Often symptoms are not severe, or may be absent, and consequently hyperglycaemia sufficient to
cause pathological and functional changes may be present for a long time before diagnosis is
made (WHO, 1999).
Types of Diabetes mellitus
Diabetes mellitus is classified into four main classes.
 Type 1 diabetes mellitus (T1DM) also called insulin dependent diabetes mellitus
(IDDM) or juvenile onset diabetes mellitus is usually due to autoimmune destruction of
the pancreatic beta cells which produce insulin. Type 1 diabetes tends to occur in young,
lean individuals, usually before 30 years of age. Approximately 10% of the patients with
diabetes mellitus have T1DM. Onset is marked by polyuria, polydypsia and weight loss.
Persons with T1DM do not synthesize insulin and are susceptible to life threatening
ketoacidosis. The patient relies on insulin medication for survival. Dietary and other
lifestyle adjustments are part of management (Tinker, 1994).
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 Type II diabetes mellitus also referred to as non-insulin dependent diabetes mellitus
(NIDDM) or obesity related diabetes or adult onset diabetes mellitus (AODM) is a
heterogeneous, multifactorial, polygenic disease characterized by insulin resistance in
target tissues, due to some impairment in beta cells function, which results in
hyperglycaemia and is commonly accompanied by other cardiovascular risk factors
(Hayden, 2002). Type II diabetes mellitus is a metabolic disorder that is primarily
characterized by insulin resistance and hyperglycaemia. It is rapidly increasing in the
developing world (Lam, 2002).
 Other specific types of diabetes due to other causes, e.g., genetic defects in β-cell
function, genetic defects in insulin action, diseases of the exocrine pancreas (such as
cystic fibrosis), and drug- or chemical-induced diabetes (such as in the treatment of AIDS
or after organ transplantation).
 Gestational diabetes mellitus (GDM). Diabetes that comes with pregnancy and faces
out after pregnancy.
Complications of Diabetes Mellitus

Diabetes is defined by blood glucose levels, much of the attention in diabetes care
focuses on the management of hyperglycaemia. The effects of hyperglycaemia include long-term
damage, dysfunction and failure of various organs. Serious long-term complications include
cardiovascular disease, chronic renal failure, retinal damage (leading to blindness), nerve damage
and microvascular damage, which may cause erectile dysfunction and poor healing. In order to
reduce these complications, aggressive treatment is recommended, such as medication and
medical nutrition therapy. Pre-meal blood glucose should be kept as close to 90 to 130mg/dL
(midpoint: 110mg/dL) as possible giving clinical situation and a postprandial blood glucose level
less than 180mg/dL (American Diabetes Association, 2006).
The Nutrition Care Process and Model (NCPM)
The NCPM is a systematic problem-solving method that food and nutrition
professionals use to think critically and make decisions that address practice-related problems.
The NCPM contains four distinct but interrelated and connected steps: nutrition assessment,
nutrition diagnosis, nutrition intervention, and nutrition monitoring and evaluation. The NCPM is
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designed to incorporate a scientific base that moves food and nutrition professionals beyond
experience-based practice to evidence based practice (Bueche, 2008).
DIABETES NUTRITION ASSESSMENT

Data sources/tools for assessment
Where to obtain nutrition assessment data depends on the practice setting. For
individuals, data can come from screening and referral form, patient/client interview, observation
and measurements, medical or health records and consultation with caregivers including family
members. For population groups, data from community-based surveys and focus groups,
statistical reports, administrative data sets, and epidemiological or research studies are used.
Types of data collected:
1. Food- and nutrition-related history: a. Food and nutrient intake, b. food and nutrient
administration, c. medication/herbal supplement use, d. knowledge/beliefs, e. food and
supplies availability.
2. Anthropometric measurements: Height, weight, body mass index (BMI) and weight
history.
3. Biochemical data, medical tests, and procedures: Lab data (e.g., electrolytes, glucose) and
tests (e.g., gastric emptying time, resting metabolic rate)
4. Nutrition-focused physical examination findings: Physical appearance, muscle and fat
wasting, swallow function, appetite and effect.
5. Client history. Personal history, medical/health/family history, treatments and
complementary/alternative medicine use and social history.
Diabetes Nutrition Diagnosis

This new model calls for dietetics professionals to incorporate a new step—making a
nutrition diagnosis—which involves working with defined terminology. It also asks dietetics
professionals to chart their diagnosis in the form of a statement that establishes the patient’s
Problem (diagnostic label), Etiology (cause/contributing risk factors), and Signs and Symptoms
(defining characteristics). Nutrition diagnosis includes: inadequate oral/beverage intake,
inadequate energy intake, inadequate intake from enteral/parenteral nutrition, excessive intake
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from enteral/parenteral nutrition, altered gastrointestinal function, inadequate protein/energy
intake, altered nutrition related laboratory value and swallowing difficulty. (Mathieu, 2005).
Diabetes Nutrition Intervention

Energy intake and diabetes: Energy intake should be balanced with energy consumption.
Recommended energy allowance for adult female is 2200Kcal/day and that for adult males is
2500Kcals/day.
Carbohydrate and Diabetes
Carbohydrate intake and available insulin are the primary determinants of postprandial glucose
levels. Managing carbohydrate intake is, therefore, a primary strategy for achieving glycemic
control (Franz et al, 2010). Day-to-day consistency in distribution of carbohydrate intake
resulted in improved glycemic control (Boden et al, 2005). Simple sugars should be substituted
with complex carbohydrates.
Sucrose and diabetes mellitus
Research consistently reported that the total amount of carbohydrate consumed at meals,
regardless of whether the source is sucrose or starch, is the primary determinant of postprandial
glucose levels. There is no effect of sucrose intake on glycemic control compared to a lower
sucrose intake when total carbohydrate is similar (Nadeau et al, 2001).
Non-Nutritive Sweeteners (NNS) and diabetes mellitus
Five NNS (sometimes called artificial sweeteners) are approved by the US Food and Drug
Administration (FDA): aspartame, saccharin, acesulfame K, neotame, and sucralose. They are
regulated as food additives and, therefore, must be approved as safe before being marketed. The
FDA also sets a sweetener Acceptable Daily Intake (ADI)—the level a person can safely
consume on average every day over a lifetime without risk (Position of the American Dietetic
Association, 2004). In December 2008, the FDA stated that the stevia-derived sweetener
rebaudioside A is generally recognized as safe as a food additive (Franz et al, 2010).
Fiber intake and diabetes mellitus
Dietary fiber describes the nondigestible carbohydrates and lignin that are intrinsic and intact in
plants, whereas functional fiber consists of the isolated nondigestible carbohydrates that have
beneficial physiological effects in human beings. Total fiber would then be the sum of dietary
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fiber and functional fiber. Dietary fiber was divided into soluble and insoluble fiber in an attempt
to assign physiologic effects to chemical types of fiber. Oat bran, barley bran, and psyllium,
legumes, mostly soluble fiber, have health claims for their ability to lower blood lipid levels.
Wheat bran and other more insoluble fibers are typically linked to laxation (Slavin, 2008).
Dietary fiber includes plant nonstarch polysaccharides (eg, cellulose, pectin, gums,
hemicellulose, β-glucans, and fiber contained in oat and wheat bran), plant carbohydrates that are
not recovered by alcohol precipitation (eg, inulin, oligosaccharides, and fructans), lignin, and
some resistant starch. Potential functional fibers include isolated, nondigestible plant (eg,
resistant starch, pectin, and gums), animal (eg, chitin and chitosan), or commercially produced
carbohydrates (eg, resistant starch, polydextrose, inulin, and indigestible dextrins) (Institute of
Medicine, Food and Nutrition Board, 2002).
Based on the current data, diets providing 30 to 50 g fiber per day from whole food sources
consistently produce lower serum glucose levels compared to a low-fiber diet. Fiber supplements
providing doses of 10 to 29 g/day may have some benefit in terms of glycemic control. A fiber-
rich meal is processed more slowly and nutrient absorption occurs over a greater time period.
Further, a diet of foods providing adequate fiber is usually less energy dense and larger in
volume than a low-fiber diet that may limit spontaneous intake of energy. This larger mass of
food takes longer to eat and its presence in the stomach may bring a feeling of satiety sooner,
although this feeling of fullness is short term. A diet of a wide variety of fiber-containing foods
also is usually richer in micronutrients (Jenkins et al, 2002).
When viscous fibers are added to a diet, theoretically, the rate of glucose appearance in the blood
is slowed and insulin secretion is subsequently reduced. Considerable experimental evidence
demonstrates that the addition of viscous dietary fibers slow gastric emptying rates, digestion,
and the absorption of glucose to benefit immediate postprandial glucose metabolism and long-
term glucose control in individuals with diabetes mellitus. Glucagon-like peptide 1 reduced
gastric emptying rates, promoted glucose uptake and disposal in peripheral tissues, enhanced
insulin-dependent glucose disposal, inhibited glucagon secretion, and reduced hepatic glucose
output in animals and human beings. These multiple effects of glucagon-like peptide 1 may
reduce the amount of insulin required by individuals with impaired glucose metabolism when
consuming a high-fiber diet (Cummings and Overhuin, 2007).
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Some soluble fibers increase the viscosity of the contents of the stomach and digestive tract.
Higher molecular weight fibers increase viscosity. This altered viscosity may be responsible for
effects on body weight and attenuated glucose and insulin response because nutrients become
trapped and emptying from the stomach is delayed. Few studies have been published on the
effectiveness of isolated β-glucans and glucose and insulin control (Kim et al, 2006). Poppitt and
colleagues (2007) found that a high dose, barley β-glucan supplement improved glucose control
when added to a high-carbohydrate starch food, but not when added to a high-carbohydrate
beverage. Compared to control, 5 g β-glucans from oats significantly lowered postprandial
concentrations of glucose and insulin, while barley β-glucan did not. Barley β-glucan reduced
plasma glucose and insulin responses in male subjects (Ostman et al, 2006).
Two studies compared high-fiber (40 to 60 g) to low-fiber (10 to 20 g) diets with similar
macronutrient percentages of energy. One study showed no significant differences between diets
on HbA1c; one study showed a 2% reduction in HbA1c only in participants compliant with the
50-g fiber diet. Two studies found 24-hour glycemic profiles lower on the higher fiber compared
to lower-fiber diets (Chandalia et al, 2003).
Protein Intake and diabetes mellitus
In persons with diabetes with normal renal function, usual protein intake of approximately 15%
to 20% of daily energy intake does not need to be changed. Although protein intake has an acute
effect on insulin secretion, usual protein intake in longer-term studies has minimal effects on
glucose, lipid levels, and insulin concentrations. Exceptions for change in protein intake are in
persons who consume excessive protein choices high in saturated fatty acids, in those who have a
protein intake less than the Recommended Dietary Allowance, or in patients with diabetic
nephropathy.
Cardiovascular disease and diabetes mellitus
Persons with diabetes are at a three- to fourfold increased risk for CVD, which is particularly
evident in younger age groups and in women. Persons with diabetes have the equivalent CVD
risk as persons with pre-existing CVD and no diabetes. Thus, it is essential that diabetes MNT
interventions address this risk. Primary goals of MNT for persons with CVD are to limit
saturated and trans-fatty acids and cholesterol intake. Beneficial effects of fiber,
phytostanols/phytosterols, n-3 fatty acids, a Mediterranean diet, and other plant-based food
approaches are reported (Buse et al, 2007).
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Weight management and diabetes mellitus
In individuals with diabetes and insulin resistance, weight loss generally improves glycemic
outcomes and contributes to beneficial effects on blood pressure and blood lipids. However, as
the disease progresses and insulin deficiency as compared to insulin resistance becomes more
prominent, weight loss is less likely to be effective in improving glycemic outcomes. With
insulin deficiency, additional anti-diabetes medications combined with MNT are necessary and
prevention of weight gain becomes important.
Physical activity and diabetes mellitus
Studies in persons with diabetes have reported improvements in blood glucose control, reduced
cardiovascular risk, assistance with weight management, and improved well-being from regular
physical activity. Improvements in glycemia are reported to be independent of weight loss (Sigal
et al, 2004).
Diabetes Nutrition Monitoring and Evaluation
Nutrition monitoring and evaluation identifies patient outcomes relevant to the nutrition
diagnosis and intervention plans and goals. The purpose is to determine the amount of progress
made and whether goals/expected outcomes are being met. The change in specific nutrition care
indicators between assessment and reassessment can be measured and compared to the patient’s
previous status, nutrition intervention goals or reference standards and evaluate the overall
impact of the nutrition intervention on patient’s health outcomes. The aim is promote more
uniformity in assessing the effectiveness of nutrition intervention. The use of standardized
indicators and criteria increases the validity and reliability in how outcome data are collected.
Outcomes used in nutrition monitoring and evaluation are organized in four categories.
1. Food- and nutrition-related history: a. Food and nutrient intake, b. food and nutrient
administration, c. medication/herbal supplement use, d. knowledge/beliefs, e. food and
supplies availability.
2. Anthropometric measurements: Height, weight, body mass index (BMI) and weight
history.
3. Biochemical data, medical tests, and procedures: Lab data (e.g., electrolytes, glucose) and
tests (e.g., gastric emptying time, resting metabolic rate)
4. Nutrition-focused physical examination findings: Physical appearance, muscle and fat
wasting, swallow function, appetite and effect.
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American Diabetes Association 2004. Diagnosis and classification of Diabetes Mellitus.
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Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. 2005. Effect of a low-carbohydrate diet
on appetite, blood glucose levels, and insulin resistance in obese patients with type 2
diabetes. Ann Intern Med. 2005; 142:403–411.
Bueche, J; Charney, P., Pavlinac,J., Skipper, A., Elizabeth Thompson, E., Myers, E., .2008.
Nutrition Care Process and Model Part I: The 2008 Update. Journal of the American
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Buse J.B, Ginsberg H.N, Barkis G.L, Clark N.G, Costa F, Eckel R, Fonseca V, Gerstein H.C,
Grundy S, Nesto R.W, Pignone M.P, Plutzky J, Porte D, Redberg R, Stitzel K.F, Stone
N.J. 2007. Primary prevention of cardiovascular disease in people with diabetes mellitus:
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Association. Diabetes Care. 30:162-172.
Chandalia M, Garg A, Lutjohann D, von Bergmann K, Grundy S.M, Brinkley L.J. 2000.
Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N
Engl J Med. 342:1392-1398.
Cummings D.E, Overhuin J. 2007. Gastrointestinal regulation of food intake. J Clin Invest.
117:13–23.
Franz M.J.,Powers M.A., Leontos C., Holzmeister L.A., Kulkami K., Monk A. Wedel N.,
Gradwell E. 2010. The Evidence for Medical Nutrition Therapy for Type 1 and Type 2
Diabetes in Adults. Journal of American Dietetic Association.110; 12:1852-1889.
Hayden, M.R., 2002. Islet amyloid, metabolic syndrome and the natural progressive history of
type 2 diabetes mellitus (http://www.joplonk.net/)jop o. pancreas (online) 3; 5:86-108.
Institute of Medicine, Food and Nutrition Board. 2002. Dietary Reference Intakes: Energy,
Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids.
Washington, DC: National Academies Press.
Jenkins D.J, Kendall C.W, Augustin L.S, Vuksan V. 2002. High-complex carbohydrate or
lente carbohydrate foods?. Am J Med. 113(suppl 9B):30S–37S
Kim S.Y, Song H.J, Lee Y.Y, Cho K, Roh Y.K. 2006. Biomedical issues of dietary fiber β-
glucan. J Korean Med Sci. 21:781–789.
Lam, M. 2002. Diabetes. Dr. Lam.com. An Insiders Guide to Natural
Medicine.www.lamMD.com.
Mathieu J., Foust M., Ouellette P. 2005. Implementing Nutrition Diagnosis, Step Two in the
Nutrition Care Process and Model: Challenges and Lessons Learned in Two Health Care
Facilities. Journal of American Dietetic Association.7:15; 1636.
Nadeau J, Koski K.G, Strychar I, Yale J.F. 2001. Teaching subjects with type 2 diabetes how to
incorporate sugar choices into their daily meal plan promotes dietary compliance and
does not deteriorated metabolic profile. Diabetes Care. 24:222-227.
Ostman E, Rossi E, Larsson H, Brighenti F, Bjorck I. 2006. Glucose and insulin responses in
healthy men to barley bread with different levels of (1-3; 1-4)-β-glucans; predictions
using fluidity measurements of in vitro enzyme digests. J Cereal Sci. 43:230–235.
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Poppitt S.D, van Drunen J.D, McGill A.T, Mulvey T.B, Leahy F.E. 2007. Supplementation of a
high-carbohydrate breakfast with barley β-glucan improves postprandial glycaemic
response for meals but not beverages. Asia Pac J Clin Nutr. 16:16–24.
Sigal R.J, Kenny G.P, Boulé N.G, Wells G.A, Prud’homme D, Fortier M, Reid R.D, Tulloch H,
Coyle D, Phillips P, Jennings A, Jaffey J. 2007. Effects of aerobic training, resistance
training, or both on glycemic control in type 2 diabetes. A randomized trial. Ann
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Slavin, J. L. 2008. Position of the American Dietetic Association: Health Implications of Dietary
Fiber. Journal of the American Dietetic Association.108:10; 1716-1731.
Tinker, I.F. 1994. Diabetes mellitus. A priority health care issue for Women. Journal of the
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ONCOLOGY
Introduction
Oncology is a branch of medicine that deals with the prevention, diagnosis, and treatment
of cancer. A medical professional who practices oncology is an oncologist. The name's
etymological origin is the Greek word ὄγκος (ónkos), meaning "tumor", "volume" or "mass" and
the word λόγος (logos), meaning "speech" (McCutcheon, 2001). Cancer is a term used to
describe a group of more than 100 multifactorial diseases in which abnormal cells reproduce in
an uncontrolled manner and are able to spread to other parts of the body and invade healthy
tissues. One defining feature of cancer is the rapid creation of abnormal cells that grow beyond
their usual boundaries, and which can then invade adjoining parts of the body and spread to other
organs, the latter process is referred to as metastasizing. Metastases are a major cause of death
from cancer. Cancer is the second leading cause of death globally, and was responsible for 8.8
million deaths in 2015. Globally, nearly 1 in 6 deaths is due to cancer. Approximately 14 million
new cases of cancer were recorded in 2012. The total annual economic cost of cancer in 2010
was estimated at approximately US$ 1.16 trillion. Approximately 70% of deaths from cancer
occur in low- and middle-income countries. Advanced age is a risk factor for many cancers. The
median age of cancer diagnosis is 66 years. Around one third of deaths from cancer are due to
the 5 leading behavioral and dietary risks: high body mass index, low fruit and vegetable intake,
lack of physical activity, tobacco use, and alcohol use (Stewart et al, 2014).
Causes of cancer
Cancer arises from the transformation of normal cells into tumour cells in a multistage
process that generally progresses from a pre-cancerous lesion to a malignant tumour. These
changes are the result of the interaction between a person's genetic factors and 3 categories of
external agents, including:
 physical carcinogens, such as ultraviolet and ionizing radiation;

 chemical carcinogens, such as asbestos, components of tobacco smoke, aflatoxin (a food
contaminant), and arsenic (a drinking water contaminant); and
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 biological carcinogens, such as infections from certain viruses, bacteria, or parasites.
Types of Cancer
There are more than 100 types of cancer. Types of cancer are usually named for the
organs or tissues where the cancers form. For example, lung cancer starts in cells of the lung, and
brain cancer starts in cells of the brain. Cancers also may be described by the type of cell that
formed them, such as an epithelial cell or a squamous cell.
Here are some categories of cancers that begin in specific types of cells:
Carcinoma
Carcinomas are the most common type of cancer. They are formed by epithelial
cells, which are the cells that cover the inside and outside surfaces of the body. There are many
types of epithelial cells, which often have a column-like shape when viewed under a microscope.
Carcinomas that begin in different epithelial cell types have specific names:
Adenocarcinoma is a cancer that forms in epithelial cells that produce fluids or mucus. Tissues
with this type of epithelial cell are sometimes called glandular tissues. Most cancers of the breast,
colon, and prostate are adenocarcinomas.
Basal cell carcinoma is a cancer that begins in the lower or basal (base) layer of the epidermis,
which is a person’s outer layer of skin.
Squamous cell carcinoma is a cancer that forms in squamous cells, which are epithelial cells that
lie just beneath the outer surface of the skin. Squamous cells also line many other organs,
including the stomach, intestines, lungs, bladder, and kidneys. Squamous cells look flat, like fish
scales, when viewed under a microscope. Squamous cell carcinomas are sometimes called
epidermoid carcinomas.
Transitional cell carcinoma is a cancer that forms in a type of epithelial tissue called transitional
epithelium, or urothelium. This tissue, which is made up of many layers of epithelial cells that can
get bigger and smaller, is found in the linings of the bladder, ureters, and part of the kidneys
(renal pelvis), and a few other organs. Some cancers of the bladder, ureters, and kidneys are
transitional cell carcinomas.
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Sarcoma
Sarcomas are cancers that form in bone and soft tissues, including muscle, fat, blood vessels,
lymph vessels, and fibrous tissue (such as tendons and ligaments). Osteosarcoma is the most
common cancer of bone. The most common types of soft tissue sarcoma are leiomyosarcoma,
Kaposi sarcoma, malignant fibrous histiocytoma, liposarcoma, and dermatofibrosarcoma
protuberans.
Leukemia
Cancers that begin in the blood-forming tissue of the bone marrow are called leukemias.
These cancers do not form solid tumors. Instead, large numbers of abnormal white blood cells
(leukemia cells and leukemic blast cells) build up in the blood and bone marrow, crowding out
normal blood cells. The low level of normal blood cells can make it harder for the body to get
oxygen to its tissues, control bleeding, or fight infections.
Lymphoma
Lymphoma is cancer that begins in lymphocytes (T cells or B cells). These are disease-
fighting white blood cells that are part of the immune system. In lymphoma, abnormal
lymphocytes build up in lymph nodes and lymph vessels, as well as in other organs of the body.
There are two main types of lymphoma:
Hodgkin lymphoma – People with this disease have abnormal lymphocytes that are called
Reed-Sternberg cells. These cells usually form from B cells.
Non-Hodgkin lymphoma – This is a large group of cancers that start in lymphocytes. The
cancers can grow quickly or slowly and can form from B cells or T cells.
Multiple Myeloma
Multiple myeloma is cancer that begins in plasma cells, another type of immune cell. The
abnormal plasma cells, called myeloma cells, build up in the bone marrow and form tumors in
bones all through the body. Multiple myeloma is also called plasma cell myeloma and Kahler
disease.
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Melanoma
Melanoma is cancer that begins in cells that become melanocytes, which are specialized
cells that make melanin (the pigment that gives skin its color). Most melanomas form on the
skin, but melanomas can also form in other pigmented tissues, such as the eye.
Brain and Spinal Cord Tumors

There are different types of brain and spinal cord tumors. These tumors are named based
on the type of cell in which they formed and where the tumor first formed in the central nervous
system. For example, an astrocytic tumor begins in star-shaped brain cells called astrocytes,
which help keep nerve cells healthy. Brain tumors can be benign (not cancer) or malignant
(cancer).
Other Types of Tumors
Germ Cell Tumors

Germ cell tumors are a type of tumor that begins in the cells that give rise to sperm or
eggs. These tumors can occur almost anywhere in the body and can be either benign or
malignant.
Neuroendocrine Tumors
Neuroendocrine tumors form from cells that release hormones into the blood in response
to a signal from the nervous system. These tumors, which may make higher-than-normal
amounts of hormones, can cause many different symptoms. Neuroendocrine tumors may be
benign or malignant.
Carcinoid Tumors
Carcinoid tumors are a type of neuroendocrine tumor. They are slow-growing tumors that
are usually found in the gastrointestinal system (most often in the rectum and small intestine).
Carcinoid tumors may spread to the liver or other sites in the body, and they may secrete
substances such as serotonin or prostaglandins, causing carcinoid syndrome (National Cancer
Institute, 2017).
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Cancer Prevention
Nutrition guidelines for cancer prevention are similar to those for preventing other
diseases including heart disease and diabetes. The general diet guidelines for the prevention of
cancer risk include:
 Keep a healthy weight. Obese individuals have an increased risk of cancers of the
breast, colon, rectum, endometrium, oesophagus, kidney, pancreas, and gallbladder.
Obesity can negatively affect inflammation in the body, the immune system, the way in
which cells grow and levels of certain hormones. Weight in the belly is most closely
connected with an increased risk of colorectal cancer and cancers of the pancreas and
uterus and breast in postmenopausal women. Other cancers associated with obesity
include: esophageal, rectal, kidney, thyroid, gallbladder, liver, ovarian and prostate. Limit
foods with added sugars and fats that provide a lot of calories but few nutrients.
 Eat vegetables, fruits, whole grains and legumes. Fill half the plate with fruits and
vegetables and make at least half the grains whole grains. Eating plenty of fruits and
vegetables, including beans, is linked with a lower risk of lung, oral, esophageal, stomach
and colon cancer. Also, eating a diet rich in these plant-based foods can help you stay at a
healthy weight.
 Limit Calorie-Dense, Nutrient-Deficient Foods. Reduce intake of foods with added

sugars and solid fats that provide a lot of calories but few nutrients. These foods include:
sugar-sweetened beverages, processed snack foods and desserts. Calories add up fast with
these sorts of calorie-dense foods, which can lead to weight gain and leaves little room
for more healthful, cancer-preventive foods.
 Limit meat portions. Choose a variety of protein foods, including seafood, poultry, lean
meat, legumes, eggs and nuts. There is a link between colon cancer and eating large
amounts of meat especially processed meat such as ham, bacon and hot dogs. Protein
should be enjoyed in moderation and to include lean protein foods. Plant based source of
protein such as beans should be consumed more often and the rest of the plate filled with
whole grains and vegetables.
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 Limit alcohol. Alcohol can increase risk of cancer of the mouth, throat, oesophagus,
larynx, liver and breast. The risk of cancer is much higher for those who drink alcohol
and also use tobacco. If consumed at all, limit alcoholic drinks to no more than one drink
daily for women and two for men. A standard drink contains about 14grams alcohol. This
roughly corresponds to a 350ml glass of beer, 150ml glass of 12% wine and 44ml glass
of spirit.
 Consume less salt (sodium). In cultures where people eat a lot of salt preserved, salt-
cured and salt-pickled food, the risk for stomach, nasopharyngeal and throat cancer may
be higher. Individuals should reduce their sodium intake to less than 2300milligrams of
sodium a day (about a teaspoon of salt). Adults with hypertension or prehypertension
should further reduce their sodium intake to 1500milligrams a day. Read food labels to
learn exactly how much sodium is in a product.
 Avoid Tobacco. Tobacco is the leading cause of cancer and of death from cancer.
Smoking is associated with increased risk of cancers of lung, larynx, mouth, oesophagus,
throat, bladder, kidney, liver, stomach, pancreas, colon, rectum, cervix and acute myeloid
leukemia. Smokeless tobacco (snuff or chewing tobacco) is associated with increased
risks of cancers of the mouth, oesophagus, and pancreas.
 Exercise. Men who had prostate cancer and exercised vigorously had a 61 percent lower
risk of dying from the disease. Vigorous exercise was defined as more than three hours
per week (Kohn, 2016).
References
Kohn, J. 2016. 7 Cancer Prevention Tips for Your Diet.
http://www.eatright.org/resource/health/diseases-and-conditions/cancer/diet-and-cancer-
prevention.
McCutcheon, M. 2001. Where Have My Eyebrows Gone? Cengage Learning.
ISBN 0766839346.P5
National Cancer Institute. 2017. What is cancer?
https://www.cancer.gov/about-cancer/understanding/what-is-cancer
83
Stewart BW, Wild CP, editors 2014. World cancer report. Lyon: International Agency for
Research on Cancer; 2014
PROTEIN ENERGY
MALNUTRITION
HYDRATION FOR CHILDREN
PAEDIATRIC WEIGHT
MANAGEMENT
BY
DTN. ONWUKA-KALU NKEIRU
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PROTEIN ENERGY MALNUTRITION
OUTLINE
 INTRODUCTION
 DEFINITION
 EPIDEMIOLOGY
 RISK FACTORS
 CLASSIFICATION
 CLINICAL FEATURES
 MANAGEMENT
 PREVENTION
INTRODUCTION
 Protein Energy Malnutrition (PEM) is a serious often lethal disease that is common in
poor countries. It is a major contributor of death in children aged under 5.
 It is in this backdrop that MDG 1 is anchored on i.e. eradicate poverty and extreme
hunger.
 In 2010, it is estimated that 650,000 deaths of children under 5 is directly or indirectly
caused by PEM.
DEFINITION
 Protein Energy Malnutrition is a spectrum of disease that includes kwashiorkor,
marasmus and marasmic-kwashiorkor.
 Marasmus: inadequate intake of protein and calorie.
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 Kwashiorkor: inadequate protein intake with reasonable calorie intake. While Marasmus
represents an adaptive response to starvation, kwashiorkor is a maladaptive response.
EPIDEMIOLOGY
 PEM is more common in tropical countries (Northern Nigeria) and Asian countries.
 It occurs in poor families found in these regions especially children age under 5 (male
children).
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RISK FACTORS
 Inadequate diet
 Disease the above two can result from
 Household food insecurity
 Poverty
 Unequal access to resources
 Gender discrimination
 Conflicts
CLASSIFICATION OF PEM
There are different classification systems;
 Gomez
 Welcome
 Modified welcome
 WHO
MODIFIED WELCOME
Generally, clinical features include symptoms and signs.
SYMPTOMS INCLUDE;
 Weight loss
 Skin rash
 Diarrhea
 Poor food intake
 Lethargy
 Generalized body swelling
 Inadequate nutritional history as regards FADU.
 Poor parent income
SIGNS
 Central Nervous System: Apathy, irritability, wisened old man face, moon face
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 Musculoskeletal System: severe wasting, generalized edema, hanging skin fold
 HAIR: brittle and sparse, thin, and flag sign
 MOUTH: angular stomatitis, cheilosis
 SKIN: flaky paint dermatosis, wrinkled skin
 Dehydration
 Anemia
 Hypothermia
 Enlarged liver
However, while the above features (signs and symptoms) of PEM are common to both
kwashiorkor and marasmus. There are features constant in each.
CONSTANT FEATURES OF MARASMUS

 Edema is absent
 The following are present
 Poor growth muscle wasting
 Has intact appetite unlike kwashiorkor with poor appetite
DIFFERENCES BETWEEN KWASHIORKOR AND MARASMUS

 Signs and symptoms of severe PEM MARASMUS.
 Occurs in infants (under 1year old).
 Low weight for age (<60% of standard weight).
 Nearly always infant looks like wisened old man or has a monkey face.
 There is no edema and there may be no change in the hair colour.
 There may be associated signs of specific vitamin and mineral deficiencies.
 A child with marasmus is usually hungry.
 Biochemical changes are less severe than kwashiorkor.
KWASHIORKOR
 This occurs most in children aged 1-3years.
 There is always edema, mainly on the feet and lower legs and the child appears moon
faced.
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 Child may look fat because of edema.
 The hair often turns red, brown or grey pluck able and curly hair grows straight.
 Skin may be pale and usually, child is anemic.
 They have no appetite and have difficult to feed.
MANAGEMENT OF PEM
Successful management of the severely malnourished child requires that both medical and social
problems be recognized and corrected and if the illness is viewed as being only a medical
disorder the child is likely to relapse when he or she returns home and other children in that
family will remain at risk of developing the same problem
 The mother must be helped to improve the child’s diet by;
 Increasing the concentration of energy and protein in the child’s meals
 Feeding more frequently
 Increasing the variety of foods offered
 Monitoring of the child’s height and weight
There is a time for the management of child with severe malnutrition. This involves three phases;
 Initial treatment
 Rehabilitation
 Follow up
Initial treatment:
 Here the problem is identified and treated in the hospital or residential care facility
 Specific deficiencies are corrected, metabolic abnormalities are reserved and feeding is
begun
Rehabilitation
 Intensive feeding is given to recover most of the lost weight, emotional and physical
stimulation are increased, the mother or care giver is trained to continue care at home and
then prepared are made for discharge
Follow up
 After discharge, the child and his/her family are followed up to be assured of the
continual physical, mental and emotional development of the child.
PREVENTION AND TREATMENT
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 Keep a growth chart in the home
 Promote breastfeeding aggressively (bottle feeding using powdered milk, over diluted
with sometimes polluted water and given in unsanitary bottles should be discouraged)
 Immunize infants and children
 Nutrition education of mothers on adequate nutrition of infants and children
 Improvement of the locally available food supplies and income
REFERENCES
Ghai et al.,(2010). Essential Paediatrics, 7th ed. Pg62
Nkangineme et al.,(2007). Textbook of Paediatrics, 3rd ed.
Yinka et al.,(2011). Rule of Thumb, pg 20
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HYDRATION FOR CHILDREN
Infant and young children have a higher proportion of body water than adults. They are also less
heat tolerant and may be more likely to get dehydrated, especially when being physically active
and in hot climates. They have a higher water requirements in relation to their body weights than
adults. Encouraging children to drink fluids regularly is very important as children may not
remember to have a drink by themselves.
Teachers, parent/guardians and care providers need to make sure that there are drinks available
for children regularly through the day and that children are encouraged to drink plenty of fluids.
Kids don’t always recognize the early stages of thirst which can make them particularly
vulnerable to becoming dehydrated, especially during time that can drive up their body fluid
losses, for example when they are playing sports or during warm weather. Dehydration, even if
only mild can cause tiredness, headaches, lack of concentration, reduced mental performance and
dry skin.
HOW MUCH DO CHILDREN NEED?
The amount of fluids a child needs depends on many factors. These include: Age, weather,
physical activity and gender. Generally, they should aim to drink about 6-8 glasses of fluid per
day (on top of the water provided by foods in their diets---for kids aged 4-13). Younger children
need relatively smaller drinks (e.g 120-150ml serving) and older children need larger drinks (e.g
250-300ml serving).
APPROPRIATE DRINK FOR CHILDREN
When choosing drinks for children, it is important to be aware although the all provide water,
and some also contain essential vitamins and minerals, they may also provide sugars and
therefore energy (calorie/kilojoules). Energy in drinks contributes to our daily energy intake in
the same way as food. Eating too much energy from fluids over time could cause weight gain.
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Gender Age Group Amount of fluid Amount of fluid
from drinks and from drinks
food(Litres/day) only(Litres/day)
Boys and Girls 4-8 yrs 1.6 (4-6 glasses) 1.1-1.3
Girls 9-13 yrs 1.9 (6-8 glasses) 1.3-1.5
Boys 9-13 Yrs 2.1 1.5-1.7
In addition, drinking sugar-sweetened drinks too often can potentially lead to tooth decay,
especially if consumed frequently between meals, or if teeth are not brushed regularly with
fluoride toothpaste. Dental guideline recommends consuming sugar-containing food and drinks
on no more than four occasions per day. It is also important to be aware that some drinks are
acidic (e.g fruit juice, squash and some carbonated drinks) and that this may cause dental erosion
(damage to tooth enamel) if they are drunk often. Some drinks such as tea, coffee and some soft
drinks may also contain caffeine which is a mild stimulant. Too much caffeine can make children
irritable and keep them awake at night if consumed in the evening. So it is advisable not to give
children caffeine-containing drinks at this time.
Water
Water hydrates without providing extra energy (calories/kilojoules) or risking harm to the teeth;
and so a healthy choice.
Milk
Milk is a useful source of nutrients such as B-vitamins and calcium. Most children should drink
reduced fat milks. Fruit and vegetable juices and smoothies, sugar-free drinks, tea and coffee,
sugary drinks, sports and energy drinks.
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PAEDIATRIC WEIGHT MANAGEMENT
Overweight--------10-20% above ideal body weight.
Obesity-------------20% or more above ideal body weight.
The most cause is excess calorie intake over energy expenditure with resultant storage of fat. It is
common in childhood and there is often a family pattern of overweight. Disabilities which
restrict physical activity and some hormonal disorders lead to obesity in few children.
Health education and dietary guidelines for health professionals and parents/caregivers plus a
greater awareness of overweight and obesity and its effect on child health can help to reduce its
incidence.
Overweight and obesity in infancy
An overfed baby will develop extra fat cells which then continuously demand to be filled. The
effects of this may include:
 Delayed motor development(rolling, crawling, walking, climbing, running)

 Mechanical disorders of hips, legs and feet.
 Greater risk of accidents.
 Recurrent chest infections.
 Chafing and soreness where skin surfaces rub together.
 Breathlessness.
 Greater expectations by adults because baby looks older.
Possible Causes are:
 Over concentrated bottle feeds, encouraging baby to finish up bottle when he/she is
clearly satisfied.
 Addition of sugar and /or cereal to bottle feed.
 Early introduction of weaning foods.
 Insisting baby eats everything up.
 Too many snacks.
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 Lack of opportunity and encouragement for physical activity----long periods of time
spent in lot, pram, bouncing chart or play pen.
Prevention and management
The aim is to slow down the rate of weight gain or temporarily halt it. A slow weight loss may be
desirable in the older baby (9-12 months) if there is marked obesity, but remember that babies
need a nutritious diet at all times.
Practical measures include:
 Encouraging mothers to breast feed.

 Making up bottle feeds correctly- no added sugar or solids.
 Avoidance of early weaning (not before 4 months).
 Allowing the baby’s appetite to dictate how much food is eaten—encourage finger food
and self-feeding.
 Providing opportunity and encouragement for physical activity.
 Avoid offering sugary foods drinks.
Overweight and Obesity in Childhood
The effects may include:
 Appearance----the child looks fat, plump abdomen, thighs and upper arms.
 Above ideal weight and height measurements—a child may be taller than expected due
to increased protein intake.
 Difficulty with gross motor skills—PE, games and sports.
 Social /school isolation
 Difficulty in buying and choosing clothes.
Possible Causes are:
 A pattern of eating large meals.

 Snacking and grazing on high calorie foods.
 Lack of physical exercise.
 Economical and psychological factors.
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Prevention And Management
 Prevention of diet adequate in all nutrients. Reduction of calorie intake, especially fatty
and empty calorie foods.
 Adequate opportunity for indoor and outdoor physical activity for all age groups.
 Encourage independence in skills such as feeding, dressing and undressing.
 Monitor time spent watching TV and playing computer games.
 Growth should be measured and recorded at regular intervals.
 Rewards for progress may be given, for example a special outing or a new item of
clothing.
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HYGIENE
CHRONIC RENAL FAILURE
BY
OKWY-NWEKE
96
HYGIENE
Hygiene is the practice of measures designed to promote and preserve health. Hygiene cannot
fully be discussed without involving food and handlers.
PERSONAL HYGIENE:
This refers to the state of a person’s body and clothing. Food handler play an important role in
food safety and in the transmission of food poisoning because they may introduce pathogens into
the food during production, processing, distribution and even preservation.
Having a good understanding of food safety procedures and potential factors that causes food
borne illness is very important to all handlers.
A food handler should adopt the following practices:
 Report to work in good health, clean and properly dressed.
 Change into a clean appropriate uniform and apron; Change it when it’s soiled during
working hours. Clean uniform includes hairnet / cap, apron, flat sandals and hand towels.
 Washing hands properly, frequently and at the appropriate time which involves : before
commencing food preparation; before and after touching raw foods; before touching
cooked food; after visiting the toilet, sneezing into your hands, blocking a cough,
scratching & rubbing of hair, nose, ears and touching of refuse bin or even sweeping.
 Keeping the fingers nail properly trimmed without polish on or artificial nails. NO
BITTING OF NAILS.
 No long sleeve shirt or blouse; no jewelry except a plain wedding ring while handling the
food.
 Treat and bandage all wounds and sores immediately. When hands are bandaged single
glove should be use.
 Food handlers should never taste food directly from the cooking spoon or ladle. Taste the
food in a correct manner: use a tea/table spoon; put small quantity into a plate to taste;
step away from the exposed food ; don’t reuse the plate / spoon again wash off as you
wait for another tasting time.
 Do not handle food with hands unless when absolutely necessary. Use tongue, spoons,
forks, scoops or other implement that can easily be washed.
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 Do not use same implement, container or surface for raw and cooked food under any
circumstances.
Report any that is sick to the appropriate authorities and ensure that anyone suffering from
communicable diseases (cough & cather, septic wounds, diarrhea) should not prepare or dish out
or even serve foods.
KITCHEN HYGIENE:
Kitchen hygiene comprises of cleanliness of the cooking area, kitchen utensils, tables, cookers,
walls & ceiling, doors & windows, gutters etc. the aim of cleaning these items of course is to
ensure that all sources of infection are removed/reduced; that there can been no transfer of
bacteria to our food. Dirty utensils beside from poisoning the food, it also makes the food
unappealing especially to the patients we serve.
The ideal thing is that all utensils should be washed with soap, sponge and water before and after
use. They should not be left with dirty water or food particles that will attract flies and rodent.
Table surface should be washed thoroughly before and after use then dried with clean cloth.
Cookers should be cleaned after each meal when still warm to be able to remove the stains.
Windows and doors should be cleaned or dusted daily and the kitchen must be cobweb regularly;
scrub the floor regularly especially after preparing each meal.
The cooking utensils should be orderly kept in a shelf.
Improper food storage may be hazardous to health. The raw food and cooked food should be
kept in fluid unit.
All the kitchen hygiene must be observed in every unit of the medical food administration.
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CHRONIC KIDNEY DISEASE
Chronic kidney disease (CKD) is typically a progressive disease which is characterized by the
inability of the kidney function to return to normal after acute kidney failure or progressive renal
decline from a disease.
CKD causes permanent reduction in functioning which finally leads to end stage renal disease
(ESRD).
Signs and symptoms of Chronic Kidney Disease:
 Weakness; Decreased/ loss of Appetite;
 Nausea/ vomiting; Noctouria;
 Polyuria; blood in the urine or dark coloured urine; foamy or bubbly urine;
 Edema; Hypertension;
 Pale skin, unintentional weight loss etc.
Some underlying causes of Chronic Kidney Disease:
Chronic kidney disease can be caused by the following:
 History of myocardial infraction
 Evidence of autoimmune disease
 Frequent urinary track infection
 History of hepatitis
 Long standing hypertension
 Glomerunephritis in early childhood
 Previous Acute kidney injuring episode
 Previous urologic intervention
 Frequent use of NSAIDs or pain killers
 Along term exposure to nephrotoxic antibiotics
 CKD diagnosis among first degree relatives etc.
Early stages of CKD can be detected through the following:
 Laboratory measurement of albumin creatinine ratio,
 Glomenular filtration ratio (GFR),
 Imaging which includes Ultra sound, Computerized tomography (CT) scan & Magnetic
resonance imaging (MRI)
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ESTIMATING OR MEASURING GLOMERULAR FILTRATION RATIO (eGFR) IN
CKD
Glomerular Filtration Ratio (GFR) is usually accepted as the best index of kidney function;
persistently decreased GFR (L60ml/mm/1.73m2) is a hallmark for CKD, even in the absence of
any marker for kidney damage. GFR usually correlates well with the prognosis & complication
of CKD like anemia, mineral bone disorder & cardiovascular diseases. GFR should be
determined for confirming diagnosis, staging the disease, estimating the prognosis and making
decision about treatment in all CKD Patients.
GFR level may also be used to decide appropriate timing to start renal replacement therapies.
GFR should be monitored in CKD patient according to the stages and severity of the CKD.
There is however no consensus on the monitoring frequency and GFR in various stages.
This measured GFR is considered the gold standard but is not practical for daily clinical use due
to complexity of the measurement procedure.
Formular for measuring GFR=
Stages of Chronic Kidney Disease.

Stages EGFR Description
1 90-130ml/min Kidney damage but normal to increase
2 60-89ml/min Mild decrease in kidney function
3 30-59ml/min Moderately decrease in kidney function
4 15-29ml/min Severe decrease in kidney function
5 Less than 15ml/min Kidney failure with treatment necessary, which can be defined
as end stage renal disease.
EGFR estimated Glomerular filtration rate.
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Medical Nutrition Therapy (MNT)
The purpose of diet therapy for Chronic Kidney Disease is to maintain good nutritional status,
slow progression and to treat complications.
MNT.
- A different nutritional therapy will be proposed for each level of CKD.
- The primary objectives of MNT is to manage the symptoms associated with the syndrome
(edema, hypoalbuniemia, hyperlipidemia) decrease the risk of progression to renal failure
and maintain nutritional stores.
- Patients are primarily treated with statins to correct hyperlipidemia, low sodium diet (Ls) and
diuretics Appeal 2006.
Medical Nutrition Therapy

Nutrition Assessment Data:
 Dietary recall (Dietary Ass)
 Intake/ output records (BA)
 flow chart (BA)
 Check lab results (if available) (Biochem Ass)
 Weight /BMI etc (Anthrop. Ass)
 Signs / Symptoms (Clinical Ass)
Nutrition Diagnosis
Some of the more common nutrition diagnosis in the CKD population includes:
 Inadequate mineral intake
 Excessive mineral intake
 Imbalance of nutrients
 Excessive fluid intake
 Impaired nutrient utilization
 Altered nutrition – related lab values
 Food medication interaction
 Food and nutrition – related knowledge deficit.
Depending on the nut diagnosis MNT intervention are adjusted.
101
Nutrition Intervention: Patients with progressive CKD should have individualized diet
Energy intake:
Recommend 23kcal -35kcal /k g /body wt. considering the weight status and goals, Age and
gender, level of physical activity, metabolic stressors. This will help prevent signs of
malnutrition and spare protein for tissue repairs.
Protein Intake:
- Adults with CKD without diabetes, not on dialysis, with EGFR below 50ml/men/1.73m 2
should be on a protein controlled diet providing 0.6g – 0.8g /kg/body wt/day.
- For an optimal protein use 50% - 60% of protein should be from sources of high
biological value (HBV).
- Patients with established severe protein deficiency, who continue to loose protein may
require a diet with sufficient protein and energy to maintain a positive nitrogen balance
and to produce an increase in plasma concentration and disappearance of edema.
- Sufficient carbohydrate and fat intake are needed to spare protein for anabolism.
Potassium Intake:
For adult with CKD who exhibit hyperkalaemia should be prescribe a potassium intake of less
than 2.4g. Adjustments on potassium intake can be done based on:
- Serum potassium
- Blood pressure
- Medications
- Kidney function
- Glycemic control,
- Acidosis
- Diarrhea
- Constipation
- Vomiting
Some fruits high in potassium include:
1. Avocado – 975mg
2. Banana – 422mg
3. Dates 1cup – 964mg
4. Guava – 688mg
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5. Water melon – 320mg
6. Pomegranate – 666mg
7. Passion fruit – 821mg
Phosphorus intake:
Recommended level (3 – 5) a low – phosphorus diet providing 800mg – 1000mg / day or 10mg -
12mg phosphorus /gram of protein. CKD patients have a predisposition for mineral and bone
disorders. Phosphorus control is the cornerstone for treat and prevention of secondary
hyperparathyroidism renal bone disease and soft tissue calcification.
Dietary fiber:
Adults with early CKD should consume diet rich in dietary fiber that is associated with reduction
of inflammation and mortality in patients.
Education patients on self management behaviors
1. Engaging in appropriate physical exercises or activities
2. Avoid smoking to reduce progression of CKD
3. Reduce alcohol intake
4. Reduce carbonated beverage intake e.g. cola
5. Fluid should be taken in moderation.
Nutrition Monitoring / Evaluation
- Food and nutrient intake (diet History, diet experience, intake of micro / macro nutrient
quantity consumed).
- Medication: Use of herbal or botanical supplement, dietary supplements (prescribed or not
prescribe
- Knowledge, beliefs or attitudes readiness to change nutrition and lifestyle behaviours
- Factors affecting access to food.
REFERENCES
B. Srilakshmi. (2011). Dietetics 6th ed.
Maria Chan and David Johnson. (2012). Modification of lifestyle and nutrition interventions for
management of early chronic kidney diseases. Kidney health Australia.
103
FOOD PROCESSING
ENERGY EXPENDITURE
ENERGY CONSERVATION
BY
DIETITIAN AFIEROHO MERCY C.
104
FOOD PROCESSING
Processing is a procedure in which food is prepared for consumption, It means processing raw
ingredients to edible product. Food processing means primarily from raw materials to finished
product.
There are several purposes to food processing. This can include processing ingredients which are
not safe to eat raw, flavouring foods to make them more interesting and making dishes which
comply with cultural and religious norms surrounding food, in addition to addressing issues such
as allergies.
Food processing is also usually intended to make food and include activities such as food
fortification.
FERMENTATION
Fermentation usually implies that the action of microorganisms is desirable. Fermentation of

foods serves several functions:
- Enrichment of the diet by improving palatability and acceptability through development

of a diversity of flavours, aroma’s and textures in food substrates.
- Preservation of substiantial amounts of food through lactic acid, alcohol, acetic acid, and
alcohol fermentation.
- Enrichment of food substrate biologically with protein, essential amino acids, essential
fatty acids and vitamins.
- Detoxification during food fermentation, removal of antinutrient, natural toxicant and
microtoxins.
- A decrease in cooking time and fuel requirements.
IMPORTANCE OF FOOD FERMENTATION
Fermented foods contribute to about one third of the diet worldwide, causes changes in food
quality including texture, flavor, appearance, nutrition and safety.
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PROCESSING OF FOODS
Processing of cereal products like corn, wheat usually begin with soaking the grain to soften it
and make the bran easier to remove. Soaking decreases the length of time the meal will last
before it goes bad. The process involved in cereals processing (Agidi, Pap) include: Cleaning,
soaking, dehulling and grinding.
Processing of Legumes
Soyabean are part of the legume family, very high in protein and contains essential acids like
phytic acid and alpha linolenic acid. The word soy comes from the Japanese word
shoyu.Soyabean is known by various names including: soya, soybean and glycine max.
NUTRIENT COMPOSITION
Soyabean consists of 40% protein, 35% carbohydrate, 5% ash, 20% oil which contains omega -
3- fatty acid which is good for the heart. Soyabean also contains excellent amount of dietary
fiber, vitamins and mineral
ANTINUTRITIONAL FACTORS
Soyabean contains some potent antinutritional factors that inhibit the absorption of protein and
some nutrients present in soyabean and there are components in it that is toxic to the body and
also inhibits the utilization of some nutrients present in the body as well. These components are
Protease inhibitors and lectins. Protease exert their nutritional effect by causing pancreatic
hypertrophy/hyperplasia which ultimately results in an inhibition of growth. Lectin by virtue of
its ability to bind to glycoprotein receptors on the epithelial cells linning the intestinal mucosa
inhibits growth by interfering with the absorption of nutrients.Antinutritional effects is also
caused by some relatively heat stable factors such as goitrogens, phytoestrogens and tannins
(Wijeratne W.B.,1999)
PROCESSING OF SOYABEAN
Due to the presence of all these antinutritional factors in soyabean, soyabean it’s being subject to
intense heat treatment and fermentation to greatly reduce the antinutritional effects. Soyabean
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like other legumes has a fair proportion of unavailable starch which can be removed by various
processing and cooking methods. These processes also remove the natural toxin to make them
digestible and palatable for young children. It must be soaked, skinned, well cooked and then
finely mashed or ground to smooth paste or flour after drying. Soyabean flour and other
soyabean products (drinks, isomil) could be useful foods for children like (Lucas E.W.,2000)
ENERGY EXPENDITURE
Energy expenditure is the amount of energy (or calories) that a person needs to carry out a
physical function such as breathing, circulating blood, digesting food, or physical movement.
Your total daily energy expenditure (TDEE) is the total number of calories you burn each day.
Total daily energy expenditure can vary from person to person depending on body size, gender,
body composition and activity level. Energy is expended for one’s basal metabolism, ability to
participate in physical activities, and even to consume food (Whitney & Rolfs, 2013).
BASAL METABOLIC RATE
The basal metabolic rate (BMR) is the rate at which the body expends energy for activities that
support the body. The process involved include maintaining a heartbeat, respiration, kidneys
filtering wastes (Whitney & Rolfs, 2013),ion transport, maintaining the normal turnover of
enzymes, temperature and other functions. BMR accounts for 60-80% of one’s daily energy
expenditure small deficits or excess in BMR can add up to a large number of calories over
time.BMR accounts for about 1kcal/kg body weight per hour for an adult male and 0.9Kcal/kg
body weight per hour for an adult female.
FACTORS THAT DETERMINE BMR
AGE: BMR is highest in people who are growing such as children and pregnant women
(Whitney & Rolfs, 2013). One’s BMR peaks in the infancy stage and declines rapidly through
one’s childhood and adolescent years. With increasing age, one’s BMR starts to fall slowly. This
decline is largely due to the loss of muscle. The loss of muscle is not inevitable and is often
caused by absolute or relative inactivity. Weight-bearing exercises can help prevent some muscle
loss among the elderly (Baggott, 2008).
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BODY COMPOSITION: Lean body mass is a major determinant of one’s BMR. Women tend
to have more body fat and less lean muscle mass compared to men; thus, women tend to have a
lower BMR than those of comparable men.
BODY TEMPERATURE: Additionally, BMR is high in those who have a fever, are under
stress, or have highly active thyroid glands.
EXERCISE: One-way to increase one’s BMR is to participate in endurance and strength-training

activities regularly in order to maximize lean body mass (Whitney & Rolfs, 2013).
NUTRITIONAL STATE: Along the same note, from a nutritional standpoint, decreased caloric
requirements can lead to decreased food intake, and a lower calorie intake can lead to a
deficiency of essential nutrients (Baggott, 2008).
Other factors that determine BMR include the amount of body surface (the greater the area, the
greater the heat loss), gender (Male average higher energy use because of greater lean body
mass), caffeine and tobacco use (increase metabolic rate).
Basal metabolic rate is very important in everyday life, and maintaining a healthy lifestyle is
important to keeping one’s basal metabolic rate in an ideal range.
Energy expenditure from physical activity
Physical activity is the most variable component of energy expenditure since it is dictated by
intentional lifestyle choices involving skeletal muscle action and the body systems that support
these actions. Ranging from 5-40% of daily energy expenditure, this percentage will remain in
the lower end of the spectrum for those with sedentary jobs who incorporate little physical
activity and at the higher end of the spectrum for those who have physically strenuous jobs and
use their leisure time to exercise (Powers, Scott K.; Howley, Edward T.; 2015)). This increases
energy expenditure beyond BMR by as much as 25% to 40%. Climbing stairs rather than riding
the elevator, walking rather than driving, standing in buses rather than sitting increases physical
activity and hence energy use. Estimating the amount of energy expended during physical
activity relies on two categories:
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1. Body composition (specifically muscle mass and body weight)
2. The nature of the activity (Whitney, Ellie; Rolfes, Sharon Rady; 2016). body fat is more
equally distributed in those who are consistently active (Rising R et al., 1994). Other body
systems, including the nervous system, cardiovascular system, endocrine system, and pulmonary
system, are all highly involved in regulating and supporting skeletal muscle activity, inhalation
of oxygen and exhalation of carbon dioxide, also deliver oxygen and nutrients to skeletal muscle
cells (Schoeller, Dale A., 2009).
THERMIC EFFECT OF FOOD
This is the energy the body uses to digest, absorb and further process the macronutrients you eat
through absorption, transportation, storage and your metabolism. This used to be known as the
Specific Dynamic Action. Everything you eat will give you calories that are burned through
digestion and increase your metabolism. This process happens about 2 hours after you eat a
meal. This type of energy expenditure accounts for about 10% of the total calories you ingest
(Whitney, E., & Rolfes, S., 2013). The amount varies, however, with:
1. The different types of macronutrients.
Carbohydrates have a thermic effect of food of 5-30%.
Proteins have a thermic effect of food of 30%.
Fats have a thermic effect of food of 0-5% (Whitney, E., & Rolfes, S., 2013).
The TEF for CHO rich or protein rich meal is higher than a fat rich meal. It takes less energy to
transfer absorbed fat into adipose stores than to convert glucose into glycogen or metabolise
amino acids into fat.
2. This amount can also vary with how much food you eat at once (eating large loads of food
versus eating smaller),
3. More frequent meals have an effect on thermic effect of food.
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4. Meals with more calories have a higher thermic effect of food than smaller meals
ADAPTIVE THERMOGENESIS
Adaptive thermogenesis is the change in basal metabolic rate of the body to compensate for the
adjustment of energy expenditure based on changes in the environment, such as diet
(Overfeeding), trauma, stress, and extreme weather.
To determine caloric requirements to maintain current weight (TDEE), follow step 1. and then
step 2. to calculate your TDEE.
1. Calculate BMR (Basal Metabolic Rate)
Women BMR = 655 + (9.6 X weight in kg) + (1.8 x height in cm) – (4.7 x age in yrs)
Men BMR = 66 + (13.7 X weight in kg) + (5 x height in cm) – (6.8 x age in yrs)
Note: Multiply the number in brackets first, then you can add and subtract.
For example:
1. Female
2. Age: 27 years
3. Height: 178 cm (5’10’’)
4. Weight: 69kg (151lbs.)
Therefore,
BMR = 665 + (9.6 X 69) + (1.8 x 178) – (4.7 x 27)
= 1520.9 calories/ day
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2. Calculate Total Daily Energy Expenditure (TDEE)
TDEE = BMR x Activity Factor
Determine your activity factor from the table below and multiply this number by the BMR you
just calculated above, to determine your TDEE.
Activity Factor Table
Amount of
Description TDEE/ Maintenance
Exercise/Activity
Sedentary Little or no Exercise/ desk job TDEE = 1.2 x BMR
Light exercise/ sports 1 – 3 days/ TDEE = 1.375 x

Lightly active
week BMR
Moderate Exercise, sports 3 – 5 days/ TDEE = 1.55 x

Moderately active
week BMR
Heavy Exercise/ sports 6 – 7 days/ TDEE = 1.725 x

Very active
week BMR
Very heavy exercise/ physical job/

Extremely active TDEE = 1.9 x BMR
training 2 x/ day
Therefore,
TDEE = BMR x Activity Factor
TDEE = 1520.9 x 1.375
= 2091
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This 27 year old woman needs 2091 calories per day to maintain her current weight.
ENERGY CONSERVATION
Reduction in the amount of energy consumed in a process or system, or by an organization or
society, through economy, elimination of waste, and rational use.
Individuals and organizations that are direct consumers of energy may want to conserve energy
in order to reduce energy costs and promote economic, political and environmental
sustainability. Industrial and commercial users may want to increase efficiency and thus
maximize profit.
Sources of energy
1. Solar
2. Water like hydroelectricity (dams like kanji,)
3. Fossil fuel, crude oil and its derived products like kerosene, petrol or gasoline
4. Wind (windmill rotates to turn turbines to generate electricity)
ENERGY USAGE: .
The energy usage is categorized in four broad sectors: transportation, residential, commercial,
and industrial
Energy usage in the transportation and residential sectors is largely controlled by individual
domestic consumers. Commercial and industrial energy usage are controlled by businesses.
Transportation sector
The transportation sector includes all vehicles used for personal or freight transportation. Of the
energy used in this sector, approximately 65% is consumed by gasoline-powered vehicles,
primarily personally owned. Diesel-powered transport (trains, merchant ships, heavy trucks, etc.)
consumes about 20%, and air traffic consumes most of the remaining 15%.
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Residential sector
The residential sector refers to all private residences, including single-family homes, apartments,
manufactured homes and dormitories. Energy use in this sector varies significantly across the
country, due to regional climate differences and different regulation. example
space conditioning, 44%(heating and cooling)
 water heating, 13%

 lighting, 12%
 refrigeration, 8%
 home electronics, 6%
 laundry appliances, 5%
 kitchen appliances, 4%
 other uses, 8%
Energy usage in some homes may vary widely from these averages.
Commercial sector
The commercial sector consists of retail stores, offices (business and government), restaurants,
schools and other workplaces. Energy in this sector has the same basic end uses as the residential
sector, in slightly different proportions. Space conditioning is again the single biggest
consumption area, but it represents only about 30% of the energy use of commercial buildings.
Lighting, at 25%, plays a much larger role than it does in the residential sector . Lighting is also
generally the most wasteful component of commercial use.
Industrial sector
The industrial sector represents all production and processing of goods, including manufacturing,
construction, farming, water management and mining.
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Ways of conserving energy
1. Taxes
Some countries employ energy or carbon taxes to motivate energy users to reduce their
consumption.
2. Building Design
One of the primary ways to improve energy conservation in buildings is to use an energy audit.
An energy audit is an inspection and analysis of energy use and flows for energy conservation in
a building, process or system to reduce the amount of energy input into the system without
negatively affecting the output(s).
3. Transportation
Zoning reforms that allow greater urban density as well as designs for walking and bicycling can
greatly reduce energy consumed for transportation. The use of telecommuting by major
corporations is a significant opportunity to conserve energy.
4. Consumer products
LED lamps use at least 75% less energy, and last 25 times longer, than traditional incandescent
light bulbs.
Consumers are often poorly informed of the savings of energy efficient products. A prominent
example of this is the energy savings that can be made by replacing incandescent light bulbs with
more modern alternatives.
Energy conservation in Nigeria

Conserve Energy, Save Money. The initiative is designed to sensitize everyone by connecting
with and influencing their behavior through do-it-yourself tips .
In addition, the members of the public were encouraged to calculate their current household
energy consumption and discover ways to save money. Example:
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Why would someone be using an appliance that takes say 400w/h when an alternative appliance
can take just 80w/h and yet deliver the same service
10 bulbs(60w) costs #4.00 per kw/h of electricity
10 bulbs for 8 hours / day in a home will consume
Daily: 10 (60w bulbs)x 8hrs =4800w
Monthly : 10(60w bulbs)x 8hrs x 30days =144000w
Yearly : 10 (60w bulbs) x8 x 30days x 12 months=1728000w
If 1kw of electricity cost #4.00/hr; then in 1 year, this household would have spent :
#4.00 x 1728kw =# 6912.00.
If the same household decide to replace the 10 bulbs with energy saving bulbs rated at 10w; This
household would have spent #1152 and saved #6912 – #1152 =#5760 per year
Assuming we have 1 million House holds connected to Electricity distribution company (EDC)
using 60w bulbs
EDC will have to generate 1728000000kw
Nigeria would have spent 1728000000kw x 4.00 =# 6912000000.00
But for 10w bulbs, EDC will generate 288000000kw
Nigeria would have spent 288000000 x# 4.00 =# 1152000000.00 to conserve energy.Energy is

conserved spending 11 billion a year to 69 billion for the same Household.
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HEALTH AND SAFETY
PRACTICES IN THE HOSPITAL
HYPERTENSION
MICROWAVE OVEN AND SAFETY
BY
DTN. OKWARA C.C.
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HEALTH AND SAFETY PRACTICES IN THE HOSPITAL
WHAT IS SAFETY
1. Safety is the condition of being protected against physical, social spiritual financial,
political, emotion, occupational, psychological, education or other types or consequences
of failure, damage, error, accident, harm or any other event which could be considered
non desirable.
2. Safety can also be defined to be the control of recognized hazard to achieve an accepted
level of risk.
3. Safety means keeping oneself or others free from harm or danger.
HEALTH AND SAFETY PRACTICES FOR HEALTH CARE PERSONNEL & WASTE
WORKERS.
An evaluation of health workers safety at Bugardo medical centre (BMC) was made by BMC
health workers safety initiative in collaboration with Medicare through a base line survey done in
July and August 2009. This survey indentifies key guidelines needed to project hospital workers
in different areas of the hospital. This guideline respond to those need by providing key
information to use for training reference for health workers on best medical safety practices in
hospital settings.
CONTENT:
The hospital guide contains necessary information to be used in high lighting workers safety and
advising out what should be done to create a safety working environment.
The guideline covered the following areas:
1. Infection prevention and control in the context of health workers safety
2. Management of occupational exposures to HIV & recommendation.
3. Health care waste management
4. The use of chemicals in a hospital fire
5. Electrical safely and first aid
6. Safely for health workers in laboratory and radiology
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OVERALL OBJECTIVE:
To provide guidance to health workers in protecting against occupation hazards and exposure to
pathogens in the hospital setting.
SPECIFIC OBJECTIVES:
1. To assist health workers in protecting against occupation hazards and exposure to blood
and body fluids.
2. To reduce injuries and illness due to needle sticks and exposure to blood and body fluids
3. To strengthen knowing of disposal system for sharp and other infectious waste
4. To increase awareness about personal and hospital hygiene, infection control and good
health for hospital staff.
5. To increase the knowledge and skills of hospital staff on electrical and fire safety
6. To increase the safety of workers working in laboratory and radiology
MODES OF TRANSMISSION
1. Contract (direct & indirect): touching a person or contaminated surface, sexual

contact. Examples of illnesses that can be contacted through this mode include
haemorrhagic fever virus like Ebola, Laser fever; enteric pathogen.
2. Drop let: infected droplets come into contact with eyes, nose or mouth. Examples of
illnesses include Influenza and Rubella viruses, corynebacterium diphtheria.
3. Air born: residue from infected droplets or contaminated dust particles remains in air for
long periods of time and enter the body through the respiratory tract. Examples of
illnesses here includes TB (Kocks disease), chicken pox , and measles.
4. Fecal oral route: Organisms infect the digestive system through contaminated food or
water. Examples of illnesses here are: salmonellosis, cholera, typhoid fever, Hepatitis A.
5. Vector: Animals capable of transmitting disease are rats, mosquito’s fleas. Examples of
illnesses spread by these vectors include malaria, yellow fever, and dengue fever.
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PERSONAL PROTECTIVE EQUIPMENT
Specific for personal protective equipment Specification
Gloves Embossed grip for a secure Skin resistance grip.
Neoprene shell is tough and flexible.
Common liner resists punctures, cuts and abrasion.
Boots Molded ply vinyl or other plastic to ensure that it is water proof.
Anti skid tread prevents slipping.
Resistant to sharps puncture.
Aprons Longer length extends to overlap with the boots.
Cotton ties and neck loop for each on/off.
Moisture proof and chemical resistant.
Reusable, non sterile.
Eye protection 100% polycarbonate materials resists impact vented side shields
allow air to flow through durable and cleanable design.
Mask Property fit and comfortable.
Mask with cartridge (for incinerator operator) or ordinary mask.
MEANING AND CAUSES OF WORKSHOP ACCIDENTS

Accidents are defined as events occurring by chance, which result in injury to people or damage
to property.
Causes of accidents in the workshop can be grouped into two major headings:
1. Unsafe actions
2. Unsafe condition
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Unsafe actions:
Many accidents happen because people are careless in the workshop. When people attempt to do
the wrong thing or when laid -down procedures are not followed, accidents often happen.
Examples of unsafe actions include
1. Entering the workshop in disorderly manner
2. Failure to use safety devices
3. Failure to follow laid down procedures for handling tools, machines, and other facilities
4. Failure to obey workshop rules and regulations.
Unsafe conditions:
When a tool or equipment is faulty, or the working environment constitutes a danger to the users,
an unsafe condition exists.
Examples of unsafe conditions are:
1. Slippery or wet floors
2. The absence of safety devices
3. Non maintenance of tools, equipment and other facilities
4. Working in the workshop when one is sick or fatigued.
HOW TO PREVENT ACCIDENTS IN A WORKSHOP

Accidents in the workshop can be prevented. This can be achieved when people obey simple
rules and regulations in workshops. It is therefore important to note that:
1. You are responsible for your own safety.
2. You are also responsible for the safety of other people and equipment in the
workshop.
DRESSING SAFELY FOR WORK

People should observe the following dressing safety rules
1. Dress correctly for workshop practice
2. Do not wear watches, bracelets, rings or long- sleeve shirts. They can cause very serious
injuries to the arm if caught in the machine.
3. Long- sleeve shirts must be rolled above the elbows if they are to be worn in a workshop
4. If hair is long, tie or cover it up before walking into a workshop
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5. Wear special shoes for foot protection.
6. Wear gloves for hand protection
Basic Kitchen Safety

Kitchen safety includes (among other things):
 Electrical and grease fires
 Scalding (to burn or affect painfully with or as if with hot liquid or steam)
 Food safety and preparation
 Cleanliness
 Handling hot items (water, hot pans, etc.)
 Electrical safety
 Handling small appliances safely
 Handling sharp objects safely
 Child proofing and well.
BASIC KITCHEN SAFETY TIPS

1. Make sure all wires, cords and plugs on your appliances are not frayed and that the plugs
have 3-prong grounded connections. This would include coffee makers, toasters, blenders,
microwaves, mixers, etc.
2. Don’t use extension cords. You can obtain a junction box that has built-in GFI (ground fault
interrupters). This will allow you extra plug in space and the GFI will kick in if there is a
power shortage. Helps avoid water/electrical shock accidents.
3. Get rid of any appliance that is broken or damaged. New ones are very inexpensive these
days. If a new one would bust your budget, try garage and tag sales (just make sure you’re not
buying somebody else’s broken appliance).
4. Put a childproof lock not only on the cabinets with your medicines and cleaning
supplies, but also your oven.
5. Don’t leave the kitchen with pots & pans cooking on the stove. Make sure to turn off
burners as soon as you take the pot off.
6. Avoid wearing inappropriate clothing while cooking. That means loose sleeves and sweaters.
7. Keep dish towels, pot holders and oven mitts away from the stove.
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8. Keep matches and lighters in high places where curious little hands can’t reach them.
9. If using candles in the kitchen, don’t leave the room (or home) while they’re burning. Make
sure they are in a safe place and are in flame proof containers.
10. Check furniture, curtains, dish towels, etc. to be sure they are not blocking heaters or vents.
11. Keep a fire extinguisher in or near the kitchen, but not near the stove or the heater.
12. In case of a grease fire, salt and/or baking soda will help if you do not have a fire
extinguisher.
13. Keep emergency numbers handy – 911 is easy to remember, but phone numbers to
Poison Control might take longer.
14. Scalding is one of the most common injuries in the kitchen. Make sure to turn pot handles
away from the front of the stove and away from little curious hands.
15. Scalding can occur from hot steam as well. Be careful when lifting lids from hot food
(including opening that hot bag of microwave popcorn)!
16. Handling Knives: (a) Always cut away from your body when using a knife. It can slip and cut
you, (b) Always use a cutting board, (c) Protect your counter tops, (d) Keep blades sharp, (e)
Keep knives clean (including handle) – slippery handles can cause injuries, (f) Don’t put
knives in a sink of soapy water – they may not be seen and accidents can occur, (g) Wash and
dry carefully keeping sharp edge away from your hands, (h) Always lay them flat, never on
the back or edge, (i) Don’t attempt to catch a knife as it falls – better it hits the floor than cut
your hand, (j) Wash knives with warm soapy water after each use.
17. Be sure appliances are unplugged before touching sharp edges (blenders, can openers, mixers,
etc.).
18. Never stick a fork in a toaster to retrieve trapped toast – you may get shocking results.
19. Always be sure the blender is unplugged before touching the blades.
20. Be careful about sharp edges: scissors, broken glass, potato peeler, etc.
21. Never ever, ever leave cooking foods unattended – not even for a minute.
22. Casualness causes casualties – don’t answer or talk on the phone while cooking – you can be
distracted and injuries can result.
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23. Clean up spills immediately – wet floors are slippery when wet.
24. Keep the kitchen floor clear of toys and other items.
25. Be certain that walking areas are always clear of toys and other items.
26. Keep young children out of the kitchen while cooking.
27. Always use a step-stool to reach high places.
28. Store cleaning supplies and all chemicals in a safe place
29. Use safety latches.
REFERENCES
Central Board of Health (2003). Zambia infection prevention guidelines. JHPIEGO.
Damani, N.N.(2003). Manual Of Infection Control Procedures: 2nd edition
Obioma, G and Nwagbara, C (2008). NERDC Basic Technology for Junior Secondary Schools.
Rubin, J.N (2004). Recurring Pitfalls in Hospital Preparedness and Response.
U.S.Department of Labor Occupational Safety & Health Administration. 2000.
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HYPERTENSION
WHAT IS HYPERTENSION?
Hypertension also referred as high blood pressure is a condition in which the arteries have
persistently elevated blood pressure.
Blood pressure is the force of blood pushing up against the blood vessel walls. The higher the
pressure, the harder the heart pumps. Blood pressure above 140/90mmHg is considered
hypertension.
Hypertension can lead to damaged organs, as well as several illnesses, such as renal failure,
aneurism, heart failure, stroke or heart attack.
Classification of hypertension:
a) Essential
b) Secondary
Essential hypertension is the term for high blood pressure with unknown cause. This accounts for
about 95% of cases. It is the most common chronic disease of industrialized societies,
particularly among the middle and old age group. It is the major contributor to the development
of cardiovascular disease, stroke and renal failure. The higher the systolic or diastolic pressure,
the greater the risk of coronary heart disease. Systolic blood leads to congestive heart failure and
stroke.
Secondary hypertension is the type of HBP with a known direct cause, such as Kidney diseases,
tumors or birth control pills.
RISK FACTORS ASSOCIATED WITH HIGH BLOOD PRESSURE

1) Smoking
Nicotine raises blood pressure by constricting the blood vessels. This occurs because the
oxygen in y blood decreases and because nicotine directly stimulates the production of a
hormone, epinephrine (also known as adrenaline), in the adrenal gland. Epinephrine
raises blood pressure by constricting blood vessels. After tobacco use raises blood
pressure, they are at risk of all the medical consequences of high blood pressure.
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2) Obesity or being over weightt
Researchers found out that obesity /over - weight children are much more likely to suffer
from hypertension during adulthood.
3) Diabetes
4) Sedentary life style
5) Lack of Physical activity
6) High level of salt intake (sodium sensitivity). According to American heart
Association, sodium consumption should be limited to 1500mg per day and that’s include
everybody; even healthy people without high blood pressure, diabetes, or cardiovascular
diseases.
7) Insufficient calcium, potassium and magnesium consumption.
8) High level of alcohol consumption.
9) Stress
10) Aging
11) Medicines such as birth control drugs.
12) Genetics and a family history of hypertension/heredity. Scientist in 2011 from the
university of Leicester England reported in the journal hypertension that some genes in
the kidneys may contribute to hypertension.
13) Chronic kidney disease.
14) Adrenal and thyroid problems or tumors. Statistic in the USA indicates that African
Americans have a higher incidence of hypertension than those other ethnicities.
15) Sex males have high BP than females.
16) Increased Low density lipoprotein Cholesterol.
17) Insulin resistance
18) Hyperlipidaemia
19) Race
MODIFIABLE RISK FACTORS

 Obesity
 Cigarette smoking
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 Alcohol
 Stress
SYMPTOMS OF HYPERTENSION
About 33% of people with hypertension do not know that they have high blood pressure and this
ignorance can last for years, for this reason, it is advisable to undergo periodic blood pressure
screenings even when no symptoms are present.
(a) Severe headache
(b) Fatigue or confusion
(c) Dizziness
(d) Nausea
(e) Problems with vision
(f) Chest pain
(g) Breathing problems
(h) Irregular heart beat
(i) Blood in urine.
Classification of blood pressure for adult age of 18 yrs or older

Category Systolic Bp (mmHg) Diastolic Bp (mmHg)
Optional <120 <80
Normal 120-129 80-84
High normal 130-139 85-89
Hypertension
Stage 1 140-179 70-99
Stage 2 160-179 100-109
Stage 3 180-209 110-119
Stage 4 > > 120
Source: Whelton PK. Epidemiology of hypertension. Lancet. 1994; 44:401-6
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MANAGEMENT OF HIGH BLOOD PRESSURE
Non Drug Treatment

1. Weight reduction – weight reduction in the obese lowers blood pressure.
2. Aerobic exercises like jogging, cycling, and swimming reduces HBP, increases High
Density Lipoprotein, and reduces obesity. Jogging reduces the diastolic pressure by about
15-20mmHg; this effect was independent of weight change.
3. Improve life style/modification:
i. Stop smoking
ii. Stop intake of alcohol
Dietetic Management
DASH Diet
i. Low Sodium Diets
2.3g = 100mmol = mild low sodium diet
1.2g = 50mmol = moderately low sodium diet
0.6g = 25mmol = restricted low sodium diet
ii. Increase Potassium Intake

Low serum potassium values in a patient with HBP points to an aldosterone –
Secretery suprarenal tumor (Conn’s syndrome).
Dietary potassium restriction decreases blood pressure in patients with hypertension.
If patient is on diuretics, supplements of fruit juices should be given.
iii Increase Vegetable Intake
REFERENCES
Anita, F.P and Abraham. P (2002). Clinical Dietetics and Nutrition.
Green, M.S., Jucha E., and Lz, Y. (1986). Blood pressure in smokers and non-smokers:
epidemiologic findings. Am Heart J; 111:932–940.
Whelton PK, Epidemiology of hypertension; 44: 401 -6.
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MICROWAVE OVEN AND SAFETY
A microwave oven (commonly referred to as a microwave) is a kitchen appliance that heats and

cooks food by exposing it to microwave radiation in the electromagnetic spectrum. This
induces polar molecules in the food to rotate and produce thermal energy in a process known
as dielectric heating (an electromagnetic heating effect). Microwave ovens heat foods quickly
and efficiently because excitation is fairly uniform in the outer 25–38 mm (1–1.5 inches) of
a homogeneous, high water content food item; food is more evenly heated throughout (except in
heterogeneous, dense objects) than generally occurs in other cooking techniques. Microwave
ovens are popular for reheating previously cooked foods and cooking a variety of foods. Unlike
conventional ovens, microwave ovens usually do not directly brown or caramelize food, since
they rarely attain the necessary temperatures to produce Millard reaction. Exceptions occur in
rare cases where the oven is used to heat frying-oil and other very oily items (such as bacon),
which attain far higher temperatures than that of boiling water. Microwave ovens have a limited
role in professional cooking, because the boiling-range temperatures produced in especially
hydrous foods impede flavors produced by the higher temperatures of frying, browning, or
baking. However, additional heat sources can be added to microwave ovens, or
into combination microwave ovens, to produce these other heating effects, and microwave
heating may cut the overall time needed to prepare such dishes. Some modern microwave ovens
are part of over-the-range units with built-in extractor hoods. A microwave oven heats food by
passing microwave radiation through it. Microwaves are a form of non-ionizing electromagnetic
radiation with a frequency higher than ordinary radio waves but lower than infrared light.
Microwave ovens use frequencies in one of the ISM (industrial, scientific, medical) bands, which
are reserved for this use, so they do not interfere with other vital radio services. Consumer ovens
usually use 2.45 gigahertz (GHz)—a wavelength of 12.2 centimeters (4.80 in)—while large
industrial/commercial ovens often use 915 megahertz (MHz)—32.8 centimeters
(12.9 in). Water, fat, and other substances in the food absorb energy from the microwaves in a
process called dielectric heating. Microwave heating is more efficient on liquid water than on
frozen water, where the movement of molecules is more restricted.
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Compared to liquid water, microwave heating is less efficient on fats and sugars (which have a
smaller molecular dipole moment). Sugars and triglycerides (fats and oils) absorb microwaves
due to the dipole moments of their hydroxyl groups or ester groups. However, due to the
lower specific heat capacity of fats and oils and their higher vaporization temperature, they often
attain much higher temperatures inside microwave ovens. This can induce temperatures in oil or
very fatty foods like bacon far above the boiling point of water, and high enough to induce some
browning reactions, much in the manner of conventional broiling ), braising, or deep fat frying.
Foods high in water content and with little oil rarely exceed the boiling temperature of water.
For cooking or reheating small amounts of food, the microwave oven may use less energy than a
cook stove. Although microwave ovens are touted as the most efficient appliance, the energy
savings are largely due to the reduced heat mass of the food's container. The amount of energy
used to heat food is generally small compared to total energy usage in typical residences in the
United States.
COMPONENTS OF A MICROVAVE OVEN
A microwave oven consists of:
 A high voltage power source, commonly a simple transformer or an electronic power

converter, which passes energy to the magnetron
 A high voltage capacitor connected to the magnetron, transformer and via a diode to the
chassis
 A cavity magnetron, which converts high-voltage electric energy to microwave radiation
 A magnetron control circuit (usually with a microcontroller)
 A short waveguide (to couple microwave power from the magnetron into the cooking
chamber)
 A metal cooking chamber
 A turntable or metal wave guide stirring fan.
 A digital / manual control panel
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Modern microwave ovens use either an analog dial-type timer or a digital control panel for
operation. Control panels feature an LED, liquid crystal or vacuum fluorescent display, numeric
buttons for entering the cook time, a power level selection feature and other possible functions
such as a defrost setting and pre-programmed settings for different food types, such as meat, fish,
poultry, vegetables, frozen vegetables, frozen dinners, and popcorn. In most ovens, the
magnetron is driven by a linear transformer which can only feasibly be switched completely on
or off. As such, the choice of power level does not affect the intensity of the microwave
radiation; instead, the magnetron is cycled on and off every few seconds, thus altering the large
scale duty cycle. Newer models have inverter power supplies that use pulse-width
modulation to provide effectively continuous heating at reduced power, so that foods are heated
more evenly at a given power level and can be heated more quickly without being damaged
by uneven heating
There are traits unique to microwave cooking that affect how evenly and safely food is cooked.
“Cold spots” can occur because of the irregular way the microwaves enter the oven and are
absorbed by the food. If food does not cook evenly, bacteria may survive and cause food borne
illness.
Defrosting Food
• Remove food from its store wrap before defrosting in the microwave oven. Foam trays and
plastic wraps are not heat stable at high temperatures. Melting or warping from hot food may
cause chemicals to leach into food.
• Cook meat and poultry immediately after microwave thawing. Some areas of frozen food may
begin to cook during the defrosting time. Holding partially cooked food is not recommended
because any bacteria present would not have been destroyed.
• Remember to take food out of the microwave Do not forget about a food item that has been
thawing in the microwave. Food should not be left out of refrigeration more than two hours.
Wraps & Bags: Wax paper, oven cooking bags, parchment paper and white microwave paper
towels are safe to use. Put microwave-safe plastic wrap loosely over food so that steam can
escape, and do not let it directly touch your food. The moist heat will help destroy harmful
bacteria. Never use brown paper or plastic grocery bags, newspapers, metals, aluminum foil, or
thin plastic storage bags in the microwave. They can get too hot and burn.
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Containers Not Intended for the Microwave Oven:
Margarine tubs, whipped topping bowls, cheese containers and others can wrap or melt from hot
food, possibly causing harmful chemicals to get in the food.
Reheating Foods
• Foods that were cooked and stored safely can be reheated to any temperature.
• Reheating foods that were not cooked to proper temperatures or not stored safely must be
thrown out. Reheating them will not make them safe to eat.
• Cover foods to hold in moisture and provide even heating. Covering food helps protect against
contamination, keeps moisture in, and allows food to cook evenly.
• Microwaving baby food and formula is not recommended because uneven heating can result in
scalding a baby’s mouth. If micro waved, stir food, shake bottles and test. What containers and
wraps are safe to use in the microwave oven?
Only use cookware that is specially manufactured for use in the microwave oven. Glass, ceramic
containers, and all plastics that are safe to use usually will be labeled for microwave oven use.
Utensils Safe to Use
If you are not sure if pottery or dinnerware is microwave safe, place the empty utensil in the
microwave alongside a cup of water in a glass measure. Microwave on high temperature for 1
minute. If the dish remains cool, it is safe to microwave. If the dish gets warm or hot to the
touch, do not use. Safe utensils for microwave cooking include glass and glass ceramic cookware
and those labeled for microwave use. Some current plastic containers and food wraps are
specifically designed to resist radiation from microwaves. Products may use the term
"microwave safe", may carry a microwave symbol (three lines of waves, one above the other) or
simply provide instructions for proper microwave use. Any of these is an indication that a
product is suitable for microwaving when used in accordance with the directions provided.
SAFE TO USE:
 Any utensil labeled for microwave use.

 Heatproof glass (such as Pyrex, Anchor Hocking, etc.).
 Glass-ceramic (such as Corning Ware).
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 Oven cooking bags.
 Baskets (straw and wood) for quick warm-ups of rolls or bread. Line the basket with napkins to
absorb moisture from food.
 Most paper plates, towels, napkins and bags. For optimal safety use white, unprinted materials.
 Wax paper, parchment paper, heavy plastic wrap. Do not allow plastic wrap to touch food; vent
it to allow a steam escape.
 Heat-susceptor packaging.
NOT SAFE TO USE:
 Cold storage containers: margarine tubs, cottage cheese and yogurt cartons, etc. These materials
are not approved for cooking and chemicals can migrate into food.
 Brown paper bags and newspapers.
 Metal pans.
 Foam-insulated cups, bowls, plates or trays.
 China with metallic paint or trim.
 Chinese "take-out" containers with metal handles.
 Metal "twist ties" on package wrapping.
 Food completely wrapped in aluminum foil.
 Food cooked in any container or packaging that has warped or melted during heating.
EFFECTS OF MICROWAVE ON FOODS AND NUTRIENTS
Comparative cooking method studies generally find that, if properly used, microwave cooking
does not affect the nutrient content of foods to a larger extent than conventional heating, and that
there is a tendency towards greater retention of many micronutrients with microwaving, probably
due to the reduced preparation time.[36] Microwaving human milk at high temperatures is
contraindicated, due to a marked decrease in activity of anti-infective factors.
Any form of cooking will destroy some nutrients in food, but the key variables are how much
water is used in the cooking, how long the food is cooked, and at what temperature. [38] Nutrients
are primarily lost by leaching into cooking water, which tends to make microwave cooking
healthier, given the shorter cooking times it requires. [39] Like other heating methods,
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microwaving converts vitamin B12 from an active to inactive form; the amount of inactivation
depends on the temperature reached, as well as the cooking time. Boiled food reaches a
maximum of 100 °C (212 °F) (the boiling point of water), whereas microwave food can get
locally hotter than this, leading to faster breakdown of vitamin B 12. The higher rate of loss is
partially offset by the shorter cooking times required. [40] A single study indicated that
microwaving broccoli loses 74% or more of phenolic compounds (97% of flavonoids), while
boiling loses 66% of flavonoids, and high-pressure boiling loses 47%, [41] To minimize phenolic
losses in potatoes, microwaving should be done at 500W.[43]
Spinach retains nearly all its folate when cooked in a microwave; in comparison, it loses about
77% when boiled, leaching out nutrients. Bacon cooked by microwave has significantly lower
levels of carcinogenic nitrosamines than conventionally cooked bacon.[38] Steamed vegetables
tend to maintain more nutrients when micro waved than when cooked on a
stovetop. Microwave blanching is 3-4 times more effective than boiled water blanching in the
retaining of the water-soluble vitamins folic acid, thiamin and riboflavin, with the exception of
ascorbic acid, of which 28.8% is lost (vs. 16% with boiled water blanching).
MICROWAVE SAFE COOKING BASICS

• Arrange food items evenly in a covered dish and add a little liquid. Cover the dish loosely with
a microwave-safe lid or plastic wrap to allow steam to escape. Steam helps destroy bacteria and
ensures uniform heating. Oven cooking bags also promote safe, even cooking.
• Foods and liquids are heated unevenly in the microwave, so stir or rotate food midway through
cooking, and turn large food items upside down. This prevents cold spots where harmful bacteria
can survive.
• Pierce hot dogs and baking potatoes with a fork before putting them into the microwave oven to
keep them from exploding. Reheat hot dogs until they are hot and steaming.
• To prevent burns, carefully remove food from the microwave oven. Use potholders and
uncover foods away from your face so steam can escape.
• Always allow the recommended standing time to complete cooking.
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MICROWAVING MEAT & POULTRY
 All raw meat, poultry and egg dishes cooked in a microwave oven must be cooked to at
least 165 °F in all parts of the food and allowed to stand covered for at least two minutes.
Use a food thermometer or the oven’s temperature probe and check food in several
places. Cooking times may vary because microwave ovens vary in power and efficiency.
• De-bone large pieces of meat. Bone can shield the meat around it from thorough cooking.
• Cook large pieces of meat on medium power (50 percent) for longer times. This allows heat
to conduct deeper into meat without overcooking outer areas. Turn large food items upside
down so foods cook more evenly and safely.
• Do not microwave whole, stuffed poultry. Cooking of meat is so rapid, the stuffing inside
might not reach a sufficient temperature to be safe.
 Never partially cook raw meat or poultry to finish cooking later. When microwaving food
partly done to finish cooking on the grill or conventional oven, transfer the microwave
food to another heat source immediately.
BENEFITS AND SAFETY FEATURES
All microwaves use a timer for the cooking time, at the end of cooking time, the oven switches
itself off. Microwave ovens heat food without getting hot themselves. Taking a pot off stove,
unless it is an induction cook top, leaves a potentially dangerous heating element or trivet that
will stay hot for some time. Likewise, when taking a casserole out of a conventional oven, one's
arms are exposed to the very hot walls of the oven. A microwave oven does not pose this
problem.
1. Food and cookware taken out of a microwave oven are rarely much hotter than 100 °C
(212 °F). Cookware used in a microwave oven is often much cooler than the food
because the cookware is transparent to microwaves; the microwaves heat the food
directly and the cookware is indirectly heated by the food. Food and cookware from a
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conventional oven, on the other hand, are the same temperature as the rest of the oven; a
typical cooking temperature is 180 °C (356 °F). That means that conventional stoves and
ovens can cause more serious burns.
2. The lower temperature of cooking (the boiling point of water) is a significant safety
benefit compared to baking in the oven or frying, because it eliminates the formation of
tars and char, which are carcinogenic. Microwave radiation also penetrates deeper than
direct heat, so that the food is heated by its own internal water content. In contrast, direct
heat can burn the surface while the inside is still cold. Pre-heating the food in a
microwave oven before putting it into the grill or pan reduces the time needed to heat up
the food and reduces the formation of carcinogenic char.
3. Unlike frying and baking, microwaving does not produce acryl amide in potatoes,

[30]
however unlike deep-frying, it is of only limited effectiveness in reducing
glycoalkaloid (i.e. solanine) levels. Acryl amide has been found in other micro waved
products like popcorn.
HAZARDS
1. High temperatures
Homogeneous liquids can superheat when heated in a microwave oven in a container with a

smooth surface. That is, the liquid reaches a temperature slightly above its normal boiling point
without bubbles of vapour forming inside the liquid. The boiling process can
start explosively when the liquid is disturbed, such as when the user takes hold of the container to
remove it from the oven or while adding solid ingredients such as powdered creamer or sugar.
This can result in spontaneous boiling (nucleation) which may be violent enough to eject the
boiling liquid from the container and cause severe scalding.
Closed containers, such as eggs, can explode when heated in a microwave oven due to the
increased pressure from steam. Intact fresh egg yolks outside the shell will also explode, as a
result of superheating. Insulating plastic foams of all types generally contain closed air pockets,
and are generally not recommended for use in a microwave, as the air pockets explode and the
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foam (which can be toxic if consumed) may melt. Not all plastics are microwave-safe, and some
plastics absorb microwaves to the point that they may become dangerously hot.
Products that are heated for too long can catch fire. Though this is inherent to any form of
cooking, the rapid cooking and unattended nature of the use of microwave ovens results in
additional hazard.
2. Metal objects
Any metal or conductive object placed into the microwave will act as an antenna to some
degree, resulting in an electric current. This causes the object to act as a heating element. This
effect varies with the object's shape and composition, and is sometimes utilized for cooking.
Any object containing pointed metal can create an electric arc (sparks) when micro waved. This
includes cutlery, crumpled aluminum (though some foil used in microwaves are safe), twist-ties
containing metal wire, the metal wire carry-handles in paper Chinese take-out food containers, or
almost any metal formed into a poorly conductive foil or thin wire; or into a pointed shape. Forks
are good example: the tines of the fork respond to the electric field by producing high
concentrations of electric charge at the tips.
What is "standing time"?
Microwaves cause water, fat, and sugar molecules to vibrate 2.5 million times per second,
producing heat. After the oven is off or food is removed from the oven, the molecules continue
to generate heat as they come to a standstill. This additional cooking after microwaving stops is
called "carryover cooking time," "resting time," or "standing time." It occurs for a longer time in
dense foods such as a whole turkey or beef roast than in less-dense foods like breads, small
vegetables and fruits. During this time, the temperature of a food can increase several degrees.
For that reason, directions may advise to let a food "rest" for a few minutes after turning off the
oven or removing food from the oven.
Use a food thermometer or the oven's temperature probe to verify the food has reached a safe
internal temperature. Unless the food thermometer is labeled safe for microwave cooking, do not
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leave the thermometer in the food during microwaving. Instead, use an instant read food
thermometer to test the temperature of the food after removing it from the microwave oven.
What are the USDA recommended temperatures for microwaving food safely?
Place the thermometer in the thickest area of the meat or poultry — not near fat or bone — and
check the temperature in the innermost part of the thigh and wing and in the thickest part of the
breast of whole poultry. Cooking times may vary because ovens vary in power and efficiency.
 Cook ground meats to 160 °F as measured with a food thermometer.

 Cook all raw beef, pork, lamb and veal steaks, chops, and roasts to a minimum internal
temperature of 145 °F as measured with a food thermometer before removing meat from the heat
source. For safety and quality, allow meat to rest for at least three minutes before carving or
consuming. For reasons of personal preference, consumers may choose to cook meat to higher
temperatures.
 Cook all poultry to a safe minimum internal temperature of 165 °F as measured with a food
thermometer.
 Eggs and casseroles containing eggs, 160 °F.
 Fish should reach 145 °F.
After removing food from the microwave, always allow standing time of at least 3 minutes. This
completes the cooking process. Then check the internal temperature with a food thermometer
WHAT IS THE BEST WAY TO THAW FROZEN FOOD IN A MICROWAVE OVEN
Remove food from its packaging before defrosting. Do not use foam trays and plastic wraps
because they are not heat stable at high temperatures. Melting or warping from the heat of the
food may cause harmful chemicals to migrate into it.
Select the "defrost" setting or 30% power. During microwave defrosting, rotate and turn food
upside down where possible. For individual pieces such as chicken parts, break them apart when
possible, rotate and turn upside down several times during defrosting. When thawing ground
meats, scrape the thawed portion off as it softens; remove it from the oven. Continue to
microwave defrost the remaining portion.
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Cook meat, poultry, egg casseroles, and fish immediately after defrosting in the microwave oven
because some areas of the frozen food may begin to cook during the defrosting time.
HOW TO CLEAN THE INSIDE OF A MICROWAVE OVEN
Consult the manufacturer's use and care manual for the best advice for your model of microwave
oven. Some manufacturers recommend unplugging the microwave before cleaning it to minimize
the possibility of electric shock. If you can't locate the manual, follow these general instructions.
 Remove spatters and spills as they occur so food residue won't become dried on.
 Wipe with a soft cloth or clean paper towel dampened with warm water.
 For heavier soil, use baking soda, a mild soap, or dishwashing liquid.
 Do not use steel wool, scouring pads, abrasive cleaners, or oven cleaners.
To remove food odors or loosen baked-on food residue, mix 6 tablespoons of baking soda OR
1/2 cup lemon juice with one cup of water in a microwave-safe glass measure. Microwave the
mixture until it boils. Then leave the mixture in the microwave without opening the door until
the mixture cools. The steam will help loosen food residue and remove odors. Wipe the surfaces
with a soft cloth or paper towel.
Always consult the owner's manual of your microwave oven and heed the manufacturer's
recommendations for the use of aluminum foil. It can be safe to use small amounts of aluminum
foil in a microwave oven.
Microwaves cannot pass through metal but are absorbed by food. No food completely covered
by aluminum foil or in a covered metal pan should be put in a microwave oven because food
wouldn't be available to absorb the microwaves. Operating the oven empty or when the food is
completely wrapped in aluminum foil can cause damage to the oven and the food won't heat.
However, small pieces of aluminum foil can be used to "shield" areas of foods, such as poultry
drumsticks and wings, to prevent overcooking.
Some food packaged in foil containers can be safe to microwave. Read the package heating
instructions to see if the food manufacturer has specific recommendations for microwaving the
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product. Because food in these containers will only heat from the top, it's best to microwave
foods only 1-2 inches in depth so food near the bottom will be heated thoroughly before food on
top dries and overcooks.
GENERAL RULES FOR SAFE USE OF ALUMINUM FOIL:
 Use new, smooth foil only. Wrinkled foil can cause arcing (sparks).
 Cover no more than 1/4 of the food with foil.
 Shape the foil smoothly to the food so no edges stick out.
 It makes no difference which side of foil (shiny or dull) is facing out.
 Do not place the foil closer than one inch from the oven walls.
 If the microwave oven has metal shelves OR a metal turntable, don't microwave food in foil
containers or metal pans, and don't let foil used for shielding touch or be close to the shelves or
turntable.
 If you see arcing (sparks), immediately remove the foil shielding; transfer frozen food from foil
container to a microwave-safe utensil.
REFERENCES
Hervé This, Révélations gastronomiques, Éditions Belin. 7011-1756-9
"Litton — For Heat, Tune to 915 or 2450 Megacycles". Litton Industries, 1965. Southwest

Museum of Engineering, Communications and Computation. 2007. Retrieved 12
December 2006.
Chaplin & Martin 2012). "Water and Microwaves". Water Structure and Science. London South
Bank University..
Stove versus Microwave: Which Uses Less Energy to Make Tea? Retrieved , 2012
"Heating and cooling no longer majority of U.S. home energy use - Today in Energy - U.S. Energy
Information Administration (EIA)". www.eia.gov. Retrieved 2016-02-22.
"FAQs: Using Plastics in the Microwave". American Chemistry Council.
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"The Five Worst Foods to Grill". Physicians Committee for Responsible Medicine. 2005. Archived
from the original on 30 December 2010.
"Acrylamide: Information on Diet, Food Storage, and Food Preparation". Food. U.S. Food and
Drug Administration. 22 May 2008.
Tice, R; Brevard & Brigette (February 1999), 3-Picoline [108-99-6]: Review of Toxicological

Literature(PDF), Research Triangle Park, North Carolina: Integrated Laboratory Systems
Lassen, A; Ovesen, L ( 1995). "Nutritional effects of microwave cooking". Nutrition & Food

Science. 95 (4): 8–10. doi:10.
Quan R, Yang C, Rubinstein S, et al. (April 1992). "Effects of microwave radiation on anti-
infective factors in human milk". Pediatrics. 89 (4 Pt 1): 667–9. PMID 1557249.
O'Connor & Anahad ( 2006). "The Claim: Microwave Ovens Kill Nutrients in Food". The New York
Times.
"Microwave cooking and nutrition". Family Health Guide. Harvard Medical School.

Retrieved 23 July 2011
Fumio Watanabe; Katsuo Abe; Tomoyuki Fujita; Mashahiro Goto; Miki Hiemori and Yoshihisa
Nakano ( 1998). "Effects of Microwave Heating on the Loss of Vitamin B(12) in Foods". Journal
of Agricultural and Food Chemistry. 46 (1): 206–210.
Vallejo, F, Tomás-Barberán, F.A, García-Viguera, C (2003). "Phenolic compound contents in

edible parts of broccoli inflorescences after domestic cooking". J Sci Food Agric. 83 (14):1511–6.
Osinboyejo, M. A.; Walker, L. T; S. Ogutu & Verghese, M.. "Effects of microwave blanching vs.
boiling water blanching on retention of selected water-soluble vitamins in turnips, foods, and
greens using HPLC". National Center for Home Food Preservation, University of Georgia.
Retrieved 23 July 2011.
FDA. Food Code 2009.

http://www.fda.gov/Food/FoodSafety/RetailFoodProtection/FoodCode/FoodCode2009/
ucm186451.htm
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USDA Food Safety and Inspection Service. ( 2011). Cooking Safely in the Microwave Oven.
http://www.fsis.usda.gov/factsheets/cooking_safely_in_the_microwave/index.asp
USDA/FSIS ( 2004.). Home Alone? After School Snacks and Food Safety USDA Quiz for
Parents and Kids. http://www.fsis.usda.gov/News_& _Events/NR_090704_01/index.asp
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NUTRITION IN PREGNANCY
AND LACTATION
MEDICAL NUTRITION
THERAPY
CLINICS AND TALKS
BREASTFEEDING
BY
DTN. ONYIA BLESSING.
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Nutrition in pregnancy and Lactation
A woman who has been well nourished before conception begins her pregnancy with
reserves of several nutrients so that the needs of the growing foetus can be met without affecting
her health. When infants are well nourished in the womb, they have an enhanced chance of being
born in good physical and mental health. The effect of under nutrition during reproduction will
vary depending on the nutrients involved, length of time it is lacking, and at what stage of
gestation it occurs. Mother’s diet should be adequate so that maternal stores do not get depleted
and there is sufficient milk production to nourish her child after delivery. Adolescent mothers
have more nutritional demands than others.
Women with low body weight and poor nutritional status before pregnancy have more
Low birth weight babies, premature spontaneous rupture of membranes, infection and anaemia.
A pre-pregnancy weight of <40kg will be useful in determining women who will deliver low
birth weight and Small for Gestational Age (SGA) babies. Maternal nutrition plays a role in
certain types of fetal malformation or spontaneous abortion. Since these abnormalities can occur
so early in pregnancy (during organogenesis), diet modifications must begin before pregnancy
occurs.
On the other hand, overweight women are prone to having fetal deaths, diabetes,
hypertensive disorders and abnormal labour. Because these abnormalities / maladies are difficult
to correct once pregnancy occurs, a woman should strive to have a body mass within 90-120% of
ideal weight prior to conception.
Energy needs during pregnancy increases because of the:
- Growth and physical activity of the foetus

- Growth of the placenta and maternal tissue
- Normal increase in maternal size
- Additional work in carrying the weight of the foetus and extra maternal tissues
- Slow but steady rise in BMR during pregnancy which increases by about 5% in 1 st and 2nd
trimester and by about 12% during the 3rd trimester.
Any decrease in the maternal activity decreases the caloric requirements.
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ICMR recommended dietary allowances for a pregnant and lactating woman
Nutrient Normal Adult Pregnant woman 2nd Lactation

Woman and 3rd trimester
Energy (kcals) 0-6mth 6-12mth
Sedentary 1875 + 300 + 550 + 400
Moderate 2225 + 300 + 550 + 400
Heavy 2925 + 300 + 550 + 400
Protein (g) 50 + 15 + 25 + 18
Fat (g) 20 30 45 45
Calcium (mg) 400 1000 1000 1000
Iron (mg) 30 38 30 30
Retinol (µg) 600 600 950 950
B Carotene (µg) 2400 2400 3800 3800
Thiamin (mg)
Sedentary 0.9 + 0.2 + 0.3 + 0.2
Moderate 1.1 + 0.2 + 0.3 + 0.2
Heavy 1.2 + 0.2 + 0.3 + 0.2
Riboflavin (mg)
Sedentary 1.1 + 0.2 + 0.3 + 0.2
Moderate 1.3 + 0.2 + 0.3 + 0.2
Heavy 1.5 + 0.2 + 0.3 + 0.2
Niacin (mg)
Sedentary 12 +2 +4 +3
Moderate 14 +2 +4 +3
Heavy 16 +2 +4 +3
Pyridoxine (mg) 2.0 2.5 2.5 2.5
Ascorbic acid (mg) 40 40 80 80
Folic acid (µg) 100 400 150 150
Vitamin B12 (µg) 1 1 1.5 1.5
Water 2300ml + 400ml + 700ml
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PROTEIN
Additional protein during pregnancy is essential for:
- Rapid growth of the foetus
- The enlargement of the uterus, mammary glands and placenta
- Increase in maternal circulating blood volume and subsequent demand of increased
plasma protein to maintain colloidal osmotic pressure and circulation of tissue fluids.
- Formation of amniotic fluid and storage reserves for labour, delivery and lactation.
- The transfer of amino-acids from the mother to foetus (up to 20wks, all amino acids must
be provided to the foetus as it cannot oxidize amino acids as a source of energy).
Protein Deficiency during pregnancy can lead to:
- Increased pregnancy risk.
- Foetus may grow at the expense of mother.
- Maximum growth of the baby cannot be attained.
- Number of tissue cells particularly brain cells may be less.
Protein and caloric deficiency may result in poor utilization of food by the off-spring after birth
and failure to ever compensate for early food deprivation.
Essential Fatty Acids (EFA)
Helps in relaxing muscles and blood vessels of the uterus and makes delivery easier. It adversely
affects pregnancy outcome.
Sources: - corn, cotton seed, soya bean oil are good sources of linoleic acid.
α- linolenic acid is present in fish oils, green leafy vegetables, soya bean and walnuts.
CALCIUM
Essential not only for the calcification of foetal bones and teeth, but also for protection of
mother’s calcium reserves to meet high demands during lactation.
To prevent ‘Osteomalacia’, mother’s diet should contain less of phytic acid, adequate amounts of
Vitamin D and sufficient amount of calcium.
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IRON
- Infants are born with high Haemoglobin levels of 18-22g/dl (18-22g/100ml). Iron stores
in the liver of an infant last from 3-6mths.
- Iron is also required for the growth of the foetus and placenta.
- For the formation of haemoglobin as there is 40-50% increased maternal blood volume.
- Loss of maternal iron through skin and sweat is about 170mg of iron and should be
replaced.
The actual iron increase is required only in the 2nd and 3rd trimester.
IODINE
Deficiency in pregnancy can lead to abortion, still births, congenital anomalies, increased
perinatal mortality, cretinism and psychomotor defects.
ZINC
Deficiency in pregnancy can lead to foetal mortality, foetal malformation including CNS
teratogenecity and reduced intra uterine growth rate. It also doubles the risk of preterm delivery.
FOLIC ACID
- Prevents macrocytic anaemia in pregnancy.
- Promotes normal foetal growth.
- Needed for the synthesis of essential components of DNA and RNA which increases
rapidly during growth, (prevents neural tube defects: closes by 28days gestation).
- Essential for the development of RBCS which increases as the mother’s blood volume
increases.
Deficiency can lead to spontaneous abortion, preterm labour and LBW (Low Birth
Weight).
- Neural tube defects e.g spina bifida
- Anencephaly (absence of brain)
- PIH (Pregnancy Induced Hypertension).
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- Selective promotion of spontaneous abortion of defective fetuses (Terathanasia).
PROBLEMS ASSOCIATED WITH PREGNANCY

Nausea and vomiting, constipation, heart burn, pica, anaemia, PIH, gestational diabetes etc.
NUTRITION IN LACTATION
Factors Affecting the volume and composition of Breast milk:

1. Maternal nutritional status:- Fat and energy concentration in milk are significantly
related to fat stores.
2. Parity: - Milk of primiparae has a higher fat concentration than that of multiparae.
3. Supplementary Feeding: - No significant effect of supplementary feeding on the
production of milk.
4. Infant Demand: - The frequency of milk removal is an important determinant of the
volume of the milk secreted. Sucking stimulates the release of the hormones that
stimulate milk production. Frequent feeding removes the locally active inhibitor.
5. Under-nourished mother produces less quantity but same quality of milk.
6. Lactose, protein, calcium, iron, copper and fluorine content of milk are independent of
the mother’s diet.
7. Selenium, Iodine and B-Vitamins content of milk is dependent on mother’s diet.
8. Lactational capacity is a function of genetic heritage.
9. Maternal physical activity, the thermic effect of food or maternal and infant illness may
affect the amount and content of milk.
10. Milk production may also be affected by the inadequate fluid intake.
11. Unusual flavor compounds may be present in the breast milk, if the mother consumes
strong flavoured foods.
Nutritional Requirements:-
- Should meet her own daily needs

- Provide enough nutrients for the growing infant.
- Furnish the energy for the mechanics of milk production.
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Diet of lactating mother and her nutritional status during pregnancy affect to a certain extent
quality and quantity of breast milk. In 6months, a normally developing infant doubles the birth
weight accumulated in 9months of pregnancy.
Milk content: - An average daily milk production for a lactating woman is 650ml though some
may produce as much as 1000ml. Calorie value of human milk is 65kcal/100ml. Hence, calorie
value of 650ml = 420kcal.
Milk Production: - The metabolic work involved in producing this amount of milk requires about
400kcal.
The additional energy needed for lactation is drawn from maternal adipose tissue stores laid
down during pregnancy.
Also, an additional energy may be required if the lactating mother is a teenager, feeding more
than one child, under weight, or if she is also pregnant.
FLUID
An increased fluid intake is necessary for adequate milk production, since milk is a fluid tissue.
Water and beverages such as juices, soups, butter milk and milk, all add to the fluid necessary to
produce milk. A lactating mother should take 2-3 litres of fluid per day.
CLINICS AND TALKS

There are different clinics that are run by the department in this hospital.
They include: - MOP (Medical Out Patient Clinics), Ante-Natal, CHOP (Children Out Patient
Clinics), ARV (Anti-retroviral Clinic) and DM (Diabetic Clinic)
Whenever a patient is referred to a Dietitian in any of the clinics, this patient will be
assessed and proper dietary counseling done.
Assessment of a patient using
NUTRITION CARE PROCESS
(1) ASSESSMENTS:-
(a) Nutritional Assessment which includes:-
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(i) Client History: - Get the social, Medical or Health history, Medication (drug) and
supplement history and personal history. Most often, these are gotten from the folder but can be
confirmed by asking the patient or care-giver.
(ii) Food and Nutrition related History (Dietary intake/Assessment):- This is gotten using Diet
history which can be for a month or more. Here, the patient is asked the number of meal
eaten/day, his or her appetite, food likes and dislikes, presence or absence of Nausea and
vomiting. Use of any nutritional supplements, cigarette smoking, habits related to sleep, rest,
work, physical activity and exercise, chewing and swallowing ability etc.
This is then followed by a 24-hour diet recall which involves:-
Client’s usual pattern of eating during and between meals, beginning with the 1 st food or drink
of the day. Types of food, serving sizes, frequency and timing and significant seasonal
variations. Ask specific questions on dietary preferences and habits.
The above is for adult patients or clients, but for infant’s diet history, ask the mother
about the following:-
When was breast feeding initiated i.e at birth (immediately) or delayed. If delayed, why and
what was given. Then, was the baby Exclusively breastfed or Predominately breastfed and for
how long.
- Exclusive breast feeding: - Only breast milk.
- Predominate breast feeding: - Breast milk + water.
When was Complementary feeding started i.e what Age, what kind of food and the quantity.
E.g if pap, how and what was it fortified (quantity) and how frequently the baby was fed.
(b) Biochemical Data, Medical Tests and Procedures
Laboratory data e.g Electrolytes, Glucose (FBS), Lipid etc. Then, compare with the normal
indices.
(c) Anthropometric Measurements: - Height, weight, length, BMI, Growth rate and rate of
weight gain.
LENGTH: - For children < 24months of age or children between 24-36 months who cannot
stand erect without assistance. This is measured in a recumbent position using an
infantometer and two persons are required to measure this.
INFANTOMETER: - A stationary headboard and moveable footboard. One person holds the
child’s head against the headboard; the other person keeps the child’s legs straight and
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against the bottom of the feet with the toes pointing upwards and then reads the measurement
to the nearest 0.1 cm.
HEIGHT: - Children 2-3yrs or older.
The child stands with heels together, arm to the sides, legs straight, shoulders relaxed and
looking straight ahead. Heels, buttocks, scapulae and back of head should if possible be
against the vertical surface of the STADIOMETER. Some people may not be able to touch
all four points against the stadiometer because of obesity, protruding buttocks or curvature of
the spine, then, have the subject touch two or three points to the vertical surface of the
stadiometer. Then lower the headboard on the highest point of the head with enough pressure
to compress the hair and read off to 0.1cm.
HEAD CIRCUMFERENCE:-
This is important to detect abnormalities of head and brain growth, especially in the 1 st
year of life. This is measured from birth – 36 months of age because head circumference
increases rapidly during the 1st 12months of life but by 36months, growth is much slower.
Have the child sit on the lap of the care-giver, although older child can stand. Use a non-
stretchable measuring tape, placing it just above (not over) the ears, and around the back of
the head, so that the maximum circumference is measured, then pull the tape to compress the
hair. Read off to the nearest 0.1cm.
MUAC: - Mid-Upper Arm Circumference is also taken.
WEIGHT: - Weigh the adult patient using Electronic Scale or Balance–beam scale. Weigh
infant’s nude using pan type or platform weighing scale or subtract the weight of the diaper
from the patient’s weight. The infant is weighed lying down in the middle of the pan. Read
off the to the nearest 0.01 kg and plot on the growth chart.
Adults and children who can stand are weighed and recorded to the nearest 0.1 kg.
N/B: - For children: - Compare with growth chart for Height/Length or with percentiles for
Length- for- age and Weight- for – age.
To Calculate Expected Weight of Children:-

0-1yr = n +9 (n = age in months)
2
1-6yrs = 2(n) + 8 where n = age
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7-12yrs = 7n -5
2
% Weight Loss
= Current wt x 100
Expected wt
FAO / WHO % Weight Loss
% Wt Loss Oedema
Under weight 80-60 % 0
Marasmus 60% 0
Kwashiorkor 80- 60 % +
Marasmic Kwashiorkor 60 % +
Adults:- Calculate the BMI and classify if underweight, overweight, Normal or obese.
BMI(kg/m2) Obesity class Men≤102cm Men>102cm

Women≤88cm Women>88cm
Disease risk Factor
Relative to Normal weight and
Waist circumference.
Under weight <18.5 - -
Normal 18.5-24.9 - -
Overweight 25.0-29.9 Increased High
Obesity 30.0-34.9 I High Very High
35.0-39.9 II Very high Very High
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Morbid/Extreme ≥40.0 III Extremely high Extremely High
obesity
WAIST CIRCUMFERENCE/BODY FAT

Body fat distribution can be classified as Android/Male type (Upper body) and Gynoid
Obesity / Female type (Lower body).
Android obesity: - Fat within the upper part of the body especially within the abdomen.
Gynoid obesity: - Body fat within the hips and thighs.
Fat distribution is a more important risk factor for Morbidity and Mortality than obesity
per se.
MEASUREMENT/ASSESSMENT OF TOTAL ABDOMINAL FAT:-
(A) Waist- hip- ratio (WHR):- Should be less than 1.

Males (Adult) = < 0.9
Adult Females = < 0.8
(B) Waist circumference is actually a better predictor of total abdominal fat content than the
WHR and a better predictor of disease risk.
The subject should wear light clothing, then locate the right iliac crest by using the
fingertips to gently feel for the highest point of the hip bone on the subject’s right side, then
use an inelastic tape to measure. The tape should be snug against the skin but not so tight as to
compress the skin. The subject should stand erect, abdominal muscles relaxed and arms at the
sides.
Adult Male = < 102cm
Adult Female = < 88cm
High risk Waist Circumference for Adult Males and Females.
Male > 40 inch or >102cm
Female > 35 inch or > 88cm
(d) Clinical Examination or Nutrition-Focused Physical Findings: - Check for oral health,
general physical appearance, muscle and subcutaneous fat wasting, Signs and symptoms of
malnutrition, Anaemia, Dehydration, Oedema, Hair colour and Loss etc.
(2) Nutrition Diagnosis
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After all these assessments, a nutritional diagnosis is made.
(3) Nutrition Intervention: - Outline the nutritional interventions aimed at correcting or
reducing the above made nutritional diagnosis.
(4) Nutritional Monitoring and Evaluation: - This is routinely done to determine whether
nutrition intervention goals and objectives are being achieved. It is also the process used to
quantify the amount of progress the client/patient has made as a result of specific nutrition
intervention.
ADVANTAGES/BENEFITS OF BREAST FEEDING.
Breastfeeding/Nursing is the art of feeding of babies and young children with milk from a
woman’s breast. It is recommended that breastfeeding begins within the first hour of a baby’s life
continues often and as much as the baby wants (ie feeding on demand)
(https:iien.m.wikipedia.org).
W.H.O recommends Exclusive breastfeeding up to 6months of age, with continued breast

feeding along with appropriate complementary foods up to 2years of age or beyond. (www.
Who.int).
1. It confers immunity or antibiotics (immunoglosulin A (igA) against diseases to the baby

(ie the colostrums which is the first milk produced by the mother, forming a protective
layer on the mucous lining/membranes of the intestines, nose and throat.
2. It is also specially tailored for your baby that is Ideal Nutritions for the baby.
3. Breastfeeding also helps the baby avoid many diseases later in life eg. Type I & 2 Dim,
Hypercholesterolaemia, inflammatory bowel diseases, HTN etc.
4. It can also protect your baby from developing allergies and asthma.
N.B :- Vit. D can be lacking in breast milk except the mother has a very high intake.
5. Breastfed babies have lower obesity rates. They also have more leptin and more
beneficial gut bacteria.
- leptin a key hormone for regulating appetite and fat storage.
6. it may also affect a baby’s brain development and reduces the risk of future behaviour
and learning problems.
7. it also helps mother to loose weight especially after the 1st 3months of lactating.
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8. it also helps the uterus to contract by increased secretion of oxytocin which helps the
uterus to return to its previous size.
9. mothers who breastfeed have a lower risk of depression by oxytocin which encourages
caregiving, relaxation and bonding between mother and child.
10. it reduces disease risk in mothers especially Ovarian and breast cancer.
11. it can also act as a contraceptive method by delaying ovulation and menstruation.
12. Breastfeeding saves time and money.
PROBLEMS ASSOCIATED WITH BREASTFEEDING
1. Breast Pain: This often interfers with successful breastfeeding. It is cited as the 2 nd most
common cause for the abandonment of Exclusive breastfeeding after perceived low milk
supply.
2. Inverted Nipples: Inverted/retracted nipples sometimes make attachment to the breast
difficult. Treatment:- The nipple is manually stretched out several times a day. A pump or
a plastic syringe is used to draw out the nipple and the baby is then put to breast.
3. Enlargement: is the sense of breast fullness experienced by most women within 36hrs of
delivering.
Prevention:- Breastfeeding on demand. Engorgement may affect the arcola, the periphery
of the breast or the entire breast and may interfere with breastfeeding both from the pain
and also from the distortion of the normal shape of the areola/nipple. This makes it harder
for the baby to latch properly for feeding .
Causes: - Nipple pain, improper feeding technique infrequent feeding or infant – mother
separation.
4. Nipple pain:- this may occur by the 2nd day after delivery but improves within 5 days.
Sore Nipple which is a common cause of pain, often results from baby not latching on the
nipple properly.
Factors include:- too much pressure on the nipple when not enough of the areola is
latched unto and an improper release of suction at the end of the feeding. Improper use of
breast pumps.
Infection can also cause Nipple pain.
5. Candidiasis: - symptoms of breast candidiasis include pain, itching, burning and redness,
and or a shiny or white patching appearance.
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- Milk Stasis: This is when a milk duct is blocked and cannot drain properly. It may affect
only a part of the breast and is not associated with any infection. Treatment is by varying
the baby’s feeding position and applying heat before feeding.
- Mastitis:- Inflammation of the breast causing local pain (dolor), redress (rubor), swelling
(tumor), and warmth (calor). It mostly occurs 2-3 weeks after delivery but can happen at
any time.
Treatment:- Continued breastfeeding, plenty of rest and adequate fluid supply are the best
treatment for light cases.
INFANT HEALTH PROBLEMS AFFECTING BREASTFEEDING.
Infants with classic Galactosemia cannot digest lactose and therefore can not benefit from
breast milk.
- Mother’s active untreated Pulmonary Tubercluosis except where BCG has been given to
the baby. (WHO)
- Taking certain medications that suppress the Immune system(26)
- Mother using potentially harmful substance such as Cocaine, Heroin, Amphetamine
EFFECTS OF SMOKING ON BREASTFEEDING.
- Infants may have smoking – induced reductions of the milk Iodine Content.
- Smoking can adversely affect the lactation process by decreasing milk production and
altering the milk composition. Smoking reduces the daily milk output by roughly 250 –
300ml, which can cause the mother to wean her baby early.
- The alterd milk composition can also cause infants to have colic and crying which lead to
early weaning.
- Nicotice can also be secreted in the breast milk.
- Heavy smoking can also cause vomiting, diarrhoea, rapid heart rate, restlessness in
breastfed infants.
- Sudden infant Death syndrome (SIDS) is also common in babies exposed to a smoky
environment
N/B. Counsel mothers not to smoke during or immediately before feeding their infants
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ALCOHOL:- Heavy alcohol consumption harms the infant by causing problems with the
development of motor skills and decreasing the speed of weight gain.
CAFFEINE: Too much of this can cause irritability, sleeplessness, nervoursness and increased
feeding in the breastfed infant. Stop or restrict using coffee, tea or cola if your baby reacts
negatively to them.
DIET
Mothers in famine conditions can produce milk with highly nutritional content, a Malnourished
mother may produce milk with decreased levels of several Micronutrients eg. Iron, Zinc and Vit.
B12
- She may also have a lower supply than a well nourished mother.
- There are no foods that are absolutely contra-indicated during breastfeeding, but a baby
may show sensitivity to particular foods that the mother eats.
REFERENCES
Gartner L M; et al (2005) “Breastfeeding and the use of human milk” Paediatrics. 115(2) : 496 -
506 doi:10. 1542/peds. 2004 - 2491. PMID 15687461
Woolridge M (1986). “Aetiolose of sore nipples”.Midwifery. 2(4) : 172 – 6.
Hill P, Humenick S (1994). “The occurrence of breast engorgement”. JHum Lact. 10 (2); 79-86.
Calbe B, Stewart M, Davis J (1997). “Nipple wound care: a new approach to an old problem”. J
Hum Lact. 13(4): 313-8.
Amir L; Garland S; Dennerstein L; Fanish S (1996). “Candida albicans: Is it associated with
nipple pain in lactating women?”. Gynecol Obstet Invest. Karger. 41 (1): 30-34.
Mead MN (2008). “ Contaminants in human milk: weighing the risks against the benefits of
breastfeeding”. Envriron Health Perspect. 116 (10): A426 – 34.
Menella J.A; et al. (2007). “Breastfeeding and Smoking: Short – term Effects on infant feeding
and sleep” Paediatrics. 120: 497 – 502.
Najdawi, F. and Faouri, M, 1999. Maternal smoking and breast feeding.
Eastern Mediterranean Health Journal. 5(3); 450 – 465.
The U.S surgeon General’s Report. (Chapter 5; pages 180-194).
157
Gunn A, Gunnt, Mitchell E (2000). “clinical Review Article: Is changing the sleep environment
enough ?” Current recommendations for SIDS”. Sleep Med Rev. 4(5): 453-69
BILLING AND COSTING

NUTRITION CARE PROCESS
NUTRITION IN HIV/AIDS
VEGETARIAN NUTRITION
BY
DIETITIAN VIVIAN OKOYEH
158
BILLING AND COSTING
OUTLINE:
 INTRODUCTION
 PROCEDURE FOR ESTIMATING PATIENT’S BILL
 BILLING CHECK LIST
 MONTHLY COSTING
 PROCEDURE FOR MAKING A MONTHLY COSTING (Medical food administration
unit nutrition and dietetics department UNTH)
INTRODUCTION
Billing is the act of estimating and writing out a note to pay for expended good(s) or services.
This can be done by issuing out an official document stating the time, type and amount of
good(s) or service(s) given, unit cost and total cost incurred etc. followed by a note stating
amount to pay after deduction has been made for deposits made. This is used when the point of
payment is different from point of purchase or when the good(s) or service(s) supplier is a
different unit from the revenue collecting unit in a single operational chain.
The nutrition and dietetics department is one of the commercialized units in the hospital. Though
commercialized, it is not completely autonomous. The hospital has staff posted from accounts
department managing and overseeing the funds generated such that when poorly managed, bottle
necks are formed and effective service delivery jeopardized. To aid the billing process, the
department designed a form which is inserted in the folders of in-patients once feeding is
commenced. This form is adequately filled by the dietitian indicating date of commencement of
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feeding, type of feeding, deposits made etc. Upon discharge, the folder is brought to the
department for estimation of bill for onward payment to the commercialized nutrition and
dietetics account.
Below is a sample of a filled billing form.
*PLEASE SEND FOLDER TO THE DEPARTMENT OF NUTRITION AND DIETETICS ON

DISCHARGE FOR COSTING OF FLUID/SOLID DIETS CONSUMED.
DEPARTMENT OF NUTRITION AND DIETETICS
UNIVERSITY OF NIGERIA TEACHING HOSPITAL ITUKU OZALLA ENUGU
IN-PATIENT DIET BILLING FORM
NAME:____Mr X_____________________________
WARD:_________MMW_______________________
DATE ADMITTED:_________06/03/15____________
DATE DISCHARGED:_____20/4/15_(Death)_______
A. FLUID DIET
DATE FLUID DIET TOTAL AMOUNT RECEIP BA SIGN.

ADMINISTRATION COST DEP. ON T NO L.
ADMISSION
TYPE VOL. STRENTH
06/03/15 NG 2L/day Full #450 per #2000 042356 O.V.O

Liter
08/03/15 ORAL 2L/day Full
12/03/15
160
161
B. SOLID DIET
DATE STANDARD DIET HIGH COST DIET
13/3/15 #900/day #3600/day
20/4/15
PROCEDURE FOR ESTIMATING PATIENT’S BILL
The form above is usually inserted into patient’s folder by the dietitian in charge of the ward;
duly filled with patient data during the course of her ward visits (this applies to patients in the
surgical wards generally on high protein diet) or following a referral to attend to a patient.
Upon discharge, the patient’s bill is estimated thus:
A Fluid diet:
There are basically three main types of fluid diets prepared in the therapeutic diet kitchen
viz: nasogastric, oral and gastrostomy feeds. Currently, they are all cost at 450 naira per liter flat.
To estimate amount of feed consumed on discharge, total volume of feed consumed throughout
stay is summed up from the fluid diet register. This is a register where daily inventory of fluid
diets prepared is recorded. Then the total volume multiplied by the unit price.
If patient X in sample billing form above consumed 2L of nasogastric fluid diet daily on the
6/3/15 and 7/3/15, then progressed to 2L oral high protein fluid diet daily from the 8 th to 12th of
March 2015. Estimated bill would be as follows
Total volume of feed: 7days x 2L= 14L
Total cost of feed: 14 x 450 = N6300
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B Solid diet:
There are various therapeutic solid diets ranging from diabetic diet, low sodium diet, low
protein diet, low fat diet, high protein diet, gastric diet, low residue diet and varying
combinations. In the solid diet session, standard diets are cost currently at 900 naira per day and
high cost option cost at 3600 naira per day.
To estimate cost of solid diet consumed on discharge, total amount of food consumed throughout
stay is summed up from the diet requisition sheet. This is a daily diet sheet sent from the wards
requesting that the outlined diets be prepared for the under listed patients. Then the total number
of meals served (number of days fed) is multiplied by the unit price. Remember that the unit
price of standard diet is different from high cost. The high cost diet is usually an elaborate menu
with options to make choice from.
If patient X in sample billing form above consumed standard solid diet daily from the 13 th to 20th
of April 2015. Estimated bill would be as follows
Total meals served: 39meals (19days in March and 20 days in April)
Total cost of food: 39 x 900 = N35100
NB-If this patient was on high cost diet, estimated bill would be as follows
Total cost of food: 39 X 3600 = N140, 400
Therefore, to estimate cost of therapeutic diet received within duration of hospital stay
(admission to discharge). The various diets received and other services received in the ward are
summed up.
For patient X above Total bill in the light of following diet progression from the 6 th of March to
20th April 2015 would be
Standard: N6300 + N35100 = N42800
OR
High cost: N6300 + 140400 = N1406700
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After bill estimation, any diet feeding deposit paid would be deducted to get final amount patient
is still owing the hospital. This amount is written out with the note patient is to pay…with this
final note to pay patient goes to the revenue point to pay the stated amount.
If patient X was on standard diet and paid a diet feeding deposit of 2000 naira.
The summary of the bill would be
N42800 - N2000 =N40800
Patient is to pay N40800
BILLING CHECK LIST
At the end of the billing exercise, it is important to cross check using the following points to
avoid over or under billing patient.
 Death case: in the event of death a patient is exempted from paying for meal served on
that day. Therefore while estimating bill, it is stated minus 1 day death. In case above
patient would pay N40800 – N900(minus 1day death) = 39900
 Surgery: 1 day, 2days or 3days is exempted in view of minor, sub major and major
surgeries respectively if NPO (nothing by mouth) was observed.
 Breaks in admission stay: this happens when patient is allowed home and later re
admitted. Only days for which patient was on admission is cost, taking note of when
feeding commenced.
 Other services: services like counseling and issuing of diet guide is usually added to bill.
The dietitian notes on the billing forms that such services were rendered.
 Neonates: new born admitted in New Born Special Care Unit (NBSCU) receive infant
formula. Currently they are cost N350 per day for pre term and N700 for full term. NB:
Those neonates that are breast fed are not cost.
At the end of the billing process, relevant information is filled into the costing registers to
preserve departmental records of bills and movement of folders.
NOTE
Care must be taken to estimate bills to avoid error. Any under billed patient incurs sub
charge on the staff who under billed to get back the short fall.
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COSTING
Food service is one of the top highly profitable businesses. It is a highly competitive market
since food is a basic necessity of life. A delicious meal alone would not be enough to deliver
success in business. To succeed one need a good location, sensible marketing and factors like
reasonable pricing (offering affordable product with optimum profit) in addition to great tasting
food. There are many factors to consider but the most basic strategy is to come up with the
costing template for the recipe from which one can easily determine and adjust retail price. This
should be such that the cost would fit target market without compromising the income.
PROCEDURE FOR COSTING
STEP 1
Write down the recipe including all the ingredients and quantities as well as average yield. It
helps to convert the quantities to measurable equivalent. In the therapeutic diet unit an ingredient
register is used to collate ingredient use daily for ease at the end of the month.
STEP 2
Determine the price of each ingredient and calculate cost per recipe. This is achieved by simply
dividing the ingredient price by total volume and multiplies by equivalent measure in the recipe.
In the therapeutic diet unit, a costing template is used and entries done in a monthly costing
register.
STEP 3
Add up the total cost of the ingredients per recipe to determine the total recipe cost. In the
therapeutic diet unit, costing is done not as per recipe but meal type- fluid diet, solid diet and
infant formula. Ingredients are usually bought in bulk.
STEP 4
Divide the total recipe cost by the total yield to get cost per serving.
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STEP 5
Add mark up to cost per serving. For a 130% profit margin in a make and sell item. 100% would
cover production cost and 30% the production mark up.
Other things that could be considered in large food service include depreciation cost of
equipments and price fluctuation (seasonality of inflation can affect price). It is better to use the
upper limit of cost in planning the costing so that one doesn’t have to increase price consistently.
Though when price of materials generally increase (inflation) product price has to increase too.
MONTHLY COSTING
The medical food administration unit, Nutrition and dietetics dept UNTH; on a monthly base,
evaluate the cost of providing the various therapeutic diets; calculate the revenue accruing to
estimate the profit obtained. This helps the medical food administrator to monitor profit and
make plans to maintain current meal pricing, evaluate wastage, adjust current recipe or introduce
areas of revenue generation in order to provide patient with affordable product at optimum cost.
The food service in the hospital is more of a therapeutic unit than profit maximizing unit.
Within the first week of the next month the person in charge of the monthly costing sums up all
ingredients used within the previous month, transfers the values to the monthly costing register
following the template provided. Other non food items used regularly like matches, nylon, cost
of gas, transport incurred etc is also entered into the appropriate column in the register. The unit
price of each item is inserted and used to generate the amount spent on solid diet, fluid diet and
infant formula for the month. Total number of patient served is collected from the solid diet
register, total volume of feed provided is taken from the fluid register and total number of tins
infant formula issued and number of babies fed collected from the infant formula register. This
information is also inserted in the appropriate column in the template and used to estimate
income generated by multiplying through with the unit cost of each item. Profit is estimated by
difference. Amount realized from each section minus amount spent. The gross profit (ie. profit
minus overhead cost) is calculated by summing up individual profit from the various sections.
It is expected that before the 14th the personnel in charge of the monthly costing would have
completed the work and submitted it to the computer analyst to key into the computer for
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documentation and onward dispatch to concerned parties after vetting and submission to the head
of department.
PROCEDURE FOR MAKING A MONTHLY COSTING
A SOLID DIET
The total ingredients used are compiled at the end of the month and transferred to the costing
template using the outline below.
S/N Ingredient Quantity(Kg) Unit price(N) Cost(N)

1 Egg 940 pcs 23.34 21939.60
2 Meat 140kg 1000 140000
3 Chicken
4 Milk small sachet 640 sach 35 22400
5 Milk big sachet 24 sach 750 18000
6 Milo small sachet 580 sach 30 17400
7 Granulated sugar
8 Bread rolls
9 Corn flakes
10 Ugu
11 Carrot 3.8Kg 200 760
12 Tomatoes
13 Rice
14 Okpa
15 Brown beans
16 Yam
17 Water melon
… matches 5 packets 10 50
81 Transport 11340
Total a 611278.54
The costing is done as follows:
The quantity of each ingredient used is entered into the table above in Kilogramme, crate,
sachet, rolls, bundle or appropriate units. The unit price is derived for each ingredient and value
entered in relation to the unit of choice. To arrive at the total cost, the quantity utilized is
multiplied by the unit cost (both need to be in the same unit either in grammes or kilogrammes,
rolls or loaves, rolls or bundles etc.)
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Unit cost of item =Total cost of the item purchased that month
Total quantity purchased
Total cost = Quantity of ingredient X Unit cost
After the above has been achieved, the total number of patient fed within the time period is
entered into a template as follows
Patients fed Total no. of Unit cost(N) Total cost(N)

patient
Number of patient on standard

diet
743 900 668700
Number of patient on High cost

diet
8 3600 28800
Total b 751 697500
The standard and high cost diet served is summed up from the solid diet summary register and
the value obtain inserted in the table above accordingly. The current unit cost of each meal is
also inserted accordingly.
Total revenue generated is calculated by summing up total cost of standard and high cost diets.
Total cost = number served X unit price of meal.
Profit Solid diet A: Difference A = (b-a):- 697500 – 611278.54 = 86221.46
B INFANT FORMULA
Below is a template used for assessing turn over from provision of infant formula.
Commercial infant Total amount Unit cost(N) Total cost(N)

formula consumed
Number of babies fed(c) 49 700 34300
Number of tins used 18 1250 22500
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Profit Infant formula B: Difference B = (c-d):- 34300 - 22500 = 11800
C FLUID DIET
High energy mixture: Below is a sample of the template used to estimate revenue generated from
the fluid diet section. Like the solid diet, total cost is derived by multiplying the volume
consumed with unit cost per volume.
Type of feed No. of patient Vol. of feed Unit cost Total cost
NG children 26 22.8 300 6840
NG adult 362 803.2 450 361440
Oral children 43 481 400 19240
Oral adult 52 73.6 450 33120
Gastrostomy - - - -
Total(e) 420640
Total revenue generated – Total (e) = sum of individual feed cost.
The cost incurred in providing the ingredients used for the month is also estimated and profit
deduced by difference. Below is a sample of the template used.
Ingredient Quantity Unit cost (N) Total cost(N)

Glucose 37 430 15910
Sugar 8.3 211.79 1757.86
Milk 79 610.56 48234.24
Soyabean 12.1 666.67 8066.71
Vegetable oil 4 1350 5400
Vitamin Bco 300 1 300
Vitamin C 300 1 300
Pap 103.2 150 15480
Total (f) 95448.81
Profit Fluid diet C: Difference C = (e-f):- 420640–95448.81 = 325191.19
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At the end, gross profit is derived from sum of individual unit profit and stated as follows;
Total profit made for the time period under review excluding overhead cost
A = 86221.46
B = 11800.00
C = 325191.19
423212.65
Four hundred and twenty three thousand two hundred and twelve naira sixty five kobo.
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NUTRITON CARE PROCESS
DEFINITION OF TERMS
NUTRITION
Nutrition is the science that interprets the interaction of nutrients and other substances in food
(phyto-nutrients) in relation to maintenance, growth, reproduction, health and disease of an
organism. It includes food intake, absorption, assimilation, biosynthesis, catabolism and
excretion. Nutrition in summary is all that has to do with the food we eat and how the body
utilizes it.
An adequate well balanced diet combined with regular physical activity is a cornerstone of good
health. Poor nutrition on the contrary can lead to low immunity, high susceptibility to disease,
impaired physical/mental development and reduced productivity.
CARE
Care is an effort made to do something correctly, safely or without causing damage. It is a

combination of action done to keep someone from harm.
PROCESS
Process is a systematic series of actions directed to some end.
Nutrition care process (NCP) therefore is an organized or systematic group of activities that
allows a professional (dietitian) to identify nutritional needs and provide care to meet these needs
for optimum nutrition and health. The house of delegates of the American Dietetic Association
(ADA) in 2003 adopted the NCP in an effort to provide dietetic professionals with a framework
for critical thinking and decision making in patient and client management. The use of a care
process provides a frame work for registered Dietitians (RD) to individualize care, taking into
account the patient/client’s needs and values using the best evidence available to make decisions.
It is hoped that at the end of the lecture one would
 Know what the NCP is
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 Identify the four basic aspects of the NCP
 Understand different ways of carrying out a nutrition assessment
 Make a nutrition diagnosis using PES statement
 Critically think up appropriate nutrition intervention objective
 Understand monitoring and evaluation protocol
 Document cases using ADIME style.
The Nutrition care process (NCP) using the ADIME approach consists of four basic steps.
Assessment: This refers to nutrition assessment data. It is a comprehensive evaluation carried

out by a RD using medical and health, social, nutrition and medication histories; physical
examination, anthropometric measurement; and laboratory data to obtain adequate information in
which to make a professional judgment about nutrition status (ASPEN 2009). This is collected
by the RD in order to ascertain the nutrition diagnosis a patient/client presents with. The nutrition
assessment (NA) step allows a RD to devise a plan of action to prevent or correct nutrient
imbalance, nutrition related problem or to evaluate if a particular care plan is working. The NA
done has to be sensitive enough to detect subtle nutrition problem and specific enough to identify
problem nutrients.
The goals of nutrition assessment are to:
 Identify individuals who require aggressive nutrition support

 Restore or maintain an individual’s nutrition wellness
 Identify appropriate medical nutrition therapy (MNT)
Information needed would include:
(A) Historical information (Client history)
(a) Medical/health history (MH): As an assessment tool, this gathers information on patients
current complain, past medical condition, surgical history, family medical history,
chronic disease risk, mental/emotional health to obtain a general view of patients health
and disease risk.
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(b) Medication/supplement history (MS): Obtains information on prescription drug and over
the counter drug use, dietary/herbal supplement, alcohol intake, cigarette/tobacco and
illegal drug use. This gives one an idea of a patient’s life style and inkling to possible
medication/ supplement disposed problem or benefit.
(c) Personal/social history (PS): Usually obtains information personal/socio economic status
as possible indicator of wellbeing or problem. This includes information on age,
occupation, educational level, ethnic identity, religious belief, home situation, cognitive
abilities, etc.
(d) Food/nutrition history (FN): This is geared towards obtaining information on food
intake/problem and food security. Food intake history could be obtained using 24 hour
diet recall, food frequency questioner and food portion size estimations. Other
information obtained includes food allergies and intolerance, food availability, nutrition/
health knowledge, and physical activity and exercise pattern (helps in offering
information on energy use and requirement).
(B) Anthropometric data
Anthropometry is the measurement of the different physical dimensions of the body. The
physical dimensions of the body mostly used include weight, height (length in children), mid
upper arm circumference (MUAC), skin fold thickness, waist and hip circumference (adult),
head and chest circumference (under 5’s). Usually, these measurements are use to derive indices
that give various biological interpretations that are age dependent. These values are often
compared with national and international standards eg. WHO Growth reference CHART children
5-19years 2007, NCHS/WHO 1995 and NHANES1994.
Assessment of weight measurement:
In children
Weight of an individual can be expressed in terms of standard deviation or Z scores or

percentage of expected weight for age.
Underweight is low weight for age at <-2SD of the median value of the WHO 2007 international
reference standard (<-3SD=severe)
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Wasting is low weight for height at <-2SD of the median value of the WHO 2007 international
reference standard (<-3SD=severe)
Assessment of height measurement
Height of an individual can be expressed in terms of standard deviation or Z scores or percentage

of expected height for age.
Stunting is low height for age at <-2SD of the median value of the WHO 2007 international
reference standard (<-3SD=severe). It is linear growth that has failed to reach genetic potential
due to poor diet of disease.
BMI
In children and adolescents the BMI is both sex and age specific. The BMI classification chart
WHO 2007 international reference standard is a helpful tool.
In adult
BMI RANGE INTERPRETATION
<16.0Kg/m2 Severe underweight
16.0-16.99Kg/m2 Moderate underweight
17.0-18.49Kg/m2 Mild underweight
18.5-24.9Kd/m2 NORMAL
25.0-29.9Kg/m2 Overweight and @ risk of being obese
30.0-39.9Kg/m2 Obese with increased health risk
>40.0Kg/m2 Severely obese with major health risk
Source: WHO, 1995
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Assessment using body circumferences
In children
Head and chest circumferences (usually for under 5’s)
Below 6months- head circumference should be larger than chest circumference
Above 6months- chest circumference should be larger than head circumference. The head/chest
ratio of less or more than 1 indicates abnormality.
Interpretation of MUAC
<12.0cm Severe malnutrition
12.0-13.5cm Moderate malnutrition
>13.5cm NORMAL
In adults
Assessment using waist circumferences
Waist circumference >102cm (40inches) in men and
>88cm (35inches) in non pregnant women
= abdominal fat accumulation and increased risk for cardiovascular disease.
Interpretation of waist/hip ratio
>0.95 WHR in Men and
>0.8 in Women
= android obesity (excess fat deposition around waist and upper abdomen). Increased risk of
diabetes and cardiovascular disorders (Okeke et al 2011 and O’Dea 2002)
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(C) Laboratory data: laboratory data is useful in detecting early changes in body metabolism
and nutrition even before the appearance of overt clinical signs. It is useful to validate data
obtained from dietary methods, like comparing intake of fatty foods with lipid profile. Below are
some tests for assessing nutritional status.
NUTRIENT SENSITIVE LESS SENSITIVE

PROTEIN Plasma amino acid, hair root, Total protein
serum albumin, urinary
creatinine
LIPIDS Serum cholesterol, serum
triglycerides, lipoproteins
VITAMIN A Serum Vit.A
VITAMIN B1 Urinary thiamin, erythrocyte
transketolase activity
VITAMIN B2 Urinary riboflavin, erythrocyte
glutathione reductase
NICOTINIC ACID N1 methyl nicotinamide Urinary pyridine
FOLIC ACID Red blood cell folate Serum folate, bone marrow
film, thin blood film, urinary
exretion
VITAMIN B6 Tryptophan load test, Urinary pyridoxine excretion,
xanthurenic acid excreted in blood transaminase
urine
VITAMIN B12 Serum Vit. B12, Bone marrow film, schilling
serumthimidylate synthetase, test
urine methylmalonic acid
VITAMIN C Serum ascorbic acid Urinary ascorbic acid
VITAMIN D Serum 25-OH-Vit.D , serum
3
alkaline phosphate
VITAMIN E Hydrogen peroxide
erythrocyte hemolysis test,
serum or plasma tocopherol
VITAMIN K Prothrombin time
IRON Iron deposit in bone marrow, Hemoglobin, hematocrit, thin
serum iron, % saturation of blood film
transferring
IODINE Urinary iodine, thyroid
function test
ZINC Serum and plasma zinc Hair zinc
MAGNESIUM Serum magnesium
Adapted from Okeke et al 2011- source Krause and Mahan (1979)
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In addition to these there are other lab investigations in the clinical setting used to detect organ
failure. These are guide to the RD in proffering MNT in many chronic and debilitating diseases
with nutritional implication. This include renal function test(SEUCR), liver function test, serum
glucose test etc.
(D) Clinical observation (signs of good or poor nutrition)
Body Normal Clinical sign Nutrient Non nutrient

part/system appearance deficient confounders
Hair Shiny, firm and Lacks luster (natural Protein/energy Excessive
not easilyshine), dull and dry, bleaching,
plunked thin and sparse, alopecia
dyspigmented, easily
plunked (Kwashiokor
and less common in
marasmus)
Face Uniform skin Nasolabial dyssebacea Riboflavin. Iron acne
colour, smooth (scaling of skin around
healthy the nostrils)
appearance, not Protein/energy
swollen Swollen face (moon
face), paleness, diffuse
depigmentation
(Kwashiokor)
Eyes Bright, clear, Pale conjunctiva Iron

shiny, no sores (Anemia)
at corners of Red membrane, bitot Vitamin A
eye lids, health spot, conjunctival
pink and moist xerosis(dryness),
conjunctiva, no corneal xerosis
prominent (dullness) Riboflavin,
blood vessel keratomalacia (softness pyridoxine
of cornea)
Redness of corners of
eyelids, corneal arcus
(white ring around the
eye)
Xanthelasma (small
yellowish lumps
around the eye)
(hyperlipidemia)
Lips Smooth, not Angular stomatitis Riboflavin Excessive
cracked or (lesions at the corners salivation
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swollen of the mouth), cheilosis from
(redness or sweeing of improper
lips and mouth) fitted
denture,
cracking
from
exposure to
harsh climate
Tongue Deep red in Scarlet/purplish and Nicotinic acid Leucoplakia
appearance, not raw tongue
swollen or Swollen tongue Niacin
smooth
Teeth No cavities, no Mottled enamel, dental Fluoride Health
pain and bright caries, missing habits,
teeth(fluorosis) periodontal
disease
Gums Healthy, red, Spongy, bleeding Vitamin C Periodontal
no bleeding, disease
not swollen
Glands Face not Thyroid enlargement Iodine Allergy or
swollen (swollen front neck) thyroid
Parotid enlargement inflammation
(cheeks swollen)
(starvation)
Skin No rashes, not Xerosis (dryness), Vitamin A Environment
swollen, no follicular al exposure
dark or light Hyperkerotosis Vitamin C
spots (sandpaper skin) Vitamin C
Petechiae (skin
hemorrhages) Nicotinic acid
Pellagrous dermatosis Physical
(red swollen areas) Vitamin K abuse
Excessive bruising, Riboflavin
Srotal and vulval
dermatosis
Xanthomas (fat deposit
under skin joint)
(hyperlipidemia)
Nails Firm, pink Koilonchias (spoon Iron

shaped, brittle,ridged)
Subcutaneous Normal fat Edema (kwashiorkor) Protein
tissue Fat below standard
(starvation, marasmus)
fat above standard
(obesity)
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Muscular and Good muscle Muscle wasting Protein/energy
skeletal systems tone,walk/run (starvation, marasmus)
without pain Craniotabes (thin, soft, Vitamin D
skull bone) under
Frontal and parietal Vitamin D
bossing (round
swelling front and side
bones) Vitamin C/D
Epiphyseal
enlargement (swelling
of front and side head/ Vitamin D
end of bones) Vitamin D
Open anterior
fontanelle (soft area on Vitamin C
head closing late) Thiamin
Knock knee or bow leg Vitamin D
Musculoskeletal
hemorrhages,
Calf muscle tenderness,
Thoracic rosary
Fracture in elderly
(Osteoporosis)
Cardiovascular Normal heart Cardiac enlargement, Thiamin
system rate, no tachycardia
murmurs
Gastrointestinal No organ Hepato-splenomegaly Protein/energy
system palpable (kwashiorkor)
Nervous system Psychological Psychomotor changes Thiamin,
stability Mental confusion nicotinic acid
Depression
Sensory loss
Loss of position sense
Loss of vibration
Loss of ankle and knee-
jerks, burning and Vitamin B12
tingling hands and feet Thiamin
These would usually provide information on the following
(a) Nutrition adequacy - dietary history and detailed nutrient intake eg. 24 hour diet recall or
food frequency questioner.
(b) Health status - anthropometric and biochemical measurements, physical and clinical
conditions, physiological disease status.
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(c) Functional and behavioural status – social and cognitive function, psychological and
emotional factors, quality of life measures, change in readiness
In order to carry out a nutrition assessment, the following components can be reviewed.
 Dietary intakes in other to evaluate factors that affect health condition and nutrition risk.
 Health and disease condition for nutrition related consequence.
 Psychological, functional and behavioral factors related to food assess selection,
preparation, physical activity and understanding of health condition.
 Patients’, clients’, or groups’ knowledge, readiness to learn, and potential for changing
behaviours.
 Identify standards by which data will be compared.
 Identify possible problem areas for making nutrition diagnoses.
Diagnosis: This is the identification and labeling of a nutrition problem that a RD is

responsible for treating independently. Nutrition diagnosis (ND) is different from a medical
diagnosis because unlike a medical diagnosis the ND is usually resolved with appropriate
nutrition intervention. It is suggested that the RD use a PES (P-Problem, E-Etiology and S-
Signs/Symptoms) statement to communicate the nutrition diagnosis. The ND requires careful and
objective analysis of the pattern of relationships among the assessment data. This includes
specific problem eg. Inadequate energy intake (problem) related to a history of avoidance of
carbohydrate rich foods (etiology) as evidenced by involuntary weight loss (loose cloth fitting).
Each nutrition problem receives separate diagnosis.
This second step of NCP involves identifying the appropriate diagnosis. It includes an analysis of
the factors affecting adequacy of the current nutritional intake and overall nutritional status. In
most cases institutions use standards of care or nutritional practice guidelines that describe
recommended actions in the NCP. The ND exists in three main domains.
Intake diagnoses:
This involves nutrient related diagnoses either inadequate or excessive ingestion of nutrients,
energy, fluid, alcohol, dietary supplements, food ingredients. For example
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 Excessive alcohol intake
 Inadequate energy intake
 Inadequate fluid intake
 Inappropriate infusion of PEN
 Increased calcium needs
 Inconsistent carbohydrate intake
Clinical diagnoses:
This involves medical or physical condition that disrupts nutrition status such as disruption in
physiological/mechanical functioning, altered nutrient metabolism and body weight problems
like
 Altered blood potassium levels

 Altered GI function (constipation)
 Breastfeeding difficulty
 Food medication interaction
 Involuntary weight gain
 Swallowing difficulty
Behavioural-Environmental diagnoses:
This includes problems related to patients’ knowledge, attitudes or beliefs; physical environment;
access to food and food safety. Examples include
 Disordered eating pattern

 Impaired ability to prepare meals
 Limited access to food
 Physical inactivity
 Self feeding difficulty
 Undesirable food choices
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Intervention: This is a purposeful action of the RD aimed at ameliorating or lessening the
nutrition diagnosis. The nutrition intervention (NI) attempts to modify dietary and life style
practices or environmental conditions that interfere with nutrition status or health. NI targets
etiology as identified in ND when possible. Often times, it includes nutrition education and
nutrition counseling which require close interaction with patient. To be successful, patient/client
dietary and lifestyle preferences are put into consideration. Goals are stated in measurable
outcomes eg. Weight gain of 0.5- 1kg weekly till IBW is achieved. A nutrition diagnosis can
change after a successful nutrition intervention (NI).
This third step of the NCP requires planning and goal setting, followed by the selection of an
intervention that fits the cause of the problem. For example nutrition education is an appropriate
intervention for the person who has little knowledge of how to manage gluten free diet. Outside
education, any other nutrition diagnosis needs to be addressed as well. Dietary modification,
provision of enteral or parenteral nutrition or in depth nutrition counseling may be also needed.
Monitoring and Evaluation: The final step of the NCP is specific to individual patient or
client and is related to the signs and symptoms identified in the assessment. Monitoring and
evaluation would be developed according to nutrition diagnosis, assessment factors and
outcomes for individual being served. As dietary management progresses, measurable goals set
need to be assessed and outcome evaluated for effective care. The nutrition problem must be
evaluated periodically. Original goal and outcome measures should be reviewed and compared
with updated assessment data and patient/client progress monitored carefully. If progress is slow
or patient unwilling the NCP should be redesigned and take into account reason for poor success
of earlier plan.
 The 1st step in monitoring and evaluation is to determine indicators that should be
monitored
 2nd Match these indicators with the sign and symptoms identified during the assessment
process
 Finally compare observations with previous indicators, sign and symptom and expected.
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For example if excessive carbohydrate intake was identified during assessment, monitoring and
evaluation would entail evaluating the carbohydrate intake at a designated time for follow up
probably by requesting a 3 day food record.
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NUTRITION IN HIV/AIDS
OUTLINE:
Nutrition and HIV/AIDS: Basic Facts What is HIV?
What is AIDS?
How HIV Is Transmitted
How HIV Is NOT Transmitted
Nutrition and HIV/AIDS
Anorexia
Diarrhea Fever
Nausea/Frequent Vomiting
Thrush
Anemia
Other Nutritional Impacts of HIV
How to Maintain Good Nutrition
Macronutrients
Micronutrients
Safe Hygienic Practices: Proper Storage and Handling of Food and Water
Planning Meals for PLWHAs
References
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Nutrition and HIV/AIDS: Basic Facts what is HIV?
This lecture provides basic facts on HIV/AIDS, the relationship between HIV/AIDS and
nutrition and basic elements to maintain good nutrition in adults. It is designed to provide you
with basic information on HIV/AIDS. The information is focused on sub-Saharan Africa.
What is HIV?
H = Human (who is affected)
I = Immunodeficiency (the result)
V = Virus (the causal agent)
What is AIDS?
A = Acquired (from bodily fluids through a behavior or action, including from the mother
during pregnancy, during delivery or through breastmilk)
I = Immune (where the virus attacks)
D= Deficiency (resulting effect of virus)
S = Syndrome (series of illnesses; not just one)
Acquired Immune Deficiency Syndrome, or AIDS, is a disease caused by a retrovirus known as

the Human Immunodeficiency Virus (HIV), which attacks and impairs the body’s natural
defense system against disease and infection. HIV is a slow-acting virus that may take years to
produce illness in a person. During this period, an HIV-infected person’s defense system is
impaired, and other viruses, bacteria and parasites take advantage of this “opportunity” to further
weaken the body and cause various illnesses, such as pneumonia, tuberculosis and oral thrush.
This is why the infections and cancers seen in HIV-infected individuals are called
“opportunistic”.
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When a person starts having opportunistic infections, he/she has AIDS. The amount of time it
takes from HIV infection to become full-blown AIDS depends on the general health and
nutritional status before and during the time of HIV infection. The average time for an adult is
approximately ten years.
There is no cure for HIV/AIDS. Some therapies can prevent, treat or even cure many of the
opportunistic infections and relieve the symptoms associated with them, which include fever,
coughing, itching, and difficulty in breathing or swallowing and chronic diarrhea. Other drugs,
developed more recently, directly attack HIV. These antiretroviral (ARV) drugs attack the virus
and may slow its replication in the body, but they are not cures. The cost of the ARV drugs is
declining but, unfortunately, the treatments are not affordable or accessible for most people
living with HIV/AIDS (PLWHA). One of the cost-effective drugs (nevirapine), used to prevent
mother to child transmission of the virus during delivery, currently costs approximately US$138
per case.
How HIV is Transmitted?
HIV is transmitted through three primary routes:
● Unprotected sex with a person already carrying the HIV virus;
● Transfusions of contaminated blood and its by-products; or use of non-sterilized instruments

such as sharing non-sterilized needles, razors and other instruments for surgical procedures;
● Transmission from infected mother to her child (mother-to-child transmission, MTCT) during
pregnancy, childbirth or breastfeeding.
In most of the developing world, HIV is mostly transmitted through sexual contact with an
infected person. Women are more likely to be infected with HIV than men. Children are also at
risk. A pregnant woman who is HIV-infected has about a 15-40 percent risk of infecting her
baby with HIV in the absence of antiretroviral medication. Of children who become infected, 25-
40 percent will contract HIV during pregnancy or during labor, and 15 percent through
breastfeeding.
HIV Infected Babies
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Q: How many babies will become HIV-infected if about 20% of the mothers are HIV-infected?
A: Of 100 women, 20 mothers will be HIV infected.
Out of the 20 who are infected, 12 will not pass the virus to their infant (60%).
Out of the 8 (40%) infants that are HIV-infected, about 3 (15%) got infected by breast milk. The
remainder (5 babies) was infected during pregnancy and delivery.
In other words, in a high HIV prevalence community, if 20% of mothers are HIV-infected; the
number of babies infected by breast milk will be less than 4 percent.
Conclusion: The vast majority of babies and mothers are not HIV-infected. Breastfeeding is a
safe option for this majority of babies and should therefore not be discouraged.
How HIV Is Not Transmitted
HIV is not transmitted through the following means:
● Handshakes,
● Hugging,
● Eating food from the plate of an HIV infected person,
● Mosquitoes or other insects bites,
● Kissing,
● Sharing latrines or toilet facility.
Many people do not know that they are infected with the virus. They may appear healthy, but
still be capable of transmitting the virus through unprotected sexual intercourse or by reusing
contaminated sharp objects like injection needles, razors or other devices, or in the case of a
pregnant or lactating mother, during labor and delivery or through breastfeeding her child.
REMINDER!
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HIV is only contracted through the exchange of bodily fluids. Anyone who suspects that he or
she has been exposed to HIV should consult the nearest health center for voluntary counseling
and testing services.
Nutrition and HIV/AIDS
Figure 1. Relationship between HIV/AIDS and Nutrition
HIV
Immune Impairments
“Weak body”
“Body can’t fight Illness”
Malnutrition
“Swollen body
and feet” Infectious Disease
“Pale skin, eyes, Diarrhea

hair”
Tuberculosis (TB)
“Lack of blood”
Malaria
“Underweight”
Pneumonia
1. “Thinness”
“Muscle wasting”
An HIV-infected person is more at risk for malnutrition for the following reasons:
1. Reduced food intake. Adults with HIV/AIDS suffer from appetite loss (anorexia) and have
difficulty eating; thus they eat less and fail to meet their dietary requirements. There are several
reasons for a person to reduce their intake in food. The person may be suffering from an
infection, such as mouth sores or fever. Side effects from medications used to treat an illness
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may cause a reduction in appetite. Depression from dealing with a fatal disease and possible
social stigma can also cause people to lose their appetite and reduce their food intake.
2. Poor absorption. HIV/AIDS affects how the body uses the foods that are consumed, resulting
in poor absorption of nutrients (protein, carbohydrates, fats, vitamins, minerals and water). Poor
absorption of nutrients accompanies diarrhea, which is common with HIV infection. Parasites
like giardia and other infections caused by bacteria and viruses cause diarrhea and reduce
absorption. HIV may also damage intestinal cells that affect the absorption of fats and
carbohydrates. Poor fat absorption also affects absorption of micronutrients like Vitamins A and
E, which are important for the proper functioning of the immune system.
3. Changes in metabolism. With poor nutrient absorption, individuals may not be able digest
foods efficiently and therefore the body may not be able to use the nutrients properly,
particularly fats, carbohydrates and proteins.
4. Chronic infections and illnesses. Fevers and infections that accompany an HIV infection lead
to greater nutrient requirements and poor use of the nutrients by the body. Furthermore, people
who are chronically ill may also have a reduced appetite, which leads to reduced food intake and
weight loss.
The results of these factors include weight loss, loss in lean muscle tissue and increased damage
to the immune system. These factors are most common for adults but they are also prevalent in
children infected with HIV.
A number of other symptoms and illnesses commonly caused by HIV infection have nutritional
consequences that can lead to malnutrition.
Anorexia:
Anorexia, or loss of appetite, occurs during many different infections and when fever is present.
It leads to general weight loss, and is common when individuals are depressed or are living in
socially and emotionally unfavorable environments.
Diarrhoea:
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Diarrhoea occurs when a person has several watery or loose bowel movements in a day. There
are several causes for diarrhea: unclean drinking water, infections, parasites or even some
medical treatments. It results in losses of water, nutrients and minerals and leaves a person at
greater risk of dehydration. Diarrhoea also reduces appetite and leads to poor nutrient
absorption. If diarrhoea continues for a prolonged period of time, it leads to severe malnutrition.
Fever:
Fever means that the body feels warmer than normal. People with fever may have the chills,
sweat more, have muscle and joint aches or be fatigued. Fever is common in people living with
HIV/AIDS, and does not necessarily indicate a serious illness. There are many reasons for fever,
and it is often hard to determine whether fever is due to HIV or to other illnesses such as malaria.
From a nutritional point of view, fever may result in increased nutrient requirements, since the
body utilizes nutrients poorly when fever is present.
Nausea/Frequent Vomiting:
Nausea and frequent vomiting can result from the drugs used to treat HIV/AIDS or from the
opportunistic infections. Nausea also leads to reduced appetite and poor utilization of the food
consumed.
Thrush:
Thrush is a fungal (candida yeast) infection common in HIV-infected people who have damaged
immune systems. Thrush refers to whitish spots on the inside of the mouth, tongue, vagina or
anus. Although these sores are uncomfortable, they are not life threatening. The danger is that
these sores can result in difficulty eating foods, loss of appetite and reduced food intake and thus
lead to weight loss.
Anaemia:
Anaemia results from an inadequate number or quality of red blood cells in the body. This is
most often due to a lack of iron in the diet and to infections such as malaria and hookworm,
which destroy red blood cells and may lead to bleeding and/or loss of blood. Women and
190
children are especially prone to anaemia. Persons who are anaemic often experience tiredness
and weakness and may have pallor
In summary Nutritional Impacts of HIV is as follows:
● Poor food intake
● Poor nutrient absorption
● Disruption of metabolism
● Chronic infection
● Muscle wasting or loss in lean body tissue
Illnesses Associated with Nutritional Impacts
● Anorexia
● Diarrhoea
● Fever
● Nausea
● Thrush
● Anaemia
Excerpted from Network of African People Living with AIDS (November 1997).
Summary of Nutritional Impacts of HIV
(paleness) in the eyes, tongue, palms and nail-beds. The relationship between HIV and anemia is
not clearly understood, although it is known that HIV-infected persons who are anemic generally
progress faster to AIDS than those who are not.
Other Nutritional Impacts of HIV
191
In households with HIV-infected members, others may also experience nutritional impacts,
particularly young children and orphans. Sometimes when adults become infected with the
virus, they are too sick to work and cannot continue to provide for themselves and their families.
This can result in reduced income for the household and hence fewer resources (labor and
money) to obtain food. In addition, other family members suddenly find themselves working
more, either to produce income or to provide care for the HIV-infected individual, which can
also lead to deterioration in nutritional status for themselves and their children.
How to Maintain Good Nutrition
Good nutrition for all individuals, but especially PLWHAs, requires the consumption of an
adequate amount of:
● Macronutrients (proteins, carbohydrates and fats), and
● Micronutrients (vitamins and minerals)
Macronutrients: A deficiency in macronutrients, also known as “protein-energy malnutrition,”

manifests itself in the weight loss and wasting that is typical of AIDS patients. These symptoms
occur as a result of reduced food intake; poor absorption of nutrients; and changes in metabolism
that affect cell growth, enzymatic processes and immune system reactions.
Because of these effects, an HIV-infected person has additional nutrient requirements: 10-15
percent additional energy intake and 50 to 100 percent increase in protein intake as compared to
a non HIV infected person.
Energy Needs
An active non-HIV-infected adult requires approximately 2070 kcal/day.
An HIV-infected adult requires 10 to 15 percent more energy per day (or approximately 400
additional kcal for men and 300 kcal for women).
Protein needs: A non-HIV-infected man requires about 57 grams/day of protein and a woman
requires 48 grams/day.
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An HIV-infected adult needs approximately 50 to 100 percent more protein for a total of 85
grams/day for men and 72 grams/day for women.
Sources: Woods (1999); James and Shofield (1990); WHO (1985).
Micronutrients: Consuming micronutrients (especially Vitamins A, B6 and B12, iron and zinc)
is important for building a strong immune system and fighting infections. For example, Vitamin
A deficiency is associated with higher maternal-child transmission rates, faster progression from
HIV to AIDS, higher infant mortality and child growth failure. The B-group vitamins play
important roles in immune regulations, and deficiencies play a role in disease progression.
Micronutrient consumption can be increased through eating specific foods or through special
supplements. In many settings, establishing home and community gardens to grow local foods
and vegetables is important to improve intake of vitamin and mineral rich foods. Also, raising
small animals (e.g., chickens) should be considered to help improve the consumption of protein,
fat, as well as micronutrients such as iron and Vitamin A.
The impact of taking micronutrient supplements on HIV infection is not well known. The most
promising results are for Vitamin A and the B-group vitamins. Vitamin B6 (niacin) and B12
supplementation have been shown to improve survival and reduce disease progression, although
only in healthy populations where micronutrient deficiencies are not common and when intakes
were high. Vitamin B6 (10 mg daily) supplementation is also recommended for TB patients
being treated with isoniazid. Vitamin A supplementation for children of HIV infected mothers
has been shown to reduce illness, particularly diarrhoea. Vitamin A supplements are also
recommended for mothers immediately after delivery and for infants 6 months and older.
Yet in many African settings, taking micronutrient supplements may be difficult due to lack of
availability and high cost. Establishing links to health services and private-sector sources for a
regular supply of micronutrient supplements is beneficial to communities.
Optimal nutrition helps all people feel better, stay healthier and live longer, whether they are
HIV-infected or not.
Multiple Positive Impacts for PLWHA
193
Adequate nutrition has multiple positive effects for a PLWHA
● Prevents malnutrition and wasting,
● Achieves and maintains optimal body weight and strength,
● Enhance the body’s ability to fight opportunistic infections,
● May help delay the progression of HIV,
● Improve the effectiveness of drug treatments,
● Improve the quality of life.
Safe Hygienic Practices:
Proper Storage and Handling of Food and Water PLWHAs are more vulnerable to infection
because their immune systems have already been weakened. Properly handling food and water
is especially important. Listed below are guidelines for handling water, animal products, fruits
and vegetables and general food storage.
Water
● Be sure water is clean! Boil water for at least 5 - 10 minutes to kill germs.
● Always keep water stored in a container with a lid to cover it.
● Always wash your hands with soap before and after touching foods.
Animal Products
● Cook all animal products (meat, chicken, pork, fish and eggs) at high temperatures until
thoroughly cooked.
● Do not eat soft-boiled eggs or meat that still has red juice.
● Thoroughly wash utensils and surfaces where you placed uncooked foods, particularly meats,
before you handle other foods.
194
● Cover meat, poultry or fish with a clear cover or cloth and keep separate from other foods to
avoid contamination.
Fruits and Vegetables
● Use clean water to thoroughly wash all fruits and vegetables that are to be eaten raw to avoid
contamination.
● If it is not possible to wash fruits and vegetables properly, remove the skin to avoid
contamination.
● Remove the bruised parts of fruits and vegetables to remove any molds and bacteria that are
growing.
General Foods Storage and Handling
● Make sure that the areas where you prepare and eat food are free of flies.
● Cover leftover food to avoid contamination.
● Keep hot foods hot and cold foods cold.
● If food products have expiration labels, do not eat after the “best before” date has expired.
● Store cooked food at most for one day and re-heat before eating.
● If you have a refrigerator, put all leftover foods in refrigerator.
Planning Meals for PLWHAs
Select foods available to the household that can be prepared, cooked and served in a given time.
In planning meals, the following elements should be considered:
● Good nutrient value and variety of the available foods (animal foods, legumes, nuts, fruits,
vegetables, staples and fats);
● The needs of the person(s);
● The time available; and
195
● The costs of foods.
Persons caring for PLWHAs need to plan meals that are adequate and satisfy the needs of the
body. It is estimated that PLWHAs need 10-15 percent additional energy and 50-100 percent
more protein than a non-HIV-infected person. Meals should contribute to good health, be
attractive and stimulate the appetite.
In planning a meal for an HIV-affected household, the following guidelines are useful:
1) Always select body-building foods (such as proteins) to form the core of the meal.
Proteins are the elements that make other cells work and help to absorb all nutrients in the body.
Protein dishes include:
● All legumes such as beans, soya, cowpeas, pigeon peas, groundnuts or peanuts and sauces, and
● Meat (chicken, pork or beef), dairy products, fish, eggs and insects
2) Choose available vegetables, such as carrots, raip and tomatoes. Dark green leafy vegetables
and yellow fruits and vegetables like pumpkin are very important.
3) Use energy foods (such as meals based on cereals, including maize, rice, matooke or banana
and roots and tubers such as cassava) to fill up the body.
4) When possible, increase the energy value during food preparation by, for example,
● Adding sugar to porridge or juice, or
● Adding a teaspoon per person of oil to porridge.
5) Add fruits such as mangos and papayas (paw paw) to enhance nutrient intake.
References
Bijlsma, Marlou. July 2000 (draft). “Nutritional Care and Support for People with HIV: Review
of the Literature, Initiatives and Educational Materials in Sub-Saharan Africa and
Recommendations for Developing National Programmes.” Report to FAO.
196
James, W.P.T., and E. C. Schofield 1990. Human Energy Requirements: A Manual for Planners
and Nutritionists. Oxford: Oxford University Press. Food and Agriculture Organization.
Joint United Nations Program on HIV/AIDS (UNAIDS) and World Health Organization (WHO).
December 2000. AIDS Epidemic Update. Document No.: UNAIDS/00.44E or
WHO/CDS/CSR/EDC/2000.9. Geneva.
Marseille, E., J. Kahn, F. Mmiro, et al. “Cost Effectiveness of Single Dose Nevirapine Regimen
for Mothers and Babies to Decrease Vertical HIV-1 Transmission in Sub-Saharan Africa.”
Lancet. 354, No. 9181, September 4, 1999, p. 803-809.
Ministry of Agriculture, Animal Industry and Fisheries, Republic of Uganda, and United Nations
Development Programme (UNDP). 1998. “Nutrition and HIV/AIDS: A Handbook for Field
Extension Agents.”
National AIDS Control Program, Ministry of Health and Population, Malawi. 2000 (draft).
“Home-Based Care Providers Handbook.” Lilongwe.
Network of African People Living with HIV/AIDS. November, 1997. “A Healthy Diet for Better
Nutrition for People Living with HIV/AIDS.” Nairobi, Kenya.
Piwoz, E.G., and E.A. Preble. November 2000. HIV/AIDS and Nutrition: A Review of the
Literature and Recommendations for Nutritional Care and Support in Africa. Washington, DC:
Academy for Educational Development.
197
Objectives
At the end of the lecture, students should be able to
 Define at least 6 different types of vegetarian diets

 Name at least 6 nutrients to be aware of while following a vegetarian diet
 Name at least 3 major concern throughout the life circle
 Name at least 3 chronic diseases that may improve or be prevented with a
vegetarian diet
Outline:
Introduction
Types of vegetarian diet
Vegetarian nutrition
Vegetarian diets
Health implications of vegetarian diets
Conclusions
References
Appendices
198
INTRODUCTION
There is much interest in a range of dietary practices followed by vegetarians, both in terms of
the nutritional content of vegetarian diets, and health and mortality rates among vegetarians. In
the U.S 3% of adults indicated they never eat meat, poultry and fish/seafood. (Christina N. 2009)
Of this group, one percent also never eat dairy, eggs, and honey. Recent estimates show that
between 3 and 7% of the UK population are vegetarian (Povey et al . 2001; Robinson 2001) and
in parallel with this, there is a growing awareness of the potential benefit of plant based diets
(BNF 2003), and even those who include meat in the diet are advised to eat more plant-derived
foods.
Vegetarianism has become more popular in recent years, and a body of information is now
emerging that provides an insight into the differences between those following an omnivorous
diet and those following plant-based diets. Despite the popular opinion that vegetarianism is a
healthy option, there are some areas for concern and careful planning is necessary to ensure that
the diet is well balanced.
MOTIVE FOR A VEGETARIAN LIFESTYLE
The choice to become vegetarian could be as a result of one or more of the following reasons.
Religious: people at times choose to follow a particular lifestyle option due to their religious
preferences. Various religions promote certain dietary observances due reverence for an animal
e.g. Hindu Indians abhor eating beef because the cow is a sacred animal in their religion. The
Jews practicing Judaism abhor eating pork because they feel it is an unclean animal. The
seventh day Adventist promote a vegetarian lifestyle for its health benefits.
Ethical and ecological issues: wild life promoters and animal lovers for ecological and at times
psychological reasons refrain from consuming animals for food. Some would have only products
that do no harm to the animal e.g. Milk and/or eggs, others would only eat plant products that do
not kill the parent tree e.g. Fruits etc.
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Health: in recent times, animal products have been implicated for certain cancers and non
communicable diseases like gall stones, gout, diverticulitis etc. Health conscious individuals
sometimes choose to become vegetarian for the health benefits it proposes to give. The high
fiber, phyto chemical and anti oxidant content of vegetarian diets marks it out as a health booster.
Other motives include:
Environmental
Animal Welfare
Economical
Sensory and taste preferences
Philosophical teachings
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CLASSES OF VEGETARIAN DIET
Class of Description of dietary pattern

Diet
Demi/semi- Occasionally eats meat/poultry/fish

vegetarian
Pesco- Excludes meat and poultry, but includes fish (and possibly other seafood).
vegetarian
May include dairy products and eggs.
Lacto-ovo- Excludes all flesh foods. Includes dairy produce and eggs.
vegetarian
Ovo- Excludes all flesh foods and dairy produce. Includes eggs.
vegetarian
Lacto- Excludes all flesh foods and eggs. Includes dairy produce.
vegetarian
Vegan Avoids all foods of animal origin.
Macrobiotic 10 dietary regimens of increasing restrictions. Usually vegetarian,
but may eat meat or fish if wild/hunted in the lowest (least restricted) dietary
regimens.Diet is usually based on brown rice with some fruit, vegetables and
pulses.
The final stage of the diet consists of wholegrains and limited liquids.
Fruitarian Diet is usually based on fresh and dried fruits, nuts, seeds and a few
vegetables.
The diet generally consists only of foods that do not kill the plant of origin.
Adapted from Robinson and Hackett (1995).
201
202
The term ‘vegetarian’ encompasses a spectrum of dietary patterns, some of which are more
restrictive than others. Consequently, nutrient intake can vary considerably, depending on which
foods are selected. Even within subgroups, for example lacto-vegetarians, the diets of individuals
within the group may still differ markedly. Nutritional status is at risk when any group of foods
is regularly omitted from the diet, for whatever reason, whether it be an altruistic reason for
avoiding meat, or, in response to an allergy to a particular food, such as cows’ milk. Whatever
the motive for avoiding any food group, care must be taken to ensure that the diet remains
balanced and nutritionally complete so as to avoid any deficiencies and to ensure optimal
nutritional status.
A recent survey of the diets of UK adults (Henderson et al . 2003a, 2003b) showed that meat
and meat products provide a major contribution to a range of nutrients. When meat and meat
products, and other animal derived foods, such as fish, dairy products and eggs, are not eaten, the
nutrients which they contain need to be derived from other sources that are naturally rich in those
nutrients, or are fortified. Compared with omnivorous diets, plant based diets are reported to
contain less saturated fatty acids, animal protein and cholesterol, and more folate, fibre,
antioxidants, phytochemicals and carotenoids (Bingham 1999; American Dietetic Association
and Dietitians Canada 2003).
However, vegans may have low intakes of vitamin B 12 , vitamin D, calcium and iodine.
NUTRITION CONSIDERATIONS FOR VEGETARIANS
Protein: this is the building block for many structural structures of the body. It is important for
growth and development in all stages of life. Therefore an important component of an adequate
diet. Proteins are of two major types, the animal proteins and plant proteins. Plant proteins are
usually limiting in one or more essential amino acid. It is therefore necessary to make good
combinations to provide all essential amino acids if animal proteins are excluded from the diet.
Good Sources of Protein for vegetarians include Beans, Tofu, Veggie burger or other meat
substitutes, Soymilk, Peanut butter and nuts, Dairy products.
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Iron: like protein, animal products contain heam form of iron which is easily absorbed; while
plant sourced iron the non heam form require vitamin C to enhance iron absorption. Other factors
that might affect iron absorption in a vegetarian diet include presence of high fiber and phytic
acid that bind iron, making them unavailable. Good sources of iron include: enriched bread and
cereal, whole wheat bread and other whole grains, dried apricots, figs, prunes, leafy green
vegetables, tomato juice, beans, nuts, soybeans and tofu. Vitamin C rich foods include: melons,
citrus fruits, pineapple, strawberries, kiwi fruit, broccoli, peppers, tomatoes.
Zinc: absorption of zinc is also impaired by phytate in plant based foods. Good sources of zinc
include: Soybeans and other beans, whole grains (refined grains don't have it unless they are
fortified) and foods like nuts, seeds, fortified ready-to-eat cereals, and nut and seed butters.
Breads are better sources of zinc than crackers or muffins because yeast makes zinc more
absorbable.
Calcium: Good sources of calcium are dairy products, green leafy vegetables such as Bok choy,
Broccoli, Chinese/ Napa cabbage, Collards, Kale, Okra, Turnip greens, calcium fortified orange
juice, calcium-fortified soymilk and calcium-set tofu. Calcium is an essential component of
bones and teeth. It is of paramount importance in planning of meals for children, pregnant and
lactating mothers and the elderly.
Vitamin D: vitamin D is also necessary for strong bones and teeth. Good sources include
fortified cereals, fortified soy milk, fortified orange juice, egg yolks, cow’s milk
Vitamin B12: Vitamin B12 is necessary for energy metabolism. Good sources include fortified
breakfast cereals and some brands of soymilk, some brands of nutritional yeast are rich in
vitamin B12 (Red Star Vegetarian Support Formula), cow’s milk, eggs.
Vitamin A/Beta carotene: vitamin A is needed for good eye sight and a fat soluble vitamin.
Presence of fat is necessary for proper absorption. Good sources of vitamin A and beta-carotene
include apricots, cantaloupe, mango, pumpkin, butternut squash, sweet potatoes, spinach, carrots
Omega-3 fatty acids: good sources of omega 3 fatty acids include Flaxseeds and flaxseed oil,
canola oil, soybeans and soybean oil, tofu, walnuts and walnut oil.
Iodine: good sources of iodine include dairy products, seafood, iodized salt.
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VEGAN FOOD PYRAMID
Adapted from J Am Diet Assoc. 2003;103:771-775)
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VEGETARIAN DIETS
 A well-balanced vegetarian diet can provide adequate amounts of all of the nutrients
required by the body throughout the lifecycle. However, more attention and careful
dietary planning may be required for specific vulnerable subgroups.
 Restrictive dietary patterns, such as some extreme macrobiotic diets, have been found to
lead to poor growth and malnutrition; such diets are not recommended for infants and
children.
Infancy and childhood
 Lacto- and lacto-ovo-vegetarian diets can be completely adequate during infancy and
childhood.
 Weaning should follow the same principles as for nonvegetarian infants.
 Careful dietary planning is needed for infants who are weaned onto vegan diets to ensure
that adequate energy, essential fatty acids, protein, calcium and foods fortified with
vitamin B12 (or supplements), are included.
Demerits:
 large quantities of raw or cooked fruits and vegetables, and water-based cereal ‘gruels’
such as
 ‘kokoh’ (a dilute porridge made from ground rice, wheat, oats, beans and sesame flour,
which is often used as a weaning food in macrobiotic infant diets)
 Are bulky and can lead to reduced energy density of the diet, and the presence of high
levels of phytate in these foods may have an adverse effect on the mineral content of the
diet.
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Important dietary considerations:
 It is recommended that all children under 2 years of age (and up to 5 years of age if
nutritional status is low) receive supplements of vitamin drops containing vitamins A, C
and D.
 Foods fortified with vitamin B12 should be included in a vegan diet and, if necessary, a
vitamin B12 supplement.
 Restrictive dietary patterns such as some macrobiotic diets, characterised by a reluctance

to use proprietary infant formulae, fortified foods and vitamin supplements could lead to
lower weight gain in children compared with the omnivorous infants, and slower motor
and language development .
 In the absence of supplementation with Vitamin D, there should be regular inclusion of

oily fish.
 If dairy product is excluded for a child's diet, the infant diet need to be combined with the
use of calcium-fortified products and caution with use of high fibre cereal foods.
 Ensure adequate vitamin B12 intakes, the use of foods fortified with B12 and/or B12
supplements is strongly advised.
Pregnancy and lactation
 Particular attention to dietary requirements for vitamins and minerals is needed during
pregnancy and lactation.
 Guidelines on what to eat during pregnancy and lactation are essentially the same for
vegetarians as for meat-eaters.
 Women on restricted diets may need to consume supplements or fortified food in order to
meet these needs.
Athletics
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 Data on the effects of a vegetarian diet on athletic performance are few.
 It is therefore important for female vegetarian athletes to eat sufficient iron-containing

foods and foods that promote absorption of iron.
 A poorly planned vegetarian diet can have an adverse effect on physical performance and
long-term health.
Elderly
 A well-planned vegetarian diet can easily provide all the nutrients needed by elderly
people.
 Particular attention should be paid to mineral adequacy, folate, vitamin B12 and vitamin
D, especially for elderly vegetarians and vegans who are housebound or living in an
institution.
Health implications of vegetarian diets
 Well-balanced vegetarian diets reduce risks of many chronic diseases, and may treat,
improve or reverse obesity, heart disease, high blood pressure, type 2 diabetes, and some
digestive problems. They also offer promise in treatment for cancer and kidney disease.
Overweight / Obesity
 The high fiber and nutrient density (more nutrients for fewer calories) of vegetarian diets
may support healthy weight loss.
 The fiber in beans, whole grains, fruits and vegetables may slow eating speed and food
intake, which may provide longer-term fullness after meals; nutrient density may help
limit hunger and cravings.
 Since obesity is a risk factor for most conditions discussed below, losing weight aids
treatment of these other conditions.
Heart Disease
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 Vegetarian diets help treat heart disease by addressing obesity, and the low saturated fat
content of plant foods helps the body reduce cholesterol production.
 Eating foods with soluble fiber, in foods like beans, barley, oats, and apples, reduces
blood cholesterol levels.
 Plants contain thousands of phytochemicals and healthy oils that limit key steps in the
disease process, thus reducing risk of heart attack and stroke.
Type 2 Diabetes
 Weight loss helps treat diabetes as well; in fact, losing only 5-10% of your body weight
tends to lower blood sugar.
 The high fiber content found in a vegetarian diet helps control blood sugar swings after
meals, and the resulting fullness helps control portions, hunger cravings, and blood sugar
spikes.
 Eating more whole grains may also supply greater amounts of nutrients essential to help
your body use blood sugar more efficiently.
Hypertension
 Losing weight also reduces blood pressure.
 Choose unprocessed plant foods as they are naturally low in sodium. Emphasize home-
prepared foods with minimal added salt or salty ingredients.
 Reduce high-sodium foods like bread, breakfast cereals, cheese, bottled sauces, salad
dressings, soups, processed foods and restaurant meals.
 Additionally, most fruits, vegetables and especially beans are high in potassium,
magnesium and other compounds that help support healthy blood pressure.
Constipation and Diverticular Disease
 High fiber foods reduce constipation and result in regular, smooth bowel movements.
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 Soluble fiber attracts water to the colon, making stools soft and easy to pass, and supports
healthy gut bacteria.
 It also helps to trap small inedible food particles that may otherwise become trapped in
these pouches, causing pain and inflammation of diverticulosis, an out-pouching of the
colon wall from using excessive force to move the bowels.
 Movement of stool is further enhanced with insoluble fiber found in the more sturdy parts
of plant foods.
Chronic Kidney Failure
 Diabetes and hypertension together significantly increase risk for chronic kidney disease.
 When vegetarian diets reduce blood sugar and blood pressure, kidney disease prognosis
improves, more so in early on-set cases.
 A well-planned vegetarian diet is lower in protein and sodium and that limits further
damage and may slow disease progression.
Cancer
 Nutrition guidelines for cancer recovery from national and worldwide cancer research
focus on prevention strategies of dietary principles: whole grains, beans, fruits and
vegetables, and significantly limit red and processed meats.
 This approach also helps cancer patients who are obese or have heart disease. While
research is ongoing, no data on cancer remission or death rates are available yet.
 Despite exaggerated concerns about the use of soy foods during breast cancer recovery,
research now shows either no effect or small benefits.
SUMMARY
 Well-designed vegetarian diets can help to reverse major chronic diseases, or at least
limit the damage from these diseases.
210
 The potential benefits of using a well-balanced vegetarian diet as primary or adjunct
therapy for chronic disease are almost unlimited.
 A registered dietitian nutritionist (RDN) can help you develop a healthy vegetarian
dietary plan that meets your needs.
CONCLUSION
 There is no evidence that being vegetarian per se confers a protective effect.
 More research is needed to establish whether vegetarianism has a role to play in

protection against a range of other diseases that are less prevalent amongst vegetarian
populations.
 Following a vegetarian diet does not automatically equate to being healthier; vegetarians
and meat-eaters alike need to be mindful of making appropriate dietary and lifestyle
choices.
211
REFERENCES
 American Dietetic Association and Dietitians Canada (2003) Position of the American
Dietetic Association and Dietitians of Canada: vegetarian diets. Journal of the American
Dietetic Association 103 (6): 748–62.
 BNF (British Nutrition Foundation) (2003) Plants: Diet and Health. The Report of the
British Nutrition Foundation Task Force. Blackwell Publishing, Oxford.
 British Nutrition Foundation (2005) Vegetarian nutrition. Briefing paper Nutrition

Bulletin, 30, 132–167
 Bingham S (1999) High-meat diets and cancer risk. Proceedings of the Nutrition Society
58: 243–8.
 Henderson L, Gregory J, Irving K et al. (2003a) The National Diet and Nutrition Survey:
Adults Aged 19–64 Years. Volume 2: Energy, Protein, Carbohydrate, Fat and Alcohol
Intake. HMSO, London.
 Henderson L, Irving K, Gregory J et al. (2003b) The National Diet and Nutrition Survey:
Adults Aged 19–64 Years. Volume 3: Vitamin and Mineral Intake and Urinary Analytes.
HMSO, London.
 Robinson F & Hackett A (1995) Vegetarianism: What’s in a name? Vegetarianism and

Health: a Discussion of Current Ideas. Liverpool John Moores University, Liverpool.
212
CORONARY HEART DISEASE
BARIATRIC SURGERY
MICRONUTRIENT DEFICIENCY
BY
DTN. IGBANUGO VIVIAN
213
CORONARY HEART DISEASE
CORONARY HEART DISEASE (CHD) is also known as ISCHEMIC HEART DISEASE

(IHD) and CORONARY ARTERY DISEASE (CAD).
Coronary Heart Disease is when your coronary arteries become narrowed by a gradual build – up
of fatty materials within their walls. Coronary arteries are the arteries that supply the heart
muscle with oxygen – rich blood. The condition whereby the walls of the coronary arteries
become narrowed by the gradual build – up of fatty material is called arterosclerosis and the
fatty material is called atheroma.
In time the arteries may become so narrow that they cannot deliver enough oxygen – rich blood
to the heart. The pain and discomfort is called angina (chest pain).
If a piece of the artheroma breaks off, it may cause a blood clot (blockage) to form. This may
block the coronary arteries and cut off the supply of oxygen to the heart muscle, the heart may
become permanently damaged. This is known as heart attack.
Risk factors of coronary heart disease
 A risk factor is something that increases the likelihood of getting a disease.

 Smoking
 High blood pressure
 High blood cholesterol
 Diabetes
 Physical inactivity
 Overweight or obesity
Family history of heart disease
 Ethnic background
 Sex – men are more likely to develop coronary heart disease at an earlier age than women
 Age – the older one gets, the more likely one is to develop coronary heart disease
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 Even if there is already have a heart condition, it is important to protect the heart by
living a healthy lifestyle by
 Healthy eating – a healthy diet can help reduce the risk of developing coronary heart
disease and stop weight gain, reducing the risk of diabetes and high blood pressure. It can
also help lower the cholesterol levels and reduce the risk of some cancers.
A healthy diet can benefit the heart even if there is already a heart condition
 Eat adequate diet -

 Eat plenty of fruits and vegetales
 Choose whole grain legumes and cereals
 Choose low fat milk and diary products
 Eat non – fatty meat, fish and eggs, beans and other non dairy sources of protein
 Avoid drinks high in sugar and foods high in fat
Fats
Choose the right type of fats.
 Replace saturated fats with small amounts of mono and poly unsaturated fats.
 Cut down on foods containing trans – fats. All fats and oil are high in calories so even the
unsaturated fats should only be used in small amounts.
 Too much saturated fat can increase the amount of cholesterol in the blood which can
increase the risk of developing coronary heart disease.
 Trans – fat can also raise the amount of cholesterol in the blood.
Salt
1. Eating too much salt can increase the risk of developing high blood pressure which increases
the risk of developing coronary heart disease.
2. Reduce alcohol intake
3. Stop smoking – this can help to lower the cholesterol and improve the heart health.
4. Be physically active
5. Controlling blood sugar and blood cholesterol
6. Maintaining normal blood pressure
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ATHEROSCLEROSIS
Atherosclerosis is a potentially serious condition where arteries become clogged up by fatty
substances known as plaques or atheroma. The plaques cause the affected arteries to harden and
narrow. Restricted blood flow can damage organs and stop them functioning properly. If a
plaque ruptures, it can cause a blood clot which can block the blood supply to the heart triggering
a heart attack or it can block the blood supply to the brain triggering a stroke.
Cholesterol is a fatty substance carried around the body by proteins. When cholesterol and
proteins are combined, they are called lipoproteins.
There are two major cholesterol
1. Low – density lipoprotein (LDL) cholesterol which is known as the bad type of
cholesterol. LDL cholesterol carries cholesterol from the liver to the cells that need it.
2. High – density lipoprotein (HDL) is known as the good type of cholesterol. HDL carry
cholesterol away from the cells and back to the liver to be broken down. Too much LDL
(bad cholesterol) in the blood can cause fatty materials to build up in the walls of the
artery. The risk is very high if there is high level of LDL and low level of HDL.
Cholesterol is measured in units called millimols per litre of blood (mmol/L).
Total cholesterol should be under 4mmol/L especially if there is a risk of heart and circular
disease.
LDL should be under 2mmol/l
HDL should be above 1mmol
Triglyceride is another type of fatty substance in the blood. Like LDL, triglycerides are also
bad. They are found in foods such as dairy products, meat, cooking oils. They can also be
produced in the body either by the body’s fat stores or in the liver.
Ideally, triglyceride levels should be less than 1.7mmol/L. High triglycerides predispose one to
cardiovascular diseases.
Being overweight or obesity, fatty foods, sugary foods, fatty meats, fatty foods, lead to high
triglyceride level. Smoking, physical inactivity, kidney or liver diseases can lead to high
triglycerol as well as familial hypercholesterolemia (FH) can also cause exceptionally high
cholesterol even if you have a healthy lifestyle.
216
Familial hypercholesterolemia FH, is a genetic condition resulting in exceptionally high levels of
cholesterol in the blood.
Familial hypercholesterolemia is an inherited condition and one might have had high cholesterol
from birth. There is a higher risk of having heart disease at an early age if left untreated. In FH,
the liver cannot remove enough of the bad cholesterol LDL from the blood, so the LDL remains
high. This can cause gradual build – up of fatty materials (antheroma) in the coronary arteries.
Foods high in saturated fat can increase the risk of atherosclerosis.
Dietary Risks of atherosclerosis

Diet is used to minimize the risk of atherosclerosis by avoiding foods that could clog the arteries.
 Cholesterol: High fat dairy products or egg y[ok, animal protein, liver , shellfish and
other meats. Daily dose cholesterol should not be more than 300mg a day.
 Saturated fats: products such as hot dogs, high fat dairy products or animal products
such as beef, sausages and bacon all contain saturated fats.
 Trans fats should be avoided completely. Trans fats are found in margarine, processed
snacks and baked goods.
 Sodium: should be less than 2.3 mg of sodium a day.
Recommended foods
 Good fats – All fats are high on calories. Foods containing polyunsaturated and
monounsaturated fats can help cholesterol levels. Pecans, avocados, almonds,
walnuts, olives, olive oil and peanut oil.
 Fish: Fish are great sources of proteins and omega-3 fatty acids that help lower the
blood triglycerides. Cod fish and tuna fish have less fat than poultry or red meat.
Salmon, sardines are rich with omega-3 fatty acids which promote heart health.
 Healthy carbohydrates: fruits and vegetables, whole grains and legumes (peas,
beans and lentils), low – fat dairy products.
 Fiber rich foods: such foods can help decrease the risk of atherosclerosis. Foods rich
in fiber are whole wheat flour, wheat bran, nuts and legumes.
Physical activity also helps to reduce coronary heart diseases.
Medical Nutrition Therapy
217
High fiber, low fat, low sodium (<2g/day) is recommended. Not more than 6g a day as too much
salt increases blood pressure.
6g salt = 1 teaspoon full
Bariatric Surgery
Bariatric Surgery (weight loss surgery) includes a variety of procedures performed on people
who have obesity. Weight loss is achieved by reducing the size of the stomach with a gastric
band or through removal of a portion of the stomach (Sleeve gastrostomy or biliopancreatic
diversion with duodenal switch) or by resecting and re-routing the small intestine to a small
stomach pouch (gastric bypass surgery). Long term studies show that the procedures cause
significant long term loss of weight, recovering from diabetes, improvement of cardiovascular
risk factors and a reduction in mortality from 40% to 23%. The U.S National Institutes of Health
recommends bariatric surgery for obese people with BMI of at least 40 and for people with BMI,
of at least 35 and serious coexisting medical condition such as diabetes. The recent guidelines
suggest that any patient with a BMI of more than 30 with comorbidities is a candidate for
bariatric surgery.
Indication
A medical guideline by the American College of physician concluded that Surgery should be
considered a treatment option for patient with a BMI of 40kg/m², or more who instituted but
failed an adequate exercise and diet program and who present with obesity-related comorbid
condition such as hypertension, impaired glucose tolerance, diabetes mellitus, hyperlipidemia
and obstructive sleep apnea. A doctor-patient discussion of surgery should include the long term
side effect, such as possible need for reoperation, gall bladder diseases and malabsorption.
Adverse Effect of Bariatric surgery
A study of insurance claim of 2522 people who had undergone bariatric surgery showed 21-9%
complication during the initial hospital stay and a total of 40% risk of complication in the
subsequent 6 months. This was more in those over 40years and led to an increased health care
expenditure.
Common problem were:
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1. Gastric dumping syndrome in about 20% (bloating and diarrhoea after eating,
necessitating small meal or medication)
2. Leaks at the surgical site (12%)
3. Incisional hernia (7%)
4. Infection (6%)
5. Pneumonia (4%)
The rate of complications appears to be reduced when the procedure is performed by an

experienced surgeon.
6. Metabolic bone disease manifesting as osteopenia and secondary hyper-parathyroidism

have been reported after Roux-en-y gastric by pass surgery due to reduced calcium
absorption. The highest concentration of calcium transporters is in the duodenum. Since
the ingested food will not pass though the duodenum after a bypass procedure, calcium
levels in the blood may decrease causing secondary hyperparathyroidism, increase in
bone turnover, and a decrease in bone. Increased risk of fracture has also been linked to
bariatric surgery. Rapid weight loss after obesity surgery can contribute to the
development of gall stones as well as increasing the lithogenicity of bile.
Adverse effects on the kidneys have been studied:
1. Hyperoxaluria that can potentially lead to oxalate nephropathy and irreversible renal
failure is the most significant abnormality seen on urine chemistry studies
2. Rhabdomyolysis leading to acute kidney injury and impaired renal handling of acid and
base has been reported after bypass surgery
Nutritional derangements due to deficiencies of micronutrients like iron, vitamin B12, fat
soluble vitamins, thiamine and folate are especially common after malabsorptive bariatric
procedures.
Seizures due to hyperinsulinemic hypoglycemia have been reported. Inappropriate insulin

secretion secondary to islet cell hyperplasia called pancreatic nesidioblastosis might explain this.
A study published in JAMA-surgical reports that self-harm behaviors and suicide are increased
in those having bariatric surgery.
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Eating after bariatric Surgery immediately after bariatric surgery, the patient is restricted to
clear liquid diet which includes foods such as clear broth, diluted fruit juices or sugar-free drinks
and gelatin desserts. This diet is continued until the GIT has recovered somewhat from the
surgery.
Blended or puréed sugar-free diet for at least 2 weeks
This may consist of high protein liquid or soft foods such as protein shakes, soft meat and dairy
products. Foods high in carbohydrates are usually avoided when possible. Post-surgery over
eating is curbed because exceeding the capacity of the stomach causes nausea and vomiting.
Diet restriction after recovery from surgery will depend on the type of Surgery. Many patients
will need to take a daily multi vitamin pill for life to compensate for reduced absorption of
essential nutrients because patients cannot eat a large quantity of food. A diet that is relatively
high in protein, low in carbohydrate, low in fat and low in alcohol is recommended.
Fluid recommendation
It is very common within the first month post surgery for a patient to undergo volume depletion
and dehydration. Patients have difficulty drinking appropriate amount of fluids as they adapt to
their new gastric volume.
Limitation on oral fluid intake, reduced calorie intake and a higher incidence of vomiting and
diarrhoea are all factors that contribute to dehydration. In order to prevent fluid volume depletion
and dehydration a minimum of 1.4-1.9 litres should be taken in small sips all day.
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MICRONUTRIENT DEFICIENCY
Micronutrient deficiency is a lack of essential vitamin and minerals
required in small amount by the body for proper growth and development. Micronutrients
include: Vitamin A, B, C and D, Calcium, Folate, Iodine, Iron, Zinc
Iron deficiency
Iron deficiency is the most common form of malnutrition worldwide. A lack of iron in the diet
results in iron deficiency.
What is iron?
Iron is a micronutrient that is essential to the structure of every cell in the body, particularly the
red blood cells (Hemoglobin) which transport oxygen in the blood to the tissues of the body. Iron
is also a key component of protein in muscle tissue and is critical for the normal development of
the central nervous system.
Iron rich foods are
 Meat, poultry fish

 Fortified cereals and oatmeal
 Legumes (e.g. soybeans and lentils)
 Leafy green vegetables
 Seeds (e.g. sesame and pumpkin)
Lack of iron causes iron Deficiency Anaemia (IDA)
Iron Deficiency
This is when the iron stored away for later use is reduced as indexed by a low ferritin level
Treatment
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1. Oral iron supplement can be used for both prevention and treatment of IDA. Oral iron
supplements are usually best absorbed on an empty stomach. However because iron can
irritate a Childs stomach, supplements may need to be taken with food.
2. Eat iron rich foods
3. Vitamin C enhances iron absorption eg a citrus juice. It usually takes months of iron
supplementation to correct the IDA.
Iodine Deficiency
Goitre iodine deficiency is the worlds most common but preventable cause of mental retardation
a lack of iodine in the diet can affect the thyroid gland function resulting in a condition called
goitre.
What is Iodine?
Iodine is a nutrient essential for normal functioning of the thyroid gland, production of thyroid
hormone and metabolism. Iodine is typically found in small ants, in foods and varies depending
on environmental factors such as soil concentration of iodine and the use of fertilizers.
Sources of dietary iodine: Fortified Bread, Iodized table salt, Dairy products eg cheese, yoghurt
cow milk, Egg, Soy milk and soy sauce, Shell fish.
What is Iodine deficiency?
Iodine is not produced by the body, so it must be obtained through the diet. Sufficient thyroid
hormone is not produced without enough iodine. Iodine deficiency can lead to goitre
(enlargement of the thyroid gland)
Hypothyroidism
Mental retardation in infants &children whose mothers were iodine deficient during pregnancy
TREATMENT
1. Iodized salt
2. Iodized oil
3. Iodized water have been effective in preventing iodine deficiency
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4. Consuming foods high in iodine can help treat and prevent iodine deficiency.
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VITAMIN D DEFICIENCY – RICKETS
Vitamin D is a fat soluble vitamin naturally produced by the body. It is essential in the
absorption of calcium for proper bone development and function. Vitamin D is found in Cod and
cod liver oil, Egg yolks, Milk and butter, Salmon and shrimp and fortified cereals. Vitamin D
deficiency can lead to abnormalities in bone development and a condition in children called
rickets, in which bones are not mineralized. In rickets bone become soft and may bend, distort
and or fracture eg bow leg and K leg. Rickets is one of the most common children diseases in
many developing countries.
TREATMENT OF RICKETS
1. Vitamin D supplementation
2. Increasing dietary intake of calcium, phosphate and vitamin D
3. Daily exposure to small of sunlight (15 minutes/day for lighter skinned children)
4. Special braces to position the bones (severe cases)
5. Surgery (for very severe skeletal deformities)
SELENIUM
Selenium is a trace mineral needed by the body in small amounts for good health. Selenium is
incorporated into protein to make antioxidant enzymes. These enzyme help prevent cellular
damage from free radicals that can cause the development of chronic diseases such as cancer and
heart diseases
Food sources of selenium
1. Brazel nuts
2. Canned tuna and cod
3. Beef and poultry
4. Enriched pasta and rice
5. Eggs
6. Cottage cheese
7. Oatmeal
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What is Selenium Deficiency?
Selenium deficiency is a result of too little selenium in the diet
Though rare, it can lead to 3 specific diseases
1. Keshan Disease – results in an enlarged heart and poor heart function in selenium-
deficient children
2. Kashin-Beck Disease results in osteoarthritis and weakened immune system in children.
3. Myxedematous Endemic Cretinism results in mental retardation in infants born to
mothers deficient in both selenium and iodine
Treatment
Selenium supplementation protects people from developing keshan disease but cannot reverse
heart muscle damaged once it occurs. There is little evidence that improving selenium nutritional
Kashin–Beck disease.
Vitamin A – Night Blindess
Is a group of compound that play significant role in vision, bone development, immune support
and normal bodily foundation
Retinol and beta-carotene are forms of pre-vitamin A which are converted to vitamin A in the
body.
Food sources of vitamin A include: Eggs, Milk and butter, Liver, Fish (eg heiring, sardines, and
tuna. Sources of beta carotene include spinach, Carrots, Orange and Sweet potatoes.
What is vitamin A deficiency? This exists when a child regularly fails to eat sufficient amounts
of vitamin A or beta-carotene which leads to low levels of blood serum vitamin A. Serious lack
of vitamin A leads to Night blindness
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Treatment
The night blindness associated with vitamin A deficiency can be reverse with treatment. Total
blindness however cannot be reversed or treated
Treatment for vitamin A deficiency
1. Oral and injectable supplementation

2. Food fortification eg fortifying veg oil
3. Increasing consumption of vitamin A rich foods both animal and fruits and vegetables
VITAMIN B12 DEFICIENCY Pernicious Anaemia
Vitamin B12 is a water soluble vitamin that exists in several forms. Vitamin B12 is needed for
proper red blood cells formation and the maintenance of healthy nerve cells. It is also essential to
making DNA, the genetic material in cells. Vitamin B12 is found in fortified cereals and in foods
from animal origin such as fish, meat, poultry, Eggs milk and milk product
What is vitamin b12 deficiency?
Vitamin B12 deficiency results from inadequate dietary intake or impaired absorption
Treatment
1. Supplements or oral pills, under the tongue pills, liquid, nasal sprays or injection
2. Increased consumption of animal products
FOLATE
Also known as vitamin B9 is a water soluble vitamin naturally found in foods. Folate is
necessary for the production and maintenance of new cells. It is essential important during
periods of cell division and growth such as infancy and pregnancy. Both adults and children need
folate to make normal red blood cells and prevent anaemia.
Food sources of folate are leafy green vegetable eg (Spinach and turning greens), Peas and
Beans, Fruits and vegetables. Folic acid (synthetic folate) in commonly added to enrich grain
products such as cereals, Rice, Pasta, Bread, Flour.
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Megalobastic anaemia.
Folate deficiency can slow growth rate in infants and children. Advanced folate deficiency can
lead to anaemia in adults.
Treatment
Supplementation of the diet with vitamins and foods rich in folate or folic acid can help prevent
and treat folate deficiency
ZINC
Zinc is an essential mineral found in over 200 enzymes that are involved in a wide range of
function in the body. This zinc – containing enzymes play a role in immune function wound
healing and making other proteins. Zinc supports normal growth and development during
childhood and adolescence and is required for proper sense of taste and smell
Foods sources of zinc include: Meats, Sea foods (eg crabs, shrimp, crayfish), Eggs, Whole
grains and oats, Nuts and seeds eg walnuts, tiger nuts leafy green vegetable, Yoghurt. Because
zinc play so many roles on the body including brain development a deficiency of zinc can impact
multiple bodily function and result in a wide variety of symptoms such as Dandruff, eczema and
skin rashes, Behavioral and sleep disturbances, Delayed would healing, Joint pain, Growth
retardation, Hair loss, Hyperactivity, Increased allergic sensitivity, Inflammatory bowed disease
and diarrhea, Loss of appetite, Mild anaemia, Poor nail growth, white spots on fingernails and
transverse lines on finger nails and Hang nails.
Risk factors
Low intake of dietary zinc, intestinal parasites, intake of foods that prevents zinc absorption (eg
foods high in iron, calcium, vitamin D and fibre)
Treatment
Zinc deficiency can be managed
1. By supplements (zinc sulfate or zinc gluconate
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2. Increasing dietary intake vitamin and mineral supplement to aid zinc absorption (egVit A,
E, B6, Mg, P and Ca)
FOLATE
Folate (vitamin B9) in involved is cell multiplication and tissue growth (through methylation of
nucleotides). It functions closely with vitamin B12 in protein synthesis and metabolism.
Prevalence of deficiency
Folate deficiency is more prevalent in populations who consume large amounts of refined cereals
(which are low in folate) and small amounts of leafy greens and fruits (which are high in folate)
E.g. in Germany, lacto-ovo vegetarian (vegetarian who also consume eggs and dairy) had higher
levels of red blood cell folate than non-vegetarian. This findings was likely due to a high
consumption of folate- rich vegetables by the vegetarian
- Malabsorption and infection with intestinal parasites

- Genetic disorder of folate metabolism
Bacterial over growth
Deficiency of folate
- Megaloblastic anaemia (low hemoglobin with large immature red blood cells
- Increase susceptibility to infection decreased blood clotting, intestinal malabsorption
- Risk for cardiovascular disease (associated with increased homocysteine levels)
- Neural tube defects in infants exposed prenatally (soon after conception) to inadequate
folate
- Birth defects in infants exposed prenatally (eg oro-facial clefts)
- Cognitive impairment
- Depression
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NUTRITIONAL GENOMICS
NUTRITION IN CRITICAL CARE
BY
DTN ENUKA H.C
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INTRODUCTION
Nutrition and genetics both play an important role in human health as well as the development of
chronic diseases such as cancer, osteoporosis, diabetes and cardiovascular disease.
Nutrigenomics describes the scientific approach that integrates nutritional sciences and genomics
and includes the application of other high-throughput ‘omics’ technologies such as
transcriptomics, proteomics and metabolomics to investigate the effects of nutrition on health.
The purpose of this bulletin is to describe the current state of knowledge using key examples and
assess the potential role of nutrigenomics in developing personalized dietary advice tailored to an
individual’s unique genetic profile.
Variability between individuals in response to dietary intervention is a well-known phenomenon
in nutrition research and practice (Ordovas 2008). For example, the effect of dietary changes on
phenotypes such as blood cholesterol, body weight and blood pressure can differ significantly
between individuals (Ordovas et al.2007). There are many factors that can influence the response
to diet such as age, sex, physical activity, smoking and genetics. The goal of personalized
nutrition is to identify individuals who benefit from a particular nutritional intervention
(responders), and identify alternatives for those who do not (non-responders).
Individuals should no longer be subjected to unnecessary diets they find unpleasant and
ineffective when there may be an alternate dietary approach that is more effective. Personalized
nutrition could be useful in both the prevention and treatment of chronic diseases by tailoring
dietary advice to an individual’s unique genetic profile.
The daily ingestion, absorption, digestion, transport, metabolism and excretion of nutrients and
food bioactives involve many proteins such as enzymes, receptors, transporters, ion channels and
hormones. Variations in genes encoding proteins that affect any of these processes can alter both
the amount of the protein produced as well as how well that protein functions. If a genetic
variation leads to altered production or function of these proteins then nutritional status might be
affected. The study of the relationship between genes and diet is called nutrigenomics (or
nutritional genomics), which is an umbrella term for two complimentary approaches: how
nutrients affect gene function and how genetic variation affects nutrient response. The latter is
sometimes referred to as nutrigenetics (El-Sohemy 2007), and includes the study of how genetic
variations affect food intake and eating behaviours (Eny and El-Sohemy 2010; Garcia-Bailo et
al. 2009).
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Although the term nutrigenomics is relatively new, the concept has been around for some time.
Perhaps the most familiar example is lactose intolerance, which is a condition resulting from an
inadequate production of lactase in the small intestine due to genetic variation in the lactase gene
(Swallow 2003). Individuals with lactose intolerance are unable to efficiently break down the
primary milk sugar (lactose) from dairy products. Consequently, the dietary recommendation is
to limit lactose-containing foods or to use lactase supplements or lactose-free dairy products to
prevent gastrointestinal discomfort (Swagerty et al. 2002). Phenylketonuria (PKU) is an inborn
error of metabolism, which represents another classic example of nutrigenomics. PKU can result
from a genetic variation in phenylalanine hydroxylase (the enzyme needed to convert
phenylalanine to tyrosine), which leads to a decrease in phenylalanine hydroxylase activity
(DiLella et al. 1986). Individuals with PKU can develop neurological damage (severe mental
retardation and seizures) from excess phenylalanine (Surtees and Blau 2000) unless they follow
the recommended low-phenylalanine diet (National Institutes of Health Consensus Development
Conference Statement: Phenylketonuria: screening and management, October 16-18, 2001).
Lactose intolerance and PKU are examples that involve a single genetic defect along with a
single dietary exposure. A major challenge of nutrigenomics, however, is to identify gene-
nutrient interactions that affect complex polygenic disorders such as obesity, diabetes, cancer and
cardiovascular disease that take several years – or even decades – to develop and have
multifactorial etiologies.
As such, it is often difficult to determine the role of specific dietary factors and gene variants in
the development of these diseases. The concept of diet-gene interactions involves a genetic
variant modulating the effect of a dietary factor on a specific phenotype or health outcome
measure such as serum lipid concentrations, high blood glucose or obesity. Conversely, diet-gene
interactions can refer to the dietary modification of the effect of a genetic variant on the
phenotype or health outcome measure (Ordovas 2008).
A major goal of nutrigenomics is the prevention of the onset and progression of chronic disease.
Research strategies currently contribute to this goal by building the body of evidence linking
nutrients to metabolic pathways that affect disease outcomes. The incorporation of genetics into
nutritional epidemiologic studies aims to improve their consistency. Current research could lead
to the development of personalized nutrition guidelines for individuals and specific sub-
populations, which could decrease the risk of chronic diseases.
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DEFINITIONS AND PRINCIPLES
Nutrigenomics is both the examination of how nutrients affect genes (i.e. influence gene
expression and function) and how genes affect diet (i.e. what an individual eats and how an
individual responds to nutrients), with the latter sometimes being referred to as nutrigenetics.
Nutrigenomics can include the full spectrum of research strategies from basic cellular and
molecular biology to, clinical trials, epidemiology and population health. These different
experimental approaches can be used to improve our understanding of how nutrition affects
various health outcomes, and current trends in personalized nutrition have focused on the role of
genetic variation to understand why some individuals respond differently from others to the same
nutrients consumed.
Genes are segments of DNA that contain the information for making a specific protein. The gene
is the functional and physical unit of heredity passed from parent to offspring. When variations
in the DNA occur the result can be changes to the structure and function of the protein. There are
several different types of genetic variations, including single nucleotide polymorphisms (SNPs),
which are alterations in a single nucleotide.
Alleles are the variant forms of a gene at a particular location on a chromosome.
The genotype is the genetic identity of an individual for a genetic site, determined from the
combination of maternal and paternal alleles. Genotypes do not necessarily show as outward
characteristics, and as such are different from phenotypes.
A phenotype is an observable trait in an individual such as hair color, high blood sugar
concentrations, or the presence of a disease. Individuals with the same genotype may have
different phenotypes, in part, because of their different environments.
A haplotype is a group of alleles that are inherited together and, therefore, groups of genetic
polymorphisms are often inherited together.
Using examples of specific dietary factors such as alcohol, caffeine, fat, and fruits and
vegetables, this lecture will highlight the importance of incorporating genetics into the field of
nutrition and also address some of the questions and methods associated with the development of
personalized nutrition.
ALCOHOL
Incorporating data on genetic variability into a nutrition study can clarify whether or not a
specific dietary compound is linked to a particular health outcome. This diet-disease connection
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is made by the observation of whether the association between the disease and the dietary factor
is influenced by functional variants in genes involved in the metabolism of the dietary factor. For
example, moderate alcohol consumption has been associated with a lower risk of heart disease.
The primary mechanism proposed for this association is the higher levels of high-density-
lipoprotein (HDL) cholesterol found among moderate drinkers. However, it is possible that the
protective effect of moderate alcohol consumption is due to some confounding lifestyle factor
associated with moderate alcohol intake that differs from abstainers or heavy drinkers.
The enzyme alcohol dehydrogenase 1C (ADH1C), also known as alcohol dehydrogenase type 3
(ADH3) oxidizes alcohol to acetaldehyde. It has two polymorphic forms with distinct kinetic
properties. The ADH1C*1 allele produces!1 and the ADH1C*2 allele produces !2. The rate of
alcohol metabolism (ethanol oxidation) in !1!1 individuals is more than twice as high as in !2!2
individuals, with heterozygous individuals metabolizing alcohol at an intermediate rate.
Therefore, if there is a causal protective effect of moderate alcohol on risk of heart disease, this
effect would be expected to be stronger in individuals with the slow ADH1C genotype compared
to those with fast metabolism.
An early gene-diet interaction study examined data from the Physicians Health Study and the
Nurses’ Health Study to determine whether the effect of moderate alcohol consumption on HDL
levels and the risk of myocardial infarction (MI) vary according to ADH3 genotype
(Hines et al. 2001). The study reported evidence of a dose response decrease in heart disease as
alcohol metabolism slows according to genotype, for a marked 86% reduction in heart disease
risk in subjects with the slow-alcohol-metabolizing genotype who consumed at least 1 alcoholic
drink per day (Hines et al. 2001). The polymorphism was also associated with higher levels of
HDL (Hines et al. 2001).
The finding of an effect of the functional ADH1C polymorphism on the relation between alcohol
consumption and the risk of heart disease suggests that the protective effect is due to the alcohol
and not some associated lifestyle factor since those with the slow-alcohol-metabolizing genotype
who did not consume alcohol were not at a lower risk.
A key step in nutrigenomics research is to identify the sub-set(s) of the population that have
different reactions to dietary factors. In the case of alcohol, those groups were identified based
on genetic differences in alcohol metabolism. The extent to which this knowledge is being or
will be incorporated into nutrition practice remains unknown.
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CAFFEINE
Knowledge gained by incorporating genetic variation into a nutrition study not only provides a
more rational basis for giving personalized dietary advice, but will also improve the quality of
evidence used for making population-based dietary recommendations for the prevention of
specific diseases. This can be illustrated by considering recent studies that explore the effects of
caffeine on certain health outcomes (Cornelis et al. 2006). These studies have helped pinpoint
caffeine as the bioactive in coffee that affects certain diseases. These studies have also identified
how a response to coffee by a specific genotype can be beneficial or detrimental depending on
the disease being examined.
Caffeine is metabolized primarily by the cytochrome P450 1A2 (CYP1A2) enzyme, and a
polymorphism in the CYP1A2 gene determines whether individuals are‘rapid’ caffeine
metabolizers (those who are homozygous for the –163 A allele) or ‘slow’ caffeine metabolizers
(carriers of the -163 C allele). Intake of coffee is associated with an increased risk of MI only
among individuals with slow caffeine metabolism (Cornelis et al. 2006), suggesting that caffeine
increases risk of MI since it is the only major compound in coffee that is known to be detoxified
by CYP1A2. Furthermore, a protective effect of moderate coffee consumption was observed
among the fast metabolizers, suggesting that other components of coffee might be protective and
their effects are ‘unmasked’ in those who eliminate caffeine rapidly. This coffee-CYP1A2
genotype interaction has since been supported by a prospective study investigating the effect of
coffee intake on the risk of developing hypertension in individuals stratified by CYP1A2
genotype (Palatini et al. 2009). That study also measured epinephrine and norepinephrine in the
urine of the subjects, because these chatecholamines have been shown to increase after caffeine
administration in humans. Urinary epinephrine was significantly higher in coffee drinkers than
abstainers, but only among slow caffeine metabolizers, which is of interest because increased
sympathetic activity is considered an important mechanism through which caffeine raises blood
pressure.
A similar concept was utilized in an observational study of coffee and breast cancer
(Kotsopoulos et al. 2007). By dividing subjects into CYP1A2 genotypes, this study aimed to
determine if caffeine was the compound in coffee that explains the protective effect that had
previously been observed between coffee and risk of breast cancer (Nkondjock et al. 2006;
Baker et al. 2006). Indeed, a diet-gene interaction was present. However, unlike the studies on
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risk of MI and hypertension in which slow caffeine metabolizers were at increased risk from
drinking coffee, in this study coffee was associated with a lower risk of breast cancer among
slow metabolizers (Kotsopoulos et al. 2007). No protective effect was observed among fast
metabolizers, implicating caffeine as the protective component of coffee. This is consistent with
findings from animal studies showing that caffeine inhibits the development of mammary tumors
(Wolfrom et al. 1991; Yang et al. 2004).
DIETARY FAT
Considerable research efforts have been devoted to studying dietary fat in relation to biomarkers
of chronic disease such as concentrations of blood lipids. There is growing evidence that the
optimal amount and type of dietary fat intake depends ,in part, on an individual’s unique genetic
profile (Ordovas, 2008). A major focus has been placed on the epidemiological diet-gene
interaction studies, but clinical dietary trials that examine the difference in response to treatment
among genotypes have also been conducted based on the findings from observational studies.
For example, plasma omega 3 fatty acid responses to an omega 3 fatty acid supplement was
found to be modulated by apoE4, but not by the common PPAR-! L162V polymorphism
(Plourde et al. 2009). After supplementation, only non-carriers of E4 had increased omega-3 in
their plasma (Plourde et al. 2009).
After 3 months of supplementation with 3.6 g of omega 3 fatty acids/day (containing 2.4 g of
EPA and DHA) or placebo capsules containing olive oil, changes in cholesterol, including HDL
cholesterol concentrations, were similar among the PPAR-! L162V genotypes (Lindi et al. 2003).
In another study, subjects followed a low-fat diet for 8 weeks and then were supplemented daily
with 5 g of fish oil for 6 weeks, and the decrease in plasma triglyceride concentrations was
comparable for both PPAR-! L162V genotype groups, although a significant diet-gene
interaction was observed for plasma C-reactive protein (Caron-Dorval et al. 2008). Such clinical
studies are often limited by small sample sizes and short durations to assess physiological
changes. However, such limitations could be overcome with partnerships and collaborations
among researchers (McCabe-Sellers et al. 2008).
The replication of diet-gene interactions is an important step towards personalized nutrition
because it strengthens the evidence that will be used to design clinical trials and subsequent
nutrition recommendations based on genotype. It is widely recognized that nutrigenomics
provides industry with an incentive to develop functional foods and novel nutritional products
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(Kaput, 2007). Concern exists that functional foods created for prevention of chronic diseases
may incorporate bioactive compounds, such as PUFAs, without considering the interaction with
genetic polymorphisms (Ferguson 2009). Even where diet-gene interactions are well established
there may be a lag between the science and the evidence-based development and promotion of
functional foods optimized to certain genotypes. For example, the consumption of a food
containing added PUFA could lead to a range of responses in individuals, from significant
benefit, to an adverse effect (Ferguson 2009).
FRUITS AND VEGETABLES

Fruits and vegetables can affect multiple pathways and biological processes in the human body
because they are sources of water, fibre, vitamins, minerals, and numerous phytochemicals.
Evidence derived from epidemiological studies has suggested that high fruit and vegetable intake
is associated with a reduced risk of a variety of cancers (Kim and Park 2009) as well as
cardiovascular disease (He et al. 2006). However, a protective role has not been established
conclusively in clinical studies. This may be due to general challenges associated with
conducting long-term clinical trials, or to differences in dietary treatments and controls.
However, human genetic variation could also be one of the factors modifying response to plant
foods and their constituents. It has been observed that dietary intake of a phytochemical might
not necessarily result in comparable exposure levels in the circulation or target tissues of interest
(Lampe 2009). This variation in individual response may explain, in part, the observed
heterogeneity across different study populations. Characterizing how genetic factors modify the
effects of a high plant- based diet or specific components in plant foods on human health
outcome could clarify how plant foods influence disease risk and help to identify populations
that might benefit most from high fruit and vegetable intake.
Variations in genes affecting phytochemical absorption, distribution, utilization,
biotransformation and excretion potentially influence nutrient exposure at the tissue level
(Lampe, 2009). For example, the protein expression and activity of many nutrient metabolizing
enzymes are modulated by several compounds, including the substrates they act on. Therefore,
genetic variations in the pathways that these compounds act could alter biological response to
dietary factors.
Although few studies have addressed these potential genetic differences (Lampe, 2009), some
studies have explored the effects of genetic variation in biotransformation enzymes such as
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glutathione transferases (GSTs) (Probst-Hensch et al. 1998) (Lampe et al. 2000b) (Lampe et al.
2000a).
In addition to determining how an individual responds to an ingested amount of a specific dietary
bioactive, genetic variation can also influence our food preferences and ingestive behaviours.
Flavor including taste is an important determinant of how much a food is liked or disliked and
subsequently eaten or not. Common polymorphisms in genes involved in flavor perception may
account for differences in food preferences and dietary habits (Eny and El-Sohemy 2010). This
variability could affect food choices, which may influence health status and the risk of chronic
disease (Garcia-Bailo et al. 2009). For example, there are several vegetables that are disliked by
many because they are experienced as tasting extremely bitter, yet many of these vegetables are
rich sources of nutrients that have been associated with improved health outcomes.
The TAS2R38 receptor is known to detect two bitter substances called phenylthiocarbamide
(PTC) and 6-n-propylthiouracil (PROP) (El-Sohemy et al. 2007; Kim et al. 2003), which are not
found in foods, but have structural similarities to bitter compounds in certain foods. Carriers of
the PAV haplotype have been classified as “super-tasters” because they have a higher sensitivity
to PTC and PROP in comparison to individuals homozygous for AVI (Wooding et al. 2004;
Drayna 2005).
TAS2R50 has been associated with risk of MI, which has been hypothesized to be due to
differences in dietary preferences for bitter foods that appear to offer cardiovascular protection
(Shiffman et al.2005).
Establishing a genetic basis for food likes and dislikes may partially explain some of the
inconsistencies among epidemiologic studies relating diet to risk of chronic diseases because the
genetic makeup of a group of individuals could be a confounder to the nutritional exposure of
interest. Additionally, polymorphisms strongly associated with taste perception may potentially
be useful as surrogate markers of dietary exposure in gene–disease association studies where
information on dietary habits is not available. Finally, an understanding of the genetics of taste
perception may lead to the development of realistic personal and public health strategies for
providing dietary advice.
Fruit and vegetables are generally regarded as healthy foods to be consumed by all. However, it
may be beneficial for certain individuals, based on genetics, to focus on specific fruits and
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vegetables. For example, genotypes associated with more favourable metabolism of carcinogens
may be associated with less favourable metabolism of phytochemicals (Lampe, 2009).
Research findings to date suggest a complex association between consumption of several
vegetables and biotransformation enzyme activities in humans (Lampe et al. 2000b).
Genetic variation in pathways affecting nutrient absorption, transport, utilization and excretion,
taste preference, and food tolerance all potentially influence the effect of plant-based diets on
risk of disease.
Nutrigenomics is just in the very beginning of its existence. Only large and systematic studies
will determine how important nutrigenomics will be in the future clinical practice. The final goal
of nutrigenomics is to find an optimum dietary regimen for a given individual respecting not
only the quantitative and qualitative nutritional needs and health status, but also the genetic
predispositions in order to prevent the onset of many western-type diseases, or to help to cure
them more effectively.
The nutritional genomics focuses on the bioactive substances found in regular food and how
those substances affect the balance between health and disease via the interaction with the
individual's genome. The pandemics of obesity, cardiovascular disease, diabetes, etc. emerged
only recently so we can't presume that important changes of the genome are to blame. The more
probable cause of the above mentioned diseases can be found in the change of the outcomes of
genome x environment interactions. The environment is represented mainly by the lifestyle and
diet, and as such it indeed dramatically changed during the last century in both qualitative and
quantitative ways of physical activity, stress levels and diet.
On the empirical level it is well known that the quantity as well as the diet composition affects
the onset, incidence, severity and progression of majority of chronic diseases. Opposed to the
pharmacotherapy with well defined doses and target structures and mechanisms of action, our
diet consists of heterogeneous mixture of many biologically active substances, some of which
can be direct ligands of receptors affecting transcription of huge amount of genes (1). Moreover,
it is becoming evident that maternal diet during the pregnancy is important, as it "Metabolically
programs" through epigenetic modulations the homeostatic systems of the fetus.
These are 5 basic principles of nutrigenomics.
1. Substances contained in the food (micro- and macro-nutrients) can directly or indirectly
affect the human genome through changes in its structure and gene expression.
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2. Under certain circumstances and in some individuals the diet can be an important risk
factor for the development of the number of diseases.
3. Some genes regulated by active substances in the diet probably play a crucial role in the
onset, incidence, progression and severity of the disease.
4. The degree to which diet influences the balance between health and disease may depend
on individual's genetic makeup.
5. Nutritional intervention is based on the knowledge of individual's nutritional status and
needs as well as genotype (individualized nutrition) and can be used for prevention,
mitigation or healing the chronic diseases.
The fact, that common diet contains many bioactive substances that can through the interaction
with receptors activate or modulate the transcription of target genes or directly cause the
rearrangement of chromatin structure, is widely accepted, but not often recognized in the design
and interpretation of genetic and epidemiologic studies. The studies that follow the effect of a
certain diet often disregard the possible effect of genetic variability within the studied cohort, on
the other hand, some studies analyzing the effect of candidate gene. Polymorphism on the
studied trait (for example blood pressure, obesity) does not include the diet interference, which
can dramatically influence the resulting association. Nutritional genomics aims to resolve this
evident discrepancy.
NUTRIGENETIC INTERACTIONS
In real life situations, the interactions can be even more complicated as the pharmacotherapy will
influence the gene-diet interactions and the phenotypical outcomes. This dietary modulated
pharmacogenomic interaction was recently described in a system of several genetically defined
animal models of insulin resistance and dyslipidemia. We observed a significant difference in
antidiabetic action of rosiglitazone on metabolic parameters. This action was dependent on
dietary combination of carbohydrates and fats in diet and the genetic predisposition of tested
individual.
Classical example of nutrigenetic interaction leading to the clinical manifestation is persisting
tolerance of lactose in adult age. Point mutation C13910T emerged probably 9000 years ago in
north European population and caused long-term expression of lactose hydrolase and prevented
thus the natural gradual loss of function of this enzyme leading to physiological hypolactasia in
239
adulthood. Except for this "static" interaction there are also "dynamic" interactions that lead to
different responses to the dietary change according to the genetic makeup of the individual.
During the follow-up of men cohort in Czech MONICA study it was found that in response to
dramatic dietary change between years 1988 - 1996 only the carriers of CC-204 variant of
cholesterol-7alpha-hydroxylase (CYP-7A1) gene reduced the cholesterol levels. The carriers of
AA-204 variant of the gene were resistant to the dietary changes. It is also necessary to have in
mind the gene-gene interactions, the overall genetic makeup on which the given allele operates
as it can significantly modulate the given phenotype. The effect of a given allele is henceforth
more easily studied on genetically defined models. Haluzík et al. verified this concept in a study
where the introgression of mutation (ob/ob) of the leptin gene to the genome of two distinct
mouse strains C57BL/6J and FVB/N caused significantly different manifestation of insulin
resistance under identical dietary conditions.
CONCLUSION
Dietary intake of a nutrient does not necessarily result in the same concentrations in the blood or
tissue because substantial individual variability in the absorption, distribution, metabolism and
elimination can exist. The mechanisms responsible for the between-person differences in dietary
response are very complex and have been poorly understood. Research to date has indicated that
diet-gene interactions play a significant role in this between-person variability, and has clarified
some of these genetic differences.
The interaction between genetic and dietary influences can result in a higher risk of disease in
certain individuals and populations. Currently, diet-gene association studies are revealing
evidence on which to base gene-specific dietary intervention trials to confirm results. Replication
of current findings and further research in the form of genotype-specific nutritional intervention
studies are necessary. The future of nutrigenomics research promises to provide additional
knowledge of biological function and individual response to diet. This iterative approach to
health research is paving the road towards personalized nutrition.
Nutrigenomic practices for specific monogenic conditions such as PKU are currently being
successfully used in health care interventions in the form of newborn screening programs. The
application of nutrigenomics by healthcare professionals for the prevention and treatment of
complex chronic diseases, however, has not yet been widely adopted. Whether such practice will
be feasible for the population-at-large in the immediate future remains to be determined, but the
240
principles and tools of nutrigenomics are expected to soon allow for earlier and more targeted
interventions than currently exist (DeBusk 2009). As the current research in nutrigenomics often
focuses on how diet-gene interactions influence phenotypes found to be predictive biomarkers of
disease (Kaput et al. 2007), it is likely that the path from research to applications will proceed
into clinical practice using these markers of chronic disease as outcome measures. Recent
developments in genome-wide approaches have already identified many susceptibility alleles for
common complex diseases (Office of Population Genomics et al.), including several previously
unknown etiologic pathways in disease pathogenesis (Ding and Kullo 2009), and have the
potential to identify novel targets for prevention or treatment with dietary factors.
Diet is an important environmental factor that interacts with the genome to modulate disease
risk. A clear understanding of these interactions has the potential to support disease prevention
through optimization of dietary recommendations. The extent to which nutrigenomics will be
incorporated in nutrition therapy and promotion remains unknown. However, nutrigenomics has
emerged as a rapidly developing research area with great potential to yield findings that could
change the way dietary guidelines for populations and recommendations for individuals are
established and advised in the future.
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NUTRITION IN CRITICAL CARE
Introduction
Critically ill patients have complex nutritional needs and require intensive nutritional input.
As part of the metabolic response to injury, resting energy expenditure may be raised,
leading to extensive catabolism, hyperglycaemia, and progressive lean body mass loss,
changes in serum trace element levels, fluid retention, and reduced synthesis of visceral
proteins such as albumin. Contributing to poorer outcome is the previously reported high
prevalence of malnutrition (40%) in Intensive Care Unit (ICU) patients. Catabolism
combined with malnutrition can lead to several unwanted clinical sequelae:
 Impaired wound healing.
 Impaired immune response.
 Impaired coagulation capacity.
 Impaired gut function.
 Muscle wasting.
 Reduced respiratory muscle function.
Evidence suggests that nutrition support can slow catabolism in ICU patients. This can
improve patient outcome and reduce subsequent duration of recovery, thereby leading to a
reduced length of hospital stay and reduced overall hospital costs. A number of studies
have shown that survival from intensive care improves with better nutritional adequacy and
with the use of evidence-based nutrition support guidelines.
The overall goal of feeding ICU patients is to provide nutrition support to those who need
it, consistent with their medical condition, nutritional status, metabolic capability and
available route of administration.
Impact of an intensive care dietitian
The dietitian is considered central to the provision of nutrition support to those patients in
need of it, and is ideally placed to provide nutritional screening and assessment. Dedicated
dietetic staffing to ICU has been associated with better provision of nutrition support and
may result in improved patient outcomes.
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A recent international multicentre prospective observational study outlined best achievable
nutrition practices in participating ICUs relative to evidence based critical care nutrition
clinical practice guidelines. Analysis of the data showed that the presence or absence of a
dietitian in intensive care had a significant effect on determining performance with respect
to nutrition practices. The presence of a dietitian is associated with top performance, and is
considered a primary enabling factor that affects adherence to internationally recognized
nutrition guidelines in ICU. Another recent study showed improvements in early
introduction and route of feeding, as well as better achievement of nutritional targets
associated with the presence of an ICU dietitian.
Assessment and requirements
Nutritional screening
All ICU admissions should be screened to assess their need for nutrition support.
Recommend nutrition support within 24 to 48 hours of ICU admission (or once
haemodynamically stable) for:
 Undernourished or hyper catabolic patients.
 Patients expected to stay in ICU for 3 days or more.
 Patients not expected to commence diet within next 5 days or more.
A ‘nutrition risk in the critically ill score’ (NUTRIC Score) has recently been validated for
screening ICU patients. Further validation studies are needed.
Assessment/requirements
Before initiation of feeding, nutritional assessment should consider:
 Recent weight loss.
 Nutrient intake prior to admission.
 Level of disease severity.

 Co-morbid conditions.
 Function of gastrointestinal tract.

In the critical care setting, the traditional protein markers such as albumin, prealbumin,
transferrin and retinol binding protein are a reflection of the acute phase response and do
not accurately represent nutritional status in the ICU setting.
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Requirements should be assessed individually and provided according to tolerance.
Overfeeding critically ill patients can have detrimental effects on outcome. Conversely,
persistent underfeeding has been associated with increasing complications. Over aggressive
feeding during the acute phase of injury may also promote adverse outcome effects
Recommended macronutrient requirements are summarized in table below. Some validated
equations used to calculate energy requirements in the critically ill are shown in Table 2.
Recommended macronutrient requirements for use in ICU.
(per kg recommendations infer per kg per 24 hours.)
Individualized.
Use validated equations, in the absence of indirect calorimetry.
Energy
 20-25kcal/kg in acute phase of critical illness.
 25-30kcal/kg in recovery phase.
 25kcal/kg
 Consider hypocaloric feeding in critically ill obese (BMI >30kg/m2), e.g. 60-70% of target
energy requirements, or 11-14kcal/kg actual body weight, or 22-25kcal/kg ideal body weight.
Protein
 1.3-1.5g protein/kg.
 1.2-2.0g protein/kg if BMI<30kg/m2.

 2g/kg ideal weight if BMI 30-40kg/m2.
 2.5g/kg ideal weight if BMI >40kg/m2.
 Caution with excess nitrogen in severely ill.
Glucose
 Minimum 2g/kg
 3-5 (maximum 7) g/kg.

Fat/lipid
 0.7-1.5g/kg.
 0.8-1g/kg in sepsis/SIRS.
 Consider lipid source.
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Sample validated requirement Equation
equations used in ICU Author &
Year
Ireton-Jones 1992 EEE (s) = 629 - 11(A) + 25(W) -
(for spontaneously breathing 609(O)
patients)
Ireton-Jones 2002 EEE (v) = 1784 - 11(A) + 5(W) +
(for ventilated patients) 244(G) + 239(T) + 804(B)
Penn State 2003/2004 RMR= Mifflin-St Jeor (0.96) +
(using Mifflin St. Jeor) Tmax(167) + VE(31) - 6212
Modified Penn State 2011 RMR = Mifflin-St Jeor (0.71) +
(for ≥60year olds with BMI Tmax(85) + VE(64) - 3085
≥30kg/m2)
Mifflin St. Jeor 1990 for use with Men: 10(weight) + 6.25(height) –
Penn State equation 5(age) + 5
Women: 10 (weight) +
6.25(height) ) – 5(age) - 161
EEE is estimated energy expenditure (kcal/24hr.); v is ventilator dependent; s is

spontaneously breathing; A is age (years); W is body weight (kg); G is gender
(male=1, female=0); T is diagnosis of trauma (present=1, absent=0); B is diagnosis
of burn (present=1, absent=0); O is obesity (>30% above IBW from Metropolitan
Life Insurance Tables, present=1, absent=0); RMR= Resting Metabolic Rate; Tmax
is maximum body temperature in the previous 24 hours (degrees Celsius); Ve is
minute ventilation (litres per minute)at the time of measurement read from the
ventilator. Height in cm.
Whether kcal/kg, indirect calorimetry or use of predictive equations should be used to
assess requirements in ICU remains unclear. For extremely overweight or
underweight patients, or patients with severe sepsis and/or multi-organ dysfunction
syndrome (MODS), estimating requirements is more difficult. Indirect calorimetry
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may be beneficial for these patients, but is often unavailable and is not appropriate for
certain patients. Clinical judgement and close monitoring of these patients is
paramount.
Feeding the malnourished patient
Refeeding syndrome is a life threatening condition encompassing acute micronutrient
deficiencies, fluid and electrolyte imbalances, and disturbances of organ function and
metabolic regulation that may result from over-rapid or unbalanced nutrition support
provision to malnourished patients. Effects include
 Severe hypophosphataemia (whole body depletion).
 Fluid balance abnormalities (acute overload/depletion).
 Hypokalaemia.
 Hypomagnesaemia.
 Altered glucose metabolism.
 Vitamin deficiency.
 Cardiac failure, pulmonary oedema and dysrhythmias.
 Risk of death.
At risk patients
People who have not eaten for more than 5 days should have nutrition support
introduced at no more than 20kcal/kg/24 hours initially. Increase feeding rates to
meet full needs if clinical and biochemical monitoring reveals no refeeding problems.
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High risk patients
NICE 2006 criteria for determining which patients are at high risk of developing refeeding
problems
One or more of the following:
- BMI less than 16 kg/m2
- unintentional weight loss greater than 15% within the last 3–6 months
- little or no nutritional intake for more than 10 days
- low levels of potassium, phosphate or magnesium prior to feeding.
Two or more of the following:

- BMI less than 18.5 kg/m2
- unintentional weight loss greater than 10% within the last 3–6 months
- little or no nutritional intake for more than 5 days
- A history of alcohol abuse, or drugs including chemotherapy.
Nutrition support in patients at high risk of refeeding syndrome
Start nutrition support at ≤10 kcal/kg/day, increase levels slowly to meet or exceed
full requirements by day 4 to 7 (consider 5 kcal/kg/day in extreme cases, e.g. anorexia
nervosa patients).
Restore circulatory volume and monitor fluid balance and overall clinical status
closely.
Providing immediately before and during the first 10 days of feeding: oral thiamine
200–300 mg daily, or full dose daily intravenous vitamin B preparation, Pabrinex®
1and 2, one to two pairs once to three times daily for 3 to 5 days (use the higher more
frequent dose for chronic alcohol abusers).
Give a balanced multivitamin/trace element supplement once daily.
Provide oral, enteral or intravenous supplements of potassium, phosphate and
magnesium unless pre-feeding plasma levels are high (in accordance with local
hospital policies/protocols on electrolyte replacement).
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Pre-feeding correction of low plasma levels is unnecessary, but low levels must be
supplemented as they occur throughout refeeding.
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Providing nutrition support
Enteral nutrition
Enteral feeding is the preferred route of feeding for ICU patients. Evidence suggests
enteral feeding helps to:
 Maintain gut integrity.
 Prevent gut stasis.
 Maintain gut mass.
 Maintain gut associated lymphoid tissue.
 Prevent stress ulceration.

Early enteral feeding (within 24-48 hours of ICU admission) benefits ICU patients.
Enteral feeds
Enteral feeds are more nutritionally complete, are better metabolically handled, and
often cost less than parenteral solutions.
Standard feeds are appropriate for most ICU patients.
Arginine supplemented feeds are not recommended in severely septic patients due to
possible adverse effects on outcome.
Standard feed formulations are appropriate for the majority of patients with AKI on
CRRT. Consider renal feeds if uncontrolled electrolyte derangements.
An enteral feed rich in eicosapentaenoic acid, gamma-linolenic acid and antioxidants
conferred a 19.4% risk reduction in mortality rate in ARDS and ALI ICU patients
with severe sepsis. A recent meta-analysis evaluated outcome data from studies using
this feed and reports significantly more ventilator-free days; 83% risk reduction in
developing new organ failures (p<0.0001); 60% risk reduction in 28-day in-hospital
all-cause mortality (p=0.001). Recent guidelines on nutrition support in Intensive
Care patients encourage use of this feed in patients with ARDS and severe ALI.
Enteral Glutamine
Enteral supplementation of glutamine has demonstrated outcome benefits in burns,
and trauma patients. There are conflicting recommendations over use of enteral
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glutamine in other critically ill patients. Glutamine powder mixed with water can be
given enterally in 2-3 divided doses to provide 0.3-0.5g glutamine per kg per day.
Bowel sounds
The presence of bowel sounds is not a necessary prerequisite for commencing enteral
feeding in an ICU setting. Normal myoelectric activity in the bowel returns after
surgery in the absence of bowel sounds. Bowel sounds are not necessarily correlated
with bowel peristalsis. Enteral nutrition can commence in surgical patients without
waiting for flatus or a bowel motion.
Gastric aspirate volumes

With large bore NG tubes, initially aspirate the stomach of critically ill patients every
4 hours. Gastric aspirate/residual volume measurement correlates poorly with gastric
emptying, as well as incidence of regurgitation and aspiration. Once clinical
condition stabilizes and gastric aspirate/residual volumes are consistently normal,
consider fine bore NG tube for feeding. Review feeding policy if raised gastric
aspirate/residual volumes. Acceptable gastric residual volume levels of between 250
and 500ml have been advocated for ICU patients.
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Cut off values for gastric aspirate Source of recommendation
volumes Gastric aspirate/residual
volume cut off recommendation
for enteral feeding in ICU
250-500ml American Society for Parenteral
and Enteral Nutrition (ASPEN)
Guidelines 2009
≥250ml Canadian Clinical Practice (CPG)
Guidelines 2003 and 2009
>500ml – withhold feed & reassess North American Summit on
aspiration in the Critically Ill
Patient: Consensus statement 2002;
ASPEN 2009
<500ml – avoid withholding feed American Society for Parenteral
unless other signs of intolerance and Enteral Nutrition (ASPEN)
Guidelines 2009
Confirming nasogastric tube position

Radiographic confirmation of correct positioning of any blindly-placed tube (small or
large bore) should be obtained prior to its initial use for administration of feed or
medications.
Bedside pH checks can also be used to check position. Gastric acid suppression
therapy may affect pH readings. The NPSA recommends that a pH of <5.5 confirms
gastric position. A recent study, however, recommends a pH of 5.0 as a safer, reliable,
and practical cut-off. An Irish study in 2008 reported a high correlation between using
pH strips and using a calibrated pH meter to check pH of enteral aspirates with r-
values approaching 1 in all cases. The NPSA recommend radiological confirmation of
nasogastric tubes if pH is >5.5.
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The exit site of a feeding tube should be marked at the time of initial placement.
Observe for a change in the external tube length during feeding.
In adult patients the auscultatory method should not be relied upon to differentiate
between gastric and respiratory placement of feeding tubes.
Feed administration guidelines

Closed enteral feeding systems should be used where possible.
Administration sets for closed system enteral nutrition formulas should be changed
per manufacturer guidelines. Giving sets for open systems should be changed at least
every 24 hours.
Use sterile water for flushing tubes or for enteral water infusion. Flush feeding tubes
regularly.
Sterile liquid formulas should be used in preference to powdered reconstituted feeds.
Closed-system enteral nutrition formulas can hang for 24 hours.
Sterile decanted formulas should have a maximum 8 hour hang-time.
Reconstituted powdered feeds should have a maximum 4 hour hang-time.
Store unopened liquid enteral feeds as per manufacturer’s guidelines and use before
expiry date.
Enteral nutrition prescriptions should include: patient identifiers, the feed formula, the
enteral access device/site, and the administration method and rate.
A head-of-bed elevation of 30 to 45o is recommended during feeding, unless contra-
indicated.
Feed rate guidelines:

There are limited prospective data to form strong recommendations about initial
starting rates for enteral feeding. Formulas are frequently commenced at full strength
at a lower rate and advanced to goal rate in set increments, e.g. 20ml/hour, over set
timeframes, e.g. every 8 hours, until target rate is achieved. Feeds should not be
diluted (with rare exceptions).
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Some authors recommend commencing feeds at full target rate in stable patients.
Aiming for target feed volumes per 24 hours has also been advocated to improve
nutritional adequacy.
A recent ARDSNET randomised trial (EDEN trial) 50 showed that early trophic
enteral feeds (25% of goal calories) were associated with similar outcome benefits to
full enteral feeds in younger, normo-well nourished patients with a relatively short
ICU stay. Other studies, have shown that the most significant outcome benefits from
full nutrition therapy occur in patients with low BMI, high BMI, and with prolonged
stays in ICU (>7days). A large observational study showed that reaching >80% of
nutritional target was associated with improved mortality.
Strategies to improve enteral feeding tolerance

 For patients with inadequate feed tolerance:
 Consider use of prokinetics, e.g. metaclopramide and/or erythromycin, unless
contraindicated. Efficacy declines after 2-3 days when prescribed alone, or after 6
days when prescribed as a combination. Routine use of prokinetics is not
recommended unless signs of feed intolerance are present, Significant side-effects can
occur with use of either prokinetic (seek advice from pharmacy).
 Consider use of laxatives if no bowel motions, where there is no contraindication.
 Reduce use of opiates where possible.
 Consider patient positioning. Ensure head of patient is elevated to 30 to 45 degrees,
where possible.
 Consider post-pyloric access for feeding
 Control hyperglycaemia if present.
 Correct abnormal electrolytes and avoid hypokalaemia, where possible.
Post-pyloric feeding
Routine nasojejunal feeding in ICU patients is not required unless gastric feeding
intolerance is present. Critically ill patients at high risk of aspiration, or who have
demonstrated gastric feed intolerance, should be fed via post-pyloric route.
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Small bowel nasoenteric feeding tubes can migrate upward into the stomach. Monitor
pH, changes in external tube length, and changes in gastric residuals. Check X-rays to
confirm location of feeding tube tip initially, and as needed.
Success rates with nasoenteric tube placement are high via endoscopic (96%) and
fluoroscopic techniques (94%). Sonographic and magnet-assisted placement has
success rates of 85% and 60%, respectively. Placement using tip pH-sensors is
between 50% and 97% successful.
Blind bedside placement is variable with reported levels of between 15% and 100%
in the literature. An Irish study reported an 86% success rate in blind bedside
insertion of nasojejunal tubes (mainly placed by a nurse specialist or dietitian). A
recent study using an electromagnetically guided nasointestinal tube system in ICU
patients with gastric feed intolerance was successful in post-pyloric tube placement in
87% of cases.
2. Parenteral nutrition
Consider Parenteral nutrition when Enteral feeding is not possible or adequate.
Standard bags can be tailored to the individual by adjusting infusion rates. Daily
micronutrients should be provided routinely in PN regimen or as a separate
intravenous infusion. Micronutrients above the normal recommendation may be
needed in case of excess loss/need. Consider Parenteral glutamine.
Some authors recommend initiating PN in the critically ill if enteral feeding cannot
commence within 24 to 48 hours of ICU admission. When used to supplement
insufficient enteral feeding, late parenteral nutrition (day 8) was associated with
improved outcomes compared with early PN initiation in one study. Another study
found that supplemental PN on day 4 of insufficient enteral feeding, to reach 100% of
nutrition needs, had significant outcome benefits. A reasonable trigger time of 72
hours for commencing PN in ICU, could be used where EN has failed or is
contraindicated.
Central venous access device (CVAD)
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The use of femoral vein for PN is relatively contraindicated, since this is associated
with a high risk of contamination at the exit site, and a high risk of venous
thrombosis.
Intravenous Glutamine
Significant improvements in six month mortality rates, and length of stay have been
demonstrated in ICU patients on parenteral feeding who were supplemented with
intravenous glutamine68. Significant cost savings were also noted69. Parenteral doses
of 0.5g L-glutamine/kg/day2 and 0.2 to 0.4g L-glutamine/kg/day17 have been
recommended. Several international guidelines recommend the use of IV glutamine
in parenterally fed ICU patients. The outcome benefits of supplemental IV glutamine,
however, are not consistently demonstrated, as evidenced by the recent SIGNET trial. See
local intensive care unit guidelines for current practice.
Addition of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) to

lipid emulsions in PN regimens used in ICU
High circulating levels of inflammatory mediators such as eicosanoids, cytokines and
reactive species, are seen in very critically ill patients and have been associated with
poor outcomes. Intravenous fish oil can decrease synthesis of inflammatory mediators
and can improve EPA and DHA levels in cell membranes. This may be associated
with improved outcomes such as mortality, infection rate, antibiotic usage and length
of ICU or hospital stay, although results are inconsistent.
Lipid emulsions should be an integral part of PN in ICU for energy and to ensure
essential fatty acid provision, especially in longer-term PN. There is currently
insufficient data to recommend a particular lipid type for to be used in PN for
critically ill patients. Avoidance of lipids high in soybean oil has been advocated by
some for use in short-term PN, but clinical judgement is needed. Triglyceride levels
should be measured to assess lipid clearance - see local guidelines.
Other considerations
Glycaemic control
In 2001, Van den Berghe’s group demonstrated that intensive insulin therapy to
strictly control blood glucose levels between 4.4 and 6 mmol/l, significantly reduced
ICU mortality in surgical ICU patients. Mortality benefits were not seen in medical
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ICU patients in a 2006 study by the same group (although morbidity benefits were
shown).
In 2009, the NICE-SUGAR study investigators recommended a blood glucose target
of 10mmol/l. Strict glycaemic control (target blood glucose of 4.5-6 mmol/l),
increased the absolute risk of death at 90 days by 2.6%. Severe hypoglycaemia (blood
glucose less than 2.2mmol/l) was significantly more common with intensive glucose
control.
Systems that can offer continuous glucose monitoring are being investigated. All ICU
patients should have their blood glucose levels maintained at or below 10 mmol/l15.
Feeding over 24 hours may aid glycaemic control in ICU. See local intensive care
unit intravenous insulin infusion protocols for achieving glycaemic control.
Feeding the obese critically ill patient
There is an increasing prevalence of obesity in hospitalised patients. A consensus
workshop on nutrition therapy in the severely obese critically ill patient published
conclusions and consensus recommendations in 2011. These may provide guidance
for patient management in the absence of large randomised trials. Recommendations
include:
 The obese, critically ill patient may be expected to have a greater number of
underlying co-morbidities and subsequently more complications than lean
counterparts. The effect of obesity on ICU and hospital mortality is both controversial
and uncertain.
 Critically ill patients at increased health risk due to obesity-related conditions may be
identified by the presence and extent of comorbidities and functional limitations.
 Specialised equipment should be acquired to manage the unique impact of obesity on
delivery of care in the ICU.
 At initial assessment weight and BMI should be considered “vital signs” for the obese
patient and carefully recorded in the medical record.
 Initial assessment of biomarkers of the metabolic syndrome (serum levels of
triglyceride, cholesterol, and glucose) is also recommended.
 Prolonged periods of NPO (nil by mouth) are not justified.
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 Basic principles of critical care nutrition should be applied to the obese critically ill
patient. The need for and the benefit gained from early enteral nutrition (EN) is no
different from that of their lean counterparts.
 Optimal enteral access and level of feeding within the gastrointestinal tract may
require post-pyloric feeding into the small bowel.
 Caloric requirements should be measured when possible by indirect calorimetry. In
the absence of indirect calorimetry, use predictive equations validated in patient
populations that include critically ill obese patients.
 High-protein hypocaloric feeding should be provided to the obese ICU patient.
Consider the use of prebiotics or probiotics to beneficially alter the gut microflora.
Additional micronutrients
 Evidence supporting routine supplementation of micronutrients in addition to meeting
recommended daily intakes by nutrition support, is unclear. Some guidelines do exist
 Avoid toxicity in patients with hepatic and renal insufficiency.
Micronutrient supplementation Source of recommendation

in ICU Additional micronutrient
supplementation
Supplemental combined vitamins Canadian Clinical Practice (CPG)
and trace elements should be Guidelines 2009
considered in critically ill patients American Society for Parenteral
receiving nutrition support.* and Enteral Nutrition (ASPEN)
Guidelines 2009
*Additional studies to delineate optimal dosage, route and combination of

micronutrients are needed.
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Infusions commonly used in ICU with nutritional implications
The outlines commonly used medication infusions in ICU and potential nutritional
implications.
Medication infusions used in ICU
and possible nutritional Possible nutritional implications
implications Medication
Inotropes e.g. noradrenaline - Increasing levels indicate severity
infusion, adrenaline infusion, of illness/unstable patient.
vasopressin. - Inotropes can lead to
hyperglycaemia.
- Inotropes can increase energy
requirements.
- Avoid overfeeding patients with
raised or increasing inotropic
requirements.
Sedatives e.g. midazolam infusion, - Sedatives reduce energy
propofol infusion. requirements.
- Sedatives reduce gut motility by
relaxing visceral smooth muscle.
- Propofol contains lipid which must
be considered when devising.
Nutrition support prescription, e.g. Lipuro contains MCT/LCT fat (0.01g fat/ml) and
1.058kcal/ml; Diprivan contains LCT fat (0.01g fat/ml) and 1.1kcal/ml.
Opioid analgesics e.g. morphine - Reduce gastric emptying and lead
infusion. to disordered motility in the
duodenum.
Dopamine infusion. - Decreases proximal gastric tone
and decreases contractions in gastric
antrum.
Gastric acid reducing agents. - Can stimulate gastrin which
inhibits gastric emptying.
Intravenous 5% Dextrose - Gives 50g carbohydrate per litre,
equivalent to 200kcal per litre.
Dialysate - Consider energy derived from
glucose containing dialysates.
When significant amounts of nutrients are provided or lost through means other than
the nutrition support formula (e.g. intravenous infusions, drugs, dialysis mode), the
nutrition care plan should be adjusted accordingly.
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Monitoring of Nutrition Support:
An interdisciplinary approach is advised. See local guidelines for monitoring of
nutrition support. Monitoring guidelines should include regular:
 Nutritional assessments.
 Measurement and interpretation of relevant biochemistry and haematological

parameters.
 Clinical assessment (including gastrointestinal function, and changes in clinical

condition that may have implications for requirements, fluid status, presence of organ
failure, mode of dialysis, etc.).
 Dietary assessment if applicable.
 Nutrition support assessment (including nutritional adequacy, feed tolerance, etc.).
 Other patient-specific factors.
Swallow assessment and Speech and Language Therapist input:

The provision of diagnostic and therapeutic support is fundamental to the care
pathway of critically ill people. Patients with critical care needs are frequently
intubated due to respiratory failure, need for mechanical ventilation, assistance with
secretion management and pulmonary hygiene and airway obstruction80. Intubation,
by itself, can impair swallowing over a period of up to three days post extubation in
patients with no other cause for dysphagia.
The current literature demonstrates a large amount of clinical evidence demonstrating
that a tracheostomy tube influences swallowing. The highest dysphagia frequencies
occur following prolonged intubation. Current research suggests dysphagia frequency
ranges from 3%- 62% as the period of intubation increases from 124.8- 346.6 mean
hours.
Furthermore, patients with a tracheostomy may have communication problems that
affect their ability to be involved in their own care. All people with critical care needs
who have communication and / or swallowing difficulties due to organic, concomitant
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or psychogenic disorders should have access to a timely and responsive speech and
language therapy service.
CARDIOVASCULAR DISEASES
BY
DIETITIAN AJAEBILI NGOZI .A.
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CARDIOVASCULAR DISEASES
The heart is a muscular organ about size of a closed fist that functions as the body’s circulatory
pump. It takes in deoxygenated blood through the veins and delivers it to the lungs for
oxygenation before pumping it into various arteries. The heart is located in the thoracic cavity
medial to the lungs and posterior to the sternum, on superior end, the base of the heart is attached
to the aorta, pulmonary arteries and veins and vena cava. The heart sits within a fluid filled
cavity called pericardial cavity. The heart wall is made up of three layers:
Epicardium which is the outermost part
Myocardium which is the middle part and it’s responsible for pumping of blood
Endocardium which is the innermost part
The heart has four chambers: right atrium, left atrium, right ventricle and left ventricle. The atria
are smaller than the ventricles and have thinner, less muscular walls than the ventricle. The atria
act as receiving chambers for blood, so they are connected to the veins that carry blood to the
heart. The ventricles are larger, stronger, pumping chambers that send blood out of the heart. The
ventricles are connected to the arteries that carry blood away from the heart.
The heart weighs between 200g to 425g. Each day, the average heart beats 100,000 times,
pumping about 2000gallons (7571 litres) of blood.
 CVD has been the leading cause of death in the United States for every year since 1900
except 1908
 CVD kills almost as many people yearly as the next seven causes of death combined
 CVD includes hypertension, coronary heart disease, heartfailure, congenital heart defects
and stroke
PREVALENCE AND INCIDENCE
CVD accounts for almost 50% of all deaths in industalized nations. Estimates for the year 2006
are that 80,000,000 people in the United states have one or more forms of CVD (American Heart
265
Association, 2009). Seventy percent of CVD can be prevented or delayed with dietary choices
and lifestyle modification (Forman and Bulwer, 2006). There are 12 modifiable dietary, lifestyle
and metabolic risk factors: high blood glucose, LDL, Cholesterol, Blood pressure, overweight-
obesity, high dietary trans fatty acid and salt, low dietary polyunsaturated fatty acids, omega 3
fatty acids, fruits and vegetables, physical inactivity, alcohol use and tobacco smoking. Other
risk factors include age, male gender, low socio economic status, family history.
ANGINA PECTORIS
Angina pectoris involves chest pain or discomfort from decreased blood flow to the myocardium
from decreased oxygen supply (often during exertion). It can also be defined as chest pain caused
by myocardial ischemia from reduced blood flow and/or reduced oxygen supply to the
myocardium. Angina is a warning sign that a heart attack (MI) may occur.
RISK FACTORS
They include:
Tobacco use, hypertension, diabetes mellitus, dyslipidaemia, obesity, sedentary lifestyle,

lipoprotein, elevated homocysteine, congestive heart failure, congenital heart defects, narrowing
of the aortic valves, ventricle wall thickening and atheroma leading to arterial narrowing. The
above causes decreased oxygen supply to the myocardium.Angina can also occur from anemia,
hyperthyroidism, aortic stenosis or vasospasm, exercise and emotional stress. These causes
increased oxygen demand on the myocardium.
TYPES OF ANGINA PECTORIS

Stable:
̶ Caused by specific amount of activity
̶ Predictable
̶ Relieved with rest and nitrates
Unstable:
̶ Pain occurs with increasing frequency, severity, and duration over time
̶ Unpredictable
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̶ May occur at rest
̶ High risk for MI
Prinzmetal’s (variant):
̶ Has no identified cause
̶ May occur at same time of day
̶ May intensify or worsen over time
̶ Is usually caused by coronary artery spasm
Angina decubitus:
̶ Occurs when a person is lying down with no cause
̶ Occurs because gravity redistributes body fluids
SIGNS AND SYMPTOMS OF ANGINA PECTORIS
Pressure or heaviness in chest beneath breastbone—women are likely to have unusual types of
chest discomfort
• Pain may occur down shoulder or inside of arms, or in the throat, jaw, or teeth
• Stomach pain, especially after eating
• Sweating
• Light-headedness
• Hypotension
• Pulse changes
• Indigestion
OBJECTIVES OF MEDICAL NUTRITION THERAPY
 Relieve chest pain. Improve circulation to the heart

 Increase activity as tolerated. Gradually increase exercise, especially through programs in
cardiac rehabilitation
 Maintain weight or lose weight if obese. A conventional dietetic intervention with weight
loss helps to reduce pain frequency
 Reduce symptoms of metabolic syndrome where present
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 Avoid constipation with straining
 Control BP and lower elevated serum cholesterol
MEDICAL NUTRITION THERAPY
 Small, frequent feedings rather than three large meals are indicated
 Increase fiber as tolerated; include an adequate fluid intake. Increase intake of fruits
 Restrict saturated fats, dietary cholesterol and sodium as necessary according to the
individual profile. A very low fat diet can be quite effective
 Limit stimulants such as caffeine
 Promote calorie control if overweight; modify by age and sex
 It is prudent to increase intake of olive, soybean and canola oils, seeds and nuts, including
walnuts, almonds, peanuts and pistachio.
MYOCARDIAL INFARCTION
Myocardial infarction is the technical name for a heart attack. A heart attack occurs when an
artery leading to the heart becomes completely blocked and the heart does not get enough blood
or oxygen. Without oxygen, cells in that area of the heart die. Therefore, M.I is necrosis in the
heart muscle caused by prolonged inadequate blood supply or oxygen deficit.
RISK FACTORS/ CAUSES
 Atherosclerosis
 Family history of heart disease
 Patient history of heart disease
 Diabetes or elevated blood glucose even in non-Diabetes
 Hypertension
 Advanced age
 Elevated LDL (bad ) cholesterol and triglyceride
 Stress, smoking , sedentary lifestyle
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 Poor diet (high sodium, high fat, high intake of alcohol, low intake of B- complex
vitamins, calcium, magnesium and potassium, low intake of fruits and vegetables)
 Lack of exercise
 Obesity
 Embolus
 Thrombosis
SIGNS AND SYMPTOMS
 Pain, typically in middle of chest, radiating to jaws, arms (usually the left), abdomen,
and/or shoulders, and lasting 20 minutes:Possible to have no pain (particularly in
females)Sudden onset of pain, not associated with activity
 Tachycardia
 Excessive perspiration
 Painful breathing and/or difficulty breathing
 Anxiety/panic
 Nausea/vomiting
 Fever
 Stomach pain, often confused with indigestion
PREVENTIVE CARE
You can reduce the risk of heart attack by;
 Stopping smoking
 Getting aerobic exercise (such as walking, biking or swimming) for at least 30 minutes, 5
days per week
 Reduce stress
 Eating a diet low in saturated fat and rich in fruits, vegetables and wholegrain
 Losing weight or maintaining a proper weight
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 Promote rest to reduce heart strain. Avoid the distension of heavy meals
 Prevent arrhythmias by serving food at body temperature
 Avoid both constipation and flatulence
 Avoid excessive heart stimulation from caffeine
 Reduce elevated levels of lipids
 Decrease energy required to chew prepared meals, perform activities of daily living
during convalescence
 Identify modifiable risk factors and complications; reduce risk when possible e.g. lose
weight if obese.
 Use liquids at initial stage to promote rest while reducing the dangers of aspiration or
vomiting
 Reduce fluid and caffeine intake to that recommended by Physician
 As treatment progresses, diet should include soft, easily digested foods that are low in
saturated fats, cholesterol and gas forming foods
 Limit diet to 2g of sodium or remove salt from table
 The DASH DIET and MEDITERANEAN DIET are useful.
DASH DIET(DIETARY APPROACHES TO STOP HYPERTENSION)
This emphasizes a diet rich in fruits, vegetables and low fat or non-fatdairy products that provide
high intake of potassium, magnesium and calcium sources. Sodium intake should be between
1500mg to 2400mg per day,(the lower the better). Weight loss, regular exercise and limiting
alcohol.
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MEDITERRANEAN DIET
Mediterranean diet concentrates on whole grains, fresh fruits and vegetables, fish, oliveoil and
moderate wine consumption. The Mediterranean style diet is not low fat, it is low in saturated fat
but high in monounsaturated fat. It appears to be heart healthy.
 Adequate calcium, magnesium and potassium will be needed but not in excess
 Decrease intake of whole milk products, red meats, visible fats on meat/ poultry and
commercial baked products. Limit egg yolks to 4-5 times weekly if lipids are elevated
 Increase food sources of vitamin E and K, Folic acid and Vitamin B6 and B12
 Fiber is especially important, choose vegetables, fruits and cereal grains
 Include judicious use of nuts, such as walnuts,almonds, pecans and pistachios.
HYPERTENSIVE HEART DISEASE
Hypertensive heart disease includes a number of complications ofhigh blood pressure that affect
the heart. The cause of hypertensive heart disease is chronically elevated blood pressure (BP);
however, the causes of elevated BP are diverse. Hypertensive heart disease refers to heart
problems that occur because of high blood pressure. These problems include:
 Coronary artery disease and angina

 Heart failure
 Thickening of the heart muscle (called hypertrophy)
Essential or primary hypertension accounts for 90% of cases of hypertension in adults.

Secondary causes of hypertension account for the remaining 10% of cases of chronically
elevated BP. High blood pressure means the pressure inside the blood vessels (called arteries) is
too high. As the heart pumps against this pressure, it must work harder. Over time, this causes
the heart muscle to thicken. Without treatment, symptoms of heart failure may develop.
Sometimes the muscle can be so thick that it does not get enough oxygen. This can cause angina
(chest pain). High blood pressure also leads to thickening of the blood vessel walls. When
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combined with cholesterol deposits in the blood vessels, the risk of heart attacks and stroke
increases. Hypertensive heart disease is the leading cause of illness and death from high blood
pressure.Uncontrolled and prolonged elevation of BP can lead to a variety of changes in the
myocardial structure, coronary vasculature, and conduction system of the heart. These changes in
turn can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease
(CAD), various conduction system diseases, and systolic and diastolic dysfunction of the
myocardium, complications that manifest clinically as angina or myocardial infarction, cardiac
arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF).Thus,
hypertensive heart disease is a term applied generally to heart diseases, such as LVH, coronary
artery disease, cardiac arrhythmias, and CHF that are caused by the direct or indirect effects of
elevated BP. Although these diseases generally develop in response to chronically elevated BP,
marked and acute elevation of BP can lead to accentuation of an underlying predisposition to any
of the symptoms traditionally associated with chronic hypertension.
SIGNS AND SYMPTOMS OF HYPERTENSIVE HEART DISEASE
The symptoms and signs of hypertensive heart disease will depend on whether or not it is
accompanied by heart failure. In the absence of heart failure, hypertension, with or without
enlargement of the heart (left ventricular hypertrophy) is usually symptomless. Symptoms and
signs of chronic heart failure can include:
 Fatigue
 Irregular pulse or palpitations
 Swelling of feet and ankles
 Weight gain
 Nausea
 Shortness of breath
 Difficulty sleeping flat in bed (orthopnea)
 Bloating and abdominal pain
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 Greater need to urinate at night
 Altered mentation (in severe cases)
 An enlarged heart (cardiomegaly)
Patients can present acutely with heart failure and pulmonary edema due to sudden failure of
pump function of the heart. Acute heart failure can be precipitated by a variety of causes
including myocardial ischemia, marked increases in blood pressure, or cardiac dysrhythmias,
especially atrial fibrillation. Alternatively heart failure can develop insidiously over time.
DIAGNOSIS
Stages of elevated BP and hypertension:
Category Systolic BP (mm Hg) Diastolic BP (mm Hg)
Optimal < 120 < 80
Prehypertension 120-139 80-89
Stage I 140-159 90-99
Stage II >160 >100
From: National Heart, lung andblood Institute. Accessed July16, 2009, at

http/www.nhlbi.nih.gov/hbp/detect/categ.htm.
PREVENTION
Because there are no symptoms with high blood pressure, people can have the condition without
knowing it. Diagnosing high blood pressure early can help prevent heart disease, stroke, eye
problems, and chronic kidney disease.The risk of cardiovascular disease and death can be
reduced by lifestyle modifications, including dietary advice, promotion of weight loss and
regular aerobic exercise, moderation of alcohol intake and cessation of smoking. Drug treatment
may also be needed to control the hypertension and reduce the risk of cardiovascular disease,
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manage the heart failure, or control cardiac arrhythmias. Patients with hypertensive heart disease
should avoid taking over the counter non-steroidal anti-inflammatory drugs (NSAIDs), or cough
suppressants, and decongestants containing sympathomimetics, unless otherwise advised by
their physician as these can exacerbate hypertension and heart failure.
 Assess medical risk factors, co morbidities and identifiable causes of hypertension. For
example, essential hypertension affects 1 billion people worldwide and has a genetic
basis(Mein et al, 2004)
 Reduce cardiovascular (heart failure and stroke) and renal morbidity and mortality (ADA,
2009) by lowering high BP. The DASH dietary pattern reduces SBP by 8-14mmhg
(ADA,2009)
 For individuals with hypertension and diabetes or renal disease, maintain BP goal of
<130/80mmhg (ADA, 2009)
 Increase vascular responsiveness. Dietary sodium intake should be limited to no more

than 2300mg sodium per day; this level can lower SBP by approximately 2-8mmHg
(ADA,2009)
 Achieve and maintain an optimal body weight (BMI 18.5- 24.9); weight reduction lowers
SBP by 5-20mmHg per 10kg body weight loss(ADA, 2009)
 Increase magnesium, calcium, vitamin D, E and K where serum levels or dietary intake is
low
 Encourage adequate intake of fluids unless contraindicated. Avoid excesses of alcohol

that may increase BP
 Dietitians should encourage individuals to engage in aerobic physical activity for at least
30mins per day on most days of the week, as it reduces systolic BP by approximately 4-
9mmHg (ADA, 2009).
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 The DASH diet works within 14 days of initiation. This diet rich in fruits, vegetables and
low fat dairy foods; it is low in SFA and total fat. Adequate amount of potassium from
skim milk, baked potatoes, grapefruit, oranges, bananas, lima beans and other fruits and
vegetables should be planned daily
 Tips on eating the DASH way: Start small; make gradual changes in eating habits.
Organize meals around carbohydrates such as pasta, rice, beans or vegetables.
Carbohydrates such as beans, whole grain, oat bran, and fruits (apples, blueberries) and
vegetables should make up 50% of the diet.
 Treat meat as one part of the whole meal, instead of the main focus. Use fruits or low fat,
low-calorie foods such as sugar-free gelatin for desserts and snacks.
 Increase fruits and vegetables (5 – 10 servings daily) for their flavonoid, phytochemical,
potassium content and properties (ADA, 2009). Besides the DASH diet, Mediterranean
and vegetarian diet patterns tend to lower BP and can be beneficial.
 Limit sodium intake. Only 20 – 50% of patients with hypertension are sodium sensitive.
Patients with EH are more sodium sensitive than patients whose conditions are secondary
to other disorders (Houben et al, 2005).
 Read label carefully. If something is sodium free, it has 5mg or less per serving.
Something that is light in sodium has 50% less than the usual recipe. A food that is
labeled low sodiummust be 149mg or less per serving. About 77% of salt in the diet
comes from processed foods, 12% naturally, and the remainder is either added during
cooking or at the table.
 Use an energy-controlled diet if weight loss is needed.
 Olive, soybean, and canola oils can be substituted for some saturated fats in cooking.
Pistachios, sunflower kernels, sesame seeds, and wheat germ are good sources of
phytosterols: use them often.
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 Limit alcoholic beverages to one drink for women and to two drinks for men.
 Use sources of omega-3 fatty acids, such as mackerel, haddock, sardines, andsalmon,
several times weekly. Tuna should be usedless often because potential mercury content
could elevate BP.
 Higher intake of dairy products seems to reduce serum uric acid levels: high uric acid
levels are often correlated with BP and stroke (Choi et al, 2005).
 Increase food sources of folic acid, vitamins B 12, and B6 for overall cardiovascular health.
Vitamin D is also important. Vitamin D deficiency is associated with increased risk of
developing incident hypertension or sudden cardiac death in individuals with pre-existing
CVD (Judd and Tangpricha, 2009).
 Green tea, cocoa and chocolate should be encouraged.
ATHEROSCLEROSIS, CORONARY ARTERY DISEASE AND DYSLIPIDAEMIA
Atherosclerosis
Atherosclerosis involves progressive narrowing and loss of elasticity in the blood vessel wall
caused by accumulation of plaques. The heart, brain and leg arteries are most often affected.
Coronary Artery Disease
CAD occurs when the coronary arteries that supply blood to the heartmuscle become hardened
and narrowed due to the build up of plaque on the inner walls or lining of the arteries. Blood
flow to the heart is reduced as plaque narrows the coronary arteries and diminishes oxygen
supply to the heart muscle. CAD is common and is most often caused by smoking, high BP, low
HDL cholesterol, family history of early CHD and age. Obesity , diabetes and insulin resistance
are also risks.
Ischemia
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It is a local and temporary deficiency of blood caused by obstruction, as from thrombosis. People
with ischemic heart disease benefit from diets high in monounsaturated fatty acid (MUFA),
omega 3 fatty acids, whole grains, vitamin E, wine, vegetables and fruits
Dyslipidaemia
It involves hypertriglyceridaemia, high LDL cholesterol and low levels of high density
lipoprotein cholesterol. These imbalances in individual lipd components contribute to increased
risk of coronary artery disease.
Objectives of Medical Nutrition Therapy
 Improve LDL and HDL Cholesterol levels to prevent formation of new lesions. (lower
elevated chol levels to less than 200mg/dl and Trig level to less than 200mg/dl)
 Treat metabolic syndrome. Address underlying causes like overweight, obesity and
physical inactivity
 Initiate and maintain weight loss if overweight. Obesity with a high waist circumference
is especially important to correct in both men and women
 Moderate carbohydrate restriction and weight control can improve dyslipidaemia
 Use more flavonoids, phytochemicals, soy products and fruits and vegetables
1. A diet rich in fruits , vegetables, low fat diary products, and low sodium and saturated
fat can decrease BP
2. Replace saturated fatty acid with MUFA and PUFA; include olive oil and canola oil
in cooking (less than 7% satirated fat)
3. Consume half cup of nuts daily with a diet low in saturated fat and cholesterol to
decrease total cholesterol. Nuts contains flavonoids, phenols, sterols, saponins, folic
acid, magnesium, copper, potassium and fiber eg almond, walnut, cashewnut,
groundnut, pistachio.
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4. Consume antioxidants from dietary sources. Supplemental antioxidants alone or in
combination with other antioxidant may act as pro- oxidant and have no protection
for CVD
5. Use flavonoids from tea, yellow onions, redwine, grapefruit, apples, cocoa
6. Consume a diet high in total fiber (17-30g/day)
7. Regular consumption of an average of two servings of fatty fish per week reduces risk
of death from cardiac events. However, a low to moderate fat diet is also needed
8. Use fewer animal proteins and more legumes or vegetable protein sources. Fish and
shell fish may be used 3 or 4 times weekly, especially sources rich in omega 3 fatty
acids. Remove chicken skin before cooking or just before serving. Lean beef and
chicken are considered to be comparable
9. Trans fatty acids should be avoided
10. The mediteranean diet tends to be quite acceptable to most people and works well in
lowering coronary risk factors. The DASH diet is also very useful
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HEART VALVE DISEASES
The heart has 4 valves (triscupid, pulmonary, aortic and mitral). Inflammation of any or several
of these valve can cause stenosis with thickening (which narrows the opening) or incompetence
(with distortion and inability to close fully).
If mitral valve is not functioning properly, due to injury or disease, blood leaks back into the left
atrium (regurgitates) when the left ventricle contracts and backs up into the lungs
Mitral valve prolapse is the most common cause of severe mitral regurgitation. Overall prognosis
of patients is excellent but a small subset will develop serious complications including infective
endocarditis or sudden cardiac death. Mitral stenosis (stiffening) can cause lung congestion,
breathlessness afterv exercise or while lying down, hemoptysis,brochial infections, chest pains
and right heart failure.
Aortic stenosis can cause symptoms of angina, vertigo, fainting on exertion and left heart failure
Tricuspid stenosis increases the risk of heart failure.
Pulmonary stenosis is rare and occurs in only 2% of all valve disorders
 Prevent heart failure, bacterial endocarditis, embolic or artrial fibrillation and sudden
death
 Prepare if necessary for valve replacement surgery
 Prevent or correct cardiogenic shock with tachycardia and other symptoms
 Correct or manage atherosclerosis
1) Avoid excesses of calories, sodium and fluid. In some patients with vertigo, fluid and
sodium restriction may actually be detrimental.
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2) If weight loss has taken place, add extra calories and snacks to return to a more desirable
body weight
3) The DASH diet is useful. Encourage use of flavonoids such as chocolate, cocoa, grape
juices, apples, onions, tea or red wine. Flavonoids may help to reduce blood clot
formation
4) Ensure adequate intake of omega 3 fatty acids. However, avoid high fat diets as the
benefits of omega 3 are reduced with those diets
5) Control intake of vitamin K while on warfarin
SODIUM AND SALT MEASUREMENT EQUIVALENTS
Sodium chloride is approximately 40% (39.3%) sodium and 60% chloride. To convert a
specified weight of sodium chloride to its sodium equivalent, multiply the weight by 0.393. Na is
also measure in miliequivalent (mEq). To convert miligrams of sodium to mEq, divide by atomic
weight of 23. To convert sodium to sodium chloride (salt), multiply by 2.54 Millimoles (mmol)
and miliequivalents (mEq) of sodium are the same. For example:
1 tsp of salt = approximately 6g NaCl= 6096 mg NaCl
6096 mg NaCl x 0.393= 2396mg Na (approximately 2400mg)
2396mg Na/ 23 = 104mEq Na
1g Na = 1000mg/23 = 43mEq or mmol
1tsp of salt = 2400mg or 104mEq Na
TOP TEN CATEGORIES OF HIGH –SODIUM FOODS
1) Smoked, processed, or cured meats and fish (eg., ham, bacon, corned beef, cold cuts, hot
dogs, sausage, salt pork, chipped beef, pickled herring, anchovies, tuna and sardines).
2) Tomato juices and tomato sauce, unless labeled otherwise.
3) Meat extracts, bouillon cubes, meat sauces, Monosodium glutamate and taco seasoning.
4) Salted snacks (potato chips, tortilla chips, cornchips, pretzels, salted nuts, popcorn and
crackers).
280
5) Prepared salad dressings, condiments, relishes, ketchup, barbecue sauce, cocktail sauce,
soy sauce, commercial salad dressings, salsa, pickles, olives and sauerkraut.
6) Packaged mixes for sauces, gravies, casseroles, and noodle, rice, or potato dishes;
macaroni and cheese; stuffing mix.
7) Cheese (processed and cheese spreads).
8) Frozen entrees and pot pies.
9) Canned soups.
10) Foods eaten away from home.
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IN LIVER DISEASE
BY
DIETITIAN ONOJA IFEOMA
282
LECTURE OUTLINE
 Review the functions of the liver
 Review diseases of the liver
 Major complications of liver disease
 Nutritional features of end stage liver disease
 Nutritional management of end stage liver disease
 Nutritional management of non alcoholic fatty liver disease (NAFLD)
FUNCTIONS OF THE LIVER
 Major role of the liver is the regulation of solutes in the blood that affect the functions of
other organs for example: the brain, heart, muscle and kidneys.
 Strategically placed such that all blood passing from the small intestine must travel
through the liver.
 Storage and metabolism of macronutrients such as protein, carbohydrates and lipids.
 Metabolism of micronutrients – vitamins and minerals.
 Metabolism and excretion of drugs and toxins – endogenous and exogenous.
ROLE OF THE LIVER IN NUTRIENT METABOLISM
Storage and metabolism of macronutrients such as protein, carbohydrates and lipids
Carbohydrate
 Storage of carbohydrate as glycogen
 Gluconeogenesis
 Glycogenolysis
Protein
 Synthesis of serum proteins e.g. albumin
 Synthesis of blood clotting factors
 Formation of urea from ammonia
 Oxidation of amino acids
 Deamination or transamination of amino acids
Fat
 Hydrolysis of triglycerides, cholesterol and phospholipids to fatty acids and glycerol
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 Formation of lipoproteins
 Ketogenesis
 Fat storage
 Cholesterol synthesis
 Production of bile necessary for digestion of dietary fat
Vitamins
 Site of the enzymatic steps in the activation of vitamins : thiamine, pyridoxine, folic acid,
vitamin D(25 hydroxycholecalciferol)
 Site of the synthesis of carrier proteins for vitamins: A, B12, E
 Storage site for fat soluble vitamins A, D, E, K, B12
Minerals
 Storage site for copper iron and zinc
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Clinical Manifestations of Cirrhosis
© 2004, 2002 Elsevier Inc. All rights reserved.
DISEASES OF THE LIVER HEPATITIS

 Inflammation of hepatocytes
 Reversible
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Precipitants include:
 Viral infections such as hepatitis A, B, C
 Drugs such as paracetamol
 Some herbal preparations
 Alcohol
Fatty Liver:
 Infiltration of the liver by fat
Possible causes include:
 alcohol
 obesity
 type 2 diabetes mellitus
 hyperlipidaemia
 sudden rapid weight gain
 hepatitis C
 TPN
NAFLD (Non Alcoholic Fatty Liver Disease)
 Resembles alcohol induced fatty liver
 Occurs in people who do not abuse alcohol
 Has the potential to progress to cirrhosis and liver failure
 Simple steatosis (fat infiltration)
 Steatohepatitis (NASH) (fat infiltration + Inflammation)
 Fibrosing steatohepatitis
 Cirrhosis
Risk Factors include:
 Overweight
 Obesity
 Central Obesity
Factors involved in the development of NAFLD:

 Lifestyle:
 Weight gain
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 Weight loss
 Reduced activity
 Childhood and adult obesity
 Type 2 diabetes
The major underlying risk factor for the development of NAFLD is insulin resistance.
NAFLD (Non Alcoholic Fatty Liver Disease)
 Prevalence of obesity in patients with NAFLD reported between 30% and 100%
 Prevalence of type 2 diabetes in patients with NAFLD reported between 10% and 75%
 Prevalence of hyperlipidaemia in patients with NAFLD reported between 20% and 92%
NAFLD - Symptoms
 Often asymptomatic of liver disease at time of diagnosis
 Fatigue or malaise and/or a feeling of fullness or discomfort on the right side of the
abdomen
 Mild to moderate elevation of the enzymes: aspartate amino transferase and alanine
amino transferase
 Diagnosis confirmed on biopsy
Autoimmune liver diseases
 Diseases of the biliary tract and include primary sclerosing cholangitis (PSC) and primary
biliary cirrhosis (PBC)
 PSC often occurs in association with ulcerative colitis
 Serum cholesterol levels may be elevated and unresponsive to medication or dietary
manipulation
Fulminant Hepatic Failure
 Sudden massive necrosis of hepatocytes
 The patient rapidly becomes encephalopathic and comatosed
 Causes may be viral or a reaction to a drug such as paracetamol, sulphathiazone or some
herbal remedies
Alcoholic liver disease
 Alcohol is toxic to the liver
 Caused by chronic alcohol abuse
 All stages of the disease process – hepatitis, fatty liver fibrosis and cirrhosis
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 Cessation of alcohol may result in recovery in the early stages of liver disease
 Cessation of alcohol in patient with cirrhosis may result in an improvement in liver
function and may also result in a slowing down of the disease progression
Cirrhosis
 Refers to chronic scarring of the liver
 Clearly delineated nodules form within the liver which contain connective tissue
 This leads to a significant reduction in liver function
Normal Liver vs. Damaged Liver
PORTAL HYPERTENSION
Occurs as a result of fibrous infiltration of the liver which in turn causes increased pressure in the
portal vein.
This pressure continues back through the system to the abdominal capillaries which then leak
serous fluid into the abdominal cavity due to this increased pressure and low serum albumin
levels.
Surgical interventions may be undertaken to alleviate this pressure. There are risks associated
with these procedures – infection, failed shunts, encephalopathy.
Ascites
 Refers to the accumulation of fluid in the abdominal cavity
 It contains protein, sodium and potassium
 It is considered to be an active metabolic unit
Jaundice
 Refers to the yellow colour seen in patients with liver disease
 It is caused by high circulating levels of bilirubin
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 Severe itching may be present. May be alleviated by Questran/cholestyramine or by
phenergan
Varices
 Distended/engorged veins that can occur at any point in the venous system of the GIT.
 May bleed readily as patients with end stage liver disease (ESLD) have poor coagulation
secondary to impaired synthesis of clotting factors.
Encephalopathy
 Impaired mental state that results in impaired mentation and coordination
 May result in coma.
 Believed to be caused by increases in plasma ammonia and other nitrogenous waste
products.
 These toxins cross the blood brain barrier and interfere with neuromuscular function and
behavior.
Precipitants of encephalopathy include:
 Peritoneal infection (subacute bacterial peritonitis – SBP)
 GIT bleeding
 Poor compliance with lactulose (marketed as Duphalac) therapy
 Nitrogen overload
 Fluid and electrolyte imbalance
 Medications
 Acid-base imbalance
There are four classifications of encephalopathy:
Grade1. foetor, impaired coordination, tremor, altered handwriting, reduced attention span, mild
confusion, mood swings and altered sleep pattern
Grade 2. asterixis (impaired ability to draw a star), slurred speech, ataxia inappropriate
behaviour, lethargy, impaired memory and mild disorientation
Grade3. bizarre behaviour, confusion, moderate to severe disorientation, uncharacteristic anger,
paranoia, somnolence, stupor and muscle rigidity
Grade 4. comatosed, dilated pupils.
Common Causes of Cirrhosis
•Hepatitis C (26%)
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•Alcoholic liver disease (21%)
•Hepatitis C plus alcoholic liver disease (15%)
•Cryptogenic causes (18%)
•Hepatitis B, which may be coincident with hepatitis D (15%)
•Miscellaneous (5%)
Miscellaneous causes of chronic liver disease and cirrhosis
†Nonalcoholic steatohepatitis (NASH)
†Autoimmune hepatitis
†Primary biliary cirrhosis
†Secondary biliary cirrhosis (associated with chronic extrahepatic bile duct obstruction)
†Primary sclerosing cholangitis
†Hemochromatosis
†Cystic fibrosis
†Wilson’s disease
†Alpha-1 antitrypsin deficiency
†Granulomatous disease (e.g., sarcoidosis)
†Type IV glycogen storage disease
†Drug-induced liver disease (e.g., methotrexate, alpha methyldopa, amiodarone)
†Venous outflow obstruction (e.g., Budd-Chiari syndrome, veno-occlusive disease)
†Chronic right-sided heart fa
MEDICAL NUTRITION THERAPY (MNT) FOR CIRRHOSIS

•NUTRITIONAL IMPLICATIONS
Patients with cirrhosis may be unable to consume adequate amounts of food due to:
 Early satiety caused by the effect of ascites on the stomach’s capacity to expand.
 They may also experience impaired nutrient digestion and absorption due to portal
hypertension,
 Decreased pancreatic enzyme production and/or secretion, and villus atrophy.
 Cirrhosis increases energy expenditure because of vasodilation and expanded blood
volume.
290
 Blood sugar levels can be erratic. When cirrhosis reaches levels at which 80% of
hepatocytes are dysfunctional, hypoglycemia is a frequent occurrence due to
hyperinsulinemia.
 The lack of adequate amounts of glycogen reserves as a result of the liver damage may
cause hypoglycemia after an overnight fast and also prompt mobilization of amino acids
from the skeletal muscles for gluconeogenesis.
 However, 40%–50% of all patients with end-stage liver disease suffer from insulin-
resistant diabetes mellitus. Therefore, hyperglycemia may also be evident.
NUTRITIONAL ASSESSMENT
 As with alcoholic hepatitis, assessment should include attention to food/liquid intake and
intolerances;
 Lifestyle factors including alcohol intake; lab values related to liver function and
vitamin/mineral status; and current and past medical diagnoses and treatments.
 Many of the methods often used for anthropometric and biochemical assessment of
nutritional status are not reliable for individuals with cirrhosis. Due to the edema and
ascites, dry weight may not be obtainable, and electrical impedance analysis will not be
accurate.
 Many of the liver protein lab values used to determine visceral protein status will be
abnormal because of hepatic dysfunction.
 In 2006, the European Society for Parenteral and Enteral Nutrition (ESPEN)
recommended that the Subjective Global Assessment (SGA) and measurement of mid-
arm muscle circumference (MAMC) or mid-arm circumference (MAC) and triceps skin
fold thickness (TST) be used to nutritionally assess the patient.
 The 2009 ASPEN guidelines for critical care recommend that, in addition, calorie
requirements be assessed using indirect calorimetry.
291
MALNUTRITION IN LIVER DISEASE—CAUSE
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.
Updated by Jeanette M. Hasse and Laura E. Matarese, 2002
NUTRITION DIAGNOSIS
Nutrition Diagnoses Associated With Cirrhosis Include:
1. Increased Energy Expenditure;
2. Inadequate Energy Intake;
3. Inadequate Oral Food/Beverage Intake;
4. Inadequate Protein-energy Intake;
5. Malnutrition
6. Inappropriate Intake Of AAA/BCAA
7. Inadequate Vitamin/Mineral Intake (E.G. Thiamin, Etc.);
8. Altered GI Function
9. Impaired Nutrient Utilization;
10. Underweight
11. Altered Nutrition Related Laboratory Values
12. Food-medication Interactions
13. Involuntary Weight Loss
292
Nutrition diagnoses for cirrhosis may relate to particular complications of the disorder; for
example:
1.Ascites—excessive sodium intake; excessive fluid intake
2.Esophageal varices—swallowing diffi culty; inadequate oral/food beverage intake; disordered
eating patterns
3.Encephalopathy—excessive protein intake; inappropriate intake of AAA/BCAA
4.Hepatorenal syndrome—excessive sodium intake
NUTRITION INTERVENTION
Objective
 The primary objective is to spare the liver and provide it with the nutrients needed for
regeneration
 To ensure adequate rest, fluids, good nutrition, and in particular, to prevent or avoid
further damage to the liver eg avoidance of alcohol.
 To provide adequate diet for patients suffering from anorexia and frequently unable to
consume an adequate diet
 To increase dietary intake through the use of foods.
IMPLEMENTATION
 Energy Nutrients: Calorie and protein recommendations for patients with liver cirrhosis
are 35–40 kcal/kg per day with a protein intake up to 1.6 g/kg per day depending on the
degree of malnutrition and other medical complications.
 Protein should only be restricted with severe forms of encephalopathy, and in the case of
a coma that does not respond to standard treatment, an enteral product high in branched-
chain amino acids should be administered
 Greater amounts of protein from vegetable and dairy sources have been
recommended for patients with mild encephalopathy because these sources are lower in
aromatic amino acids.
 Fat restriction to less than 30% of calories (with or without medium-chain triglyceride
supplements) is commonly recommended for patients with steatorrhea.
293
 Carbohydrate intake should be spread out by offering multiple meals throughout the day
in order to minimize hypo and hyperglycemia. Because diabetes is common in patients
with cirrhosis.
 Vitamins And Minerals
 Management of ascites usually requires a sodium restriction of 2 grams per day; fluids,
however, are not usually restricted.
 Use of a multivitamin/mineral supplement as indicated by nutrition assessment and blood
chemistry information is appropriate
OTHER CONSIDERATIONS
 Adequate nutrition should be provided through meals and supplements whenever
possible, but enteral and parenteral support should be considered in situations that result
in inadequate oral intake and certainly are indicated for those patients who are
comatose.
 For esophageal varices, a mechanically soft diet may be recommended as a preventative
measure to reduce risk of bleeding, even if there are no evident nutrition diagnoses
related to this complication.
MONITORING AND EVALUATION
 Monitoring and Evaluation In general, the patient should be monitored for:
 Tolerance to feedings,
 Amount of nutrients consumed
 Dry weight changes
 Laboratory values
 Cognitive status.
MNT FOR ASCITES
 Ascites is accumulation of fluid in the abdominal (peritoneal) cavity causing a distension.
 Restrict sodium to 2 grams or less
 Supplement protein and calorie if frequent paracentesis (a procedure involving the
removal of fluid from the abdomen using a needle).
 Ensure adequate intake of vitamins and mineral through supplementation
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 A low fat diet by enteral feeding is needed in some cases, with MCT’s as preferred fat
sources; addition of EFA’s will also be necessary.
MNT FOR HYPONATREMIA

 Hyponatremia is an electrolyte disturbance in which the sodium ion concentration in the
serum is lower than normal.
 It occurs because of the decreased ability of the body to excrete water as a result of;
persistent release of anti-diuretic hormone, sodium loss via paracentesis as well as
sodium restriction(rear). It can also be caused by over hydration from drinking too much
water (polydipsia).
 Fluid intake should be restricted to 1 to 1.5 liter per day and in some cases as low as 500-
750 ml + urinary loss.
 Moderate sodium intake.
OESOPHAGEAL VARICES: Oesophageal Varices are extremely dilated sub-mucosal veins in
the lower third of the esophagus. They are most often a consequence of portal hypertension,
commonly due to cirrhosis; patients with oesophageal varices have a strong tendency to develop
bleeding.
MNT: OESOPHAGEAL VARICES
1. Cannot feed enterally during acute bleeding episodes.
2. May require PN if patient unable to eat
MNT FOR SPECIFIC LIVER DISEASES

MNT: alcoholic liver disease
 Avoid alcohol to allow liver to heal
295
 Malnourished alcoholics should consume a well balanced meal with adequate protein and
carbohydrate
 Micronutrient deficiencies requires supplementation
MNT: HEPATITIS
 For patients with all forms of hepatitis, provide a complete and balanced meal.
 Fat should be moderate to liberal depending on tolerance
 Extra fluid should be encouraged unless contraindicated
 Supplement diet with multivitamins, especially the B-complex vitamins
 Plants like dandelion and artichoke are good for cell liver injuries because of high
phytochemicals and antioxidants
MNT IN END-STAGE LIVER DISEASE
 Energy needs are highly variable; 30% of patients are hypo metabolic and 20% hyper
metabolic
 Use indirect calorimetry where available
 Energy: 25 to 30 kcal/kg dry weight
 Ascites increases REE by 10%, thus may need increased energy (calorie)
 How? read Hasse et al. ASPEN Nutrition Support Practice Manual, 2nd Edition, 2005, p.
238.
 Cont’d: End-Stage Liver Disease
 Fat: from 25% to 30% of kcal from fat.
 May try MCT if steatorrhea is present; with severe case, fat may be restricted and
discontinue if accompanying diarrhea does not improve
 Protein: 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption,
metabolic stress
 CHO: high intake of both complex and simple carbohydrates
 Vitamin and mineral supplements may be needed
 Electrolytes: restrict sodium with edema or ascites (1500-2000 mg/day)
 Fluid: restrict fluid if hyponatremia is present 1000-1500 ml
 Hasse. ASPEN Nutrition Support Practice Manual, 2nd edition, 2500, p. 239.
296
NUTRITIONAL MANAGEMENT OF END STAGE LIVER DISEASE
Restricting protein intake did not have any positive effect on the evolution of episodic hepatic
encephalopathy.
Protein
 Protein restriction is contra - indicated for patients with decompensated cirrhosis
 Recommended protein intake for cirrhotics is 1.0 – 1.5g protein/kg/day¹
 Dietary protein restriction does not appear to be of any benefit in episodic hepatic
encephalopathy.
¹Plauth M, Merlim, Kondrup J, Weimann A, Ferenci P, Muller MJ.ESPEN Guidelines for

nutrition in Liver Disease and Transplantation. Clinical Nutrition 1997; 16: 43-55²
²Cordoba J, Lopez-Hellin J et al. Normal protein diet for episodic hepatic encephalopathy:
results of a randomised study. J of Hepatology 41 (2004) 38-43.
NUTRITIONAL MANAGEMENT OF END STAGE LIVER DISEASE

Does the type of protein matter?
Amino Acids in Encephalopathy
 Patients with advanced liver disease have an altered ratio of branched chain amino
(leucine valine, isoleucine) acids to aromatic amino acids (phenylalanine, tyrosine)
 Aromatic amino acids are catabolised in the liver and their metabolism is impaired in
cirrhosis resulting in an increase in circulating levels of AAAs
 Branched chain amino acids (BCAA) are metabolised predominantly in the skeletal
muscle and fat
297
 Plasma BCAA levels fall due to their utilisation as an energy substrate and a substrate in
gluconeogenesis
 The alteration in the ratio of BCAA: AAA has been proposed as an aetiological factor in
the development of encephalopathy.
 Marchesini et al carried out a multicentre double blind randomised trial in which BCAA
supplementation was compared with an isocaloric casein supplementation in 64 patients
with encephalopathy*
 16/34 patients in the BCAA group regained normal mental state compared with 9/30 in
the casein treated group (p<0.05)
 After 6 months on BCAA treatment nitrogen balance improved and was suggestive of
decreased nitrogen catabolism in the BCAA treated group
 Long-term oral BCAA supplementation (6 months) resulted in an increase in body weight
 15 centres over up to 15.5 months*
 174 patients with Childs B or C cirrhosis
Fischer JE, Rosen HM, Ebeid AM et al. The effect of normalisation of plasma amino acids on
hepatic encephalopathy in man. Surgery. 1976 Jul. 80 (1): 77-91.
G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid
treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101.
Marchesini G, Bianchi G, Merli M et al. Nutritional supplementation with branched chain amino
acids in advanced cirrhosis: a double blind randomised trial. Gastroenterology 2003;
124:1792-1801.
Methods:
Three types of nutritional supplements. Each 10g package supplied:
 14.4g BCAA/day (leucine, isoleucine, valine and saccharose providing 37.5 kcal)
 2.1g lacto-albumin/day (lacto-albumin, saccharose and mannitol providing 33.6 kcal)
 2.4g maltodextrose/day (maltodextrose, saccharose providing 34.9 kcal)
 All subjects were instructed to take 2 packets three times daily dissolved in 200ml water
half an hour before meals
 Patients were maintained on self selected diet. No new dietary restrictions were
recommended or prescribed
298
 Standard therapies (albumin, diuretics, lactulose) were allowed but registered
Results:
 115 patients remained in the study
 59 patients were withdrawn for a variety reasons:
a. Death
b. Deterioration in liver function
c. Non-compliance (palatability, nausea, gastrointestinal discomfort and diarrhoea)
d. Psychiatric disease
 Patients treated with BCAAs were admitted to hospital less frequently:
a. 195 days in BCAA group;
b. 327days in L-ALB group and
c. 520days in M-DXT group
 Length of stay varied within the treated groups:
a. 0-24 days in BCAA group
b. 0-31 days in the L-ALB group
c. 0-77 days in the M-DXT group.
 Improved triceps skinfold thickness in the BCAA group
 Improved midarm fat area in the BCAA group
 Reduction in the prevalence and severity of ascites in the BCAA group
 Shift towards better scoring of health only in the BCAA group
 M-DXT supplementation therapy did not require increase in insulin therapy
 Total bilirubin levels decreased in the BCAA group and increased in the M-DXT group
 Improvement in the CTP score in the BCAA group
 CTP was stable in the L-Alb group and M-DXT group
 Reduced prevalence of anorexia in the BCAA group
To summarise:
 There are benefits to routinely supplement patients with advanced cirrhosis with
branched chain amino acids
 Patient compliance
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Current Criteria for use of Oral BCAA Supplementation at RPAH:
 chronic encephalopathy
 frequent hospital admissions due to encephalopathy
 severe depletion of fat and muscle stores
 elevated blood sugar levels
Books for further reading:
Escott-Stump Sylvia., Nutrition and Diagnosis related care,7th ed
Kathleen Mahan L, Escott-Stump S., Krause’s Food and Nutrition Therapy, 12th ed, Saunders
Elsevier, 11830 west line industrial drive, St Louis Missouri 63146, USA
Thomas B, Bishop J., Manual for Dietetics Practice, 4th ed, Blackwell publishing Ltd, UK.
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A LECTURE ON
HEPATIC ENCEPHALOPATHY
DISORDERS OF LIPID
METABOLISM
ENTERAL AND PARENTERAL

FEEDING
BY
DTN. UGWUANYI, M.C.

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Meaning of some Terminologies:
Hepat Liver, Encephalo brain, pathy disease.
Hepatic Encephalopathy (Portosystemic encephalopathy)
Is a condition in which brain function is impaired by the presence of toxic substances absorbed
from the intestine (colon) which are normally removed or detoxified by the liver. It is a complex
syndrome characterized by neurological disturbances, resulting from the entrance of certain
nitrogenous substances which suppose to be detoxified or removed by the liver (if the liver is
functioning well). These nitrogenous substances move directly to the brain to cause
hyperammonemia.
Hepatic encephalopathy can be precipitated (caused) by GIT bleeding severe infection, abnormal
electrolytes or electrolyte imbalance, renal failure, diuretic therapy, use of sedatives or
medications that affect the central nervous system; and constipation.
Hepatic Encephalopathy can be induced by porta caval shunting. The spectrum of HE ranges
from minimal cerebral functional deficits which can only be found by sensitive tests, to coma
with signs of decerebration. Acute H.E. may be reversible and chronic one may worsen or lead to
coma.
The Pathogenesis of Hepatic Encephalopathy (H.E) (origin and development)
The Pathogenesis of H.E is multifactorial. The basis of neurotoxicity of ammonia,

gammaminobutyric acid (GABA) or other agents implicated in this condition is not clear.
Astrocytes are the most abundant cell type in the brain; the buffer extracellular K, regulate
neuro-transimitter release, form the blood-brain barrier, release growth factors and regulate the
brain immune response.,
Acute exposure of the astrocyte to ammonia results in alkalinization, with calcium-dependent

glutamate release and dysfunction. Glutamine, a byproduct of ammonia detoxification, is found
elevated in brain in Hepatic encephalopathy. Zinc deficiency may be involved in the
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pathogenesis of encephalopathy because it is a cofactor in Ornithine transcarbamylase (OTC)
activity and also influences ammonia production from aspartate.
STAGES OF HEPATIC ENCEPHALOPHATHY AND THEIR SYMTOMS
Grade O: Minimal Hepatic Encephalophathy lack of detectable changes in personality or

behavior, minimal changes in memory, concentration, intellectual function and co-ordination.
Grade I: Decreased attention, mild confusion, euphoria or depression; slowing of ability to

perform mental tasks, irritability and disordered sleep pattern such as inverted sleep cycle.
Grade II: Lethargy or apathy, gross deficits in ability to perform mental tasks, obvious
personality changes, inappropriate behaviour or intermitted disorientation usually regarding time.
Grade III: Somnolent but can be aroused, unable to perform mental task disorientation about
time and place, market confusion, amnesia, occasional fits of range and present but
incomprehensible speech.
Grade IV: Coma with or without response to painful stimuli.
MEDICATION USED FOR HEPATIC ENCEPHALOPATHY
1. Neomycin – Orally administered antibiotics, kills some of the bacteria present within the
intestines that produce the dangerous toxins.
2. Rifaximin – is a non-absorbed antibiotic with abroad spectrum of activity against aerobic and
anaerobic Gram-positive and Gram-negative organism. It has a better and tolerability profile
than that of lactulose and neomycin.
3. Cholestyramine or ursodeoxycholic acid – for itching.
4. Laxatives: Lactulose eg. Chronulac, duphalac, cholac syrup, constulose –lactulose is a
synthetic sugar used to treat constipation. Certain medications can increase the brain
sensitivity to ammonia and other toxins and should not be taken. Sedative drugs (Valium,
Atrivan, Xanax).
5. Zinc sulfate or acetate – zinc supplement is recommended.
6. Invasive approaches such as surgical shunts: - intrahepatic portal systemic venous shunt is
a rare spontaneous communication between the portal and systemic venous circulation,
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measuring more than 1mm indiameter and least partially located inside the liver. Pt who has
been given a portal-caval shunts are at increased risk of encephalopathy and may benefit from
mild protein restriction.
1. Formerly, the use of protein management of H.E was said to be protein of diary product.
Milk and egg tend to produce less ammonia than meat or poultry. Some text will recommend
protein restriction to begin at a dose of 0.5g/kg/day. But researchers currently found out that
vegetable protein is more tolerated than animal proteins like soya bean and soya bean products
(like soya oil, soy milk), green peas, nuts and nut butter (eg. Groundnut, cashew nut, beans,
leafy greens, sesame, sunflower seeds and unsweetened cocoa powder.
2. Alcoholic beverages should be avoided.
3. Large meals increase portal pressure, recommend use of small but frequent meal.
4. Adequate intake of carbohydrate and fat is needed to avoid muscle catabolism.
5. Avoid high dose of vitamin A & D which may be toxic to the diseased liver.
6. Foods reach in zinc also help to improve neurological symptoms and signs of malnutrition.
REFERENCES
F.P Anita, Philip Abraham (2002). Clinical Dietetics and Nutrition 4th Edition page 305-309.
L. Kathleen Mahan, Sylvia Escoth-Stump, Janicel Raymond (2012). Food and the nutrition care
process. 13th Edition pp 661-662
Sharon Raddy Rolfes, Kathryn Pinna, Ellie Whitney (2006). Understanding Normal and Clinical
Nutrition, International Student Edition PP 774
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DISORDERS OF LIPID METABOLISM
Outlines
- What are lipids
- Types of lipids
- Sources of lipids
- Importance of lipids
- Lipids digestion & metabolism
- Disorders of lipids metabolism
- Dietary management (NCP)
WHAT ARE LIPIDS?
Lipids are organic substances soluble in solvents such as alcohol, either and chloroform but not
in water. Lipids embraces fatty acids, neutral fats, phospholipids, steroids and waxes. The are
important source of energy for the body.
TYPES OF LIPIDS
Lipids generally are grouped into three types:-
1. Simple lipids: This consists of fatty acids, triacylglycerol or triglycerides waxes (esters
of fatty acids with higher alcohol, cholesterol (fatty acids esters)
2. Compound lipids: Consists of phospholipids, glycolipids, lipoprotein.
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3. Derived lipid: derivatives such as sterols & straight – chain alcohol obtained by
hydrolysis of these lipids in simple and compound lipids.
Fatty Acids (simple lipids)
The animal and vegetable fats eaten by man are mixed triglycendes containing different fatty
acids. There are over 40 naturally occurring fatty acids. Fatty acids may be saturated or
unsaturated. Cis – and Trans- fatty acids.
Saturated and unsaturated fat:
Saturated fats: are usually solid at room temperature. They are mainly short-chain fatty acids
with no double bond. The common saturated fatty acids are palmitic, stearic, lauric and myristic
acids.
Palmitic – fat of animal like sheep
Stearic – fat from beef tallow and lard.
Lauric & myristis acids – fat from vegetable particularly coconut & palm oils.
Unsaturated fat: are usually liquid at room temperature. They are made up of medium & long-
chain fatty acids with double bond. They are present in marine oils (whale, shark etc) and
vegetable oil (expect coconut & palm oils). Poly unsaturated fatty acids (PUFA) cannot be
synthesized by human and obtained entirely from diet.
CIS - & TRANS – FATTY ACID
CIS – Fatty acids: Oleic acid (18:1) is the principal naturally occurring unsaturated fatty acid. It
has one double bond in the CIS – configuration (ie the two hydrogen atoms attached to the
double bond on the same side). The CIS configuration maintain liquidity of the oil.
Trans-fatty acids: Elaidic (18:1). It has 18 carbon atom with one double bond 9ie the two
hydrogen atoms at the double bond lies on opposite sides. It solidifies fat & behave like a
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saturated fat. Trans-mono unsaturated fatty acids are formed when vegetable or marine oil are
hydrogenated.
Polyunsaturated fatty acids (PUFA)
There are two main classes of PUFA:
1. The omega-6 fatty acid (n-6 class) – this include linoleic acid, derived primarily from
plant oil such as com, stufflower, soybean and sunflower oil.
2. The omega-3 fatty acid (n-3 class) – this include linolenic acid derived from plants and
long-chain fatty acids obtained from fish oil PUFA are also essential fatty acids.
Essential fatty acids are fatty acids that cannot be synthesized by the body and have to be
supplied in the diet. Egs of EFA are linoleic, linolenic and arachidonic acids.
Linoleic and Linolenic acids are of vegetable origin and are present in cotton seeds, groundnut,
linseed oils while Arachidonic acids is synthesized from Linolenic acid in fish and animals.
Cholesterol
Normal humans have about 2g cholesterol per kg body nut. Cholesterol exist both free and as its
esters. Esters are formed by the liver and are markedly dinished in severe liver cell damage. The
sources of cholesterol are:
1. Exogenous: From animal foods mainly eggs & butter.
2. Endogenous: Synthesis from acetate by liver & the intestine (ileum) with the help of
acetyle co A enzyme. A major part of serum cholesterol is synthesized in the river,
mainly from carbohydrate.
IMPORTANCE OF LIPIDS IN THE BODY ARE:
1. Fatty acids provides energy to the body. (Fat supplies 9 kcal/ gram while protein/ CHO is
4kcal/grame.
2. Fats serve as a vehicle for absorption of fat soluble vitamins A, D, E & K.
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3. It stays longer in the stomach and helps delay the set of hunger due to the society value.
4. Fats supply essential fatty acids which are necessary for growth & function.
5. Fat (cholesterol) helps in formation of cell membrane & functioning of hormones

(testosterone)
6. It impact flavour to food.
7. Fat has other functions like insulation effect.
8. If fats & CHOs are utilized as energy sources, proteins are spared for tissue growth &
repair. This is known as the protein sparing effect.
DIGESTION & ABSORPTION OF FATS
Fat floats in the stomach. Fat emptying is therefore considerably delayed. The entry of fat into
the duodenum releases: secretin, panocreozynin and cholecystokinim which stimulate the flow of
bile and pancreatic juice.
Dietary truglycende is emulsified by bile salts, is brokem down by the pancreatic & intestinal
mucosal lipase into monoglyarides and fatty acids prior to absorption.
Bile salt
- Emulsify fats (breakdown)
- Provide optimum PH for pancreatic lipase
- Activate lipase to split fats into monoglycendes & fatty acids. The absorption takes place
in the small intestine.
Oxidation & storage of fat
Fat may be oxidized to carbon dioxide & water or stored in the fat depots. Glycerol from
hydrolyzed triglycendes returns to the liver. Glucose in the cell is converted to glycerol which
combines with fatty acids to form triglycerides for deposition in the cells.
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Fat stores can also be stored in adipose tissues. These stored fat is released & utilized by the
tissues during exercise or fasting.
After the energy requirement of the body have been met, excess fat is stored in fat depots. Under
the skin, in the pentoneal cavity, b/w the muscles and around the kidney & ovaries. Women have
a higher proportion of fatty tissue than men.
DISORDERS OF LIPID METABOLISM
The body’s store of fat is constantly broken down & reassembled to balance the body’s energy
needs with the food available. The metabolized fats calmed by the blood vessels occurs in the
following forms:
HDL - High Density Lipoprotein
VLDL - Very Low Density Lipoprotein
LDL - Low Density Lipoprotein triglycendes
Cholesterol
HDL is good to the body and helps in functioning of the muscles of the heart hence reduces the
chance of CVD (Coronary Heard Disease). So when HDL is high, it is good for the body.
But when others like VLDL, LDL, triglycendes, cholesterol are higher than required by the body,
it result in disorders of lipid metabolism called Lipidosis. Disorders of lipid metabolism includes:
1. Hypercholesterolemia
2. Hypertriglycerolemia or hypertriacylglycerolemia
3. Hyperlipidemia – when all the fats in the blood are higher than normal (ie when both
VLDL, LDL, cholesterol & triglyceride are high, the term hyper lipidemia covers it)
There are other disorders of lipid metabolism that occur as a result of enzyme
abnormalities. These types of lipid disorders are inborn defeat and is genetic. Lack of lipid
enzymes in such individuals prevent the body from converting fats into energy. Those
abnormalities are called fatty acid oxidation disorders. Examples are:
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1. Gaucher’s disease
2. Tay-Sachs disease
3. Miemann-pick disease
4. Fabry’s disease.
1. Gaucher’s disease: is caused by accumulation of glucocerebrosides in tissue. It leads to

an enlarged liver and spleen and a brownish pigmentation of the skin, etc. It is common
among the Eastern Europes.
2. Tay-Sachs Disease: Is caused by the accumulation of ganglosides in tissue. The

(ganglosides are product of fat metabolism that contains oligosacchandes unit such as
galactosamine which provides the CHOs determinant of the human blood groups A, B, &
O). Children with this disease becomes progressively intellectually disabled floppy
muscle tone, paralysis, dementia & blindness. These children usually die by age of 3 or 4.
The disease cannot be treated or cured.
3. Niemann-pick disease: Is called by accumulation sphingomyelin or cholesterol

(Sphingomelins are sphinqolipids which contain no phosphate but possess a carbohydrate
that are important in the nervous system (especially the myelin sheath). It causes retarded
growth in children. Fatty growth in the skin, dark pigmentation and an enlarge liver,
mental retardation etc. It is common among Jewish people & cannot be cured.
4. Fabry’s disease: Is caused by accumulation if glycolipids in tissues. This disease causes

skin growths, poor vision, recurrent episodes of fever and kidney or heart failure.
These disorders can be diagnosed in the fetus by chorionic vitlus sampling or

amniocentesis during pregnancy. And a new born baby can also be tested using a New born
screening test.
DIETARY MGT OF LIPID METABOLISM DISORDER USING N.C.P METHOD
Nutrition Assessment
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Dietary Assessment:- Check the patients intake; fd habit, feeding patterns, food frequency, fd
likes & dislikes & estimated caloric intake and note.
Biochemical Assessment:- Check lipid profile test, HDL, LDL, VLDL, triglycendes or total
cholesterol and match with the normal ranges if high, indicate with this arrow (increase), if low,
indicate with (decrease) if normal do not write any arrow
Clinical Assessment:- Check the pt’s physical features/findings, whether the pt is obese or
overuit, afebril or febrile, anicteric or icteric, edema present or nil, etc.
Anthropometric Assessment:- Check the pt, wt, Ht, BMI = Wt Kg

Ht(2)m
Waist Hip ratio = Waist cm
Hip m
Male normal range 0. 95 – 1cm
Female normal range 0.8 – 0.85cm
Consider jointly all your findings in the nutritional Assessments and darw a nutrition diagnosis.
Nutritional Diagnosis: Eg. Hypercholesterolemia or hypertriglerol emila or hyperlipidemia

related to food & nutrition knowledge deficit or excessive intake of fined food or inactive life
style etc as evidenced by BMI above normal, lipid profile test raised and diet history.
Nutrition Intervention
- Counsel the pt adequately and place on high fibre, low fat diet if obese or overwit, place
on high fibre, moderate fat & CHO intake.
- Avoid fried foods or frying of foods or oil.
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- Avoid or reduce intake of foods rich in saturated fats: palm oil
coconut/groundnut/groundnut oil. Egg yolk, full cream milk, organ meats, fatty meats e.g
Kanda.
- Increase fibre intake
- Increase pits activity level
- Reduce intake of refined CHO’s (soft drinks)
- Encourage intake of fds like malmit (Ykpa) it has fat good in lowering the cholesterol
- & cucumber help stimulates liver fxn hence help to enhance fat metabolism as most of
the livers are in the liver.
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ENTERAL AND PARENTERAL FEEDING
Outlines
- Definition of terms
i. Enteral feeding
ii. Parenteral feeding
iii. Blenderized foods
iv. Polymeric diets
v. Elemental diets
vi. Hyperalimentation
vii. Osmolality
viii. Enteric
ix. Feed
- Enteral Feeding
a. Meaning/types of enteral feeding
b. Conditions that demand for enteral reeding
c. Reason why pt should be fed enterally (indication)
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d. Properties of a good enternal feeds
e. Requirement/food composition of enteral feeds
f. Complication/Hazards of Enteral feeding (tube feeding)
- Parenteral feeding
a. Meaning/types of parenteral feeding
b. Disease conditions that demand for the use parenteral feeding
c. Complication of patenteral feeding
d. All in one (AIO) system.
- Advantages of Enteral feeding over parenteral feeding
DEFINITION OF TERMS
- Enteral feeding – is supplying nutrition into the digestive tract of a pt either by mouth or
by passing a tube through the nose or abdominal walls of the stomach. Enteral feeding is
also known as Tube Feeding.
- Parenteral feeding – also known as intravenous feeding is a method of getting food

nutrients into the body through vein. It is commonly known as TPN (Total Parenteral
Nutrition)
- Blenderized foods – are ordinary food items which cannot be swallowed are blenderized
to make them liquid for feeding through a tube.
- Polymeric diets – are commercially prepared mixtures of undigested protein, fat and
CHOs that are thus lower in osmolarity and require normal digestive juices.
- Elemental diets – are commercially predigested mixtures of foods like amino acids,
sugar, minerals & vitamins usually with a small amount of fat.
- Hyperlmentation – providing more nutrition than is normally supplied.
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- Osmolality – is the contraption of body fluid (eg pleasure urine) measured in terms of the
amount of dissolved substances per unit mass of water. It is usually measured in mole kg -
1
.
- Enteric – relating to small intestine.
- Feed – is any fluid diet that can be taken orally or through tubes such as NG tubes or
Gastrostomy tubes.
ENTERAL FEEDING
This is the type of feed or fluid diet given to a patient that have difficultly in swallowing solid
diet. Enteral feeding can be given by mouth or by passing a tube through the nose. The tube may
be passed into the stomach (nasogastric), duodenum (nasoduodenal), or jejunum (nasojejunal).
When there is an obstruction in the esophagus, eternal feeding is dene by passing a tube
surgically through an incision in the abdominal wall into the stomach (gastrostemy), duodenum
(duodenostomy), or jejunum (jejunostomy).
TYPES OF ENTERAL FEEDING
The route of administering fluid diet is the base for the classification of enteral feeding. Types of
enteral feeding are:
1. Oral feeding – This is the type of feeding given to a patient orally or through mouth with
consistency that will allow for easy swalling such as oral HPF, blenderized fds. The
consistency fro children oral feeds on the pt condition.
2. Nasogastric feeding – This is the types of feeding given to a pt through tube inserted
through the nose via esophagus to the stomach. It is given to pt who have difficult in
chewing and swallowing or have poor appetite. Nasogastric feeds have lighter
consistency. In a pt that have problem with gastric enzymes, the tube can be inserted
direct to duodenum or jejunum hence the name nasoduodenum & Nasojejunal.
3. Gastrostomy feeding – This is the type of feeding given to a pt through an opening into
the stomach from the abdominal wall. This is used when Nasogastric feeding is not
possible either because of the disease condition of the or aspiration pneumonia, or reflux
315
esophagitis or sinusitis related to pt previous history of tube related ones can as well lead
to dwedenostomy, jejunostomy.
Percutaneous endoscopic Gastrostomy (PEG)
This is the type of gastrostomy with the help of an endoscope, without surgical cutting of
the abdomen or the stomach. This is sued when a pt requires prolonged tube feeding. It is also
called enterostomy.
CONDITIONS OR ILLMENTS THAT DEMANDS FOR ENTERAL FEEDING
Who should be feed enterally?
- Pt with partial or full G.I function damage
- Critically ill pt eg trauma, from surgery, burns
- Unconscious and semi unconscious pt.
- Pts with Neck/facial injuries pt with sepsis
- Pt in coma
- Persistent anorexia requiring forced feeding
- Inability to swallow due to paralysis (diphtheria, poliomyelitis etc)
INDICATION (REASONS WHY WE SHOULD FEED ENTERALLY)
A. For nutrition support – for maintaining or improving organ function & for prevention of
PEM and its associated energy effect.
B. For maintaining the structure of GIT and it’s function.
C. It help to blunting the hypermetabolic effect of the injury.
D. Helping to prrebnt translocation on bacteria and toxin there by reducing sepsis.
E. Supporting the immune system
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F. Stimulating the nutritive bloods flow
G. Preventing paralytic ileus.
PROPERTIES OF A GOOD ENTERAL FEEDS ARE:
- Nutritionally adequate
- A pouring consistency
- Palatable depending on the route of feeding
- Appetizing
- Cheap – using locally available food stuff
- Well tolerated eg not causing vomiting, diarrhea
- It should supply satiety
REQUIREMENT/FOOD COMPOSITION OF ENTERAL FEEDING
Osmolality of enteric feeds:- Can be described as the rate at which the substance in the feed
consumed dissolves in the walls of intestine as well as how they affects the concentration of the
body fluids depending on the degree of tolerance.
Osmolality of a feed is affected by the concentration of protein, CHOs, Vitamins &

electrolytes etc. Feeds with higher osmolality than that of normal body fluids produces an
osmotic effect in the stomach and small intestine. The hyperosomolality draws water into the
GIT to dilute the concentration of the feed. A pressure of water into the gastro intestinal tract
may cause diarrhea, nausea / vomiting, cramping and abdominal distention. Isotomic feeds are
designed to reduce these problems. Isotomic feeds is similar to the osomolality of normal body
fluids.
Requirement
Every requirement increase during critical illness. Use mixed fuel sources eg glucose  sugar 
vege oil. Estimated energy we use 25-30 kcal/kg/Bw for normal person. Sources of energy is
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carbohydrates which is very important for critically ill pt because it is readily digested and
absorbed. Glucose is the preferred fuel for some tissue including the brain  RBC. Pap, millet,
rice & yam blenderized can be used.
Fat:- Another major energy source which provides EFA carries fat soluble vitamin ; use PUFA
such as soya bean oil, com oil, fish oil, sunflower oil etc 4-5% of EFA is recommended to
prevent EFA deficiency.
Protein:- Provide in the the range of 0.8-1.5kg/kg/Bw will meet the need of ill patients.
Protein in the form of peptides is absorbed more rapidly than protein from A as. Sources:
milk, Casilan, meat either fresh or dried grinded, groundnut grinded etc.
Vitamin & minerals
Supplementation of vitamins & minerals should take into the consideration nutrition status at the
on set of illness it A, B, C, Complex, famous sulphate and fruit juices can be used.
Fluid  water
Most adult need at least 1500 – 2000 mls fluid daily, therefore enteral feed mixture should be as
follows:
1. NG’S = 1kcal is to 1ml
2. Gastro = 1 – 1.5kcal is to 1ml
3. Oral Hemix = 1.3kcal is to 1ml
4. Oral HPF = 1 – 1.5kcal is to 1ml
This means that if you are to place a pt on 2000kcal on fluid diet, for NG it is to be
supplied in 2000mls ie 2 liters and so on.
COMPLICATION/HAZARDS OF ENTERAL FEEDING
- Contamination – should be prepared using meticulous technique to prevent microbial

contamination which can affect immuno compromise patient.
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- Dehydration (when too concentration)
- Diarrhea
- Rupture of tube during flushing
- Regurgitation of fluid/Aspiration
- Electrolyte imbalance
- Upper GIT bleeding
- Blockage of tube with clotted formular, undissolved medication or foreign bodies.
- Misplacement of tube in esophagus
- Injury or ulceration of nasal or pharyngeal mucosa etc.
PARENTAL FEEDING
This is a method of getting food nutrients into the body through vein. In parental feeding,
the end products of the food nutrients like glucose, amino acids and fatty acids & glycerol and
other nutrients goes directly into the blood stream for circulation through intravenous catheter.
Types of parenteral feeding
Parenteral feeding (also known as Total Parenteral Nutrition) can be administered intravenously
either through;
1. CPN – a large – diameter vein, usually the superior vena cava adjacent to the right
atrium, this is called central Parenteral Nutrition (CPN).
2. PPN – a Peripheral vein, usually of the hand or forearm called Peripheral Parenteral
Nutrition (PPN).
NOTE: Parenteral Feeding is used when there is a completely dysfunctional or

inaccessible GIT; TPN is then used to by-pass the GIT.
Disease conditions that demand for the use parenteral feeding are:
319
1. Complete bowel obstruction or Paralytic iteus (iteus is where the villu is situated)
2. Abdominal distention or inability to absorb nutrient via the GIT.
3. Severe post – Prandial pain (pain after eating oral or tube)
4. Inability of the practitioner to obtain enteral means etc.
5. Gastrointestinal fistula
6. Short bowel syndrome.
7. Croln’s disease ( condition in which segments of the alimentary tract become inflamed,
thickened and ulcerated.
In administering IPN proper care is needed to avoid infection & blood clothing.
Complication of parenteral feeding are:
- Venous thrombosis
- Catheter obstruction
- Puncture of the subclavion
- Pneumothorax, hemothorax etc.
All in one (AIO) systems
Intravenous nutrition used to be delivered as individual nutrients in separate glass bottles.

This system need multiple manipulation and was time – consuming & resulted in greater rate of
infections. The AIO system is currently used to avoid these problems; it also prevents sudden
high and lo-blood sugar (hyper- and hypoglycemia and enables easy management of diabetic
patient.
ADVANTAGES OF ENTERAL FEEDINGS OVER PARENTERAL FEEDING:
- Convenient
- Inexpensive
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- Easily tolerated
- Avoid metabolic disturbances
- Laboratory estimation of blood electrolytes not necessary
- Avoid catheter sepsis & infection
- No sterilization of tubes & nutrient.
REFERENCES
Sylvia Escott – Stump (2012) Nutrition and Diagnosis – Reealted care. Lippincott Willians &
Williams, a Wolters Kluwer business. 351 West Camden Street Balthmore M.D 21201.
China 7th edition pp (897-911).
F.P. Antia and Philip Abraham (2002). Clinical Dietetics and Nutrition. Oxford University Press
YMCA Library building Jaisingh Road, New Delhi/10001, India 4 th edition pp (433 –
442).
Sareen S. Gropper, Jack L. Smith James L Groff (2005) Advanced nutrition and human
metabolism Wadasworth, a division of Thompsa Learning, inc in the USA 4 th edition pp
(128 – 157).
Gordon, M and Jeffrey, S. (2007). Perspectives in Nutrition. Mc Graw Hill companies Inc. 1221
Avenue of the Americans, New York. Ny 10020 7th edition pp (674 – 681).
Oxford Concise medical dictionary.
www.britannica.com/science/metabolsim.
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ACUTE RENAL FAILURE
OBESITY
CASE STUDIES
BY
DTN AZURUNWA CHIGOZIE.A.

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ACUTE RENAL FAILURE (ACUTE KIDNEY INJURIES)
Acute kidney injury (AKI) formerly Acute Renal Failure (ARF) is characterized by a sudden
reduction in glomerular filtration rate (GFR), the amount of filtrate per unit in the nephrons, and
altered ability of the kidney to excrete the daily production of metabolic waste.
Acute renal failure is a sudden loss of kidney function. In the presence of acute renal failure
(ARF), the kidneys are unable to remove waste and concentrate urine without losing electrolytes.
ARF can occur in days to weeks and is defined as an acute elevation in serum creatinine levels.
Azotemia, an accumulation of nitrogenous wastes in the blood, and fluid and electrolyte
imbalances occur. It is common to see hyperkalemia, hyperphosphatemia and fluid overload in
patients with acute renal failure, possibly resulting in pulmonary edema. In some cases, ARF
results in permanent kidney damage, while in others it is resolved and kidney function is not
compromised.
Acute renal failure is rapid deterioration of kidney function resulting in accumulation in the body
of nitrogenous waste products of protein metabolism. This is accompanied by scanty urine or
suppression of urine (anuria).
In anuria, without excessive trauma, fever or infection, the blood urea nitrogen rises by 10 –
15mg per 100ml (3.57 – 5.36 mmol/l) daily. The serum potassium level rises by 0.7mEq (mmol)
per day, its release from the breakdown of glycogen or tissue proteins in order to provide
calories.
The usual cause of death in anuria is not the rise in blood urea, but either potassium intoxication
which occurs after about a fortnight when the serum level rises over 10mEq(mmol) per litre, or
water intoxication due to overzealous treatment with fluids with a view to stimulating urinary
flow.
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CAUSES OF ARF: This is caused by (a) Pre-renal (b) Renal (c) Post-renal factors
a. Pre renal: Kidney failure may be due to the following factors:
i. Decreased blood volume (hypovolemia) with reduced flow to the kidney. As
kidney function is normal in the early stages, there is scanty urine (less than
400ml) with high specific gravity (over 1025). Decreased blood volume occurs in
severe burns.
ii. Decreased kidney blood flow and perfusion (with or without dehydration)
with trauma, surgery, anesthesia, handling of viscera, liver and kidney
failure (hepatorenal syndrome). Urinary sodium concentration of less than
20mEq (mmol) per litre suggests that the kidneys have retained the power to
reabsorb sodium and are capable of reasonable function, while the scanty urine is
due to decreased renal perfusion. Prolonged blood volume deficiency ultimately
produces renal damage. The kidneys then lose the ability to reabsorb sodium,
resulting in urinary sodium excretion of over 20mEq/L.
b. Renal: Renal failure can occur with (i) acute kidney damage in acute glomerulonephritis,
weil’s disease and acute pyelonephritis; (ii) acute tabular necrosis because of continued
prerenal failure, mismatched transfusion, crush injuries, blood loss in pregnancy, acute
ischemic vascular damage and toxins damaging the kidneys. Sometimes it result from the
use of contrast media for x-rays or the kidney.
*Necrosis: a localized death of tissue.
c. Post-renal: kidney failure also occurs when there is obstruction to urinary flow due to
enlarged prostate, kidney stones or stricture of the urethra. Kidney function is known to
recover up to six weeks after acute urinary suppression if the patient is kept on peritoneal
dialysis or hemodialysis with an artificial kidney.
SYMPTOMS OF ARF
1. Decrease in urine output (oliguria)
2. Cessation of urination (anuria)
3. Edema and fluid retention
4. Decreased appetite
5. Change in mental
6. Change in mental status or mood.
324
It can be diagnosed using:
1. Laboratory testing for serum creatinine, blood urea nitrogen (BUN) and potassium
2. Arterial blood gases indicating metabolic acidosis.
3. Abdominal x-ray
4. Ultra sound
5. Magnetic resonance imaging (MRI) and
6. Computed tomography (CAT Scan or CT Scan).
MEDICAL MANAGEMENT
The ratio of blood nitrogen (BUN) to Cr (creatinine) can be used diagnostically to assess the
location of damage to the kidney. Depending on where the insult occurs, BUN is increased
because of poor filtration and is more actively reabsorbed. When BUN/Cr ratio is greater than
20:1, damage is prerenal (before the kidney)when damage is intrinsic (within the kidney), the
BUN/Cr ratio decreases to less than 10:1. If careful attention is directed at diagnosing and
correcting the prerenal or obstructive causes, acute kidney injury is short lived and requires no
particular nutritional intervention.
These patients are highly catabolic, and extensive tissue destruction occurs in the early stages.
Hemodialysis (HD) is used to reduce the acidosis, correct the uremia and control hyperkalemia.
If recovery is to occur, it generally takes place within 2 – 3 weeks after, the insult is corrected.
The recovery (diuretic) phase is characterized first by an increase in urine output and later by a
return of waste elimination. During this period dialysis may still be required, and careful
attention must be paid to fluid and electrolyte balance and appropriate replacement.

Nutrition care is important because the patients not only has uremia metabolic acidosis and fluid
and electrolyte imbalance, but also usually suffer from physiologic stress (e.g infection or tissue
destruction) that increases protein needs. The problem of balancing protein and energy needs
with treatment of acidosis and excessive nitrogenous waste is complicated and delicate. Early
attention to nutritional support and early dialysis improves patient survival.
a. Protein: the amount of protein recommended is influenced by the underlying causes of
AKI and the presence of other conditions. A range of recommended levels can be found
in the literature, from 0.5 – 0.8g/kg for non-dialysis patient, to 1-2g/kg for dialyzed
325
patients. With continuous renal replacement therapy (CRRT) protein losses are high and
estimated protein needs increase to 1.5 – 2.5g/kg. As the patient’s overall medical status
stabilizes and improves, metabolic requirements decrease. During this stable period
before renal function returns a minimum protein intake of 0.8 – 1g/kg of body weight
should be given.
b. Energy: energy requirements are determined by the underlying cause of AKI and
comorbidity. Energy needs can be measured at the bedside by indirect calorimetry in
most ICUs. If this equipment is not available, calorie needs should be estimated at 30 –
40kcal/kg of dry body weight per day. Excessive calorie intake can lead to excess Co 2
production, depressing respiration. Large intakes of CHO and fat are needed to prevent
the use of protein for energy production. If peritoneal dialysis (PD) or (CRRT) with a
glucose containing solution is used, the amount of glucose absorbed can add significantly
to the daily energy intake and should be calculated. For patients who receive (PN)
Parenteral nutrition, high concentration of both CHO and lipid can be administered to
fulfill these needs as long as respiratory status is monitored. A high-calorie, low protein
diet may be used in cases in which dialysis or hemofiltration is unavailable.
c. Fluid and sodium: fluid and electrolyte intake should balance the net output with
negligible urine output, significant contributions to total body water output include
emesis and diarrhea body cavity drains, and skin and respiratory losses. Sodium is
restricted, based on decreased urinary production. In the oliguric phase when the sodium
output is very low, intake should be low as in perhaps as low as 20-40mg/day. Limiting
sodium is often impossible because of the requirements for many IV solutions (including
IV antibiotic, medications for blood pressure and PN). The administration of these
solutions in electrolyte- free water in the face of oliguria quickly leads to water
intoxication (hyponatremia). Because of this reason, all fluid above the daily calculated
water loss should be given in a balanced salt solution.
d. Potassium: most excretion of potassium (K+) and the control of K+ balance are normal
functions of the kidney. When renal function is impaired, potassium balanced should be
scrutinized carefully. In dietary sources, all body tissues containing large amount of K +
thus tissue destruction can lead to tremendous k + overload. Potassium intake needs to be
individualized according to serum levels. Control of serum K + levels between dialysis
326
administered rely mainly on IV infusions of glucose, insulin and bicarbonate, all of which
serve to drive K+ into cells
327
The Academy of Nutrition and Dietetics; Nutrition Care Manual® recommends the
following.
NUTRIENTS SUGGESTED PRESCRIPTION REASONING
Protein  0.8 -1.2g: No catabolism without  Base recommendation on degree of
dialysis catabolism, renal function and treatment.
 1.0 – 1.5g: catabolism and/or  As degree of catabolism increases protein
initial dialysis needs increase.
Energy  25 – 35kcal/kg of body weight  Base recommendation on stress and
nutritional status.
 As degree of catabolism increases, energy
needs increase.
Sodium  2.0 – 3.0g/day  Base recommendation on blood pressure
and edema. Replace losses if necessary.
Potassium  2.0 – 3.0g/day  Replace Loses if necessary.
Phosphorus  8 – 15mg/kg body weight.
 Maintain serum value to within
normal limits
Calcium  Maintain, serum value to within
normal limits.
Fluid  500ml + urine output replace
output from previous day
Vitamins/  Dietary references intakes,
Minerals adjusting to level of catabolism if
needed
REFERENCES
Academy of Nutrition and Dietetics. Nutrition care manual. Available at
www.nutritioncaremanual.org. Accessed Jan 3, 2014.
Sylvia Escott-stump. (2012). Nutrition and diagnosis related care. Chronic kidney disease and
renal failure. 7th edition. pp 864 -869.
328
OBESITY
CASE STUDIES
BY
DTN AZURUNWA CHIGOZIE.A.
329
OUTLINES
- OBESITY
- ASSESMENT OF OBESITY
- TYPES /CLASSIFICATION OF OBESITY
- CAUSES OF OBESITY
- FACTORS THAT CONTRIBUTE TO OBESITY
- SYMPTOMS AND COMPLICATIONS
- MANAGEMENT OF OBESITY
a. Goal of treatment
- DIETING
REFERENCE
330
OBESITY
One can’t talk about obesity without talking about overweight. Overweight is a condition where
the body weight is 10 – 20% greater than the mean standard weight for age, height and sex.
There are different definitions of obesity.
1. It can be defined as a condition of abnormal or excessive fat accumulation in adipose

tissue, to the extent that health is impaired (Garrow, 1988).
2. WHO (2015) defines obesity as a medical condition in which excess body fat has
accumulated to the extent that it may have a negative effect on health.
If one consume high amounts of energy, particularly fat and sugars but don’t burn off the energy
through exercise and other physical activity, much of the surplus energy will be stored by the
body as “fat”.
ASSESMENT OF OBESITY
A. Body Mass Index (BMI) :is a simple index of weight – for – height that is commonly
used to classify underweight, overweight and obesity in adults.
It is defined as the weight in kilograms divided by the square of the height in meters
(kg/m2).
BMI = =kg/m2 (WHO, 1995).
Table 1. The International Classification of adult underweight, overweight and obesity

according to BMI
Classification BMI(kg/m2)
Principal cut-off point Additional cut-off point
Underweight < 18.50 <18.50 <18.50
Severe thinness <16.00 <16.00
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Moderate thinness 16.00 – 16.99 16.00 – 16.99
Mild thinness 17.00 – 18.49 17.00 – 18.49
Normal range 18.50 – 24.99 18.50 – 22.99
23.00 – 24.99
Overweight ≥25.00 ≥25.00
Pre obese 25.00 – 29.99 25.00 – 27.49
27.50 – 29.99
Obese ≥ 30.0 ≥ 30.00
Obese Class I 30.00- 34.00 30.00 – 37.49
30.50 – 34.99
Obese Class II 35.00 – 39.99 35.00 – 37.49
37.50 – 39.99
Obese Class III ≥ 40.00 ≥40.00
Source: Adapter from WHO 1995, WHO 2000 and WHO 2004.
B. Body Weight: For lack of a better database, life insurance industry statistics have been
used to develop so-called tables of normality. These tables give ideal or desirable weight
ranges for height, frame size, and sex, and are associated with greatest longevity. The
definition of overweight is accepted as 10% above ideal body weight, and the definition
of obesity is 20% above ideal body weight. The tables have been used on the assumption
that whatever weight is desirable at age 21 years is also desirable at age 65. In western
society, there is generally an increase in body weight as well as a change in body
composition with age (Vishwanath, 2003).
Therefore it is not clear whether the desirable weight should be the same from ages 21 to
65 years.
332
C. Another method of assessing obesity is through “Body fat distribution”. Having
increased waist circumference suggests that you have increased amounts of fat in your
abdomen. An increased waist circumference is a sign of obesity and can increase your
risk for obesity-related complications. Recent research shows that in some cases, certain
genetic factors may cause the changes in appetite and fat metabolism that lead to obesity.
For a person who is genetically prone to weight gain (e.g has a lower metabolism) and
who leads an inactive and unhealthy lifestyle, the risk of becoming obese is high.
D. Skinfold Thickness: About half of the body fat is deposited under the skin and the rest is
around organs and between muscle fibers. By measuring the subcutaneous fat it is
possible to evaluate one’s fat levels. The measurement should be made at some selected
sites to reveal information about the individual’s fat content. Fat is not distributed evenly
(under the skin) throughout the body. A skinfold caliper is used. The skin is pinched
together and pulled away from the muscles. The thickness of the skin and the underlying
fat tissue is then measured with the caliper and expressed in millimeter, several sites can
be choose but the tricep skinfold is the most commonly used. This is taken midway
between the shoulder and the elbow at the back of the dominant arm held in a relaxed
position. Average readings for those between the ages of 25 and 45 years are about 18mm
for men and 23mm for women. It is also advisable not to rely on tricep skinfold
measurement alone because fat arms appears to run in families even when the rest of the
body may have a much lower level of fat. But if the thickness at other sites is also above
average, the individual is considered to have a higher fat level. Other sites commonly
used are the suprailiac skinfold (the top of the hip bone just above the crest) and the
abdominal skinfold.
The skinfold thickness provides a more direct estimation of body fat than weight-for-height
values alone, but skinfold thickness measurements vary significantly between observers and
within a single observer at different sites in the body. Accurate assessment requires
measurements of multiple skin sites (Vishwanath, 2003).
TYPES /CLASSIFICATION OF OBESITY
There are multiple classifications of obesity.
333
1. Depending on the area of fat deposition, there
are three forms of obesity.
a. Peripheral: Accumulation of
excess fat in the hips, buttocks and
thighs. (This is found mostly
females. Gynoid, pear-shaped,
lower body obesity).
b. Central: Accumulation of excess fat in the abdominal area. (Mostly found in
males. Android, apple-shaped, upper body obesity)
c. Combination: this is the combination of both peripheral and central obesity.
Abdominal area is considered the most dangerous area for the accumulation of fat
because it is closely located the vital organs and their blood supply.
2. Depending on the association with other diseases there are two types.
A. Type I – Obesity: It is not caused by any disease. It is due to excessive intake of calories
and lack of physical activity.
B. Type – 2- Obesity: It is caused by a disease (like cushing syndrome, hypothyroidism,
polycystic ovarian disease and insulionma are some internal secretion diseases). It
accounts for less than 1% of obesity cases and is observed that there is abnormal weight
gain with type – obesity even on little intake of food.
3. Depending on the size and number of fat cells, obesity can be divided into:
334
A. Adult- type: In this type of obesity, only the size of fat cells in increased, it may happen
mostly in middle age.
b. Child – type: In this type of obesity, the number of fat cells is increased. It is extremely
difficult to reduce the number of fat cells which are already made.
The human body has two kinds of fat:
1. Essential fat: is vital to health in many ways e.g it cushions and protects the body’s
organs. It is needed for normal physiological function. Without essential fat the human
health and physical performance. (Muscle, bone marrow, intestine, heart, liver, lungs and
nerve cells).
2. Storage fat: Is fat stored in adipose tissue, mostly beneath the skin and around major
organs in the body.
CAUSES OF OBESITY
Obesity is caused when there is a combination of excessive food energy intake and a lack of
physical activity (Lau DC, et al., 2007). Other causes of obesity:
A. Diet/Calorie: consuming too many calories, particularly fatty and sugary kind of foods.
Some food habits like fructose-containing beverages interfere with lipid metabolism
causing lipid accumulation (hypertriglyceridemia) and fatty liver which further leads to
diabetes and obesity. Vitamin D deficiency is related to diseases associated with obesity
(Wamberg, et al., 2015).
B. Sedentary/inactivity lifestyle: A sedentary lifestyle which does not promote to burn off
the fats cause obesity (Patients Engage, 2016). If one is not very active and doesn’t burn
as many calories with a sedentary lifestyle, one can easily take in more calories everyday
than he/she use through exercise and normal daily activities. (Mayo Clinic staff, 2017).
Worldwide there has been a large shift towards less physically demanding work and
currently at least 30% of the world’s population gets insufficient exercise (WHO, 2008;
WHO, 2009; Ness-Abramof and Apovian 2006). This is primarily due to increasing use
of mechanized transportation and a greater prevalence of labor-saving technology in the
home.
335
c. Inadequate/Not sleeping enough: Sleep deprivation leads to increase in appetite through
elevating appetite stimulating hormones and suppressing the appetite hormones. This
causes hormonal changes and thereby obesity (Patients Engage, 2007).
336
FACTORS THAT CONTRIBUTE TO OBESITY
Age, gender, genes, psychological make – up, socio-economic and environmental factors etc all
contribute.
Gene: This plays a role in efficiency of metabolism and storage and distribution of body fat.
Family lifestyle: Obesity tends to run in families. This is caused both by genes and by shared
diet and lifestyle habits. If one of your parents is obese, you have a higher risk of being obese.
Emotions: some people over eat because of depression, hopelessness, anger, boredom and many
other reasons that have nothing to do with hunger. This doesn’t mean that overweight and obese
people have more emotional problems than other people. It just means that their feelings
influence their eating habits, causing them to over eat.
Environmental factors: The most important environmental factor is lifestyle. Your eating habits
and activity levels are partly learned from the people around you. Overeating and sedentary
habits (inactivity) are the most important risk factors for obesity.
Socio economic factors: When one live where it is not saves to exercise outdoor services. One
tends to become obese. More access to recreation, food and restaurants can increase obesity.
Gender/Sex: Men have more muscles than women, on average. Because muscle burns more
calories than other types of tissue, men use more calories than women, even at rest. Thus, women
are more likely than men to gain weight with the same calorie intake.
Age: People tend to lose muscle and gain fat as they age, their metabolism also slows down.
Both of these lower their calorie requirements. Advancing age result in changes in hormonal
balance and less active life styles.
Pregnancy: Women tend to weigh more after a pregnancy than they did before the pregnancy.
This can compound with each pregnancy.
Medical Problems and Medication: This can promote obesity though they are less common
causes of obesity that overeating and inactivity. Some of these are; cushing’s syndrome, Prader-
Willi syndrome, Arthritis, depression, Polycystic ovarian syndrome.
337
Medications like; steroids, antidepressants, birth control pills, anti-seizure, beta blockers,
antipsychotic drugs, diabetes etc (www.emedicine health, 2017).
SYMPTOMS AND COMPLICATIONS
The health risk associated with obesity includes:
 Breathing disorders (e.g sleep apnea, chronic obstructive pulmonary disease)

 Certain types of cancers (e.g prostrate and bowel cancer in men, breast and uterine cancer
in women)
 Coronary artery (heart) disease
 Depression
 Diabetes
 Gallbladder or liver disease
 Gstroesophageal reflux disease (GERD)
 High blood pressure
 High cholesterol
 Joint disease (e.g Osteorthritis)
 Stroke
Aside from the medical complications, obesity is also linked to psychosocial problems such as
low-self esteem, discrimination, difficulty finding employment and reduced quality of life.
MANAGEMENT OF OBESITY
The major management of obesity is through diet, exercise and lifestyle modification. The use of
pharmacologic treatment and surgical intervention are appropriate in some circumstances but are
not a substitute for the necessary changes in eating and physical activity pattern(Lau Dc et al.,
2007).
Diet programs may produce weight loss over a short term but maintaining this weight loss is
frequently difficult and often requires making exercise and a lower calorie diet a permanent part
of an individual’s lifestyle. (Strychar, 2006; Shick et al., 1998, Tate DF et al., 2007).
338
Goal of treatment
The goal of obesity treatment should focus on weight management, attaining the best weight
possible in the context of overall health. Achieving and “Ideal” body weight or percentage of
body fat is not always realistic under some circumstances, it may not be appropriate at all.
Depending on the type and severity of the obesity and the age and lifestyle of the individual,
successfully reducing bodyweight varies from a being relatively simple to being virtually
impossible.
DIETING
Diets to promote weight loss are generally divided into four categories:
a. Low-fat,
b. Low- carbohydrates
c. Low- calories and
d. Very low calories (Strychar I, 2006)
A meta-analysis of six randomized controlled trials found no difference between three of the
main diet types (low calorie, low carbohydrate, and low fat), with a 2 – 4 kilograms (4.4 – 8.8 ib)
weight loss in all studies (Strychar I, 2006). At two years these three methods resulted in similar
weight loss irrespective of macronutrients emphasized (Sacks FM, Bray GA, Carey VJ, et al.,
2009). High protein diets do not appear to make any difference ( Schwingshackl and Hoffmann,
2013). A diet high in simple sugars such as those in soft drinks increases weight (Te Morenga,
L; Mallard, S; and Mann, J, 2012).
Very low calorie diets provide 200 – 800 kcal/day, maintaining protein intake but limiting
calories from both fat and carbohydrates. They subject the body to starvation and produce an
average weekly weigh loss of 1.5 – 2.5 kilograms (3.3 – 5.5 Ib). These diets are not
recommended for general use as they are associated with adverse side effects such as loss of lean
muscle mass, increased risks of gout and electrolyte imbalances. People attempting these diets
must be monitored closely by a physician to prevent complications (Strychar, I, 2006).
339
REFERENCES
Garrow, JS (1988). Obesity and related diseases. London. Churchill Living stone. Pp 1 – 16.
Lau DC; Douketis JD; Morrison, KM; Hramiak IM; Sharma AM; UrE (April 2007). “2006
Canadian Clinical practice guidelines on the management and prevention of obesity in
adults and children summary”. CMAJ (Practice Guideline, Review). 176 (8): S1 – 13.
Doi:10.1503/cmaj.061409. PMC. 1839777, PMID 17420481.
Mayo clinic. Diseases and conditions of obesity 1998 – 2017. Mayo Foundation for Medical
Education and Research (MFMER). All rights reserved.
Ness-Abramof R, Apovian CM (February 2006). “ Diet medication for treatment and prevention
of obesity”. Endocrine (Review). 29(1): 5 – 9. Doi:10.1385/ENDO: 29: 1:135. PMID
16622287.
Patients Engage.com 2007. Obesity signs and symptoms.
Sacks FM, Bray GA, Carey VJ, et al., (February 2009). “Comparison of weight-loss diets with
different compositions of fat, protein and carbohydrates:. N. Engl. J. Med 360 (9): 859 –
73 PMC 2763382. PMID 19246357. Doi:10.1056/NEJMoa0804748
Schwingshackl, L; Hoffmann, G (April 15, 2013). “Long-term effects of low-fat diets either low
or high in protein on cardiovascular and metabolic risk factors: a systematic review and
meta-analysis”. Nutrition Journal. 12:48. PMC 3636027. PMID 23587198. Doi:10.
1186/1475-2891-12-48.
Shick, SM; Wing RR; Klem ML; McGure MI; Hill JO; Seagle H (April 1998). “Persons
successful at long-term weight loss and maintenance continue to consume a low-energy,
low-fat diet”. J.Am Assoc 98 (4): 408 – 13. Doi:10.1016/S0002-8223 (98) 00093-5.
PMID 9550162
strychar I (January 2006). “Diet in the management of weight loss: CMAJ. 174 (1): 56 – 63.
Doi:10.1503/cmaj.045037. PMC 1319349. PMID 16389240.
340
Tate DF, Jeffery RW, Sherwood NE, Wing RR, Jeffery Sherwood; Wing (1 April, 2007). “Long-
term weight losses associated with prescription of higher physical activity goals. Are
higher levels of physical activity protective against weight regain?”. Am J. Clin Nutr. 85
(4): 954 – 9. PMID 17413092
Te Morenga, L; Mallard, S; Mann, L 9Jan 15, 2012). “Dietary sugars and body weight:
systematic review and meta-analyses of randomized controlled trials and cohort studies”
BMJ (Clinical research ed). 346:e7492. PMID 23321486. Doi:10.1136/bmj.e7492
Vishwanath, M. Sardesai (2003). Introduction to Clinical Nutrition: Obesity and Eating Disorder.
2nd edition. Pp 324 – 325. Wayne State University. Detroit Michigan, USA. Copy right
2003 by Marcel Dekker. Inc. ISBN: 0-8247-4093-9.
Wamberg, Louise; Pedersen, Steen B; Rejnmark, Lars; Richelsen, Bjorn (2015). ‘Causes of
vitamin D Deficiency and Effect of vitamin D Supplementation on Metabolic
Complications in Obesity: A Review” Current obesity Reports. 4 (4): 429 – 440.
Doi:10.1007/s 13679-015-0176-5. ISSN 2162 -4968. PMID 26353882.
WHO (1995). Physical status: The use and interpretation of anthropometry. Report of a WHO
Expert Committee. WHO Technical Report Series. 854. Geneva.
WHO (2008). Obesity and overweight. World Health Organization. Archived from the original
on December 18, 2008. Retrieved January 10, 2009.
WHO (2009). “WHO/Physical Inactivity: A Global Public Health Problem”. World Health
Organisation. Retrieved February 22, 2009.
WHO (January, 2015). “Obesity and Overweight Fact Sheet N0311”. Retrieved 2 February 2016.
www.emedicinehealth.com 2017.
341
CASE STUDY
Case study is a research method involving an up-close, in-depth and detailed examination of a
subject of study (the case) as well as its related contextual conditions. Case studies can be
produced by following a formal research method. These case studies are likely to appear in
formal research venues, as journals and professional conferences, rather than popular works
In presenting a case study for a medical research method, the following are involved:
a. Name of the presenter

b. Name of the patient
c. Diagnosis
d. Ward
e. Age
f. Marital status
g. Date admitted
h. Date discharged
i. Doctors in charge (Consultants)
j. Dietitian in-charge
Other formalities in presenting a case includes
a. Brief Overview of the Diagnosis

b. Social History of the Patient
c. Past Medical History
d. Present Medical History
e. Nutrition Assessment:
342
EXAMPLE OF A CASE STUDY PRESENTATION
NAME OF PRESENTER: OKAFOR BISOLA KITAN

CASE STUDY COMMENCEMENT: 11/3/2016
NAME OF PATIENT: MrS ALAHAJA SEUN ADA-ENO
DIAGNOSIS: Congestive Cardiac Failure secondary to hypertension (NYHA IV).
WARD: Female Medical Ward
SEX: Female
DATE OF ADMISSION: 7/3/2016
DATE OF DISCHARGE: 21/3/2016
ORIGIN: Uwani in Isi-Uzo L.G.A of Enugu state.
RELIGION: Christian
OCCUPATION: House wife
AGE: 78years
RESIDENCE: Trans-ekulu
PHYSICIAN: Dr. XXXXXXXXXXX
DIETITIAN: Dtn XXXXXXXXXXX
WHAT IS CONGESTIVE HEART FAILURE?

Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power
of your heart muscles. While often referred to simply as “heart failure”, CHF specifically refers
to the stage in which fluid builds up around the heart causing it to pump inefficiently.
CHF develops when your ventricles can’t pump blood in sufficient volume to the body.
Eventually, blood and other fluids back up inside your:
• lungs
• abdomen
• liver
• lower body
343
WHAT ARE THE CAUSES OF CHF
CHF may result from other health conditions that directly affect your cardiovascular system.
That’s why it’s important to get annual checkups to lower your risk for heart health problems,
including high blood pressure (hypertension), coronary artery disease, and valve conditions.
HYPERTENSION
When your blood pressure is higher than normal, it may lead to CHF. Hypertension occurs when
your blood vessels become restricted by cholesterol and fat. This makes it harder for your blood
to pass through them.
PATIENTS FAMILY/SOCIAL HISTORY
Patient is the first child in the family of four (Two dead and two alive). She is married in a
polygamous setting with eight children out of which one is dead. There is no family history of
hypertension and diabetes
MEDICAL HISTORY
A 78 years old woman known to have hypertension for two years with poor drug adherence.
Presented to the hospital on account of recurrent cough which started gradually ten(10) years ago
and recurrent body swelling being two(2) years ago with associated breathlessness, mild exertion
an oligouria. Patient has a history of prolonged use of biomass and tobacco.
Coughing is aggravated by lying supine and relieved by sitting up and it produces whitish
sputum. There is associated hemophysis.
DATE READING(mmHg)
11/3/2016 80/50
12/3/2016 80/50
13/3/2016 80/50
344
14/3/2016 90/50
15/3/2016 90/50
16/3/2016 80/60
17/3/2016 90/60
18/3/2016 80/50
19/3/2016 80/50
20/3/2016 80/50
21/3/2016 50/40
FLUID CHART
DATE INTAKE (ml) OUTPUT (ml)
11/3/2016 1,100 750
12/3/2016 200 800
13/3/2016 950 200
14/3/2016 700 100
15/3/2016 2,250 450
16/3/2016 710 1,050
17/3/2016 1,100 750
18/3/2016 2,000 8oo
19/3/2016 950 200
20/3/2016 700 100
21/3/2016 1,250 1,000
345
Nutrition Assessment
Anthropometry
Skin fold thickness = 6mm (underweight)
Biochemical
Fasting lipid profile and S/E/U/Cr were noted
FASTING LIPID PROFILE (MMOL/L)
INVESTIGATIONS READINGS REFERENCE RANGES
Total cholesterol 2.9 3.6 – 6.2
HDL 1.5 0.8 – 1.7
LDL 1.2 1.9 – 3.6
VLDL 0.2 0.4 – 1.3
Triglycerides 0.5 0.5 – 1.0
S/E/U/Cr
INVESTIGATIONS READINGS REFERENCE RANGES
Sodium 129 138 – 146
Potassium 4.1 3.5 – 4.9
346
Calcium 2.2 2.2 – 2.8
Creatinine 1.2 0.6 – 1.3
Urea 18 2.5 – 8.5
CLINICAL
On examination, an elderly woman with oedema up to the thigh, having difficulty in breathing
although conscious and alert.
BP-80/50mmHg
DIETARY
Using 24-hour dietary recall, patient was found to have taken tea (2tbspn of milo with half tin of
peak milk) for breakfast, 2 spoons of white rice and stew for lunch and nothing for breakfast.
The estimated caloric intake from the 24-hour dietary recall is estimated to be about
1000kcal/day.
Using the food frequency questionnaire patients likes were as follows: tea, pap, pounded yam,
egusi soup, ogbono soup and bitterleaf soup.
Nutrition Diagnosis
 Loss of appetite related to generalized body swelling (oedema) as evidenced by the 24-
hour dietary recall.
Nutrition Intervention
 Patient was counseled and placed on Oral Fluid Diet Low Fat Low Protein (LFLP) of
1,500kcal/day
Estimated Caloric Intake Of Patient Based On Dietary Modification
INGREDIENT QUANTITY ENERGY(Kcal) CHO (g) PROTEIN FAT (g)
347
(g)
Pap 800ml 708 154 16 3
Milk 50g 34 72 66 72
Vegetable oil 20mls 180 - - 20
Monitoring and Evaluation
 Daily monitoring of blood pressure.
 Oedema regression monitored.
 Monitored acceptance and tolerance of dietary regime.
 Monitored adherence to dietary regimen.
Review
 Patient accepted, tolerated and adhered to dietary regimen. Due to the fluctuating blood
pressure which impaired the administration of diuretics, the patients fluid intake was
asked to be reduced by the doctor.
 Patients oral fluid was reduced to one litre a day to see if the Bp can be stabilized.
 Patient was confirmed clinically dead on the 21/3/2016 lying supine on a chair with no
respiratory movement.
348

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DIETETIC INTERNSHIP PROGRAMME

Anatomy and Physiology by Ms Ekechukwu, Frances A. 18

Overweight and Obesity by Rev. Sr. Odinakachukwu Nwosu 30

Nutrition counseling and geriatric nutrition, by Dtn. Mbomi 55

Diabetes mellitus and oncology, by Dtn Dr. Nnadi Ihuoma M. 67

Hygiene and Chronic renal failure by Dtn. Okwy-Nweke 94

Food Processing, energy expenditure and Energy Conservation, by Dtn. Afieroho

Billing and Costing, Nutrition Care Process, Nutrition in HIV/AIDS and,

Coronary Heart Disease, bariatric surgery and micronutrient deficiency

Cardiovascular diseases: Angina Pectoris, Myocardial Infraction &

Medical nutrition therapy in liver disease by Dtn. Onoja Ifeoma 272

Hepatic Encephalopathy, Disorders of lipid metabolism, enteral and parenteral feeding,

DTN OLEBU JUSTINA

Profitability and budget

Collagenous sprue is an extremely rare entity and is characterized by a lack of response to

Supplementation, food fortification and dietary diversification- a three prolonged

1. Short – term supplementation

2. Medium – term food fortifications and

3. A long –term focus on balance nutrition (dietary diversification)

Factors that trigger symptoms include:

Endoscopy/gastroscopy and biopsy

Goals of Dietary management

1) Control gluten intake.

1. Use of gluten – controlled diet.

ANATOMY OF THE LIVER

ANATOMY AND PHYSIOLOGY OF GIT

***READ UP THE TEETH

***(Read up Structure of the large Intestine.)

REV. SR. ODINAKACHUKWU NWOSU

Effects in the Body

Fat Cell Enlargement

Mortality and Morbidity Associated with Obesity

Excess body weight

Excess Body Weight

Regional Fat Distribution

How can children avoid being obese?

Let’s talk about each one…

WEIGHT MANAGEMENT STRATEGIES: MEDICAL AND NUTRITIONAL THERAPY

Who Should Consider A Weight Management Intervention?

How Much and How Fast?

Rates of Weight Loss Vary

Role of Physical Activity in Weight Management

Diet After Surgery

EFFECTS OF THESE CHANGES ON FOOD INTAKE AND UTILIZATION

NUTRITIONAL REQUIREMENT OF ELDERLY PEOPLE

THE GOAL OF NUTRITION INTERVENTION

CHALLENGES IN MEETING NUTRITIONAL NEEDS IN THE ELDERLY

CAUSES OF UNWANTED WEIGHT-LOSS IN ELDERLY PEOPLE

DTN DR. NNADI I.M

Complications of Diabetes Mellitus

DIABETES NUTRITION ASSESSMENT

Diabetes Nutrition Diagnosis

Diabetes Nutrition Intervention

 physical carcinogens, such as ultraviolet and ionizing radiation;

Brain and Spinal Cord Tumors

Other Types of Tumors

Germ Cell Tumors

 Limit Calorie-Dense, Nutrient-Deficient Foods. Reduce intake of foods with added

DTN. ONWUKA-KALU NKEIRU

CONSTANT FEATURES OF MARASMUS